Matthew J.

Budoff
Jerold S. Shinbane
Editors

Cardiac CT Imaging

Diagnosis of
Cardiovascular Disease

Third Edition

123
Cardiac CT Imaging
Matthew J. Budoff • Jerold S. Shinbane
Editors

Cardiac CT Imaging
Diagnosis of Cardiovascular Disease

Third Edition
Editors
Matthew J. Budoff Jerold S. Shinbane
Division of Cardiology Keck School of Medicine
Harbor-UCLA Medical Center University of Southern California
Torrance, CA Los Angeles, CA
USA USA

Additional material to this book can be downloaded from http://extras.springer.com.

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DOI 10.1007/978-3-319-28219-0

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Foreword to the Second Edition

Cardiac CT has finally come of age. After nearly 30 years of development and growth,
tomographic X-ray is being embraced by cardiologists as a useful imaging technology. Thirty
years ago, Doug Boyd envisioned a unique CT scanner that would have sufficient temporal
resolution to permit motion-artifact-free images of the heart. In the late 1970s, I had the good
fortune to work closely with Dr. Boyd, Marty Lipton, and Bob Herkens who had the vision to
recognize the potential of CT imaging for the diagnosis of heart disease. In the early 1980s,
when electron beam CT became available, others, including Mel Marcus (deceased), John
Rumberger, Arthur Agatston, and Dave King (deceased), were instrumental in making clinical
cardiologists aware of the potential of cardiac CT.
In 1985, several investigators recognized the potential of cardiac CT for identifying and
quantifying coronary artery calcium. Now, 20 years later, there is wide recognition of the value
of coronary calcium quantification for the prediction of future coronary events in asymptomatic
people. It has been a long and arduous road, but finally, wide-spread screening may significantly
reduce the 150,000 sudden deaths and 300,000 myocardial infarctions that occur each year in
the United States as the first symptom of heart disease
In the late 1970s, it was thought that a 2.4-s scan time was very fast CT scanning. With the
development of electron beam technology, scan times of 50 ms became possible, giving rise to
terms such as fast CT, ultrafast CT, and RACAT (rapid acquisition computed axial tomography).
Now, with the development of multidetector scanners capable of 64, 128, 256, and beyond
simultaneous slices, spatial resolution is approaching that of conventional cineangiography,
and the holy grail, noninvasive coronary arteriography, appears attainable.
In this book, Drs. Matthew Budoff and Jerold Shinbane, preeminent leaders in the field of
cardiac CT, have described the many and varied uses of the technology in the diagnosis of
cardiovascular disease. The book clearly documents that cardiac CT has not only arrived but
has become a very valuable and potent diagnostic tool.

Bruce H. Brundage, MD, MACC

Heart Institute of the Cascades, Bend, OR, USA
UCLA School of Medicine, Los Angeles, CA, USA

v
Preface

It is a testament to the intellect and diligence of the physician-scientists and engineers involved
in the field of cardiovascular computed tomography that a third edition of this text is necessary
in so short a time since this field was created. Our first cardiac CT angiogram was performed
in January 1995, over 20 years ago. The trials and tribulations that we faced over the introduction
of this modality are reminiscent of a quote by the philosopher Arthur Schopenhauer:

All truth passes through three stages.

First, it is ridiculed.
Second, it is violently opposed.
Third, it is accepted as being self-evident.

Cardiovascular CT has now matured into a firmly established subspecialty of radiology and
cardiovascular medicine with a multidisciplinary society with 4000 members, a board examina-
tion, dedicated journals, numerous scientific statements from leading national societies, focused
national and international meetings, and clear education and training pathways. The foundation
has been provided by a sound medical literature, which continues to grow at an astounding pace.
We hope that research maintains the same forward momentum fueled by the intellectual curios-
ity and passion to increase the understanding of the cardiovascular system and improve patient
care. As we look ahead, we also continue to look back and acknowledge our debt to the pioneers
of this technology who dedicated their careers to forwarding this discipline, who persevered the
ridicule and violent opposition, and may or may not be enjoying the current acceptance and
utilization in this “self-evident” era of cardiac CT.
Cardiovascular CT has become a powerful risk stratifying tool for the early detection of
atherosclerosis, used as a calcium score to identify asymptomatic persons at risk of CVD. It
has also developed into the de facto noninvasive angiogram, a measure of coronary stenosis, a
substitute for coronary angiography or noninvasive exercise testing in certain clinical situa-
tions, and a powerful tool to image the heart for congenital heart disease, trans-aortic valve
procedures, perfusion imaging, and coronary anomalies. There has been a paradigm shift in its
role related to cardiovascular therapies, with progress from pre- and postprocedure assessment
to use in the actual guidance of a variety of invasive procedures.
Advances in CT scanners, imaging techniques, postprocessing workstations, and
interpretation for diagnostic and therapeutic applications have now made the field relevant to
the entire spectrum of physicians who diagnose and treat cardiovascular disease. As such, a
thorough knowledge of cardiovascular CT is required for the thoughtful and individualized
application in patient care. We hope that this text will provide the substrate for a detailed
understanding of the art and science of this technology.

Torrance, CA, USA Matthew J. Budoff, MD

Jerold S. Shinbane, MD, FACC, FHRS, FSCCT

vii
Contents

Part I Overview

1 Computed Tomography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Matthew J. Budoff
2 Cardiovascular Computed Tomography: Current and Future
Scanning System Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
Rine Nakanishi, Wm. Guy Weigold, and Matthew J. Budoff
3 Radiation Dosimetry and CT Dose Reduction Techniques . . . . . . . . . . . . . . . . . . . 33
Kai H. Lee
4 Orientation and Approach to Cardiovascular Images . . . . . . . . . . . . . . . . . . . . . . 47
Jerold S. Shinbane and Antreas Hindoyan

Part II Cardiac CT

5 Assessment of Cardiovascular Calcium: Interpretation,

Prognostic Value, and Relationship to Lipids and Other
Cardiovascular Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
Harvey S. Hecht
6 Natural History and Impact of Interventions on CAC . . . . . . . . . . . . . . . . . . . . . 121
Paolo Raggi
7 Methodology for CCTA Image Acquisition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
Mathew J. Budoff, Jerold S. Shinbane, and Songshao Mao
8 Post-processing and Reconstruction Techniques
for the Coronary Arteries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
Swaminatha V. Gurudevan
9 Coronary CT Angiography: Native Vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
Stephan Achenbach
10 Coronary CT Angiography After Revascularization . . . . . . . . . . . . . . . . . . . . . . 179
Joachim Eckert, Marco Schmidt, Thomas Voigtländer, and Axel Schmermund

Part III CT Angiography Assessment for Cardiac Pathology

11 Assessment of Cardiac Structure and Function by Computed

Tomography Angiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
John A. Rumberger
12 Cardiovascular CT for Perfusion and Delayed Contrast
Enhancement Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Ravi K. Sharma, Ilan Gottlieb, and João A.C. Lima

ix
x Contents

13 Cardiovascular CT for Assessment of Pericardial/Myocardial

Disease Processes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
Muhammad Aamir Latif and Khurram Nasir
14 Computed Tomography Evaluation in Valvular Heart Disease . . . . . . . . . . . . . . 241
Nada Shaban, Javier Sanz, Leticia Fernández Friera,
and Mario Jorge García
15 Transcatheter Aortic Valve Implantation (TAVI) . . . . . . . . . . . . . . . . . . . . . . . . . 255
Chesnal Dey Arepalli, Christopher Naoum, Philipp Blanke,
and Jonathon A. Leipsic
16 Assessment of Cardiac and Thoracic Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275
Jabi E. Shriki, Patrick M. Colletti, and Suresh Maximin

Part IV CT Vascular Angiography

17 CT Angiography of the Peripheral Arteries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297

Jabi E. Shriki, Leonardo C. Clavijo, and Gale L. Tang
18 Aortic, Renal, Mesenteric and Carotid CT Angiography . . . . . . . . . . . . . . . . . . . 319
Anas Alani and Matthew J. Budoff
19 Assessment of Pulmonary Vascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
Bradley S. Messenger and Ronald J. Oudiz

Part V Multidisciplinary Topics

20 Value Based Imaging for Coronary Artery Disease: Implications

for Nuclear Cardiology and Cardiac CT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349
Daniel S. Berman, Alan Rozanski, Piotr Slomka, Rine Nakanishi, Damini Dey,
John D. Friedman, Sean W. Hayes, Louise E.J. Thomson, Reza Arsanjani,
Rory Hachamovitch, James K. Min, Leslee J. Shaw, and Guido Germano
21 Coronary Computed Tomographic Angiography for Detection
of Coronary Artery Disease: Analysis of Large-Scale Multicenter
Trials and Registries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381
Leslee J. Shaw
22 Cardiothoracic Surgery Applications: Virtual CT Imaging
Approaches to Procedural Planning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
Jerold S. Shinbane, Craig J. Baker, Mark J. Cunningham,
and Vaughn A. Starnes
23 Computed Tomographic Angiography in the Assessment of Congenital
Heart Disease and Coronary Artery Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . 429
Priya Pillutla and Stephen C. Cook
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification,
Virtual Procedural Planning, and Procedural Facilitation . . . . . . . . . . . . . . . . . . 455
Jerold S. Shinbane, Leslie A. Saxon, Rahul N. Doshi, Philip M. Chang,
and Matthew J. Budoff
25 Cardiovascular CT: Interventional Cardiology Applications. . . . . . . . . . . . . . . . 487
Jeffrey M. Schussler
Contents xi

26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical

Applications in the Context of Cardiovascular CT . . . . . . . . . . . . . . . . . . . . . . . . 507
Jerold S. Shinbane, Jabi E. Shriki, Antreas Hindoyan, and Patrick M. Colletti
27 Cardiovascular CT in the Emergency Department . . . . . . . . . . . . . . . . . . . . . . . . 549
Asim Rizvi and James K. Min

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 561
Contributors

Stephan Achenbach, MD University of Erlangen, Erlangen, Germany

Anas Alani, MD Department of Medicine, University of Florida – Gainesville, Gainsville,
FL, USA
Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA
Chesnal Dey Arepalli, MBBS, DNB Department of Radiology, St. Paul’s Hospital,
Vancouver, BC, Canada
Reza Arsanjani, MD Departments of Imaging and Medicine, Cedars-Sinai Medical Center
and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Craig J. Baker, MD, FACS Department of Surgery, Keck Hospital of the University of
Southern California, Los Angeles, CA, USA
Daniel S. Berman, MD Departments of Imaging and Medicine, Cedars-Sinai Medical Center
and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Philipp Blanke, MD Department of Medicine, St. Paul’s Hospital, Vancouver, BC, Canada
Matthew J. Budoff, MD David Geffen School of Medicine at UCLA, Los Angeles Biomedical
Research Institute, Torrance, CA, USA
Phillip M. Chang, MD Department of Medicine, Keck Medical Center of USC/Keck School
of Medicine at USC, Los Angeles, CA, USA
Leonardo C. Clavijo, MD, PhD, FACC, FSCAI, FSVM Department of Medicine,
Division of Cardiovascular Medicine, Department of Clinical Medicine, University of
Southern California, Los Angeles, CA, USA
Patrick M. Colletti, MD Department of Radiology, University of Southern California,
Los Angeles, CA, USA
Stephen C. Cook, MD, FACC Adult Congenital Heart Disease Center, Heart Institute,
Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA
Mark J. Cunningham, MD Department of Surgery, Keck Hospital of the University of
Southern California, Los Angeles, CA, USA
Damini Dey, PhD Departments of Imaging and Medicine, Cedars-Sinai Medical Center and
the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Rahul N. Doshi, MD, FACC, FHRS Department of Medicine, Keck Medical Center of USC,
Los Angeles, CA, USA
Joachim Eckert, MD Department of Cardiology, Cardioangiologisches Centrum Bethanien,
Frankfurt, Hessen, Germany

xiii
xiv Contributors

John D. Friedman, MD Departments of Imaging and Medicine, Cedars-Sinai Medical Center

and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Leticia Fernández Friera, MD Department of Medicine, Division of Cardiology, Mount
Sinai Medical Center, New York, NY, USA
Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
Mario Jorge Garcia, MD, FACC, FACP Division of Cardiology, Montefiore Medical Center,
Bronx, NY, USA
Guido Germano, PhD Departments of Imaging and Medicine, Cedars-Sinai Medical Center
and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Ilan Gottlieb, MD, MSc, PhD Casa de Saude Sao Jose, Rio de Janeiro, RJ, Brazil
Swaminatha V. Gurudevan, MD, FACC Department of Medicine, Healthcare Partners
Medical Group, Pasadena, CA, USA
Rory Hachamovitch, MD Department of Nuclear Medicine, Cleveland Clinic, Heart and
Vascular Institute, Cleveland, OH, USA
Sean W. Hayes, MD Departments of Imaging and Medicine, Cedars-Sinai Medical Center
and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Harvey S. Hecht, MD, FACC, FSSCT Department of Medicine, Icahn School of Medicine
at Mount Sinai, New York, NY, USA
Mount Sinai Medical Center, New York, NY, USA
Antreas Hindoyan, MD Division of Cardiovascular Medicine, Department of Internal
Medicine, Keck School of Medicine of the University of Southern California, Los Angeles,
CA, USA
Muhammad Aamir Latif, MD Department of Medicine, Center for Healthcare Advancement
and Outcomes, Baptist Health South Florida, Miami, FL, USA
Kai H. Lee, PhD Associate Professor of Clinical Radiology, Department of Radiology, Keck
School of Medicine, University of Southern California, Los Angeles, CA, USA
Jonathon A. Leipsic, MD, FRCPC, FSCCT Department of Radiology, St. Paul’s Hospital,
Vancouver, BC, Canada
João A.C. Lima, MD Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD, USA
Songshou Mao, MD Department of Medicine, Los Angeles Biomedical Research Institute,
Los Angeles, CA, USA
Suresh Maximin, MD Department of Radiology, University of Washington,
Seattle, WA, USA
Bradley S. Messenger, MD Division of Cardiology, Department of Medicine, Harbor-UCLA
Medical Center, Torrance, CA, USA
James K. Min, MD, FACC Department of Radiology, Dalio Institute of Cardiovascular
Imaging, Weill Cornell Medical College and the NewYork Presbyterian Hospital, New York,
NY, USA
Rine Nakanishi, MD, PhD Department of Medicine, Cardiac CT, Los Angeles Biomedical
Research Institute at Harbor-UCLA, Torrance, CA, USA
Christopher Naoum, MBBS, FRACP Department of Radiology, St. Paul’s Hospital,
Vancouver, BC, Canada
Contributors xv

Khurram Nasir, MD, MPH Department of Medicine, Center for Healthcare Advancement
and Outcomes, Baptist Health South Florida, Miami Beach, FL, USA
Ronald J. Oudiz, MD Department of Medicine, Los Angeles Biomedical Research
Institute, The David Geffen School of Medicine at UCLA, Harbor-UCLA Medical Center,
Torrance, CA, USA
Priya Pillutla, MD Adult Congenital Heart Disease Program, Harbor-UCLA Medical Center,
Torrance, CA, USA
Paolo Raggi, MD Department of Medicine, Mazankowski Alberta Heart Institute, University
of Alberta, Edmonton, AB, Canada
Asim Rizvi, MD Department of Radiology, Dalio Institute of Cardiovascular Imaging, Weill
Cornell Medical College and the NewYork Presbyterian Hospital, New York, NY, USA
Alan Rozanski, MD Division of Cardiology, Mt. Sinai Saint Luke’s and Roosevelt Hospitals,
New York, NY, USA
John A. Rumberger, PhD, MD Cardiac Imaging, The Princeton Longevity Center, Princeton,
NJ, USA
Javier Sanz, MD Department of Medicine, Division of Cardiology, Mount Sinai Medical
Center, New York, NY, USA
Leslie A. Saxon, MD Department of Medicine, USC Center for Body Computing, Keck
Medical Center of USC, Los Angeles, CA, USA
Axel Schmermund, MD Department of Cardiology, Cardioangiologisches Centrum
Bethanien, Frankfurt, Hessen, Germany
Marco J.M. Schmidt, MD Department of Cardiology, Cardioangiologisches Centrum
Bethanien, Frankfurt, Hessen, Germany
Jeffrey M. Schussler, MD, FACC, FSCAI, FSCCT, FACP Division of Cardiology,
Department of Internal Medicine, Baylor University Medical Center, Dallas, TX/Jack and Jane
Hamilton Heart and Vascular Hospital, Dallas, TX, USA
Division of Cardiology, Department of Medicine, Texas A&M College of Medicine,
Dallas, TX, USA
Nada Shaban, MD Department of Medicine, Division of Cardiology, North Shore University
Hospital, Manhasset, NY, USA
Ravi K. Sharma, MD Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD, USA
Leslee Shaw, PhD Department of Medicine, Emory Clinical Cardiovascular Research
Institute, Emory University School of Medicine, Atlanta, GA, USA
Jerold S. Shinbane, MD, FACC, FHRS, FSCCT Division of Cardiovascular Medicine,
Department of Internal Medicine, Keck School of Medicine of the University of Southern
California, Los Angeles, CA, USA
Jabi E. Shriki, MD Department of Radiology, Puget VA Health System, University of
Washington, Seattle, WA, USA
Piotr Slomka, PhD Departments of Imaging and Medicine, Cedars-Sinai Medical Center and
the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Vaughn A. Starnes, MD H. Russell Smith Foundation, Cardiovascular Thoracic Institute,
Keck Hospital of the University of Southern California, Los Angeles, CA, USA
xvi Contributors

Gale L. Tang, MD Department of Surgery, University of Washington, Seattle, WA, USA

Louise E.J. Thomson, MBChB Departments of Imaging and Medicine, Cedars-Sinai
Medical Center and the Cedars-Sinai Heart Institute, Los Angeles, CA, USA
Thomas Voigtländer, MD Department of Cardiology, Cardioangiologisches Centrum
Bethanien, Frankfurt, Hessen, Germany
Wm. Guy Weigold, MD, FACC, FSCCT Department of Medicine, Department of Medicine
(Cardiology), Cardiac CT, MedStar Washington Hospital Center, Washington, DC, USA
Cardiac CT Core Lab, MedStar Health Research Institute, Washington, DC, USA
MedStar Cardiovascular Research Network, Washington, DC, USA
 Part I
Overview
 Computed Tomography
1
Matthew J. Budoff

Abstract
Cardiac CT scanners are rapidly improving, each major vendor has introduced a state of the
art scanner every 2–3 years. The basic applications, terminology and acquisition has not
changed dramatically, however, improvements in hardware and software continue to reduce
radiation exposure, scan times, artifacts and improve image quality. This chapter outlines
the basic CT terminology, functions and background behind the current state of CT scan-
ners for cardiac applications. It reviews spatial, temporal and contrast resolution limits of
the CT scanners. An overview of common terms, radiation exposure and protocols are
included. This acts as an introductory chapter to be expanded by subsequent chapters that
will each go into more details on specific topics. Comparison to magnetic resonance for
image quality and functionality, and dose comparisons to mammography, nuclear and
fluoroscopy are included.

Keywords
Cardiac CT • Angiography • MDCT • MRI • Coronary calcium • Protocols • Radiation •
Spatial resolution • Temporal resolution

Overview of X-ray Computed Tomography computer reconstruction, allowing for ultimately nearly an
infinite number of projections. From a cardiac perspective,
The development of computed tomography (CT), resulting the increased spatial resolution is the reason for its increase
in widespread clinical use of CT scanning by the early 1980s, in sensitivity for atherosclerosis, plaque detection and
was a major breakthrough in clinical diagnosis across coronary artery disease (CAD). With CT, smaller objects can
multiple fields. The primary advantage of CT was the ability be seen with better image quality. Localization of structures
to obtain thin cross-sectional axial images, with improved (in any plane) is more accurate and easier with tomography
spatial resolution over ultrasound, nuclear medicine, and than with projection imaging like fluoroscopy. The excep-
magnetic resonance imaging. This imaging avoided super- tional contrast resolution of CT (ability to differentiate fat,
position of three-dimensional (3-D) structures onto a planar air, tissue and water), allows visualization of more than the
2-D representation, as is the problem with conventional lumen or stent, but rather the plaque, artery wall and other
projection X-ray (fluoroscopy). CT images, which are cardiac and non-cardiac structures simultaneously.
inherently digital and thus quite robust, are amenable to 3-D The basic principle of CT is that a fan-shaped, thin X-ray
beam passes through the body at many angles to allow for
cross-sectional imaging. The corresponding X-ray trans-
M.J. Budoff, MD mission measurements are collected by a detector array.
David Geffen School of Medicine at UCLA,
Information entering the detector array and X-ray beam
Los Angeles Biomedical Research Institute,
Torrance, CA, USA itself is collimated to produce thin sections while avoiding
e-mail: [email protected] unnecessary photon scatter (to keep radiation exposure and

© Springer International Publishing 2016 3

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_1
4 M.J. Budoff

Table 1.1 Typical Hounsfield unit values

Air ~ −1000 HU
Fat −100 to −40
Water – zero
Non-enhanced myocardium and blood – 40–60
Contrast enhanced myocardium 80–140
Calcium >130 (to about 1000)
Enhanced blood pools (lumen, aorta, LV) 300–500
Metal >1000

image noise to a minimum). The x-ray tub and detector

array rotate around the patient separated by 180°, allowing
continuous acquisition of data. The data recorded by the
detectors are digitized into picture elements (pixels) with
known dimensions. The gray-scale information contained
in each individual pixel is reconstructed according to the
attenuation of the X-ray beam along its path using a stan-
dardized technique termed “filtered back projection.” Gray-
scale values for pixels within the reconstructed tomogram
are defined with reference to the value for water and are
called “Hounsfield units” (HU; for the 1979 Nobel Prize
winner, Sir Godfrey N. Hounsfield), or simply “CT num-
bers.” These CT numbers are the attenuation or brightness
of the individual pixel (smallest definable unit on CT) of
data. A three dimensional pixel is called a voxel. Typical Fig. 1.1 A non-contrast CT scan of the heart. Quite a bit of information
pixel values for studies commonly seen on cardiac CT are can be garnered without contrast. The pericardium is visible as a thin
listed in Table 1.1. line just below the R and L. The coronary arteries can be seen, and
diameters and calcifications are present. The right coronary artery is
Dr Hounsfield is credited with the invention of the CT seen near the R, the left anterior at the L, and the circumflex at the
scanner in late 1960s. Since CT uses X-ray absorption to cre- C. The four chambers of the heart are also seen, and relative sizes can
ate images, the differences in the image brightness at any be measured from this non-contrast study. The interatrial septum is
point will depend on physical density and the presence of clearly seen (red arrow). The ascending aorta is also present on this
image and can be evaluated. Ao aorta, L left anterior descending artery,
atoms with a high difference in anatomic number like cal- LA left atrium, LV left ventricle, RA right atrium, RV right ventricle
cium, and soft tissue and water. The absorption of the X-ray
beam by different atoms will cause differences in CT bright-
ness on the resulting image (contrast resolution). Blood and pool is not possible (Fig. 1.1). Investigators have validated
soft tissue (in the absence of vascular contrast enhancement) the measurement of “LV size” with cardiac CT, which is the
have similar density and consist of similar proportions of the sum of both left ventricle (LV) mass and volume [1]. Due to
same atoms (hydrogen, oxygen, carbon). Bone has an abun- the thin wall which does not contribute significantly to the
dance of calcium and is thus brighter on CT. Fat has an abun- total measured volume, the left and right atrial volumes can
dance of hydrogen. Lung contains air which is of extremely be accurately measured on non-contrast CT [2].
low physical density and appears black on CT (HU −1000). Because contrast resolution uses attenuation or density to
The higher the density, the brighter the structure on visualize structures in gray scale, limitations of contrast res-
CT. Calcium is bright white, air is black, and muscle or olution exist even on contrast enhanced studies. These
blood is gray. There are over 5000 shades of this gray scale include differentiating the cardiac vessels from cardiac cavi-
represented on CT, centered around zero (water-gray). ties with same density (such as when the arteries run become
Computed tomography, therefore, can distinguish blood intra-myocardial), and differentiating non-calcified plaque
from air, fat and bone but not readily from muscle or other from surrounding low density structures, including throm-
soft tissue. The densities of blood, myocardium, thrombus, bus. Even with good contrast enhancement, differentiating
and fibrous tissues are so similar in their CT number, that different types of plaque (lipid-laden and fibrous) can some-
non-enhanced CT cannot distinguish these structures. Thus, times be challenging, although it is always easy to differenti-
the ventricles and other cardiac chambers can be seen on ate the bright white plaques (calcified) from non-calcific
non-enhanced CT, but delineating the wall from the blood plaques.
1 Computed Tomography 5

Fig. 1.2 Sequential 3 mm slices from a non-contrast CT scan are easily seen (red arrows) and quantitated by the computer to
study (calcium scan). This study depicts the course and calcifications derive a calcium score, volume or mass with high inter-reader
of the left anterior descending (LAD) artery. The white calcifications reproducibility

The higher spatial resolution of CT allows visualization of (bone cortex), Table 1.1. Coronary artery calcium in coronary
coronary arteries both with and without contrast enhance- atherosclerosis (consisting of the same calcium phosphate as
ment. The ability to see the coronary arteries on a non- in bone) has CT number >130 HU, typically going as high as
contrast study depends upon the fat surrounding the artery (of +1000 HU. It does not go as high as the bony cortex of the
lower density, thus more black on images), providing a natu- spine due to the smaller quantity and mostly inhomogeneous
ral contrast between the myocardium and the epicardial distribution in the coronary artery plaque. Metal, such as that
artery (Fig. 1.1). Usually, the entire course of each coronary found in valves, wires, stents and surgical clips, typically
artery is visible on non-enhanced scans (Fig. 1.2). The major have densities of +1000 HU or higher.
exception is bridging, when the coronary artery delves into
the myocardium and cannot be distinguished without con-
trast. The distinction of blood and soft tissue (such as the left Cardiac CT
ventricle, where there is no air or fat to act as a natural con-
trast agent) requires injection of contrast with CT. Similarly, Cardiac computed tomography (CT) provides image slices
distinguishing the lumen and wall of the coronary artery also or tomograms of the heart. CT technology has significantly
requires contrast enhancement. The accentuated absorption improved since its introduction into clinical practice in 1972.
of X-rays by elements of high atomic number like calcium Current conventional scanners used for cardiac and cardio-
and iodine allows excellent visualization of small amounts of vascular imaging now employ either a rotating X-ray source
coronary calcium as well as the contrast-enhanced lumen of with a circular, stationary detector array (spiral or helical
medium-size coronary arteries (Fig. 1.3). Air attenuates the CT) or a rotating electron beam (EBCT). The attenuation
X-ray less than water, and bone attenuates it more than water, map recorded by the detectors is then transformed through a
so that in a given patient, Hounsfield units may range from filtered back-projection into the CT image used for diagno-
−1000 HU (air) through 0 HU (water) to above +1000 HU sis. The biggest issue with cardiac imaging is the need for
6 M.J. Budoff

labs and cardiac catheterization labs use 1024 × 1024 matrix

resolution. The best resolution reported by a cardiac MR
study (using the 3 Tesla magnet) demonstrated resolution in
the x-, y- and z-axes of 0.6 × 0.6 × 3 mm [3]. The best resolu-
tion offered by cardiac CT is 0.35 × 0.35 × 0.5 mm, which is
almost a factor of 10 better spatial resolution and approach-
ing the ultimate for 3-D tomography of nearly cubic (isotro-
pic) “voxels” – or volume elements (a three dimensional
pixel). As we consider non-invasive angiography with either
CT or MR, we need to remember that both spatial and tem-
poral resolution is much higher with traditional invasive
RCA
angiography (discussed in more detail below).
LAD
Reconstruction algorithms and multi-“head” detectors
Collateral
common to both current electron beam and spiral/helical CT
Ramus have been implemented enabling volumetric imaging, and
multiple high-quality reconstructions of various volumes of
interest can be done either prospectively or retrospectively,
depending on the method. The details of each type of scanner
and principles of use will be described in detail.

Fig. 1.3 A contrast-enhanced CT of the coronary arteries, with excel-

lent visualization of a high-grade stenosis in the mid-portion of the MDCT Methods
LAD. A large collateral vessel is seen from the RCA, but this is quite
rare, as usually the collaterals are too small to be well seen on cardiac
CT. A large ramus intermedius is well visualized, and the dominant Sub-second MDCT scanners use a rapidly rotating X-ray
RCA is present. This is but one view of many that can be visualized tube and several rows of detectors, also rotating. The tube
with cardiac CT, allowing for near-complete visualizations of the coro- and detectors are fitted with slip rings that allow them to
nary tree continuously move through multiple 360° rotations. The
“helical” or “spiral” mode is possible secondary to
both spatial and temporal resolution. Cardiac magnetic the development of this slip-ring interconnect. This allows the
resonance (MR) has been an emerging technique for almost X-ray tube and detectors to rotate continuously during image
two decades, making little progress toward widespread utili- acquisition since no wires directly connect the rotating and
zation over this time. Temporal resolution (how long it takes stationary components of the system (i.e., no need to unwind
to obtain an image) is inversely related to spatial resolution the wires). This slip-ring technology was considered the
with cardiac MR. Improving the MR spatial resolution most fundamental breakthrough for CT, allowing
requires prolonging the imaging time. This greatly limits the advancement from conventional CT performing single slice
ability to focus with precision on moving objects, as the scanning in the 1980s to rapid multislice scanning in the
viewer needs to settle for either a high resolution image 1990s. With the gantry continuously rotating, the table
plagued by cardiac motion, or a low resolution image with moves the patient through the imaging plane at a
no motion artifacts. Cardiac CT does not suffer from this predetermined speed (table speed). The relative speed of the
inverse relationship, and allows for both high spatial and gantry relative to the rotation of the detectors is the scan
temporal resolution simultaneously. Multidetector CT pitch. Pitch is calculated as table speed divided by collimator
(MDCT), with improved spatial resolution, allows for rota- width. The collimator width is simply the number of detectors
tion speeds now on the order of 130–220 ms. The most dis- multiplied by the detector width. A typical 64 detector
tinct advantage of cardiac CT over cardiac MR is the system with 0.625 mm detectors will thus have a collimation
improved spatial resolution and thinner slice thickness width of 64 × 0.625 mm = 40 mm. Thus, each rotation of the
achievable with current systems. CT has the ability to image detector array will ‘cover’ 40 mm of the body. If the pitch is
every 0.5 mm (submillimeter slices), providing high z-axis 1, than the table is moving at 40 mm and the coverage is
(through plane resolution). In-plane resolution is dependent 40 mm, allowing for no overlapping data and acquisition of
upon the number of pixels that can be seen by a given detec- 0.625 mm data per slice. Moving the table faster will lead to
tor array. Resolution of current CT systems uses a matrix of wider slices, as a pitch of 1.5 will infer that the table is
512 × 512, allowing x- and y-axis (in plane) resolution down moving at 60 mm/rotation, while the detector array only cov-
to 0.35 mm. MR systems use a matrix of 256 × 256, and flat ers 40 mm, so each of the 64 detectors will be responsible for
plate technology currently used in advanced fluouroscopy almost 1 mm of the 60 mm that was covered during the
1 Computed Tomography 7

rotation. A low pitch (low table speed, typically used in now increasingly 100 kV and even 80 kV studies are being
cardiac imaging) allows for over-lapping data from adjacent reported, especially in children, where radiation issues are
detectors. A typical pitch for cardiac CT is 0.25, meaning much more acute.
that the table is moved at 10 mm per rotation, while the For example, the calcium scanning protocol employed in
detectors cover 40 mm, allowing thin slice acquisition and the National Institutes of Health (NIH) Multi-Ethnic Study
overlapping datasets. The heart is literally moved only ¼ of of Atherosclerosis is complex [4]. Scans were performed
the way through the detector array each rotation, so it takes using prospective ECG gating at 50 % of the cardiac cycle,
4 rotations to completely cover any portion of the heart. The 120 kV, 106 mAs, 2.5 mm slice collimation, 0.5 s gantry
pitch is varied based upon the heart rate of the patient, to rotation, and a partial scan reconstruction resulting in a
allow optimal timing of image acquisition. Most commonly, temporal resolution of 300 ms. Images were reconstructed
physicians use a low table speed and thin imaging, leading to using the standard algorithm into a 35 cm display field of
a lot of images, each very thin axial slices which are of great view. For participants weighing 100 kg (220 lb) or greater,
value for visualizing the heart with the highest resolution. the milliampere (mA) setting was increased by 25 %.
The downside is that the slower the table movement (while However, the kV is typically not currently reduced for
still rotating the X-ray tube), the higher the radiation expo- calcium scoring for two reasons. First, the radiation dose of
sure (See Chap. 3). calcium scoring is generally low (approximately 0.7
The smooth rapid table motion or pitch in helical scanning milliSieverts), similar to mammography (0.75 milliSieverts)
allows complete coverage of the cardiac anatomy in 5–25 s, and lower than annual background radiation (3–6
depending on the actual number of multi-row detectors. The milliSieverts per year). Secondly, as the kV is lowered,
current generation of MDCT systems complete a 360° calcium and contrast appear brighter, and this would change
rotation in about 3 tenths of a second (300 ms) and are the calcium scores, which up until this point, have only been
capable of acquiring 64–640 sections of the heart obtained using 120 kV acquisitions. As more data is available
simultaneously with electrocardiographic (ECG) gating in on the algorithms for scoring with lower kV scans, calcium
either a prospective or retrospective mode. MDCT differs scoring may undergo a radiation reduction of up to 40 % by
from single detector-row helical or spiral CT systems lowering the kV from 120 to 100 for the acquisition. This
principally by the design of the detector arrays and data will require new thresholds for definitions of calcium (for
acquisition systems, which allow the detector arrays to be example- 147 HU instead of 130 HU as the definition of
configured electronically to acquire multiple adjacent calcium, and 228 instead of 200 HU for the next threshold,
sections simultaneously. For example, in 64-row MDCT etc.). The exact thresholds will have to be developed for each
systems, 64 sections can be acquired at either 0.5–0.75 or CT system prior to use. Thus, while calcium score dose can
1–1.5 mm section widths or 16 sections 2.5 mm thick be reduced by iterative reconstruction, use of 100 kVp will
(commonly used for calcium scoring). need to wait for further validation. This is not an issue with
In MDCT systems, like the preceding generation of CT angiography, as lower kVp will brighten the contrast,
single-detector-row helical scanners, the X-ray photons are raising the signal to noise quality of the study.
generated within a specialized X-ray tube mounted on a MDCT systems can operate in either the sequential (pro-
rotating gantry. The patient is centered within the bore of the spective triggered) or helical mode (retrospective gating).
gantry such that the array of detectors is positioned to record These modes of scanning are dependent upon whether the
incident photons after traversing the patient. Within the patient on the CT couch is stationary (axial, or sequential
X-ray tube, a tungsten filament allows the tube current to be mode) or moved at a fixed speed relative to the gantry rota-
increased (mA), which proportionately increases the num- tion (helical mode). The sequential mode utilizes prospective
ber of X-ray photons for producing an image. Thus, heavier ECG triggering at predetermined offset from the ECG-
patients can have increased mA, allowing for better tissue detected R wave analogous to EBCT and is the current mode
penetration and decreased image noise. One of the advan- for measuring coronary calcium at most centers using
tages of MDCT is the variability of the mA settings, thus MDCT, and increasingly being used for CT angiography
increasing the versatility for general diagnostic CT in nearly when heart rates are stable and slow. This mode utilizes a
all patients and nearly all body segments. The other variable “step and shoot modality,” which reduces radiation exposure
on the acquisition is the voltage, commonly expressed as by “prospectively” acquiring images, as compared to the
killivoltage (kv or kVp). The voltage was not varied on car- helical mode, where continuous radiation is applied (and
diac CT for the first 20 years of use, but more recently it has thousands of images created) and images are “retrospectively”
been noted that by reducing the kV, exponential reduction in aligned to the ECG tracing. In the sequential mode, a 64-slice
radiation exposure can be achieved. As the kV goes down, scanner can acquire 64 simultaneous data channels of image
image noise goes up, so it is important that the kV only be information gated prospectively to the ECG. Thus a
reduced on thinner patients. While 120 kV was most typical, 64-channel system (with 0.625 mm detectors) can acquire,
8 M.J. Budoff

within the same cardiac cycle, 40 mm in coverage per (discussed below), lowers this to 130 ms acquisitions. This
heartbeat (collimation). The promise of improved cardiac remains suboptimal in faster heart rates (>70 bpm), as
imaging from the 64–640 slice scanners is mostly larger imaging during systole (or atrial contraction during late
volumes of coverage simultaneously (up to 160 mm of diastole) will be plagued by motion artifacts. Reconstruction
coverage per rotation with a 320 slice scanner with 0.5 mm algorithms have been developed that permit the use of data
detectors), allowing for less z-axis alignment issues (cranial– acquired during a limited part of the X-ray tube rotation
caudal), and improved 3-D modeling with only 2–5 s of (e.g., little more than one half of one rotation or smaller
imaging, although each vendor has a different array of sections of several subsequent rotations) to reconstruct one
detectors, with different slice widths and capabilities cross-sectional image (described below). Simultaneous
(Table 1.2). As coverage speeds increase, breath-hold and recording of the patient ECG permits the assignment of
contrast requirements will also diminish. reconstructed images to certain time instants in the cardiac
Modern MDCT systems have currently an X-ray gantry cycle. Image acquisition windows of approximately 200 ms
rotation time of less than 500 ms. The fastest available can be achieved without the necessity to average data
rotation time is 260 ms, by using half scan reconstruction acquired over more than one heartbeat (Fig. 1.4). This may
be sufficient to obtain images free of motion artifacts in
Table 1.2 Sample protocols for MDCT angiography: contrast- many patients if the data reconstruction window is positioned
enhanced retrospectively ECG-gated scan in suitable phases of the cardiac cycle, and the patient has a
4-Slice scanner: 4 × 1.0 mm collimation, table feed 1.5 mm/rotation, sufficiently low heart rate. Motion-free segments on four-
effective tube current 400 mAs at 120 kV. Pitch =1.5/4.0 slice MDCT decrease from approximately 80 to 54 % with
collimation =0.375. Average scan time =35 s
increasing heart rates [5], and similar observations have been
16-Slice scanner (1.5 mm slices): 16 × 1.5 mm collimation, table
made with both 16- and 64-detector systems. Dual source
feed 3.8 mm/rotation, effective tube current 133 mAs at
120 kV. Pitch =3.8/24 mm collimation =0.16. Average scan time CT, utilizing two x-ray tubes and two detector arrays moving
=15–20 s simultaneously around the body, can utilize partial images
16-Slice scanner (0.75 mm slices): 16 × 0.75 mm collimation, from each detector array to effectively ‘half’ the temporal
table feed 3.4 mm/rotation, effective tube current 550–650 mAs resolution, allowing motion free images up to heart rates of
at 120 kV. Pitch =3.4/12 mm collimation =0.28. Average scan
70 bpm or more. However, the system is limited by 32
time = 15–20 s
64-Slice scanner (0.625 mm slices): 64 × 0.6.25 mm collimation,
detectors, so collimation or coverage is only 19.2 mm per
table feed 10 mm/rotation, effective tube current 685 mAs at rotation (32 × 0.6 mm).
120 kV. Pitch =10/40 mm collimation =0.25. Average scan
time = 5 s
Dual Source scanner (0.6 mm slices): 32 × 0.6 mm collimation, MDCT Terminology
table feed 6 mm/rotation, effective tube current 685 mAs at
120 kV. Pitch =6/19.2 mm collimation =0.3. Average scan
time = 10–12 s Isotropic Data Acquisition
320-Slice scanner (0. 5 mm slices): 320 × 0.5 mm collimation, table The biggest advance that the newest systems provide is
feed 12 mm/rotation, effective tube current 685 mAs at 120 kV. Pitch thinner slices, important for improving image quality as well
=12/40 mm collimation =0.3. Average scan time = 2–3 s as diminishing partial volume effects. The current systems

Detector 1
Detector 2
Fig. 1.4 A typical acquisition using the Detector 3
“halfscan” method on multidetector CT
Detector 4
(Light-Speed16, GE Medical Systems,
Milwaukee Wisconsin). This
demonstrates an acquisition starting at
approximately 50 % of the R-R interval.
A scanner with a rotation speed of Segment: ~250 ms
200 ms takes approximately 250 ms to
complete an image, as depicted on LightSpeed16 /Ultra/Plus
1 Computed Tomography 9

allow for slice thick-nesses between 0.5 and 0.625 mm there is no overlap, the pitch is 1. If 50 % overlap is desired,
(depending on manufacturer and scan model). Thus, the the pitch is 0.5, as the table is moved slower to allow for
imaging voxel is virtually equal in size in all dimensions overlapping images. This is necessary with multisector
(isotropic). The spatial resolution of current CT systems is reconstruction. Typical pitch values for cardiac work are
0.35 × 0.35 mm, and has always been limited by the z-axis 0.25–0.4, allowing for up to a 4-fold overlap of images. If the
(slice thickness). Current systems theoretically allow for collimation with 64-row scanners increases to 40 mm, the
isotropic resolution (as reconstructed images can be seen at table can move four times faster than the 16-slice scanner,
0.4 mm), allowing for no loss of data by reconstructing the without affecting slice thickness. Thus, the coverage with
data in a different plane. This is very important for imaging increased numbers of detectors can go up dramatically over
the coronary, peripheral, and carotid arteries, as they run a short period of scanning time, by imaging more detectors
perpendicular to the imaging plane (each slice only and increasing the speed of table movement in concert.
encompasses a small amount of data) and to follow these
arteries, one must add multiple slices together in the z-axis. Field of View
The old limitations of CT (better interpretation for structures Another method to improve image quality of the CT
that run within the plane it was imaged, i.e., parallel to the angiograph (CTA) is to keep the field of view small. The
imaging plane) are no longer present. There is now no loss of matrix for CT is 512 × 512, meaning that is the number of
data with reformatting the data with multiplanar reformation voxels in a given field of view. This is significantly better
(MPR) or volume rendering (VR). This differs significantly than current MR scanners, accounting for the improved
from MR, which due to thick slice acquisition (still > 1 mm), spatial resolution. If the field of view is 15 cm, than each
does not allow free rotation of the resultant in-plane images. pixel is 0.3 mm. Increasing the field of view to 45 cm (typical
Thus, acquisition for CT is quite simple, obtaining axial for encompassing the entire chest) increases each pixel
slices through the area of interest, with the ability to dimension to 0.9 mm, effectively reducing the spatial resolu-
reconstruct a three-dimensional image that can be free tion of each data-point 3-fold.
rotated. MR requires acquisition of data within the plane of
interest, so if a short axis image of the left ventricle is Contrast
required, it must be obtained in that plane, not reconstructed Finally, the high scan speed allows substantial reduction in
from the axial data. Furthermore, the thinner slice imaging the amount of contrast material. The high speed of the scan
allows for less partial volume artifacts (different densities allows one to decrease the amount of contrast administered;
overlying one another, causing a mixed picture of brightness by using a 64-channel unit with a detector collimation of
on the resultant scan) and less streaking and shadowing, 0.625 mm and a tube rotation of 0.35 s (typical values for a
prevalent from dense calcifications and metal objects (such 64-detector coronary CTA), the acquisition interval is around
as bypass clips, pace-maker wires, and stents). 5–6 s, which allows one to reduce the contrast load to approx-
imately 50 mL. For a faster acquisition protocol, the contrast
Pitch delivery strategy needs to be optimized according to the scan
In the helical or spiral mode of operation, a 64-MDCT duration time. Use of a 320 detector scanner (which currently
system can acquire 64 simultaneous data channels while has 0.5 mm slices), covers the entire heart with one rotation,
there is continuous motion of the CT table. The relative further reducing the contrast needs (although some minimal
motion of the rotating X-ray tube to the table speed is called amount of contrast will be required to fill the heart and arter-
the scan pitch and is particularly important for cardiac gating ies in question). The general rule is the duration of scanning
in the helical mode. Increased collimator coverage allows for (scan acquisition time) equals the contrast infusion time. So,
decreasing the pitch, without losing spatial resolution. The if an average rate of 4 mL/s is used, a 15-s scan acquisition
definition of pitch for the multidetector systems is the would require 60 mL of contrast. With volume scanners (64-
distance the table travels per 360° rotation of the gantry, and greater detector systems), the scan times are reduced to
divided by the dimension of the exposed detector array (the 5–8 s, and contrast doses are subsequently reduced as well.
collimation, which is the slice thickness times the number of
imaging channels). For example, a 64-slice system, with 64 Prospective Triggering
equal detectors each of 0.625 mm, gives a collimation of The prospectively triggered image uses a “step and shoot”
40 mm. Thus, if the table is moving at 40 mm/rotation, the system, used for calcium scoring for years, now widely
pitch is 1.0. The pitch remains 1.0 if the table moves at available for all MDCT scanners. This obtains images at a
60 mm/rotation and the slices are thicker (0.975 mm each), certain time of the cardiac cycle (see Chap. 2), which can
or if the number of channels (detectors utilized) increases. be chosen in advance, and then only one image per detec-
Moving the table faster will lead to thicker slices, which will tor per cardiac cycle is obtained. This reduces (radiation)
decrease resolution and lead to partial volume effects. If requirements, and does allow for CT angiographic images
10 M.J. Budoff

only when heart rates are slow, as motion artifacts may aligned to the ECG tracing to create images at any point of
plague these images. When performing prospective gating, the R-R interval (cardiac cycle). This allows for all phases
the temporal resolution of a helical or MDCT system is (1–100 %) to be recreated as needed, allowing for many
proportional to the gantry speed, which determines the phases to overcome motion artifacts, correct for stair-step
time to complete one 360° rotation. To reconstruct each (misalignment) artifacts, and calculate ejection fraction and
slice, data from a minimum of 180° plus the angle of the wall motion. However, radiation doses are higher than
fan beam are required, typically 210° of the total 360° rota- prospective imaging, even when using dose modulation.
tion. For a 64-row system with 0.35-s rotation, the tempo-
ral resolution is approximately 0.20 s or 200 ms. By
reducing the display field of view to the 20 cm to encom- Halfscan Reconstruction
pass the heart, the number of views can be reduced to fur-
ther improve temporal resolution to approximately 200 ms A multislice helical CT halfscan (HS) reconstruction
per slice. The majority of MDCT systems now have gantry algorithm is most commonly employed for cardiac
rotation speeds of 250–330 ms and temporal resolution of applications. Halfscan reconstruction using scan data from a
83–167 ms per image when used for measuring coronary 180° gantry rotation (180–250 ms) for generating one single
calcium or creating individual images for CT angiography. axial image (Fig. 1.4). The imaging performances (in terms
Although physically faster rotational times may be possi- of the temporal resolution, z-axis resolution, image noise,
ble in the future, this is still rotation of an X-ray source and image artifacts) of the heartscan algorithm have
(with or without attached detectors) within a fixed radius demonstrated improvement over utilizing the entire rotation
of curvature. This is subject to the forces and limitations of (full scan). It has been shown that the halfscan reconstruction
momentum. While interpretation can be limited by the results in improved image temporal resolution and is more
phase chosen (i.e.- 75 % of the R-R interval), there is an immune to the inconsistent data problem induced by cardiac
ability to add padding. Padding allows for additional motions. The temporal resolution of multislice helical CT
phases to be imaged, but is dependent upon the heart rate. with the halfscan algorithm is approximately 60 % of the
With slower heart rates, padding can be increased, to typi- rotation speed of the scanner. The reason it is not 50 % of the
cally include an additional 10–15 % of the cardiac cycle on rotation speed is that slightly more than 180° is required to
each side of the phase chosen (allowing for phases from 60 create an image, as the fan beam width (usually 30°) must be
to 85 % to be acquired), so acquisition may be widened to excluded from the window (Fig. 1.4). Thus approximately
allow extra phases to allow for some correction of motion 210° of a rotation is needed to reconstruct an entire image.
artifacts. However, the more padding applied, the higher Central time resolution (the point in the center of the image)
the radiation exposure. is derived by the 180° rotation. MDCT using the standard
halfscan reconstruction method permits reliable assessment
Retrospective Gating of the main coronary branches (those in the center of the
The ECG is used to add R peak markers to the raw data set. image field) in patients with heart rates below 65 beats/min
A simultaneous ECG is recorded during the acquisition of [6,7]. The necessity of a low heart rate is a limitation of
cardiac images. The ECG is retrospectively used to assign MDCT coronary angiography using this methodology.
source images to the respective phases of the cardiac cycle With halfscan reconstruction, the proportion of the
(ECG gating). The best imaging time to minimize coronary acquisition time per heartbeat is linearly rising from 20 % at
motion is from 40 to 80 % of the cardiac cycle (early to 60 beats/min to 33 % at 100 beats/min. When evaluating the
mid-diastole). diastolic time, the proportion is much greater. Slower heart
The interval between markers determines the time of each rates have longer diastolic imaging. The diastolic time useful
scanned cardiac cycle. Retrospective, phase-specific, short for imaging for a heart rate of 60 beats/min is on the order of
time segments of several R-R intervals are combined to 400 ms (excluding systole and atrial contraction). Thus, a
reconstruct a “frozen axial slice.” During helical scanning, 250 ms scan will take up 70 % of the diastolic imaging time.
the patient is moved through the CT scanner to cover a body Increase the heart rate to 100 beats/min (systole remains
volume (i.e., the heart). An advantage of the helical acquisi- relatively fixed) and the biggest change is shortening of
tion mode is that there is a continuous model of the volume diastole. Optimal diastolic imaging times are reduced to
of interest from base to apex, as opposed to the sequential/ approximately 100 ms, clearly far too short for a motion-free
cine mode in which there are discrete slabs of slices which MDCT scan acquisition of 250 ms (Fig. 1.5, left panel).
have been obtained in a “step and shoot” prospective fashion. Thus, heart rate reduction remains a central limitation for
The obvious detriment to the helical acquisition is the motion-free imaging of the heart using MDCT. This can be
increase in radiation dose delivered to the patient, as partially overcome by multisegment reconstruction,
continuous images are created, and then “retrospectively” described below.
1 Computed Tomography 11

Fig. 1.5 LightSpeed16 CT angiography images. On the left is the half- motion artifacts in the distal right (green arrow), but much improved
scan reconstruction. On the right, is a reconstructed image using the over the halfscan image, which is not interpretable (red arrow)
same dataset, using multisegment reconstruction. There are still some

Fig. 1.6 A demonstration of a theoretical

image using multisegment reconstruction.
The resulting image is constructed of four
equal segments from four different
detectors. Each is reconstructed from the
same point in the cardiac cycle
(approximately 50 % in this depiction).
Four different detectors, each visualizing
the same portion of the heart in the same Detector 1
portion of the cardiac cycle, can be used to Detector 2
add together to create one image. In
Detector 3
practice, the segments are not always of
equal length, and four images are not Detector 4
always available for reconstruction
Det 2

Det 3
Det 1

Det 4

4 sectors: ~65 ms
Temporal resolution

Multisegment Reconstruction reconstruction can typically use up 2–4 different segments

correlated to the raw data. By using four heartbeats to create
The scan window refers to the time when the volume of an image, the acquisition time can be reduced to a minimum
interest is present in the scan field and is therefore “seen” by of 65 ms (Fig. 1.6).
the detector. It is the limiting factor for temporal resolution. During retrospective segmented reconstruction, views
In multisegment reconstruction, it defines the number of from different rotations are combined to simulate one half-
cardiac cycles available and hence the maximum number of scan rotation (approximately 210° of data is needed to create
segments that can be used to reconstruct one slice. an image). To calculate the number of segments that can be
Multisegment reconstruction utilizes a helical scanning extracted from a scan window, the number of positions avail-
technique coupled with ECG synchronization (images are able for reconstruction is determined automatically by a
retrospectively aligned to the ECG data acquired to keep workstation. Each position is extended into a wedge so that
track of systolic and diastolic images). Multisegment the combination of all wedges simulates a halfscan tube
12 M.J. Budoff

Fig. 1.7 The figure on the left demonstrates a standard halfscan recon- cal scan data but processed with a two-sector reconstruction algorithm
struction with a rotation speed of 400 ms (approximate 260 ms image resulting in an effective temporal resolution of 180 ms. Note how the
temporal resolution), with image data acquired on a four-channel proximal right coronary artery (white arrows), as well as the left cir-
MDCT system, 1.25 mm slice collimation, 0.6 gantry speed and a heart cumflex and great coronary vein, are now distinguishable (white arrow-
rate of 72 beats/min. The image to the right demonstrates the same heli- head) and motion-free on the multisector reconstructed image

rotation. The raw data acquired in this virtual halfscan rota- together, making a non-diagnostic image. Thus, there is
tion is sufficient for the reconstruction of one slice. The size still need for regular rhythms with CT angiography,
of the largest wedge (largest segment) defines the temporal although with higher detector systems (i.e., 64–640 detec-
resolution within the image (Fig. 1.6). In other words, the tors), the number of heartbeats needed to cover the entire
subsegment with the longest temporal data acquisition deter- heart goes down to 1–4, reducing the chance of significant
mines the temporal resolution of the overall image. If the changes in heart rates due to premature beats, breath-hold-
four segments used to create an image were of the following ing, vagal or sympathetic tone.
size (65 ms, 65 ms, 50 ms, and 100 ms), then the temporal By combining information from each of the detector
resolution of the reconstructed image is 100 ms. rows, the effective temporal resolution of the images can
The use of multisegment reconstruction has allowed for theoretically be reduced to as low as 65 ms. However, to do
markedly improved effective temporal resolution and this requires four perfectly regular beats consecutively and a
image quality. Just to be clear about how this works, let’s fast baseline heart rate, and usual reconstructions allow for
use an analogy of a pie. Imagine needing just over half of a two to three images to be utilized, yielding an effective
pie for a picture. To create an image, you can either add temporal resolution of 130–180 ms per slice (Fig. 1.7), but
together one small slice from several pies (Fig. 1.6) or you with a direct proportional increase in radiation exposure to
can take one large piece from one pie (Fig. 1.4). The advan- the patient. This method of segmenting the information of
tage of taking small pieces from each heartbeat is that the one image into several heartbeats is quite similar to the
temporal resolution goes down proportionally. The diffi- established prospective triggering techniques used for MRI
culty in using this technique is that the pieces of the pie of the coronary arteries [8,9]. With multisegment
must align properly. Patients with even very slight arrhyth- reconstruction the length of the acquisition time varies
mias (especially atrial fibrillation, sinus arrhythmia, or between 10 and 20 % of the R-R interval. Since the
multifocal atrial rhythms), changing heart rates (increased reconstruction algorithm is only capable of handling a
vagal tone during breath-holding, catecholamine response limited number of segments, the pitch (table speed) is often
after getting a contrast flush, etc.), or premature beats will increased for patients with higher heart rates. Thus, fewer
cause misregistration (misalignment) to occur. If the heart- images are available with higher heart rates, decreasing the
beats used are not perfectly regular, the computer will inad- potential success rate with this methodology (see section
vertently add different portions of the cardiac cycle “Speed/temporal resolution” below).
1 Computed Tomography 13

Multisegment reconstruction has been shown to for halfscan reconstruction, resulting from the lower pitch
improve depiction of the coronary arteries as compared to (slower table speed, increasing the time the X-ray beam is
halfscan reconstruction [10,11] (Fig. 1.5). This methodol- on) needed with multisegment reconstruction. The results of
ogy will improve temporal resolution, but high heart rates studies indicate that multi-segment reconstruction has
will still increase the motion of the coronaries, increasing superior diagnostic accuracy and image quality compared
the likelihood of image blurring and non-diagnostic with halfscan reconstruction in patients with normal heart
images (Fig. 1.5, right panel still demonstrating some rates (Fig. 1.7). Thus, multisegment reconstruction holds
blurring of the mid-distal right coronary artery with heart promise to make the routine use of beta blockers to reduce
rates of 70–75 beats/min). It is fairly common for patients the heart rate before CT coronary angiography less necessary
with low heart rates at rest to increase the heart rate sig- as a routine. One further limitation is that certain heart rates
nificantly at the time of CT angiography. This can occur cannot undergo multisegment reconstruction if the R-R
due to three factors: anxiety about the examination, the interval (in milliseconds) is an even multiple of the scanner
breath-hold, or the warmth of the contrast infusion to the rotational speed. If the heart rate and the rotation of the
patient. Thus, there is still a need for somewhat reduced scanner are synchronous, the same heart phase always
heart rates during MDCT angiography with all current corresponds to the same angle segment, and a partial-scan
reconstruction systems. interval cannot be divided into smaller segments. Finally, if
Studies examining the image quality of multisegment the heart rate is unexpectedly irregular (i.e., Premature
and halfscan reconstruction in CT with four [12] and eight Ventricular Contractions (PVCs) or stress reaction to the dye
[11] detector rows showed similar image quality in both causing increased heart rate during imaging), multi-segment
phantoms and patients. However, Dewey et al. [13] demon- reconstruction will not be successful and the diagnostic
strated that the accuracy, sensitivity, specificity, and rate of image quality will have to rely on the halfscan reconstruction.
non-assessable coronary branches were significantly better Some scanners (Philips Medical Systems is the first to
using multisegment reconstruction in a 16-slice MDCT introduce such proprietary software) have intrinsic programs
scanner. The authors attributed the difference to the higher which improve the success rate with multisegment
image quality and resulting longer vessel length free of reconstruction at increased heart rates. How well these
motion artifacts with multisegment reconstruction. The systems work and how often are clinical questions still being
obvious advantage of multisegment reconstruction is answered.
achieved by reducing the acquisition window per heartbeat
to approximately 160 ms on average, particularly useful for
diagnostic images of the right coronary artery and circum- EBCT Methods
flex artery (the two arteries that suffer the most from motion
artifacts) [14]. Therefore, MDCT in combination with mul- While now discussion is included mostly for historical rea-
tisegment reconstruction does not always require adminis- sons, it is important to remember that the origins of cardiac
tration of beta blockers to reduce heart rate. This imaging with CT lies firmly with the Electron beam com-
improvement simplifies the procedure and expands the puted tomography (GE Healthcare, Waukegan, WI). This is
group of patients who can be examined with non-invasive a tomographic-imaging device developed over 25 years ago
coronary angiography using MDCT. The potential is for specifically for cardiac imaging. At Harbor-UCLA, we
even greater application with aligning these multiple seg- started performing CT angiography of the coronary arteries
ments together with 64+ detector scanners, further improv- in January 1995, literally 10 years earlier than MDCT sys-
ing the diagnostic rate with MDCT angiography, and tems were able to image the coronary tree with similar accu-
coverage for more widespread applications such as gating racy. To date, and specifically over the past decade, there has
the entire aorta or triple-rule out imaging (imaging the entire been a huge increase in diagnostic and prognostic data
chest to evaluate pulmonary embolism, aorta and coronaries regarding coronary artery imaging. To this day, most of the
simultaneously). prognostic and diagnostic work done with coronary artery
calcium scanning was done with EBCT. In order to achieve
Limitations of Multisegment Reconstruction rapid acquisition times useful for cardiac imaging, these
Heart rates above 65 beats/min demonstrate the biggest fourth-generation CT scanners have been developed with a
benefit of multisegment reconstructions. The benefit of non-mechanical X-ray source. This allows for image
multisegment reconstruction in low heart rates has not been acquisition on the order of 50–100 ms, and with prospective
demonstrated, and some experts recommend avoiding this in ECG triggering, the ability to “freeze” the heart. Electron
lower heart rates to minimize radiation exposure. A drawback beam scanners use a fixed X-ray source, which consists of a
of multisegment reconstruction is the effective radiation 210° arc ring of tungsten, activated by bombardment from a
dose, which is estimated to be 30 % higher than necessary magnetically focused beam of electrons fired from an
14 M.J. Budoff

vascular study in one-half the total examination time required

by the C-150 and C-300 scanners. The e-Speed, in addition
to the standard 50 and 100 ms scan modes common to all
EBCT scanners, is capable of imaging speeds as fast as
33 ms. A major limitation of this modality currently is the
slice width, which is limited to 1.5 mm. Current MDCT
scanners can obtain images in 0.5–0.75 mm per slice.
Three imaging protocols are used with the EBCT scanner.
They provide the format to evaluate anatomy, cardiovascular
function, and blood flow. The imaging protocol used to study
cardiovascular anatomy is called the volume scanning mode
and is similar to scanning protocols employed by conventional
CT scanners. Single or dual scans are obtained and then the
Fig. 1.8 Depiction of the e-Speed electron beam computed tomogra- scanner couch is incremented a predetermined distance. For
phy scanner. The electron source emits a beam, which is steered mag- non-contrast studies, the table increment is usually the width
netically through the detection coil, then reflected to tungsten targets (A of the scan slice, so that there is no overlap imaging of
B C D), where a fan-shaped X-ray beam is created and, after passing
anatomy. For contrast studies, especially those to be
through the area of interest, seen by the detectors
reconstructed three-dimensionally, table incrementation is
usually less than the slice width, giving overlap of information
electron source “gun” behind the scanner ring. The patient is to improve spatial resolution (see Chaps. 3 and 4). For
positioned inside the X-ray tube, obviating the need to move example, moving the table forward 1 mm, while taking a
any part of the scanner during image acquisition (Fig. 1.8). 1.5 mm slice, gives 33 % overlap per image. Using the older
EBCT is distinguished by its use of a scanning electron beam scanners, with slice thickness of 3 mm, moving the table
rather than the traditional X-ray tube and mechanical rotation only 1.5 mm gives overlap to improve spatial resolution.
device used in current “spiral” single and multiple detector This scanning mode is utilized with and without contrast
scanners (requiring a physically moving X-ray source around enhancement and provides high spatial resolution of
the patient). EBCT requires only that the electron beam is cardiovascular anatomy. This technique provides high
swept across the tungsten targets to create a fan beam of resolution axial images, and is ideal for evaluation of the
X-ray, possible in as short as 50 ms per image (20 frames/s). aorta, coronary arteries, and congenital heart disease. A 3-D
The electron beam is emitted from the cathode, which is arteriogram reconstructed from tomographic images has the
several feet superior to the patient’s head, and then passes potential for more complete visualization of the coronary
through a magnetic coil, which bends the beam so that it will arteries (Figs. 1.3 and 1.9). The end-systolic images can be
strike one of four tungsten anode targets. The magnetic coil compared to the end-diastolic images, allowing for accurate
also steers the beam through an arc of 210°. The X-rays are measurement of regional wall thickening and motion,
generated when the electron beam strikes the tungsten anode myocardial mass (utilizing the known specific gravity of
target, then passes through the patient in a fan-shaped X-ray cardiac tissue), global and regional ejection fraction [15].
and strikes the detector array positioned opposite the anodes. Importantly, since blood is being injected into the venous
This stationary multisource/split-detector combination is system, simultaneous enhancement of the right and left
coupled to a rotating electron beam and produces serial, ventricle allows for excellent visualization of all cardiac
contiguous, thin section tomographic scans in synchrony chambers simultaneously, and measure of both right and left
with the heart cycle. ventricular function and structure [16].
There have been four iterations for EBCT since it was The flow mode imaging protocol acquires a single image
introduced clinically in the early 1980s. Since its initial gated to the electrocardiogram at a predetermined point in
introduction in 1982, it has been known as “rapid CT,” “cine the cardiac cycle (e.g., end-diastole (peak of the R-wave)).
CT,” “Ultrafast CT©,” Electron Beam CT, and “Electron Images can be obtained for every cardiac cycle or multiples
Beam Tomography©.” The overall imaging methods have thereof. Scanning is initiated before the arrival of a contrast
remained unchanged, but there have been improvements in bolus at an area of interest (e.g., left ventricular (LV)
data storage, data manipulation and management, data myocardium) and is continued until the contrast has washed
display, and spatial resolution. The original C-100 scanner in and out of the area. Time density curves from the region of
was replaced in 1993 by the C-150, which was replaced by interest can be created for quantitative analysis of flow
the C-300 in 2000. The current EBCT scanner, the e-Speed (Fig. 1.10). The filling of different chambers can be visualized
(GE/Imatron) was introduced in 2003. The e-Speed is a sequentially, allowing for visualization of flow into and out
multislice scanner and currently can perform a heart or of any area of interest. This was the original methodology
1 Computed Tomography 15

Fig. 1.9 A contrast-enhanced electron beam angiogram demonstrating long segments of the left anterior descending (arrow). Images such as seen
here can be created which are much more similar to a conventional coronary angiogram, if desired. C circumflex artery

employed to assess for graft patency, prior to the ability to the measurement of the slice width for individual images).
create 3-D images. It should be noted that early studies This is a “voxel” or volume element and it has the potential
dating back to 1983 have demonstrated saphenous vein graft to be nearly cubic using MDCT. Current coronary artery cal-
patency with this technique, achieving an accuracy of cification (CAC) scanning protocols vary between manufac-
approximately 90 % as compared to invasive angiography turers from 2.5 to 3.0 mm for MDCT. For CT angiography,
[17]. This technique is still commonly employed to detect MDCT obtains images with 0.5–0.625 mm per axial slice.
shunts (Chap. 23), as well as to deter-mine the length of time Thus, MDCT has a significant advantage in terms of spatial
it takes for contrast to travel from the arm vein at the site of resolution, and results in less partial volume averaging than
injection to the central aortic root (allowing for accurate all other modalities. Also the principles of resolution of say
image acquisition of the high resolution contrast-enhanced a 1 mm vessel require that the slice width be 1 mm or less.
images, Chap. 7). Partial volume averaging occurs when a small plaque has
dramatically different CT numbers related to whether it is
MDCT Scanners Spatial Resolution centered within one slice or divided between two adjacent
Spatial resolution compares the ability of the scanners to slices. Thus, thinner slices will have less partial volume aver-
reproduce fine detail within an image, usually referred to as aging. The visualization of smaller lesions is only possible
the high contrast spatial resolution. Spatial resolution is with smaller slice widths (Fig. 1.11). Modern MDCT sys-
important in all three dimensions when measuring coronary tems permit simultaneous data acquisition in 64–640 parallel
plaque. Even if limited to the proximal coronary arteries, the cross-sections with 0.50–0.625 mm collimation each. The
left system courses obliquely within the x–y imaging plane, in-plane spatial resolution is now as high as 17 line pairs/cm
while the right coronary artery courses through the x–y with new high definition detector arrays. However, conven-
imaging plane. Simply put, one axial image may demonstrate tional CT angiography still has higher temporal and spatial
5 or more centimeters of the left anterior descending, while resolution, allowing for better visualization of the smaller
most images will demonstrate only a cross-section of the arteries and collateral vessels. Modern angiographic equip-
right coronary artery. For more on cardiac anatomy with ment has a resolution of 40 line pairs per centimeter with a
examples, see Chap. 4. The in-plane resolution of MDCT six-inch field of view, the usual image magnification for
systems are among the best of any imaging modality, higher coronary angiography [18]. Thus, invasive coronary angiog-
than echocardiography, nuclear imaging and magnetic reso- raphy still has a 3–4-fold better resolution than current
nance imaging. The resolution in z dimension is determined MDCT systems. It is likely to remain this way until the per-
by the detector width in MDCT (this may be thought of as fection of flat panel detectors for CT – which would be akin
16 M.J. Budoff

Search region of interest

250

200

150

100

50

Fig. 1.11 Spatial resolution as measured on computed tomography. A

0
1 1 1 1 1 2 2 2 2 2 3 3 3 3 3 4 phantom is imaged, and the smaller line pairs per centimeter are evalu-
0 2 4 6 8 0 2 4 6 8 0 2 4 6 8 0 ated. Somewhat similar to an eye chart, the thinnest lines clearly seen
CT VALUE VS . TIME ( S ) define the spatial resolution of the scanner

Fig. 1.10 A flow or timing study. This study images the same level
over time. A region of interest (in this study, the circle is placed in the tissue penetration. Other approaches to overcome image
ascending aorta) defines the anatomy to be measured. The graph below noise in obese patients, beyond increasing mA and kV
measures the Hounsfield units (HU) of that region of interest on each include reconstructing thicker slices (slice thickness is
subsequent image. Initially, there is no contrast enhancement, and the
measures are of non-enhanced tissue, around 50–60 HU. Contrast starts inversely proportional to image noise) and use of iterative
to arrive on this study around 16 s, and peaks at 22 s. The bright white reconstruction (discussed below).
structure next to the ascending aorta is the superior vena cava, filled
with unmixed contrast Speed/Temporal Resolution
Cardiac CT is dependent upon having a high temporal resolu-
to the current state of the art in conventional angiography tion to minimize coronary motion-related imaging artifacts.
devices. However, three dimensional reconstructions and By coupling rapid image acquisition with ECG gating,
better contrast resolution (ability to see different densities) of images can be acquired in specific phases of the cardiac cycle.
CT over fluoroscopy, helps improve diagnostic accuracy of Studies have indicated that temporal resolutions of 19 ms are
MDCT. needed to suppress all pulmonary and cardiac motion [19].
Generally, the higher X-ray flux (mAs = tube current × Interestingly, temporal resolution needs to be faster to sup-
scan time) and greater number and efficiency of X-ray press motion of the pulmonary arteries than for cardiac imag-
detectors available with MDCT devices leads to images with ing. The study by Ritchie et al. demonstrated the need for
better signal-to-noise ratio and higher spatial resolution 19 ms imaging to suppress pulmonary motion (despite breath-
when compared to earlier scanners. Early detection of holding), while needing 35 ms imaging to fully suppress
calcified plaque is dependent upon distinguishing the plaque motion for cardiac structures. This is most likely due to the
from image noise. Newer MDCT systems (64 detector +) accordion motion of the pulmonary arteries, whereby the
have reduced image noise compared to older systems (8–18 motion of the heart causes the surrounding pulmonary arter-
noise/HU versus 24 noise/HU). Image noise CT has been ies to be pulled in and out with each beat. This has led to
shown to have an association with body mass index which some physicians to use cardiac gating during pulmonary
may result in falsely identifying noise as calcified plaque or embolism studies to improve resolution down to fourth and
overestimation of true plaque burden. Typical values for fifth generation branches of the pulmonary system.
mAs for MDCT angiography is on the order of 300–400. Cardiac MR motion studies of the coronary arteries dem-
While CT scanners have difficulties with the morbidly obese onstrate that the rest period of the coronary artery (optimal
patient, MDCT can increase the mAs (and kV) to help with diastolic imaging time) varies significantly between individ-
1 Computed Tomography 17

utilizing more detectors (i.e., 4- versus 8- versus 16- versus

64-detector/channel systems) reduces scan time (i.e., breath-
hold time) and section misregistration (misalignment), but
has no effect on temporal resolution.

Radiation Dose

Computed tomography utilizes X-rays, a form of ionizing

radiation, to produce the information required for generating
CT images. Although ionizing radiation from natural sources
is part of our daily existence (background radiation including
air travel, ground sources, and television), a role of healthcare
professionals involved in medical imaging is to understand
Fig. 1.12 A typical motion artifact seen with calcium scans on MDCT potential risks of a test and balance those against the potential
images. The limited reproducibility of this technique is due to the star benefits. This is particularly true for diagnostic tests that will
artifacts seen on this image (RCA, white arrow). Prospective gating is be applied to healthy individuals as part of a disease screening
done, with halfscan reconstruction techniques. In cases of faster heart
or risk stratification program. In order for healthcare
rates, motion artifacts seen here are commonplace. To limit radiation to
a reasonable level for this screening text, no overlap or retrospective professionals to effectively advise individuals they must
images are obtained, so multisegment reconstruction is not possible have an understanding of the exposure involved. The use of
radiological investigations is an accepted part of medical
practice, justified in terms of clear clinical benefits to the
uals with a range of 66–333 ms for the left coronary artery patient which should far outweigh the small radiation risks.
and 66–200 ms for the right coronary artery [20] and that for Diagnostic medical exposures, being the major source of
mapping coronary flow, temporal resolution of 23 ms may be man-made radiation exposure of the population, add up to
required for segments of the right coronary artery [21,22]. 50 % of the radiation exposure to the population. However,
Current generation cardiac CT systems which create images even small radiation doses are not entirely without risk. A
for measuring calcified plaque at 135–220 ms (prospectively small fraction of the genetic mutations and malignant
gated MDCT) cannot totally eliminate coronary artery diseases occurring in the population can be attributed to
motion in all individuals. Motion artifacts are especially natural background radiation. The concept of “effective
prominent in the mid-right coronary artery, where the bal- dose” was introduced in 1975 to provide a mechanism for
listic movement of the vessel may be as much as two to three assessing the radiation detriment from partial body
times its diameter during the twisting and torsion of the heart irradiations in terms of data derived from whole-body
during the cardiac cycle (Fig. 1.12). It should be noted that irradiations. The effective dose for a radiological investigation
the motion of the coronary artery during the cardiac cycle is is the weighted sum of the doses to a number of body tissues,
a 3-D event with translation, rotation, and accordion type where the weighting factor for each tissue depends upon its
movements. Thus portions of the coronary artery pass within relative sensitivity to radiation-induced cancer or severe
and through adjacent tomographic planes during each R-R hereditary effects. It thus provides a single dose estimate
cycle. Blurring of plaques secondary to coronary motion related to the total radiation risk, no matter how the radiation
increases in systems with slower acquisition speeds. The dose is distributed around the body. Adoption of the effective
resulting artifacts tend to increase plaque area and decrease dose as a standard measure of dose allows comparability
plaque density and thus alter the calcium measurements. The across the spectrum of medical and non-medical exposures.
artifacts may make those segments of the CT angiogram “The effective dose is, by definition, an estimate of the
non-diagnostic, a problem that plagued up to 70 % of the uniform, whole-body equivalent dose that would produce the
early four-slice MDCT system studies [5,12]. same level of risk for adverse effects that results from the
The image quality achieved with cardiac CT is deter- non-uniform partial body irradiation. The unit for the
mined not only by the 3-D spatial resolution but also by the effective dose is the sievert (Sv)” (www.fda.gov/cdrh/ct/rqu.
temporal resolution. The spatial resolution is directly related html). Although it has many limitations, the effective dose is
to the scan slice thickness and the reconstruction matrix. The often used to compare the dose from a CT examination, a
temporal resolution, which determines the degree of motion fluoroscopic examination, and the background radiation one
suppression, is dependent on the pitch factor (which is deter- experiences in a year. Units are either millirem (mrem) or
mined by the table speed), the gantry rotation time, and the millisievert (mSv); 100 mrem equals 1 mSv. The estimated
patient’s heart rate during the examination. As stated above, dose from chest X-ray is 0.04 mSv, and the average annual
18 M.J. Budoff

Table 1.3 Common tests with estimated radiation exposures The other variable involved in dose is the protocol used.
Test Radiation dose (mSv) The lowest radiation and most commonly applied is acquired
1 Stress MIBI 6 by prospective triggering; that is, the X-rays are only on
1 LC spine 1.3 during the acquisition of data that will be used for the image.
1 Barium enema 7 MDCT, however, can use prospective triggering or
1 Upper GI 3 retrospective gating, 120 or 140 kilovolts (kV) (with
1 Abdominal X-ray 1 protocols possible with lower kV depending upon future
1 Dental X-ray 0.7 research and tube current improvements), and a wide range
1 Cardiac catheterization 2.5–10 of mA. Retrospective gating means that the X-rays are on
Radiation dose Radiation dose throughout the heart cycle. One drawback of MDCT is the
for MDCT (mSv) for EBCT (mSv) potential for higher radiation exposure to the patient,
Calcium scan 1–1.5 0.6 depending on the tube current selected for the examination.
CT angiography 8–13 1–1.5 The X-ray photon flux expressed by the product of X-ray
CTA dose modulation 5–8 –
tube current and exposure time (mAs). For example, 200 mA
Lung CT 8 1.5
with 0.5 s exposure time yields 100 mAs in MDCT. In
Abdomen/pelvis 10 2
millisieverts, calcium scanning leads to an approximate dose
Body scan 12 2.6
of 0.9 mSv for MDCT (similar to the dose of another
Virtual colon 8–14 2–3
screening test, mammography – 0.7 mSv). This is in
comparison to a conventional coronary angiogram, with
back-ground radiation in the United States is about 300 mean doses of 8 mSv [23].
mrem or 3 mSv [23]. Table 1.3 shows the estimated radiation There are primary three factors that go into radiation
doses of some commonly used tests. dosimetry. The X-ray energy (kV), tube current (mA), and
The Food and Drug Administration (FDA) in describing exposure time. The distance of the X-ray source from the
the radiation risks from CT screening in general used the patient is a fourth source, but, unlike fluoroscopy, this
following language (www.fda.gov/cdrh/ct/risks.html): distance is fixed in all current CT scanners. Since MDCT
In the field of radiation protection, it is commonly angiography at the time utilized retrospective imaging, and
assumed that the risk for adverse health effects from cancer since radiation is continuously applied while only a fraction
is proportional to the amount of radiation dose absorbed and of the acquired data is utilized, high radiation doses from
the amount of dose depends on the type of X-ray examination. retrospective CT studies (doses of 6–10 mSv/study) still play
A CT examination with an effective dose of 10 millisieverts a role in decisions to utilize this modality in heart failure and
(abbreviated mSv; 1 mSv =1 mGy in the case of x rays) may atrial fibrillation, where retrospective studies are largely
be associated with an increase in the possibility of fatal required [24–26]. The American Heart Association wrote a
cancer of approximately 1 chance in 2000. This increase in scientific statement for radiation doses [23] from cardiac
the possibility of a fatal cancer from radiation can be studies and cited the following doses: retrospective CTA
compared to the natural incidence of fatal cancer in the US with dose modulation – 9 mSv; prospective triggered CTA –
population, about 1 chance in 5. In other words, for any one 3 mSv; stress-rest Sestamibi – 9 mSv; FDG PET scan 14 mSv
person the risk of radiation-induced cancer is much smaller and invasive coronary angiogram – 7 mSv [23]. Doses have
than the natural risk of cancer. Nevertheless, this small come down dramatically with MDCT due to multiple
increase in radiation-associated cancer risk for an individual approaches, including lower kVp (i.e. 100), dose modulation,
can become a public health concern if large numbers of the and prospective triggering, now averaging 2.1 mSev for
population undergo increased numbers of CT procedures for MDCT angiography in clinical practice [24]. Since the
screening purposes. publication by Choi et al. [24], new detectors, iterative
Since CT is the most important source of ionizing radia- reconstruction and more aggressive use of ‘fast-pitch’
tion for the general population, dose reduction and avoidance imaging has further reduced doses. It is conceivable that
is of the utmost importance, especially for the asymptomatic mean doses will dip below 1 mSv once use of these new
person undergoing risk stratification, rather than diagnostic techniques becomes widespread.
workup. Already, 50 % of a person’s lifetime radiation expo- Theoretically, since narrow collimation (beam widths)
sure is due to medical testing, and this is expected to go up causes “overbeaming,” the dose efficiency is lower with
with increased exposure to nuclear tests and CT scanning. four-slice scanners than with more detectors. Estimated
Used as a tool in preventive cardiology, cardiac CT is increas- efficiency goes from 67 % with 4 slices (1.25 mm, 5 mm
ingly being performed in the population of asymptomatic coverage) to 97 % with 16 slices (at 1.25 mm, covering
persons, a priori healthier individuals, where use of exces- 20 mm). However, obtaining thinner slices will offset this
sive radiation is of special concern. gain, as obtaining more images will lead to higher radiation
1 Computed Tomography 19

doses. Typical studies with four-slice MDCT scanners of MDCT angiography, despite the higher radiation doses.
obtained 600 images, while 16-slice scanners typically This is due to the requirement during retrospective imaging
produce about 1200 scans, and 64-detector scanners are for slower table movement to allow for oversampling, for
reporting over 2000 images produced per study. Newer gap-less and motion-reduced imaging, as well as the possi-
MDCT studies report continue to show dramatic radiation bility of multisegment reconstruction. Retrospective imag-
reductions from the early 4-slice MDCT scanners and even ing allows the clinician to have multiple phases of the
from the more recent 64-MDCT studies [27]. cardiac cycle available for reconstruction, to find the por-
The energy used can be altered in MDCT studies, and tion of the study with the least coronary motion. Many cli-
while typical imaging is done in the range of 120–140 kV, nicians utilize multiple phases for reconstruction, with
this can be varied with MDCT. The attenuation (densities) of different phases used for different coronary arteries.
calcium and iodine contrast agents increases with reduced However, constant irradiation is redundant, as most images
X-ray energy (reduced kV settings). This can reduce the are reconstructed during the diastolic phases of the heart
X-ray exposure, as the X-ray power emitted by the tube cycle. Thus, a new method for reducing radiation dose with
decreases considerably with reduced kV settings. To MDCT is to implement tube current modulation. Tube cur-
compensate for the lower power (and resultant increased rent is reduced during systole, when images are not utilized
noise of the image), the tube current (mA) can be increased. for reconstruction of images for MDCT angiography, by
Scans with less than 120 kV tube voltage (i.e., 80 kV) can 80 %, and then full dose is utilized during diastole. Depending
potentially maintain contrast-to-noise ratios that have been upon the heart rate, this may reduce radiation exposure by
established for coronary calcium and CT angiography as much as 47 % [28], but with slower heart rates, this
images, and significant lower radiation expo-sure. reduction will be less, as systole encompasses a shorter and
Preliminary experiments have demonstrated a reduction in shorter fraction of the cardiac cycle. Dose modulation pro-
radiation exposures of up to 50 % with use of 80 kV. Jakobs tocols reduce radiation doses with MDCT by attempting to
et al. demonstrated that the radiation dose for CAC scoring decrease beam current during systole, when images are not
with use of 80 kV may be as low as 0.6 mSv [28]. As the used for interpretation, and should be employed whenever
noise will go up with 80 kV imaging, this may be too low for possible [29]. Most of these protocols turn down the beam
CT angiography in larger patients, but for children and slim current (mA) during systole, so that diagnostic images are
adults, this affords a sub-millisievert dose for the first time still available from roughly 40–80 % of the R-R interval
with CTA. CT angiography protocols are much more (cardiac cycle).
common with 100 kV protocols, providing a reduction in Dose modulation widely, but not universally employed,
radiation of 40 %, as the dose reduction from kV reduction is as it is harder to use with very fast heart rates, as the time to
exponential, so a 20 % kV reduction affords a 40 % dose ramp up and ramp down the radiation dose becomes signifi-
reduction. A very low kV (i.e.- 80) is most often used for cant, and the ever shortening diastole becomes a smaller
pediatric patients. Similarly, for obese patients, where target. Also, irregular heart rates (frequent premature beats
penetration is important, a kV of 135 or 140 can be utilized, or atrial fibrillation) makes anticipation of the next R-R
but the dose will go up exponentially, so this is not widely interval challenging, so most often dose modulation is
employed. The power (mAs) used is directly proportional to turned off in this setting. The routine use of beta blockers
the radiation dose. Higher mAs results in lower image noise, makes even more sense in this setting, given the increased
following the relationship: noise is inversely proportional to ability to use dose modulation more effectively and fre-
the square root of the mAs. Thus, limiting mAs can result in quently with lower heart rates. A misconception is the
lower radiation, but higher noise. It is important to remember potential loss of wall motion and other functional data with
that reducing mAs too much to save radiation will increase dose modulation. If dose modulation is used, there are sys-
noise to the point where the scan is non-diagnostic. Most tolic images, and while they are somewhat noisier (harder
centers use either an “automatic” mAs system, which adjusts to read plaque), the image quality is still excellent for wall
the mAs based upon the image quality, or leave the mAs rela- motion and ejection fraction assessment. An image from
tively fixed. end-systole (early diastole) and end-diastole can be com-
Prospective triggering or “sequential” mode is typically pared to calculated wall thickening, ejection fraction, and
used and strongly recommended for coronary calcium cardiac motion.
assessment with MDCT, due to the lower radiation doses to Another method to decrease radiation exposure is to
which the patient is exposed. However, the drawback of increase the pitch. The pitch is usually very low, on the order
using MDCT prospective triggering is the inability to per- of 0.20–0.25 for CT angiography cases, and usually 1 for
form overlapping images, and longer image acquisition coronary calcium scanning. This low pitch raises radiation
times. Thus, all CT vendors currently recommend retrospective exposure, but is partially compensated by the more efficient
image acquisition in the “helical” mode for performance dose of using the larger collimation available with increased
20 M.J. Budoff

detectors. For individuals with different heart rates, different

pitches can be used to obtain similar datasets. Thus, for those
with slower heart rates, a faster pitch may allow for some
reduction in cardiac exposure during these studies, and thus
proportionally less radiation with dose modulation than for
those with higher heart rates. The newest scanners available
in 2014 now allow for the first time, acquisition of retrospec-
tive imaging with ‘fast-pitch’ acquisitions, moving the gan-
try very fast during the cardiac cycle and acquiring multiple
datasets with a much lower radiation profile and improved
resolution. This likely represents the next great breakthrough
in cardiac CT imaging, allowing for full datasets to calculate
ejection fraction, wall motion and plaque with radiation
doses of <1 milliSievert.
One must be careful and cognizant of the dose being
given. In one study using 16-slice MDCT, the pitch was
reduced based upon the patient being able to hold their breath
for 20 s, so very high overlap was obtained (very small
pitch). The mean irradiation dose received by the patients
Fig. 1.13 A contrast-enhanced (top image) and non-contrast study
during this MDCT angiography study was 24.2 mSv [30].
(bottom image) of the left main and proximal LAD. The soft plaque is
Understanding the physics and implications of higher mAs visible (dark region, representing fat density) with calcified plaque
and kV and thinner slices will help the clinician choose the (white regions). A computer program can be applied (Acculmage, San
necessary parameters, without over-irradiating the patient. Francisco, CA) to the individual pixels to measure lower density (pink
squares, fat density), intermediate density (red squares, fibrous den-
This concept, called “information/ milliSv,” causes one to
sity), and high density (white squares, calcified plaque). This can theo-
think about the benefit garnered from each mSv given. retically quantitate the volume of soft plaque, fibrous plaque, and
calcified plaque in any given CT image

Clinical Applications of Cardiovascular CT

more accurate representation of coronary artery anatomy
Cardiac CT has several unique diagnostic capabilities appli- and be more amenable to quantitation, thereby improving
cable to the many facets of CAD, worth the radiation expo- the diagnosis and treatment of CAD [40]. There is rapidly
sures and time needed to learn these applications. Each will accumulating data with MDCT to visualize the coronary
be discussed at length in chapters throughout this book. The arteries accurately and reliably (CT angiography) [41–
presence of coronary calcium is invariably an indicator of 44]. Looking beyond the lumen by visualizing the wall
atherosclerosis [31,32]. Non-contrast studies can accurately and its constituents (including fat, calcium, and fibrous
identify and quantify coronary calcification (a marker of tissue) is now possible with cardiac CT (Fig. 1.13).
total plaque burden) [33], while contrast-enhanced studies Coronary plaque composition evaluation is being actively
can define ventricular volumes, ejection fraction, and wall investigated [45,46]. This so-called “soft plaque” or ‘high-
motion and wall thickening with high accuracy [34]. Studies risk plaque’ evaluation has demonstrated to have prognos-
can be performed at rest, and during exercise can identify tic significance over coronary calcium or risk factors
reversible ischemia [35]. alone, as well as helping to target revascularization better
Coronary angiography during cardiac catheterization is than luminography alone [46].
the clinical gold standard for definitive diagnosis and
determination of coronary lesions. Pathologic studies
have demonstrated that the severity of coronary stenosis is Future of CT and MR
underestimated by visual analysis during clinical coro-
nary angiography [36–39]. This may result from the limi- The strengths of magnetic resonance cardiovascular imaging
tations of resolution based upon fluoroscopy and the 2-D include greater definition of tissue characteristics, perfusion,
imaging inherent in coronary angiography, as well as the valvular function, lack of X-ray radiation, and lack of need
inability to see beyond the lumen with conventional angi- for potentially nephrotoxic contrast media, compared to CT
ography. The true promise of cardiovascular CT is to visu- technologies. Several studies have been reported comparing
alize the coronary artery, including the lumen and wall. this modality to coronary angiography [47–49]. Limited tem-
Three-dimensional digital coronary images may provide poral and spatial resolution [50], partial volume artifacts (due
1 Computed Tomography 21

to push this diagnostic tool to the forefront of cardiology. For

MDCT, increased numbers of detectors will allow for better
collimation and spatial reconstructions. Having more of the
heart visualized simultaneously will also allow for reduc-
tions in the contrast requirements and breath-holding, further
improving the methodology. Multisector reconstruction
(combining images from consecutive heart beats) and dose
modulation (to reduce radiation exposure during systole,
when images are not used for reconstruction) are increas-
ingly being applied, which will continue to improve the
image quality and diagnostic rate of these machines.
Functional data, now being made available with the advent
of fractional flow reserve estimates from CT (FFRct) and
transluminal attenuation gradients (TAG) will continue to
push the frontier of CT angiographic imaging forward
quickly [54].

References
1. Mao S, Budoff MJ, Oudiz RJ, Bakhsheshi H, Wang S, Brundage BH.
A simple single slice method for measurement of left and right
ventricular enlargement by electron beam tomography. Int J Card
Imaging. 2000;16:383–90.
Fig. 1.14 A contrast-enhanced study demonstrating the abdominal 2. Budoff MJ, Mao SS, Wang S, Bakhsheshi H, Brundage BH. A
aorta, renal arteries and kidneys, and iliac circulation. This study can be Simple single slice method for measurement of left and right atrial
done with 40 cm3 of iodinated contrast, taking between 5 and 10 s volume by electron beam computed tomography. Acad Radiol.
depending on the scanner used. Highly diagnostic vascular imaging is 1999;6:481–6.
quite routine with CT scanners 3. Stuber M, Botnar RM, Fischer SE, et al. Preliminary report of
in-vivo coronary MRA at 3 Tesla in humans. Magn Reson Med.
2002;48:425–8.
4. Carr JJ, Nelson JC, Wong ND, et al. Calcified coronary artery
to slice thickness limitations) [51], reliance on multiple plaque measurement with cardiac CT in population-based studies:
breath-holds, and poor visualization of the left main coro- standardized protocol of Multi-Ethnic Study of Atherosclerosis
nary artery [52] all reduce the clinical applicability of MR (MESA) and Coronary Artery Risk Development in Young Adults
angiography. Reported sensitivities for MR angiography (CARDIA) study. Radiology. 2005;234:35–43.
5. Nieman K, Rensing BJ, van Geuns RJ, et al. Non-invasive coronary
range from 0 to 90 % [9,47]. MR angiography remains a angiography with multislice spiral computed tomography: impact
technically challenging technique with certain limitations of heart rate. Heart. 2002;88(5):470–4.
hindering its clinical use. CT angiography offers advantages 6. Ropers D, Baum U, Pohle K, et al. Detection of coronary artery
over MR angiography, including single breath-hold to reduce steno-sis with thin-slice multi-detector row spiral computed tomog-
raphy and multiplanar reconstruction. Circulation. 2003;107:664–6.
respiratory motion, higher spatial resolution, reduced slice 7. Nieman K, Cademartiri F, Lemos PA, Raaijmakers R, Pattynama
thickness and overall study time of 35–50 s with CT tech- PM, de Feyter PJ. Reliable noninvasive coronary angiography with
niques as compared to 45–90 min for MR angiography [9]. fast submillimeter multislice spiral computed tomography.
The rapidity and ease with which CT coronary angiography Circulation. 2002;106:2051–4.
8. Regenfus M, Ropers D, Achenbach S, et al. Noninvasive detection
can be performed suggest possible cost advantages compared of coronary artery stenosis using contrast-enhanced three-
with MR angiography and selective coronary angiography dimensional breath-hold magnetic resonance coronary angiography.
[53]. Thus, for most applications (in the absence of renal J Am Coll Cardiol. 2000;36:44–50.
insufficiency or contrast allergy), CT will be the preferred 9. Kim WY, Danias PG, Stuber M, et al. Coronary magnetic reso-
nance angiography for the detection of coronary stenoses. N Engl
method to evaluate anatomy, be it coronary, renal, carotid or J Med. 2001;345:1863–9.
peripheral vascular beds (Fig. 1.14). MR, in the foreseeable 10. Blobel J, Baartman H, Rogalla P, Mews J, Lembcke A. Spatial and
future, will remain a better test for intercranial imaging, as temporal resolution with 16-slice computed tomography for cardiac
the bony structures cause some scatter with CT imaging. imaging. Fortschr Roentgenstr. 2003;175:1264–71.
11. Lembcke A, Rogalla P, Mews J, et al. Imaging of the coronary arter-
For cardiovascular CT in general, better workstations ies by means of multislice helical CT: optimization of image quality
(ease of use and diagnostic capabilities), as well as improve- with multisegmental reconstruction and variable gantry rotation
ments in both spatial and temporal resolution will continue time. Fortschr Roentgenstr. 2003;175:780–5.
22 M.J. Budoff

12. Wicky S, Rosol M, Hoffmann U, Graziano M, Yucel KE, Brady using 320 MDCT. ScientificWorldJournal. 2013:731590.
TJ. Comparative study with a moving heart phantom of the impact doi:10.1155/2013/731590.
of temporal resolution on image quality with two multidetector 28. Jakobs TF, Becker CR, Ohnesorge B, et al. Multislice helical CT of
electrocardiography-gated computed tomography units. J Comput the heart with retrospective ECG gating: reduction of radiation
Assist Tomogr. 2003;27:392–8. exposure by ECG-controlled tube current modulation. Eur Radiol.
13. Dewey M, Laule M, Krug L, et al. Multisegment and halfscan 2002;12:1081–6.
reconstruction of 16-slice computed tomography for detection of 29. Trabold T, Buchgeister M, Kuttner A, et al. Estimation of radiation
coronary artery stenosis. Invest Radiol. 2004;39:223–9. exposure in 16-detector row computed tomography of the heart
14. Mao S, Lu B, Oudiz RJ, Bakhsheshi H, Liu SCK, Budoff with retrospective ECG-gating. Rofo. 2003;175:1051–5.
MJ. Coronary artery motion in electron beam tomography. 30. Leta R, Carreras F, Alomar X, et al. Non-invasive coronary
J Comput Assist Tomogr. 2000;24:253–8. angiography with 16 multidetector-row spiral computed tomogra-
15. Baik HK, Budoff MJ, Lane KL, Bakhsheshi H, Brundage phy: a comparative study with invasive coronary angiography. Rev
BH. Accurate measures of ejection fraction using electron beam Esp Cardiol. 2004;57:217–24.
tomography, radionuclide angiography, and catheterization angiog- 31. Janowitz WR, Viamonte M, Agatston AS. Comparison of serial
raphy. Int J Card Imaging. 2000;16:391–8. quantitative evaluation of calcified coronary artery plaque by
16. Mao SS, Budoff MJ, Oudiz RJ, et al. Effect of exercise on left and ultrafast computed tomography in persons with and without
right ventricular ejection fraction and wall motion in patients with obstructive coronary artery disease. Am J Cardiol. 1991;68:1–6.
coronary artery disease: an electron beam computed tomography 32. Blankenhorn DH. Coronary artery calcification: a review. Am
study. Int J Cardiol. 1999;71:23–31. J Med Sci. 1961;242:1–9.
17. McKay CR, Brundage BH, Ullyot DJ, et al. Evaluation of early 33. Breen JF, Sheedy PF, Schwartz RS, et al. Coronary artery
post-operative coronary artery bypass grafts patency by contrast- calcification detected with ultrafast CT as an indication of coronary
enhanced computed tomography. J Am Coll Cardiol. 1983;2: artery disease. Radiology. 1992;185:435–9.
312–7. 34. Lipton MJ, Higgins CB, Boyd DP. Computed tomography of the
18. Nissen SE, Gurley GL. Assessment of coronary angioplasty results heart: evaluation of anatomy and function. J Am Coll Cardiol.
by intravascular ultrasound. In: Serruys PW, Straus BH, King III 1985;5:555–95.
SB, editors. Restenosis after intervention with new mechanical 35. Roig E, Chomka EV, Castaner A, et al. Exercise ultrafast computed
devices. Dordrecht: Kluwer; 1992. p. 73–96. tomography for the detection of coronary artery disease. J Am Coll
19. Ritchie CJ, Godwin JD. Minimum scan speeds for suppression of Cardiol. 1989;13:1073–81.
motion artifacts in CT. Radiology. 1992;185:37–42. 36. Marcus ML, Armstrong MD, Heistad DD, Eastham CL, Mark AL.
20. Wang Y, Vidan E. Cardiac motion of coronary arteries: variability Comparison of three methods of evaluating coronary obstructive
in the rest period and implications for coronary MR angiography. lesions: postmortem arteriography, pathologic examination and
Radiology. 1999;213(3):751–8. measurement of regional myocardial perfusion during maximal
21. Hofman MB, Wickline SA. Quantification of in-plane motion of vasodilation. Am J Cardiol. 1982;49:1688–706.
the coronary arteries during the cardiac cycle: implications for 37. Grondin CM, Dyrda I, Pasternac A, Campeau L, Bourassa MG,
acquisition window duration for MR flow quantification. J Magn Les-perance J. Discrepancies between cineangiographic and
Reson Imaging. 1998;8(3):568–76. postmortem findings in patients with coronary artery disease and
22. Marcus JT, Smeenk HG. Flow profiles in the left anterior descend- recent myocardial revascularization. Circulation. 1974;49:703–8.
ing and the right coronary artery assessed by MR velocity 38. Thomas AC, Daview MJ, Dilly S, Dilly N, Franc F. Potential errors
quantification: effects of through-plane and in-plane motion of the in estimation of coronary arterial stenoses from clinical coronary
heart. J Comput Assist Tomogr. 1999;23(4):567–76. arteriography with reference to the shape of the coronary arterial
23. Gerber TC, Carr JJ, Arai AE, et al. Ionizing radiation in cardiac lumen. Br Heart J. 1986;55:129–39.
imaging: a science advisory from the American Heart Association 39. Mintz GS, Painter JA, Pichard AD, et al. Atherosclerosis in
Committee on Cardiac Imaging of the Council on Clinical angiographically normal coronary artery reference segments: an
Cardiology and Committee on Cardiovascular Imaging and intravascular ultrasound study with clinical correlations. J Am Coll
Intervention of the Council on Cardiovascular Radiology and Cardiol. 1995;25:1479–85.
Intervention. Circulation. 2009;119:1056–65. 40. Budoff MJ, Nakazato R, Mancini GBJ, et al. CT angiography for
24. Choi TY, Malpeso J, Li D, Sourayanezhad S, Budoff MJ. Radiation the prediction of hemodynamic significance in intermediate and
dose reduction with increasing utilization of prospective gating in severe lesions: head-to-head comparison with quantitative coronary
64-multidetector cardiac computed tomography angiography. angiography using fractional flow reserve as the reference standard.
J Cardiovasc Comput Tomogr. 2011;5:264–70. J Am Coll Cardiol Img. 2016. doi:10.1016/j.jcmg.2015.08.021.
25. Gopal A, Mao SS, Karlsberg D, Young E, Waggoner J, Ahmadi N, 41. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert E,
Pal RS, Leal J, Karlsberg RP, Budoff MJ. Radiation reduction with Scherer M, Bellinger R, Martin A, Benton R, Delago A, Min
prospective ECG-triggering acquisition using 64-multidetector JK. Diagnostic performance of 64-detector row coronary computed
computed tomographic angiography. Int J Cardiovasc Imaging. tomographic angiography of individuals undergoing invasive
2009;25(4):405–16. coronary prospective multicenter ACCURACY (assessment by
26. Mark DB, Berman DS, Budoff MJ, Carr JJ, Gerber TC, Hecht HS, coronary computed individuals without known coronary artery dis-
Hlatky MA, Hodgson JM, Lauer MS, Miller JM, Morin RL, ease: results from the tomographic angiography for evaluation of
Mukherjee D, Poon M, Rubin GD, Schwartz RS. ACCF/ACR/ coronary artery stenosis in angiography) trial. J Am Coll Cardiol.
AHA/NASCI/SAIP/SCAI/SCCT 2010 expert consensus document 2008;52(21):1724–32.
on coronary computed tomographic angiography: a report of the 42. Pagali SR, Madaj P, Gupta M, Nair S, Hamirani YS, Min JK, Lin F,
American College of Cardiology Foundation Task Force on Expert Budoff MJ. Interobserver variations of plaque severity score and
Consensus Documents. J Am Coll Cardiol. 2010;55(23): segment stenosis score in coronary arteries using 64 slice multide-
2663–99. tector computed tomography: a substudy of the ACCURACY trial.
27. Khosa F, Khan A, Nasir K, Shuaib W, Budoff M, Blankstein R, J Cardiovasc Comput Tomogr. 2010;4(5):312–8.
Clouse ME. Influence of image acquisition on radiation dose 43. Hamirani YS, Isma’eel H, Larijani V, Drury P, Lim W, Bevinal M,
and image quality: full versus narrow phase window acquisition Saeed A, Ahmadi N, Karlsberg RP, Budoff MJ. The diagnostic
1 Computed Tomography 23

accuracy of 64-detector cardiac computed tomography compared technique and preliminary results. Br Heart J. 1993;70:
with stress nuclear imaging in patients undergoing invasive cardiac 315–26.
catheterization. J Comput Assist Tomogr. 2010;34(5):645–51. 49. Paschal CB, Haache EM, Adler LP. Coronary arteries: three-
PMID: 20861764. dimensional MR imaging of the coronary arteries: preliminary
44. Abdulla J, Pedersen KS, Budoff M, Kofoed KF. Influence of coro- clinical experience. J Magn Reson Imaging. 1993;3:491–501.
nary calcification on the diagnostic accuracy of 64-slice computed 50. Duerinckx AJ, Urman MK. Two dimensional coronary MR angiog-
tomography coronary angiography: a systematic review and meta- raphy: analysis of initial clinical results. Radiology. 1994;193:
analysis. Int J Cardiovasc Imaging. 2012;28(4):943–53. 731–8.
doi:10.1007/s10554-011-9902-6. 51. Duerinckx AJ, Urman MK, Atkinson DJ, Simonetti OP, Sinha U,
45. Alani A, Nakanishi R, Budoff MJ. Recent improvement in coronary Lewis B. Limitations of MR coronary angiography. J Magn Reson
computed tomography angiography diagnostic accuracy. Clin Imaging. 1994;4:81.
Cardiol. 2014;37(7):428–33. doi:10.1002/clc.22286. PMID: 52. Duerinckx AJ, Atkinson DP, Mintorovitch J, Simonetti OP, Urman
24756932. MK. Two-dimensional coronary MRA: limitations and artifacts.
46. Min JK, Edwardes M, Lin FY, Labounty T, Weinsaft JW, Choi JH, Eur Radiol. 1996;6:312–25.
Delago A, Shaw LJ, Berman DS, Budoff MJ. Relationship of 53. Chernoff DM, Ritchie CJ, Higgins CB. Evaluation of electron
coronary artery plaque composition to coronary artery stenosis beam CT coronary angiography in healthy subjects. AJR Am
severity: results from the prospective multicenter ACCURACY J Roentgenol. 1997;169:93–9.
trial. Atherosclerosis. 2011;219:573–8. PMID: 21696739. 54. Leipsic J, Yang TH, Thompson A, Koo BK, Mancini GB, Taylor C,
47. Manning WJ, Li W, Edelman RR. A preliminary report comparing Budoff MJ, Park HB, Berman DS, Min JK. CT angiography (CTA)
magnetic resonance imaging with conventional angiography. N and diagnostic performance of noninvasive fractional flow reserve:
Engl J Med. 1993;328:828–32. results from the determination of fractional flow reserve by ana-
48. Pennell DJ, Keegan J, Firmin DN, Gatehouse PD, Underwood SR, tomic CTA (DeFACTO) study. AJR Am J Roentgenol.
Longmore DB. Magnetic resonance imaging of coronary arteries: 2014;202(5):989–94. doi:10.2214/AJR.13.11441.
 Cardiovascular Computed Tomography:
Current and Future Scanning System 2
Design

Rine Nakanishi, Wm. Guy Weigold, and Matthew J. Budoff

Abstract
Since the heart is continually in motion, cardiac computed tomography (CT) has capabili-
ties required to scan the heart with high spatial resolution, high temporal resolution, larger
detector coverage and fast scan speed. Recent technology enabled current versions of car-
diac CT to display the heart with much fewer artifacts and less radiation dose. In this chap-
ter, we will address the current and future scanning system design of cardiac CT.

Keywords
Cardiac CT • Spatial resolution • Temporal resolution • Detector coverage • Scan speed

Introduction be in place because the heart is continually in motion, the

structures of interest (i.e., coronary arteries) are small, and
The heart can be visualized in gross form on any standard their curvilinear course requires multi-planar reformatting
chest CT, but for a detailed evaluation of cardiac anatomy for analysis.
exact specifications of scanner hardware and software must For these specifications to be met, the scanner hardware
must be robust, the scanner must be fitted with ECG-
monitoring equipment, and cardiac-specific software and
image reconstruction servers must be installed.

R. Nakanishi, MD, PhD

Department of Medicine, Cardiac CT, Los Angeles BioMedical
Research Institute at Habor-UCLA Medical Center,
Elements of Scanner Design
Torrance, CA, USA
e-mail: [email protected] The general design of a CT scanner equipped for cardiac
W.G. Weigold, MD, FACC, FSCCT imaging is the same as that of any modern scanner: an x-ray
Department of Medicine, MedStar Washington Hospital Center, tube mounted on a rotating gantry opposite a detector array
Washington, DC, USA generates x-rays which are emitted across the bore, are atten-
Cardiac CT Core Lab, MedStar Health Research Institute, uated as they pass through the patient’s chest, and are scintil-
Washington, DC, USA lated by the detectors as the gantry rotates around the patient
MedStar Cardiovascular Research Network, obtaining attenuation data from multiple view angles. These
Washington, DC, USA data are transmitted to an image reconstruction server which
e-mail: [email protected]
then computes the axial images. To perform cardiac CT,
M.J. Budoff, MD (*) however, a number of additional capabilities are required,
David Geffen School of Medicine at UCLA,
namely, high spatial resolution, high temporal resolution,
Los Angeles Biomedical Research Institute,
Torrance, CA, USA and fast scan speed, while delivering an acceptable radiation
e-mail: [email protected] exposure.

© Springer International Publishing 2016 25

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_2
26 R. Nakanishi et al.

Special Design Considerations Temporal Resolution

for Cardiac CT
In order to reconstruct an axial image, attenuation data from
Spatial Resolution multiple view angles that encompass half a rotation around
the patient are required. The amount of time needed to obtain
Spatial resolution is the product of multiple variables this data is the nominal, heart-rate independent temporal
including detector characteristics and collimation, sam- resolution of the scanner. Hence, a gantry that requires
pling rate, and reconstruction methods. State of the art 330 ms to make one complete rotation has a baseline tempo-
scanners use thin 0.5–0.625 mm collimation. This reduces ral resolution of 165 ms. This is analogous to shutter speed:
volume averaging thus increasing image detail of small just as shutter speed must be sufficiently fast to capture
objects, and allows reconstruction of isotropic datasets, motion-free images of a moving subject, temporal resolution
thereby preserving z-axis resolution and permitting multi- must be sufficiently fast to capture the data needed for image
planar reformatting necessary for analysis of cardiac reconstruction within the relatively brief period of cardiac
anatomy. diastasis. If temporal resolution is insufficient, motion arti-
GE Healthcare has focused their system development fact occurs (Fig. 2.2). A temporal resolution of 165 ms is
on spatial resolution, developing a new detector scintilla- relatively slow for cardiac imaging, so systems overcome
tion material with a fast decay time (30 ns), minimal this by various means: faster gantry rotation, multi-cycle
afterglow (one-quarter that of conventional Gd2O2S crys- reconstruction, and a second x-ray tube.
tals), and increased efficiency. This new detector is one Multi-cycle reconstruction combines data from multiple
element of a multi-pronged approach to increasing image contiguous heart beats to complete the half-scan of views
resolution, which also includes new electronics that per- (Fig. 2.3). This technique is heart-rate dependent: it can only
mit increased sampling, and a new iterative reconstruc- be used within certain ranges of heart rates, since the cardiac
tion algorithm [1] (Fig. 2.1). These innovations increase cycle and gantry rotation must be asynchronous.
spatial resolution by 3–4.5 line pairs per cm (lp/cm), An approach adopted by Siemens in 2006 uses two x-ray
which is substantial given that current resolution of sys- tubes mounted on the gantry at 90° angles; therefore, only a
tems is approximately 12–15 lp/cm. The enhanced resolu- quarter turn of the gantry is required to collect the 180° of
tion is particularly useful for imaging stented and/or attenuation data. Hence, a most recent dual-source system
calcified coronary arteries, while lowering radiation with a gantry rotation time of 250 ms has a baseline central
requirements. temporal resolution of approximately 66 ms. This obviates

Fig. 2.1 Increased sampling improves image quality. Axial images resolution of the line pairs of the image derived from the high den-
of line-pair phantom demonstrate improved spatial resolution using sity sampling dataset (Reproduced with permission from Chandra
increased sampling density (on the right) compared to standard sam- [2])
pling frequency (on the left). Note the improved edge detail and
2 Cardiovascular Computed Tomography: Current and Future Scanning System Design 27

Fig. 2.2 Better temporal resolution improves image quality of moving artifact, when temporal resolution is insufficient (far left), while
structures. 3D volume reconstructions of the right coronary artery in 3 motion artifact is minimally present, and small anatomic details are
CT scans representing 3 generations of CT scanner (4-, 16-, and clearly imaged when temporal resolution is improved (far right)
64-slice, from left to right, respectively), possessing temporal (Reproduced with the kind permission of Springer Science + Business
resolution of 400, 250, and 180 ms from left to right, respectively. Media from Hurlock et al. [3])
Note that the vessel appears distorted and disjointed, due to motion

the need for multi-cycle reconstruction, making the system by increasing coverage or faster temporal resolution, scan
less susceptible to variation in heart rate, and providing high times have been recently reduced to just < 1 s, resulting in
heart rate independent temporal resolution. Several reports the minimization of the radiation exposure. The Toshiba’s
demonstrated very good image quality [4, 5] and, in a com- Aquilion One scanner (Aquilion One Dynamic Volume
parison of 64 MDCT and DSCT scans, the dual-source sys- CT; Toshiba Medical System, Tochigi-ken, Japan) has 320
tem produced better image quality at higher heart rates [6]. rows of detectors, with 0.5 mm collimation, 16 cm of cov-
Image quality is still improved, however, by reducing heart erage, and can perform an axial 1-beat acquisition of the
rate before scanning. The improvement of temporal resolu- entire heart when the rate is well controlled. The GE revo-
tion is not the only way to solve the issue for motion artifact. lution also demonstrated a wider coverage of 16 cm and
As a post image processor, GE currently provides the motion- 0.23 mm collimation, with gantry rotation 280 mm. The
correction algorithm (Snapshot Freeze; GE Healthcare) Philips iQon (Philips Healthcare, Cleveland, OH), is a 256-
which improves image quality using coronary motion arti- row scanner, which allows axial acquisition of the entire
fact and supplements interpretability for diagnostic problems heart in 2 beats.
of CAD [7].

Radiation Exposure
Detector Coverage and Scan Speed
Traditional cardiac CT uses a helical scan mode and very low
The several novel multi-slice CTs have achieved wider pitch to perform retrospective ECG-gated reconstructions.
z-axis coverage. The scan length is 16 cm, which is mostly This delivers an undesirably high radiation exposure, so vari-
enough to scan the whole heart in a single heart beat, ous methods have been designed to reduce radiation
avoiding breathing or misalignment artifact. In addition, exposure.
28 R. Nakanishi et al.

z approach is now offered by all manufacturers. Using a

64-slice system, the entire heart can be covered in 3–4
acquisitions; however this leaves the system vulnerable to
fluctuations in heart rate and rhythm during the scan. Larger
t coverage mitigates this vulnerability by reducing the number
180° of beats required for data acquisition. However, larger cover-
age lends to higher radiation doses, as the detectors are less
efficient when having to expose a wider detector array.
Hence, Philips’ 128-row iCT system can cover the entire
heart in 2 beats, with a reported radiation exposure of
3–5 mSv. Toshiba’s 320-row Aquilion One scanner can
cover the entire heart in one beat, with a reported radiation
exposure of approximately 6 mSv. However, lower radiation
doses and dependable coronary scanning using 1-beat
z acquisition requires heart rate reduction. At higher heart
rates (>65 bpm), optimal image quality requires a 2- or
3-beat acquisition (and use of multi-cycle recon) which
increases radiation exposure to approximately 13 (2-beat) to
19 (3-beat) mSv [11, 12]. Acquiring with a wide exposure
45° window (“padding”) can ensure the capture of motion-free
45° t data, but increases radiation exposure (Fig. 2.6). A narrower
45° 45° exposure window can be used with preservation of image
quality if heart rate is controlled and reduces radiation
exposure.

Fig. 2.3 Multi-cycle reconstruction. Single cycle recon (a): The dura- High Pitch Helical Scanning
tion of the acquisition window (gray bar) is approximately equivalent
to one-half the gantry rotation time, since this is the time required to
obtain 180° of attenuation data. Multi-cycle recon (b): When multiple
Radiation exposure is inversely proportional to pitch in
detector rows are present, the axial slice position in the z-position can ECG-gated helical CT. Thus, increasing the pitch could
be imaged at multiple different times, using multiple, shorter, acquisi- dramatically lower radiation requirements in cardiac
tion windows distributed across multiple contiguous beats. This data CT. In 2009, Siemens introduced an innovative scanning
can then be combined to provide 180° of attenuation data and used to
reconstruct the axial image. Temporal resolution of the image is
method using a high pitch helical mode which takes advan-
improved because the duration of the each acquisition window is tage of the dual-source design [13, 14] (Fig. 2.7). The high
shorter (Reproduced with permission of Wolters Kluwer from Vembar pitch (3.2–3.4) would normally produce gaps in the attenu-
et al. [8]) ation data using a single-source system, but, in a dual-
source system, these gaps are compensated for by gathering
One of the first was ECG-based tube current modulation, data from the second detector. Scan time is less than one
which fluctuates tube current in sync with the heart rate, second, with radiation exposures now reported less than
maintaining high tube current during diastasis and providing 1 mSv. Initial studies performed on the first-generation
the best image quality in that phase, then lowering tube cur- dual-source system proved the feasibility of the method,
rent during other phases when high-resolution detail is not though the authors noted that these first-generation sys-
required (Fig. 2.4). This results in a dose savings of tems are not suitable for this high pitch technique. High
approximately 40 %. pitch scanning with their new scanner, with faster gantry
A great advance in dose reduction was made with the rotation (250 ms) and larger coverage (96 rows), has been
advent of prospective, ECG-triggered, axial cardiac CT reported to produce very good coronary image quality with
(Fig. 2.5). By keeping the x-ray tube off during most of the radiation exposure of <1 mSv [4, 15, 16], or even lower,
scan, and only turning it on during diastasis, as triggered by with <0.1 mSv [17]. Of note, in this initial investigational
the ECG, radiation exposure is dramatically reduced. GE phase, low heart rates (<60 bpm) are absolutely required,
first published results using this method [9] with good clini- as the entire data collection takes place within a 250–
cal results and radiation doses of 1–2 mSv [10], and this 270 ms acquisition window of one heart beat; hence
2 Cardiovascular Computed Tomography: Current and Future Scanning System Design 29

Fig. 2.4 ECG-based tube current

modulation reduces radiation
exposure. Once the desired
acquisition phase is determined,
based on heart rate, in this case
75 % phase, scanning proceeds
with maintenance of 100 % tube
output during that phase, while
tube current is reduced outside of
that phase. This can reduce
effective radiation dose by 40 %
or more; however, note that
images reconstructed from the
low tube output phases (left
image) will be excessively noisy,
and are usually considered
unusable for coronary 100 %
interpretation (Reproduced with
Tube output

permission of Wolters Kluwer

from Vembar et al. [8])

20 %

Time

diastasis must be at least this long to provide motion free

data acquisition.
The GE Revolution can now utilize the new detector
and reconstruction system, along with a fast pitch algo-
rithm, to lower radiation exposure by preserving image
quality while scanning with less radiation (<1 mSv),
because images are of higher resolution and lower noise
than would otherwise be achievable with a low-exposure
scan.

Table move
Future Directions

Future scanner designs are closely guarded industry secrets,

but some concepts have been openly discussed. Flat-panel
volume CT systems replace detector rows with a large area
75 % 75 %
detector, and provide coverage of the entire heart in one
axial acquisition and extremely high spatial resolution of up
Fig. 2.5 Prospective ECG-triggered acquisition method. Cardiac to 26 lp/cm, comparable to invasive angiography [19].
rhythm is monitored while table remains stationary. When cardiac cycle However, the contrast resolution is inferior to that of multi-
reaches pre-determined acquisition phase (in this case 75 %, diastolic,
detector CT, a high radiation exposure is needed to achieve
phase), x-ray source is briefly turned on (<1 s, blue bars) and acquires
attenuation data of a length equivalent to the craniocaudal coverage of a sufficient contrast-to-noise ratio, scintillation times are
the detector array, and is then turned off. The table is advanced almost slow and temporal resolution is insufficient for cardiac
the length of craniocaudal coverage (minus a small amount of overlap), imaging.
and the process repeats again. Depending on the craniocaudal coverage
Dual energy scanning is being developed by all vendors
of the scanner, the entire heart can be scanned in 1–4 acquisitions
(Reproduced with the kind permission of Springer Science + Business by various means, including rapid fluctuation of tube energy,
Media from Weigold et al. [18]) stacked detectors, or the dual-tube design in which each tube
30 R. Nakanishi et al.

emits photons of different energy levels. Dual energy CT breakthroughs, but at the least it has the potential to enhance
could take the field to a new level of diagnostic power if it coronary lumen visualization in heavily calcified vessels by
can be used for refined tissue characterization, such as dif- differentiating calcium and iodine [20, 21] (Fig. 2.8). Dual-
ferentiating plaque characteristics. This is difficult to do in energy CT may also yield new applications for non-coronary
the coronary arteries, and initial studies have not yielded any imaging, such as imaging of myocardial perfusion [22].

a Low heart rate

Table move

75 % 75 %

b High heart rate

Table move

40 % 40 %

Fig. 2.6 Prospective CCTA phase selection and padding. Acquisition but ability to reconstruct adjacent cardiac phases is obliterated.
phase and padding depend on heart rate: For low heart rates (a), target Widening the acquisition window (“padding,” light gray shading)
late diastole (75 % phase) for prospective acquisition, but if heart rate is allows reconstruction of a small number of additional phases, which
high (b) (>75 bpm), target end-systole (40 % phase) which is more can help interpretation of motion artifact, but increases the radiation
likely to produce motion-free images. By restricting acquisition to the dose (Reproduced with the kind permission of Springer
minimum exposure window (dark gray), radiation dose is minimized, Science + Business Media from Weigold et al. [18])

83 ms

Fig. 2.7 Method of high-pitch coronary CCTA. Single source helical single heartbeat (right panel). If the image acquisition is triggered
CT requires a pitch ≤ 1.5; a faster pitch results in gaps in the data (left appropriately to synchronize acquisition with diastasis, and the heart
panel). A dual-source system can scan at a higher pitch (up to 3.2), rate is sufficiently low, motion-free images can be obtained with a very
using the second x-ray source-detector system to fill in what would oth- low radiation dose (Reproduced with permission of Elsevier from
erwise be gaps in the data. Since the table speed is so high, the entire Achenbach et al. [14])
heart can be imaged in a fraction of a second, from data derived from a
2 Cardiovascular Computed Tomography: Current and Future Scanning System Design 31

a a

c d

Fig. 2.8 Dual energy CT. Dual energy CT can be used to characterize isk) appears high-density in both images. In the subtracted image (c),
tissue: Vessel cross sectional images derived from high- (140 keV) and dense calcification has been “removed.” By adding in the low-energy
low-energy (90 keV) attenuation profiles (a and b, respectively) demon- (90 keV) attenuation data to this subtracted image, depiction of the
strate the influence of photon energy on photoattenuation. The contrast- lumen edge is enhanced (because of reduced contrast blooming), and
filled lumen (arrow) exerts greater photoattenuation on low-energy visualization of a small side branch (arrowhead) is improved (d)
photons, and hence appears brighter in (b), while calcification (aster- (Reproduced with permission of Wolters Kluwer from Boll et al. [23])

Conclusions References
Since the turn of the twenty-first century, there has been
an explosion in technological development of cardiac CT 1. Thibault JB, Sauer KD, Bouman CA, Hsieh J. A three-dimensional
systems, with concomitant gain in reliability and accu- statistical approach to improved image quality for multislice helical
racy, especially of coronary imaging. The theme has been CT. Med Phys. 2007;34:4526–44.
2. Reproduced with permission from Chandra N. CT sampling tech-
one of progressively improved spatial and temporal reso- nology [white paper]. Waukesha: GE Healthcare; 2008.
lution, reduced scan time, and, most recently, a focus on 3. Hurlock GS, Higashino H, Mochizuki T. History of cardiac com-
driving down radiation exposure. In appropriately selected puted tomography: single to 320-detector row multislice computed
patients, using careful technique, it is easily achievable to tomography [Review]. Int J Cardiovasc Imaging. 2009;25:31–42.
4. Hell MM, Bittner D, Schuhbaeck A, et al. Prospectively ECG-
perform a cardiac CT using less radiation exposure than triggered high-pitch coronary angiography with third-generation
that of a standard chest CT or an invasive coronary angio- dual-source CT at 70 kVp tube voltage: feasibility, image quality,
gram. The goal of future systems will be to make this radiation dose, and effect of iterative reconstruction. J Cardiovasc
more widely achievable in a larger group of patients with- Comput Tomogr. 2014;8:418–25.
5. Achenbach S, Ropers D, Kuettner A, et al. Contrast-enhanced
out requiring patient selection or stringent patient prep. coronary artery visualization by dual-source computed tomogra-
Given the history of rapid technological advancement, we phy – initial experience. Eur J Radiol. 2006;57:331–5.
can expect to see this goal achieved in the near future.
32 R. Nakanishi et al.

6. Achenbach S, Ropers U, Kuettner A, et al. Randomized compari- 16. Layritz C, Schmid J, Achenbach S, et al. Accuracy of pro-
son of 64-slice single- and dual-source computed tomography spectively ECG-triggered very low-dose coronary dual-source
coronary angiography for the detection of coronary artery disease. CT angiography using iterative reconstruction for the detec-
JACC Cardiovasc Imaging. 2008;1:177–86. tion of coronary artery stenosis: comparison with invasive
7. Leipsic J, Labounty TM, Hague CJ, et al. Effect of a novel vendor- catheterization. Eur Heart J Cardiovasc Imaging. 2014;15:
specific motion-correction algorithm on image quality and diag- 1238–45.
nostic accuracy in persons undergoing coronary CT angiography 17. Schuhbaeck A, Achenbach S, Layritz C, et al. Image quality of
without rate-control medications. J Cardiovasc Comput Tomogr. ultra-low radiation exposure coronary CT angiography with an
2012;6:164–71. effective dose <0.1 mSv using high-pitch spiral acquisition and raw
8. Vembar M, Walker MJ, Johnson PC. Cardiac imaging using data-based iterative reconstruction. Eur Radiol. 2013;23:
multislice computed tomography scanners: technical consider- 597–606.
ations. Coron Artery Dis. 2006;17:115–23. 18. Weigold W, Olszewski M, Walker MJ. Low-dose prospectively
9. Hsieh J, Londt J, Vass M, Li J, Tang X, Okerlund D. Step-and-shoot gated 256-slice coronary computed tomographic angiography. Int
data acquisition and reconstruction for cardiac x-ray computed J Cardiovasc Imaging. 2009;25 Suppl 2:217–30.
tomography. Med Phys. 2006;33:4236–48. 19. Gupta R, Cheung AC, Bartling SH, et al. Flat-panel volume CT:
10. Earls JP, Berman EL, Urban BA, et al. Prospectively gated trans- fundamental principles, technology, and applications.
verse coronary CT angiography versus retrospectively gated helical Radiographics. 2008;28:2009–22.
technique: improved image quality and reduced radiation dose. 20. Andreini D, Pontone G, Mushtaq S, et al. Diagnostic accuracy of
Radiology. 2008;246:742–53. rapid kilovolt peak-switching dual-energy CT coronary angiogra-
11. Hoe J, Toh KH. First experience with 320-row multidetector CT phy in patients with a high calcium score. JACC Cardiovasc
coronary angiography scanning with prospective electrocardiogram Imaging. 2015;8:746–8.
gating to reduce radiation dose. J Cardiovasc Comput Tomogr. 21. Barreto M, Schoenhagen P, Nair A, et al. Potential of dual-energy
2009;3:257–61. computed tomography to characterize atherosclerotic plaque:
12. Steigner ML, Otero HJ, Cai T, et al. Narrowing the phase window ex vivo assessment of human coronary arteries in comparison to
width in prospectively ECG-gated single heart beat 320-detector row histology. J Cardiovasc Comput Tomogr. 2008;2:234–42.
coronary CT angiography. Int J Cardiovasc Imaging. 2009;25:85–90. 22. Ruzsics B, Schwarz F, Schoepf UJ, et al. Comparison of dual-
13. Hausleiter J, Bischoff B, Hein F, et al. Feasibility of dual-source energy computed tomography of the heart with single photon emis-
cardiac CT angiography with high-pitch scan protocols. sion computed tomography for assessment of coronary artery
J Cardiovasc Comput Tomogr. 2009;3:236–42. stenosis and of the myocardial blood supply. Am J Cardiol.
14. Achenbach S, Marwan M, Schepis T, et al. High-pitch spiral acqui- 2009;104:318–26.
sition: a new scan mode for coronary CT angiography. J Cardiovasc 23. Boll DT, Hoffmann MH, Huber N, Bossert AS, Aschoff AJ, Fleiter
Comput Tomogr. 2009;3:117–21. TR. Spectral coronary multidetector computed tomography angiog-
15. Gordic S, Desbiolles L, Sedlmair M, et al. Optimizing radiation dose raphy: dual benefit by facilitating plaque characterization and
by using advanced modelled iterative reconstruction in high-pitch enhancing lumen depiction. J Comput Assist Tomogr. 2006;30(5):
coronary CT angiography. Eur Radiol. 2016;26(2):459–68. 804–11.
 Radiation Dosimetry and CT Dose
Reduction Techniques 3
Kai H. Lee

Abstract
Increasing radiation exposure to the population from widespread use of multi-row detector
CT necessitates efforts to limit the x-rays applied in CT procedures. Options are available
on CT scanners to modulate the patient dose. This chapter describes the metrics of radiation
dose, and the influence of various technical parameters in the scan and dose modulation
options on patient dose and image quality. With that information, practitioners of CT will
be better prepared to optimize the scan protocols to reduce the patient dose without sacrific-
ing the image quality necessary for interpretation.

Keywords
CT radiation metrics • Dose modulation • Scanning parameters

Introduction entific and lay journals found fewer than three million CT
examinations done in 1980, which rose to 62 million in 2007,
The ability of modern multi-detector CT scanners with and to 80 million at the end of 2014 [2–4]. Based on our
­sub-­millimeter resolution, sub-second rotation time, and large ­current knowledge of radiation biology, the deleterious effects
volume imaging has resulted in widespread use of of radiation are cumulative and medical radiation is increas-
CT. However, the widespread use of CT has also raised con- ingly a significant contributor to the amount of radiation accu-
cerns about the risks of radiation to patients. The National mulated in a person’s lifetime [5, 6]. The risk of cancer from
Council on Radiation Protection, NCRP Report No. 160, in radiation exposure is especially worrisome to children and
2006 [1] reported that radiation exposure to the United States young women who received multiple CT examinations early
population due to medical sources increased more than seven in their life. For example, studies found that one CT examina-
times in the 20 years between 1986 and 2006. According to tion of the female chest gives as much radiation as 10 mam-
the NCRP report, CT constituted about 10 % of the diagnostic mograms to each breast [7]. In addition to radiation from CT,
examinations that utilize x-rays in 2006, it contributed to cardiac patients may be exposed to radiation from nuclear
nearly 50 % of the population dose. The use of CT continued medicine perfusion studies and coronary angiography.
to rise since publication of NCRP Report 160. Reports in sci- Therefore, the practitioners of CT must be constantly aware
of the risks of radiation, and strive toward applying the lowest
dose to the patient consistent with the clinical study.
One of the difficulties confronting the clinicians when
evaluating the radiation safety of a CT procedure is the pleth-
ora of terms used to quantify the amount of radiation given to
K.H. Lee, PhD the patient. Thus, this chapter sets out on two aims. The first
Associate Professor of Clinical Radiology, aim is to explain the fundamental concepts of radiation
Department of Radiology, Keck School of Medicine,
University of Southern California, dosimetry associated with CT scans. The second aim is to
1200 North State Street, Los Angeles, CA 90033, USA describe the scanning techniques and available technologies
e-mail: [email protected] to reduce radiation dose to patients.
© Springer International Publishing 2016 33
M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_3
34 K.H. Lee

Fundamentals of Radiation Dosimetry Table 3.1 Biological damage weighting factors

Type of radiation Weighting factor
Absorbed Dose X- and gamma rays, electrons, positrons 1
Protons 2
The damaging health effects of radiation are commonly Neutrons 10
called radiation effects. Our current knowledge of radiation Alpha particles 20
effects was derived from animal studies, atom bomb
survivors, and victims of radiation accidents [6]. There were
many contributing factors to the observed radiation effects, milli-Sievert equals to one thousandth of a Sievert. The
but the outcomes ultimately depended on the amount of equivalent dose in mSv is calculated by multiplying the
radiation received. The radiation dose, or dose in short, is radiation absorbed dose D in mGy by a quality factor Q, also
the amount of energy deposited by the ionizing radiation per called the biological damage weighting factor Wr [9], for the
unit mass of tissue. Radiation dosimetry is the field of study type of radiation absorbed in tissue, i.e.,
which measures and quantifies the radiation dose. Of the
H ( mSv ) = D ( mGy ) ´ Wr .
bewildering number of terms to quantify radiation dose,
there are three related terms fundamental to radiation
protection. The three terms are the absorbed dose, the The biological damage weighting factors for four types of
equivalent dose, and the effective dose. radiation are given in Table 3.1.
The International System (SI units) of radiation dose The values of Wr are proportional to the density of ioniza-
measurements is the Gray [8]. One Gray (Gy) of radiation is tion created by the incident radiation along its path of travel
defined as 1 J of energy deposited in 1 kg of tissue, i.e., in tissue. For x-rays, gamma rays, beta particles, and elec-
trons from radioactive materials, the density of ionization
1 joule
Dose( Gy ) = created in tissue is relatively low. The weighting factor Wr
1 kg tissue. equals 1. Thus, when working with x-rays from CT, the
equivalent dose and absorbed dose are numerically equal,
The Gray is a large dose of radiation. When evaluating i.e., 1 mSv = 1 mGy. For neutrons, the weighting factor
radiation dose from CT examinations, a sub-unit of the Gray Wr = 10. The equivalent dose for 1 mGy of neutron absorbed
is used. The Gray sub-unit commonly used to quantify dose equals
radiation dose from CT examinations is the milli-Gray
H( mSv ) = 1( mGy ) × 10
(mGy). One mGy is one thousandth of a Gray. That is,
= 10 mSv.
1 mGy = 10-3 Gy.
The above example shows that neutrons are ten times more
damaging to the human body than x-rays for the same
Equivalent Dose absorbed dose.
In summary, the absorbed dose in mGy is the quantity of
The severity of biological damage depends not only on the radiation energy deposited per unit mass of tissue. The
dose of radiation absorbed in tissue, but also on the type of equivalent dose in mSv is a measure of biological damage
radiation absorbed. For example, 1 mGy of neutron radia- equal to the absorbed dose modified by a weighting factor
tion produces far greater tissue damages than 1 mGy of according the relative effectiveness of the absorbed radiation
x-rays. We therefore need a unit of measurement that to produce biological damage.
accounts for both the quantity of radiation absorbed in the Given this metric to quantify radiation, Table 3.2 lists
tissues and the effectiveness of the absorbed radiation in the average equivalent dose received annually to the
producing biological damages. The equivalent dose was total body by workers in various occupations [10–13].
devised to incorporate both the physical factors and the The table also gives the natural background radiation
effectiveness of the absorbed radiation in producing bio- and the regulatory limits on radiation exposure for ref-
logical damage. The equivalent dose is a biological scale for erence. It is interesting to note that the transcontinental
measuring the deleterious health effects of radiation. The flight crews who are not classified as occupational radi-
same biological damage is expected for the same equivalent ation workers receive an annual equivalent dose from
dose regardless of the type of radiation absorbed in tissue. the cosmic rays higher than the nuclear medicine tech-
The equivalent dose (H) is measured in Sievert (Sv). nologists who routinely handle radioactive materials on
A sub-unit of Sievert is the milli-Sievert (mSv). One the job.
3 Radiation Dosimetry and CT Dose Reduction Techniques 35

Table 3.2 Typical annual whole-body radiation dose Table 3.3 Tissue/organ sensitivity
mSv Tissue/organ Weighting factor, Wr
Nuclear medicine technologists 1.7 Gonads 0.20
Airline flight crews between Los Angeles and 2.2 Bone marrow, colon, lung, stomach 0.12
New York City Bladder, breast, liver, esophagus, thyroid 0.05
Nuclear power plant workers 2.3 Skin, bone surface 0.01
Intervention radiologists 18
Cardiologists (catheterization) 16
Natural background radiation at sea level 2.5 The effective dose translates a partial body exposure to an
Regulatory limit on the occupational workers 50 equivalent uniform dose of radiation delivered to the total
Regulatory limit on the general public 1 body. The purpose for calculating the effective dose is to pro-
vide a common denominator for the assessment of stochastic
risks using our database of whole-body exposures. Unlike
Radiation Effects to the Patient the absorbed dose and the equivalent dose, the effective dose
is not a physically measurable quantity. The effective dose is
The goal of protecting patients undergoing radiological pro- an imaginary total body dose. It is calculated from the
cedures is to prevent the occurrence of deterministic effects, absorbed dose given to any region or regions of the body.
and to minimize the risk of stochastic effects. Deterministic If we wish to estimate the stochastic risks from CT of the
effects are radiation induced somatic injuries. Examples of chest, we must translate the partial body irradiation to an
radiation induced somatic injuries are skin erythema, epila- equivalent whole-body dose in order to utilize the database
tion, and cataracts. The FDA has documented severe deter- for risk estimates. To do so, a mathematical model is used to
ministic effects such as hair loss and skin necrosis on patients compute the doses to other organs resulting from radiation
from CT and prolonged fluoroscopy guided procedures. scattered from CT of the chest. These computed organ doses
Deterministic effects are preventable. There is ample clinical are then multiplied by a risk factor according to the suscepti-
evidence of threshold doses below which such effects are not bility of each organ to radiation. Summation of the product
seen. Once the threshold dose is reached, severity of the of these computed organ doses and their associated risk
injury increases with the radiation dose. weighting factor is called the effective dose. That is, the
Stochastic risks are probabilistic occurrences of carcino- effective dose E is computed using the equation
genesis and genetic mutations. The current concept of sto-
E = ∑ Hi wi
chastic risks assumes no threshold dose for its occurrence.
Exposure to any amount of ionizing radiation is harmful. The
probability of the occurrence of stochastic effects, rather Where E is the effective dose
than its severity, increases in direct proportion to the radia- Hi is the dose equivalent to a given organ
tion absorbed dose. This is in contrast to deterministic effects wi is the risk weighting factor for that organ.
in which the severity increases as the dose increases above
the threshold. This concept of stochastic risks is called linear The effective dose is thus a weighted sum of the com-
no threshold model, and is the basis of radiation protection puted equivalent doses to all organs in the body. Table 3.3 is
regulations. a partial list of weighting factors for different body organs
published in the International Commission on Radiation
Protection Report 103 [14].
Effective Dose One may interpret the effective dose as a calculated
equivalent dose of radiation given to the entire body that
Our knowledge of stochastic risks is based on data collected would be required to produce the same risk of cancer and
from total body exposure to radiation. If we wish to estimate genetic damage as a dose of radiation delivered to a localized
the stochastic risks to a person after a partial body exposure region of the body, such as in a CT examination. In other
such as a chest CT, we must translate the chest CT dose to an words, the risk from a part of the body exposed to a given
equivalent whole-body dose in order to utilize the database dose of radiation is the same as the total body uniformly
for risk estimates. The effective dose was devised for this receiving the effective dose. The effective dose is an extrapo-
purpose. The effective dose is the dose of radiation that when lated whole-body dose from a partial body dose. As such, the
given uniformly to the whole-body will produce the same effective dose is a computed value rather than a physically
stochastic risk as the dose of radiation delivered to only a part measurable quantity. The effective dose is calculated to serve
of the body, such as the chest dose from a cardiac CT study. as a common denominator for comparing stochastic risks
36 K.H. Lee

between different medical or non-medical exposures to where CTDIw is the weighted average of CTDI100 in the phan-
radiation. Now that we understand the concept of the
­ tom. The constant 0.87 is a conversion factor to relate dose
absorbed dose, equivalent dose, and effective dose, the next measured in air to dose in soft tissues. The CTDIw is inter-
step is to learn how to calculate the effective dose from CT. preted as the average absorbed dose in the cross section of the
phantom being measured. The CTDIw is not the dose to the
patient [19]. It is an index of the amount of x-rays used in a
CT Dosimetry CT examination expressed in terms of a dose to a phantom.
CTDIw was developed during the infancy of CT scanners
CT Dose Metrics in the 1970s, when patients were scanned sequentially
section by section. This mode of operation is called axial
Special dosimetric techniques had to be developed for scan. In an axial scan, the x-ray tube rotates 360° around the
measuring CT doses because the geometry of the x-ray field patient to measure x-rays transmitted through the patient one
in CT scans is very different from conventional radiographic cross section at a time. The x-ray tube in the early models of
or fluoroscopic exposures. The fundamental metric developed CT scanners had to rewind upon completing each rotation to
for CT dosimetry is the Computed Tomography Dose untangle the electrical cables. While the x-ray tube was
Index (CTDI). From the CTDI, the dose-length product returning to the starting position, the table advanced the
(DLP) is calculated, and is in turn used to derive the effective patient to the next section to scan. There was no data
dose (E) for risk comparison [15–18]. acquisition while the patient table was in motion. Axial scans
followed a “scan-stop-scan” pattern. The advent of slip ring
technology in the early 1990s enabled the development of
CTDI helical CT scanners. Slip rings are electro-mechanical
devices for providing electrical power to the generator, x-ray
The CTDI, or specifically the CTDI100, is measured using a tube, x-ray detectors, and computers on the gantry from the
dosimeter of 100 mm length in a cylindrical acrylic phantom power source in the building. The rotating x-ray tube,
of 16-cm diameter to simulate a head, or 32-cm diameter to generator, x-ray detectors, and computers draw power from
simulate the body (Fig. 3.1). the slip rings much like electric street cars draw power from
Four measurements are made in the periphery and one in the stationary overhead cables. The slip rings enable the
the center of the phantom. The four peripheral measurements gantry assembly to rotate continuously for data acquisition
and the central measurement are used to compute the without having to rewind and pause after each rotation to
weighted average of the CTDI100 in the phantom as follows: untwist the cables, thus eliminating the inter-scan delay and
shortening the total examination time.
100 (
 2 / 3 CTDI periphery )  In a helical scan, the table translates the patient
CTDI w = 0.87 *  ,
 +1 / 3 CTDI100 ( center )  continuously through the gantry during rotation of the x-ray
tube and detectors. The scanning motion is called a helical
because the x-ray beam paints a spiral or helical pattern
around the patient as shown in Fig. 3.2.
The relative motion of the x-ray beam and the patient
table is described by the term pitch. Pitch is a dimensionless
unit equal to the distance the table moved in one rotation of
the x-ray tube divided by the width of the x-ray beam at the
axis of rotation. That is,
Distance moved by patient table in one tube rotation
Pitch =
X − ray beam width at axis of rotation.

The higher the pitch, the faster the patient translates through
the gantry, and the greater is the distance of separation
between two loops of the x-ray beam. We need a good grasp
of the concept of pitch because pitch has a strong influence on
Fig. 3.1 A typical setup of the dosimeter, ionization chamber, and the image resolution, noise, and patient dose. In an axial scan,
16-cm diameter acrylic phantom for measuring the CTDI of the head.
There are 4 holes 1 cm from the surface, and one hole in the center of
there is no table motion so the pitch equals zero. For helical
the phantom for insertion of the ionization chamber for dose scans with pitch equals to 1, the patient moved a distance in
measurements one rotation of the x-ray tube equal to the width of the x-ray
3 Radiation Dosimetry and CT Dose Reduction Techniques 37

Fig. 3.2 The x-ray beam traces a

helical pattern on the patient with
the x-ray tube rotating while the
patient table translates through
the gantry at the same time

Pitch = 0 Pitch = 1 Pitch > 1 Pitch < 1

Fig. 3.3 In an axial scan, there is no table motion during tube rotation beam leaves a gap between rotations. With a pitch < 1, the x-ray beam
and the pitch = 0. With a pitch = 1, the loops of x-ray beam are contigu- overlaps between rotations
ous and abutting each other with each rotation. With a pitch > 1, the

beam. The borders of the x-ray beams abut each other in total amount of x-ray energy deposit in the scan volume.
­successive rotations. If the table moves a distance greater DLP is defined as:
than the width of the x-ray beam in one rotation, the pitch is
DLP = CTDI vol ´ scan length.
greater than 1. There is a gap between two loops of the x-ray
beam when scanning with a pitch greater than 1. In scans with DLP is an important risk indicator because radiation risks
a pitch less than 1, the patient table moves a distance less than depend not only on the quantity and type of radiation given,
the width of the x-ray beam, and the x-ray beam overlaps in but on the volume of tissue irradiated as well. For example, a
successive loops. The x-ray beam pattern on the patient for radiation oncologist could deliver 70 Gy (70,000 mGy) of
different values of pitch is illustrated in Fig. 3.3. x-rays to a small region surrounding the prostate gland to
With the development of helical CT, the CTDIw was mod- cure a patient with prostate cancer. If 70 Gy was delivered
ified to account for variable overlaps in the spiral path of the over the entire body, the person will most certainly die. For
x-ray beam in helical scans. The currently used index of the same dose of radiation the deleterious effects increase
radiation dose to the patient is the CTDIvol. The CTDIvol is with the volume of tissue irradiated. The CTDIvol is an index
calculated by dividing the CTDIw by the pitch, i.e., of the average amount of x-ray energy deposited per unit
mass of tissue. It does not provide information regarding the
CTDI vol = CTDI w / pitch.
total amount of radiation energy deposited or the volume of
As shown in the above equation, CTDIvol is inversely tissue irradiated. The value of CTDIvol is unchanged whether
proportional to the pitch. A higher pitch leads to a lower the the scan length is 1 cm or 100 cm, but the volume of tissue
CTDIvol, as there is less overlapping of the x-ray beam in the irradiated and the biological effects from the exposure would
scan volume. be quite different. Because it is difficult to measure the mass
of tissue irradiated in a CT scan, the CTDIvol is multiplied by
the scan length to obtain the DLP as an indirect measure of
Dose-Length Product the irradiated volume and the total amount of x-ray energy
deposited in the patient. The two descriptors of CT dosimetry,
One final measurable dosimetric parameter for CT is the CTDIvol and DLP, are widely used as indices of the amount
dose-length product (DLP). The DLP is proportional to the of x-rays utilized for a CT scan, the volume of tissue exposed
38 K.H. Lee

to radiation, and the total amount of energy deposited in the cylindrical methylmethacrylate (trade names: Acrylic,
scan volume. Because CTDIvol and DLP are such important Lucite, Plexiglas) phantom. The dose metric was later refined
indicators of the risks, the values of CTDIvol and DLP are to account for helical scans. The CTDIvol as utilized today
displayed on the control console in all CT systems manufac- offers a standardized method to conveniently characterize
tured since year 2000. the x-ray output of a CT scanner for a given CT examination.
Because the CTDIvol is highly reproducible and can be easily
measured with high degrees of consistency, it is widely used
The Effective Dose from CT as an index to compare the amount of x-rays used for differ-
ent scan protocols, and even for comparing scanners made
The effective dose is not a measured dose, but can be by different manufacturers. However, many users misinter-
calculated from the DLP using a simple formula developed preted the CTDIvol as the radiation dose the patient received
by the ICRP [20, 21]. The effective dose is conveniently [19]. The misinterpretation can be traced to the CTDIvol and
calculated by multiplying the DLP by the corresponding DLP being shown on the computer console as soon as a scan
conversion factor shown in Table 3.4, i.e., protocol is selected for the patient to be scanned, and some
state laws require the two indices be recorded in the patient’s
E ( mSv ) = DLP ´ CF
examination report. An astute user may notice that the values
of CTDIvol and DLP are unchanged so long as the technical
where CF is the conversion factor for the corresponding CT parameters for the scan protocol remain the same regardless
procedure. of the size of patient placed on the table and the section of
By using the CTDIvol, DLP, and conversion factors in the body to be scanned. The CTDIvol is only an index of the
Table 3.4, some typical values of the effective dose from x-ray output for a given scan protocol, not the actual dose to
different CT procedures are shown in Table 3.5. The effective the patient.
doses from other radiologic examinations are also shown in The conversion factors applied to the DLP to calculate the
the table for comparison [22, 23]. effective dose were based on a mathematical model of a
standard man of 70 kg. If the conversion factors were applied
to a patient having a body mass index very different from
Uses and Misuses of CTDIVOL that of a standard man, the calculated effective dose can be
very different. For pediatrics there are separate tables of
The CTDI was originally developed to quantify the x-rays conversion factors for different age groups to account for
used for an axial CT scan in terms of radiation dose to a differences in their body sizes [24]. If the body sizes and
other related parameters are carefully adjusted, the calculated
Table 3.4 CT effective dose conversion factors effective dose serves as a useful metric to compare the
relative risks of different scan protocols and different imaging
Region of body Conversion factor
modalities utilizing ionizing radiation. For example, this
Head 0.0021
metric allows comparison of the relative risks of radionuclide
Neck 0.0059
perfusion studies with cardiac CT angiography. The effective
Chest 0.0140
doses that the patient received from other imaging modalities
Abdomen 0.0150
can also be added together for assessment of stochastic risks.
Pelvis 0.0150

Table 3.5 Typical effective doses of radiological examinations Updating the CTDIVOL
Radiologic examination Typical effective dose (mSv)
Head/neck CT 2–5 The CTDI was developed when CT scans were performed
Chest CT 5–7 using a narrow beam of x-rays to scan the patient axially one
Abdomen/pelvis CT 3–7 slice at a time. CT technologies and its applications have
Coronary CT angiogram 5–15 since advanced far beyond the scan pattern on which the
Coronary bi-plane angiogram 3–10 CTDI was developed 30 years ago. For example, a 320-row
MIBI cardiac stress/rest per 1.3 GBq 10.6 CT scanner has an axial scan length of 160 mm. The 100 mm
PA chest x-ray 0.02 length ionization chamber used to measure the CTDIvol is too
Skull x-ray 0.07 short even to intercept the x-ray field from edge to edge,
Lumbar spine 1.3 much less the tail ends of the beam in adjacent sections. The
I.V. urogram 2.5 assumption that all the primary and scattered x-rays were
Upper GI 3.0 collected by the ionization chamber is clearly not valid for
3 Radiation Dosimetry and CT Dose Reduction Techniques 39

the large cone beam and multi-row CT systems. The latest applied to it. Using a lower tube voltage would result in
proposed paradigm adopts the dosimetric techniques utilized applying less x-rays to the patient for the study, however
in radiation oncology to measure the equilibrium dose as an there are negative aspects of using lower kV x-rays. Use of a
index of the x-ray output from a CT scan [25, 26]. The equi- lower tube voltage must take in consideration of the patient’s
librium dose methodology can be used to quantify x-ray out- body mass to counter the potential negative effects on image
put for axial, helical, narrow or broad beam scanning in air or quality. One of the negative effects is the increase in image
in phantom with or without table translation. Perhaps due to noise and reduction of the soft tissue image contrast due to
its drastic departure from the CTDIvol concept and lack of a less x-rays passing through the patient. In fact, applying
standardized procedure to measure the equilibrium dose, the lower kV x-rays to a large patient could actually increase the
new metric has not gained wide acceptance to replace the patient dose. The reason is because low energy x-rays are
conventional CTDIvol as an index of the x-ray output from more easily absorbed in the patient and unable to reach the
CT scans. image receptor. The user then applies a higher beam current
or a longer scan time to compensate for the reduced
transmission of x-rays to the detectors in order to keep the
Methods to Reduce CT Dose image noise to an acceptable level. This results in negating
the dose reduction benefits of using lower kV. With that
Dose Reduction Techniques caution in mind, several studies reported that for coronary
CT angiography of patients weighing 185 lb or less, reducing
A number of studies reported that radiation dose from CT the voltage from 120 to 100 kV reduces the effective dose by
examinations can be reduced by more than 50 % simply by 30–40 % to the range 5–12 mSv from 9 to 17 mSv without
modifying the basic technical parameters in the scanning degrading the diagnostic accuracy [27–32]. Other studies
protocols [27–31]. The parameters selectable by the users for have shown that for thin patients, the tube voltage can be
dose reduction include the scan length, x-ray tube voltage, further reduced to 80 KV with a dose savings as high as 80 %
x-ray tube current, acquisition thickness, pitch, ECG gating, [33, 34]. The above studies demonstrated that considerable
and image reconstruction algorithms. dose savings can be achieved with overall preservation of
image quality when tube voltage reduction is matched with
the size of the patient.
Limiting the Scan Length Reducing the tube voltage for CT angiography has a
bonus advantage in addition to lowering the patient dose.
Users have the tendency to liberally scan beyond the region Contrast agents have higher probability of interaction with
of interest just to be sure nothing is missed. However, the low energy x-rays by photoelectric effect. Arterial vessels
effective dose to a patient is proportional to the dose-length-­ containing contrast agent attenuate the x-rays more strongly
product DLP which in turn is proportional to the craniocaudal and show up with higher contrast against the soft tissue
length being scanned. Hence, it is essential to establish background in spite of more noise in the overall image.
scanning protocols to limit the scan length to include only
the region of interest. A study [32] reported use of the scan
for calcium score as a guide to determine the minimum scan Modulating the Tube Current and Time
length for the individual patient in CT angiography studies. Product
Prior to CT angiography, the patient was given a pre-scan
using the calcium score protocol. The beginning of the scan Radiation dose to the patient is directly proportional to the
was determined from the calcium score images at 1 cm above product of the tube current measured in mA and the tube
the visualized most cranial aspect of the coronary arteries rotation time in seconds (mAs). While options for varying
and the end of the scan at 1 cm below the posterior descending the tube rotation time are limited for cardiac CT, there is
artery. The dose savings from limiting the scan length more great latitude in the choice of tube current. Similar to
than offsetting the dose from the calcium score scan. The reducing the tube voltage, there is a delicate balance between
effective dose was reported to be reduced by as much as the desire to lower the mA for dose reduction, and the need
30 %. to apply sufficient mA to keep the subsequent increase in
image noise from interfering with clinical interpretation.
When the mA is reduced, the intensity of the x-ray beam
Reducing the Tube Voltage passing through the patient is lessened, resulting in decreased
patient dose. Reducing the mA has the undesirable effect of
The intensity of x-rays emitted from an x-ray tube is approx- increasing the image noise and reducing the overall quality
imately proportional to the square of the kilovoltage (kV) of the images because less x-rays, and therefore less data, are
40 K.H. Lee

received by the detectors to reconstruct the images. The dose modulation options are described in greater detail here
question becomes one of deciding the optimum mA to because the operator has to make a selection when setting up
minimize dose to the patient without compromising the a scan.
image quality for accurate diagnosis. Answer to this question
depends on the comfort level of the interpreting physician to
image noise, and this subjectivity obviously varies from AEC Guided by Image Noise
physician to physician.
CT manufacturers responded to this question by Image noise can be described qualitatively as graininess of
incorporating dose modulation options into their system to the image. Low noise images appear smooth with continu-
assist the users in making the trade-off between the patient ous shades of gray from the darkest to the lightest portions
dose and image quality. The dose modulation options in of the image. High noise images show characteristic salt
various trade names are actually different implementations and pepper grains interspersed through out the image.
of the automatic exposure control (AEC) technique that has Resolution of low contrast objects can be greatly impaired
been in use for decades in fluoroscopy and radiography. In a by image noise. Image noise is influenced by a number of
nutshell, AEC controls dose to the patient by modulating the factors, but is most strongly influenced by the number of
x-ray beam intensity according to the patient’s anatomy to x-ray photons that contribute to the image. A simple way to
produce the desired image quality. The intensity of the x-ray quantify noise in an image is to calculate the percentage
beam emitted from the x-ray tube and subsequently sent standard deviation. The standard deviation of an image is
through the patient is directly proportional to the mA across the square root of the total number of counts or dots that
the tube. By modulating the electron current mA according make up the image. The resulting standard deviation is then
to the thickness of tissues that the x-ray beam must pass divided by the total counts in the image to arrive at the per-
through, the desired image quality can be maintained without centage standard deviation. The standard deviation of the
imparting unnecessary radiation to the patient. For example, number of counts in an image is a measure of noise in the
the CT scanner could automatically raise the mA to produce image. The percentage standard deviation as computed by
a more intense x-ray beam to pass through the abdomen, and the ratio of the standard deviation to the total number of
reduce qthe mA to produce a less intense x-ray beam to pass counts in the image indicates what fraction of the image is
through the lungs. occupied by noise.
There are three conditions under which the AEC can be The number of counts in a given CT image is directly
called upon to modulate the tube current (mA) to produce the proportional to the number of x-ray photons available for
desire image quality, and in the process reduce unnecessary image formation, which in turn depends on the intensity of
radiation to the patient. First, the AEC could be programmed the x-ray beam passing through the patient to strike the
to adjust the mA along the long axis of the patient so that the detectors, and the length of time the x-ray beam is on. The
mA is reduced when the x-ray beam passes through large AEC modulates the beam intensity by varying the tube
volume of air in the thorax, and is raised when the beam goes current. The exposure time is determined by the speed of the
through the more attenuating soft tissues in the abdomen and x-ray tube to make one rotation around the patient. The
pelvis. Second, the mA is adjusted in the transverse plane of product of the tube current in mA and the rotation time in
the patient according to the tube angle during its rotation seconds is commonly called the mAs. The mAs selected for
around the patient. That is, the mA is reduced when the x-ray a CT scan determines the number of x-ray photons striking
beam is passing through the patient in the thinner AP and PA the patient. The higher the mAs, the greater the number of
directions, and increased in the thicker lateral directions. photons available to pass through the patient to reach the
Third, the overall tube current is adjusted according to the detectors, and lower is the noise in the reconstructed images.
patient’s size such that a lower mA would be used on When all the other technical factors are held constant, the
pediatric than adult patients, and on the thinner than heavy image noise is inversely proportional to the square root of the
set patients. mAs, i.e.,
There are three general methods by which manufacturers
use in their dose reduction options [35, 36], each with their Noise ~ 1 / Ö mAs
advantages and disadvantages. Implementation of the dose
reduction option changes frequently in keeping with the state During CT scans, the tube rotation time is fixed. The image
of technology, but the principles behind the methodology noise guided AEC continually adjusts the mAs by adjusting
remain essentially the same. The three common dose the mA to maintain the same number of photons reaching
modulation algorithms employed by manufacturers of CT the detectors, and hence keeping the image noise at a
scanners are AEC guided by image noise, AEC guided by pre-­selected level. For example, the AEC can reduce the
reference image, and AEC guided by reference mAs. The mA when the beam is passing through in the thinner
3 Radiation Dosimetry and CT Dose Reduction Techniques 41

anterior-­posterior direction of the patient, and increases the on a scout view of the patient being scanned, the AEC adjusts
mA when passing through laterally. the tube current at each tube position to compensate for the
CT users have great flexibility in patient dose optimization difference in attenuation between the actual and reference
by providing the AEC a target image noise appropriate for patients. The image noise is not maintained for different
the particular CT procedure. The disadvantage is that the patient size. The technique relies on the experience of the
user may select a target noise level lower than necessary to user to select the proper level of tube current modulation for
obtain the diagnostic information, and results in giving a given patient and CT procedure.
unnecessary dose to the patient. A simple rule to remember
is that reducing the mAs and hence the patient dose by a
factor of 4, increases the image noise only by a factor of 2. Prospective Gating

The most dramatic reduction of dose was reported by using

AEC Guided by Reference Image the prospective gating technique in combination with tube
voltage reduction [27, 37, 38]. Prospective gating is a dose
This method of AEC is an extension of the constant image modulation technique guided by the patient’s ECG. It is also
noise algorithm. Here, the target image noise is set on the known as the ECG guided step-and-shoot technique. The
AEC using a clinical image that is selected by the reader as technique is based on the finding that the least amount of
of adequate quality for the given CT procedure. During motion artifacts were found in the images reconstructed from
scanning, the mA is adjusted at each tube position by the data in the ventricular diastolic phase. The AEC raises the
AEC to yield an image noise approximating the noise level x-ray intensity to a high level during mid-diastole to acquire
in the reference image. The advantage of the reference image the image data, and reduces to a low level during the other
approach is that the target image noise is derived from a phases of the cardiac cycle.
database of clinical images rather than some abstract To implement the prospective gating technique, the x-ray
percentage standard deviation. The major disadvantage of tube current and consequently the x-ray beam intensity is
the reference image approach is the user inclination to select modulated by the ECG tracings to synchronize with the
the a more aesthetic image as the reference image even patient’s cardiac cycle. Signals from the ECG monitor trigger
though a less visually appealing image will suffice. This the tube current to increase for data acquisition during
approach results in application more radiation to the patient diastole, and drop down when data is not acquired during the
than is necessary for diagnostic images. systolic and early diastolic phases. During the quiescent
period with no data acquisition, the table steps to the next
position to prepare for scanning. The heart is thus scanned
AEC Guided by Reference mAs sequentially in a step-and-shoot fashion as shown in Fig. 3.4.
Immediately before the scan, a sample of the ECG traces
This approach uses the mAs of a reference patient as a guide is taken to measure the average R-R time interval. When the
to modulate the mA for the actual patient. For a given CT CT is set to scan, the computer sets the clock to zero upon
procedure, a certain mAs that was found to produce images receiving an R-wave from the ECG monitor. The R-wave
of acceptable quality on a reference patient is used as the simultaneously triggers the AEC system to reduce the tube
standard of reference. From the attenuation profiles measured current to a low value until, for example, after 70–80 % of

Prospective Gating Technique

Low High Low High Low High Low High

Delay Table Moves Delay

0 70 80 0 70 80
Percent R-R Interval

Fig. 3.4 In prospective gating, the ECG signals of the patient modulate the x-ray beam intensity to high levels only for a short duration in the R-R
interval
42 K.H. Lee

the cardiac cycle has elapsed. After this initial delay, the tube contributing information to the slice images. In other words,
current is raised to a high level and maintains the high output the ­acquisition protocol used only one third of the applied
for the next 10–20 % of the cardiac cycle, corresponding to x-rays for imaging; whereas two thirds were wasted and
the time during which the heart is in the diastolic phase. At contributed unnecessary radiation to the patient. If the pro-
the 80–90 % mark that approximates the end of the diastolic tocol is set to acquire 4 slices of 1 mm wide (4 × 1) with the
phase, the system returns the tube current to the minimum same 2 mm over-scan beyond the first and the fourth row of
and stops data acquisition. The time marker is reset to zero detectors. With the slice thickness increased to 1 mm, 56 %
upon receiving the next R-wave. While the x-ray beam is at of the x-rays were used for imaging; therefore the amount
the low level, the table moves the patient to the next scanning of wasted x-rays was reduced to 44 %. This example shows
position. This step-and-shoot cycle repeats until the scan that thick slice acquisition should be used whenever possible
length is completed. By turning the x-ray beam intensity to to make over-beaming a smaller proportion of the applied
high during 10–20 % of the cardiac cycle for data acquisition, x-rays. Another reason for giving preference to thick slice
the patient dose was reported to reduce by 50–70 % in acquisition is that the x-ray intensity or imaging time must
comparison with the retrospective gating which requires the be increased to provide a sufficient number of photons for
x-ray beam on the high level continuously for the entire the reconstruction of thin slice images to keep image noise at
scan length [39]. acceptable levels. In the interest of reducing radiation to the
patient, the slice thickness should be chosen consistent with
the axial resolution required for diagnosis; therefore thinner
Slice Thickness and Patient Dose slices are not always better.

Unlike single slice scanners in which the x-ray beam is com-

pletely intercepted by the detectors, multi-slice scanners Pitch and Patient Dose
extend the x-ray beam beyond the rows of detectors in the
axial direction. The geometry in which the x-ray beam opens The pitch has an inverse relationship with the patient dose, as
beyond the active rows of detectors is called over-beaming a higher the pitch lowers the patient dose [38, 40, 41]. If
[38, 40]. Over-beaming is needed for multi-slice scanners to scans were performed using a pitch greater than 1, x-rays
ensure each row of detectors is exposed to uniform intensity sweep around the patient with gaps between successive loops
of x-rays to minimize helical artifacts. Unfortunately, the of the beam. Because less tissue is exposed to x-rays, dose to
over-beam geometry exposes patients to x-rays not used for the patient is lower. There are many advantages to using high
image formation. In general, the x-ray over beams the lead- pitch in order to lower patient dose. High pitch allows greater
ing row of detectors by about 2 mm and the trailing row by volume coverage in less time. Short scan time is obviously
2 mm. Figure 3.5 shows how over-beam gives higher dose to desirable for pediatric and trauma patients. High pitch is also
the patient from thin than thick slice imaging. If the scanner desirable in CT angiography to ensure capture of the first
is set to acquire 4 slices of 0.5 mm thickness (4 × 0.5), the pass of the contrast agent through the vessels. The
x-ray beam over scans the first row of detectors by 2 mm disadvantages of high pitch are higher image noise, poorer
and the last row by 2 mm. From a pure geometric consid- image resolution, and appearance of helical artifacts due to
eration, only a 2 mm strip of the x-ray beam is used for fewer photons in the images. Conversely, for scans performed
imaging, while the other 4 mm exposed the patient without with a pitch less than 1, the table moves the patient slowly

Over-beam Over-beam Over-beam

Fig. 3.5 For thin slice

acquisition with narrow
collimation, over-beaming causes
a greater fraction of the x-ray
beam to irradiate the patient
without contributing to the image 4 × 0.5 mm 4 × 1.0 mm
3 Radiation Dosimetry and CT Dose Reduction Techniques 43

through the gantry. Dose to the patient is higher due to In addition, the pitch may be increased from 0.2 to 0.46 for
redundant exposure from the x-ray beam overlapping in
­ higher heart rates to effect dose reduction of as much as
­successive rotations around the patient. Coronary angiogra- 50 %, because the dose is inversely proportional to the pitch
phy requires low pitch for high image resolution and low [45, 46].
noise. In this case, the patient table traverses slowly through
the gantry at incremental distances less than the width of the
x-ray beam in each gantry rotation. Redundant exposure Iterative Reconstruction
reduces image noise and increases the low contrast resolu-
tion but gives higher dose to the patient. Recent advances in CT image reconstruction by iterative algorithm is not new.
CT technology mitigate some of the issues with patient dose Until recently, though, filtered backprojection was the
in coronary CT angiography. algorithm of choice. The advantage of filtered backprojec-
tion is the rapidity with which images can be reconstructed
without elaborate computers. The reconstructed images
Recent Advances in Cardiac CT suffer, however, from problems such as amplification of
noise, beam hardening, scatter, streaks, and ring artifacts.
Expanding Rows of Detectors Noise imbedded in the data amplifies by the backprojection
algorithm during reconstruction and becomes a limiting
Development of MSCT scanners beyond 64 rows of detec- factor on patient dose reduction by methods described
tors to 128, 256 and 320 rows brought drastic changes to above. As the number of photons, the amount of x-rays
cardiovascular imaging techniques and lowering radiation used to make up the image, decreases, image noise
dose to the patient. Of particular interest to cardiologists is increases. Dose reduction becomes limited when noise
the introduction of 320-detector row CT. When using a tradi- begins to interfere with visualization of the image details.
tional 64-row scanner for coronary CT angiography, about Iterative reconstruction algorithms overcome many of the
4 cm is covered with each tube rotation. A complete scan of shortcomings of the filtered backprojection methods [47,
the heart would require a minimum of 4 gantry rotations. The 48]. Iterative reconstruction starts with a filtered backpro-
320-slice CT with a 16 cm axial view could scan the entire jection image. The projection profiles of the backprojection
heart in one rotation. It obviates helical scans, table indexing, image are next computed and compared with the actual
and artifacts in images reconstructed from data acquired over projection profiles measured during the CT scan. Various
several cardiac cycles. Dose savings are realized due to no correction methods are then applied to correct discrepan-
overlapping helical scans and less over-­beam dose. When cies between the computed and the measured projection
used in combination with kV reduction, prospective gating, profiles. The corrected projection profiles are placed back
elimination of scan overlaps, and minimization of over- to reconstruct a new image. The comparison, correction,
beaming, the patient dose can be reduced up to 90 % com- and reconstruction processes repeat in loops until errors
pared to a 64-row scanner without compromising image between the acquired and the computed projection profiles
quality [42–44]. converge to a prescribed level. The number of iterations
required to reconcile the differences between the computed
and measured profiles is substantial. Long computation
Dual Source Scanners times previously precluded its use clinically. With the
advent of computers in recent years with vastly improved
Another development in CT technology leading to an speed, time is no longer a deterrent for implementing itera-
increase in temporal resolution and reduction in patient dose tive reconstruction algorithms.
is the dual source CT scanner. A dual source CT scanner has One reason why iterative reconstruction is superior to
two sets of x-ray tube and detectors mounted at 90° angles. filtered backprojection for patient dose reduction is that the
For reconstruction of CT images, the algorithm requires reconstructed images present much lower levels of noise.
projection profiles acquired at least over 180° plus the arc Lower image noise permits the user to apply less radiation
angle of the detectors, translating to approximately 240° of to the patient to obtain the same quality images. Studies
gantry rotation. This scan mode is called half scan. For a dual found that for images reconstructed with the same noise
source scanner, the two sets of detectors only need to perform level as filtered backprojection, the iterative algorithms
a quarter scan. The two sets of quarter scan data sets are enabled use of lower beam current and therefore reduced
joined together by software to satisfy the 180° angular the patient dose by up to 65 % [29]. However, for many of
requirement. Because sufficient data can be acquired in only the CT systems in use today, implementation of iterative
one fourth of a gantry rotation, temporal resolution as short reconstruction requires major upgrading of their computing
as 80 ms is achievable for a gantry rotation time of 330 ms. equipment.
44 K.H. Lee

Conclusion 9. ICRP. ICRP publication 92: relative biological effectiveness (RBE),

High speed multi-slice CT with its high temporal and quality factor (Q), and radiation weighting factor (wR). Oxford,
UK: Elsevier Science Ltd; 2003. ISBN 0-08-044311-7.
­spatial resolution is increasingly applied for a wide spec- 10. 2007 report on occupational radiation exposures in Canada. Health
trum of cardiac studies. Because of the high radiation Canada. http://www.hc-sc.gc.ca/ewh-semt/alt_formats/hecs-sesc/
dose associated with cardiac CT examinations, it is neces- pdf/pubs/occup-travail/2007-report-rapport-eng.pdf.
sary for the clinicians to become familiar with the dosi- 11. Feng YJ, et al. Estimated cosmic radiation doses for flight personnel.
Space Med Med Eng. 2002;15(4):265–9.
metric principles, and to adopt dose reduction techniques 12. Department of Transportation Report – DOT/FAA/AM-03/16.
in their clinical practice. This chapter reviewed the basic What aircrews should know about their occupational exposure to
dosimetry parameters necessary to understand the terms ionizing radiation; 2003.
and concepts invariably brought up in any discussion of 13. NCRP Report No. 101. Exposure of the U.S. population from occu-
pational radiation; 1989.
radiation dose optimization methods. The abstract con- 14. ICRP. The 2007 recommendations of the International Commission
cept of effect dose should be well understood in order to on Radiological Protection. ICRP Publication 103. Ann ICRP.
explain to the patients the relative risks of different medi- 2007;37(2–4):1–332.
cal procedures that involve the use of radiation, such as 15. Huda W, Ogden KM, Khorasani MR. Converting dose-length prod-
uct to effective dose at CT. Radiology. 2008;248(3):995–1003.
the comparative risks of coronary CT angiography, chest 16. NcNitt-Gray MF. AAPM/RSNA physics tutorial for residents: top-
x-rays, and radionuclide perfusion studies. ics in CT, radiation dose in CT. Radiographics. 2002;22:1541–53.
Patient dose reduction can be obtained on all CT sys- 17. Goldman LW. Principles of CT: radiation dose and image quality.
tems by judiciously selecting the proper tube voltage, J Nucl Med Technol. 2007;35:213–25.
18. Bauhs JA, Vriezze TJ, Primak AN, Bruesewitz MR, McCollough
current-time product, and scan length. The numerous CH. CT dosimetry: comparison of measurement techniques and
trade-names of dose modulation techniques offered by devices. Radiographics. 2008;28:245–53.
CT manufacturers can be confusing. However, the guid- 19. Christner JA, Kofler JM, McCollough CH. Estimating effective
ing principle of all techniques involves reducing the tube dose for CT using dose-length product compared with using organ
doses: consequences of adopting international commission on
voltage, tube current, beam-on time, and scan volume to radiological protection publication 103 or dual-energy scanning.
produce acceptable quality image with the less radiation Am J Roentgenol. 2010;194:881–9.
to the patient. New systems on the market have incorpo- 20. European Commission Study Group. European guidelines on qual-
rated many of the dose reduction principles and technolo- ity criteria for computed tomography. Publication no. EUR 16262
EN. Brussels: Office for Official Publications of European
gies into their systems, but users without the benefits of Communities; 2000.
the new technologies can still minimize their patient dose 21. Radiation Exposure From Medical Exams and Procedures. https://
by matching patient’s size and weight with the dose hps.org/documents/Medical_Exposures_Fact_Sheet.pdf. Last
reduction parameters discussed in this chapter. accessed 25 July 2015.
22. Einstein AJ, Moser KW, Thompson RC, Cerqueira MD, Henzlova
MJ. Radiation dose to patients from cardiac diagnostic imaging.
Circulation. 2007;116:1290–305.
23. McCollough CH, Leng S, Yu L, Cody DD, Boone JM, McNitt-
References Gray MF. CT dose index and patient dose: they are not the same
thing. Radiology. 2011;259(2):311–6.
24. Report No. 204. Size-Specific dose Estimates (SSDE) in pediatric
1. NCRP Report No. 160. Ionizing radiation exposure of the popula- and adult body CT examinations, 2011. College Park: American
tion of the United States; 2009. Association of Physicists in Medicine. https://www.aapm.org/pubs/
2. Brinjikji W, Kallmes D, Cloft H. Rising utilization of CT in adult reports/RPT_204.pdf. Last accessed 25 July 2015.
fall patients. Am J Roentgenol. 2015;204:558–62. 25. Dixon RL, Anderson JA, Bakalyar DM, et al. Comprehensive
3. ConsumerReport.org, “Consumer reports warns against the risks of methodology for the evaluation of radiation dose in X-ray computed
radiation overexposure from unnecessary CT scans”. Release Date: tomography. AAPM Report No. 111, College Park; 2010.
27 Jan 2015. Last accessed 16 May 2015. 26. IAEA Human Health Reports 5. Status of computed tomography
4. Watson SJ, Jones AL, Oatway WB, Hughes JS. Ionizing radiation dosimetry for wide cone beam scanners, 2011, Vienna.
exposure of the UK population: 2005 review. Health Protection 27. Budoff MJ, et al. Substantial radiation dose reduction in 64-multi-
Agency, Report HPA-RPD-001; 2005. detector cardiac computed tomography by using lower X-ray
5. United Nations Scientific Committee on the Effects of Atomic energy during scanning. J Am Coll Cardiol. 2008;51:A148.
Radiation. Sources and effects of atomic radiation: ionizing 28. Budoff MJ. Maximizing dose reductions with cardiac CT. Int
radiation, Publication n. E.00.IX4. New York: United Nations; J Cardiovasc Imaging. 2009;25:279–87.
2000. 29. Maldjian PD, Goldman AR. Reducing radiation dose in body CT: a
6. BEIR VII. Health risks from exposure to low levels of ionizing primer on dose metrics and Key CT technical parameters. Am
radiation: BEIR VII-Phase 2. Washington DC: National Academies J Roentgenol. 2013;200:741–7.
Press; 2006. 30. Raff GL, et al. radiation dose from cardiac computed tomography
7. Parker MS, Hui FK, Camacho MA, et al. Female breast radiation before and after implementation of radiation dose reduction
exposure during CT pulmonary angiography. Am J Roentgenol. techniques. JAMA. 2009;301:2340–8.
2005;185(5):1228–33. 31. McCollough CH, Primak AN, Braun N, Kofler J, Yu L, Christner
8. NCRP Report No. 82. SI units in radiation protection and measure- J. Strategies for reducing radiation dose in CT. Radiol Clin North
ments; 1985. Am. 2009;47(1):27–40.
3 Radiation Dosimetry and CT Dose Reduction Techniques 45

32. Gopal A, Budoff MJ. A new method to reduce radiation exposure impactscan.org/download/msctdose.pdf. Last accessed 25 July
during multi-row detector cardiac computed tomographic angiogra- 2015.
phy. Int J Cardiol. 2009;132:435–6. 41. Primak AN, McCollough CH, Bruesewitz MR, Zhang J,
33. Pflederer T, et al. Image quality in a Low radiation exposure Fletcher JG. Relationship between noise, dose, and pitch in cardiac
­protocol for retrospective ECG-gated coronary CT angiography. multi-­detector row CT. Radiographics. 2006;26:1785–94.
Am J Roentgenol. 2009;192:1045–50. 42. Wong DTL, et al. Superior CT coronary angiography image quality
34. Gopal A, et al. Radiation reduction with prospective ECG- at lower radiation exposure with second generation 320-detector
triggering acquisition using 64-multidetector computed tomo- row CT in patients with elevated heart rate: a comparison with first
graphic angiography. Int J Cardiovasc Imaging. 2009;25: generation 320-detector row CT. Cardiovasc Diagn Ther. 2014;4(4):
405–16. 299–306.
35. Goodman TR, Brink JA. Adult CT: controlling dose and image 43. Chen MY, Shanbhag SM, Arai AE. Submillisievert median radia-
quality. In: From invisible to visible – the science and practice of tion dose for coronary angiography with a second-generation
X-ray imaging and radiation dose optimization; 2006. Categorical 320-detector row CT scanner in 107 consecutive patients.
course syllabus, Radiological Society of North America, Oak Radiology. 2013;267(1):76–85.
Brook, IL. 44. Steigner ML, et al. Narrowing the phase window width in prospec-
36. Lee CH, et al. Radiation dose modulation techniques in the multi- tively ECG-gated single heart beat 320-detector row coronary CT
detector CT era: from basics to practice. Radiographics. angiography. Int J Cardiovasc Imaging. 2009;25:85–90.
2008;28:1451–9. 45. Yu L, Liu X, et al. Radiation dose reduction in computed tomogra-
37. Sun Z. Coronary CT angiography with prospective ECG-triggering: phy: techniques and future perspective. Imaging Med. 2009;1(1):
an effective alternative to invasive coronary angiography. 65–84.
Cardiovasc Diagn Ther. 2012;2(1):28–37. 46. McCollough CH, et al. Dose performance of a 64-channel
38. Mahesh M, Cody DD. Physics of cardiac imaging with multiple- dual-source CT scanner. Radiology. 2007;243:775–84.
row detector CT. Radiographics. 2007;27:1495–509. 47. Tomizawa N, et al. Adaptive iterative dose reduction in coronary
39. Takakuwa KM, et al. Radiation dose in a “triple rule-Out” coronary CT angiography using 320-row CT: assessment of radiation dose
CT angiography protocol of emergency department patients using reduction and image quality. J Cardiovasc Comput Tomogr.
64-MDCT: the impact of ECG-based tube current modulation on 2012;6:318–24.
age, sex, and body mass index. Am J Roentgenol. 2009;192: 48. Kalendar W. Computed tomography: fundamentals, system
866–72. technology, image quality, applications. Erlangen: Publicis
­
40. Lewis M. Radiation dose issues in multi-slice CT scanning. Corporate Publishing; 2005.
ImPACT technology update no. 3, Jan 2005. http://www.
 Orientation and Approach
to Cardiovascular Images 4
Jerold S. Shinbane and Antreas Hindoyan

Abstract
Mastery of conventional anatomy and physiology is essential as a template for understanding
of cardiovascular variation and pathology. A multitude of analysis and reconstruction tools
including orthogonal, double oblique, and curved multiplanar reformatted 2-D, and volume-
rendered 3-D views can be utilized for comprehensive diagnosis of cardiovascular pathology.
The goal of this chapter is orientation to review and analysis of cardiovascular structure from
CCTA image sets using a systematic approach.

Keywords
Cardiovascular Computed Tomographic Angiography • Computed Tomography •
Curved Multiplanar Reformatted • Double-Oblique • Orientation • Orthogonal Views •
Volume-Rendered

Abbreviations LIMA Left Internal Mammary Artery

LM Left Main Coronary Artery
AAO Ascending Aorta LS Left Sinus of Valsalva
DAO Descending Aorta MV Mitral Valve
AV Aortic Valve PA Pulmonary Artery
CS Coronary Sinus PDA Posterior Descending Coronary Artery
GCV Great Cardiac Vein PV Pulmonary Vein
IVC Inferior Vena Cava RA Right Atrium
LA Left Atrium RAA Right Atrial Appendage
LAA Left Atrial Appendage RCA Right Coronary Artery
LAD Left Anterior Descending Coronary Artery RIMA Right Internal Mammary Artery
LV Left Ventricle RV Right Ventricle
LCx Left Circumflex Coronary Artery TV Tricuspid Valve

Electronic supplementary material The online version of this

chapter (doi:10.1007/978-3-319-28219-0_4) contains supplementary
material, which is available to authorized users.
Introduction

J.S. Shinbane, MD, FACC, FHRS, FSCCT (*) • A. Hindoyan, MD A systematic and comprehensive approach to analysis of
Division of Cardiovascular Medicine, Department of Internal visualized structures is essential to interpretation of CCTA
Medicine, Keck School of Medicine of the University
utilizing the multitude of analysis and reconstruction tools.
of Southern California, 1520 San Pablo Suite 300,
Los Angeles, CA 90033, USA The underpinning of this approach is an understanding of
e-mail: [email protected] the 3-D anatomy and physiology of structures and their

© Springer International Publishing 2016 47

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_4
48 J.S. Shinbane and A. Hindoyan

interrelation in the acquired tomographic data cube. Imagers resolution superior to other planes. This is not the case for
will ultimately find their own individualized algorithm for scanners providing imaging with isotropic voxels, as the vox-
image analysis, but this approach ultimately needs to be els possess uniform resolution in all axes. The reader should
complete, methodical, and efficient. The goal of this chapter visualize the patient in the supine position with the patient’s
is orientation to viewing and analyzing cardiovascular struc- feet coming out towards the reader. The sternum (anterior) and
ture from CCTA image sets, with mastery of conventional spine (posterior) can also be used to orient the reader in the
anatomy and physiology serving as a template for under- axial plane (Fig. 4.136). The reader should never try to analyze
standing of cardiovascular variation and pathology. a structure using one axial slice. Assessment of adjacent axial
An important factor prior to image analysis is review of slices to establish anatomic continuity should be performed
relevant clinical history and questions to be answered by the for comprehensive identification of a structure and its
study. Before evaluation of individual structures, the image connections.
set needs to be assessed for limitations to analysis due to the Non-coronary artery cardiovascular structure analysis
field of view, percentage of the cardiac cycle imaged, and includes: the size and architecture of the aorta and branch
image quality based on degree of target region of interest vessels at all visualized levels, the size and architecture of
contrast opacification and artifacts. Analysis should be sys- the main pulmonary artery and pulmonary artery branches,
tematic rather than focused on the most prominent findings. the 3-D relationships between the aorta and the pulmonary
One systematic approach to analysis involves comprehensive arteries, presence of anomalous thoracic vascular anatomy,
evaluation through serial assessment of: (1) Non-coronary location, number, and course of the pulmonary veins, atrio-
artery cardiovascular structure cranial to caudal with axial ventricular and ventriculo-arterial concordance, continuity
scrolling followed by additional 2- and 3-D analysis, (2) of the atrial septum, continuity of the ventricular septum,
Coronary artery cardiovascular structure cranial to caudal the presence of filling defects or masses in the left atrial
with axial scrolling as an anchor followed by additional 2- appendage, atria and ventricles, valvular structure, myocar-
and 3-D analysis, and (3) Non-cardiovascular structures in dial thickness and tissue attenuation, and pericardial thick-
the available field of view by physicians with expertise in ness and presence of effusion.
evaluation of these structures. The thorax is viewed from anterior to posterior by scroll-
ing through serial coronal images (Fig. 4.137) and from right
to left on sagittal images (Fig. 4.138). In these reconstruc-
Image Views tions, multiple stacks of images are viewed at once, and
therefore thin collimation lines can be seen. If the data sets
Orthogonal Views: Axial, Sagittal and Coronal are not aligned properly due to motion, step artifacts can
Planes (Figs. 4.1–4.134 shown at the end occur. These artifacts would not be present using scanners
of the chapter; Videos 1, 2, and 3) which have an acquisition volume imaging the field of view
in one gantry rotation, allowing single beat imaging.
Even with the advent of a multitude of imaging software Respiratory motion artifacts are well seen on sagittal views.
options, the axial images remain an anchor for analysis with In the sagittal and coronal views, assessment of contrast
additional information obtained from 2-D coronal sagittal, opacification of the descending aorta can be used as a
double oblique, curved multi-planar, and 3-D reconstruc- marker of the adequacy of timing for contrast opacification
tions useful for confirmation and specialized analysis of spe- of the distal coronary arteries. Measurement of contrast den-
cific structures. In addition to structure, tissue characteristics sity and homogeneity measured by HU at serial levels of the
related to the radiodensity of the tissue can be assessed descending aorta can be performed. If the HUs decrease sig-
through measurement of HUs (Fig. 4.135). The Hounsfield nificantly as the aorta descends, the distal coronary arteries
unit (HU) is based on an attenuation scale in which the may be poorly opacified and more difficult to analyze
radiodensity of water is 0 HU and air 1000 HU. Tissues have (Fig. 4.139).
a spectrum of HU ranges depending on their radiodensity The sagittal and coronal views display certain structures
with approximate values for fat of −50 to −100 HU, muscle well in their natural planes. Sagittal images are helpful for
10–40 HU, and wide spectrum for bone of 400–3000 HU viewing the right ventricular outflow tract, aorta in a “candy
based on architecture. cane” view, and origins of venous coronary artery bypass
Analysis of CCTA relies significantly on evaluation of the grafts off of the aorta (Fig. 4.140). Coronal images facilitate
axial plane images. In the axial plane, the thorax is viewed in display of the sternum, course of the left and right internal
serial cranial to caudal slices, with visualization of thinner mammary arteries, mid-segment of the right coronary artery,
slices enabling evaluation with greater resolution than thicker left ventricular outflow tract, pulmonary veins and atrial
slices. If the CT system used does not provide true isotropic appendage entering the left atrium, and descending aorta
voxels due to limited Z axis resolution, the axial plane provides (Fig. 4.141).
4 Orientation and Approach to Cardiovascular Images 49

a b

Fig. 4.135 Panel (a): A 2-D non-contrast axial view showing the right atrium (with inhomogeneity due to mixing of contrast enhanced
Hounsfield Units of various tissues including subcutaneous fat, air in and non-contrast enhanced blood), right ventricle, left atrium, left ven-
the lungs, bone, skeletal muscle and left ventricular myocardium. Panel tricle, and aorta. Ao aorta, HU Hounsfield units, LA left atrium, LV left
(b): A 2-D contrast-enhanced axial view showing the Hounsfield Units ventricle, RA right atrium, RCA right coronary artery, RV right
of various tissues including subcutaneous fat, air in the lungs, bone, ventricle
skeletal muscle, and left ventricular myocardium, and contrast enhanced

Fig. 4.136 A 2-D axial view showing anterior (sternum), posterior

(spine), right and left orientation

Fig. 4.137 2-D coronal view showing cranial, caudal, left and right
orientation. Motion artifacts are seen as thin collimation lines (arrows)
50 J.S. Shinbane and A. Hindoyan

a b

Fig. 4.138 2-D sagittal views showing anterior (sternum) and posterior (spine) orientation. Panel (a) Respiratory motion artifacts are seen as
discontinuity of the sternum with thin collimation lines (arrows). Panel (b) Sternum with no evidence of respiratory motion (arrow)

a b

Fig. 4.139 Panel (a): A 2-D contrast-enhanced sagittal view showing dose to visualize the distal segments coronary arteries. Panel (b): A 3-D
decreased contrast density and homogeneity at serial levels of the contrast-enhanced reconstruction with lack of visualization of the mid
descending aorta (arrow) as a marker of inadequate timing and contrast to distal left anterior descending coronary artery (arrow)

Double Oblique 2-D Views than circular shapes, allowing the maximum and minimum
diameters as well as the area of these structure to be
The axial, coronal, or sagittal views can be used as a starting quantified.
point for rotation into planes providing coaxial long and
short axis views of specific vascular structures (Fig. 4.142).
“En face” measurements at various levels of the aorta (aor- Curved Multiplanar Reformatted Views
tic annulus, sinus of Valsalva, sinotubular junction, ascend-
ing, arch, and descending aorta), pulmonary arteries, Curved MPR images can evaluate an entire vascular struc-
pulmonary vein ostia, and atrial or ventricular septal defects ture in one view (Fig. 4.143). The plane of a specific artery
are important, as these structures often have ovoid rather can be chosen and displayed as a “curved surface” from
4 Orientation and Approach to Cardiovascular Images 51

a b c

Fig. 4.140 Panel (a): A 2-D sagittal view displaying aorta in a “candy coronary artery bypass graft off of the aorta in a patient with coronary
cane” view in a patient with atherosclerotic disease of the aorta. Panel artery bypass graft surgery (arrow). Panel (c): Axial view demonstrat-
(b): A 2-D sagittal view showing the origin of a saphenous venous ing the same saphenous vein graft (arrow)

a b c

d e

Fig. 4.141 Serial 2-D coronal images. Panel (a): Sternum with left and (arrow). Panel (d): Left atrium (arrow), pulmonary veins and left atrial
right internal mammary arteries (arrow). Panel (b): Mid-segment of the appendage. Panel (e): Descending aorta (arrow)
right coronary artery (arrow). Panel (c): Left ventricular outflow tract
52 J.S. Shinbane and A. Hindoyan

Fig. 4.142 Long (a) and short axis (b) 2-D double oblique views for coaxial assessment of the aorta at the sinuses of Valsalva (arrows)

Fig. 4.143 Curved multiplanar reformatted views of the aorta with long axis (a) and serial coaxial cross sectional views (b)

within the 3D volume. This view also creates cross sectional Volume-Rendered 3-D Views
cuts of each vascular segment. The thickness of the cross
sectional cuts can be adjusted using workstation software. The volume rendered technique relies on identification of all pix-
All other structures are automatically eliminated, including els within a specified attenuation range. The 3-D views may be
the side branches, and separate reconstructions can be ren- helpful to obtain an overall sense of 3-D cardiovascular anatomy,
dered for each side-branch. but measurements related to structure should be performed using
4 Orientation and Approach to Cardiovascular Images 53

Fig. 4.144 Volume rendered 3-D reconstructions of the thorax with serial editing from thorax to cardiovascular structures to coronary arteries

2-D images in the appropriate plane. A variety of automatic and tions for morphology, atherosclerotic and non-atherosclerotic
manual editing softwares allow visualization of specific struc- plaque, mural thrombus, penetrating ulcer, dissection, aneu-
tures and relationships in the 3-D data cube, but require care in rysm and pseudoaneurysm. After review of the aorta in the
utilization in order to avoid over or under editing of structures axial position, double oblique views can be created so that
(Fig. 4.144). coaxial measurements can be made at multiple levels includ-
ing: the aortic annulus, sinuses of Valsalva, sinotubular junc-
tion, ascending aorta, arch, descending thoracic aorta, and
Orientation to Analysis of Cardiovascular potentially the upper abdominal aorta (Fig. 4.146). Due to
Structure limitation of the field of view for radiation dose reduction,
portions of the aorta may not visualized. Recognition of the
Orientation of the Great Vessels segments of the aorta not visualized is therefore important
for analysis and reporting of findings.
Review of the spatial relationship between the aorta and
main pulmonary artery is essential for analysis of rotational
abnormalities of the great vessels. In the normal relationship Pulmonary Arteries
of the aorta and main pulmonary artery, these vessels are per-
pendicular with the aorta rightward and posterior to the main The initial axial assessment of the aortic to pulmonary artery
pulmonary artery (Fig. 4.145). In D-transposition of the relationship will bring the main pulmonary artery into view.
great arteries, the aorta is usually anterior to the main pulmo- The main pulmonary artery as well as proximal right and
nary artery, while in L-transposition, the aorta is usually left pulmonary arteries can subsequently be assessed for
anterior and rightward to the main pulmonary artery. In the morphology and measured coaxially using double oblique
setting of transposition of the great arteries, these vessels can views, assessing for evidence of pulmonary arterial hyper-
be parallel with coaxial visualization in the same plane lead- tension or aneurysm (Fig. 4.147). The pulmonary arterial
ing to a “double barrel shotgun” appearance. tree is then assessed on the available full field of view on
serial slices for vessel caliber and any evidence of filling
defects, recognizing limitations if the contrast bolus has
Aorta been focused on left-sided structures. Again, due to limited
field of view for radiation dose reduction in studies per-
The aorta can be followed in the axial plane from the aortic formed for purposes such as coronary artery analysis, por-
root through the ascending aorta, arch and descending por- tions of the pulmonary arterial tree may not be visualized or
54 J.S. Shinbane and A. Hindoyan

a b

Fig. 4.145 2-D axial views demonstrating the spatial relationship posterior to the main pulmonary artery. Panel (b): D-transposition of
between the aorta and main pulmonary artery for assessment of rota- the great arteries, with parallel relationship of the great arteries with the
tional abnormalities of the great arteries. Panel (a): Normal relationship aorta anterior and rightward to the main pulmonary artery. Ao aorta, PA
of the aorta and main pulmonary artery with the aorta rightward and pulmonary artery

a adequately contrast opacified and therefore analysis is lim-

ited. Recognition of the portions of the pulmonary arterial
tree not visualized is therefore important to analysis and
reporting of findings.

Cardiac Chambers

Axial images should be reviewed for the spatial relationship

between the heart and the thorax (Fig. 4.148). With normal
anatomy, the heart is in the left hemithorax (levocardia), as
b opposed anomalous location in the right hemithorax (dex-
trocardia), or midline (mesocardia). The ventricles are nor-
mally D-looped, with the right ventricle rightward and
anterior to the left ventricle, whereas in L-looped ventricles
the relationship is inverted.

Right Atrium/SVC/IVC/Coronary Venous System

Visualization of the right atrium is dependent on the injec-
tion protocol. Even in circumstances where there is signifi-
cant contrast bolus in the right atrium, there is still
non-contrast enhanced blood flow from the contralateral
arm venous drainage as well as the inferior vena cava. The
Fig. 4.146 2-D double oblique views demonstrating coaxial display of presence of contrast and non-contrast enhanced blood
the aorta at multiple levels. Panel (a): The aortic annulus, sinuses of
causes Hounsfield Unit heterogeneity in the right atrium
Valsalva, sinotubular junction, ascending aorta, Panel (b): Descending
thoracic aorta and upper abdominal aorta. Ao aorta, Ao V aortic valve, making endocardial assessment more challenging. The right
ST sinotubular atrium has a triangular shaped appendage as opposed to the
4 Orientation and Approach to Cardiovascular Images 55

a b

Fig. 4.147 2-D axial view of the main pulmonary artery. Panel (a): Pulmonary artery enlargement associated with pulmonary arterial hyperten-
sion. Panels (b, c): Large pulmonary artery emboli (arrows). Ao aorta, PA pulmonary artery

vermicular, “worm like”, morphology of the left atrial

appendage (Fig. 4.149). Familiarity with the division of the
right atrium into a trabeculated lateral portion separated by
the crista terminalis from a smooth walled septum is essen-
tial to avoid misinterpretation of structures as masses.
Characteristics of the septum such as lipomatous hypertro-
phy (Fig. 4.150), atrial septal aneurysm, patent foramen
ovale, and atrial septal defect require analysis of the entire
septum. The size, shape and morphology of atrial septal
defects including the surrounding rim require detailed
assessment in double oblique views. Analysis for the pres-
ence, morphology and patency of the superior and inferior
vena cavae should also include a search for any anomalous
connections from the pulmonary veins as well as for the
presence of other venous connection to the right atrium. The
coronary sinus ostium is usually seen in the inferoposterior
right atrium. The coronary sinus/great cardiac vein should
be evaluated for continuity throughout course as well as for
evidence of enlargement due to either right-sided pressure
and volume overload or a left-sided superior vena cava with
Fig. 4.148 2-D axial views of the normal orientation of the heart in the aneurysmal coronary sinus connection. The coronary sinus
thorax (levocardia). ostium may have a variable degree of presence of a remnant
56 J.S. Shinbane and A. Hindoyan

Fig. 4.149 Views of the triangular shaped, wide based right atrial appendage. Panel (a): 3-D reconstruction. Panel (b): 2-D double oblique image.
RAA right atrial appendage

flow back from the myocardium through the coronary

venous branches, great cardiac vein and then to the coronary
sinus. Adequate opacification of a left-sided superior vena
cava requires images obtained with a left arm venous con-
trast injection.

Left Atrium/Pulmonary Veins

The left atrium and its relationship to the pulmonary
veins and other thoracic structures can be characterized
with multiple CCTA reconstruction modalities
(Figs. 4.151 and 4.152). The left atrium is often trapezoi-
dal in shape and becomes progressively more spherical
when enlarged. The complex shape makes single plane
assessment challenging and therefore volumetric assess-
ment more completely characterizes size. The left atrial
volume can be quantitated at end systole and end-dias-
tole. The left atrial appendage is a complex structure,
with variation in shape, size, lobulation, and the presence
of pectinate muscles. Characterization of the left atrial
appendage ostial characteristics, length of the main body,
and number and morphology of lobes can be important to
Fig. 4.150 2-D axial view of the atrial septum demonstrating lipoma- procedures such as left atrial appendage occlusion
tous hypertrophy (arrows) devices. Assessment should be made for filling defects in
the left atrial appendage. Filling defects can be due to
Thebesian valve. Evaluation of the entire coronary venous thrombus, mass, or inadequate opacification due to
system necessitates a delay in timing of image acquisition decreased left atrial appendage velocity. The left atrium
from contrast injection as contrast-enhanced blood must should be assessed for masses as well as other anomalies
4 Orientation and Approach to Cardiovascular Images 57

a b c

Fig. 4.151 Multimodal views of the left atrium. Panel (a): 3-D poste- LAA left atrial appendage, LLPV left lower pulmonary vein, LUPV left
rior view of the left atrium. Panel (b): Endovascular view of the left upper pulmonary vein, RLPV right lower pulmonary vein, RUPV right
upper and lower pulmonary veins and the left atrial appendage. Panel upper pulmonary vein
(c): Endovascular view of the right upper and lower pulmonary veins.

a b

Fig. 4.152 2-D double oblique views of the left atrium. Panel (a): form or “wormlike” with a narrow ostium. The ridge between the left
Relationship of the esophagus, left lower pulmonary vein and aorta. atrial appendage and left upper pulmonary vein can be prominent and
Panel (b): Relationship between the left atrial appendage, left upper misdiagnosed as an atrial mass. Ao aorta, LAA left atrial appendage,
pulmonary vein, and the ridge between these structures. In contradis- LLPV left lower pulmonary vein, LUPV left upper pulmonary vein
tinction to the right atrial appendage, the left atrial appendage is verin-

such as accessory atrial appendages and diverticulae. The the interface of the left atrium and pulmonary vein using a dou-
ridge between the left atrial appendage and left atrium, ble oblique approach. Multiple variations in pulmonary venous
sometimes referred to as the “Coumadin ridge” can be anatomy occur, commonly with three right and two left pulmo-
prominent and misdiagnosed as an atrial mass. nary veins. Pulmonary veins can coalesce into a single trunk at
The pulmonary veins can be assessed as they course to the the atrial interface. Each vein should be followed from its ori-
left atrium on the coronal and axial views, with subsequent gin in the lungs and assessment should be made for any evi-
measurement of the pulmonary vein orifices made coaxially at dence of anomalous pulmonary venous return.
58 J.S. Shinbane and A. Hindoyan

a b

Fig. 4.153 2-D double oblique views of the right ventricle. Panel (a): and pulmonic valve annulus (double black arrows), separated by the
Trabeculation of the septum and a moderator band (black arrow). Panel conus, creating divisions into an inflow, body, and outflow
(b): Non-adjacent location of the tricuspid annulus (single black arrow)

on an adequately opacified right ventricle, volumetric assess-

ment of size and function can be measured. The right ven-
tricle though is ovoid in shape and therefore can be more
challenging to quantitate than the left ventricle.

Left Ventricle
Morphologic features of the left ventricle include a smooth-
walled septum, adjacent location of the mitral valve and aor-
tic valve annuli, and prominent papillary muscles (Fig. 4.154).
Assessment can be made for wall thinning as well as lipoma-
tous metaplasia associated with myocardial infarction. The
ventricular septum can be assessed for continuity versus
presence of a ventricular septal defect with characterization
of location, shape, and size. The ventricle can be assessed for
thrombi and masses. For retrospectively gated studies, func-
tional views can be reformatted for assessment of left ven-
tricular volumes, wall thicknesses and thickening, myocardial
mass, regional wall motion and global ventricular function
Fig. 4.154 2-D double oblique view of the left ventricle with the
anatomic features of a smooth-walled septum (black arrow) and (Fig. 4.155, Video 4).
continuity between the aortic and mitral valve annuli (white arrows)

Valvular Structure and Function

Right Ventricle
Similar to the right atrium, heterogeneous opacification of On retrospectively-gated studies, aortic and mitral valve anat-
the contrast can occur in the right ventricle. Morphologic omy and motion including annular dimensions, valve leaflet
features of the right ventricle include trabeculation of the number, morphology, degree of calcification, valve excur-
septum, moderator band, and non-adjacent location of the sion, apposition, prolapse, valve area, and regurgitant orifice
tricuspid valve and pulmonary valve annuli as they are sepa- can be assessed (Figs. 4.156 and 4.157). Additionally, large
rated by the conus arteriosus, therefore creating right ven- vegetations or other masses, can be visualized. Functional
tricular divisions into an inflow, body, and outflow image sets can be formatted following the traditional echo-
(Fig. 4.153). When retrospectively-gated images are acquired cardiographic views, with the ability to view motion
4 Orientation and Approach to Cardiovascular Images 59

Fig. 4.155 2-D retrospectively-gated end-diastolic and end-systolic short axis ventricular views used for assessment of wall thickness, volumes,
and ejection fraction

a b

Fig. 4.156 2-D contrast-enhanced double oblique aortic valve images. Panel (a): Trileaflet calcific aortic stenosis. Panel (b): Planimetry of aortic
valve area demonstrating severe aortic stenosis

through the entire cardiac volume in these views. Functional Pericardium

views can also be viewed in oblique planes for dynamic
analysis of specific structures. Tricuspid and pulmonic The pericardium should be assessed for evidence of
valve assessment requires adequate contrast opacification regional or global thickening, calcification, pericardial
of the right heart for analysis. With prospectively gated effusion, and pericardial masses. This may be particularly
images more limited data related to valve morphology can helpful in scenarios of posterior pericardial effusions,
be obtained (Fig. 4.158). where echocardiographic imaging may be more challeng-
60 J.S. Shinbane and A. Hindoyan

a b

Fig. 4.157 2-D double oblique mitral valve images. Panel (a): Short axis view. Panel (b): 4 chamber view

a b

Fig. 4.158 2-D double oblique pulmonary valve images. Panel (a): Long axis view of right ventricular outflow tract. Panel (b): Coaxial view
showing the pulmonary valve regurgitant orifice. LV left ventricle, PA pulmonary artery, RA right atrium
4 Orientation and Approach to Cardiovascular Images 61

ing. Small pericardial effusion can be appreciated on coro- course and termination of each coronary artery should be
nal images with the fluid layering in the pericardial space analyzed for coronary artery dominance and for anomalies.
just above the diaphragm. The HU cursor, if placed on the Viewing the aortic root in the axial plane as a clock face, the
effusion, can confirm that the attenuation of the fluid is right coronary artery arises from the right sinus of Valsalva
near water attenuation (0 HU). at approximately 11:30 on the clock face and the left main
coronary artery arises off of the left sinus of Valsalva at
approximately 3:30 on the clock face (Fig. 4.159).” The right
Coronary Artery Assessment coronary artery should be followed in the right AV groove,
the left anterior descending coronary artery in the anterior
Assessment of the coronary arteries requires a multimodal interventricular groove and the left circumflex coronary
approach to reconstruction and analysis. Prior to assessment artery in the left AV groove with branches of each artery
for coronary arterial atherosclerotic disease, the origin, coursing out of their respective grooves. The posterior

a b

c d

Fig. 4.159 Axial Images demonstrating the normal location of the ori- main coronary artery (arrow). Panel (b): 2-D axial view showing the
gins of the coronary arteries. Viewing the aortic root in the axial plane as origin of the right coronary artery (arrow). Panel (c): Thick maximal
a “clock face,” the right coronary artery arises from the right coronary intensity projection showing the origin of the left main and right coro-
sinus at approximately 11:30 on the “clock face” and the left main coro- nary arteries (arrows). Panel (d): Thick maximal intensity projection
nary artery arises off of the left coronary sinus at approximately 3:30 on showing the origin of the left main and right coronary arteries (arrows)
the “clock face.” Panel (a): 2-D axial view showing the origin of the left
62 J.S. Shinbane and A. Hindoyan

descending artery can be visualized either from the right perpendicular to the axial plane will appear linear. The lim-
coronary artery or circumflex in the posterior interventricular itation is that an arterial segment coursing in any other
groove, defining vessel dominance. direction will be out of plane and therefore challenging to
Anomalous coronary arteries can be characterized by review. Therefore, other modalities including 2-D double
ostial location and morphology, course and termination. An oblique and curved multiplanar reconstructions are
anomalous coronary artery can arise off of a shared ostium employed to follow the course of the arterial segment being
with another coronary artery, as its own separate ostium, off analyzed.
of another coronary artery, or off of another vascular struc- Double oblique views allow each coronary artery to be fol-
ture such as the pulmonary artery. For a coronary artery off lowed in plane coaxially throughout its course (Fig. 4.160).
of the contralateral aortic sinus, the course can be pre-pul- Use of double oblique views allows the reader to follow the
monic, inter-arterial, intra-septal, or retro-aortic. Termination course of each coronary artery, which is especially useful for
can occur in an anomalous myocardial vascular distribution tortuous segments. The optimal assessment plane for the most
or into another arterial or venous vascular structure. proximal segment of a coronary artery can be identified in its
Beginning at the most cranial slices, maximum intensity long and short axis and then rotated 360 degrees. The oblique
projections can be viewed at 5 mm slice thickness. These plane is then moved at small increments for serial assessment
thicker slices facilitate visualization of the longitudinal course of segments and branches from proximal to distal artery.
of the vessels, with one limitation being that the brightest Curved multiplanar reformatted images are extremely
pixel dominates the image. Therefore, in the presence of useful to evaluate an entire coronary artery in one view. The
heavily calcified segments, one might miss a non-calcified reader can choose the plane of a specific artery which is
plaque causing a significant narrowing of the coronary vessel. displayed as a “curved surface” from within the 3-D volume
Adjusting the slice thickness back to 0.5 mm, each coronary (Fig. 4.161). With curved multiplanar reformatted views, a
artery segment can subsequently be followed, assessing for centerline is created and the artery “straightened out” and
the presence of calcified, mixed, and non-calcified plaque in viewed as a cylinder. The software also creates cross sec-
the vessels of mild, moderate, or severe grades. The coronary tional cuts of each coronary arterial segment of the cylinder,
artery calcium images should also be referenced, as they with the ability to adjust the thickness of the cross sections.
demonstrate the presence and location of calcium without The arterial segment of interest (coronary artery stenosis)
contrast in the coronary arteries. can be compared to the segments above and below it as a
In the axial view, the vessels are visualized in the plane reference. All other structures are automatically eliminated,
of image acquisition. As previously mentioned, if the CT including the side branches, and separate reconstructions
system used does not provide true isotropic voxels due to can be rendered for every side branch. The long axis luminal
limited Z axis resolution, the axial view provides greater view can be rotated 360° around its central axis in order to
resolution than other reconstructed planes. Each individual assess eccentric plaques and stenoses. With curved multipla-
artery should be followed through the cranial to caudal nar reformatted images, the computer software could create
axial slices rather than attempting to view multiple arteries the appearance of a stenosis by following an area of dense
on one axial slice. The left main coronary artery, left ante- calcium rather than the center of the vessel lumen.
rior descending artery, circumflex coronary artery, and Additionally, the centerline can jump from the coronary
right coronary artery are analyzed individually along with artery to follow an adjacent cardiac vein. The centerline
their branches. A coronary arterial segment coaxial to the should therefore be viewed in order to ensure that it remains
axial plane will appear as a circle, while an artery coursing within the center of the vessel of analysis.

a b c

Fig. 4.160 2-D double oblique identification of a segment of the left anterior descending coronary artery with long (a, b) and short axis (c) views
of the arterial segment
4 Orientation and Approach to Cardiovascular Images 63

a b

Fig. 4.161 Curved multiplanar reformatted view of a left anterior descending coronary artery. (a) The left anterior descending coronary artery is viewed
as serial coaxial cross sections. (b) The centerline (yellow line) is used to determine the center of each arterial segment

The volume rendered technique relies on identifying all images. The 3-D volume rendered images in CCTA help in
pixels above a certain threshold with various degrees of identification of coronary anomalies as well as to assess the
attenuation. The results are most similar in orientation to dominance of the coronary arterial tree. In patients with pre-
invasive coronary angiography images (Figs. 4.162 and vious coronary artery bypass graft surgery, the origin of
4.163, Videos 5 and 6). The coronary arteries are seen as grafts from the aorta can be counted and the courses fol-
relatively smooth structures with other cardiovascular land- lowed to the native vessels. Stumps of occluded grafts can
marks present. The image can be rotated, allowing the inter- also be easily identified. As there are potential artifacts with
preter some flexibility in visualizing the segment from all these additional techniques, the thin axial slices should
multiple angles. A stenotic coronary artery segment will always be used to confirm or exclude any potential lesions
appear darker as well as narrowed on volume rendered that might be seen with other reconstructions.
64 J.S. Shinbane and A. Hindoyan

a b

c d

Fig. 4.162 3-D images of the right coronary artery (arrows) in the right Panels (c, d): Images of coronary arteries with varying degree of trans-
anterior oblique 30 degree/ caudal 0 degree view. Panel (a): Image with parency of the heart. As opposed to invasive angiography, the left coro-
skeletal structures. Panel (b): Image of heart and coronary arteries. nary artery is also visualized. CAU caudal, RAO right anterior oblique

Artifacts Affecting Assessment be performed. If the HUs decrease significantly as the aorta
of The Coronary Arteries descends, the distal coronary arteries may be poorly opaci-
fied and more difficult to analyze. Additionally, inadequate
A spectrum of artifacts may limit interpretation of the coro- flushing of contrast out of the superior vena cava can cause
nary arteries. Recognition of artifacts related to acquisition “streak artifact” potentially obscuring the mid right coro-
and reconstruction is important in order to avoid misinterpre- nary artery.
tation of coronary artery findings.
Artifacts Due to Overlap of HU Attenuation
Coronary Artery Artifacts Due to Contrast Dose Between Coronary Artery Lumen and Other
and Timing Relative to Image Acquisition Structures
In the setting of right heart greater than left heart enhance- Blooming artifacts can occur due to coronary artery or
ment, the images may have been acquired too early after cardiac calcification, stents, clips, wires, pacemakers,
contrast administration. This early acquisition of images implantable cardiac defibrillators and other radiopaque
can also lead to the distal segments of the coronary arteries implanted materials. The non- contrast coronary artery
not being opacified, which can be misinterpreted as signifi- calcium images can be used to assess for coronary artery
cant stenosis or occlusion. Measurement of contrast density segments which may be problematic prior to analysis of
and homogeneity at serial levels of the descending aorta can the CCTA images. Changing contrast level can diminish
4 Orientation and Approach to Cardiovascular Images 65

a b

c d

Fig. 4.163 3-D images of the right coronary artery (arrows) in the left d): Images of coronary arteries with varying degree of transparency of
anterior oblique 30°/ caudal 0° view. Panel (a): Image with skeletal the heart. As opposed to invasive angiography, the left coronary artery
structures. Panel (b): Image of heart and coronary arteries. Panels (c, is also visualized. CAU caudal, LAO left anterior oblique

these artifacts, and viewing of thin slices can decrease traction. The motion of the right coronary artery is particu-
volume averaging artifact, but some arterial segment larly complex and therefore images may appear blurred,
evaluation may be non-diagnostic. appear as a “cashew nut” like shape or appear as a complete
double image, depending on the phase of the R-R interval
Coronary Artery Artifacts Due to Motion chosen to view. All available phases of the R-R interval
Artifacts can occur due to patient motion, respiratory motion, should be assessed for each coronary artery segment with
motion due to ectopic atrial and ventricular beats and other motion artifact in order to choose the most optimal images
arrhythmias, and cardiac/coronary artery motion (Fig. 4.164). for analysis.
Respiratory and patient motion artifacts are well seen on sag-
ittal views by viewing the sternum and other skeletal struc- Coronary Artery Artifacts Due to 3-D
tures. In coronal images and sagittal reconstructions, multiple Reconstruction
stacks of images are viewed simultaneously, and therefore Although the 3-D images are intuitive regarding the
thin collimation lines can be seen. If the data sets are not gross location, orientation and relationships of the coro-
aligned properly due to motion, step artifact can occur. nary arteries to cardiovascular structures, reconstruc-
Cardiac motion is complex, with contraction from apex to tion can lead to the artifactual appearance of coronary
base as well as rotational movement of the heart during con- artery stenosis or obstruction. The automated editing
66 J.S. Shinbane and A. Hindoyan

a b

Fig. 4.164 Coronary artery artifacts due to curved multiplanar refor- motion (arrow). Panel (b): Areas of coronary artery discontinuity due
mats of a left anterior mammary artery graft to the left anterior descend- to motion (white arrows). Additional blooming artifacts due to surgical
ing coronary artery. Panel (a): Double image of the LIMA graft due to clips are present (black arrow)

software may have edited out too much of the artery or racic masses, and assessment of abdominal structures
left in overlying tissue obstructing view of the coronary which may be in the field of view. Assessment of the non-
artery (Fig. 4.165 ). The variety of motion artifacts men- cardiovascular structures in the field of view should be per-
tioned above can lead to the discontinuous appearance formed by physicians with expertise in analysis of these
of the artery. Intra-myocardial bridging can also appear structures.
as coronary artery occlusion as the artery courses inter-
nal to the epicardium. Due to these issues related to 3-D Conclusion
reconstruction, the volume rendered images are not CCTA workstations and software provide multiple
used as the primary modality to document the presence modalities to assess cardiovascular structure and func-
of coronary artery stenoses. tion. Although axial images are most commonly relied on
for final interpretation, other planes and reconstruction
modalities, if used with a thorough knowledge of their
Non-cardiovascular Structure strengths and limitations, are important to analysis. The
employment of these modalities in an organized approach
Additional assessment of appropriately windowed full field coupled with an understanding of the spatial relationships
of view images need to be performed to assess: visceral between cardiovascular structures allow for comprehen-
situs, skeletal structure, lung parenchyma, presence of tho- sive diagnosis of cardiovascular pathology.
4 Orientation and Approach to Cardiovascular Images 67

a b c

Fig. 4.165 Coronary artery artifacts due to 3-D reconstruction. Panel the left anterior descending coronary artery without overlying tissue
(a): Over editing of a portion of the left anterior descending coronary demonstrating a patent left anterior descending coronary artery
artery (arrows). Panel (b): Under editing with overlying tissue (arrows)
obstructing view of the coronary artery (arrow). Panel (c): 3-D view of
68 J.S. Shinbane and A. Hindoyan

Orientation to Axial Images

a b

Fig. 4.1 (a–m) Serial axial 3-D CCTA images beginning at the level of the pulmonary artery with slices proceeding in a cranial to caudal
direction
4 Orientation and Approach to Cardiovascular Images 69

e f

g h

Fig. 4.1 (continued)

70 J.S. Shinbane and A. Hindoyan

i j

k l

Fig. 4.1 (continued)

4 Orientation and Approach to Cardiovascular Images 71

Fig. 4.1 (continued)

72 J.S. Shinbane and A. Hindoyan

Orientation to Sagittal Images

a b

Fig. 4.2 (a–j) Serial sagittal 3-D CCTA images beginning Serial sagittal CT angiography images beginning at the sternum and proceeding
leftward
4 Orientation and Approach to Cardiovascular Images 73

f g

h i

Fig. 4.2 (continued)

74 J.S. Shinbane and A. Hindoyan

Orientation to Coronal Images

a b

Fig. 4.3 (a–g) Serial coronal CCTA angiography images beginning at the sternum and proceeding posteriorly
4 Orientation and Approach to Cardiovascular Images 75

f g

Fig. 4.3 (continued)

Serial 2-D Axial, Coronal, and Sagittal Images

Fig. 4.4 Fig. 4.5

76 J.S. Shinbane and A. Hindoyan

Fig. 4.6
Fig. 4.9

Fig. 4.7 Fig. 4.10

Fig. 4.8 Fig. 4.11

4 Orientation and Approach to Cardiovascular Images 77

Fig. 4.15
Fig. 4.12

Fig. 4.13 Fig. 4.16

Fig. 4.14 Fig. 4.17

78 J.S. Shinbane and A. Hindoyan

Fig. 4.18 Fig. 4.21

Fig. 4.19 Fig. 4.22

Fig. 4.20 Fig. 4.23

4 Orientation and Approach to Cardiovascular Images 79

Fig. 4.24 Fig. 4.27

Fig. 4.25 Fig. 4.28

Fig. 4.26 Fig. 4.29

80 J.S. Shinbane and A. Hindoyan

Fig. 4.30 Fig. 4.33

Fig. 4.31 Fig. 4.34

Fig. 4.32 Fig. 4.35

4 Orientation and Approach to Cardiovascular Images 81

Fig. 4.36
Fig. 4.39

Fig. 4.37
Fig. 4.40

Fig. 4.41
Fig. 4.38
82 J.S. Shinbane and A. Hindoyan

Fig. 4.45

Fig. 4.42

Fig. 4.46

Fig. 4.43

Fig. 4.47
Fig. 4.44
4 Orientation and Approach to Cardiovascular Images 83

Fig. 4.48 Fig. 4.51

Fig. 4.49 Fig. 4.52

Fig. 4.50 Fig. 4.53

84 J.S. Shinbane and A. Hindoyan

Fig. 4.54 Fig. 4.57

Fig. 4.55 Fig. 4.58

Fig. 4.56 Fig. 4.59

4 Orientation and Approach to Cardiovascular Images 85

Fig. 4.60
Fig. 4.63

Fig. 4.61
Fig. 4.64

Fig. 4.62
Fig. 4.65
86 J.S. Shinbane and A. Hindoyan

Fig. 4.66

Fig. 4.69

Fig. 4.67

Fig. 4.70

Fig. 4.68
4 Orientation and Approach to Cardiovascular Images 87

Fig. 4.73
Fig. 4.71

Fig. 4.74
Fig. 4.72
88 J.S. Shinbane and A. Hindoyan

Fig. 4.75 Fig. 4.78

Fig. 4.79
Fig. 4.76

Fig. 4.80
Fig. 4.77
4 Orientation and Approach to Cardiovascular Images 89

Fig. 4.81 Fig. 4.84

Fig. 4.82 Fig. 4.85

Fig. 4.83 Fig. 4.86

90 J.S. Shinbane and A. Hindoyan

Fig. 4.87 Fig. 4.90

Fig. 4.88 Fig. 4.91

Fig. 4.92
Fig. 4.89
4 Orientation and Approach to Cardiovascular Images 91

Fig. 4.93 Fig. 4.96

Fig. 4.94 Fig. 4.97

Fig. 4.95 Fig. 4.98

92 J.S. Shinbane and A. Hindoyan

Fig. 4.99 Fig. 4.102

Fig. 4.100 Fig. 4.103

Fig. 4.101 Fig. 4.104

4 Orientation and Approach to Cardiovascular Images 93

Fig. 4.105 Fig. 4.108

Fig. 4.106
Fig. 4.109

Fig. 4.107
Fig. 4.110
94 J.S. Shinbane and A. Hindoyan

Fig. 4.111 Fig. 4.114

Fig. 4.112 Fig. 4.115

Fig. 4.113 Fig. 4.116

4 Orientation and Approach to Cardiovascular Images 95

Fig. 4.117 Fig. 4.120

Fig. 4.118 Fig. 4.121

Fig. 4.119 Fig. 4.122

96 J.S. Shinbane and A. Hindoyan

Fig. 4.123
Fig. 4.126

Fig. 4.124 Fig. 4.127

Fig. 4.125 Fig. 4.128

4 Orientation and Approach to Cardiovascular Images 97

Fig. 4.132
Fig. 4.129

Fig. 4.133
Fig. 4.130

Fig. 4.134
Fig. 4.131
 Part II
Cardiac CT
 Assessment of Cardiovascular Calcium:
Interpretation, Prognostic Value, 5
and Relationship to Lipids and Other
Cardiovascular Risk Factors

Harvey S. Hecht

Abstract
Coronary artery calcium scanning has proven to be the most powerful predictor of cardiac
risk in the primary prevention population, far exceeding conventional risk factors in
prognostic value. It has also proven superior to all markers of inflammation, ankle brachial
index, carotid intima-media thickness and flow mediated vasodilation. Its most accepted
application is in the intermediate risk cohort, with an outcome based net reclassification
index of the Framingham Risk Score exceeding 50 %. Application to young patients with a
family history of premature coronary disease and to all diabetics older than 40 years of age
is also appropriate.

Keywords
Coronary artery calcium • Primary prevention • Coronary artery disease • Risk factors •
Risk prediction • Atherosclerosis

Cardiac risk assessment has traditionally been based on Background

conventional risk factors; the shortcomings of this approach
are all too often highlighted by major cardiac events occur- CAC is pathognomonic for atherosclerosis [2–4].
ring in presumably low-risk people. The annual presentation Mönckeberg’s calcific medial sclerosis does not occur in the
of 650,000 previously asymptomatic patients with an acute coronary arteries [5]; atherosclerosis is the only vascular dis-
coronary event as the initial manifestation of coronary artery ease known to be associated with coronary calcification.
disease (CAD) [1] is a testimony to the failure of our current Calcium phosphate (in the hydroxyapatite form) and choles-
risk assessment model. Consequently, there has been a focus terol accumulate in atherosclerotic lesions. Circulating pro-
on markers of subclinical atherosclerosis that may be utilized teins that are normally associated with bone remodeling play
for risk assessment of individuals, rather than extrapolating an important role in coronary calcification, and arterial cal-
from risk factors that reflect trends in large groups of patients cium in atherosclerosis is a regulated active process similar
in epidemiologic studies. The most powerful of these sub- to bone formation, rather than a passive precipitation of cal-
clinical markers is coronary artery calcium (CAC). cium phosphate crystals [6–9]. Rumberger et al. [10] demon-
strated that the total area of coronary artery calcification is
highly correlated (r = 0.9) in a linear fashion with the total
H.S. Hecht, MD, FACC, FSSCT area of coronary artery plaque on a segmental, individual,
Department of Medicine, Icahn School of Medicine at Mount
and whole coronary artery system basis (Fig. 5.1), and the
Sinai, New York, NY, USA
areas of coronary calcification comprise approximately one
Mount Sinai Medical Center,
fifth that of the associated coronary plaque. Additionally,
One Gustave L. Levy Place, Box 1030,
New York, NY 10029-6574, USA there were plaque areas without associated coronary cal-
e-mail: [email protected] cium, suggesting that there may be a coronary plaque size

© Springer International Publishing 2016 101

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_5
102 H.S. Hecht

most commonly associated with coronary calcium but, in the Methodology

smaller plaques, the calcium is either not present or is
undetectable. Technical
Intravascular ultrasound [11, 12] measures of combined
calcified and non-calcified plaque confirm the strong In the beginning, the data substantiating the importance of
relationship (Fig. 5.2). CAC were derived through the use of electron beam
tomography (EBT), utilizing a rotating electron beam to
acquire prospectively triggered, tomographic 100-ms
X-ray images at 3 mm intervals in the space of a 30- to
16
40-s breathhold. The multidetector computed tomography
Square root sum of plaque areas

14 n = 38
(MDCT) technology has replaced EBT and employs a
r = 0.90
12 rotating gantry with a special X-ray tube and variable
p < 0.001
10 number of detectors (from 4 to 320), with 75–375-ms
8 images at 0.5,1.5, 2.0, or 3.0 mm intervals, depending on
6 the protocol and manufacturer.
4
2
Scoring
0
0 1 2 3 4 5 6 7
Square root sum of calcium areas
The presence of CAC is sequentially quantified through the
entire epicardial coronary system. Coronary calcium is
defined as a lesion above a threshold of 130 Hounsfield units
Fig. 5.1 Correlation between calcified and total plaque burden in
(which range from −1000 (air), through 0 (water), and up to
histopathologic coronary artery specimens (Reproduced from
Rumberger et al. [10], with permission from Wolters Kluwer +1000 (dense cortical bone)), with an area of three or more
Health) adjacent pixels (at least 1 mm2). The original calcium score

Fig. 5.2 Coronary artery

calcium scan (left) demonstrating
areas of extensive calcification
corresponding to heavily
calcified plaque on intravascular
ultrasound (upper right), and less
extensive calcification
corresponding to less heavily
calcified plaque on intravascular
ultrasound (lower right), AO
aorta, RVOT right ventricular
outflow tract
5 Assessment of Cardiovascular Calcium 103

developed by Agatston et al. [13] is determined by the Epidemiology

product of the calcified plaque area and maximum calcium
lesion density (from 1 to 4 based upon Hounsfield units). By comparing a person’s calcium score to others of the same
Standardized categories for the calcium score have been age and gender through the use of large databases of asymp-
developed with scores of 0 indicating absence of calcified tomatic subjects, a calcium percentile is generated [16]. This
plaque, 1–10 considered minimal, 11–100 mild, 101–400 is an index of the prematurity of atherosclerosis; for exam-
moderate, and >400 severe. Examples are shown in Fig. 5.1. ple, a 50-year-old man in the 76th percentile has more plaque
The calcium volume score [14] is a more reproducible than 75 % but less plaque than 24 % of asymptomatic
parameter that is independent of calcium density and may be 50-year-old men. Although there is an increasing incidence
the parameter of choice for serial studies to track progression of coronary calcification with increasing age, this simply
or regression of atherosclerosis, but is rarely used. Phantom- parallels the development of coronary atherosclerosis.
based calcium mass scores are applicable to any CT scanner Table 5.1 shows coronary calcification incidence in an
[15], but are never clinically used. Examples of CAC scans unselected patient population of men and women [17]. The
are shown in Fig. 5.3. amount of CAC in women is similar to that in men a decade

Fig. 5.3 Examples of coronary artery calcium scans. Left normal with- involving the left main (LM), anterior descending, and circumflex
out CAC. Center moderate CAC involving the left anterior descending coronary arteries, LADD left anterior descending diagonal branch
(LAD) and circumflex (LCx) coronary arteries. Right extensive CAC

Table 5.1 Calcium percentile database for asymptomatic men and women: coronary calcium scores as a function of patient age at the time of
examination
Percentiles 40–45 years 46–50 years 51–55 years 56–60 years 61–65 years 66–70 years 71–75 years
Men (n = 28,250)
10 0 0 0 1 1 3 3
25 0 1 2 5 12 30 69
50 2 3 15 54 117 166 350
75 11 36 110 229 386 538 844
90 69 151 346 588 933 1151 1650
Women (n = 14,540)
10 0 0 0 0 0 0 0
25 0 0 0 0 0 1 4
50 0 0 1 1 3 25 51
75 1 2 6 22 68 148 231
90 4 21 61 127 208 327 698
104 H.S. Hecht

younger, paralleling the 10-year lag in women of the focused on the low specificity as a critical flaw. While the
development of clinical atherosclerosis. presence of CAC is nearly 100 % specific for atherosclerosis,
Useful though these current nomograms are, variations it is not specific for obstructive disease since both obstructive
according to ethnicity have been described, and data regard- and non-obstructive lesions have calcification present in the
ing these variations are still being collected and separated. intima. Comparisons with pathology specimens have shown
In earlier studies, Blacks were noted to have either lower that the degree of luminal narrowing is weakly correlated
[18, 19] or similar [20, 21] amounts of CAC as Caucasians with the amount of calcification on a site-by-site basis [28–
of the same age; Hispanics had less CAC than Caucasians 30], whereas the likelihood of significant obstruction
[18]. In the more recent Multi-Ethnic Study of increases with the total CAC score [4, 31, 32]. Shavelle et al.
Atherosclerosis (MESA) of 6110 asymptomatic patients [33] reported a 96 % sensitivity and 47 % specificity for a
with 53 % female and an average age of 62 years, men had calcium score >0, with a relative risk for obstructive disease
greater calcium levels than women, and calcium amount of 4.5, compared to a 76 % sensitivity and 60 % specificity
and prevalence continually increased with increasing age for treadmill testing, with a relative risk of 1.7. Bielak et al.
[22]. In men, Caucasians and Hispanics were the first and [34] noted a sensitivity and specificity of 99.1 % and 38.6 %
second highest respectively; Blacks were lowest at the for a calcium score >0. However, when corrected for
younger ages, and Chinese were lowest at the older ages. In verification bias, the specificity improved to 72.4 %, without
women, whites were highest, Chinese and Black were loss of sensitivity (97 %). The likelihood ratio for obstruc-
intermediate, and Hispanics were the lowest except for tion ranged from 0.03–0.07 in men and women ≥50 years of
Chinese in the oldest age group. Thus, predictive indices age for 0 scores to 12.85 for scores >200. In the <50 years
should be extrapolated to non-whites with caution. cohort, the likelihood ratios ranged from 0.1–0.29 for 0
However, MESA demonstrated very strong CAC predictive scores to 54–189 for scores >100.
for all groups [23]. Rumberger et al. [35] demonstrated that higher calcium
Younger patients with a family history of premature CAD scores are associated with a greater specificity for obstruc-
have significantly higher CAC scores than similar aged tive disease at the expense of sensitivity; for example, a
individuals without this risk factor, particularly if there is a threshold score of 368 was 95 % specific for the presence of
sibling history of premature CAD [24]. In MESA, the odds obstructive CAD. In 1764 persons undergoing angiography,
ratios for the presence of CAC independent of all risk factors the sensitivity and negative predictive value in men and
in those with compared to those without a family history of women were >99 % [36]; a score of 0 virtually excluded
premature CAD were 2.74 with premature CAD in both a patients with obstructive CAD. In a separate study of 1851
parent and a sibling, 2.06 in a sibling alone, and 1.52 in a patients undergoing CAC scanning and angiography [37],
parent alone [25]. CAC scanning by EBT in conjunction with pretest probabil-
ity of disease derived by a combination of age, gender, and
risk factors, facilitated prediction of the severity and extent
Radiation of angiographically significant CAD in symptomatic
patients.
The vast majority of CAC scanning is performed on MDCT In a recent meta-analysis of 10,355 symptomatic patients
scanners. The radiation exposure should not exceed 1.0 mSv who underwent cardiac catheterization and CAC, 0 CAC was
[26]. Iterative reconstruction techniques that decrease noise noted in 1941. Significant obstructive disease, defined as
will lead to even lower radiation exposure. Appropriate >50 % diameter stenosis, was noted in 5805 (56 %). For
perspective is obtained by comparing this exposure to the CAC >0 and the presence of >50 % diameter stenosis, the
0.75 mSv of the annual mammographic examination following were reported: sensitivity 98 %, specificity 40 %,
recommended for women 45 years and older. positive predictive value 68 %, and negative predictive value
93 % [38].

Coronary Artery Calcium and Obstructive

Disease Prognostic Studies in Symptomatic Patients

Incidence The prognostic value of extensive CAC (>1000) in symp-

tomatic males with established advanced CAD was demon-
The relationship of CAC to obstructive disease has been strated in a 5-year follow-up study of 150 patients [39]. More
extensively investigated, and was misunderstood by the 2000 recently, in a meta-analysis of 3924 symptomatic patients
ACC/AHA Consensus Document on EBT [27], which with a 3.5 year follow up, the cardiac event rate was
5 Assessment of Cardiovascular Calcium 105

2.6 %/year in those with CAC >0 and 0.5 %/year in 0 CAC smoking, respectively. In women, only CAC was linked to
patients [38]. However, in this era of coronary computed events, with a relative risk of 2.6; risk factors were not
tomographic angiography (CCTA), CAC alone is not justi- related. The presence of CAC provided prognostic informa-
fied in the symptomatic population; CCTA will identify the tion incremental to age and other risk factors.
noncalcified plaque and obstructive disease that may be Shaw et al. [44] retrospectively analyzed 10,377 asymp-
noted in these patients, even with 0 CAC. tomatic patients with a 5-year follow-up after an initial EBT
evaluation. All-cause mortality increased proportional to
Clarification CAC, which was an independent predictor of risk after
Despite the apparently reasonable specificities, which are adjusting for all of the Framingham risk factors (p < 0.001).
similar to those of stress testing, it must be understood that Superiority of CAC to conventional Framingham risk factor
the purpose of CAC scanning is not to detect obstructive assessment was demonstrated by a significantly greater area
disease and, therefore, it is inappropriate to even use under the ROC curves (0.73 versus 0.67, p < 0.001).
“specificity” in the context of obstruction. Rather, its purpose Greenland et al. [45] analyzed a population-based study
is to detect subclinical atherosclerosis in its early stages, for of 1461 prospectively followed, asymptomatic subjects who
which it is virtually 100 % specific.

CAC in Asymptomatic Patients

Percent/year cardiac events

4.8
4.1
Key Prognostic Studies in Primary Prevention 4
and Comparisons with Standard Risk Factor
Paradigms
2.1
The utility of CAC for risk evaluation in the asymptomatic 2
primary prevention population is dependent on prognostic
studies documenting the relative risk conferred by calcified
plaque quantitation compared to conventional risk factors. 0.11
0
Raggi et al. [40] demonstrated, in 632 asymptomatic patients
0 1-90 100-400 >400
followed for 32 months, an annualized event rate of 0.1 %/
Calcium scores
year in patients with 0 scores, compared to 2.1 %/year with
scores of 1–99, 4.1 %/year with scores of 100–400, and Fig. 5.4 Relationship of coronary artery calcium score to annual hard
4.8 %/year with scores >400. Thus, the annualized event cardiac event rates in 632 asymptomatic patients undergoing EBT cal-
rates associated with coronary calcium were in the range cified plaque imaging. The solid line indicates the 2 %/year event rate
consistent with secondary prevention risk
considered to warrant secondary prevention classification by
the Framingham Risk Score (Fig. 5.4).
The odds ratio conferred by a calcium percentile >75 % 25
was 21.5 times greater than for the lowest 25 %, compared to 21.5
an odds ratio of 7 for the highest versus lowest quartiles of 20 EBT
National Cholesterol Education Program (NCEP) risk fac-
All NCEP risk factors
tors (Fig. 5.5).
Odds ratio

15
Wong et al. [41], in 926 asymptomatic patients followed
for 3.3 years, noted a relative risk of 8 for scores >270, after
10
adjusting for age, gender, hypertension, high cholesterol,
7
smoking, and diabetes. Arad et al. [42], in 1132 subjects fol- 6.2
lowed for 3.6 years, reported odds ratios of 14.3–20.2 for 5
3.1 3.1
scores ranging from >80 to >600; these were 3–7 times 1 1 1
greater than for the NCEP risk factors. In a retrospective 0
analysis of 5635 asymptomatic, predominantly low to mod- 1st 2nd 3rd 4th
erate risk, largely middle-aged patients followed for Calcium percentile quartiles
37 ± 12 months, Kondos et al. [43] found that the presence of
Fig. 5.5 Odds ratios of coronary artery calcium and NCEP risk factor
any CAC by EBT was associated with a relative risk for quartiles for annual hard cardiac event rates in asymptomatic patients
events of 10.5, compared to 1.98 and 1.4 for diabetes and undergoing coronary artery calcium imaging
106 H.S. Hecht

3.5 3.3 Table 5.2 Risk of coronary events associated with increasing coronary
artery calcium after adjusting for standard risk factors in MESA
3 2.4
2.5 CAC Annual rate Events/no at risk HR P
2 0 0.11 % 15/3409 1.0 <0.001
2
1–100 0.59 % 39/1728 3.61 <0.001
1.5
101–300 1.43 % 41/752 7.73 <0.001
1 0.7 >300 2.87 % 67/833 9.67 <0.001
0.5 0.12 Doubling 1.26 <0.001
0

35 32 12.5 Coronary-artery calcium score

Cumulative incidence of coronary

30
>300
25 101−300
10.0
20 1−100
16
15 0

events (%)
12
75
10
5 1 2.5
0 50

2.5

Fig. 5.6 Annual event rates and relative risks for cardiac events in 0.0
5585 asymptomatic patients at different levels of coronary artery cal- 0.0 1.0 2.0 3.0 4.0 5.0
cium (St. Francis Heart Study). The solid line indicates the 2 %/year Years to event
event rate consistent with secondary prevention risk
Fig. 5.7 Coronary events at different CAC levels in MESA

were predominantly moderate to high risk, and found that population (71 years), Vliegenthart et al. found a hazard ratio
CAC scores >300 significantly added prognostic information of 4.6 for CAC 400–1000 compared to <100 after 3.3 years
to Framingham risk analysis in the 10–20 % Framingham of follow up [49].
risk category. The results of the St Francis Heart Study by Subsequently, even more powerful data have emerged.
Arad et al. [46] in a prospective, population-based study of Budoff et al. [50] in another all cause mortality study, with
5585 asymptomatic, predominantly moderate- to moderately- retrospective analysis of 25,203 asymptomatic patients
high-risk men and women, mirrored previous retrospective after 6.8 years, found that CAC >400 was associated with a
studies [7, 18–20], and confirmed the higher event rates hazard ratio of 9.2. In the largest study using coronary
associated with increasing CAC scores. CAC scores >100 calcium percentile rather than absolute scores, Becker et al.
were associated with relative risks of from 12 to 32, and were [51] in 1724 patients followed prospectively for 3.4 years,
secondary prevention equivalent, with event rates >2 %/year reported hazard ratios for CAC percentile >75 % versus
(Fig. 5.6). Incremental information over Framingham scores 0 % of 6.8 for men and 7.9 for women. The area under the
was documented with areas under the ROC curves of 0.81 ROC curve for CAC percentile (0.81) was significantly
for CAC and 0.71 for Framingham (p < 0.01). superior to the Framingham (0.66), European Society of
The prognostic significance of very high calcium scores Cardiology (0.65), and PROCAM risk scores (0.63). Eighty
was provided in a study of 98 asymptomatic patients with a two percent of patients who developed myocardial infarc-
CAC score >1000 who were followed for 17 months [47] tion or cardiac death were correctly classified as high risk
during which 35 patients (36 %) suffered a hard cardiac by CAC percentile, compared to only 30 % by Framingham,
event (myocardial infarction or cardiac death). The annual- 36 % by the European Society of Cardiology, and 32 % by
ized event rate of 25 % refuted the erroneous concept that PROCAM.
extensive calcified plaque may confer protection against Perhaps the most important study is the Multiethnic
plaque rupture and events. Study of Atherosclerosis, an NHLBI sponsored prospective
In a younger cohort of 2000 asymptomatic Army person- evaluation of 6814 patients followed for 3.8 years [23].
nel, Taylor et al. [48] demonstrated the powerful predictive Compared to patients with 0 CAC, the hazard ratios for a
value of CAC. There was a relative risk of 11.8 in patients coronary event were 7.73 for those with CAC 101–300,
with CAC >44 compared to those with 0 CAC, after correct- and 9.67 among participants for CAC >300 (P < 0.001)
ing for the Framingham Risk Score. In a much more elderly (Table 5.2; Fig. 5.7).
5 Assessment of Cardiovascular Calcium 107

Table 5.3 Characteristics and risk ratio for follow-up studies using coronary artery calcium in asymptomatic persons
Mean age Follow-up Calcium score Comparator group Relative risk
Author N (years) duration (years) cutoff for RR calculation ratio
Arad [42] 1173 53 3.6 CAC >160 CAC <160 20.2
Park [108] 967 67 6.4 CAC >142.1 CAC <3.7 4.9
Raggi [40] 632 52 2.7 Top quartile Lowest quartile 13
Wong [41] 926 54 3.3 Top quartile (>270) First quartile 8.8
Kondos [43] 5635 51 3.1 CAC No CAC 10.5
Greenland [45] 1312 66 7.0 CAC >300 No CAC 3.9
Shaw [44] 10,377 53 5 CAC ≥400 CAC ≤10 8.4
Arad [46] 5585 59 4.3 CAC ≥100 CAC <100 10.7
Taylor [48] 2000 40–50 3.0 CAC >44 CAC = 0 11.8
Vliegenthart [49] 1795 71 3.3 CAC >1000 CAC < 100 8.3
Budoff [50] 25,503 56 6.8 CAC >400 CAC 0 9.2
Lagoski [53] 3601 45–84 3.75 CAC >0 CAC 0 6.5
Becker [51] 1726 57.7 3.4 CAC >400 CAC 0 6.8 men
7.9 women
Detrano [23] 6814 62.2 3.8 CAC >300 CAC 0 14.1
Erbel [55] 4487 45–75 5 >75th % <25th % 11.1 men
3.2 women
CAC coronary artery calcium score

Among the four racial and ethnic groups (Caucasian, Table 5.4 Summary of CAC absolute event rates from 14,856 patients
Chinese, Hispanic, Black), doubling the CAC increased risk in five prospective studies
of any coronary event by 18–39 %. The ROC curve areas CAC FRS risk Ten years event rate
were significantly higher (p < 0.001) with the addition of 0 Very low 1.1–1.7 %
CAC to standard risk factors. CAC was more predictive of 1–100 Low 2.3–5.9 %
coronary disease than carotid intima-media thickness; the 100–400 Intermediate 12.8–16.4 %
hazard ratios per 1-SD increment increased 2.5-fold (95 % >400 High 22.5–28.6 %
CI, 2.1–3.1) for CAC and 1.2-fold (95 % CI, 1.0–1.4) for >1000 Very high 37 %
IMT [52]. Abbreviations: CAC coronary artery calcium, FRS Framingham risk
In the 2684 patients in the female component of MESA score
[53], Lagoski et al. reported a 6.5 hazard ratio for the 32 %
with a CAC >0 versus the 68 % with 0 CAC, even though
90 % were low risk by Framingham. In an analysis of all the AUC from 0.602 to 0.727 in men and from 0.660 to
cause mortality in 44,052 asymptomatic patients followed 0.723 in women, and led to a reclassification of 77.1 % of
for 5.6 years [54], the deaths/1000 patient years were 7.48 intermediate risk individuals (62.9 % into low risk, and
for CAC >10, compared to 1.92 for CAC 1–10, and 0.87 for 14.1 % into high risk group). The relative risk associated
0 CAC. Finally, in a meta-analysis of 64,873 patients fol- with doubling of the CAC score was 1.32 (95 % CI: 1.20–
lowed for 4.2 years, the coronary event rate was 1 %/year for 1.45, p < 0.001) in men and 1.25 (95 % CI: 1.11–1.42,
the 42,283 with CAC >0, compared to 0.13 %/year in the p < 0.0001) in women.
25,903 patients with 0 CAC [38]. In all of these studies, receiver operator characteristic
Finally, in the Heinz Nixdorf Recall Study [55], 4487 curves for CAC were superior to the Framingham Risk Score
subjects without CAD were followed for 5 years. Low ATP and the annual event rate for CAC >100–400 exceeded the
III risk was noted in 51.5 %, while 28.8 % and 19.7 % were coronary artery disease equivalent of >2 %/year. Table 5.3
at intermediate and high risk, respectively. The prevalence summarizes the relative risk results of the largest published
of low (<100), intermediate (100–399) and high (≥400) outcome studies.
CAC scores was 72.9 %, 16.8 % and 10.3 %, respectively Amalgamation of data from five large prospective ran-
(p < 0.0001). The relative risk of CAC >75th vs ≤25th per- domized studies [23, 46, 49, 51, 55] yields 10 year event
centile was 11.1 (p < 0.0001) for men and 3.2 (p = 0.006) for rates that can be translated into Framingham Risk Score
women. Adding CAC to the ATP III categories improved equivalents (Table 5.4). CAC >400 is a CAD equivalent,
108 H.S. Hecht

Table 5.5 Reclassification of FRS risk by CAC primary prevention 4.2 years [54], the coronary event rate was 0.13 %/year in
outcome studies the 25,903 patients with 0 CAC compared to 1 %/year for
Study % reclassified N Age Follow up (years) the 42,283 with CAC >0. In an analysis of all cause mortal-
MESA 5878 62.2 5.8 ity in 44,052 asymptomatic patients followed for 5.6 years
FRS 0–6 % 11.6 % [54], the deaths/1000 patient years for the 19,898 with 0
FRS 6–20 % 54.4 % CAC was 0.87, compared to 1.92 for CAC 1–10, and 7.48
FRS >20 % 35.8 % for CAC >10.
NRI 25 % While non-calcified, potentially “vulnerable” plaque is by
Heinz Nixdorf 4487 45–75 5.0 definition not detected by CAC testing, CAC can identify the
FRS <10 % 15.0 % pool of higher-risk asymptomatic patients out of which will
FRS 10–20 % 65.6 % emerge approximately 95 % of the patients presenting each
FRS >20 % 34.2 % year with sudden death or an acute myocardial infarction
Rotterdam 2028 69.6 9.2 (MI). While the culprit lesion contains calcified plaque in
FRS <10 % 12 % only 80 % of the acute events [57], of greater importance is
FRS 10–20 % 52 %
the observation that exclusively soft, non-calcified plaque
FRS >20 % 34 %
has been seen in only 5 % of acute ischemic syndromes in
NRI 19 %
both younger and older populations [12, 58]. In a more recent
Abbreviations: CAC coronary artery calcium, FRS Framingham risk meta-analysis [38], only 2 of 183 (1.1 %) 0 CAC patients
score, MESA multiethnic study of atherosclerosis
were ultimately diagnosed with an acute coronary syndrome
after presenting with acute chest pain, normal troponin, and
with 10 year event rates exceeding 20 % in asymptomatic equivocal EKG findings. CAC >0 had 99 % sensitivity, 57 %
patients. The absence of calcified plaque conveys an extraor- specificity, 24 % positive predictive value, and 99 % negative
dinarily low 10 year risk (1.1–1.7 %), irrespective of the predictive value for ACS. Thus, while it is uncommon that a
number of risk factors [56]. patient with an imminent acute ischemic syndrome would
Of critical importance is the net reclassification index have had a 0 CAC score, further evaluation, particularly with
(NRI) conferred by CAC in the asymptomatic population by CCTA, is mandatory.
three major prospective population based studies [23, 49, 55]
(Table 5.5). The percentage of patients with FRS risk esti-
mate correctly reclassified by CAC based on outcomes Adherence to Therapeutic Interventions
ranged from 52 to 65.6 % in the intermediate risk population,
34–35.8 % in the high risk group and 11.6–15 % in the low With the exception of a single study flawed by insufficient
risk cohort, with NRI’s for the entire study population from power [59], CAC has been shown to have a positive effect
19 to 25 %. on initiation of and adherence to medication and life style
changes. In 505 asymptomatic patients, statin adherence
3.6 years after visualizing their CAC scan was 90 % in
Zero Coronary Artery Calcium Scores those with CAC >400 compared to 75 % for 100–399,
63 % for 1–99, and 44 % for 0 CAC (p < 0.0001) [60].
Individuals with zero CAC scores have not yet developed Similarly, in 980 asymptomatic subjects followed for
detectable, calcified coronary plaque but they may have fatty 3 years, ASA initiation, dietary changes, and exercise
streaking and early stages of plaque. Non-calcified plaques increased significantly from those with 0 CAC (29 %,
are present in many young adults. Nonetheless, the event 33 %, 44 %, respectively) and was lowest (29 %) in those
rate in patients with CAC score 0 is very low [40, 45, 46]. with CAC >400 (61 %, 67 %, 56 %, respectively [61].
Raggi et al. [40] demonstrated an annual event rate of 0.11 % Finally, after a 6 year follow up in 1640 asymptomatic sub-
in asymptomatic subjects with 0 scores (amounting to a jects, the odds ratios for those with CAC >0 compared to 0
10-year risk of only 1.1 %), and in the St Francis Heart CAC for usage of statins, ASA, and statin + ASA were
Study [46], scores of 0 were associated with a 0.12 % annual 3.53, 3.05 and 6.97, respectively [62]. In the Eisner
event rate over the ensuing 4.3 years. Greenland et al. [45], (Early Identification of Subclinical Atherosclerosis by
in a higher-risk asymptomatic cohort, noted a higher annual Noninvasive Imaging Research) trial, 2137 asymptomatic
event rate (0.62 %) with 0 CAC scores; a less sensitive CAC patients were randomized to using CAC to guide treatment
detection technique and marked ethnic heterogeneity may or employing usual care [63]. CAC directed care produced
have contributed to their findings. In the definitive MESA significant improvement in systolic blood pressure, LDL-
study [23], 0 CAC was associated with a 0.11 % annual C, weight and waist size compared to usual care, without
event rate. In a meta-analysis of 64,873 patients followed for an increase in downstream testing. Patients with CAC >400
5 Assessment of Cardiovascular Calcium 109

Apparently healthy population men >45 year women > 55 year1

Step 1 Very low risk3 Exit Exit All >75year receive uncondtional treatment2

. Coronary Artery Calcium Score (CACS)

Atherosclerosis test or
. Carotid IMT (CIMT) & Carotid Plaque4

Step 2 Negative test Positive test

.CACS = 0 . CACS = 1
. CIMT <50th percentile . CIMT ≥50th percentile or carotid plaque
No risk factors5 + risk factors . CACS<100 & <75th% . CACS100-399 or >75th% . CACS >100& >90th%
. CIMT<100 & <75th% .CIMT ≥1 mm or >75th% or CACS ≥400
&no carotid plaque or <50 % stenotic plaque . ≥50% stenotic plaque5

ABI <0.9
Step 3 CRP >4 mg
Lower Moderate Moderately High Very
risk risk high rish Optional rish high rish

LDL <160 mgdl <130 mgdl <130 mgdl <100 mgdl <70 mgdl
target <100 Optional <70 Optional
Re-test interval 5–10 years 5–10 years Individuaized Individuaized Individuaized

My ocardial
Follow existing ischemia test
guidelines

Angiography Yes No

Fig. 5.8 The SHAPE guideline (Towards the National Screening for Heart Attack Prevention and Education Program)

had significantly greater improvement in all parameters recommendation for low intermediate risk (<7.5 %), similar
than those with 0 CAC. to the 2010 guidelines for low-intermediate risk (6–10 %,
class IIb). CAC is now recommended when clinical deci-
sion making is unclear (by physician or patient), for those
Coronary Artery Calcium and Guidelines with risk <7.5 % and they state “assessing CAC is likely to
be the most useful of the current approaches to improving
In 2006, the SHAPE guidelines (Fig. 5.8) recommended risk assessment among individuals found to be at interme-
CAC or carotid intima-media thickening for all but the diate risk after formal risk assessment.” This however does
lowest risk asymptomatic men >45 years and women essentially exclude the intermediate risk population for
>55 years, with subsequent treatment based upon the which the NRI by CAC in three major population-based
amount of CAC [64]. prospective outcome studies [23, 49, 55] has ranged from
The 2010 ACCF/AHA Guideline for Assessment of 52 to 66 % (see Table 5.3). The outcomes on which the
Cardiovascular Risk in Asymptomatic Adults appropri- 2013 guidelines were based were changed by the addition
ately assigned a class IIa recommendation to CAC for of stroke, for which the investigators believed there was
evaluation of the asymptomatic intermediate-risk popula- not sufficient CAC data, even though the Heinz Nixdorf
tion and for all patients older than 40 with diabetes melli- Recall Study of 4180 patients demonstrated hazard ratios
tus [65]. On the basis of flawed assumptions, the 2013 of CAC for stroke to be similar to age, hypertension, and
American College of Cardiology (ACC)/AHA Guideline smoking (Table 5.6) [68]. Further, the MESA data shows
on the Treatment of Blood Cholesterol to Reduce CVD (including stroke) performs as well as CAD [69].
Atherosclerotic Cardiovascular Risk in Adults [66] and Erroneous cost and radiation exposure concerns were also
the 2013 ACC/AHA Guideline on the Assessment of used to justify the classification, despite the $100 CAC
Cardiovascular Risk [67] assigned CAC to a class IIb cost and the decrease in radiation to <1 mSv.
110 H.S. Hecht

Table 5.6 Relationship between coronary artery calcium and events in asymptomatic diabetic patients
Study n Prevalence Hazard ratio AUC Event rates ⁄ year
Wong [85] 1823 Any CAC
No DM: 53 %
DM: 73.5 %
Becker [86] 716 DM 0 CAC: 15 % CAC: 0.77 0 CAC: 0.2 %
CAC >400: 42 % FRS: 0.68 CAC >400:5.6 %
UKPDS: 0.71
P < 0.01
Eikeles [87] 589 DM Compared to CAC 0–10 CAC: 0.73 CAC <10: 0 %
CAC >1000: 13.8 UKPDS: 0.63
CAC 401–1000: 8.4 P < 0.03
CAC 101–400: 7.1
CAC 11–100: 4.0
Anand [88] 510 DM CAC <10: 53.7 % Compared with CAC <100 CAC: 0.92
CAC >1000: 58 UKPDS: 0.74
CAC 401–1000: 41 FRS: 0.60
CAC 101–400: 10 P < 0.001
CAC 0–100: 1
Malik [89] 881 DM Inc. CAC: 2.9–6.5 CAC + RF: 0.78–0.80 1.5 %
4036 No DM Inc. CAC: 2.6–9.5 RF: 0.72–0.73 0.5 %
P < 0.001
Source: Wiley from Hecht and Narula [107]
AUC area under curve, CAC coronary artery calcium, DM diabetes mellitu, FRS Framingham risk score, Inc. increasing, MetS metabolic syn-
drome, RF risk factors, UKPDS UK prospective diabetes study

Correlation with Risk Factors Framingham Risk Scores between postmenopausal women
with and without calcified plaque, rendering therapeutic
Correlation in Individual Patients decisions that are not plaque- imaging-based extremely
with Conventional Risk Factors problematic.
The very limited value of individual risk factors for risk
Conventional risk factors do correlate with CAC [70–72], prediction was illustrated by Nasir et al. [56] in 44,952
even though CAC is superior to conventional risk factors in primary prevention patients followed for 5.6 years. The
predicting outcomes. There is a clear association of CAC decrease in survival in 0 CAC subjects with increasing
with a premature family history of CAD, diabetes, and lipid numbers of risk factors was trivial, declining from 99.7 %
values in large groups of patients. However, the difficulty with no risk factors to 99.0 % with ≥3 risk factors. Patients
equating risk factors with CAC in individual patients has with a CAC >400 and no risk factors had 7× the risk of 0
been highlighted by the work of Hecht et al. in 930 consecu- CAC patients with ≥3 risk factors (16.9 vs 2.7 events per
tive primary prevention subjects undergoing EBT [71]. They 1000 patients years.
found increasing likelihoods of CAC with increasing levels
of low-density lipoprotein cholesterol (LDL-C) and decreas-
ing levels of high-density lipoprotein cholesterol (HDL-C) Correlation with Novel Risk Factors
in the population as a whole, but found no differences in
the amount of plaque between groups and demonstrated a MESA extended the risk factor inferiority to more novel risk
total lack of correlation in individual patients between the factors, including hs-CRP, carotid IMT, ankle bracial index,
EBT calcium percentile and the levels of total, LDL- and flow mediated vasodilation and family history of premature
HDL-cholesterol, total/HDL-cholesterol, triglycerides, CAD, (Table 5.7). In 1330 intermediate risk patients followed
lipoprotein(a) (Lp(a)), homocysteine, and LDL particle size. for 7.6 years in the Multiethnic Study of Atherosclerosis,
Postmenopausal women presented a striking example of CAC had the highest HR and correctly reclassified 66 % of
the inability of conventional risk analysis to predict the FRS predicted outcomes [69]. Similarly, in 1286 asymptom-
presence or absence of subclinical atherosclerosis [73]. atic patients with a 4.1 year follow up, a combination of five
There were no differences in any lipid parameters or in the blood biomarker risk factors, including hs-CRP, interleuk-6,
5 Assessment of Cardiovascular Calcium 111

myeloperoxidase, beta natriuretic protein and plasminogen Genetics

activator-1, did not significantly increase the FRS c-statistic.
CAC, on the other hand, increased it from 0.73 to 0.84 The lack of clear relationship between lipid levels and
(p < 0.003) [74]. subclinical plaque in individual patients does not negate the
The poor risk prediction performance of hs-CRP and its atherogenic effect of these metabolic disorders. Rather, it
lack of correlation with CAC do not challenge the highlights the variations in individual susceptibility to the
inflammatory aspects of the disease process. Rather, it atherogenic effects at a given plasma level, very likely
emphasizes the greater value of evidence of the disease itself, mediated by as yet undetermined genetic factors. O’Donnell
namely CAC, compared to a risk marker, such as et al. [76], in an analysis of abdominal aortic calcium in 2151
hs-CRP. Moreover, inflammation is the central commonality patients in 1159 families in the Framingham Study, noted a
for a host of diseases characterized by higher incidences of heritability component accounting for up to 49 % of the
both subclinical and clinical atherosclerosis (Fig. 5.9). variability in calcified plaque, and concluded that “AAC
There is much less data regarding lipoprotein-associated deposits are heritable atherosclerotic traits. A substantial
phospholipase A2 (Lp-PLA2). In a nested case–control portion of the variation is due to the additive effects of genes,
study among 266 CARDIA participants [75], Lp-PLA2 mass which have yet to be characterized.” Peyser et al. [77],
was significantly higher in subjects with CAC compared to analyzing coronary calcium in 698 patients in 302 families,
those without CAC (OR 1.28). The numbers are too small to found a variance of up to 48 % associated with additive
provide meaningful conclusions. polygenes after adjustment for covariates. They concluded
that there is a: substantial genetic component for subclinical
CAD variation . . . even after accounting for effects of genes
Table 5.7 Comparison of novel risk markers for improvement in acting through measured risk factors. These genes may act
cardiovascular risk assessment in 1330 intermediate-risk individuals
through other measurable risk factors or through novel
Marker Multivariate HR p NRI vs FRS pathways that have not or cannot be measured in vivo.
ABI 0.79 .01 .036 Identification of such genes will provide a better basis for
Brachial FMD 0.82 .52 .024 prevention and treatment of subclinical CAD.
CAC 2.60 <.001 .659 Unfortunately, the single nucleotide polymorphism arena
Carotid IMT 1.33 .13 .102 has not yet delivered any clinically concrete options.
Family history 2.18 .001 .160 The inevitable conclusion of the consistent lack of rela-
hs-CRP 1.26 .05 .079 tionship between risk factors and disease and the superiority

Fig. 5.9 Inflammatory diseases associated with a higher risk of coronary artery disease. Abbreviations: COPD chronic obstructive pulmonary
disease, CVD cardiovascular disease, HIV human immunodeficiency virus, PVD peripheral vascular disease, SLE systemic lupus erythematosus
112 H.S. Hecht

of CAC in individual patients was summarized by Hecht family history, while an NCEP risk factor, does not contrib-
[78]: “The most important role of risk factors may be to iden- ute points to the Framingham score. In 222 young patients
tify the modifiable targets of risk reduction in patients with presenting with an MI as the first sign of CAD (mean age
risk already established by clinical events or significant 50 years), Akosah et al. [82] demonstrated that 70 % were in
CAC.” these lesser risk categories and would not have been started
on a statin using NCEP guidelines. Data from Schmermund
et al. [12] and Pohle et al. [58] indicate that 95 % of acute MI
Clinical Applications patients would have been identified by CAC plaque imaging
irrespective of age. On the basis of these observations, the
Patient Selection use of CAC scoring should be considered in patients with a
family history of premature CAD, irrespective of the FRS, as
Intermediate Risk recommended by the 2009 CAC Appropriate Use Criteria
Hecht et al. [79] proposed recommendations for the [83]. Irrespective of family history, the NRI in the low risk
application of CAC scanning (Table 5.8). The Framingham population ranges from 11.6 to 16 %; approximately one of
Risk Score [80], incorporating both age and gender, was every eight low risk patients will miss the opportunity for
recommended as the initial step in selecting the appropriate recognition of their increased risk and upgrading of therapy
test populations. Asymptomatic patients in the National in the absence of CAC scanning.
Cholesterol Education Adult Treatment Program III [81]
classified 10–20 % Framingham 10-year risk category Higher Risk
(intermediate risk) comprise the group that presents the With an NRI of 35 % for the FRS >20 % group, scanning of
greatest challenge to the treating physician, and are those in this cohort appears appropriate, with treatment and goals to
whom the application of CAC scoring is most appropriate; be determined by the CAC level. Whether or not clinicians
the CAC score can assist the physician in decisions regarding will consider downgrading intensity of treatment is quite
the initiation of statin therapy and lifestyle modifications. As problematic, since it is not guideline based.
previously noted, the NRI for this group ranges from 52 % to Examples of risk transformation are shown in Figs. 5.10,
66 %, with subsequent appropriate downgrading or upgrading 5.11, and 5.12. A 57-year old man with hypertension, total
of medical therapy for this majority of the intermediate risk cholesterol 235 mg/dL, LDL-C 150 mg/dL, HDL-C 75 mg/
group. dL, and a 10-year Framingham risk of 12 %, was referred for
CAC scanning. The CAC score was 1872, in the >99th % for
Lower Risk his age, placing him in the highest risk category with LDL-C
Patients with less than 10 % Framingham risk may also ben- treatment goal of <70 mg/dL (Fig. 5.10).
efit from CAC scoring to guide management decisions. For Figure 5.11a displays the CAC scan of a 41-year-old
instance, most young patients with a family history of prema- woman whose mother experienced a myocardial infarction at
ture CAD will not have sufficient risk factors to even warrant age 55. The total cholesterol was 188 mg/dL, LDL-C
Framingham scoring (lower NCEP risk) or will be in the 112 mg/dL, HDL-C 50 mg/dL and triglycerides 132 mg/
moderate (1–10 % 10-year Framingham risk group), since dL. She was in the 0–1 risk factor group in which a

Table 5.8 Recommendations for treatment in asymptomatic, NCEP classified moderately high-risk patients based upon CAC score
CAC score/percentile Framingham risk group equivalent LDL goal (mg/dL) Drug therapy (mg/dL)
0 Lower risk; 0–1 risk factors; Framingham risk assessment not <160 ≥190
required
160–189: drug optional
1–10 and ≤75th % Moderate risk; 2 + risk factors (<10 % Framingham 10-year <130 ≥160
risk)
11–100 and ≤75th % Moderately high risk; 2 + risk factors (10–20 % Framingham <130 ≥130
10-year risk)
100–129: consider drug
101–400 or >75th % High risk; CAD risk equivalent (>20 % Framingham 10-year <100 Optional goal <70 ≥100
risk)
<100: consider drug
>400 or >90th % Highest riska <100 Optional goal <70 Any LDL level
a
Based on CAC score; consider beta blockers
5 Assessment of Cardiovascular Calcium 113

a b

c d

Fig. 5.10 A 57-year-old man with hypertension, total cholesterol aorta. Ao aorta, LAD left anterior descending coronary artery,
235 mg/dL, LDL-C 150 mg/dL, HDL-C 75 mg/dL, and a 10-year LADD diagonal branch of left anterior descending coronary artery,
Framingham risk of 12 % referred for CAC scanning; CAC score was LCx left circumflex coronary artery, PDA posterior descending branch
1872, in the >99th percentile. Slices from base (a) through apex (d) of right coronary artery, RCA right coronary artery
reveal significant CAC in all coronary arteries and the ascending

Framingham Risk Score need not be calculated. The CAC Other Applications
score was 110, in the left anterior descending (LAD) and
diagonal branch, in the >99th percentile for her age, placing Diabetes
her in a high-risk category. She developed symptoms, under-
went dual isotope nuclear stress testing (Fig. 5.11b), which The 2010 ACC Guideline for Assessment of Risk in
revealed severe anteroseptal ischemia, followed by angiogra- Asymptomatic Adults awarded CAC a Class IIa recommenda-
phy and placement of a stent to treat a 95 % ostial LAD ste- tion for all adults older than 40 with diabetes [65]. While the
nosis (Fig. 5.11c). Statin therapy was implemented to reduce initial reasoning was to identify the high risk patients with CAC
the LDL-C to <70 mg/dL. >400 for further evaluation to rule out obstructive disease, CAC
A 65- year-old male hypertensive smoker, with an LDL-C prognostic data have challenged the ingrained concept of diabe-
of 140 mg/dL and a 10-year Framingham risk of 25 %, was tes mellitus as a CAD disease equivalent. Patients with diabetes
very reluctant to take a statin prescribed for his LDL-C. A and CAC have higher risks than those without diabetes and
CAC scan was performed (Fig. 5.12), which demonstrated similar CAC, but the absence of CAC conveys a similar low risk
total absence of calcified plaque, despite the presumed high in both groups [84–90]. Therefore, the more appropriate ratio-
risk. Therapeutic life changes, rather than statins, were nale is for straightforward risk classification as with any other
recommended. risk factor, allowing for the possibility of downgrading risk.
114 H.S. Hecht

a c

Fig. 5.11 A 41-year-old woman with a premature family history of revealing severe anteroseptal ischemia. (c) Angiography demonstrating
CAD, total cholesterol 188 mg/dL, LDL-C 112 mg/dL, HDL-C 50 mg/ 95 % ostial LAD stenosis and severe LADD disease. LAD left anterior
dL, and triglycerides 132 mg/dL, in the lowest Framingham risk group. descending coronary artery, LADD diagonal branch of left anterior
(a) CAC score of 110, in the left anterior descending and diagonal descending coronary artery
branch, in the >99th percentile. (b) Dual isotope nuclear stress testing

Repeat Scanning Stress Testing

The use of serial CAC scanning to evaluate the progres- Since stress testing should only be performed in symptom-
sion of disease and the effects of therapy is a powerful atic patients, in whom CAC is not indicated, the interplay
emerging indication that will be covered in greater detail between the two is limited. Nonetheless, a combination of
in Chap. 6. Asymptomatic patients with a 0 CAC score CAC and stress EKG has been advocated in symptomatic
should not undergo repeat scanning for at least 4 years. patients. However, coronary CTA is clearly the CT modality
The average time to conversion to a >0 CAC was of choice, and will very likely replace stress testing as the
4.1 ± 0.9 years and the average score at the time of conver- first test in the evaluation of symptomatic patients [92].
sion was 19 ± 19 [91]. The repeat scanning interval in In asymptomatic patients, post CAC stress testing is an
patients with >0 CAC is not data determined. Rather, issue, and the appropriateness of stress testing after CAC
logic dictates that the greater the concern, the shorter scanning is directly related to the CAC score. The data
should be the interval. The low radiation dose makes indicate that the incidence of abnormal nuclear stress testing
repeat scanning less problematic. is 1.3 %, 11.3 % and 35.2 % for CAC scores of <100,100–400
5 Assessment of Cardiovascular Calcium 115

et al. [100] reported on 105 patients. Of the 46 with positive

scores (>0), 14 had abnormal follow-up inpatient testing. Of
the 59 with 0 calcium scores, stress evaluation and/or coro-
nary arteriography were normal in the 54 who underwent
further testing and all were free of cardiac events 4 months
later (100 % negative predictive value). Georgiou et al. [101]
noted 41 cardiac events in 192 emergency room patients fol-
lowed for 37 months; all but four were associated with cal-
cium scores ≥4. However, CCTA data have clearly
demonstrated a small (5 %) but finite incidence of obstruc-
tive disease in 0 CAC patients with chest pain [102], mandat-
ing performance of CCTA rather than CAC alone in this
setting

Limitations

Frequently cited limitations of CAC are assuming much less

importance. Radiation is no longer a significant issue as the
Fig. 5.12 A 65-year-old male hypertensive smoker, LDL-C of 140 mg/
dL and a 10-year Framingham risk of 25 %. CAC scan demonstrated absorbed radiation dose falls to the level of mammography.
total absence of calcified plaque Unfortunately, irresponsible scare tactics have magnified
public concern; education is needed to counter these negative
effects. Cost has also become less of a concern as the price of
and >400, respectively [93–97]. It is only in the >400 CAC scanning has plummeted to ~ $100. “Incidentalomas”
group that the pretest likelihood is sufficiently high to and their subsequent evaluation have generated negative sen-
warrant further evaluation with functional testing. Coronary timents. The frequency of clinically significant findings is
computed tomographic angiography is appropriate in 1.2 %, with indeterminate findings at 7.0 % [103]. The asso-
patients with CAC <1000; higher CAC scores may preclude ciated costs do not negatively impact the cost effectiveness
accurate evaluation. It is never appropriate to proceed of CAC [104]. Standard guidelines on how to handle these
directly to the catheterization laboratory from a CAC scan in findings may reassure patients and physicians [98]. Patient
asymptomatic patients. anxiety related to CAC findings has also been cited as a neg-
Evaluation of incidental findings, particularly lung nod- ative. Anxiety is not an intended consequence but a certain
ules, should follow standard radiology guidelines [98]. amount is appropriate and inevitable when informed of
increased cardiac risk, and may motivate increased adher-
ence. On the other hand, for those with high anxiety of early
Cardiomyopathy ASCVD based on a severe family history or a high calcu-
lated ASCVD risk score, concern can often be calmed when
CAC may be used to differentiate ischemic from nonisch- reclassified toward significantly less risk by CAC. The most
emic cardiomyopathies. Budoff et al. [99] demonstrated in persistent criticism is the lack of randomized controlled tri-
120 patients with heart failure of unknown etiology that the als that demonstrate improved patient outcomes through the
presence of CAC was associated with a 99 % sensitivity for use of CAC. The appropriate response notes that there “… is
ischemic cardiomyopathy. Nonetheless, coronary CTA has a double standard that demands randomized controlled (out-
replaced CAC for this indication. come) trials for CAC screening while ignoring their neces-
sity for every other technology…. It is incumbent on the
cardiology community to temper the inflexible need for ran-
Emergency Department Chest Pain Evaluation domized trials with the reality of 565,000 patients presenting
with myocardial infarctions annually as their first symptoms,
Emergency department triage of chest pain patients by CAC 95 % of whom could be identified as at high risk by CAC
has been totally supplanted by CCTA. Several early studies screening and aggressively treated to significantly reduce
demonstrated potential application of CAC to the ED. Laudon events [105].”
116 H.S. Hecht

Conclusions 7. Ideda T, Shirasawa T, Esaki Y, et al. Osteopontin mRNA is

The validation of CAC scanning as a risk assessment tool expressed by smooth muscle-derived foam cells in human athero-
sclerotic lesions of the aorta. J Clin Invest. 1993;92:2814–20.
may well represent one of the most significant advances 8. Hirota S, Imakita M, Kohri K, et al. Expression of osteopontin mes-
in the history of preventive medicine. It offers the possi- senger RNA by macrophages in atherosclerotic plaques. A possible
bility of accurately identifying the vast majority of association with calcification. Am J Pathol. 1993;143:1003–8.
patients destined to suffer acute cardiac events, and, in so 9. Shanahan CM, Cary NR, Metcalfe JC, Weissberg PL. High expres-
sion of genes for calcification-regulating proteins in human athero-
doing, should allow for substantial reduction of cardio- sclerotic plaque. J Clin Invest. 1994;93:2393–402.
vascular mortality and morbidity by increasingly effective 10. Rumberger JA, Simons DB, Fitzpatrick LA, et al. Coronary artery
pharmacologic and lifestyle therapy of the underlying dis- calcium areas by electron beam computed tomography and coro-
ease process. nary atherosclerotic plaque area: a histopathologic correlative
study. Circulation. 1995;92:2157–62.
It is appropriate to conclude by quoting Dr. Scott 11. Baumgart D, Schmermund A, Goerge G, et al. Comparison of elec-
Grundy [106]: tron beam computed tomography with intracoronary ultrasound
The power of imaging for detecting subclinical athero- and coronary angiography for detection of coronary atherosclero-
sclerosis to predict future ASCVD events is increasingly sis. J Am Coll Cardiol. 1997;30:57–64.
12. Schmermund A, Baumgart D, Gorge G, et al. Coronary artery cal-
being recognized. Imaging has at least three virtues. It cium in acute coronary syndromes: a comparative study of electron
individualizes risk assessment beyond use of age, which beam CT, coronary angiography, and intracoronary ultrasound in
is a less reliable surrogate for atherosclerosis burden; it survivors of acute myocardial infarction and unstable angina.
provides an integrated assessment of the lifetime expo- Circulation. 1997;96:1461–9.
13. Agatston AS, Janowitz WR, Hildner FJ, et al. Quantification of
sure to risk factors; and it identifies individuals who are coronary artery calcium using ultrafast computed tomography.
susceptible to developing atherosclerosis beyond estab- J Am Coll Cardiol. 1990;15:827–32.
lished risk factors. Also of importance, in the absence of 14. Callister TQ, Cooil B, Raya SP, et al. Coronary artery disease:
detectable atherosclerosis, short-term risk appears to be improved reproducibility of calcium scoring with an electron-beam
CT volumetric method. Radiology. 1998;208:807–14.
very low. Thus, for primary prevention, a recommenda- 15. Becker CR, Kleffel T, Crispin A, et al. Coronary artery calcium
tion could be established that detection of significant measurement. Agreement of multirow detector and electron beam
plaque burden is a preferred strategy for initiation of CT. Am J Roentgenol. 2001;176:1295–8.
LDL-lowering drugs. With such a recommendation, major 16. Janowitz WR, Agatston AS, Kaplan G, Viamonte M. Differences in
prevalence and extent of coronary artery calcium detected by ultra-
risk factors and emerging risk factors could be used as a fast computed tomography in asymptomatic men and women. Am
guide for selecting subjects for imaging more than as a J Cardiol. 1993;72:247–54.
primary guide for therapy. Once subclinical atherosclero- 17. Hoff JA, Chomka EV, Krainik AJ, et al. Age and gender distribu-
sis is detected, intensity of drug therapy could be adjusted tions of coronary artery calcium detected by electron beam tomog-
raphy in 35,246 adults. Am J Cardiol. 2001;87:1335–9.
for plaque burden. This 2-step approach to risk assess- 18. Budoff MJ, Yang TP, Shavelle RM. Ethnic differences in coronary
ment could provide a solution to the dilemma of patient atherosclerosis. J Am Coll Cardiol. 2002;39:408–12.
selection for cholesterol-lowering drugs in primary pre- 19. Newman AB, Naydeck BL, Whittle J, et al. Racial differences in
vention. In addition, it could be applied to all population coronary artery calcification in adults. Arterioscler Thromb Vasc
Biol. 2002;22:424–30.
subgroups. It could also be useful as a guide to low-dose 20. Khuran C, Rosenbaum CG, Howard BV, et al. Coronary artery cal-
aspirin prophylaxis and cholesterol-lowering therapy. cification in black women and white women. Am Heart J. 2003;145:
724–9.
21. Jain T, Peshock R, Darren K, McGuire DK. African Americans and
Caucasians have a similar prevalence of coronary calcium in the
References Dallas Heart Study. J Am Coll Cardiol. 2004;44:1011–7.
22. McClelland RL, Chung H, Detrano R, et al. Distribution of coro-
1. Heart and stoke statistical update. Dallas: American Heart nary artery calcium by race, gender, and age. Results from the
Association; 2001. Multi-Ethnic Study of Atherosclerosis (MESA). Circulation.
2. Blankenhorn DH, Stern D. Calcification of the coronary arteries. 2006;113:30–7.
Am J Roentgenol. 1959;81:772–7. 23. Detrano R, Guerci AD, Carr JJ, et al. Coronary calcium as a predic-
3. Frink RJ, Achor RW, Brown AL, et al. Significance of calcification tor of coronary events in four racial or ethnic groups. N Engl J Med.
of the coronary arteries. Am J Cardiol. 1970;26:241–7. 2008;358:1336–45.
4. Wexler L, Brundage B, Crouse J, et al. Coronary artery calcifica- 24. Nasir K, Michos ED, Rumberger JA, et al. Coronary artery calcifi-
tion: pathophysiology, epidemiology, image methods and clinical cation and family history of premature coronary heart disease: sib-
implications. A scientific statement from the American Heart ling history is more strongly associated than parental history.
Association. Circulation. 1996;94:1175–92. Circulation. 2004;110:2150–6.
5. Faber A. Die Arteriosklerose, from Pathologische Anatomie, from 25. Khurram Nasir K, Budoff MJ, Wong ND, et al. Family history of
Pathogenese Und Actiologie. G. Fischer; 1912. premature coronary heart disease and coronary artery calcification.
6. Bostrom K, Watson KE, Horn S, et al. Bone morphogenetic protein Multi-Ethnic Study of Atherosclerosis (MESA). Circulation.
expression in human atherosclerotic lesions. J Clin Invest. 2007;116:619–62.
1993;91:1800–9. 26. Gerber TC, Carr JJ, Arai AE, et al. Ionizing radiation in cardiac
imaging: a science advisory from the American Heart Association
5 Assessment of Cardiovascular Calcium 117

Committee on Cardiac Imaging of the Council on Clinical 45. Greenland P, LaBree L, Azen SP, et al. Coronary artery calcium
Cardiology and Committee on Cardiovascular Imaging and score combined with Framingham score for risk prediction in
Intervention of the Council on Cardiovascular Radiology and asymptomatic individuals. JAMA. 2004;291:210–5.
Intervention. Circulation. 2009;119:1056–196526. 46. Arad Y, Goodman KJ, Roth M, et al. Coronary calcification, coro-
27. O’Rourke RA, Brundage BH, Froelicher VF, et al. American nary risk factors, and atherosclerotic cardiovascular disease events.
College of Cardiology/American Heart Association expert consen- The St Francis Heart Study. J Am Coll Cardiol. 2005;46(1):
sus document on electron beam computed tomography for the diag- 158–65.
nosis and prognosis of coronary artery disease. Circulation. 47. Wayhs R, Zelinger A, Raggi P. High coronary artery calcium scores
2000;102:126–40. pose an extremely elevated risk for hard events. J Am Coll Cardiol.
28. Simons DB, Schwartz RS, Edwards WD, et al. Noninvasive defini- 2002;39:225–30.
tion of anatomic coronary disease by ultrafast computed tomo- 48. Taylor AJ, Bindeman J, Feuerstein I, et al. Coronary calcium inde-
graphic scanning: a quantitative pathologic comparison study. J Am pendently predicts incident premature coronary heart disease over
Coll Cardiol. 1992;20:1118–26. measured cardiovascular risk factors mean three-year outcomes in
29. Detrano R, Tang W, Kang X, et al. Accurate coronary calcium the prospective army C\coronary C\calcium (PACC) project. J Am
phosphate mass measurements from electron beam computed Coll Cardiol. 2005;46:807–14.
tomograms. Am J Card Imaging. 1995;9:167–73. 49. Vliegenthart R, Oudkerk M, Song B, et al. Coronary calcification
30. Mautner GC, Mautner SL, Froelich J, et al. Coronary artery calcifi- detected by electron-beam computed tomography and myocardial
cation: assessment with electron beam CT and histomorphometric infarction. The Rotterdam Coronary Calcification Study. Eur Heart
correlation. Radiology. 1994;192:619–23. J. 2002;23:1596–603.
31. Budoff MJ, Georgiou D, Brody A, et al. Ultrafast computed tomog- 50. Budoff MJ, Shaw LJ, Liu ST, et al. Long-term prognosis associated
raphy as a diagnostic modality in the detection of coronary artery with coronary calcification. Observations from a registry of 25,253
disease-a multicenter study. Circulation. 1996;93:898–904. patients. J Am Coll Cardiol. 2007;49:1860–70.
32. Guerci AD, Spadaro LA, Popma JJ, et al. Electron Beam tomogra- 51. Becker A, Leber A, Becker C, Knez A. Predictive value of coronary
phy of the coronary arteries: relationship of coronary calcium score calcifications for future cardiac events in asymptomatic individuals.
to arteriographic findings in asymptomatic and symptomatic adults. Am Heart J. 2008;155:154–60.
Am J Cardiol. 1997;79:128–33. 52. Folsom AR, Kronmal RA, Detrano RC, et al. Coronary artery calci-
33. Shavelle DM, Budoff MJ, LaMont DH, et al. Exercise testing and fication compared with carotid intima-media thickness in the pre-
electron beam computed tomography in the evaluation of coronary diction of cardiovascular disease incidence the Multi-Ethnic Study
artery disease. J Am Coll Cardiol. 2000;36:32–8. of Atherosclerosis (MESA). Arch Intern Med. 2008;168:1333–9.
34. Bielak LF, Rumberger JA, Sheedy PF, et al. Probabilistic model for 53. Lakoski SG, Greenland P, Wong ND, et al. Coronary artery calcium
prediction of agiographically defined obstructive coronary artery scores and risk for cardiovascular events in women classified as
disease using electron beam computed tomography calcium score “Low Risk” based on Framingham risk score. The Multi-Ethnic
strata. Circulation. 2000;102:380–5. Study of Atherosclerosis (MESA). Arch Intern Med. 2007;167(22):
35. Rumberger JA, Sheedy PF, Breen FJ, et al. Electron beam CT coro- 2437–42.
nary calcium score cutpoints and severity of associated angiogra- 54. Blaha M, Budoff MJ, Shaw LJ, et al. Absence of coronary artery
phy luminal stenosis. J Am Coll Cardiol. 1997;29:1542–8. calcification and all-cause mortality. J Am Coll Cardiol Img.
36. Haberl R, Becker A, Leber A, et al. Correlation of coronary calcifi- 2009;2:692–700.
cation and angiographically documented stenoses in patients with 55. Erbel R, Möhlenkamp S, Moebus S, et al. Signs of subclinical coro-
suspected coronary artery disease: results of 1,764 patients. J Am nary atherosclerosis measured as coronary artery calcification
Coll Cardiol. 2001;37:451–7. improve risk prediction of hard events beyond traditional risk fac-
37. Budoff MJ, Raggi P, Berman D, et al. Continuous probabilistic tors in an unselected general population – The Heinz Nixdorf
prediction of angiographically significant coronary artery disease Recall Study five-year outcome data. J Am Coll Cardiol
using electron beam tomography. Circulation. 2002;105(15): 2009;56:1397–406. In press.
1791–6. 56. Nasir K, Rubin J, Blaha MJ, Shaw LJ, et al. Interplay of coronary
38. Sarwar A, Shaw LJ, Shapiro MD, et al. Diagnostic and prognostic artery calcification and traditional risk factors for the prediction of
value of absence of coronary artery calcification. J Am Coll Cardiol all-cause mortality in asymptomatic individuals. Circ Cardiovasc
Img. 2009;2:675–88. Imaging. 2012;5:467–73.
39. Mohlenkamp S, Lehmann N, Schmermund A, et al. Prognostic 57. Mascola A, Ko J, Bakhsheshi H, et al. Electron beam tomography
value of extensive coronary calcium quantities in symptomatic comparison of culprit and non-culprit coronary arteries in patients
males – a 5-year follow-up study. Eur Heart J. 2003;24:845–54. with acute myocardial infarction. Am J Cardiol. 2000;85:
40. Raggi P, Callister TQ, Cooil B, et al. Identification of patients at 1357–9.
increased risk of first unheralded acute myocardial infarction by 58. Pohle K, Ropers D, Mäffert R, et al. Coronary calcifications in
electron beam computed tomography. Circulation. 2000;101:850–5. young patients with first, unheralded myocardial infarction: a risk
41. Wong ND, Hsu JC, Detrano RC, et al. Coronary artery calcium factor matched analysis by electron beam tomography. Heart.
evaluation by electron beam compute tomography and its relation 2003;89:625–8.
to new cardiovascular events. Am J Cardiol. 2000;86:495–8. 59. O’Malley PG, Feuerstein IM, Taylor AJ. Impact of electron beam
42. Arad Y, Spadaro LA, Goodman K, et al. Prediction of coronary tomography, with or without case management, on motivation,
events with electron beam computed tomography. J Am Coll behavioral change, and cardiovascular risk profile: a randomized
Cardiol. 2000;36:1253–60. controlled trial. JAMA. 2003;289:2215–23.
43. Kondos GT, Hoff JA, Sevrukov A, et al. Electron-beam tomography 60. Kalia NK, Miller LG, Nasir K, Blumenthal RS, et al. Visualizing
coronary artery calcium and cardiac events: a 37-month follow-up coronary calcium is associated with improvements in adherence to
of 5,635 initially asymptomatic low to intermediate risk adults. statin therapy. Atherosclerosis. 2006;185:394–9.
Circulation. 2003;107:2571–6. 61. Orakzai RH, Nasir K, Orakzai SH, et al. Effect of patient visualiza-
44. Shaw LJ, Raggi P, Schisterman E, et al. Prognostic value of cardiac tion of coronary calcium by electron beam computed tomography
risk factors and coronary artery calcium screening for all-cause on changes in beneficial lifestyle behaviors. Am J Cardiol.
mortality. Radiology. 2003;28:826–33. 2008;101:999–1002.
118 H.S. Hecht

62. Taylor AJ, Bindeman J, Feuerstein I, et al. Community-based provi- 81. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent
sion of statin and aspirin after the detection of coronary artery cal- clinical trials for the National Cholesterol Education Program
cium within a community-based screening cohort. J Am Coll Adult Treatment Panel III guidelines. Circulation. 2004;110:
Cardiol. 2008;51:1337–41. 227–39.
63. Rozanski A, Gransar H, Shaw LJ, et al. Impact of coronary artery 82. Akosah K, Schaper A, Cogbill C, Schoenfeld P. Preventing myocar-
calcium scanning on coronary risk factors and downstream testing: dial infarction in the young adult in the first place: how do the
The EISNER (Early Identification of Subclinical Atherosclerosis National Cholesterol Education Panel III guidelines perform? J Am
by Noninvasive Imaging Research) prospective randomized trial. Coll Cardiol. 2003;41:1475–9.
J Am Coll Cardiol. 2011;57:1622–32. 83. Taylor A, Cerqueira M, Hodgson JM, et al. Appropriate use criteria
64. Naghavi M, Falk E, Hecht HS, et al. From vulnerable plaque to for cardiac computed tomography. J Am Coll Cardiol. 2010;56:
vulnerable patient—Part III: executive summary of the Screening 1864–94.
for Heart Attack Prevention and Education (SHAPE) task force 84. Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of
report. Am J Cardiol. 2006;98(Suppl 2A):2H–15. coronary artery calcium screening in subjects with and without dia-
65. Greenland P, Alpert JS, Beller GA, et al. 2010 ACCF/AHA guide- betes. J Am Coll Cardiol. 2004;43:1663–9.
line for assessment of cardiovascular risk in adults. A report of the 85. Wong ND, Sciammarella MG, Polk D, et al. The metabolic syn-
American College of Cardiology Foundation/American Heart drome, diabetes, and subclinical atherosclerosis assessed by coro-
Association Task Force on Practice Guidelines. J Am Coll Cardiol. nary calcium. J Am Coll Cardiol. 2003;41:1547–53.
2010;56:e50–103. 86. Becker A, Leber A, Becker B, et al. Predictive value of coronary
66. Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA calcifications for future cardiac events in asymptomatic patients
guideline on the treatment of blood cholesterol to reduce athero- with diabetes mellitus: prospective study in 716 patients over 8
sclerotic cardiovascular risk in adults. J Am Coll Cardiol. 2013. years. BMC Cardiovasc Disord. 2008;27:1–8.
doi:10.1016/j.jacc.2013.11.002. 87. Elkeles R, Godsland IF, Feher MD, et al. Coronary cal- cium mea-
67. Goff Jr DC, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA surement improves prediction of cardiovascular events in asymp-
guideline on the assessment of cardiovascular risk. J Am Coll tomatic patients with type 2 diabetes: the PREDICT study. Eur
Cardiol. 2013. doi:10.1016/j.jacc.2013.11.005. Heart J. 2008;29:2244–51.
68. Hermann DM, Gronewold J, Lehmann N, et al. Heinz Nixdorf 88. Anand DV, Lim E, Hopkins D, Corder R, et al. Risk stratification in
Recall Study Investigative Group. Coronary artery calcification is uncomplicated type 2 diabetes: prospective evaluation of the com-
an independent stroke predictor in the general population. Stroke bined use of coronary artery calcium imaging and selective myo-
2013;44:1008–13. cardial perfusion scintigraphy. Eur Heart J. 2006;27:713–21.
69. Yeboah J, McClelland RL, Polonsky TS, et al. Comparison of novel 89. Malik S, Budoff M, Katz R. Impact of subclinical atherosclerosis
risk markers for improvement in cardiovascular risk assessment in on cardiovascular disease events in individuals with metabolic syn-
intermediate-risk individuals. JAMA. 2012;308:788–95. drome and diabetes: the Multi-Ethnic Study of Atherosclerosis.
70. Kuller LH, Matthews KA, Sutton-Tyrrell K, et al. Coronary and Diabetes Care. 2011;34:2285–90.
aortic calcification among women 8 years after menopause and 90. Kuller LH, Velentgas P, Barzilay J, et al. Diabetes mellitus, sub-
their premenopausal risk factors: the Healthy Women Study. clinical cardiovascular disease and risk of incident cardiovascular
Arterioscler Thromb Vasc Biol. 1999;19:2189–98. disease and all-cause mortality. Arterioscler Thromb Vasc Biol.
71. Hecht HS, Superko HR, Smith LK, et al. Relation of coronary 2000;20:823–9.
artery calcium identified by electron beam tomography to serum 91. Min JK, Lin FY, Gidseg DS, et al. Determinants of coronary cal-
lipoprotein levels and implications for treatment. Am J Cardiol. cium conversion among patients with a normal coronary calcium
2001;87:406–12. scan. What is the “Warranty Period” for remaining normal? J Am
72. Daviglus ML, Pirzada A, Liu K, et al. Comparison of low risk and Coll Cardiol. 2010;55:1110–7.
higher risk profiles in middle age to frequency and quantity of coro- 92. Hecht HS. A paradigm shift: coronary computed tomographic angi-
nary artery calcium years later. Am J Cardiol. 2004;94:367–9. ography before stress testing. Am J Cardiol. 2009;104(4):613–8.
73. Hecht HS, Superko HR. Electron beam tomography and national 93. He ZX, Hedrick TD, Pratt CM, et al. Severity of coronary artery
cholesterol education program guidelines in asymptomatic women. calcification by electron beam computed tomography predicts
J Am Coll Cardiol. 2001;37:1506–11. silent myocardial ischemia. Circulation. 2000;101:244–51.
74. Rana JS, Gransar H, Wong ND, et al. Comparative value of coro- 94. Moser KW, O’Keefe JH, Bateman TM, et al. Coronary calcium
nary artery calcium and multiple blood biomarkers for prognostica- screening in asymptomatic patients as a guide to risk factor modifi-
tion of cardiovascular events. Am J Cardiol. 2012;109:1449–53. cation and stress myocardial perfusion imaging. J Nucl Cardiol.
75. Iribarren C, Gross MD, Darbinian JA, et al. Association of lipopro- 2003;10:590–8.
tein-associated phospholipase A2 mass and activity with calcified 95. Berman DS, Wong ND, Gransar H, et al. Relationship between
coronary plaque in young adults. The CARDIA Study. Arterioscler stress-induced myocardial ischemia and atherosclerosis measured
Thromb Vasc Biol. 2005;25:216–21. by coronary calcium tomography. J Am Coll Cardiol. 2004;44:
76. O’Donnell CJ, Chazaro I, Wilson PW, et al. Evidence for heritabil- 923–30.
ity of abdominal aortic calcific deposits in the Framingham Heart 96. Anand DJ, Lim E, Raval U, et al. Prevalence of silent myocardial
Study. Circulation. 2002;106:337–41. ischemia in asymptomatic individuals with subclinical atheroscle-
77. Peyser PA, Bielak LF, Chu J, et al. Heritability of coronary artery rosis detected by electron beam tomography. J Nucl Cardiol.
calcium quantity measured by electron beam computed tomogra- 2004;11:450–7.
phy in asymptomatic adults. Circulation. 2002;106:304–8. 97. Chang SM, Nabi F, Xu J, et al. The coronary artery calcium score
78. Hecht HS. Risk factors revisited. Am J Cardiol. 2003;93:73–5. and stress myocardial perfusion imaging provide independent and
79. Hecht HS, Budoff M, Ehrlich J, Rumberger J. Coronary artery cal- complementary prediction of cardiac risk. J Am Coll Cardiol.
cium scanning: clinical recommendations for cardiac risk assess- 2009;54:1872–82.
ment and treatment. Am Heart J. 2006;151:1139–46. 98. MacMahon H, Austin JH, Gamsu G, et al. Guidelines for manage-
80. Wilson PW, D’Agostino B, Levy D, et al. Prediction of coronary ment of small pulmonary nodules detected on CT scans: a state-
heart disease using risk factor categories. Circulation. 1998;97: ment from the Fleischner Society. Radiology. 2005;237:
1837–47. 395–4002101.
5 Assessment of Cardiovascular Calcium 119

99. Budoff MJ, Shavelle DM, Lamont DH, et al. Usefulness of elec- cardiac computed tomography. J Am Coll Cardiol. 2009;54:
tron beam computed tomography scanning for distinguishing 1533–4.
ischemic from non-ischemic cardiomyopathy. J Am Coll Cardiol. 104. Pletcher MJ, Pignone M, Earnshaw S, et al. Using the coronary
1998;32:1173–8. artery calcium score to guide statin therapy: a cost-effectiveness
100. Laudon DA, Vukov LF, Breen JF, et al. Use of electron-beam com- analysis. Circ Cardiovasc Qual Outcomes. 2014;7:276–84.
puted tomography in the evaluation of chest pain patients in the 105. Hecht HS. The Deadly double standard: the saga of screening for
emergency department. Ann Emerg Med. 1999;33:15–21. subclinical atherosclerosis. Am J Cardiol. 2008;101:1085–7.
101. Georgiou D, Budoff MJ, Kaufer E, et al. Screening patients with 106. Grundy SM. Is lowering low-density lipoprotein an effective strat-
chest pain in the emergency department using electron beam egy to reduce cardiac risk? Promise of low-density lipoprotein–
tomography: a follow-up study. J Am Coll Cardiol. 2001;38: lowering therapy for primary and secondary prevention.
105–10. Circulation. 2008;117:569–73.
102. Rosen BD, Fernandes V, McClelland RL, et al. The prevalence 107. Hecht HS, Narula J. Coronary calcium in diabetes mellitus.
of flow limiting stenoses in coronary arteries with previously J Diabetes. 2012;4:342–50.
documented zero calcium score: the Multi-Ethnic Study of 108. Park R, Robert Detrano R, Xiang M et al. Combined use of com-
Atherosclerosis (MESA). J Am Coll Cardiol Img. 2009;2:1175–83. puted tomography coronary calcium scores and C-reactive protein
103. MacHaalany J, Yeung Y, Ruddy TD, et al. Potential clinical and levels in predicting cardiovascular events in non-diabetic individ-
economic consequences of noncardiac incidental findings on uals. Circulation. 2002.
 Natural History and Impact
of Interventions on CAC 6
Paolo Raggi

Abstract
Coronary artery calcium is a marker of sub-clinical atherosclerosis and it is deposited via an
active process similar to bone formation. Sequential non-contrast CT has been proposed as
a method to accurately quantify and monitor progression of calcification. While interven-
tions have generally failed to slow progression of calcification, it has become apparent that
continued progression of CAC is associated with an increased risk of myocardial infarction
and cardiac death. As a consequence, researchers have implemented sequential cardiac CT
to follow the progression of coronary artery calcium in a variety of clinical settings and in
some cases have reported encouraging results.

Keywords
Coronary artery calcium • Progression • Statins • Serial CT imaging • Atherosclerosis • All-
cause mortality • Epicardial adipose tissue • Chronic kidney disease • Human immunodefi-
ciency virus

Preface ity for sequential imaging. Therefore, researchers have

investigated the utilization of cardiac CT imaging to follow
Coronary artery calcium has long been known to be associ- the progression of cardiovascular calcification in a variety of
ated with atherosclerotic plaque and its development is due clinical settings, as will be discussed in this chapter.
to an active process resembling bone formation. Similarly,
aortic valve degeneration and calcification appear to follow a
pathophysiologic process very similar to atherosclerosis. Natural History of Plaque Calcification
With non-contrast CT it is possible to detect and accurately
quantify the extent of calcification of vessels and cardiac In Western societies pre-atherosclerotic changes in the arte-
valves offering an opportunity to monitor progression of dis- rial wall begin very early in life. Necropsy data from 2876
ease. While interventions have generally failed to slow pro- subjects between the ages of 15 and 34 revealed intimal
gression of calcification, it has become apparent that lesions in the aortas of all patients and in the right coronary
continued progression of coronary artery calcium (CAC) is artery of more than half of the youngest patients (15–19 year
associated with an increased risk of myocardial infarction old). The prevalence and extent of disease increased with
and cardiac death, suggesting that there might be some util- advancing age [1]. CAC has long been known to be associ-
ated with atherosclerosis and it is now clearly established
that plaque calcification may be dependent upon an active
P. Raggi, MD process of mineralization resembling bone formation [2–5].
Department of Medicine, Mazankowski Alberta
Several enzymes necessary for the assembly of normal bone
Heart Institute, University of Alberta,
4A7.050, 8440 – 112 Street, Edmonton, AB T6G 2B7, Canada have been found in the context of human atherosclerotic
e-mail: [email protected] plaques [2–4] and cells normally found in the vessel wall,

© Springer International Publishing 2016 121

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_6
122 P. Raggi

such as smooth muscle cells [5], macrophages and pericytes typical plaques with a lipid-rich core and scattered calcific
[6] can transform into osteoblast-like cells with bone gener- granules. As plaques expanded the calcific deposits grew.
ating potential. Pericytes are of particular interest given the After exposing the animals to a diet severely restricted in
modern view that atherosclerosis is a process partially driven cholesterol, the plaques became more fibrotic, with a lower
from the outside of the arterial lumen. Pericytes are inter- cholesterol content and the calcium deposits stopped growing
spersed with endothelial cells in the vasa vasorum penetrat- [14]. In another experiment Williams et al. [15] used a
ing through the adventitia of vessels developing monkey model of atherosclerosis to study the effect of
atherosclerosis and have been shown to be able to undergo medical therapy in addition to diet on atherosclerosis
osteoblastic differentiation [6]. As vasa vasorum proliferate progression and regression. Thirty-two adult (7–10 years of
and expand in the vessel wall, bringing more pericytes in its age) male cynomolgus monkeys were fed an atherogenic diet
context, they cause a series of intramural hemorrhages [7]. for 2 years (progression phase). During the subsequent
The cellular membrane of erythrocytes is rich in cholesterol 2-year a low cholesterol diet was begun (treatment phase).
and cell death in the context of the vessel wall causes accu- Additionally, 14 monkeys received pravastatin (20 mg/kg
mulation of large amounts of lipids promoting inflammation body weight per day), while the diet of the other 18 monkeys
and possibly inducing osteoblasic changes in the pericytes. was adjusted to maintain equal plasma LDL levels between
As a result of a complex cascade of events, in advanced groups over time. At the end of the treatment phase the total,
stages of atherosclerosis true ossification can be observed in low density and high-density lipoprotein cholesterol levels
pathological specimen. It is currently unknown if arterial were similar in the two animal groups. However, histological
calcification is part of the ongoing inflammatory phenomena analysis of the coronary, carotid and iliac arteries revealed
in the plaque or an attempt at repairing the damage brought important differences between treatment groups. While the
to the vascular wall by noxious stimuli. Some investigators lumen area was not different, pravastatin treated animals
have suggested that calcium deposition simply results from showed a reduction in intimal neovascularization, plaque
recurrent hemorrhage and thrombosis with deposition of macrophage infiltration and a decrease in calcification of
minerals in the context of the plaque [8]. early as well as advanced plaques. These findings suggested
Numerous researchers have investigated what factors are that statins might benefit the arterial wall in ways that differ
associated with CAC appearance (conversion of calcium from simple lipoprotein lowering. However, Stary [16],
score from 0 to >0) and progression. In an analysis of racial Daoud [17] and Clarkson [18] did not find any reduction in
differences in disease progression, the Multi Ethnic Study of calcium deposition in the atherosclerotic plaque with
Atherosclerosis (MESA) investigators reported that all interventions in experiments conducted in swine and
traditional risk factors correlated with calcium progression monkeys. Hence, although attractive, the histological proof
in Whites, Asians, Hispanics and African Americans alike that arterial calcification may regress remains very
[9]. However, Whites showed the greatest progression and controversial.
diabetes mellitus had a stronger impact on Blacks than other
races. The European Heinz Nixdorf Recall (HNR) population
study confirmed that all traditional risk factors impact Technical Considerations
inception and progression of CAC [10]. However, the MESA
investigators further stressed the importance of family The severity of calcification is assessed by means of
history of premature coronary artery disease [11], diabetes quantitative calcium-scores. The first score was developed
mellitus and the metabolic syndrome [12], while the HNR by Agatston et al. [19]; this score holds a good correlation
researchers highlighted the importance of smoking [13] in with the underlying atherosclerotic plaque burden [20] and
promoting conversion from nil to positive calcium. has been used widely in research and clinical trials. The
As the process of calcification of a plaque appears to be Agatston score is derived by multiplying the area of a
dependent upon active phenomena of mineralization, it is calcified plaque by a density coefficient rated 1 through 4.
plausible that the formation and degradation of calcification This scoring method was shown to have a limited inter-scan
may be a dynamic phenomenon in the atherosclerotic plaque reproducibility, especially when used with the older EBCT
similar to what happens in bone, and that these processes technology, and new scoring methods were therefore
may be activated or inhibited by external interventions. introduced for the purpose of performing reliable sequential
Numerous studies have addressed atherosclerosis regression studies [21–23]. The calcium volume score (measured in
in animal models. In one experiment, 59 Rhesus monkeys picoliters) is derived using an isotropic interpolation principle
were fed a high cholesterol diet for several years and then and it represents the volume of matter denser than 130
exposed to a cholesterol restricted diet for three more years Hounsfield units (i.e. calcium) contained in an atherosclerotic
[14]. The animals were progressively sacrificed along the plaque. The inter-scan reproducibility of this score is
experimental period and histology revealed development of significantly higher than that of the Agatston method [21].
6 Natural History and Impact of Interventions on CAC 123

The mass score was the third and last score to be introduced Nonetheless, the invasive nature of coronary angiography
[22, 23]. Though reportedly more reliable and reproducible greatly limits the utility of this tool for sequential studies,
than the other two scores, to date this measurement has not especially in asymptomatic people. More modernly athero-
yet been employed extensively. Another important technical sclerosis imaging to gauge the effect of treatment has been
consideration is the method used to report change and the assessed with sequential measurements of CAC and carotid
numerous imaging platforms currently available with the artery intimal medial thickness [28–32]. This approach pre-
various brands and models of CT scanners present on sumes that limiting the progression or inducing the regres-
the market. The change in absolute score tends to minimize sion of atherosclerosis in asymptomatic individuals will
while a change in percent score exaggerates the difference at provide the same benefit observed in symptomatic patients
follow-up in the presence of small baseline scores (the who underwent sequential invasive studies. This is an obvi-
reverse is true for large baseline scores). A novel method was ous limitation as symptomatic patients may have a very dif-
therefore introduced by Hokanson based on the difference ferent substrate for their on-going atherosclerotic disease
between the square root of the follow-up and the square root compared to asymptomatic subjects harboring sub-clinical
of the baseline calcium volume score [24]. This score is not disease.
affected by the baseline score and an increase ≥2.5 is consid- Callister et al. [28] published the first report of sequential
ered a reliable indication of true change. A final word of cau- EBCT scanning to measure progression of CAC in
tion should be reserved for the type of scanner and imaging asymptomatic patients. They conducted an observational
protocol utilized for sequential imaging; it is unlikely that an study on 149 patients referred by primary care physicians for
Agatston score measured with an original EBCT scanner can calcium screening. Treatment with HMG-CoA reductase
be compared with a follow-up scan obtained years later with inhibitors (statins) was recommended for all patients, but the
a high-resolution MDCT. If possible, a patient should be re- initiation of such therapy was left to the discretion of the
scanned with the same equipment and with the same param- referring physician. Baseline and follow-up EBCT scan at a
eters (slice thickness, voltage, electrocardiographic gating minimum of 12-month interval (range 12–15 months) and
etc.) serial LDL-cholesterol measurements were obtained in all
patients. Of the 149 patients, 105 received treatment with
statins and 44 did not. Progression of CAC was seen in all
Effect of Statins on Progression of CAC untreated patients (mean LDL ± SD: 147 ± 22 mg/dl) and
averaged 52 ± 36 %/year (Fig. 6.1). In contrast, the mean
Initial human studies of atherosclerosis progression and yearly calcium volume score change for all treated patients
regression were conducted by means of quantitative coronary (mean LDL: 114 ± 23 mg/dl) was 5 ± 28 % (p < 0.001 vs.
angiography [25, 26]. The cardiovascular event reduction untreated patients). Budoff et al. [29] reported the results of
associated with luminal stenosis improvements seen on an observational study of 299 asymptomatic patients
quantitative coronary angiography far outweighed the followed for 1–6.5 years after an initial EBCT scan. All
magnitude of the regression recorded over long-term patients underwent a second scan at a minimum of 12 months.
follow-up periods [27]. This observation became germane to The follow-up scans showed an increase in CAC in all
the concept that induction of plaque regression is an untreated patients while patients treated with statins showed
important surrogate marker worth achieving since it may significant slowing of progression (15 ± 8 %/year on
translate in substantial cardiovascular risk reduction. treatment vs. 39 ± 12 %/year without treatment). Two more

2.0
Percent calcium score change

1.5 *

1.0

0.5
*
0.0

-0.5
*P < 0.001
-1.0
Therapy No therapy

Fig. 6.1 Progression of calcium volume score in 105 patients treated indicate median (line in the middle of the box), confidence intervals
for a year with statins and 44 untreated patients. There was a significant (vertical lines) as well as 25th and 75th percentile (lower and top border
difference in progression between the two groups. The box plots of the box) [28]
124 P. Raggi

Calcium volume score Calcium volume score

Median CVS:+15 %
Atorvastatin 80 mg
Mean LDL = 94 mg/dl
615 dyslipidemic 12 months follow-up
post menopausal
women
Pravastatin 40 mg Median CVS:+14.3 %
Mean LDL = 129 mg/dl

Fig. 6.2 Design of the BELLES trial and main study results. Aggressive lipid lowering therapy with atorvastatin did not slow progression of CAC
more than moderate treatment with pravastatin [37]

small studies, in 66 men treated with cerivastatin [30] and et al. [39] randomized 366 patients with no known cardiovas-
eight patients with familial hypercholesterolemia receiving cular disease to 10 mg vs 80 mg of atorvastatin daily for
LDL apheresis [31], contributed to the growing evidence that 1 year. The mean LDL levels on treatment were 109 ± 28 and
statin therapy may retard the progression of CAC. Finally, in 87 ± 33 mg/dl, respectively. Again the mean calcium volume
a subanalysis of the Women’s Health Initiative Observational score progression was not different at the end of 12 months
Study, Hsia et al. [33] evaluated prospectively the rate of pro- of follow-up (25 % vs 27 %). Finally, Houslay et al. [40] ran-
gression of CAC in healthy postmenopausal women. Of 914 domized 48 patients to atorvastatin 80 mg/daily and 54
postmenopausal women enrolled in the main study, 305 patients to placebo. After a median follow-up of 24 months
women with a baseline calcium score ≥10 were invited for a the atorvastatin group had progressed by 26 %/year from
repeat scan and 94 agreed to undergo a second scan. In mul- baseline and the placebo group by 18 %/year (P = NS).
tivariable analyses, statin use at baseline was a negative pre- In conclusion, the results of randomized trials failed to
dictor (p = 0.015), whereas the baseline calcium score was a confirm that lipid lowering therapy may slow progression of
strong positive predictor (p < 0.0001) of progression of CAC. CAC; indeed there was a trend for statin therapy to attain the
Despite these encouraging results, other observational opposite effect.
studies [34–36] and several randomized trials [37–39] failed
to confirm an association between LDL lowering and pro-
gression of CAC. The BELLES trial (Beyond Endorsed Effect of Non-lipid Lowering Interventions
Lipid Lowering With EBT Scanning) was a prospective, ran- on Progression of CAC
domized study of post-menopausal and dyslipidemic women
with a minimal calcium volume score of 30 at baseline [37]. Besides medical therapy for dyslipidemia, other treatment
After the initial EBCT scan, the 615 women enrolled were modalities have been studied to slow the progression of
randomized to treatment with atorvastatin 80 mg/day or CAC. An example of therapy of critical importance is
pravastatin 40 mg/day; a follow-up scan was performed represented by the effect of tight diabetic control on
12 months after randomization (Fig. 6.2). The mean LDL atherosclerosis progression. Snell-Bergeon et al. [41]
cholesterol level was significantly lower with atorvastatin assessed the effect of glycemic control in type 1 diabetes
(94 mg/dl) than pravastatin (129 mg/dl). Nonetheless, the patients on progression of CAC. In 109 type 1 diabetic
median percent change of the calcium volume score was not patients (22–50 year old), sequential EBCT scans were
different between the two treatment arms (15.1 % and 14.3 % performed at an interval of 2.7 years. Progression of CAC
for atorvastatin and pravastatin respectively, P = NS). The St. was noted in 21 patients and it was associated with baseline
Francis Heart Study [38] was a prospective, randomized hyperglycemia (odds ratio 7.11, 95 % CI 1.38–36.6, P = 0.02),
study of 1005 healthy individuals with a CAC score above after adjustment for baseline CAC, duration of diabetes, age
the 80th percentile for age and sex at screening. The study and sex. There was also a significant interaction between
compared the effect of 20 mg/daily of atorvastatin along with higher insulin dose and higher body mass index (P = 0.03),
vitamin C and E versus placebo on progression of CAC. At suggesting that glycemic control and insulin resistance
the end of a mean follow-up of 4.3 years the progression was affected progression of CAC. Similarly, Anand et al. fol-
similar among treatment arms (~20 %/year). Schmermund lowed 392 type-2 diabetic patients. Progression of CAC was
6 Natural History and Impact of Interventions on CAC 125

noted in 56 % of those with CAC at baseline; the best predic- either no change or an increase in score. Of interest, serum
tors of progression were the baseline CAC score, statins use lipid levels were reduced in a large proportion of patients
and hemoglobin A1c >7 % during follow-up [42]. despite the fact that most patients were already receiving
In the Women’s Health Initiative (WHI), menopausal statins prior to enrollment. No liver, renal or hematological
women between the ages of 50–59 years were randomized to side effects were recorded.
treatment with conjugated estrogens or placebo [43]. In a Obviously, these studies were very small and mainly
sub-study of the WHI, 1064 women were submitted to CAC exploratory in nature and the utility of such interventions
screening after 8.7 years from trial initiation. Women who will need to be confirmed in larger prospective studies.
had received estrogens showed a lower CAC score at follow-
up compared to those who had received placebo (83.1 vs
123.1, P = 0.02). Similarly, in a prospective observational Cardiovascular Calcification in End Stage
study, combined hormone replacement therapy (progestin Renal Disease and the Effect of Therapies
plus estrogens) and placebo were associated with a signifi- on Its Progression
cantly greater progression of CAC (22–24 %/year) then
treatment with unopposed estrogens alone (9 %/year) [44]. The cardiovascular disease rates of patients suffering from
Several other approaches have been attempted to slow end-stage chronic kidney disease receiving dialysis (CKD
CAC progression. In a small, randomized study, Rath et al. stage 5D) are 30–50 fold higher than in the general population
[45] assessed the progression rate of CAC in subjects treated [49]. However, the cardiovascular mortality and morbidity of
with a combination of vitamins, minerals and coenzymes. this patient group is only partially explained by traditional
Untreated patients showed an average annual score increase risk factors [50], and disorders of mineral metabolism may
of 44 % as assessed by the Agatston method. The rate of contribute substantially to the high incidence of events [51–
progression was slowed to 15 % yearly when patients were 56]. Hyperphosphatemia and its traditional management
given nutritional supplements. with calcium-based phosphate binders has been implicated
Budoff et al. [46] used aged garlic extract (AGE) to inhibit in the development and progression of cardiovascular
CAC progression. AGE was employed because it was previ- calcification, and the dose of oral calcium has been correlated
ously shown to reduce multiple cardiovascular risk factors, with the severity of calcification [51, 57]. Vascular and
including blood pressure, serum cholesterol levels, platelet valvular calcifications are very extensive in CKD-5D
aggregation and adhesion, while stimulating nitric oxide gen- (Fig. 6.3) and progress rapidly. In an attempt to curb the
eration in endothelial cells. In a placebo-controlled, double- rapid progression of calcification, the Treat-to-Goal Study—a
blind, randomized pilot study 23 patients were treated with randomized, multicenter clinical trial—compared the
4 ml of oral AGE or the equivalent amount of placebo per day. calcium-free, non-absorbable polymer sevelamer with
Nineteen patients completed the 1-year protocol. At the end traditional calcium-based phosphate binders [58]. Study
of follow-up the mean change in calcium volume score for outcomes included serum levels of phosphorus, calcium,
the AGE group (n = 9) was significantly smaller (7.5 ± 9.4 %) intact parathyroid hormone (PTH), and lipids, as well as
than for the placebo group (n = 10) that demonstrated an aver- change in calcification of the coronary arteries and thoracic
age increase of 22 ± 18.5 % (P = 0.046). Throughout the study aorta quantified by EBCT. Two hundred adult patients who
there were no significant differences in individual cholesterol had received hemodialysis for a median of 3 years prior to
parameters or CRP between treatment group. study entry, were enrolled at 15 medical centers in Europe
For a long time microscopic organisms called nanobacte- and the United States. During the study period, phosphate
ria were thought to be implicated in the process of athero- binders were adjusted to maintain serum phosphorus levels
sclerosis where they operated as nucleating factors for between 3.0 and 5.0 mg/dL, serum calcium levels between
CAC. More recently what was once believed to be an infec- 8.5 and 10.5 mg/dL and serum PTH levels between 150 and
tious agent has been described as a core of phosphate and 300 pg/mL. EBCT was performed at the start of the study,
calcium crystals with adherent molecules of fetuin-A; these and after 6 and 12 months of treatment. In spite of a similar
complexes have been shown to act as nucleating factors for control of serum phosphorus and calcium, coronary and
fast growth of calcification [47]. Nonetheless, before such aortic calcification progressed significantly in the calcium-
knowledge was acquired tetracyclines – as treatment for treated patients while there was no statistically significant
nanobacteria – were combined with ethylenediaminetet- change from baseline in the sevelamer group. At 1 year
raacetic acid disodium salt (EDTA) – as a chelating agent, as (Fig. 6.4), the median percent change in coronary and aorta
well as vitamins and CoQ10 and administered to 77 volun- scores were 25 % and 28 % and 6 % and 5 % in the calcium
teers with stable coronary artery disease [48]. EBT scans and sevelamer group, respectively (p = 0.02 for all intergroup
were performed at baseline and after a short follow-up of comparisons). Of note, the mean LDL cholesterol was sig-
4 months. Of the 77 patients, 44 (57 %) showed CAC score nificantly lower in the sevelamer group, than in patients
regression (average −14 %), while the remaining 33 showed treated with calcium salts, despite the fact that the latter
126 P. Raggi

Fig. 6.3 Extensive

cardiovascular calcification in a
patient suffering from end-stage
renal disease. The soft tissues
have been removed and only the
calcified portion of the aorta and
coronary arteries are shown. AA
aortic arch, LAD left anterior
descending coronary artery, CX
circumflex coronary artery, RCA
right coronary artery, TA thoracic
aorta

A second randomized study was performed with the same

30 28*
Median % calcium score change

25*
primary end-point of CAC progression in patients random-
25 ized to sevelamer or calcium-based phosphate binders within
a few weeks of beginning hemodialysis [62]. At the end of
20
18 months of follow-up calcium treated patients again
15 showed a significant 11-fold greater progression of CAC
than sevelamer treated patients (p < 0.002). The secondary
10
6 end point of this study was long-term mortality; at the end of
5
5 4.5 years of follow-up the mortality of calcium treated
patients was double that of sevelamer treated subjects (haz-
0 ard ratio: 3.2; p < 0.02) [63]. In contrast with these 2 studies,
Coronary Aorta Coronary Aorta
the investigators of the CARE-2 study were unable to con-
Calcium-salts Sevelamer firm that sevelamer and calcium-acetate phosphate binders
affect CAC progression differently and showed an approxi-
Fig. 6.4 Median percentage calcium score change for coronary arteries mate 30 % progression at the end of 1 year for both treatment
and aorta in end-stage renal disease patients randomized to 1-year arms [64]. In this protocol the investigators meant to ascer-
treatment with sevelamer or calcium-based salts. The progression was
significant for both coronary arteries and aorta only in the calcium salt
tain whether the effect of sevelamer on CAC progression is
treated patients [58] due to its lipid lowering ability; therefore they planned to
randomize patients to sevelamer or a combination of calcium
salts and statins. However, 80 % of the sevelamer treated
received statins more often. However, the changes in calcium patients also received statins and this may have caused CAC
score severity seen at 52 weeks were independent of the progression in both arms as shown in the general population
levels of LDL cholesterol, HDL cholesterol and C-reactive (see above). Furthermore, the PTH level of sevelamer treated
protein. Additionally, sevelamer therapy was accompanied patients was double that of prior studies [58, 62], suggesting
by a simultaneous improvement in bone mineral density a very poor control of mineral metabolism. In a more recent
[59]. Interestingly, an inverse relationship between CAC and trial cinacalcet and vitamin D, both used to reduce the PTH
bone mineral density has also been observed in non-uremic levels in secondary hyperparathyroidism, were compared as
individuals [60, 61] and suggests an interaction between far as their ability to slow CAC progression [65]. At the end
bone and vascular health. of 1 year of follow-up cinacalcet showed a non-significant
6 Natural History and Impact of Interventions on CAC 127

but clear trend toward slowing of calcification of the cardiac tion of traditional risk factors and HIV-specific risk factors,
valves, coronary arteries and aorta. Due to the numerous pro- such as chronic inflammation, proliferation of pro-
tocol violations committed by the participating physicians, a inflammatory lymphocytes, endothelial damage and dys-
subanalysis was performed to assess the effect of protocol function and global activation of the immune system. HIV
adherence [66]. Patients who were treated with cinacalcet in infected patients have been demonstrated to have a higher
close adherence with the protocol showed a very significant prevalence and larger than expected deposits of CAC [69–
slowing of CAC and aortic valve calcification compared to 71] and CAC seems to progress rapidly in HIV infected
controls. Although this was an unplanned sub-analysis it patients [72, 73]. In addition to traditional risk factors,
highlighted the importance of protocol adherence and the immunological factors have been associated with the preva-
possibility that many unsuccessful randomized studies may lence and progression of CAC such as nadir CD4 count [69],
be marred by poor compliance with the protocol design by HIV infection per se [72], volume of epicardial fat [73], and
the participating physicians rather than the patients. circulating CD16+ monocytes [74].

Coronary Atherosclerosis in Human Visceral Adipose Tissue and Coronary Artery

Immunodeficiency Virus Infected Patients Calcium

With the advent of highly effective anti-retroviral therapy The current epidemic of obesity, insulin resistance and dia-
(HART), the mortality due to AIDS related diseases has betes mellitus in western countries, has generated a strong
dropped dramatically. However, other diseases have surfaced interest in the potential role of visceral adipose tissue in the
and are now affecting these patients in premature age. development of atherosclerosis and its complications. The
Among the most prominent is atherosclerosis and coronary intra-abdominal and epicardial adipose tissues (EAT)
artery disease [67, 68]. Initially believed to be a consequence (Fig. 6.5) are highly inflamed in obese patients, patients with
of the dyslipidemia induced by several HART drugs, the the metabolic syndrome and in those with established
concept has now evolved to include a more complex interac- coronary artery disease; large quantities of pro-inflammatory

a b

Fig. 6.5 (a) Axial computed tomography image showing extensive in (a); the epicardial adipose tissue is encased between the visceral and
calcium deposits in the left anterior coronary artery and a small amount parietal pericardium highlighted by the orange line
of calcium at the origin of the right coronary artery. (b) Same image as
128 P. Raggi

cytokines and free fatty acids are released by these fat com- 45 %

Mean % cacium score change

partments [75]. The exact mechanisms by which EAT may P < 0.0001
predispose to atherosclerosis development are unknown,
although several plausible mechanisms may be involved in
this process. The adventitia of the coronary arteries comes in 17 %
direct contact with EAT without the interposition of a fascia.
EAT may thus exert a paracrin effect with direct exposure of
the adventitia to humoral and cellular inflammatory
mediators; this in turn may promote proliferation of vasa Event free Myocardial infarction
vasorum and growth of subendothelial atherosclerotic lesions LDL = 120 LDL = 118
[75]. Adipocytes are capable of secreting numerous cytokines
that affect metabolic, inflammatory and vascular pathways;
Fig. 6.6 Mean CAC volume score in patients treated with statins who
some of them are specifically secreted by adipocytes (such as suffered a myocardial infarction during follow-up and event-free sub-
adiponectin, leptin, and resistin), while others are also jects. Despite attaining a similar mean LDL level with treatment, the cal-
produced by other tissues (plasminogen activator inhibitor cium score progression was significantly different between groups [80]
type-1 (PAI-1), tumor necrosis factor-α, interleukin 1 and 6,
monocyte chemo-attractant protein 1 (MCP-1), angiotensin atic individuals submitted to sequential EBCT scanning
II, and cholesteryl ester transfer protein) [75]. Several studies while undergoing treatment with statins. The mean follow-
showed an association of EAT with CAC, while others have up was 3 years, men and women were enrolled in equal pro-
shown an association of EAT with plaques showing portions and the mean age of the enrolled subjects was
characteristics of vulnerability [75]. In 3 studies in the 57 ± 8 years. In spite of an identical average LDL level on
general population [76–78] and one study of HIV infected treatment (~120 mg/dl in each group), the 41 patients who
patients [73] there was a significant association between suffered a myocardial infarction showed a much greater
EAT and CAC progression. In the Heinz Nixdorf Recall yearly CAC score progression than the 454 event-free survi-
study [78], the association of EAT and CAC progression was vors (42 ± 23 % vs 17 ± 25 %, P < 0.001, Fig. 6.6). The inves-
significant in patients with a small burden of atherosclerosis tigators further applied a threshold of 15 %/year increase in
at baseline (defined as a CAC score less than 100) but not in CAC score to differentiate a true score change from a mea-
patients with more advanced disease. Additionally, the asso- surement reproducibility error [21]. Independent of the base-
ciation was stronger in younger subjects and patients with line CAC score patients with an increase smaller than 15 %/
lower body mass index. The authors hypothesized that these year (i.e no progression from baseline) suffered very few
seemingly paradoxical results suggest that EAT acts as an events (N = 5) and the events occurred late during follow-up.
initial promoter of atherosclerosis but that it may not have a On the contrary, the majority of events (N = 36) occurred in
prolonged long-term effect on CAC. patients showing a CAC score progression >15 %/year and
the events occurred early during follow-up. Figure 6.7 shows
an example of rapid progression of CAC and the occurrence
Clinical Implications of CAC Progression of an acute coronary event in a 64 year old man. In the MESA
study [81] 5862 patients had a baseline and follow-up CAC
The clinical significance of progression of CAC has been scan at approximately 2.5 year interval while the median
addressed in several observational studies and one random- clinical follow-up time was 7.5 years. Progression of CAC
ized trial to date. Raggi et al. [79] followed 817 asymptom- was a predictor of incident cardiovascular events both in
atic individuals referred by primary care physicians for patients without and those with CAC at baseline. An increase
sequential EBCT imaging at an average interval of of ≥300 Agatston score units in patients with CAC at base-
2.2 ± 1.3 years. Telephone interviews and chart reviews were line was associated with a hazard ratio of 6.3 of developing
conducted to ascertain the occurrence of myocardial infarc- hard cardiovascular events. In an observational study of 4609
tion after the second CT scan. The mean yearly CAC volume asymptomatic patients, Budoff et al. [82] performed
score change for the individuals who suffered a myocardial sequential CT scans an average of 3.5 years from baseline.
infarction was 47 ± 50 % while it averaged 26 ± 32 % in those The intent was to test whether CAC progression measured by
free of events (P < 0.001). Treatment of hyperlipidemia (a three different methods (absolute change, increase >15 %/
probable marker of greater baseline risk) and CAC score year and square root) predicted mortality and which method
change were independent predictors of myocardial was the most predictive. During follow-up there were 288
infarction. all-cause deaths and CAC progression measured by any of
In a second observation [80], the occurrence of myocar- the three methods was predictive of an event, although the
dial infarction was estimated in a cohort of 495 asymptom- square root method was the best model. Finally, three
6 Natural History and Impact of Interventions on CAC 129

incident cardiovascular events were recorded of which 49

a occurred after the second CT scan; the median absolute CAC
score increase was 4 units in event-free survivors and 247
units in those who suffered events (P < 0.0001). In multiple
logistic regression analyses, age (p = 0.03), male gender
(p = 0.04), LDL cholesterol (p = 0.01), HDL cholesterol
(p = 0.04), and 2-year change in CAC score (p = 0.0001) were
significantly associated with risk of events.
The studies reviewed above clearly indicate that CAC
progression poses a serious threat for the occurrence of
future events. Nonetheless, whether sequential CAC
screening should be recommended in clinical practice
remains controversial since available therapies are not
effective in slowing calcium accrual.

Conclusion
Despite a basic science construct, there has been no vali-
dation of the clinical utility of sequential CAC imaging to
monitor the effectiveness of lipid lowering therapy. On
the other hand, the benefit of non-calcium based therapies
b for phosphate-binding purposes in end-stage renal disease
has been clearly shown with this technique. A number of
small and preliminary studies have shown that CT can be
of potential use in monitoring the outcome of various
therapies. Nonetheless, there is an urgent need to stan-
dardize the scoring methods and assess the equivalence of
the existing CT equipment [23, 86]. Additionally, the
rigid application of a density threshold of 130 HU to
define the presence of tissue calcification in all patients
limits our ability to identify more recent and less densely
calcified plaques and may be incorrectly applied to all the
different CT brands and models available on the market.
Although there is a need for further prospective studies,
the most interesting finding that has emerged so far is that
progression of CAC is associated with a greater risk of
adverse events.
Future directions of research may include studying the
effect of novel therapies such as HDL raising drugs, new
Fig. 6.7 (a) This 64 year old man at intermediate risk of cardiovascular LDL lowering therapies (i.e. – PCSK-9 inhibitors), new
events by Framingham categories had a baseline CAC score of 106. (b)
After 18 months from the first CT his score increased to 296. Within treatments for HIV that do not affect lipid metabolism,
3 months of the second CT scan he suffered a non-ST elevation etc. If sequential CT imaging were confirmed to be useful
myocardial infarction in assessing the effectiveness of anti-atherosclerotic ther-
apies, it would greatly facilitate the conduction of preven-
independent groups of researchers made the observation that tion trials by allowing a reduction in the number of
progression of CAC is faster in patients with the metabolic patients needed to treat. Furthermore, a physician’s effort
syndrome and diabetes mellitus and it is linked with increased to implement preventive measures might be facilitated by
risk of cardiovascular events [12, 83, 84]. sharing information with his patients about the course of
The only prospective randomized trial that tested the their disease.
hypothesis of CAC progression as a predictor of an adverse With continued improvements in CT technology and
event was the St. Francis Heart Study [85]. In the natural further reduction in radiation exposure, it is hoped that the
history arm of the study 4903 patients (age 50–70) were role of sequential CT imaging may become better defined
submitted to a baseline and repeat CT scan 2 years after either for follow-up of CAC or non-calcified plaque
enrollment. After approximately 4 years of follow-up 119 changes by CT angiography [87].
130 P. Raggi

References 16. Stary HC. The development of calcium deposits in atherosclerotic

lesions and their persistence after lipid regression. Am J Cardiol.
2001;88(2A):16E–9.
1. Strong JP, Malcom GT, McMahan A, Tracy RE, Newman III WP,
17. Daoud AS, Jarmolych J, Augustyn JM, Fritz KE. Sequential mor-
Herderick EE, Cornhill F. Prevalence and extent of atherosclerosis
phologic studies of regression of advanced atherosclerosis. Arch
in adolescents and young adults. The Pathobiological Determinants
Pathol. 1981;105:233–9.
of Atherosclerosis in Youth Study. JAMA. 1999;281:727–35.
18. Clarkson TB, Bond MG, Bullock BC, Marzetta CA. A study of ath-
2. Bostrom K, Watson KE, Horn S, Wortham C, Herman IM, Demer
erosclerosis regression in Macaca mulatta. IV. Changes in coronary
LL. Bone morphogenic protein expression in human atherosclerotic
arteries from animals with atherosclerosis induced for 19 months
lesions. J Clin Invest. 1993;91:1800–9.
and then regressed for 24 months or 48 months at plasma choles-
3. Fitzpatrick LA, Severson A, Edwards WD, Ingram RT. Diffuse
terol concentrations of 300 or 200 mg/dl. Exp Mol Pathol.
calcification in human coronary arteries: association of osteopontin
1981;34:345–68.
with atherosclerosis. J Clin Invest. 1994;94:1597–604.
19. Agatston AS, Janowitz WR, Hildner JR, Zusmer NR, Viamonte Jr
4. Shanahan CM, Cary NR, Metcalfe JC, Weissberg PL. High expres-
M, Detrano R. Quantification of CAC using ultrafast computed
sion of genes for calcification-regulating proteins in human athero-
tomography scanning. J Am Coll Cardiol. 1990;15:
sclerotic plaques. J Clin Invest. 1994;93:2393–402.
827–32.
5. Proudfoot D, Davies JD, Skepper JN, Weissberg PL, Shanahan
20. Sangiorgi G, Rumberger JA, Severson A, Edwards WD, Gregoire J,
CM. Acetylated low-density lipoprotein stimulates human vascular
Fitzpatrick LA, Schwartz RS. Arterial calcification and not lumen
smooth muscle cell calcification by promoting osteoblastic
stenosis is highly correlated with atherosclerotic plaque burden in
differentiation and inhibiting phagocytosis. Circulation.
humans: a histologic study of 723 coronary artery segements using
2002;106:3044–50.
non-decalcifying methodology. Electron beam computed
6. Collett GD, Canfield AE. Angiogenesis and pericytes in the initia-
tomography and coronary artery disease: scanning for coronary
tion of ectopic calcification. Circ Res. 2005;96:930–8.
artery calcification. J Am Coll Cardiol. 1998;31:126–33.
7. Subbotin V. Neovascularization of coronary tunica intima (DIT) is
21. Callister TQ, Cooil B, Raya S, Lippolis NJ, Russo DJ, Raggi
the cause of coronary atherosclerosis. Lipoproteins invade coronary
P. Coronary artery disease: improved reproducibility of calcium
intima via neovascularization from adventitial vasa vasorum, but
scoring with electron-beam CT volumetric method. Radiology.
not from the arterial lumen: a hypothesis. Theor Biol Med Model.
1998;208:807–14.
2012;9:11.
22. Rumberger JA, Kaufman L. A rosetta stone for CAC risk stratifica-
8. Bini A, Mann KG, Kudryk BJ, Schen FJ. Noncollagenous bone
tion: agatston, volume, and mass scores in 11,490 individuals. AJR
matrix proteins, calcification and thrombosis in carotid artery
Am J Roentgenol. 2003;181:743–8.
atherosclerosis. Arterioscler Thromb Vasc Biol. 1999;19:1852–61.
23. McCollough CH, Ulzheimer S, Halliburton SS, Shanneik K, White
9. Kronmal RA, McClelland RL, Detrano R, Shea S, Lima JA,
RD, Kalender WA. CAC: a multi-institutional, multimanufacturer
Cushman M, Bild DE, Burke GL. Risk factors for the progression
international standard for quantification at cardiac CT. Radiology.
of coronary artery calcification in asymptomatic subjects: results
2007;243:527–38.
from the Multi-Ethnic Study of Atherosclerosis (MESA).
24. Hokanson JE, MacKenzie T, Kinney G, Snell-Bergeon JK, Dabelea
Circulation. 2007;115(21):2722–30.
D, Ehrlich J, Eckel RH, Rewers M. Evaluating changes in coronary
10. Erbel R, Lehmann N, Churzidse S, Rauwolf M, Mahabadi AA,
artery calcium: an analytic method that accounts for interscan
Möhlenkamp S, Moebus S, Bauer M, Kälsch H, Budde T, Montag
variability. AJR Am J Roentgenol. 2004;182:1327–32.
M, Schmermund A, Stang A, Führer-Sakel D, Weimar C,
25. Jukema JW, Bruschke AV, van Boven AJ, Reiber JH, Bal ET,
Roggenbuck U, Dragano N, Jöckel KH; on behalf of the Heinz
Zwinderman AH, Jansen H, Boerma GJ, van Rappard FM, Lie
Nixdorf Recall Study Investigators. Progression of coronary artery
KI. Effects of lipid lowering by pravastatin on progression and
calcification seems to be inevitable, but predictable – results of the
regression of coronary artery disease in symptomatic men with
Heinz Nixdorf Recall (HNR) study. Eur Heart J. 2014;pii:ehu288.
normal to moderately elevated serum cholesterol levels. The
[Epub ahead of print].
Regression Growth Evaluation Statin Study (REGRESS).
11. Pandey AK, Blaha MJ, Sharma K, Rivera J, Budoff MJ, Blankstein
Circulation. 1995;91:2528–40.
R, AlMallah M, Wong ND, Shaw L, Carr J, O'Leary D, Lima JA,
26. Brown G, Albers JJ, Fisher LD, Schaefer SM, Lin JT, Kaplan C,
Szklo M, Blumenthal RS, Nasir K. Family history of coronary heart
Zhao XQ, Bisson BD, Fitzpatrick VF, Dodge HT. Regression of
disease and the incidence and progression of coronary artery
coronary artery disease as a result of intensive lipid-lowering
calcification: Multi-Ethnic Study of Atherosclerosis (MESA).
therapy in men with high levels of apolipoprotein B. N Engl J Med.
Atherosclerosis. 2014;232:369–76.
1990;323:1289–98.
12. Wong ND, Nelson JC, Granston T, Bertoni AG, Blumenthal RS,
27. Levine GN, Keaney Jr JF, Vita JA. Cholesterol reduction in cardio-
Carr JJ, Guerci A, Jacobs Jr DR, Kronmal R, Liu K, Saad M, Selvin
vascular disease: clinical benefits and possible mechanisms. N Engl
E, Tracy R, Detrano R. Metabolic syndrome, diabetes, and
J Med. 1995;332:512–21.
incidence and progression of coronary calcium: the Multiethnic
28. Callister TQ, Raggi P, Cooil B. Effects of HMG-CoA reductase
Study of Atherosclerosis study. JACC Cardiovasc Imaging.
inhibitors on coronary artery disease. N Engl J Med. 1998;339:
2012;5:358–66.
1972–7.
13. Lehmann N, Möhlenkamp S, Mahabadi AA, Schmermund A,
29. Budoff MJ, Lane KL, Bakhsheshi H, Mao S, Grassmann BO,
Roggenbuck U, Seibel R, Grönemeyer D, Budde T, Dragano N,
Friedman BC, Brundage BH. Rates of progression of CAC by
Stang A, Mann K, Moebus S, Erbel R, Jöckel KH. Effect of
electron beam tomography. Am J Cardiol. 2000;86:8–11.
smoking and other traditional risk factors on the onset of coronary
30. Achenbach S, Dieter R, Pohle K, Leber A, Thilo C, Knez A,
artery calcification: results of the Heinz Nixdorf recall study.
Menendez T, Maeffert R, Kusus M, Regenfus M, Bickel A, Haberl
Atherosclerosis. 2014;232:339–45.
R, Stienbeck G, Moshage W, Daniel WG. Influence of lipid-
14. Stary HC. Natural history of calcium deposits in atherosclerosis
lowering therapy on the progression of coronary artery calcification.
progression and regression. Z Kardiol. 2000;89 Suppl 2:28–35.
Circulation. 2002;106:1077–82.
15. Williams JK, Sukhova GK, Herrington DM, Libby P. Pravastatin
31. Hoffmann U, Derfler K, Haas M, Stadler A, Brady TJ, Kostner
has cholesterol-lowering independent effects on the artery wall of
K. Effects of combined low density lipoprotein apheresis and
atherosclerotic monkeys. J Am Coll Cardiol. 1998;31:684–91.
6 Natural History and Impact of Interventions on CAC 131

aggressive statin therapy on coronary calcified plaque as measured 48. Maniscalco BS, Taylor KA. Calcification in coronary artery disease
by computed tomography. Am J Cardiol. 2003;91:461–4. can be reversed by EDTA-tetracycline long-term chemotherapy.
32. Taylor AJ, Kent SM, Flaherty PJ, Coyle LC, Markwood TT, Pathophysiology. 2004;11:95–101.
Vernalis MN. ARBITER: Arterial Biology for the Investigation of 49. Renal Data System US. USRDS 2004 Annual Data Report: Atlas of
the Treatment Effects of Reducing Cholesterol: a randomized trial End-Stage Renal Disease in the United States. Bethesda: National
comparing the effects of atorvastatin and pravastatin on carotid Institutes of Health, National Institute of Diabetes and Digestive
intima medial thickness. Circulation. 2002;106:2055–60. and Kidney Diseases; 2004.
33. Hsia J, Klouj A, Prasad A, Burt J, Adams-Campbell LL, Howard 50. Longenecker JC, Coresh J, Powe NR, Levey AS, Fink NE, Martin
BV. Progression of coronary calcification in healthy postmenopausal A, et al. Traditional cardiovascular disease risk factors in dialysis
women. BMC Cardiovasc Disord. 2004;4:21. patients compared with the general population: the CHOICE Study.
34. Hecht HS, Harman SM. Comparison of the effects of atorvastatin J Am Soc Nephrol. 2002;13:1918–27.
versus simvastatin on subclinical atherosclerosis in primary 51. Guérin AP, London GM, Marchais SJ, Metivier F. Arterial stiffen-
prevention as determined by electron beam tomography. Am ing and vascular calcifications in end-stage renal disease. Nephrol
J Cardiol. 2003;91:42–5. Dial Transplant. 2000;15:1014–21.
35. Hecht HS, Harman SM. Relation of aggressiveness of lipid- 52. Blacher J, Guerin AP, Pannier B, Marchais SJ, London GM. Arterial
lowering treatment to changes in calcified plaque burden by calcifications, arterial stiffness, and cardiovascular risk in end-stage
electron beam tomography. Am J Cardiol. 2003;92:334–6. renal disease. Hypertension. 2001;38:938–42.
36. Wong ND, Kawakubo M, LaBree L, Azen SP, Xiang M, Detrano 53. Raggi P, Boulay A, Chasan-Taber S, Amin N, Dillon M, Burke SK,
R. Relation of CAC progression and control of lipids according to et al. Cardiac calcification in adult hemodialysis patients. A link
the National Cholesterol Education Program guidelines. Am between end-stage renal disease and cardiovascular disease? J Am
J Cardiol. 2004;94:431–6. Coll Cardiol. 2002;39:695–701.
37. Raggi P, Davidson M, Callister TQ, Welty FK, Bachmann GA, 54. London GM, Guérin AP, Marchais SJ, Métivier F, Pannier B, Adda
Hecht H, Rumberger JA. Aggressive versus moderate lipid- H. Arterial media calcification in end-stage renal disease: impact on
lowering therapy in hypercholesterolemic post-menopausal all-cause and cardiovascular mortality. Nephrol Dial Transplant.
women: Beyond Endorsed Lipid Lowering with EBT Scanning 2003;18:1731–40.
(BELLES). Circulation. 2005;112(4):563–71. (In press). 55. London GM. Cardiovascular calcifications in uremic patients:
38. Arad Y, Spadaro LA, Roth M, Newstein D, Guerci A. Treatment of clinical impact on cardiovascular function. J Am Soc Nephrol.
asymptomatic adults with elevated calcium scores with atorvastatin, 2003;14:S305–9.
vitamin C and vitamin E. The St. Francis Heart Study randomized 56. Block GA, Klassen PS, Lazarus JM, Ofsthun N, Lowrie EG,
clinical trial. J Am Coll Cardiol. 2005;46:166–72. Chertow GM. Mineral metabolism, mortality, and morbidity in
39. Schmermund A, Achenbach S, Budde T, Buziashvili Y, Förster A, maintenance hemodialysis. J Am Soc Nephrol. 2004;15:2208–18.
Friedrich G, et al. Effect of intensive versus standard lipid-lowering 57. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D,
treatment with atorvastatin on the progression of calcified coronary et al. Coronary-artery calcification in young adults with end-stage
atherosclerosis over 12 months: a multicenter, randomized, double- renal disease who are undergoing dialysis. N Engl J Med.
blind trial. Circulation. 2006;113:427–37. 2000;342:1478–83.
40. Houslay ES, Cowell SJ, Prescott RJ, Reid J, Burton J, Northridge 58. Chertow GM, Burke SK, Raggi P. Sevelamer attenuates the pro-
DB, Boon NA, Newby DE, Scottish Aortic Stenosis and Lipid gression of coronary and aortic calcification in hemodialysis
Lowering Therapy, Impact on Regression trial Investigators. patients. Kidney Int. 2002;62:245–52.
Progressive coronary calcification despite intensive lipid-lowering 59. Raggi P, James G, Burke S, Bommer J, Taber SC, Holzer H, Braun
treatment: a randomised controlled trial. Heart. 2006;92:1207–12. J, Chertow GM. Paradoxical decrease in vertebral bone density
41. Snell-Bergeon JK, Hokanson JE, Jensen L, MacKenzie T, Kinney with calcium-based phosphate binders in hemodialysis. J Bone
G, Dabelea D, Eckel RH, Ehrlich J, Garg S, Rewers M. Progression Miner Res. 2005;20:764–72.
of coronary artery calcification in type 1 diabetes: the importance of 60. Barengolts EI, Berman M, Kukreja SC, Kouznetsova T, Lin C,
glycemic control. Diabetes Care. 2003;26:2923–8. Chomka EV. Osteoporosis and coronary atherosclerosis in asymp-
42. Anand DV, Lim E, Darko D, Bassett P, Hopkins D, Lipkin D, tomatic postmenopausal women. Calcif Tissue Int. 1998;62:
Corder R, Lahiri A. Determinants of progression of coronary artery 209–13.
calcification in type 2 diabetes role of glycemic control and 61. Sirola J, Sirola J, Honkanen R, Kroger H, Jurvelin JS, Maenpaa P,
inflammatory/vascular calcification markers. J Am Coll Cardiol. Saarikoski S. Relation of statin use and bone loss: a prospective
2007;50(23):2218–25. population-based cohort study in early postmenopausal women.
43. Manson JE, Allison MA, Rossouw JE, Carr JJ, Langer RD, Hsia J, Osteoporos Int. 2002;13:537–41.
et al. Estrogen therapy and coronary-artery calcification. N Engl 62. Block GA, Spiegel DM, Ehrlich J, Mehta R, Lindbergh J, Dreisbach
J Med. 2007;356:2591–602. A, et al. Effects of sevelamer and calcium on coronary artery calci-
44. Budoff MJ, Chen GP, Hunter CJ, Takasu J, Agrawal N, Sorochinsky fication in patients new to hemodialysis. Kidney Int. 2005;68(4):
B, Mao S. Effects of hormone replacement on progression of 1815–24.
coronary calcium as measured by electron beam tomography. 63. Block GA, Raggi P, Bellasi A, Kooienga L, Spiegel DM. Mortality
J Womens Health (Larchmt). 2005;14:410–7. effect of coronary calcification and phosphate binder choice in inci-
45. Rath M, Niedzwiecki A. Nutritional supplement program halts pro- dent hemodialysis patients. Kidney Int. 2007;7:438–41.
gression of early coronary atherosclerosis documented by ultrafast 64. Qunibi W, Moustafa M, Muenz LR, He DY, Kessler PD, Diaz-Buxo
computed tomography. J Appl Nutr. 1996;48:67–78. JA, et al. A 1-year randomized trial of calcium acetate versus
46. Budoff MJ, Takasu J, Flores FR, Niihara Y, Lu B, Lau BH, Rosen sevelamer on progression of coronary artery calcification in hemo-
RT, Amagase H. Inhibiting progression of coronary calcification dialysis patients with comparable lipid control: the Calcium Acetate
using Aged Garlic Extract in patients receiving statin therapy: a Renagel Evaluation-2 (CARE-2) study. Am J Kidney Dis.
preliminary study. Prev Med. 2004;39:985–91. 2008;5:952–65.
47. Kuro-O M. A phosphate-centric paradigm for pathophysiology and 65. Raggi P, Chertow GM, Torres PU, Csiky B, Naso A, Nossuli K,
therapy of chronic kidney disease. Kidney Int Suppl (2011). Moustafa M, Goodman WG, Lopez N, Downey G, Dehmel B,
2013;3:420–6. Floege J, on behalf of the ADVANCE Study Group. The ADVANCE
132 P. Raggi

Study: a randomized study to evaluate the effects of cinacalcet plus study using non-contrast cardiac CT. Atherosclerosis. 2011;218:
low dose vitamin D on vascular calcification in patients on 363–8.
hemodialysis. Nephrol Dial Transplant. 2011;26(4):1327–39. 77. Yerramasu A, Dey D, Venuraju S, Anand DV, Atwal S, Corder R,
66. Ureña-Torres PA, Floege J, Hawley CM, Pedagogos E, Goodman Berman DS, Lahiri A. Increased volume of epicardial fat is an
WG, Pétavy F, Reiner M, Raggi P. Protocol adherence and the independent risk factor for accelerated progression of sub-clinical
progression of cardiovascular calcification in the ADVANCE study. coronary atherosclerosis. Atherosclerosis. 2012;220:
Nephrol Dial Transplant. 2013;28:146–52. 223–30.
67. Triant VA, Lee H, Hadigan C, Grinspoon SK. Increased acute 78. Mahabadi AA, Lehmann N, Kälsch H, Robens Y, Bauer M, Dykun
myocardial infarction rates and cardiovascular risk factors among I, Budde T, Moebus S, Jöckel KH, Erbel R, Möhlenkamp
patients with human immunodeficiency virus disease. J Clin S. Association of epicardial adipose tissue with progression of
Endocrinol Metab. 2007;92:2506–12. coronary artery calcification is more pronounced in the early phase
68. Freiberg MS, Chang CC, Kuller LH, Skanderson M, Lowy E, of atherosclerosis – results from the Heinz Nixdorf Recall study.
Kraemer KL, Butt AA, Bidwell Goetz M, Leaf D, Oursler KA, JACC Cardiovasc Imaging. 2014;7(9):909–16.
Rimland D, Rodriguez Barradas M, Brown S, Gibert C, McGinnis 79. Raggi P, Cooil B, Shaw LJ, Aboulhson J, Takasu J, Budoff MJ,
K, Crothers K, Sico J, Crane H, Warner A, Gottlieb S, Gottdiener J, Callister TQ. Progression of coronary calcification on serial
Tracy RP, Budoff M, Watson C, Armah KA, Doebler D, Bryant K, electron beam tomography scanning is greater in patients with
Justice AC. HIV infection and the risk of acute myocardial infarc- future myocardial infarction. Am J Cardiol. 2003;92:827–9.
tion. JAMA Int Med. 2013;173(8):614–22. 80. Raggi P, Callister T, Budoff M, Shaw L. Progression of CAC and
69. Post WS, Budoff M, Kingsley L, Palella Jr FJ, Witt MD, Li X, risk of first myocardial infarction in patients receiving cholesterol-
George RT, Brown TT, Jacobson LP. Associations between HIV lowering therapy. Arterioscler Thromb Vasc Biol. 2004;24:
infection and subclinical coronary atherosclerosis. Ann Intern Med. 1272–7.
2014;160:458–67. 81. Budoff MJ, Young R, Lopez VA, Kronmal RA, Nasir K, Blumenthal
70. Mangili A, Gerrior J, Tang AM, O’Leary DH, Polak JK, Schaefer RS, Detrano RC, Bild DE, Guerci AD, Liu K, Shea S, Szklo M,
EJ, Gorbach SL, Wanke CA. Risk of cardiovascular disease in a Post W, Lima J, Bertoni A, Wong ND. Progression of coronary cal-
cohort of HIV-infected adults: a study using carotid intima-media cium and incident coronary heart disease events: MESA (Multi-
thickness and coronary artery calcium score. Clin Infect Dis. Ethnic Study of Atherosclerosis). J Am Coll Cardiol. 2013;61:
2006;43:1482–9. 1231–9.
71. Kingsley LA, Cuervo-Rojas J, Munoz A, Palella FJ, Post W, Witt 82. Budoff MJ, Hokanson JE, Nasir K, Shaw LJ, Kinney GL, Chow D,
MD, et al. Subclinical coronary atherosclerosis, HIV infection and Demoss D, Nuguri V, Nabavi V, Ratakonda R, Berman DS, Raggi
antiretroviral therapy: multicenter AIDS Cohort Study. Aids. P. Progression of coronary artery calcium predicts all-cause mortal-
2008;22:1589–99. ity. JACC Cardiovasc Imaging. 2010;3:1229–36.
72. Guaraldi G, Zona S, Orlando G, Carli F, Ligabue G, Fiocchi F, 83. Raggi P, Cooil B, Ratti C, Callister TQ, Budoff M. Progression of
Menozzi M, Rossi R, Modena MG, Raggi P. Human immunodefi- coronary calcification and occurrence of myocardial infarction in
ciency virus infection is associated with accelerated atherosclero- patients with and without diabetes mellitus. Hypertension.
sis. J Antimicrob Chemother. 2011;66(8):1857–60. 2005;45:1–6.
73. Zona S, Raggi P, Bagni P, Orlando G, Carli F, Ligabue G, Scaglioni 84. Kiramijyan S, Ahmadi N, Isma’eel H, Flores F, Shaw LJ, Raggi P,
R, Rossi R, Guaraldi MG. Parallel increase of subclinical athero- Budoff MJ. Impact of coronary artery calcium progression and
sclerosis and epicardial adipose tissue in patients with HIV. Am statin therapy on clinical outcome in subjects with and without dia-
Heart J. 2012;163:1024–30. betes mellitus. Am J Cardiol. 2013;111:356–61.
74. Baker JV, Hullsiek KH, Singh A, Wilson E, Henry K, Lichtenstein 85. Arad Y, Goodman KJ, Roth M, Newstein D, Guerci AD. Coronary
K, Onen N, Kojic E, Patel P, Brooks JT, Hodis HN, Budoff M, calcification, coronary risk factors, and atherosclerotic cardiovas-
Sereti I, CDC SUN Study Investigators. Immunologic predictors of cular disease events. The St. Francis Heart Study. J Am Coll
coronary artery calcium progression in a contemporary HIV cohort. Cardiol. 2005;46:158–65.
AIDS. 2014;28(6):831–40. 86. Oudkerk M, Stillman AE, Halliburton SS, Kalender WA,
75. Alexopoulos N, Katritsis D, Raggi P. Visceral adipose tissue as a Mohlenkamp S, McCollough CH, et al. CAC screening: current sta-
source of inflammation and promoter of atherosclerosis. tus and recommendations from the European Society of Cardiac
Atherosclerosis. 2014;233:104–12. Radiology and North American Society for Cardiovascular
76. Nakanishi R, Rajani R, Cheng VY, Gransar H, Nakazato R, Imaging. Int J Cardiovasc Imaging. 2008;24(6):645–71.
Shmilovich H, Otaki Y, Hayes SW, Thomson LE, Friedman JD, 87. Zeb I, Li D, Nasir K, Malpeso J, Batool A, Flores F, Dailing C,
Slomka PJ, Berman DS, Dey D. Increase in epicardial fat volume is Karlsberg RP, Budoff M. Effect of statin treatment on coronary
associated with greater coronary artery calcification progression in plaque progression – a serial coronary CT angiography study.
subjects at intermediate risk by coronary calcium score: a serial Atherosclerosis. 2013;23:198–204.
 Methodology for CCTA Image
Acquisition 7
Mathew J. Budoff, Jerold S. Shinbane,
and Songshao Mao

Abstract
Cardiovascular computed tomographic angiography (CCTA) can assess cardiovascular
pathology through visualization of gross anatomic abnormalities, characterization of tissue
attenuation, and cardiac functional analysis. As cardiac structures are in constant motion,
special attention to the methodology of image acquisition is essential to capturing high
quality images during the most quiescent stage of cardiac and coronary artery motion.
Successful imaging requires an understanding of the interplay of multiple motions, includ-
ing the complexities of cardiac motion, motion related to variation in heart rate and rhythm,
potential respiratory motion, potential patient movement, table motion, gantry rotation, and
timing and movement of the intravenous contrast bolus through the structures of interest
(Fig. 7.1).
Optimization of image acquisition is achieved through localization of target structures,
timing of scanning for capture of images during the segment of the R-R interval with rela-
tively slow cardiac motion, and injection of contrast media to enhance opacification of
structures throughout all slice levels. These techniques help to avoid or minimize motion
artifacts and suboptimal opacification of structures of interest, which would make subse-
quent image reconstruction and diagnostic analysis a challenge. Imaging methodology
must also focus on minimizing the exposure to radiation and the amount of intravenous
contrast. This chapter will focus on methods essential to acquisition of diagnostic images
for the assessment of cardiovascular pathology.

Keywords
Cardiac computed tomography • Image Acquisition • Methodology • Non-invasive angiog-
raphy • Radiation • Contrast • Calcium scoring • Scan protocols

Introduction
M.J. Budoff, MD (*)
David Geffen School of Medicine at UCLA, Los Angeles Cardiovascular computed tomographic angiography (CCTA)
Biomedical Research Institute, Torrance, CA, USA can assess cardiovascular pathology through visualization of
e-mail: [email protected] gross anatomic abnormalities, characterization of tissue
J.S. Shinbane, MD, FACC FHRS FSCCT attenuation, and cardiac functional analysis. As cardiac
Division of Cardiovascular Medicine, structures are in constant motion, special attention to the
Department of Internal Medicine,
methodology of image acquisition is essential to capturing
University of Southern California,
Keck School of Medicine, Los Angeles, CA, USA high quality images during the most quiescent stage of car-
diac and coronary artery motion. Successful imaging requires
S. Mao, MD
Department of Medicine, Division of CardiologyLos Angeles an understanding of the interplay of multiple motions,
Biomedical Research Institute, Los Angeles, CA 90713, USA including the complexities of cardiac motion, motion related

© Springer International Publishing 2016 133

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_7
134 M.J. Budoff et al.

Gantry rotation field of view is set at 20 cm, the voxel size is 20 cm divided
IV
Contrast by 512 voxels, or 0.4 mm. If the field of view is set a 50 cm
injection
velocity
to include evaluation of axilla, breast and lungs, the voxel
Heart rate and rhythm size is approximately 1 mm, or 2.5 fold worse resolution.
Cardiac motion Structures are delineated by their attenuation, as measured in
Potential respiratory motion
Hounsfield units (HU), named after Sir Godfrey Hounsfield,
the inventor of computed tomography. Each voxel is assigned
a unit of attenuation based on a scale, with the attenuation
values of different substances represented by a different HU
Table movement
value [1]. Representative HU values include: air −1000, fat
−50 to −100, water 0, muscle 10–40, contrast 80–300, cal-
Circulation time Potential patient motion cium 130–1500.

Fig. 7.1 Schematic demonstrating multiple motion factors which must

be accounted for during imaging, including the complexities of cardiac Scanner
motion, motion related to variation in heart rate and rhythm, potential
respiratory motion, potential patient movement, table motion, gantry Conceptually, multidetector computed tomography (MDCT)
rotation, and the movement of the intravenous contrast bolus to the systems work using similar principles, but vary in regard to
structures of interest
specific components and features. A MDCT system has an
x-ray tube/collimator and detector/collimator housed in a
to variation in heart rate and rhythm, potential respiratory gantry capable of extremely rapid rotation. The x-ray tube
motion, potential patient movement, table motion, gantry provides radiation energy quantified through tube current
rotation, and timing and movement of the intravenous con- (mAs) and tube voltage (kVP). Multidetector scanners have
trast bolus through the structures of interest (Fig. 7.1). multiple rows of detectors arranged in a variety of arrays
Optimization of image acquisition is achieved through with the goal of covering a specified volume during each
localization of target structures, timing of scanning for cap- gantry rotation. Advances in detector number and
ture of images during the segment of the R-R interval with arrangement have lead to increases in the volume of coverage
relatively slow cardiac motion, and injection of contrast per rotation, with imaging of the entire heart now achievable
media to enhance opacification of structures throughout all within one cardiac cycle [2].
slice levels. These techniques help to avoid or minimize The relationship between table movement, gantry rotation
motion artifacts and suboptimal opacification of structures of speed and beam collimation defines the degree volume
interest, which would make subsequent image reconstruction coverage per rotation, as well as the degree of overlap
and diagnostic analysis a challenge. Imaging methodology between rotations. The concept of “pitch” quantifies this
must also focus on minimizing the exposure to radiation and relationship, as pitch relates to coverage obtained by the
the amount of intravenous contrast. This chapter will focus x-ray beam, through beam width and table movement, during
on methods essential to acquisition of diagnostic images for one rotation of the gantry. The pitch therefore defines the
the assessment of cardiovascular pathology. amount of overlap of the acquired data and the speed at
which the study is complete. Overlapping images allow for
oversampling, permitting multisector image reconstruction,
Image Acquisition Concepts but also lead to greater radiation exposure. With a pitch value
of less than 1, there is overlap between volumes of coverage.
The ability to visualize the coronary vasculature is due to The definition of pitch has evolved with advancement of
advances in spatial and temporal resolution of scanning tech- scanner technologies, and various equations have been
nology. There are multiple factors that affect spatial and tem- proposed depending on the specific type of scanner [3].
poral resolution, many of which are interdependent. The goal Using conventional ECG-gated helical data acquisition, the
of image acquisition is to visualize the target structures in pitch values for coronary CT angiography are typically
their entirety while limiting the field of view to exclude addi- considerably less than 1 (e.g., 0.22), which indicates that the
tional structures, as a larger field of view will increase radia- table is advanced by much less than one detector row width
tion exposure and may diminish image quality. The field of during one rotation of the scanner. Thus, the same region
view defines the imaging boundaries important to ensuring within the heart is exposed during several consecutive
visualization of structures of interest. As the 512 by 512 voxel rotations, which increases radiation dose. Newer systems
matrix is assigned to a particular field of view, a smaller field enable thinner slice thickness and collimation, allowing for
of view leads to greater spatial resolution. For example, if a an even lower pitch resulting in more images, thinner
7 Methodology for CCTA Image Acquisition 135

reconstruction intervals, and better visualization of the acquisition speed is insufficient to completely freeze heart
coronary anatomy. Systems which provide enough Z axis motion, cardiac triggering is essential in order to capture and
coverage for whole heart imaging in one gantry rotation process images at times of minimal cardiac and coronary
eliminate the variable of pitch, by allowing for imaging artery motion speed to avoid blurring of images.
without table movement [2]. In contrast, the latest generation Based on ventricular and atrial contraction and relaxation,
dual-source CT technology permits ECG-triggered helical there are six phases in a cardiac cycle (R-R interval). These
scanning at very high pitch values. By inter-weaving data include: isovolumic contraction time, ejection time,
measured from two detector systems separated by isovolumic relaxation time, left ventricular rapid filling,
approximately 90°, pitch can be increased up to 3.4 [4]. diatasis, and atrial contraction time. During ventricular
Helical scanning with such high pitch values reduces the systole, the motion of right coronary artery and left circumflex
amount of redundant data collected, thus substantially mid-segment are in an anterior and inner direction, which
decreasing radiation exposure. This dual-source CT reverses in diastole. At end isovolemic contraction and
configuration allows prospectively ECG-triggered high- relaxation, the motion speed is close zero, but the time
pitch helical scan mode, first introduced in 2009. With interval for imaging is very short.
single-source CT systems, this pitch is limited to a maximum There are three relatively low speed motion segments:
value of 1.5 for gapless data acquisition in the z-axis. At isovolumic contraction, isovolumic relaxation, and diastasis.
higher pitch values, data gaps occur, which may result in The isovolumic contraction time (after the R wave) and
image artifacts and errors in image reconstruction. However, relaxation time (after the T wave) are approximately
with second-generation dual-source CT, the second tube/ 50–140 ms. Diastasis is the other slower motion segment, but
detector system is used to fill the data gaps; accordingly, the the length is more variable following heart rate changes. In
pitch can be increased to values above 3. This results in very patient with heart rates of greater than 100–110 bpm,
short CT data acquisition and radiation exposure times. diastasis is minimal [11]. The diatasis segment is the optimal
scan time in patient with a lower heart rate, and is the most
common time period for assessment in patients with regular
ECG Triggering and controlled heart rates.
With image acquisition, an ECG signal is simultaneously
ECG triggering is essential to minimize the effects of cardiac recorded with the raw data set. Two ECG gating techniques
motion on image acquisition. Cardiac and coronary motion are used for CCTA imaging, retrospective and prospective
during a single cardiac cycle is extremely complex and can triggering. With retrospective ECG gating, images are
be analyzed in the context of the X, Y, and Z axis planes. acquired throughout the cardiac cycle (Figs. 7.2 and 7.3)
Left ventricular contraction and relaxation are the main [12]. The strength of this approach is that images can be
source of cardiac motion. Multiple types of cardiac motion reconstructed using the most optimal timing for each
have been noted including: inward or outward motion of the coronary artery or arterial segment after image acquisition
endocardium with systole and diastole; rotation; torsion or has occurred. Additionally, acquisition of images throughout
wringing; translocation; and “accordion-like” base to apex the cardiac cycle allows for volumetric assessment of cardiac
motion [3]. There is greater X-Y direction motion at the mid- function. The major drawback of this approach is that
portion of the left ventricle and greater Z direction motion at radiation exposure is significantly greater than with a
the base of the heart [5]. Left ventricular endocardial maxi- prospective ECG gated approach. Retrospective gating with
mal motion speed has been reported at 41–100 mm/s [6, 7]. current tube modulation leads to a significant decrease in
Specific motion issues also relate to individual coronary radiation by decreasing radiation exposure during the systolic
arteries. Since the right coronary artery is further from the phase of the cardiac cycle [13].
center of the left ventricle than the left coronary artery, this With prospective triggering, images are obtained at a set
artery exhibits faster motion, especially in its mid-section percentage of the R-R interval. The advantage of this
[8]. Atrial systole and diastole are important factors causing technique is the limitation to radiation exposure [14]. The
motion of the right coronary artery and the left circumflex disadvantage relates to the limited dataset obtained. If the
coronary artery [9]. The right coronary artery has 50 mm/s images obtained demonstrate significant motion artifact,
motion speed by angiography [10]. The left main and there are no other images to reconstruct. Given the variability
proximal portion of left anterior descending coronary artery of heart rate with arrhythmias, prospective gating can be
have greater Z plane motion, and therefore Z axis motion can problematic with significant atrial or ventricular ectopy or
induce left main motion abnormalities [5, 7]. atrial fibrillation.
Given the imaging challenges caused by cardiac motion, In regard to variability of heart rate or rhythm, any change
appropriate collimation size and acquisition speed are factors in heart rate or rhythm can alter chamber size, and therefore
important to minimizing CCTA motion artifact. Since the change of the spatial location of target structure in axial or
136 M.J. Budoff et al.

Retrospective ECG gating

Fig. 7.2 Demonstration of motion of the right coronary artery at serial artery is seen at other phases. The arrow depicts the right coronary
decile percentages of the R-R interval during retrospective gating. The artery, which should be a round structure, but with motion, appears as a
most optimal R-R percentage is 70 %, as blurring of the right coronary ‘cashew-nut’ shape

3-D images, even if the individual axial image is not blurred. most cases), as a consistently wide diastolic time interval is
All patients have some variability in heart rate, even those needed with techniques such as ECG-based tube current
without atrial or ventricular ectopy. Scanning protocols exist modulation, prospectively ECG-triggered axial scanning,
which can withhold imaging during short R-R intervals and prospectively ECG-triggered high-pitch helical scan-
during image acquisition [15]. Post processing analysis ning. Without adequate patient preparation (generally, beta-
includes editing and deletion of images from ectopic beats blocker drugs), it is rare that this goal is achieved. Calcium
and analysis of mid-diastolic phases of the R-R interval with channel blockers with good chronotropic effects (verapamil,
an absolute rather than relative time from the preceding R diltiazem) can be used as an alternative, or in conjunction
wave when the R-R interval is variable. with, beta blockade in patients with high resting heart rates
Heart rate control is essential for image optimization. Pre- undergoing CCTA.
medication with beta blockers, or calcium channel blockers Nitroglycerin is given sublingually prior to scanning to
when beta blockers are contra-indicated, is used to achieve maximally dilate coronary arteries. Since there may be
sinus rates of 60 beats/min using most standard MDCT catecholamine stimulation with breath hold, the sound of the
systems. With dual source MDCT systems, imaging can be scanner, nitroglycerin administration, and the sensation of
performed with heart rates in a higher range (although contrast administration, a resting sinus rate that appears to be
radiation doses will still go up with faster heart rates, so good controlled without medications prior to scanning may still
justification for beta blockade with this system still exists) increase during scanning. Special attention to monitoring of
[16, 17]. heart rate and blood pressure is important, as in some cir-
High quality images on CCTA depend on a low and steady cumstances patients may not be able to tolerate medications
heart rate (below 70 bpm, and preferably below 60 bpm in for heart rate control and dilation of coronary arteries.
7 Methodology for CCTA Image Acquisition 137

Fig. 7.3 3-D reconstructions of the LAD at different phases of the R-R interval, demonstrating reconstruction at a suboptimal phase and an opti-
mal phase for artery visualization. (a) Reconstruction at 30 % of the R-R interval. (b) Reconstruction at 70 % of the R-R interval

Breath hold is essential to limit motion of structures due enhancement at all slice levels using as small a dose of con-
to respiration during image acquisition. Breath hold times trast medium as possible. Important factors to consider in
have decreased significantly with advances in technology regard to contrast media injection are circulation time and
and allow for cardiac imaging to be completed during a injection methodology.
single breath hold. There is some controversy as to the Assessment of the circulation time is important to timing
optimal phase of respiration for breath hold. Regardless of the acquisition of images, and is defined as the time from
the phase chosen in an individual lab, it is important to contrast injection to the optimal enhancement of target
practice breath hold commands and exercises prior to the structures. This sequence typically consists of repetitively
scan. The technologist, by assessing whether breath holding imaging a single slice using a low radiation serial scanning
was optimal during the scout film, calcium score and/or of the same slice to obtain the peak enhancement time
contrast timing run, can further educate the patient prior to through time density curve analysis (Figs. 7.4 and 7.5). With
the CTA scan acquisition. As an end-inspiratory breath hold CCTA, scans are obtained at the level of the takeoff of the
will move thoracic structures more caudally than an end- left main coronary artery or descending aorta, to create a
expiratory breath hold, consistent breath hold instructions time–density curve to assess the time to peak opacification.
need to be given for preview images and actual scans, and The measured transit time is then used as the delay time from
critical for the CTA for diagnostic images. the start of the contrast injection to imaging start for the
CCTA. It is important to use the same injection rate for the
circulation time as for the subsequent CCTA study.
Contrast Media Injection Another contrast timing method utilizes an automatic
bolus-triggering technique. With this method, angiography
The aim of contrast media injection is to enhance the contrast imaging is automatically activated when the CT HU reaches
differentiation between target structure and surrounding a pre-specified HU value [18]. Circulation times vary based
tissues, by increasing the CT Hounsfield Units (CT HU) of on the cardiac output. Patients with low output states having
the interest structure. Ideally, an injection protocol will increased times and high output states with decreased times.
achieve optimal enhancement with uniformity of contrast Many factors influence circulation time, including venous
138 M.J. Budoff et al.

Fig. 7.4 Serial axial images of the target slice demonstrating opacification for determination of the circulation time

tal vein. Optimal enhancement depends on the contrast

CT# (HU)
media dose and injection rate. The goal is to maintain the
150
same level of vascular enhancement throughout image acqui-
130 sition. The dose of contrast media is dependent on multiple
factors, such as patient size, scan time, and desired enhance-
110
ment level (CT HU). Multiphase contrast injectors with pre-
90 set volumes and injection velocities are used to maintain
uniformity of contrast enhancement throughout the study. A
70
first injection stage with a high velocity, often 5 ml/s, is fol-
50 lowed by saline injection to flush the remaining contrast out
0 10 20 30 40
of the intravenous line and antecubital vein using a multi-
Time (s)
phase injector. The use of a saline bolus after contrast injec-
tion moves the residual contrast in the intravenous tubing
Fig. 7.5 Graph of CT Hounsfield Units versus time, demonstrating the
and arm veins into the heart and coronary vasculature. The
time to maximal opacification of the region of interest
timing of the saline bolus is important, as in some studies
clearance of the venous circulation and right heart structures
anatomy, cardiac output, and underlying cardiac and valvular can help with visualization of arterial structures, while in
function and therefore must be individually determined. other studies, these structures are important to analysis. A
Low osmolar nonionic contrast media contrast medium is middle phase with diluted contrast can also be utilized for
usually administered via an 20-gauge needle in the antecubi- some opacification of right heart and venous structures.
7 Methodology for CCTA Image Acquisition 139

Specific injection protocols may be necessary for certain distance from carina to left main coronary artery is extremely
specialized indications including congenital heart disease. variable [19]. Also, the left anterior descending coronary
Since image quality on CT is based upon contrast to noise artery can course cranial to the left main coronary artery
ratios (CNR), maintaining good contrast opacification is (Fig. 7.6). For coronary artery imaging, scanning 10 mm cra-
important. In larger patients or more obese subjects, the nial to the left main coronary artery and 10 mm caudal to the
noise will be greater, so to ensure good image quality, faster apex is subsequently performed with CCTA. In patients with
rates of contrast injection are preferable to maintain the coronary artery bypass grafts, the starting point is the top of
CNR. Thus, for patients who are very obese, increasing the the aortic arch or 10 mm higher than the surgical metal clips.
rate of contrast to 6 ml/s is often necessary. A larger IV The mid level of the right pulmonary artery can also be used
access may be necessary to ensure good flow at higher injec- as the beginning of the scan level, if it can be defined in pre-
tion rates. view images.
After the scout images, a calcium scan is performed
(Fig. 7.7). This is a high resolution non-contrast cardiac-
Preview, Calcium, and Contrast Scans gated study which provides important prognostic information
regarding future cardiovascular risk. For the calcium scan,
CCTA is performed in the following sequence: planar scout the 2-D axial images are analyzed with the identification of
images, a non-contrast coronary artery calcium scan, a calcium either using manual or automated methods, with
timing scan for assessment of the circulation time, and a quantification of calcium score based on identification of HU
contrast scan. Planar scout images are obtained in order to units with an attenuation of at least 130 HU in the areas of
define the most cranial and caudal scanning levels (Z-axis) of identified calcium. There are two major methods of
the structures of interest. The scout images are obtained in quantifying coronary artery calcium, the Agatston score and
anteroposterior and lateral views and aligned to the patient volumetric analysis. The Agatston score is based on the
by a laser system. The scan volume is selected with the plaque number, and plaque area times a coefficient based on
structures of interest placed within the center of the scanning the peak HU units in the plaque [20]. Calcium volume score
volume. Important landmarks can be identified including the describes a volumetric analysis of calcium with calculation
left atrial appendage, which is usually the most cranial based on volumetric reconstruction and is more reproducible
structure of the heart, and the ventricular apex, which is the on serial study [21]. The calcium score is a marker of plaque
most caudal structure. Although the carina had served as a burden and is an independent risk factor for coronary artery
marker to localize the most cranial aspect of the heart, the disease beyond traditional risk factors [22, 23].

Fig. 7.6 Axial views (cranial to caudal) showing the left anterior field. (a) The cranial slice, showing the left anterior descending (arrow).
descending artery coursing cranial to the takeoff off the left main coro- (b) A more caudal slice, demonstrating the left main artery (arrow) is
nary artery. If the cranial limit of the field of view were at the level of visualized inferiorly to the left anterior descending artery
the left main, the left anterior descending could be out of the imaging
140 M.J. Budoff et al.

This may vary by the type of study, with some studies per-
formed specifically for assessment of coronary artery anat-
omy, while others are performed for additional assessment of
thoracic vasculature, such as in the case of congenital heart
disease.

Relation of Image Acquisition to Image

Analysis

Image reconstruction is dependent on image acquisition, as

the reconstructed images are only as good as the acquired
data. The raw datasets are imported to workstations with
software allowing the analysis of images in multiple 2-D and
3-D formats. Prior to reconstruction, the 2-D axial dataset
must be reviewed to ensure that the structures of interest
were scanned in their entirety and that there is uniformity of
contrast throughout the study. A decrease in contrast in the
distal vessels can appear as stenoses. Adequate and uniform
Fig. 7.7 Coronary artery calcium score axial image showing a calcifi- enhancement of the distal aorta can be helpful in ensuring
cation of the left anterior descending coronary artery that distal coronary arteries have been adequately opacified.
Interpretation of CT coronary angiography requires
The calcium scan is useful to the planning, performance, reconstruction and analysis of multiple 2-D and 3-D analyses
and interpretation of the CCTA. Assessment of the images so that findings can be confirmed on multiple views and
can be used to ensure that there is complete coverage of the artifacts related to image acquisition can be identified. Image
coronary anatomy in the image set prior to contrast angiog- reconstruction allows a 3-D understanding of cardiovascular
raphy, as well as to determine the minimum volume to be anatomy from large vessel to small vessel. The serial axial
covered to minimize radiation exposure [24]. The degree of 2-D images are reconstructed into a 3-D data cube with
coronary calcification may prohibit the accurate assessment subsequent use of software to edit out and analyze
of coronary artery stenoses. cardiovascular structure. Workstation software has
The calcium score as well as the calcium distribution dramatically reduced the time for image editing and
should be assessed prior to the performance of the CCTA to reconstruction. Systematic reconstruction, serial automated
determine whether the contrast study should be performed. editing, and analysis of this data cube allows one to glean
Different imaging centers use various cutoffs for the information important to characterization of the structure
performance of CCTA in the setting of a significantly and relationship between structures essential to clinical
elevated calcium score, with some center using >500 or diagnosis and planning and facilitation of cardiovascular
>1000. It is important though to have an understanding of the procedures. These reconstructions include: assessment of
specific goal of an individual study, as depending on the thoracic structures in relation to skeletal structures, relation
question asked and the location of calcium, some studies of large vessel vasculature and structures, cardiac chambers,
may still be performed in settings of an elevated calcium valves, and coronary vasculature (Fig. 7.8).
score. For example, in cases where the location and patency Reconstruction of coronary artery anatomy requires
of coronary artery bypass grafts are the clinical questions, assessment of the phase of the cardiac cycle during which an
calcium in the native coronary arteries may still not artery or arterial segment is most quiescent. Retrospectively
necessarily prohibit the study from being performed. In gated axial images can be reconstructed at different diastolic
addition to traditional cardiac risk factors, knowledge of the phases of the cardiac cycle and assessed for the most optimal
calcium score is helpful in assessing the pretest probability images regarding minimizing cardiac motion (Figs. 7.2 and
of coronary artery disease when interpreting the contrast 7.3). As the optimal phase of the cardiac cycle may vary by
angiography images. artery and arterial segment, different arteries or segments
After performance of the calcium scan, a contrast angiog- may need to be analyzed using multiple modalities. Once the
raphy study is performed, requiring the administration of correct phase or phases have been chosen, 2-D images can be
iodinated contrast timed to enhance the structures of interest. rapidly formatted in axial, sagittal, and coronal planes.
7 Methodology for CCTA Image Acquisition 141

Subsequent analysis is performed primarily from axial

images with additional analysis with multiple modalities of
image reconstruction (Fig. 7.9a–g). Functional analysis for
retrospectively gated scans can be formatted and assessed in
standard echo views (Fig. 7.10).
Although the 3-D reconstructed images are both aesthetic
and intuitive regarding orientation, it is essential to recognize
that the process of reconstruction has limitations. It is
essential to remember that the 2-D views provide an entire
dataset whereas the 3-D techniques lead to loss of data and
potential artifacts that adversely affect interpretation of
images. Given the limitations of reconstruction techniques, it
is essential to continually reference back to the 2-D images
and view potential findings using multiple types of
reconstructions before making a diagnosis.
There are many factors related to image acquisition that
may affect image reconstruction and analysis. With volume
rendering, pixels are assigned HU depending on their
attenuation. With automated editing, pixels below a certain
HU cutoff (lower threshold 80–100 HU) are edited out.
Volume rendering and editing software allows creation of
3-D image with structures removed to adequately visualize
structures of interest, but involves potential loss of data
through over-editing of structures. If over-edited, the
coronary arteries can appear as though stenoses are present.
Construction of 3-D images from 2-D image sets with
cardiac respiratory or patient motion between slices can lead
to artifactually discontinuous arterial segments that could be
misinterpreted as stenoses. Lack of uniformity of contrast
enhancement on serial slices may also result in the artifactual
appearance of stenoses. If only viewed on 3-D images,
myocardial bridging can be misinterpreted as obstructive
coronary artery disease. Misalignment artifacts (formed
from movement between the large acquisitions of the 64–160
detector arrays or collimation), can also form regions of
pseudo-stenosis. Misalignment artifacts have been previously
known as mis-registration, stair step, collimation or a
multitude of prior names. The Society of Cardiovascular
Computed Tomography has developed a nomenclature
document to standardize these names [25].
Partial volume effects may limit reconstruction and
analysis. The goal of scanning is to acquire isotropic data,
where the spatial resolution is equal in the X, Y, and Z axes,
allowing for accurate images with multiplane reconstructions
[26]. As spatial resolution in the Z axis may not be truly
isotropic, some volume averaging of data may occur.
Therefore, volumes averaging may occur with only a portion
of the depth of the image being represented as present
throughout the dataset.
Fig. 7.8 Reconstructions of thoracic structures in relation to skeletal
structures, relation of large vessel vasculature and structures, cardiac Calcified plaques may also limit reconstruction and
chambers, valves, and coronary vasculature analysis of images. The purpose of contrast enhanced studies
142 M.J. Budoff et al.

a b c

d e

f g

Fig. 7.9 A significant right coronary artery non-calcified stenosis is the coronary arteries; (d) Curved multiplanar reformatted view; (e)
shown using multiple reconstruction modalities. Multiple CCTA angi- Double oblique reformat; (f) Sagittal view with a thick maximum inten-
ography views are demonstrated including; (a) 3-D volume rendered sity projection; (g) Cardiac catheterization angiography emulation
view of the heart and coronary arteries; (b) 3-D volume rendered view
of the heart and coronary arteries; (c) 3-D volume rendered view of only

is to increase contrast between coronary vessel lumen and sels. Luminal enhancement though, will decrease the con-
surrounding tissues. Greater lumen enhancement (repre- trast between enhanced vessel lumen and calcified plaques.
sented by increased CT HU) will create greater contrast This can make assessment of the coronary arterial wall chal-
between the vessel lumen and non-calcified vessel wall, lenging for assessment of different tissue components of the
which is especially important for visualization of small ves- plaque wall.
7 Methodology for CCTA Image Acquisition 143

Fig. 7.10 Functional views in standard echo planes. (a) Short axis view; (b) 2 chamber view; Panel; (c) 4 chamber view; (d) 3 chamber view

Other reconstruction and viewing modalites can are use- and is helpful for differentiating calcium, contrast, and metal
ful for analysis of images that are problematic due to issues in the coronary arteries and avoids issues of volume averag-
related to image acquisition [27]. Maximal intensity ing of structures. As editing is not involved with this modal-
projections demonstrate the maximal density point at each ity, there will be overlap of structures as one moves through
point in a 3-D volume. Conceptually, this provides the ability the dataset.
to move through the 3-D data cube with a thick slab focused Multiplanar curved reformatting allows for in plane
on the maximum intensity of the images in the slab. The analysis of an individual vessel (Fig. 7.11) [28]. A
modality provides for assessment of small and distal vessels reconstruction is performed orthogonal to vessel centerline
144 M.J. Budoff et al.

Fig. 7.11 Curved multiplanar reformation of the left anterior descending coronary artery, allowing in plane analysis of the vessel

and does not require editing. Vessels can be analyzed in a References

360° rotation allowing for assessment of eccentricity of
plaque in relation to the vessel lumen. The technique requires 1. Brooks RA. A quantitative theory of the Hounsfield unit and its
application to dual energy scanning. J Comput Assist Tomogr.
accurate vessel tracking and determination of the centerline
1977;1(4):487–93.
of the vessel. Interactive display methods may provide 2. Dewey M, Zimmermann E, Deissenrieder F, et al. Noninvasive
greater diagnostic accuracy than pre-rendered images [27]. coronary angiography by 320-row computed tomography with
Virtual endoscopic views, which provide a perspective from lower radiation exposure and maintained diagnostic accuracy:
comparison of results with cardiac catheterization in a head-to-head
inside a vessel or chamber have been developed, but are very
pilot investigation. Circulation. 2009;120(10):867–75.
dependent on filtering and smoothing techniques. 3. Silverman PM, Kalender WA, Hazle JD. Common terminology for
Fluoroscopic views are helpful for assessment of metallic single and multislice helical CT. AJR Am J Roentgenol.
structures such as pacemaker leads. 2001;176(5):1135–6.
4. Hausleiter J, Bischoff B, Hein F, Meyer T, Hadamitzky M,
The evolution of CT scanners and workstations allow for
Thierfelder C, Allmendinger T, Flohr TG, Schomig A, Martinoff
rapid acquisition and reconstructions of images for the char- S. Feasibility of dual-source cardiac CT angiography with high-
acterization of cardiovascular disease processes. CCTA pitch scan protocols. J Cardiovasc Comput Tomogr. 2009;3:
imaging poses challenges due to the complex motion of the 236–42.
5. Mao S, Budoff MJ, Bin L, Liu SC. Optimal ECG trigger point in
heart, variation in heart rate and rhythm, and tissue character-
electron-beam CT studies: three methods for minimizing motion
istics of cardiovascular structures. An understanding of these artifacts. Acad Radiol. 2001;8(11):1107–15.
factors and meticulous attention to triggering techniques, 6. Ritchie CJ, Godwin JD, Crawford CR, Stanford W, Anno H, Kim Y.
contrast injection methods, and preview methods can lead to Minimum scan speeds for suppression of motion artifacts in
CT. Radiology. 1992;185(1):37–42.
images visualizing anatomy and function critical to the diag-
7. Rogers Jr WJ, Shapiro EP, Weiss JL, et al. Quantification of and
nosis and treatment of patients with cardiovascular disease. correction for left ventricular systolic long-axis shortening by
7 Methodology for CCTA Image Acquisition 145

magnetic resonance tissue tagging and slice isolation. Circulation. ultrafast computed tomography. J Am Coll Cardiol. 1990;15(4):
1991;84(2):721–31. 827–32.
8. Mao S, Lu B, Oudiz RJ, Bakhsheshi H, Liu SC, Budoff MJ. 21. Callister TQ, Cooil B, Raya SP, Lippolis NJ, Russo DJ, Raggi P.
Coronary artery motion in electron beam tomography. J Comput Coronary artery disease: improved reproducibility of calcium
Assist Tomogr. 2000;24(2):253–8. scoring with an electron-beam CT volumetric method. Radiology.
9. Achenbach S, Ropers D, Holle J, Muschiol G, Daniel WG, Moshage 1998;208(3):807–14.
W. In-plane coronary arterial motion velocity: measurement with 22. Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC.
electron-beam CT. Radiology. 2000;216(2):457–63. Coronary artery calcium score combined with Framingham score
10. Topol EJ, Nissen SE. Our preoccupation with coronary luminology. for risk prediction in asymptomatic individuals. JAMA. 2004;
The dissociation between clinical and angiographic findings in 291(2):210–5.
ischemic heart disease. Circulation. 1995;92(8):2333–42. 23. Greenland P, Bonow RO, Brundage BH, et al. ACCF/AHA 2007
11. Weyman AE. Principles and practice of echocardiography. 2nd ed. clinical expert consensus document on coronary artery calcium
Philadelphia: Lea and Febiger; 1994. p. 721–41. scoring by computed tomography in global cardiovascular risk
12. Becker CR, Knez A, Ohnesorge B, Schoepf UJ, Reiser MF. Imaging assessment and in evaluation of patients with chest pain: a report of
of noncalcified coronary plaques using helical CT with retrospec- the American College of Cardiology Foundation Clinical Expert
tive ECG gating. AJR Am J Roentgenol. 2000;175(2):423–4. Consensus Task Force (ACCF/AHA Writing Committee to Update
13. Abada HT, Larchez C, Daoud B, Sigal-Cinqualbre A, Paul JF. the 2000 Expert Consensus Document on Electron Beam Computed
MDCT of the coronary arteries: feasibility of low-dose CT with Tomography) developed in collaboration with the Society of
ECG-pulsed tube current modulation to reduce radiation dose. AJR Atherosclerosis Imaging and Prevention and the Society of
Am J Roentgenol. 2006;186(6 Suppl 2):S387–90. Cardiovascular Computed Tomography. J Am Coll Cardiol.
14. Husmann L, Valenta I, Gaemperli O, et al. Feasibility of low-dose 2007;49(3):378–402.
coronary CT angiography: first experience with prospective 24. Gopal A, Budoff MJ. A new method to reduce radiation exposure
ECG-gating. Eur Heart J. 2008;29(2):191–7. during multi-row detector cardiac computed tomographic angiogra-
15. Matsutani H, Sano T, Kondo T, et al. ECG-edit function in multide- phy. Int J Cardiol. 2009;132(3):435–6.
tector-row computed tomography coronary arteriography for 25. Weigold WG, Abbara S, Achenbach S, et al. Consensus document
patients with arrhythmias. Circ J. 2008;72(7):1071–8. on standardized nomenclature for cardiac computed tomography a
16. Brodoefel H, Burgstahler C, Tsiflikas I, et al. Dual-source CT: report of the society of cardiovascular computed tomography writ-
effect of heart rate, heart rate variability, and calcification on image ing committee. J Cardiovasc Comput Tomogr. 2011;5(3):136–44.
quality and diagnostic accuracy. Radiology. 2008;247(2):346–55. doi:10.1016/j.jcct.2011.04.004.
17. Ropers U, Ropers D, Pflederer T, et al. Influence of heart rate on the 26. Tsukagoshi S, Ota T, Fujii M, Kazama M, Okumura M, Johkoh T.
diagnostic accuracy of dual-source computed tomography coronary Improvement of spatial resolution in the longitudinal direction for
angiography. J Am Coll Cardiol. 2007;50(25):2393–8. isotropic imaging in helical CT. Phys Med Biol. 2007;52(3):
18. Cademartiri F, Nieman K, van der Lugt A, et al. Intravenous contrast 791–801.
material administration at 16-detector row helical CT coronary 27. Ferencik M, Ropers D, Abbara S, et al. Diagnostic accuracy of
angiography: test bolus versus bolus-tracking technique. Radiology. image postprocessing methods for the detection of coronary artery
2004;233(3):817–23. stenoses by using multidetector CT. Radiology. 2007;243(3):
19. Bakhsheshi H, Mao S, Budoff MJ, Bin L, Brundage BH. Preview 696–702.
method for electron-beam CT scanning of the coronary arteries. 28. Achenbach S, Moshage W, Ropers D, Bachmann K. Curved
Acad Radiol. 2000;7(8):620–6. multiplanar reconstructions for the evaluation of contrast-enhanced
20. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte Jr electron beam CT of the coronary arteries. AJR Am J Roentgenol.
M, Detrano R. Quantification of coronary artery calcium using 1998;170(4):895–9.
 Post-processing and Reconstruction
Techniques for the Coronary Arteries 8
Swaminatha V. Gurudevan

Abstract
Proper post-processing of cardiac CT images is crucial to obtain high-quality diagnostic
images of the coronary arteries. The design of acquisition protocols take into account scan-
related factors such as the temporal and spatial resolution of the scanner as well as patient-
relate factors such as the patient weight and ECG tracing. ECG gating can be performed
with either prospective or retrospective gating, with each method having distinct advan-
tages. The next phase of post-processing involves the layout of images on the cardiac CT
workstation. These reconstruction techniques enable the interpreting physician to reliably
identify the anatomy and course of the coronary arteries and interpret coronary artery
plaque and luminal obstruction.

Keywords
Reconstruction • Temporal resolution • Spatial resolution • Maximum intensity projection •
Convolution kernel • Pitch • Retrospective and prospective ECG gating

Introduction Scan-Related Post-processing Parameters

With the advent of multidetector computed tomography, Temporal and Spatial Resolution
noninvasive imaging of the coronary arteries is now pos-
sible. Attention to detail in the post-processing aspects of Two important parameters to understand when evaluating an
coronary artery imaging is crucial to obtain high-quality, imaging modality are temporal and spatial resolution.
clinically diagnostic images. This chapter will review the Temporal resolution refers to the ability of an imaging
scan-related and post-scan related post-processing param- modality to detect two distinct events in time as separate
eters that with careful adjustment can greatly aid the events, and is expressed in units of time. It can be likened to
reader in accurately interpreting cardiovascular CT the shutter speed on a camera. Fast shutter speeds have supe-
images. rior temporal resolution to slow shutter speeds and produce
superior images of rapidly moving subjects in action shots.
Slow shutter speeds, on the other hand, will produce blurring
artifacts when subjects move. The intrinsic temporal resolu-
tion of single source multidetector CT systems (using half-
scan reconstruction) ranges from 160 to 225 ms, while dual
S.V. Gurudevan, MD, FACC
source CT systems have a temporal resolution as low as 83 ms.
Department of Medicine, Healthcare Partners Medical Group,
401 S. Fair Oaks Ave., Pasadena, CA 91105, USA Two approaches to optimize temporal resolution in cardiac
e-mail: [email protected] CT include improving the imaging speed with ultrafast

© Springer International Publishing 2016 147

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_8
148 S.V. Gurudevan

gantry rotation speeds and slowing the motion of the heart where the coronary arteries move the least. Coronary artery
during the examination through effective beta blockade. Each motion occurs predictably in specific phases of the cardiac
technique is essential to produce motion-free images. cycle. The two phases of the cardiac cycle in which the coro-
Spatial resolution, on the other hand, refers to the ability nary arteries move the least are mid-diastole, during the dias-
of an imaging modality to detect two distinct objects in space tasis period between early rapid ventricular filling (the E
as separate objects, and is expressed in units of distance. wave) and atrial contraction (the A wave) and end-systole,
Smaller objects such as coronary arteries require submilli- immediately prior to the E wave [3]. At slow heart rates
meter spatial resolution to clearly define the vessel wall, (Fig. 8.1), the diastasis period (between 70 and 80 % of the
lumen, coronary plaque. The spatial resolution of multide- R-R interval) is the most optimal imaging period. At faster
tector CT ranges from 0.5 to 0.625 mm, and is most directly heart rates (Fig. 8.2), the diastasis period shrinks, making the
related to the width of the collimated beam. end-systolic period (between 30 and 50 % of the R-R inter-
val) the period of least coronary motion [4].
Due to the motion of the beating heart, ECG gating is
Cardiac CT Gating necessary to achieve consistent images of the heart that are
free of motion artifacts. Prospective ECG gating relies on
Coronary artery motion that occurs during the cardiac the scanner initiating imaging only during a pre-specified
cycle remains the greatest challenge to effective imaging interval of the cardiac cycle (Fig. 8.3), usually the mid-
of the coronary arteries with cardiovascular CT [1, 2]. diastolic interval. Systolic images are not obtained, and a
Reconstruction algorithms target phases of the cardiac cycle slow, steady heart rate is necessary to avoid motion artifacts.

Fig. 8.1 Coronary artery motion 80

velocity profile of a patient with LAD
a baseline heart rate of 72 beats
LCX
per minute (bpm). A biphasic 60 RCA
Velocity (mm/s)

pattern of rest periods was found

during end systole (at 40–50 %
of the R-R interval) and mid
diastole (at 70–80 % of the R-R
40
interval) (Modified from Lu et al.
[1] with permission from Wolters
Kluwer Health) 20

0
0 20 40 60 80 100
R-R % intervals

100
LAD
80 LCX
RCA
Velocity (mm/s)

60

40

20

0
0 20 40 60 80 100
R-R % intervals

Fig. 8.2 Coronary artery motion velocity profile of a patient with a baseline heart rate of 89 bpm. A monophasic rest period pattern was found
near end systole (at 40–60 % of the R-R interval) (Modified from Lu et al. [1] with permission from Wolters Kluwer Health)
8 Post-processing and Reconstruction Techniques for the Coronary Arteries 149

75% great vessels (20 cm or less) is selected so that the X-axis and
Reconstruction Y-axis spatial resolution matches the Z-axis resolution,
window which is related only to the collimated beam width. This
resolution ranges from 0.5 to 0.625 mm for most CT systems.
R to R interval Figure 8.6 demonstrates representative axial images from a
ECG gated thoracic CT exam with a larger field of view and a
more refined field of view.
X-ray

Convolution Kernel
Fig. 8.3 Prospective ECG-gating

The generation of interpretable cardiac CT images involves

50 % 50 % the application of a variety of reconstruction filters, the goal
of which are to maximize signal to noise ratio and improve
Percentage visualization of the object of interest. This image processing
ECG occurs on the CT scanner console and can be employed
following acquisition of the raw CT data. The convolution
X-ray kernel is defined as the image processing filter applied to the
raw data to yield a final scan image. The sharpness of the
Fig. 8.4 Retrospective ECG-gating
final image is most directly influenced by the type of filter
employed.
A soft convolution kernel will tend to smooth edges and
The greatest advantage of prospective ECG gating is the use reduce the amount of image noise. It can be advantageous
of a low radiation dose (as low as 1 mSv) [5]. to employ this kernel in obese patients where signal-to-
Retrospective ECG gating involves a continuous spiral noise ratio can be diminished secondary to attenuation
feed and scan wherein the entire heart volume is covered from adipose tissue. Sharp convolution kernels tend to
continuously. Data acquisition occurs from all phases of the enhance edges at the cost of increased overall image noise.
cardiac cycle (Fig. 8.4). The patient’s ECG is recorded These sharp kernels can be used in patients with stents or
simultaneously with the CT data acquisition and from the heavily calcified vessels [8–10] to reduce blooming arti-
raw scan data, specific phases of the cardiac cycle are facts that can occur, as shown in Fig. 8.7. For the majority
reconstructed to create multiple data sets [6]. Data overlap of coronary CT imaging applications, a neutral convolution
is necessary to capture each table position at more than one kernel is employed that balances image noise and edge
cardiac cycle. Retrospective gating enables imaging at detection.
more rapid heart rates by employing multi-segment recon-
struction to increase the effective temporal resolution of the
scanner. In addition, by overlapping data acquisition, errant Spiral Pitch
reconstruction from premature heartbeats and variations in
heart rate can be corrected through ecg-editing programs An important parameter for characterizing a spiral CT is the
(Fig. 8.5) [7]. pitch. The pitch is defined as the table feed per gantry rotation
divided by the width of the collimated beam. A pitch of
greater than 1 implies there are gaps in data acquisition,
Field of View while a pitch of less than 1 implies that there is overlap in
data acquisition (Fig. 8.8). Retrospectively gated multide-
While the scanned field of view represents the entire object tector cardiac CT data acquisitions are performed with a
scanned within the gantry, the displayed field of view is pitch of approximately 0.2, as cardiac gating is always nec-
defined as the angular size of the displayed scan on the 3 essary for motion-free images and it is necessary to image an
dimensional matrix. For a given CT application, the size of entire cardiac cycle at least once at each table position.
the matrix is 512 × 512, which limits the number of voxels Modern 64-slice CT scanners automatically determine pitch
that can be displayed within a particular field of view. For based on the scan length and heart rate. The major advan-
general thoracic CT applications, the entire chest is included tages of using a slower pitch is an improved temporal resolu-
in the field of view. However, with cardiac imaging tion due to increased data overlap while the major
applications, it is necessary to reduce the displayed field of to disadvantage is an increased radiation exposure. Multisegment
maximize X-axis and Y-axis spatial resolution. Typically a reconstruction (discussed below) requires a decreased pitch
field of view that encompasses the heart, pericardium and compared to half-scan reconstruction [6].
150 S.V. Gurudevan

Pre-ECG editing Post-ECG editing

a b

c d

Fig. 8.5 ECG editing to eliminate misregistration artifacts can be the R-R interval was notably irregular. (c) Is an oblique sagittal section at
employed on retrospectively gated CT acquisitions. (a) Is an oblique coro- the same reconstruction interval demonstrating similar misregistration
nal section taken at 40 % of the R-R interval demonstrating stairstep-like artifacts (arrows). (b and d) Demonstrate successful elimination of the
misregistration artifacts (arrows) in a patient with atrial fibrillation under- artifacts in the same oblique coronal and sagittal planes using ECG editing
going a retrospectively gated 64-slice cardiac CT examination, in whom to perform precise reconstruction at the end of the T wave (end systole)

a b

Fig. 8.6 Axial projections of two gated cardiac CT examinations at resolution in the X and Y axes. (b) Demonstrates an appropriately
different displayed fields of view. (a) Demonstrates a displayed field of limited field of view for a cardiac CT examination
view encompassing the entire chest. This will tend to limit image
8 Post-processing and Reconstruction Techniques for the Coronary Arteries 151

a b

c d

Fig. 8.7 Sharp and smooth convolution kernels are employed to kernel. (b and d) are similar projections using a sharp (B46f) convolu-
improve visualization of stents and calcified vessels while reducing tion kernel. Blooming artifacts are reduced, and the edge of the stent is
blooming artifacts. (a and c) Depict long axis and short axis oblique more clearly delineated at the expense of increased noise in the remain-
thin-slice projections of an LAD stent using a standard smooth (B26f) der of the image

Reconstruction of CT Data in 64-Detector CT

Pitch Systems

With 64-detector CT systems, each revolution of the gantry

Pitch 2
enables imaging of 3.2–4.0 cm of the heart (64 detectors
times the width of each detector). To cover the entire heart,
the required length of most cardiac scans is 9–10 cm; this
Pitch 1
necessitates combining data from multiple table positions to
yield a final volume of data. The greatest challenge in the
itch 0.5
reconstruction of this volumetric cardiac CT data is the
maintenance of temporal uniformity: that is, one should be
able to provide cardiac images at each table position from the
Table feed per rotation same part of each cardiac cycle. A breakdown of temporal
Pitch:
(in Multislice CT) Total width of collimated beam uniformity can lead to characteristic “stairstep” artifacts.
(n detectors ¥ collimation)
The most commonly used reconstruction algorithm in
Fig. 8.8 Pitch refers to the table feed per gantry rotation during a spiral spiral cardiac CT is the half-scan reconstruction method,
acquisition divided by the width of the collimated beam. A pitch of which involves the use of scan data from a single gantry
exactly 1 (central diagram) implies that there are no data gaps and there rotation to generate an axial CT image. Half-scan
is no overlap of data. When pitch is greater than 1 (top diagram), there
reconstruction excludes the fan beam width (approximately
are gaps in data acquisition, whereas when pitch is less than 1 (bottom
diagram), there is data overlap. Retrospectively gated cardiac CT exam- 30°), so that approximately 210° of rotation are necessary to
inations are performed with a pitch of approximately 0.2 generate a single axial image. Using the half-scan method,
152 S.V. Gurudevan

the temporal resolution is approximately 60 % of the position from different subsequent gantry rotations, one
rotational speed of the scanner (due to the fan beam width simulated half-scan rotation is generated. This results in
exclusion). For modern single source 64-slice CT scanners improved image quality with fewer motion artifacts. By
which have gantry rotation times ranging from 330 to combining images from 3 cardiac cycles, the effective
375 ms, the temporal resolution using the half-scan recon- temporal resolution can be improved to as much as 65 ms.
struction method is approximately 200–225 ms. In patients Multi-segment reconstruction relies heavily on a consistent
with heart rates of 60 beats per minute or less, the mid-diastolic R-R interval on the consecutive beats used to generate the
diastasis period of minimal coronary motion is long enough final axial image. Irregularities from atrial fibrillation or
to allow effective reconstructions in mid diastole in the sinus arrhythmia during breath holding may cause misregis-
majority of patients. tration artifacts.
In patients with heart rates faster than 80 beats per min-
ute, the duration of the diastasis period decreases consider-
ably and may be only 100–200 ms. This makes it nearly Reconstruction of CT Data in 320-Detector CT
impossible to reconstruct motion-free images using the half- Systems
scan reconstruction method. In these cases, multi-segment
reconstruction may be utilized to improve the effective With 320-detector CT systems, one axial rotation can cover
temporal resolution of the CT scanner. Multisegment recon- up to 16 cm of tissue, although typically all 320 detectors
struction relies on additional data overlap with slower table cannot be employed simultaneously to image the heart. To
movement and decreased pitch during CT acquisition accomplish this, the use of a wide X-ray beam and a wide
[11, 12]. This overlap results in the same table position being cone angle is required. Figures 8.10 and 8.11 demonstrate
available for imaging at multiple heart beats from multiple the concept of the fan angle and the cone angle. The cone
detectors (Fig. 8.9). By combining views at a single table angle determines the coverage of the X-ray beam in the lon-
gitudinal, or z-axis while the fan angle determines the cover-
age in the x/y plane. The use of a wide cone angle gives the
320-detector scanner the ability to cover up to 16 cm of tissue

60°
60°
60°
67 ms 67 ms 67 ms

180°

67 ms

Image data
s d
ou
t i nu & fee
n
Co scan
i r al
sp Volume
Z – Position

gaps
slower
pitch
Recon
Recon
Recon

Delay

Fig. 8.9 (a and b) Multisegment reconstruction of a CT acquisition

involves the acquisition of data at a single table position over several
cardiac cycles. The volumetric data are combined to yield a final
summed volume. The major requirement for multisegment reconstruc-
tion is data overlap, which results in a slower pitch and higher radiation
dose during the CT acquisition. Using this technique, effective temporal Fig. 8.10 The fan angle represents the spread of the X-ray beam in the
resolution can be improved to 67 ms for a scanner with a half-scan x/y plane and is a factor in determining the diameter of the field of view
acquisition time of 200 ms (Reproduced with permission from Toshiba America Medical Systems)
8 Post-processing and Reconstruction Techniques for the Coronary Arteries 153

in one axial rotation [13]. As a result, it is not necessary to

move the patient through a spiral scan line. Instead, the
patient can remain stationary and the entire heart to be
imaged in a single gantry revolution. This has the potential to
substantially improve image clarity by eliminating stairstep
and misregistration artifacts that are sometimes seen with
64-detector systems, but will have no impact on temporal
resolution, based upon the gantry rotation speed (as described
above).
While use of a wide cone angle offers the capability of
whole organ coverage, it also presents a challenge to image
reconstruction algorithms employed in 64-detector systems.
Traditional reconstruction algorithms cannot successfully
incorporate the highly tilted X-ray planes created by the cone
angle trajectory. As a result, one can get cone-beam artifacts
including shading, ghosting, and diminished resolution as
shown in Fig. 8.12a. With more advanced reconstruction
algorithms specifically designed for 320-detector systems
that account for the cone angle, these artifacts can be elimi-
nated, shown in Fig. 8.12b [14].

Post Scan Related Post-processing

Parameters

After the scan has been completed and datasets have been
generated, additional post-processing techniques on a car-
diac CT workstation are essential to accurately interpreting
cardiac morphology as well as coronary artery anatomy and
disease burden. The presence of an isotropic data set in
which the spatial resolution is identical across all planes of
Fig. 8.11 The cone angle quantifies the spread of the X-ray beam in
the z-direction, along the length of the patient (Reproduced with per- examination facilitates manipulation of the data on a
mission from Toshiba America Medical Systems) workstation.

a b

Fig. 8.12 Panel A (top) illustrates cone beam artifact. The image image reconstructed with a novel reconstruction algorithm that takes
demonstrates shading, ghosting, and diminished resolution. This is a into account the wide cone angle, thereby eliminating the artifact
result of a reconstruction algorithm that does not properly take into (Reproduced with permission from Toshiba America Medical
account the wide cone angle. Panel B (bottom) shows an identical Systems)
154 S.V. Gurudevan

The raw axial images are the most reliable for diagnosis, Objects in volume Image plane
as they reflect the source data in the order the images were
acquired. To assist the reader in processing large volumes of
data and illustrating key findings, additional rendering
techniques have been developed [15, 16]. These include the
multiplanar reformatting, maximum intensity projection,
the volume averaging and volume rendering techniques, and
the curved multiplanar projection. All involve rendering data
contained within a 3 dimensional slab (the thickness of
which the user can change) of data as a single 2-dimensional Selected “Slab” of images

projection.
Fig. 8.14 Maximum Intensity Projection (MIP)

Multiplanar Reformatting (MPR) Objects in volume Image plane

Multiplanar reformatting involves the selection of an

arbitrary image plane in a cardiac CT volume. This tech-
nique requires an isotropic volumetric data set with equal
spatial resolution in the X, Y, and Z axes. The plane may not
conform to the conventional axial, coronal, and sagittal
imaging planes and can be modified by the user, as shown in
Fig. 8.13. MPR is the mainstay for analysis of cardiac CT
data sets and is the most reliable method for the reader to Selected “Slab” of images

arrive at the correct diagnosis. It can be performed using a Fig. 8.15 Volume averaging
single slice or with differing numbers of stacked slices.
When more than one slice is selected, a rendering option
must be selected to display a composite image of the multi- are surrounded by low-attenuation epicardial fat, resulting in
ple slices. an angiogram-like image with excellent edge definition
(Fig. 8.14). Due the selection of the highest intensity voxels
within a slab, the MIP tends to overestimate stenosis severity
Maximum Intensity Projection in calcified vessels and stented segments (bright objects like
calcium and metal get further enhanced). Overreliance on
The maximum intensity projection (MIP) involves the pro- MIPs can also lead the reader to overlook subtle findings in
jection of data in a 3-dimensional slab so that only the voxels the coronary arteries, including motion and misalignment
of highest HU are displayed on a 2-dimensional image artifacts. In general, readers should always reconfirm find-
(Fig. 8.14). Initially developed by Rubin and colleagues ings on MIP with the source axial data.
[17, 18]. for use in peripheral CT angiography, the MIP is now
used for nearly all CT angiography applications and is the
mainstay of coronary artery interpretation. The MIP is ideal Volume Averaging and Volume Rendering
for the display of coronary artery images from a contrast CT
examination as the maximum intensity in the coronary arter- Volume averaging (VA) involves the projection of data in a
ies is usually the intraluminal contrast. The coronary arteries 3-dimensional slab so that the intensity of all the voxels in
the slab is averaged on a final 2-dimensional image
(Fig. 8.15). While edge definition is poorer than with MIP,
Objects in volume Image plane
VA enables the reader to “see through” a dense object in a
Selectsd plane
slab and can be useful in interpreting stenoses in calcified
vessels. When specific colors are assigned to specific ranges
of HU in a 3-dimensional volumetric slab, this is termed vol-
ume rendering (VR); this is available on virtually every car-
diac workstation. The relative position and 3-dimensional
relationship of the coronary arteries, cardiac veins, and car-
diac chambers is possible using 3-dimensional VR
Fig. 8.13 Multiplanar Reformat Projection (MPR) (Fig. 8.16). While especially helpful in evaluating coronary
8 Post-processing and Reconstruction Techniques for the Coronary Arteries 155

Objects in volume Image plane

Fig. 8.17 Curved Planar Reformat (CPR)

References
1. Lu B, Mao SS, Zhuang N, et al. Coronary artery motion during the
cardiac cycle and optimal ECG triggering for coronary artery imag-
ing. Invest Radiol. 2001;36(5):250–6.
2. Mao S, Lu B, Oudiz RJ, Bakhsheshi H, Liu SC, Budoff MJ.
Coronary artery motion in electron beam tomography. J Comput
Assist Tomogr. 2000;24(2):253–8.
3. Kim WY, Stuber M, Kissinger KV, Andersen NT, Manning WJ,
Botnar RM. Impact of bulk cardiac motion on right coronary MR
angiography and vessel wall imaging. J Magn Reson Imaging.
2001;14(4):383–90.
4. Isma’eel H, Hamirani YS, Mehrinfar R, et al. Optimal phase for
coronary interpretations and correlation of ejection fraction using
late-diastole and end-diastole imaging in cardiac computed tomog-
raphy angiography: implications for prospective triggering. Int
J Cardiovasc Imaging. 2009;25(7):739–49.
5. Gurudevan SV, Narula J. Prospective electrocardiogram-gating: a
new direction for CT coronary angiography? Nat Clin Pract
Cardiovasc Med. 2008;5(7):366–7.
6. Flohr TG, Schaller S, Stierstorfer K, Bruder H, Ohnesorge BM,
Fig. 8.16 3D volume rendering Schoepf UJ. Multi-detector row CT systems and image-
reconstruction techniques. Radiology. 2005;235(3):756–73.
7. Cademartiri F, Mollet NR, Runza G, et al. Improving diagnostic
anomalies and bypass grafts, the reader should never attempt
accuracy of MDCT coronary angiography in patients with mild
to interpret stenoses purely on the basis of a 3D VR images: heart rhythm irregularities using ECG editing. AJR Am
as calcium and intraluminal contrast have attenuation ranges J Roentgenol. 2006;186(3):634–8.
that are near one another, significant coronary artery stenoses 8. Ehara M, Kawai M, Surmely JF, et al. Diagnostic accuracy of coro-
nary in-stent restenosis using 64-slice computed tomography: com-
in calcified vessels can be misinterpreted.
parison with invasive coronary angiography. J Am Coll Cardiol.
2007;49(9):951–9.
9. Nieman K, Cademartiri F, Raaijmakers R, Pattynama P, de Feyter
Curved Multiplanar Projection P. Noninvasive angiographic evaluation of coronary stents with
multi-slice spiral computed tomography. Herz. 2003;28(2):
136–42.
The curved multiplanar projection (CMP) is a centerline 10. Maintz D, Seifarth H, Flohr T, et al. Improved coronary artery stent
method for analysis of vessels whereby a virtual plane is cre- visualization and in-stent stenosis detection using 16-slice com-
ated using the center of the column of contrast visualized on puted-tomography and dedicated image reconstruction technique.
Invest Radiol. 2003;38(12):790–5.
a series of consecutive axial slices (Fig. 8.17). A virtual
11. Kachelriess M, Ulzheimer S, Kalender WA. ECG-correlated image
plane in which the vessel is “stretched out” can then be dis- reconstruction from subsecond multi-slice spiral CT scans of the
played. CMP is useful for confirming and illustrating the heart. Med Phys. 2000;27(8):1881–902.
appearance of stenoses identified using standard axial multi- 12. Ohnesorge B, Flohr T, Becker C, et al. Cardiac imaging by means
of electrocardiographically gated multisection spiral CT: initial
planar projections. It is particularly useful for tortuous ves-
experience. Radiology. 2000;217(2):564–71.
sels and those vessels that cannot be easily tracked in a single 13. Tuy HK. An inverse formula for cone-beam reconstruction. SIAM
plane or thin slab using MIP. The CMP is only as reliable as J Appl Math. 1983;43:546–52.
the accuracy of the centerline, and should not be used as a 14. Feldkamp LA, Davis LC, Kress JW. Practical cone beam algorithm.
J Opt Soc Am. 1984;1:612–9.
first-line assessment of coronary stenosis severity. Artifacts
15. Addis KA, Hopper KD, Iyriboz TA, et al. CT angiography: in vitro
from inaccurate centerlines can lead to incorrect assessment comparison of five reconstruction methods. AJR Am J Roentgenol.
of stenosis severity. 2001;177(5):1171–6.
156 S.V. Gurudevan

16. Pavone P, Luccichenti G, Cademartiri F. From maximum intensity 18. Prokop M, Shin HO, Schanz A, Schaefer-Prokop CM. Use of maxi-
projection to volume rendering. Semin Ultrasound CT MR. mum intensity projections in CT angiography: a basic review.
2001;22(5):413–9. Radiographics. 1997;17(2):433–51.
17. Rubin GD, Dake MD, Napel S, et al. Spiral CT of renal artery ste-
nosis: comparison of three-dimensional rendering techniques.
Radiology. 1994;190(1):181–9.
 Coronary CT Angiography:
Native Vessels 9
Stephan Achenbach

Abstract
Coronary CT Angiography has become increasingly stable and robust and accuracy to iden-
tify and rule out high-grade stenosis of the coronary arteries is high. The main clinical
application is to rule out significant coronary artery disease in patients with a relatively low
pre-test likelihood of disease. For this application, several guidelines in the US and Europe
endorse the use of cardiac CT. Other applications of coronary CTA include the support of
coronary interventions, especially in the context of chronic total coronary occlusion, the
identification of coronary anomalies, and, to some extent, the assessment of non-obstructive
coronary atherosclerosis. However, the use of coronary CTA for screening purposes is cur-
rently not supported by official recommendations.

Keywords
Coronary CT Angiography • Coronary CTA • Coronary Artery Disease • Computed
Tomography • Stenosis • Atherosclerosis • Plaque

Introduction therefore be aware that artefacts can occur and may lead to
false-positive and, less frequently, to false-negative results.
Visualization of the coronary arteries has been the major Diagnostic accuracy is impaired when image quality is
focus of cardiac CT in the past years. Non-invasive “coronary reduced and image quality, in turn, is influenced by many fac-
CT angiography” has tremendous clinical potential for detect- tors such as the patient’s heart rate, body weight, ability to
ing or ruling out coronary artery stenoses in selected patients cooperate, and extent of coronary calcification. Therefore, the
(see Figs. 9.1 and 9.2). As a consequence of continuous and clinical utility of coronary CT angiography significantly
substantial progress regarding image quality and robustness depends on the specific clinical situation and patient under
of the investigation, it is incorporated in several recent official investigation. The specific advantages and disadvantages of
guidelines and recommendations. In addition, imaging of coronary CT angiography must be carefully considered
coronary atherosclerotic plaque may play a potential role in before using this method in the workup of a patient with
risk stratification. However, spatial resolution and temporal known or suspected coronary artery disease.
resolution of CT imaging, even with the latest scanner gen-
erations, are not equal to those of invasive coronary angiogra-
phy. Interpreters of coronary CT angiography data sets must Imaging Protocol

Since the small dimensions and the rapid motion of the coro-
nary vessels pose tremendous challenges for non-invasive
S. Achenbach, MD
imaging, high-end CT equipment and adequate imaging pro-
Department of Cardiology, University of Erlangen,
Ulmenweg 18, Erlangen 91054, Germany tocols must be used. Currently, 64-slice CT is considered the
e-mail: [email protected] minimum requirement for coronary artery imaging, and newer

© Springer International Publishing 2016 157

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_9
158 S. Achenbach

a b

c d

Fig. 9.1 Normal anatomy of the coronary arteries in transaxial images. (a) artery is visible (double arrows). Large arrow: Mid left anterior descending
Level of the left main origin from the aortic root. The bifurcation of the left coronary artery, small arrow: left circumflex coronary artery. (d) Mid-
main into the left anterior descending (large arrow) and left circumflex ventricular level. The left anterior descending coronary artery (large
coronary artery (small arrow) can be seen. The arrowheads point at a coro- arrow), left circumflex coronary artery (small arrow), and right coronary
nary vein. (b) A few mm further distal, the left anterior descending coro- artery can be seen (double arrows). (e) Distal segment of the right coronary
nary artery (large arrow) has given rise to a diagonal branch (arrowhead). artery (double arrow), which ends in the posterior descending artery (small
(c) Level of the right coronary ostium. A short section of the right coronary arrow). The arrowhead points at a right ventricular branch
9 Coronary CT Angiography: Native Vessels 159

a b

Fig. 9.2 Same patient as in Fig. 9.1. Various forms of post-processing artery (arrows) in a double-oblique plane. (c, d) 3-dimensional, surface-
have been used to visualize longer segments of the coronary arteries. (a) weighted Volume Rendering Technique (VRT) reconstructions in two
Curved multiplanar reconstruction (curved MPR) of the right coronary different angulations
artery. (b) Maximum Intensity projection (MIP) of the right coronary

technology [1], such as Dual Source CT and scanners that during data acquisition will cause substantial artefact and
allow simultaneous acquisition of 256 or 320 cross-sections, may render the coronary arteries (or parts of them) unevalu-
provide for more robust image quality and further improved able. Therefore, patients should be able to reliably hold their
image quality. breath for approximately 10 s. Otherwise, coronary CT
A basic prerequisite for CT imaging of the coronary angiography should not be performed. Heart rate should be
arteries is the patient’s ability to understand and follow regular and preferably low (optimally below 60/min, even
breathhold commands. Even slight respiratory motion though this is not as strictly required for Dual Source CT)
160 S. Achenbach

[1, 2]. It is usually recommended that patients receive pre- with a limited number of scanners that have either two detec-
medication with short acting beta blockers to lower the heart tors or a very wide detector. Images are acquired during con-
rate. Beta blockers can be administered orally approxi- tinuous, very fast motion of the table, and the volume of the
mately 1 hr prior to scanning, or intravenously immediately heart is typically covered within 150–250 ms. In the cranio-
before the scan. Sometimes, a combination of both is neces- caudal direction, the data for each subsequent image are
sary. Nitrates should be given to all patients who have no acquired with a very slight temporal offset as compared to
contraindications in order to achieve coronary dilatation, the previous image (approximately 0.5 ms), so that the con-
which substantially improves image quality [1]. secutive images represent ever so slightly different time
Intravenous contrast enhancement is necessary for coro- instants within the cardiac cycle. Since the transition is
nary CT angiography and typically, 50–100 ml of iodine- smooth and image acquisition is typically performed in dias-
based, high concentration contrast agent are injected. High tole with very little cardiac motion, this offset is not notice-
flow rates are recommended, injection should be between 4 able in the data set and in reconstructed images. This mode
and 7 ml/s. Synchronization of contrast injection and data of data acquisition provides high image quality at very low
acquisition can be achieved either through a “bolus tracking” doses, but requires stable heart rates below 60 beats/min to
method or by using a separate “test bolus” acquisition to avoid artefact [8–11].
measure the contrast transit time.
Subsequent data acquisition can follow various princi-
ples. The obtained data need to be synchronized with the Radiation Exposure
heart beat, and this can either be achieved through retrospec-
tive ECG gating or prospective ECG triggering [1]. Unless specific measures are taken to limit radiation dose,
Retrospectively gated scans are acquired in spiral mode the exposure during coronary CTA can be high. A landmark
and usually provide for robust and high image quality, flexi- study performed several years ago demonstrated that in
bility to choose the cardiac phase during which images are individual centers, the average estimated effective radiation
reconstructed, as well as the ability to reconstruct “func- exposure was as high as 30 mSv (while in the same study,
tional” data sets throughout the cardiac cycle in order to sites at the lower end of the spectrum performed coronary
analyse left ventricular function and regional wall motion. In CTA with an average exposure of only 4–5 mSv) [12]. Since
order to limit radiation exposure, the output of the x-ray tube then, substantial progress has been achieved regarding radi-
can be “modulated” during the acquisition, with lower out- ation exposure (see Table 9.1). ECG-based tube current
put in systole, and higher output in diastole, when the most modulation in spiral acquisition and prospectively ECG-
relevant image reconstructions are usually performed. triggered image acquisition avoid x-ray exposure during the
Prospectively triggered scans are associated with substan- entire cardiac cycle and limit x-ray tube output to those
tially lower radiation exposure. Images are acquired in axial phases of the heart beat which are likely to be used for
mode without table movement and the patient table is image reconstruction. This limits the flexibility of recon-
advanced by one detector width following the acquisition, structing images during different parts of the R-R interval,
with subsequent images acquired in the next or second to which would be desirable to assess ventricular function (a
next cardiac cycle. Less flexibility to reconstruct data at dif- question, however, that is rarely relevant in coronary CTA),
ferent time instants in the cardiac cycle as well as greater and which is also advantageous when motion artefacts are
susceptibility to artefacts caused by arrhythmia are trade-offs present, to identify a phase with no or little artefact. Hence,
for the advantage of lower dose. Especially in young low heart rates, which make it extremely likely that artefact-
patients – in whom radiation dose may be of major concern – free images are obtained in diastole, facilitate the use of
prospectively triggered scans should be strongly considered these techniques and in this way, reducing the heart rate by
[2–5]. Heart rate must be low so that artefact-free images can premedication contributes to lower radiation exposure [2].
be guaranteed at the time instant of radiation exposure. The While the tube voltage for coronary CTA used to uniformly
lowest radiation dose is achieved when the x-ray exposure be 120 kV, it has been observed that depending on patient
window in each cardiac cycle is only as long as one-half size, it is possible to reduce tube voltage to 100 or 80 kV, or
rotation of the gantry requires (just long enough to recon- in very selected cases even 70 kV [13–17]. The increase in
struct one set of transaxial slices), but “padding” (x-ray noise is tolerable depending on patient size, and to some
exposure over a longer time period in each cardiac cycle) extent is offset by higher iodine contrast. A “rule of thumb”
may be used to provide some flexibility regarding the time is that tube voltage can be reduced to 100 kV for all patients
instant of image reconstruction [6, 7]. with a body weight below 100 kg. Finally, there is a linear
A combination of spiral acquisition and prospective trig- relationship between tube current and image noise, so that
gering is the so-called “Flash Mode” (prospectively ECG again, especially in patients with low body weight there is
triggered high pitch spiral acquisition). It is only available potential to reduce exposure.
9 Coronary CT Angiography: Native Vessels 161

Table 9.1 Measures to reduce radiation exposure in coronary CTA

Method Downsides Specifics Prerequisites
Avoid x-ray exposure during the Loss of flexibility to Spiral acquisition with ECG-based Low and stable heart rate
entire cardiac cycle reconstruct data during freely tube current modulation
selectable time instants in the Prospectively ECG triggered axial CT scanner with wide detector
cardiac cycle acquisition
Reduce tube voltage (as compared Increased image noise (to some 100 kV or 80 kV, with some Low body weight
to standard 120 kV) degree offset by higher iodine scanners 70 kV
contrast)
Reduce tube current Increased image noise Scanner specific Low body weight
Iterative reconstruction Altered image impression as Various algorithms, None
compared to filtered back vendor-specific
projection

Many of the measures that decrease radiation exposure projections (approximately 5 mm slice thickness) and multi-
do, on the other hand, increase image noise. Since “iterative planar reconstructions (see Figs. 9.2 and 9.3) in oblique or
reconstruction” can reduce noise as compared to the standard curved planes that are adapted to the orientation of the coro-
“filtered back projection” (at the cost of longer computation nary arteries. 3-dimensional renderings allow quite impres-
time), it can offset the downsides of reduced exposure to sive visualization of the heart and coronary arteries, but they
some extent and therefore allows to use lower exposure pro- are not accurate for stenosis detection and play no role in
tocols [2, 18, 19]. data interpretation (see Fig. 9.3) [25].
The combination of various methods that limit exposure
permit to perform coronary CTA with doses well below
1 mSv (see Fig. 9.3). This is clinically possible with high-end Typical Findings
hardware in somewhat selected patients (low heart rate and
reasonable body weight) [17]. There are published series that In most cases, coronary CT angiography is performed to
demonstrated high accuracy for stenosis detection using such detect or rule out significant coronary artery stenoses (See
protocols [20, 21]. In a very strictly selected patient cohort, it Fig. 9.4). In most cases, presence of a “significant” luminal
has even been reported that doses below 0.1 mSv are possible stenosis is assumed when the diameter reduction of the coro-
[10], but image quality at this extreme end of the spectrum is nary lumen appears to be more than 70 %. Stenosis severity
not good and robust enough for routine clinical practice. is usually determined my visual estimation, since quantita-
Without going to the extreme and by using measures that tive approaches are not exact – the spatial resolution of coro-
are widely available, do not require special training and are nary CT angiography, approximately 0.5 mm, is not sufficient
straightforward to implement, Chinnayan et al. reported a to allow for accurate, quantitative stenosis grading. In fact,
mean effective dose of 6.4 mSv across 15 centers routinely visual estimation of stenosis degree has no downsides as
performing coronary CTA [22]. In the most recent multi- compared to quantitative approaches [26–28]. Stenosis
center trial, the average effective dose for coronary CT angi- severity in CT can appear to be less or more than invasive
ography was 3.2 mSv (as compared to 9.75 mSv for SPECT angiography – the typical margin of agreement is approxi-
and 12.0 mSv for invasive angiography) [23]. mately ±20 % [27]. Hence, stenoses that appear to be less
than 50 % in CT can be expected to be less than 70 % in
invasive angiography with a very high degree of certainty. In
Image Reconstruction and Post-processing most cases, however, there is a tendency to overestimate,
rather than underestimate, the degree of luminal stenosis in
Typical data sets for coronary artery visualization by CT coronary CT angiography as compared to catheter-based
consist of approximately 200–300 thin (0.5–0.75 mm) trans- invasive coronary angiography (Fig. 9.5). Often, high grade
axial cross-sections (see Figs. 9.1, 9.2, and 9.3). In most coronary artery stenoses appear as complete or near-complete
cases, workstations are used for data interpretation. While interruptions of the coronary artery lumen in the CT data set
many workstations provide pre-rendered reconstructions that (Fig. 9.6). Categories of stenosis severity that are recom-
are intended to show the coronary arteries over their entire mended for use in coronary CT angiography reports care
course, readers should not rely on such atomatoed post- listed in Table 9.2 [24]. The differentiation between com-
processing tools alone. In fact, official recommendations plete coronary artery occlusions and high-grade stenoses can
mandate that the reader manipulates the original data and be difficult in coronary CT angiography. Very long lesions
does not rely on pre-rendered reconstructions [24]. The most typically correspond to complete occlusions (Fig. 9.7), while
useful post-processing tools are thin-slab maximum intensity shorter lesions can either be secondary to high grade luminal
162 S. Achenbach

a b

Fig. 9.3 Very low dose coronary CT angiography. Using a combina- multiplanar reconstructions of the left anterior descending coronary
tion of a low-dose image acquisition mode (prospectively ECG- artery (a, arrow), left circumflex coronary artery (b, arrow),
triggered high-pitch spiral acquisition), low tube voltage (70 kV), and right coronary artery (c, arrow)) clearly demonstrate the absence
low tube current and iterative reconstruction, CT angiography was of coronary artery stenosis. (d) 3-dimensional surface-weighted
performed with an estimated effective dose of 0.35 mSv. Curved reconstruction

narrowing or to a complete occlusion with good distal filling especially if data acquisition is not carefully and expertly
via collateral flow [29]. Since CT only shows a static image performed. If artefacts caused by motion, calcium, or a com-
and flow in the coronary arteries can not actually be seen, bination of both cause misinterpretation, it will in most cases
retrograde filling of a coronary artery segment can not be be overestimation of stenosis degree or a false-positive read-
differentiated from antegrade flow (Fig. 9.8). ing of a stenosis [30, 31]. False-negative interpretations are
Insufficient image quality is most frequently the conse- less frequent.
quence of motion artefact (as a consequence of coronary
movement or respiration), high image noise, or a combina-
tion of both. Additional problems can be caused by severe Accuracy for Stenosis Detection
calcification, which causes partial volume effects (often
referred to as “blooming”) and aggravates motion artefacts Coronary CT angiography has high accuracy for the detection
(Fig. 9.9). In some cases, artefacts render the entire data set of coronary artery stenoses (see Fig. 9.4). In addition to
or some coronary segments unevaluable. This has become numerous small, single-center studies, four multi-center trials
less frequent with more modern scanners but can still occur, have investigated the accuracy of coronary CT angiography
9 Coronary CT Angiography: Native Vessels 163

a b

c d

Fig. 9.4 Coronary CT angiography in a patient with a very proximal, main trifurcation, can be seen (arrow). (b) Curved multiplanar recon-
high-grade stenosis of the left anterior descending coronary artery. (a) struction of the left main and left anterior descending coronary artery
Maximum intensity projection in a transaxial orientation. The stenosis (arrow: stenosis). (c) 3-dimensional reconstruction (arrow: stenosis).
of the left anterior descending coronary artery, just distal to the left (d) Invasive coronary angiogram (arrow: stenosis)

for the identification of coronary artery stenosis in compari- trials cited above), which is due to a tendency to overestimate
son to invasive coronary angiography (see Table 9.3). Two stenosis degree in coronary CTA as well as the fact that image
trials performed in patients with suspected coronary artery artefacts often result in false-positive interpretations. As in
disease using 64-slice CT have demonstrated sensitivities of any diagnostic test, there is a trade-off between sensitivity
95–99 % and specificities of 64–83 % as well as negative and specificity in coronary CT angiography: Most studies –
predictive values of 97–99 % for the identification of indi- and most clinical users – will aim to keep sensitivity high, at
viduals with at least one coronary artery stenosis [32, 33]. the cost of specificity. If, on the other hand, a high specificity
The positive predictive values were lower (64 and 86 % in the is desired, sensitivity will suffer. In a multicenter study of 291
164 S. Achenbach

a b

Fig. 9.5 Frequently, the degree of luminal narrowing appears more stenosis in the proximal right coronary artery (arrow). (b) In the corre-
severe in coronary CT angiography than in the invasive, catheter-based sponding invasive angiogram, the stenosis appears less severe (arrow)
coronary angiogram. (a) Curved multiplanar reconstruction showing a

a b

Fig. 9.6 High-grade luminal stenoses often appear as complete inter- lumen is completely interrupted. (b) Corresponding invasive coronary
ruption of the coronary artery lumen in coronary CT angiography. (a) angiogram. A small residual lumen is present (arrow). The spatial reso-
Maximum Intensity Projection in a patient with a high grade stenosis of lution of CT is not sufficient to reliably visualize such small remaining
the right coronary artery (arrow). At the site of the stenosis, the arterial lumina

Table 9.2 Recommended categories of luminal stenosis severity for patients with 56 % prevalence of coronary artery stenoses, as
reporting coronary CT angiography [24] well as 20 % of patients with previous myocardial infarction
Recommended quantitative stenosis grading and 10 % with prior revascularization, specificity was high
0 – Normal Absence of plaque and no luminal (90 %) and the positive predictive value was 91 % [34].
stenosis However, this came at the cost of decreased sensitivity (85 %)
1 – Minimal Plaque with <25 % stenosis and negative predictive value (83 %, see Table 9.3) [23].
2 – Mild 25–49 % stenosis A large meta-analysis of trials that compared coronary
3 – Moderate 50–69 % stenosis CT angiography to invasive coronary angiography for ste-
4 – Severe 70–99% stenosis nosis detection in a total of 3764 patients yielded a patient-
5 – Occluded based sensitivity of 98 % and specificity of 82 % to identify
9 Coronary CT Angiography: Native Vessels 165

a b

Fig. 9.7 Total occlusion of the left anterior descending coronary gram confirms proximal occlusion of the left anterior descending
artery. (a) Coronary CT angiography displays interruption of the coro- coronary artery (large arrow). The small arrow points at the diagonal
nary artery lumen over a long distance (arrows). (b) The invasive angio- branch

a b

Fig. 9.8 Coronary CT angiography cannot identify retrograde filling (b) Invasive coronary angiography shows chronic total occlusion of the
of a coronary artery via collaterals. (a) Maximum Intensity Projection proximal right coronary artery (arrow) and retrograde filling of the mid
of the right coronary artery showing lesion with severe impairment of and distal right coronary artery via a collateral vessel (Kugel’s
the lumen (arrow). The distal vessel segments are filled with contrast. collateral)

individuals with at least one significant coronary artery ste- Accuracy values are not uniform across all patients. Several
nosis. The negative predictive value was 99 % and the posi- trials have demonstrated that high heart rates, obesity, and
tive predictive value was 91 %. On an individual artery-based extensive calcification negatively influence accuracy [36–40].
level, sensitivity was 95 %, specificity 90 %, negative pre- Usually, degraded image will lead to false-positive rather than
dictive value 99 % and positive predictive value 75 % [35] false-negative findings. Specificity is therefore typically
(see Table 9.4) reduced when image quality is not very good (see Fig. 9.10).
166 S. Achenbach

a b

Fig. 9.9 Typical artifacts that can occur in coronary CT angiography. aggravated by the presence of calcium or other high-density material.
(a) Motion artifact due to rapid coronary artery movement. Here, the (b) “Misaligment” or “Step” artifacts (arrows). Such artifacts can occur
right coronary is affected. Motion causes blurring of the arterial contour due to respiratory or other body motion or due to arrhythmias. (c)
(large arrow). It also causes low-density artifacts that, in this case, are Severe calcification can render the coronary arteries uninterpretable
outside the actual vessel cross-section (small arrow). Such artifacts are regarding the presence of stenoses

Along with patient factors that influence image quality dictive value: 100 % in both groups), while accuracy is sub-
(such as body weight, heart rate, and the degree of calcifica- stantially lower in high-risk patients (see Table 9.5) [41].
tion), the accuracy of coronary CT angiography depends on Overall, the good diagnostic performance of coronary CT
the pre-test likelihood of disease [39, 41]. In an analysis of angiography in patients who are not at high likelihood of
254 patients referred to invasive angiography and also stud- having coronary artery stenoses, and especially the very high
ied by CT, it was demonstrated that coronary CT angiogra- negative predictive value found for such patients make coro-
phy performs best in patients with a low to intermediate nary CTA is a clinically useful tool in symptomatic patients
clinical likelihood of coronary artery stenoses (negative pre- who have a low or intermediate likelihood of coronary
9 Coronary CT Angiography: Native Vessels 167

Table 9.3 Multi-center studies that investigated the accuracy of coronary artery stenosis detection by contrast-enhanced 64-slice coronary CT
angiography in comparison to invasive coronary angiography. The last of the cited studies (Rochitte et al.) used a combined reference standard of
“At least 50 % stenosis in coronary angiography plus perfusion defect in SPECT”. All values are based on per-patient analyses
Negative Positive
Number of Number of Prevalence of Sensitivity (95 % Specificity (95 % predictive value predictive value
Author sites patients obstructive CADa CI) CI) (95 % CI) (95 % CI)
Budoff [32] 16 230 25 % 95 (85–99 %) 83 % 99 % 64 %
(76–88 %) (96–100 %) (53–75 %)
Meijboom [33] 3 360 68 % 99 % 64 % 97 % 86 %
(98–100 %) (55–73 %) (94–100 %) (82–90 %)
Miller [34] 9 291a 56 % 85 % (79–90 %) 90 % 83 % 91 %
(83–94 %) (75–89 %) (86–95 %)
Rochitte [23] 16 381b 38 % 92 %c 51 %c 92 %c 53 %c
(87–96 %) (44–57 %) (86–96 %) (47–60 %)
a
This trial included 58 patients with previous myocardial infarction and 28 patients with previously percutaneous coronary intervention
b
This trial included 104 patients with previous myocardial infarction and 109 patients with previously placed coronary stents
c
Combined reference standard of angiographic stenosis plus perfusion defect

Table 9.4 Results of a meta-analysis that investigated the accuracy of coronary artery stenosis detection by computed tomography angiography
in comparison to invasive coronary angiography [35]
Negative predictive Positive predictive
Number of trials Sensitivity (95 % CI) Specificity (95 % CI) value (range) value (range)
Per patient analysis 18 98.2 % (97.4–98.8 %) 81.6 % (79.0–84.0 %) 99.0 % (88–100 %) 90.5 %(75–100 %)
Per-artery analysis 17 94.9 % (93.9–95.8 %) 89.5 % (88.8–90.2 %) 99.0 % (93–100 %) 75.0 % (53–95 %)
Per-segment analysis 17 91.3 % (90.2–92.2 %) 94 % (93.7–94.2 %) 99.0 % (98–100 %) 69.0 % (44–86 %)

a b

Fig. 9.10 Artifacts typically lead to false-positive results of coronary rior descending coronary artery (arrows). (b) Invasive angiography
CT angiography. (a) Calcification, slight motion and somewhat high shows that no relevant stenosis is present
image noise lead to a false-positive interpretation of the mid left ante-

disease, but for clinical reasons require further workup to symptomatic patients have an extremely favourable clinical
rule out significant coronary stenoses. A negative coronary outcome when coronary CT angiography is “negative”
CT angiography will obviate the need for further testing. and hence do not require any further testing [42–46]. The
Indeed, several observational trials clearly demonstrated that large-scale, multi-center international CONFIRM registry
168 S. Achenbach

Table 9.5 Diagnostic performance of 64-slice CT depending on the clinical pre-test likelihood of coronary artery disease in 254 patients [41]
Pre-test probability N Sensitivity % Specificity % Pos. pred. value % Neg. pred. value %
High 105 98 74 93 89
Intermediate 83 100 84 80 100
Low 66 100 93 75 100

supports the extremely good prognosis of symptomatic elevation [51], and that outcome is excellent if CT demon-
patients after a normal coronary CTA examination [47]. The strates the absence of coronary stenosis in acute chest pain
registry collected data from 12 centers in 6 countries between patients [52–59]. A cost advantage of incorporating CT angi-
2005 and 2009 who underwent clinically indicated coronary ography in the workup of low-likelihood acute chest pain
CTA. Min et al. analyzed 24 775 of these patients, with fol- patients as compared to the standard of care has been demon-
low-up obtained in 23 854, of which 5594 patients had strated [54]. Most trials of coronary CTA in acute chest pain
obstructive coronary artery disease and 18 260 did not. Over patients can justifiably be criticized for including very low-
a mean period of 2.3 years, 404 deaths were recorded. The risk patients [60], but their results can likely be extrapolated
mean annualized death rate in patients with a normal coro- to patients with somewhat higher risk. In fact, both US [61]
nary CTA examination was only 0.28 % [48]. and European guidelines on acute coronary syndromes
Based on the same registry, Shaw et al. analyzed the rela- incorporate coronary CT angiography as a useful tool to rule
tionship between coronary CTA results, invasive coronary out stenosis in patients with low-risk acute chest pain [62].
angiography, and subsequent mortality [49]. They found that As for other applications, coronary CT angiography should
in patients without any obstructive stenosis in coronary CTA, be considered in acute chest pain patients only if patient
performing invasive coronary angiography was associated characteristics promise full evaluability and high image
with a relative hazard for death of 2.2 (p = 0.011), while in quality [62].
patients with obstructive stenosis in coronary CTA, invasive
angiography was associated with a relative hazard for death
of 0.61 (p = 0.047). Min et al. reported that a benefit of revas- Coronary CT Angiography and Ischemia
cularization was only present in patients with high-risk anat-
omy in coronary CTA (at least two-vessel coronary artery Coronary CTA, like invasive angiography, is a purely mor-
disease with involvement of the left anterior descending phologic imaging modality and cannot demonstrate the
coronary artery, three-vessel coronary disease or left main functional relevance of stenoses (ischemia). The correla-
stenosis) [50]. Revascularization was associated with a haz- tion of CT results with the presence of ischemia is poor
ard ratio for death of 0.38 (95 % CI: 0.18–0.83) in patients [63–65]. Especially in the case of lesions with borderline
with “high-risk CAD” in coronary CTA, but there was no degree of stenosis, this may be a limitation for the clinical
survival difference in patients without “high-risk CAD” in application of CT angiography. Not surprisingly, coronary
coronary CTA (hazard ratio 3.24 with a 95 % CI between CT angiography a better predictor of angiographic find-
0.76 and 13.89). Thus, sufficient data is available that coro- ings than testing for ischemia [63–65]. A “negative” coro-
nary CTA is an excellent prognostic tool and that it is safe to nary CT angiography result is a reliable predictor to rule
avoid any further testing in chest pain patients if coronary out the presence of coronary artery stenoses and the need
CT angiography demonstrates the absence of coronary artery for revascularization, and it may therefore be used as a
stenoses. “gatekeeper” to avoid invasive angiograms. On the other
hand, coronary CTA – like invasive angiography – should
not be performed in an unselected patient population and
Acute Chest Pain not for “screening” purposes. A positive coronary CTA
scan taken by itself does not strongly predict the need for
In the setting of acute chest pain, it is clinically very useful revascularization [66].
to reliably and quickly rule out – or identify – coronary artery Several methods are under evaluation to improve the
stenosis (see Fig. 9.11). This is especially the case if the ability of coronary CT angiography to predict ischemia.
ECG is normal and myocardial enzymes are not elevated, the They include the combination with CT-based myocardial
likelihood of coronary disease is low, but the possibility of perfusion [67, 68] assessment and specific analysis meth-
myocardial infarction requires a rapid and definite diagnosis. ods, such as the “transluminal attenuation gradient” or
Numerous trials have demonstrated that CT angiography is CT-based determination of the “fractional flow reserve”
accurate and safe to stratify patients with acute chest pain (FFR) [69, 70]. Especially the latter receives widespread
and absence of ECG changes as well as myocardial enzyme interest. Based on the anatomic CT data set, computational
9 Coronary CT Angiography: Native Vessels 169

a b

c d

Fig. 9.11 Typical findings of coronary CT angiography in patients with the site of the lesion shows ring-like enhancement with a central filling
an acute coronary syndrome. (a) Coronary CT angiography (curved mul- defect (arrow). Similar to the pronounced positive remodeling shown in
tiplanar reconstruction) shows three high-grade stenoses of the right cor- Fig. 9.11b, this finding, when present, typically indicates an acute coro-
onary artery (arrows). (b) As frequently seen in acute coronary lesions, nary lesion, but is not necessarily observed in all lesions associated with
there is pronounced “positive remodeling” of the of the lesion (arrows), a an acute coronary syndrome. (d) Invasive coronary angiogram (arrows:
consequence of plaque rupture with subsequent thrombus formation serial stenoses)
inside the vessel. (c) A cross-sectional view of the right coronary artery at

fluid dynamics are applied to model the flow and resistance

pattern under adenosine stress and to obtain the FFR value Imaging of Coronary Atherosclerotic Plaque
for all segments of the coronary artery tree Initial publica-
tions show that this is feasible, and can improve the speci- Coronary CT angiography allows to visualize non-stenotic
ficity of CT to identify ischemia causing lesions over a coronary atherosclerotic plaque if image quality is good
purely anatomic assessment alone. However, further vali- (see Fig. 9.12). Given the fact that the vast majority of car-
dation will be necessary. diac events are caused by plaque rupture, the detection and
170 S. Achenbach

a b

c d

Fig. 9.12 Visualization of non-obstructive coronary atherosclerotic present at the site of the plaque (arrow). (d) 7 years after coronary CT
plaque by CT. (a) Multiplanar reconstruction of the left anterior angiography shown in panels a and b and after the invasive angiogram
descending coronary artery. In the proximal vessel segment, a non- shown in panel c, the patient developed acute symptoms and presented
obstructive plaque which is partly calcified (small arrow) and partly with ST-elevation myocardial infarction of the anterior wall. The left
non-calcified (large arrow) can easily be detected by CT. (b) Cross- anterior descending coronary artery was occluded at the site of the for-
sectional view of the plaque (arrow) shows its eccentric position. (c) merly non-obstructive, partly calcified atherosclerotic plaque
Invasive coronary angiogram. Only a very slight luminal stenosis is

characterization not only of calcified, but also of non-calci- in selected patients. With some limitations and again under
fied plaque components is a promising tool for improved the prerequisite of excellent image quality, plaque quantifi-
risk stratification. In comparison to IVUS, accuracy for cation and characterization is possible. On average, the CT
detecting non-calcified plaque has been found to be approx- attenuation within “fibrous” plaques is higher than within
imately 80–90 % [71–73] but these studies were performed “lipid-rich” plaques (mean attenuation values of 91–116
9 Coronary CT Angiography: Native Vessels 171

HU versus 47–71 HU) [74–77] However, the variability of (HR 1.6; 95 % CI 1.2–2.2). Other trials and analyses confirm
density measurements within plaque types is large and similar findings [84, 85]. The problematic issue is that while
numerous factors, including the degree of intraluminal con- absence of plaque is clearly associated with an extremely
trast attantuation as well as various image reconstruction good prognosis, the presence of some non-obstructive plaque
parameters influence the density that is measured by CT is very frequent in the population and the positive predictive
within coronary plaques [78, 79]. Therefore, accurate clas- value regarding future cardiovascular events is very low [85].
sification of plaque composition by coronary CTA is not Also, a relevant incremental prognostic value of contrast-
currently possible. On the other hand, some parameters that enhanced coronary CT angiography over coronary calcium
are more readily available from CT might also contribute to measurements has so far not convincingly been demonstrated
the detection of “vulnerable” plaques. They include a [86]. Therefore, coronary CT angiography for the identifica-
“spotty” pattern of calcification, and a large degree of posi- tion of coronary atherosclerotic plaque is currently not rec-
tive remodelling [80–83]. ommended for risk assessment purposes in asymptomatic
Some characteristics of coronary atherosclerotic plaque individuals.
that can determined by CT, such as positive remodeling (see
Fig. 9.13) and low CT attenuation of the atherosclerotic
material (below 30 HU), are associated with the occurrence Anomalous Coronary Arteries
of future acute coronary syndromes [83]. However, the pres-
ence and extent of coronary atherosclerotic plaque seems to Coronary CT angiography is an excellent tool to investigate
be a more robust marker of risk than individual plaque char- patients with known or suspected congenital coronary artery
acteristics. Several studies and data based on large registries anomalies (Figs. 9.14 and 9.15). Coronary CT angiography
have been able to demonstrate a prognostic value of athero- can classify both the origin and also the often complex course
sclerotic lesions detected by coronary CT angiography both of anomalous coronary vessels [87–91]. While the necessity
in symptomatic and asymptomatic individuals. An analysis for contrast agent injection and radiation exposure are cer-
of the clinical CONFIRM registry, including more than tain drawbacks of CT imaging as compared to MR, which is
23,000 patients, confirmed the prognostic value of coronary also a potential diagnostic tool in coronary artery anomalies,
CT angiography, where the presence of coronary stenoses, the ease of data acquisition and the predictability with which
but also the presence of non-obstructive plaque was associ- a high-resolution data set with optimal image quality for
ated with an increased risk of mortality [48]. However, the evaluation can be expected make coronary CT angiography a
hazard ratio for non-obstructive plaque was relatively low method of choice for the workup of known or suspected
anomalous coronary vessels. Obviously, the use of low-dose
image acquisition protocols is recommendable in the often
young patients who undergo evaluation for anomalous coro-
nary arteries.

Guidelines and Recommendations

A group of US-based professional societies (both cardiology

and radiology) has jointly issued a statement of
“Appropriateness Criteria” for cardiac CT in the year 2010
(see Table 9.6). The document lists clinical situations in
which coronary CTA could be applied, and rates them as
inappropriate, appropriate, or uncertain [92]. Such situations
include the use of CT coronary angiography to rule out coro-
nary artery stenoses in patients who are symptomatic, but
who have a non-interpretable or equivocal stress test, who
are unable to exercise, or who have a non-interpretable
ECG. Furthermore, the document considers the use of coro-
nary CT angiography appropriate for patients with new onset
heart failure and for patients who present witch acute chest
pain and an intermediate pre-test likelihood of coronary
Fig. 9.13 Pronounced positive remodeling of a non-obstructive, non-
calcified coronary atherosclerotic plaque of the right coronary artery artery disease, but who have a normal ECG and absence of
(arrows) enzyme elevation (see Table 9.5) [92]. Finally, the use of CT
172 S. Achenbach

a b

Fig. 9.14 Visualization of a coronary anomaly by CT. Due to its left circumflex coronary artery. This infrequent anomaly is clinically
three-dimensional nature, coronary CT angiography allows excellent harmless. (a) Two-dimensional CT image in transaxial orientation
delineation of the origin and course of anomalous coronary arteries. which shows the position of the anomalous left main coronary artery
This patient has an anomalous left main coronary artery arising from anterior to the pulmonary artery (arrows). (b) Three-dimensional
the right coronary sinus and travelling anterior to the pulmonary reconstruction. The arrows point at the anomalous left main coronary
artery, with subsequent division into the left anterior descending and artery

a b

Fig. 9.15 “Interarterial” versus “sub-pulmonary” course of an anom- coronary artery. Surgical correction, irrespective of symptoms, is fre-
alous left main coronary artery. (a) Patient with an anomalous left quently suggested. (b) Patient with an anomalous left main coronary
main coronary artery (arrows) that arises from the right coronary sinus which also arises from the right coronary sinus but then travels below
and follows an “interarterial” course between the ascending aorta and the pulmonary artery, embedded in the septum (“subpulmonary” or
right pulmonary artery. In this location (see inset), there is potential “transseptal” course, see arrows). This anomaly is typically considered
danger of ischemia due to kinking or compression of the left main less harmful
9 Coronary CT Angiography: Native Vessels 173

Table 9.6 Appropriateness of coronary CT angiography in various clinical situations [92]

Non-acute symptoms possibly representing an ischemic equivalent – no stress test done
ECG interpretable and able to exercise
Low pre-test likelihood (<10 %) Uncertain
Intermediate pre-test likelihood (10–90 %) Appropriate
High pre-test likelihood (>90 %) Inappropriate
ECG uninterpretable or unable to exercise
Low or intermediate pre-test likelihood Appropriate
High pre-test likelihood Uncertain
Non-acute symptoms, prior ECG exercise test
Normal but continued symptoms Appropriate
Abnormal
Intermediate duke treadmill score Appropriate
Low or high duke treadmill score Inappropriate
Non-acute symptoms, prior stress imaging procedure
Equivocal Appropriate
Mildly positive Uncertain
Moderately or severely positive Inappropriate
Discordant ECG exercise and stress imaging results Appropriate
New or worsening symptoms with a past stress imaging study
Past study normal Appropriate
Past study abnormal Uncertain
Acute symptoms with suspicion of ACS (urgent presentation)
Definite MI Inappropriate
“Triple Rule Out” for acute chest pain of uncertain cause (differential diagnosis includes Uncertain
pulmonary embolism, aortic dissection, and ACS)
Cardiac biomarkers normal or equivocal and ECG normal or uninterpretable
Low or intermediate pre-test likelihood Appropriate
Intermediate pre-test likelihood Appropriate
Patient with previous revascularization by CABG and
Symptoms, assessment of bypass patency required Appropriate
No symptoms, surgery <5 years ago Inappropriate
No symptoms, surgery ≥5 years ago Uncertain
Patient with previous revascularization by PCI and
Symptoms, stent <3 mm Inappropriate
Symptoms,, stent ≥3 mm Uncertain
No symptoms, left main stent ≥3 mm Appropriate
No symptoms, other stents Inappropriate

angiography is considered “appropriate” to evaluate patients able to initially perform (without serial ECGs and
with anomalous coronary arteries [92]. CT angiography for troponins) coronary CT angiography to assess coronary
screening purposes is not endorsed. artery anatomy (Level of Evidence: A) or rest myocardial
Official guidelines issued by the European Society of perfusion imaging with a technetium-99 m radiopharma-
Cardiology assign a “Class IIa” recommendation (“should be ceutical to exclude myocardial ischemia (Level of
considered”) to coronary CTA in patients with suspected sta- Evidence: B)
ble coronary artery disease [93] and patients with acute chest ACC/AHA guidelines on stable coronary disease, in their
pain but absence of ECG changed and enzyme elevation [62]. last version dated 2012, provide the following recommenda-
United States guidelines on non-ST-elevation acute coronary tions regarding the use of coronary CTA [94]:
syndromes, jointly issued by the ACC and AHA [61], assign a
“Class IIa” recommendation to coronary CTA and state that: Class IIa (“Should be considered”)
In patients with possible ACS and a normal ECG, nor- Patients unable to exercise, with low to intermediate
mal cardiac troponins, and no history of CAD, it is reason- pretest probability of ischemic heart disease
174 S. Achenbach

Patients with intermediate pretest probability of ischemic dose-optimization strategies in cardiovascular CT. J Cardiovasc
heart disease and an inconclusive exercise test, ongoing Comput Tomogr. 2011;5:198–224.
3. Bischoff B, Hein F, Meyer T, Krebs M, Hadamitzky M, Martinoff
symptoms in spite of a normal exercise test, as well as S, Schömig A, Hausleiter J. Comparison of sequential and heli-
patients unable to undergo stress testing by myocardial cal scanning for radiation dose and image quality: results of the
perfusion imaging or stress echocardiography Prospective Multicenter Study on Radiation Dose Estimates of
Class IIb (“might be reasonable”) Cardiac CT Angiography (PROTECTION) I Study. AJR Am
J Roentgenol. 2010;194(6):1495–9.
Patients able to exercise, with intermediate pretest prob- 4. Hausleiter J, Meyer TS, Martuscelli E, Spagnolo P, Yamamoto
ability of ischemic heart disease H, Carrascosa P, Anger T, Lehmkuhl L, Alkadhi H, Martinoff
S, Hadamitzky M, Hein F, Bischoff B, Kuse M, Schömig A,
Achenbach S. Image quality and radiation exposure with prospec-
tively ECG-triggered axial scanning for coronary CT angiography:
Summary and Outlook the multicenter, multivendor, randomized PROTECTION-III study.
JACC Cardiovasc Imaging. 2012;5(5):484–93.
In spite of the impressive and continuously improving image 5. Kim JS, Choo KS, Jeong DW, Chun KJ, Park YH, Song SG, Park
quality, coronary CT angiography does not currently consti- JH, Kim JH, Kim J, Han D, Lim SJ. Step-and-shoot prospectively
ECG-gated vs. retrospectively ECG-gated with tube current modu-
tute a general replacement for invasive, catheter-based diag- lation coronary CT angiography using 128-slice MDCT patients
nostic coronary angiography. A somewhat lower spatial and with chest pain: diagnostic performance and radiation dose. Acta
temporal resolution as compared to invasive angiography, the Radiol. 2011;52(8):860–5.
requirement for regular and low heart rates, and the necessity 6. Labounty TM, Leipsic J, Min JK, Heilbron B, Mancini GB, Lin FY,
Earls JP. Effect of padding duration on radiation dose and image
for breathhold cooperation will preclude CT angiography in a interpretation in prospectively ECG-triggered coronary CT angiog-
relevant fraction of patients who require a workup for coro- raphy. AJR Am J Roentgenol. 2010;194(4):933–7.
nary artery disease. In addition, coronary CT angiography 7. Leipsic J, LaBounty TM, Ajlan AM, Earls JP, Strovski E, Madden
performs less well in patients with diffuse, severe disease, M, Wood DA, Hague CJ, Poulter R, Branch K, Cury RC, Heilbron
B, Taylor C, Grunau G, Haiducu L, Min JK. A prospective ran-
with substantial coronary calcification, or with small coro- domized trial comparing image quality, study interpretability, and
nary arteries (as encountered, for example, in some individu- radiation dose of narrow acquisition window with widened acqui-
als with diabetes). For these cases and all situations where the sition window protocols in prospectively ECG-triggered coronary
need for a revascularization procedure is expected based on computed tomography angiography. J Cardiovasc Comput Tomogr.
2013;7:18–24.
clinical grounds, an invasive approach and catheter-based 8. Lell M, Marwan M, Schepis T, Pflederer T, Anders K, Flohr T,
angiography will remain the best diagnostic option. Allmendinger T, Kalender W, Ertel D, Thierfelder C, Kuettner A,
However, there are numerous patients with a lower pre-test Ropers D, Daniel WG, Achenbach S. Prospectively ECG-triggered
likelihood of disease and with characteristics that promise high-pitch spiral acquisition for coronary CT angiography using
dual source CT: technique and initial experience. Eur Radiol.
high image quality and diagnostic accuracy. In these patients, 2009;19:2576–83.
coronary CTA, if performed expertly, is a superb test to rule 9. Achenbach S, Goroll T, Seltmann M, Pflederer T, Anders K, Ropers
out the presence of coronary artery stenosis and avoid the need D, Daniel WG, Uder M, Lell M, Marwan M. Detection of coronary
for any further testing. Data on the prognostic value of coro- artery stenoses by low-dose, prospectively ECG-triggered, high-
pitch spiral coronary CT angiography. JACC Cardiovasc Imaging.
nary CTA will continue to accumulate and the continuous 2011;4(4):328–37.
technical improvements of CT hardware will make coronary 10. Schuhbaeck A, Achenbach S, Layritz C, Eisentopf J, Hecker F,
CTA ever more robust and accurate. It can therefore be Pflederer T, Gauss S, Rixe J, Kalender W, Daniel WG, Lell M,
expected that the role of coronary CTA in clinical cardiology Ropers D. Image quality of ultra-low radiation exposure coronary
CT angiography with an effective dose <0.1 mSv using high-pitch
will continue to expand. The challenges to meet will include spiral acquisition and raw data-based iterative reconstruction. Eur
the identification of the specific patient groups that benefit Radiol. 2013;23(3):597–606.
most from coronary CTA, assuring the widespread availability 11. Neefjes LA, Dharampal AS, Rossi A, Nieman K, Weustink AC,
of high-end CT hardware, and the incorporation of training in Dijkshoorn ML, Ten Kate GJ, Dedic A, Papadopoulou SL, van
Straten M, Cademartiri F, Krestin GP, de Feyter PJ, Mollet NR.
coronary CTA into the curriculum of cardiology training. Image quality and radiation exposure using different low-dose scan
protocols in dual-source CT coronary angiography: randomized
study. Radiology. 2011;261:779–86.
12. Hausleiter J, Meyer T, Hermann F, Hadamitzky M, Krebs M,
References Gerber TC, McCollough C, Martinoff S, Kastrati A, Schömig A,
Achenbach S. Estimated radiation dose associated with cardiac CT
1. Abbara S, Arbab-Zadeh A, Callister TQ, Desai MY, Mamuya W, angiography. JAMA. 2009;301:500–7.
Thomson L, Weigold WG. SCCT guidelines for performance of 13. Bischoff B, Hein F, Meyer T, Hadamitzky M, Martinoff S, Schömig
coronary computed tomographic angiography: a report of the A, Hausleiter J. Impact of a reduced tube voltage on CT angiogra-
Society of Cardiovascular Computed Tomography Guidelines phy and radiation dose: results of the PROTECTION I study. JACC
Committee. J Cardiovasc Comput Tomogr. 2009;3:190–204. Cardiovasc Imaging. 2009;2:940–6.
2. Halliburton SS, Abbara S, Chen MY, Gentry R, Mahesh M, Raff 14. Jun BR, Yong HS, Kang EY, Woo OH, Choi EJ. 64-slice coro-
GL, Shaw LJ, Hausleiter J. SCCT guidelines on radiation dose and nary computed tomography angiography using low tube voltage
9 Coronary CT Angiography: Native Vessels 175

of 80 kV in subjects with normal body mass indices: comparative beyond binary grading of coronary arterial stenoses on coronary
study using 120 kV. Acta Radiol. 2012;53(10):1099–106. computed tomographic angiography: insights for the imager and
15. Cao JX, Wang YM, Lu JG, Zhang Y, Wang P, Yang C. Radiation referring clinician. JACC Cardiovasc Imaging. 2008;1:472–4.
and contrast agent doses reductions by using 80-kV tube voltage in 27. Cury RC, Pomerantsev EV, Ferencik M, Hoffmann U, Nieman
coronary computed tomographic angiography: a comparative study. K, Moselewski F, Abbara S, Jang IK, Brady TJ, Achenbach S.
Eur J Radiol. 2014;83(2):309–14. Comparison of the degree of coronary stenoses by multidetector
16. LaBounty TM, Leipsic J, Poulter R, Wood D, Johnson M, Srichai computed tomography versus by quantitative coronary angiogra-
MB, Cury RC, Heilbron B, Hague C, Lin FY, Taylor C, Mayo JR, phy. Am J Cardiol. 2005;96(6):784–7.
Thakur Y, Earls JP, Mancini GB, Dunning A, Gomez MJ, Min 28. Boogers MJ, Schuijf JD, Kitslaar PH, van Werkhoven JM, de Graaf
JK. Coronary CT angiography of patients with a normal body FR, Boersma E, van Velzen JE, Dijkstra J, Adame IM, Kroft LJ,
mass index using 80 kVp versus 100 kVp: a prospective, multi- de Roos A, Schreur JH, Heijenbrok MW, Jukema JW, Reiber JH,
center, multivendor randomized trial. AJR Am J Roentgenol. Bax JJ. Automated quantification of stenosis severity on 64-slice
2011;197(5):W860–7. CT: a comparison with quantitative coronary angiography. JACC
17. Hell MM, Bittner D, Schuhbaeck A, Muschiol G, Brand M, Lell M, Cardiovasc Imaging. 2010;3(7):699–709.
Uder M, Achenbach S, Marwan M. Prospectively ECG-triggered 29. von Erffa J, Ropers D, Pflederer T, Schmid M, Marwan M,
high-pitch coronary angiography with third-generation dual-source Daniel WG, Achenbach WG. Differentiation of total occlusion
CT at 70 kVp tube voltage: Feasibility, image quality, radiation and high-grade stenosis in coronary CT angiography. Eur Radiol.
dose, and effect of iterative reconstruction. J Cardiovasc Comput 2008;18(12):2770–5.
Tomogr. 2014;8:418–25. 30. Hoffmann U, Moselewski F, Cury RC, Ferencik M, Jang IK, Diaz
18. Yin WH, Lu B, Li N, Han L, Hou ZH, Wu RZ, Wu YJ, Niu HX, LJ, Abbara S, Brady TJ, Achenbach S. Predictive value of 16-slice
Jiang SL, Krazinski AW, Ebersberger U, Meinel FG, Schoepf UJ. multidetector spiral computed tomography to detect significant
Iterative reconstruction to preserve image quality and diagnos- obstructive coronary artery disease in patients at high risk for
tic accuracy at reduced radiation dose in coronary CT angiogra- coronary artery disease: patient-versus segment-based analysis.
phy: an intraindividual comparison. JACC Cardiovasc Imaging. Circulation. 2004;110:2638–43.
2013;6:1239–49. 31. Yan RT, Miller JM, Rochitte CE, Dewey M, Niinuma H, Clouse
19. Leipsic J, Nguyen G, Brown J, Sin D, Mayo JR. A prospective ME, Vavere AL, Brinker J, Lima JA, Arbab-Zadeh A. Predictors of
evaluation of dose reduction and image quality in chest CT using inaccurate coronary arterial stenosis assessment by CT angiogra-
adaptive statistical iterative reconstruction. AJR Am J Roentgenol. phy. JACC Cardiovasc Imaging. 2013;6(9):963–72.
2010;195(5):1095–9. 32. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert
20. Achenbach S, Marwan M, Ropers D, Schepis T, Pflederer T, Anders E, Scherer M, Bellinger R, Martin A, Benton R, Delago A, Min
K, Kuettner A, Daniel WG, Uder M, Lell MM. Coronary computed JK. Diagnostic performance of 64-multidetector-row coronary
tomography angiography with a consistent dose below 1 mSv using computed tomographic angiography for evaluation of coronary
prospectively ECG-triggered high-pitch spiral acquisition. Eur artery stenosis in individuals without known coronary artery dis-
Heart J. 2010;31:340–6. ease. J Am Coll Cardiol. 2008;52:1724–32.
21. Alkadhi H, Stolzmann P, Desbiolles L, Baumueller S, Goetti R, 33. Meijboom WB, Meijs MF, Schuijf JD, Cramer MJ, Mollet NR,
Plass A, Scheffel H, Feuchtner G, Falk V, Marincek B, Leschka van Mieghem CA, Nieman K, van Werkhoven JM, Pundziute G,
S. Low-dose, 128-slice, dual-source CT coronary angiography: Weustink AC, de Vos AM, Pugliese F, Rensing B, Jukema JW, Bax
accuracy and radiation dose of the high-pitch and the step-and- JJ, Prokop M, Doevendans PA, Hunink MG, Krestin GP, de Feyter
shoot mode. Heart. 2010;96(12):933–8. PJ. Diagnostic accuracy of 64-slice computed tomography coro-
22. Chinnaiyan KM, Boura JA, DePetris A, Gentry R, Abidov A, Share nary angiography: a prospective, multicenter, multivendor study.
DA, Raff GL, Advanced Cardiovascular Imaging Consortium J Am Coll Cardiol. 2008;52:2135–44.
Coinvestigators. Progressive radiation dose reduction from coronary 34. Miller JM, Rochitte CE, Dewey M, Arbab-Zadeh A, Niinuma
computed tomography angiography in a statewide collaborative qual- H, Gottlieb I, Paul N, Clouse ME, Shapiro EP, Hoe J, Lardo AC,
ity improvement program: results from the Advanced Cardiovascular Bush DE, de Roos A, Cox C, Brinker J, Lima JA. Diagnostic per-
Imaging Consortium. Circ Cardiovasc Imaging. 2013;6:646–54. formance of coronary angiography by 64-row CT. N Engl J Med.
23. Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M, 2008;359:2324–36.
Miller JM, Niinuma H, Yoshioka K, Kitagawa K, Nakamori S, 35. Paech DC, Weston AR. A systematic review of the clinical effec-
Laham R, Vavere AL, Cerci RJ, Mehra VC, Nomura C, Kofoed KF, tiveness of 64-slice or higher computed tomography angiography
Jinzaki M, Kuribayashi S, de Roos A, Laule M, Tan SY, Hoe J, Paul as an alternative to invasive coronary angiography in the investiga-
N, Rybicki FJ, Brinker JA, Arai AE, Cox C, Clouse ME, Di Carli tion of suspected coronary artery disease. BMC Cardiovasc Disord.
MF, Lima JA. Computed tomography angiography and perfusion to 2011;11:32.
assess coronary artery stenosis causing perfusion defects by single 36. Vanhoenacker PK, Heijenbrok-Kal MH, Van Heste R, Decramer I,
photon emission computed tomography: the CORE320 study. Eur Van Hoe LR, Wijns W, Hunink MG. Diagnostic performance of
Heart J. 2014;35:1120–30. multidetector CT angiography for assessment of coronary artery
24. Leipsic J, Abbara S, Achenbach S, Cury R, Earls JP, Mancini GJ, disease: meta-analysis. Radiology. 2007;244:419–28.
Nieman K, Pontone G, Raff GL. SCCT guidelines for the inter- 37. Westwood ME, Raatz HD, Misso K, Burgers L, Redekop K,
pretation and reporting of coronary CT angiography: a report of Lhachimi SK, Armstrong N, Kleijnen J. Systematic review of the
the Society of Cardiovascular Computed Tomography Guidelines accuracy of dual-source cardiac CT for detection of arterial stenosis
Committee. J Cardiovasc Comput Tomogr. 2014;8(5):342–58. in difficult to image patient groups. Radiology. 2013;267(2):387–95.
25. Ferencik M, Ropers D, Abbara S, Cury RC, Hoffmann U, Nieman 38. Chen CC, Chen CC, Hsieh IC, Liu YC, Liu CY, Chan T, Wen MS,
K, Brady TJ, Moselewski F, Daniel WG, Achenbach S. Diagnostic Wan YL. The effect of calcium score on the diagnostic accuracy
accuracy of image postprocessing methods for the detection of of coronary computed tomography angiography. Int J Cardiovasc
coronary artery stenoses by using multidetector CT. Radiology. Imaging. 2011;27 Suppl 1:37–42.
2007;243(3):696–702. 39. Arbab-Zadeh A, Miller JM, Rochitte CE, Dewey M, Niinuma
26. Cheng V, Gutstein A, Wolak S, Suzuki Y, Dey D, Gransar H, H, Gottlieb I, Paul N, Clouse ME, Shapiro EP, Hoe J, Lardo AC,
Thomson LE, Hayes SW, Friedman JD, Berman DS. Moving Bush DE, de Roos A, Cox C, Brinker J, Lima JA. Diagnostic
176 S. Achenbach

accuracy of computed tomography coronary angiography accord- diagnostic and surgical procedures: results from the multicenter
ing to pre-test probability of coronary artery disease and severity CONFIRM (coronary CT angiography evaluation for clinical out-
of coronary arterial calcification. The CORE-64 (Coronary Artery comes: an International Multicenter) registry. J Am Coll Cardiol.
Evaluation Using 64-Row Multidetector Computed Tomography 2012;60(20):2103–14.
Angiography) International Multicenter Study. J Am Coll Cardiol. 50. Min JK, Berman DS, Dunning A, Achenbach S, Al-Mallah M, Budoff
2012;59(4):379–87. MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V, Chinnaiyan
40. Kruk M, Noll D, Achenbach S, Mintz GS, Pręgowski J, Kaczmarska K, Chow BJ, Cury R, Delago A, Feuchtner G, Hadamitzky M,
E, Kryczka K, Pracoń R, Dzielińska Z, Sleszycka J, Witkowski Hausleiter J, Kaufmann P, Karlsberg RP, Kim YJ, Leipsic J, Lin FY,
A, Demkow M, Rużyłło W, Kępka C. Impact of coronary artery Maffei E, Plank F, Raff G, Villines T, Labounty TM, Shaw LJ. All-
calcium characteristics on accuracy of CT angiography. JACC cause mortality benefit of coronary revascularization vs. medical
Cardiovasc Imaging. 2014;7(1):49–58. therapy in patients without known coronary artery disease under-
41. Meijboom WB, van Mieghem CA, Mollet NR, Pugliese F, Weustink going coronary computed tomographic angiography: results from
AC, van Pelt N, Cademartiri F, Nieman K, Boersma E, de Jaegere CONFIRM (COronary CT Angiography EvaluatioN For Clinical
P, Krestin GP, de Feyter PJ. 64-slice computed tomography coro- Outcomes: An InteRnational Multicenter Registry). Eur Heart
nary angiography in patients with high, intermediate, or low pre- J. 2012;33:3088–97.
test probability of significant coronary artery disease. J Am Coll 51. Meijboom WB, Mollet NR, Van Mieghem CA, Weustink AC,
Cardiol. 2007;50:1469–75. Pugliese F, van Pelt N, Cademartiri F, Vourvouri E, de Jaegere P,
42. Gilard M, Le Gal G, Cornily JC, Vinsonneau U, Joret C, Pennec Krestin GP, de Feyter PJ. 64-slice computed tomography coronary
PY, Mansourati J, Boschat J. Midterm prognosis of patients with angiography in patients with non-ST elevation acute coronary syn-
suspected coronary artery disease and normal multislice computed drome. Heart. 2007;93:1386–92.
tomography findings. A prospective management outcome study. 52. Hoffmann U, Nagurney JT, Moselewski F, Pena A, Ferencik M,
Arch Intern Med. 2007;165:1686–9. Chae CU, Cury RC, Butler J, Abbara S, Brown DF, Manini A,
43. Lesser JR, Flygenring B, Knickelbine T, Hara H, Henry J, Kalil A, Nichols JH, Achenbach S, Brady TJ. Coronary multidetector com-
Pelak K, Lindberg J, Pelzel J, Schwartz RS. Clinical utility of coro- puted tomography in the assessment of patients with acute chest
nary CT angiography: coronary stenosis detection and prognosis in pain. Circulation. 2006;114:2251–60.
ambulatory patients. Cath Cardiovasc Interv. 2007;69:64–72. 53. Gallagher MJ, Ross MA, Raff GL, Goldstein JA, O’Neill WW,
44. Hadamitzky M, Freissmuth B, Meyer T, Hein F, Kastrati A, O’Neil B. The diagnostic accuracy of 64-slice computed tomog-
Martinoff S, Schömig A, Hausleiter J. Prognostic value of coro- raphy coronary angiography compared with stress nuclear imaging
nary computed tomographic angiography for prediction of cardiac in emergency department low-risk chest pain patients. Ann Emerg
events in patients with suspected coronary artery disease. JACC Med. 2007;49:125–36.
Cardiovasc Imaging. 2009;2:404–11. 54. Goldstein JA, Gallagher MJ, O’Neill WW, Ross MA, O’Neil BJ,
45. Ostrom MP, Gopal A, Ahmadi N, Nasir K, Yang E, Kakadiaris I, Raff GL. A randomized controlled trial of multi-slice coronary
Flores F, Mao SS, Budoff MJ. Mortality incidence and the sever- computed tomography for evaluation of acute chest pain. J Am Coll
ity of coronary atherosclerosis assessed by computed tomography Cardiol. 2007;49:863–71.
angiography. J Am Coll Cardiol. 2008;52:1335–43. 55. Coles DR, Wilde P, Oberhoff M, Rogers CA, Karsch KR,
46. Abidov A, Gallagher MJ, Chinnayan KM, Mehta LS, Wegner JH, Baumbach A. Multislice computed tomography coronary angiogra-
Raff GH. Clinical effectiveness of coronary computed tomographic phy in patients admitted with a suspected acute coronary syndrome.
angiography in the triage of patients to cardiac catheterization and Int J Cardiovasc Imaging. 2007;23:603–14.
revascularization. J Nucl Cardiol. 2009;16:701–13. 56. Litt HI, Gatsonis C, Snyder B, Singh H, Miller CD, Entrikin DW,
47. Otaki Y, Arsanjani R, Gransar H, Cheng VY, Dey D, Labounty Leaming JM, Gavin LJ, Pacella CB, Hollander JE. CT angiogra-
T, Lin FY, Achenbach S, Al-Mallah M, Budoff MJ, Cademartiri phy for safe discharge of patients with possible acute coronary syn-
F, Callister TQ, Chang HJ, Chinnaiyan K, Chow BJ, Delago dromes. N Engl J Med. 2012;366:1393–403.
A, Hadamitzky M, Hausleiter J, Kaufmann P, Maffei E, Raff G, 57. Hoffmann U, Truong QA, Schoenfeld DA, Chou ET, Woodard
Shaw LJ, Villines TC, Dunning A, Cury RC, Feuchtner G, Kim PK, Nagurney JT, Pope JH, Hauser TH, White CS, Weiner SG,
YJ, Leipsic J, Berman DS, Min JK. What have we learned from Kalanjian S, Mullins ME, Mikati I, Peacock WF, Zakroysky P,
CONFIRM? Prognostic implications from a prospective multi- Hayden D, Goehler A, Lee H, Gazelle GS, Wiviott SD, Fleg JL,
center international observational cohort study of consecutive Udelson JE, ROMICAT-II Investigators. Coronary CT angiogra-
patients undergoing coronary computed tomographic angiography. phy versus standard evaluation in acute chest pain. N Engl J Med.
J Nucl Cardiol. 2012;19:787–95. 2012;367:299–308.
48. Min JK, Dunning A, Lin FY, Achenbach S, Al-Mallah M, Budoff 58. Jones RL, Thomas DM, Barnwell ML, Fentanes E, Young AN,
MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V, Chinnaiyan Barnwell R, Foley AT, Hilliard M, Hulten EA, Villines TC, Cury
K, Chow BJ, Delago A, Hadamitzky M, Hausleiter J, Kaufmann RC, Slim AM. Safe and rapid disposition of low-to-intermediate
P, Maffei E, Raff G, Shaw LJ, Villines T, Berman DS, CONFIRM risk patients presenting to the emergency department with chest
Investigators. Age- and sex-related differences in all-cause mortality pain: a 1-year high-volume single-center experience. J Cardiovasc
risk based on coronary computed tomography angiography findings Comput Tomogr. 2014;8(5):375–583.
results from the International Multicenter CONFIRM (coronary 59. Staniak HL, Bittencourt MS, Pickett C, Cahill M, Kassop D, Slim
CT angiography evaluation for clinical outcomes: an International A, Blankstein R, Hulten E. Coronary CT angiography for acute
Multicenter Registry) of 23,854 patients without known coronary chest pain in the emergency department. J Cardiovasc Comput
artery disease. J Am Coll Cardiol. 2011;58(8):849–60. Tomogr. 2014;8(5):359–67.
49. Shaw LJ, Hausleiter J, Achenbach S, Al-Mallah M, Berman DS, 60. Redberg RF. Coronary CT, angiography for acute chest pain. N
Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Kim YJ, Cheng Engl J Med. 2012;367(4):375–6.
VY, Chow BJ, Cury RC, Delago AJ, Dunning AL, Feuchtner GM, 61. Amsterdam EA, Wenger NK, Brindis RG, Casey Jr DE, Ganiats
Hadamitzky M, Karlsberg RP, Kaufmann PA, Leipsic J, Lin FY, TG, Holmes Jr DR, Jaffe AS, Jneid H, Kelly RF, Kontos MC,
Chinnaiyan KM, Maffei E, Raff GL, Villines TC, Labounty T, Levine GN, Liebson PR, Mukherjee D, Peterson ED, Sabatine
Gomez MJ, Min JK, CONFIRM Registry Investigators. Coronary MS, Smalling RW, Zieman SJ. 2014 AHA/ACC guideline for the
computed tomographic angiography as a gatekeeper to invasive management of patients with non-ST-elevation acute coronary
9 Coronary CT Angiography: Native Vessels 177

syndromes: a report of the American College of Cardiology/ 73. Leber AW, Becker A, Knez A, von Ziegler F, Sirol M, Nikolaou
American Heart Association Task Force on Practice Guidelines. K, Ohnesorge B, Fayad ZA, Becker CR, Reiser M, Steinbeck G,
J Am Coll Cardiol. 2014;64(24):e139–228. Boekstegers P. Accuracy of 64-slice computed tomography to clas-
62. Hamm CW, Bassand JP, Agewall S, Bax J, Boersma E, Bueno sify and quantify plaque volumes in the proximal coronary system:
H, Caso P, Dudek D, Gielen S, Huber K, Ohman M, Petrie MC, a comparative study using intravascular ultrasound. J Am Coll
Sonntag F, Uva MS, Storey RF, Wijns W, Zahger D, ESC Committee Cardiol. 2006;47:672–7.
for Practice Guidelines. ESC guidelines for the management of 74. Pohle K, Achenbach S, MacNeill B, Ropers D, Ferencik
acute coronary syndromes in patients presenting without persistent M, Moselewski F, Hoffmann U, Brady TJ, Jang IK, Daniel
ST-segment elevation: the Task Force for the management of acute WG. Characterization of non-calcified coronary athero-
coronary syndromes (ACS) in patients presenting without persis- sclerotic plaque by multi-detector row CT: comparison to
tent ST-segment elevation of the European Society of Cardiology IVUS. Atherosclerosis. 2007;190:174–80.
(ESC). Eur Heart J. 2011;32(23):2999–3054. 75. Sun J, Zhang Z, Lu B, Yu W, Yang Y, Zhou Y, Wang Y, Fan
63. Schuijf JD, Wijns W, Jukema JW, Atsma DE, de Roos A, Lamb Z. Identification and quantification of coronary atherosclerotic
HJ, Stokkel MP, Dibbets-Schneider P, Decramer I, De Bondt P, plaques: a comparison of 64-MDCT and intravascular ultrasound.
van der Wall EE, Vanhoenacker PK, Bax JJ. Relationship between AJR Am J Roentgenol. 2008;190(3):748–54.
noninvasive coronary angiography with multi-slice computed 76. Nakazato R, Shalev A, Doh JH, Koo BK, Dey D, Berman DS, Min
tomography and myocardial perfusion imaging. J Am Coll Cardiol. JK. Quantification and characterisation of coronary artery plaque
2006;48:2508–14. volume and adverse plaque features by coronary computed tomo-
64. Min JK, Shaw LJ, Berman DS. The present state of coronary com- graphic angiography: a direct comparison to intravascular ultra-
puted tomography angiography – a process in evolution. J Am Coll sound. Eur Radiol. 2013;23(8):2109–17.
Cardiol. 2010;55:957–65. 77. Obaid DR, Calvert PA, Gopalan D, Parker RA, Hoole SP, West NE,
65. Hacker M, Jakobs T, Hack N, Nikolaou K, Becker C, von Ziegler Goddard M, Rudd JH, Bennett MR. Atherosclerotic plaque compo-
F, Knez A, Konig A, Klauss V, Reiser M, Hahn K, Tiling R. Sixty- sition and classification identified by coronary computed tomogra-
four slice spiral CT angiography does not predict the functional phy: assessment of computed tomography-generated plaque maps
relevance of coronary artery stenoses in patients with stable angina. compared with virtual histology intravascular ultrasound and his-
Eur J Nucl Med Mol Imaging. 2007;34:4–10. tology. Circ Cardiovasc Imaging. 2013;6(5):655–64.
66. Berman DS, Hachamovitch R, Shaw LJ, Friedman JD, Hayes SW, 78. Cademartiri F, Mollet NR, Runza G, Bruining N, Hamers R,
Thomson LE, Fieno DS, Germano G, Wong ND, Kang X, Rozanski Somers P, Knaapen M, Verheye S, Midiri M, Krestin GP, de Feyter
A. Roles of nuclear cardiology, cardiac computed tomography, and PJ. Influence of intracoronary attenuation on coronary plaque mea-
cardiac magnetic resonance: noninvasive risk stratification and surements using multislice computed tomography: observations in
a conceptual framework for the selection of noninvasive imaging an ex vivo model of coronary computed tomography angiography.
tests in patients with known or suspected coronary artery disease. Eur Radiol. 2005;15:1426–31.
J Nucl Med. 2006;47:1107–18. 79. Achenbach S, Boehmer K, Pflederer T, Ropers D, Seltmann M,
67. Bamberg F, Becker A, Schwarz F, Marcus RP, Greif M, von Lell M, Anders K, Kuettner A, Uder M, Daniel WG, Marwan
Ziegler F, Blankstein R, Hoffmann U, Sommer WH, Hoffmann VS, M. Influence of slice thickness and reconstruction kernel on the
Johnson TR, Becker HC, Wintersperger BJ, Reiser MF, Nikolaou computed tomographic attenuation of coronary atherosclerotic
K. Detection of hemodynamically significant coronary artery ste- plaque. J Cardiovasc Comput Tomogr. 2010;4(2):110–5.
nosis: incremental diagnostic value of dynamic CT-based myocar- 80. Achenbach S, Ropers D, Hoffmann U, MacNeill B, Baum U,
dial perfusion imaging. Radiology. 2011;260:689–98. Pohle K, Brady TJ, Pomerantsev E, Ludwig J, Flachskampf FA,
68. Tashakkor AY, Nicolaou S, Leipsic J, Mancini GB. The emerg- Wicky S, Jang IK, Daniel WG. Assessment of coronary remodel-
ing role of cardiac computed tomography for the assessment of ing in stenotic and nonstenotic coronary atherosclerotic lesions
coronary perfusion: a systematic review and meta-analysis. Can by multidetector spiral computed tomography. J Am Coll Cardiol.
J Cardiol. 2012;28:413–22. 2004;43:842–7.
69. Taylor CA, Fonte TA, Min JK. Computational fluid dynamics 81. Moselewski F, Ropers D, Pohle K, Hoffmann U, Ferencik M,
applied to cardiac computed tomography for noninvasive quantifi- Chan RC, Cury RC, Abbara S, Jang IK, Brady TJ, Daniel WG,
cation of fractional flow reserve: scientific basis. J Am Coll Cardiol. Achenbach S. Comparison of measurement of cross-sectional coro-
2013;61:2233–41. nary atherosclerotic plaque and vessel areas by 16-slice multide-
70. Nørgaard BL, Leipsic J, Gaur S, Seneviratne S, Ko BS, Ito H, tector computed tomography versus intravascular ultrasound. Am
Jensen JM, Mauri L, De Bruyne B, Bezerra H, Osawa K, Marwan J Cardiol. 2004;94:1294–7.
M, Naber C, Erglis A, Park SJ, Christiansen EH, Kaltoft A, Lassen 82. Gauss S, Achenbach S, Pflederer T, Schuhbäck A, Daniel WG,
JF, Bøtker HE, Achenbach S, NXT Trial Study Group. Diagnostic Marwan M. Assessment of coronary artery remodelling by dual-
performance of noninvasive fractional flow reserve derived from source CT: a head-to-head comparison with intravascular ultra-
coronary computed tomography angiography in suspected coro- sound. Heart. 2011;97(12):991–7.
nary artery disease: the NXT trial (analysis of coronary blood 83. Motoyama S, Sarai M, Harigaya H, Anno H, Inoue K, Hara
flow using CT angiography: next steps). J Am Coll Cardiol. T, Naruse H, Ishii J, Hishida H, Wong ND, Virmani R, Kondo
2014;63(12):1145–55. T, Ozaki Y, Narula J. Computed tomographic angiography
71. Achenbach S, Moselewski F, Ropers D, Ferencik M, Hoffmann U, characteristics of atherosclerotic plaques subsequently result-
MacNeill B, et al. Detection of calcified and noncalcified coronary ing in acute coronary syndrome. J Am Coll Cardiol. 2009;54:
atherosclerotic plaque by contrast-enhanced, submillimeter multi- 49–57.
detector spiral computed tomography: a segment-based comparison 84. Bittencourt MS, Hulten E, Ghoshhajra B, O’Leary D, Christman
with intravascular ultrasound. Circulation. 2004;109:14–7. MP, Montana P, Truong QA, Steigner M, Murthy VL, Rybicki FJ,
72. Leber AW, Knez A, Becker A, Becker C, von Ziegler F, Nikolaou Nasir K, Gowdak LH, Hainer J, Brady TJ, Di Carli MF, Hoffmann
K, et al. Accuracy of multidetector spiral computed tomography U, Abbara S, Blankstein R. Prognostic value of nonobstructive and
in identifying and differentiating the composition of coronary ath- obstructive coronary artery disease detected by coronary computed
erosclerotic plaques: a comparative study with intracoronary ultra- tomography angiography to identify cardiovascular events. Circ
sound. J Am Coll Cardiol. 2004;43:1241–7. Cardiovasc Imaging. 2014;7(2):282–91.
178 S. Achenbach

85. Hulten EA, Carbonaro S, Petrillo SP, Mitchell JD, Villines Association; American Society of Echocardiography; American
TC. Prognostic value of cardiac computed tomography angiogra- Society of Nuclear Cardiology; North American Society for
phy: a systematic review and meta-analysis. J Am Coll Cardiol. Cardiovascular Imaging; Society for Cardiovascular Angiography
2011;57(10):1237–47. and Interventions; Society for Cardiovascular Magnetic Resonance.
86. Cho I, Chang HJ, Sung JM, Pencina MJ, Lin FY, Dunning AM, ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010
Achenbach S, Al-Mallah M, Berman DS, Budoff MJ, Callister appropriate use criteria for cardiac computed tomography. A report
TQ, Chow BJ, Delago A, Hadamitzky M, Hausleiter J, Maffei E, of the American College of Cardiology Foundation Appropriate
Cademartiri F, Kaufmann P, Shaw LJ, Raff GL, Chinnaiyan KM, Use Criteria Task Force, the Society of Cardiovascular Computed
Villines TC, Cheng V, Nasir K, Gomez M, Min JK, CONFIRM Tomography, the American College of Radiology, the American
Investigators. Coronary computed tomographic angiography and Heart Association, the American Society of Echocardiography,
risk of all-cause mortality and nonfatal myocardial infarction in the American Society of Nuclear Cardiology, the North American
subjects without chest pain syndrome from the CONFIRM Registry Society for Cardiovascular Imaging, the Society for Cardiovascular
(coronary CT angiography evaluation for clinical outcomes: an inter- Angiography and Interventions, and the Society for Cardiovascular
national multicenter registry). Circulation. 2012;126(3):304–13. Magnetic Resonance. J Am Coll Cardiol. 2010;56:1864–94.
87. Ropers D, Moshage W, Daniel WG, et al. Visualization of coro- 93. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C,
nary artery anomalies and their course by contrast-enhanced elec- Budaj A, Bugiardini R, Crea F, Cuisset T, Di Mario C, Ferreira
tron beam tomography and three-dimensional reconstruction. Am JR, Gersh BJ, Gitt AK, Hulot JS, Marx N, Opie LH, Pfisterer M,
J Cardiol. 2001;87:193–7. Prescott E, Ruschitzka F, Sabaté M, Senior R, Taggart DP, van
88. Datta J, White CS, Gilkeson RC, Meyer CA, Kansal S, Jani ML, der Wall EE, Vrints CJ. 2013 ESC guidelines on the management
Arildsen RC, Read K. Anomalous coronary arteries in adults: depiction of stable coronary artery disease: the task force on the manage-
at multi-detector row CT angiography. Radiology. 2005;235:812–8. ment of stable coronary artery disease of the European Society of
89. Kim SY, Seo JB, Do KJ, Heo JN, Lee JS, Song JW, Choe YH, Kim Cardiology. Eur Heart J. 2013;34:2949–3003.
TH, Yong HS, Choi SI, Song KS, Lim TH. Coronary artery anoma- 94. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas
lies: classification and ECG-gated multi-detector row CT findings AP, Douglas PS, Foody JM, Gerber TC, Hinderliter AL, King SB,
with angiographic correlation. Radiographics. 2006;26:317–33. Kligfield PD, Krumholz HM, Kwong RY, Lim MJ, Linderbaum JA,
90. Duran C, Kantarci M, Durur Subais I, Gulbaran M, Sevimli S, Mack MJ, Munger MA, Prager RL, Sabik JF, Shaw LJ, Sikkema
Bayram E, Eren S, Karaman A, Fil F, Al O. Remarkable anatomic JD, Smith Jr CR, Smith Jr SC, Spertus JA, Williams SV, Anderson
anomalies of coronary arteries and their clinical importance: a mul- JL, American College of Cardiology Foundation/American Heart
tidetector computed tomography angiographic study. J Comput Association Task Force. 2012 ACCF/AHA/ACP/AATS/PCNA/
Assist Tomogr. 2006;30:939–48. SCAI/STS guideline for the diagnosis and management of patients
91. Bozlar U, Uğurel MS, Sarı S, Akgün V, Ors F, Taşar M. Prevalence with stable ischemic heart disease: a report of the American
of dual left anterior descending artery variations in CT angiogra- College of Cardiology Foundation/American Heart Association
phy. Diagn Interv Radiol. 2015;21:34–41. task force on practice guidelines, and the American College of
92. Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O’Gara P, Physicians, American Association for Thoracic Surgery, Preventive
Rubin GD, American College of Cardiology Foundation Appropriate Cardiovascular Nurses Association, Society for Cardiovascular
Use Criteria Task Force; Society of Cardiovascular Computed Angiography and Interventions, and Society of Thoracic Surgeons.
Tomography; American College of Radiology; American Heart Circulation. 2012;126(25):e354–471.
 Coronary CT Angiography After
Revascularization 10
Joachim Eckert, Marco Schmidt, Thomas Voigtländer,
and Axel Schmermund

Abstract
Because of the high number of coronary revascularizations clinicians frequently have to
assess bypass or stent function in patients presenting with chest pain or other symptoms
suggesting dysfunction. Predominantly, invasive coronary angiography is performed for
this purpose. In the last decade innovations in CT scanners, protocols and reconstructions
have led to a remarkable increase in diagnostic accuracy of coronary CT angiography for
the assessment of coronary bypass grafts and stents whereas radiation exposure has signifi-
cantly decreased. Occlusions of bypass grafts and occlusive in-stent stenoses can be ruled
out with a high negative predictive value approaching 100 %.

Keywords
Coronary CT angiography • Stents • Bypass grafts

Background Bypass Grafts

Coronary artery revascularization is one of the most frequent Venous Grafts: Anatomy and Natural History
medical procedures. In the year 2009 about 350,000 percuta-
neous coronary interventions (PCI) were performed and Venous bypass grafts still represent the majority of all
200,000 patients underwent bypass surgery in the United grafts used for bypass surgery. Due to differences in anat-
States [1]. In clinical practice, patients after coronary revas- omy and surgical techniques, their patency rates are infe-
cularization frequently present with symptoms suggesting rior to internal mammary artery grafts [2, 3]. Three modes
progression of coronary artery disease (CAD). Physicians of venous bypass graft degeneration have been described
have to reevaluate the patency of the coronary arteries, espe- which occur at different time points after surgery. Within
cially concerning an in-stent-stenosis or occluded bypass hours to weeks after surgery, technical deficiencies and
grafts. These patients often undergo invasive coronary angi- thrombotic activation lead to early thrombotic occlusion in
ography (ICA) even though there is no evidence of ischemia. approximately 5–10 % of the grafts [4]. Over the course of
As an alternative to ICA, coronary computed tomography the following year, intimal hyperplasia and thrombosis
angiography (CCTA) plays an increasing role for obtaining appear to be the major mechanisms, accounting for an over-
reliable information on coronary anatomy noninvasively. all occlusion rate of 10–15 % within the first year [4, 5].
Finally, after the first year, mechanisms known from native
coronary artery atherosclerosis predominate. Bypass attri-
J. Eckert, MD (*) • M. Schmidt, MD • T. Voigtländer, MD tion between postoperative years 1 and 5 appears to be
A. Schmermund, MD minimal. After year 5, atherothrombotic occlusion of
Department of Cardiology, Cardioangiologisches venous grafts accounts for a reduced patency rate. It has
Centrum Bethanien, Im Pruefling 23,
traditionally been estimated to range between 40 and 60 %
Frankfurt, Hessen 60389, Germany
e-mail: [email protected]; [email protected]; at 10–12 years [4, 6]. However, data from the Veteran
[email protected]; [email protected] Affairs Cooperative Study indicate that venous grafts which

© Springer International Publishing 2016 179

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_10
180 J. Eckert et al.

are open 1 week after surgery have a patency rate of 68 % Non-invasive CT Examination
after 10 years [2]. The presence of angiographic stenoses
between 50 and 99 % of graft diameter appears to be Venous bypass grafts are typically larger in diameter than the
17–22 % at 10 years [2]. As opposed to native coronary native large epicardial coronary arteries (approximately 4 –
arteries and arterial grafts, venous bypass grafts tend to 10 mm versus 2 – 5 mm), and they are less subjected to car-
develop an extensive thrombotic burden and occlude quite diac motion. Accordingly, even with older-generation
rapidly once a high-grade stenosis has formed. (“non-cardiac”) CT machines, investigators examined con-
trast enhancement along the course of the graft to establish
bypass patency [8, 9]. Due to the inherent limitations of non-
Arterial Grafts: Anatomy and Natural History gated scanning with relatively long acquisition times, overall
diagnostic accuracy regarding bypass graft patency remained
The left internal mammary artery (“IMA”) is most often at approximately 90 %, with better results for (larger) vein
used as arterial graft. Arterial vessels are by design much grafts than for the arterial grafts. It was not possible to iden-
better adapted to systemic blood pressure values and shear tify potential non-occlusive high-grade bypass body steno-
stress than venous vessels, and this translates into improved ses, the distal anastomosis of grafts, or the native coronary
patency rates [2, 3]. IMA grafts patent at 1 week after surgery arterial run-off. The advent of electron-beam computed
had a 10 year patency rate of 88 % in the Veterans Affairs tomography (EBCT) as the first dedicated cardiac CT scan-
Cooperative Study [2]. As with venous grafts, recipient ner and the development of non-invasive coronary angiogra-
vessel location and status influence graft survival. Survival is phy beginning in 1994 allowed for visualization of coronary
best for grafts to the left anterior descending coronary artery bypass grafts and three-dimensional representation of the
and a native vessel diameter ≥ 2 mm [2]. Interestingly, IMA graft vessels [10]. Still, however, image quality was in part
grafts sewed to a recipient vessel with < 50 % diameter insufficient for detailed analysis of small diameter grafts or
stenosis may have a very high rate of occlusion, probably the complex anatomy of native vessels and the anastomosis
due to competing flow through the native vessel [7]. region. Also, artifacts related to metal clips and breathing /
Regarding CT imaging, the smaller lumen diameter of arrhythmias hampered image quality. Despite these limita-
arterial grafts and frequent use of metal clips represent a tions, EBCT bypass angiography was used for some years
challenge for diagnostic image quality. for detecting venous bypass graft occlusion or stenosis

Fig. 10.1 64-row MDCT 3-dimensional image reconstruction shows two patent venous grafts coursing to a right coronary artery and an obtuse
marginal branch (Courtesy of Dr. Dieter Ropers, University Clinic Erlangen-Nürnberg, Germany)
10 Coronary CT Angiography After Revascularization 181

predictive value for ruling out high-grade bypass graft stenoses

ranging between 96 and 99 % [18–20]. However, depending
on the anatomy, the distal anastomosis can still be challeng-
ing to examine, and the degree of stenosis tends to be overes-
timated [18]. The native coronary circulation can be assessed
despite previous bypass surgery [19–21] (Fig. 10.4), how-
ever, as in a population with no previous bypass surgery,
heavy coronary calcification or a small native vessel diame-
ter can render the CT analysis difficult. Sensitivities for the
detection of significant lesions range between 86–95 % for
distal runoffs and 86–97 % for non grafted arteries.
A recent publication demonstrated the prognostic value of
CCTA in coronary bypass patients [22]. Both bypass grafts
and native coronary arteries were analyzed regarding the
number of unprotected coronary territories (UCT). The inci-
dence of myocardial infarction as well as the risk of death
increased significantly with higher numbers of UCT. Hence,
CCTA not only provides morphologic information on the
coronary anatomy but also prognostic data.

Fig. 10.2 64-row MDCT 3-dimensional image reconstruction shows a

patent left internal mammary graft with two anostomoses to the first Imaging Protocols
diagonal branch and left anterior descending coronary artery itself,
respectively
Most experts agree that consequential betablockade
should be undertaken with the aim of reaching heart
within the shaft body and proved to be helpful in a subset of rates ≤ 60–65 bpm, which improves image quality due to less
patients with unspecific symptoms after bypass surgery. motion artifacts and may reduce radiation exposure. Although
With later generations of multidetector CT systems and most recent scanner generations are less susceptible to motion
improvements in spatial and temporal resolution stenosis artifacts, practical experience dictates that this approach
detection in more difficult situations such as the bypass anas- yields superior visibility of coronary artery segments. The
tomosis region or visualization of arterial grafts surrounded administration of oral or intravenous nitrates for vasodilata-
by metal clips was enhanced. Currently, arterial grafts and tion immediately prior to the scan is recommended. A tempo-
the anastomosis region of venous and arterial grafts can be ral window of 60 % of the RR-interval appears to be best
analyzed with increased diagnostic yield [11–19] (Figs. 10.1 suited [23]. Caudo-cranial scan direction seems to be supe-
and 10.2). Even the analysis of native vessel disease progres- rior in terms of image quality and radiation exposure [24].
sion became more accurate with multidetector CT scanners The latest development in CT scanners led to a remarkable
[15] (Fig. 10.3). Regarding the exclusion of high-grade ste- decrease in radiation exposure (prospective ECG-gating,
noses, the negative predictive value was 100 % for bypass reduced tube voltage, tube current modulation, higher acqui-
grafts and 96–98 % for the native coronary arteries (grafted sition speed) which is on average lower than in ICA.
or nongrafted). Only 9 % of the native coronary arteries were Specific scanning protocols with the various scanners are
unevaluable due to severe calcifications or motion artifacts. detailed elsewhere in this book.
A meta-analysis by Hamon et al. comprised studies using
16- and 64-slice MDCT published up to May 2007 [11]. A
total of 15 studies were included, six of which used 64-slice Conclusions to Bypass Grafts
CT [12–17]. Table 10.1 gives an overview of the diagnostic
performance of 64-slice MDCT in a total of 355 patients and CCTA is increasingly used as a modality for the non-invasive
976 bypass grafts [11]. Between 87 and 100 % of the grafts assessment of bypass graft patency and stenoses. As
were fully assessable regarding the detection / exclusion of compared to ICA, a small proportion of grafts remains
angiographically significant stenoses. In particular, a high unassessable due to artifacts or anatomic complexity.
negative predictive value was obtained in the studies, However, this proportion has decreased with improvements
indicating the ability to reliably rule out high-grade stenoses in scanner technology. Bypass grafts as well as native
or obstruction of the bypass grafts using 64-slice coronary arteries can be evaluated with high diagnostic
MDCT. More recent studies have confirmed a negative accuracy. ICA remains gold standard for defining coronary
182 J. Eckert et al.

Fig. 10.3 64-row MDCT

a
3-dimensional image
reconstruction (a) shows a patent
left internal mammary graft to
the left anterior descending
coronary artery and the
corresponding selective
angiogram. Distal to the
anastomosis, the left anterior
descending coronary artery is
occluded; see corresponding
invasive angiographc image (b)

Table 10.1 Results of 64-slice MDCT examination of 976 bypass grafts as documented in a meta-analysis by Hamon et al.a
Positive predictive Negative predictive Positive likelihood Negative likelihood
Sensitivity (%) Specificity (%) value (%) value (%) ratio ratio
98.1 (96.0,99.3) 96.9 (95.3,98.1) 94.1 (91.0,96.3) 99.1 (98.0,99.7) 24.7 (12.5,47.7) 0.03 (0.01,0.06)
Numbers in parentheses = 95 % CI
a
Data from Hamon et al. [11]

bypass anatomy, but especially in patients with non-specific patent grafts in those patients without prior recent angiogra-
complaints, CCTA is an excellent alternative and provides a phy, including use of right and left internal mammaries
nice roadmap to see the origin locations and number of non-invasively.
10 Coronary CT Angiography After Revascularization 183

a b

Fig. 10.4 Patent left internal mammary graft to the left anterior descending coronary artery with normal runoff (a). Patent single vein graft to the
right coronary artery with normal runoff (b). Bypass grafts as well as the native coronary arteries can be evaluated with good image quality

Coronary Stents (BRS), on the other hand, made of magnesium or

polylactid polymer, are free of metal and may be visual-
Background ized only by radioopaque markers at the extreme ends of
the scaffold.
The majority of percutaneous coronary angioplasties are
performed with placement of a stent in the vessel wall [25].
Most stents are made of stainless steel or cobalt-chromium, Non-invasive CT Examination
which can both be challenging to visualize using CCTA due
to motion artifacts and “blooming”. Usual stent diameters Early EBCT-studies used time-density curve analysis in a
range between 2.5 and 4 mm. The widespread use of drug region of interest distal to the stent comparing it to the pattern
eluting stents has significantly reduced the risk of in-stent in the aorta [27–29]. This led to a reliable detection of com-
restenosis [26]. Vessel size, stented length, co morbidities, plete occlusions whereas high-grade and subtotal stenoses
lesion morphology, and previous bypass surgery are predic- were frequently missed because of the fact that contrast flow
tors of higher rates of restenosis [26]. may pass subtotal stenoses and collateral vessels may fill the
Depending on materials and size, stents can have a vessel lumen retrogradely.
widely different appearance in CCTA. A closed cell Apart from motion artifacts, in vitro studies revealed fur-
design with a higher metal-to-surface ratio makes it more ther stent-related problems –– in CT imaging such as
difficult to visualize the stent lumen than an open cell enhancement of the stent struts (“blooming”), apparent
design. New generations of bioresorbable scaffolds reduction of the stent lumen, attenuation of contrast values
184 J. Eckert et al.

Fig. 10.5 Ultra-high resolution images of a coronary stent using within the stented vessel model), the longer arrow a 50 % restenosis in
64-row MDCT. The two left panel pictures show the stent mounted on the same setting. The right panel shows a three-dimensional
a vessel model placed in a phantom with realistic attenuation values. reconstruction of the stent
The short arrow marks an artificial 30 % in-stent restenosis (produced

a b

Fig. 10.6 Intermediate in-stent-stenosis of a 3.25 × 16 mm bare-metal-stent in the proximal left anterior descending artery (a). Corresponding
invasive coronary angiogram of the left coronary artery (b)
10 Coronary CT Angiography After Revascularization 185

inside the lumen and beamlike artifacts adjacent to the stent

[30–33] (Fig. 10.5). Improvements in CT technology like
multi slice and dual-source scanners in recent years have
increased the accuracy of detection of in-stent stenoses
(Fig. 10.6). Nevertheless, stent artifacts are still problematic,
and they vary between different types of stents [34]. Several
studies have evaluated the accuracy of multislice CCTA in
diagnosing in-stent stenoses versus ICA (gold-standard)
[35–40], partly combined with IVUS [38] or OCT [39].
Taking all segments into account, sensitivity was 50–100 %,
specificity 57–98 %, and negative predictive value (NPV)
96–100 %. Looking only at the assessable stents (predomi-
nantly stents > 3.0 mm), sensitivity was 86–100 %, specific-
ity 93–97 %, and NPV 98–100 %.
Besides patient-related aspects that impede image quality,
in particular heart rate, vessel calcifications, motion artifacts,
and obesity, stent diameter has been identified as the most
important stent-related factor. Stent diameters of 3.0 mm or
more appear to have a significantly higher diagnostic accu-
racy on CCTA than smaller stents [38, 40] (Fig. 10.7). A
good correlation between CCTA and IVUS can be observed
in the analysis of left main coronary artery stents [41]. The
type of stent plays an essential role. A strut thickness of less
than 100 μm is associated with less artifacts und thus
improves diagnostic accuracy [38]. Due to the artifacts men-
tioned above, CCTA tends to underestimate lumen area
which may result in false positive findings. On the other
hand, stent occlusions or high-grade in-stent stenoses can be
ruled out with confidence (NPV 98–100 %). In 2010, a meta-
analysis combined 14 studies assessing diagnostic accuracy
of CCTA versus ICA [42]. In total, 89 % of all stents were
assessable. Sensitivity for assessable stents was 90 %, speci-
ficity 91 %.
Rief et al. showed improved diagnostic precision in com-
bining CCTA with myocardial CT perfusion (CTP) [43].
CTP can add functional information concerning an in-stent
stenosis and the need for revascularization (93 % sensitiv- Fig. 10.7 Patent drug-eluting stent (3.0 × 18 mm) in the proximal left
ity). Fixed perfusion deficits due to previous myocardial anterior descending artery
infarctions result, however, in a sensitivity of 65 % and PPV
of only 33 % for CTP alone.
Recent bioresorbable stents (BRS) are hardly visible in scanner technology and image reconstruction, e.g., iterative
CCTA and, unlike metal stents, do not generate artifacts. reconstruction [45, 46]. Image quality has improved due to
So far, comparative studies with other DES concerning the use of sharp, high-resolution kernels [47, 48]. Most
diagnostic yield exist only in vitro [34]. Onuma et al. patients can be scanned with prospective ECG-triggering,
demonstrated the feasibility of CCTA and fractional flow resulting in a significantly lower radiation exposure compared
reserve (FFR) in patients after implantation of an to the retrospective spiral mode. Xia et al. even examined
ABSORB BRS [44]. patients after stent implantation with high-pitch spiral mode
[49]. Diagnostic accuracy was equal to low-pitch spiral mode
and sequential mode, effective dose was in the range of
Imaging Protocols 1.0 mSv.
Preparations for CCTA are the same for stent imaging as
Over the last decade there has been a dramatic reduction in for other CCTA indications and are described elsewhere in
radiation exposure with CCTA due to improvements in CT the book.
186 J. Eckert et al.

Conclusion bypass grafts by electron beam tomography. Am J Cardiol.

Using new dual-source CT systems, coronary stents can 1997;79:856–61.
11. Hamon M, Lepage O, Malagutti P, et al. Diagnostic performance of
be visualized with high diagnostic accuracy. In stents with 16- and 64-section spiral CT for coronary artery bypass graft
diameters of 3.0 mm or more, in-stent stenoses can be assessment: meta-analysis. Radiology. 2008;247:679–86.
ruled out with reasonably high certainty. Importantly, 12. Malagutti P, Nieman K, Meijboom WB, et al. Use of 64-slice CT in
strut thickness of the stents has an impact on image qual- symptomatic patients after coronary bypass surgery: evaluation of
grafts and coronary arteries. Eur Heart J. 2007;28:1879–85.
ity. Stents with a small strut thickness are better assess- 13. Pache G, Saueressig U, Frydrychowicz A, et al. Initial experience
able by CCTA than those with thicker struts. A new with 64-slice cardiac CT: non-invasive visualization of coronary
quality has been introduced by bioresorbable stents, artery bypass grafts. Eur Heart J. 2006;27:976–80.
whose materials are partly not visible in CCTA. Such 14. Dikkers R, Willems TP, Tio RA, Anthonio RL, Zijlstra F, Oudkerk
M. The benefit of 64-MDCT prior to invasive coronary angiography
stents can only be identified by distinct radio-opaque in symptomatic post-CABG patients. Int J Cardiovasc Imaging.
markers at the extreme ends of the stent. ICA remains the 2006;23:369–77.
gold-standard for the diagnosis of in-stent stenoses. For 15. Ropers D, Pohle FK, Kuettner A, et al. Diagnostic accuracy of non-
individual patients with prior implantation of relatively invasive coronary angiography in patients after bypass surgery
using 64-slice spiral computed tomography with 330-ms gantry
large coronary stents (≥3 mm), CCTA may offer an rotation. Circulation. 2006;114:2334–41.
attractive alternative. 16. Meyer TS, Martinoff S, Hadamitzky M, et al. Improved non-
invasive assessment of coronary artery bypass grafts with 64-slice
computed tomographic angiography in an unselected patient
population. J Am Coll Cardiol. 2007;49:946–50.
References 17. Jabara R, Chronos N, Klein L, et al. Comparison of multidetector
64-slice computed tomographic angiography to coronary
1. Riley RF, Don CW, Powell W, Maynard C, Dean LS. Trends in angiography to assess the patency of coronary artery bypass grafts.
coronary revascularization in the United States from 2001 to 2009. Am J Cardiol. 2007;99:1529–34.
Circ Cardiovasc Qual Outcomes. 2011;4:193–7. 18. Feuchtner GM, Schachner T, Bonatti J, et al. Diagnostic perfor-
2. Goldman S, Zadina K, Moritz T, VA Cooperative Study Group mance of 64-slice computed tomography in evaluation of coronary
#207/297/364, et al. Long-term patency of saphenous vein and left artery bypass grafts. AJR Am J Roentgenol. 2007;189:574–80.
internal mammary artery grafts after coronary artery bypass sur- 19. Nazeri I, Shahabi P, Tehrai M, Sharif-Kashani B, Nazeri A.
gery: results from a Department of Veterans Affairs Cooperative Assessment of patients after coronary artery bypass grafting using
Study. J Am Coll Cardiol. 2004;44:2149–56. 64-slice computed tomography. Am J Cardiol. 2009;103:
3. Schwartz L, Kip KE, Frye RL, Alderman EL, Schaff HV, Detre 667–73.
KM, Bypass Angioplasty Revascularization Investigation. 20. de Graaf FR, van Velzen JE, Witkowska AJ, et al. Diagnostic per-
Coronary bypass graft patency in patients with diabetes in the formance of 320-slice multidetector computed tomography coro-
Bypass Angioplasty Revascularization Investigation (BARI). nary angiography in patients after coronary artery bypass grafting.
Circulation. 2002;106:2652–8. Eur Radiol. 2011;21:2285–96.
4. Lytle BW, Loop FD, Cosgrove DM, Ratliff NB, Easley K, Taylor 21. Weustink AC, Nieman K, Pugliese F, et al. Diagnostic accuracy of
PC. Long-term (5 to 12 years) serial studies of internal mammary computed tomography angiography in patients after bypass
artery and saphenous vein coronary bypass grafts. J Thorac grafting: comparison with invasive coronary angiography. JACC
Cardiovasc Surg. 1985;89:248–58. Cardiovasc Imaging. 2009;2:816–24.
5. Shi Y, O’Brien Jr JE, Mannion JD, Morrison RC, Chung W, Fard A, 22. Mushtaq S, Andreini D, Pontone G, et al. Prognostic value of coro-
Zalewski A. Remodeling of autologous saphenous vein grafts. The nary CTA in coronary bypass patients: a long-term follow-up study.
role of perivascular myofibroblasts. Circulation. 1997;95: JACC Cardiovasc Imaging. 2014;7:580–9.
2684–93. 23. Desbiolles L, Leschka S, Plass A, et al. Evaluation of temporal win-
6. Fitzgibbon GM, Kafka HP, Leach AJ, Keon WJ, Hooper GD, dows for coronary artery bypass graft imaging with 64-slice
Burton JR. Coronary bypass graft fate and patient outcome: CT. Eur Radiol. 2007;17:2819–28.
angiographic follow-up of 5,065 grafts related to survival and 24. Lee SK, Jung JI, Ko JM, Lee HG. Image quality and radiation expo-
reoperation in 1,388 patients during 25 years. J Am Coll Cardiol. sure of coronary CT angiography in patients after coronary artery
1996;28:616–26. bypass graft surgery: influence of imaging direction with 64-slice
7. Berger A, MacCarthy PA, Siebert U, Carlier S, Wijns W, Heyndrickx dual-source CT. J Cardiovasc Comput Tomogr. 2014;8:124–30.
G, Bartunek J, Vanermen H, De Bruyne B. Long-term patency of 25. Trikalinos TA, Alsheikh-Ali AA, Tatsioni A, Nallamothu BK, Kent
internal mammary artery bypass grafts. Relationship with DM. Percutaneous coronary interventions for non-acute coronary
preoperative severity of the native coronary artery stenosis. artery disease: a quantitative 20-year synopsis and a network meta-
Circulation. 2004;110(suppl II):II-36–40. analysis. Lancet. 2009;373:911–8.
8. Brundage BH, Lipton MJ, Herfkens RJ, Berninger WH, Redington 26. Cassese S, Byrne RA, Tada T, et al. Incidence and predictors of
RW, Chatterjee K, Carlsson E. Detection of patent coronary bypass restenosis after coronary stenting in 10 004 patients with surveil-
grafts by computed tomography. A preliminary report. Circulation. lance angiography. Heart. 2014;100:153–9.
1980;61:826–31. 27. Schmermund A, Haude M, Baumgart D, Görge G, Grönemeyer D,
9. Daniel WG, Dohring W, Stender HS, Lichtlen PR. Value and limita- Seibel R, Sehnert C, Erbel R. Non-invasive assessment of coronary
tions of computed tomography in assessing aortocoronary bypass Palmaz-Schatz stents with contrast enhanced electron beam
graft patency. Circulation. 1983;67:983–7. computed tomography. Eur Heart J. 1996;17:1546–53.
10. Achenbach S, Moshage W, Ropers D, Nossen J, Bachmann 28. Möhlenkamp S, Pump H, Baumgart D, Haude M, Gronemeyer DH,
K. Noninvasive, three-dimensional visualization of coronary artery Seibel RM, Schwartz RS, Erbel R. Minimally invasive evaluation
of coronary stents with electron beam computed tomography: In
10 Coronary CT Angiography After Revascularization 187

vivo and in vitro experience. Catheter Cardiovasc Interv. 40. Zhang J, Li M, Lu Z, Hang J, Pan J, Sun L. In vivo evaluation of
1999;48:39–47. stent patency by 64-slice multidetector CT coronary angiography:
29. Pump H, Möhlenkamp S, Sehnert CA, Schimpf SS, Schmidt A, shall we do it or not? Int J Cardiovasc Imaging. 2012;28:651–8.
Erbel R, Gronemeyer DH, Seibel RM. Coronary arterial stent 41. Roura G, Gomez-Lara J, Ferreiro JL, et al. Multislice CT for assess-
patency: assessment with electron-beam CT. Radiology. ing in-stent dimensions after left main coronary artery stenting: a
2000;214:447–52. comparison with three dimensional intravascular ultrasound. Heart.
30. Maintz D, Juergens KU, Wichter T, Grude M, Heindel W, Fischbach 2013;99:1106–12.
R. Imaging of coronary artery stents using multislice computed 42. Sun Z, Almutairi AM. Diagnostic accuracy of 64 multislice CT
tomography: in vitro evaluation. Eur Radiol. 2003;13:830–5. angiography in the assessment of coronary in-stent restenosis: a
31. Mahnken AH, Buecker A, Wildberger JE, Ruebben A, Stanzel S, meta-analysis. Eur J Radiol. 2010;73:266–73.
Vogt F, Günther RW, Blindt R. Coronary artery stents in multislice 43. Rief M, Zimmermann E, Stenzel F, et al. Computed tomography
computed tomography: in vitro artifact evaluation. Invest Radiol. angiography and myocardial computed tomography perfusion in
2004;39:27–33. patients with coronary stents: prospective intraindividual compari-
32. Schlosser T, Scheuermann T, Ulzheimer S, et al. In-vitro evaluation son with conventional coronary angiography. J Am Coll Cardiol.
of coronary stents and 64-detector-row computed tomography 2013;62:1476–85.
using a newly developed model of coronary artery stenosis. Acta 44. Onuma Y, Dudek D, Thuesen L, et al. Five-year clinical and func-
Radiol. 2008;49:56–64. tional multislice computed tomography angiographic results after
33. Schlosser T, Scheuermann T, Ulzheimer S, et al. In vitro evaluation coronary implantation of the fully resorbable polymeric everoli-
of coronary stents and in-stent stenosis using a dynamic cardiac mus-eluting scaffold in patients with de novo coronary artery dis-
phantom and a 64-detector row CT scanner. Clin Res Cardiol. ease: the ABSORB cohort A trial. JACC Cardiovasc Interv.
2007;96:883–90. 2013;6:999–1009.
34. Gassenmaier T, Petri N, Allmendinger T, et al. Next generation 45. Ebersberger U, Tricarico F, Schoepf UJ, et al. CT evaluation of
coronary CT angiography: in vitro evaluation of 27 coronary stents. coronary artery stents with iterative image reconstruction: improve-
Eur Radiol. 2014;24:2953–61. ments in image quality and potential for radiation dose reduction.
35. Rixe J, Achenbach S, Ropers D, et al. Assessment of coronary Eur Radiol. 2013;23:125–32.
artery stent restenosis by 64-slice multi-detector computed tomog- 46. Eisentopf J, Achenbach S, Ulzheimer S, Layritz C, Wuest W, May
raphy. Eur Heart J. 2006;27:2567–72. M, Lell M, Ropers D, Klinghammer L, Daniel WG, Pflederer
36. Ehara M, Kawai M, Surmely JF, et al. Diagnostic accuracy of coro- T. Low-dose dual-source CT angiography with iterative reconstruc-
nary in-stent restenosis using 64-slice computed tomography: com- tion for coronary artery stent evaluation. JACC Cardiovasc Imaging.
parison with invasive coronary angiography. J Am Coll Cardiol. 2013;6:458–65.
2007;49:951–9. 47. Oda S, Utsunomiya D, Funama Y, et al. Improved coronary in-stent
37. Pugliese F, Weustink AC, Van Mieghem C, et al. Dual source coro- visualization using a combined high-resolution kernel and a hybrid
nary computed tomography angiography for detecting in-stent iterative reconstruction technique at 256-slice cardiac CT-Pilot
restenosis. Heart. 2008;94(7):848–54. study. Eur J Radiol. 2013;82:288–95.
38. Andreini D, Pontone G, Bartorelli AL, et al. Comparison of feasi- 48. Zhou Q, Jiang B, Dong F, et al. Computed tomography coronary
bility and diagnostic accuracy of 64-slice multidetector computed stent imaging with iterative reconstruction: a trade-off study
tomographic coronary angiography versus invasive coronary angi- between medium kernel and sharp kernel. J Comput Assist Tomogr.
ography versus intravascular ultrasound for evaluation of in-stent 2014;38:604–12.
restenosis. Am J Cardiol. 2009;103:1349–58. 49. Xia Y, Junjie Y, Ying Z, et al. Accuracy of 128-slice dual-source CT
39. Kubo T, Matsuo Y, Ino Y, et al. Diagnostic accuracy of CT angiog- using high-pitch spiral mode for the assessment of coronary stents:
raphy to assess coronary stent thrombosis as determined by intra- first in vivo experience. Eur J Radiol. 2013;82:617–22.
vascular OCT. JACC Cardiovasc Imaging. 2011;4:1040–3.
 Part III
CT Angiography Assessment for Cardiac Pathology
 Assessment of Cardiac Structure
and Function by Computed 11
Tomography Angiography

John A. Rumberger

Abstract
High-resolution multi-detector CT (MDCT) scanners capable of quantitative imaging of the
heart were introduced around 2002. Initially 16-slice scanners were validated but the cur-
rent state of the art is 64+-slice scanners. This chapter discusses the use of 64+-slice MDCT
for quantitative assessment of cardiac structure and function.

Keywords
Left ventricle • Systolic function • Diastolic function • MDCT • Cardiac CT

Current State of the Art for those familiar with two-dimensional echocardiography,
these correspond to the short axis, apical four-chamber, and
CT has traditionally oriented and displayed images parallel apical two-chamber views, respectively. These cardiac imag-
or at 90° angles to the long axis of the body (i.e., transaxial, ing planes are oriented at 90°angles relative to each other
coronal, and sagittal image planes). Such presentations ori- [i.e. 3-orthogonal planes].
ented about the long axis of the body do not satisfy prior In order to employ CT to define the cardiac chambers
established presentations of cardiac images as they do not and separate them from the surrounding myocardium, it is
cleanly transect the ventricles, atria, or myocardial regions as necessary to use intravenous contrast. In general, this can
supplied by the major coronary arteries. be accomplished with <100 mL of non-ionic contrast, and
Knowledge of cardiac ejection fractions [1], absolute ven- it is possible to perform complete imaging of the heart
tricular volumes [2, 3], and location and extent of regional chambers, the coronary arteries, and the proximal great
wall motion abnormalities provides valuable diagnostic and vessels (aorta and pulmonary artery) in a single setting with
prognostic information, and non-invasive cardiac imaging a single injection of contrast. Methods for contrast admin-
has become the reference standard in routine clinical istration for MDCT scanning of the heart are found
practice. elsewhere.
The American Heart Association in 2002 [4] published Orthogonal (short and various long axes) cardiac CT
standards of myocardial segmentation and nomenclature for images after intravenous contrast allow for identification of
tomographic imaging of the heart using non-invasive imag- non-opacified intracardiac thrombi (Fig. 11.2a) and tumors
ing modalities and divided the left ventricle (LV) into 17 seg- (Fig. 11.2b) including excellent resolution of the left atrium
ments. The nomenclature for image presentation for cardiac and the left atrial appendage (Fig. 11.3), allowing localiza-
CT is: the short axis, horizontal long axis, and vertical long tion of structures smaller than 1 mm [5, 6]. Cardiac CT can
axis, as shown in Fig. 11.1. These cardiac axes are very additionally be of assistance in defining thrombi or occult
familiar to practitioners performing SPECT or PET imaging; occlusion of the venae cavae and other right-sided structures.
Cardiac CT can also be a primary method of defining intra-
J.A. Rumberger, PhD, MD cardiac shunts such as those caused by inter-ventricular
Cardiac Imaging, The Princeton Longevity Center, (Fig. 11.4a) and inter-atrial (Fig. 11.4b) congenital defects
Forestall Village, 136 Main Street, Princeton, NJ 08540, USA and other acquired defects post-infarction [7].
e-mail: [email protected]

© Springer International Publishing 2016 191

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_11
192 J.A. Rumberger

Fig. 11.1 Standardized presentation of the heart in cardiac vertical long axis, and the short axis (Reprinted from Cerqueira et al.
CT. American Heart Association 17 segment model of the left ventricle [4], with permission of Wolters Kluwer Health, Copyright 2002,
(LV); the orthogonal imaging planes are the horizontal long axis, the American Heart Association, Inc.)

Cardiac CT can be used to quantitate left and right ven- of the results. Table 11.1 shows validated norms for LV
tricular volumes [8–10], left and right atrial volumes, left and chamber size, wall thicknesses, ejection fraction, and
right ventricular muscle mass [11–14], regional left ventricu- ventricular volumes using cardiac CT. Reproducibility of CT
lar function, wall thickening and contractility [15–17], rates in performing right and left ventricular volume and function
of diastolic filling of the right and left ventricles [16, 18, 19], measurements has also been established [34, 35].
post-infarction left and right ventricular remodeling [20–24], Cardiac CT imaging using thin sections allows post-
cardiac remodeling following cardiac [25] and lung trans- processing of images into end-diastolic and end-systolic
plantation [26], and ejection fraction [27–30] in patients with short and “long” axis images at multiple ECG-phases to
no contraindication to the use of iodinated contrast medium. facilitate identification of structures and salient features of
Additional applications include quantitation of uni-valvular the ventricular anatomy (Fig. 11.6). Using short and long
regurgitation [31] and assessment of infarct size [32, 33]. axis imaging also allows identification of infarct locations
The majority of these validation studies was performed in (Fig. 11.7). Demonstrated in this latter example is a common
the 1980s and 1990s using EBT and has been adapted and/or CT finding in contrast-enhanced images from patients with
re-validated in studies using MDCT. In most instances, these remote myocardial infarction. The “negative” contrast noted
quantitative aspects can be performed or at least well- in Fig. 11.7 is actually due to lack of contrast opacification in
approximated in patients with generally normal sinus the infarcted region causing “contrast rarefaction.” Long axis
rhythm. Since the number of cardiac cycles imaged per scan (both vertical and horizontal) imaging of the left ventricle
is single (256- and 320-slice scanners) or generally limited to also allows for definition of basilar and apical infarcts, and
<5 (64-slice scanners), quantitation may be limited in those true- and pseudo-apical aneurysms (Fig. 11.8). Two-
patients with significant dysrhythmias, such as non-regular dimensional and three-dimensional reconstruction methods,
atrial fibrillation. possible in nearly an infinite number of imaging planes, also
All available post-processing workstations can provide allows for postoperative assessment of left ventricular
quantitative and often non-interactive (i.e., automatic) aneurysectomy (Fig. 11.9). Global and regional details of the
measurements of the LV in particular. Shown in Fig. 11.5a–e, LV due to ischemic cardiomyopathy and hypertrophic
is the general outline of the procedure and subsequent display cardiomyopathy using cardiac CT provide details commonly
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 193

Fig. 11.2 Examples of non-opacified cardiac thrombus and tumor. (a) non-opacified area in the LA chamber is a left atrial myxoma shown at
Modified vertical long axis tomogram of the left ventricle (LV); the area end-systole and end-diastole: note that, during diastole, the myxoma
noted by the arrow is a non-opacified thrombus at the LV apex. (b) prolapses through the mitral valve
Modified horizontal long axis image of the left atrium (LA)/LV; the

noted by other imaging methods. The right ventricle (RV) Three-dimensional calipers available on all CT worksta-
can also be imaged. Figure 11.10 shows a dilated RV in a tions allow for quantitative measures of ventricular dimen-
patient with arrhythmogenic RV dysplasia, and Fig. 11.11 sions in any axis (Fig. 11.14a). Additionally, measures of
shows fatty infiltration of the RV; cardiac CT can often be an ventricular muscle thicknesses can be done on all myocardial
alternative or a confirmatory method to MRI in the evaluation walls (Fig. 11.14b). Measures of the aorta and other chambers
of such patients [36]. Biventricular consequences to such as the left atrium (Fig. 11.14c) can also be helpful and
congenital (Fig. 11.12) and acquired heart disorders augment data on ventricular volumes, muscle mass, and func-
(Fig. 11.13) can also be imaged. tion by CT. Normal layers of fat on the epicardial surface of
194 J.A. Rumberger

Normal LA appandage LA appandage thrombus

Fig. 11.3 Definition of the left atrial appendage by cardiac CT. Left: a normal LA (left atrial) appendage (dotted circle). Right: LA appendage
with thrombus (dotted circle)

a
Membranous VSD

Ostium secundum ASD

Fig. 11.4 Examples of congenital intra-cardiac shunts as shown by cardiac CT. (a) “Peri” membranous ventricular septal defect (VSD) as noted
by the arrow. (b) Jet of contrast demonstrating a left to right shunt from an ostium secundum atrial septal defect (ASD) as noted by the arrow
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 195

Fig. 11.5 Quantitation of LV (left ventricular) function by cardiac CT. LV muscle mass and myocardial wall thicknesses can be determined.
(a) Horizontal long axis, vertical long axis, and short axis views of the (d) Lower right of the figure: a color map of the myocardial surface
left ventricle (LV); the line demonstrates the plane of the mitral valve: systolic function is defined to provide definition of regional LV function.
when performing quantitative analysis, it is necessary that the LV (e) LV chamber volume as a function of time during the cardiac cycle;
chamber be isolated. (b) Semi-quantitative edge definition of the from these data can be derived information on EF (ejection fraction),
cardiac endocardial surfaces using thresholding methods; from this EDV (end-diastolic volume), EDV (end-systolic volume), SV (stroke
information, the LV endocardial (chamber) volumes can be determined. volume), rates of systolic emptying (contractility), as well as rates of
(c) Semi-quantitative isolation of the LV myocardial epicardial and early and late diastolic filling (diastolic function)
septal surfaces using thresholding methods; from this information the
196 J.A. Rumberger

Fig. 11.5 (continued)

11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 197

Fig. 11.5 (continued)

198 J.A. Rumberger

Fig. 11.5 (continued)

11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 199

e for assessment of coronary plaque and lumen anatomy.

However, quantitation of cardiac function using MDCT can
120
only practically be performed using retrospective
ECG-gating.
Prospective ECG-gating protocols provide static images
100
of the heart and the coronary arteries and are appropriate if
the indication for performing 64 + -slice MDCT is solely
80
assessment of coronary artery anatomy. Prospectively gated
Volume (ml)

MDCT can also provide general information about cardiac

60
chamber sizes, general cardiac anatomy, and some evalua-
tions of the pericardium, but cannot be used to quantitate LV
40 and RV systolic or diastolic function. In such instances, if LV
function is also desired for overall clinical assessment, then
20 alternative methods are widely available such a gated SPECT,
MRI, and two-dimensional echocardiography. Although
MRI and ultrasound provide no ionizing radiation exposure,
0 10 20 30 40 50 60 70 80 90 100 SPECT imaging can result in radiation exposures up to 3–5
% R–R
times that of cardiac CT.
Utilization of prospective ECG gating can significantly
Fig. 11.5 (continued) reduce the effective radiation dose to the patient using
MDCT; however, if quantitation of LV function is also
the heart and the outer surface of the pericardial sac provide required, a retrospective gated cardiac CT can be performed
natural contrast and permit the examiner to reliably identify with limited radiation by lowering the kV from 120–100
the pericardium (Fig. 11.15). Contrast-enhanced CT often [and now even 80] and application of ECG-dose (mA)
allows separating chronic effusive pericarditis from gross peri- modulation. A properly planned retrospective 64 + slice
cardial thickening since the parietal and epicardial layers of cardiac CT can be performed with effective patient radiation
the pericardium have their own blood supply. CT can be used doses of 2–6 mSv versus a prospectively gated MDCT scan,
to define the entire anatomy of the pericardium and may be of which can be done generally with effective radiation doses of
greatest value in localization of loculated effusions such as 1–3 mSv (or slightly higher using 256-slice and 320-slice
those confined to the posterior areas of the heart (which are scanners).
difficult to define using surface two-dimensional echocardiog-
raphy). Tamponade can be identified with CT by right atrial or
ventricular collapse or by indirect signs such as an inappropri- Contraindications
ately enlarged inferior vena cava or enlarged hepatic veins.
High-resolution images can define the anatomic localization The contraindications to performing a retrospectively gated
and extent of pericardial thickening. In the evaluation of a MDCT for assessment of cardiac structure and function are
patient for constrictive pericarditis, CT can add considerably the same as those for performing any cardiac CT examina-
to the diagnosis. CT has an advantage over traditional echocar- tion. Beta-blockers are almost universally applied to get rest-
diography in that the entire cardiac volume is imaged very ing heart rates in the range of 60 beats/min. Individuals with
quickly, and then images of both two-dimensional and three- reactive airways disease (e.g., emphysema, asthma) should
dimensional views can be rapidly generated. Contrast is usu- only be given beta-blockers under controlled conditions.
ally not required to image the pericardium, as the natural Intravenous contrast is also required, thus reduced renal func-
delineation of the pericardial surface (usually 100 Hounsfield tion (e.g., creatinine >1.9 mg/dl) might suggest that an alter-
Units, HU) and adjacent air (<-700 HU) is dramatic. Calcified native method of evaluating the LV/RV should be considered,
pericardial tissue is even easier to image, as the calcification is but there is no absolute contraindication for MDCT cardiac
usually in the +300−400 HU range. imaging in the presence of abnormal renal function.
Issues of radiation exposure of the patient during diagnos-
tic cardiac CT examinations and have been bandied about in
Indications the press for some time; it is of course important that this
potential hazard be considered and risk versus benefit defined
The mandate for a complete cardiac CT angiogram (CCTA) by the referring physician. But the American Association of
in routine clinical practice is to include quantitative cardiac Physicists in Medicine [AAPM] issued the following state-
structure and function as part of each evaluation performed ment in 12/11 [37]:
200 J.A. Rumberger

Table 11.1 Reference values for left ventricular size, function, and muscle mass for cardiac CT in adult women and mena
Women Men
Reference Mildly Moderately Severely Reference Mildly Moderately Severely
Measurement range abnormal abnormal abnormal range abnormal abnormal abnormal
Septal wall 6–9 10–12 13–15 >16 6–10 11–13 14–16 >17
thickness (mm)a
Posterior wall 6–9 10–12 13–15 >16 6–10 11–13 14–16 >17
thickness (mm)a
LV muscle mass 66–155 156–176 177–187 >190 96–200 201–227 228–254 >260
(gm)
LV diameter 39–53 54–57 58–61 >62 42–59 60–63 64–68 >69
(mm)a
LV global EDV 60–110 111–122 123–136 >140 70–160 161–190 191–210 >210
(ml)
LV global ESV 20–50 51–60 61–70 >71 25–60 61–70 71–85 >86
(ml)
LV global EF >55 45–54 30–44 <30 >55 45–54 30–44 <30
(%)
Data from Rumberger et al. [32]; and Lang et al. [35]
EDV end-diastolic volume, ESV end-systolic volume, EF ejection fraction
a
End-diastole, mid left ventricle

Fig. 11.6 Example of LV (left ventricle) short axis images from the (end D) during a 10-phase ECG gated reconstruction of cardiac func-
apex to base of the heart and various ECG related phases defined from tion using Cardiac CT
end-diastole (End D) to end-systole (ES) and back to end-diastole
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 201

Fig. 11.7 Vertical long axis and mid-LV short axis images of a patient of transmural infarction in the inferior septum, inferior (posterior) wall,
with remote myocardial infarction. Left: vertical long axis; the arrows and lateral wall; using such presentations, estimates of myocardial
point to regions of transmural infarction in the lower septal wall, apex, infarction size can be estimated
and lateral wall. Right: mid-LV short axis; the arrows point to regions

a b

Fig. 11.8 Examples of left ventricular (LV) true aneurysm and long axis image of LV demonstrating dilation of LV apex and thinning
“pseudo” aneurysm using Cardiac CT. (a) End-systolic long axis image of myocardial with akinetic regional motion and “pseudo” aneurysm
of LV demonstrating LV apical aneurysm (arrow); (b) End-diastolic (arrows)
202 J.A. Rumberger

a b

Fig. 11.9 Cardiac CT images of patient after left ventricular (LV) arrows. (c) A maximum intensity projection (2-dimensional) of the LV
aneurysmectomy. (a, b) Volume rendering presentation from lateral and long axis showing the area of aneurysm repair: the two bright objects at
anterior views of the LV: the area of aneurysm repair is shown by the the LV apex are surgical pledgets

The American Association of Physicists in Medicine (AAPM) doses are highly speculative and should be discouraged. These
acknowledges that medical imaging procedures should be predictions are harmful because they lead to sensationalistic
appropriate and conducted at the lowest radiation dose consis- articles in the public media that cause some patients and parents
tent with acquisition of the desired information. Discussion of to refuse medical imaging procedures, placing them at substan-
risks related to radiation dose from medical imaging procedures tial risk by not receiving the clinical benefits of the prescribed
should be accompanied by acknowledgement of the benefits of procedures.
the procedures. Risks of medical imaging at effective doses
below 50 mSv for single procedures or 100 mSv for multiple Patients unable to hold their breath for 15 s or who are
procedures over short time periods are too low to be detectable
uncooperative should be avoided for cardiac CT. The pres-
and may be nonexistent. Predictions of hypothetical cancer inci-
dence and deaths in patient populations exposed to such low ence of various dysrhythmias (frequent PACs/PVCs) can
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 203

Fig. 11.10 Short axis images of

the LV (right) and RV (right
ventricle, left) from an 18 year
old woman with syncope and
ARVD (arrhythmogenic RV
dysplasia). Note the enlargement
of the RV compared to the LV
and the presence of wide
trabeculations in the RV, both
major criteria for diagnosis of
ARVD

Fig. 11.11 Cardiac CT Images of two patients with ARVD (arrhythmogenic right ventricular dysplasia). The arrows demonstrate “fatty
infiltration” of the RV wall, a major diagnostic criteria for the diagnosis of ARVD
204 J.A. Rumberger

Fig. 11.12 Cardiac CT in a patient with “non-compaction” of the LV. LV chamber and the presence of deep “sinusoids” (fenestrations) of the
Left: Long axis showing dilation of the lower (apical) one-half of the LV chamber
LV chamber. Right: a mid-LV short axis demonstrating dilation of the

make quantitation of LV function with MDCT difficult, and appropriate CT reconstructed phase. Definition of end-
individuals with pacemakers should have the ventricular rate systole is more difficult. Although using a 10-phase retro-
set to 60 beats per minute. The presence of atrial fibrillation spective reconstruction usually assigns end-systole to the
is not a contraindication, but, with uncontrollable rapid ven- smallest chamber volume, recent data suggest that at least a
tricular response, will likely result in sub-optimal data. 15 phase reconstruction might be more appropriate for tim-
ing of this event [38]. The number of phases reconstructed
from a 64+-slice MDCT retrospectively ECG gated cardiac
Strengths CT is a choice made by the physician, and going from a
10-phase to a 20-phase reconstruction only results in more
A properly planned 64+slice, retrospectively ECG-gated, images to review for analysis and the subsequent increase in
MDCT examination can provide quantitative data on LV/RV file size and image storage requirements. Also, many of the
systolic (and diastolic function) both globally and region- available image processing workstations have a limit to the
ally. It can also provide quantitative data on chamber sizes, number of images that can be placed into active memory for
valve (both natural (Fig. 11.16) and prosthetic) valve motion review.
and cross-sectional areas, visualization of intra-cardiac
shunts, definition of cardiac tumors and thrombi, quantita-
tion of LV muscle mass, regional wall thicknesses and Comparison to Other Imaging Modalities
thickening, myocardial infarct size, and the gross physio-
logic consequences of pericardial effusions and pericardial EBT and by inference 64+slice MDCT has been validated
constriction. for assessment of cardiac function in comparison to SPECT
imaging, MRI, contrast-ventriculography, and two-
dimensional echo.
Limitations

Sub-optimal assessment of cardiac structures and function Future Directions

can occur due to cardiac dysrhythmias, inadequate heart rate
control during imaging, and poor chamber contrast timing/ The quantitation of cardiac structure and function by car-
administration. Definition of end-diastole is straight-forward diac CT has been evolving for more than 25 years.
by noting the timing of the R-wave on the ECG and the Improvements in cardiac edge-detection methods have
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 205

Fig. 11.13 Cardiac CT of a patient with severe pulmonary hyperten- dilation of the right ventricle (RV) and right atrium (RA)/left atrium; the
sion as a consequence to severe, chronic mitral valve regurgitation. The short (right) axis image demonstrates a common characteristic of pul-
horizontal (left) and vertical (middle) long axis images demonstrate the monary hypertension and a “D” shaped interventricular septum (IVS)

essentially eliminated the need to laboriously trace images thickening, regional wall motion, and LV volumes from
from each tomographic plane and apply a modified 64+-slice MDCT cardiac examinations. Semi-quantitative
Simpson’s (stack of coins) rule. All current workstations information on left/right atrial volume/dimensions and RV
allow for straight-forward information on EF, regional wall volume/dimensions are also in development.
206 J.A. Rumberger

Fig. 11.14 Measurement of cardiac and chamber dimensions in car- severe cardiac hypertrophy. (c) Representative measurements of the
diac CT. (a) Long axis and short axis dimensions of the left ventricular aortic root and left atrium as measured mimicking a para-sternal mea-
long axis and at mid ventricle short axis. (b) Measurements of septal, surement that might be done using two-dimensional echocardiography
apical, and lateral wall thicknesses at end-diastole in a patient with (direction indicated by arrow)
11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 207

Fig. 11.15 Evaluation of the pericardium by cardiac CT. (a) Left – the cardiac epicardial surface; this was performed by changing the CT
Concentric, densely calcified pericardium in a patient with constrictive display window and level settings on the image presented in b, top left;
pericarditis as a consequence to tuberculosis. Right – Images from a Bottom: a maximum intensity projection of the horizontal cardiac long
patient with pericardial tamponade from a concentric pericardial axis demonstrating the opacified cardiac chambers and the surrounding
effusion. (b) Top left – Volume rendered image demonstrating entire low intensity circumferential pericardial effusion
cardiac volume; Top right: Volume rendered image demonstrating only
208 J.A. Rumberger

Fig. 11.15 (continued)

11 Assessment of Cardiac Structure and Function by Computed Tomography Angiography 209

Fig. 11.16 Evaluation of cardiac valve stenosis using cardiac CT. (a) valve area in a patient with moderate mitral valve stenosis. (b)
LV long axis and short axis images demonstrating thickened mitral Representative orthogonal views of the aortic valve and measurement
valve leaflets (arrow) and dilated left atrium and measurement of mitral of aortic valve area in a patient with known mild aortic valve stenosis

References puted tomography for the detection of left atrial thrombi in patients
with atrial fibrillation. Heart. 2004;90(12):1477–8.
6. Meinel Jr JF, Wang G, Jiang M, Frei T, Vannier M, Hoffman
1. Hammermeister KE, DeRouen TA, Dodge HT. Variables predictive E. Spatial variation of resolution and noise in multi-detector row
of survival with coronary disease: selection by univariate and multi- spiral CT. Acad Radiol. 2003;10:607–10.
variate analyses from the clinical, electrocardiographic, exercise, 7. Paul JF, Macé L, Caussin C, Fsihi A, Berthaux X, Brenot P, et al.
arteriographic and quantitative angiographic evaluation. Multirow detector computed tomography assessment of intraseptal
Circulation. 1979;59:421–50. dissection and ventricular pseudo-aneurysm in postinfarction ven-
2. Norris RW, Barnaby PF, Brandt PWT. Prognosis after recovery tricular septal defect. Circulation. 2001;104:497–8.
from first acute myocardial infarction: determinant of reinfarction 8. Reiter SJ, Rumberger JA, Feiring AJ, Stanford W, Marcus
and sudden death. Am J Cardiol. 1984;53:408–13. ML. Precision of right and left ventricular stroke volume measure-
3. White HD, Norris RM, Brown MA, Brandt PWJ, Whitlock RML, ments by rapid acquisition cine computed tomography. Circulation.
Weld CJ. Left ventricular end-systolic volume as the major deter- 1986;74:890–900.
minant of survival after recovery from myocardial infarction. 9. Yamamuro M, Tadamura E, Kubo S, Toyoda H, Nishina T, Ohba M,
Circulation. 1987;76:44–51. et al. Cardiac functional analysis with multi-detector row CT and
4. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myo- segmental reconstruction algorithm: comparison with echocardiog-
cardial segmentation and nomenclature for tomographic imaging of raphy, SPECT, and MR imaging. Radiology. 2005;234:381–90.
the heart – a statement for healthcare professions from the Cardiac 10. Halliburton SS, Petersilka M, Schvartzman PR, Obuchowski N,
Imaging Committee of the Council on Clinical Cardiology of the White RD. Evaluation of left ventricular dysfunction using multi-
American Heart Association. Circulation. 2002;105:539–42. phasic reconstructions of coronary multi-slice computed tomogra-
5. Achenbach S, Sacher D, Ropers D, Pohle K, Nixdorff U, Hoffman phy data in patients with chronic ischemic heart disease: validation
U, Muschiol G, Flachskampf PA, Daniel WW. Electron beam com-
210 J.A. Rumberger

against cine magnetic resonance imaging. Int J Cardiovasc Imaging. 26. Rensing BJ, McDougall JC, Breen JR, Vigneswaran WT, McGregor
2003;19:73–83. CGA, Rumberger JA. Right and left ventricular remodeling after
11. Feiring AJ, Rumberger JA, Reiter SJ, Skorton DJ, Collins SM, orthotopic single lung transplantation for end-stage emphysema.
Lipton MJ, et al. Determination of left ventricular mass in the dog J Heart Lung Transplant. 1997;16:926–33.
with rapid acquisition cardiac CT scanning. Circulation. 27. Gerber T, Rumberger JA, Gibbons R, Behrenbeck T. Measurement
1985;72:1355–62. of left ventricular ejection fraction by TC-99 M sestamibi first-pass
12. Hajduczok Z, Weiss RM, Marcus ML, Stanford W. Determination angiography in patients with myocardial infarction: comparison
of right ventricular mass in humans and dogs with ultrafast com- with electron beam computed tomography. Am J Cardiol.
puted tomography. Circulation. 1990;82:202. 1999;83:1022–6.
13. Kuroda T, Seward JB, Rumberger JA, Yanagi H, Tajik AJ. Left ven- 28. Schuijf JD, Bax JJ, Jukema JW, Lamb HJ, Vliegen HW, Salm LP,
tricular volume and mass: comparative study of 2-dimensional et al. Noninvasive angiography and assessment of left ventricular
echocardiography and ultrafast computed tomography. function using multislice computed tomography in patients with
Echocardiography. 1994;11:1–9. type 2 diabetes. Diabetes Care. 2004;27:2905–10.
14. Rumberger JA. Quantifying left ventricular regional and global sys- 29. Dirksen MS, Bax JJ, de Roos A, Jukema JW, van der Geest RJ,
tolic function using ultrafast computed tomography. Am J Card Geleijns K, et al. Usefulness of dynamic multislice computed
Imaging. 1991;5(1):29–37. tomography of left ventricular function in unstable angina pectoris
15. Feiring AJ, Rumberger JA, Reiter SJ, Collins SM, Skorton DJ, Rees and comparison with echocardiography. Am J Cardiol.
M, et al. Sectional and segmental variability of left ventricular func- 2002;90:1157–60.
tion: experimental and clinical studies using ultrafast computed 30. Rumberger JA, Sheedy PF, Breen JF. Use of ultrafast (cine) x-ray of
tomography. J Am Coll Cardiol. 1988;12:415. right and left ventricular volume measurements by electron-beam
16. Lanzer P, Garrett J, Lipton MJ, Gould R, Sievers R, O’Connell W, computed tomography in cardiac and cardiovascular imaging. In:
et al. Quantitation of regional myocardial function by cine com- Guiliani ER, Gersh BJ, McGoon MD, Dayes DL, Shaff HF, editors.
puted tomography: pharmacologic changes in wall thickness. J Am Mayo clinic practice of cardiology. 3rd ed. St. Louis: Mosby; 1996.
Coll Cardiol. 1986;8:682. p. 303–24.
17. Feiring AJ, Rumberger JA. Ultrafast computed tomography analy- 31. Rumberger JA, Reed JE. Quantitative dynamics of left ventricular
sis of regional radius-to-wall thickness ratios in normal and vol- emptying and filling as a function of heart size and stroke volume in
ume-overloaded human left ventricle. Circulation. 1992;85: pure aortic regurgitation and in normal subjects. Am J Cardiol.
1423–32. 1992;70:1045–50.
18. Rumberger JA, Weiss RM, Feiring AJ, Stanford W, Hajduczok ZD, 32. Weiss RM, Stark CA, Rumberger JA, Marcus ML. Identification
Rezai K, et al. Patterns of regional diastolic function in the normal and quantitation of myocardial infarction or risk area size with
human left ventricle: an ultrafast-CT study. J Am Coll Cardiol. cine-computed tomography. Am J Card Imaging. 1990;4:33–7.
1989;13:119–25. 33. Schmermund A, Gerber T, Behrenbeck T, Reed JE, Sheedy PF,
19. Lipton MJ, Rumberger JA. The assessment of left ventricular sys- Christian TF, et al. Myocardial infarct size by electron beam com-
tolic and diastolic function by ultrafast computed tomography. Am puted tomography: a comparison with 99mTc sestamibi. Invest
J Card Imaging. 1991;5:318–27. Radiol. 1998;33:313–21.
20. Rumberger JA, Behrenbeck T, Breen JR, Reed JE, Gersh BJ. Non- 34. Schmermund A, Breen JF, Sheedy PF, Rumberger
parallel changes in global chamber volume and muscle mass during JA. Reproducibility of right and left ventricular volume measure-
the first year following transmural myocardial infarction in man. ment by electron-beam CT in patients with congestive heart failure.
J Am Coll Cardiol. 1993;21:673–82. Int J Card Imaging. 1998;14(3):201–9.
21. Hirose K, Reed JE, Rumberger JA. Serial changes in left and right 35. Lang RM, et al. Recommendations for chamber quantification: a
ventricular systolic and diastolic mechanics during the first year report from the American Society of Echocardiography’s
after an initial left ventricular Q-wave myocardial infarction. J Am Guidelines and Standards Committee and the Chamber
Coll Cardiol. 1995;25:1097–104. Quantification Writing Group, Developed in Conjunction with the
22. Hirose K, Shu NH, Reed JE, Rumberger JA. Right ventricular dila- European Association of Echocardiography, A Branch of the
tation and remodeling the first year after an initial transmural wall Europena Society of Cardiology. J Am Soc Echocardiogr.
myocardial infarction. Am J Cardiol. 1993;72:1126. 2005;18:1440–63.
23. Chareonthaitawee P, Christian TF, Hirose K, Gibbons RJA. Relation 36. Soh EK, villines TC, Feuerstein IM. Sixty-four-multislice com-
of initial infarct size with the extent of left ventricular remodeling puted tomography in a patient with arrhythmogenic right ventricu-
in the year after acute myocardial infarction. J Am Coll Cardiol. lar dysplasia. J Cardiovasc Comput Tomogr. 2008;2:191–2.
1995;25:567–73. 37. Policy number: PP25-A: AAPM position statement on radiations
24. Sehgal M, Hirose K, Reed JE, Rumberger JA. Regional left ven- risks from medical imaging procedures. Policy Date 12/13/11;
tricular systolic thickening and thicknesses during the first year Sunset Date 12/31/16. http://www.aapm.org/org/policies/details.
after initial Q-wave myocardial infarction: serial effects of ventric- asp?id=318&type=PP&current=true.
ular remodeling. Int J Cardiol. 1996;53:45–54. 38. Bardo DME, Kachenoura N, Newby B, Lang RM, Mor-Avi
25. Vigneswaran WT, Rumberger JA, Rodeheffer RJ, Breen JF, V. Multidetector computed tomography evaluation of left ventricu-
McGregor CGA. Ventricular remodeling following orthotopic car- lar volumes: sources of error and guidelines for their minimization.
diac trans-plantation. Mayo Clin Proc. 1996;71:735–42. J Cardiovasc Comput Tomogr. 2008;2:222–30.
 Cardiovascular CT for Perfusion
and Delayed Contrast Enhancement 12
Imaging

Ravi K. Sharma, Ilan Gottlieb, and João A.C. Lima

Abstract
Recent advancements in multi-detector computed tomography (MDCT) imaging have dem-
onstrated the ability of MDCT to be a comprehensive imaging modality, which in a single
scan setting could provide a wide array of complementary information. Advent of MDCT
system with faster scan acquisition of entire myocardial volume has allowed assessment of
stress myocardial perfusion that has shown to provide incremental diagnostic accuracy over
coronary CT angiography (CTA) in assessing hemodynamically significant stenosis.
Detection of fibrosis by Delayed Enhanced MDCT (DE-MDCT) has been validated
against gold standards such as histology and contrast enhanced MRI. DE-MDCT can accu-
rately identify and characterize morphological features of acute and healed myocardial
infarction, including infarct size, transmurality, and the presence of microvascular obstruc-
tion and collagenous scar. In addition, recent studies have also substantiated the utility of
contrast enhanced MDCT in assessment of extracellular volume fraction (ECV) which cor-
responds to diffuse myocardial fibrosis. This has allowed comprehensive evaluation of
myocardial tissue characteristics with significant bearing on the management, prognosis
and follow-up of a myocardial disease process.

Keywords
Computed tomography perfusion • Stress CT perfusion • Delayed enhanced MDCT
• MDCT myocardial viability • Myocardial fibrosis

Electronic supplementary material The online version of this chap- Abbreviations

ter (doi:10.1007/978-3-319-28219-0_12) contains supplementary
material, which is available to authorized users.
CAD Coronary Artery Disease
R.K. Sharma, MD • J.A.C. Lima, MD (*) CTA Coronary CT Angiography
Division of Cardiology, Johns Hopkins Hospital, DE-MDCT Delayed enhanced MDCT
Blalock 524D, 600 N. Wolfe St, Baltimore, MD 21287, USA ECV Extracellular Volume Fraction
e-mail: [email protected]; [email protected]
LAD Left Anterior Descending
I. Gottlieb, MD Msc, PhD LV Left Ventricle
Casa de Saúde São José – Radiologia,
R. Macedo Sobrinho, 21 – Humaitá, Rio de Janeiro,
MDCT Multi-Detector Computed Tomography
RJ 22271-080, Brazil MRI Magnetic Resonance Imaging
e-mail: [email protected] PET Positron Emission Tomography
SPECT Single Photon Emission Computed Tomography

© Springer International Publishing 2016 211

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_12
212 R.K. Sharma et al.

Subject Overview perfusion assessment had to wait until spiral CT technology

progressed sufficiently to enable the acquisition of 64 slices
A 54 year old male with diabetes and family history of coro- simultaneously [2]. Advent of wide array single source (256
nary artery disease (CAD) comes to a cardiologist for the or 320) and dual source detector scanning system with faster
first time for atypical chest pain. The patient reports “having gantry rotation time has allowed rapid acquisition of entire
to grasp for air” while in chest pain. A rest electrocardio- cardiac volume with low radiation exposure, making MDCT
gram (ECG) is done at the office, in which non-specific T perfusion imaging more feasible and safe to perform.
wave changes were the only abnormality. Besides blood Currently, the greatest limitations to CT coronary angiog-
tests, the cardiologist orders an echocardiogram that shows raphy are the presence of severely calcified coronary seg-
reduced left ventricle (LV) function and akinesis of the mid ments, stents, or other artifacts that limit luminal visualization.
and apical anterior-septal walls and a stress single photon Patients with calcified arteries tend to be older and/or have
emission computed tomography (SPECT) study that shows advanced CAD. Their studies are challenging from a diagnos-
a perfusion defect in the same regions, with little reversibil- tic viewpoint because vulnerable plaques and stenotic lesions
ity on the rest images. Thinking this is most likely ischemic may be hidden underneath large amounts of calcium accumu-
coronary disease, the cardiologist orders a cardiac magnetic lated in the atherosclerotic plaques encompassing one or
resonance imaging (MRI) for viability evaluation prior to more segments. While progress in multidetector technology
the invasive coronary angiography, which showed an has improved our ability to study such patients, greater cover-
occluded mid left anterior descending (LAD) artery with age and improved temporal resolution are unlikely to elimi-
distal filling via collaterals. Given the presence of viability nate the problem, which is in large part intrinsic to the
on the MRI scan, the patient successfully underwent percu- pathogenesis of atherosclerosis, namely, plaques grow out-
taneous coronary intervention of the mid-LAD lesion and wardly first and tend to accumulate calcium as part of the
two months later LV function shows improvement and the healing process, therefore creating a natural shield to X-ray
patient is asymptomatic. penetration. That is a particular limitation to the study of
Cardiologists are familiar with relying on a number of dif- older persons, patients with advanced CAD, and patients who
ferent imaging modalities for a thorough assessment of car- underwent coronary artery bypass graft surgery or multiple
diovascular diseases and further decision making. Coronary stent implantation, as well as patients with diseases such as
anatomy evaluation is usually performed using invasive cath- chronic renal failure that accelerate plaque calcification.
eterization or more recently by non-invasive MDCT scans. Furthermore, coronary anatomic information is much
Global and regional myocardial function as well as structural more valuable when combined with a functional test, since
abnormalities can be assessed with echocardiography, MRI some decisions regarding treatment are based on the detec-
and MDCT. Subclinical atherosclerosis is usually assessed tion of myocardial ischemia [3]. Corresponding perfusion
via detection of coronary calcium using MDCT or electron deficit related to an anatomic stenosis also confers worse
beam CT scanners or via measuring carotid intima-media clinical prognosis [4]. The poor correlation between ana-
thickness with ultrasound; while ischemia detection and tomic modalities such as invasive coronary angiography [5,
quantification at stress are usually performed with nuclear 6] and MDCT [7] with stress perfusion tests underscores the
SPECT or positron emission tomography (PET), echo or fact that one cannot substitute for the other.
MRI imaging. Finally myocardial fibrosis for viability and Myocardial perfusion measurements by MDCT are
prognosis assessment is usually detected and quantified by derived from the upslope differences in contrast enhance-
MRI and nuclear techniques. ment between the ischemic and remote areas (Fig. 12.1).
Recent advancements in MDCT imaging have demon- Previous generation 64-detector scanners had limited cover-
strated the feasibility of MDCT to be a comprehensive imaging age of the heart, resulting in the base of the heart being
modality, which in a single scan setting could provide a wide scanned earlier in time than the apex, making comparisons in
array of complementary information. Ideally, using one imag- signal intensities between the two areas problematic. In this
ing modality to perform all these assessments during a single regard, the introduction of wide coverage MDCT technology
scan setting could have substantial economic implications, may allowed the entire heart to be imaged in one gantry rotation
serve to reduce patient anxiety, and improve workflow. (Fig. 12.2) combined with the capability of programming
such gated image acquisitions to occur only during specific
portions of a given cardiac cycle (Fig. 12.3). This created a
Ischemia Detection by MDCT brand new horizon of possibilities to reduce radiation expo-
sure enough to enable the performance of combined angiog-
The notion that CT could provide information on myocardial raphy and myocardial perfusion assessment during stress,
perfusion has been documented in the past by investigators which associated with the angiographic and delayed
using electron beam CT [1]. However, the combination of a enhanced images, should provide a comprehensive cardiac
reliable coronary angiogram with stress-induced myocardial assessment. Also, with more coverage and faster acquisition,
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging 213

a 700
b
Signal Density Curve (HU)

600 LV
Stenosed
500
Remote
400

300

200

100

0
1
4
7
10
13
16
19
22
25
28
31
34
37
40
43
46
49
Time (seconds)

Fig. 12.1 Myocardial enhancement upslope curves for the left ventric- circle) and remote (open circle) areas present a delta in myocardial
ular cavity, remote and ischemic region (a). The usual timing of a coro- enhancement intensity (b) that can be measured, as shown inside the
nary CT angiogram is shown as the region between the vertical bars. dashed box (a)
following the contrast bolus with an ROI placed at the ischemic (filled

Fig. 12.2 Schematic coverage of a 256-detector as compared to a 64-detector MDCT scanner

scan times have decreased, reducing the amount of contrast Using iodine molecules as a tracer, current research has
material per scan [8]. Such techniques are ideal for the demonstrated that by measuring the concentration in time of
assessment of patients with chest pain who also have calci- the tracer in the myocardium, MDCT can determine absolute
fied coronaries, as well as the follow up of patients with blood flow in different regions of the myocardium [2].
advanced heart disease post coronary artery bypass surgery Recent attention to patients with chest pain but no obstruc-
or multiple stent implantations. tive epicardial CAD (syndrome X) has demonstrated that in
214 R.K. Sharma et al.

Fig. 12.3 Schematic

demonstration of the radiation
exposure time differences
between retrospective gating
(single heart beat) and
prospective triggering used in
wide coverage MDCT scanners

a substantial proportion of these individuals microvascular MDCT for Detection of Myocardial Fibrosis
processes can be identified by perfusion reserve measure- and Viability
ments in association with traditional CAD risk factors such
as hypercholesterolemia, hypertension and smoking as well The ability to distinguish dysfunctional but viable myocar-
as with diabetes [9]. The possibility of quantifying epicardial dium from nonviable tissue after acute or chronic ischemia
coronary plaque while also assessing microvascular disease has important implications for the therapeutic management
during maximal vasodilatation enables coronary MDCTA – of patients with coronary artery disease [19, 20]. Image-
armored with high spatial resolution – to characterize macro- based characterization of myocardial scar morphology can
vascular atherosclerosis as well as microvascular dysfunction identify those patients with hibernating myocardium who
secondary to atherosclerosis or other disease processes. The may achieve functional systolic recovery with revasculariza-
capability of quantifying myocardial blood flow by contrast tion [21]. The assessment of myocardial viability and infarct
enhanced MDCT represent a “quantum leap” in our ability to morphology with delayed contrast-enhanced MRI has been
assess and characterize the entire process of cardiac well validated over the past several years and is performed
atherosclerosis. routinely at several clinical cardiac MRI centers.
Single center studies [10–12] have demonstrated the The recent advent of MDCT technology has expanded its
incremental diagnostic performance of MDCT stress perfu- potential for a more comprehensive evaluation of cardiovas-
sion imaging in addition to coronary CTA in assessing cular diseases. While hypo attenuation in the non-contrasted
flow-limiting stenosis. Subsequently, the CORE320 study scan (due to fatty degeneration of the infarcted area) or dur-
[13], a multicenter, international study also validated ing the contrast enhanced coronary angiography scan has
improved diagnostic accuracy of coronary CTA plus MDCT been shown to demonstrate areas of previous MI, it is largely
perfusion imaging compared to the reference standard of underestimated by MDCT [22, 23]. Delayed enhanced
invasive coronary angiography plus a corresponding perfu- MDCT (DE-MDCT) myocardial imaging can accurately
sion deficit on SPECT imaging. On head to head compari- identify and characterize morphological features of acute
son, the ability of stress MDCT perfusion imaging to detect and healed myocardial infarction, including infarct size,
myocardial ischemia was similar to SPECT imaging, with transmurality, and the presence of microvascular obstruction
better MDCT sensitivity for left main and multivessel ste- and collagenous scar (Fig. 12.4) [24, 25]. Infarcted myocar-
noses [14]. This enhanced sensitivity is attributed to better dial tissue by DE-MDCT is characterized by well-delineated
spatial resolution of MDCT and favorable kinetics of iodine hyper-enhanced regions, whereas regions of microvascular
dye which serves as a tracer in MDCT perfusion imaging. obstruction by MDCT are characterized by hypo-
Previously limited to single center experience [10, 15– enhancement on imaging early after MI [24, 25]. Detection
17], current efforts are directed towards expanding this tech- of fibrosis by DE-MDCT has been validated against gold
nique to different MDCT scanner systems (including 64-, standards such as histology and contrast enhanced MRI [24,
128-, 256-, and 320-slice) and across multivendor platform 26–28]. In addition, recent studies [29, 30] have also sub-
using different stress agents. The ongoing multicenter, mul- stantiated the utility of contrast enhanced MDCT in assess-
tivendor study of Regadenoson in Subjects Undergoing ment of extracellular volume fraction (ECV), a measurement
Stress Myocardial Perfusion Imaging Using Multidetector of interstitial myocardial volume expansion which corre-
Computed Tomography Compared to Single Photon sponds to diffuse myocardial fibrosis.
Emission Computed Tomography [18] (www.clinicaltrials. Introduction of delayed contrast enhanced MDCT imag-
gov, NCT01334918) is a step in this direction. ing in assessment of hypertrophic cardiomyopathy has been
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging 215

a b c

Fig. 12.4 Typical contrast-enhanced myocardial MDCT images show- 5 min after contrast injection. the infarcted region is represented by the
ing axial slices (a) at baseline (preinfarct) 5 min after contrast, subendocardial anterior hyperintense region (arrows)
(b) postinfarct during first-pass contrast injection, and (c) postinfarct

a b c

d e

Fig. 12.5 Multiplanar reconstruction of the left ventricular basal (a), rior, basal to mid septal, and apical septal walls (arrows). A small aneu-
mid (b), and apical short-axis (c) views and horizontal (d) and vertical rysm is noted in the apical septum (c, d) (Reprinted from Gore R et al.
long-axis (e) views show delayed hyperenhancement in the basal ante- [41] with permission from Elsevier)
216 R.K. Sharma et al.

of particular interest where it has shown comparable accuracy after iodinated contrast administration is similar to that pro-
to delayed contrast enhanced MRI in detecting myocardial posed for delayed gadolinium-enhanced MRI [19]. Under
fibrosis (Fig. 12.5) [31–33]. This has allowed comprehensive conditions of normal myocyte function, sarcolemmal mem-
evaluation of myocardial tissue characteristics with signifi- branes serve to exclude iodine from the intracellular space.
cant bearing on the management [31], prognosis [34], and After myocyte necrosis, however, membrane dysfunction
follow-up in these patients who may not be ideal candidates ensues, and iodine molecules are able to penetrate the cell.
for MRI given significant proportion of them have implant- Because 75 % of the total myocardial volume is intracellu-
able cardiac defibrillator. lar, large increases in the volume of distribution are achieved,
The mechanism of myocardial hyperenhancement and which results in marked hyperenhancement relative to the
hypo-enhancement in acutely injured myocardial territories non-injured myocytes. The mechanism of hyperenhance-

a b

Fig. 12.6 Multiplanar reconstruction images showing normal left anterior descending (a), left circumflex (b), and right coronary artery (c)
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging 217

ment of healed myocardial infarction or collagenous scar is rality of delayed enhancement predicts functional recovery
thought to be related to an accumulation of contrast media after revascularization [21], the better spatial resolution of
in the interstitial space between collagen fibers and thus an MDCT as compared to CMR may influence the accuracy of
increased volume of distribution compared with that of viability assessment, but no study thus far has tested this
tightly packed myocytes. The low signal intensity of micro- hypothesis.
vascular obstruction regions despite restoration of normal
flow through the infarct-related artery is explained by the
death and subsequent cellular debris blockage of intramyo- Integrating All Methodologies into One
cardial capillaries at the core of the damaged region. These Examination
obstructed capillaries do not allow contrast material to flow
into the damaged bed, which results in a region of low signal The number of scans to be performed varies for individual
intensity compared with normal myocardium. In minutes to patients, depending on the clinical questions to be answered.
hours, contrast material is able to penetrate this relatively For a comprehensive cardiac evaluation, in the future four
“no reflow” region, and the necrotic myocytes that reside in consecutive scans should be performed, with acceptable
that myocardial territory then become hyperenhanced as radiation dose. The first one would be a low dose prospec-
iodine is internalized by the cell. In weeks the microvascular tively unenhanced calcium score scan (<1 mSv) [35], the
obstruction area is replaced by collagenous scar tissue and second one also prospectively gated and contrasted for the
the former dark area now become bright. Since the transmu- acquisition of coronary angiography and morphology
(approximately 1–4 mSv) [36], the third would be the stress
perfusion study during maximum vasodilation, which could
be performed as a “static” perfusion acquisition, i.e. one
acquisition at peak contrast opacification of the myocardium
(approximately 1–4 mSv); or alternatively as a “dynamic”
perfusion acquisition, i.e. several low dose prospective
acquisitions representing the contrast passage through the
heart (approximately 3–7 mSv) (Fig. 12.6 and 12.7, Videos
12.1, 12.2, 12.3, and 12.4).[16] Static perfusion has been
more validated and can be performed in scanners with 4 cm
coverage or more, but dynamic perfusion might improve
accuracy, by allowing construction of contrast wash in curves
in the myocardium. For that, one would need a scanner with
at least 8 cm coverage, multiple “shots” are acquired during
contrast administration and at least a large portion of the
myocardium needs to be imaged at each “shot”. Finally, a
low dose prospectively triggered delayed enhancement scan
would be performed 5–10 min after the stress study
(1–3 mSv) [36]. The final result would be calcium score,
coronary anatomy, morphology, stress perfusion and viabil-
ity in a “one stop shop” scan that lasts around 20 min.
(Fig. 12.8) shows a timeline for a comprehensive cardiac
Fig. 12.7 Multiplanar reconstruction image showing obstructive evaluation. Employing dose reduction techniques [37] like
coronary artery stenosis of left anterior descending artery (a)

Prospectively
triggered scan
with contrast for
Calcium score scan Helical stress perfusion coronary anatomy
1-2mSv scan (7-9 mSv) (3–4 mSv) Prospectively triggered
no contrast delayed
Start adenosine enhancement scan
infusion End adenosine (3–4 mSv)

3–4 min 3–4 min

Fig. 12.8 Proposed timeline for a

comprehensive MDCT scan Time approximately 20 minutes
218 R.K. Sharma et al.

limiting scan length, prospective scan acquisition, post pro- profile and proved efficacy in diverging blood from isch-
cessing methods such as iterative reconstruction and filtered emic to non-ischemic territories. Utility of regadenoson is
back projection [38], and availability of next generation currently being explored.[18]
scanners with faster gantry rotation time and wide volume 3. Since adenosine usually increases heart rate, aggressive
coverage could result in substantial reduction in the amount beta-blockade should be pursued. Adequate hydration
of radiation exposure, allowing one to acquire enhanced prior to the scan may potentially blunt the reflex increase
information at the cost of less than 10 mSv of radiation. in heart rate from the adenosine infusion.
4. Nitroglycerin should not be given concomitantly to ade-
nosine, since it can reverse the ischemic effects of the lat-
Clinical Pearls DE ter, as well as decrease blood pressure and increase heart
rate even further.
1. The optimal contrast dose to be used for DE images is 5. The visual contouring of the underperfused myocardial
still not defined, but studies in humans [23, 25] showed areas is the method currently being applied in addition to
that the usual amount used for a 16-detector coronary the semi-automated software. However, the best thresh-
CTA (120–140 ml) provide good enhancement and old for quantitatively discriminating ischemia from
could be as low as 80–90 ml using advanced scanner remote myocardium is still not defined.
system.[31] 6. The problem of balanced ischemia will potentially be
2. For optimal contrast between the infarcted and the remote solved with wide coverage MDCT scanners by allowing
regions, the delayed enhanced scan should be done absolute quantification of myocardial blood flow.
between 5 and 10 min after contrast injection.[24] 7. Whether stress perfusion scans will be recommended to
3. Most of the studies done so far reconstructed the images everyone or just selected patient populations (such as the
in end-diastole for DE analysis. ones with high calcium scores) is still under
4. The delayed enhancement pattern is important to differ- investigation.
entiate between ischemic and non-ischemic etiologies,
the earlier being found as a wave front from the endocar-
dium to the pericardium. Non-ischemic cardiomyopa- References
thies can also result in myocardial scar that appears on
DE images, but those tend to be patchy and do not follow 1. Lerman LO, Siripornpitak S, Maffei NL, Sheedy 2nd PF, Ritman
the endocardium-to-epicardium pattern seen in ischemic EL. Measurement of in vivo myocardial microcirculatory function
cardiomyopathy.[39] with electron beam CT. J Comput Assist Tomogr. 1999;23:390–8.
2. George RT, Jerosch-Herold M, Silva C, Kitagawa K, Bluemke DA,
5 Molecular size of the iodinated contrast material may
Lima JA, Lardo AC. Quantification of myocardial perfusion using
affect the uptake of the tissue by that agent. Two trials dynamic 64-detector computed tomography. Invest Radiol.
used a smaller molecule with high iodine concentration 2007;42:815–22.
(iomeprol) [23, 25] while another one used a larger mol- 3. Smith Jr SC, Feldman TE, Hirshfeld Jr JW, Jacobs AK, Kern MJ,
King SB, Morrison DA, O'Neil WW, Schaff HV, Whitlow PL,
ecule with a lower iodine concentration (iodixanol).[24]
Williams DO, Antman EM, Adams CD, Anderson JL, Faxon DP,
It is still unclear which one is the best, if any, or whether Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Nishimura R, Ornato
other factors (such as ionic polarization) are important. JP, Page RL, Riegel B. ACC/AHA/SCAI 2005 guideline update for
6. DE imaging by MDCT can be obtained both in patients percutaneous coronary intervention: a report of the American
College of Cardiology/American Heart Association Task Force on
with an acute MI as well as patients that had infarcts more
Practice Guidelines (ACC/AHA/SCAI Writing Committee to
than 6 months prior to imaging.[23–25] Update 2001 Guidelines for Percutaneous Coronary Intervention.
7. Microvascular obstruction can be imaged in the early Circulation. 2006;113:166–286.
phase after MI, and it is gradually replaced by fibrous tis- 4. van Werkhoven JM, Schuijf JD, Gaemperli O, Jukema JW, Boersma
E, Wijns W, Stolzmann P, Alkadhi H, Valenta I, Stokkel MP, Kroft
sue that appears bright on the DE images 2–4 weeks after
LJ, de Roos A, Pundziute G, Scholte A, van der Wall EE, Kaufmann
the MI.[40] PA, Bax JJ. Prognostic value of multislice computed tomography
and gated single-photon emission computed tomography in patients
with suspected coronary artery disease. J Am Coll Cardiol.
2009;53:623–32.
Clinical Pearls Ischemia 5. Rodes-Cabau J, Candell-Riera J, Angel J, de Leon G, Pereztol O,
Castell-Conesa J, Soto A, Anivarro I, Aguade S, Vazquez M,
1. MDCT myocardial perfusion is shown to have incremen- Domingo E, Tardif JC, Soler-Soler J. Relation of myocardial perfu-
tal diagnostic accuracy in identifying or excluding hemo- sion defects and nonsignificant coronary lesions by angiography
with insights from intravascular ultrasound and coronary pressure
dynamically significant stenosis.
measurements. Am J Cardiol. 2005;96:1621–6.
2. Adenosine is the drug most often tested for stress perfu- 6. Ragosta M, Bishop AH, Lipson LC, Watson DD, Gimple LW,
sion in MDCT, due to its short onset and offset, safety Sarembock IJ, Powers ER. Comparison between angiography and
12 Cardiovascular CT for Perfusion and Delayed Contrast Enhancement Imaging 219

fractional flow reserve versus single-photon emission computed Loureiro R, Feuchtner G, Gewirtz H, Hoffmann U, Mamuya WS,
tomographic myocardial perfusion imaging for determining lesion Brady TJ, Cury RC. Adenosine-induced stress myocardial perfu-
significance in patients with multivessel coronary disease. Am sion imaging using dual-source cardiac computed tomography.
J Cardiol. 2007;99:896–902. J Am Coll Cardiol. 2009;54:1072–84.
7. Schuijf JD, Wijns W, Jukema JW, Atsma DE, de Roos A, Lamb HJ, 18. Cury RC, Kitt TM, Feaheny K, Akin J, George RT. Regadenoson-
Stokkel MP, Dibbets-Schneider P, Decramer I, De Bondt P, van der stress myocardial CT perfusion and single-photon emission CT:
Wall EE, Vanhoenacker PK, Bax JJ. Relationship between noninva- rationale, design, and acquisition methods of a prospective, multi-
sive coronary angiography with multi-slice computed tomography center, multivendor comparison. J Cardiovasc Comput Tomogr.
and myocardial perfusion imaging. J Am Coll Cardiol. 2014;8:2–12.
2006;48:2508–14. 19. Wu KC, Lima JA. Noninvasive imaging of myocardial viability: cur-
8. Hein PA, May J, Rogalla P, Butler C, Hamm B, Lembcke rent techniques and future developments. Circ Res. 2003;93:1146–58.
A. Feasibility of contrast material volume reduction in coronary 20. Pagley PR, Beller GA, Watson DD, Gimple LW, Ragosta
artery imaging using 320-slice volume CT. Eur Radiol. M. Improved outcome after coronary bypass surgery in patients
2010;20:1337–43. with ischemic cardiomyopathy and residual myocardial viability.
9. Buchthal SD, den Hollander JA, Merz CN, Rogers WJ, Pepine CJ, Circulation. 1997;96:793–800.
Reichek N, Sharaf BL, Reis S, Kelsey SF, Pohost GM. Abnormal 21. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O,
myocardial phosphorus-31 nuclear magnetic resonance spectros- Klocke FJ, Bonow RO, Judd RM. The use of contrast-enhanced
copy in women with chest pain but normal coronary angiograms. N magnetic resonance imaging to identify reversible myocardial dys-
Engl J Med. 2000;342:829–35. function. N Engl J Med. 2000;343:1445–53.
10. Cury RC, Magalhaes TA, Borges AC, Shiozaki AA, Lemos PA, 22. Sanz J, Weeks D, Nikolaou K, Sirol M, Rius T, Rajagopalan S,
Junior JS, Meneghetti JC, Rochitte CE. Dipyridamole stress and Dellegrottaglie S, Strobeck J, Fuster V, Poon M. Detection of
rest myocardial perfusion by 64-detector row computed tomogra- healed myocardial infarction with multidetector-row computed
phy in patients with suspected coronary artery disease. Am tomography and comparison with cardiac magnetic resonance
J Cardiol. 2010;106:310–5. delayed hyperenhancement. Am J Cardiol. 2006;98:149–55.
11. George RT, Arbab-Zadeh A, Miller JM, Vavere AL, Bengel FM, 23. Mahnken AH, Koos R, Katoh M, Wildberger JE, Spuentrup E,
Lardo AC, Lima JA. Computed tomography myocardial perfu- Buecker A, Gunther RW, Kuhl HP. Assessment of myocardial via-
sion imaging with 320-row detector computed tomography bility in reperfused acute myocardial infarction using 16-slice com-
accurately detects myocardial ischemia in patients with puted tomography in comparison to magnetic resonance imaging.
obstructive coronary artery disease. Circ Cardiovasc Imaging. J Am Coll Cardiol. 2005;45:2042–7.
2012;5:333–40. 24. Lardo AC, Cordeiro MA, Silva C, Amado LC, George RT,
12. Rief M, Zimmermann E, Stenzel F, Martus P, Stangl K, Greupner J, Saliaris AP, Schuleri KH, Fernandes VR, Zviman M, Nazarian S,
Knebel F, Kranz A, Schlattmann P, Laule M, Dewey M. Computed Halperin HR, Wu KC, Hare JM, Lima JA. Contrast-enhanced
tomography angiography and myocardial computed tomography multidetector computed tomography viability imaging after
perfusion in patients with coronary stents: prospective intraindi- myocardial infarction: characterization of myocyte death,
vidual comparison with conventional coronary angiography. J Am microvascular obstruction, and chronic scar. Circulation.
Coll Cardiol. 2013;62:1476–85. 2006;113:394–404.
13. Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M, 25. Gerber BL, Belge B, Legros GJ, Lim P, Poncelet A, Pasquet A,
Miller JM, Niinuma H, Yoshioka K, Kitagawa K, Nakamori S, Gisellu G, Coche E, Vanoverschelde JL. Characterization of acute
Laham R, Vavere AL, Cerci RJ, Mehra VC, Nomura C, Kofoed KF, and chronic myocardial infarcts by multidetector computed tomog-
Jinzaki M, Kuribayashi S, de Roos A, Laule M, Tan SY, Hoe J, Paul raphy: comparison with contrast-enhanced magnetic resonance.
N, Rybicki FJ, Brinker JA, Arai AE, Cox C, Clouse ME, Di Carli Circulation. 2006;113:823–33.
MF, Lima JA. Computed tomography angiography and perfusion to 26. Bauer RW, Kerl JM, Fischer N, Burkhard T, Larson MC, Ackermann
assess coronary artery stenosis causing perfusion defects by single H, Vogl TJ. Dual-energy CT for the assessment of chronic myocar-
photon emission computed tomography: the CORE320 study. Eur
Heart J. 2014;35:1120–30. dial infarction in patients with chronic coronary artery disease: com-
14. George RT, Mehra VC, Chen MY, Kitagawa K, Arbab-Zadeh A, parison with 3-T MRI. AJR Am J Roentgenol. 2010;195:639–46.
Miller JM, Matheson MB, Vavere AL, Kofoed KF, Rochitte CE, 27. Schuleri KH, Centola M, George RT, Amado LC, Evers KS,
Dewey M, Yaw TS, Niinuma H, Brenner W, Cox C, Clouse ME, Kitagawa K, Vavere AL, Evers R, Hare JM, Cox C, McVeigh ER,
Lima JA, Di Carli M. Myocardial CT perfusion imaging and Lima JA, Lardo AC. Characterization of peri-infarct zone heteroge-
SPECT for the diagnosis of coronary artery disease: a Head-to- neity by contrast-enhanced multidetector computed tomography: a
Head comparison from the CORE320 multicenter diagnostic per- comparison with magnetic resonance imaging. J Am Coll Cardiol.
formance study. Radiology. 2014;272:407–16. 2009;53:1699–707.
15. Rocha-Filho JA, Blankstein R, Shturman LD, Bezerra HG, Okada 28. Senra T, Shiozaki AA, Salemi VM, Rochitte CE. Delayed enhance-
DR, Rogers IS, Ghoshhajra B, Hoffmann U, Feuchtner G, Mamuya ment by multidetector computed tomography in endomyocardial
WS, Brady TJ, Cury RC. Incremental value of adenosine-induced fibrosis. Eur Heart J. 2008;29:347.
stress myocardial perfusion imaging with dual-source CT at cardiac 29. Nacif MS, Kawel N, Lee JJ, Chen X, Yao J, Zavodni A, Sibley CT,
CT angiography. Radiology. 2010;254:410–9. Lima JA, Liu S, Bluemke DA. Interstitial myocardial fibrosis
16. George RT, Arbab-Zadeh A, Miller JM, Kitagawa K, Chang HJ, assessed as extracellular volume fraction with low-radiation-dose
Bluemke DA, Becker L, Yousuf O, Texter J, Lardo AC, Lima cardiac CT. Radiology. 2012;264:876–83.
JA. Adenosine stress 64- and 256-row detector computed tomogra- 30. Nacif MS, Liu Y, Yao J, Liu S, Sibley CT, Summers RM, Bluemke
phy angiography and perfusion imaging: a pilot study evaluating DA. 3D left ventricular extracellular volume fraction by
the transmural extent of perfusion abnormalities to predict athero- low-radiation dose cardiac CT: assessment of interstitial myocar-
sclerosis causing myocardial ischemia. Circ Cardiovasc Imaging. dial fibrosis. J Cardiovasc Comput Tomogr. 2013;7:51–7.
2009;2:174–82. 31. Zhao L, Ma X, Delano MC, Jiang T, Zhang C, Liu Y, Zhang
17. Blankstein R, Shturman LD, Rogers IS, Rocha-Filho JA, Okada Z. Assessment of myocardial fibrosis and coronary arteries in
DR, Sarwar A, Soni AV, Bezerra H, Ghoshhajra BB, Petranovic M, hypertrophic cardiomyopathy using combined arterial and delayed
220 R.K. Sharma et al.

enhanced CT: comparison with MR and coronary angiography. Eur enhanced multidetector computed tomography accurately quanti-
Radiol. 2013;23:1034–43. fies infarct size and reduces radiation exposure. JACC Card
32. Langer C, Lutz M, Eden M, Ludde M, Hohnhorst M, Gierloff C, Imaging. 2009;2:412–20.
Both M, Burchert W, Faber L, Horstkotte D, Frey N, Prinz 37. Halliburton SS, Abbara S, Chen MY, Gentry R, Mahesh M, Raff
C. Hypertrophic cardiomyopathy in cardiac CT: a validation study GL, Shaw LJ, Hausleiter J. SCCT guidelines on radiation dose and
on the detection of intramyocardial fibrosis in consecutive patients. dose-optimization strategies in cardiovascular CT. J Cardiovasc
Int J Cardiovasc Imaging. 2014;30:659–67. Comput Tomogr. 2011;5:198–224.
33. Berliner JI, Kino A, Carr JC, Bonow RO, Choudhury L. Cardiac 38. Chen MY, Steigner ML, Leung SW, Kumamaru KK, Schultz K,
computed tomographic imaging to evaluate myocardial scarring/ Mather RT, Arai AE, Rybicki FJ. Simulated 50 % radiation dose
fibrosis in patients with hypertrophic cardiomyopathy: a compari- reduction in coronary CT angiography using adaptive iterative dose
son with cardiac magnetic resonance imaging. Int J Cardiovasc reduction in three-dimensions (AIDR3D). Int J Cardiovasc
Imaging. 2013;29:191–7. Imaging. 2013;29:1167–75.
34. Shiozaki AA, Senra T, Arteaga E, Martinelli Filho M, Pita CG, 39. Gottlieb I, Macedo R, Bluemke DA, Lima JA. Magnetic resonance
Avila LF, Parga Filho JR, Mady C, Kalil-Filho R, Bluemke DA, imaging in the evaluation of non-ischemic cardiomyopathies: cur-
Rochitte CE. Myocardial fibrosis detected by cardiac CT predicts rent applications and future perspectives. Heart Fail Rev.
ventricular fibrillation/ventricular tachycardia events in patients 2006;11:313–23.
with hypertrophic cardiomyopathy. J Cardiovasc Comput Tomogr. 40. Wu KC, Kim RJ, Bluemke DA, Rochitte CE, Zerhouni EA, Becker
2013;7:173–81. LC, Lima JA. Quantification and time course of microvascular
35. Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu obstruction by contrast-enhanced echocardiography and magnetic
K, Shea S, Szklo M, Bluemke DA, O'Leary DH, Tracy R, Watson resonance imaging following acute myocardial infarction and
K, Wong ND, Kronmal RA. Coronary calcium as a predictor of reperfusion. J Am Coll Cardiol. 1998;32:1756–64.
coronary events in four racial or ethnic groups. N Engl J Med. 41. Gore R, Abraham T, George RT. CT characterization of myocardial
2008;358:1336–45. substrate in hypertrophic cardiomyopathy. J Cardiovasc Comput
36. Chang HJ, George RT, Schuleri KH, Evers K, Kitagawa K, Lima Tomogr. 2014;8(22):166–9.
JA, Lardo AC. Prospective electrocardiogram-gated delayed
 Cardiovascular CT for Assessment
of Pericardial/Myocardial Disease 13
Processes

Muhammad Aamir Latif and Khurram Nasir

Abstract
Pericardial and myocardial diseases represent an important cause of morbidity and mortality.
Although echocardiography remains the initial standard diagnostic tool for identifying
these diseases it has limited detail for the morphological and functional analysis of the
pericardium and myocardium. Cardiac CT (CCT) and MR (CMR) are the primary modalities
of choice when comprehensive functional assessment of the heart is required. These imaging
techniques provide advanced information on anatomy and cardiac function to optimize
diagnosis and treatment. However, as CMR is relatively more costly and time consuming, it
is often only used when diagnosis is not clear. Due to the volumetric nature of image
acquisition, cardiac CT provides an accurate and reproducible method for assessing both
myocardial and pericardial morphology and function. The excellent spatial resolution and
contrast to noise ratio of CT allows for the detection of mural thrombi in patients with
severely reduced left ventricular function. CCT can easily help identify pericardial diseases
such as inflammation, effusion, pericardial cyst, benign or malignant masses, as well as
pericardial calcification in the case of constrictive pericarditis. CCT is also proficient in
diagnosing the functional assessment of the heart. As most of cardiomyopathies have
functional compromise, CCT is best suited for cardiomyopathies in terms of functional
analysis. With the advancement of CT technology, radiation exposure is minimal, and with
continued improvement in post-processing software, it is able to produce a variety of high-
quality images in multiple reformats with historically low radiation and contrast dose. The
new General Electric (GE) Revolution CT scanner has made it possible to image the heart
with abnormal rate and rhythm without compromising image quality. It is especially useful
for patients who have contraindications to beta-blockers or who have atrial fibrillation.

Electronic supplementary material The online version of this

chapter (doi:10.1007/978-3-319-28219-0_13) contains supplemen-
tary material, which is available to authorized users.

M.A. Latif, MD
Department of Medicine, Center for Healthcare Advancement and
Outcomes, Baptist Health South Florida, 6262 Sunset Dr. Suite
200, Miami, FL 33143, USA
e-mail: [email protected]; [email protected]
K. Nasir, MD, MPH (*)
Department of Medicine, Center for Healthcare Advancement and
Outcomes, Baptist Health South Florida, 1691 Michigan Avenue
Suite 500, Miami Beach, FL 33139, USA
e-mail: [email protected]; [email protected]

© Springer International Publishing 2016 221

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_13
222 M.A. Latif and K. Nasir

Keywords
Pericardial • Myocardial • Computed Tomography • Cardiomyopathies • Dilated
Cardiomyopathy • Restrictive Cardiomyopathy • Takotsubo Cardiomyopathy •
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

Introduction ogy, including refinements in temporal resolution and dra-

matic reductions in radiation exposure, CCT may play a
The twenty first century has already seen extensive research larger role in the evaluation of patients with known or sus-
to benefit human civilization. Theories and concepts previ- pected diseases of the myocardium and pericardium. The
ously considered imaginary and magical are now being main concern of cardiac CT is radiation exposure. With
implemented in a practical way with the help of technology. recent advancement in technology, radiation exposure has
Cardiac CT is one such technology. It started as an imaging been minimized. Newer CT protocols have been developed
machine to augment x-ray radiography and give detailed to do selective gating images that lower the dose delivered
three-dimensional images of the body’s internal organs. during non-diagnostic portions of the cardiac cycle. Most
Cardiac CT use for heart images has received great attention recently the General Electric Revolution CT scanner has the
worldwide because previously it was hard to image a con- ability to even further reduce the radiation dose by selective
tinuously moving structure in the body. Cardiac CT is able to retrospective imaging. Previously for gating purposes, it was
freeze the image in each phases of the cardiac cycle and with required to use either retrospective or prospective gating
high temporal and spatial resolution give a detailed anatomi- synchronized with the patient ECG monitor. The newer
cal and physiological picture of the heart. Although the cur- scanners no longer require a decision for which mode (retro-
rent primary clinical use of contrast-enhanced cardiac spective or prospective) to be used but rather the focus is
computed tomography (CCT) remains the exclusion of coro- primarily on when to image within the cardiac cycle accord-
nary artery disease in low to intermediate risk symptomatic ing to the ECG strip as interpreted by the scanner. This has
patients, this modality also offers a unique opportunity to further reduced radiation exposure. Technological advance-
assess both the pericardium and myocardium. Given the ment has also overcome the dependence on low heart rate,
associated contrast and radiation exposure, CCT presently beat-to-beat variability and their relation to image quality.
serves as an adjunct to echocardiography and cardiac MRI Now excellent image quality can be obtained with heart rates
for this purpose. However, CCT provides superb delineation ranging from 70 to 90 bpm by using newer CT protocols.
of the pericardium and can precisely localize lesions as well The Revolution CT scanner has robust, high performance
as aid in their characterization. Further, CCT can effectively cardiac imaging based on three points of excellence: tempo-
evaluate morphology and function in various myocardial dis- ral resolution (0.28 s gantry rotation, intelligent motion
eases, including the various cardiomyopathies. The volumet- correction), spatial resolution and whole organ coverage
ric nature of image acquisition with CCT provides an (160 mm detector). With these improvements the cardiac CT
accurate and reproducible method for quantifying ventricu- exam provides the best possible overall picture of the heart,
lar mass, volumes, and function. This chapter will discuss including the pericardium and myocardium. The cinematic
the application of CCT in the assessment of various myocar- mode is a feature of cardiac CT software to provide func-
dial and pericardial disease processes. tional global assessment of the myocardium. These imaging
modalities can also play an important role in prognosis, as
well as direct treatment and further management.
Cardiac CT Advancement

Due to the volumetric nature of image acquisition, cardiac CT Imaging of Myocardial Disease
CT provides an accurate and reproducible method for assess-
ing both myocardial and pericardial morphology and func- Myocardial diseases or cardiomyopathies can be classified
tion. The excellent spatial resolution and contrast to noise based on their origin, anatomy, physiology, histopathology
ratio of CT allows for the detection of mural thrombi in or genetics. The World Health Organization (WHO) defines
patients with severely reduced left ventricular function. the cardiomyopathies as diseases of myocardial tissue asso-
While echocardiography remains the primary noninvasive ciated with cardiac dysfunction and subdivides them mainly
imaging modality for evaluation of the myocardium and into four categories: dilated, restrictive, hypertrophic, and
pericardium, CCT serves as a valuable tool for further evalu- arrhythmogenic right ventricular cardiomyopathy (ARVC)
ation due to its inherently superb spatial resolution and soft [1]. Non-invasive imaging can determine whether abnormal-
tissue contrast. With further improvements in CCT technol- ities are present in the myocardium, valves, pericardium, or
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 223

vessels. Echocardiography is the most common imaging patients with dynamic left ventricular outflow obstruction,
technique used for the initial diagnosis and management of CCT delineates the systolic anterior motion of the anterior
cardiomyopathy; however, other imaging modalities, includ- mitral valve leaflet on the multiphase images. While poor
ing nuclear cardiac imaging, cardiac magnetic resonance acoustic windows may limit echocardiography, CCT can
imaging, and cardiac computed tomography, may play an reliably identify all areas of the myocardium and provide
important role depending on the underlying etiology of the accurate, reproducible measurements of wall thickness.
cardiomyopathy [2].

Arrhythmogenic Right Ventricular

Dilated Cardiomyopathy Cardiomyopathy (ARVC)

Dilated cardiomyopathy is characterized by ventricular ARVC is an unusual cardiomyopathy characterized by

enlargement and decreased systolic function. Besides the abnormal right ventricular function, fibrofatty deposition
reconstructed CT data at specific diastolic (and/or systolic) into the right ventricular myocardium, and abnormal elec-
phases of the cardiac cycle for evaluation of the coronary trocardiographic changes, which predispose these patients
arteries and cardiac morphology, a multiphase data set, to sudden cardiac death. CCT has an advantage over echo-
which reconstructs the entire cardiac cycle at 5–10 % inter- cardiography in its ability to visualize the right ventricle
vals, allows for viewing images in cinematic mode. This and thus to evaluate right ventricular morphology and sys-
multiphase reconstruction allows for assessment of left and tolic function, similar to MRI. However, MRI has superior
right ventricular systolic function in any orientation, tissue characterization capabilities and remains the modal-
including all of the standard echocardiographic planes [3]. ity of choice for evaluating suspected ARVC. CCT becomes
Thus, CCT can assess myocardial thickness (Video 13.1), the modality of choice when metal implants or claustropho-
ventricular shape and volume, and global and regional bia preclude MRI. When performing CCT in these patients,
ventricular function with excellent correlation to it is important to ensure adequate opacification of the right
echocardiography and cardiac MRI [4, 5]. Additionally, ventricle at the time of image acquisition. This can be
patients with severely reduced left ventricular function are at achieved by either prolonging the contrast administration
risk for the development of mural thrombus. Given its by several seconds (4–6 s) or by empirically utilizing a
inherently high contrast to noise ratio and excellent spatial shorter delay time. Alternatively, placing a region of inter-
resolution, CCT can readily identify such mural thrombi. est in the main pulmonary artery and triggering the scan at
its peak opacification can consistently achieve preferential
right-sided opacification. CCT can reliably characterize
Restrictive Cardiomyopathy right ventricular dimensions as well as focal aneurysms of
the myocardium, increased trabeculations, and/or areas of
Restrictive cardiomyopathy is characterized by increased right ventricular dysfunction, all confirmatory findings in
ventricular stiffness and associated diastolic dysfunction. RV dysplasia. Importantly, CCT can also detect fatty infil-
Ventricular size and systolic function are usually normal, but tration as areas of hypoattenuation, confirmed by CT atten-
the atria and systemic veins (superior and inferior vena cavae, uation measurements. However, the finding of fat is
hepatic veins, coronary sinus) are often dilated due to sensitive but not specific for ARVC [6]. Hence, CCT find-
increased filling pressures. These features are easily depicted ings must be correlated with clinical and electro-cardio-
by CCT but are nonspecific. While CCT is not indicated graphic data to establish the diagnosis of ARVC.
solely for the evaluation of possible restrictive cardiomyopa-
thy, it is useful in differentiating it from constrictive pericar-
ditis by excluding pericardial abnormalities. This distinction Left Ventricular Noncompaction
leads to important therapeutic consequences.
Left ventricular noncompaction is a cardiomyopathy charac-
terized by a 2-layered myocardium: a thin compacted layer
Hypertrophic Cardiomyopathy and a thick noncompacted layer. The ratio of noncompacted to
compacted myocardium has been reported to be greater than
Hypertrophic cardiomyopathy is a genetic disorder of vari- or equal to 2.3:1 by cardiac MRI in cases of non-compaction
ous sarcomeric proteins resulting in cardiac myocyte disar- [7]. The hypertrabeculations of the noncompacted myocar-
ray and left ventricular hypertrophy with or without dium, as well as thrombi that may form within the recesses,
obstruction. This most commonly involves asymmetric are easily delineated with CCT due to its favorable contrast-to-
septal hypertrophy, although other variants exist, including noise ratio (Fig. 13.2). Left ventricular noncompaction fre-
apical and mid-ventricular hypertrophy (Fig. 13.1). In quently manifests itself as a dilated cardiomyopathy with
224 M.A. Latif and K. Nasir

a b c

d e f

g h i

j k l

Fig. 13.1 The most common form of hypertrophic cardiomyopathy myopathy, muscle thickening occurs predominantly at the apex of the
manifests as asymmetric septal hypertrophy with or without obstruc- left ventricle, as can be seen in end-diastolic images in the four-and
tion. This three-chamber view in end-diastole (a) demonstrates abnor- two-chamber views (e, f). The corresponding end-systolic images dem-
mal thickening of the mid-and basal interventricular septum. The onstrate complete obliteration of the left ventricular apex (g, h). When
short-axis view in end-diastole (b) demonstrates normal mitral valve the left ventricular hypertrophy primarily affects the mid-ventricular
morphology and opening. In systole, the three-chamber view (c) dem- level, there can be mid-cavitary obliteration with an associated gradient
onstrates systolic anterior motion of the anterior mitral valve leaflet at the level of obstruction. End-diastolic images in the short-axis (i),
(arrow) causing a gradient across the left ventricular outflow tract. This two-chamber (j), and four-chamber (k) views, and the 3-D volume-
is consistent with hypertrophic obstructive cardiomyopathy. The short- rendered image (l) demonstrate prominent thickening at the mid-ven-
axis view in systole (d) also demonstrates systolic anterior motion of tricular level. The corresponding end-systolic images
the mitral valve as well as incomplete coaptation of the leaflets (arrow), (m–p) demonstrate complete obliteration of the mid-cavity and early
causing mitral regurgitation. In the apical form of hypertrophic cardio- apical outpouching
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 225

m n

o p

Fig. 13.1 (continued)

reduced left ventricular function, which can also be assessed Due to edema of the myocardium, CCT may also show low
by CCT. Clinically, noncompaction is associated with both attenuation at ventricular wall and interventricular septum
heart failure and sudden death. [8], which can be confirmed with Cardiac MR as increased
signal on T2-weighted imaging. There may also be delayed
myocardial enhancement on contrast-enhanced CCT images
Myocardial Inflammation (Myocarditis) in acute myocarditis [9]. The morphologic features of the
on CT Scan enhancement are similar to the myocardial enhancement of
myocarditis with gadolinium contrast on CMR, and different
Acute myocarditis is a relatively uncommon disease but may from the enhancement patterns seen in patients with myocar-
well be under diagnosed. CCT can be helpful in the diagno- dial infarction [9]. On CMR there is a subepicardial delayed
sis of myocarditis. With the typical history of chest pain and contrast enhancement (DCE) pattern typical of acute myo-
elevated serum troponin-I level in young patients, myocardi- carditis in comparison to an ischemic DCE pattern, which is
tis on CCT will show normal epicardial coronary arteries. transmural or subendocardial [10].
226 M.A. Latif and K. Nasir

a b c

d e f

Fig. 13.2 The morphological hallmark of left ventricular noncompac- these characteristically prominent trabeculations that form the noncom-
tion is the presence of hypertrabeculations. These hypertrabeculations are pacted layer (white arrows). End-diastolic images in the short-axis view
often most prominent toward the left ventricular apex. End-diastolic at the base (d), mid-ventricular (e), and apical levels (f) again demon-
images in the two-(a), three-(b), and four-chamber (c) views demonstrate strate these hypertrabeculations, most prominently at the apex

CT Imaging of Pericardial Disease Anatomy of Pericardium and CT Scan

Pericardial diseases represent an important cause of morbid- The pericardium is a double-layered membrane normally
ity and mortality in patients with cardiovascular disease and measuring <2 mm in thickness that forms a sac which sur-
constitute a spectrum ranging from benign to malignant rounds the heart and the origins of the great vessels (Fig. 13.3)
causes. Pericardial diseases can present clinically as acute [11]. It is made of two sacs in one. The outer sac is the fibrous
pericarditis, pericardial effusion, cardiac tamponade, and pericardium and inner sac is the double-layered serous peri-
constrictive pericarditis. Patients can subsequently develop cardium. Layers of serous pericardium are divided by the
chronic or recurrent pericarditis. Structural abnormalities pericardial space, which usually only contains 15–50 mL of
including congenitally absent pericardium and pericardial serous fluid. They have quite different structures—the
cysts are usually asymptomatic and are uncommon. fibrous pericardium is a tough connective tissue continuous
Advances in multimodality noninvasive cardiac imaging with and bound to the central tendon of the diaphragm, the
have enhanced its role in the management of patients with roots of the great vessels, the pretracheal layer of the deep
suspected pericardial disease. Structural and functional cervical fascia and the sternum via the superior sterno-peri-
information obtained from echocardiography and the ana- cardiac ligaments (to manubrium) and inferior sterno-peri-
tomic detail provided by cardiac computed tomography and cardiac ligaments (to xiphoid process). The serous
magnetic resonance have led to growing interest in the com- pericardium is composed of a single layer of flattened cells
plementary use of these techniques. Management of the forming a closed sac and in turn also forms two continuous
patient with suspected pericardial disease requires expertise layers. The visceral serous pericardium (or epicardium) cov-
with the key imaging modalities and the ability to choose the ers heart and great vessels. The parietal serous pericardium
appropriate imaging tests for each patient. lines the fibrous pericardium and is inseparable from it.
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 227

a b

Fig. 13.3 Due to its excellent spatial resolution, cardiac CT can image (white arrowheads). The pericardium is often best visualized over the
the pericardium, which is normally <2 mm thick. These short-axis (a) right side of the heart, as the more abundant epicardial fat located there
and four-chamber (b) views demonstrate the normal, thin pericardium provides good tissue contrast

The serous pericardium is invaginated by the heart and pericardium as a well-defined, linear structure that is easily
great vessels to form two sinuses: the oblique sinus is detectable in both contrast and noncontrast-enhanced exami-
formed by the indentations of the superior and inferior vena nations because of its visibility against the low attenuation of
cavae and the four pulmonary veins (blind-ending) and thus the surrounding fat. Visualization of the pericardium varies
sits posterior to the left atrium where it may be mistaken for with location and is sometimes difficult at the lateral, poste-
an esophageal mass or bronchogenic cyst. The transverse rior, and inferior left ventricular walls because of a paucity of
sinus lies between the aorta and pulmonary artery anteriorly pericardial fat in these locations.
and the atria posteriorly, surrounding the ascending aorta. It
includes several recesses (superior aortic recess, inferior aor-
tic recess, pulmonic recesses and post caval recess) that may Inflammation of Pericardium on CT Scan
be mistaken for dissection or lymphadenopathy [12]. These
recesses are important when evaluating for pericardial meta- To evaluate for pericardial inflammation, a noncontrast CT
static disease in oncology patients. can be performed prior to the contrast-enhanced CT.
While echocardiography is conventionally used for the Enhancement of the pericardium after contrast administra-
evaluation of pericardial diseases, CCT offers a number of tion is indicative of pericardial inflammation, and may be
distinct advantages. CCT provides a larger imaging field seen in cases of pericarditis. The current reference stan-
allowing assessment of concomitant pathology. In addition, dard for the noninvasive evaluation of pericardial constric-
CCT offers a superior soft tissue contrast, and thus character- tion is cardiac MRI. The characteristic anatomic changes
ization of specific pericardial processes is sometimes possi- associated with constrictive pericardial disease (elongated
ble. CCT is exquisitely sensitive to the detection of calcium and narrow RV, enlargement of the right atrium and infe-
and thus can be useful in identifying pericardial calcification, rior cava, and pericardial thickening) are clearly identified
a finding that can be associated with constrictive pericarditis with both MRI and CCT. However, since patients with true
(Fig. 13.4). One of the limitations of CCT in evaluating the constrictive pericarditis typically present with orthopnea,
pericardium, however, is its occasional difficulty in differen- it is often difficult for them to lie flat in the MRI scanner
tiating pericardial fluid from a thickened pericardium. for up to 1 h. CCT may offer another option for evaluating
With CCT, the normal pericardium (Video 13.2) is best constrictive pericarditis, with short examination times rep-
imaged in systole and appears as a line of average thickness resenting one of its major advantages. The excellent spa-
of 1.3–2.5 mm (almost always <4 mm). CCT delineates the tial resolution of CCT allows for accurate measurement of
228 M.A. Latif and K. Nasir

a b

Fig. 13.4 Cardiac CT is exquisitely sensitive for the detection of cal- noted on the short-axis view (a) and 3-D volume-rendered image (b).
cium. In this case of pericardial constriction, the patient was found to The volume rendered image demonstrates circumferential pericardial
have a thickened, heavily calcified pericardium (white arrowheads) as calcification at the base

pericardial thickness. A pericardial thickness >4 mm is Pericardial Effusion on CT Scan

considered pathological and, in the appropriate clinical
context, is suggestive of pericardial constriction [13, 14]. Echocardiography remains the modality of choice for the ini-
However, it is important to note that neither pericardial tial evaluation of pericardial effusion (Fig. 13.5b). However,
calcification nor thickening is diagnostic of constrictive several findings make further evaluation with CCT useful,
pericarditis. Besides these morphological characteristics, such as a loculated effusion, hemorrhagic effusion, or equivo-
the demonstration of an early diastolic septal bounce on cal findings on echocardiography. Pericardial effusions may
the multiphase cine images is suggestive of constrictive be characterized with CCT by measuring their CT attenuation.
physiology [15]. A CT attenuation close to water (e.g., 0 Hounsfield Units, HU)
The normal pericardium is a double-layered membrane suggests a simple pericardial effusion. If the CT attenuation is
that is <2 mm thick. A pericardial thickness >4 mm is con- greater than that of water, the effusion may represent hemor-
sidered pathological. Pericardial thickening may be found in rhage, purulence, or a malignant/cellular process.
the absence of constriction (e.g., acute pericariditis, uremia,
collagen vascular diseases). Enhancement of the pericar-
dium, indicative of pericardial inflammation, may be found Pericardial Masses
in cases of pericarditis. Pericardial inflammation can be eval-
uated by performing CCT with and without contrast. The Pericardial masses include cysts and neoplasms. Pericardial
inflamed pericardium will demonstrate a significant increase cysts are congenital and are usually found at the right cos-
in CT attenuation after contrast administration. tophrenic angle [16]. They tend to be asymptomatic
smooth-walled simple cysts that do not enhance after con-
trast administration (Fig. 13.5c). However, sometimes
Congenital Absence of Pericardium pericardial cyst can present on left side and can compress
the left atrium with clinical symptoms of dyspnea [17].
Rare individuals demonstrate a congenital absence of the With regard to neoplasms, metastases are far more com-
pericardium. While this can present as a complete absence of mon than primary pericardial tumors. Neighboring struc-
pericardial tissue, most cases demonstrate only partial peri- tures, such as the lung and breast, are most commonly the
cardial defects, typically on the left side (Fig. 13.5a). Clues source of metastatic disease to the pericardium. Other
on CCT that suggest this diagnosis are rotation of the heart to findings associated with metastatic disease include peri-
the left, interposition of lung tissue in the aortopulmonary cardial effusion and an irregularly thickened pericardium
window, and bulging of the left atrial appendage through the [18]. Primary neoplasms of the pericardium occur infre-
pericardial defect. Infrequently, the left atrial appendage can quently and may be benign (fibroma, teratoma, lipoma,
be incarcerated in the defect requiring surgical enlargement hemangioma) or malignant (mesothelioma, lymphoma,
or closure. sarcoma, and liposarcoma) [19].
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 229

a b c

Fig. 13.5 Partial absence of the pericardium (a). In this example, nor- case, the pericardium also enhanced after administration of iodinated
mal pericardium is found over the right ventricular free wall (white contrast (white arrowheads), suggesting pericardial inflammation.
arrowheads), but there is absence of the pericardium over the right ven- Pericardial cysts (asterisk) are benign fluid-filled pericardial masses,
tricular apex and left ventricle (black arrowheads). Pericardial effu- typically found at the right cardio-phrenic angle (c)
sions (asterisks) are often found in the context of pericarditis (b). In this

Volumetric quantification of epicardial fat and thoracic fat

require the following steps: demarcation of the heart bound-
aries on CT images, and tracing of the inner thoracic cavity
and pericardium, which can be manual [21, 28] or semi-
automated [20]. The superior most slice is typically chosen
at the bifurcation of the pulmonary artery. The anatomic
landmark for the inferior limit of the heart is typically the
most inferior slice of the myocardium [26] or the most infe-
rior slice with the posterior descending artery [29]. With
semi-automated measurement, pericardial fat contours are
generated by spline interpolation through several control
points, which are placed manually on the visceral pericar-
dium [30], and the inner thoracic cavity is segmented auto-
matically [31]. CT uses standard fat attenuation values to
define fat attenuation; for non-contrast CT typically an
attenuation range of (−30, −190) Hounsfield Units is used.
Fat voxels within this attenuation range within the visceral
pericardium are classified as epicardial fat, and within the
inner thoracic cavity classified as thoracic fat.
Fig. 13.6 Axial view of heart with normal pericardium on Revolution
CT calcium scan (yellow arrowhead)
Comparison to Other Imaging Modalities

Pericardial Fat Assessment with CT Scan Generally cardiac computed tomography is superior to
echocardiography and cardiac MRI because of its supe-
Recent studies have shown that increased pericardial fat is rior and ultrasensitive resolution and excellent field of
strongly associated with increased coronary artery calcium, view. Echocardiography is good for a quick assessment of
coronary plaque burden and major adverse cardiovascular pericardium but it does not give the detail of pericardial
events (MACE) [20, 21]. These findings suggest that peri- disease as clearly as CT/MRI. Cardiac MRI is limited in
cardial fat may play a role in causing coronary atherosclero- use because of high cost and time duration of the scan that
sis [22–26]. Due to distinct attenuation values of fat on CT, make it less suitable for emergent pericardial conditions
fat can be readily measured around the heart with cardiac such as cardiac tamponade. Table 13.1 [32, 33] compares
CT, both with and without contrast [27]. Cardiac CT, with pericardial disorder assessment with CCT, echocardiogra-
its high spatial resolution, allows accurate measurement of phy and CMR. Table 13.2 [34–90] compares myocardial
epicardial and thoracic fat distances and volumes (Fig. 13.6). disorder assessment with these imaging modalities.
Table 13.1 Pericardial disorders assessment with cardiac imaging modalities
230

Pericardial condition Definition CT angiographic diagnostic finding Echocardiographic diagnostic finding MRI diagnostic finding
Pericarditis Pericarditis is an Normal pericardial thickness is Only helpful if a pericardial effusion is present Most sensitive method for the diagnosis of acute
inflammation of the less than 4 mm and is usually with pericarditis. pericarditis is delayed enhancement of the
pericardium. 1–2 mm Can determine whether the effusion is limiting pericardium on cardiac MR (CMR) [33].
Pericardial thickening/ the filling of the heart (i.e., causing cardiac On CMR, the pericardium normally appears
enhancement (the most accurate tamponade). black because of its low water content;
single parameter for pericarditis, However, in patients with pericarditis, enhanced
with sensitivity of 54–59 % and gadolinium uptake in the inflamed pericardium
specificity of 91–96 %) [32]. is present on delayed images
Cardiac Tamponade Cardiac Tamponade is a Enlargement of the SVC and IVC RV diameters are reduced. CMR has a limited role in the setting of cardiac
clinical syndrome caused Periportal lymphedema Early diastolic collapse of RV tamponade owing to the emergent and
by the accumulation of Reflux of contrast material within RA free-wall collapse during late diastole. RA life-threatening nature of this condition.
fluid in the pericardial the IVC and azygos vein, and isovolumic contraction is prolonged to occupy CMR findings with other imaging modalities
space, resulting in reduced enlargement of hepatic and renal one third of the cardiac cycle. include; swinging heart and paradoxical septal
ventricular filling and veins. LA free-wall compression in patients with fluid bounce seen on short-or long-axis cine MR
subsequent hemodynamic Flattened heart sign. posterior to the left atrium. LV free-wall may images.
compromise. The Compression of the coronary sinus. exhibit paradoxical movement CMR imaging can help differentiate the nature
condition is a medical Angulation or bowing of SVC & IVC may show congestion (unless of the pericardial effusion (transudative,
emergency, the interventricular septum. patient is relatively volume depleted) exudative, and or hemorrhagic) in addition to
complications of which IVC is usually greater than 2.2 cm in diameter the effects on cardiac functioning and diastolic
include pulmonary edema, with less than 50 % inspiratory compression filling.
shock, and death. Exaggerated inspiratory effects, especially with
pulsus paradoxus, may include RV expansion,
interventricular septum shift to the left, and LV
compression
Mitral changes, with reduced D-E amplitude or
E-F slope and delayed mitral opening time
Aortic valve with premature closure
Echocardiographic stroke volume diminished
RV epicardial notching during isovolumic
contraction
Coarse vibrations of LV posterior wall.
Pseudohypertrophy or apparent wall thickening
due to compression
M.A. Latif and K. Nasir
 13

Constrictive Constrictive pericarditis is Diffuse thickening of anterior Cardiac echograms show normal contraction Cardiac MRI can detect constrictive physiology.
Pericarditis a reduction in the pericardium upto the vascular root and systolic function. MRI allows precise measurement pericardial
elasticity, or stiffening, of best seen on multiplanar Special procedures, including an assessment of thickness; the ideal views for measuring
the pericardium, a reformats. Doppler velocities across the mitral and pericardial thickness are short axis views
sack-like covering that Size of all 4-heart chambers tricuspid valves during inspiration and Measure chamber sizes at successive 50-msec
surrounds the heart, should be within the normal range. expiration, are needed to demonstrate delays after the R wave and to determine
resulting in impaired -IVC is dilated to more than ventricular interdependence. whether or not a filling plateau is present.
filling of the heart with double the size of aortic diameter. Newer echocardiographic procedures, such as Assess volumetric flow and regurgitant flow to
blood. Poor opacification of liver the evaluation of the early diastolic Doppler the pulmonary veins and the hepatic vein.
parenchyma due to congestion and myocardial velocity gradients at the posterior Fast imaging with deep respiration help to
no contrast enhancement in the wall, echocardiographic TDI, and color M mode establish whether filling is concordant or
portal vein. flow propagation, have been reported to discordant. CP restriction creates discordance
No progression of the contrast- enhance the differentiation between CP and with reduced left ventricular filling, which
agent bolus through the vascular restrictive cardiomyopathy corresponds to increased right ventricular
system, and evidence of filling.
significant systolic dysfunction MRI shows reversed curvature of the
should be absent intraventricular septum.
MRI does not depict pericardial calcifications.
Pericardial effusion Pericardial effusion is an Differentiation of the pericardial Echo-free space: (1) posterior to LV (small-to- On spin-echo images, the pericardial effusion or
abnormal accumulation of line from the myocardium is moderate effusion); (2) posterior and anterior portions of it may appear as a signal void (dark)
fluid in the pericardial enabled by the presence of a small (moderate-to-large effusion); (3) behind left sac because of moving fluid in the pericardial
cavity. Because of the amount of epicardial and atrium large-to-very large effusion and/or cavity. In gradient-echo sequences, effusions are
limited amount of space in pericardial fat. This fat may be anterior adhesion. hyperintense.
the pericardial cavity, fluid visible on CT scans. Diminished mobility of posterior pericardium- Hemorrhagic effusions have the opposite
accumulation leads to an CT demonstrates the superior to-lung interface. appearance; they have high signal intensity on
increased intrapericardial recesses of the pericardium Enhanced RV wall mobility unmasked in T1-weighted spin echo images and low intensity
pressure which can extending over the ascending aorta presence of anterior fluid on gradient echo images.
negatively affect heart and lateral to the main pulmonary Swinging heart (large effusions, usually Depict pericardial recesses, mediastinal fat, and
Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes

function artery. These recesses may be tamponade): (1) RV and LV walls move in other similar anatomic structures within the
distended in the presence of a synchrony; (2) periodicity 1:1 or 2:1 (one or pericardial sac.
pericardial effusion. two swings per cardiac cycle); (3) 2:1 swing is Dark-blood (double inversion recovery) imaging
Attenuation of the effusion on CT characteristic of cardiac Tamponade; (4) can measure pericardial thickness accurately.
may be helpful in suggesting the pseudoparadoxic motion of LV posterior wall; Fat-sensitive imaging (based on chemical shift
etiology. (5) mitral and/or tricuspid pseudoprolapse; (6) or on T1 values) can discern pericardial fat from
mitral systolic anterior motion; (7) alternating other materials.
mitral E-F slope and aortic opening excursion; Dynamic MRI can identify constrictive disease
(8) aortic valve exhibiting midsystolic closure; (failure to expand for the last 6/20 frames of
(9) pulmonic valve with midsystolic notch diastole).
Hemopericardium with blood clots identifiable MRI can also assess for adhesions by placing
by echocardiography demagnetization stripes to observe for
Inspiratory decrease in LV ejection time (with translational motion at the pericardium, and it
effusion can assess for restrictive disease by strain
mapping.
CT computed tomography, MRI magnetic resonance imaging, CMR cardiac MR, SVC superior vena cava, IVC inferior vena cava, RV right ventricle, LV left ventricle, RA right atrium, LA left
atrium, CP Contrictive Pericarditis, TDI tissue Doppler imaging
231
232 M.A. Latif and K. Nasir

Table 13.2 Myocardial disorder assessment with cardiac imaging modalities

Myocardial CT Angiographic Echocardiographic diagnostic
condition Definition diagnostic finding finding MRI diagnostic finding
Dilated Dilated Gated CT scanning is Left ventricular spherical MRI and magnetic resonance
cardiomyopathy cardiomyopathy is an accurate means of dilatation. angiography (MRA) are the most
a condition in evaluating cardiac Normal or reduced wall thickness. accurate methods for assessing cardiac
which the function, especially Poor systolic wall thickening, and/ anatomy or function. MRI/MRA is
ventricular with the use of or reduced inward endocardial used when echocardiography is
chambers show ultrafast CT scanning systolic motion. inadequate, as this study is often not
increased systolic and 50-millisecond All of the systolic indices are used because of its relatively high cost
and diastolic image acquisition. reduced, including left ventricular and limited availability, as well as
volume and a low Only 1 short fractional shortening, fractional contraindications if ferromagnetic
Ejection Fraction breath-hold period is area change, and ejection fraction. metallic foreign bodies are present in
(<40 %) [1, 34]. required, and Four chamber cardiac enlargement the patient.
definition of the is often present.
endocardial margins is On M-mode, additional features
excellent, allowing a related to systolic dysfunction are
degree of automation increased separation of the mitral
for defining the leaflet E point from the septum,
ventricular volumes. poor mitral valve opening, poor
Increased in left aortic valve opening and early
ventricular end- closure from a reduced stroke
diastolic and volume, and poor systolic aortic
end-systolic volume. root motion.
Left ventricular wall Doppler has been used in dilated
thinning. cardiomyopathy to measure
Decrease ejection decreased stroke volume
fraction.
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 233

Table 13.2 (continued)

Myocardial CT Angiographic Echocardiographic diagnostic
condition Definition diagnostic finding finding MRI diagnostic finding
Hypertrophic Hypertrophic MDCT is an excellent LV wall thickness of 13 mm in the Either spin-echo MRI or cine MRA
cardiomyopathy cardiomyopathy is method for observing anterior septum or posterior wall or help to views 4 chamber and short axis
characterized by irregular wall 15 mm in the posterior septum or [44].
left ventricular hypertrophy, apical free wall, in the absence of LV Accurately characterize the
hypertrophy (wall morphology, and wall dilatation or other cardiac and distribution and degree of myocardial
thickness motion dynamics [35]. systemic causes of increased mass hypertrophy & asymmetric septal
>12–15 mm) Criterion for LV wall [38]. hypertrophy.
without obvious hypertrophy is an LV Asymmetric septal hypertrophy Visualize apical and posterolateral
etiology. wall thicker than (defined as a ratio of septal myocardial hypertrophy that is not
Associated right 13-mm. Right thickness to posterior wall always evident on 2D echograms [45].
ventricular ventricular thickness of at least 1.3–1.5) [39]. MRI helps to calculate hypertrophic
hypertrophy may hypertrophy is Ground-glass appearance is noted scores [46].
be seen in 15 % of considered when the either visually or by using Hypertrophy in HCM is usually
cases. right ventricular wall quantitative texture analysis in both asymmetric and is typically most
is thicker than 6 mm hypertrophied and evident in the anteroseptal
(Fig. 13.8). nonhypertrophied regions of the myocardium [47].
Wall thickening ventricle [40], used to distinguish Basal IVS at end diastole is
during systole can be HCM from other causes of disproportionately thickened, ratio of
calculated with secondary hypertrophy [41]. IVS thickness to posterolateral wall
MDCT. Most patients Narrowing or obstruction of the thickness is significantly increased.
(71 %) have decreased LVOT caused by IVS and the Decreased systolic myocardial
wall thickening at the anterior leaflet of the mitral valve, thickening [48]. Long-axis show
hypertrophic site and which results in a dynamic typical spade-shaped deformity of the
normal or increased pressure gradient. LV cavity and the apical distribution of
thickening at the Abnormal systolic anterior motion myocardial hypertrophy.
nonhypertrophic site (SAM) of the anterior leaflet and, Diffuse hypertrophy of RV wall,
[35]. occasionally, the posterior leaflet of increased RV wall index [49].
Late enhancement of the mitral valve may be present; LV mass can be reliably estimated
the myocardium on severe SAM, with septal-leaflet with spin-echo MRI, ECG-gated MRI,
EBCT has been contact, has been proposed as a or multilevel cine MRA; however, LV
reported in major diagnostic criterion. mass, indexed to body surface area, is
approximately 47 % Mitral valve abnormalities in HCM normal in about 20 % of patients with
of HCM patients [36]; patients include increased leaflet HCM [50].
this finding suggests area, elongation of the leaflet, and LVH in HCM often decreases the LV
the presence of anomalous insertion of papillary volume and increases the ejection
abnormal tissue muscle directly into the anterior fraction, without significantly
Degree of regional mitral leaflet. changing stroke volume. Cine MRA
wall thickening also is Prasad et al. have reported pitfalls can be used to calculate these
significantly less in in the echocardiographic diagnosis parameters
areas of late of HCM [42]. Obstruction of LVOT results in a
enhancement, which Approximately 70 % of HCM subaortic pressure gradient (can be
reflects the abnormal patients have an LV outflow detected on cine MRA as signal void).
myocardial gradient of 30 mmHg (2.7 m/s by Although areas of physiologic signal
architecture [37]. Doppler) [43]. void can be seen on scans in healthy
individuals, signal voids are larger and
persist longer in the cardiac cycle in
patients with pathologic conditions
that cause obstruction [51].
Mitral regurgitation appears on cine
MRAs as a signal void in the left
atrium during ventricular systole
which may be associated with mitral
valve prolapse [52–54].
Gadolinium enhancement can detect
myocardial fibrosis [55].
MRI can differentiate between HCM
and amyloidosis [56, 57].
(continued)
234 M.A. Latif and K. Nasir

Table 13.2 (continued)

Myocardial CT Angiographic Echocardiographic diagnostic
condition Definition diagnostic finding finding MRI diagnostic finding
Restrictive Restrictive CT is not useful in the Echocardiography is often part of MRI is a sophisticated, accurate,
cardiomyopathy cardiomyopathy is evaluation of the patient's evaluation Normal noninvasive tool that is well suited to
characterized by a restrictive ventricular size and systolic the evaluation of the morphology and
marked decrease in cardiomyopathy but functions usually are evident in function of the heart. In restrictive
ventricular can help in multi- cases of restrictive cardiomyopathy cardiomyopathy, the thickness of the
compliance. It is modality imaging for [59–63]. pericardium (<4 mm) is a key finding
predominantly a exclusion of other Findings that have been described [64–71].
disease of diastolic diagnoses. as helpful in diagnosing restrictive Diagnosis of constrictive pericarditis
dysfunction where Presence of cardiomyopathy include mid- (excluding restrictive cardiomyopathy)
the systolic pericardial diastolic reversal of flow across the may be made on the basis of
(contractile) calcification on CT mitral and tricuspid valves. Atrial pericardial thickness. The sensitivity is
function of the along with appropriate enlargement with normal left 88 %; the specificity is 100 %; and the
myocardium is hemodynamics may ventricular end-diastolic accuracy is 93 %.
usually unaffected. indicate pericardial dimensions may also be seen. Ventricular hypertrophy is not
constriction [58]. Typically, patients with constrictive associated with restrictive
Although calcification pericarditis have a thickened cardiomyopathy, but some degree of
of the pericardium is pericardium and marked thickening may be seen on both
associated with respiratory variation during cross-sectional imaging and
constrictive diastole. One study showed that echocardiography in cases of
pericarditis, not with Doppler myocardial velocity infiltrative restrictive cardiac disease
restrictive gradients, as measured from the (e.g., amyloidosis or
cardiomyopathy, the left ventricular posterior wall hemochromatosis).
absence of calcium is during the predetermined phases of Patients with a history of cardiac
not a diagnostic the cardiac cycle, are lower in surgery or pericardiotomy may have a
finding. In 50 % of patients with restrictive thickened pericardium without a
cases of constrictive cardiomyopathy than in patients constrictive physiologic pattern.
pericarditis, there are with constrictive pericarditis [60]. Conversely, in the postoperative
no findings of a Restrictive cardiomyopathy might patient, the visceral pericardium may
calcified pericardium; not be distinguishable from constrict the heart without being
however, although a constrictive pericarditis on the abnormally thick.
thickened pericardium basis of echocardiography alone.
(>4 mm) is associated Inadequate acoustic windows may
with constrictive limit echocardiography, and it may
pericarditis, some not be sufficient for the evaluation
patients with of pericardial thickness. In such
restrictive cases, use of CT or MRI is the next
cardiomyopathy also step.
have a mildly
thickened pericardium
in the absence of
calcification (see the
image below).
Advanced imaging
techniques may not be
sufficient to make the
diagnosis of restrictive
cardiomyopathy,
necessitating
myocardial biopsy.
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 235

Table 13.2 (continued)

Myocardial CT Angiographic Echocardiographic diagnostic
condition Definition diagnostic finding finding MRI diagnostic finding
Arrhythmogenic Disorder of the Dilatation of the right Tricuspid annular measurements Revised CMR criteria now require
right ventricular heart muscle of ventricle is one are valuable, easy to obtain, and presence of both qualitative findings
cardiomyopathy unknown origin. It criterion for diagnosis allow quantitative assessment of (RV regional akinesia, dyskinesia,
(ARVC) is characterized by of ARVC and it is right ventricular function [73]. dyssynchronous contraction) and
electrical commonly seen in ARVC patients showed an quantitative metrics (decreased
instability of the patients with ARVC. abnormal velocity pattern that may ejection fraction or increased indexed
heart as a result of Fatty tissue in be an early but non-specific sign of RV end-diastolic volume) [74].
replacement of the conspicuous the disease. Major criteria (RV ejection fraction
right ventricular trabeculae of the right Normal right ventricular ≤40 % or indexed RV end-diastolic
myocardium with ventricle, especially in dimensions do not exclude ARVC, volume ≥110 mL/m2 for men and
fatty or fibrous the anterior wall, and subjective detection of early ≥100 mL/m2 for women) are chosen to
fatty tissue. apex, and inferior changes in wall motion may be achieve approximately 95 %
(diaphragmatic) wall; difficult [73]. specificity. Cutoffs with high
and a scalloped specificity invariably result in lower
appearance (bulging) sensitivity; major CMR criteria have a
of the right ventricular sensitivity of 68–76 % [75].
wall are characteristic Minor criteria (RV ejection fraction
findings at helical 40–45 % or indexed RV end-diastolic
computed tomography volume 100–110 mL/m2 for men and
(CT) that may be used 90–100 mL/m2 for women) had a
to diagnose ARVC higher sensitivity (79–89 %), but a
[72]. consequently lower specificity
Fatty tissue in the left (85–97 %) [76].
ventricle and
ventricular septum is
seen relatively
frequently in ARVC,
and fat in the
ventricular septum is
another useful finding
for diagnosis of
ARVC with helical
CT.
When evaluating
dilatation of the right
ventricle, it is
important to rule out
pulmonary
hypertension. A
dilated right ventricle
with an ectatic
pulmonary trunk may
indicate pulmonary
hypertension rather
than ARVC [72].
(continued)
236 M.A. Latif and K. Nasir

Table 13.2 (continued)

Myocardial CT Angiographic Echocardiographic diagnostic
condition Definition diagnostic finding finding MRI diagnostic finding
Takotsubo Takotsubo Normal coronary Echocardiography plays a key role in Late gadolinium enhancement (LGE)
cardiomyopathy cardiomyopathy, arteries. diagnostic assessment of Takotsubo on CMRI is generally absent in stress
also known as Left ventricular apical cardiomyopathy (TTC) [76]. cardiomyopathy in contrast to
transient apical hypokinesis with During the acute phase, TTE may myocardial infarction in which intense
ballooning systolic ballooning. detect a large area of dysfunctional subendocardial or transmural LGE is
syndrome is a type Useful to rule out myocardium usually extended seen [85–89].
of non-ischemic acute coronary chest beyond the territory of distribution LGE is also useful in differentiating
cardiomyopathy in pain causes including of a single coronary artery. stress cardiomyopathy from
which there is a the aorta and Wall motion analysis reveals a myocarditis, which is characterized by
sudden temporary pulmonary arteries. typical pattern of LV myocardial patchy late gadolinium enhancement.
weakening of the CT is usually not contractility characterized by However, when a low threshold for
muscular portion performed in these symmetrical regional abnormalities LGE is used (e.g., three standard
of the heart patients unless the extending equally into the anterior, deviations above the mean signal
diagnosis is uncertain. inferior, and lateral walls. This intensity of remote myocardium), LGE
‘circumferential pattern’ can be is occasionally detected in stress
considered a hallmark of TTC [77]. cardiomyopathy [87].
Echocardiography reveals LV CMR evidence of myocardial edema is
morphology allowing the commonly seen in stress
recognition not only the classic LV cardiomyopathy. However, myocardial
apical dysfunction, but also variant edema is also seen in acute MI and
forms, such as midventricular myocarditis. In one series, 81% of
dysfunction and apical sparing patients had evidence of focal
[76]. It also plays an important role myocardial edema on CMR and these
in the early detection of severe regions corresponded to areas of wall
potential complications such as motion abnormality [90].
right ventricular (RV) involvement CMR may also enable identification of
(biventricular dysfunction), LVOT thrombus in the left or right ventricle,
obstruction, thrombus formation, which may not be detected by
MR, and ventricular rupture echocardiography [90].
[77–80].
Helps at follow-up to confirm
recovery of LV function. Finally,
non-conventional echocardiographic
techniques (tissue Doppler, strain
imaging, real-time three-dimensional
[3D] echocardiography), coronary
flow velocity reserve, and
myocardial contrast
echocardiography may provide new
insights in the assessment of LV and
RV myocardial function and
coronary microcirculation
physiopathology [78, 81].
Symmetric pattern of wall motion
abnormalities (WMA) characteristic
of typical TTC is sometimes
difficult to assess by transthoracic
echo (use of contrast agent for LV
opacification could magnify this
pattern). This peculiar pattern of
WMA could also be evaluated by
myocardial deformation imaging
using the speckle tracking method,
which demonstrates a transient
circular impairment of not only
longitudinal LV function but also
circumferential and radial LV
function as well as LV twist
mechanics deficiency [82–84].
CT computed tomography, MRI magnetic resonance imaging, CMR cardiac MR, SVC superior vena cava, IVC inferior vena cava, RV right
ventricle, LV left ventricle, RA right atrium, LA left atrium, CP Contrictive Pericarditis, TDI tissue Doppler imaging, MRA magnetic resonance
angiography, ECG electrocardiography, TTE trans-thoracic echocardiography, LVOT left ventricular outflow tract
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 237

Future Directions

CT scan has revolutionized cardiac diagnostic and prognostic

capabilities, not only to diagnose the disease but also to monitor
the progression and or regression of the disease. With current
advancement of the CT technology, radiation exposure is very
limited and continues to diminish with ongoing development of
CT protocols. The Revolution CT scanner is one of the newer
developments by GE healthcare. It can acquire excellent image
quality despite high heart rates and with less radiation and con-
trast dose than typical CT scanners (Fig. 13.7). The pericardium
may be secondarily involved with ischemic or other heart dis-
ease. Implementation of CT scanning in ER protocols for chest
pain may help identify pericardial disease. Future molecular
imaging will be another addition to the current CT protocol for
pericardial and myocardial disease evaluation.

References
Fig. 13.7 Revolution CT Angiography produces excellent image qual- 1. Richardson P, McKenna W, Bristow M, Maisch B, Mautner B,
ity with reduce radiation dose. Thinning of the left ventricular wall O’Connell J, et al. Report of the 1995 World Health Organization/
(blue arrowhead) a sign of dilated cardiomyopathy in this patient. Note International Society and Federation of Cardiology Task Force on
the right coronary artery (white arrowhead) and pericardium (yellow the definition and classification of cardiomyopathies. Circulation.
arrowhead) 1996;93(5):841–2.
2. Tummala LS, Young RK, Singh T, Jani S, Srichai MB. Role of non-
invasive imaging in the work-up of cardiomyopathies. Curr
Atheroscler Rep. 2015;17(3):486.
3. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S,
Laskey WK, et al. Standardized myocardial segmentation and
nomenclature for tomographic imaging of the heart. A statement
for healthcare professionals from the Cardiac Imaging Committee
of the Council on Clinical Cardiology of the American Heart
Association. Circulation. 2002;105(4):539–42.
4. Annuar BR, Liew CK, Chin SP, Ong TK, Seyfarth MT, Chan WL,
et al. Assessment of global and regional left ventricular function
using 64-slice multislice computed tomography and 2D
echocardiography: a comparison with cardiac magnetic resonance.
Eur J Radiol. 2008;65:112–9. Ireland.
5. Halliburton SS, Petersilka M, Schvartzman PR, Obuchowski N,
White RD. Evaluation of left ventricular dysfunction using
multiphasic reconstructions of coronary multi-slice computed
tomography data in patients with chronic ischemic heart disease:
validation against cine magnetic resonance imaging. Int
J Cardiovasc Imaging. 2003;19(1):73–83.
6. Tandri H, Bomma C, Calkins H, Bluemke DA. Magnetic resonance
and computed tomography imaging of arrhythmogenic right ven-
tricular dysplasia. J Magn Reson Imaging. 2004;19(6):848–58.
7. Petersen SE, Selvanayagam JB, Wiesmann F, Robson MD, Francis
JM, Anderson RH, et al. Left ventricular non-compaction: insights
from cardiovascular magnetic resonance imaging. J Am Coll
Cardiol. 2005;46:101–5. United States.
8. Brett NJ, Strugnell WE, Slaughter RE. Acute myocarditis demon-
Fig. 13.8 55 year old African American female with zero calcium strated on CT coronary angiography with MRI correlation. Circ
score (scanning heart rate of 53 beat per minute and body mass index of Cardiovasc Imaging. 2011;4:e5–6. United States.
43). Apical variant hypertrophic Cardiomyopathy with marked thicken- 9. Brooks MA, Sane DC. CT findings in acute myocarditis: 2 cases.
ing of the apical walls of the left ventricle (white arrowhead). Very J Thorac Imaging. 2007;22:277–9. United States.
small left ventricular cavity (yellow arrowhead) due to hypertrophy of 10. Codreanu A, Djaballah W, Angioi M, Ethevenot G, Moulin F,
the left ventricle. Felblinger J, et al. Detection of myocarditis by contrast-enhanced
238 M.A. Latif and K. Nasir

MRI in patients presenting with acute coronary syndrome but no 29. Tamarappoo B, Dey D, Shmilovich H, Nakazato R, Gransar H,
coronary stenosis. J Magn Reson Imaging. 2007;25(5):957–64. Cheng VY, et al. Increased pericardial fat volume measured from
11. Roberts WC, Spray TL. Pericardial heart disease: a study of its noncontrast CT predicts myocardial ischemia by SPECT. JACC
causes, consequences, and morphologic features. Cardiovasc Clin. Cardiovasc Imaging. 2010;3:1104–12. United States American
1976;7(3):11–65. College of Cardiology Foundation. Published by Elsevier Inc.
12. Truong MT, Erasmus JJ, Gladish GW, Sabloff BS, Marom EM, 30. Saura D, Oliva MJ, Rodriguez D, Pascual-Figal DA, Hurtado JA,
Madewell JE, et al. Anatomy of pericardial recesses on multidetec- Pinar E, et al. Reproducibility of echocardiographic measurements
tor CT: implications for oncologic imaging. AJR Am J Roentgenol. of epicardial fat thickness. Int J Cardiol. 2010;141:311–3.
2003;181(4):1109–13. Netherlands.
13. Soulen RL, Stark DD, Higgins CB. Magnetic resonance imaging of 31. Dey D, Suzuki Y, Suzuki S, Ohba M, Slomka PJ, Polk D, et al.
constrictive pericardial disease. Am J Cardiol. 1985;55:480–4. Automated quantitation of pericardiac fat from noncontrast
United States. CT. Invest Radiol. 2008;43:145–53. United States.
14. Spodick DH. Pericardial disease. JAMA. 1997;278(9):704. 32. Hammer MM, Raptis CA, Javidan-Nejad C, Bhalla S. Accuracy of
15. Himelman RB, Lee E, Schiller NB. Septal bounce, vena cava pleth- computed tomography findings in acute pericarditis. Acta Radiol.
ora, and pericardial adhesion: informative two-dimensional echo- 2014;55:1197–202. England: The Foundation Acta Radiologica
cardiographic signs in the diagnosis of pericardial constriction. 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.
J Am Soc Echocardiogr. 1988;1(5):333–40. nav.
16. Oyama N, Komuro K, Nambu T, Manning WJ, Miyasaka 33. Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN,
K. Computed tomography and magnetic resonance imaging of the Melduni RM, et al. Pericardial disease: diagnosis and management.
pericardium: anatomy and pathology. Magn Reson Med Sci. Mayo Clin Proc. 2010;85:572–93. United States.
2004;3:145–52. Japan. 34. Boffa GM, Thiene G, Nava A, Dalla VS. Cardiomyopathy: a neces-
17. Seo GW, Seol SH, Jeong HJ, Seo MG, Song PS, Kim DK, et al. A sary revision of the WHO classification. Int J Cardiol. 1991;30(1):
large pericardial cyst compressing the left atrium presenting as a 1–7.
pericardiopleural efussion. Heart Lung Circ. 2014;23(12):e273–5. 35. Yoshida M, Takamoto T. Left ventricular hypertrophic patterns and
18. O’Leary SM, Williams PL, Williams MP, Edwards AJ, Roobottom wall motion dynamics in hypertrophic cardiomyopathy: an electron
CA, Morgan-Hughes GJ, et al. Imaging the pericardium: appear- beam computed tomographic study. Intern Med. 1997;36(4):
ances on ECG-gated 64-detector row cardiac computed tomogra- 263–9.
phy. Br J Radiol. 2010;83:194–205. England. 36. Naito H, Saito H, Ohta M, Takamiya M. Significance of ultrafast
19. Luk A, Ahn E, Vaideeswar P, Butany JW. Pericardial tumors. Semin computed tomography in cardiac imaging: usefulness in assessment
Diagn Pathol. 2008;25(1):47–53. of myocardial characteristics and cardiac function. Jpn Circ
20. Dey D, Wong ND, Tamarappoo B, Nakazato R, Gransar H, Cheng J. 1990;54(3):322–7.
VY, et al. Computer-aided non-contrast CT-based quantification of 37. Saito H, Naito H, Takamiya M, Hamada S, Imakita S, Ohta M. Late
pericardial and thoracic fat and their associations with coronary enhancement of the left ventricular wall in hypertrophic
calcium and Metabolic Syndrome. Atherosclerosis. 2010;209:136– cardiomyopathy by ultrafast computed tomography: a comparison
41. Ireland. with regional myocardial thickening. Br J Radiol. 1991;64(767):
21. Ding J, Kritchevsky SB, Harris TB, Burke GL, Detrano RC, Szklo 993–1000.
M, et al. The association of pericardial fat with calcified coronary 38. McKenna WJ, Spirito P, Desnos M, Dubourg O, Komajda M.
plaque. Obesity (Silver Spring). 2008;16:1914–9. United States. Experience from clinical genetics in hypertrophic cardiomyopathy:
22. Ding J, Kritchevsky SB, Hsu FC, Harris TB, Burke GL, Detrano proposal for new diagnostic criteria in adult members of affected
RC, et al. Association between non-subcutaneous adiposity and families. Heart. 1997;77(2):130–2.
calcified coronary plaque: a substudy of the Multi-Ethnic Study of 39. Maron BJ, Pelliccia A, Spirito P. Cardiac disease in young trained
Atherosclerosis. Am J Clin Nutr. 2008;88:645–50. United States. athletes. Insights into methods for distinguishing athlete’s heart
23. Mazurek T, Zhang L, Zalewski A, Mannion JD, Diehl JT, Arafat H, from structural heart disease, with particular emphasis on hypertro-
et al. Human epicardial adipose tissue is a source of inflammatory phic cardiomyopathy. Circulation. 1995;91(5):1596–601.
mediators. Circulation. 2003;108:2460–6. United States. 40. Lattanzi F, Spirito P, Picano E, Mazzarisi A, Landini L, Distante A,
24. Greif M, Becker A, von Ziegler F, Lebherz C, Lehrke M, Broedl et al. Quantitative assessment of ultrasonic myocardial reflectivity
UC, et al. Pericardial adipose tissue determined by dual source CT in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1991;17:1085–
is a risk factor for coronary atherosclerosis. Arterioscler Thromb 90. United States.
Vasc Biol. 2009;29:781–6. United States. 41. Naito J, Masuyama T, Tanouchi J, Mano T, Kondo H, Yamamoto K,
25. Alexopoulos N, McLean DS, Janik M, Arepalli CD, Stillman AE, et al. Analysis of transmural trend of myocardial integrated ultra-
Raggi P. Epicardial adipose tissue and coronary artery plaque sound backscatter for differentiation of hypertrophic cardiomyopa-
characteristics. Atherosclerosis. 2009;210:150–4. Ireland: Elsevier thy and ventricular hypertrophy due to hypertension. J Am Coll
Ireland Ltd. Cardiol. 1994;24:517–24. United States.
26. Cheng VY, Dey D, Tamarappoo B, Nakazato R, Gransar H, 42. Prasad K, Atherton J, Smith GC, McKenna WJ, Frenneaux MP,
Miranda-Peats R, et al. Pericardial fat burden on ECG-gated Nihoyannopoulos P. Echocardiographic pitfalls in the diagnosis of
noncontrast CT in asymptomatic patients who subsequently hypertrophic cardiomyopathy. Heart. 1999;82 Suppl 3:III8–15.
experience adverse cardiovascular events. JACC Cardiovasc 43. Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn
Imaging. 2010;3:352–60. United States: American College of HJ, Seidman CE, et al. American College of Cardiology/European
Cardiology Foundation. Published by Elsevier Inc. Society of Cardiology clinical expert consensus document on
27. Dey D, Nakazato R, Li D, Berman DS. Epicardial and thoracic fat – hypertrophic cardiomyopathy. A report of the American College of
Noninvasive measurement and clinical implications. Cardiovasc Cardiology Foundation Task Force on Clinical Expert Consensus
Diagn Ther. 1949–2012;2:85–93. China Republic. Documents and the European Society of Cardiology Committee for
28. Rosito GA, Massaro JM, Hoffmann U, Ruberg FL, Mahabadi AA, practice guidelines. J Am Coll Cardiol. 2003;42:1687–713. United
Vasan RS, et al. Pericardial fat, visceral abdominal fat, States.
cardiovascular disease risk factors, and vascular calcification in a 44. Park JH, Kim YM, Chung JW, Park YB, Han JK, Han MC. MR
community-based sample: the Framingham Heart Study. imaging of hypertrophic cardiomyopathy. Radiology. 1992;185(2):
Circulation. 2008;117:605–13. United States. 441–6.
13 Cardiovascular CT for Assessment of Pericardial/Myocardial Disease Processes 239

45. Sardanelli F, Molinari G, Petillo A, Ottonello C, Parodi RC, 62. Sengupta PP, Krishnamoorthy VK, Abhayaratna WP, Korinek J,
Masperone MA, et al. MRI in hypertrophic cardiomyopathy: a mor- Belohlavek M, Sundt 3rd TM, et al. Comparison of usefulness of
phofunctional study. J Comput Assist Tomogr. 1993;17(6): tissue Doppler imaging versus brain natriuretic peptide for differen-
862–72. tiation of constrictive pericardial disease from restrictive cardiomy-
46. Posma JL, Blanksma PK, van der Wall EE, Hamer HP, Mooyaart opathy. Am J Cardiol. 2008;102:357–62. United States.
EL, Lie KI. Assessment of quantitative hypertrophy scores in 63. McCall R, Stoodley PW, Richards DA, Thomas L. Restrictive
hypertrophic cardiomyopathy: magnetic resonance imaging cardiomyopathy versus constrictive pericarditis: making the dis-
versus echocardiography. Am Heart J. 1996;132:1020–7. United tinction using tissue Doppler imaging. Eur J Echocardiogr.
States. 2008;9:591–4. England.
47. Hansen MW, Merchant N. MRI of hypertrophic cardiomyopathy: 64. White CS. MR evaluation of the pericardium. Top Magn Reson
part I. MRI appearances. AJR Am J Roentgenol. 2007;189: Imaging. 1995;7(4):258–66.
1335–43. United States. 65. White CS. MR evaluation of the pericardium and cardiac malignan-
48. Maron BJ, Bonow RO, Cannon 3rd RO, Leon MB, Epstein cies. Magn Reson Imaging Clin N Am. 1996;4(2):237–51.
SE. Hypertrophic cardiomyopathy. Interrelations of clinical mani- 66. Celletti F, Fattori R, Napoli G, Leone O, Rocchi G, Reggiani LB,
festations, pathophysiology, and therapy (1). N Engl J Med. et al. Assessment of restrictive cardiomyopathy of amyloid or idio-
1987;316(13):780–9. pathic etiology by magnetic resonance imaging. Am J Cardiol.
49. Maron MS, Hauser TH, Dubrow E, Horst TA, Kissinger KV, 1999;83:798–801, A10. United States.
Udelson JE, et al. Right ventricular involvement in hypertrophic 67. Masui T, Finck S, Higgins CB. Constrictive pericarditis and restric-
cardiomyopathy. Am J Cardiol. 2007;100:1293–8. United States. tive cardiomyopathy: evaluation with MR imaging. Radiology.
50. de Roos A, Doornbos J, Luyten PR, Oosterwaal LJ, van der Wall 1992;182(2):369–73.
EE, den Hollander JA. Cardiac metabolism in patients with dilated 68. Schulz-Menger J, Friedrich MG. Magnetic resonance imaging in
and hypertrophic cardiomyopathy: assessment with proton- patients with cardiomyopathies: when and why. Herz. 2000;25(4):
decoupled P-31 MR spectroscopy. J Magn Reson Imaging. 384–91.
1992;2(6):711–9. 69. Shehata ML, Turkbey EB, Vogel-Claussen J, Bluemke DA. Role of
51. Mirowitz SA, Lee JK, Gutierrez FR, Brown JJ, Eilenberg SS. cardiac magnetic resonance imaging in assessment of nonischemic
Normal signal-void patterns in cardiac cine MR images. Radiology. cardiomyopathies. Top Magn Reson Imaging. 2008;19:43–57.
1990;176(1):49–55. United States.
52. Aurigemma G, Reichek N, Schiebler M, Axel L. Evaluation of 70. Westenberg JJ, Braun J, Van de Veire NR, Klautz RJ, Versteegh MI,
mitral regurgitation by cine magnetic resonance imaging. Am Roes SD, et al. Magnetic resonance imaging assessment of reverse
J Cardiol. 1990;66:621–5. United States. left ventricular remodeling late after restrictive mitral annuloplasty
53. Utz JA, Herfkens RJ, Heinsimer JA, Shimakawa A, Glover G, Pelc in early stages of dilated cardiomyopathy. J Thorac Cardiovasc
N. Valvular regurgitation: dynamic MR imaging. Radiology. Surg. 2008;135:1247–52; discussion 52–3. United States.
1988;168(1):91–4. 71. Harris SR, Glockner J, Misselt AJ, Syed IS, Araoz PA. Cardiac MR
54. Wagner S, Auffermann W, Buser P, Lim TH, Kircher B, Pflugfelder imaging of nonischemic cardiomyopathies. Magn Reson Imaging
P, et al. Diagnostic accuracy and estimation of the severity of valvu- Clin N Am. 2008;16:165–83, vii. United States.
lar regurgitation from the signal void on cine magnetic resonance 72. Kimura F, Sakai F, Sakomura Y, Fujimura M, Ueno E, Matsuda N,
images. Am Heart J. 1989;118:760–7. United States. et al. Helical CT features of arrhythmogenic right ventricular car-
55. O’Hanlon R, Assomull RG, Prasad SK. Use of cardiovascular mag- diomyopathy. Radiographics. 2002;22(5):1111–24.
netic resonance for diagnosis and management in hypertrophic car- 73. Lindstrom L, Wilkenshoff UM, Larsson H, Wranne B.
diomyopathy. Curr Cardiol Rep. 2007;9(1):51–6. Echocardiographic assessment of arrhythmogenic right ventricular
56. Hansen MW, Merchant N. MRI of hypertrophic cardiomyopathy: cardiomyopathy. Heart. 2001;86(1):31–8.
part 2, Differential diagnosis, risk stratification, and posttreatment 74. te Riele AS, Tandri H, Bluemke DA. Arrhythmogenic right ven-
MRI appearances. AJR Am J Roentgenol. 2007;189:1344–52. tricular cardiomyopathy (ARVC): cardiovascular magnetic
United States. resonance update. J Cardiovasc Magn Reson. 2014;16:50. England.
57. Fattori R, Rocchi G, Celletti F, Bertaccini P, Rapezzi C, Gavelli 75. Bluemke DA. ARVC: Imaging diagnosis is still in the eye of the
G. Contribution of magnetic resonance imaging in the differential beholder. JACC Cardiovasc Imaging. 2011;4:288–91. United States.
diagnosis of cardiac amyloidosis and symmetric hypertrophic 76. Citro R, Piscione F, Parodi G, Salerno-Uriarte J, Bossone E. Role of
cardiomyopathy. Am Heart J. 1998;136:824–30. United States. echocardiography in takotsubo cardiomyopathy. Heart Fail Clin.
58. Mastouri R, Sawada SG, Mahenthiran J. Noninvasive imaging tech- 2013;9(2):157–66, viii.
niques of constrictive pericarditis. Expert Rev Cardiovasc Ther. 77. Citro R, Rigo F, Ciampi Q, D’Andrea A, Provenza G, Mirra M,
2010;8(9):1335–47. et al. Echocardiographic assessment of regional left ventricular
59. Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma GP, Beller GA, wall motion abnormalities in patients with tako-tsubo cardiomyop-
Bierman FZ, et al. ACC/AHA guidelines for the clinical application of athy: comparison with anterior myocardial infarction. Eur
echocardiography: executive summary. A report of the American J Echocardiogr. 2011;12:542–9. England.
College of Cardiology/American Heart Association Task Force on 78. Parodi G, Del Pace S, Salvadori C, Carrabba N, Olivotto I, Gensini
practice guidelines (Committee on Clinical Application of GF. Left ventricular apical ballooning syndrome as a novel cause of
Echocardiography). Developed in collaboration with the American acute mitral regurgitation. J Am Coll Cardiol. 2007;50:647–9.
Society of Echocardiography. J Am Coll Cardiol. 1997;29(4):862–79. United States.
60. Palka P, Lange A, Donnelly JE, Nihoyannopoulos P. Differentiation 79. Haghi D, Athanasiadis A, Papavassiliu T, Suselbeck T, Fluechter S,
between restrictive cardiomyopathy and constrictive pericarditis by Mahrholdt H, et al. Right ventricular involvement in Takotsubo car-
early diastolic doppler myocardial velocity gradient at the posterior diomyopathy. Eur Heart J. 2006;27:2433–9. England.
wall. Circulation. 2000;102(6):655–62. 80. de Gregorio C, Grimaldi P, Lentini C. Left ventricular thrombus
61. Rajagopalan N, Garcia MJ, Rodriguez L, Murray RD, Apperson- formation and cardioembolic complications in patients with
Hansen C, Stugaard M, et al. Comparison of new Doppler echocar- Takotsubo-like syndrome: a systematic review. Int J Cardiol.
diographic methods to differentiate constrictive pericardial heart 2008;131:18–24. Netherlands.
disease and restrictive cardiomyopathy. Am J Cardiol. 2001;87: 81. Meimoun P, Clerc J, Vincent C, Flahaut F, Germain AL, Elmkies F,
86–94. United States. et al. Non-invasive detection of tako-tsubo cardiomyopathy vs.
240 M.A. Latif and K. Nasir

acute anterior myocardial infarction by transthoracic Doppler 86. Dec GW. Recognition of the apical ballooning syndrome in the
echocardiography. Eur Heart J Cardiovasc Imaging. 2013;14: United States. Circulation. 2005;111:388–90. United States.
464–70. England. 87. Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I,
82. Mansencal N, Abbou N, Pilliere R, El Mahmoud R, Farcot JC, Muellerleile K, Aldrovandi A, et al. Clinical characteristics and
Dubourg O. Usefulness of two-dimensional speckle tracking echo- cardiovascular magnetic resonance findings in stress (takotsubo)
cardiography for assessment of Tako-Tsubo cardiomyopathy. Am cardiomyopathy. JAMA. 2011;306:277–86. United States.
J Cardiol. 2009;103:1020–4. United States. 88. Handy AD, Prasad A, Olson TM. Investigating genetic variation of
83. Meimoun P, Passos P, Benali T, Boulanger J, Elmkies F, Zemir H, adrenergic receptors in familial stress cardiomyopathy (apical
et al. Assessment of left ventricular twist mechanics in Tako-tsubo ballooning syndrome). J Cardiol. 2009;54:516–7. Japan.
cardiomyopathy by two-dimensional speckle-tracking echocar- 89. Sharkey SW, Maron BJ, Nelson P, Parpart M, Maron MS,
diography. Eur J Echocardiogr. 2011;12:931–9. England. Bristow MR. Adrenergic receptor polymorphisms in patients with
84. Heggemann F, Weiss C, Hamm K, Kaden J, Suselbeck T, stress (tako-tsubo) cardiomyopathy. J Cardiol. 2009;53:53–7.
Papavassiliu T, et al. Global and regional myocardial function quan- Japan.
tification by two-dimensional strain in Takotsubo cardiomyopathy. 90. Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG,
Eur J Echocardiogr. 2009;10:760–4. England. Lesser JN, et al. Natural history and expansive clinical profile of
85. Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol.
H. Assessment of clinical features in transient left ventricular apical 2010;55:333–41. United States: 2010 American College of
ballooning. J Am Coll Cardiol. 2003;41:737–42. United States. Cardiology Foundation. Published by Elsevier Inc.
 Computed Tomography Evaluation
in Valvular Heart Disease 14
Nada Shaban, Javier Sanz, Leticia Fernández Friera,
and Mario Jorge García

Abstract
Valvular heart disease commonly affects patients evaluated in the cardiology practice.
Although Echocardiography is the primary modality for the evaluation of patients with
suspected or known valvular heart disease, cardiac CT has distinct advantage in the evalua-
tion of several anatomical features of the cardiac valves, including the extent of calcifica-
tion, the geometry of the annulus and the evaluation of biological and mechanical prostheses.
It is important for cardiologists, radiologists and other cardiac imaging specialists to recog-
nize the features of normal and abnormal valves in patients who are referred for cardiac CT
evaluation.

Keywords
Cardiac valve • Aortic stenosis • Aortic regurgitation • Mitral Stenosis • Mitral Regurgitation
• Bioprosthetic valves • Mechanical prosthetic valves • Trans-aortic valve replacement (TAVR)

Introduction mitral regurgitation (MR) is the most prevalent abnor-

mality [1]. Doppler echocardiography is the initial imag-
Valvular heart disease (VHD) affects 2.5 % of U.S. adults ing modality of choice, allowing for comprehensive
and predominantly involves the left cardiac chambers. diagnosis in the majority of patients [2, 3]. In cases of
Regurgitant lesions are more common than stenotic, and poor acoustic window and/or disparate results regarding
disease severity, additional tests may be required. Cardiac
Electronic supplementary material The online version of this chap- catheterization is a time-honored modality, but is limited
ter (doi:10.1007/978-3-319-28219-0_14) contains supplementary by its invasive nature. Magnetic resonance imaging (MRI)
material, which is available to authorized users. has become an excellent noninvasive alternative for both
valvular insufficiency and stenosis [4]. Due to the need
N. Shaban, MD for radiation and contrast, computed tomography (CT)
Department of Medicine, Division of Cardiology, North Shore
has a limited role for the evaluation of VHD as the pri-
University Hospital, Manhasset, NY, USA
mary indication. It may occasionally be employed as such
J. Sanz, MD
when echocardiographic results are inconclusive and the
Department of Medicine, Division of Cardiology, Mount-Sinai
Medical Center, New York, NY, USA patient is not a good candidate for MRI. Table 14.1 out-
lines the strengths and weaknesses of the different imag-
L.F. Friera, MD
Department of Medicine, Division of Cardiology, Mount-Sinai ing modalities used to assess VHD [5]. CT is increasingly
Medical Center, New York, NY, USA being used for preoperative evaluations for noninvasive
Centro Nacional de Investigaciones Cardiovasculares, coronary angiography and for workup for transcatheter
Madrid, Spain heart valve replacement. Useful information on valve
M.J. García, MD, FACC, FACP (*) anatomy and function can simultaneously be obtained
Division of Cardiology, Montefiore Medical Center, from a coronary CT examination.
111 East 210th St, Bronx, NY 10467, USA
e-mail: [email protected]

© Springer International Publishing 2016 241

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_14
242 N. Shaban et al.

Table 14.1 Strengths and weaknesses of the different imaging modalities used to assess VHD
Transthoracic Transesophageal
Parameter echocardiography echocardiography Cardiac CT Cardiac MRI
Spatial resolution Very good. Pixel size Excellent. Pixel sizes Excellent. Pixel sizes Good. In plane resolution
1–2 mm. 0.5–1.0 mm. 0.6–0.75 mm is good, but through-plane
resolution is fair, 6–8 mm.
Temporal resolution Excellent. 30–60 frames/s Excellent. 30–60 frames/s Dependent on scanner Depends on pulse
in real time. in real time. technology. 10–20 frames sequence and heart rate.
per beat if ECG gating 20–30 frames per beat if
applied. ECG gating applied.
Flow velocity and Excellent with Doppler Excellent with Doppler Poor. No current Good with cine phase-
volume measurements ultrasound. ultrasound. validated clinical method contrast imaging. Not as
for measuring flow widely used or
velocity or flow volume standardized as Doppler
at CT. measurements.
Patient specific Poor acoustic windows in Invasive and requires Images are easily Requires compliant
limitations some patients. sedation. acquired in many patient. Claustrophobia
patients, but uses limits uses.
radiation and contrast Cannot be used with
material, which limits pacemakers or
use. defibrillators.
Ancillary information Good. Cardiac dimensions Good. Cardiac dimensions Excellent. Quantitatively Superior.
can be measured, although can be measured, although measures left ventricular
with less precision than with less precision than dimensions and volumes.
with CT or MRI. with CT or MRI.

General Considerations or regurgitation of the atrioventricular valves usually results

in atrial enlargement. Significant regurgitation of any valve
A diagram summarizing the potential applications of CT for eventually causes ipsilateral ventricular dilatation, often
the evaluation of patients with VHD is shown in Fig. 14.1. accompanied by eccentric hypertrophy. Stenotic lesions of
The Society for Computed Cardiac Tomography recently the semilunar (aortic and pulmonary) valves lead to concen-
released consensus guidelines for the appropriate use of car- tric hypertrophy and later may also lead to ventricular dilata-
diac CT to evaluate non-coronary structures including car- tion. Post-stenotic dilatation of the pulmonary trunk or the
diac valves. It is appropriate to use cardiac CT to evaluate ascending aorta may be present as well.
native and prosthetic valves with suspected clinically CT can provide important information regarding hemody-
significant valvular dysfunction if the images from other namic repercussions of valvular lesions. Enlargement of the
noninvasive methods are inadequate. It is not recommended right heart chambers can be caused by tricuspid/pulmonary
as the initial imaging modality to assess valvular anatomy abnormalities or secondary pulmonary hypertension, and
and function [6]. typically leads to posterior rotation of the cardiac axis
Valvular assessment includes the detection of calcifica- (Fig. 14.2). Pulmonary vein dilatation and interstitial and
tion on non-contrast scans and of other aspects of valvular alveolar lung edema are all signs of increased left atrial pres-
anatomy and cardiac function using contrast enhancement. sures and left-sided heart failure. Similarly, dilatation of the
Quantification of valve calcification follows the same prin- pulmonary arteries, right heart chambers, superior and infe-
ciples as coronary calcium scoring, and the “Agatston”, vol- rior vena cava, pleuro-pericardial effusions and ascites, are
umetric and mass scores have been proposed. Regarding suggestive of pulmonary hypertension and/or right ventricu-
contrast-enhanced CT, detailed evaluation of valvular func- lar heart failure [9].
tion and anatomy is possible for both regurgitant and, par- Cardiac CT has had a major emergence in the realm of
ticularly, stenotic lesions through planimetry of the valve preoperative assessment of transcatheter aortic valve replace-
area. ment (TAVR). It is crucial in the assessment of annular area
CT also allows for accurate quantification of ventricular (Fig. 14.3), diameter, valve leaflet morphology/calcification
volumes, ejection fraction and mass [7], all of which carry (Fig. 14.4), optimum deployment angles, and peripheral vas-
important prognostic and therapeutic implications in patients cular assessment (Figs. 14.5 and 14.6). The severity of the
with VHD. In isolated regurgitant lesions, the regurgitant vol- aortic valve Agatston calcium score, calculated by cardiac
ume and regurgitant fraction can be derived from the differ- CT, has been shown to correlate with degree of paravalvular
ence between the left and right stroke volumes [8]. Stenosis leak following transcatheter heart valve implantation.
14 Computed Tomography Evaluation in Valvular Heart Disease 243

Fig. 14.1 Comprehensive evaluation of valvular heart disease (VHD) with CT

a b

Fig. 14.2 Four chamber (panel a) and short-axis (panel b) views of a hypertrophy and enlargement, together with abnormal interventricular
contrast-enhanced CT scan in an young patient with congenital mitral septal bowing indicative of right ventricular pressure/volume overload
stenosis (“parachute mitral valve”; arrowhead and asterisk) and sec- (arrows)
ondary pulmonary hypertension. There is severe right ventricular

CT coronary angiography for preoperative evaluation selected patients with low or intermediate pre-test
in VHD is also increasingly being used. A high accuracy probability.
for the detection of significant coronary stenoses has A typical imaging protocol is summarized in Table 14.2.
been reported, with slightly lower diagnostic yield in Contrast infusion is routinely followed by saline, resulting in
cases of aortic stenosis (AS) due to frequent aortic and a more compact bolus and easier evaluation of the right coro-
coronary calcifications [ 10 – 13 ]. These studies have nary artery; however, it may also impair the visualization of
demonstrated high negative and moderate positive pre- right chambers and valves. This can be overcome by employ-
dictive value; thus, patients referred for valvular surgery ing dual- or triple-phase injection protocols [15, 16].
without significant coronary stenoses by CT may safely Retrospective ECG gating is advantageous in patients with
avoid the need for invasive angiography [14 ]. On the VHD at the expense of higher radiation dose. ECG-based
other hand, patients with greater than a mild degree of tube current modulation can be used, but it may limit the
luminal stenosis or extensive calcifications need to have assessment of both ventricles and valves, particularly in obese
a confirmatory catheterization. For this reason, it seems patients and in the cardiac phases with lower output. If such
prudent to consider CT for this application only in evaluation is intended, it may be necessary to avoid its use.
244 N. Shaban et al.

Fig. 14.3 Axial-oblique image of the aortic annulus in a patient evalu-

ated for trans-aortic valve replacement (TAVR) demonstrating an ellip-
tical geometry. Green is antero-posterior and blue is transverse diameter Fig. 14.5 3-D Volume-rendered image of the iliac and femoral arteries
of the LV outflow tract in a patient evaluated for trans-aortic valve replacement (TAVR)
demonstrating moderate calcification and tortuosity

Fig. 14.4 Axial-oblique image of the aortic valve in a patient evalu-

ated for trans-aortic valve replacement (TAVR) demonstrating moder-
ate leaflet calcification Fig. 14.6 Axial image of the proximal femoral arteries in a patient
evaluated for trans-aortic valve replacement (TAVR)

malities (i.e. bicuspid valves). Severe calcification associated

Specific Valvular Abnormalities with faster rates of stenosis progression and increased car-
diac event rates [17]. Aortic valve calcification can be accu-
Aortic Stenosis rately quantified using CT (Fig. 14.7), and interscan
reproducibility is >90 % [18–20]. The amount of calcifica-
Aortic stenosis (AS) is often accompanied by cusp calcifica- tion is directly correlated with the severity of AS [19–22],
tion and tends to occur in patients with trileaflet valves above although the relationship is curvilinear with stenosis severity
65 years of age or in younger patients with congenital abnor- increasing more rapidly at lower than higher calcium loads.
14 Computed Tomography Evaluation in Valvular Heart Disease 245

Table 14.2 Imaging protocol

Scanning protocol (for a 256-slice scanner)
Tube voltage (kV) 100–120
Tube output (mA) 500–800
Detector number 128
Detector collimation (mm) 0.6
ECG gating Retrospective/Prospective
Helical pitcha 0.16–0.18
Rotation time (ms) 270–330
Tube current modulationa
(HR ≤ 65) On
(HR > 65) Off
Contrast protocol (370 mgI/cc)
Contrast amount (cc) 80–100
Contrast infusion rate (cc/s) 4–5
Saline amount (cc) 50
Saline infusion rate (cc/s) 4–5
Image reconstruction
Reconstruction filter Intermediate
Slice width (mm) 0.6
Increment (mm) 0.3 mm
Matrix 512 × 512
Reconstruction interval Every 5–10 %
Image analysis: Axial images, MPR, MIP (cine loops and still frames)
Typical scanning protocol for MDCT coronary angiography employed in our institution
ECG electrocardiogram, HR heart rate, MPR: multiplanar reformation, MIP maximum intensity projection
a
If retrospective gating

The incremental value of the information derived from the

aortic valve calcium score may be particularly useful in
patients with low cardiac output and reduced transvalvular
gradients.
Contrast-enhanced CT can precisely evaluate valve mor-
phology, accurately differentiating trileaflet from bicuspid
valves (Fig. 14.8a, b). Planimetric determinations of the
aortic valve area (Fig. 14.8c) have shown excellent correla-
tion with echocardiographic and invasive measurements
[23–29].
CT has emerged as the integral imaging modality for
transcatheter heart valve replacement. As opposed to con-
ventional aortic valve replacement, direct visualization of
the valve and annulus is lacking during the TAVR proce-
dure. As a result, imaging is necessary to allow for appro-
priate valve sizing. CT is used to assess valve morphology,
location and degree of calcification, annular sizing, optimum
deployment angles, and for presence of peripheral vascular
disease. These assessments play a role in predicting success
of valve implantation and risk of paravalvular leak in these
Fig. 14.7 Axial, non-contrast CT image in a patient with moderate patients.
aortic stenosis, demonstrating the quantification of aortic valve calcium Expert consensus documents have been released on the
(arrow) using the same approach as for coronary calcium scoring. The use of CT before TAVR stating that CT should be used in the
valvular calcium score (“Agatston”) was 2227
246 N. Shaban et al.

a b c

Fig. 14.8 Double oblique systolic reconstructions of contrast- sinuses; panel b). Planimetry of the valve can be performed subse-
enhanced CT scans showing a tri-leaflet (panel a) and a bicuspid aortic quently (red contour, panel c): the figure shows a bicuspid aortic valve
valve (the arrowhead indicates the fusion of the right and left coronary with moderate stenosis (valve area = 1.2 cm2)

assessment of all patients being considered for TAVR unless commissures, sub-valvular apparatus or even the left atrial
contraindicated and that datasets should be interpreted wall. MS is often accompanied by marked atrial enlargement
jointly within a multidisciplinary team [30]. involving the appendage. The presence or absence of throm-
bus in the left atrial appendage can be determined after con-
trast administration with very high sensitivity although lower
Aortic Regurgitation specificity since slow flow may impair opacification, which
may be increased by adding delayed imaging [34, 35].
CT may be useful in evaluating the mechanism leading to Planimetry of mitral valve opening by CT provides accurate
aortic regurgitation (AR). AR caused by degenerative valve assessment of MS severity (Fig. 14.11) [36].
disease is characterized by thickened and/or calcified leaflets,
and the area of lack of coaptation may be visualized in
diastolic phase reconstructions centrally or at the Mitral Regurgitation
commissures. In cases of AR secondary to enlargement of
the aortic root, the regurgitant orifice is typically located Both echocardiography and cardiac CT have high sensitivi-
centrally (Fig. 14.9). Other etiologies that can be depicted ties (92.3 % and 84.6 %, respectively) and specificities
include interposition of an intimal flap in cases of dissection, (100 % each) for assessing mitral valve abnormalities com-
valve distortion or perforation in cases of endocarditis, or pared with intraoperative findings, and echocardiography is
leaflet prolapse observed in dissection and in Marfan more sensitive than CT for depicting each prolapsed leaflet
syndrome. Regurgitant orifice areas measured by planimetry of the mitral valve [37]. Echocardiography has been consid-
using MDCT correlate well with echocardiographic ered the reference imaging modality for mitral valve evalu-
parameters of AR severity, such as the vena contracta width ation given the radiation dose exposure and inferior temporal
and the ratio of regurgitant jet to left ventricular outflow tract resolution of CT. In mitral valve prolapse, for example, the
height, and allow for the detection of moderate and severe use of echocardiography alone to identify the exact site of
AR with high accuracy [31–33]. prolapse is clinician dependent and sometimes difficult,
even for those with expertise, because of the limited acous-
tic window and the complex structure of the mitral
Mitral Stenosis apparatus.
In patients with mitral valve prolapse, CT can demon-
As in the case of aortic valve calcification, the presence of strate the presence of leaflet thickening or the degree and
calcium in the mitral annulus is associated with systemic location of prolapse (Fig. 14.12 and Video 14.1). In cases of
atherosclerosis and carries negative prognostic implica- MR secondary to annular enlargement, often accompanying
tions. The amount of mitral annular calcium can also be dilated cardiomyopathy, dimensions of the annulus can be
quantified with CT (Fig. 14.10), although reproducibility accurately quantified, and a central area of insufficient leaflet
appears to be somewhat lower [18]. In rheumatic mitral coaptation may be observed. Although quantifying MR
stenosis (MS), calcification can extend to the leaflets, degree may be difficult, preliminary data suggests that
14 Computed Tomography Evaluation in Valvular Heart Disease 247

Fig. 14.9 Contrast-enhanced MDCT in a patient with an aneurysmal the ascending aorta (red and green lines). A large, central area of insuf-
aorta and aortic insufficiency. The valvular plane (yellow line; left lower ficient leaflet coaptation during diastole (right lower panel; arrowhead)
panel) is oriented perpendicular to two orthogonal planes aligned with can be visualized

planimetry of the regurgitant orifice by CT correlates well to evaluate by echocardiography in the adult patient.
with echocardiographic grading of severity [38]. Therefore, CT and MRI, due to their good spatiotemporal
resolution, large field of view, and multiplanar reconstruction
techniques, are playing increasingly important roles in the
Pulmonic Valve Disease evaluation of this valve.
For visualizing the pulmonary valve, the CT intravenous
Pathology of the pulmonic valve, whether from idiopathic contrast medium injection protocol should be optimized to
causes, infective endocarditis, thrombus, regurgitation/ ensure that there is adequate contrast opacification in the right
stenosis, or secondary to congenital heart disease is difficult cardiac chambers. For morphological evaluation of the valve,
248 N. Shaban et al.

prospective electrocardiography (ECG) triggered acquisition Vegetations are often mobile and tend to be on the atrial
should be used to minimize radiation dose. However, if func- aspect of atrioventricular valves, and on the ventricular
tional analysis of the valve or the RV is desired, retrospective aspect of semilunar valves (Fig. 14.13). CT can be particu-
ECG-gated multi-phasic acquisition with tube current modu- larly useful in the demonstration of perivalvular abscesses
lation is the ideal scanning mode [39]. as fluid-filled collections (Fig. 14.14) that may retain con-
trast in delayed imaging [41]. In a recent study, MDCT cor-
rectly identified 26 out of 27 (96 %) patients with valvular
Infective Endocarditis vegetations and 9 out of 9 (100 %) patients with abscesses,
which were better characterized by MDCT than with trans-
Studies have shown that cardiac-gated CTA has excellent esophageal echocardiography [42]. Intravascular contrast
sensitivity, specificity, and positive predictive and negative administration should be optimized, and intravascular
predictive values in the preoperative evaluation for suspected attenuation can be further accentuated by the use of 100-kV
infective endocarditis, in addition to excellent correlations scan protocols whenever possible. Although the maximal
with preoperative TEE and intraoperative findings [40]. temporal resolution of a scanner cannot be altered, the
reconstruction frame of the dataset can and should be opti-
mized when assessing valvular function. Reconstruction of
20- or 25-phase datasets (at 5 % or 4 % increments of the
R-R interval) provides improved temporal depiction of
valve motion that facilitates cine evaluation of valvular
pathology, such as hypermobile vegetations. In addition,
advanced image processing techniques, such as blood pool
inversion (BPI) volume-rendering, can be used to allow
3-Dimensional/4-Dimensional (3-D/4-D) assessment of
valvular structure and function [43]. In patients with aortic
valve endocarditis with highly mobile vegetations, CT may
be especially attractive as an alternative to invasive coro-
nary angiography for preoperative evaluation.

Prosthetic Valves

Many of the aforementioned features of native VHD apply

also to the evaluation of cardiac bioprostheses. Transthoracic
echocardiography is useful for prosthetic valve evaluation, but
can be limited by acoustic shadowing and poor acoustic win-
Fig. 14.10 Short-axis view at the level of the mitral valve, showing dowing. Recently, cardiac CT has been recognized as a viable
extensive annular calcification (arrows)
alternative to evaluation of prosthetic valve complications

a b c

Fig. 14.11 Contrast-enhanced CT scan in the four-chamber and short- opening of the leaflets can be observed (arrows and asterisk). Planimetry
axis views (panels a and b, respectively) from a patient with rheumatic of the valve (panel c) demonstrated moderate stenosis (red contour;
mitral stenosis. The typical thickening and restricted dome-shaped area = 1.3 cm2)
14 Computed Tomography Evaluation in Valvular Heart Disease 249

including valve thrombosis, dehiscence, pannus development, able windowing adjustments is to minimize beam hardening is
endocarditis, and paravalvular leak. However, careful atten- certainly possible [44].
tion to CT technique, achieving prescan target heart rates, Recent work suggests iterative reconstructions may
extensive windowing adjustments, and awareness of normal reduce beam-hardening artifact from prosthetic valves
postoperative paravalvular structures is imperative. Some compared with filtered back projection reconstruction tech-
valves, such as ball in cage valves, are not readily evaluable by niques [45]. Motion artifact can be adequately reduced by
CT because of extreme beam hardening artifact from the administration of beta-blockade to achieve heart rates
thicker metal struts found in these models. Whereas evaluation between 50 and 60 bpm. Motion artifact is worst for aortic
of most other valves using a very soft window with consider- valve prosthesis during ventricular systole and for mitral
valve prosthesis during end-diastole. Thus, it has been found
that imaging in mid-diastole is the most ideal for prosthetic
valve evaluation [46]. CT is particularly useful for the evalu-
ation of some types of mechanical valves. In Prostheses with
two discs should open symmetrically (Fig. 14.15 and Video
14.2). In those with a single disc, the angle of opening can
also be measured [47]. Finally, heterografts and homografts
can be evaluated completely, including the distal anastomo-
sis and the patency of the coronary arteries if these were
reimplanted.

Imaging Pearls

• Plan ahead; as this will allow for imaging protocol

optimization if valvular evaluation will be attempted.
• If simultaneous assessment of the right heart structures is
Fig. 14.12 End-systolic three-chamber view of the left ventricle dem-
intended, the contrast protocol should be optimized. An
onstrating prolapse of the posterior mitral leaflet (arrow) initial bolus of 80–100 cc followed by a mixture of

a b

Fig. 14.13 Diastolic (panel a) and systolic (panel b) reconstructions ascending aorta in systole can be noted (black arrows). In addition,
of a contrast-enhanced MDCT study in a patient with a bioprosthesis in perivalvular thickening and fluid-filled collections can be noted (white
the aortic position. A large, mobile vegetation that prolapses into the arrows) indicating the presence of a perivalular abscess
250 N. Shaban et al.

a b

c d

Fig. 14.14 Evaluation of mechanical prostheses by CT. The top row (panel d) reconstructions of a non-contrast CT evaluation of a dysfunc-
shows contrast-enhanced images (systole, panel a; diastole, panel b) of tional mitral prosthesis. One of the discs does not open in diastole
a normal-functioning mechanical prosthesis in the mitral position. The (white arrowhead). Subsequent surgical intervention demonstrated
two discs close and open completely and symmetrically (white arrows) prosthetic thrombosis
during the cardiac cycle. Comparable systolic (panel c) and diastolic

contrast and saline (1:1) at 4–5 cc/s will result in adequate tube output can be timed to end-systole, which will
coronary evaluation and sufficient right-heart opacification provide adequate depiction of mitral closure and aortic
without excessive enhancement. Alternatively, a second opening, as well as potentially motionless coronary
infusion of contrast administered at a slower rate images, particularly at higher heart rates.
(2–3 cc/s) can be employed [15, 16]. • If the entire thoracic aorta needs to be imaged (i.e. in
• Quantification of ventricular end-systolic volumes and cases of aneurysm with associated AR) and coronary
the degree of MR and AS requires adequate image quality evaluation is not required, using thicker detector
during systole. It may be necessary to avoid tube current collimation will enable reductions in radiation dose and
modulation in these cases. Alternatively, the maximal breath-hold duration.
14 Computed Tomography Evaluation in Valvular Heart Disease 251

entire aorta and iliofemoral arteries with ECG

synchronization. For these sections, non-gated
acquisitions will allow lower radiation exposure and
faster volume coverage requiring lower contrast volumes.
Since detailed dimensions of the aortic root and of the
iliofemoral arteries must be obtained, spatial resolution
must be high enough to provide adequate imaging. The
optimal acquisition protocol is that which obtains a
reconstructed slice width of <1.0 mm throughout the
entire imaging volume.
• Variability of the quantification of aortic valve calcium is
lowest in mid-diastole [49].
• A valvular “Agatston” score ≥1100 resulted in respective
sensitivity and specificity of 93 and 82 % for the diagno-
sis of severe AS [20]. A score >3700 has a positive predic-
tive value of near 100 % [25].
• The optimal plane to perform planimetry of the valvular
area is parallel to the annulus as determined from two
orthogonal double-oblique views perpendicular to the
valve plane. The optimal level of that plane is the one
showing the smallest area during the phase of maximum
valve opening (Fig. 14.9).
Fig. 14.15 Contrast-enhanced CT in a patient with pulmonary infun-
dibular stenosis (arrowheads). The contrast protocol was optimized to • Quantification of the regurgitant volume/fraction from the
provide adequate opacification of right heart chambers difference in right and left stroke volumes is only accurate
for isolated regurgitant lesions.
• A score evaluating leaflet mobility and thickening,
• Most patients with VHD can tolerate beta-blockers for subvalvular thickening and calcification, as well as the
optimal coronary evaluation. However, caution and presence of left atrial thrombus, may determine whether
smaller doses are recommended in cases with severe MS can be treated percutaneously or surgically. CT can
degrees of left ventricular dysfunction/dilatation, AS, AR provide useful information for all of these features.
or pulmonary hypertension. • The mitral valve is divided into the anterolateral
• Atrial fibrillation is common in patients with VHD. It commissure, posteromedial commissure, anterior leaflet
may lead to a decrease in image quality and accuracy of and posterior leaflet. The leaflets are subdivided into three
valvular and ventricular assessment, although this is segments each (A1, A2 and A3; and P1, P2, and P3, from
typically more significant for evaluation of the coronary lateral to medial). Determination of which segments are
arteries. affected and to what degree determines in part the
• For the evaluation of ventricular or valvular function with likelihood of successful surgical repair in mitral valve
MDCT, reconstructions at every 10 % of the RR interval prolapse.
are usually sufficient. In specific cases, a more detailed • Sharper reconstruction filters and increasing window
evaluation of the valve can be obtained by reconstructing level of the image display facilitates evaluation of
images at smaller intervals (i.e. every 5 %) in the cardiac mechanical prosthetic valves.
phase of interest (for example, during systole for AS) • Optimum valve evaluation for both aortic and mitral
[48]. prosthetic valves is best achieved during mid-diastole.
• The combination of cine loops and still frames facilitates
the detection of valvular abnormalities.
• CT imaging in the evaluation for TAVR should include
imaging of the aortic root, aorta, and iliac, as well as References
common femoral arteries. To achieve the desired accuracy
and to allow for adequate motion-free images, imaging of 1. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG,
Enriquez-Sarano M. Burden of valvular heart diseases: a population-
the aortic root must be synchronized to the
based study. Lancet. 2006;368(9540):1005–11.
electrocardiogram (ECG) either by retrospective ECG 2. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd,
gating or by prospective ECG triggering, depending on Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM
patient characteristics. It is not necessary to image the 3rd, Thomas JD. 2014 AHA/ACC guideline for the management of
252 N. Shaban et al.

patients with valvular heart disease: executive summary: a report of 16. Takakuwa KM, Halpern EJ. Evaluation of a “triple rule-out” coro-
the American College of Cardiology/American Heart Association nary CT angiography protocol: use of 64-Section CT in low-to-
Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63(22): moderate risk emergency department patients suspected of having
2438–88. acute coronary syndrome. Radiology. 2008;248(2):438–46.
3. Bonow RO, Carabello BA, Chatterjee K, de Leon Jr AC, Faxon DP, 17. Rosenhek R, Binder T, Porenta G, Lang I, Christ G, Schemper M,
Freed MD, et al. 2008 Focused update incorporated into the ACC/ et al. Predictors of outcome in severe, asymptomatic aortic stenosis.
AHA 2006 guidelines for the management of patients with valvular N Engl J Med. 2000;343(9):611–7.
heart disease: a report of the American College of Cardiology/ 18. Budoff MJ, Takasu J, Katz R, Mao S, Shavelle DM, O’Brien KD,
American Heart Association Task Force on Practice Guidelines et al. Reproducibility of CT measurements of aortic valve
(Writing Committee to Revise the 1998 Guidelines for the calcification, mitral annulus calcification, and aortic wall
Management of Patients With Valvular Heart Disease): endorsed by calcification in the multi-ethnic study of atherosclerosis. Acad
the Society of Cardiovascular Anesthesiologists, Society for Radiol. 2006;13(2):166–72.
Cardiovascular Angiography and Interventions, and Society of 19. Koos R, Kuhl HP, Muhlenbruch G, Wildberger JE, Gunther RW,
Thoracic Surgeons. Circulation. 2008;118(15):e523–661. Mahnken AH. Prevalence and clinical importance of aortic valve
4. Cawley PJ, Maki JH, Otto CM. Cardiovascular magnetic resonance calcification detected incidentally on CT scans: comparison with
imaging for valvular heart disease: technique and validation. echocardiography. Radiology. 2006;241(1):76–82.
Circulation. 2009;119(3):468–78. 20. Messika-Zeitoun D, Aubry MC, Detaint D, Bielak LF, Peyser PA,
5. Bennett CJ, Maleszewski JJ, Araoz PA. CT and MR imaging of the Sheedy PF, et al. Evaluation and clinical implications of aortic
aortic valve: radiologic-pathologic correlation. Radiographics Rev valve calcification measured by electron-beam computed
Publ Radiol Soc North Am Inc. 2012;32(5):1399–420. tomography. Circulation. 2004;110(3):356–62.
6. Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O’Gara P, 21. Koos R, Mahnken AH, Sinha AM, Wildberger JE, Hoffmann R,
et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR Kuhl HP. Aortic valve calcification as a marker for aortic stenosis
2010 appropriate use criteria for cardiac computed tomography. A severity: assessment on 16-MDCT. AJR Am J Roentgenol.
report of the American College of Cardiology Foundation 2004;183(6):1813–8.
Appropriate Use Criteria Task Force, the Society of Cardiovascular 22. Shavelle DM, Budoff MJ, Buljubasic N, Wu AH, Takasu J, Rosales
Computed Tomography, the American College of Radiology, the J, et al. Usefulness of aortic valve calcium scores by electron beam
American Heart Association, the American Society of computed tomography as a marker for aortic stenosis. Am J Cardiol.
Echocardiography, the American Society of Nuclear Cardiology, 2003;92(3):349–53.
the North American Society for Cardiovascular Imaging, the 23. Alkadhi H, Wildermuth S, Plass A, Bettex D, Baumert B, Leschka
Society for Cardiovascular Angiography and Interventions, and the S, et al. Aortic stenosis: comparative evaluation of 16-detector row
Society for Cardiovascular Magnetic Resonance. J Am Coll CT and echocardiography. Radiology. 2006;240(1):47–55.
Cardiol. 2010;56(22):1864–94. 24. Bouvier E, Logeart D, Sablayrolles JL, Feignoux J, Scheuble C,
7. Orakzai SH, Orakzai RH, Nasir K, Budoff MJ. Assessment of car- Touche T, et al. Diagnosis of aortic valvular stenosis by multislice
diac function using multidetector row computed tomography. cardiac computed tomography. Eur Heart J. 2006;27(24):3033–8.
J Comput Assist Tomogr. 2006;30(4):555–63. 25. Cowell SJ, Newby DE, Burton J, White A, Northridge DB, Boon
8. Reiter SJ, Rumberger JA, Stanford W, Marcus ML. Quantitative NA, et al. Aortic valve calcification on computed tomography
determination of aortic regurgitant volumes in dogs by ultrafast predicts the severity of aortic stenosis. Clin Radiol.
computed tomography. Circulation. 1987;76(3):728–35. 2003;58(9):712–6.
9. Boxt LM. CT of valvular heart disease. Int J Cardiovasc Imaging. 26. Feuchtner GM, Dichtl W, Friedrich GJ, Frick M, Alber H, Schachner
2005;21(1):105–13. T, et al. Multislice computed tomography for detection of patients
10. Gilard M, Cornily JC, Pennec PY, Joret C, Le Gal G, Mansourati J, with aortic valve stenosis and quantification of severity. J Am Coll
et al. Accuracy of multislice computed tomography in the Cardiol. 2006;47(7):1410–7.
preoperative assessment of coronary disease in patients with aortic 27. Feuchtner GM, Muller S, Bonatti J, Schachner T, Velik-Salchner C,
valve stenosis. J Am Coll Cardiol. 2006;47(10):2020–4. Pachinger O, et al. Sixty-four slice CT evaluation of aortic stenosis
11. Meijboom WB, Mollet NR, Van Mieghem CA, Kluin J, Weustink using planimetry of the aortic valve area. AJR Am J Roentgenol.
AC, Pugliese F, et al. Pre-operative computed tomography coronary 2007;189(1):197–203.
angiography to detect significant coronary artery disease in patients 28. LaBounty TM, Sundaram B, Agarwal P, Armstrong WA, Kazerooni
referred for cardiac valve surgery. J Am Coll Cardiol. EA, Yamada E. Aortic valve area on 64-MDCT correlates with
2006;48(8):1658–65. transesophageal echocardiography in aortic stenosis. AJR Am
12. Reant P, Brunot S, Lafitte S, Serri K, Leroux L, Corneloup O, et al. J Roentgenol. 2008;191(6):1652–8.
Predictive value of noninvasive coronary angiography with multide- 29. Lembcke A, Thiele H, Lachnitt A, Enzweiler CN, Wagner M, Hein
tector computed tomography to detect significant coronary stenosis PA, et al. Precision of forty slice spiral computed tomography for
before valve surgery. Am J Cardiol. 2006;97(10):1506–10. quantifying aortic valve stenosis: comparison with echocardiography
13. Scheffel H, Leschka S, Plass A, Vachenauer R, Gaemperli O, and validation against cardiac catheterization. Invest Radiol.
Garzoli E, et al. Accuracy of 64-slice computed tomography for the 2008;43(10):719–28.
preoperative detection of coronary artery disease in patients with 30. Achenbach S, Delgado V, Hausleiter J, Schoenhagen P, Min JK,
chronic aortic regurgitation. Am J Cardiol. 2007;100(4):701–6. Leipsic JA. SCCT expert consensus document on computed
14. Russo V, Gostoli V, Lovato L, Montalti M, Marzocchi A, Gavelli G, tomography imaging before transcatheter aortic valve implantation
et al. Clinical value of multidetector CT coronary angiography as a (TAVI)/transcatheter aortic valve replacement (TAVR). J Cardiovasc
preoperative screening test before non-coronary cardiac surgery. Comput Tomogr. 2012;6(6):366–80.
Heart (Br Cardiac Soc). 2007;93(12):1591–8. 31. Alkadhi H, Desbiolles L, Husmann L, Plass A, Leschka S, Scheffel
15. Litmanovich D, Zamboni GA, Hauser TH, Lin PJ, Clouse ME, H, et al. Aortic regurgitation: assessment with 64-section
Raptopoulos V. ECG-gated chest CT angiography with 64-MDCT CT. Radiology. 2007;245(1):111–21.
and tri-phasic IV contrast administration regimen in patients with 32. Feuchtner GM, Dichtl W, Muller S, Jodocy D, Schachner T, Klauser
acute non-specific chest pain. Eur Radiol. 2008;18(2):308–17. A, et al. 64-MDCT for diagnosis of aortic regurgitation in patients
14 Computed Tomography Evaluation in Valvular Heart Disease 253

referred to CT coronary angiography. AJR Am J Roentgenol. 42. Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J,
2008;191(1):W1–7. Scheffel H, et al. Multislice computed tomography in infective
33. Jassal DS, Shapiro MD, Neilan TG, Chaithiraphan V, Ferencik M, endocarditis: comparison with transesophageal echocardiography
Teague SD, et al. 64-slice multidetector computed tomography and intraoperative findings. J Am Coll Cardiol. 2009;53(5):
(MDCT) for detection of aortic regurgitation and quantification of 436–44.
severity. Invest Radiol. 2007;42(7):507–12. 43. Entrikin DW, Gupta P, Kon ND, Carr JJ. Imaging of infective endo-
34. Kim YY, Klein AL, Halliburton SS, Popovic ZB, Kuzmiak SA, Sola carditis with cardiac CT angiography. J Cardiovasc Comput
S, et al. Left atrial appendage filling defects identified by multidetec- Tomogr. 2012;6(6):399–405.
tor computed tomography in patients undergoing radiofrequency 44. O’Neill AC, Martos R, Murtagh G, Ryan ER, McCreery C, Keane
pulmonary vein antral isolation: a comparison with transesophageal D, et al. Practical tips and tricks for assessing prosthetic valves and
echocardiography. Am Heart J. 2007;154(6):1199–205. detecting paravalvular regurgitation using cardiac CT. J Cardiovasc
35. Hur J, Kim YJ, Lee HJ, Ha JW, Heo JH, Choi EY, et al. Left atrial Comput Tomogr. 2014;8(4):323–7.
appendage thrombi in stroke patients: detection with two-phase car- 45. Sucha D, Willemink MJ, de Jong PA, Schilham AM, Leiner T,
diac CT angiography versus transesophageal echocardiography. Symersky P, et al. The impact of a new model-based iterative recon-
Radiology. 2009;251(3):683–90. struction algorithm on prosthetic heart valve related artifacts at
36. Messika-Zeitoun D, Serfaty JM, Laissy JP, Berhili M, Brochet E, reduced radiation dose MDCT. Int J Cardiovasc Imaging.
Iung B, et al. Assessment of the mitral valve area in patients with 2014;30(4):785–93.
mitral stenosis by multislice computed tomography. J Am Coll 46. Symersky P, Budde RP, Westers P, de Mol BA, Prokop
Cardiol. 2006;48(2):411–3. M. Multidetector CT imaging of mechanical prosthetic heart
37. Ghosh N, Al-Shehri H, Chan K, Mesana T, Chan V, Chen L, et al. valves: quantification of artifacts with a pulsatile in-vitro model.
Characterization of mitral valve prolapse with cardiac computed Eur Radiol. 2011;21(10):2103–10.
tomography: comparison to echocardiographic and intraoperative 47. Konen E, Goitein O, Feinberg MS, Eshet Y, Raanani E, Rimon U,
findings. Int J Cardiovasc Imaging. 2012;28(4):855–63. et al. The role of ECG-gated MDCT in the evaluation of aortic and
38. Alkadhi H, Wildermuth S, Bettex DA, Plass A, Baumert B, Leschka mitral mechanical valves: initial experience. AJR Am J Roentgenol.
S, et al. Mitral regurgitation: quantification with 16-detector row 2008;191(1):26–31.
CT--initial experience. Radiology. 2006;238(2):454–63. 48. Abbara S, Pena AJ, Maurovich-Horvat P, Butler J, Sosnovik DE,
39. Rajiah P, Nazarian J, Vogelius E, Gilkeson RC. CT and MRI of Lembcke A, et al. Feasibility and optimization of aortic valve pla-
pulmonary valvular abnormalities. Clin Radiol. 2014;69(6):630–8. nimetry with MDCT. AJR Am J Roentgenol. 2007;188(2):356–60.
40. Gahide G, Bommart S, Demaria R, Sportouch C, Dambia H, Albat 49. Ruhl KM, Das M, Koos R, Muhlenbruch G, Flohr TG, Wildberger
B, et al. Preoperative evaluation in aortic endocarditis: findings on JE, et al. Variability of aortic valve calcification measurement with
cardiac CT. AJR Am J Roentgenol. 2010;194(3):574–8. multislice spiral computed tomography. Invest Radiol.
41. Gilkeson RC, Markowitz AH, Balgude A, Sachs PB. MDCT evalu- 2006;41(4):370–3.
ation of aortic valvular disease. AJR Am J Roentgenol. 2006;
186(2):350–60.
 Transcatheter Aortic Valve
Implantation (TAVI) 15
Chesnal Dey Arepalli, Christopher Naoum, Philipp Blanke,
and Jonathon A. Leipsic

Abstract
Computerized tomography (CT) plays a pivotal role in selection of patients’, appropriate
device size and pre-procedural guidance in successful outcome of transcatheter aortic valve
implantation (TAVI). CT based vascular and non-vascular evaluation and integration of
relevant measurements into TAVI work up has been shown to reduce morbidity and mortal-
ity. Post-procedural device assessment and complications could also be reliably evaluated
with CT. Utilization of CT is not just confined to TAVI but it is also increasingly being used
for any transcatheter valvular assessment.

Keywords
AS – Aortic Stenosis • AVC – Aortic Valvular Calcifications • AA – Aortic Annulus • SOV –
Sinus of Valsalva • Coronary Artery Ostium • PAR – Paravalvular Regurgitation • CT –
Computerized tomography • TTE – Transthoracic Echocardiography • TEE – Transesophageal
Echocardiography • TAVI – Transcatheter Aortic Valve Implantation

Introduction The most common cause for AS is age related progressive

calcification of a normal aortic valve (Fig. 15.1a–c) [1, 2].
Transcatheter aortic valve implantation (TAVI) is an alterna- Additionally, congenital causes like bicuspid aortic valve or
tive treatment option for symptomatic severe aortic stenosis inflammatory conditions like rheumatic heart disease are
(AS) patients who are deemed inoperable or at high risk for also common causes of AS [1]. The prevalence of senile AS
surgical aortic valve replacement (AVR). TAVI as the name is increasing as the mean age of Western societies is increas-
suggests is a procedure where in a bio-prosthetic device is ing [3, 4]. Current data has documented the prevalence of AS
implanted without removing the diseased valve via a trans- in the elderly population (age ≥ 75 years) as 12.4 % and
catheter approach. severe AS is 3.4 % [3]. Although senile or degenerative aor-
tic stenosis occurs primarily in the elderly population, with
C.D. Arepalli, MBBS, DNB • C. Naoum, MBBS, FRACP mean age of 65–70 years, congenital bicuspid aortic valve
Department of Radiology, St Paul’s Hospital UBC, Vancouver, BC, (BAV) with significant aortic stenosis tends to occur slightly
Canada earlier between 15 and 65 years of age (Fig. 15.1d) [5, 6]. In
P. Blanke, MD one study it was observed that BAV was the commonest
Department of Medicine, St Paul’s Hospital UBC, Vancouver, BC, cause of AS between the ages of 60 and 75 years (59 % of
Canada
cases) and those aged less than 60 years, BAV was a caus-
J.A. Leipsic, MD, FRCPC, FSCCT (*) ative factor in 40 % [7]. BAV AS were found to require AVR
Department of Radiology, St. Paul’s Hospital,
5 years before than those with a tricuspid valve [8].
Room P2214 – 2nd Floor Providence Building 1081 Burrard
Street, Vancouver, BC V6Z 1Y6, Canada Importantly, the natural clinical progression of symp-
e-mail: [email protected] tomatic AS is rapid and associated with a poor clinical

© Springer International Publishing 2016 255

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_15
256 C.D. Arepalli et al.

a b

c d

Fig. 15.1 Aortic valvular calcification (AVC). AVC of varying with a larger non-coronary cusp and raphae between the right and
degrees – (a) mild, (b) moderate, (c) severe, (d) Bicuspid aortic the left coronary cusps in keeping with a Type 1 A Bicuspid Valve
valve (BAV) with calcification. Note the asymmetry of the cusps

outcome with an average time of death shown to be within co-morbidities in the elderly population that make surgical
5 years after onset of angina, 3 years after onset of syn- risk prohibitive [3, 10].
cope and within 1–2 years after onset of heart failure TAVI is a new alternate therapy that has been shown
symptoms [9]. through many registries, meta-analyses, and a number of
Until the advent of TAVI, the sole effective treatment randomized trials to be an effective therapy for severe symp-
option for symptomatic AS was surgical AVR. Medical treat- tomatic AS who were deemed inoperable and high risk sur-
ment alone had very poor prognosis with a mortality rate of gical patients [11, 12]. TAVI was first pioneered by Cribier
50 % at 2 years. Unfortunately, many patients with severe et al. in 2002 through transvenous transeptal approach [13].
symptomatic AS are denied this surgery owing to associated However, over the past decade, alternative procedures have
15 Transcatheter Aortic Valve Implantation (TAVI) 257

been developed and at present retrograde transarterial trans- various anatomical measurements are critical in the determi-
femoral path, first described by Webb and colleagues in nation of patient eligibility, bioprosthesis size, procedural
2005, is the most favored approach. planning and to anticipate procedural complications.
As opposed to surgical AVR where it is possible to directly
visualize and measure the size of the aortic root; TAVI relies
indirectly on imaging measurements before implantation. Anatomy
Based on these measurements; device selection and the pro-
cedural approach are planned. Pre-procedural imaging plays Aortic Root
a critical role in ensuring the success of the procedure and
also to minimize the peri and post-procedural complications. The Aortic root is a further extension of the left ventricular
outflow tract (LVOT). As a result, the LVOT should be con-
sidered an anatomical segment between the left ventricle and
Imaging Modalities ascending aorta.
As the aortic root is a complex dynamic structure; under-
Historically, TAVI imaging was reliant on measurements standing the morphology and kinesis of the aortic root sub-
derived form 2-dimensional echocardiography and invasive components helps in better appreciation of interplay of different
angiography. However, multidetector computed tomography sub-components with each other and also with adjacent struc-
(MDCT) has grown to become an essential tool for the tures. This not only helps in procedural success but also has the
assessment of aortic root/annulus, evaluation of thoracic and potential in refinement of the bio-prosthesis devices.
abdominal aorta and ilio-femoral vessels. Moreover, MDCT Aortic root sub-components include aortic annulus (AA),
is being used to predict optimal co-planar projection angles aortic sinus and the valvular leaflets, the coronary ostia and
for device deployment. the sinotubular junction.
Current state of the art CT scanners acquire data volu-
metrically with isotropic spatial and high temporal resolu-
tion. Post processing of data provide multiplanar and curved Aortic Annulus
planar reformations (MPR and CPR), volume rendered tech-
nique images (VRT), minimum and maximum intensity pro- Broadly, two terms define the aortic annulus – (a) anatomic
jections (MIPmin and MIPmax respectively) which are essential annulus and (b) virtual basal ring. The Anatomical Aortic
to accurately size the aortic annulus, aortic root and other annulus is more of a histological demarcation that is defined
vascular access sites. Integration of CT data into sizing algo- as a fibrous structure that attaches the aortic root to the left
rithms and work flow has consistently demonstrated signifi- ventricle. It consists of three coronets like structures that
cant reduction in the incidence of paravalvular and vascular support the valvular leaflets. The Virtual basal annulus is
complications [14–16]. Thus CT has become an accepted defined by nadir (lowest depth) plane of each of the coronets
integral part in the overall work flow of TAVI patients. Of and it corresponds to the aortic-ventricular junction.
late, CT has also been shown to play an important additional Although the term annulus suggests a circular shape,
role in valve in valve procedures. with the use of 3-D MDCT imaging , it has been found to be
The role of MDCT for valvular intervention can be fairly consistently to be of a non-circular geometry with
broadly discussed under three headings: often elliptical and sometimes oval shaped configuration
[17, 18].
(a) Pre-procedural, It has been also observed that there are considerable
(b) Peri-procedural and variations in shape, size and direction of the annulus dur-
(c) Post procedural. ing the cardiac cycle (Fig. 15.2). These are influenced by
deformation, stretch, compliance of the aortic root as well
Although the focus of this chapter is on pre-procedural as left ventricular geometry, mitral valve anatomy and
role of CT; it is equally pertinent to understand the peri and pathology [19, 20]. Further, Nakai et al. [21] showed that
post procedural complications as they play an important role there is cranial displacement of aortic annulus during early
in understanding the dynamics of TAVI and thus indirectly systole and in diastole whereas in rest of the systole and in
influence the pre-procedural work up. isovolumetric relaxation there is caudal displacement. It
Before one can proceed with CT based ‘Sizing of the aor- has been observed in multiple studies, that the aortic annu-
tic annulus’ and procedural planning in the work up of TAVI lus measurements in cohorts without and with aortic steno-
patients, it is important to understand the complex aortic sis show largest size (area) and diameter in systole and
valve and root anatomy. Knowledge of the 3 dimensional smallest measurements during diastole due to cyclical
(3 D) complex aortic root geometry and consideration of changes [22–26].
258 C.D. Arepalli et al.

Imaging Modalities and Aortic Annulus echocardiography (TEE) are routinely used. In fact, the cur-
Assessment rent TAVI device sizes provided by vendors are based on 2D
echocardiography measurements. However, it was noted in
Strengths and Limitations several studies that echocardiography measurements under-
of Echocardiography and MDCT estimated the true aortic annular size and were smaller in
size when compared to MDCT.
Accurate and reproducible pre-operative measurements of In a meta-analysis, MDCT aortic annulus diameter mea-
annulus are of paramount importance that helps in patient surements on coronal view were 25.3 ± 0.52 mm which were
selection, device selection and size for TAVI procedure and larger than sagittal view measurements by MDCT
also forecasting the outcome of the geometrical configura- (22.7 ± 0.37 mm), TTE (22.6 ± 0.28 mm), and TEE
tion of aortic annulus-prosthesis after implantation. In (23.1 ± 0.32 mm) [27]. In a study by Mizia-Stec at el, the
addition, better understanding of the aortic root complex and mean aortic annulus diameter on TTE was 24 ± 3.6 mm,
precise measurements would help in predicting and 26 ± 4.2 mm using TEE, and 26.9 ± 3.2 mm on MDCT
mitigating peri and post procedural complications. (P = 0.04 vs. TTE) [28]. Messika-Zeitoun and colleagues
Owing to the complex 3D aortic root geometry, measure- [29] observed larger differences between CT and TTE
ments in a single plane have been shown to lead to both (1.22 ± 1.3 mm) or TEE (1.52 ± 1.1 mm) than the difference
under or overestimation (depending upon the plane used) between TTE and TEE (0.6 ± 0.8 mm; and p < 0.0001, respec-
and have therefore been shown to be limited value for TAVI tively p = 0.03).
sizing. Two dimensional (2D) measurements as provided by Early experiences with the integration of CT not only
transthoracic echocardiography (TTE) and transesophageal documented differences in annular measurements between

a b c

d e f

Fig. 15.2 Dynamic nature of Aortic Annulus over the course of shape of the aortic annulus changes from elliptical in diastole
cardiac cycle (75–25 %) (a–f) and corresponding measurements (75 %) to near circular in systole (25 %). The perimeter size
(g–l). Note the variation in the shape and size of the aortic annulus increased from 74 to 79 mm (~5 mm difference – ~6 %) variation,
from diastole (65–75 %) through systole (25–35 %). Measurement whereas area size increased from 4.24 to 4.84 cm2 (~0.6 cm2 differ-
of aortic annulus is usually performed in systole. The Geometrical ence – ~variation of 13 %)
15 Transcatheter Aortic Valve Implantation (TAVI) 259

g h i

j k l

Fig. 15.2 (continued)

MDCT and echocardiography but also differences in poten- 3D modalities in measurement of aortic root including aortic
tial sizing recommendations. Koos et al. evaluated the annulus and left ventricular outflow tract.
impact of 3D imaging methods (Cardiac magnetic reso- Ng et al. evaluated 2D circular, 3D circular and 3D pla-
nance – CMR and dual source CT – DSCT) versus 2D TEE nimetered annular and LVOT areas by TEE and compared
methods on TAVI selection [30]. In their cohort of 58 with MSCT planimetered areas [23]. In their cohort, the
patients, different measurements would have changed TAVI mean annular area by MSCT planimetry was 4.65 ± 0.82 cm2
strategy in 22–24 % patients. DSCT coronal measurements whereas by 2D TEE circular (3.89 ± 0.74 cm2, P < 0.001), 3D
when compared to 2D TEE would have changed strategy in TEE circular (4.06 ± 0.79 cm2, P < 0.001), and 3D TEE pla-
16 patients. Further in 14/16 of those patients, the prosthe- nimetered annular areas (4.22 ± 0.77 cm2, P < 0.001). They
sis size would have been larger and in the rest of the two, it observed 3D TEE derived planimetered annular areas had
was too large to implant. In a related similar study of 45 the narrowest limits of agreement and least bias when com-
patients comparing 2D TTE and TEE and MSCT measure- pared to MDCT. Although the circular geometric assump-
ments, Messika-Zeitoun et al. observed that a decision tions made by 2D and 3D circular measurements were
based on MSCT would have modified TAVI strategy in overcome by 3D TEE; Ng et al. observed 3D TEE when
40–42 % [29]. compared to MDCT still underestimated annular areas by up
The limitations of 2-D imaging largely reflect the complex to 10 %.
almost uniformly non-circular configuration of the annulus. It MSCT has also been shown to be highly discriminatory of
is not that 2-D diameters derived from echocardiography or those patients that historically experienced paravalvular
MSCT are inaccurate but it is simply a geometrical reality regurgitations owing to undersizing secondary to device siz-
that the complex morphology of a non-circular structure can- ing on the basis of 2-dimensional echocardiography. Willson
not be accurately characterized with a single 2-D measure- and colleagues noted that the annular area in particular on
ment. The growing appreciation of the limitations of 2-D MDCT was highly discriminatory of PAR [31]. This was
imaging has driven and increased focus on the utilization of important knowledge as it has been well established the
260 C.D. Arepalli et al.

paravalvular regurgitation is associated with increased mor- area derived ED showed a significant mean difference
bidity and mortality [28–30, 32, 33]. (0.4 ± 0.6 mm; p = 0.009), thus reconfirming influence of the
Building upon this retrospective knowledge multiple cardiac cycle on aortic annulus area measurements [38]. It is
groups have shown that the integration of MDCT in device likely that the diseased valves/tissues leave little scope for
selection allows for the reduction in the burden of stretch and therefore perimeter derived aortic annulus mea-
PAR. Jilaihawi et al, prospective integration of CT guided surements are least subjected to variation in cardiac cycle
algorithm reduced worse than mild paravalvular regurgita- (Fig. 15.2). However, it is being noted smoothing algorithms
tion (PAR) from 21.9 to 7.5 % when compared to 2D TEE used for perimeter derived measurements are inconsistent
[24]. Building upon this single center data Binder et al. in a across work station platforms and might cause measurement
prospective, multicenter controlled trial, evaluated the effects errors. Although area based ED measurements are smaller
of the integration of an area based sizing algorithm on the than perimeter derived ED, both approaches showed good
clinical outcomes post TAVI [34]. With a non-randomized agreement [38].
trial design half of the subjects (n = 133) underwent TAVI Whether perimeter or area is chosen for transcatheter
with the integration of MDCT measurements and sizing heart valve (THV) selection it is essential to understand the
recommendations and the other half underwent TAVI without impact that the geometrical variable (area or perimeter
the integration of MDCT. They observed more than mild derived measurements) may have on the prosthesis size that
PAR (primary endpoint) was present in 5.3 % (7 of 133) of would be selected. Blanke et al. showed assuming a perfect
the MDCT group and in 12.8 % (17 of 133) in the control circle with ellipticity index of 1, with increase in nominal
group (p = 0.032). The combined secondary endpoint (com- diameter, area increases exponentially whereas perimeter
posite of in-hospital death, aortic annulus rupture, and severe increases proportionally [39]. Thus, for e.g. 10 % diameter
PAR) occurred in 3.8 % (5 of 133) of the MDCT group and oversizing would translate to 10 % increase in perimeter
in 11.3 % (15 of 133) of the control group (p = 0.02). Finally whereas it would increase area by 21 %. These geometrical
the recently published large multicenter high risk CoreValve truths are essential to understand and of clinical importance
(Medtronic, Minneapolis, MN) trial showed excellent clini- when certain degree of annular oversizing is contemplated
cal outcomes as compared to surgical aortic valve replace- during TAVI.
ment with the THV selection supported almost exclusively In summation, 3D MDCT measurements play a critical
by MDCT perimeter measurements [35]. role in annular sizing and THV selection. MDCT measure-
ments are accurate, reproducible and choice of area or perim-
eter derived measurements need to be tailored depending
Dynamism of the Aortic Annulus upon the choice of prosthesis devices, allowing for dyna-
mism of the aortic annulus and based on the available tools
It is to be noted that aortic annulus is a dynamic structure (software) available at the sites.
with variation during systole and diastole phases of the car-
diac cycle. The aortic annulus is often elliptical and assumes
more circular shape during systole (Fig. 15.2). Further, it has MDCT Measurement of the Aortic Annulus
been observed that there is increased asymmetrical deforma-
tion during diastole which especially affects the right coro- Approach to Aortic Annulus Measurement
nary cusp portion of the annulus [36]. The ellipticity index
(EI) defined as ratio of maximum to minimum diameters We recommend using the phase of the cardiac cycle with best
substantially decreased from diastole to systole due to sig- image quality and in systolic phases (25–45 %) to allow for
nificant increase in antero-posterior minor diameter [25]. consistent assessment of the annulus when it is the largest.
Significant changes in area and radius were observed in both Aortic annulus measurements are performed orthogonally in
non-diseased annulus and stenotic annulus [37]. This has relation to the plane of 3 hinge points on a dedicated work
been attributed to annular reshaping than stretch with corre- station. Manual multiplanar reformats of the annulus is pre-
sponding increase in systolic area [25]. ferred as it helps in better understanding of the annulus and
Although cross-sectional area (CSA) derived measure- the annular plane rather than relying on automated tools
ments varied during cardiac cycle, it was found perimeter which should ideally only be used by highly experienced
based diameter measurements show negligible increase in operators. Briefly, the steps to achieve ‘optimal’ sizing of the
patients with calcified valves (0.56 ± 0.85 %; p < 0.001) and aortic annulus are mentioned below (Fig. 15.3), however,
very small changes in normal subjects (2.2 ± 2.2 %, p = 0.01) reader should look into expert consensus documents/recom-
[25]. In another study by Aspern et al., no significant differ- mendations for further in-depth information [15, 40].
ence was observed with perimeter-derived effective diame- The first step is to lock the orthogonal planes at 90° to
ters (ED) (mean difference: 0.2 ± 0.4; p = 0.07), however, each other. The cross hairs in the coronal and sagittal images
15 Transcatheter Aortic Valve Implantation (TAVI) 261

a b c

d e f

g h i

Fig. 15.3 Steps to achieve optimal sizing of aortic annulus. Step 1: hairs on the rest of the two oblique planes correspond to aortic annulus
Volumetric data is loaded onto the workstation and in a standard 3D for- plane (panel 6 – p–r). Any adjustments, if necessary, are made by follow-
mat (panel 1), the views are transverse (a), Coronal (b) and sagittal (c). ing the above steps. Step 6: Once a satisfactory plane is achieved (panel
The first step is to lock the orthogonal planes at 90° to each other (a–c). 7 – s–u), it is further confirmed by toggling the transverse oblique set of
Step 2: The cross hairs in the coronal and sagittal images are moved to the images cranially and caudally across the aortic root (panel 7 – s and panel
level of aortic valves and adjusted so that the cross hairs on the transverse 8 – v, red arrows). If a true aortic annular plane has been achieved, then
plane are positioned at the level of aortic valve (panel 2 – d–f). Step 3: one would observe that the valve hinge points would disappear or appear
Then the cross hairs on the coronal and sagittal views are rotated and symmetrically all at once (panels 7 – s–u and 8 – v–x). Utmost focus is
adjusted so as to correspond to the aortic annulus plane (panel 3). Now the given so that cross hairs are just touching the nadir points (panel 7 – s–u).
corresponding views are oblique set of images, for e.g. transverse/coronal/ If this plane is not achieved, then the coronal (panel 7 – t) and sagittal
sagittal oblique (g–i). Step 4: The cross hairs on the transverse oblique are oblique (panel 7 – u) planes needs to be further fine-tuned so as to achieve
rotated either clockwise or anticlockwise (panel 3 g) so as to check desired plane and again cross checked by rotating the cross hairs on the
whether the cross hairs correspond to aortic annular plane i.e. nadir point transverse oblique view (panel 7 – s). Step 7: Once an optimal view is
of the coronary cusps (panel 4 – j–l). In this panel views, the cross hairs achieved then the cross hairs are at the true aortic annular plane (panel
cuts across the cusp rather than located at the hinge/nadir point (panel 4 – 9 – y, z, A). Then a ROI trace is made along the circumference of the aortic
k). Step 5: The cross hairs are further adjusted by placing the cross hairs at annulus to calculate the major and minor diameters, mean diameters, area
the aortic annular plane (panel 5 – m–o). Once again the cross hair on the and circumference of the aortic annulus (panel 9 – y). Corresponding
transverse oblique view is rotated and again investigated to see the cross coronal and sagittal oblique planes are shown (panel 9 – z, a)
262 C.D. Arepalli et al.

j k l

m n o

p q r

Fig. 15.3 (continued)

15 Transcatheter Aortic Valve Implantation (TAVI) 263

s t u

v w x

y z

Fig. 15.3 (continued)

should be moved to the level of aortic valves and adjusted so across the transverse oblique so that to visualize the nadir
that the transverse plane is positioned at the level of aortic point of the valves in coronal oblique and sagittal oblique
valve. This would correspond to coronal and sagittal oblique planes. Utmost focus is given so that cross hairs are just
planes respectively. Next the transverse oblique plane is touching the nadir points and they disappear equally in all
moved up and down across the aortic root so as to visualize planes. Once this is confirmed, the specific position of aortic
the valve hinge points. The valve hinge points should disap- annulus in the transverse oblique plane is identified and a
pear or appear symmetrically all at once, if not, coronal and ROI trace is made along the circumference of the aortic
sagittal oblique planes need to be further fine-tuned so as to annulus. Majority of the present day work stations have auto-
achieve desired plane. Again, the cross hairs are rotated matic tools that would calculate diameters (D) – Dmin,
264 C.D. Arepalli et al.

Dmax, Dmean, area and perimeter once the tracing is made. angiographic projections and MDCT of aortic root [44]. It is
If these features are not available, diameter (D) can be calcu- important to recognize that correlation with the fluoroscopic
lated from circumference (D = circumference / π). (π = Pi). angles in the hybrid operating room relies on comparable posi-
Area is calculated from π.D2/4. tioning at the time of CT and during the procedure.

Implantation View – CO Planar Angle Evaluation of Aortic Annulus and Aortic Valve
Prediction Leaflets

The Aortic annulus is not orthogonal to the body axis/planes. Apart from annulus sizing, assessment of the aortic annulus, left
For a successful implantation, the prosthetic device needs to ventricular outflow tract and aortic valve leaflets is equally
be deployed coaxially to the centerline of the aorta. important for a successful TAVI procedure. Valve calcifications
Inappropriate deployment might lead to complications [41]. may be distributed focally or diffusely over the surface of the
This plane can be achieved on both CT workstation and fluo- valve cusps or they may present along the leaflet edges. Presence
roscopy units. However to achieve the same plane in fluoros- of severe calcium is likely to cause important peri and post pro-
copy unit, multiple aortograms are to be performed in a cedural complications. Post dilatation techniques might need to
stepwise approach. be employed in patients with severe calcification.
This situation offers an opportunity for pre-procedural CT In TAVI cohorts, it is not uncommon to see sub annular or
to help predict the co-planar angles of deployment prior to the LVOT calcification (Figs. 15.4 and 15.5) or aorto-mitral calci-
procedure. At here are innumerable co-planar angles of deploy- fication as a continuum (Fig. 15.4a, b). Distribution of calcium
ment typically ranging from RAO Caudal to LAO Cranial. Pre- in each of these locations has been shown to have important
procedural co-planar angle guidance has been shown to help prognostic implications. In a study by Barbanti et al., 31 con-
reduce procedure fluoroscopy time and the volume of contrast secutive TAVI patients who had LVOT/annular/aortic con-
needed for the procedure [42, 43]. Binder et al. have demon- tained/noncontained rupture were caliper-matched to control
strated significant correlation (r = 0.682, p < 0.001) between group of 31 patients without annular injury [45]. They
the predicted optimal deployment projections using 3D observed at least 2 features were significantly associated with

a b

Fig. 15.4 (a) Left ventricular out flow tract (LVOT) (green arrow) and function and geometry. It should be noted that deployment of a balloon
(b) Mitral annular calcification (MAC) (yellow chevron). Severe LVOT expandable prosthesis is contraindicated in concomitant significant
calcification is associated with increased annular rupture. The impact of mitral stenosis with significant mitral annular calcification. LVEF left
MAC on TAVI procedure and outcomes is unclear. Presence of MAC ventricle ejection fraction
might cause stenosis and/or regurgitation and that influences LV
15 Transcatheter Aortic Valve Implantation (TAVI) 265

a b

Fig. 15.5 Factors influencing annular rupture. (a) Subannular (yellow chevrons) and (b) LVOT calcification (green arrow). Note the relatively low
left coronary ostial-aortic annulus height (measured 9.6 mm) (red double arrow)

annular rupture: 1. Moderate/severe LVOT/subannular calcifi- (Fig. 15.1a–c) or could also be quantified analogous to the
cation ((odds ratio, 10.92; 95 % CI, 3.23–36.91; P < 0.001) and concept of the Agatston score that is being used in assessment
2. ≥20 % area oversizing (odds ratio, 8.38; 95 % CI, 2.67– of coronary artery calcifications.
26.33; P = <0.001). Area oversizing ≥20 % was found to be Haensig et al. assessed for association between native
the strongest predictor of aortic rupture and presence of sig- AVC and paravalvular leak in 120 consecutive patients who
nificant LVOT/subannular calculation seems to compound to proceeded with Edwards SAPIEN prosthesis. No paraval-
increased risk. Additionally, presence and characteristics of vular leaks (n = 66) were noted with mean AVC score of
annular calcification such as protruding, round and asymmet- 2704 ± 1510, mild paravalvular leaks (n = 31) with
rical distribution at the coronary cusps seems to predict PAR 3804 ± 2739 (P = 0.05); and moderate paravalvular leaks
(Fig. 15.5a). In a study by Feuchtner et al., protruding annular (n = 4) with AVC score of 7387 ± 1044 (P = 0.002) [48]. A
calcification >4 mm, adherent annular calcification >6 mm significant association between the AVC score and paraval-
predicted significant PAR (p = 0.03 and 0.009 respectively). vular leaks [odds ratio [(OR; per AVC score of 1000),
Further, it was observed total left and non-coronary and left 11.38; 95 % confidence interval (CI) 2.33–55.53; P = 0.001)]
coronary calcium size score predicted relevant leaks (p = 0.004 was noted. It is not only the amount of calcification but
and p = 0.001, resp.) but not right or non-coronary cusps location/distribution at each separate cusp or commissure
calcium [46]. has been found to be associated with PAR [48]. Their study
During the procedure, severe calcification may offer identified significant association for the right and left coro-
resistance to the expansion caused by balloon or self- nary cusp, for right-left and left non coronary commissure,
expandable devices and may prevent appropriate alignment and there was no significant association for non-coronary
and/or complete apposition of the sealing skirt to the native right commissure and for non-coronary cusp. Interestingly
commissures. Further, incomplete apposition of the device a number of other studies evaluating patients who under-
with commissures may potential lead to development of went TAVI using a self-expanding system,, did not find an
paravalvular regurgitation (PAR). It has been shown that association between PAR and the degree of calcification
even mild paravalvular leaks are associated with increased [49, 50]. It is likely the distribution of radial force at differ-
mortality [47, 48] ent locations due to the nature of the device with balloon
Aortic valve calcifications (AVC) distribution is better expandable at the annulus whereas the self-expandable at
visualized on the cross-sectional view of the sinus of Valsalva. the ascending aorta cause varied propensity towards devel-
AVC can be assessed qualitatively as mild, moderate or severe opment of PAR.
266 C.D. Arepalli et al.

a b

Fig. 15.6 Coronary ostial-aortic annulus heights. (a) Low left coronary ostial height (~8 mm) and (b) adequate right coronary ostial height
(~13 mm)

Coronary Arteries and Ostial Heights predispose to coronary obstruction. This registry allowed
the field to understand mechanisms of coronary occlusion
In general, the right and left coronary arteries arise from their beyond coronary height that the majority of patients (~
respective right and left coronary cusps. They usually arise 65 %) who had coronary obstruction had aortic root efface-
below the sinotubular junction with the right coronary artery ment and also SOV diameter of <30 mm when compared
typically at a higher level than left. Given the nature of TAVI, to the control group. Coronary artery obstruction was more
where in the native aortic leaflets are displaced and the bio- frequently observed in female patients (>80 %) likely
prosthesis is implanted in the aortic root; the coronary ostial related to the female anatomy with smaller aortic root/
height clearance measurement is important to understand shallow aortic sinus and also relatively due to low lying
and discriminate those at risk of coronary arterial occlusion. coronary ostia (Figs. 15.5b and 15.6a). In addition, a sig-
Coronary ostial height measurements are performed in a per- nificant difference in SOV/AA ratios was also observed
pendicular fashion from the annular plane to the coronary between those who had coronary obstruction when com-
ostia (Fig. 15.6a, b). pared to control groups (1.25 + _0.04 vs. 1.34 + _0.03;
A coronary ostial cut off of 10 mm was suggested p = 0.003) [53].
by the American College of Cardiology Foundation/ It is also interesting to note that coronary obstruction was
American Association for Thoracic Surgery/Society for more often observed in patients with balloon expandable
Cardiovascular Angiography and Interventions/Society of devices than those who had self-expandable devices [53, 54].
Thoracic Surgeons expert consensus [15, 51]. However, in It is unknown whether makeup of the device or mechanism
a study of reported cases of coronary obstruction, the mean of deployment has any role in the observed obstructions.
height was 10.3 mm (range 7–12 mm) and 60 % of cases Other causes which predispose to coronary obstruction
with obstruction had a height >10 mm [52]. In a multi- include bulky calcification of the native aortic leaflets, long
center registry study, it was observed majority of the mobile leaflets and specifically presence of leaflet length
patients who had coronary obstruction (~80 % overall and more than the coronary ostial heights.
96 % of women) had a left ostial height <12 mm [53]. Although, at present there are no standard guidelines for a
Further, adding to the complexity and importance of ostial ‘safe’ coronary ostial height; various factors that predispose
measurements, in the same registry study, even though the to coronary obstruction need to be taken into account. These
coronary ostial heights were more than >12 mm, 21.4 % include patient’s sex, the size of the aortic root, sinus of
had a coronary obstruction implying that there are factors Valsalva diameter, coronary ostial heights, and the ratio of
beyond ‘safety cutoff’ of coronary ostial height that might SOV/AA (Fig. 15.7).
15 Transcatheter Aortic Valve Implantation (TAVI) 267

a b

c d

Fig. 15.7 Unfavorable anatomy of aortic root (same patient as in diameters (d) (Cusp – yellow triangles, Commissure – notched
Fig. 15.5). (a, b) Aortic annulus is smaller in size and it shows green arrow). This TAVI patient is female and there is relatively
subannular and LVOT calcification (yellow chevron’s). (Even low left coronary ostial height (9.6 mm) (Fig. 15.5b). Multiple
though aortic valvular calcification is of mild degree (c), the aortic confounding factors increase risk of peri-procedural complications
sinus is shallow as it measures <30 in all cusp-commissure

Evaluation of Aortic Arch, Thoraco- Academic Research Consortium (VARC) [60, 61]. In a
Abdominal Aortic Assessment and Ilio- meta-analysis study of 16 outcomes based on VARC 2011,
Femoral Arterial Assessment the pooled estimated rate for major and minor vascular
complications were 11.9 % (range 5–23.3 %) and 9.7 %
Vascular related complications are one of the most frequent (range 5.6–28.3 %) with an overall vascular complication
adverse events associated with TAVI procedure [11, 12, rate of 18.8 % (range 9.5–51.6 %) [56]. Occurrence of
55–59]. TAVR related complications are defined by Valve major vascular complication was associated significantly
268 C.D. Arepalli et al.

with higher rates of 30 day and 1 year all-cause and cardiac Arterial Lumen Diameter Assessment
mortality Owing to the increased risk associated with vas-
cular injury the assessment of the vascular pathway and Ideally the delivery system needs to be smaller than vascular
risk factors for vascular injury are important steps in pre- luminal diameter. Due to relatively larger delivery systems
TAVI work up. that are used (>18 F), accurate assessment of the vascular
access and pathway is critical. As most TAVI cohorts are
elderly, it is not uncommon to see vessels which are tortuous
Peripheral Vascular Accesses and have considerable atherosclerotic burden. In a study of
100 TAVI patients for peripheral artery disease, one-third
Access routes can be broadly classified into retrograde (35 %) had at least one criterion of unsuitable iliofemoral anat-
(transfemoral [TF], transaortic, transsubclavian etc.), ante- omy and out of those more than 75 % had a luminal diameter
grade (tranapical) approach or a combination of both (trans- of less than 8 mm [62]. The other unfavorable factors included
caval-transaortic). Each of the access sites for delivery of severe circumferential calcification at the iliac bifurcation
TAVI has advantages and limitations. (>60 %), and severe angulation of the iliac arteries (<90°).
The risk factors for vascular injury include small cali- Although the arterial lumen can be assessed on the source
ber vessels (Fig. 15.8), presence of significant occlusive axial or transverse set of images, assessment in this view
disease, burden and pattern of calcification, excessive tends to inaccurately measure the true minimal luminal
iliac tortuosity. Dual plane angiography can be used in diameter. Areas of significant stenosis can be under appreci-
the assessment of vessel caliber and also for presence of ated due tortuous course of the vessels. Further, the presence
significant stenosis; however, it is limited in the evalua- of dense calcium causes blooming artifacts which tend to
tion of plaque burden and vessel tortuosity. Similarly, overestimate stenosis.
although ultrasound could be used in the assessment of Accurate measurements of lumen diameter are obtained
plaque burden and assessment of luminal diameter, it is through multiplanar reformations. Due to MDCT volumetric
limited in evaluation of tortuosity and if the calcific acquisition, orthogonal planes to the center line of arterial
plaque burden is high. MDCT with its superior spatial lumen can be obtained to determine the true short and long
and temporal resolution, volumetric acquisition and rel- axis diameter measurements. Modern post processing work
atively simple post-processing techniques helps in eval- stations have curved planar reformations tool which would
uation of the risk factors for vascular injury and thus help in extracting the entire course of the vessel and thus a
is considered gold standard modality for vascular visual and quantitative measurements could be obtained.
screening. A potential limitation in assessment of arterial lumen arises

a b

Fig. 15.8 Narrow Ilio-femoral luminal diameters. Although Common iliac arteries measure <6 mm and the common femoral
calcification in the ilio-femoral arteries is minimal; bilateral arteries access sites measures <5 mm. Alternative access sites
ilio-femoral arteries show narrow minimal lumen diameter. need to be considered in this patient
15 Transcatheter Aortic Valve Implantation (TAVI) 269

in the presence of dense calcium which tends to overestimate minimal lumen area [MLA]) in 255 patients and found
stenosis and thus undermines the luminal diameter. This is SFAAR of 1.35 was predictive of vascular complications
overcome by choosing proper window level and width set- (sensitivity 78.6 %, specificity 62.9 %) [63]. In comparison,
tings or by using bone algorithm settings during measure- although a diameter ratio cutoff of 1.45 was predictive but it
ments. Some of the modern work stations have a full width had lower sensitivity and specificity (64.2 % and 67.4 %,
half maximum built in tool which could be used for accurate respectively). These findings highlight the importance of
diameter measurements. Hayashida et al. were the first to lumen diameter and area measurements and their relation to
introduce the concept of sheath to femoral artery ratio sheath diameter/areas in predicting vascular complications.
(SFAR) and defined it as the ratio of the sheath outer diam-
eter (in millimeters-mm) to the minimal femoral artery
diameter (in mm) [58]. In their study, a SFAR threshold of Vessel Wall Calcifications
1.05 (area under the curve = 0.727) predicted a higher rate of
VARC major complications (30.9 % vs. 6.9 %, p = 0.001) Arterial luminal or area measurements need to be determined
and 30-day mortality (18.2 % vs. 4.2 %, p = 0.016). A SFAR in concurrence with the presence of atherosclerotic plaques,
≥1.05 was also associated with an increased incidence of more specifically calcifications. Calcifications are broadly
30-day mortality (18.2 % vs. 2.8 %, p = 0.004). Using this defined as follows: 0-no calcification; 1-mild calcification;
SFAR threshold, the minimal femoral artery diameter neces- 2-moderate calcification; and 3-severe calcification
sary for the 19- and 18-F introducer sheaths was calculated (Fig. 15.9) [64]. Presence of circumferential calcification
as 7.1 and 6.9 mm, respectively. (>75 % vessel circumference) and/or horseshoe (>180°) cal-
Another series looked into both SFAR and sheath: femo- cifications with decreased luminal diameter are at a higher
ral artery area ratio (SFAAR – sheath area to the femoral risk of complications. In a study of 132 patients, the presence

a b c

d e f

Fig. 15.9 Iliofemoral calcifications. They are broadly classified derived from MDCT (d–f) could be used to calculate SFAR and
as: 0-no calcification; (a) 1-mild calcification; (b) 2-moderate SFAAR depending upon the sheath device used. SFAR > 1.05 and
calcification; and (c) 3-severe calcification [66]. Presence of SFAAR > 1.35 were associated with increased vascular
horseshoe or circumferential calcification increases risk of vascular complications. SFAR Sheath to Femoral Artery Ratio (Diameter),
complications. Further, the diameter and area measurements SFAAR Sheath Area to Femoral Minimal Lumen Area Ratio
270 C.D. Arepalli et al.

of circumferential ilio-femoral calcifications was an impor- access vessel diameter (TT/AD) index and observed that a
tant risk factor for vascular complications and also an inde- value 27.89 predicts vascular complications with 50.8 %
pendent predictor of increased mortality after TF-TAVI [65]. sensitivity and 70.6 % specificity (AUC: 0.22, P = 0.008)
Further, incorporation of this MSCT derived parameter in [66]. TT/AD ratio defined as sum of angles (TT) divided by
the workup algorithm of patients with a sheath-to-iliofemoral the minimum femoral arterial diameter (AD) at the access
artery ratio – SIFAR ≥1 on angiographic screening improved site. Even though, the indexed values were primarily based
the specificity for prediction of major vascular complications on 2D invasive angiography, nevertheless, a small subset of
to 62 % without altering the sensitivity (100 %). their cohort were evaluated with 3D MDCT and found to
In another series, arterial calcification (Grade > 2) at punc- have good correlation (r = 0.66, p = 0.013).
ture site was found to be independent predictor of major vas- Chiam et al. assessed iliofemoral dimensions and charac-
cular complication, p < 0.001 [66] . The authors also noted teristics by ultrasonography in 549 Asian patients [68]. They
despite the use of a pigtail catheter for an ideal puncture, observed female gender, lower body surface area, and pres-
arterial wall calcification could not be evaluated by fluoros- ence of diabetes mellitus; dyslipidemia and smoking history
copy and recommended assessment through MDCT. Kurra were independent factors for smaller iliofemoral dimensions.
et al. proposed presence of more than 60 % circumferential Thus for the same degree of tortuosity, a smaller intraluminal
calcification at the external–internal iliac bifurcation as an diameter might predispose to increased vascular risk, if TT/
unsuitable iliofemoral anatomy [62]. AD index is incorporated.

Iliofemoral Arterial Tortuosity Alternative Access

Iliofemoral Arterial Tortuosity have implications for transfem- Alternative access routes should be considered in patients
oral TAVI approach as excess tortuosity might increase the where reconstructed CT images reveal unfavorable
access site complication rates and thus would affect procedural ilio-femoral anatomy. Description of various access sites
success. The degree of tortuosity could be graded as – 0-no is beyond the scope of this chapter; however, the underly-
tortuosity; 1-mild tortuosity (30–60°); 2-moderate tortuosity ing principles would remain the same as mentioned
(60–90°); and 3-severe tortuosity (≥90°) (Fig. 15.10) [62, 64]. above. Access routes need to be assessed holistically
Although it was observed that iliofemoral tortuosity alone depending upon patient’s condition and also the device
does not predict vascular complications [58, 67]; Vavuranakis that is likely to be deployed with minimal complications
et al. in their study incorporated total arterial tortuosity/ (Fig. 15.11).

a b c

Fig. 15.10 Ilio-femoral tortuosity. Multiple panels show mild, 3-severe tortuosity (≥90°) [64, 66]. Although, the degree of
moderate and severe tortuosity of peripheral vascular access (a–c). tortuosity per se might not significantly influence increased risk for
Degree of tortuosity is graded as: 0-no tortuosity; (a) 1-mild vascular complications; a combination of increased tortuosity and
tortuosity (30–60°); (b) 2-moderate tortuosity (60–90°); and (c) small luminal diameter predisposes to vascular risk
15 Transcatheter Aortic Valve Implantation (TAVI) 271

a b

Fig. 15.11 Structural overlay of peripheral access sites. MDCT vascular access sites were assessed (b, c). VRT images provide visual
volumetric acquisition provides VRT images which help in better depiction of prior bypass graft procedure and presence of left bra-
anatomical understanding of the overlying structures. For e.g. (a). chiocephalic vein overlying the ascending aorta (b, c). If a transaortic
Overlay of Iliofemoral arteries against the backdrop of pelvic bones access is contemplated relevant knowledge of anatomy and their rela-
helps in easy assessment of tortuosity. In another TAVI patient, an tions to each other help in proper planning. VRT volume rendered
unfavorable iliofemoral access was noted and hence alternate technique

Conclusion from simply being a tool for the assessment of iliofemoral

The integration of computed tomography into transcathe- access to now being the non-invasive test of choice for pre-
ter aortic valve replacement planning and guidance has procedural annular sizing and transcatheter heart valve
seen rapid progression over the last 5 years. CT has gone selection. With ongoing evolution of the transcatheter
272 C.D. Arepalli et al.

devices and the procedure, as well as the introduction of 15. Achenbach S, Delgado V, Hausleiter J, Schoenhagen P, Min
other transcatheter valvular solutions CT will almost cer- JK, Leipsic JA. SCCT expert consensus document on com-
puted tomography imaging before transcatheter aortic valve
tainly grow in its utilization and help us further understand implantation (TAVI)/transcatheter aortic valve replacement
how to appropriately size transcatheter devices and hope- (TAVR). J Cardiovasc Comput Tomogr. 2012;6(6):366–80. Epub
fully reduce procedural related complications. 2012/12/12.
16. Neragi-Miandoab S, Michler RE. A review of most relevant com-
plications of transcatheter aortic valve implantation. ISRN Cardiol.
2013;2013:956252. Epub 2013/07/12.
References 17. Tops LF, Wood DA, Delgado V, Schuijf JD, Mayo JR, Pasupati
S, et al. Noninvasive evaluation of the aortic root with multislice
computed tomography implications for transcatheter aortic valve
1. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Borden
replacement. JACC Cardiovasc Imaging. 2008;1(3):321–30. Epub
WB, et al. Heart disease and stroke statistics – 2013 update: a report
2009/04/10.
from the American Heart Association. Circulation. 2013;127(1):e6–
18. Schultz CJ, Moelker A, Piazza N, Tzikas A, Otten A, Nuis RJ,
245. Epub 2012/12/15.
et al. Three dimensional evaluation of the aortic annulus using mul-
2. Thaden JJ, Nkomo VT, Enriquez-Sarano M. The global burden of
tislice computer tomography: are manufacturer’s guidelines for siz-
aortic stenosis. Prog Cardiovasc Dis. 2014;56(6):565–71. Epub
ing for percutaneous aortic valve replacement helpful? Eur Heart
2014/05/20.
J. 2010;31(7):849–56. Epub 2009/12/10.
3. Osnabrugge RL, Mylotte D, Head SJ, Van Mieghem NM, Nkomo 19. Blanke P, Russe M, Leipsic J, Reinohl J, Ebersberger U, Suranyi
VT, LeReun CM, et al. Aortic stenosis in the elderly: disease P, et al. Conformational pulsatile changes of the aortic annulus:
prevalence and number of candidates for transcatheter aortic valve impact on prosthesis sizing by computed tomography for transcath-
replacement: a meta-analysis and modeling study. J Am Coll eter aortic valve replacement. JACC Cardiovasc Interv. 2012;5(9):
Cardiol. 2013;62(11):1002–12. Epub 2013/06/04. 984–94. Epub 2012/09/22.
4. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott 20. Ng AC, Yiu KH, Ewe SH, van der Kley F, Bertini M, de Weger A,
CG, Enriquez-Sarano M. Burden of valvular heart diseases: a et al. Influence of left ventricular geometry and function on aortic
population-based study. Lancet. 2006;368(9540):1005–11. Epub annular dimensions as assessed with multi-detector row computed
2006/09/19. tomography: implications for transcatheter aortic valve implanta-
5. Fedak PW, Verma S, David TE, Leask RL, Weisel RD, Butany tion. Eur Heart J. 2011;32(22):2806–13. Epub 2011/07/26.
J. Clinical and pathophysiological implications of a bicuspid aortic 21. Nakai H, Takeuchi M, Yoshitani H, Kaku K, Haruki N, Otsuji
valve. Circulation. 2002;106(8):900–4. Epub 2002/08/21. Y. Pitfalls of anatomical aortic valve area measurements using two-
6. Beppu S, Suzuki S, Matsuda H, Ohmori F, Nagata S, Miyatake dimensional transoesophageal echocardiography and the poten-
K. Rapidity of progression of aortic stenosis in patients with con- tial of three-dimensional transoesophageal echocardiography. Eur
genital bicuspid aortic valves. Am J Cardiol. 1993;71(4):322–7. J Echocardiogr. 2010;11(4):369–76. Epub 2009/12/22.
Epub 1993/02/01. 22. Bertaso AG, Wong DT, Liew GY, Cunnington MS, Richardson
7. Pomerance A. Pathogenesis of aortic stenosis and its relation to JD, Thomson VS, et al. Aortic annulus dimension assessment by
age. Br Heart J. 1972;34(6):569–74. Epub 1972/06/01. computed tomography for transcatheter aortic valve implantation:
8. Mautner GC, Mautner SL, Cannon 3rd RO, Hunsberger SA, differences between systole and diastole. Int J Cardiovasc Imaging.
Roberts WC. Clinical factors useful in predicting aortic valve 2012;28(8):2091–8. Epub 2012/02/10.
structure in patients >40 years of age with isolated valvu- 23. Ng AC, Delgado V, van der Kley F, Shanks M, van de Veire NR,
lar aortic stenosis. Am J Cardiol. 1993;72(2):194–8. Epub Bertini M, et al. Comparison of aortic root dimensions and geom-
1993/07/15. etries before and after transcatheter aortic valve implantation by
9. Ross Jr J, Braunwald E. Aortic stenosis. Circulation. 1968;38(1 2- and 3-dimensional transesophageal echocardiography and mul-
Suppl):61–7. Epub 1968/07/01. tislice computed tomography. Circ Cardiovasc Imaging. 2010;
10. Salinas P, Moreno R, Lopez-Sendon JL. Transcatheter aortic 3(1):94–102. Epub 2009/11/19.
valve implantation: current status and future perspectives. World 24. Jilaihawi H, Kashif M, Fontana G, Furugen A, Shiota T, Friede
J Cardiol. 2011;3(6):177–85. Epub 2011/07/21. G, et al. Cross-sectional computed tomographic assessment
11. Panchal HB, Ladia V, Desai S, Shah T, Ramu V. A meta-analysis improves accuracy of aortic annular sizing for transcatheter aortic
of mortality and major adverse cardiovascular and cerebrovascu- valve replacement and reduces the incidence of paravalvular aor-
lar events following transcatheter aortic valve implantation versus tic regurgitation. J Am Coll Cardiol. 2012;59(14):1275–86. Epub
surgical aortic valve replacement for severe aortic stenosis. Am 2012/03/01.
J Cardiol. 2013;112(6):850–60. Epub 2013/06/13. 25. Hamdan A, Guetta V, Konen E, Goitein O, Segev A, Raanani E,
12. Cao C, Ang SC, Indraratna P, Manganas C, Bannon P, Black D, et al. Deformation dynamics and mechanical properties of the aor-
et al. Systematic review and meta-analysis of transcatheter aortic tic annulus by 4-dimensional computed tomography: insights into
valve implantation versus surgical aortic valve replacement for the functional anatomy of the aortic valve complex and implica-
severe aortic stenosis. Ann Cardiothorac Surg. 2013;2(1):10–23. tions for transcatheter aortic valve therapy. J Am Coll Cardiol.
Epub 2013/08/27. 2012;59(2):119–27. Epub 2012/01/10.
13. Cribier A, Eltchaninoff H, Bash A, Borenstein N, Tron C, Bauer 26. Buellesfeld L, Stortecky S, Kalesan B, Gloekler S, Khattab AA,
F, et al. Percutaneous transcatheter implantation of an aortic valve Nietlispach F, et al. Aortic root dimensions among patients with
prosthesis for calcific aortic stenosis: first human case description. severe aortic stenosis undergoing transcatheter aortic valve replace-
Circulation. 2002;106(24):3006–8. Epub 2002/12/11. ment. JACC Cardiovasc Interv. 2013;6(1):72–83. Epub 2013/01/26.
14. Leipsic J, Yang TH, Min JK. Computed tomographic imaging of 27. Zhang R, Song Y, Zhou Y, Sun L. Comparison of aortic annulus
transcatheter aortic valve replacement for prediction and prevention diameter measurement between multi-detector computed tomog-
of procedural complications. Circ Cardiovasc Imaging. 2013;6(4): raphy and echocardiography: a meta-analysis. PLoS One. 2013;
597–605. Epub 2013/07/19. 8(3):e58729. Epub 2013/03/22.
15 Transcatheter Aortic Valve Implantation (TAVI) 273

28. Mizia-Stec K, Pysz P, Jasinski M, Adamczyk T, Drzewiecka- 41. Kurra V, Kapadia SR, Tuzcu EM, Halliburton SS, Svensson L,
Gerber A, Chmiel A, et al. Preoperative quantification of aortic Roselli EE, et al. Pre-procedural imaging of aortic root orienta-
valve stenosis: comparison of 64-slice computed tomography with tion and dimensions: comparison between X-ray angiographic
transesophageal and transthoracic echocardiography and size of planar imaging and 3-dimensional multidetector row computed
implanted prosthesis. Int J Cardiovasc Imaging. 2012;28(2):343– tomography. JACC Cardiovasc Interv. 2010;3(1):105–13. Epub
52. Epub 2011/02/01. 2010/02/05.
29. Messika-Zeitoun D, Serfaty JM, Brochet E, Ducrocq G, Lepage L, 42. Gurvitch R, Wood DA, Leipsic J, Tay E, Johnson M, Ye J, et al.
Detaint D, et al. Multimodal assessment of the aortic annulus diam- Multislice computed tomography for prediction of optimal angio-
eter: implications for transcatheter aortic valve implantation. J Am graphic deployment projections during transcatheter aortic valve
Coll Cardiol. 2010;55(3):186–94. Epub 2010/02/02. implantation. JACC Cardiovasc Interv. 2010;3(11):1157–65. Epub
30. Koos R, Altiok E, Mahnken AH, Neizel M, Dohmen G, Marx 2010/11/23.
N, et al. Evaluation of aortic root for definition of prosthesis size 43. Leipsic J, Gurvitch R, Labounty TM, Min JK, Wood D, Johnson M,
by magnetic resonance imaging and cardiac computed tomogra- et al. Multidetector computed tomography in transcatheter aortic
phy: implications for transcatheter aortic valve implantation. Int valve implantation. JACC Cardiovasc Imaging. 2011;4(4):416–29.
J Cardiol. 2012;158(3):353–8. Epub 2011/02/15. Epub 2011/04/16.
31. Willson AB, Webb JG, Labounty TM, Achenbach S, Moss R, 44. Binder RK, Leipsic J, Wood D, Moore T, Toggweiler S, Willson A,
Wheeler M, et al. 3-dimensional aortic annular assessment by et al. Prediction of optimal deployment projection for transcatheter
multidetector computed tomography predicts moderate or severe aortic valve replacement: angiographic 3-dimensional reconstruction
paravalvular regurgitation after transcatheter aortic valve replace- of the aortic root versus multidetector computed tomography. Circ
ment: a multicenter retrospective analysis. J Am Coll Cardiol. Cardiovasc Interv. 2012;5(2):247–52. Epub 2012/03/23.
2012;59(14):1287–94. Epub 2012/03/01. 45. Barbanti M, Yang TH, Rodes Cabau J, Tamburino C, Wood DA,
32. Altiok E, Koos R, Schroder J, Brehmer K, Hamada S, Becker M, Jilaihawi H, et al. Anatomical and procedural features associated
et al. Comparison of two-dimensional and three-dimensional imag- with aortic root rupture during balloon-expandable transcatheter
ing techniques for measurement of aortic annulus diameters before aortic valve replacement. Circulation. 2013;128(3):244–53. Epub
transcatheter aortic valve implantation. Heart (Br Cardiac Soc). 2013/06/12.
2011;97(19):1578–84. Epub 2011/06/28. 46. Feuchtner G, Plank F, Bartel T, Bonaros N, Müller S, Leipsic J,
33. Husser O, Rauch S, Endemann DH, Resch M, Nunez J, Bodi V, et al. TCT-836 prediction of paravalvular leaks after transcatheter
et al. Impact of three-dimensional transesophageal echocardiogra- aortic valve implantation by valvular or annular calcification? J Am
phy on prosthesis sizing for transcatheter aortic valve implantation. Coll Cardiol. 2012;60(17_S).
Catheter Cardiovasc Interv. 2012;80(6):956–63. Epub 2012/03/16. 47. Kodali SK, Williams MR, Smith CR, Svensson LG, Webb JG,
34. Binder RK, Webb JG, Willson AB, Urena M, Hansson NC, Makkar RR, et al. Two-year outcomes after transcatheter or surgical
Norgaard BL, et al. The impact of integration of a multidetector aortic-valve replacement. N Engl J Med. 2012;366(18):1686–95.
computed tomography annulus area sizing algorithm on outcomes Epub 2012/03/27.
of transcatheter aortic valve replacement: a prospective, multi- 48. Haensig M, Lehmkuhl L, Rastan AJ, Kempfert J, Mukherjee C,
center, controlled trial. J Am Coll Cardiol. 2013;62(5):431–8. Epub Gutberlet M, et al. Aortic valve calcium scoring is a predictor of
2013/05/21. significant paravalvular aortic insufficiency in transapical-aortic
35. Adams DH, Popma JJ, Reardon MJ, Yakubov SJ, Coselli JS, Deeb valve implantation. Eur J Cardiothorac Surg. 2012;41(6):1234–40.
GM, et al. Transcatheter aortic-valve replacement with a self- discussion 40-1. Epub 2012/01/14.
expanding prosthesis. N Engl J Med. 2014;370(19):1790–8. Epub 49. John D, Buellesfeld L, Yuecel S, Mueller R, Latsios G, Beucher
2014/04/01. H, et al. Correlation of Device landing zone calcification and acute
36. Lehmkuhl L, Foldyna B, Von Aspern K, Lucke C, Grothoff M, procedural success in patients undergoing transcatheter aortic valve
Nitzsche S, et al. Inter-individual variance and cardiac cycle depen- implantations with the self-expanding CoreValve prosthesis. JACC
dency of aortic root dimensions and shape as assessed by ECG-gated Cardiovasc Interv. 2010;3(2):233–43. Epub 2010/02/23.
multi-slice computed tomography in patients with severe aortic ste- 50. Koos R, Mahnken AH, Dohmen G, Brehmer K, Gunther RW,
nosis prior to transcatheter aortic valve implantation: is it crucial Autschbach R, et al. Association of aortic valve calcification sever-
for correct sizing? Int J Cardiovasc Imaging. 2013;29(3):693–703. ity with the degree of aortic regurgitation after transcatheter aor-
Epub 2012/09/19. tic valve implantation. Int J Cardiol. 2011;150(2):142–5. Epub
37. de Heer LM, Budde RP, van Prehn J, Mali WP, Bartels LW, Stella PR, 2010/03/31.
et al. Pulsatile distention of the nondiseased and stenotic aortic valve 51. Holmes Jr DR, Mack MJ, Kaul S, Agnihotri A, Alexander KP, Bailey
annulus: analysis with electrocardiogram-gated computed tomogra- SR, et al. 2012 ACCF/AATS/SCAI/STS expert consensus docu-
phy. Ann Thorac Surg. 2012;93(2):516–22. Epub 2011/12/06. ment on transcatheter aortic valve replacement: developed in col-
38. von Aspern K, Foldyna B, Etz CD, Hoyer A, Girrbach F, Holzhey laboration with the American Heart Association, American Society
D, et al. Effective diameter of the aortic annulus prior to trans- of Echocardiography, European Association for Cardio-Thoracic
catheter aortic valve implantation: influence of area-based versus Surgery, Heart Failure Society of America, Mended Hearts, Society
perimeter-based calculation. Int J Cardiovasc Imaging. 2015;31: of Cardiovascular Anesthesiologists, Society of Cardiovascular
163–9. Epub 2014/08/29. Computed Tomography, and Society for Cardiovascular Magnetic
39. Blanke P, Willson AB, Webb JG, Achenbach S, Piazza N, Min Resonance. J Thorac Cardiovasc Surg. 2012;144(3):e29–84. Epub
JK, et al. Oversizing in transcatheter aortic valve replacement, a 2012/08/18.
commonly used term but a poorly understood one: dependency on 52. Ribeiro HB, Nombela-Franco L, Urena M, Mok M, Pasian S, Doyle
definition and geometrical measurements. J Cardiovasc Comput D, et al. Coronary obstruction following transcatheter aortic valve
Tomogr. 2014;8(1):67–76. Epub 2014/03/04. implantation: a systematic review. JACC Cardiovasc Interv. 2013;
40. Kasel AM, Cassese S, Bleiziffer S, Amaki M, Hahn RT, Kastrati 6(5):452–61. Epub 2013/04/23.
A, et al. Standardized imaging for aortic annular sizing: implica- 53. Ribeiro HB, Webb JG, Makkar RR, Cohen MG, Kapadia SR,
tions for transcatheter valve selection. JACC Cardiovasc Imaging. Kodali S, et al. Predictive factors, management, and clinical out-
2013;6(2):249–62. Epub 2013/03/16. comes of coronary obstruction following transcatheter aortic valve
274 C.D. Arepalli et al.

implantation: insights from a large multicenter registry. J Am Coll for transcatheter aortic valve implantation: the Valve Academic
Cardiol. 2013;62(17):1552–62. Epub 2013/08/21. Research Consortium-2 consensus document. J Am Coll Cardiol.
54. Khatri PJ, Webb JG, Rodes-Cabau J, Fremes SE, Ruel M, Lau K, 2012;60(15):1438–54. Epub 2012/10/06.
et al. Adverse effects associated with transcatheter aortic valve 62. Kurra V, Schoenhagen P, Roselli EE, Kapadia SR, Tuzcu EM,
implantation: a meta-analysis of contemporary studies. Ann Intern Greenberg R, et al. Prevalence of significant peripheral artery dis-
Med. 2013;158(1):35–46. Epub 2013/01/02. ease in patients evaluated for percutaneous aortic valve insertion:
55. Genereux P, Webb JG, Svensson LG, Kodali SK, Satler LF, Fearon preprocedural assessment with multidetector computed tomography.
WF, et al. Vascular complications after transcatheter aortic valve J Thorac Cardiovasc Surg. 2009;137(5):1258–64. Epub 2009/04/22.
replacement: insights from the PARTNER (Placement of AoRTic 63. Krishnaswamy A, Parashar A, Agarwal S, Modi DK, Poddar KL,
TraNscathetER Valve) trial. J Am Coll Cardiol. 2012;60(12):1043– Svensson LG, et al. Predicting vascular complications during
52. Epub 2012/08/14. transfemoral transcatheter aortic valve replacement using com-
56. Genereux P, Head SJ, Van Mieghem NM, Kodali S, Kirtane AJ, puted tomography: a novel area-based index. Catheter Cardiovasc
Xu K, et al. Clinical outcomes after transcatheter aortic valve Interv. 2014;84(5):844–51. Epub 2014/03/25.
replacement using valve academic research consortium definitions: 64. Eltchaninoff H, Kerkeni M, Zajarias A, Tron C, Godin M, Sanchez
a weighted meta-analysis of 3,519 patients from 16 studies. J Am Giron C, et al. Aorto-iliac angiography as a screening tool in select-
Coll Cardiol. 2012;59(25):2317–26. Epub 2012/04/17. ing patients for transfemoral aortic valve implantation with the
57. Mwipatayi BP, Picardo A, Masilonyane-Jones TV, Larbalestier R, Edwards SAPIEN bioprosthesis. EuroIntervention. 2009;5(4):438–
Thomas S, Turner J, et al. Incidence and prognosis of vascular com- 42. Epub 2009/09/17.
plications after transcatheter aortic valve implantation. J Vasc Surg. 65. Reinthaler M, Aggarwal SK, De Palma R, Landmesser U, Froehlich
2013;58(4):1028–36.e1. Epub 2013/09/03. G, Yap J, et al. Predictors of clinical outcome in transfemoral
58. Hayashida K, Lefevre T, Chevalier B, Hovasse T, Romano M, TAVI: Circumferential iliofemoral calcifications and manufacturer-
Garot P, et al. Transfemoral aortic valve implantation new criteria derived recommendations. Anadolu kardiyoloji dergisi: AKD
to predict vascular complications. JACC Cardiovasc Interv. 2011; Anatol J Cardiol. 2015;15:297–305. Epub 2014/11/22.
4(8):851–8. Epub 2011/08/20. 66. Vavuranakis M, Kariori M, Voudris V, Kalogeras K, Vrachatis D,
59. Lange R, Bleiziffer S, Piazza N, Mazzitelli D, Hutter A, Tassani- Aznaouridis C, et al. Predictive factors of vascular complications
Prell P, et al. Incidence and treatment of procedural cardiovascular after transcatheter aortic valve implantation in patients treated with
complications associated with trans-arterial and trans-apical inter- a default percutaneous strategy. Cardiovasc Ther. 2013;31(5):e46–
ventional aortic valve implantation in 412 consecutive patients. Eur 54. Epub 2013/06/15.
J Cardiothorac Surg. 2011;40(5):1105–13. Epub 2011/04/26. 67. Toggweiler S, Gurvitch R, Leipsic J, Wood DA, Willson AB,
60. Leon MB, Piazza N, Nikolsky E, Blackstone EH, Cutlip DE, Binder RK, et al. Percutaneous aortic valve replacement: vascular
Kappetein AP, et al. Standardized endpoint definitions for outcomes with a fully percutaneous procedure. J Am Coll Cardiol.
Transcatheter Aortic Valve Implantation clinical trials: a consensus 2012;59(2):113–8. Epub 2012/01/10.
report from the Valve Academic Research Consortium. J Am Coll 68. Chiam PT, Koh AS, Ewe SH, Sin YK, Chao VT, Ng CK, et al.
Cardiol. 2011;57(3):253–69. Epub 2011/01/11. Iliofemoral anatomy among Asians: implications for transcatheter
61. Kappetein AP, Head SJ, Genereux P, Piazza N, van Mieghem NM, aortic valve implantation. Int J Cardiol. 2013;167(4):1373–9. Epub
Blackstone EH, et al. Updated standardized endpoint definitions 2012/04/24.
 Assessment of Cardiac and Thoracic
Masses 16
Jabi E. Shriki, Patrick M. Colletti, and Suresh Maximin

Abstract
Cardiac masses are uncommonly encountered, but can pose a perplexing diagnostic
dilemma when present. Familiarity with cross-sectional imaging of the heart can provide a
number of tools to enable diagnosis. In this chapter, we discuss the varied appearances of
cardiac masses. Thrombi tend to occur in characteristic locations include the left atrial
appendage and left ventricular apex. Benign neoplastic masses, tend to be pedunculated and
have narrow attachments to the myocardial walls. For example, atrial myxomas tend to have
narrow attachments at the left atrial side of the interatrial septum. Malignant neoplastic
masses tend to grow in an infiltrative pattern with broad attachments to the myocardium.

Keywords
Myocardial masses • Cardiac mass • Thrombus • Myxoma • Angiosarcoma • Cardiac
metastases

Overview istics of normal myocardium and of masses. Two approaches

to cardiac gating may be applied: prospective ECG trigger-
Excellent spatial and contrast resolution make cardiovascu- ing and retrospective ECG gating [1].
lar computed tomographic angiography (CCTA) an ideal Pre-contrast CT imaging may help to identify some fea-
method for the detection and evaluation of cardiac masses tures, such as calcifications, which appear as foci of punctu-
and masses adjacent to the heart. Suspended respiration and ate or coarse hyperattenuation, typically in the range of 130
cardiac gating techniques employed with CCTA enhance Hounsfield units (HU), and hemorrhage, which may have a
delineation of planes between masses and normal structures. more modest and ill-defined hyperattenuation relative to
While many cardiac masses are well demonstrated with non- normal myocardium. CT without contrast is the imaging
gated CT, the ability to freeze cardiac motion enables clearer modality of choice for demonstrating calcification.
evaluation of tissue attenuation and enhancement character- Demonstration of low attenuation prior to contrast adminis-
tration may be helpful
The amount of iodinated contrast agent required for satis-
J.E. Shriki, MD (*) factory CT evaluation of cardiac masses depends on patient
Department of Radiology, Puget VA Health System, University mass, with 0.5–1.0 g of iodine per kilogram body mass as the
of Washington, 1660 S. Columbian Way, Seattle, WA 98101, USA
usual dose [2]. Most clinically used contrast agents have low
e-mail: [email protected]
osmolality, with concentrations of 300–400 mg iodine/ml.
P.M. Colletti, MD
Typically, 100 ml of contrast agent is administered at
Department of Radiology, University of Southern California,
Los Angeles, CA, USA 4–5 ml/s via a programmable injector system. This is fol-
lowed by a bolus flush of 50 ml of normal saline [3].
S. Maximin, MD
Department of Radiology, University of Washington, Timing CT image acquisition to the arrival of the con-
Seattle, WA, USA trast bolus in the left atrium or left ventricle is typically

© Springer International Publishing 2016 275

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_16
276 J.E. Shriki et al.

identical to the timing used for coronary artery CT exami- detection region of interest (ROI) within a chamber or a
nations [4]. Optimal left atrial appendage enhancement vessel which contains internal thrombus or tumor. Such an
may, however, be somewhat difficult, since the left atrial error may result in failure to detect the bolus as shown in
appendage may opacify somewhat more slowly or hetero- Fig. 16.1.
geneously. In addition, there may be considerable variabil- Opacification of the right heart with contrast may be
ity in circulation time from patient to patient, particularly more challenging. Without appropriate acquisition timing
in patients with cardiac tumors or thrombi. The time for right heart visualization, there may be insufficient con-
between intravenous contrast injection and appearance of trast for delineation of right atrial and right ventricular endo-
contrast in the aorta can be determined using a small vol- cardial borders. Excessive contrast within the right heart
ume test contrast agent bolus of 20 ml and rapid, repeated may result in streaking and obscuration of subtle masses.
imaging of a single trans-aortic plane [5]. Alternatively, Even when the right heart is well opacified, there is fre-
with bolus tracking, a Hounsfield unit (HU) threshold may quently swirling of contrast with non-opacified blood arriv-
be set such that the volume acquisition is triggered to ing from the inferior vena cava. The mixture of opacified
begin once a certain HU value is detected in the ascending and non-opacified blood can make delineation of masses in
aorta. A uniform, programmed injection requires 10–25 s the right heart difficult. Optimal timing and technique for
for delivery of intravenous contrast agent and up to 50 right heart examination usually differs from that used for
additional seconds for the saline flush. One potential pit- routine CCTA. In most patients, optimal right ventricular
fall in employing automatic bolus detection in cardiac opacification is achieved by placing the ROI for bolus track-
masses is that it is possible to inadvertently place the bolus ing in the main pulmonary artery.

a b

H 120
U
100
E
n 80
h
60
a
n 40
c
e 20
m
e 0 1 1
n 1 1 1
-20
t 1
0 5 10 15 20
c Elapsed Time (sec)

Fig. 16.1 (a, b) Pitfall of automated bolus detection. Automatic bolus detection fails due to tumor replacing the blood pool in the selected region-
of-interest in the main pulmonary artery
16 Assessment of Cardiac and Thoracic Masses 277

Right ventricular delineation in congenital heart disease Interpreting Cardiac Masses: Key Descriptors
with transposition or other abnormal great vessel relationships
requires some a priori knowledge of the anatomy and relevant Location
surgical history to select the correct region for timing prescrip-
tion. When opacification of multiple chambers is needed, Lesion location relative to the specific, involved chambers
more complex injection protocols can be utilized with multi- should be noted and may provide a hint as to the nature of a
phasic contrast administration, including injection of mixtures particular mass. Masses related to the heart itself which are
of saline and contrast [6]. cardiac in origin have a unique differential diagnosis. Masses
One advantage cardiac magnetic resonance imaging immediately adjacent to the heart and intimately involving
(CMR) holds over cardiac CT for cardiac masses is the abil- the pericardium should be described as pericardial (Fig. 16.2).
ity to obtain excellent contrast for both the right ventricle and Masses which are external to the heart should be described as
left ventricle in the same examination due to the ability to paracardial (within the mediastinum, adjacent to the heart).
image the heart in multiple phases of contrast administration, For lesions within the mediastinum, a separate set of diag-
with no radiation dose. Venous or equilibrium phase imaging nostic possibilities should be included in the differential.
on CMR can help to homogeneously opacify the right heart A full discussion of mediastinal masses, however, is beyond
chambers. the scope of this text. Although some tumors may violate
Clinical [7–19] and imaging [20–28] features of car- planes and make identification of the organ of origin diffi-
diac masses are summarized in Tables 16.1, 16.2, 16.3, cult, in most cases, cardiac masses, pericardial masses, and
and 16.4. mediastinal masses can be separated.

Table 16.1 Benign cardiac neoplasms

Location Features
Myxoma (40 % of all benign tumors) (Fig. 16.16) LA septum 75 %; RA 18 %; ventricles 10 % calcified; frequent systemic emboli;
7 %; multiple 5 % may protrude through mitral valve during
diastole
Fibroelastoma Lipoma Arise from valves; project into aorta or Derived from endocardium; may be multiple;
MPA Varies often an incidental finding at surgery
Encapsulated adipose tissue (fat attenuation);
asymptomatic; negative CT density; 25 %
are multiple; consider tuberous sclerosis;
should not be confused with fat in
paracardiac folds
Lipomatous hypertrophy Atrial septum; protrudes into RA Fat attenuation
Fibroma Myocardium Well delineated, calcified; enhance
minimally
Hemangioma Myocardium Calcifications; delayed enhancement
Lymphangioma Myocardium Diffuse proliferation; minimally enhancing
Paraganglioma, dysembryoma, pheochromocytoma Paracardiac; AV groove Sympathetic plexus; hyper-enhancing;
correlate with urinary catecholamines;
alpha-and beta-blockade for surgery
Teratoma Pericardial; attach to the aorta or PA Multi-cystic; frequently calcify; moderate
roots enhancement

Table 16.2 Cystic cardiac masses

Location Features
Pleuro-pericardial cyst 75 % in right paracardiac angle Asymptomatic (avascular/calcified); unilocular,
sharply marginated, 20–40 HU; may communicate
with pericardium; change shape with body position
Echinococcal cysts Myocardial or pericardial (Avascular/calcific rim); nearly always also in liver,
lung, eyes, brain
Tuberculoma Myocardial or pericardial Calcified; constrictive pericarditis
Hematoma Posterior recesses at the aortic root Acutely hyper-dense; may calcify; traumatic or
or left atrium post-surgical
Thrombosed coronary aneurysm Course of coronary arteries Calcified rim; thrombus
278 J.E. Shriki et al.

Table 16.3 Malignant cardiac tumors

Location Features
Metastasis (20 × as common as Pericardial; intravascular; Seen in 10 % of end-stage cancers; lung (36 %), breast
primary tumor) (Fig. 16.2) intra-myocardial (7 %), esophagus (6 %); lymphoma, melanoma, Kaposi’s
sarcoma, leukemia (20 %); modes of dissemination: direct
or lymphatic; hematogenous; direct venous extension
(pulmonary veins or inferior vena cava)
Lung, breast, melanoma, sarcoma, Pericardial; direct or lymphatic; Lung cancer may extend to the left atrium along the
leukemia, thyroid, kidney hematogenous; direct venous extension pulmonary veins
Renal, urothelial, hepatocellular, Extend up the inferior vena cava to the Enhancing intravascular mass; primary tumor identified
adrenal, retroperitoneal sarcoma right atrium
Lymphoma Pericardium; myocardium; commonly May infiltrate epicardial fat; 50 % associated with HIV
basal in location
Angiosarcoma (Fig. 16.1) Pericardium; RV, RA, myocardium Angiosarcoma of the pericardium or right ventricle is most
common; poor prognosis; distribution is similar to
lymphoma
Osteosarcoma RA, RV Ossification
Rhabdomyosarcoma, fibrosarcoma Myocardium Most common primary cardiac malignancy in infants and
children
Always involves the myocardium; pericardial involvement
is typically in the form of nodular masses rather than
sheet-like spread
Mesothelioma Pericardium Intra-pericardial mass; effusions; constrictive physiology

Table 16.4 Other cardiac masses

Location Features
Endo-myocardial fibrosis Pericardium; myocardium Thickened pericardium; thickened myocardium with
patchy enhancement restrictive and constrictive
physiology
Erdheim-Chester disease Pericardium; myocardium Thickened pericardium; thickened (non-langherans
fibrosis) myocardium with patchy enhancement
restrictive and constrictive physiology
RA thrombus (Fig. 16.12) Right atrium Associated with indwelling catheters and devices
RV thrombus Right ventricle Associated with severe coagulopathy; dilated
cardiomyopathy
LA thrombus (Fig. 16.11) Left atrium Seen in atrial fibrillation and mitral stenosis; attached
to posterior or superior atrial wall; may be calcified
LV thrombus (Fig. 16.8) Left ventricle Common complication of myocardial infarction
(20–40 % of anterior MIs); contiguous to akinetic
myocardium; most common at the apex
Vegetations Valves; catheters EKG-triggered cine views of valves helpful

Chamber Involvement wall. A mass at the apex of the left ventricle, which appears
separate from the wall, has a higher probability of being a
The chamber of origin and location within the chamber thrombus. Attention should be given to associated wall
should be noted. For example, a mass in the left atrium motion abnormalities or aneurysms. Severe metastatic
attached along the interatrial septum has a higher chance of involvement of the myocardial wall may result in a wall
being an atrial myxoma. A mass in the left atrial appendage motion abnormality. However, a thrombus may present as a
has a higher probability of being a thrombus. Some authors mass closely associated with a wall motion abnormality
have suggested that, on imaging, metastases are more com- such as dyskinetic aneurysmal segment. Transiently, throm-
mon in the right heart. boemboli with a peripheral origin, such as deep vein
However, this could be due to the earlier detection of thrombi, may be seen in the right atrium and right ventricle
right heart masses, since the wall of the right ventricle is (Fig. 16.3), and are called “in transit thrombi”. A mass
thinner than the wall of the left ventricle. A mass in the left which arises from the crista terminalis of the right atrium
ventricle may be neoplastic, if it is felt to be arising from the may be a prominent network of Chiari. Elastofibromas are
16 Assessment of Cardiac and Thoracic Masses 279

a b

c d

Fig. 16.2 A 22-year-old female with a primary pericardial primitive restriction of cardiac motion, and as a result artifacts due to cardiac
neuroectodermal tumor. Images obtained are obtained as part of a post- motion are mild. There is heavy neoplastic infiltration of the atrioven-
contrast non-gated CT scan of the chest. Transverse and oblique tricular groove with invasion of the right atrium and ventricle (black
4-chamber views are shown (a–d). In this case, the tumor was causing arrowheads)

common lesions which occur along the valve surfaces, but example of valvular pathology mimicking a cardiac mass is
are usually small and not well-seen on CCTA. Valvular veg- caseous mitral annular calcification, where an ovoid mass of
etations may rarely grow to a size where they may mimic a caseous calcifications develops in close proximity to the
cardiac mass, although this diagnosis should be considered mitral annulus as a result of liquefactive necrosis of mitral
in some cases where a mass is closely related to a valve. An valvular calcifications (Fig. 16.4).
280 J.E. Shriki et al.

a b

Fig. 16.3 A 44 year-old female with shortness of breath. The sagittal, or from the pelvic venous system. MinIP views are useful in
minimum intensity projection (MinIP) view shows a vermiform, low- demonstrating low attenuation structures, when surrounded by rela-
attenuation filling defect (black arrow, a), representing a thrombus in tively high attenuation. A transverse view on the same study shows
the right ventricle, which had likely migrated from the lower extremities multiple, separate pulmonary emboli (white arrows, b)

Lesion Morphology

Masses should also be described as intramural (within the

myocardial wall) or intracameral (within the cardiac cham-
ber). Metastatic and malignant primary tumors usually have
a significant intramural component or a very broad-based
attachment to the wall of the myocardium, whereas benign
masses are more commonly pedunculated and intracameral,
often having a narrow attachment. Masses arising from the
myocardium tend to have more obtuse angles with the endo-
cardial surface, whereas masses within chambers or with
pedunculated attachments tend to have more acute angles
with the endocardium. This rubric is commonly helpful in
identifying pedunculated masses as benign. Thrombi which
are adherent to the internal wall of the ventricle are, however,
an important exception to this rule. Lesion shape is less help-
ful as both benign and malignant masses may be lobulated or
appear round.

Fig. 16.4 An 81 year-old male with caseous mitral annular calcifica- Attenuation
tions. A mass was seen near the region of the mitral annulus on echo-
cardiography. CT was performed for further evaluation. A non-contrast, Attenuation can be characterized by Hounsfield unit (HU)
transverse image shows the classic morphology of caseous mitral measurement. Care should be taken to ensure that cardiac
annular calcifications, with central homogeneous hyperattenuation
representing liquified calcifications and denser, peripheral shell-like gating is adequate, as the presence of motion may alter or
calcifications (white arrow) artifactually elevate measured attenuation. Attenuation
16 Assessment of Cardiac and Thoracic Masses 281

values from −100 to −10 HU are generally associated with Lesion Number
fatty masses such as intracardiac lipomas or lipomatous
hyperplasia of the interatrial septum. Frequently, mea- Multiple lesions are more likely to be due to metastatic dis-
surement of attenuation is not needed. For example, fatty ease or to multiple thrombi. Metastatic disease typically
intracardiac masses can be compared to the attenuation of appears as multiple lesions in the myocardial wall in differ-
subcutaneous or mediastinal fat. Cystic masses will ent locations. Multiple thrombi may be encountered as
tend to have attenuation values between −10 and well, especially when masses are located in characteristic
10 HU. Calcifications have an attenuation value of 130 HU locations, such as the left atrial appendage or the left ven-
or greater. Coarse calcifications may be seen in myxomas, tricular apex.
although many other lesions may calcify, including some
thrombi and many treated metastases. Attenuation relative
to muscle or specifically myocardium is frequently used Commonly Encountered Masses
to describe lesions as hypoattenuating or hyperattenuat-
ing. Frequently, attenuation relative to the blood pool is Although a complete discussion of all cardiac masses is
also described, although it should be noted that patients beyond the scope of this chapter, familiarity with the most
with anemia may have depressed pre-contrast attenuation common causes of cardiac masses assists in arriving at the
values within vascular structures. correct diagnosis.

Enhancement Thrombi

Enhancement should be reported with respect to the degree Thrombi are the most common cause of intracardiac masses.
of enhancement and to the phase at which enhancement is On pre-contrast CT, thrombi may either present as hypoat-
seen. Lesions which show no or minimal enhancement are tenuating or hyperattenuating masses relative to blood pool
more likely to be benign. This is true of thrombi, which usu- (Figs. 16.6 and 16.7). Attenuation relative to blood pool is
ally show no enhancement. Myxomas usually show minimal influenced by the patient’s hematocrit, since more anemic
or mild post-contrast enhancement, particularly in the arte- patients will have relatively lower attenuation of blood pool.
rial phase of contrast administration, when CCTA imaging is The degree of attenuation within a thrombus may also be
performed. Angiosarcomas, the most common malignant dependent on thrombus age. Most thrombi will show no
primary neoplasm of the heart, may have very avid enhance- enhancement after administration of contrast. However,
ment, to the extent that the borders of these masses may be some chronic thrombi, described as being more organized,
indistinguishable from contrast within the chamber of the have been reported to have some peripheral enhancement
heart. Other neoplastic lesions, including metastases, may after contrast administration [29]. This is most commonly
show more modest enhancement. seen in the setting of chronic thrombi adherent to the wall,
and has been reported mostly on MRI. On CCTA, essentially
no contrast enhancement will be shown within thrombi. In
Involvement of Other Vascular Structures the case of small thrombi, Hounsfield units may be elevated
after administration of contrast when comparison between
Numerous masses may invade the heart from the great ves- pre- and post-contrast CCTA is made, although this is more
sels. Tumors of the upper abdomen may grow into the right likely related to pseudoenhancement, whereupon beam hard-
atrium via the inferior vena cava (Fig. 16.5). Hepatocellular ening effects cause false elevation of attenuation values due
carcinoma, adrenocortical carcinoma, and renal cell carci- to adjacent hyperattenuating structures or contrast.
noma are among the most common tumors of the upper Pseudoenhancement tends to occur in lesions less than 1 cm
abdomen to invade into the right atrium. Bronchogenic car- in size. On MRI, thrombi are most commonly dark on all
cinomas may invade into the heart through the pulmonary sequences. Thrombi can also be recognized by the character-
veins and present as a left atrial mass. Mediastinal tumors istic locations in which they occur, including at the left ven-
and bronchogenic carcinomas that involve the mediastinum tricular apex and in the left atrial appendage.
may extend into the heart via the superior vena cava. Tumors Ventricular thrombi can be recognized by their charac-
of the mediastinum may grow directly into the heart with teristic location, most commonly at the apex of the left ven-
external myocardial invasion. Thrombi along catheters may tricle (Fig. 16.8). Morphologically, they may either present
track along venous structures, most commonly the superior as one or many ovoid structures within the chamber or may
vena cava. appear pedunculated (Fig. 16.9). Many thrombi may also
282 J.E. Shriki et al.

a b

Fig. 16.5 A 24 year-old male with retroperitoneal malignant germ cell into the inferior vena cava and right atrium (black arrows on b and c,
tumor. Post-contrast CT images are obtained of the abdomen in the por- respectively). Note other sites of metastatic disease including a right
tal venous phase and are shown from caudal (a) to cranial (c). There is lower lobe metastasis (white arrow, c) and a left retrocrural lymph node
extensive left periaortic lymphadenopathy, with invasion of tumor into (white arrowhead, b). This tumor exhibits a common appearance of
the left renal vein (black arrow on a). There is also extension of tumor metastatic disease from germ cell tumor with low internal attenuation

be flat and layered against the endocardial surface of the infarctions, in comparison to inferior infarctions [30, 31].
left ventricular wall. Association with an underlying wall Visualization of multiple thrombi is not uncommon in the
motion abnormality, such as an area of aneurysm formation post-infarction setting.
or an area of infarction, is also an important hint to the cor- Atrial thrombi can be very problematic to confidently
rect diagnosis. Ventricular thrombi have been reported in diagnose, particularly when present in the left atrial
up to one third of transmural infarctions [30], and are asso- appendage, where contrast opacification is often nonuni-
ciated much more commonly with apical and anterior form. Patients at risk for atrial thrombi commonly have
16 Assessment of Cardiac and Thoracic Masses 283

a b

Fig. 16.6 A 56 year-old male with rheumatic heart disease and a echocardiogram (not shown) and was consistent with an atrial thrombus
hyperattenuating left atrial appendage thrombus. Oblique MPR views (white arrows). Note the presence of atrial wall calcifications, which are
are shown from a non-contrast scan (a, b). A focal mass with hyperat- encountered commonly in the setting of rheumatic heart disease. The
tenuation is present in the left atrial appendage, which was also seen on left atrium is massively enlarged and forms the right heart border (a)

a b

Fig. 16.7 A 62 year-old male admitted with a recent myocardial infarc- (white arrow). A thrombus was suspected. A repeat scan 1 week later
tion with a hypoattenuating left ventricular thrombus. A transverse, obtained with a small amount of intravenous contrast (b) demonstrates
non-contrast view (a) obtained to evaluate the extent of pleural effusion clear delineation of the large thrombus at the left ventricular apex
demonstrates an area of low attenuation at the left ventricular apex (white arrow)
284 J.E. Shriki et al.

a b

Fig. 16.8 A 45-year-old woman with a recent myocardial infarction. Four-chamber (a) and two-chamber (b) views from a cardiac CT show a left
ventricular apical aneurysm with thrombus

a b

Fig. 16.9 A 55 year-old male with a mass at the ventricular apex on intracameral, low attenuating, non-enhancing, apical mass is seen, con-
transthoracic echocardiogram. Images from a cardiac CT scan obtained sistent with a thrombus. A small area of apical septal late gadolinium
in the two-chamber (a) and short axis (b) planes are shown. A mobile, enhancement was demonstrated on the patient’s CMR (not shown)

enlarged atria with heterogeneous enhancement as a result appendage may make exclusion of thrombus very difficult
of circulatory stasis within the left atrium. This smoke- (Fig. 16.10). As a result, transesophageal echocardiogra-
like enhancement can be especially prominent in the left phy is still considered the gold standard for the evaluation
atrial appendage, and, in patients with severe atrial of a thrombus in the left atrium or left atrial appendage.
enlargement, this poor opacification of the chamber and Imaging protocols with a delayed phase or with the patient
16 Assessment of Cardiac and Thoracic Masses 285

a b

Fig. 16.10 A 47 year-old female with atypical chest pain. Orthogonal appendage. No thrombus was identified on echocardiography.
MPR views of the left atrium from a CCTA (a, b) demonstrate left atrial Heterogeneous opacification of the left atrial appendage is a significant
enlargement with heterogeneous enhancement of the left atrial pitfall in the identification or exclusion of atrial thrombi on CCTA

ment and dysfunction. Right atrial thrombi may form in

the atrial appendage, and can be difficult to delineate due
to the inherently heterogeneous opacification of the nor-
mal right heart (Fig. 16.12). There are however lower
risks of thrombus development in the right atrial append-
age, since this structure tends to be flatter and more broad-
based, compared to the left atrial appendage, which is a
more lobulated or tubular structure and has a neck. These
morphologic differences make the left atrial appendage
more prone to the development of thrombi compared to
the right atrial appendage.

Metastatic Disease

Metastatic disease is the most common cause of a malignant

Fig. 16.11 A 48 year-old female with left atrial enlargement and atrial neoplastic mass in the heart. Metastatic disease has been
fibrillation. On a contrast-enhanced CT scan, a filling defect is clearly reported as more common in the right heart, but, as previ-
identified in the left atrial appendage (white arrowhead). When such a ously mentioned, this may be due to the earlier recognition
defect is clearly delineated by contrast as in this case, thrombus can be of metastatic lesions in the right ventricle, since the wall is
more definitively identified
thinner than that of the left ventricular wall. Most metastatic
lesions are isoattenuating to the myocardium on pre-con-
in the prone position have been reported as techniques for trast CT imaging. Contrast enhancement of metastatic
improved opacification of the atrial appendage, although lesions is somewhat variable depending on the degree of
these techniques are not yet widely employed [32, 33]. vascularity of the neoplasm. Most metastases enhance less
When a non-enhancing filling defect is clearly delineated than the myocardium initially after administration of con-
by contrast, however, a left atrial appendage thrombus can trast, but will slowly accumulate and retain contrast.
be more easily diagnosed (Fig. 16.11). Differentiation of Metastases may also show retention of contrast on late-
atrial thrombus from other cardiac masses is usually made phase imaging. This pattern of enhancement may be less
on the clinical basis in patients with known atrial enlarge- well-characterized on CT, since multiphasic imaging with
286 J.E. Shriki et al.

a b

Fig. 16.12 A 38 year-old female with recent resection of gastric carci- large parenchymal hepatic hematoma, related to her recent surgery,
noma. Transverse (a) and four-chamber (b) views are shown from a CT which may have contributed to the development of a right atrial throm-
scan of the chest. There is some heterogeneous opacification of the right bus. CMR (not shown) demonstrated features consistent with a throm-
atrium with some streaking, although the thrombus can be seen through bus, and this structure resolved on subsequent studies
these artifacts (black arrowheads, (a) and (b)). The patient also had a

CT is uncommonly performed (Fig. 16.13). It should also be Myxomas characteristically occur in the atria, and are more
noted that the optimal phase for CCTA during coronary commonly left atrial rather than right atrial, with a reported
arterial enhancement is earlier than the optimal phase for predominance of 80 % in the left atrium compared to 20 % in
demonstrating myocardial wall enhancement. As a result, the right atrium. Masses which arise in the atria may also
the differential enhancement between a metastatic lesion prolapse into the ventricular chambers [14]. Myxomas have
and normal myocardium may not be as clearly seen on also, however, been reported to occur in both ventricles. The
CCTA (Fig. 16.14). most common imaging appearance is that of a lobulated
The most common morphology of cardiac metastatic dis- mass with pre-contrast hypoattenuation relative to blood
ease is an intramural mass or a mass with a broad-based pool and relative to myocardium. Masses are commonly lob-
attachment, in contradistinction to benign masses, which ulated in appearance and predominantly intracameral. The
tend to be intracameral and have a narrow attachment. Many most common site of attachment for either right or left atrial
metastases which invade the heart from the adjacent medias- myxomas is at the fossa ovalis, a feature which can be help-
tinal or pericardial spaces may, however, involve the epicar- ful in arriving at the correct diagnosis [9]. Correct identifica-
dium first, and subsequently invade into the myocardium. tion of the site of attachment is also helpful in presurgical
Metastatic disease to the heart is found in up to 10 % of planning. Atrial myxomas commonly demonstrate punctate
patients with a primary malignancy at the time of autopsy or coarse calcifications, which is also useful in establishing
[34]. Although numerous neoplasms have been reported to the diagnosis. Pre-contrast hypoattenuation is commonly
be metastatic to the heart, the lung is the most common site seen relative to blood pool and normal myocardium
of a primary tumor, occurring in up to 36.7 % of patients (Fig. 16.16). Rarely, atrial myxomas may be diffusely and
[35]. Melanoma is however, an important source of hema- densely calcified [17].
togenous spread of disease to the heart from a distant pri- The classic triad of clinical symptoms reported with myx-
mary site [36]. An example of metastases involving the right omas includes constitutional symptoms, manifestations of
ventricle is shown in Fig. 16.15. obstructive valvular disease, and embolic phenomenon.
Constitutional symptoms include fever, malaise, weight loss,
and anemia, among others. These symptoms are likely
Myxomas related to an autoimmune response initiated by the tumor
[37]. Cardiac-related symptoms of atrial myxomas vary
Myxomas are the most common benign neoplasm of the depending on the chamber of involvement. Atrial myxomas
heart and comprise 50 % of all primary cardiac masses. have been commonly reported to mimic mitral valve disease
16 Assessment of Cardiac and Thoracic Masses 287

a b

Fig. 16.13 A 45 year-old female with metastatic melanoma. A trans- after intravenous injection of gadolinium (b) demonstrates areas of
verse view from a contrast-enhanced CT scan (a) shows irregular thick- relatively decreased enhancement related to the perfused myocardium
ening of the ventricular walls and a moderate-sized pericardial effusion. (white arrows). A delayed, 4-chamber view obtained 10 min after con-
The ventricular metastases are not well-delineated due to the early trast administration (c) demonstrates late enhancement within the car-
phase of contrast administration, which was in part, due to the patient’s diac metastases (white arrows)
poor cardiac function. A post-contrast CMR sequence obtained at 70 s

and rheumatic heart disease by clinical presentation [38]. embolize, although this difference in embolization rate could
Involvement of other valves may, however, produce manifes- be related to the more apparent manifestations of systemic
tations of aortic, pulmonic, or tricuspid valvular disease. emboli [39].
Embolization is another common feature of myxomas, and A genetic predisposition to myxomas has been postulated
may occur to either the pulmonic or systemic circulation, and suggested by case reports of families with multiple
depending on the chamber of involvement. Up to 35 % of left members with myxomas and in patients with several myxo-
atrial myxomas and up to 10 % of right atrial myxomas may mas [40]. Notably, Carney’s Syndrome may be associated
288 J.E. Shriki et al.

Fig. 16.14 A 56 year-old male with high-grade urothelial malignancy are better seen in the portal venous phase images (bottom row), where
and cardiac metastases. Transverse views from an arterial phase of a the myocardium is more well-enhanced. Note that other metastases are
post-contrast CT scan (top row) faintly show metastases to the left ven- also better seen on the later phase study, including pleural metastases
tricular myocardium (white arrows). These areas of hypoenhancement (black arrows)

a b

Fig. 16.15 A 48 year-old female with right ventricular metastases due ventricle, with broad-based attachments to the ventricular wall, consis-
to thymic carcinoma. Transverse (a) and coronal (b) views from a post- tent with metastatic disease
contrast CT scan show large masses arising from the wall of the right
16 Assessment of Cardiac and Thoracic Masses 289

a b

Fig. 16.16 A 52 year-old male with treated colorectal carcinoma and enhancement, and delineates the pedunculated nature of the mass,
a left atrial mass. A pre-contrast CT scan (a) demonstrates the low which arises from the region of the fossa ovalis
attenuation left atrial mass. The post-contrast study (b) shows no

with atrial myxomas, occurring in two thirds of patients, in tumors may be difficult to delineate from the ventricular
addition to other manifestations including mammary myxoid chamber on later phases due to bright enhancement. Venous
fibroadenomas, pigmented cutaneous lesions, endocrine dis- lakes and linear vascular structures within masses may be
orders, testicular tumors, and schwannomas [41]. seen, resulting in what has been likened to a “sunray pattern”
[43]. Two morphological appearances of angiosarcomas
have been reported, including a focal mass arising from the
Cardiac Sarcomas myocardium itself or a diffuse infiltrating process involving
the myocardium and pericardium [44, 45]. Undifferentiated
Cardiac sarcomas comprise the most common primary sarcomas are tumors with no specific histological staining
malignant tumors of the heart, but are a rare entity overall, patterns. The nature and definition of tumors in this category
with a prevalence at autopsy as low as 0.0001 % [42]. has changed over time as histological techniques have
Metastases to the heart outnumber malignant primary lesions improved. Similar to angiosarcomas, these tumors may
by a ratio of 20–40 to 1. Among subtypes of sarcoma, angio- either present as a focal mass or as a diffusely infiltrative
sarcomas are most common, comprising approximately myocardial and pericardial process. The common site of ori-
37 %. This tumor subtype in particular tends to occur com- gin is the left atrium, with a predisposition reported at 80 %
monly in the right atrium. Other subtypes tend to arise most [13]. A propensity for valvular involvement has also been
commonly from the left atrium, although all types of sarco- reported [46–48]. Rhabdomyosarcomas are very uncommon
mas may occur in any chamber [13]. For most cardiac sarco- in adults, but are the most common form of cardiac sarcomas
mas, survival is reported as very poor, with metastases and the most common primary cardiac malignancy in pediat-
commonly detected shortly after clinical presentation [10]. ric populations [13]. Embryonal rhabdomyosarcomas occur
On CCTA and CMR, angiosarcomas may show areas of in pediatric patients, whereas tumors in adults tend to be
hemorrhage and necrosis and may appear heterogeneous. more pleomorphic [49]. Osteosarcomas of the heart are rare
Avid enhancement is commonly seen (Fig. 16.17), and neoplasms, and are distinguished by their propensity to form
290 J.E. Shriki et al.

Fig. 16.17 (a, b) A 33 year-old female with angiosarcoma. Sequential pre-contrast, early, and late contrasted images demonstrate vascular
enhancement within the angiosarcoma. Note the enhancing right lower lobe pulmonary nodule (arrowhead), consistent with a metastasis

dense calcifications [50], although some tumors of this type intracardiac lymph nodes. Tumors likely arise from primi-
may demonstrate only minimal calcification [13]. Other tive, totipotential mesenchymal cells, and usually consist of
tumor subtypes include leiomyosarcoma, fibrosarcoma, and high grade B-cell lymphomas. Strictly defined, cardiac lym-
liposarcoma, although these are even rarer than the afore- phoma includes lymphoma involving the heart and pericar-
mentioned neoplasms. dium without other areas of lymphomatous involvement.
Anecdotal reports suggest that there is increased risk for car-
diac lymphoma in AIDS and in other immune deficiency
Cardiac Lymphoma states [51]. Given the rarity of this entity, the radiologic
findings are not well-established, although reports indicate
Cardiac lymphoma is a very rare entity, and in a series of 533 that tumors are usually relatively isoattenuating on CT and
cardiac tumors and cysts, it accounted for only 1.3 % of isointense on CMR, with heterogeneous enhancement after
tumors [11]. These tumors are rare since there are no true contrast administration [52].
16 Assessment of Cardiac and Thoracic Masses 291

Lipoma the third most common benign neoplasms behind myxomas

and lipomas. Ninety percent of papillary fibroelastomas
Cardiac lipomas are the second most common cause of a occur on valves, with the aortic valve being the most com-
benign cardiac neoplasm, after myxomas. Lipomas are eas- mon location. When associated with the atrioventricular
ily recognized as benign by the homogeneously low, pre- valves, these tumors tend to occur along the atrial side, which
contrast attenuation consistent with fat, which demonstrate may help to differentiate these lesions from thrombi [56].
essentially no enhancement after contrast administration. Associated valvular dysfunction is common, although many
Tumors are soft and may be large at the time of initial diag- of these lesions are detected incidentally [57]. An additional,
nosis. Symptoms are usually due to mass effect, although common presentation is the occurrence of embolic phenom-
commonly cardiac lipomas are detected incidentally and enon to the systemic or pulmonary circulation [58]. These
prior to onset of clinical manifestations. Some tumors may tumors are, however, uncommonly reported on CCTA, and
encase coronary arteries, resulting in mass effect and dis- as a result no characteristic CCTA features of this entity have
placement, making resection difficult [53]. Although there is emerged.
seldomly diagnostic uncertainty, some entities may mimic
lipomas, including lipomatous hypertrophy of the interatrial
septum (Fig. 16.18). Rarely, lipomatous metaplasia within Pediatric Cardiac Masses
chronic myocardial infarctions may be misdiagnosed as a
lipoma [54]. In pediatric patients who present with cardiac masses, a sep-
arate set of diagnostic possibilities should be considered.
Pediatric patients will less commonly present for CCTA
Papillary Fibroelastoma evaluation, due to radiation concerns. Additionally, since
there is sparse literature on CCTA in pediatric patients, the
Papillary fibroelastomas, also known as Lambl’s excres- typical appearances of many masses are difficult to delin-
cences, are avascular masses comprised of fronds of dense eate. However, some familiarity with masses which may
connective tissue. These masses may be either reactive in present in pediatric patients is useful to physicians involved
nature or may be related to a hamartoma [55]. The true prev- in cardiac imaging.
alence of this entity is not known, and these tumors have In infants and children, the most common masses encoun-
been postulated to be under-recognized and under-diagnosed tered are rhabdomyomas. These masses tend to occur in the
due to their small size. Most sources refer to these lesions as walls of the ventricles, and the vast majority of these masses

a b

Fig. 16.18 A 78 year-old male with lipomatous hypertrophy of the lipomatous hypertrophy in the wall of the interatrial septum (white
interatrial septum. Images from a CT scan of the chest obtained in the arrows). Note the characteristic sparing of the region of the fossa ovalis
transverse plane (a) and in the short axis plane of the heart (b) show (black arrow)
292 J.E. Shriki et al.

are multiple. A strong association with tuberous sclerosis is at dynamic CT involving injection protocol with dose tailored to
present, although many patients do not manifest other signs patient weight. Radiology. 2004;230(1):142–50.
5. Cademartiri F, Nieman K, van der Lugt A, et al. Intravenous con-
of tuberous sclerosis until many years later. Spontaneous trast material administration at 16-detector row helical CT coronary
regression of tumors is common, although the initial clinical angiography: test bolus versus bolus-tracking technique. Radiology.
presentation may be severe. When these lesions regress, they 2004;233:817–23.
may leave behind foci of myocardial fat attenuation [59]. 6. Bae KT, Tran HQ, Heiken JP. Uniform vascular contrast enhance-
ment and reduced contrast medium volume achieved by using
Cardiac fibromas constitutes the second most common cause exponentially decelerated contrast material injection method.
of pediatric cardiac masses, and usually are seen as large, Radiology. 2004;231:732–6.
solitary lesions. Some of these may grow to an enormous 7. Boyd DB. Computerized transmission tomography of the heart
size. Symptoms may include heart failure, chest pain, using scanning electron beams. In: Higgins CH, editor. Computed
tomography of the heart and great vessels. Mount Kisco/New York:
arrhythmias, and sudden cardiac death [60]. Myxomas are Futura Publishing Company; 1983. p. 45–55.
very rare in the pediatric population, but have been reported 8. Newhouse JH. Fluid compartment distribution of intravenous
in large series in older pediatric patients and adolescents iothalamate in the dog. Invest Radiol. 1977;12:364–7.
[17]. As described earlier, the most common malignant neo- 9. Prichard RW. Tumors of the heart. Arch Pathol. 1951;51:98–128.
10. Glancy DL, Morales JB, Roberts WC. Angiosarcoma of the heart.
plasm in pediatric patients is a cardiac rhabdomyosarcoma, Am J Cardiol. 1968;21:413–9.
which often has embryonal features at histology. Additional 11. McAllister HA, Fenoglio Jr JJ. Tumors of the cardiovascular sys-
rare tumors are encountered in pediatric populations includ- tem: atlas of tumor pathology, vol. 2. Washington, DC: Armed
ing cardiac angiomas, cardiac teratomas, and Purkinje cell Forces Institute of Pathology; 1978.
12. Lund JT, Ehman RL, Julsrud PR, et al. Cardiac masses: assessment
tumors. by MR imaging. AJR Am J Roentgenol. 1989;152(3):469–73.
13. Burke AP, Cowan D, Virmani R. Primary sarcomas of the heart.
Cancer. 1992;69:387–95.
Mimics of Cardiac Masses 14. Tazelaar HD, Locke TJ, McGregor CG. Pathology of sur-
gically excised primary cardiac tumors. Mayo Clin Proc.
1992;67(10):957–65.
Several normal structures in the heart may mimic a mass 15. Lam KY, Dickens P, Chan AC. Tumors of the heart. A 20-year
even to an experienced reader. Misidentification of normal experience with a review of 12,485 consecutive autopsies. Arch
structures as masses can lead to unnecessary biopsies, sur- Pathol Lab Med. 1993;117(10):1027–31.
16. Marx GR. Cardiac tumors. In: Emmanouilides GC, Gutgesell HP,
geries, and subsequent morbidity. Notably, in the right Riemenschneider TA, Allen HD, editors. Moss and Adams heart
atrium, a prominent crista terminalis may mimic a cardiac disease in infants, children, and adolescents: including the fetus and
mass. When a small and reticulated mass is present along young adult, vol. 2. 5th ed. Baltimore: Williams & Wilkins; 1995.
this structure in the right atrium, a network of Chiari may be p. 1773–86.
17. Burke A, Virmani R. Tumors of the heart and great vessels: atlas of
present. Uncommonly, prominence of the Eustachian valve tumor pathology. Fasc 16, ser 3. Washington, DC: Armed Forces
or juxtacaval lipomatous tissue may mimic a lower right Institute of Pathology; 1996.
atrial mass. Usually, the contrast timing for the right ventri- 18. Takach TJ, Reul GJ, Ott DA, Cooley DA. Primary cardiac tumors
cle is such that some saline is being injected at the time of in infants and children: immediate and long-term operative results.
Ann Thorac Surg. 1996;62(2):559–64.
scanning of the heart. However, in some cases, unopacified 19. Ludomirsky A. Cardiac tumors. In: Bricker JT, Fisher DJ, editors.
blood flow entering the right atrium from the inferior vena The science and practice of pediatric cardiology, vol. 2. 9th ed.
cava may simulate a mass when the right atrium is otherwise Baltimore: Williams & Wilkins; 1998. p. 1885–93.
filled with contrast. In the left atrium, the “coumadin ridge,” 20. Araoz PA, Eklund HE, Welch TJ, Breen JF. CT and MR imaging of
primary cardiac malignancies. Radiographics. 1999;19(6):1421–34.
located between the atrial appendage ostium and the superior 21. Chiles C, Woodard PK, Gutierrez FR, Link KM. Metastatic
pulmonary vein, may appear mass-like. involvement of the heart and pericardium: CT and MR imaging.
Radiographics. 2000;20:1073–103.
22. Grebenc ML, Rosado de Christenson ML, Burke AP, Green CE,
Galvin JR. Primary cardiac and pericardial neoplasms: radiologic–
References pathologic correlation. Radiographics. 2000;20:1073–103; quiz
1110–1071, 1112.
1. Desjardins B, Kazerooni EA. ECG-gated cardiac CT. Am 23. Grebenc ML, Rosado-de-Christenson ML, Green CE, Burke AP,
J Roentgenol. 2004;182:993–1010. Galvin JR. Cardiac myxoma: imaging features in 83 patients.
2. Newhouse JH, Murphy RX. Tissue distribution of soluble contrast: Radiographics. 2002;2(3):673–89.
effect of dose variation and changes with time. Am J Roentgenol. 24. Piazza N, Chughtai T, Toledano K, et al. Primary cardiac tumours:
1981;136:463–7. eighteen years of surgical experience on 21 patients. Can J Cardiol.
3. Cademartiri F, Mollet N, van der Lugt A, et al. Non-invasive 16-row 2004;20(14):1443–8.
multislice CT coronary angiography: usefulness of saline chaser. 25. Tatli S, Lipton MJ. CT for intracardiac thrombi and tumors. Int
Eur Radiol. 2004;14:178–83. J Cardiovasc Imaging. 2005;21(1):115–31.
4. Awai K, Hiraishi K, Hori S. Effect of contrast material injec- 26. Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: diagnosis
tion duration and rate on aortic peak time and peak enhancement and management. Lancet Oncol. 2005;6(4):219–28.
16 Assessment of Cardiac and Thoracic Masses 293

27. Leipsic JA, Heyneman LE, Kim RJ. Cardiac masses and myocardial 44. Bruna J, Lockwood M. Primary heart angiosarcoma detected by
diseases. In: McAdams HP, Reddy GP, editors. Cardiopulmonary computed tomography and magnetic resonance imaging. Eur
imaging syllabus—2005. Leesburg: American Roentgen Ray Radiol. 1998;8:66–8.
Society; 2005. p. 1–13. 45. Jannigan DT, Husain A, Robinson NA. Cardiac angiosarcomas: a
28. Sparrow PJ, Kurian JB, Jones TR, Sivananthan MU. MR imaging review and a case report. Cancer. 1986;57:852–9.
of cardiac tumors. Radiographics. 2005;25:1255–76. 46. Herhusky MJ, Gregg SB, Virmani R, Chun PKC, Bender H, Gray Jr
29. Barkhausen J, Hunold P, Eggebrecht HH, et al. Detection and GF. Cardiac sarcoma presenting as metastatic disease. Arch Pathol
characterization of intracardiac thrombi on MR imaging. AJR Am Lab Med. 1985;109:943–5.
J Roentgenol. 2002;179:1539–42. 47. Ludomirsky A, Vargo TA, Murphy DJ, Gresik MV, Ott DA, Mullins
30. Weinreich DJ, Burke JF, Ferrel JP. Left ventricular mural thrombi CE. Intracardiac undifferentiated sarcoma in infancy. J Am Coll
complicating acute myocardial infarction long-term follow-up with Cardiol. 1985;6:1362–4. Abstract 37.
serial echocardiography. Ann Intern Med. 1984;100(6):789–94. 48. Itoh K, Matsumura T, Egawa Y, et al. Primary mitral valve sarcoma
31. Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left in infancy. Pediatr Cardiol. 1998;19:174–7.
ventricular thrombosis after acute transmural myocardial infarc- 49. Hwa J, Ward C, Nunn G, et al. Primary interventricular cardiac
tion: serial evaluation by two-dimensional echocardiography. tumors in children: contemporary diagnostic and management
N Engl J Med. 1981;305(6):297–302. options. Pediatr Cardiol. 1994;15:233–7.
32. Hur J, Kim YJ, Nam JE, Choi EY, Shim CY, Choi BW, et al. 50. Chaloupka JC, Fishman EK, Siegelman SS. Use of CT in the
Thrombus in the left atrial appendage in stroke patients: detection evaluation of primary cardiac tumors. Cardiovasc Intervent Radiol.
with cardiac CT angiography--a preliminary report. Radiology. 1986;9:132–5.
2008;249(1):81–7. 51. Holladay AO, Siegel RJ, Schwartz DA. Cardiac malignant
33. Hur J, Kim YJ, Lee HJ, et al. Left atrial appendage thrombi in stroke lymphoma in acquired immune deficiency syndrome. Cancer.
patients: detection with two-phase cardiac CT angiography versus 1997;70(8):2203–7.
transesophageal echocardiography. Radiology. 2009;251(3):683–90. 52. Dorsay TA, Ho VB, Roviera MJ, Armstrong MA, Brissette
34. Abraham KP, Reddy V, Gattuso P. Neoplasms metastatic to the MD. Primary cardiac lymphoma: CT and MR findings. J Comput
heart: review of 3314 consecutive autopsies. Am J Cardiovasc Assist Tomogr. 1993;17:978–81.
Pathol. 1990;3:195–8. 53. Hananouchi GI, Goff WB. Cardiac lipoma: six-year follow-up with
35. Klatt EC, Heitz DR. Cardiac metastases. Cancer. 1990;65:1456–9. MRI characteristics, and a review of the literature. Magn Reson
36. MacGee W. Metastatic and invasive tumours involving the heart in Imaging. 1990;8(6):825–8.
a geriatric population: a necropsy study. Virchows Arch A Pathol 54. Banks KP, Lisanti CJ. Incidental finding of a lipomatous lesion
Anat Histopathol. 1991;419:183–9. involving the myocardium of the left ventricular wall. AJR Am
37. Bjessmo S, Ivert T. Cardiac myxoma: 40 years’ experience in 63 J Roentgenol. 2004;182:261–2.
patients. Ann Thorac Surg. 1997;63:697–700. 55. Rubin MA, Snell JA, Tazelaar HD, Lack EE, et al. Cardiac pap-
38. Markel ML, Waller BF, Armstrong WF. Cardiac myxoma: a review. illary fibroelastoma: an immunohistochemical investigation and
Medicine. 1987;66:114–25. unusual clinical manifestations. Mod Pathol. 1995;8:402–7.
39. Castells E, Ferran V, Octavio-de-Toledo MC. Cardiac myxomas: 56. Klarich KW, Enriquez-Sarano M, Gura GM, et al. Papillary fibro-
surgical treatment, long-term results and recurrence. J Cardiovasc elastoma: echocardiographic characteristics for diagnosis and
Surg. 1993;34:49–53. pathologic correction. J Am Coll Cardiol. 1997;30:784–90.
40. Carney JA. Differences between nonfamilial and familial cardiac 57. Edward FH, Hale D, Cohen A, et al. Primary cardiac valve tumors.
myxoma. Am J Surg Pathol. 1985;9:53–5. Ann Thorac Surg. 1991;52:1127–31.
41. Carney JA, Gordon H, Carpenter PC, Shenoy BV, Go VW. The 58. McFadden PM, Lacy JR. Intracardiac papillary fibroelastoma:
complex of myxomas, spotty pigmentation and endocrine overac- an occult cause of embolic neurologic deficit. Ann Thorac Surg.
tivity. Medicine. 1985;64:270–83. 1987;43:667–9.
42. McCallister Jr HA. Primary tumors of the heart and pericardium. 59. Bosi G, Lintermans JP, Pellegrino PA, et al. The natura history of
Curr Probl Cardiol. 1979;4:1–51. cardiac rhabdomyoma with and without tuberous sclerosis. Acta
43. Yahata S, Endo T, Honma H, et al. Sunray appearance on enhanced Paediatr. 1996;85:928–31.
magnetic resonance image of cardiac angiosarcoma with pericar- 60. Turi GK, Albala A, Fenoglio Jr JJ. Cardiac fibromatosis: an ultra-
dial obliteration. Am Heart J. 1994;127:468–71. structural study. Hum Pathol. 1980;11:577–9.
 Part IV
CT Vascular Angiography
 CT Angiography of the
Peripheral Arteries 17
Jabi E. Shriki, Leonardo C. Clavijo, and Gale L. Tang

Abstract
The application of CT angiography to the systemic vascular tree poses a number of unique
challenges, but offers the ability to noninvasively depict a wide array of arterial pathology.
CT of the peripheral arterial tree also has a number of specific advantages relative to other
modalities, including conventional angiography, MRI, and ultrasound. Peripheral CT angi-
ography has particularly important applications in imaging extremities in the setting of
acute ischemia or trauma. While some of the skills in performing CT angiography in other
body parts are applicable to peripheral CT angiography, several technical considerations
should be recognized in incorporating peripheral imaging into a CT angiography practice.

Keywords
Peripheral computed tomography • Peripheral vascular ct angiography • Peripheral angio-
gram • Peripheral vascular disease • Systemic arterial disease • Vascular cta • Peripheral
ct angiogram

Introduction disease entities. Additionally, the skills of 3-D data manip-

ulation useful in evaluation of coronary arteries and vascu-
CT angiography is a useful modality in imaging the periph- lar structures elsewhere in the body can be translated into
eral arterial tree and has become an integral component in skills in interpreting peripheral CT angiographic studies.
many cardiovascular imaging practices. Large portions of Advancements in CT angiography, including the dissemi-
the arterial system can be easily imaged with excellent nation of multislice, dual source, and dual energy scan-
spatial resolution, low radiation dose, and minimal risk to ners, have made submillimeter isotropic voxel resolution
the patient. Peripheral CT angiography has particular possible, and have enabled more detailed visualization of
advantages as a non-invasive means of depicting the sys- arterial structures. Simultaneous increases in computa-
temic arterial tree and is able to demonstrate a number of tional speed and widespread availability of dedicated 3-D
software make visualization and evaluation of peripheral
arterial anatomy much more facile.
J.E. Shriki, MD (*)
Department of Radiology, Puget VA Health System, University of
Washington, 1660 S. Columbian Way, Seattle, WA 98101, USA
e-mail: [email protected] Acquisition and Scanning Techniques
L.C. Clavijo, MD, PhD, FACC, FSCAI, FSVM
Department of Medicine, Division of Cardiovascular Medicine, Special Considerations Regarding Peripheral
Department of Clinical Medicine, University of Southern CT Angiography
California, Los Angeles, CA, USA
G.L. Tang, MD Several technical considerations should be recognized in
Department of Surgery, University of Washington, making the transition from cardiac to peripheral vascular CT
Seattle, WA, USA

© Springer International Publishing 2016 297

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_17
298 J.E. Shriki et al.

angiography. First, while the coronary arteries are usually

opacified along with the aorta even in the presence of steno-
ses, the peripheral vasculature may have a variable relation-
ship with aortic opacification. In patients with severe
atherosclerotic disease, the presence of stenoses, occlusions,
and aneurysms may delay optimal opacification of the
peripheral arteries. In thoracic, abdominal, and neuroimag-
ing applications, higher detector row CT scanners provide a
number of advantages. However, for peripheral CT angiog-
raphy, the high speed of scanning with multi-detector row
CT scanners may result in outpacing of the bolus of contrast,
with images obtained prior to arrival of the contrast bolus
into the area of interest. As a result, the timing of peripheral
CT angiography has separate considerations that differ from
scanning other, more proximal, body parts (Fig. 17.1).
Also, the reconstructed field of view for peripheral appli-
cations is frequently larger in transverse axial dimension
than that employed for cardiac CT. This is because of the
wider distribution of peripheral arterial structures in the
transverse plane. As a result, images may have lower in-
plane spatial resolution. This loss of in-plane resolution may
be offset by the use of separate, reconstructed fields of view
for each lower extremity or for different parts of the anatomy
scanned. When imaging the lower extremities, the feet
should be kept straight and positioned as closely together as
possible, so that the reconstructed field of view closely
matches the anatomy being imaged. This can be achieved by
securing the feet into a table extension or harness, which is
usually attachable or built into the table (Fig. 17.2).
In comparison to cardiac CT, there is a longer craniocaudal
extent of anatomy imaged with peripheral CT angiography.
As a result, data sets may be much larger for comparable
slice thickness. For example, whereas a single phase of a
cardiac CT reconstruction at 0.5 mm may comprise 1–200 or
more images, a data set from a peripheral CT angiogram of
the lower extremities might include several thousand images,
due to the craniocaudal extent of imaging from the diaphragm
to the toes. As a result, some readers prefer thicker slices or
coronal plane images for initial evaluation, and reserve the
use of thin slices for a more limited, adjunctive role in
problem solving. Alternatively, most 3-D workstations have
options for subvolume selection, which enables evaluation of
the arterial tree in an incremental fashion, allowing larger Fig. 17.1 A 3-D reconstruction demonstrating that the run-off vessels
data sets to be evaluated, with enhanced multiplanar are less well opacified than the popliteal arteries, likely related to slight
outpacing of the contrast bolus by the speed of the scanner
reformatting capabilities.

interchangeably, although there are differences between the

Dual Energy and Dual Source CT terms. Dual source CT is a technique of scanning with
orthogonally positioned CT acquisition systems (including
The advent of dual source and dual energy scanning has x-ray source and x-ray detector) mounted to the same gantry.
enabled a new set of advantages of CT imaging for the This enables fast and essentially simultaneous acquisition of
peripheral vascular tree. It should be noted that the descriptors scan data with two separate energies. The main advantage of
of “dual energy” and “dual source” CT are sometimes used dual source CT is that scanning at two different energies can
17 CT Angiography of the Peripheral Arteries 299

smaller or more peripheral venous access site. Most studies

for peripheral CT angiography report contrast rates of 3.5–
4.0 ccs per second as optimal [4–6]. Since the area scanned
in imaging the peripheral arterial tree is significantly larger
in craniocaudal extent compared to the coronary tree, a more
prolonged bolus of contrast, with a slightly slower rate of
delivery is preferable to ensure homogeneous, persistent,
bright opacification of the peripheral arteries. This injection
rate is slightly slower than the rate employed for imaging the
heart, which may be as high as 5–6 ccs per second [7], since
Fig. 17.2 Reconstructed volume projections can demonstrate the soft the aim of peripheral CT angiography is a sustained peak of
tissue anatomy. The lower extremities should be closely apposed to one bright opacification, whereas in coronary CT, prolongation
another in order to minimize the dimensions of the reconstructed field of peak contrast opacification is a less important factor.
of view. In this case, this is achieved by use of a table extension (white
arrow)
Patients are usually given a formulation of intravenous con-
trast with 300–400 mg of iodine per mL, with 120–180 ccs
of contrast given depending on each patient’s body surface
be obtained rapidly, resulting in excellent temporal resolu- area [8]. The total amount of contrast, however, may be
tion with minimal mismatch between acquisitions. However, reduced when scanners with higher numbers of detectors are
dual source CT scanning is one means of obtaining scan data used [9, 10]. Higher iodine concentrations have been demon-
at two different energies, and is therefore, best considered a strated to have higher attenuation levels when the aortic
subtype of dual energy CT. Other means of scanning at two enhancement is compared [11]. Larger amounts of contrast
energies are available, including rapid switching of kilovolt are needed in patients who are taller or are more obese [8].
potentials (kVp) of the x-ray generating tube, or selective Administration of a saline chaser is useful in ensuring a
detector arrays which are sensitive to different types of higher degree of opacification, and also in prolonging the
radiation. plateau of attenuation once the peak is reached. A saline
Dual energy scanning using sequential scanning with two chaser is also useful in diminishing the total amount of con-
different energies has been a research tool since soon after the trast needed for optimal opacification [12, 13]. Saline injec-
advent of CT [1]. The development of more advanced CT tion can also clear residual contrast from the central venous
acquisition techniques has enabled dual energy CT using dual system. Central venous? stasis of contrast can impede imag-
source CT scanners and other techniques to be commercially ing of the central upper extremity arteries due to streaking as
available since 2006 [2]. A further, more extensive discussion a result of dense contrast in the superior vena cava, brachio-
of the physics of dual energy and dual source CT is beyond cephalic veins, or other venous structures. When imaging the
the scope of this chapter, but typically, the two energies dur- upper extremities, contrast injection should be made via the
ing which scanning is performed are 80 and 140 kV. extremity contralateral to the area of interest to avoid this
There are several potential advantages of dual energy CT, pitfall. Optimal timing for acquisition varies significantly in
including plaque characterization and improvement of con- each patient. In patients with normal cardiac function, a
trast visualization. In peripheral CT angiography, the main rapid acquisition of images may outpace the bolus of con-
advantage of scanning at two energies is that higher energy trast. In patients with depressed cardiac function or arterial
scan data can be obtained, resulting in selective subtraction pathology, the scanning time should be prolonged to ensure
of higher attenuation materials, such as calcium or stent scanning is not performed before arrival of the contrast bolus
material [3]. As a result, the contrast column within the ves- [14]. At our institution, in patients with suspected athero-
sel can be depicted more easily, without obscuration or sclerotic disease, the lower extremities are scanned twice,
blooming from high attenuation calcium or stent wall with a second acquisition beginning just above the knees and
(Fig. 17.3). timed immediately after the first acquisition. This second
acquisition enhances visualization of arterial structures,
although there may be significant venous contamination at
Contrast Administration the time of a second scan, which may make 3-D reconstruc-
tions somewhat difficult to evaluate.
As with imaging other vasculature, rapid rates of contrast Several techniques for ensuring optimal arterial timing
administration are critical in obtaining optimal peripheral may be employed. A timing bolus utilizes injection of a
vascular opacification. Consequently, a more central, large small amount of contrast with serial images through a region
bore, venous access line (usually consisting of an 18-gauge of interest (ROI) in order to predict the timing of bolus
catheter in the antecubital fossa) is highly preferable to a arrival. This is somewhat problematic in evaluating the
300 J.E. Shriki et al.

a b

Fig. 17.3 Frontal, thick volume, maximum intensity projection CT bilateral common iliac artery stents (white arrows) and calcified plaque
images are shown with bone removal. The scan is obtained with dual in the aorta (white arrowheads). Subtraction of high attenuation struc-
energy CT, enabling subtraction imaging. Images are shown before (a) tures, including stents and vascular calcifications is one of the advan-
and after (b) subtraction of high attenuation materials, including the tages of dual energy, dual source CT

peripheral arterial tree, since different portions may be opaci- the attenuation value reaches a particular, preset threshold,
fied at different times, depending on the degree of upstream scanning of the remainder of the field of view is initiated. At
disease. This technique also necessitates two separate injec- our institution, for peripheral CT angiography of the lower
tions with an initial, small bolus. Because only a small, initial extremities, an attenuation value of 180 Hounsfield units (HU)
dose of contrast is used though, the total amount of contrast is employed, and the ROI is placed in the infrarenal aorta.
is generally not significantly impacted. This technique may Alternatively, the ROI can also be placed in the lower extremity
also help in preparing the patient for the clinical, physiologic arteries, such as the femoral arteries. This technique has the
manifestations such as sensory warmth and a metallic taste pitfall of being affected by patient motion, and may require
which commonly ensue after contrast administration. some technologist expertise in identifying the vessel. When
Alternatively, bolus tracking can be performed with the bolus triggering is used, the ROI is generally positioned to
main contrast injection. With this technique, an ROI within the include approximately half of the diameter of the vessel.
aorta is serially scanned during the injection of contrast. When Different vendor-specific protocols are available for automated
17 CT Angiography of the Peripheral Arteries 301

contrast monitoring. For slower scanners, a lower threshold images [17, 18]. In many early studies, only the transverse
(100 HU) may be used to ensure that the speed of scanning axial data set was evaluated. The transverse plane of the
matches arrival of the contrast bolus [15]. A significant limita- body is in a relatively perpendicular axis to the long arteries
tion of the bolus tracking technique is that the ROI may be of the extremities, resulting in views which approximate the
placed within an area of thrombus or in the false lumen of a short axis plane of much of the vascular tree with minimal
dissection. If this occurs, opacification within the ROI may not technical manipulation of data sets. For a more accurate
be achieved, and scanning might be incorrectly delayed. interpretation, final review of studies at a dedicated 3-D
Preset timing of scanning uses a fixed time interval workstation is commonly employed. Key images for demon-
between initiation of contrast administration and scanning. strating stenoses or other vascular pathology are subse-
This is less commonly employed at most institutions, espe- quently also sent to archiving and communication systems
cially for imaging peripheral arteries. This technique may be (PACS) to illustrate important findings.
especially problematic in patients with atherosclerotic dis- In addition to the evaluation of transverse axial data sets,
ease and in patients with low cardiac output, where the bolus review of long and short axis planes utilizing multiplanar
will be circulated through the arteries more slowly. For the reformatted views (MPR), thick maximum intensity projec-
upper extremities, scanning may be initiated 20 s after the tion views (MIP) (Fig. 17.4), and curvilinear plane refor-
start of contrast injection. For the lower extremities, scanning matted views (CPR) (Fig. 17.5) result in a more thorough
may be initiated 50 s after the beginning of injection [16]. assessment of the peripheral vascular tree and in improved
sensitivity and specificity for depicting disease [19]. Review
of the transverse axial views is the usual starting point for
Techniques for Interpreting Studies most readers. Reformatting data along the plane of the ves-
sel utilizing MPR views introduces few artifacts, as long as
Several studies have demonstrated an excellent accuracy of scans are obtained using isotropic voxels. MIP views gener-
CT in comparison to conventional digital subtraction angiog- ally demonstrate the higher attenuation values within a thick
raphy (DSA), based solely on evaluation of transverse slab of the data set, and are useful for demonstrating the

Fig. 17.4 A reformatted view through the radial artery is shown (a). length of the arterial anatomy is demonstrated. MIP views are also
On the progressively thicker maximum intensity projection (MIP) useful for demonstrating high attenuation structures such as bones and
views obtained with a thickness of 2 cm (b) and 4 cm (c), a greater stents
302 J.E. Shriki et al.

Fig. 17.5 Curved planar reformatted views show the long axis, orthogonal (white arrows) and short axis (closed arrowhead) of arterial structures.
This is contrasted with the MIP MPR view (open arrowhead)

course of a tortuous vessel. MIP views are also useful for Newer tools enable color-coding of vessels to bring atten-
demonstrating other high attenuation structures such as tion to areas of plaque. Techniques are also available for
stents (Fig. 17.6a), surgical clips, calcifications, and osse- characterization of atherosclerotic lesions with respect to
ous structures. CPR images introduce some potential arti- attenuation values in order to classify lesions as fatty, fibrous,
facts, as computer algorithms select the center line to be or calcified. These tools may be used adjunctively to the
followed. Frequently, computer-generated center lines may techniques described earlier, but have yet to be rigorously
drift into an area of calcification in the wall, and may make evaluated or validated.
a stenosis appear more severe. User-directed CPR images
may be created, but are commonly time consuming and
require some expertise to generate. Unlike evaluation of the Validation of Peripheral CT Angiography
coronary arteries, CPR images are less susceptible to arti-
facts in the large vessels of the extremities, where arteries Advancement in CT technology has been rapid, with the
course in relatively straight planes. Three-dimensional recent advent of isotropic voxel imaging and multi-detector
views are usually demonstrated with a lit projection and are CT. The pace of technological advancement has surpassed
helpful in demonstrating anatomic relationships, though the rate at which newer technologies are validated. For this
they are problematic for demonstrating or grading stenoses reason, large multicenter studies and meta-analyses likely
(Fig. 17.6b). underestimate the accuracy of CT angiography as a tool.
17 CT Angiography of the Peripheral Arteries 303

Fig. 17.6 The thick MIP view (a) demonstrates the aortic stents. They are also well-seen on the volume rendered view (b) in this patient who is
status post aortic stenting after repair for aortic coarctation and a bicuspid aortic valve

Large studies have, however, demonstrated several sig- detecting stenoses by CT angiography were 99 % and 98 %,
nificant advantages of CT angiography in comparison to respectively [21]. Moreover, the use of advanced imaging tools,
DSA, including a fourfold lower radiation dose and a much including 3-D reconstructions and multiplanar reformatted
lower risk of complications. Moreover, studies have shown views, provide detailed visualization of stenotic lesions, normal
an excellent accuracy for the diagnosis of atherosclerotic dis- vasculature, or previously revascularized lower extremity arter-
ease as well as excellent correlation with DSA [20]. ies along with nearby extravascular structures. Augmenting
Diagnostic CT angiography performs comparably to DSA axial images with reformatted views has been shown to improve
and favorably compares to duplex ultrasound and MR angi- accuracy of interpretation [22].
ography for the evaluation in patients with chronic periph- Due to the speed and accessibility of imaging, CTA is also
eral arterial disease or traumatic vascular injuries [21]. extremely useful in diagnosing acute limb ischemia and criti-
Compared to other non-invasive imaging modalities such cal limb ischemia, helping clinicians to promptly and effec-
as ultrasonography and MRA, CTA possesses several advan- tively formulate treatment plans. CTA also possesses
tages. CTA reproducibility does not significantly depend on advantages in depicting peripheral vascular aneurysms, pro-
variability of technical skills as is oftentimes the limitation viding clear, comprehensive images and precise dimensions
of ultrasonography. In patients with multilevel peripheral along with delineating involvement of adjacent vessels and
arterial disease, ultrasonography assessment has poor speci- structures. Thus, CTA is a useful diagnostic and surveillance
ficity to localize lesions, and is hindered by an impractical tool for aneurysm detection and follow-up.
amount of time consumed in such extensive clinical evalua-
tion. MRI angiography may have limitations in patients with
stents, surgical clips, or other devices, and is problematic in Role of Peripheral CT Angiography
patients with non-MR conditional cardiac devices. for the Vascular Physician
A study evaluating CT angiography with 64-row detector
scanners for the detection of peripheral vascular disease evalu- The most important application of CT angiography for the
ated 840 segments of the systemic arteries in 28 patients with vascular interventional specialist is pre-procedure planning,
lower extremity claudication. This study found an overall diag- including: selection of patients best treated with endovascu-
nostic accuracy of 98 % in the detection of lesions with a degree lar intervention versus open surgical procedures, identifica-
of stenosis of 50 % or higher. The sensitivity and specificity for tion of vascular access sites, pre-procedure selection of
304 J.E. Shriki et al.

Table 17.1 Advantages of CT angiography in patients with peripheral emia may arise from stenosis as far proximal as the aorta.
arterial disease prior to endovascular interventions Since disease anywhere in the arterial tree may produce
1. Selection of patients for endovascular versus open surgical symptoms, knowledge of normal anatomy of the entire arte-
revascularization. rial tree is necessary in order to accurately interpret periph-
2. Vascular access selection. eral CT angiography.
3. Lesion characterization (thrombus, degree of calcification, lesion
length, vessel size).
4. Arterial vascular inflow and outflow.
5. Selection of interventional angiographic views and angulations.
Upper Extremities
6. Equipment selection based on lesion characteristics and vessel
size (thrombolysis, sheaths, wires, balloons, stents, atherectomy, The normal upper extremity arterial supply begins with the
distal embolic protection). subclavian arteries. The left subclavian artery typically arises
7. Decreased contrast use. directly from the aortic arch. The right subclavian artery most
8. Decreased radiation exposure. commonly arises from the brachiocephalic (innominate)
9. Evaluation of extravascular arterial disease (popliteal entrapment, artery, which typically gives off a right common carotid artery
cystic adventitial disease, bony exostosis, thoracic outlet syndrome). as well a right subclavian artery. In 15 % of patients, the
innominate artery also gives off the left common carotid artery,
a variant described as a bovine arch. In these patients, the left
appropriate angiographic views, and pre-procedural lesion common carotid artery commonly arises as the first vessel off
characterization (thrombus burden, dissection, calcification, of the bovine innominate, although it may arise more cranially
tortuosity, etc.). CT angiography also provides valuable as a trifurcation vessel of the innominate artery [24].
information for tailoring the most appropriate endovascular Other commonly encountered variants of aberrant origina-
therapy, including: thrombolysis, laser, directional or orbital tion of the subclavian artery exist. An aberrant right subcla-
atherectomy, reentry device, distal embolic protection vian artery may either arise from a left sided aortic arch, as
device, balloon angioplasty, self-expanding or balloon the last major vessel from the arch (left arch with aberrant
expandable stents, and covered stents (Table 17.1). right subclavian artery) (Fig. 17.7). In the case of a right aor-
Patients who undergo intervention for peripheral arterial tic arch, the left subclavian artery may arise as the last major
disease have a higher incidence of vascular access site compli- vessel from the arch (right arch with aberrant left subclavian
cations compared to patients who undergo percutaneous coro- artery). In either case, the aberrant subclavian artery usually
nary intervention [23]. Patients with peripheral atherosclerotic takes a course posterior to the esophagus and may produce
disease commonly have a high burden of diffuse, often densely dysphagia, which is commonly referred to as dysphagia luso-
calcified, atherosclerotic plaques. As a result, vascular access ria. A double aortic arch may also cause dysphagia lusoria
selection is important to ensure safe and successful peripheral [25]. In addition, an aberrant subclavian artery may arise
interventions. The atherosclerotic burden in some patients from a dilated trunk, termed a diverticulum of Kommerel.
may prevent adequate hemostasis, which predisposes these This is a true aneurysm that likely results from an embryo-
patients to hemorrhagic complications at access sites. CT logical remnant of a separate, incompletely formed aortic
angiography offers an overall view of the arterial system and, arch. Both the double aortic arch and the right arch with an
therefore, may allow for identification of the most appropriate aberrant left subclavian artery represent vascular rings. In the
access site for peripheral interventions. In patients with severe, latter case, the ring is completed by the ligamentum arterio-
diffuse disease, alternative access sites or techniques (brachial, sum. Clinically significant atherosclerotic occlusive compli-
popliteal, antegrade, bypass grafts) may be utilized. cation rates resulting from aberrant subclavian arteries are
CT angiography also helps in the decision to use distal likely similar to rates of atherosclerotic complications
embolic protection devices, especially in cases where there observed in normal arteries, although aberrant subclavian
is heavy atherosclerotic burden, soft or unstable plaque, or arteries are more prone to aneurysmal degeneration.
thrombus. The choice of an appropriate device for the pro- Anatomically, the subclavian artery is divided into proxi-
tection against distal embolization may be guided by vessel mal, middle, and distal portions. The proximal portion of the
anatomy, tortuosity, and landing zone anatomy. subclavian artery is defined as the portion medial to the ante-
rior scalene muscle. The mid portion of the subclavian artery
is located posterior to the anterior scalene muscle and usu-
Normal Peripheral Arterial Anatomy ally contains the most cranial portion of the subclavian arch.
and Variants The distal portion of the subclavian artery lies lateral to the
lateral border of the anterior scalene muscle and ends at the
Symptomatic manifestations of arterial diseases may appear lateral border of the first rib. At this point the subclavian
in the distal extremities, but may also arise from disease artery changes name to become the axillary artery.
which is proximal and remote to the site of symptoms. For The vertebral artery is usually the first vessel that arises
example, non-healing ulcers in the toes as a result of isch- from the subclavian artery and most commonly arises from the
17 CT Angiography of the Peripheral Arteries 305

Fig. 17.7 On this CT scan of the chest performed to evaluate for an etiology of shortness of breath, a right-sided aortic arch with an aberrant left
subclavian artery (white arrow) is incidentally noted. This is shown on the transverse view (a) and volume rendered (b) view

first portion of the subclavian artery, usually within 1.2–2.5 cm Lower Extremity
of the vessel origin. The other vessels include the internal
mammary artery (Fig. 17.8), thyrocervical trunk, and costo- The aortic bifurcation most commonly occurs at the level of
cervical trunk. These vessels also most commonly arise from the L4 vertebral body, although some patients may have an
the first portion of the subclavian artery and are usually clus- unusually high aortic bifurcation as a normal variant. The
tered near the medial border of the anterior scalene muscle. common iliac arteries are usually 4–5 cm in length, although
At the lateral border of the first rib, the subclavian artery the right common iliac artery is usually slightly longer than
transitions to become the axillary artery, which proceeds to the left. The common iliac arteries course medial to the psoas
predominantly supply arterial blood flow to the upper chest muscles and beneath the ureters to the inferior pelvic brim
wall and the proximal portion of the upper extremity. In the before bifurcating into external and internal branches. The
case of axillary artery occlusion proximal to the origin of the common iliac artery may give rise to an iliolumbar trunk,
subscapular artery, collateral flow may be provided through which can be a source of endoleak in patients who have
chest wall and scapular collaterals. By definition, the axillary undergone aortic aneurysm repair. Accessory renal arteries
artery ends at the lateral border of the teres major, where it may rarely arise from the common iliac arteries, especially
changes name to become the brachial artery. The axillary when a pelvic or ptotic kidney is present.
artery is surrounded by the brachial plexus. The internal iliac artery runs posteriorly from the com-
The brachial artery is the main vessel to the upper extrem- mon iliac artery, and subsequently gives off anterior and pos-
ity. Most commonly, the brachial artery gives off a profunda terior divisions. The main branch of the posterior division is
branch in the upper portion of the upper extremity. Below the the superior gluteal artery, which exits the sciatic foramen.
elbow, the brachial artery usually trifurcates into a radial The posterior division may also give rise to an iliolumbar
artery laterally and a common trunk that gives off an interos- artery. The anterior division gives off several important
seous artery and an ulnar artery medially. In 15 % of patients, branches including the internal pudendal artery, and the uter-
the brachial artery gives off the radial artery proximal to the ine artery in women. The external iliac artery courses more
elbow as it courses in the upper arm. The radial or ulnar artery anteriorly in comparison to the internal iliac artery. Below
may rarely arise aberrantly from the axillary artery. There is a the inguinal ligament, it changes name to become the com-
close relationship with the median nerve which normally runs mon femoral artery. Vascular landmarks for the inguinal lig-
just medial to the brachial artery throughout the upper arm. ament are the origins of the deep circumflex iliac artery and
The median nerve may overlie the brachial artery rendering it the inferior extent of the inferior epigastric artery, which also
vulnerable to injury during brachial artery access. mark the delineation between external iliac artery and
306 J.E. Shriki et al.

a b

Fig. 17.8 CT angiography is useful in demonstrating the internal volume rendered view (b). In evaluating the subclavian artery and its
mammary arteries in patients in whom aortocoronary bypass is planned. branches, injection of contrast should be made via the contralateral
The course of the left internal mammary artery (white arrows) is extremity in order to ensure that streaking from dense venous contrast
demonstrated on the curved plane reformatted view (a) and also on the does not occur

common femoral artery. The external iliac artery gives off from the femoral vein can avoid confusion as the vein is part
other small branches, such as small muscular branches and of the deep venous system.
the cremasteric artery, which runs in the spermatic cord. The femoral artery courses anteromedially in the thigh. In
The common femoral artery, which begins below the the middle third of the thigh, the femoral artery enters the
inguinal ligament, is a short vessel which usually has a length adductor canal or eponymously, Hunter’s canal. This is a
of 4 cm and gives off the superficial femoral artery and deep frequent site of atherosclerotic disease. At the junction of the
femoral artery at approximately the level of the lesser tro- middle and lower third of the thigh, the femoral artery exits
chanter of the femur. Most commonly, there is also a slightly the adductor canal and changes name to the popliteal artery.
more lateral branch given off at the same level, which is the The popliteal artery is a common site of several unique
circumflex femoral artery. The term “superficial femoral diseases including cystic adventitial disease and popliteal
artery” is still used commonly by physicians, whereas anato- artery entrapment syndrome. Knee dislocation injuries may
mists favor the name “femoral artery”. In regard to femoral damage the popliteal artery. At approximately the level of
venous anatomy, there has been some shift in nomenclature the knee, the popliteal artery gives off medial and lateral
among physicians in order to avoid confusion when thrombi geniculate branches. These branches may serve as important
of the vein are reported. Drop of the descriptor “superficial” collaterals for reconstitution of the popliteal artery from the
17 CT Angiography of the Peripheral Arteries 307

profunda using geniculate collateral pathways in the setting CT has an advantage in comparison to conventional
of femoral artery occlusion. angiography in demonstrating 3-D vascular anatomy and
The popliteal artery continues behind the knee and gives variants in the context of muscular and osseous anatomy.
off the anterior tibial artery. In most patients, the anterior Variants which contribute to clinically significant arterial
tibial artery gives off the dorsalis pedis artery, which courses disease are rare and some variants may not cause significant
along the dorsal aspect of the foot. The other main branch of vascular pathology. Rarely, for example, the external iliac
the popliteal artery is the tibioperoneal trunk. This divides artery may be absent, and the common femoral artery arises
into the posterior tibial artery and peroneal artery. Variations from the internal iliac artery (Fig. 17.9). This common
in this conventional anatomy occur approximately 10 % of variant would not be expected to cause clinically significant
the time, with the most common variant being a high takeoff manifestations of arterial disease [26].
of the anterior tibial at or above the level of the knee joint. A Rarely, the main lower extremity artery may arise from
true trifurcation followed by a hypoplastic or absent posterior the internal iliac artery, and courses posteriorly to the ischial
tibial artery are the next most common variants, while high tuberosity. This variant is known as a persistent sciatic artery.
origin of the posterior tibial artery is rare. The peroneal The anomalous course of the artery along the ischial tuberos-
artery runs in the deep compartment of the lower portion of ity can result in premature atherosclerotic disease (Fig. 17.10)
the lower extremity and usually terminates above the ankle and also in formation of aneurysms (Fig. 17.11). Typically,
in collateral branches to the posterior tibial and dorsalis occlusion or aneurysm formation occurs where the artery
pedis arteries. The posterior tibial artery runs posterior to the courses behind the ischial tuberosity. Vascular pathology is
medial maleolus of the ankle and frequently can be palpated thought to occur due to repetitive underlying trauma due to
at this point. The plantar arch is an arcade of vessels which impact of the ischial tuberosity onto the artery [27].
may be primarily served by either the dorsalis pedis artery or For variants where abnormal muscular anatomy may con-
the posterior tibial artery. The main vessel supplying the tribute to pathology, the arterial tree may be better imaged
plantar arch should be noted and included in CT angiography with MRI. In general imaging of the muscular structures of the
reports. extremities, MRI has advantages relative to CT angiography,

a b

Fig. 17.9 (a, b) An unusual variant is shown in which there is anterior and posterior divisions, before continuing anteriorly to give off
congenital absence of the external iliac artery. The internal iliac artery the common femoral artery
(white arrow) in this case takes a course posteriorly to give off the
308 J.E. Shriki et al.

a b

Fig. 17.10 (a, b) Images of the right lower extremity are shown in a probable occlusion of the persistent sciatic artery in the thigh. There is,
patient with bilateral persistent sciatic arteries. Note that the persistent however, reconstitution of the vessel via large profunda collaterals after
sciatic artery (white arrows) is occluded at the level of the ischial both occlusions
tuberosity (white arrowhead). There is also a second long segment of

including better resolution of soft tissue structures such as as their initial manifestation. The presence of peripheral
musculature and joints. Non-contrast MR angiography tech- arterial disease significantly contributes to worsened
niques also permit imaging with the extremity in different morbidity and mortality, likely because it is a marker of
positions, without the use of ionizing radiation. systemic atherosclerotic disease burden. Patients with
peripheral arterial disease have a four to fivefold increase
in risk of myocardial infarction or stroke [29, 30].
Abnormalities and Diseases of the Peripheral Peripheral arterial disease is a common condition, occur-
Arteries ring in 10–25 % of patients over the age of 55. The incidence
increases with age at a rate of 0.3 % per year in men aged
Atherosclerotic Disease 40–55 and at a rate of 1 % per year in men over the age of 75.
Up to 70–80 % of affected individuals are symptomatic,
Atherosclerosis is by far the most common disease of the although only a minority of patients will eventually require
peripheral arterial tree [28]. At times, patients may present revascularization. Twenty five percent of patients with
with concomitant cerebrovascular disease and coronary peripheral arterial disease will require some medical or sur-
atherosclerotic disease, although some patients with ath- gical treatment. Because of their increased morbidity and
erosclerotic disease may present with peripheral ischemia mortality, all patients with peripheral arterial disease should
17 CT Angiography of the Peripheral Arteries 309

a b c

Fig. 17.11 (Same patient as in Fig. 16.9). (a–c) Images of the left just above the ischial tuberosity (white arrowhead). Note also that the
lower extremity are shown in a patient with bilateral persistent sciatic vessel is less well opacified distal to the aneurysm due to stagnant flow
arteries (white arrows). Note the presence of a large aneurysm extending

have aggressive control of their atherosclerotic risk factors; that patients with a ‘coral reef aorta’ should not undergo
however, only about 25 % of patients are actually treated endovascular interventions which necessitate crossing of the
[31, 32]. juxtamesenteric aorta should be avoided in patients with a
Peripheral CT angiography can demonstrate atherosclero- “coral reef aorta” [35, 36].
sis at a very early stage in the disease process. Low attenua- In the peripheral tree, atherosclerotic disease may be multi-
tion plaques, likely related to an early phase of plaque focal and usually consists of mixed attenuation plaques. CT
evolution, may be seen [33]. Plaques may be calcified or angiography is useful in demonstrating stenoses of 50 % or
non-calcified, and may not cause stenosis until very late in greater, which may contribute to patient symptoms. Specific
the disease course (Fig. 17.12). Densely calcified atheroscle- features of each plaque that should be described include the
rotic plaques in the peripheral arterial tree may somewhat location of the lesion, degree of stenosis, and length of the
degrade CT angiography image quality, although this is less plaque. When CT angiography is used for plaque characteriza-
of a concern when imaging the extremities compared to the tion, descriptors for plaque attenuation may be added, with
coronary arteries due to the larger caliber of vessels and the reporting of plaques as calcified, non-calcified, or mixed
lower potential for motion and other artifacts. plaque. Further evaluation of lesions with stenoses is com-
Atherosclerotic plaques may be present throughout the monly pursued with catheterization for measurement of pres-
vascular tree. Typically aortic atherosclerotic disease begins sure gradients. Specific criteria for intervention have also been
in the infrarenal aorta and becomes more severe closer to the delineated, based on the degree of patient symptoms [37].
aortic bifurcation. A rarer variant in some patients with ath- Atherosclerotic disease may cause a number of symptoms
erosclerotic disease is the development of arborified, endo- depending on the site of involvement. Several syndromes
aortic calcified plaques, which predominantly protrude into have been characterized based on the distribution of athero-
the lumen, and are usually most pronounced in the juxtames- sclerotic disease. For example, subclavian steal syndrome
enteric and juxtarenal aorta. This variant has been termed a results from proximal stenosis in the subclavian artery
“coral reef” aorta (Fig. 17.13) [34]. Recognition of this vari- (Fig. 17.14). As a result of stenosis, the distal subclavian
ant of atherosclerotic disease is important since patients with artery may receive collateral flow from the vertebral arteries.
endoaortic calcific proliferation are at higher risk for post- Reversal of flow through the ipsilateral vertebral artery com-
catheterization embolic phenomenon. It has been suggested monly ensues. Because of the relatively rich brain collateral
310 J.E. Shriki et al.

a b

Fig. 17.12 (a, b) Multifocal atherosclerosis is demonstrated on these volume rendered views of the lower extremities. The femur, tibia, and fibula
have been subtracted from the field of view in order to better demonstrate the arterial anatomy

system, only a small percentage of patients with this reversal Grafts and Stents in the Arterial Tree
of flow will present with symptoms related to vertebrobasilar
insufficiency. These symptoms are commonly worsened dur- In addition to being a non-invasive modality with excellent
ing exercise of the upper extremity, which results in increased spatial resolution, CT angiography has several other
flow to the extremity and worsened steal from the cerebro- advantages in the evaluation of the treated vascular sys-
vascular circulation. Leriche syndrome is a constellation of tem. In comparison to MRI and MR angiography, CT angi-
symptoms which results from aortic and bilateral iliac artery ography is advantageous for visualization of stents. On
disease, including gluteal and lower extremity claudication, MRI, stents may be visualized only as artifacts and the
penile impotence, and lower extremity atrophy. internal lumen may be non-visualized due to susceptibility
Similar to assessment of aortic aneurysms, duplex ultra- effects. Even when the internal lumen is visualized, the
sound is the most cost effective strategy for surveillance of stented segment generally is incompletely evaluated by
popliteal or femoral aneurysms. CT angiography, however, is MR angiography. Other metallic structures including sur-
also favored over other imaging modalities for accurate siz- gical clips may also induce artifacts on MRI, including
ing of the proximal and distal arterial landing zones prior to signal void and failure of fat saturation, whereas artifacts
endovascular peripheral aneurysm repair. Evaluation of from surgical devices are generally less significant on
thrombus and patency of runoff vessels is also easily accom- CT. Dual source or dual energy CT further potentiates
plished by preoperative CT angiography. visualization of high attenuation, metallic structures with
17 CT Angiography of the Peripheral Arteries 311

a b

Fig. 17.13 Views from a CT angiogram of the abdomen are shown calcified, endoluminal, arborified plaques are present (white arrows) in
with transverse (a, b) and sagittal (c) images shown. A “coral reef” the juxtamesenteric aorta
aorta is present with dense endoaortic calcific proliferation. Densely

less significant obscuration of adjacent anatomy due to high attenuation of metallic stents, and because of the
minimizing of streaking. phenomenon of “blooming” on CT, a very bright stent
Stents in peripheral arterial structures are typically may appear to be outside the confines of the wall of a ves-
well-seen using thick MIP images (Fig. 17.15). This sel. The limitations of stent depiction on coronary CT are
allows visualization of stent struts and exclusion of strut less significant in evaluation of the peripheral arterial tree
fractures. Stents are easily depicted as high attenuation due to the larger internal diameter of stents commonly
structures. Stents are frequently well-evaluated on post- employed in the peripheral vessels and also due to the
contrast and non-contrast images. In the short axis view, absence of motion and other artifacts that can limit the
stent struts are frequently seen as regularly spaced, hyper- evaluation of stented coronary arteries. In-stent restenosis
attenuating foci at the rim of the artery, commonly in a in the peripheral vasculature is usually easily evaluated
hexagonal array (Fig. 17.16). Because of the relatively using CT angiography.
312 J.E. Shriki et al.

Fig. 17.14 Images from a CT

angiogram are shown in a patient a b
with known coronary artery
disease and concomitant
symptoms of subclavian steal.
The oblique sagittal (a) and
volume rendered (b) views show
a focal, shelf-like area of
narrowing near the origin of the
left subclavian artery (arrow, (a)
and (b)). In this case,
identification of this stenosis was
useful as an explanation of the
patient’s symptoms. Preoperative
identification of subclavian
stenosis is also important in
patients in whom aortocoronary
bypass is planned, as this
condition may impede optimal
flow through the internal
mammary artery

a b

Fig. 17.15 Stents are well-depicted on CT angiography. In this case, the stent is seen on the volume rendered view (yellow arrow, a) and also on
the orthogonal, curved plane reformatted views (white arrows, b)
17 CT Angiography of the Peripheral Arteries 313

a b c

Fig. 17.16 A stent is the left common iliac artery is shown. The stent is present on the volume rendered view (a) and also on the curved plane
reformatted views (b). Note that, in the short axis of the vessel (c), the stent is seen as a hexagonal array of hyperattenuating struts

a b d

Fig. 17.17 Bilateral, aortofemoral bypass grafts are present (white not opacified. Enlargement and irregularity may be present at anasto-
arrows) and are seen as unusually smooth appearing structures connect- motic sites as shown in this transverse CT image taken at the level of the
ing portions of the vascular tree. The occluded, native vessels are visu- patient’s anastomoses (white, open arrowheads, c). Note that the patient
alized on the transverse view (b, white arrowheads), but are not also has aortic and celiac stents (black arrows, d)
visualized on the volume rendered view (a) since the native arteries are

Graft material is also well evaluated on CT. Bypass grafts enlarged and irregular, as a result of the patch angioplasty
are commonly recognized as long, smooth, branchless tubes frequently performed at anastomosis sites. Grafts commonly
connected to the native vasculature on 3-D colored, lit pro- are comprised of either interposed veins, Dacron, or
jections (Fig. 17.17). On axial views, the excluded, unopaci- expanded polytetrafluoroethylene (PTFE). In some cases,
fied, native vessels are frequently visible. The connections where increased torsional effects are anticipated and may
between graft material and native vessel lumen may be compromise grafts, reinforced graft material is commonly
314 J.E. Shriki et al.

a b

Fig. 17.18 A bifemoral bypass graft (white arrows) is evident with a typical, corrugated appearance, which is well seen on the volume rendered
view (a) and the curved planar reformatted view (b)

employed. The rings of such grafts are typically visible as involving the peripheral arteries, fibromuscular dysplasia
corrugated on CT angiography (Fig. 17.18). most commonly occurs in the external iliac artery, which is
the third most common site of fibromuscular dysplasia in the
body. As in other parts of the body, the classification system
Trauma for fibromuscular dysplasia is based on the layer of the artery
involved, with medial fibroplasia being the most common
CT angiography as a modality has multiple features that form. The most typical appearance of fibromuscular dyspla-
make it ideal for imaging of the arterial tree in the setting of sia is apparent beading of the vessel and is due to several,
trauma. First, intimal flaps and abnormalities of the wall of closely approximated weblike areas of narrowing with inter-
the artery are better depicted by CT angiography compared vening outpouchings of the vessel from post-stenotic dilata-
to MR angiography, and may be better seen on CT than on tion (Fig. 17.20) [38]. Other forms of fibromuscular dysplasia
ultrasound, especially within the bony pelvis where bowel may have a variety of appearances [39]. Conventional angi-
gas and patient body habitus may limit duplex evaluation. ography may have an advantage in demonstrating this entity
CT angiography is also useful in demonstrating the entire compared with CT, due to the inherently higher spatial reso-
arterial tree in a less time-intensive fashion than ultrasound lution of conventional angiographic images.
or MR angiography. Concomitant post-traumatic deformities
to the muscles and bones may also be simultaneously dem-
onstrated on CT (Fig. 17.19). Other Diseases of the Systemic Arteries
CT signs of arterial injury include contrast extravasation,
vessel non-opacification, abrupt vessel occlusion, focal ves- Cystic adventitial disease is a rare entity, which may affect
sel narrowing/spasm, pseudoaneurysm, intimal flap, or arte- any artery adjacent to a joint and presents as a smooth nar-
riovenous fistula. Traumatic injury to vessels may ensue rowing without atherosclerotic disease. The narrowing is
after blunt or penetrating trauma and may be seen in associa- accompanied by cystic structures along the course of the
tion with fractures which displace vessels [16]. artery. The most common artery affected is the popliteal.
MRI is the preferred modality for depicting the cysts which
occur along the vessel, although low attenuation cysts are
Fibromuscular Dysplasia commonly observed on CT [40, 41].
Popliteal artery entrapment syndrome can occur due to a
Although fibromuscular dysplasia is a common cause of ste- number of abnormalities in the relationship between the
nosis in the renal or carotid arteries, it is less commonly popliteal artery and the muscles of the popliteal space. The
encountered elsewhere in the peripheral arterial tree. When most common abnormal muscle in this case is the medial
17 CT Angiography of the Peripheral Arteries 315

Fig. 17.19 CT angiography is useful in the setting of trauma. A structures may be subtracted, however, in order to better demonstrate
surface-rendered view (a) shows the deformity in the outer contour of the underlying arterial anatomy (d). In this case, resultant occlusion of
the extremity. CT angiography simultaneously demonstrates osseous the popliteal artery is also present (white arrow, d)
structures, demonstrating a dislocation at the knee (b, c). The osseous

a b

Fig. 17.20 Fibromuscular dysplasia is shown in the external iliac external iliac artery (arrow) is demonstrated on a reformatted view from
artery, which is the third most common site for this entity, following the the patient’s abdominal CT (a), but is more clearly demonstrated on the
internal carotid and renal arteries. The classic, beaded appearance of the conventional angiography (b), due to the higher spatial resolution
316 J.E. Shriki et al.

head of the gastrocnemius, although a number of abnormal MRI and MR angiography have several advantages in
relationships have been described. This syndrome usually patients, including the ability to perform imaging without
causes some degree of fixed narrowing of the popliteal contrast. Non-contrast MR angiography techniques have
artery, although there is commonly a dynamic component of advanced dramatically, although there is still considerable
narrowing, usually during plantar flexion or dorsiflexion. variability between institutions and MR technology. Clinically
Repetitive trauma to the artery as a result of the abnormal useful imaging of tibial and pedal vessels using non-contrast
relationship to the muscle may cause aneurysmal dilatation, MR is generally not possible except in highly specialized
thrombosis, or thromboembolism. MRI is useful in demon- centers. Because calcium does not interfere with contrast-
strating popliteal artery entrapment syndrome, where an enhanced MR angiography, evaluation of tibial vessels with
abnormal muscular slip courses medial to the popliteal MRA, when a separate tibial imaging bolus is used instead of
artery. In this case, the lower extremity may need to be a bolus-chase technique, is frequently superior to CTA in
imaged in several positions including dorsiflexion and plan- patients with critical limb ischemia. In particular, the ade-
tarflexion [40]. This is also more easily performed with MR quacy of MR sequences for imaging the arterial tree are
angiography, since MR angiography is less sensitive to opti- dependent on the scanner, sequences, and vendor-specific
mal vascular opacification and images can be obtained at techniques used. MR angiography has significant limitations
different time-points. Also, as non-contrast means of per- in evaluating the post-surgical arterial tree, due to artifacts
forming MRA become more robust, some vascular pathol- such as failure of fat saturation and susceptibility artifacts due
ogy may be imaged without the administration of contrast. to surgical clips, stents, or other foreign material. MR angiog-
Since the common femoral artery is a common site of vas- raphy is also contra-indicated in patients with non-MR condi-
cular access, it is subject to iatrogenic complications includ- tional pacemakers or ICDs. Likewise, certain stents and
ing chiefly pseudoaneurysm and arteriovenous fistula stent-grafts are MR conditional, such that patients with these
formation. Because of the focal nature of these complica- implants cannot undergo MR in 3 T machines. Patients with
tions, and because the portion of the artery involved is fre- claustrophobia or significant back pain may not tolerate lying
quently very superficial, ultrasound with Doppler is usually still for the hour-long exam. Because of these limitations MR
an adequate modality for the diagnosis and follow-up of iat- is contraindicated in approximately 30 % of patients.
rogenic femoral artery complications. On the other hand, In the past, MR has been preferable in patients with renal
when a deep or retroperitoneal hematoma is suspected, CT disease due to relatively lower nephrotoxicity of gadolinium,
may be a more robust technique than ultrasound. compared to iodinated contrast media. However, the recent
recognition of nephrogenic systemic fibrosis as a complica-
tion of gadolinium administration has decreased the utility of
Other Modalities for Imaging the Peripheral MR angiography in patients with chronic, severe renal dis-
Arteries ease [42]. Gadolinium should generally not be given to
patients with a creatinine clearance of 30 ccs per minute or
Advancements in imaging of the peripheral arteries have less. In patients who are already dialysis-dependent, iodin-
occurred in virtually every modality. As a result, the decision ated contrast may be a better choice. CT has an advantage to
between modalities is more complex. Physical exam and MR angiography in superior spatial resolution and depiction
ankle-brachial index measurement is an adequate means of of smaller vessels. Evaluation of the patency of circumferen-
making an initial diagnosis of peripheral arterial disease [37]. tially calcified tibial vessels remains challenging for CTA,
Further evaluation with ultrasound is also useful in demon- however, and is one of the few circumstances where DSA
strating and localizing atherosclerotic disease. Complete eval- may be required.
uation of the entire extremity with ultrasound is, however, very
time-intensive and detection of disease is technologist depen-
dent. Detection and measurement of stenoses with ultrasound Radiation Dose in Peripheral CT
is also dependent on technical factors, such as the angle of Angiography
insonation employed. Evaluation of the pelvic vasculature by
ultrasound is much more difficult, and portions of the vascula- The radiation dose in CT angiography remains high and is
ture may not be easily demonstrated with ultrasound due to increasingly a consideration in most CT applications.
overlying bowel gas and osseous structures. In very obese Concerns of radiation are somewhat mitigated by the fact
patients, ultrasound may be significantly limited. Heavy or cir- that the extremities contain less radiosensitive tissues. When
cumferential calcification, such as that found within patients imaging the extremities, breast and abdominal shielding can
with diabetes or renal insufficiency also significantly limits easily be employed with no compromise to image quality.
ultrasound. Determination of severity of disease by ultrasound Shielding significantly decreases scatter and is under-utilized
also has difficulty in determining the severity of disease in in patients undergoing CT in general, including peripheral
arterial segments distal to a high-grade stenosis. CT angiography.
17 CT Angiography of the Peripheral Arteries 317

The radiation dose for conventional angiography is, how- 14. Becker CR, Wintersperger B, Jakobs TF. Multi-detector-row CT
ever, much higher than for CT angiography [43]. This is in angiography of peripheral arteries. Semin Ultrasound CT MR.
2003;24:268–79.
contradistinction to radiation doses in the heart, where cath- 15. Fleischmann D. Use of high concentration contrast media:
eterization results in lower radiation doses compared to principles and rationale—vascular district. Eur J Radiol.
CT. One study found that for a 16-slice CT scanner, the aver- 2003;45:S88–93.
age radiation dose for a peripheral CT angiogram was 16. Miller-Thomas MM, West OC, Cohen AM. Diagnosing traumatic
arterial injury in the extremities with CT angiography: pearls and
3.0 mSv in men, whereas the radiation dose for a conven- pitfalls. Radiographics. 2005;25:S133–42.
tional angiogram had an average of 11.0 mSv. Other studies 17. LawrenceJ A, Kim D, Kent KC, et al. Lower extremity spiral
have shown similar results, with CT angiography generally CT angiography versus catheter angiography. Radiology. 1995;
found to have a fourfold lower radiation dose in comparison 194:903–8.
18. Rieker O, Duber C, Schmiedt W, et al. Prospective comparison of
with peripheral angiography [44]. Although peripheral CT CT angiography of the legs with intraarterial digital subtraction
angiography has a relatively low radiation dose and rela- angiography. AJR Am J Roentgenol. 1996;166:269–76.
tively less radiosensitive tissues are exposed, the risks of 19. Otah KE, Takase K, Igarashi K, et al. MDCT compared with digital
radiation should not be taken lightly. subtraction angiography for assessment of lower extremity arterial
occlusive disease: importance of reviewing cross-sectional images.
AJR Am J Roentgenol. 2004;182:201–9.
20. Willman JK, Baumert T, Chandler P. Aortoiliac and lower extrem-
ity assessed with 16 detector row CT angiography respective com-
References parison with distal subtraction angiography. Radiology. 2005;236:
1083–93.
1. Chiro GD, Brooks RA, Kessler RM, et al. Tissue signatures with 21. Shareghi S, Gopal A, Gul K, et al. Diagnostic accuracy of 64 mul-
dual-energy computed tomography. Radiology. 1979;131:521–3. tidetector computed tomographic angiography in peripheral vascu-
2. Flohr TG, McCollough CH, Bruder H, et al. First performance lar disease. Catheter Cardiovasc Interv. 2010;75:23–31.
evaluation of a dual-source CT (DSCT system). Eur Radiol. 22. Fishman EK, Ney DR, Heath DG, et al. Volume rendering versus
2005;16(2):256–68. maximum intensity projection in CT angiography: what works best,
3. Kau T, Eicher W, Reiterer C, et al. Dual-energy CT angiography in when, and why. Radiographics. 2006;26:905–22.
peripheral arterial occlusive disease-accuracy of maximum inten- 23. Shammas MW, Lemke JH, Dipple EG. In-hospital complications of
sity projections in clinical routine and subgroup analysis. Eur peripheral vascular interventions using fractionated heparin as the
Radiol. 2011;21(8):1677–86. primary anticoagulant. J Invasive Cardiol. 2003;15:242–6.
4. Rubin GD, Schmidt AJ, Logan LJ, Sofilos MC. Multi-detector row 24. Lippert H, Pabst R. Aortic arch. In: Arterial variations in man: classi-
CT angiography of lower extremity arterial inflow and runoff: ini- fication and frequency. Munich: JF Bergmann-Verlag; 1985. p. 3–10.
tial experience. Radiology. 2001;221:146–58. 25. Janssen M, Baggen MGA, Veen HF, et al. Dysphagia lusoria: clini-
5. Ofer A, Nitecki SS, Linn S, et al. Multidetector CT angiography of cal aspects, manometric findings, diagnosis, and therapy. Am
peripheral vascular disease: a prospective comparison with intraar- J Gastroenterol. 2000;95:1411–6.
terial digital subtraction angiography. Am J Roentgenol. 26. Koyama T, Tadanori T, Kitanaka Y, Katagiri K, et al. Congenital
2003;180:719–24. anomaly of the external iliac artery: a case report. J Vasc Surg.
6. Jakobs TF, Wintersperger BJ, Becker CR. MDCT-imaging of 2003;37(3):683–5.
peripheral arterial disease. Semin Ultrasound CT MR. 2004; 27. Brantley SK, Rigdon EE, Raju S. Persistent sciatic artery: embryol-
25:145–55. ogy, pathology, and treatment. J Vasc Surg. 1993;18(2):242–8.
7. Johnson PT, Pannu HK, Fishman EK. IV contrast infusion for coro- 28. Mesurolle B, Qanadli SD, El Hajjam M, Goeau-Brissonniere OA,
nary artery CT angiography: literature review and results of a Mignon F, Lacombe P. Occlusive arterial disease of abdominal
nationwide survey. Am J Roentgenol. 2009;192:W214–21. aorta and lower extremities: comparison of helical CT angiography
8. Bae KT, Seeck BA, Hildebolt CF, et al. Contrast enhancement in with transcatheter angiography. Clin Imaging. 2004;28:252–60.
cardiovascular MDCT: effect of body weight, height, body surface 29. Ness J, Aronow WS. Prevalence of coexistence of coronary artery
area, body mass index, and obesity. Am J Roentgenol. 2008; disease, ischemic stroke, and peripheral arterial disease in older per-
190:777–84. sons, mean age 80 years, in an academic hospital-based geriatrics
9. Fleischmann D. Aorto-popliteal bolus transit time in peripheral CT practice. Brief reports. J Am Geriatr Soc. 1999;47(10):1255–6.
angiography: can fast acquisition outrun the bolus? Eur Radiol. 30. Newman AB, Shemanski L, Manolio TA, et al. Ankle-arm index as
2003;13:S268. a predictor of cardiovascular disease and mortality in the cardiovas-
10. Heuschmid M, Krieger A, Beierlein W, et al. Assessment of periph- cular health study. Arterioscler Thromb Vasc Biol. 1999;
eral arterial occlusive disease: comparison of multislice-CT angiog- 19:538–45.
raphy (MS-CTA) and intraarterial digital subtraction angiography 31. “Peripheral arterial disease prevention and prevalence”. Peripheral
(IA-DSA). Eur J Med Res. 2003;8:389–96. arterial disease. 2007. http://www.3-rx.com/ab/more/peripheral-
11. Cademartiri F, Mollet NR, Van der Lugt A, et al. Intravenous con- arterial-disease-prevention-and-prevalence/. Retrieved on 03 Sept
trast material administration at helical 16–detector row CT coro- 2009.
nary angiography: effect of iodine concentration on vascular 32. Sharrett AR. “Peripheral arterial disease prevalence”. Peripheral
attenuation. Radiology. 2005;236:661–5. arterial disease. 2007. http://www.health.am/vein/more/peripheral-
12. Orlandini FA, Boini S, Iochum-Duchamps S, et al. Assessment of arterial-disease-prevalence/. Retrieved on 03 Sept 2009.
the use of a saline chaser to reduce the volume of contrast medium 33. Cordeiro M, Lima J. Atherosclerotic plaque characterization by
in abdominal CT. Am J Roentgenol. 2006;187:511–5. multidetector row computed tomography angiography. J Am Coll
13. Cademartiri F, Mollet NR, Van der Lugt A, et al. Non-invasive Cardiol. 2006;47(8):C40–7.
16-row multislice CT coronary angiography: usefulness of saline 34. Rosenberg GD, Killewich LA. Case report: blue toe syndrome from
chaser. Eur Radiol Vol. 2004;14(2):178–83. a “coral reef” aorta. Ann Vasc Surg. 1995;9(6):561–4.
318 J.E. Shriki et al.

35. Levien LJ, Veller MG. Popliteal artery entrapment syndrome: more and cystic adventitial disease. Am J Roentgenol. 2003;180:
common than previously recognized. J Vasc Surg. 1999; 627–32.
30(4):587–98. 41. Tsolakis CS, Walvatne CS. Cystic adventitial disease of the popli-
36. Qvarfordt PG, Reilly LM, Sedwitz MM, Ehrenfeld WK, Stoney RJ. teal artery: diagnosis and treatment I.A. Eur J Vasc Endovasc Surg.
“Coral reef” atherosclerosis of the suprarenal aorta: a unique clini- 1998;15(3):188–94.
cal entity. J Vasc Surg. 1984;1(6):903–9. 42. Sadowski EA, Bennett LK, Chan MR, et al. Nephrogenic systemic
37. Hirsch AT, et al. ACC/AHA guidelines for the management of fibrosis: risk factors and incidence estimation. Radiology.
patients with peripheral arterial disease (lower extremity, renal, 2007;243:148–57.
mesenteric, and abdominal aortic). J Vasc Interv Radiol. 43. Kocinaja D, Cioppaa AA, Ambrosinia GT, et al. Radiation dose
2006;17(9):1383–98. exposure during cardiac and peripheral arteries catheterization. Int
38. Walter JF, Stanley JC, Mehigan JT, et al. External iliac artery fibro- J Cardiol. 2006;113(2):283–4.
dysplasia. Am J Roentgenol. 1978;31(1):125–8. 44. Martin ML, Tay KH, Borys F, et al. Multidetector CT angiography
39. Sauer L, Reilly LM, Goldstone J, et al. Clinical spectrum of symp- of the aortoiliac system and lower extremities: a prospective com-
tomatic external iliac fibromuscular dysplasia. J Vasc Surg. parison with digital subtraction angiography. Am J Roentgenol.
1990;12(4):488–95. Discussion 495–6. 2003;180:1085–91.
40. Elias DA, White LM, Rubenstein JD, et al. Pictorial essay, clinical
evaluation and MR imaging features of popliteal artery entrapment
 Aortic, Renal, Mesenteric and Carotid CT
Angiography 18
Anas Alani and Matthew J. Budoff

Abstract
Computed tomography angiography has an increasing role in vascular imaging of the aorta,
renal, mesenteric, and carotid arteries. There has been tremendous improvement in com-
puted tomography technology that has made such images the preferred choice for diagnos-
ing various acute and chronic vascular diseases and replacing non-invasive and invasive
tests.

Keywords
Computed Tomography Angiography • Aorta CT Angiography • Renal CT Angiography •
Mesenteric CT Angiography • Carotid CT Angiography • Vascular CT Angiography •
Aortic Dissection • CT Angiography Acquisition and Protocol

Introduction coronary arteries, as well as less tortuous courses. The renal

and carotid arteries are usually straight structures, so recon-
Computed tomographic angiography (CTA) of vascular structions are significantly less complicated than coronary
beds is significantly easier to perform and interpret than imaging. Also, due to the increased speed of newer systems
coronary studies. There is no cardiac motion to contend (electron beam tomography (EBT) and 16+ row multi-
with, so gating is most often not necessary. The exception is detector computed tomography (MDCT)), venous enhance-
the ascending aorta, where pseudodissections (an appear- ment is less common, so it is easier to see the arteries
ance of a dissection caused by motion of the aortic root – without superimposed contrast-filled structures (venous
Fig. 18.1) have plagued earlier studies with single-slice contamination). This is another reason why CT is most often
computed tomography (CT) due to motion artifacts [1]. superior to magnetic resonance imaging (MRI) in these vas-
Most of the large vessels of interest (the carotid, renal, and cular beds.
mesenteric arteries) have significantly larger diameters than In regard to the aorta, CTA can diagnose aneurysm, dis-
section, and wall abnormalities such as ulceration, calcifica-
tion, or thrombus throughout the full length of the aorta, as
well as the involvement of branch vessels. Disease of the
A. Alani, MD aorta or great vessels can present with a broad clinical spec-
Department of Medicine, University of Florida – Gainesville, trum of symptoms and signs. The accepted diagnostic gold
Gainsville, FL, USA standard, selective digital subtraction angiography, is now
Los Angeles Biomedical Research Institute at Harbor-UCLA, being challenged by state-of-the-art CTA and magnetic res-
1124 W Carson Street, Torrance, CA 90502, USA onance (MR) angiography. Currently, in many centers,
e-mail: [email protected]
cross-sectional imaging modalities are being used as the
M.J. Budoff, MD (*) first line of diagnosis to evaluate the vascular system, and
David Geffen School of Medicine at UCLA, Los Angeles
conventional angiography is reserved for therapeutic
Biomedical Research Institute, Torrance, CA USA
e-mail: [email protected] intervention.

© Springer International Publishing 2016 319

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_18
320 A. Alani and M.J. Budoff

The following broad approach is a guide to CT scan acquisi-

tion for various scanners. For peripheral imaging, where elec-
trocardiogram (ECG) gating is not required, 16–320-slice
scanners are more than adequate to image the entire volume.
In addition, there is no need for the speed that is required for
cardiac work (temporal resolution or rotation speed).

1. Intravenous injection of 35–70 mL of a nonionic contrast

agent (300–370 mg I/mL), decreasing with scanners with
higher numbers of detectors.
2. Monophasic or biphasic injection rate: most commonly a
monophasic injection at 4 mL/s (followed by a saline
bolus). Three phase injections (pure contrast, followed by
mixed contrast saline and pure saline) are more important
and common with cardiac applications.
3. Scan delay is determined by test injection (10 mL at
4 mL/s) or by automated triggering (to achieve imaging to
coincide with contrast arrival in the aortic root close to the
area of interest). The scan delay should be determined
near the start of the section being imaged (transverse
Fig. 18.1 Axial view of pseudo-dissection of aorta caused by motion aorta for carotids, abdominal aorta for renals or runoffs).
artifact in an ungated computed tomography (CT) scan of the chest 4. Pitch:
• For 16-detector MDCT: 16 × 0.625 mm detector
Principles of Imaging configuration with 1.25-mm reconstruction thickness
and pitch = 1.7 (table speed 17.5 mm/rotation divided
In aortic imaging, the volume coverage capabilities of by 10-mm detector coverage (16 × 0.625 = 10 mm)),
MDCT have come to full use without having to compromise reconstructed retrospectively with 0.37-mm intervals
on resolution or detail [2, 3]. With the current configuration for 3D and multi-planar reconstruction (MPR).
of 64-row (or greater) CT scanners, the entire abdominal • For 64-detector MDCT: 64 × 0.625 mm detector con-
aorta and the iliac arteries can be covered within seconds and figuration with 0.625–1.25-mm reconstruction thick-
with isotropic resolution (Chap. 1). Investigation of the ness and pitch = 1 (moving the table 40 mm and covering
dataset can now be done on the anteroposterior (coronal) and 40 mm with each rotation) up to a pitch of 1.375 (table
lateral (sagittal) planes, which has been the convention with speed 55 mm/rotation divided by 40-mm detector
invasive angiography. A few important technical advances width), reconstructed retrospectively with 0.3-mm
have further improved aorta imaging using CTA. First is the intervals for 3D and MPR (the 40-mm detector width
increased number of detector rows for the acquisition of coverage per rotation used is currently available in the
images over greater z-axis lengths with one gantry rotation. GE and Phillips 64 systems. The Siemens single- or
With up to 320 detectors, volume coverage per rotation is as dual-source has a collimation of 19.2–38.4 mm, increas-
much as 160 mm. The typical distance needed for the ing with the Philips 256 (128 detectors of 0.625 mm
abdominal aorta is on the order of 400 mm, so two to three allowing 80 mm of coverage per rotation; the Toshiba
rotations would cover the entire abdomen. Using a rotation 320 allows 160 mm of coverage per rotation)).
speed of <500 ms, this could be accomplished in 1–2 s.
Second, the use of dual-source technology allows for further
reduction of acquisition times, since the entire aorta can be Aortic CTA
scanned in one breath hold. This technology has considerably
improved temporal resolution compared to single-source The speed and ease of modern CTA make it the technique of
acquisition (for which resolution approaches 0.4 mm) [4]. choice for diagnosing chronic and acute aortic pathologic
findings, such as intramural hematoma, aneurysm, traumatic
injuries, atherosclerosis, and dissection (Fig. 18.2). With the
CT Technique current configuration of 64-row CT scanners, the entire
abdominal aorta and the iliac arteries can be covered with
Understanding the principles of CTA techniques is essential to isotropic resolution. Moreover, the high scan speed allows
acquire diagnostic images consistently. This section reviews substantial reduction of the amount of contrast material used
current CTA methods used in the evaluation of great vessels. in earlier studies, hence reducing the adverse effects.
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 321

radiation-sensitive organs such as the thyroid and orbits) and

contrast (which is more significant for renal artery imaging
due to the frequent coexistence of renal insufficiency and
renal artery stenosis) make MR more attractive for selective
cases. New scanners with more detectors reduce contrast,
since the imaging territory is covered in a shorter period. If
there is no ECG gating, contrast requirements are minimal
(30–40 cc per study). Another technique to minimize contrast
is using saline to flush the contrast through the system (Chap.
2). The saline chaser offers two significant benefits with CTA
imaging. One is that the contrast is forced from the tubing
and extremity veins into the central circulation, allowing for
a reduction in the total contrast dose. A second benefit is that
the contrast sitting in the vein during imaging can cause
partial volume (beam hardening) artifacts. Moving the
contrast out of the venous system is important for cardiac
imaging (where the scatter from the superior vena cava can
cause artifacts in the right atrium and right coronary artery),
carotid imaging (obscuring the proximal brachiocephalic
artery or carotid base), and pulmonary imaging.
With fast imaging, the venous circulation is not filled;
reducing venous contamination (large veins obscuring
Fig. 18.2 A volume-rendered image depicting an aortic dissection smaller arteries). This could be problematic in renal beds and
involving the abdominal aorta (arrow), starting below the renal arteries runoff studies, as is often seen with MRI. Thus, using new
and ending prior to the iliac arteries scanners, large areas can be scanned with minimal contrast
use. The most common protocols employed increase the
Gated vs. Non-ECG Gated CTA image acquisition time from 100 ms per image to 200–
300 ms per image to improve tissue penetration and reduce
Non-gated CTA allows for very fast acquisition, and inter- image noise. Still, 50–60 mL of contrast at most is all that is
pretation is significantly less complicated. Without ECG gat- necessary to complete a thoracic and abdominal aortic study.
ing or breath-holding, artifacts such as misregistration do not The radiation dose of CTA has improved dramatically
occur, which improves image quality compared to cardiac over the last few years [9]. Using a low and reasonably
studies. Non-ECG-gated CT is performed in parts of the achievable dose to obtain a diagnostic image can be done by
aorta without much aortic dynamics, such as the abdominal decreasing tube current, tube voltage, scan coverage, and
aorta. ECG gating means that the scan is synchronized to the other dose-saving strategies. Newer-generation scanners
cardiac beat. This will lead to decreased motion artifacts with a large detector array can cover a larger area of the aorta
from cardiac movement and aortic dynamics [5] (Fig. 18.1). with each gantry rotation and provide prospective triggering
Such motion artifacts may mimic the appearance of a dissec- over a larger span of the aorta, resulting in less radiation.
tion in the ascending aorta and lead to misdiagnosis [6]. This
ECG triggering should be considered in the ascending aorta,
the aortic arch, and the descending thoracic aorta [7]. ECG- Aortic Dissection
gated CTA requires longer acquisition to obtain the specific
phase of the ECG cycle, which will result in more contrast The superior temporal resolution of current MDCT systems
media [8]. The possibility of applying ECG-controlled significantly improves imaging of the aorta, because motion
X-ray-tube dose modulation is another step forward for artifacts are eliminated in the ascending aorta. CT is often
reducing radiation exposure rates. considered a superior method over other imaging methods
for the identification of aortic dissection, as the intimal flap
is usually well delineated, even in branches of the aorta. The
Challenges 3D nature and the ability to see the outer wall, false lumens,
and the presence of a clot make this technique superior to
CTA application can be limited due to radiation doses and even invasive angiography for the evaluation of dissection
nephrotoxicity. Of course, the requirements of radiation (Fig. 18.3). The extent of the dissection, including the
(which are more significant for carotid imaging due to proximal entry and distal re-entry sites, the involvement of
322 A. Alani and M.J. Budoff

of the entire thoracic aorta is indicated to demonstrate the

maximal aortic diameter and to detect associated disease in
other segments of the aorta. In the situation of an acute life-
threatening event, CT can provide extensive information
concerning the heart, aorta, and great vessels with a single
scan protocol (Fig. 18.4). In addition, during the same
examination, the brain and spinal canal can be evaluated if
necessary. The entire global CT examination (head, cervi-
cal spine, chest, abdomen, and pelvis) can be completed on
modern MDCT systems with scan times of 20 s and exam
times of <15 min [13].

Comparison to Other Methods

Although MRI and transesophageal echocardiography can

provide excellent and unique information, the robust nature
of CT often makes it preferable. Advantages are the ability
to image the entire aorta and beyond, the demonstration of
surrounding structures and organs, quantitative measures of
Fig. 18.3 Spiral aortic dissection seen on a sagittal view of a gated aneurysm size and location, and a rapid examination time.
64-multidetector computed tomography (MDCT) cardiac scan Limitations are the negative effects of iodinated contrast on
renal function, the rare adverse reactions to iodinated con-
adjacent branch vessels, and the potential comprise of the trast, and the inability to directly measure blood flow (which
true lumens are thoroughly evaluated. is useful for determining true and false lumens). A current
The ability to visualize the great vessels in the transverse MDCT protocol for CTA provides high-resolution arterial
aorta, neck, and arms makes CT significantly more robust than phase images from the thoracic inlet to the femoral arteries.
transthoracic and transesophageal echocardiographic imaging This coverage incorporates the entire aorta, as well as the
and tolerance by patients is significantly better. Transthoracic organs of the chest, abdomen, and pelvis. Beyond classify-
echocardiography visualizes the aortic root well but is poor at ing dissections as involving the ascending (Stanford type A)
imaging the mid-ascending and descending thoracic aorta. or descending (type B), CT can demonstrate associated find-
Transesophageal echocardiography is minimally invasive but ings that are critical to patient care, such as mediastinal
does not image the distal ascending thoracic aorta or arch well. hematoma, pericardial effusions, pseudoaneurysm forma-
Because imaging protocols for MDCT can be performed in tion, and active extravasation of contrast from the aorta.
less than 10 min (significantly shorter than MR or transesoph- Quantitative measurement of aneurysm size, location, and
ageal echocardiography), even unstable patients can be evalu- relation to branch vessels can be used for planning operative
ated and triaged quickly. With the use of flow modes (usually or intravascular repair and for monitoring post-procedure
used for timing of contrast), assessing luminal flow in the true anatomy.
and false lumens is possible. The need for precise and quantitative measurements with
CT has become more critical with continued advancements
in endovascular repair with stent grafts [14, 15]. CTA is less
Thoracic Imaging operator-dependent than transesophageal echocardiography,
it allows for complete organ visualization, and it is faster and
Diseases of the thoracic aorta present a diagnostic chal- more convenient for patients than MRI and digital subtrac-
lenge. Many aortic conditions such as aneurysms typically tion angiography. The latter issues are especially important
cause no symptoms and often go clinically unrecognized with severely ill patients. In the setting of blunt and penetrat-
until a life-threatening complication occurs. CT is the pri- ing trauma, CT of the chest can be extremely useful in diag-
mary means of imaging the lung, thoracic trauma (blunt nosis and as an aid to surgical management [16]. Another
and penetrating), aneurysms, and aortic dissections [10]. major advantage over MR is that these examinations are per-
CT is playing an increasingly important role in the diagno- formed in critically ill patients who may require mechanical
sis and management of thoracic aortic pathology [11, 12]. ventilation, invasive monitoring, intravenous infusion
Once aortic disease is detected, a comprehensive evaluation pumps, and cardiac pacing.
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 323

Fig. 18.4 Thoracic aortic dissection extending into the transverse aorta (left) and descending thoracic aorta (right). The intramural thrombus is
easily identified by the arrow

Abdominal Aorta

Aortic aneurysm is associated with risk of sudden death due

to aortic dissection or ruptures. It can occur in association
with connective tissue disorders or acquired cardiovascular
disease [17]. The ability to measure the diameter, wall throm-
bus, and calcification makes CT an ideal modality for
sequentially following patients and making accurate assess-
ments for surgical planning or medical therapy (Fig. 18.5).
Aortic endovascular stenting is gaining acceptance as an
alternative to traditional open surgical repair for abdominal
aortic aneurysms. CT imaging is the predominant method
used for preoperative planning to assess the feasibility of
endovascular aortic stenting and to select the appropriate
aortic stent graft. The abdominal aorta is usually scanned
before and following intravenous contrast enhancement,
which enables detection of calcification of the arterial wall
that will be partly obscured following contrast enhancement.
It also provides a baseline for evaluating any vascular injury
with hemorrhage or thrombus that will be seen in the post-
contrast acquisition. 3D sagittal and coronal reconstructions
are routinely performed (Figs. 18.6 and 18.7). Maximum
intensity projection (MIP) provides images similar to con-
ventional angiography and is useful to visualize calcification
Fig. 18.5 Aortic wall calcification (arrow) and aneurysm on an axial
and the relationship of the aneurysm to adjacent vessels. image at the level of abdominal aorta
324 A. Alani and M.J. Budoff

Fig. 18.6 A representation of the 2D axial images (top left), curved the volume-rendered image. The thrombus, however, is only visible on
multiplanar reformat (top right), and volume-rendered images (bottom) the 2D images and curved MIP image (green arrows). The white arrow
of a patient with an abdominal aortic aneurysm. The iliacs and femoral demonstrates the iliac aneurysm
bifurcations can be seen best in their true anatomic 3D orientation with
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 325

4. Follow-up for the size and progression or regression of

abdominal aortic aneurysms.
5. Diagnosis of the presence and severity of complications
following aortic stent-graft placement, including
endoleaks, aneurysm expansion, rupture, and pseudoan-
eurysm, thrombus, and graft migration [18].
6. Detection and depiction of aortic dissection.
7. Detection of the presence of aortic aneurysm rupture.

Accurate measurements of the aortic root diameter can be

made easily, and the extent of the aneurysm can be defined.
Luminal thrombus is easily identified by differences in tissue
density during contrast enhancement. The tomographic
format of CT provides excellent definition of the relationship
of aortic aneurysms to adjacent structures. Blood leakage
from the aneurysm or stent may be recognizable with contrast
enhancement of surrounding tissues.
The 2D images (axial data), MIP, and multiplanar imaging
allow accurate measurement of the length, location, and
diameter of aneurysms. The involvement of branch vessels
(renals, mesenterics, iliacs, etc.) is also easily assessed with
minimal contrast requirements. CTA has become the first-line
modality for evaluation to plan stent-graft deployment
(Fig. 18.7) and post-procedural assessment (Fig. 18.8).
Cephalocaudal coverage from the celiac trunk to the proximal
thighs provides a suitable study volume to detect aortic dis-
ease. Although the preoperative assessment requires a true
early arterial phase to investigate all preoperative necessities
(e.g., aortic neck diameters, angle and distance from the renal
arteries), postoperative study requires a biphasic scan proto-
col for more detailed inspection of the perigraft space to rule
out possible endoleaks. High-resolution thin-slice protocols
are preferable, especially for the post-processing task.

Comparison to Other Modalities

Like CT, magnetic resonance angiography (MRA) of the

abdomen is always acquired as part of a routine lower-
Fig. 18.7 Abdominal aortic aneurysm with large intramural thrombus, extremity runoff procedure most commonly performed for
seen on maximal intensity projection image (top, green arrow) and symptoms of claudication. With CT, the renals can be
volume-rendered (bottom, blue structure) routinely evaluated during an abdominal aorta study. For
MR, the evaluation of the renal arteries for characterizing
Common Indications for CTA potential renal artery stenosis in patients with hypertension
of Abdominal Aorta must be done as a separate procedure with different imaging
protocols. This is also true for the evaluation of a potential
1. Detection and depiction of atherosclerotic occlusive renal donor. In these patients, dedicated abdominal MRA
disease or aneurysmal dilatation of the abdominal aorta acquisition is required with greater contrast enhancement,
and iliac arteries. which is not feasible when the legs and feet must also be
2. Preoperative assessment of aortoiliac aneurysms to imaged at the same time. This is because there is a limit on
determine whether open repair or stent grafting is the total volume of gadolinium, which is usually 30–45 mL
indicated. for an adult. An abdominal MRA performed for the
3. Preoperative measurement of the aneurysm for selecting indications listed is often scanned as part of the same proce-
the appropriate stent graft. dure as a thoracic MRA, as it is for CT.
326 A. Alani and M.J. Budoff

interpreted as negative for acute aortic disorder. The resulting

sensitivity was 99 % (67 of 68), specificity was 100 % (304
of 304), the positive predictive value was 100 % (67 of 67),
the negative predictive value was 99.7 % (304 of 305), and
the accuracy was 99.5 % (371 of 373). Stueckle et al. [21]
compared conventional angiography to CTA in the diagnosis
of morphologic changes in the abdominal aorta and its
branches in 52 patients who underwent both MDCT and
invasive angiography before surgical treatment. All CT
examinations were performed after the administration of
100 mL of contrast medium with a collimation of 4 × 1 mm
and a pitch of 7. All aneurysms, occlusions, stenoses, and
calcifications were diagnosed correctly by CTA in axial and
multiplanar projections (sensitivity 100 %; specificity
100 %). The degree of stenosis was overestimated in three
cases when using axial projections. 3D volume-rendered
(VR) CTA showed a sensitivity of 91 % for aneurysms, 82 %
for stenoses, 75 % for occlusions, and 77 % for calcifica-
tions. The specificity was 100 % in all cases.
With more detector systems, imaging improves. Multislice
CTA is similar to invasive angiography for abdominal vessels
if multiplanar projections are used. Yoshida et al. [22]
evaluated 57 individuals who underwent emergency CTA
and surgery for type A aortic dissection or intramural
hematoma. The diagnosis by CTA was correct as type A
aortic dissection (45 patients) or intramural hematoma (12
patients) according to surgical pathology. The accuracy of
Fig. 18.8 A patient status post repair of a thoracic aortic aneurysm. CTA was 100 % (57 of 57), the sensitivity was 100 % (49 of
The stent can be seen without scatter artifact or partial volume effect
49), and the specificity was 100 % (eight of eight). In addi-
tion, all values were 100 % for diagnosis of aortic arch
Triple Rule-Out CTA anomalies.
These findings demonstrated that CTA is a highly accu-
CTA can be used as the first choice in the emergency room to rate imaging method in all kinds of thoracic and abdominal
rule out aortic dissection, acute coronary syndrome, pulmo- aorta diseases. CTA produces excellent 3D images that are
nary embolism, and adjacent intrathoracic structure pathol- competitive in quality with interventional angiography. In
ogy in patients with chest pain in an appropriate clinical some instances, CTA images can give more information
setting. Triple rule-out requires an ECG-gated study. This about the aortic diseases due to visualization of lumen,
can eliminate further testing in 75 % of the patients and pro- thrombus, and wall disease simultaneously as compared to
vide a cost-effective evaluation [19]. interventional angiography.

CTA Accuracy in Diagnosis of Aortic Disease Conclusion

Several studies have demonstrated the accuracy of CT for the The simultaneous acquisition of multiple thin collimated
diagnosis of aortic diseases. Hayter et al. [20] investigated slices in combination with enhanced gantry rotation speed
373 patients who underwent CTA in the emergency room for offers thin-slice coverage of extended volumes without any
suspected aortic disorders. The diagnosis of acute aortic loss in spatial resolution. Early limitations of four-slice
disorder was confirmed using surgical/pathologic diagnoses scanners required restricting the scan volume and focusing
or any imaging as the reference standard (aortography, MRA, on dedicated abdominal vessel territories in order to provide
or echocardiography). In total, there were 23 acute aortic high spatial resolution (1–2 mm). 16+ detector-row
dissections, 14 acute aortic intramural hematomas, 20 acute technology now enables full abdominal coverage from the
penetrating aortic ulcers, 44 new or enlarging aortic diaphragm to the groin without compromising spatial
aneurysms, and 11 acute aortic ruptures, and 305 cases were resolution. This technique enables the evaluation of the
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 327

whole arterial visceral vasculature (e.g., hepatic vessels,

mesenteric vessels, renal arteries) and the aortic-iliac axis in
a single data acquisition. More detectors allow faster volume
coverage (and reduce the contrast requirements).

Renal CT Angiography

Important indications for directed renal artery imaging

comprise the assessment of patients with suspected renal
vascular hypertension to exclude hemodynamically
significant renal artery stenosis, as well as a complete
preoperative assessment for renal transplant candidates.
Current CT systems with 64+ channels permit rapid
acquisition of large volumes of submillimeter data with
isotropic resolution (equal resolution in the X, Y, and Z
dimensions). This allows 3D data to be reconstructed in any
plane. Wide ranges of functional techniques are now
available with CTA, which may help us to identify patients
who would or would not benefit from renal artery
revascularization [23]. CTA of the renal arteries is performed Fig. 18.9 A volume-rendered image of the abdominal aorta and ves-
with a high-resolution protocol (with thickness as low as sels (including exquisite detail of the mesenteric and iliac arteries)
0.5–0.625 mm). Achieving adequate coverage to encompass using 64-detector MDCTA
the entire kidneys and the origins of accessory renal arteries
is easily accomplished in a scan with a duration of <3 s, or as
part of the aortic evaluation (described previously). With
adequate selection of the acquisition parameters (thin
collimation), high-spatial-resolution volumetric datasets for
subsequent 2D and 3D reformation can be acquired
(Fig. 18.9). Whereas fast acquisitions allow for a reduction
of total contrast volume in the setting of CTA, this is not the
case when CTA is combined with a second-phase abdominal
MDCT acquisition for parenchymal (e.g., hepatic) imaging.

Comparison to Other Modalities

Although renal artery duplex ultrasound (US) is often the first Fig. 18.10 Renal artery aneurysm
examination performed, there are a number of well-recognized
limitations, the most important of which is the challenge of complicated. Renal CTA is an accurate and reliable test for
optimally visualizing these vessels in obese patients. Catheter visualizing vascular anatomy (Fig. 18.10) and renal artery
angiography has been the traditional gold standard for renal stenosis, and it is therefore a viable alternative to MRA in the
artery evaluation [24], but limitations include invasiveness of assessment of patients with renovascular hypertension and in
the procedure, contrast allergy, nephropathy, and plaque potential living related renal donors.
embolization. The improvements in spatial resolution and
image quality of cross-sectional techniques have allowed MR
and CTA to replace this invasive examination in most circum- CTA Accuracy in Diagnosis of Renal Artery
stances. MRA has also benefited from a number of recent Stenosis
developments, including improvements in gradient hardware
and the recent introduction of parallel imaging, both of which Several studies investigated the diagnostic accuracy of CTA
permit reduced acquisition times and improved spatial resolu- in the diagnosis of renal artery stenosis. CTA has been
tion. However, thicker slices with MRA require acquisition in reported as having 94–100 % sensitivity and 79–97 % spec-
the plane of interest, making scanning protocols much more ificity [25]. Rountas et al. [26] compared the diagnostic
328 A. Alani and M.J. Budoff

accuracy of renal artery duplex US, CTA, and MRA to the Tepe et al. [30] used 3D EBT angiography to evaluate
gold standard, digital subtraction angiography, for the detec- renal artery lesions as well as vascular variants that are
tion of renal artery stenosis in 58 patients with clinically sus- crucial to detect before surgery. Forty patients underwent
pected renovascular hypertension. There were 132 renal EBT (GE-Imatron, C 150 ultrafast CT scanner, San
arteries. The sensitivity and specificity were 75 % and 89.6 % Francisco, CA) of the renal arteries. The study demonstrated
for renal artery duplex US, 94 % and 93 % for CTA, and 90 % that both MIP and VR images were excellent in demonstrating
and 94.1 % for MRA, respectively. Willmann et al. [27] stenosis of the renal arteries. Accessory and main renal
obtained excellent-quality CT angiograms (92 % sensitivity arteries were easily depicted, and stenosis was shown with
and 99 % specificity) for the detection of hemodynamically high accuracy. Among 40 renal angiography patients, 21 had
significant arterial stenosis of aortoiliac and renal arteries. In stenosis of the renal arteries with different percentages. A
this study, they used a half-second MDCT scanner and a total of 12 accessory renal arteries (five left, seven right)
nominal section thickness of 1 mm. Compared to MRA, there were detected. With its noninvasive VR and MIP techniques,
is no statistically significant difference between 3D MRA and CT is easy to apply and is functional and accurate for neo-
CTA in the detection of hemodynamically significant arterial plasms, renal vascular anatomy, and renal artery stenosis.
stenosis of the aortoiliac and renal arteries. This study also Another study evaluated findings in 50 main and 11
demonstrated that patient acceptance of the CT study is accessory renal arteries [31]. All arteries depicted in
higher than that of either invasive angiography or MRA. conventional angiograms were visualized in MIP and VR
images. Receiver operating characteristic (ROC) analysis for
MIP and VR images demonstrated excellent discrimination
Methods of Renal CTA for the diagnosis of stenosis of at least 50 % (area under the
ROC curve, 0.96–0.99). Sensitivity was not significantly
As a rule of thumb, the injection duration should match the different for VR and MIP (89 % vs. 94 %, p > 0.1), and
acquisition time in routine clinical practice. Biphasic specificity was greater with VR (99 % vs. 87 %, p = 0.008–
injection protocols with an initially high injection rate 0.08). Stenosis of at least 50 % was overestimated with CTA
followed by a slower continuing injection phase ensure in four accessory renal arteries, but three accessory renal
optimal opacification of the renal arteries (Chap. 2). Note arteries that were not depicted in conventional angiography
that high-concentration contrast material requires only were depicted in CTA. In the evaluation of renal artery
moderate injection flow rates (with a maximum of 4.5 mL/s) stenosis, CTA with VR is faster and more accurate than CTA
to achieve high iodine administration rates [28]. with MIP. Accessory arteries that were not depicted with
conventional angiography were depicted with both CT angi-
ographic algorithms.
Image Post-processing Techniques

While most vascular beds have demonstrated an advantage of Conclusion

MIP imaging over VR for accurate stenosis detection (espe-
cially coronary artery imaging), renal vasculature seems more CTA is a highly reliable technique for the detection of renal
amenable to quantitation with VR. One study specifically artery stenosis and for morphologic assessment. CTA can sur-
compared overall image quality and vascular delineation in pass conventional angiography in terms of diagnostic accu-
MIP and VR images. The authors found that all main and racy and reduced exposure to iodinated contrast (Fig. 18.11).
accessory renal arteries depicted in invasive angiography In patients with renal insufficiency, color-coded duplex US or
were also demonstrated in MIP and VR images [29]. VR per- gadolinium-enhanced MRA should remain as the initial
formed slightly better than MIP for quantification of stenoses examination performed, depending on local expertise and
>50 % (VR: r2 = 0.84, p < 0.001; MIP: r2 = 0.38, p = 0.001) and availability. However, new warnings regarding systemic
significantly better for severe stenoses (VR: r2 = 0.83, fibrosis with gadolinium make this agent contraindicated in
p < 0.001; MIP: r2 = 0.21, p = 0.1). For detection of stenosis, patients with glomerular filtration rates of <30 mg/mL/mm2.
VR yielded a substantial improvement in positive predictive
value (for stenoses >50 and 70 %, VR: 95 and 90 %; MIP: 86
and 68 %, respectively). The image quality obtained with VR Mesenteric CT Angiography
was not significantly better than that with MIP, but vascular
delineation in VR images was significantly better (Fig. 18.11). CTA has become a valuable minimally invasive tool for the
The VR technique of renal MRA enabled more accurate visualization of normal vascular anatomy and its variants, as
detection and quantification of renal artery stenosis than MIP, well as for pathologic conditions affecting the mesenteric
with significantly improved vascular delineation. vessels (Figs. 18.12 and 18.13) [32, 33]. CTA is considered
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 329

the first-line imaging test in the diagnosis of mesenteric isch- CTA Accuracy in Diagnosis of Mesenteric
emia [34]. Indications for CTA include not only acute and Ischemia
chronic ischemia, aneurysm, and dissection, but also preop-
erative vascular assessment for patients undergoing liver According to a recent review and meta-analysis that included
lesion embolization and in the setting of liver transplantation eight studies, CTA has a high diagnostic accuracy in the diag-
[35, 36]. In addition, mesenteric CTA can assist in the evalu- nosis of mesenteric ischemia. Sensitivity ranged from 83 to
ation of abdominal pain by ruling out other intra-abdominal 100 % with a pooled sensitivity of 94 %, and specificity ranged
pathology. from 67 to 100 % with a pooled specificity of 95 % [37].

Methods and Image Post-processing

Techniques

Protocols for typical aortic imaging (described previously)

are used to image the mesenteric vasculature. Mesenteric
CTA has been facilitated by rapid image acquisition with
64-slice scanners, which reduce artifacts from respiratory
variation. This allows for the visualization of lesions at the
mesenteric orifice and evaluation of distal reconstitution.
Multiple axial images and rotational views may be necessary
to evaluate mesenteric lesions at the aortic orifice. The
reconstructed images allow for easy evaluation of all
abdominal vasculature. VR is most often used, predominantly
Fig. 18.11 A volume-rendered electron beam tomography (EBT)
study of the renal arteries, depicting a high-grade stenosis of the left
due to complex anatomy that makes MIP imaging more
renal artery (arrow). The left kidney also opacifies less (darker color) difficult (Fig. 18.13). Since the arteries are highly tortuous,
than the right kidney, suggesting decreased blood flow and significance leaving the 2D plane often (and traveling both caudally and
of the visualized stenosis

Fig. 18.12 Maximal intensity projection of the abdominal aorta, demonstrating severe calcifications at the iliac bifurcation (arrow, left image).
The right image demonstrates a normal arterial bed in another patient, displayed using volume rendering (VR)
330 A. Alani and M.J. Budoff

radiation and iodinated contrast agents make it the best tech-

nique for children and patients with azotemia [40].

Carotid Artery CT Angiography

Ischemic cerebrovascular events are often due to atheroscle-

rotic narrowing of the carotid bifurcation (Fig. 18.14) [41].
Carotid disease contributes to stroke, transient ischemic
attacks, amaurosis figax through sudden occlusion, and cere-
bral or ocular embolization. Invasive angiography is the cur-
rent reference standard for the evaluation of obstructive
carotid artery disease. CTA is a robust technique in assessing
carotid artery stenosis, allowing for excellent visualization of
the lumen of the carotid artery using intravenous contrast
(Fig. 18.15). Subsequent refinement of US, CT, and MRI
techniques has led to changes in clinical practice, such that
many centers have now abandoned conventional angiography
in favor of safer imaging modalities [42].
CTA offers details of the entire relevant neurovascular axis
by excluding significant carotid disease and intracranial dis-
Fig. 18.13 3D image demonstrating the ability of CT to visualize
the abdominal arteries, including the gastric arteries in this case ease [43]. Coupling non-contrast-enhanced cranial CT imag-
ing with CT perfusion imaging and CTA of the entire
cerebrovascular axis is both safe and feasible [44]. The even-
cranially at different times), these vessels pose the most chal- tual ability to preemptively identify asymptomatic plaques
lenge with axial interpretations. With coronary imaging, the with high likelihood to produce symptoms is the most practi-
arteries run cranial to caudal, without significant exception. cal goal of the CTA imaging technique, which would allow
Thus, interpreting with MIP or axial imaging is fairly for appropriate intervention prior to a disabling or fatal neu-
straightforward, as the operator needs to systematically start rologic event. CTA and gadolinium-enhanced MRA have
from the most cranial images to the most caudal to follow the both proved to be reliable and fast techniques to evaluate the
respective arteries. With mesenteric imaging, the arteries degree of internal carotid artery (ICA) stenosis [45]. Apart
commonly turn both cranially and caudally, and VR enables from a hemodynamically significant luminal stenosis, com-
visualization of the entire dataset with one reconstruction. plexities in extracranial carotid artery plaque morphology
No studies of the diagnostic potential of the different recon- have also been shown to increase the risk of thromboembolic
struction methods have been reported. events, including surface irregularities/ulcerations due to
plaque rupture, calcification, fibrous cap thinning, intraplaque
hemorrhage, and the presence of necrotic core. Out of all the
Comparison to Other Modalities modalities, luminal surface irregularities and ulcerations are
most frequently seen in CTA.
Invasive angiography allows for diagnosis and treatment in a The North American Symptomatic Carotid
single test and is thus considered the reference standard test Endarterectomy Trial and European Carotid Surgery Trial
to evaluate acute and chronic mesenteric ischemia [38]. CTA demonstrated a large reduction in strokes by performing
and contrast-enhanced MRA are excellent noninvasive carotid endarterectomy [46, 47] in symptomatic patients
screening techniques for patients suspected of having with a stenosis of more than 70 %. Thus, an accurate
mesenteric ischemia from all causes. CTA has higher spatial assessment of carotid disease is important. Furthermore,
resolution and faster acquisition times, allowing assessment endarterectomy in patients with a symptomatic moderate
of the peripheral visceral branches and the inferior mesenteric carotid stenosis of 50–69 % produced a moderate reduction
artery with greater accuracy than contrast-enhanced MRA. In in the risk of stroke [33]. Current practice is to use CTA to
addition, it allows for the identification of calcified plaques. facilitate patient triage and provide specific information to
Contrast-enhanced MRA has a longer examination time that rule out large vessel stenosis in patients with transient
may result in delay therapeutic intervention. In addition, it ischemic attacks, suspected stroke, or carotid bruits
has limited use in the diagnosis of distal stenosis and (Fig. 18.16) [42]. Common indications include evaluation of
nonocclusive mesenteric ischemia [39]. MRA is therefore patients with carotid bruits, symptoms of vertebral insuffi-
the clear second choice in this clinical setting, but the lack of ciency, borderline carotid US examinations, or insufficient
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 331

Fig. 18.14 Two patients with carotid stenosis at the bifurcation. The also seen (arrow). The right image demonstrates a maximal intensity
left image is a volume- rendered image, with a high-grade stenosis at projection image of the same region, with a tight stenosis and thrombus
the proximal portion of the internal carotid, with a dense calcification present (arrow)

Fig. 18.15 3D images of normal carotid arteries bilaterally

332 A. Alani and M.J. Budoff

a1 a2

b1 b2

c1 c2 c3

Fig. 18.16 (a1) Right external carotid artery stenosis. (a2) Volume image of right ICA stent. (c1) Axial view of left carotid artery dissec-
rendered image of right external carotid artery stenosis. (b1) Coronal tion. (c2) Coronal view of left carotid artery dissection. (c3) Volume
view of right internal carotid artery (ICA) stent. (b2) Volume rendered rendered image of left carotid artery dissection

MRA examinations of the carotid system. Many vascular Given that a large proportion of patients with carotid
surgeons will not operate based upon carotid US, requiring artery disease will be evaluated for potential carotid artery
confirmation with either CTA or invasive angiography. stenting, CT imaging should focus on assessment of the
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 333

following: (1) stenosis severity, (2) disease within the aor- combination of optimal tracking volume placement and
tic arch and at the origin of the common carotid arteries, (3) adjustment of tracking volume size ensures optimal sensitiv-
the size of the common carotid artery at the lesion location, ity to the contrast material bolus. By choosing a 20-mm
(4) the size of the distal ICA, and (5) the presence of con- tracker volume placed in the aortic arch, bolus arrival was
tralateral disease. always detected. Careful timing is very important, with arte-
rial enhancement being critical. It is vital to make sure that
there is no venous filling when images are obtained.
CTA Accuracy in Diagnosis of Carotid Artery Obtaining images too early will lead to non-enhanced
Stenosis images, and obtaining images late allows for venous enhance-
ment. Large jugular veins filled with contrast in close prox-
According to previous research and reviews that included old imity to the carotid arteries can make the interpretation of
CT scanners, contrast-enhanced MRA is more accurate than carotid arteries more difficult.
MDCT in diagnosing carotid artery stenosis [48, 49].
However, MDCT is quickly developing, and more high-
quality images are being produced. A recent prospective Image Post-processing Techniques
study by Anzidei et al. evaluated 170 patients with suspected
carotid artery disease. They compared the diagnostic accu- Precision in the length and degree of stenosis has been
racy of US Doppler, steady-state contrast-enhanced MRA, reported to depend more on measurement technique than on
and CTA with invasive angiography as the reference stan- acquisition parameters [52]. The accuracy of stenosis mea-
dard. CTA has slightly better accuracy, sensitivity, and speci- surement depends on the scanning plane, which ideally
ficity than MRA (97 %, 95 %, and 98 % vs. 95 %, 93 %, and should be perpendicular to the carotid artery used to obtain
97 %, respectively). CTA has a greater accuracy than US magnified transverse oblique images. Most authors consider
(97 % vs. 76 %). Moreover, CTA and MRA have an identical MIP or curved multiplanar reconstructions as the most accu-
ability in plaque morphology and composition analysis with rate techniques for measurements. VR is considered the least
no statistical difference between the two tests [50]. accurate technique for measurement. CTA allows data to be
reconstructed into 2D and 3D images with cross-sectional
views that can accurately depict plaque morphology. The
Methods for Carotid CTA images are analyzed with axial images and MIP or curved
multiplanar reconstruction. Total post-processing is now
Carotid CT angiographic images are obtained with patients done in real time (<1 min). MIP techniques allow data to be
placed in the supine position with the head tilted back as far reconstructed into images that closely resemble conventional
as possible to avoid inclusion of dental hardware. Spiral data catheter-based angiograms that can be rotated 360° to be
can be acquired with a slice thickness of 0.5–0.625 mm start- viewed from any angle. This helps to delineate the unstable
ing at the seventh cervical vertebra and proceeding as far plaques that are less stenotic but at high risk of producing
cephalad as required. Transverse source images are recon- symptomatic embolization or carotid occlusion.
structed in 1-mm increments using a small field of view
(15 cm). These parameters allowed for a spatial resolution of
0.3 × 0.3 × 0.6 mm. Total coverage was approximately 18 cm. Plaque Composition
In general, good image quality is essential. A CT angio-
graphic image of good quality is easily obtained if the patient Plaques that are more prone to disruption fracture or fissur-
does not move during the study. Given the faster scan times ing may be associated with a higher risk of embolization,
with increased detector systems, this is even easier. A breath- occlusion, and consequent ischemic neurologic events [53].
hold acquisition is not necessary. Compared with invasive The degree of arterial stenosis is the main determinant of
angiography and CTA, a major limitation of gadolinium- stroke risk in carotid artery disease, and it has been used to
enhanced MRA is spatial resolution. select patients who will benefit from surgical intervention
With a power injector, 30–40 mL of nonionic contrast [54]. However, with recent advances in MRI and CTA imag-
medium is injected at a rate of 2.5 mL/s into an antecubital ing, there has been interest in atherosclerotic plaque features
vein. Administration of each bolus was followed immedi- (vulnerable plaque) beyond the degree of stenosis in risk
ately by a 20-mL saline flush. The acquisition is initiated stratification for stroke. Wintermark el al. [55] found a good
after the start of the administration of contrast medium, the correlation between the plaque composition evaluated by
time of which was determined by a test of circulation time. CTA and histopathological findings.
By using automatic triggering with detection of the contrast A recent study by Gupta et al. [56] evaluated patients with
material bolus, it is straightforward to selectively obtain an high-grade ICA disease. There was a strong relation between
arterial phase image. Previous studies [51] have shown that a increasing soft plaque thickness measurements and ipsilateral
334 A. Alani and M.J. Budoff

ischemic stroke (each 1-mm increase in plaque thickness making the measurement of stenosis much easier. Almost all
corresponded to 2.7 times more likelihood of ipsilateral authors consider that calcified plaque is a limitation of
ischemic events). A cutoff thickness of 3.5 mm of the soft CTA. This can be minimized by using multiplanar volume
plaque can differentiate between asymptomatic and reconstruction to visualize the entire bifurcation initially
symptomatic individuals. In contrast, calcified plaque was with a large-volume reconstruction. By reducing volume
associated with a lower risk of disease, with maximum reconstruction, we can clearly visualize the residual lumen at
thickness substantially higher in asymptomatic patients. the maximal part of stenosis, even when circumferential
Acute carotid ischemic events were associated certain plaque calcified plaques are present. Moreover, CTA is able to
morphology found by CT imaging. Increased wall volume, a differentiate mural calcifications and contrast material,
thinner fibrous cap, a greater number of lipid clusters, and because the attenuations of intraluminal contrast and
lipid clusters closer to the lumen were associated with calcifications are not similar. Therefore, calcifications should
increased risk of stroke [57]. not be considered limitations of CTA [64]. In addition,
carotid arteries tend to calcify less than either coronary or
peripheral arteries (perhaps because carotid arteries are more
Comparison to Other Modalities elastic and less muscular), so dense circumferential
calcifications occur less frequently in this vascular bed.
Invasive angiography has long been considered the standard Detection of ulcerated plaques may prove to be important,
for evaluation of carotid stenosis, but it has well-known risks since it has been suggested that the presence of plaque
and limitations. Invasive angiography allows only a limited ulceration is a risk factor for embolism [65]. Most studies
number of views, which can lead to an underestimation of suggest that CTA is the best modality for analyzing plaque
the degree of stenosis by as much as 40 % [58] compared morphology. Plaque irregularities are more frequent in CTA
with histological correlation. Invasive angiography is also a than in invasive angiography or contrast-enhanced
relatively expensive technique that uses numerous resources. MRA. However, the inability of invasive angiography to
Most importantly, there is a small but definite risk of major depict plaque ulceration is well documented [65, 66], partly
complications secondary to the procedure itself. The because of the limited number of views typically obtained.
Asymptomatic Carotid Atherosclerosis Study Committee The case of CTA depicting an ulceration that is not depicted
reported a 1.2 % risk of persisting neurologic deficit or death in gadolinium-enhanced MRA could be due to a lack of
following invasive angiography, while the surgical risk was spatial resolution in gadolinium-enhanced MRA.
1.5 %. The risks associated with CTA are markedly lower
with similar or lower radiation exposures and no catheter-
induced risks. Conclusion
Carotid artery CTA has substantial benefits, including its
accuracy, lack of invasiveness [59], and improved spatial and Carotid CTA has matured and can be used to quantify
temporal resolution compared with MRA. Gadolinium- stenoses more precisely than US, to detect tandem stenoses,
enhanced MRA is an appropriate technique for evaluating and for the workup of acute stroke patients. The newer
ICA stenosis [60–62]. Clinically relevant stenosis and occlu- scanners and multiple dose-saving strategies have the
sions of the ICA were correctly detected with good sensitiv- additional advantage of a very low radiation profile, allowing
ity, specificity, and interobserver agreement. Most studies for minimal risk to the patient and maximum visualization of
with gadolinium-enhanced MRA demonstrate overestimation the arteries in question.
of the degree of stenosis [53, 61, 62]. Artifacts due to the
excessive section thickness necessary with current MR sys-
tems cause a partial volume effect [58, 63]. The signal loss Vertebral Artery CT Angiography
can also be explained by the presence of hemodynamic modi-
fications. The decreased flow caused by stenosis leads to a Although conventional intra-arterial angiography remains
reduced concentration of contrast agent in the distal arterial the gold standard method for imaging the vertebral artery,
lumen, which may also explain why overestimation of steno- noninvasive modalities such as MDCT, MRA, and US are
sis with gadolinium-enhanced MRA can occur [64], espe- constantly improving and are playing an increasingly
cially for evaluating the degree of stenosis in small-vessel important role in diagnosing vertebral artery pathology in
lumens. MRA can replace invasive angiography in most clinical practice. Normal anatomy, normal variants, and a
patients. However, it has been proved that CTA is highly number of pathologic entities such as vertebral
accurate and can replace invasive angiography [44, 64]. atherosclerosis, arterial dissection, arteriovenous fistula,
In contrast to the other two modalities, CTA allows direct subclavian steal syndrome, and vertebrobasilar dolichoectasia
visualization of the arterial wall and atheromatous plaque, can be seen.
18 Aortic, Renal, Mesenteric and Carotid CT Angiography 335

Chapter Summary 18. Hobo R, Buth J, EUROSTAR Collaborators. Secondary interven-

tions following endovascular abdominal aortic aneurysm repair
using current endografts. A EUROSTAR report. J Vasc Surg.
During the past decade, we have been witness to a tremen- 2006;43(5):896–902.
dous development in the field of CT imaging. CTA has 19. Halpern EJ. Triple-rule-out CT angiography for evaluation of acute
gained remarkably by improvements in scan time and image chest pain and possible acute coronary syndrome. Radiology.
2009;252(2):332–45.
quality, replacing diagnostic angiography in many cases of 20. Hayter RG, et al. Suspected aortic dissection and other aortic disor-
aorta, renal, mesenteric, and carotid angiography. In addi- ders: multi-detector row CT in 373 cases in the emergency setting.
tion, there has been an exciting advance in techniques for Radiology. 2006;238(3):841–52.
reducing radiation dose that have achieved dramatic results 21. Stueckle CA, et al. Multislice computed tomography angiography
of the abdominal arteries: comparison between computed
and decreased radiation concerns. These vascular beds suffer tomography angiography and digital subtraction angiography
from fewer motion artifacts (except for the ascending aorta), findings in 52 cases. Australas Radiol. 2004;48(2):142–7.
so imaging with CTA is ideal. CTA is less expensive and less 22. Yoshida S, et al. Thoracic involvement of type A aortic dissection
invasive, and it allows for simultaneous visualization of large and intramural hematoma: diagnostic accuracy – comparison of
emergency helical CT and surgical findings. Radiology.
anatomic areas from multiple angles using 3D display. 2003;228(2):430–5.
23. Glockner JF, Vrtiska TJ. Renal MR and CT angiography: current
concepts. Abdom Imaging. 2007;32(3):407–20.
References 24. Kim D, et al. Renal artery imaging: a prospective comparison of
intra-arterial digital subtraction angiography with conventional
angiography. Angiology. 1991;42(5):345–57.
1. Stanford W, Rooholamini SA, Galvin JR. Ultrafast computed
25. Sarkodieh JE, Walden SH, Low D. Imaging and management of
tomography in the diagnosis of aortic aneurysms and dissections.
atherosclerotic renal artery stenosis. Clin Radiol. 2013;68(6):
J Thorac Imaging. 1990;5(4):32–9.
627–35.
2. Katz DS, Hon M. CT angiography of the lower extremities and aor-
26. Rountas C, et al. Imaging modalities for renal artery stenosis in
toiliac system with a multi-detector row helical CT scanner: promise
suspected renovascular hypertension: prospective intraindividual
of new opportunities fulfilled. Radiology. 2001;221(1):7–10.
comparison of color Doppler US, CT angiography, GD-enhanced
3. Kim JK, et al. Living donor kidneys: usefulness of multi-detector
MR angiography, and digital substraction angiography. Ren Fail.
row CT for comprehensive evaluation. Radiology.
2007;29(3):295–302.
2003;229(3):869–76.
27. Willmann JK, et al. Aortoiliac and renal arteries: prospective intra-
4. Kalender WA, Quick HH. Recent advances in medical physics. Eur
individual comparison of contrast-enhanced three-dimensional MR
Radiol. 2011;21(3):501–4.
angiography and multi-detector row CT angiography. Radiology.
5. Roos JE, et al. Thoracic aorta: motion artifact reduction with retro-
2003;226(3):798–811.
spective and prospective electrocardiography-assisted multi-
28. Fleischmann D. Multiple detector-row CT angiography of the renal
detector row CT. Radiology. 2002;222(1):271–7.
and mesenteric vessels. Eur J Radiol. 2003;45 Suppl 1:S79–87.
6. Qanadli SD, et al. Motion artifacts of the aorta simulating aortic
29. Mallouhi A, et al. 3D MR angiography of renal arteries: compari-
dissection on spiral CT. J Comput Assist Tomogr. 1999;23(1):1–6.
son of volume rendering and maximum intensity projection algo-
7. Gotway MB, Dawn SK. Thoracic aorta imaging with multisclice
rithms. Radiology. 2002;223(2):509–16.
CT. Radiol Clin North Am. 2003;41(3):521–43.
30. Tepe SM, Memisoglu E, Kural AR. Three-dimensional noninvasive
8. Blanke P, et al. Thoracic aorta: prospective electrocardiographically
contrast-enhanced electron beam tomography angiography of the
triggered CT angiography with dual-source CT--feasibility, image
kidneys: adjunctive use in medical and surgical management. Clin
quality, and dose reduction. Radiology. 2010;255(1):207–17.
Imaging. 2004;28(1):52–8.
9. Raff GL. Radiation dose from coronary CT angiography: five years
31. Johnson PT, et al. Renal artery stenosis: CT angiography – com-
of progress. J Cardiovasc Comput Tomogr. 2010;4(6):365–74.
parison of real-time volume-rendering and maximum intensity pro-
10. Fishman JE. Imaging of blunt aortic and great vessel trauma.
jection algorithms. Radiology. 1999;211(2):337–43.
J Thorac Imaging. 2000;15(2):97–103.
32. Laghi A, et al. Multislice spiral computed tomography angiography
11. Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl
of mesenteric arteries. Lancet. 2001;358(9282):638–9.
J Med. 1997;336(26):1876–88.
33. Lawler LP, Fishman EK. Celiomesenteric anomaly demonstration
12. Rubin GD. Helical CT angiography of the thoracic aorta. J Thorac
by multidetector CT and volume rendering. J Comput Assist
Imaging. 1997;12(2):128–49.
Tomogr. 2001;25(5):802–4.
13. Rubin GD, et al. Aorta and iliac arteries: single versus multiple
34. Oliva IB, et al. ACR Appropriateness Criteria (R) imaging of mes-
detector-row helical CT angiography. Radiology.
enteric ischemia. Abdom Imaging. 2013;38(4):714–9.
2000;215(3):670–6.
35. Erbay N, et al. Living donor liver transplantation in adults: vascular
14. Galla JD, et al. Identification of risk factors in patients undergoing
variants important in surgical planning for donors and recipients.
thoracoabdominal aneurysm repair. J Card Surg. 1997;12(2
AJR Am J Roentgenol. 2003;181(1):109–14.
Suppl):292–9.
36. Byun JH, et al. Evaluation of the hepatic artery in potential donors
15. Semba CP, et al. Acute rupture of the descending thoracic aorta:
for living donor liver transplantation by computed tomography
repair with use of endovascular stent-grafts. J Vasc Interv Radiol.
angiography using multidetector-row computed tomography:
1997;8(3):337–42.
comparison of volume rendering and maximum intensity projection
16. Zinck SE, Primack SL. Radiographic and CT findings in blunt chest
techniques. J Comput Assist Tomogr. 2003;27(2):125–31.
trauma. J Thorac Imaging. 2000;15(2):87–96.
37. Cudnik MT, et al. The diagnosis of acute mesenteric ischemia: a
17. Lu B, et al. Electron beam tomography with three-dimensional
systematic review and meta-analysis. Acad Emerg Med.
reconstruction in the diagnosis of aortic diseases. J Cardiovasc Surg
2013;20(11):1087–100.
(Torino). 2000;41(5):659–68.
336 A. Alani and M.J. Budoff

38. Brandt LJ, Boley SJ. AGA technical review on intestinal ischemia. 51. Castillo M, Wilson JD. CT angiography of the common carotid
American Gastrointestinal Association. Gastroenterology. artery bifurcation: comparison between two techniques and con-
2000;118(5):954–68. ventional angiography. Neuroradiology. 1994;36(8):602–4.
39. Laissy JP, Trillaud H, Douek P. MR angiography: noninvasive vas- 52. Cinat M, et al. Helical CT angiography in the preoperative evalua-
cular imaging of the abdomen. Abdom Imaging. tion of carotid artery stenosis. J Vasc Surg. 1998;28(2):290–300.
2002;27(5):488–506. 53. Cronqvist M, et al. Evaluation of time-of-flight and phase-contrast
40. Shih MC, Hagspiel KD. CTA and MRA in mesenteric ischemia: MRA sequences at 1.0 T for diagnosis of carotid artery disease.
part 1, role in diagnosis and differential diagnosis. AJR Am I. A phantom and volunteer study. Acta Radiol. 1996;37(3 Pt
J Roentgenol. 2007;188(2):452–61. 1):267–77.
41. Kannel WB. Current status of the epidemiology of brain infarction 54. Halliday A, et al. 10-year stroke prevention after successful carotid
associated with occlusive arterial disease. Stroke. endarterectomy for asymptomatic stenosis (ACST-1): a multicentre
1971;2(4):295–318. randomised trial. Lancet. 2010;376(9746):1074–84.
42. North American Symptomatic Carotid Endarterectomy Trial 55. Wintermark M, et al. High-resolution CT imaging of carotid artery ath-
Collaborators. Beneficial effect of carotid endarterectomy in erosclerotic plaques. AJNR Am J Neuroradiol. 2008;29(5):875–82.
symptomatic patients with high-grade carotid stenosis. N Engl 56. Gupta A, et al. Evaluation of computed tomography angiography
J Med. 1991;325(7):445–53. plaque thickness measurements in high-grade carotid artery steno-
43. Smith WS, et al. Safety and feasibility of a CT protocol for acute sis. Stroke. 2014;45(3):740–5.
stroke: combined CT, CT angiography, and CT perfusion imaging 57. Wintermark M, et al. Carotid plaque computed tomography imaging
in 53 consecutive patients. AJNR Am J Neuroradiol. in stroke and nonstroke patients. Ann Neurol. 2008;64(2):149–57.
2003;24(4):688–90. 58. Levy RA, Prince MR. Arterial-phase three-dimensional contrast-
44. Na DG, et al. Multiphasic perfusion computed tomography in enhanced MR angiography of the carotid arteries. AJR Am
hyperacute ischemic stroke: comparison with diffusion and perfu- J Roentgenol. 1996;167(1):211–5.
sion magnetic resonance imaging. J Comput Assist Tomogr. 59. Marro B, et al. Computerized tomographic angiography scan fol-
2003;27(2):194–206. lowing carotid endarterectomy. Ann Vasc Surg. 1998;12(5):451–6.
45. Runge VM, Kirsch JE, Lee C. Contrast-enhanced MR angiography. 60. Leclerc X, et al. Contrast-enhanced three-dimensional fast imaging
J Magn Reson Imaging. 1993;3(1):233–9. with steady-state precession (FISP) MR angiography of supraaortic
46. MRC European carotid surgery trial: interim results for symptom- vessels: preliminary results. AJNR Am J Neuroradiol.
atic patients with severe (70-99%) or with mild (0-29%) carotid 1998;19(8):1405–13.
stenosis. European Carotid Surgery Trialists’ Collaborative Group. 61. Slosman F, et al. Extracranial atherosclerotic carotid artery disease:
Lancet. 1991;337(8752):1235–43. evaluation of non-breath-hold three-dimensional gadolinium-enhanced
47. Barnett HJ, et al. Benefit of carotid endarterectomy in patients with MR angiography. AJR Am J Roentgenol. 1998;170(2):489–95.
symptomatic moderate or severe stenosis. North American 62. Scarabino T, et al. MR angiography in carotid stenosis: a compari-
Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl son of three techniques. Eur J Radiol. 1998;28(2):117–25.
J Med. 1998;339(20):1415–25. 63. Remonda L, Heid O, Schroth G. Carotid artery stenosis, occlusion,
48. U-King-Im JM, Young V, Gillard JH. Carotid-artery imaging in the and pseudo-occlusion: first-pass, gadolinium-enhanced, three-
diagnosis and management of patients at risk of stroke. Lancet dimensional MR angiography – preliminary study. Radiology.
Neurol. 2009;8(6):569–80. 1998;209(1):95–102.
49. Chappell FM, et al. Carotid artery stenosis: accuracy of noninvasive 64. Randoux B, Marro B, Marsault C. Carotid artery stenosis: competi-
tests – individual patient data meta-analysis. Radiology. tion between CT angiography and MR angiography. AJNR Am
2009;251(2):493–502. J Neuroradiol. 2004;25(4):663–4; author reply 664.
50. Anzidei M, et al. Diagnostic accuracy of colour Doppler ultraso- 65. Hatsukami TS, et al. Carotid plaque morphology and clinical
nography, CT angiography and blood-pool-enhanced MR angiog- events. Stroke. 1997;28(1):95–100.
raphy in assessing carotid stenosis: a comparative study with DSA 66. Comerota AJ, et al. The preoperative diagnosis of the ulcerated
in 170 patients. Radiol Med. 2012;117(1):54–71. carotid atheroma. J Vasc Surg. 1990;11(4):505–10.
 Assessment of Pulmonary Vascular
Disease 19
Bradley S. Messenger and Ronald J. Oudiz

Abstract
Pulmonary hypertension (PH) is defined as an abnormal elevation of pulmonary arterial
pressure (PAP), with a mean PAP ≥25 mmHg. A classification system organizes this het-
erogeneous patient population into five groups based on the underlying etiology, pathogen-
esis, and pathophysiology associated with the PH. A thorough diagnostic workup is
necessary to determine the precise etiology, treatment strategy, and prognosis for patients
with PH. Cardiac Computed Tomography is a useful tool in PH for detection of disease,
workup, and characterization of the underlying etiologies as it describes the cardiac struc-
tures and functional abnormalities seen with PH.

Keywords
Pulmonary Arterial Hypertension • Pulmonary Artery • Right Ventricle • Pulmonary
Embolism • Right Heart Catheterization • Cardiac Structure

Pulmonary hypertension (PH) is defined as an abnormal ele- capillary hemangiomatosis. (See section “Classification of
vation of the pulmonary arterial pressure with diverse etiolo- PH”, below) In this chapter, we provide an overview of PH
gies and pathogenesis. It is hemodynamically defined as a characteristics seen on cardiac CT.
mean pulmonary artery pressure ≥25 mm Hg and pulmonary
vascular resistance >3 Wood units. The presence of PH typi-
cally leads to the right ventricular failure syndrome [1] of Classification of PH
dyspnea, fluid overload, and untimely death, and is respon-
sible for millions of US hospital admissions annually. The simplicity of defining pulmonary hypertension with
Diseases of the pulmonary circulation span a variety of dis- hemodynamic data belies the challenges of diagnosing and
ease entities including pulmonary arterial hypertension (PAH), managing this disorder. The patient population is heteroge-
pulmonary venous hypertension, chronic thromboembolic neous with multiple potential etiologies, prognoses, and
pulmomary hypertension (CTEPH), pulmonary arteriovenous treatment options. The modified classification from the 5th
malformation, pulmonary arterial stenosis, pulmonary arterial World Symposium on PH held in Nice, France in 2013
aneurysm, pulmonary venoocclusive disease, and pulmonary (revised from the previous revision in 2008) divides PH into
five groups, shown in Table 19.1. The largest groups in the
B.S. Messenger, MD (*) Western world are Groups 2 and 3, respectively the left sided
Division of Cardiology, Department of Medicine, heart disease and hypoxic lung disease [2].
Harbor-UCLA Medical Center,
k1000 West Carson Street, Torrance, CA 90502, USA
e-mail: [email protected]
Group 1 PH: PAH
R.J. Oudiz, MD
Department of Medicine, Los Angeles Biomedical Research
Institute, The David Geffen School of Medicine at UCLA, Group 1 pulmonary hypertension is referred to as pulmonary
Harbor-UCLA Medical Center, Torrance, CA, USA arterial hypertension (PAH), a disease of the precapillary

© Springer International Publishing 2016 337

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_19
338 B.S. Messenger and R.J. Oudiz

Table 19.1 Summary of CT findings in pulmonary hypertension telangiectasia. BMPR2 mutations, however, have also been
Pulmonary arteries detected in 11 % to 40 % of apparently idiopathic cases with-
Enlarged proximal vessels out a family history [10, 11], so the distinction between idio-
Pruning of the distal vessels pathic and familial BMPR2 mutations may be artificial.
Calcification of the proximal pulmonary arteries Interestingly, in up to 30 % of families with PAH, no BMPR2
Thrombosis mutation has been identified. Thus, heritable forms of PAH
Aneurysms include IPAH with germline mutations and familial cases
Heart with or without identified germline mutations [12, 13].
RA, RV, and IVC dilation Genetic testing is not mandatory in heritable PAH, genetic
RV hypertrophy testing should only be performed after genetic counseling,
Decreased RV systolic function with a discussion of the risks, benefits, and limitations of
Flattened interventricular septum (“D-shaped” and undersized left such testing [14].
ventricle)
Pericardial thickening and/or effusion
PAH Associated with Connective Tissue Diseases
Others
The prevalence of PAH has been well established for patients
Hypertrophy of bronchial arteries
with systemic sclerosis (SSc). Two recent prospective studies
Segmental bronchial artery to bronchus ratio > 1:1 in 3 or 4 lobes
using echocardiography as a screening method and right heart
Retrograde opacification of the inferior vena cava or hepatic vein
catheterization for confirmation found a prevalence of PAH in
SS of between 7 % and 12 % [15, 16]. The prevalence of PAH
pulmonary circulation due to a complex process intrinsic to in systemic lupus erythematosis and mixed connective tissue
the pulmonary vasculature. As many entities clinically disease remains unknown; although its incidence is greater
mimic PAH, it is a diagnosis of exclusion, requiring a thor- than IPAH, it occurs less frequently than in SSc [17–20]. In the
ough workup and proper consideration of more common eti- absence of fibrotic lung disease, PAH has also been reported
ologies such as left-sided heart disease and hypoxic lung infrequently in Sjögren syndrome [21], polymyositis [22], and
disease. PAH, like PH, is similarly defined hemodynamically rheumatoid arthritis [23]. Approximately one half of patients
as a mean pulmonary artery pressure ≥25 mmHg at rest and with PH and connective tissue diseases will die within 1 year
PVR >3 Wood units, but the pulmonary capillary wedge if left untreated [24]. PH is also a frequent complication of
pressure measures ≤15 mmHg [3]. idiopathic pulmonary fibrosis (IPF). IPF patients with con-
The natural history of PAH is variable based upon etiology comitant PH have a two to threefold increase in mortality
but it typically follows a progressive course with a poor prog- compared to IPF patients with normal pulmonary arterial pres-
nosis if left untreated [4]. Most patients with PAH present with sures [25]. However, the presence or severity of PH does not
exertional dyspnea that worsens over months to years. correlate with the level of IPF disease seen on high resolution
Exertional angina, syncope, and peripheral edema appear later CT [26]. It is increasingly being recognized that PH in patients
in the course when increasing pulmonary vascular resistance with IPF is the sequelae of a “primary” occlusive pulmonary
strains and ultimately impairs right ventricular function. The vasculopathy, rather than being purely secondary to fibrotic
diagnosis of PAH is often delayed due to the nonspecific destruction of the vascular bed [27].
symptoms and subtle findings on physical examination {5].
PAH Associated with Congenital Heart
Idiopathic and Heritable PAH Disease (CHD)
Idiopathic PAH (IPAH) is a diagnosis of exclusion in which PAH related to CHD results from the effects of a long-
no etiology nor family history can account for the disease. standing abnormal increase in pulmonary blood flow which
The incidence of IPAH is rare, with an estimated incidence leads to pathologic changes in the pulmonary vasculature,
of 1–2 cases per million per year worldwide [6]. The disor- particularly in the smaller vessels. This results in increased
der is approximately 4 times more common in women [7, 8], pulmonary vascular resistance, which in turn has deleterious
presenting in the third decade for women and in the fourth effects upon the heart and larger pulmonary vascular struc-
decade for men without racial or ethnic predisposition [6]. tures. Direct shunts can increase pulmonary blood flow and
PAH has a familial component is some patients. Germline pressure (patent ductus arteriosis) (Fig. 19.1).
mutations in the bone morphogenetic protein receptor type 2 Eisenmenger syndrome is defined as CHD with an ini-
(BMPR2) gene can be detected in approximately 70 % of tially large systemic-to-pulmonary shunt that induces pro-
cases [8, 9]. Mutations in activin receptor-like kinase type 1 gressive pulmonary vascular disease and PAH, resulting in
(ALK-1 or endoglin have been found in familial PH with a reversal of the shunt and central cyanosis [28, 29].
strong association for concomitant hereditary hemorrhagic Eisenmenger syndrome represents the most advanced form
19 Assessment of Pulmonary Vascular Disease 339

systemic-to-pulmonary shunts in Europe and North America

ranges between 1.6 and 12.5 cases per million adults, with
25–50 % of this population affected by Eisenmenger syn-
drome [33].

PAH Associated with Schistosomiasis

Though not prominent in industrialized nations, schistoso-
miasis may be the most common cause of PAH in the world
given the expected 200 million people infected with the para-
site [34]. The mechanism of PH is probably multifactorial,
and includes mechanical obstruction, local vascular inflam-
mation related to eggs, and portal hypertension [35, 36].
These cases can have a similar clinical presentation to IPAH
[37], with similar histopathologic findings [38], and thus
similar radiographic appearance. PAH occurs almost exclu-
sively in the 10 % of infected patients who develop hepato-
splenic schistosomiasis [39].

Pulmonary Veno-Occlusive Disease

and Pulmonary Capillary Hemangiomatosis
Pulmonary veno-occlusive disease (PVOD) accounts for a
small number of pulmonary hypertension cases, most com-
Fig. 19.1 64 slice multi-detector CT in a 20 year-old woman with pat-
ent ductus arteriosis (black arrow), seen well in this sagittal view with monly in children and young adults [40]. The estimated
resultant dilation of the main pulmonary artery annual incidence rate is 0.1–0.2 cases of PVOD per million
persons in the general population [41, 42].
Patients with PH due to PVOD frequently present with
congestive heart failure symptoms of dyspnea on exertion,
peripheral edema, and radiographic signs of pulmonary
edema with Kerley B lines that is expected with post-
capillary PH. However, the hemodynamics at right heart
catheterization similar to pre-capillary PH and may lead cli-
nicians to diagnose idiopathic PH [40]. Vasodilator therapy,
as used to treat a subset of idiopathic PH patients, can cause
acute pulmonary edema, so distinguishing PVOD from IPAH
has important clinical significance.
CT imaging may help raise a clinician’s suspicion for
PVOD. The CT findings of the disease includes smooth sep-
tal thickening, diffuse or mosaic ground-glass opacities,
multiple small nodules, and pleural effusion [43–47]. PVOD
and pulmonary capillary hemangiomatosis (PCH) also show
the presence of crackles and clubbing on physical examina-
tion, hemosiderin-laden macrophages on bronchoalveolar
lavage [48], as well as lower carbon monoxide diffusing
capacity and PaO2 [47]. In a comparison study, PVOD
Fig. 19.2 CT scan in a 22 year-old woman with Eisenmenger syn- patients had peripheral ground glass opacities (GGO) in
drome due to atrial septal defect and pulmonary hypertension. Right 93 % of cases compared with 13 % incidence of GGO in
cardiac chambers are enlarged with marked right ventricular hypertro-
phy (black arrow) patients with PAH [49]. Thickened interlobular septa and
mediastinal adenopathy were also strongly correlated with
PVOD compared with PAH patients [41].
of PAH associated with CHD (Fig. 19.2). A large proportion The only effective treatment for PVOD is lung transplant
of patients with CHD develop some degree of PAH [30–32]. with most diagnoses being made at time of transplant or
The prevalence of PAH associated with congenital autopsy.
340 B.S. Messenger and R.J. Oudiz

Group 2 PH: Pulmonary Hypertension Diagnostic Workup of PE

due to Left Heart Disease Many diagnostic tests have been suggested for the evaluation
of patients with suspected VTE. These include the history
One of the most commonly seen forms of PH is pulmonary and physical examination to the electrocardiogram, chest
hypertension due to left heart disease. Since the etiology of radiography, echocardiography, ventilation-perfusion scin-
their PH is distal to the pulmonary arterial system, Group 2 tigraphy, pulmonary angiography, CT and MR angiography,
patients have “post-capillary” PH. Like other forms of PH, it lower-extremity venography, and sonography. Although the
manifests clinical signs and symptoms of the right heart fail- diagnostic accuracy of laboratory tests such as D-dimer has
ure syndrome. Group II PH includes patients with preserved increased (a negative result in combination with a low-prob-
or reduced ejection fraction, valvular heart disease and cer- ability clinical assessment provides reasonable certainty for
tain forms of congenital heart disease affecting left ventricu- excluding PE), radiographic imaging plays an important role
lar flow and/or performance. in the diagnosis of PE, especially with the development of
multi-detector CT (MDCT) and increased use of CT pulmo-
nary angiography.
Group 3 PH: Pulmonary Hypertension Although normal chest x-ray findings are observed in
due to Lung Diseases and/or Hypoxia 24 % of patients with PE, an elevated hemidiaphragm can be
observed in 20 % of patients with acute PE [58]. An elevated
A subcategory of lung disease characterized by a mixed hemidiaphragm, consolidation, pleural effusion, or atelecta-
obstructive and restrictive pattern includes chronic bronchi- sis occurs in about 2/3 of patients with acute PE. Especially
ectasis, cystic fibrosis [50], and a newly identified syndrome in a massive PE (Fig. 19.3), local hyperlucency is seen when
characterized by the combination of pulmonary fibrosis, a lobar or segmental artery is occluded (Westermark sign),
mainly of the lower zones of the lung, and emphysema, and engorgement of a major hilar artery (Fleischner sign)
mainly of the upper zones of the lung [51]. The prevalence of can be detected [59, 60]. Abrupt tapering or termination of a
PH in all of these conditions remains largely unknown. pulmonary vessel (knuckle sign), a pleural-based density or
However, in a recent retrospective study of 998 patients with costophrenic density (Hampton’s hump), and alveolar or
chronic obstructive pulmonary disease who underwent right interstitial pulmonary edema may occur. Most of the above
heart catheterization, only 1 % had severe pulmonary hyper- chest x-ray findings are nonspecific. Nuclear scintigraphy
tension (mean PA pressure >40 mm Hg) [52]. In the syn- (ventilation-perfusion or V/Q scanning) is useful if multide-
drome of combined pulmonary fibrosis and emphysema, the tector CT angiography (MDCTA) is not available. The V/Q
prevalence of PH is almost 50 % [51]. scan in a patient with an acute PE will demonstrate an area

Group 4 PH: Chronic Thromboembolic

Pulmonary Hypertension (CTEPH)

Pulmonary embolism (PE) is an obstruction of a pulmonary

artery caused by a blood clot, air, fat, or tumor tissue. The
most common cause of the obstruction is a blood clot
(thrombus) usually from a peripheral vein. The average
annual incidence of venous thromboembolism (VTE) in the
United States is 1 per 1000, with about 250,000 incident
cases occurring annually [53–55]. The challenge in under-
standing the real disease is that an additional equal number
of patients are diagnosed with PE at autopsy [53, 56]. It is
estimated that between 650,000 and900,000 fatal and non-
fatal VTE events occur in the US annually [57]. The classic
triad of signs and symptoms of PE (hemoptysis, dyspnea,
chest pain) are neither sensitive nor specific, and many Fig. 19.3 64 slice multi-detector CT in a patient with pulmonary
embolism. An axial section at the level of the main pulmonary artery
patients with PE are initially asymptomatic; most patients
shows the filling defect (white arrows) of bilaterally enlarged pulmo-
who have symptoms often have atypical and/or nonspecific nary arteries with massive thromo-emboli. A small amount of right
symptoms. pleural effusion (white arrowhead) is observed
19 Assessment of Pulmonary Vascular Disease 341

distal to thrombus that is not properly per fused, increasing

the V/Q mismatch.
Perfusion defects appear the same on a VQ scan whether
the pulmonary embolus is acute or chronic. In contrast, CT
findings of acute versus chronic emboli differ. In CTEPH,
there may be intraluminal thrombi and dilated bronchial
arteries. Furthermore, a mosaic pattern of hyperattenuation
and hypoattenuation is frequently seen, representing the
variation in perfusion between pulmonary segments [40].
Other evidence of CTEPH on CT includes abrubt narrowing
of vessels, intimal irregularities, or total occlusions. Yet,
there is greater concern that CT findings may be difficult to
detect. A study from Tunariu, et al. found a sensitivity of
51 % for CTPA compared with 96 % sensitivity for VQ scans
[61]. The specificity of CTPA can also be limited by the sub-
tly distinct mosaic pattern of hyperattenuation and hypoat-
tenuation found in Group 1 PAH. With improved ECG-gated
CT imaging, recent studies have shown much improved sen-
sitivity. He, et al found the sensitivity of VQ scan to be 100 %
if high and intermediate risk results were interpreted as posi-
tive for a PE with sensitivity declining to 96 % but specificity
rising to 95 % if only high risk results were counted as
abnormal [62]. CT had a sensitivity of 92 % with specificity
of 95 % in the same patient cohort [62]. While V/Q scan
remains slightly more sensitive, CT imaging now serves as a Fig. 19.4 64 slice multi-detector CT in a 58 year-old man with multi-
viable alternative given improvements in sensitivity and ple bilateral pulmonary embolism. (a) “Saddle embolus” (black arrow)
specificity with newer scanners. at the bifurcation of right pulmonary Artery (PA). (b) “Tram line”
Pulmonary angiography, the gold standard for diagnosing (white arrow) and “ring shape” (black arrowhead) features of emboli at
both peripheral PAs
PE, is being replaced in many institutions with MDCTA,
which is less invasive, easier to perform, and has high sensi-
tivity (83 %-100 %) and specificity (89 %-97 %) [63–65]. Methods of Detecting and Characterizing PH
The PIOPED studies (large multicenter trials for CCTA in
suspected PE) report negative predictive values as high as The appropriate classification of patients with suspicion of
99 %. PAH requires a rigorous diagnostic approach. PH symptoms
The newest noninvasive method for the evaluation and are nonspecific and progress slowly over months to years.
diagnosis of PE is MRI. Although not as extensively studied Exertional dyspnea is the most common symptom with
as other imaging techniques, it can be utilized for the patients fatigue occurring in a minority of cases. Manifestations of
with renal dysfunction or an iodine contrast allergy. CT angi- syncope, peripheral edema, and angina may be more con-
ographic findings are shown (Figs. 19.3 and 19.4). cerning and frequently appear in patients with evidence of
Chronic thromboembolic pulmonary hypertension impaired right ventricular function. Clinicians should have a
(CTEPH) represents a frequent cause of PH (Fig. 19.4). The higher index of suspicion for PAH in patients using amphet-
incidence of CTEPH is uncertain; however, it is known to amines or diet pills, a history of autoimmune disease, or a
occur in up to 4 % of patients after an acute pulmonary known family history of PH.
embolism [66, 67]. It is strongly recommended that patients Guidelines put forth from the AHA/ACCF recommend a
with suspected or confirmed CTEPH be referred to a center rigorous workup for pulmonary hypertension which includes
with expertise in the management of this disease to consider the diagnostic algorithm as shown in Table 19.2 [3].
the feasibility of performing pulmonary thromboendarterec- Transthoracic echocardiography (TTE) is often used as a
tomy, currently the only curative treatment. The decision first-line screening test to exclude or identify patients with
depends on the location of the obstruction (central vs. more severe PH by estimating systolic PA pressure and looking for
distal pulmonary arteries), the correlation between hemody- evidence of the cardiac hemodynamic perturbations seen
namic findings, and the degree of mechanical obstruction. with PAH, such as right-sided cardiac and great vessel
342 B.S. Messenger and R.J. Oudiz

Table 19.2 Clinical classification of pulmonary hypertension peripheral arteries, and right-sided cardiac chamber enlarge-
1. Pulmonary arterial hypertension (PAH) ment [3, 5]. The chest radiograph may suggest an underlying
1. Idiopathic PAH cause for PH and is thus recommended in the workup of sus-
2. Heritable pected PH.
BMPR2 mutation (familial or isolated) Right-sided heart catheterization (RHC) is the most accu-
ALK1, endoglin (with or without hereditary hemorrhagic rate test for determining cardiopulmonary hemodynamics
telangiectasia) and remains the gold standard by which the diagnosis of PH
Unknown is made and hemodynamic severity is calculated. A RHC is
3. Drug- and toxin-induced required not only to confirm the presence and the severity of
4. Associated with PH, but also to exclude left-sided heart disease, potentially
Connective tissue diseases correctable intracardiac left-to-right shunting, and to per-
HIV infection form acute vasodilator testing.
Portal hypertension Because the signs and symptoms of PH are non-specific
Congenital heart diseases
and there is no reliable non-invasive test for its detection,
Schistosomiasis
patients often undergo computed tomography (CT) as part of
Chronic hemolytic anemia
their diagnostic work-up. CT is able to evaluate the lung
5. Persistent pulmonary hypertension of the newborn
parenchyma (for interstitial or emphysematous changes), the
6. Pulmonary veno-occlusive disease (PVOD)
pulmonary artery (calcification, dilation, embolism, patent
and/or pulmonary capillary hemangiomatosis (PCH)
ductus), the pulmonary veins, the cardiac chambers (hyper-
2. Pulmonary hypertension due to left heart disease
trophy, dysplasia, enlargement, thrombus, septal defects),
1. Systolic dysfunction
the coronary vessels, and the IVC simultaneously.
2. Diastolic dysfunction
It is important to be aware of the CT findings that may
3. Valvular disease
suggest the diagnosis of PH, such as an enlarged main pul-
3. Pulmonary hypertension due to lung diseases and/or hypoxia
1. Chronic obstructive pulmonary disease
monary artery (Figs. 19.5). Radiographically, PH is said to
2. Interstitial lung disease
be more likely when the main pulmonary artery diameter
3. Other pulmonary diseases with mixed restrictive and (MPAD) is ≥29 mm (sensitivity 69 %, specificity 100 %) [6,
obstructive pattern 7] and/or the ratio of the main pulmonary artery to ascending
4. Sleep-disordered breathing aorta diameter is >1 (sensitivity 70.8 % and specificity
5. Alveolar hypoventilation disorders 76.5 %) [8, 68]. Others have reported that the most specific
6. Chronic exposure to high altitude CT findings for the presence of PH were both a MPAD
7. Developmental abnormalities ≥29 mm and segmental artery-to-bronchus ratio of >1:1 in
4. Chronic thromboembolic pulmonary hypertension (CTEPH) three or four lobes (specificity 100 %) [9]. In addition, the
5. Pulmonary hypertension with unclear multifactorial MPAD correlates with the severity of pulmonary hyperten-
mechanisms sion; two studies have defined the upper limit of normal for
1. Hematologic disorders: myeloproliferative disorders, main pulmonary artery diameter as 32 mm [6, 10]. An addi-
splenectomy
tional feature of PH is rapid tapering or “pruning” of the dis-
2. Systemic disorders: sarcoidosis, pulmonary Langerhans cell
histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, tal pulmonary vessels (Fig. 19.5).
vasculitis With improvements in ECG-gated CT technology, newer
3. Metabolic disorders: glycogen storage disease, Gaucher methods have been developed with similar accuracy in pre-
disease, thyroid disorders dicting the presence of PH. Revel et al. demonstrated that a
4. Others: tumoral obstruction, fibrosing mediastinitis, chronic reduction in distensibility of the right pulmonary artery has a
renal failure on dialysis high specificity for PH[69]. Distensibility is determined by
ALK1 activin receptor-like kinase type1, BMPR2 bone morphogenetic evaluating the change in cross-sectional area of the right PA
protein receptor type2
during systole compared with diastole. The difference in
maximum area from the minimum area is divided by the
chamber enlargement and dysfunction, flattening of the maximum area and multiplied by 100 to get a percentage of
interventricular septum, and pericardial effusion. distensibility. A value of less than 16.5 % had 86 % sensitiv-
Echocardiography is also useful for evaluating congenital ity and 96 % specificity for PH [69]. RV thickness is a known
heart disease and left-sided heart disease. finding in PH with RV free wall thickness >6 mm (81 % sen-
Suggested radiographic imaging includes a chest x-ray sitivity and 91 % specificity), RV/LV lumen ratio >1.28 (sen-
and, depending on the need, CT radiography. The chest sitivity of 85 % and specificity of 86 %), and RV wall/LV
radiographic findings of PH are hilar fullness characteristic wall ratio >0.32 as accurate predictors of PH [70]. With a
of dilated central pulmonary arteries, pruning of the high degree of specificity, CT imaging provides important
19 Assessment of Pulmonary Vascular Disease 343

Fig. 19.6 64 slice multi-detector CT in a 44 year-old man with secon-

dum atrial septal defect (ASD) and pulmonary hypertension demon-
strating right atrial (RA) and right ventricular (RV) enlargement

Fig. 19.5 Electron Beam CT scan in a 22 year-old woman (a) and 64

slice multi-detector CT in a 40 year-old man (b), both with pulmonary
hypertension. Pulmonary arteries (PA) are enlarged and tapering dis-
tally, with an increased main PA to aorta ratio

evidence for pulmonary hypertension that should prompt cli-

nicians to pursue a workup for pulmonary hypertension.
The presence of calcification in the pulmonary arteries
suggests more severe disease [9], as does pericardial thicken-
ing and/or effusion [12]. Some studies have reported that
hypertrophy of the bronchial artery occurs frequently in
patients with idiopathic PAH (IPAH) and Eisenmenger’s Fig. 19.7 64 slice multi-detector CT in a 31 year-old man with sinus
syndrome [13, 14]. These studies also reported that pulmo- venosum atrial septal defect (ASD) and pulmonary hypertension dem-
nary artery thromboses and aneurysms were common in onstrating right atrial (RA) dilation and right ventricular (RV) hypertro-
phy, and flattening of the inter-ventricular septum (black arrow),
patients with congenital heart disease (CHD) as compared to indicating high right sided pressures
patients with IPAH, while dilation and mural calcification
was seen in similar frequency in both groups [13].
It is generally accepted that in patients with chronic, unre- As the right ventricle enlarges, the interventricular sep-
paired systemic-to-pulmonary shunts the CT findings can tum becomes flattened (Fig. 19.7) and eventually convex to
appear very similar to those found in precapillary pulmonary the left side [15–17], and thus septal flattening is a com-
hypertension such as IPAH and PAH associated with connec- monly noted cardiac abnormality found in patients with PH
tive tissue disease, portal hypertension, and HIV infection. [18]. If cine-CT is performed, reduced right ventricular sys-
Commonly, right (or pulmonic) ventricular hypertrophy is tolic function may also be present. The presence of retro-
seen, with right ventricular enlargement and associated right grade opacification of the inferior vena cava or hepatic vein
atrial enlargement (Fig. 19.6). during contrast-enhanced CT may be a nonspecific sign of
344 B.S. Messenger and R.J. Oudiz

echocardiographic data, but cine-CT provides the necessary

axial images of the LV in systole and diastole to calculate the
index.
Although CT imaging of the great vessels is a simple and
straightforward noninvasive methodology, it has not gained
widespread acceptance as a screening test for PH [1].
Table 19.1 summarizes the CT findings of PH. While CT
cannot diagnose pulmonary hypertension, clinicians should
be aware that a wealth of information regarding the end
result of the chronic hemodynamic effect of PH upon cardio-
vascular anatomy. A diagnosis and its underlying etiology
may be highly suggested by closely evaluating the pulmo-
nary vasculature and cardiac anatomy on CT imaging.

References
1. Vonk-Noordegraaf A, Haddad F, Chin KM, Forfia PR, Kawut SM,
Lumens J, Naeije R, Newman J, Oudiz RJ, Provencher S, Torbicki
A, Voelkel NF, Hassoun PM. Right heart adaptation to pulmonary
arterial hypertension: physiology and pathobiology. J Am Coll
Cardiol. 2013;62(25 Suppl):D22–33.
2. Simonneau G, Gatzoulis MA, Adatia I. Updated clinical classifica-
Fig. 19.8 64 slice multi-detector CT in a 26 year-old man with anola-
tion of pulmonary hypertension. J Am Coll Cardiol.
mous pulmonary venous return and pulmonary hypertension demon-
2013;62(25_S):D34–41.
strating right atrial dilation and right ventricular hypertrophy, and
3. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009
dilated inferior vena cava with swirling of white contrast (black arrow),
expert consensus document on pulmonary hypertension a report of
indicating severe tricuspid regurgitation
the American College of Cardiology Foundation Task Force on
Expert Consensus Documents and the American Heart Association
developed in collaboration with the American College of Chest
significant pulmonary hypertension and/or right ventricular Physicians; American Thoracic Society, Inc.; and the Pulmonary
dysfunction [19] (Fig. 19.8). Hypertension Association. J Am Coll Cardiol. 2009;53:1573–619.
4. McLaughlin VV, Presberg KW, Doyle RL. Prognosis of pulmonary
Although hemodynamics cannot be directly measured
arterial hypertension: ACCP evidence-based Clinical Practice
with CT, the sequelae of chronic pulmonary hypertension Guidelines. Chest. 2004;126(1_suppl):78S–92.
can be seen with structural cardiac changes. The increased 5. Brown LM, Chen H, Halpern S, Taichman D, McGoon MD, Farber
pulmonary vascular resistance that occurs with PH places HW, Frost AE, Liou TG, Turner M, Feldkircher K, Miller DP,
Elliott CG. Delay in recognition of pulmonary arterial hyperten-
greater strain on the right ventricle. Right ventricular hyper-
sion: factors identified from the REVEAL Registry. Chest.
trophy (>6 mm thickness) is a common finding, and as the 2011;140:19–26.
RV begins failing in the setting of persistently elevated after- 6. Rich S, Dantzker DR, Ayres SM, et al. Primary pulmonary hyper-
load, an increased in RV end diastolic volume will occur tension: a national prospective study. Ann Intern Med. 1987;
107:216–23.
[71]. RV enlargement leads to increasing RV pressure and
7. Loyd JE, Butler MG, Foroud TM, Conneally PM, Phillips JA,
volume, which are reflected in the bowing of the interven- Newman JH. Genetic anticipation and abnormal gender ratio at
tricular septum. CT findings of RV/LV >1 and LV septal flat- birth in familial primary pulmonary hypertension. Am J Respir Crit
tening are sensitive and specific markers for PH. In small Care Med. 1995;152:93–7.
8. Cogan JD, Pauciulo MW, Batchman AP, et al. High frequency of
studies by Contractor et al and Lim et al, found these signs
BMPR2 exonic deletions/duplications in familial pulmonary arte-
had a sensitivity of 78 %–92 % and a specificity of 100 % for rial hypertension. Am J Respir Crit Care Med. 2006;174:590–8.
echocardiographic findings of RV dysfunction. [71–73] 9. Aldred MA, Vijayakrishnan J, James V, et al. BMPR2 gene rear-
Systolic eccentricity index (sEi) correlates well with pulmo- rangements account for a significant proportion of mutations in
familial and idiopathic pulmonary arterial hypertension. Hum
nary hypertension severity [74]. In normal conditions, the
Mutat. 2006;27:212–3.
LV cavity is shaped like a circle. With increasing RV pres- 10. Machado RD, Aldred MA, James V, et al. Mutations of the TGF- β
sure and volume overload, the septal wall flattening leads to type II receptor BMPR2 in pulmonary arterial hypertension. Hum
a deformed, D-shaped left ventricle. The length of the sep- Mutat. 2006;27:121–32.
11. Thomson JR, Machado RD, Pauciulo MW, et al. Sporadic primary
tum (D1) becomes longer than the width of the LV cavity
pulmonary hypertension is associated with germline mutations of
(D2), with a ratio of D1/D2 >1 (normal score is 1) that is the the gene encoding BMPR-II, a receptor member of the TGF-β fam-
eccentricity score [74]. Most studies have evaluated sEi with ily. J Med Genet. 2000;37:741–5.
19 Assessment of Pulmonary Vascular Disease 345

12. Chaouat A, Coulet F, Favre C, et al. Endoglin germline mutation in 32. Hoffman JI, Rudolph AM. The natural history of ventricular septal
a patient with hereditary haemorrhagic telangiectasia and dexfen- defects in infancy. Am J Cardiol. 1965;16:634–53.
fluramine associated pulmonary arterial hypertension. Thorax. 33. Galiè N, Manes A, Palazzini M, et al. Management of pulmonary
2004;59:446–8. arterial hypertension associated with congenital systemic-to pul-
13. Trembath RC, Thomson JR, Machado RD, et al. Clinical and monary shunts and Eisenmenger’s syndrome. Drugs.
molecular genetic features of pulmonary hypertension in patients 2008;68:1049–66.
with hereditary hemorrhagic telangiectasia. N Engl J Med. 34. Fernandes C, Jardim C, Honanian A, Hoette S, Morinaga LK,
2001;345:325–34. Souza R. Schistosomiasis and Pulmonary Hypertension. Pulmonary
14. McGoon M, Gutterman D, Steen V, et al. Screening, early detec- Vascular Disorders. Prog Respir Res. Basel. Karger.
tion, and diagnosis of pulmonary arterial hypertension: ACCP evi- 2012;41:143–8.
dencebased clinical practice guidelines. Chest. 2004;126:14S–34. 35. Shaw AP, Ghareed A. The pathogenesis of pulmonary schistoso-
15. Hachulla E, Gressin V, Guillevin L, et al. Early detection of pulmo- miasis in Egypt with special reference to Ayerza’s disease. J Pathol
nary arterial hypertension in systemic sclerosis: a french nation- Bacteriol. 1938;46:401–24.
wide prospective multicenter study. Arthritis Rheum. 36. de Cleva R, Herman P, Pugliese V, et al. Prevalence of pulmonary
2005;52:3792–800. hypertension in patients with hepatosplenic mansonic schistosomi-
16. Mukerjee D, St George D, Coleiro B, et al. Prevalence and outcome asis- prospective study. Hepatogastroenterology. 2003;50:
in systemic sclerosis associated pulmonary arterial hypertension: 2028–30.
application of a registry approach. Ann Rheum Dis. 2003; 37. Lapa MS, Ferreira EV, Jardim C, Martins Bdo C, Arakaki JS, Souza
62:1088–93. R. Clinical characteristics of pulmonary hypertension patients in
17. Tanaka E, Harigai M, Tanaka M, Kawaguchi Y, Hara M, Kamatani two reference centers in the city of Sao Paulo. Rev Assoc Med Bras.
N. Pulmonary hypertension in systemic lupus erythematosus: eval- 2006;52:139–43.
uation of clinical characteristics and response to immunosuppres- 38. Chaves E. The pathology of the arterial pulmonary vasculature in
sive treatment. J Rheumatol. 2002;29:282–7. Manson’s schistosomiasis. Chest. 1966;50:72–7.
18. Asherson RA, Higenbottam TW, Dinh Xuan AT, Khamashta MA, 39. Papamatheakis DG, Mocumbi AOH, Kim NH, Mandel
Hughes GR. Pulmonary hypertension in a lupus clinic: experience J. Schistosomiasis-associated pulmonary hypertension. Pulmonary
with twenty-four patients. J Rheumatol. 1990;17:1292–8. Circulation. 2014;4:596–611.
19. Burdt MA, Hoffman RW, Deutscher SL, Wang GS, Johnson JC, 40. Grosse C, Grosse A. CT findings in diseases associated with pulmo-
Sharp GC. Long-term outcome in mixed connective tissue disease: nary hypertension: a current review. Radiographics. 2010;30(7):
longitudinal clinical and serologic findings. Arthritis Rheum. 1753–77.
1999;42:899–909. 41. Mandel J, Mark EJ, Hales CA. Pulmonary veno-occlusive disease.
20. Jaïs X, Launay D, Yaici A, et al. Immunosuppressive therapy in Am J Respir Crit Care Med. 2000;162:1964–73.
lupus- and mixed connective tissue disease-associated pulmonary 42. Frazier AA, Franks TJ, Mohammed TL, Ozbudak IH, Galvin
arterial hypertension: a retrospective analysis of twenty-three cases. JR. From the archives of the AFIP: pulmonary veno-occlusive dis-
Arthritis Rheum. 2008;58:521–31. ease and pulmonary capillary hemangiomatosis. Radiographics.
21. Launay D, Hachulla E, Hatron PY, Jaïs X, Simonneau G, Humbert 2007;27:867–82.
M. Pulmonary arterial hypertension: a rare complication of primary 43. Holcomb Jr BW, Loyd JE, Ely EW, Johnson J, Robbins
Sjögren syndrome: report of 9 new cases and review of the litera- IM. Pulmonary veno-occlusive disease: a case series and new
ture. Medicine (Baltimore). 2007;86:299–315. observations. Chest. 2000;118:1671–9.
22. Bunch TW, Tancredi RG, Lie JT. Pulmonary hypertension in poly- 44. Resten A, Maitre S, Humbert M, et al. Pulmonary hypertension: CT
myositis. Chest. 1981;79:105–7. of the chest in pulmonary veno-occlusive disease. Am J Roentgenol.
23. Dawson JK, Goodson NG, Graham DR, Lynch MP. Raised pulmo- 2004;183:65–70.
nary artery pressures measured with doppler echocardiography in 45. Lantuéjoul S, Sheppard MN, Corrin B, Burke MM, Nicholson
rheumatoid arthritis patients. Rheumatology (Oxford). AG. Pulmonary veno-occlusive disease and pulmonary capillary
2000;39:1320–5. hemangiomatosis: a clinicopathologic study of 35 cases. Am J Surg
24. Coghlan JG, Handler C. Connective tissue associated pulmonary Pathol. 2006;30:850–7.
arterial hypertension. Lupus. 2006;15:138–42. 46. Ozsoyoglu AA, Swartz J, Farver CF, Mohammed TL. High resolu-
25. Lettieri CJ, Nathan SD, Barnett SD, et al. Prevalence and outcomes tion computed tomographic imaging and pathologic features of pul-
of pulmonary arterial hypertension in advanced idiopathic pulmo- monary veno-occlusive disease: a review of three patients. Curr
nary fibrosis. Chest. 2006;129:746–52. Probl Diagn Radiol. 2006;35:219–23.
26. Corte TJ, et al. Pulmonary hypertension in idiopathic pulmonary 47. Montani D, Achouh L, Dorfmuller P. Pulmonary venoocclusive dis-
fibrosis: a review. Sarcoidosis Vasc Diffuse Lung Dis. 2009; ease: clinical, functional, radiologic, and hemodynamic character-
26:7–19. istics and outcome of 24 cases confirmed by histology.
27. Zisman DA, Karlamangla AS, Ross DJ, et al. High-resolution chest Medicine(Baltimore). 2008;87:220–33.
CT findings do not predict the presence of pulmonary hypertension 48. Rabiller A, Jaïs X, Hamid A, et al. Occult alveolar haemorrhage in
in advanced idiopathic pulmonary fibrosis. Chest. 2007; pulmonary veno-occlusive disease. Eur Respir J. 2006;27:108–13.
132:773–9. 49. Resten A, Maitre S, Humbert M, Rabiller A, Sitbon O, Capron F,
28. Eisenmenger V. Die angeborene defecte der kammersheidewand Simonneau G, Musset D. Pulmonary hypertension: CT of the chest
das herzen. Z Klin Med. 1897;132:131. in pulmonary venoocclusive disease. AJR Am J Roentgenol.
29. Wood P. The Eisenmenger syndrome or pulmonary hypertension 2004;183:65–70.
with reversed central shunt. Br Med J. 1958;2:701–9. 50. Fraser KL, Tullis DE, Sasson Z, Hyland RH, Thornley KS, Hanly
30. Daliento L, Somerville J, Presbitero P, et al. Eisenmenger syn- PJ. Pulmonary hypertension and cardiac function in adult cystic
drome: factors relating to deterioration and death. Eur Heart fibrosis: role of hypoxemia. Chest. 1999;115:1321–8.
J. 1998;19:1845–55. 51. Cottin V, Nunes H, Brillet PY, et al. Combined pulmonary fibrosis
31. Besterman E. Atrial septal defect with pulmonary hypertension. Br and emphysema: a distinct underrecognised entity. Eur Respir
Heart J. 1961;23:587–98. J. 2005;26:586–93.
346 B.S. Messenger and R.J. Oudiz

52. Chaouat A, Bugnet AS, Kadaoui N, et al. Severe pulmonary hyper- 64. Qanadli SD, Hajjam ME, Mesurolle B. Pulmonary embolism detec-
tension and chronic obstructive pulmonary disease. Am J Respir tion. Prospective evaluation of dual-section helical CT versus selec-
Crit Care Med. 2005;172:189–94. tive pulmonary arteriography in 157 patients. Radiology.
53. Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, 2000;217:447–55.
Melton 3rd LJ. Trends in the incidence of deep vein thrombosis and 65. Winer-Muram HT, Rydberg J, Johnson MS, et al. Suspected acute
pulmonary embolism: a 25-year population-based study. Arch pulmonary embolism: evaluation with multi-detector row CT ver-
Intern Med. 1998;158:585–93. sus digital subtraction pulmonary arteriography. Radiology.
54. Tapson VF. Acute pulmonary embolism. N Engl J Med. 2004;233:806–15.
2008;358:1037–52. 66. Tapson VF, Humbert M. Incidence and prevalence of chronic
55. Heit JA. The epidemiology of venous thromboembolism in the thromboembolic pulmonary hypertension: from acute to chronic
community. Arterioscler Thromb Vasc Biol. 2008;28:370–2. pulmonary embolism. Proc Am Thorac Soc. 2006;3:564–7.
56. Sandler DA, Martin JF. Autopsy proven pulmonary embolism in 67. Pengo V, Lensing AW, Prins MH, et al. Incidence of chronic throm-
hospital patients: are we detecting enough deep vein thrombosis? boembolic pulmonary hypertension after pulmonary embolism. N
J R Soc Med. 1989;82:203–5. Engl J Med. 2004;350:2257–64.
57. Kumar A, Ouriel K. Handbook of endovascular interventions. 68. Wells JM, Dransfield MT. Pathophysiology and clinical implica-
New York: Springer Science & Business Media; 2012. p. 404. tions of pulmonary arterial enlargement in COPD. Int J Chron
58. Elliott CG. Chest radiographs in acute pulmonary embolism: results Obstruct Pulmon Dis. 2013;8:509–21.
from the international cooperative pulmonary embolism registry. 69. Revel MP, Faivre JB, Remy-Jardin M, Delannoy-Deken V, Duhamel
Chest. 2000;118:33–8. A, Remy J. Pulmonary hypertension: ECG-gated 64-section CT
59. Stein PD, Terrin ML, Hales CA, Palevsky HI, Saltzman HA, angiographic evaluation of new functional parameters as diagnostic
Thompson BT, Weg JG. Clinical, laboratory, roentgenographic and criteria. Radiology. 2009;250:558–66.
electrocardiographic findings in patients with acute pulmonary 70. Chan AL, Juarez MM, Shelton DK, MacDonald T, Li CS, Lin C,
embolism and no pre-existing cardiac or pulmonary disease. Chest. Albertson TE. Novel computed tomographic chest metrics to detect
1991;100:598–603. pulmonary hypertension. BMC Med Imaging. 2011;11:7.
60. Stein PD, Willis III PW, DeMets DL, Greenspan RH. Plain chest 71. Ghaye B, Ghuysen A, Bruyere PJ, D'Orio V, Dondelinger RF. Can
roentgenogram in patients with acute pulmonary embolism and no CT pulmonary angiography allow assessment of severity and prog-
pre-existing cardiac or pulmonary disease. Am J Noninvas Cardiol. nosis in patients presenting with pulmonary embolism? What the
1987;1:171–6. radiologist needs to know. Radiographics. 2006;26:23–39.
61. Tunariu N, Gibbs SJ, Win Z, Gin-Sing W, Graham A, Gishen P, 72. Contractor S, Maldjian PD, Sharma VK, Gor DM. Role of helical
Al-Nahhas A. Ventilation-perfusion scintigraphy is more sensitive CT in detecting right ventricular dysfunction secondary to acute
than multidetector CTPA in detecting chronic thromboembolic pul- pulmonary embolism. J Comput Assist Tomogr. 2002;26:587–91.
monary disease as a treatable cause of pulmonary hypertension. 73. Lim KE, Chan CY, Chu PH, Hsu YY, Hsu WC. Right ventricular
J Nucl Med. 2007;48:680–4. dysfunction secondary to acute massive pulmonary embolism
62. He J, Fang W, Lv B, et al. Diagnosis of chronic thromboembolic detected by helical computed tomography pulmonary angiography.
pulmonary hypertension: comparison of ventilator/perfusion scan- Clin Imaging. 2005;29:16–21.
ning and multidetector computed tomography pulmonary angiogra- 74. López-Candales A, Bazaz R, Edelman K, Gulyasy B. Apical
phy with pulmonary angiography. Nucl Med Commun. systolic eccentricity index: a better marker of right ventricular com-
2012;33:459–63. promise in pulmonary hypertension. Echocardiography. 2010;
63. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed 27:534–8.
tomography for acute pulmonary embolism. N Engl J Med.
2006;354:2317–27.
 Part V
Multidisciplinary Topics
 Value Based Imaging for Coronary
Artery Disease: Implications for Nuclear 20
Cardiology and Cardiac CT

Daniel S. Berman, Alan Rozanski, Piotr Slomka,

Rine Nakanishi, Damini Dey, John D. Friedman,
Sean W. Hayes, Louise E.J. Thomson, Reza Arsanjani,
Rory Hachamovitch, James K. Min, Leslee J. Shaw,
and Guido Germano

Abstract
Technology in cardiac computed tomography (CT) and nuclear cardiology is constantly
improving. In single photon emission CT (SPECT), new cameras, reconstruction methods,
and protocols have dramatically reduced radiation doses to patients. In positron emission
tomography (PET), application of quantitative measurements of myocardial perfusion
reserve is improving assessment of prognosis. PET/CT is routinely performed in conjunc-
tion with coronary artery calcium (CAC) scanning in many centers, extending the ability of
myocardial perfusion imaging (MPI) studies to impact patient management. In cardiac CT,
marked improvements in equipment and reconstruction software have also dramatically
reduced the patient radiation associated with cardiac testing, and have reduced the fre-
quency of non-diagnostic studies. New methods for combining anatomic and functional
assessment with CT—CT perfusion and FFRCT measurements—are beginning to be used
clinically. With the expanding capabilities of each technology, their opportunities to provide
value increases. Given the changing reimbursement paradigm from a volume-based to a
value-based system, the applications of each technology that will survive are those that
improve relationship between outcomes and costs. With respect to coronary artery disease
(CAD), a growing body of evidence exists regarding the value of specific tests in the various
clinical settings in which CAD is considered. For prevention, data is strong in that CAC
scanning can provide value by improving outcomes. In the patient with acute chest pain,
CCTA appears to be able to shorten time in the hospital and reduce costs. In patients with

D.S. Berman, MD (*) • P. Slomka, PhD • D. Dey, PhD

J.D. Friedman, MD • S.W. Hayes, MD • L.E.J. Thomson, MBChB
R. Arsanjani, MD • G. Germano, PhD R. Hachamovitch, MD
Departments of Imaging and Medicine, Department of Nuclear Medicine, Cleveland Clinic,
Cedars-Sinai Medical Center and the Cedars-Sinai Heart Institute, Heart and Vascular Institute, Cleveland, OH, USA
Los Angeles, CA, USA
J.K. Min, MD, FACC
e-mail: [email protected]
Department of Radiology, Dalio Institute of Cardiovascular Imaging,
A. Rozanski, MD Weill Cornell Medical College and the NewYork Presbyterian
Division of Cardiology, Mt. Sinai Saint Luke’s Hospital, New York, NY, USA
and Roosevelt Hospitals, New York, NY, USA
L.J. Shaw, PhD
R. Nakanishi, MD, PhD Department of Medicine, Emory Clinical Cardiovascular
Department of Medicine, Los Angeles Biomedical Research Research Institute, Emory University School of Medicine,
Institute at Harbor-UCLA, Torrance, CA, USA Atlanta, GA, USA

© Springer International Publishing 2016 349

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_20
350 D.S. Berman et al.

suspected stable ischemic heart disease and an intermediate pre-test likelihood of CAD, the
use of CCTA appears to be valuable. In patients who have known CAD or in whom a
nondiagnostic CCTA is likely, improvement in outcomes based on CCTA is less likely and
testing for ischemia may be preferred. In patients with a very high likelihood of CAD or
known CAD, registry data suggests that ischemia testing, such as that provided by SPECT-
or PET-MPI studies, may improve outcomes by improving selection of patients for revascu-
larization. The ISCHEMIA trial will test whether a strategy basing decisions for
revascularization on noninvasive assessment of ischemia improves outcomes. Test selection
is highly dependent on accurate pretest risk assessment. An updated method for assessment
of pre-test risk has developed which may lead to improved utilization of cardiac imaging
procedures. In all of the applications of noninvasive imaging, value can only be achieved if
the appropriate patients are selected for testing and if the test result changes management,
such that outcomes can be improved or costs reduced.

Keywords
SPECT-MPI • PET-MPI • Myocardial perfusion imaging • Single photon emission computed
tomography • Positron emission tomography • Cardiac CT • Coronary CT angiography •
Coronary artery calcium scanning

Introduction to the study, including cost increases due to downstream

testing and therapies and cost decreases due to more effi-
The rapid evolution of new medical technologies and ther- cient care from reduced unnecessary downstream testing
apies and the increasing numbers of patients being studied and therapies. In the future, whether the payer is the gov-
or treated based on these developments are leading to an ernment, insurance companies, or the patients themselves,
unsustainable increase in health care costs. In the United it is likely that only those approaches that provide value
States, through legislation such as the Affordable Care will be purchased. In imaging, this implies an increasing
Act, a transition from a volume-based health care reim- penetrance of value-based imaging, with growth in testing
bursement to a value-based reimbursement. Over the past in areas of proven value and reduction of testing in areas in
few decades, there has been a rise in the use of imaging which value has not been shown.
that parallels that of the overall rise in healthcare costs. In this chapter, we review the technologic developments
While efforts such as implementation of Appropriate Use in the nuclear cardiology and cardiac CT in light of advances
Criteria have slowed the rise in these expenses, a contin- that are likely to improve value and then to explore the poten-
ued increase in overall imaging costs is still occurring. It is tial “value proposition” of these modalities in the various
virtually inevitable that value-based medical care reim- clinical settings of suspected or known CAD in which they
bursement will be increasingly the norm and will apply to are applied.
most of the use of medical imaging.
What is value in imaging? Inherently, as with any com-
modity, value is a function of quality and cost (Fig. 20.1).
In cardiology, quality ultimately implies improvement in
patient outcomes. In the patient with coronary artery dis-
ease (CAD), these outcomes might reduce cardiac events
such as death or myocardial infarction or improvement in
quality of life. Other measures of quality include accuracy
of diagnosis, efficiency of service for the patient, and
reduction of any harm that might be associated with the
care such as radiation, or complications from unnecessary
invasive diagnostic or therapeutic procedures. Value is
inversely related to costs, which are not only the costs of
the imaging studies themselves, but all of the costs related Fig. 20.1 Value-based imaging: concepts
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 351

Technologic Developments Added value of machine learning combining supine and prone
SPECT-MPI and clinical data
a
Nuclear Cardiology Entire population: (N = 1181)
1.0
In the last several years, there have been several advances in 0.9
the technology of nuclear cardiology including single photon 0.8
emission computed tomography (SPECT) and positron emis- 0.7 Area

Sensitivity
sion tomography (PET) for myocardial perfusion imaging 0.6 ML: Quantitative + Clinical 0.94 ± 0.01**
(MPI). One of the primary areas of advantage of nuclear car- 0.5 ML: Quantitative Only 0.90 ± 0.01*
diology methods is the degree to which automated, objective 0.4
quantitative analysis is available and implemented in practice. TPD 0.88 ± 0.01
0.3
These methods are becoming increasingly automatic. They 0.2 *Better than TPD (p<0.001)
reduce the dependence on local expertise in interpretation, **Better than TPD and ML Quantitative (p<0.0001)
0.1 ML – Machine Learning
leading to increased reliability of the measurements across 0.0
TPD – Total Perfusion Deficit

laboratories. Importantly, automated assessment has a dra- 0.0 0.2 0.4 0.6 0.8 1.0
matic effect on reproducibility of measurements, which is 1 - Specificity
highly important in serial assessment. While the reproduc-
ibility of subjective visual assessment is poor, very high Entire population: (N = 1181)
reproducibility of quantitative measurements has been shown b
1.0
by documented in multiple patient populations [1–3]. 0.9
Recently, advanced automated quantitation has been shown 0.8
to improve accuracy of diagnosis of CAD compared to expert 0.7 Area
visual interpretations [4]. Further, the introduction of machine
Sensitivity

0.6
ML: Quantitative + Clinical 0.94 ± 0.01*
learning, in which the computer is provided all of the vari- 0.5
ables available to the clinician, SPECT MPI has been shown Expert 1: MPS + Clinical 0.89 ± 0.01
0.4
to provide greater accuracy for CAD detection than either Expert 2: MPS + Clinical 0.85 ± 0.01
0.3
expert visual or quantitative perfusion defect assessment [4]
0.2 *Better than Expert 1 and Expert 2 (p < 0.0001)
(Fig. 20.2; Courtesy Ref. [4]). It is likely that quantitative ML – Machine Learning
0.1 MPS – Myocardial Perfusion SPECT
analysis with machine learning will become routine in nuclear
0.0
cardiology laboratories. 0.0 0.2 0.4 0.6 0.8 1.0
Specifically pertinent to SPECT, recent camera and 1 - Specificity
computer developments have been introduced that improve
image quality [5]. The introduction of CZT detector cameras Fig. 20.2 ROC curves comparing the machine learning (ML) algo-
has resulted in increased counting efficiency (sensitivity), rithm of quantitative + clinical data (red): (a): vs ML of quantitative
SPECT-MPI data alone (blue) and total perfusion deficit alone (green).
which can be employed to reduce time of procedures or (b): vs expert visual analysis of supine and prone SPECT-MPI (MPS)
administered radiation doses, while at the same time including clinical data by expert 1 (blue) and expert 2 (green) for the
improving resolution [6]. With these cameras, the ability to detection of obstructive coronary artery disease (Reprinted from
perform SPECT MPI with as little as 3 mCi of Tc-99m has Arsanjani et al. [4] with permission from Springer)
been reported, with an associated radiation dose of approxi-
mately 1 mSv to the patient [7, 8]. One of these cameras has
been shown to be accurate for detection of CAD even in the possible. To accomplish this, either attenuation correction
morbidly obese patient (Fig. 20.3; Courtesy Ref. [9]), imaging or two view (prone supine or upright/supine) is
allowing cardiac imaging of patients up to 500 lb—perhaps important to reduce the effects of soft tissue attenuation,
unachievable with any other modality at this time [9]. New particularly important when a rest and stress examination
approaches to reconstruction of raw data have also become cannot be compared [12, 13]. Numerous publications have
available for use with standard sodium-iodide detector documented that a normal stress only study is associated
Anger cameras, which allow for shorter imaging time or with excellent patent prognosis, which is equal to that asso-
reduced radiation dose [10, 11]. Protocols have also ciated with rest/stress studies (Fig. 20.4; Courtesy Ref. [14])
changed, with stress first sequences, as were used in the ini- [14, 15]. In 2015 at Cedars-Sinai, stress only studies, with a
tial SPECT imaging applications with Tl-201, becoming radiation dose to the patients of <2 mSv, was performed in
more common. With these, stress only studies become nearly 40 % of cases.
352 D.S. Berman et al.

Fig. 20.3 Case example of high SPECT-MPI image quality obtained with a CZT camera using moving detectors in a 48 year old male with body
mass index (BMI) 60. U upright; S supine; TPD total perfusion deficit (Reprinted from Nakazato et al. [9] with permission from Springer)

Prognosis of normal stress-only

vs standard stress/rest SPECT-MPI

1.0

0.9
% Survival

0.8
Log-rank p = 0.02 (unadjusted)
0.7 p = 0.89 (adjusted)

0.6
Stress-Only
0.5 Stress + Rest

0 2 4 6 8
Fig. 20.4 Kaplan-Meier survival curves according to SPECT-MPI Years
protocol for patients undergoing stress-only (red; n = 8034) or Number at risk
stress + rest (blue; n = 8820) imaging (Reprinted from Chang et al. Stress-only 8034 6996 4981 3243 1196
[14] with permission from Elsevier) Stress+rest 8820 7413 4525 2107 732
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 353

Fig. 20.5 Unadjusted

annualized cardiac mortality by
tertiles of CFR and categories of
stress PET-MPI perfusion defect
(PD). CD cardiac mortality. 9
(Reprinted from Murthy et al.
[18] with permission from
Wolters Kluwer Health, Inc)

Important advances have also been made in PET. For identification of diffuse epicardial disease and microvascular
PET-MPI, perhaps the most important of these has been the dysfunction, which have their own prognostic and therapeu-
incorporation of absolute quantitative myocardial perfusion tic implications beyond those associated with assessment of
measurement. Referred to as myocardial perfusion reserve an individual coronary lesion [20, 21].
(MFR) or coronary flow reserve (CFR)—or absolute peak The existing PET or SPECT myocardial perfusion tracers
stress perfusion measurements—these assessments have are not ideal. One problem of the existing myocardial perfu-
now become available through the major software vendors sion tracers is that their uptake in the myocardium is not lin-
and excellent correlation between the methods has been ear with respect to flow at high flow rates. A new
shown [16, 17]. These methods, using the widely available radiopharmaceutical currently in clinical trials overcomes
tracer Rb-82, have also validated by comparison with N-13 this and other limitations of the currently used tracers.
ammonia PET [17]. The prognostic value of these absolute Flurpiridaz F-18 is linearly extracted across the range of
flow measurements has been documented in a large number flow, providing greater contrast within a perfusion defect
of clinical studies. Importantly, the added prognostic value compared to a normal zone than is achieved with Tc-99m
of these measurements when combined with standard rela- sestamibi [22–24] (Fig. 20.6; Courtesy Ref. [24]). This is
tive perfusion PET-MPI assessments has been shown [18, also likely to be true with respect to Rb-82, which has shown
19]. For any degree of relative perfusion defect abnormality, a similar plateauing of uptake with respect to flow as the
mortality has been shown to increase according to the degree SPECT agents. F-18 provides superior resolution compared
of abnormality of MFR (Fig. 20.5; Courtesy Ref. [18]). to Rb-82, and due to its 110 min half-life can be used with
These absolute flow measurements provide added value in exercise. It also lends itself to stress only application and
many respects, including the ability to recognize when there does not require an on-site cyclotron [23] or expensive gen-
has been inadequate vasodilation stimulus due to caffeine erator. It has the potential, depending on pricing, to become
intake by the patient—seen as no increase in flow between the PET-MPI agent of choice.
rest and stress. These measurements provide an overall Increasingly, PET-MPI and SPECT-MPI are combining
assessment of myocardial perfusion, which is related not functional and anatomic assessment of patients with sus-
only to the presence of significant epicardial stenosis or ste- pected CAD. PET-MPI is currently almost exclusively per-
noses, but also the status of the microvasculature. This capa- formed with PET/CT scanners [10]. SPECT/CT scanners are
bility provides information that is complementary to the also growing in their use. The use of these hybrid scanners
assessment of fractional flow reserve (FFR), allowing the provides the capability to routinely measure and report the
354 D.S. Berman et al.

Fig. 20.6 Case example of Flurpiridaz F 18 PET (top two rows) vs Flurpiridaz F 18 images. Coronary angiography subsequently demon-
Tc-99m rest SPECT (bottom two rows). The patients was an 87 year old strated subtotal in-stent stenosis. ADENO adenosine; VLA vertical long
woman with shortness of breath 3 months after stenting the left anterior axis; HLA horizontal long axis; MIBI sestamibi (Reprinted with permis-
descending coronary artery. An anterior wall stress perfusion defect is sion from Berman et al. [24] with permission from Elsevier)
seen on both types of scans but is shows greater contrast on the

coronary artery calcium (CAC) score on patients undergoing tions of MPI in detection of epicardial CAD: its reliance on
MPI. This addition of the CAC score has several major the presence of a hemodynamically significant lesion. Over a
advantages. From the standpoint of interpretation, the pres- decade ago, it was recognized that high CAC scores are com-
ence of CAC and its extent provide additional powerful mon in patients with normal SPECT-MPI [25]. By adding
information which can improve the accuracy of interpreta- CAC assessment, the combined MPI/CAC study allows both
tion of MPI when borderline perfusion defects are noted: the assessment of the coronary atherosclerotic burden as well
when the CAC score is 0, the interpreter is able to be confi- as the flow limiting disease [26–28].
dent in considering an “equivocal” perfusion scan as “prob- Finally, molecular imaging is an area of particular strength
ably normal”, while when the CAC is high, the equivocal for nuclear cardiology, taking advantage of the ability of
scan can be considered to be “probably abnormal” (Fig. 20.7). minute amounts of tracer to be employed, such that the
Perhaps most importantly, combining CAC with PET- or administered tracer has no effect on the physiologic effect of
SPECT-MPI assessments overcomes one of the major limita- the molecule. Virtually any biologically active molecule can
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 355

Fig. 20.7 Case example of combined SPECT-MPI and coronary artery fusion study alone. The finding that the CAC score was 1463 (97th per-
calcium scanning (CAC). The patient was a 57 year old male. The centile) resulted in increased observer certainty in interpreting the study
SPECT-MPI study was considered probably abnormal based on the per- as abnormal

be labelled with a PET radioisotope, providing the opportu- they do not assess the activity of disease. It is widely recog-
nity for PET molecular imaging (and for some molecules nized that coronary inflammation plays a pivotal role in the
SPECT imaging) to provide unique insights into pathophysi- development of plaque rupture—the process that triggers
ologic processes. From a practical perspective of broad most myocardial infarctions [32]. Severe coronary stenoses
application in medicine, it must be realized that each tracer can be completely stable, with only fibrous or calcified
developed would need to go through a long and costly devel- plaque, and have minimal likelihood of causing a coronary
opment to reach standard clinical use. However, there are thrombosis. On the other hand large inflamed plaques may
two tracers that are approved by the FDA and widely avail- not cause a coronary stenosis, but could be at high risk of
able that can be applied to the assessment of the patient with rupture [33] (Fig. 20.8). Imaging of coronary plaque inflam-
atherosclerosis. F-18 FDG is widely used for assessment of mation with PET has the potential to assess the activity of
cancer. It has also been used for over 30 years for the assess- CAD. Recently, exciting development has been reported
ment of myocardial viability. Multiple studies have shown with the use of the simple salt-F-18 sodium fluoride—for
that F-18 FDG can also be used for imaging of arterial identification of high risk coronary artery plaque [34, 35].
inflammation, with well-developed application in carotid This agent was used over 40 years ago as a bone scanning
imaging [29]. While not yet a routine clinical tool, FDG tracer. It tracks the active deposition of calcium. In a series of
carotid assessment is already playing an important role in reports, Dweck, Joshi, and Newby have reported that F-18
assessing novel therapies [30, 31]. F-18 FDG can also be fluoride can localize in coronary plaque. In an important
effective in imaging of infection, including infected cardiac study of F-18 fluoride imaging in 80 patients, these investi-
devices and intravenous lines. gators studied 40 patients with acute ischemic syndromes
One of the problems of CAD that is not routinely (ACS) and 40 with stable angina [35]. The found that 93 %
addressed by any of the standard imaging methods is that of the patients with ACS had F-18 fluoride uptake in the area
356 D.S. Berman et al.

Fig. 20.8 Left: Cross-section of a stable atheroma associated with high grade coronary stenosis. Right: Cross-section of an fatal inflamed, lipid
rich plaque which had ruptured, associated with a mild coronary stenosis (Reprinted from Moreno et al. [33] with permission from Elsevier)

found to be the culprit plaque on invasive coronary angiogra- coronary stenosis, not possible with non-contrast CT, CCTA
phy (ICA) (Fig. 20.9; Courtesy Ref. [27]). In the patients allows assessment of noncalcified plaque. Motoyama et al.
with stable angina, 45 % had F-18 fluoride uptake, in each demonstrated that certain adverse characteristics of coronary
corresponding to a lesion with adverse plaque characteristics plaques were associated with increased ACS events [36]
on IVUS. The current paradigm for guiding revasculariza- (Fig. 20.10). Subsequently, considering positive remodeling
tion of patients with stable ischemic heart disease (SIHD) is and low attenuation plaque (associated with lipid content and
to revascularize based on the presence of hemodynamically the size of the necrotic core), these authors demonstrated in
significant stenosis. It is possible that if CAD can be charac- a series of over 1000 patients without obstructive CAD that
terized by the degree of inflammation associated with it, that patients with the number of adverse plaque features as asso-
patients with stenoses but inactive disease might be safely ciated with the frequency of ACS events [37]. Shmilovich
guided toward conservative management rather than toward et al. demonstrated that adverse plaque characteristics added
revascularization. to % stenosis in prediction of myocardial ischemia [38]
(Fig. 20.11 Shmilovich). Subsequently, Nakazato et al. dem-
onstrated that the aggregate plaque volume on CCTA added
Cardiac CT to diameter stenosis in prediction of reduced FFR in interme-
diate coronary lesions [39]. More recently, Park et al. dem-
Cardiac CT has been employed for 20 years for CAC mea- onstrated that positive remodeling on CCTA was associated
surements—performed with minimal radiation, in a single with ischemia-causing lesions across the degrees of coronary
breath, and no contrast. As discussed below, this is a power- artery stenosis [40]. These adverse plaques characteristics
ful tool for prevention in CAD. Coronary CT angiography can be appreciated visually, but their manual measurement is
(CCTA) is a younger method—with its use being accepted time consuming and tedious, and not likely to become com-
only in 64 detector row scanners or more, scanners that were monly performed. Importantly, automated software
introduced in 2005. This method provides exquisite images approaches to assessment of coronary plaque have been
of the coronary arteries. Beyond allowing assessment of developed allowing assessing of a wide variety of plaque
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 357

Fig. 20.9 Illustration of F-18 NaF uptake superimposed on CCTA lesion in the left circumflex coronary artery that was stented but was not
(right) and corresponding culprit lesions on invasive coronary angio- the culprit vessel had no increase in uptake of F-18 NaF (white arrows,
grams (left) in a patient with recent anterior ST elevation MI (top) and lower panel) (Reprinted from Joshi et al. [35] with permission under a
non-ST elevation MI (bottom). Intense uptake of F-18 NaF (orange/ Creative Commons Attribution license)
red) is seen at the site of the culprit plaques (red arrows). A bystander

characteristics (Fig. 20.12 Dey). Automated assessment of in digital subtraction angiography initially evaluated in the
plaque characteristics (Autoplaq®; Cedars-Sinai Medical 1970s. With cardiac CT, it has now been applied to assess
Center, Los Angeles, California) has been shown by Dey perfusion defects at rest and during vasodilator stress, pro-
et al. to correlate highly with measurements by intravascular viding assessments of regional hypoperfusion. The approach
ultrasound [41]. More recently, Diaz-Zamudio, Dey and has recently been assessed in two large multicenter trials.
associates have shown these automated plaque measure- The CORE64 study evaluated rest/adenosine CTP using the
ments to be predictive of abnormal FFR and more predictive combination of stenosis ≥50 % on ICA and SPECT myocar-
than stenosis grading in intermediate coronary lesions, with dial perfusion defect as the comparator of hypoperfusion. A
total, noncalcified, and low-attenuation being significant pre- high receiver operating characteristic (ROC) curve area was
dictors of ischemia [42]. The automated assessments have reported [43]. Comparable accuracy for detection of ICA
the potential of becoming practical clinical tools that could stenosis was subsequently reported in the trial between ade-
augment the assessment of coronary stenosis by CCTA. nosine CTP and pharmacologic SPECT assessments. In
Beyond the anatomic assessments of plaque and stenosis, another multicenter trial, Cury et al. reported a high ROC
CCTA acquisitions can be used to assess physiologic pro- curve area for the assessment of perfusion defect comparing
cesses. Two major developments have been recently reported regadenoson CTP to regadenoson SPECT [44]. These reports
in this regard. The first is the assessment of myocardial per- suggest that CCTA might effectively be used clinically for
fusion with CT (CT perfusion or CTP). CTP has its origins assessment of vasodilator stress myocardial perfusion and
358 D.S. Berman et al.

Fig. 20.10 CCTA (volume rendering, right; curved multiplanar recon- maximal luminal obstruction. On CCTA the plaque is seen to be large,
struction (middle) and ICA showing adverse plaque characteristics with positive remodeling (yellow arrows; remodeling index 1.43) and to
associated with moderate stenosis in a culprit left anterior descending have a low attenuation component (red arrow), consistent with lipid in
coronary artery lesion in a 40-year-old male patient presenting with necrotic core (Reprinted from Motoyama et al. [36] with permission
acute coronary syndrome. The blue arrow on ICA shows the site of from Elsevier)

coronary plaque and stenosis. Potentially, this combination tion and potentially allowing them to reduce the need for
could allow adjudication of borderline stenoses with respect FFR measurements in the catheterization laboratory as well
to their hemodynamic significance without need for a second as to reduce the proportion of times that ICA is performed
stress test on a separate occasion. and revascularization is not needed. How well the approach
An exciting even more recent development has been that will perform in standard clinical practice is currently under-
of estimating FFR from a resting CCTA study FFRCT. This going evaluation.
approach uses computational fluid dynamics, assessing the
CCTA studies through the use of an off-site supercomputer.
The method does not require a second acquisition with its Value-Based Imaging
attendant radiation and work-flow complexity, and has no
additional contrast or radiation, since it uses the standardly All of these assessments now available due to the techno-
acquired CCTA study (Fig. 20.13). Three large multicenter logic assessments must now be addressed in terms of how
trials have demonstrated the high accuracy of this method in they will fit in with the migration to value-based imaging. In
predicting FFR by ICA [45–47]. In the NXT study, the accu- this section, we address consideration of the “value proposi-
racy of FFRCT exceeded that of coronary stenosis measured tion” in four different settings in which CAD is considered or
by ICA in prediction of FFR [47] (Fig. 20.14; Courtesy being evaluated: prevention, detection/assessment of ACS,
NXT). This promising technique could be of high value to assessment of patients with suspected or known SIHD, and
interventionalists in determining the need for revasculariza- patients with heart failure related to CAD.
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 359

Fig. 20.11 Case examples

illustrating the relationship of
coronary stenosis on CCTA
(top) to ischemia on
SPECT-MPI polar maps
(bottom) in patients with high
grade coronary stenosis by
quantitative coronary analysis
(QCA). The patient on the left
had an 81 % stenosis,
associated with a plaque
without adverse features
(green arrow) and had no
evidence of ischemia. The
patient on the right had a
70 % stenosis by QCA,
associated with a plaque with
adverse characteristics of
large volume, positive
remodeling (yellow arrow)
and low attenuation plaque
(red arrow) and demonstrated
clear evidence of ischemia
(Reprinted from Shmilovich
et al. [38] with permission
from Elsevier)

Fig. 20.12 Features which

can be assessed by automated
quantitative plaque
characterization (AutoPlaq®;
Cedars-Sinai Medical Center;
Los Angeles, California).
NCP non-calcified plaque,
CP calcified plaque
(Reprinted from Dey et al.
[41] copyright RNSA® with
permission from the
Radiological Society of North
America)
360 D.S. Berman et al.

Fig. 20.13 Illustration of CCTA (left) ICA (middle) and FFRCT (right) the correspondence between the FFR and the FFRCT measurements and
in: a patient with a moderate coronary stenosis (top) associated with a the discordance with the visually appreciated degree of stenosis (red
reduced FFR and FFRCT (top) and a patient with a higher grade coro- arrows) (Reprinted from Min et al. [45] with permission from the
nary stenosis associated with a normal FFR and FFRCT (bottom). Note American Medical Association)

Prevention and aspirin therapy [48, 49]. There are multiple limitations
More lives could be saved by appropriate implementation in the use of global risk scores in the individual patient.
of preventive therapies such as the use of statin and aspirin They do not take into account individual variations of the
than through the use of revascularization. Yet the manner biologic effects of the risk factor, the chronicity of the fac-
in which prevention strategies are chosen is imprecise. tor, and cannot account for all risk factors. On the other
Increasingly, modern concepts are that medicine is migrat- hand, the CT CAC score is a marker of CAD in an indi-
ing toward “precision medicine,” in which the therapy for a vidual patient, representing the integrated effect of all risk
patient is chosen based on the characteristics of that indi- factors on the individual’s coronary vasculature. It thus
vidual. The standard guidelines for implementation of overcomes the imprecision of the global risk scores. Recent
aggressive prevention strategies employ the use of global analysis of patients from the Multi-Ethnic Subclinical
risk scores, such as the Framingham Risk Score (FRS) to Atherosclerosis (MESA) study has shown that the new
place patients into treatment groups. These scores are AHA-ACC-ASCVD score overestimated risk by 25–115 %,
based on risk factors that are known in populations to be with substantial implications for individual patients and the
independently associated with atherosclerotic cardiovascu- health care system [50].
lar disease (ASCVD) [48]. The current ACC/AHA guide- Hundreds of studies have evaluated the prognostic value
lines from 2014 essentially result in nearly 100 % of men of the CAC in asymptomatic subjects. They have consis-
over age 55 having a recommendation for being on statin tently documented that CAC score provides incremental
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 361

Fig. 20.14 Accuracy, NXT: Per-Vessel Prediction of Invasive FFR:

sensitivity, and specificity of FFRCT vs. CT and ICA:
FFRCT (red) and percent
diameter stenosis [black:
CCTA; pink: ICA] in FFRCT£.80cv N=484
prediction of invasive FFR CT≥50 ICA≥50
(Reprinted with permission 100 95
from Nørgaard et al. [47] 91 92 93
with permission from 90 81 84 83 86
Elsevier)
80

70 65 64
60 61
60
51
50 46

40
33
30

20

10

0
Accuracy Sensitivity Specificity PPV NPV

FFRCT diagnostic accuracy superior to both CT and ICA stenosis

information over a global risk scores, mainly the FRS. Among and weight maintenance was associated with lower coronary
most important of these studies to date are the MESA study calcium incidence, slower calcium progression, and lower
[51] and the Heinz-Nixdorf Recall study [52]. These were all-cause mortality over 7.6 years [60].
large, population based studies in which CAC and multiple The largest randomized trial to date assessing the value of
other tests were compared to global risk scores for assessing CAC scanning is the Early Identification of Subclinical
patient prognosis. The results of the trials were very similar. Atherosclerosis by Noninvasive Imaging Research (EISNER)
They showed strong incremental value of CAC over the FRS, trial [56]. It was designed to test the primary hypothesis that
and a high net reclassification index (NRI). Each trial has performing CAC scanning would lead to a beneficial sus-
had numerous substudies reported. In a recent report from tained 4-year effect on individuals’ CAD risk factors—using
the MESA trial, the CAC score was the only assessment of the FRS as a composite of these—as a surrogate for improved
many including CRP to add to the FRS in assessment of outcomes. Secondarily, we assessed the impact of CAC
prognosis [53]. Further interesting work from the MESA scanning on downstream medical resource utilization and
trial has been to show that the CAC score could be used to healthcare costs. The trial involved assigning 2137 volunteers
more effectively target statin and aspirin therapy than the to groups that did versus did not undergo CAC scanning
FRS. With respect to aspirin, Miedema et al. [54] demon- before risk factor counseling (2:1 scan/control randomiza-
strated from MESA that in patients with a low FRS (<10 %), tion). Compared to the no-scan group, the scan group showed
the use of aspirin would result in net patient harm, whereas a net favorable change in systolic blood pressure (p = 0.02),
the use of aspirin in patients with CAC >100 would be asso- LDL-cholesterol (p = 0.04), waist circumference for those
ciated with patient benefit. Similarly, regarding statin ther- with increased abdominal girth (p = 0.01), and tendency to
apy, it was projected that it is both cost-saving and more weight loss among overweight subjects (p = 0.07). While
effective to scan intermediate-risk patient for CAC and to mean FRS rose in the no-scan group, it remained static in the
treat those with CAC ≥1 with a statin than basing treatment scan group (0.7 ± 5.1 versus 0.002 ± 4.9, p = 0.003). Within
on standard risk-assessment guidelines [55]. the scan group, increasing baseline CAC score was associ-
The CAC scan can affect the degree to which the patient ated with a dose–response improvement in systolic and dia-
adopts heart healthy behaviors including improvement in stolic blood pressure (p <0.001), total cholesterol (p <0.001),
risk factor profile [56], intensification of Rx [57], better LDL-cholesterol (p <0.001), triglycerides (p <0.001), weight
adherence to Rx [58], dietary modifications [58], and (p <0.001) and FRS (p = 0.003). Downstream medical testing
increased exercise [59]. Interesting work from MESA and costs in the scan group were comparable versus the no-
demonstrated that improvement in healthy lifestyle behavior scan group, balanced by lower and higher resource utiliza-
including regular exercise, healthy diet, smoking avoidance, tion for those with normal CAC scans and CAC scores ≥400,
362 D.S. Berman et al.

respectively. Improvement in the global risk score, associ- MPI was abnormal in 22 %, concordant with the results of
ated with no increase in overall costs, provided evidence that the DIAD study. Major adverse cardiac events (MACE,
there is value in testing this population at intermediate risk. defined as cardiac death, myocardial infarction, or symptom-
Of note, this study had several components that were acting driven coronary revascularization) occurred in 2.9 % of
to underestimate the potential of the CAC scan to improve patients with normal baseline SPECT-MPI compared to
outcomes. The only difference between the control and treat- 9.8 % of patients with an abnormal MPI (p = 0.011). Patients
ment groups was a one-time counselling session in which the with abnormal SPECT-MPI were randomized to an approach
patients in the scan group were shown their scans and a nurse of catheterization with intended revascularization vs nonin-
practitioner discussed the scan implications (those that were vasive management; there was no difference in outcomes in
known at that early time) along with the patients risk factor those randomized to medical therapy only vs combined
profile with the patient, while the control group patients medical therapy and revascularization. Overall, the findings
received the risk factor counseling alone. There were no suggest a lack of outcome benefit of stress testing of asymp-
treatments recommended by the nurse practitioner; specifi- tomatic diabetic patients. Whether such testing might have
cally, the only treatment guidelines that were discussed were been beneficial if the definition of high-risk had been based
those of the NCEP III—with no specific recommendation for on elevated CAC levels would be of interest.
change in treatment based on scanning. Subsequently, A recent multicenter RCT has evaluated the application of
patients were sent by mail an anonymized report of their CCTA in the high risk asymptomatic diabetic patient. In this
study; however, their physicians were not sent reports. regard, the FACTOR-64 trial evaluated whether routine cor-
onary CTA screening of high risk asymptomatic diabetics
Application in Diabetes affects changes in treatment that leads to a reduction in car-
Assessment of the asymptomatic patient with diabetes is an diac events [64]. Nine hundreds patients were randomized to
important subgroup with generally a higher risk of cardiac CT screening (n = 452) with protocol specific recommenda-
events than patients in most other asymptomatic groups. tions for management after testing or standard care (n = 448).
Comparing the potential value of the various noninvasive CCTA showed no CAD in 31 %, mild plaque <50 % stenosis
tests in these patients casts further light on their effectiveness in 46 %, moderate stenosis in 12 %, and severe stenosis in
in the asymptomatic patient population. CAC scanning may 11 % of the patients. CCTA prompted a stress test in 14 % of
be of value in this application. the cases, and angiography in 8 %, of whom 53 % underwent
Extensive data has shown that a CAC score of 0 is found subsequent PCI and 19 % underwent coronary artery bypass
in a high proportion of adult asymptomatic diabetics—38 % graft (CABG). There was a trend for a lower rate of events in
in the MESA study [61]. The possibility that this finding the CT group: for the primary composite endpoint of death,
might improve patient outcomes, particularly in the psycho- MI, or hospitalization for unstable angina, the rate was 6.2 %
logic well being of the diabetic patient, if of interest in this in the CT arm vs. 7.6 % in the standard care group (HR 0.80,
regard. There is a greater increase of risk of events in every 95 % CI 0.49–1.32, p = 0.38). At the end of the trial, the CT
category of increased CAC score when compared to the non- group showed improvements in statin use and intensity, lipid
diabetic population. CAC scanning has the potential of defin- fractions, and blood pressure levels. The composite primary
ing a high risk group that might benefit from ischemia end point was less than half of expected and there was a non-
testing. significant trend toward lower composite events. While not
Randomized clinical trials (RCTs) have suggested that yet proven statistically in this trial, the results suggest that a
routine SPECT-MPI in the asymptomatic diabetic patient strategy based on screening high risk asymptomatic diabet-
may not be of value. In the Detection of Ischemia in ics using CCTA might be of value.
Asymptomatic Diabetics (DIAD) study [62], 1143 asymp-
tomatic diabetics were randomized to either a screening Value of Noninvasive Imaging for Prevention
approach using SPECT-MPI (n = 522), or a non-imaging Given the plethora of CAC studies demonstrating the adverse
regimen. The patients were not selected to be high risk. Over prognosis of a high CAC score, it is questionable whether a
a 4.8 year follow-up, the cardiac event rates were low and sufficiently powered randomized clinical trial demonstrating
there was no outcome benefit in the group undergoing that CAC improves outcomes be performed. Nonetheless, a
SPECT-MPI. While the prevalence of any perfusion or LV vast amount of consistent observational data suggest that
function abnormality was 22 %, a moderate-to-large perfu- CAC scanning in the appropriate asymptomatic patient at low
sion defect was present in ischemia only 6 %. In the small to intermediate risk would result in improved outcomes that
group that did have moderate-to-large perfusion defects, the would outweigh any increase in costs associated with the test
event rate was elevated. The Basel Asymptomatic High-risk and downstream testing and treatments, thus providing value
Diabetes Outcome (BARDOT) trial [63] studied 400 patients (Fig. 20.15). The possibility that coronary CTA or stress
with type 2 diabetes who had no history or symptoms of myocardial perfusion imaging might prove of value in very
CAD, but who were defined as high risk. Baseline SPECT- high risk asymptomatic patients has not been fully explored.
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 363

Use of SPECT-MPI in the Evaluation of Acute

Chest Pain

Noninvasive imaging has become part of the standard of

care in assessing patients with low to intermediate risk of an
ACS in the ED. A common approach is to use rest or rest/
stress Tc-99m sestamibi or tetrofosmin SPECT-MPI for this
purpose. A 99 % negative predictive value of rest SPECT-
MPI, when the radiopharmaceutical is injected during or
shortly after chest pain, has been reported [69]. A prospec-
Fig. 20.15 Hypothesized value of using CAC scanning for prevention tive, randomized, controlled multicenter trial examined
in patients with an intermediate risk of ASCVD
whether incorporating acute rest SPECT-MPI into an ER
evaluation strategy of patients presenting with suspected
Evaluation of the Symptomatic Patient acute ischemia improved initial ER triage [71]. A signifi-
cant reduction in hospitalization was noted in patients with
In the symptomatic patient without known CAD, the first normal SPECT-MPI studies. When the radiopharmaceutical
question that arises addresses what is the cause of the is injected after pain has subsided and the SPECT-MPI
symptoms (i.e., establishing the diagnosis) and, after it is study is normal, stress SPECT-MPI studies or stress only
answered, what is the appropriate treatment, which involves SPECT-MPI protocols are common and have been shown to
assessment of short term as well as long term risk. While be effective [72]. The comparative use of SPECT-MPI to
use of 50 % stenosis on ICA for establishing diagnosis of CCTA is discussed below. Below, evidence that CCTA may
CAD as the cause of symptoms is questioned, it has been be superior in this application will be presented; however,
the usual standard for establishing the presence of “signifi- there are settings in which CCTA would be expected to be
cant” CAD—a standard that might be common to assess- nondiagnostic in which SPECT-MPI might be preferred.
ment of the patients with either acute or stable chest pain These include patients with known dense coronary calcifi-
syndromes. In this regard, the sensitivity and specificity for cation, elderly patients in whom dense coronary calcifica-
detection of “angiographically significant” CAD has long tions are likely, patients with prior bypass surgery, possibly
been a standard for test assessment. Extensive evidence has with prior percutaneous coronary intervention (PCI), and
shown that direct visualization of the coronary stenosis known ischemic cardiomyopathy, and with contraindica-
with CCTA is superior to all other forms of noninvasive tions to CCTA.
testing, on a per patient, per vessel, and per segment basis
[65–68]. Beyond detection of stenosis, CCTA has been
studied extensively in risk prediction and effect on patient Use of CCTA in the Evaluation of Acute
outcomes. Chest Pain

Three large randomized clinical trials have evaluated the

Evaluation of Patient with Acute Chest Pain application of CCTA to patients in with suspected ACS in the
emergency department in comparison to a standard of care
Almost eight million individuals are evaluated each year for approach (SOC). In all of these studies, the patients evalu-
acute chest pain in the emergency department (ED) [69]. ated were defined as being in a low to intermediate group
Despite standardized protocols and high vigilance, between regarding the likelihood of having an ACS at the time of their
2 and 6 % of patients are erroneously discharged with missed ED visit. The first of these was the CT-STAT trial comparing
myocardial infarction [70] with higher mortality rates than CCTA to rest/stress SPECT-MPI [73]. In 16 centers, 699
patients who are hospitalized. For patients with normal or patients were randomly assigned to CCTA (n = 361) or MPI
nondiagnostic initial ECGs and troponin levels on presenta- (n = 338) as the index noninvasive test. CCTA resulted in a
tion to the ED, an important clinical problem is to distinguish 54 % reduction in time to diagnosis (2.9 h vs. 6.3 h)
those with acute coronary syndromes requiring hospital compared with MPI (p <0.0001). Costs of care were 38 %
admission from those who may be safely discharged. It is lower (p <0.0001). The diagnostic strategies had no differ-
now standard in many EDs and chest pain centers to evaluate ence in major adverse cardiac events after normal index test-
such patients with a “rule-out myocardial infarction” strat- ing (0.8 % in the CCTA arm vs. 0.4 % in the MPI arm,
egy followed by stress testing and/or cardiac imaging; how- p = 0.29). The ACRIN-PA trial [74] evaluated 1392 low-to-
ever, it has been estimated that the diagnosis of acute ED intermediate risk patients (TIMI score 0–2) presenting to the
chest pain costs $10–$12 billion annually in the United ED to CCTA or the physician elected traditional approach to
States [69]. standard care in a 2:1 ratio. Patients evaluated with coronary
364 D.S. Berman et al.

CTA had a shorter mean hospital stay and were also dis-
charged more rapidly (total length of stay 18 vs 25 h; p
<0.0001) and more frequently (50 vs 23 %) than patients
undergoing the standard care evaluation. Of 640 patients
with a negative CCTA examination, none died or had a myo-
cardial infarction within 30 days [74]. The ROMICAT II trial
[75] randomly assigned patients 40–74 years of age with
symptoms suggestive of acute coronary syndromes but with-
out ischemic electrocardiographic changes or an initial posi-
tive troponin test to early CCTA or to standard evaluation in
the emergency department. The rate of acute coronary syn-
dromes among 1000 patients with a mean (±SD) age of
54 ± 8 years (47 % women) was 8 %. Compared with stan-
dard evaluation, in the CCTA group, the mean length of hos-
pital stay was reduced by 7.6 h (p <0.001). Fifty percent of Fig. 20.16 Hypothesized value of using CCTA in patients with acute
the patients in the CCTA arm were discharged by 8.6 vs chest pain. ED emergency department
26.7 h in the standard ED evaluation arm (p <0.001). A
higher proportion of patients were discharged directly from
the emergency department (47 vs. 12 %, p <0.001). Sixty- symptoms. In this regard, the downstream long term effects
two percent of patients were in the ED for 12 h or less in the of knowledge about the presence of non-obstructive CAD—
CCTA arm vs 21 % in the control arm. There were no signifi- if effectively explained to the patient—may have the effect
cant differences in major adverse cardiovascular events at 28 of increasing preventive treatment and improving outcomes.
days. The cumulative mean cost of care was similar in the Thus, the “value proposition” for the use of CCTA in the ED
CCTA group and the standard-evaluation group ($4289 and is likely to be positive for application in the correctly selected
$4060, respectively; p = 0.65). patient (Fig. 20.16). It is of great interest, however, that as of
The CT-COMPARE trial [76] was a single center large 2015, the largest insurance carrier in the United States—
randomized trial comparing CCTA to exercise ECG testing Wellpoint—has a national medical policy (with effective
(ExECG) in 562 patients with low-intermediate risk chest date 10/08/2013) that the use of CCTA “is considered inves-
pain subjects. ACS occurred in 24 (4 %) patients. Despite tigational and not medically necessary for…diagnosis of
higher odds of downstream testing in the CCTA arm (OR CAD, in individuals with acute or non-acute symptoms” [77]
2.0), 30 day per-patient cost was significantly lower in the (reference “Anthem; Medical Policy #: RAD 00035 Last
CCTA group ($2193 vs $2704, p < 0.001). The length of stay Review Date: 02/05/2015”).
of patients in the CCTA arm was significantly shorter
(p < 0.0005). No patient had post-discharge cardiovascular
events at 30 days. Evaluation of the Symptomatic Patient
with Suspected Stable Ischemic Heart Disease
Value of CCTA in the Patient with Suspected ACS (SIHD)
How might the results of these four trials be interpreted with
respect to “value”? In aggregate, the results are consistent Chest discomfort or other symptoms raising the possibility
with respect to the major findings. Overall, both CCTA and of angina are among the most common problems confronting
standard of care approaches are successful in assuring a low primary care physicians and cardiologists. While stress
risk of missed events or of early events after discharge. testing, usually with imaging, is the most common manner in
Regarding outcomes, while “hard outcomes” of death or which patients with suspected SIHD are evaluated, the use of
myocardial infarction were not different, improved outcomes CCTA is rapidly growing in this setting. In these patients, the
would include the patient benefit of rapid discharge and the reason for testing is twofold: (1) establishing the diagnosis
effect of their rapid discharge on improved care of other explaining the symptoms so as to institute the appropriate
patients in a busy ED environment. An effect that has not yet medical therapy and (2) assessing potential benefit from
been adequately assessed is the potential of the CCTA revascularization. Despite the youth of the method—with
approach to reduce both short term and long term costs. CCTA being introduced with 64 slice scanners only in
Since extensive data has now shown that patients with com- 2005—an impressive body of evidence has been accumulated
pletely normal CCTA studies have an extremely low rate of documenting the effectiveness of CCTA not only for estab-
subsequent ACS over a prolonged period of time, there may lishing the diagnosis but in assessing the risk of events.
be fewer repeat visits to the ED by patients with normal stud- As noted above, CCTA has higher sensitivity and speci-
ies, who might be less concerned about their recurrent chest ficity for angiographically significant disease noted above
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 365

when compared to other forms of testing. Regarding risk of Prognostic Value of CCTA CAD Extent / Severity
cardiac events, strong prognostic power of CCTA has been
consistently demonstrated. A large number of manuscripts 1.00
Normal
have been published from the CONFIRM registry, which as Non-Obstructive
p<0.0001
of 2015 was comprised of more than 32,000 patients evalu- 0.98

ated in six countries, in whom comprehensive clinical, scan, 1-Vessel

Survival Probability
CAD
and outcome data were recorded [78]. Data elements 0.96 p<0.0001
2-Vessel
included risk factors, symptom type, CCTA results inter- CAD
p<0.001
preted in 16 coronary segments for plaque, plaque type, and 0.94

stenosis severity (0 = normal; 1 = 1 to <50 % stenosis; 2 = 50 3-Vessel/Left Main

p<0.0001
to <70 % stenosis, and 3 = ≥70 % stenosis). The number of 0.92 23,854 patients w/o known CAD (57±13 years), 2.3 year f/u
vessels with ≥50 % stenosis, a modified Duke score which
added the location of the stenosis, a segment involvement 0.90
0.0 0.5 1.0 1.5 2.0 2.5 3.0
score (SIS)—the number from 0 to 16 of segments with Survival Time (Years)
plaque, and a summed severity score (SSS), accounting for
the severity of stenosis and the number of segments involved, Fig. 20.17 Unadjusted All-Cause Kaplan-Meier Survival by the pres-
ence, extent, and severity of CAD by CCTA. Note the dose-response
ranging from 0 to 48. In the seminal article from CONFIRM, relationship of mortality to increasing numbers of vessels with obstruc-
Min et al. reported analysis of 23,854 patients without known tive coronary artery disease (CAD). f/u follow-up (Reprinted from Min
CAD who underwent a 2.3 year follow-up [78]. This early et al. [78] with permission from Elsevier)
study demonstrated that the mortality rate in patients with
entirely normal CCTA studies was extremely low, and that
with every degree of increasing abnormality, mortality rate due to CHD. At 6 weeks, CTCA reclassified the diagnosis of
increased. Importantly, there was significant increase in mor- CHD in 558 (27 %) patients and the diagnosis of angina due
tality in the patients with non-obstructive CAD progressively to CHD in 481 (23 %) patients (p <0.0001). Regarding the
increasing according to anatomic extent and severity of non- presence of CHD, physician certainty increased (p < 0.0001)
obstructive CAD (Fig. 20.17). This increase was noted for and the frequency of CHD increased (p = 0·0172). Regarding
the number of vessels with greater than 50 % stenosis, the diagnosis of angina due to CHD, the certainty increased (p
modified Duke score, the SIS, and the SSS. These increases < 0.0001). The findings changed planned investigations (in
in mortality with each increasing degree of anatomic abnor- 15 vs 1 %; p <0.0001) and treatments (23 vs 5 %; p <0.0001)
mality were observed in men and women. Since this publica- (Fig. 20.18), but did not affect 6-week symptom severity or
tion, consistent findings have been reported from CONFIRM subsequent admittances to hospital for chest pain. After
across multiple patient subgroups, ranging from patients 1.7 years, CTCA was associated with a 38 % reduction in
with no risk factors [79] to patients with abnormal left ven- fatal and non-fatal myocardial infarction (26 vs 42, HR 0.62,
tricular function [80]. In a group of 15,187 patients from 95 % CI 0.38–1.01; p = 0.053), close to, but missing, statisti-
CONFIRM in whom MACE events were recorded (death, cal significance (Fig. 20.18). The overall conclusion of the
myocardial infarction, and late revascularization), this trial was the CCTA changed and clarified diagnosis in one of
graded relationship between events and observed degree of four patients, altered subsequent investigations in one of six,
CAD by CCTA was also seen [81]. A long “warranty period” changed treatment in one of four and showed a trend toward
for patients with a normal has been described: the annual reduction of fatal and non-fatal MI.
event rate of patients with a normal CCTA study has been The PROMISE trial [83] evaluated 10,003 symptomatic
reported in multiple studies to be less than 0.25 %. patients (60.8 ± 8.3 years, 52.7 % were women, 87.7 %
Two large randomized clinical trials comparing CCTA to symptomatic) with no prior CAD who were referred for
a SOC approach have recently been reported. The Scot-Heart noninvasive testing, randomizing them to CCTA (n = 4686)
Trial [82] examined 4138 patients aged 18–75 presenting to or functional testing (n = 4692) with stress nuclear (67.3 %),
12 rapid access chest pain centers in Scotland who were ran- stress echo (22.5 %), or stress ECG alone (10.2 %). The
domized to CCTA vs a SOC approach. The median follow up composite primary end point was death, myocardial infarc-
time was 1.7 years. Of note, 85 % of the patients had already tion, hospitalization for unstable angina, or major procedural
had stress ECG testing at the time of randomization. The pri- complication. Secondary end points included invasive car-
mary endpoint was certainty of the diagnosis of angina sec- diac catheterization that did not show obstructive CAD and
ondary to coronary heart disease at 6 weeks. From 2010 to radiation exposure. The mean pretest likelihood of obstruc-
2014, the study randomized 4146 (42 %) of 9849 patients tive CAD by the Diamond-Forrester classification was
who had been referred for assessment of suspected angina 53.3 ± 21.4 %. However, the observed prevalence of ≥50 %
due to CHD. At baseline, 47 % of participants had a clinic stenosis on CCTA in the CCTA arm was only 11.3 %.
diagnosis of CHD and 36 % were considered to have angina Over a median follow-up period of 25 months, a primary
366 D.S. Berman et al.

Fig. 20.18 Results of the CTCA and Clinical Outcome

Scot Heart Trial. Kaplan- 1.7 Years of Follow-up
Meier curves for CHD death
and myocardial infarction
(left) and CHD death, CHD Death and Non-Fatal MI CHD Death, Non-Fatal MI
myocardial infarction, and
stroke (right) in patients and Non-fatal Stroke
assigned to CTCA (blue) and 5 5
standard care (red) (Adapted HR 0.62 [0.38-1.01], P=0.053 HR 0.64 [0.41-1.01], P=0.056

Proportion of patients

Proportion of patients
with permission from the
4

with an event (%)

with an event (%)

Newby et al. Lancet, 2015 4
under a Creative Commons Standard Care
Attribution license) 3 Standard Care 3

2 2
CTCA
CTCA 1
1

0 0
CTCA 2073 1571 853 323 CTCA 2073 1569 851 321
Standard Care 2073 1550 837 316 Standard Care 2073 1547 835 315

0 1 2 3 0 1 2 3
Follow up Follow up
(years) (years)

end-point event occurred in 3.3 % of the CCTA group and approach to the symptomatic patient with an intermediate
3.0 % in the functional-testing group (p = ns). No significant pretest likelihood of CAD, based on using CCTA as the ini-
difference was also shown in subsequent death or non-fatal tial test is shown schematically in Fig. 20.20.
MI. While invasive coronary angiography was more com-
mon within 90 days after testing in the CCTA group (12.2 vs. Value of CCTA and Stress Imaging in the Patient
8.1 %), CCTA was associated with fewer catheterizations with Suspected Stable Ischemic Heart Disease
showing no obstructive CAD than was functional testing (3.4 How might the results of these the current evidence be inter-
vs. 4.3 %, P = 0.02). Although the trial was not powered for preted with respect to “value” of CCTA and stress imaging in
non-inferiority, this large trial suggests that a strategy of ini- suspected SIHD? A conceptual approach to the symptomatic
tial CCTA is not inferior to the more commonly employed patient with an intermediate pretest likelihood of CAD,
functional strategy with respect to short term cardiac events based on using CCTA as the initial test, is shown in Fig. 20.21.
in a relatively low risk, symptomatic population. The value will likely depend on the correct selection of
The influence of CCTA on subsequent management is patients for testing. Consistent large registry data provide
illustrated in case examples on Fig. 20.19. When the findings evidence of excellent risk stratification by CCTA. The Scot-
of CCTA are completely normal, treatment and subsequent Heart trial suggested a possible benefit with respect to out-
testing is clear. The very high negative predictive value—the comes, and important changes in confidence of diagnosis
definitive ability to rule out CAD and the associated long and changes in therapy. The PROMISE trial provided evi-
“warranty period”—is a principal driving force in the dence that CCTA has similar outcomes compared to a func-
application of CCTA. As with CAC scanning, the finding of tional approach in a patient group with a low prevalence of
non-obstructive CAD may prompt the use of aggressive CAD. It is reasonable to hypothesize that in the low-interme-
preventive measures, which is likely to ultimately improve diate likelihood of obstructive CAD group, there may be an
long term outcomes. When a proximal high grade stenosis is outcome benefit as suggested by Scot-Heart, or outcomes
found, direct referral for invasive coronary angiography might be unchanged as suggested by PROMISE. CCTA
would likely follow. Stress imaging after CCTA may be strategy will likely be less costly than a functional strategy,
useful in guiding the decisions in patients with borderline despite an increase in the rate of revascularization
coronary stenosis (50–69 %), non-diagnostic CCTA results, (Fig. 20.21). The greatest cost savings might be in patients
and possibly patients with significant but not critical stenosis with entirely normal studies—as the benign prognosis asso-
to evaluate the presence and extent and severity of ischemia ciated with the completely normal study, commonly seen in
as a guide to potential benefit from revascularization. As dis- the patients being sent for testing, becomes more widely
cussed above, FFRCT is an alternative approach to assess- appreciated. In these patients, it is likely that the frequency
ment of lesions associated with diagnostic uncertainty. An repeat functional tests will be lower than with the functional
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 367

Fig. 20.19 Curved multiplanar reconstructions of CCTA from patients representing different levels of risk based on CCTA findings (top) and
possible subsequent management. The arrow points to an intermediate-to-high finding on CCTA. ICA invasive coronary angiography

Fig. 20.20 Conceptual

approach based on initial
CCTA to diagnosis and
management of coronary
artery disease in symptomatic
patients with an intermediate
pre-test likelihood of CAD.
Abnl abnormal, revasc
revascularization (Adapted
from Schuijf et al. [84] with
permission from Springer)
368 D.S. Berman et al.

testing approach—unless functional testing is combined CCTA—such as stress CT perfusion or FFRCT might extend
with anatomic assessment such as performing an adjunctive the population in whom the initial CCTA approach will
CAC scan—potentially often stopping a cycle of multiple likely be of value.
repeat tests. The cost-effectiveness CCTA in this patient Stress imaging with SPECT-MPI remains by far the most
population has recently been reviewed [85]. At the other end common approach to testing of the patient with an intermedi-
of the spectrum of likelihood of hemodynamically signifi- ate likelihood of hemodynamically significant CAD. Given
cant disease, a reasonable hypothesis would be that if ana- the wide availability of stress imaging methods compared to
tomic approach to assessment of CCTA alone is used—not the current less widely available CCTA imaging, the predomi-
taking advantage of functional information that might be nance of the stress imaging approach is likely to remain for a
derived from CCTA—CCTA might not prove to be of value considerable amount of time (Fig. 20.22). With the initial
(Fig. 20.21). For example, if a very high CAC score is pres- stress imaging approach, CCTA could be used as a second test
ent in a substantial proportion of patients—leading to a high when the results of stress testing are equivocal or discordant
proportion of nondiagnostic studies—CCTA might be asso- (e.g., severe ST depression with a normal MPI study) [86].
ciated with an increase in downstream testing, either func- A drawback of stress imaging without anatomic assessment
tional testing or invasive coronary angiography, potentially in patients with an intermediate likelihood of CAD is that the
not changing outcomes compared to a functional approach methods detect only patients with hemodynamically signifi-
but increasing costs. Adding “functional” information to cant lesions and fail to identify patients with subclinical ath-
erosclerosis in whom aggressive medical and lifestyle
modification might prevent subsequent cardiac events. While
SPECT-MPI assessment of ischemia is an excellent test of
short-term prognosis, CAC scanning may be a better test of
long-term prognosis. Over a decade ago, it was recognized that
high CAC scores are common in patients with normal SPECT-
MPI [25] (Fig. 20.23). Thus, patients with non-obstructive
CAD, previously unknown, could be afforded effective pre-
ventive therapies, such as statins and aspirin. In this regard, the
coupling of CAC scanning with SPECT- or PET-MPI dis-
cussed above could provide an effective alternative to the
CCTA as a first choice approach to management of the patient
with suspected SIHD. It has further been suggested [87] that a
Fig. 20.21 Hypothesized value of using CCTA in symptomatic powerful, inexpensive alternative that may prove to be of value
patients with suspected stable ischemic heart disease (SIHD)

Fig. 20.22 MPI approach to

diagnosis and management of
CAD in symptomatic patients
with an intermediate-to-high
pre-test likelihood of CAD or
known CAD (*Indicates that
there may be benefit from
CAC scanning to assess
underlying subclinical
atherosclerosis). Int
intermediate, ICA invasive
coronary angiography, CCS
coronary calcium scan)
(Adapted from Schuijf et al.
[84] with permission from
Springer)
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 369

Fig. 20.23 Distribution of

coronary artery calcium (CAC)
scores for 1119 patients
manifesting a normal myocardial
perfusion single-photon emission
computed tomography (MPS)
(left) and the 76 patients with an
ischemic MPS (right) (Adapted
from Berman et al. [25] with
permission from Elsevier)

is the combination of an ECG stress test without imaging with perform PCI—resulted in improved outcomes in patients
a CAC scan—the “coronary calcium treadmill test.” with multivessel CAD compared to a strategy based on ana-
tomic assessment alone [96, 97]. Patients with FFR guided
revascularization had a lower event rate (death, non-fatal MI,
Patients with a High Likelihood of CAD repeat revascularization) than the group in the angiographi-
or Known CAD cally guided strategy. Subsequently, the FAME II trial ran-
domized stable patients with FFR ≤0.80 to PCI vs medical
In contrast to patients with an intermediate likelihood of management [98]. The trial was stopped before reaching its
CAD, patients with a high likelihood of CAD are generally target sample size due to excessive events—death, non-fatal
considered by their clinicians to have CAD and are treated MI, and unstable angina—in the medical therapy arm. While
accordingly. If limiting symptoms are present, the patient is there were no differences between the FFR guided and the
usually directly sent for invasive angiography. In patients medical management approaches with respect to hard events
without limiting symptoms, stress imaging is performed to alone, the results demonstrated an outcome benefit of isch-
assess the extent and severity of ischemia in order to guide emia driven decisions for revascularization using the com-
the decision for revascularization. An extensive body of posite endpoint (p <0.001). The ability of an FFR-guided
information has demonstrated the prognostic power of isch- approach to reduce cardiac events was also demonstrated in
emia testing with SPECT- or PET-MPI as well as with stress a large registry of 7358 patients with stable disease studied at
echocardiography and stress cardiac magnetic resonance the Mayo Clinic [99].
imaging [88–91]. For SPECT and PET, risk has been shown Registry data with SPECT-MPI has provided evidence
to increase as a function of stress perfusion abnormality in that supports the approach of ischemia driven revasculariza-
virtually all subsets of patients with known or suspected tion. The potential that the amount of ischemia on SPECT-
CAD [89, 92]. Importantly, as noted above, these include the MPI to predict benefit with revascularization was first
categories of patients in whom CCTA is contraindicated or described in a single center registry by Hachamovitch et al.
likely to be non-diagnostic. in 1998 [100]. Subsequently, this benefit was documented in
Large randomized clinical trials have suggested that ana- a larger population of 10,627 patients without prior CAD
tomic assessment of disease alone does not provide evidence who underwent SPECT MPI. A “proof-of-principle” ques-
of revascularization benefit in most patients [93]. Most fre- tion was asked: can imaging identify appropriate and benefi-
quently quoted in this regard are the results of the COURAGE cial treatment strategies and at what threshold of abnormality
trial [94] and the BARI 2D trial [95] which did not demon- does therapeutic efficacy shift [101]. After adjusting for dif-
strate benefit over optimal medical therapy as an initial ferences between medically treated and revascularized
strategy. patients—including a propensity score adjustment to correct
There is evidence, however, that an ischemia guided for differences in referral patterns to treatment options—
approach to revascularization can be of benefit. Noteworthy patients with extensive myocardial ischemia by SPECT MPI
in this regard are the results of the FAME studies. The FAME exhibited a survival benefit with myocardial revasculariza-
trial provided evidence that a revascularization strategy tion for the intermediate-term occurrences of cardiac death
based on the use of ischemia testing as assessed by invasive (Fig. 20.24). By contrast, among those with no myocardial
FFR—with a cut-off of ≤0.80 considered as the criterion to ischemia, the cardiac death rate was higher with myocardial
370 D.S. Berman et al.

Fig. 20.24 Relationship

between %myocardium
ischemic and log of the
hazard ratio in 10,647
patients treated either with
medical therapy (dashed line)
or early revascularization
(<60 days post-SPECT MPS;
solid line) based on
multivariable modeling. In
the setting of little or no
ischemia, medical therapy is
associated with superior
survival; with increasing
amounts of ischemia a
progressive survival benefit
with revascularization over
medical therapy is present.
95 % confidence intervals are
shown by the closely dotted
lines (*Indicates p <0.001.)
(Adapted from Hachamovitch
et al. [101] with permission
from Wolters Kluwer Health,
Inc)

revascularization than with medical therapy. The “cross-over vascular death or heart failure over a follow up of 3.1 years.
point” at which myocardial ischemia tipped the balance Overall, only patients with reduced CFR had a significant
towards myocardial revascularization appeared to be more improvement with revascularization. Further, a significant
than 10 % ischemic myocardium. Thus, this study provided interaction between CFR and early CABG was noted, but not
insight into a potential linkage between cardiac imaging with PCI, such that patients with reduced CFR who under-
results, patient treatment, and patient clinical outcomes. This went CABG had much greater freedom from event rate than
linkage was further examined in higher-risk patient subsets patients those with low CFR who underwent PCI (Fig. 20.26)
including those with prior revascularization or small prior [105]. Gould et al. have recently expanded on the concepts
MI [102], elderly [103], and high risk diabetic patients by a suggested by the results of this small study [106], noting the
recent study [104]. In long-term follow-up of 5200 elderly importance of diffuse CAD in increasing the risk of myocar-
patients (≥75 years old) undergoing MPI, over 25 % of dial infarction and decreasing the likelihood that stent place-
whom had prior MI, the threshold for benefit from revascu- ment across individual lesions will prevent MI. They further
larization appeared 15 % myocardium ischemic [103]. In note that diffuse CAD can be assessed with CFR measure-
another long-term follow-up study of 13,969 patients from ments by PET but are not assessed by FFR and conclude that
the same registry, those with moderately to severely exten- consideration of CFR might improve selection of patients for
sive ischemia appeared to benefit from revascularization revascularization.
even in the presence of known CAD or prior revasculariza- While registry data suggests a benefit of revascularization
tion, providing they did not have extensive prior MI (>10 % in patients with moderate to severe ischemia, this benefit has
fixed defect by MPI) [102]. The threshold for this apparent not yet been validated in a randomized controlled trial.
benefit was between 10 and 15 % myocardium ischemic Whether an ischemia guided approach in SIHD improves
(Fig. 20.25). outcomes is currently being evaluated in the ISCHEMIA
A small but provocative study has suggested that addition trial (the International Study of Comparative Health
of quantitative myocardial blood flow reserve measurements Effectiveness with Medical and Invasive Approaches). This
may be associated with cardiac events independently and study is randomizing patients with moderate-to-severe
may modify prediction of benefit from early revasculariza- ischemia based on the 10 % ischemia criterion suggested
tion. In a study of 329 patients referred for invasive coronary from the Cedars-Sinai data—as the entry criterion. Patients
angiography after PET scanning with CFR measurements, with left main CAD—assessed by blinded CCTA—are
Taqueti et al. evaluated the relationship between CFR and excluded. The remaining patients are being randomized to an
observed benefit from revascularization. Patients were stud- invasive approach of catheterization with intent for ischemia
ied for the interaction between CFR findings and whether or guided revascularization + optimal medical therapy (OMT)
not the patients were revascularized with respect to cardio- vs a no catheterization approach with OMT alone.
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 371

Fig. 20.25 Hazard ratio

associated with early Ischemia and Scar and Therapeutic Benefit
revascularization compared
with medical therapy at a b
specific values of 2.00 2.00

(Early revascularization vs. medical therapy)

(Early revascularization vs. medical therapy)

n = 8,791 n = 1,542
%myocardium ischemic. 1.75
1.75 No Known CAD Prior Revasc
(a) patients with no prior 1.51
1.50 1.50
coronary artery disease, 1.29
(b) patients with prior 1.25

Hazard ratio

Hazard ratio
1.25 1.10 1.18
revascularization but no prior 0.93
1.07
0.98
1.00 1.00
myocardial infarction, 0.80 0.89
0.80
0.68 0.74
(c) patients with prior MI, 0.75 0.75

and (d) patients with <10 % 0.50

0.50
fixed defect. P-values as per
0.25
Cox proportional hazards 0.25

model (Adapted from 0.00 0.00

0 5 10 15 20 25
Hachamovitch et al. [102] 0 5 10 15 20 25
%myocardium ischaemic %myocardium ischaemic
with permission from Oxford
University Press) c d 2.00
2.00
(Early revascularization vs. medical therapy)

(Early revascularization vs. medical therapy)

n = 3,216 1.75
1.75 Prior MI <10% fixed defect n = 11,880
1.49
1.50
1.50
1.28
1.25
Hazard ratio

Hazard ratio
1.25 1.10
0.95
1.00 0.92 1.00
0.89 0.87 0.85 0.80
0.80 0.80
0.70
0.75 0.75

0.50 0.50

0.25
0.25

0.00
0 5 10 15 20 25 0.00
0 5 10 15 20 25
%myocardium ischaemic
%myocardium ischaemic
n = 13,969; FU 8.7±3.3 yrs

Value of Ischemia Testing in the Patient Sinai laboratories, Rozanski et al. have shown that there has
with a High Likelihood of or Known CAD been a dramatic reduction in the frequency of abnormal test
A reasonable hypothesis is that the value of ischemia testing results over time [107]. Whereas in 1991 approximately
will depend on the pre-test risk (Fig. 20.27). If the ischemia 40 % of patients referred for testing had ischemia by SPECT-
guided management approach is confirmed in randomized MPI, by 2009 this rate was less than 10 % (Fig. 20.28).
clinical trials, there will be an opportunity for the value of Similar findings have now been reported from other centers.
ischemia testing to be shown; however, this value would What could be the explanation of the very low observed
likely be strongly dependent on the pre-test risk. If the pre- prevalence of abnormal SPECT-MPI studies? One answer
test risk is sufficiently high, ischemia testing might lead to is that the widely used Diamond-Forrester criteria for
improved outcomes by appropriately guided revasculariza- determining pre-test likelihood of angiographically signifi-
tion. Costs might be decreased compared to an approach cant CAD may not be applicable in the types of patients cur-
without ischemia testing—such as that of using coronary rently being referred for noninvasive testing. Data from the
CTA to guide the decision for proceeding to catheterization CONFIRM registry are enlightening in this regard. Cheng
in this high risk group—since the use of CCTA alone might et al. reported that the Diamond-Forrester criteria markedly
be associated with an excessive number of catheterizations overestimated pretest likelihood of CAD [108]. In 8106
and revascularizations as discussed above. As noted above, patients in with nonanginal chest pain, atypical angina, or
the use of CT perfusion of FFRCT measurement in conjunc- typical angina, the Diamond-Forrester pre-test likelihood of
tion with CCTA might provide a means by which CCTA as angiographically significant CAD was 51 %. However, the
the initial test could be of value in this patient group. observed frequency of ≥50 % stenosis was 18 %. Based on
If used in a population of low risk, however, the ischemia the pooled data from CCTA studies, approximately 90 % of
testing is likely not to be of value. In this regard, there is an patients with CCTA stenosis have ICA stenosis. Based on the
indication that the risk of patients currently undergoing test- report by Tonino et al. from the FAME trial, only 57 % of
ing may be too low for the testing to be of value. In a study lesions judged visually to have ≥50 % stenosis have isch-
of 39,515 patients referred for SPECT-MPI to the Cedars- emia by FFR [109]. Further, it a meta-analysis by Zhou et al.,
372 D.S. Berman et al.

CFR is Associated with Cardiac Events Independently of Stenosis and

Modifies the Effect of Early Revascularization
CFR + or – vs Revasc + or – CFR + or – vs Type of Revasc
Adjusted‡ Adjusted‡
CFR low, revasc + CFR low, CABG
100 100
n = 193
N = 329
p = 0.002
90 90
Freedom from Event§ (%)

Freedom from Event¶ (%)

p = 0.61

80 80

CFR low, revasc –

CFR low, PCI
70 70 p = 0.01

60 CFR high, Revasc (+) 60 CFR high, CABG

CFR high, Revasc (–) CFR high, PCI
CFR low, Revasc (+) CFR low, CABG
CFR low, Revasc (–) CFR low, PCI
50 50
0 200 400 600 800 1000 1200 0 200 400 600 800 1000 1200
Days Days

Fig. 20.26 Freedom from events according to coronary flow reserve the subgroup of patients who underwent revascularization (right), there
(CFR) and early revascularization (Revasc) (left) and type of revascu- was no difference in event-free survival among those with high CFR
larization (revasc) right. Freedom from cardiovascular death or heart (log-rank P = 0.76; adjusted P = 0.61), but in those with low CFR, only
failure admission differed significantly among subgroups stratified by those who also underwent coronary artery bypass grafting (CABG), vs
CFR and revascularization (left) (overall log-rank P = 0.03; adjusted percutaneous coronary intervention (PCI), experienced lower rates of
P = 0.002) Patients with high CFR, independently of revascularization, events (log-rank P = 0.02; adjusted P = 0.01) (Adapted from Taqueti
experienced lower rates of events, whereas those with low CFR who did et al. [105] with permission from Wolters Kluwer Health, Inc)
not undergo revascularization experienced the highest rate of events. In

would have ischemia by SPECT—very similar to what was

reported by Rozanski et al. [107]. The results of the
PROMISE trial confirm these calculations. While the pretest
likelihood of CAD using the Diamond-Forrester criteria was
53.3 %, only 11.7 % had stenosis by CCTA and only 10.7 %
had abnormal functional studies [83].
An updated approach to assessment of the pretest likeli-
hood of CAD as well as of risk—the “CONFIRM Risk
Score” in patients referred to noninvasive testing has recently
been described based on an analysis of the CONFIRM data
[111] with validation in the Cedars-Sinai nuclear cardiology
database. The simple to implement score is illustrated in
Fig. 20.29. An intuitive number is assigned for age (e.g., 4
for 40–49 years, 7 for >70 years), and 1 or 0 are assigned
based on sex, angina, diabetes, hypertension, family history
Fig. 20.27 Hypothesized value of using SPECT- or PET-MPI (isch- of premature CAD, and smoking. With a simple table the
emia testing) in symptomatic patients with suspected stable ischemic number converts to a risk of death or MI or a pre-test likeli-
heart disease (SIHD) hood of CAD. The CONFIRM risk score was better cali-
brated than the Framingham Risk Score or the
it has been shown that only 77 % of patients with ischemia Diamond-Forrester pre-test likelihood calculations. Use of
by FFR have ischemia by SPECT-MPI [110]. Multiplying the CONFIRM risk score could lead to a more effective deci-
these rates together, the result is that if the patients sent for sion as to whether to use an imaging test in a given patient
testing have an intermediate pre-test likelihood of CAD by and which test to choose, and, ultimately, to a greater oppor-
Diamond-Forrester criteria, it would be expected that 8.6 % tunity of noninvasive testing to demonstrate value.
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 373

Fig. 20.28 Year by year

prevalence of abnormal and
ischemic SPECT-MPI studies
between 1991 and 2009
among 39,515 diagnostic
patients tested at Cedars-Sinai
Medical Center (Adapted
from Rozanskiet al. [107]
with permission from
Elsevier)

Assessment of Patients with Heart Failure nary artery disease and an intermediate to high likelihood of
and Known or Suspected CAD CAD undergoing cardiac SPECT- or PET-MPI or CCTA
[113]. These results were classified as normal (or non-
At the end of the spectrum of patients with CAD who are obstructive for CCTA), mildly abnormal, and moderately or
referred for testing are the patients with heart failure. In this severely abnormal. Baseline medication use was relatively
population, CCTA has a limited role—predominantly being infrequent. At 90 days, 9.6 % of patients underwent catheter-
to rule out ischemic cardiomyopathy in patients presenting ization. While the rates of catheterization and medication
with heart failure of unknown cause and in whom the likeli- changes increased in proportion to test abnormality findings,
hood if CAD is considered to be relatively low [112]. among patients with the most severe test result findings,
In the patient with an ischemic cardiomyopathy, myocardial 38–61 % were not referred to catheterization, 20–30 % were
viability imaging (PET or CMR) would be more likely than not receiving aspirin, and 20–25 % were not receiving a lipid-
CCTA to be of value in guiding the decision for revascular- lowering agent at 90 days after the index test. Risk-adjusted
ization or transplantation. analyses revealed that changes in use of aspirin and lipid low-
ering agent were greater after CCTA. The authors concluded
Value of Imaging Depends on the Effect that overall, noninvasive testing had only a modest impact on
of Imaging on Patient Management clinical management of patients referred for clinical testing.
The fundamental value equation is quality divided by cost. Although post-imaging use of cardiac catheterization and
Test quality ultimately rests in beneficial patient outcomes. medical therapy increased in proportion to the degree of
Costs relate not only to the cost of testing but also to all of the abnormality findings, the frequency of catheterization and
costs resulting from the test. In consideration of the value of medication change suggests possible under-treatment of
noninvasive imaging, there can be no value if the test does not higher risk patients. Even in the severely abnormal group,
improve the relationship between outcomes and costs, and only 27 % had no catheterization or medication change.
this is dependent on the manner in which test results change As noted above, in the Scot-Heart trial, changes in treat-
patient management. The test itself has no effect. Unfortunately, ment after CCTA testing compared to the non-imaging arm
there is evidence that often this last link-the link between the were clear, with 18 vs 4 % of patients being placed on preven-
test and treatment change-is not as strong as it needs to be. tive therapy in the CCTA and control arms, respectively. As
The SPARC (Study of Myocardial Perfusion and Coronary noted, there was also a trend toward improved hard outcomes
Anatomy Imaging Roles in Coronary Artery Disease) in the CCTA arm of the study. The effects of the CCTA vs
addressed these issues by evaluating 90-day post-test rates of functional testing in the PROMISE trial regarding changes in
catheterization and medication changes in a prospective reg- therapy have not yet been reported. The results of the
istry of 1703 patients without a documented history of coro- FACTOR-64 study provide promising results regarding the
374 D.S. Berman et al.

Fig. 20.29 Table illustrating the CONFIRM risk score. Illustrated is of death or MI and a 31 % likelihood of CAD (≥ 50% stenosis)
scoring for a 65 year old male with a history of hypertension and smok- (Reprinted from Min et al. [111] with permission from Elsevier)
ing. The CONFIRM risk score (*) is 9, which would predict an 8.02 risk

influence of test results on patient therapy and possibly on hard ning [114]. In this study, 430 patients in 9 centers with heart
outcomes; however, it should be noted, that changes in therapy failure, known or suspected CAD and LVEF ≤35 % were
in this study based on test results were part of the study design. randomized to a management plan assisted by FDG PET
The principal manner in which SPECT-MPI or PET-MPI stud- (n = 218) or standard care (n = 212), with specific recommen-
ies alter patient management is principally in guiding deci- dations regarding the use of FDG PET information for revas-
sions to consider revascularization. Regarding institution of cularization decisions. The outcome was a composite of
preventive management measures after testing, the combined cardiac death, myocardial infarction, and recurrent hospital
use of CAC with SPECT- or PET-MPI could allow similar stay for cardiac cause within 1 year. In the overall trial, there
effects as observed with CCTA with the use of MPI. Whether was no significant difference in the hazard ratio for the com-
the ability of PET-MPI to assess myocardial blood flow posite outcome in the PET vs SOC arm (p = 0.15). For
reserve, with its prognostic implications, and potential added patients in whom the PET recommendations were followed,
information regarding benefit from revascularization, will the hazard ratio was significant (p = 0.019), illustrating that a
affect changes in patient management has yet to be examined. test results can have a beneficial effect on outcome only if the
The ability of a test to affect outcomes is dependent on test appropriately changes therapy. The further reliance of
and degree to which the test to the manner in which test the outcome benefit of testing was subsequently illustrated in
results change therapy. The steps involved in this potential of this study when expertise in performance and clinical use of
testing to affect outcomes are well exemplified by the the testing is present. A post-hoc analysis was performed
PARR-2 study (Fig. 20.30), which involved FDG PET scan- comparing a subgroup of patients studied in five hospitals
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 375

Influence of Adherence to Strategies and Expertise on Impact of

FDG-PET on Patient Outcomes: Results of the PARR-2 Study
1.0
0.8
0.6
0.4

Overall Adhering to strategy

0.2

Standard arm Standard arm

P=0.15 PET arm P=0.019 ADHERE arm
0.0

0 100 200 300 100 200 300

Days Days
Cardiac event free survival probability

0.8 PET

0.6
Standard

0.4 More experienced center

0.2 P=0.005

0.0
0 50 100 150 200 250 300 350 400
Days

Fig. 20.30 Influence of adherence to strategies and expertise on impact planned therapeutic strategy of the trial based on PET viability results
of FDG-PET on patient outcomes as shown in two publications from the was followed (right), a significant survival benefit in the PET arm was
PARR-2 Trial. The top two illustrations illustrate composite outcome of seen. When patients who were tested in a center with greater experience
cardiac death, myocardial infarction, recurrent hospital stay for cardiac with FDG-PET were assessed (lower illustration), an even greater sur-
cause within 1 year. Green PET arm, Orange Standard arm. In the over- vival benefit in the PET arm was shown (Top two panels: (Adapted from
all trial (left), no survival benefit was shown. In the subset in whom the Beanlands et al. [114] with permission from Elsevier))

able to shorten time in the hospital and reduce costs. In

with greater experience in and access to the use of the PET patients with suspected SIHD and an intermediate pre-test
assisted strategy in the PARR-2 trial [115]. There was a sig- likelihood of CAD, the use of CCTA appears to be valu-
nificant reduction in cardiac events in the patient population able. In patients who have known CAD or in whom a non-
studied at the five sites with expertise (p = 0.005) that had not diagnostic CCTA is likely, improvement in outcomes is
been seen in the overall trial. less likely and testing for ischemia may be preferred. In
patients with a very high likelihood of CAD or known
Conclusion CAD, registry data suggests that ischemia testing, such as
Technology cardiac CT and nuclear cardiology is con- that provided by SPECT- or PET-MPI studies, may improve
stantly improving, such that the information provided be outcomes by improving selection of patients for revascular-
each form of testing is expanded, potentially decreasing the ization. The ISCHEMIA trial will test whether a strategy
need for layered testing. The value of cardiac imaging basing decisions for revascularization on noninvasive
depends on impact on outcomes and all costs related to per- assessment of ischemia is improves outcomes. In patients
formance of a test. In clinical applications, the potential with heart failure, the use of CCTA is primarily to rule out
value of the modalities is related to the setting in which ischemic cardiomyopathy. As with any form of testing,
they are employed. For prevention, data is strong in that assessing the pre-test likelihood of disease is of paramount
CAC scanning can provide value by improving outcomes. importance in determining the need for a test which could
In the patient with acute chest pain, CCTA appears to be be of value. Recent data show that the pretest likelihood of
376 D.S. Berman et al.

CAD and pretest risk is markedly overestimated by tradi- view towards reduced radiation exposure. Curr Cardiol Rep.
tional approaches, most likely explaining a marked increase 2012;14:208–16.
11. Dey D, Slomka PJ, Berman DS. Achieving very-low-dose radia-
in frequency of normal stress SPECT-MPI studies. Updated tion exposure in cardiac computed tomography, single-photon
methods for assessment of pre-test risk may lead to emission computed tomography, and positron emission tomogra-
improved utilization of cardiac imaging procedures. In phy. Circ Cardiovasc Imaging. 2014;7:723–34.
selected heart failure patients, of myocardial viability using 12. Arsanjani R, Hayes SW, Fish M, Shalev A, Nakanishi R, Thomson
LE, Friedman JD, Germano G, Berman DS, Slomka P. Two-
PET or MRI may prove to provide value. In all of the appli- position supine/prone myocardial perfusion SPECT imaging
cations of noninvasive imaging, value can only be achieved improves visual inter-observer correlation and agreement. J Nucl
if the appropriate patients are selected for testing and if the Cardiol. 2014;21:703–11.
test result changes therapy, such that cost savings or 13. Slomka PJ, Nishina H, Abidov A, Hayes SW, Friedman JD,
Berman DS, Germano G. Combined quantitative supine-prone
improved outcomes can follow the testing strategy. myocardial perfusion SPECT improves detection of coronary
artery disease and normalcy rates in women. J Nucl Cardiol.
Acknowledgement Supported in part by the Adelson Family 2007;14:44–52.
Foundation and the Diane and Guilford Glazer Foundation 14. Chang SM, Nabi F, Xu J, Raza U, Mahmarian JJ. Normal stress-
only versus standard stress/rest myocardial perfusion imaging:
similar patient mortality with reduced radiation exposure. J Am
Coll Cardiol. 2010;55:221–30.
References 15. Duvall WL, Wijetunga MN, Klein TM, Razzouk L, Godbold J,
Croft LB, Henzlova MJ. The prognosis of a normal stress-only
1. Mahmarian JJ, Cerqueira MD, Iskandrian AE, Bateman TM, Tc-99m myocardial perfusion imaging study. J Nucl Cardiol.
Thomas GS, Hendel RC, Moye LA, Olmsted AW. Regadenoson 2010;17:370–7.
induces comparable left ventricular perfusion defects as adenos- 16. Dekemp RA, Declerck J, Klein R, Pan XB, Nakazato R, Tonge C,
ine: a quantitative analysis from the advance MPI 2 trial. JACC Arumugam P, Berman DS, Germano G, Beanlands RS, Slomka
Cardiovasc Imaging. 2009;2:959–68. PJ. Multisoftware reproducibility study of stress and rest myocar-
2. Xu Y, Hayes S, Ali I, Ruddy TD, Wells RG, Berman DS, Germano dial blood flow assessed with 3d dynamic PET/CT and a 1-tissue-
G, Slomka PJ. Automatic and visual reproducibility of perfusion compartment model of 82-Rb kinetics. J Nucl Med. 2013;54:
and function measures for myocardial perfusion SPECT. J Nucl 571–7.
Cardiol. 2010;17:1050–7. 17. Slomka PJ, Alexanderson E, Jacome R, Jimenez M, Romero E,
3. Berman DS, Kang X, Gransar H, Gerlach J, Friedman JD, Hayes Meave A, Le Meunier L, Dalhbom M, Berman DS, Germano G,
SW, Thomson LE, Hachamovitch R, Shaw LJ, Slomka PJ, Yang LD, Schelbert H. Comparison of clinical tools for measurements of
Germano G. Quantitative assessment of myocardial perfusion abnor- regional stress and rest myocardial blood flow assessed with
mality on SPECT myocardial perfusion imaging is more reproduc- 13N-ammonia PET/CT. J Nucl Med. 2012;53:171–81.
ible than expert visual analysis. J Nucl Cardiol. 2009;16:45–53. 18. Murthy VL, Naya M, Foster CR, Hainer J, Gaber M, Di Carli G,
4. Arsanjani R, Xu Y, Dey D, Vahistha V, Shalev A, Nakanishi R, Blankstein R, Dorbala S, Sitek A, Pencina MJ, Di Carli
Hayes S, Fish M, Berman D, Germano G, Slomka PJ. Improved MF. Improved cardiac risk assessment with noninvasive measures
accuracy of myocardial perfusion SPECT for detection of coro- of coronary flow reserve. Circulation. 2011;124:2215–24.
nary artery disease by machine learning in a large population. 19. Ziadi MC, Dekemp RA, Williams KA, Guo A, Chow BJ,
J Nucl Cardiol. 2013;20:553–62. Renaud JM, Ruddy TD, Sarveswaran N, Tee RE, Beanlands
5. Slomka PJ, Pan T, Berman DS, Germano G. Advances in SPECT RS. Impaired myocardial flow reserve on rubidium-82 positron
and pet hardware. Prog Cardiovasc Dis. 2015;57:566–78. emission tomography imaging predicts adverse outcomes in
6. Sharir T, Slomka PJ, Hayes SW, DiCarli MF, Ziffer JA, Martin patients assessed for myocardial ischemia. J Am Coll Cardiol.
WH, Dickman D, Ben-Haim S, Berman DS. Multicenter trial of 2011;58:740–8.
high-speed versus conventional single-photon emission computed 20. Gould KL, Johnson NP. Physiologic stenosis severity, binary
tomography imaging: quantitative results of myocardial perfusion thinking, revascularization, and “hidden reality”. Circ Cardiov
and left ventricular function. J Am Coll Cardiol. 2010;55: Imag. 2015;8:e002970.
1965–74. 21. Gould KL, Johnson NP, Bateman TM, Beanlands RS, Bengel FM,
7. Nakazato R, Berman DS, Hayes SW, Fish M, Padgett R, Xu Y, Bober R, Camici PG, Cerqueira MD, Chow BJ, Di Carli MF,
Lemley M, Baavour R, Roth N, Slomka PJ. Myocardial perfusion Dorbala S, Gewirtz H, Gropler RJ, Kaufmann PA, Knaapen P,
imaging with a solid-state camera: simulation of a very low dose Knuuti J, Merhige ME, Rentrop KP, Ruddy TD, Schelbert HR,
imaging protocol. J Nucl Med. 2013;54:373–9. Schindler TH, Schwaiger M, Sdringola S, Vitarello J, Williams Sr
8. Einstein AJ, Blankstein R, Andrews H, Fish M, Padgett R, Hayes KA, Gordon D, Dilsizian V, Narula J. Anatomic versus physiologic
SW, Friedman JD, Qureshi M, Rakotoarivelo H, Slomka P, assessment of coronary artery disease. Role of coronary flow
Nakazato R, Bokhari S, Di Carli M, Berman DS. Comparison of reserve, fractional flow reserve, and positron emission tomography
image quality, myocardial perfusion, and left ventricular function imaging in revascularization decision-making. J Am Coll Cardiol.
between standard imaging and single-injection ultra-low-dose 2013;62:1639–53.
imaging using a high-efficiency spect camera: the Millisievert 22. Yu M, Guaraldi MT, Mistry M, Kagan M, McDonald JL, Drew K,
study. J Nucl Med. 2014;55:1430–7. Radeke H, Azure M, Purohit A, Casebier DS, Robinson SP.
9. Nakazato R, Slomka PJ, Fish M, Schwartz RG, Hayes SW, Bms-747158-02: a novel PET myocardial perfusion imaging
Thomson LE, Friedman JD, Lemley Jr M, Mackin ML, Peterson agent. J Nucl Cardiol. 2007;14:789–98.
B, Schwartz AM, Doran JA, Germano G, Berman DS. Quantitative 23. Maddahi J. Properties of an ideal PET perfusion tracer: new PET
high-efficiency cadmium-zinc-telluride SPECT with dedicated tracer cases and data. J Nucl Cardiol. 2012;19 Suppl 1:S30–7.
parallel-hole collimation system in obese patients: results of a 24. Berman DS, Maddahi J, Tamarappoo BK, Czernin J, Taillefer R,
multi-center study. J Nucl Cardiol. 2015;22:266–75. Udelson JE, Gibson CM, Devine M, Lazewatsky J, Bhat G,
10. Slomka PJ, Dey D, Duvall WL, Henzlova MJ, Berman DS, Washburn D. Phase II safety and clinical comparison with single-
Germano G. Advances in nuclear cardiac instrumentation with a photon emission computed tomography myocardial perfusion
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 377

imaging for detection of coronary artery disease: Flurpiridaz f 18 38. Shmilovich H, Cheng VY, Tamarappoo BK, Dey D, Nakazato R,
positron emission tomography. J Am Coll Cardiol. 2013;61:469–77. Gransar H, Thomson LE, Hayes SW, Friedman JD, Germano G,
25. Berman DS, Wong ND, Gransar H, Miranda-Peats R, Dahlbeck J, Slomka PJ, Berman DS. Vulnerable plaque features on coronary
Hayes SW, Friedman JD, Kang X, Polk D, Hachamovitch R, CT angiography as markers of inducible regional myocardial
Shaw L, Rozanski A. Relationship between stress-induced myo- hypoperfusion from severe coronary artery stenoses.
cardial ischemia and atherosclerosis measured by coronary cal- Atherosclerosis. 2011;219:588–95.
cium tomography. J Am Coll Cardiol. 2004;44:923–30. 39. Nakazato R, Shalev A, Doh JH, Koo BK, Gransar H, Gomez MJ,
26. Berman DS, Hachamovitch R, Shaw LJ, Friedman JD, Hayes SW, Leipsic J, Park HB, Berman DS, Min JK. Aggregate plaque
Thomson L, Fieno DS, Germano G, Slomka P, Wong ND, Kang volume by coronary computed tomography angiography is
X, Rozanski A. Roles of nuclear cardiology, cardiac computed superior and incremental to luminal narrowing for diagnosis of
tomography, and cardiac magnetic resonance: assessment of ischemic lesions of intermediate stenosis severity. J Am Coll
patients with suspected coronary artery disease. J Nucl Med. Cardiol. 2013;62:460–7.
2006;47:74–82. 40. Park HB, Heo R, o Hartaigh B, Cho I, Gransar H, Nakazato R,
27. Schenker MP, Dorbala S, Hong EC, Rybicki FJ, Hachamovitch R, Leipsic J, Mancini GB, Koo BK, Otake H, Budoff MJ, Berman
Kwong RY, Di Carli MF. Interrelation of coronary calcification, DS, Erglis A, Chang HJ, Min JK. Atherosclerotic plaque charac-
myocardial ischemia, and outcomes in patients with intermediate teristics by CT angiography identify coronary lesions that cause
likelihood of coronary artery disease: a combined positron ischemia: a direct comparison to fractional flow reserve. JACC
emission tomography/computed tomography study. Circulation. Cardiovasc Imaging. 2015;8:1–10.
2008;117:1693–700. 41. Dey D, Schepis T, Marwan M, Slomka PJ, Berman DS, Achenbach
28. Berman DS. Fourth annual Mario s. Verani, md memorial lecture: S. Automated three-dimensional quantification of noncalcified
noninvasive imaging in coronary artery disease: changing roles, coronary plaque from coronary CT angiography: comparison with
changing players. J Nucl Cardiol. 2006;13:457–73. intravascular us. Radiology. 2010;257:516–22.
29. Rudd JH, Warburton EA, Fryer TD, Jones HA, Clark JC, Antoun 42. Diaz-Zamudio M, Dey D, Schuhbaeck A, Nakazato R, Gransar H,
N, Johnstrom P, Davenport AP, Kirkpatrick PJ, Arch BN, Pickard Slomka PJ, Narula J, Berman DS, Achenbach S, Min JK, Doh JH,
JD, Weissberg PL. Imaging atherosclerotic plaque inflammation Koo BK. Automated quantitative plaque burden from coronary
with [18f]-fluorodeoxyglucose positron emission tomography. CT angiography noninvasively predicts hemodynamic signifi-
Circulation. 2002;105:2708–11. cance by using fractional flow reserve in intermediate coronary
30. Rudd JH, Myers KS, Bansilal S, Machac J, Rafique A, Farkouh M, lesions. Radiology. 2015;276(2):408–15.
Fuster V, Fayad ZA. 18-fluorodeoxyglucose positron emission 43. Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M,
tomography imaging of atherosclerotic plaque inflammation is Miller JM, Niinuma H, Yoshioka K, Kitagawa K, Nakamori S,
highly reproducible: implications for atherosclerosis therapy Laham R, Vavere AL, Cerci RJ, Mehra VC, Nomura C, Kofoed
trials. J Am Coll Cardiol. 2007;50:892–6. KF, Jinzaki M, Kuribayashi S, de Roos A, Laule M, Tan SY, Hoe
31. Tawakol A, Fayad ZA, Mogg R, Alon A, Klimas MT, Dansky H, J, Paul N, Rybicki FJ, Brinker JA, Arai AE, Cox C, Clouse ME, Di
Subramanian SS, Abdelbaky A, Rudd JH, Farkouh ME, Nunes Carli MF, Lima JA. Computed tomography angiography and
IO, Beals CR, Shankar SS. Intensification of statin therapy results perfusion to assess coronary artery stenosis causing perfusion
in a rapid reduction in atherosclerotic inflammation: results of a defects by single photon emission computed tomography: the
multicenter fluorodeoxyglucose-positron emission tomography/ core320 study. Eur Heart J. 2014;35:1120–30.
computed tomography feasibility study. J Am Coll Cardiol. 44. Cury RC, Kitt TM, Feaheny K, Blankstein R, Ghoshhajra BB,
2013;62:909–17. Budoff MJ, Leipsic J, Min JK, Akin J, George RT. A randomized,
32. Burke AP, Farb A, Malcom GT, Liang Y, Smialek JE, Virmani R. multicenter, multivendor study of myocardial perfusion imaging
Plaque rupture and sudden death related to exertion in men with with regadenoson CT perfusion vs single photon emission CT.
coronary artery disease. JAMA. 1999;281:921–6. J Cardiovasc Comput Tomogr. 2015;9:103–12.e101–2.
33. Moreno PR, Narula J. Thinking outside the lumen: fractional flow 45. Min JK, Leipsic J, Pencina MJ, Berman DS, Koo BK, van
reserve versus intravascular imaging for major adverse cardiac Mieghem C, Erglis A, Lin FY, Dunning AM, Apruzzese P, Budoff
event prediction. J Am Coll Cardiol. 2014;63:1141–4. MJ, Cole JH, Jaffer FA, Leon MB, Malpeso J, Mancini GB, Park
34. Dweck MR, Chow MW, Joshi NV, Williams MC, Jones C, SJ, Schwartz RS, Shaw LJ, Mauri L. Diagnostic accuracy of frac-
Fletcher AM, Richardson H, White A, McKillop G, van Beek EJ, tional flow reserve from anatomic CT angiography. JAMA.
Boon NA, Rudd JH, Newby DE. Coronary arterial 18F-sodium 2012;308:1237–45.
fluoride uptake: a novel marker of plaque biology. J Am Coll 46. Koo BK, Erglis A, Doh JH, Daniels DV, Jegere S, Kim HS,
Cardiol. 2012;59:1539–48. Dunning A, DeFrance T, Lansky A, Leipsic J, Min JK. Diagnosis
35. Joshi NV, Vesey AT, Williams MC, Shah AS, Calvert PA, of ischemia-causing coronary stenoses by noninvasive fractional
Craighead FH, Yeoh SE, Wallace W, Salter D, Fletcher AM, van flow reserve computed from coronary computed tomographic
Beek EJ, Flapan AD, Uren NG, Behan MW, Cruden NL, Mills angiograms. Results from the prospective multicenter discover-
NL, Fox KA, Rudd JH, Dweck MR, Newby DE. 18F-fluoride flow (diagnosis of ischemia-causing stenoses obtained via
positron emission tomography for identification of ruptured and noninvasive fractional flow reserve) study. J Am Coll Cardiol.
high-risk coronary atherosclerotic plaques: a prospective clinical 2011;58:1989–97.
trial. Lancet. 2014;383:705–13. 47. Nørgaard BL, Leipsic J, Gaur S, Seneviratne S, Ko BS, Ito H,
36. Motoyama S, Kondo T, Sarai M, Sugiura A, Harigaya H, Sato T, Jensen JM, Mauri L, De Bruyne B, Bezerra H, Osawa K, Marwan
Inoue K, Okumura M, Ishii J, Anno H, Virmani R, Ozaki Y, M, Naber C, Erglis A, Park SJ, Christiansen EH, Kaltoft A, Lassen
Hishida H, Narula J. Multislice computed tomographic JF, Bøtker HE, Achenbach S, NXT Trial Study Group. Diagnostic
characteristics of coronary lesions in acute coronary syndromes. performance of non-invasive fractional flow reserve derived from
J Am Coll Cardiol. 2007;50:319–26. coronary ct angiography in suspected coronary artery disease: the
37. Motoyama S, Sarai M, Harigaya H, Anno H, Inoue K, Hara T, nxt trial. J Am Coll Cardiol. 2014;63(12):1145–55.
Naruse H, Ishii J, Hishida H, Wong ND, Virmani R, Kondo T, 48. Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum
Ozaki Y, Narula J. Computed tomographic angiography character- CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones
istics of atherosclerotic plaques subsequently resulting DM, McBride P, Schwartz JS, Shero ST, Smith Jr SC, Watson K,
in acute coronary syndrome. J Am Coll Cardiol. 2009;54: Wilson PW. 2013 ACC/AHA guideline on the treatment of blood
49–57. cholesterol to reduce atherosclerotic cardiovascular risk in adults:
378 D.S. Berman et al.

a report of the American College of Cardiology/American Heart calcium, cardiovascular events, and mortality: results from mesa.
Assocication task force on practice guidelines. J Am Coll Cardiol. Am J Epidemiol. 2013;178:12–21.
2014;63:2889–934. 61. Malik S, Budoff MJ, Katz R, Blumenthal RS, Bertoni AG, Nasir
49. Kavousi M, Leening MJ, Nanchen D, Greenland P, Graham IM, K, Szklo M, Barr RG, Wong ND. Impact of subclinical atheroscle-
Steyerberg EW, Ikram MA, Stricker BH, Hofman A, Franco rosis on cardiovascular disease events in individuals with meta-
OH. Comparison of application of the ACC/AHA guidelines, bolic syndrome and diabetes: the multi-ethnic study of
adult treatment panel iii guidelines, and European Society of atherosclerosis. Diabetes Care. 2011;34:2285–90.
Cardiology guidelines for cardiovascular disease prevention in a 62. Wackers FJ, Young LH, Inzucchi SE, Chyun DA, Davey JA,
European cohort. JAMA. 2014;311:1416–23. Barrett EJ, Taillefer R, Wittlin SD, Heller GV, Filipchuk N,
50. DeFilippis AP, Young R, Carrubba CJ, McEvoy JW, Budoff MJ, Engel S, Ratner RE, Iskandrian AE. Detection of silent myocar-
Blumenthal RS, Kronmal RA, McClelland RL, Nasir K, Blaha dial ischemia in asymptomatic diabetic subjects: the diad study.
MJ. An analysis of calibration and discrimination among multiple Diabetes Care. 2004;27:1954–61.
cardiovascular risk scores in a modern multiethnic cohort. Ann 63. Zellweger MJ, Maraun M, Osterhues HH, Keller U, Muller-Brand
Intern Med. 2015;162:266–75. J, Jeger R, Pfister O, Burkard T, Eckstein F, von Felten S, Osswald
51. Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, S, Pfisterer M. Progression to overt or silent cad in asymptomatic
Liu K, Shea S, Szklo M, Bluemke DA, O’Leary DH, Tracy R, patients with diabetes mellitus at high coronary risk: main findings
Watson K, Wong ND, Kronmal RA. Coronary calcium as a pre- of the prospective multicenter bardot trial with a pilot randomized
dictor of coronary events in four racial or ethnic groups. treatment substudy. JACC Cardiovasc Imaging. 2014;7:1001–10.
N Engl J Med. 2008;358:1336–45. 64. Muhlestein JB, Lappe DL, Lima JA, Rosen BD, May HT,
52. Erbel R, Möhlenkamp S, Moebus S, Schmermund A, Lehmann N, Knight S, Bluemke DA, Towner SR, Le V, Bair TL, Vavere AL,
Stang A, Dragano N, Grönemeyer D, Seibel R, Kälsch H, Bröcker- Anderson JL. Effect of screening for coronary artery disease using
Preuss M, Mann K, Siegrist J, Jöckel KH, Group HNRSI. Coronary CT angiography on mortality and cardiac events in high-risk
risk stratification, discrimination, and reclassification improve- patients with diabetes: the factor-64 randomized clinical trial.
ment based on quantification of subclinical coronary atherosclero- JAMA. 2014;312:2234–43.
sis: the Heinz Nixdorf recall study. J Am Coll Cardiol. 65. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert E,
2010;56:1397–406. Scherer M, Bellinger R, Martin A, Benton R, Delago A, Min JK.
53. Yeboah J, McClelland RL, Polonsky TS, Burke GL, Sibley CT, Diagnostic performance of 64-multidetector row coronary com-
O’Leary D, Carr JJ, Goff DC, Greenland P, Herrington DM. puted tomographic angiography for evaluation of coronary artery
Comparison of novel risk markers for improvement in cardiovas- stenosis in individuals without known coronary artery disease:
cular risk assessment in intermediate-risk individuals. JAMA. results from the prospective multicenter accuracy (assessment by
2012;308:788–95. coronary computed tomographic angiography of individuals
54. Miedema MD, Duprez DA, Misialek JR, Blaha MJ, Nasir K, undergoing invasive coronary angiography) trial. J Am Coll
Silverman MG, Blankstein R, Budoff MJ, Greenland P, Folsom Cardiol. 2008;52:1724–32.
AR. Use of coronary artery calcium testing to guide aspirin utili- 66. Meijboom WB, Meijs MF, Schuijf JD, Cramer MJ, Mollet NR,
zation for primary prevention: estimates from the multi-ethnic van Mieghem CA, Nieman K, van Werkhoven JM, Pundziute G,
study of atherosclerosis. Circ Cardiovasc Qual Outcomes. Weustink AC, de Vos AM, Pugliese F, Rensing B, Jukema JW,
2014;7:453–60. Bax JJ, Prokop M, Doevendans PA, Hunink MG, Krestin GP, de
55. Roberts ET, Horne A, Martin SS, Blaha MJ, Blankstein R, Budoff Feyter PJ. Diagnostic accuracy of 64-slice computed tomography
MJ, Sibley C, Polak JF, Frick KD, Blumenthal RS, Nasir K. Cost- coronary angiography: a prospective, multicenter, multivendor
effectiveness of coronary artery calcium testing for coronary heart study. J Am Coll Cardiol. 2008;52:2135–44.
and cardiovascular disease risk prediction to guide statin 67. Miller JM, Rochitte CE, Dewey M, Arbab-Zadeh A, Niinuma H,
allocation: the multi-ethnic study of atherosclerosis (mesa). PLoS Gottlieb I, Paul N, Clouse ME, Shapiro EP, Hoe J, Lardo AC,
One. 2015;10:e0116377. Bush DE, de Roos A, Cox C, Brinker J, Lima JA. Diagnostic per-
56. Rozanski A, Gransar H, Shaw LJ, Kim J, Miranda-Peats L, Wong formance of coronary angiography by 64-row CT. N Engl J Med.
ND, Rana JS, Orakzai R, Hayes SW, Friedman JD, Thomson LE, 2008;359:2324–36.
Polk D, Min J, Budoff MJ, Berman DS. Impact of coronary artery 68. Neglia D, Rovai D, Caselli C, Pietila M, Teresinska A, Aguade-
calcium scanning on coronary risk factors and downstream testing Bruix S, Pizzi MN, Todiere G, Gimelli A, Schroeder S, Drosch T,
the eisner (early identification of subclinical atherosclerosis by Poddighe R, Casolo G, Anagnostopoulos C, Pugliese F, Rouzet F,
noninvasive imaging research) prospective randomized trial. J Am Le Guludec D, Cappelli F, Valente S, Gensini GF, Zawaideh C,
Coll Cardiol. 2011;57:1622–32. Capitanio S, Sambuceti G, Marsico F, Perrone Filardi P,
57. Nasir K, McClelland RL, Blumenthal RS, Goff Jr DC, Hoffmann Fernandez-Golfin C, Rincon LM, Graner FP, de Graaf MA,
U, Psaty BM, Greenland P, Kronmal RA, Budoff MJ. Coronary Fiechter M, Stehli J, Gaemperli O, Reyes E, Nkomo S, Maki M,
artery calcium in relation to initiation and continuation of cardio- Lorenzoni V, Turchetti G, Carpeggiani C, Marinelli M, Puzzuoli
vascular preventive medications: the multi-ethnic study of athero- S, Mangione M, Marcheschi P, Mariani F, Giannessi D, Nekolla S,
sclerosis (mesa). Circ Cardiovasc Qual Outcomes. 2010;3: Lombardi M, Sicari R, Scholte AJ, Zamorano JL, Kaufmann PA,
228–35. Underwood SR, Knuuti J. Detection of significant coronary artery
58. Orakzai RH, Nasir K, Orakzai SH, Kalia N, Gopal A, Musunuru disease by noninvasive anatomical and functional imaging. Circ
K, Blumenthal RS, Budoff MJ. Effect of patient visualization of Cardio Imag. 2015;8:e002179.
coronary calcium by electron beam computed tomography on 69. Amsterdam EA, Kirk JD, Bluemke DA, Diercks D, Farkouh ME,
changes in beneficial lifestyle behaviors. Am J Cardiol. Garvey JL, Kontos MC, McCord J, Miller TD, Morise A, Newby
2008;101:999–1002. LK, Ruberg FL, Scordo KA, Thompson PD. Testing of low-risk
59. Taylor AJ, Bindeman J, Feuerstein I, Le T, Bauer K, Byrd C, Wu patients presenting to the emergency department with chest pain:
H, O’Malley PG. Community-based provision of statin and aspirin a scientific statement from the American heart association.
after the detection of coronary artery calcium within a community- Circulation. 2010;122:1756–76.
based screening cohort. J Am Coll Cardiol. 2008;51:1337–41. 70. Pope JH, Aufderheide TP, Ruthazer R, Woolard RH, Feldman JA,
60. Ahmed HM, Blaha MJ, Nasir K, Jones SR, Rivera JJ, Agatston A, Beshansky JR, Griffith JL, Selker HP. Missed diagnoses of acute
Blankstein R, Wong ND, Lakoski S, Budoff MJ, Burke GL, Sibley cardiac ischemia in the emergency department. N Engl J Med.
CT, Ouyang P, Blumenthal RS. Low-risk lifestyle, coronary 2000;342:1163–70.
20 Value Based Imaging for Coronary Artery Disease: Implications for Nuclear Cardiology and Cardiac CT 379

71. Udelson JE, Beshansky JR, Ballin DS, Feldman JA, Griffith JL, Chang HJ, Cademartiri F, Chinnaiyan K, Chow BJ, Delago A,
Handler J, Heller GV, Hendel RC, Pope JH, Ruthazer R, Spiegler Hadamitzky M, Hausleiter J, Kaufmann P, Raff G, Shaw LJ,
EJ, Woolard RH, Selker HP. Myocardial perfusion imaging for Villines T, Cury RC, Feuchtner G, Kim YJ, Leipsic J, Berman DS,
evaluation and triage of patients with suspected acute cardiac isch- Min JK. Age-related risk of major adverse cardiac event risk and
emia: a randomized controlled trial. JAMA. 2002;288:2693–700. coronary artery disease extent and severity by coronary ct
72. Duvall WL, Savino JA, Levine EJ, Baber U, Lin JT, Einstein AJ, angiography: results from 15 187 patients from the international
Hermann LK, Henzlova MJ. A comparison of coronary cta and multisite CONFIRM study. Eur Heart J Cardiovasc Imag. 2014;15:
stress testing using high-efficiency spect MPI for the evaluation of 586–94.
chest pain in the emergency department. J Nucl Cardiol. 82. The SCOT-HEART Investigators. CT coronary angiography in
2014;21:305–18. patients with suspected angina due to coronary heart disease
73. Goldstein JA, Chinnaiyan KM, Abidov A, Achenbach S, Berman (SCOT-HEART): an open-label, parallel-group, multicentre trial.
DS, Hayes SW, Hoffmann U, Lesser JR, Mikati IA, O’Neil BJ, Lancet. 2015;385:2383–91.
Shaw LJ, Shen MY, Valeti US, Raff GL. The CT-STAT (coronary 83. Douglas PS, Hoffmann U, Patel MR, Mark DB, Al-Khalidi HR,
computed tomographic angiography for systematic triage of acute Cavanaugh B, Cole J, Dolor RJ, Fordyce CB, Huang M, Khan
chest pain patients to treatment) trial. J Am Coll Cardiol. MA, Kosinski AS, Krucoff MW, Malhotra V, Picard MH, Udelson
2011;58:1414–22. JE, Velazquez EJ, Yow E, Cooper LS, Lee KL. Outcomes of
74. Litt HI, Gatsonis C, Snyder B, Singh H, Miller CD, Entrikin DW, anatomical versus functional testing for coronary artery disease. N
Leaming JM, Gavin LJ, Pacella CB, Hollander JE. CT angiogra- Engl J Med. 2015;372:1291–300.
phy for safe discharge of patients with possible acute coronary 84. Schuijf JD, Jukema JW, van der Wall EE, Bax JJ. The current
syndromes. N Engl J Med. 2012;366:1393–403. status of multislice computed tomography in the diagnosis and
75. Hoffmann U, Truong QA, Schoenfeld DA, Chou ET, Woodard prognosis of coronary artery disease. J Nucl Cardiol. 2007;14(4):
PK, Nagurney JT, Pope JH, Hauser TH, White CS, Weiner SG, 604–12.
Kalanjian S, Mullins ME, Mikati I, Peacock WF, Zakroysky P, 85. Zeb I, Abbas N, Nasir K, Budoff MJ. Coronary computed tomog-
Hayden D, Goehler A, Lee H, Gazelle GS, Wiviott SD, Fleg JL, raphy as a cost-effective test strategy for coronary artery disease
Udelson JE. Coronary CT angiography versus standard evaluation assessment – a systematic review. Atherosclerosis. 2014;
in acute chest pain. N Engl J Med. 2012;367:299–308. 234:426–35.
76. Hamilton-Craig C, Fifoot A, Hansen M, Pincus M, Chan J, 86. Abidov A, Gallagher MJ, Chinnaiyan KM, Mehta LS, Wegner JH,
Walters DL, Branch KR. Diagnostic performance and cost of CT Raff GL. Clinical effectiveness of coronary computed tomographic
angiography versus stress ECG – a randomized prospective study angiography in the triage of patients to cardiac catheterization and
of suspected acute coronary syndrome chest pain in the emer- revascularization after inconclusive stress testing: results of a
gency department (ct-compare). Int J Cardiol. 2014;177:867–73. 2-year prospective trial. J Nucl Cardiol. 2009;16:701–13.
77. Anthem. Coronary artery imaging: contrast-enhanced Coronary 87. Rozanski A, Cohen R, Uretsky S. The coronary calcium treadmill
Computed Tomography Angiography (CCTA), Coronary test: a new approach to the initial workup of patients with
Magnetic Resonance Angiography (MRA) and Cardiac Magnetic suspected coronary artery disease. J Nucl Cardiol. 2013;20:
Resonance Imaging (MRI). Medical Policy #: RAD 00035; 719–30.
Current Effective Date: 04/077/2015; Last Review Date: 88. Cremer P, Hachamovitch R. Assessing the prognostic implications
02/05/2015. of myocardial perfusion studies: identification of patients at risk
78. Min JK, Dunning A, Lin FY, Achenbach S, Al-Mallah M, Budoff vs patients who may benefit from intervention? Curr Cardiol Rep.
MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V, Chinnaiyan 2014;16:472.
K, Chow BJ, Delago A, Hadamitzky M, Hausleiter J, Kaufmann P, 89. Shaw LJ, Hage FG, Berman DS, Hachamovitch R, Iskandrian
Maffei E, Raff G, Shaw LJ, Villines T, Berman DS, Investigators A. Prognosis in the era of comparative effectiveness research:
C. Age- and sex-related differences in all-cause mortality risk where is nuclear cardiology now and where should it be? J Nucl
based on coronary computed tomography angiography findings Cardiol. 2012;19:1026–43.
results from the international multicenter confirm (coronary ct 90. Bourque JM, Beller GA. Stress myocardial perfusion imaging for
angiography evaluation for clinical outcomes: an international assessing prognosis: an update. JACC Cardiovasc Imaging.
multicenter registry) of 23,854 patients without known coronary 2011;4:1305–19.
artery disease. J Am Coll Cardiol. 2011;58:849–60. 91. Dorbala S, Di Carli MF, Beanlands RS, Merhige ME, Williams
79. Leipsic J, Taylor CM, Grunau G, Heilbron BG, Mancini GB, BA, Veledar E, Chow BJ, Min JK, Pencina MJ, Berman DS, Shaw
Achenbach S, Al-Mallah M, Berman DS, Budoff MJ, Cademartiri LJ. Prognostic value of stress myocardial perfusion positron
F, Callister TQ, Chang HJ, Cheng VY, Chinnaiyan K, Chow BJ, emission tomography: results from a multicenter observational
Delago A, Hadamitzky M, Hausleiter J, Cury R, Feuchtner G, registry. J Am Coll Cardiol. 2013;61:176–84.
Kim YJ, Kaufmann PA, Lin FY, Maffei E, Raff G, Shaw LJ, 92. Berman DS, Shaw LJ, Min JK, Hachamovitch R, Abidov A,
Villines TC, Min JK. Cardiovascular risk among stable individuals Germano G, Hayes SW, Friedman JD, Thomson LE, Kang X,
suspected of having coronary artery disease with no modifiable Slomka P, Rozanski A. SPECT/PET myocardial perfusion imag-
risk factors: results from an international multicenter study of ing versus coronary ct angiography in patients with known
5262 patients. Radiology. 2013;267:718–26. or suspected CAD. Q J Nucl Med Mol Imaging. 2010;54:
80. Arsanjani R, Berman DS, Gransar H, Cheng VY, Dunning A, Lin 177–200.
FY, Achenbach S, Al-Mallah M, Budoff MJ, Callister TQ, Chang 93. Berman DS, Hachamovitch R, Shaw LJ, Hayes SW, Germano G.
HJ, Cademartiri F, Chinnaiyan KM, Chow BJ, DeLago A, Nuclear cardiology. In: Fuster VAR, O’Rourke RA, Roberts R,
Hadamitzky M, Hausleiter J, Kaufmann P, LaBounty TM, Leipsic King SB, Wellens HJJ, editors. Hurst’s the heart. New York:
J, Raff G, Shaw LJ, Villines TC, Cury RC, Feuchtner G, Kim YJ, McGraw-Hill Companies; 2004. p. 563–97.
Min JK. Left ventricular function and volume with coronary ct 94. Boden WE, O’Rourke RA, Teo KK, Hartigan PM, Maron DJ,
angiography improves risk stratification and identification of Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL,
patients at risk for incident mortality: results from 7758 patients in Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G,
the prospective multinational confirm observational cohort study. Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS,
Radiology. 2014;273:70–7. Mancini GB, Weintraub WS. Optimal medical therapy with or
81. Nakazato R, Arsanjani R, Achenbach S, Gransar H, Cheng VY, without PCI for stable coronary disease. N Engl J Med. 2007;
Dunning A, Lin FY, Al-Mallah M, Budoff MJ, Callister TQ, 356:1503–16.
380 D.S. Berman et al.

95. Frye RL, August P, Brooks MM, Hardison RM, Kelsey SF, revascularization to reduce myocardial infarction and mortality:
MacGregor JM, Orchard TJ, Chaitman BR, Genuth SM, Goldberg new lessons from randomized trials, coronary physiology, and sta-
SH, Hlatky MA, Jones TL, Molitch ME, Nesto RW, Sako EY, tistics. Circ Cardio Imag. 2015;8:e003099.
Sobel BE, Group BDS. A randomized trial of therapies for type 2 107. Rozanski A, Gransar H, Hayes SW, Min J, Friedman JD, Thomson
diabetes and coronary artery disease. N Engl J Med. 2009;360: LE, Berman DS. Temporal trends in the frequency of inducible
2503–15. myocardial ischemia during cardiac stress testing: 1991 to 2009.
96. Tonino PA, De Bruyne B, Pijls NH, Siebert U, Ikeno F, van’ t Veer J Am Coll Cardiol. 2013;61:1054–65.
M, Klauss V, Manoharan G, Engstrøm T, Oldroyd KG, Ver Lee 108. Cheng VY, Berman DS, Rozanski A, Dunning AM, Achenbach S,
PN, MacCarthy PA, Fearon WF, FAME Study Investigators. Al-Mallah M, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ,
Fractional flow reserve versus angiography for guiding percutane- Chinnaiyan K, Chow BJ, Delago A, Gomez M, Hadamitzky M,
ous coronary intervention. N Engl J Med. 2009;360:213–24. Hausleiter J, Karlsberg RP, Kaufmann P, Lin FY, Maffei E,
97. Pijls NH, Fearon WF, Tonino PA, Siebert U, Ikeno F, Bornschein B, Raff GL, Villines TC, Shaw LJ, Min JK. Performance of the tradi-
van’t Veer M, Klauss V, Manoharan G, Engstrøm T, Oldroyd KG, tional age, sex, and angina typicality-based approach for estimat-
Ver Lee PN, MacCarthy PA, De Bruyne B, Investigators FS. ing pretest probability of angiographically significant coronary
Fractional flow reserve versus angiography for guiding percutane- artery disease in patients undergoing coronary computed tomo-
ous coronary intervention in patients with multivessel coronary graphic angiography: results from the multinational coronary ct
artery disease: 2-year follow-up of the fame (fractional flow reserve angiography evaluation for clinical outcomes: an international mul-
versus angiography for multivessel evaluation) study. J Am Coll ticenter registry (CONFIRM). Circulation. 2011;124:2423–32.
Cardiol. 2010;56:177–84. 109. Tonino PA, Fearon WF, De Bruyne B, Oldroyd KG, Leesar MA,
98. De Bruyne B, Pijls NH, Kalesan B, Barbato E, Tonino PA, Piroth Z, Ver Lee PN, MacCarthy PA, Van’t Veer M, Pijls NH. Angiographic
Jagic N, Mobius-Winkler S, Rioufol G, Witt N, Kala P, MacCarthy P, versus functional severity of coronary artery stenoses in the FAME
Engstrom T, Oldroyd KG, Mavromatis K, Manoharan G, Verlee P, study: fractional flow reserve versus angiography in multivessel
Frobert O, Curzen N, Johnson JB, Juni P, Fearon WF. Fractional flow evaluation. J Am Coll Cardiol. 2010;55(25):2816–21.
reserve-guided pci versus medical therapy in stable coronary disease. 110. Zhou T, Yang LF, Zhai JL, Li J, Wang QM, Zhang RJ, Wang S,
N Engl J Med. 2012;367:991–1001. Peng ZH, Li M, Sun G. SPECT myocardial perfusion versus frac-
99. Li J, Elrashidi MY, Flammer AJ, Lennon RJ, Bell MR, Holmes tional flow reserve for evaluation of functional ischemia: a meta
DR, Bresnahan JF, Rihal CS, Lerman LO, Lerman A. Long-term analysis. Eur J Radiol. 2014;83:951–6.
outcomes of fractional flow reserve-guided vs. Angiography- 111. Min JK, Dunning A, Gransar H, Achenbach S, Lin FY, Al-Mallah
guided percutaneous coronary intervention in contemporary M, Budoff MJ, Callister TQ, Chang HJ, Cademartiri F, Maffei E,
practice. Eur Heart J. 2013;34:1375–83. Chinnaiyan K, Chow BJ, D’Agostino R, DeLago A, Friedman J,
100. Hachamovitch R, Berman DS, Shaw LJ, Kiat H, Cohen I, Cabico Hadamitzky M, Hausleiter J, Hayes SW, Kaufmann P, Raff GL,
JA, Friedman J, Diamond GA. Incremental prognostic value of Shaw LJ, Thomson L, Villines T, Cury RC, Feuchtner G, Kim YJ,
myocardial perfusion single photon emission computed Leipsic J, Berman DS, Pencina M. Medical history for prognostic
tomography for the prediction of cardiac death: differential risk assessment and diagnosis of stable patients with suspected
stratification for risk of cardiac death and myocardial infarction. coronary artery disease. Am J Med. 2015;128(8):871–8.
Circulation. 1998;97:535–43. 112. Levine A, Hecht HS. Cardiac CT angiography in congestive heart
101. Hachamovitch R, Hayes SW, Friedman JD, Cohen I, Berman failure. J Nucl Med. 2015;56 Suppl 4:46s–51.
DS. Comparison of the short-term survival benefit associated with 113. Hachamovitch R, Nutter B, Hlatky MA, Shaw LJ, Ridner ML,
revascularization compared with medical therapy in patients with Dorbala S, Beanlands RS, Chow BJ, Branscomb E,
no prior coronary artery disease undergoing stress myocardial Chareonthaitawee P, Weigold WG, Voros S, Abbara S, Yasuda T,
perfusion single photon emission computed tomography. Jacobs JE, Lesser J, Berman DS, Thomson LE, Raman S, Heller
Circulation. 2003;107:2900–7. GV, Schussheim A, Brunken R, Williams KA, Farkas S, Delbeke
102. Hachamovitch R, Rozanski A, Shaw LJ, Stone GW, Thomson LE, D, Schoepf UJ, Reichek N, Rabinowitz S, Sigman SR, Patterson
Friedman JD, Hayes SW, Cohen I, Germano G, Berman DS. R, Corn CR, White R, Kazerooni E, Corbett J, Bokhari S, Machac
Impact of ischaemia and scar on the therapeutic benefit derived J, Guarneri E, Borges-Neto S, Millstine JW, Caldwell J, Arrighi J,
from myocardial revascularization vs. Medical therapy among Hoffmann U, Budoff M, Lima J, Johnson JR, Johnson B, Gaber
patients undergoing stress-rest myocardial perfusion scintigraphy. M, Williams JA, Foster C, Hainer J, Di Carli MF, SPARC
Eur Heart J. 2011;32:1012–24. Investigators. Patient management after noninvasive cardiac
103. Hachamovitch R, Kang X, Amanullah AM, Abidov A, Hayes SW, imaging results from sparc (study of myocardial perfusion and
Friedman JD, Cohen I, Thomson LE, Germano G, Berman coronary anatomy imaging roles in coronary artery disease). J Am
DS. Prognostic implications of myocardial perfusion single- Coll Cardiol. 2012;59:462–74.
photon emission computed tomography in the elderly. Circulation. 114. Beanlands RS, Nichol G, Huszti E, Humen D, Racine N, Freeman
2009;120:2197–206. M, Gulenchyn KY, Garrard L, de Kemp R, Guo A, Ruddy TD,
104. Sorajja P, Chareonthaitawee P, Rajagopalan N, Miller TD, Frye Benard F, Lamy A, Iwanochko RM. F-18-fluorodeoxyglucose
RL, Hodge DO, Gibbons RJ. Improved survival in asymptomatic positron emission tomography imaging-assisted management of
diabetic patients with high-risk SPECT imaging treated with coro- patients with severe left ventricular dysfunction and suspected
nary artery bypass grafting. Circulation. 2005;112:I311–6. coronary disease: a randomized, controlled trial (parr-2). J Am
105. Taqueti VR, Hachamovitch R, Murthy VL, Naya M, Foster CR, Coll Cardiol. 2007;50:2002–12.
Hainer J, Dorbala S, Blankstein R, Di Carli MF. Global coronary 115. Abraham A, Nichol G, Williams KA, Guo A, deKemp RA,
flow reserve is associated with adverse cardiovascular events Garrard L, Davies RA, Duchesne L, Haddad H, Chow B, DaSilva
independently of luminal angiographic severity and modifies the J, Beanlands RS. 18F-FDG pet imaging of myocardial viability in
effect of early revascularization. Circulation. 2015;131:19–27. an experienced center with access to 18f-fdg and integration with
106. Gould KL, Johnson NP, Kaul S, Kirkeeide RL, Mintz GS, Rentrop clinical management teams: the Ottawa-five substudy of the parr 2
KP, Sdringola S, Virmani R, Narula J. Patient selection for elective trial. J Nucl Med. 2010;51:567–74.
 Coronary Computed Tomographic
Angiography for Detection of Coronary 21
Artery Disease: Analysis of Large-Scale
Multicenter Trials and Registries

Leslee J. Shaw

Abstract
The field of coronary computed tomographic angiography (CCTA) has evolved dramatically
with an ever increasing and robust evidence base to support its clinical utility in terms of an
unparalleled diagnostic accuracy and effective risk stratification rivaling the more commonly
applied, comparative stress imaging procedures. This chapter seeks to highlight the available
high quality effectiveness evidence, including large observational and randomized trial data,
that support the utility of CCTA as a valuable tool in the diagnosis of coronary artery
disease.

Keywords
Quality Research • Effectiveness Research • Multicenter Trial • Randomized Trials

Introduction given the enormity of this task, we cannot be all inclusive but
hope to provide readers with a smattering of the available
The field of coronary computed tomographic angiography evidence within selective indications which strongly support
(CCTA) has evolved dramatically with an ever increasing CCTA as clinically effective and enhancing patient care.
and robust evidence base to support its clinical utility in Moreover, we will highlight specific leadership on the part of
terms of an unparalleled diagnostic accuracy and effective CCTA investigators to provide a clinically effective tool
risk stratification rivaling the more commonly applied, com- while enhancing radiation safety profiles.
parative stress imaging procedures. It is difficult to fathom
but, in 2005, 64-slice CCTA was introduced and, in less than
a decade, all of our knowledge base on the strengths and Coverage with Evidence Development
limitations of this noninvasive, anatomic procedure have
been revealed. The CCTA community, including combined In 2008, the Centers for Medicaid and Medicare Services
expertise in cardiology and radiology, has strategically reviewed the available evidence with CCTA and recom-
sought to answer both technical and clinical questions with mended that there be no national coverage determination due
regards to the accuracy and effectiveness of this procedure to to a paucity of evidence in certain indications. Although one
guide optimal patient care strategies. may argue that none of the other competitive and commonly-
In this chapter, we will highlight the current high quality employed models were held to such a high standard, these
evidence based on the clinical utility of CCTA. Importantly, new standards reflect our current state of affairs for payer
policies. In today’s challenging healthcare environment, cov-
erage policies are garnered by a sufficiently high level of evi-
L.J. Shaw, PhD dence noting that an imaging modality is capable of
Department of Medicine, Emory Clinical Cardiovascular
improving clinical outcomes of patients. This new standard
Research Institute, Emory University School of Medicine,
1462 Clifton Rd NE, Rm 529, Atlanta 30324, GA, USA has been termed patient-centered imaging and places the
e-mail: [email protected] core aims of imaging aligned with each patient and the

© Springer International Publishing 2016 381

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_21
382 L.J. Shaw

ultimate goal of improved quality or quantity of life as stratification of major adverse cardiac events (MACE) (i.e.,
initiated based on anatomic markers identified during the cardiac death or nonfatal myocardial infarction). These
CCTA procedure. Given this new standard, where are we results were confirmatory of prior findings noting a directly
today in evidence for clinical indications? proportional relationship between CAC scores and MACE
risk. That is, there is a very low risk of MACE in patients
with no CAC or a zero score. As the CAC score increases
Growth in CCTA Research (i.e., becomes more extensive), the overall MACE risk
increases; such that for patients with a CAC score of 300–
Since 2005, there has been an explosion in published research on 400 or higher, the MACE risk is at least 10 % over 5 years
CCTA. Based on statistics from Thomson Reuters’ Web of [2]. This risk is exceedingly high for asymptomatic
Knowledge which collects data on all published manuscripts, individuals and has been consistently reported across
approximately 30 peer-reviewed manuscripts were published in numerous patient and population cohorts [3, 4].
2004 and this number has grown to over 180 for 2013. This is One may actually quantify the added contribution to risk
dramatic growth and reflects the fact that, in 2013, CCTA articles estimation using the net reclassification improvement (NRI)
were cited over 3500 times. This acceleration in the published statistic [5]. Two reports have been published on the calcula-
literature, as we will highlight, reflects not only the expansive- tion of the NRI using the MESA population registry [6, 7]. In
ness of the evidence but also high quality evidence supporting the first of these series, the NRI was 0.25 revealing that CAC
CCTA as a highly effective diagnostic test procedure. findings improve the detection of lower or higher risk status
for 1 in 4 individuals when compared to risk estimation using
the Framingham risk score [6]. This NRI statistic for CAC is
Specific Clinical Indications for CCTA much higher than for other markers, such as high sensitivity
with High Level Evidence Supporting Clinical C-reactive protein (CRP) [8]. An updated report from MESA,
Effectiveness in intermediate risk individuals, compared the NRI for CAC
as compared to other markers such as a family history of pre-
In this chapter, we will highlight specific evidence on three mature coronary heart disease, CRP, ankle brachial index, and
specific clinical indications for the use of CCTA including: carotid intima-media thickness (Fig. 21.1) [7]. If one exam-
ines the NRI results for a prognostic model estimating 7-year
1. Diagnostic Testing for the Detection of High Risk Patients incidence of MACE (defined as myocardial infarction, coro-
with Coronary Artery Calcium (CAC) Scoring nary heart disease death, resuscitated cardiac arrest, or angina
2. Acute Evaluation of Low Risk Chest Pain in the followed by coronary revascularization), the statistic for CAC
Emergency Department (ED) was 0.66 and at least 6-fold higher than for many of the other
3. Diagnosis and Risk Stratification of Patients with Stable risk markers [7].
Chest Pain A limitation with the available CAC evidence is the lack
of randomized trials noting improved outcomes. Despite this
there are several additional publications that are relevant to
Detecting High Risk Patients with CAC answering this question. In a related secondary analysis from
Scoring the MESA registry, Blaha and colleagues reported on the
number needed to treat (NNT) to save a life if CAC screening
Let us begin our review of the CCTA evidence by focusing was employed to target treatment with statin therapy (in this
on the available and high quality evidence on screening of case, 20 mg of rosuvastatin) [9]. This result revealed that if
apparently healthy individuals. In 2010, the American all patients with a 0 CAC score were treated with statins, the
College of Cardiology published a thorough review of the NNT would be over 500. However, if only patients with a
available evidence across all cardiovascular screening CAC score of 100 or higher were targeted, then the NNT
modalities [1]. We will highlight the results of this guideline would be dramatically reduced to 24 [9].
but also discuss more recent publications which have There have been several intermediate outcome trials which
extended these findings on the use of CAC screening. have randomized patients to CAC scanning versus no scanning
Although numerous reports were published using patient with primary outcomes of change in the Framingham risk score
series, the National Institutes of Health – National Heart, [10, 11]. In the Early Identification of Subclinical Atherosclerosis
Lung, and Blood Institute-sponsored Multi-Ethnic Study of by Noninvasive Imaging Research (EISNER) trial, a 2:1 ran-
Atherosclerosis (MESA) published 5-year outcome data domization had 1311 patients receiving CAC scanning and 623
following CAC scoring in 6724 asymptomatic apparently did not receive CAC scanning [10]. The primary findings from
healthy people ages 45–84 years [2]. The evidence from this this trial revealed that CAC scanning resulted in minimal change
population cohort revealed that CAC scoring was in the Framingham risk score (0.002 %) by comparison there
independently predictive and highly effective at risk was a marked worsening of this risk score in patients not
21 Coronary Computed Tomographic Angiography for Detection of Coronary Artery Disease 383

1.8

1.6

1.4

1.2

0.8
0.659
0.6

0.4

0.16
0.2 0.102
0.079
0.024 0.036
0
FRS + Brachial FMD FRS + Ankle Brachial FRS + CRP FRS + Family History FRS + C-IMT FRS + CAC
Index

Fig. 21.1 Net reclassification improvement (NRI) results form the intima media thickness (C-IMT), and coronary artery calcium (CAC).
NIH-NHLBI-sponsored MESA registry including intermediate The NRI compares the added value of each of the sreening tests when
Framingham risk score (FRS) patients. The results indicate the NRI compared to the FRS alone. The endpoint for this analysis is 7-year
based on an array of screening tests including brachial flow mediate myocardial infarction, coronary heart disease death, resuscitated car-
dilation (FMD), high sensitivity C-reactive protein (CRP), carotid diac arrest, or angina followed by coronary revascularization

receiving the CAC scan (0.7 %, p = 0.0003). As well, patients largely include patients with a low risk Thrombolysis in
randomized to receive the CAC scan showed net favorable Myocardial Ischemia (TIMI) risk score whose index tropo-
changes in systolic blood pressure (p = 0.02), LDL cholesterol nin level was negative. For this indication, there are three
(p = 0.04), and for improvements in waist circumference for relatively large randomized clinical trials which have been
those with an increased abdominal girth (p = 0.01) [10]. published and include a total of 3069 patients [12–14]. Each
The compilation of evidence is quite strong and does of the trials compared a CCTA-driven strategy as compared
reveal that CAC scoring is highly effective at identifying to the current standard of care (SOC); with this largely
high risk patients. Yet, to date, this body of evidence has not including some form of stress testing [12–14]. The most
been compelling to support universal coverage for CAC prominent finding from all 3 trials has been the time to
scoring. Medicare covers CAC for asymptomatic persons in diagnosis, length of stay, and the proportion of patients that
17 states, however, most current Medicare policies are based were discharged from the ED [12–14]. For all trials, time
on treatment for illness and not screening of the well. All efficiency was demonstrably superior with CCTA as
screening coverage policies, such as mammography, must be compared to the SOC. For example, from one trial, 47 % of
legislated. To date, there is a lack of trial evidence, similar to patients in the CCTA arm were discharged from the ED as
that recently reported for lung cancer, which demonstrates compared to only 12 % of the SOC arm [12]. Thus, CCTA
improved outcomes for patients randomized to CAC scoring reduced the overall length of stay in the ED by 7.6 h [14].
as compared to those without CAC scanning. Figure 21.2 depicts the proportional rate of discharge across
the length of time spent in the ED [12].
The longer length of stay in those receiving the SOC led
Efficiency of CCTA in the Acute Evaluation to higher costs of care for one trial (on average $1321 cost
of Low Risk Chest Pain in the Emergency savings with CCTA) but in another trial, the CCTA arm led
Department (ED) to more intensive care and resulted in similar ED costs
(p = 0.7) [13, 14]. To this extent, it remains uncertain as to
As we turn to the available evidence in symptomatic patients, whether the CCTA-guided diagnostic efficiency can lead to
our initial review of the evidence is on the use of CCTA for economic savings for the healthcare system. Moreover, we
the evaluation of low risk chest pain in the ED. This would may learn that the prevalence of CAD identified by CCTA in
384 L.J. Shaw

Fig. 21.2 An approximation of 1

the proportion of patients
discharged from the ED for those 0.9
patients randomized to CCTA as
compared with SOC. The 0.8
medianlength of stay was 8.6 h
for patients receiving CCTA as 0.7
compared to 26.7 h for those
0.6
within the SOC arm of the
ROMICAT II trial 0.5 CCTA
SOC
0.4

0.3

0.2

0.1

0
0 6 12 18 24 30 36 42 48

the ED may be the key factor in defining cost savings. That Despite the limitations, this robust body of evidence is supe-
is, should the likelihood of CAD be elevated, the higher rior to the stress imaging data. For example, there is but one
prevalence of CAD may require more intensive follow-up large clinical trial on the impact of stress nuclear in the (ER
including invasive angiography or stress imaging studies that Assessment of Sestamibi for Evaluation of Chest Pain [ERASE]
increase the overall costs of care. By comparison, should we Trial). The ERASE trial enrolled a total of 2127 patients who
be able to define patients with largely negative CCTA were randomized to receive an index resting nuclear scan as
findings, then the lack of anatomic findings may prove to compared to usual care [18]. In 2127 patients, a total of 52 %
impact on cost savings to a greater extent when compared to of the usual care arm were discharged as compared to 42 % of
higher risk populations. Of course, with this latter statement, those randomized to the nuclear scan arm (odds ratio: 0.68,
one has to take care not to employ CCTA in too low risk 95 % confidence intervals = 0.57–0.82) [18]. Similar to CCTA,
patients where the radiation exposure would be unwarranted. the extent to which patients have prior CAD which impacts on
Suffice it to say that additional explorations of the potential resting perfusion abnormalities are likely the critical factor in
for cost minimization in the ED by selectively employing early discharge for patients presenting with acute chest pain.
CCTA remains an area of active exploration. Despite this, the differential in discharge appears greater for
An additional challenge with the current evidence base is CCTA as compared to that of the ERASE trial.
the lack of longterm data on clinical effectiveness of random- A point worth making in this discussion is the extent to
ization to CCTA versus SOC. The randomized trials employed which identification of an obstructive lesion is the source of
thus far have largely examined near-term outcomes of 1–6 the presenting symptoms. Despite a stenosis, the presence of
months [12–14]. From the ACRIN-PA trial, none of the 640 collateral flow or the distal site of the stenosis may not
patients with a negative CCTA died or had a nonfatal myocar- prompt presenting symptoms and this remains an important
dial infarction within one month of discharge from the ED [13]. consideration and challenge for CCTA. However, issues
The UK’s National Health Service technology assessment sup- related to soft tissue attenuation with stress nuclear can result
ported the use of CCTA in the ED as a cost effective strategy in a false positive rate of follow-up angiography that is
for troponin negative patients [15]. A recent meta-analysis unacceptably high [19]. The incorporation of CT fractional
revealed that the near-term odds of readmission for an acute flow reserve (CT-FFR) calculations in conjunction with the
coronary syndrome were non-significant with an odds ratio of anatomic findings may prove optimal for guiding patient
1.2 (95 % confidence intervals: 0.7–2.2) [16]. In one recent care in the acute evaluation of chest pain [20]. The addition
report examining long-term (i.e., ~4 years follow-up) of 506 of FFR improves the diagnostic accuracy of anatomy defined
discharged patients without plaque and patients with nonob- by CCTA but is limited by the length of time required for the
structive plaque, only 1 % were readmitted for chest pain and complex calculations and remote calculation of the FFR
none of the patients underwent revascularization, died, or had measurement. Despite this, improvements in the technology
an acute coronary syndrome [17]. Data such as this on the long- and the addition of this FFR measurement in the near-term
term consequences of CCTA-guided discharge will surely help post-discharge may prove optimal for long-term effectiveness
to ensure confidence and define the warranty period of the of a CCTA-guided strategy following acute evaluation of
index diagnosis as to the presence and extent of CAD. chest pain in the ED.
21 Coronary Computed Tomographic Angiography for Detection of Coronary Artery Disease 385

Fig. 21.3 Annual rate of major 1.00 %

CAD events for patients with a
negative CCTA and stress
nuclear result 0.80 %

0.66 %

0.60 %

0.40 %

0.20 %
0.20 %

0.00 %
CCTA Stress Nuclear

We highlighted the high quality of evidence on the use of and nonobstructive CAD findings on CCTA [26–31]. The
CCTA in the ED and it is worth noting that the depth of evi- largest of the registry data is that from the COronary CTA
dence far exceeds that of other modalities. Likely, when EvaluatioN For Clinical Outcomes: An InteRnational
additional clinical practice guidelines are updated on acute Multicenter (CONFIRM) multicenter and multinational
coronary syndrome care that CCTA will garner a high level registry enrolling more than 30,000 patients who have been
recommendation based on these three randomized trials followed for approximately 3–5 years for the occurrence of
[12–14]. death from all-causes and nonfatal myocardial infarction
[32]. Several important findings have been revealed by
examining risk stratification data in a diverse and expansive
Diagnostic and Prognostic Value of CCTA group of patients. First, in all of these reports, CCTA findings
in Multicenter Trials and Registries of the extent and severity of CAD provide effective means to
risk stratify patients [28]. Reports have been published
Our next set of indications is to examine the available evi- across an array of age and gender subsets of diverse race/
dence supporting the use of CCTA in the evaluation of ethnicity [28, 33, 34], in the diabetic [35, 36], post-coronary
patients with stable chest pain. Notably, the evidence with bypass surgery [37], in patients with a family history of CAD
CCTA is largely based on large, multicenter registries and [38], to name a few. The extensiveness of this evidence and
several controlled clinical trials. If we start with the early evi- its rapid accrual is a testimony to the CCTA’s community of
dence that examined the correlation of findings between investigators who are eager to define the strengths and limi-
CCTA and invasive coronary angiography, there are three tations of CCTA as an index diagnostic procedure.
controlled clinical trials that have been published [21–23]. Secondly, from this evidence base, multiple reports from
These trials represented pivotal evidence that the anatomic diverse countries now report that patients with a normal
findings that we commonly observe with invasive angiogra- CCTA have a very low rate of CAD events [28, 39–41]. A
phy were concordant with the newly introduced CCTA ana- synthesis of this evidence examining follow-up through 7
tomic findings. In fact, the results revealed a high degree of years reveals that the major CAD event rate is approximately
accuracy for CCTA when compared to invasive anatomic 0.2 % per year (Fig. 21.3) [28, 39–41]; similar to that of the
findings. From one cohort with a low-intermediate risk of general population. For stress echocardiography and nuclear
CAD, the diagnostic sensitivity and specificity for obstructive imaging, the annual rate of major CAD event rates is gener-
CAD on invasive angiography was 94 and 83 % [3]. From the ally <1 % per year but exceeds that for CCTA; generally in
CorE64 trial, the diagnostic sensitivity and specificity was 85 the range of 0.4–0.9 % [25, 42].
and 90 % [22]. As well, from one meta-analysis of the data on Third, several reports now reveal that the presence of mild
64 slice CCTA, the diagnostic sensitivity and specificity was but nonobstructive CAD is associated with an elevated hazard
94 and 85 % [24]. These data reveal an overall higher diag- for death above and beyond that of patients with a normal
nostic accuracy for CCTA in the detection of obstructive CCTA [26–28, 31]. From one series of 2583 symptomatic
CAD when compared to that of stress imaging [25]. patients with <50 % stenosis on CCTA and followed for
Extending beyond these trials, there have been numerous approximately 3 years, the mortality hazard for all-cause
reports on the prognostic relationship between obstructive death was elevated 2- to 6-fold for patients with 1–3 vessel
386 L.J. Shaw

Fig. 21.4 Observational

evidence on the impact of 6.00%
coronary revascularization
5.3%
based on CCTA-defined high
risk CAD 5.00%

4.00%

3.00%
2.3%
2.00%

1.00%

0.00%
Coronary Revascularization Medical Therapy

High Risk CAD

nonobstructive CAD [31]. In ground-breaking work by 2012 Stable Ischemic Heart Disease Clinical
Motoyama and Narula [26, 27], the presence of high risk Practice Guidelines: Indications for CCTA
plaque, defined as positive arterial remodeling and low atten-
uation plaque, was associated with a very high risk of incident Recently, a culmination of evidence among patients with sta-
acute coronary syndromes. In patients without any high risk ble chest pain was published in the 2012 American College of
plaque, the acute coronary syndrome rate was 0.5 % at 4-years Cardiology’s Stable Ischemic Heart Disease clinical practice
of follow-up. By comparison, for patients with both positive guideline [44]. Based on this sizeable evidence base with
remodeling and low attenuation plaque, the acute coronary CCTA, there are now 6 indications for CCTA in low-interme-
syndrome rate was an astonishing 22 % at 4-years of follow- diate probability patients. There has been confusion on the
up. These data, as exploratory as they are, represent very part of readers of this guideline because the indications for
exciting findings that we are only beginning to unfold. If we CCTA mirror that of stress imaging. Despite this, all of the
can further define and more reliably measure the burden of indications are Class IIa – IIb levels of evidence and the result
nonobstructive plaque and its relationship to acute coronary of this strong body of evidence highlighted above.
events, then this could revolutionize the field of diagnostic
testing. We await further explorations from these groups that
will help to improve risk detection of symptomatic patients. Stable Ischemic Heart Disease Trials
A fourth important finding on the use of CCTA in the index
evaluation of symptomatic patients is the identification of There are a number of stable ischemic heart disease trials
severe CAD, including multivessel and left main CAD, and which have recently been completed and provide high
the associated high risk status of these anatomic subsets. In quality evidence for CCTA (Table 21.1). One of these tri-
patients with multivessel CAD, the annualized CAD event als is the NIH-NHLBI-sponsored PROspective Multicenter
rates often are in the range of 8–10 % or higher [43]. Important Imaging Study for Evaluation of Chest Pain (PROMISE)
observational findings from CONFIRM reveal that patients Trial which has enrolled 10,000 patients who were fol-
with high risk CAD receive a proportional risk reduction with lowed for ~2.5 years. The PROMISE trial randomized
coronary revascularization as compared to medical therapy patients to CCTA as compared to functional testing
[43]. Over 2 years of follow-up, the all-cause mortality rate for including stress electrocardiography, echocardiography,
patients with high risk CAD was 5.3 % for those treated medi- and nuclear imaging. Results from the PROMISE trial
cally as compared to 2.3 % for those undergoing coronary revealed no difference in the primary endpoint of
revascularization (Fig. 21.4, p = 0.0075). Additional data are death, acute coronary syndrome or major procedural
required from a randomized trial setting to further unfurl the complications, with a hazard ratio of 1.04 (95% confi-
possibilities for therapeutic risk reduction based on CCTA dence interval: 0.83–1.29, p=0.75) [48]. The challenge
findings. This latter point should also entail the initiation and with the PROMISE trial was the enrollment of low risk
intensification of preventive therapies and their impact on out- patients with few reported events and including a popula-
come among patients with nonobstructive CAD. tion with the majority of patients having atypical chest
21 Coronary Computed Tomographic Angiography for Detection of Coronary Artery Disease 387

pain symptoms. From a second trial, similar non-signifi- patients who will be randomized to invasive coronary
cant but trending results were reported in the SCOT-Heart angiography-guided treatment as compared to prompt
trial with a hazard for coronary heart disease death or medical therapy (without invasive coronary angiography).
nonfatal myocardial infarction of 0.62 (95% confidence These trials will and have demonstrably improved the
interval: 0.38–1.01, p=0.053). Based on the SCOT-Heart quality of evidence and provide important information to
trial, there appears to be a trend toward improve outcomes guide selection of candidates and those who may or may
for CCTA and this requires further exploration but may be not receive a benefit from testing with CCTA.
due to the greater reported initiation of preventive medi-
cations that is frequently observed. Both of these trials Conclusions
establish CCTA as equally effective as functional imaging The evidence base on the clinical utility of CCTA has
(Fig. 21.5) [49]. A second NIH-NHLBI-sponsored trial in grown substantially over the past few years. This evidence
patients with CCTA-defined CAD is the International emulates an important development and will be a path to
Study of Comparative Health Effectiveness with Medical rationally guiding healthcare coverage decisions using
& Invasive Approaches Trial which will enroll 8000 quality evidence from large registries and clinical trials.

Table 21.1 Stable ischemia heart disease trials

Sponsor Trial N= Endpoint
Suspected CAD AHRQ Randomized evaluation 4300 CAD death, MI, & RANa vs. MPI
of patients with stable revascularization
angina comparing
utilization of diagnostic
examinations
NIH-NHLBI PROspective 10,000 2.5 years death, ACS, RANa vs. functional
multicenter imaging complications testing
study for evaluation of
chest pain trial
Known CAD NIH-NHLBI International study of 8000 4–6 years CV death or MI Blinded CCTA to r/o
comparative health LM & normal
effectiveness with coronaries
medical & invasive Completion: 7/19
approaches trial
Source: www.rescuetrial.org, www.promisetrial.org, www.ischemiatrial.org [45–47]
a
RAN Randomization

1.2

0.8

0.6
Hazard Ratio

0.4

0.2

Fig. 21.5 Primary results 0

from the PROMISE and PROMISE SCOT-HEART
SCOT-HEART trials revealing
that CCTA was equally Hazard Ratio: 1.04 Hazard Ratio: 0.62
effective at near-term clinical (95% CI: 0.83, 1.29) (95% CI: 0.38, 1.01)
outcomes p=0.750 p=0.053
388 L.J. Shaw

Table 21.2 A synopsis of the available evidence with CCTA for multicenter registries and from randomized or controlled clinical trials
Randomized clinical or controlled clinical trials
High quality: Multicenter registries Near-term outcomes Long-term outcomes
Diagnostic accuracy **** ***
Risk assessment ***** *****
ED *****
A total of 5 stars are available for this ranking

The upcoming large clinical trials can further refine our Comparison of novel risk markers for improvement in cardiovascu-
evidence on the clinical utility of CCTA. The public and lar risk assessment in intermediate-risk individuals. JAMA. 2012;
308:788–95.
private payer community has largely been unresponsive 8. Wilson PW, Pencina M, Jacques P, Selhub J, D’Agostino Sr R,
to this evidence base and it may be that the evidence has O’Donnell CJ. C-reactive protein and reclassification of cardiovas-
been amassed so rapidly and that their ability to maintain cular risk in the Framingham Heart Study. Circ Cardiovasc Qual
current knowledge base has been slow to respond. Despite Outcomes. 2008;1:92–7.
9. Blaha MJ, Budoff MJ, DeFilippis AP, Blankstein R, Rivera JJ,
this, certainly the evidence supports a re-evaluation of the Agatston A, O’Leary DH, Lima J, Blumenthal RS, Nasir K.
national and private payer policies for CCTA. This Associations between C-reactive protein, coronary artery calcium,
author’s opinion on the quality of evidence with CCTA is and cardiovascular events: implications for the JUPITER popula-
reported in Table 21.2. tion from MESA, a population-based cohort study. Lancet. 2011;
378:684–92.
10. Rozanski A, Gransar H, Shaw LJ, Kim J, Miranda-Peats L, Wong
ND, Rana JS, Orakzai R, Hayes SW, Friedman JD, Thomson LE,
Polk D, Min J, Budoff MJ, Berman DS. Impact of coronary artery
References calcium scanning on coronary risk factors and downstream testing
the EISNER (Early Identification of Subclinical Atherosclerosis by
1. Greenland P, Alpert JS, Beller GA, Benjamin EJ, Budoff MJ, Fayad Noninvasive Imaging Research) prospective randomized trial.
ZA, Foster E, Hlatky MA, Hodgson JM, Kushner FG, Lauer MS, J Am Coll Cardiol. 2011;57:1622–32.
Shaw LJ, Smith Jr SC, Taylor AJ, Weintraub WS, Wenger NK, 11. O’Malley PG, Feuerstein IM, Taylor AJ. Impact of electron beam
Jacobs AK, Smith Jr SC, Anderson JL, Albert N, Buller CE, Creager tomography, with or without case management, on motivation,
MA, Ettinger SM, Guyton RA, Halperin JL, Hochman JS, Kushner behavioral change, and cardiovascular risk profile: a randomized
FG, Nishimura R, Ohman EM, Page RL, Stevenson WG, Tarkington controlled trial. JAMA. 2003;289:2215–23.
LG, Yancy CW, American College of Cardiology Foundation/ 12. Hoffmann U, Truong QA, Schoenfeld DA, Chou ET, Woodard PK,
American Heart Association Task Force on Practice Guidelines. Nagurney JT, Pope JH, Hauser TH, White CS, Weiner SG, Kalanjian
2010 ACCF/AHA guideline for assessment of cardiovascular risk in S, Mullins ME, Mikati I, Peacock WF, Zakroysky P, Hayden D,
asymptomatic adults: a report of the American College of Cardiology Goehler A, Lee H, Gazelle GS, Wiviott SD, Fleg JL, Udelson JE,
Foundation/American Heart Association Task Force on practice Investigators R-I. Coronary CT angiography versus standard evalu-
guidelines. J Am Coll Cardiol. 2010;56:e50–103. ation in acute chest pain. N Engl J Med. 2012;367:299–308.
2. Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu 13. Litt HI, Gatsonis C, Snyder B, Singh H, Miller CD, Entrikin DW,
K, Shea S, Szklo M, Bluemke DA, O’Leary DH, Tracy R, Watson Leaming JM, Gavin LJ, Pacella CB, Hollander JE. CT angiography
K, Wong ND, Kronmal RA. Coronary calcium as a predictor of for safe discharge of patients with possible acute coronary syn-
coronary events in four racial or ethnic groups. N Engl J Med. dromes. N Engl J Med. 2012;366:1393–403.
2008;358:1336–45. 14. Goldstein JA, Chinnaiyan KM, Abidov A, Achenbach S, Berman
3. Budoff MJ, Shaw LJ, Liu ST, Weinstein SR, Mosler TP, Tseng PH, DS, Hayes SW, Hoffmann U, Lesser JR, Mikati IA, O’Neil BJ,
Flores FR, Callister TQ, Raggi P, Berman DS. Long-term prognosis Shaw LJ, Shen MY, Valeti US, Raff GL, Investigators C-S. The
associated with coronary calcification: observations from a registry CT-STAT (coronary computed tomographic angiography for sys-
of 25,253 patients. J Am Coll Cardiol. 2007;49:1860–70. tematic triage of acute chest pain patients to treatment) trial. J Am
4. Erbel R, Mohlenkamp S, Moebus S, Schmermund A, Lehmann N, Coll Cardiol. 2011;58:1414–22.
Stang A, Dragano N, Gronemeyer D, Seibel R, Kalsch H, Brocker- 15. Goodacre S, Thokala P, Carroll C, Stevens JW, Leaviss J, Al
Preuss M, Mann K, Siegrist J, Jockel KH, Heinz Nixdorf Recall Khalaf M, Collinson P, Morris F, Evans P, Wang J. Systematic
Study Investigative Group. Coronary risk stratification, discrimina- review, meta-analysis and economic modelling of diagnostic strat-
tion, and reclassification improvement based on quantification of egies for suspected acute coronary syndrome. Health Technol
subclinical coronary atherosclerosis: the Heinz Nixdorf Recall Assess. 2013;17:v–vi, 1–188.
study. J Am Coll Cardiol. 2010;56:1397–406. 16. D’Ascenzo F, Cerrato E, Biondi-Zoccai G, Omede P, Sciuto F,
5. Pencina MJ, D’Agostino Sr RB, D’Agostino Jr RB, Vasan Presutti DG, Quadri G, Raff GL, Goldstein JA, Litt H, Frati G,
RS. Evaluating the added predictive ability of a new marker: from Reed MJ, Moretti C, Gaita F. Coronary computed tomographic
area under the ROC curve to reclassification and beyond. Stat Med. angiography for detection of coronary artery disease in patients pre-
2008;27:157–72; discussion 207–12. senting to the emergency department with chest pain: a meta-
6. Polonsky TS, McClelland RL, Jorgensen NW, Bild DE, Burke GL, analysis of randomized clinical trials. Eur Heart J Cardiovasc
Guerci AD, Greenland P. Coronary artery calcium score and risk Imaging. 2013;14:782–9.
classification for coronary heart disease prediction. JAMA. 2010; 17. Nasis A, Meredith IT, Sud PS, Cameron JD, Troupis JM,
303:1610–6. Seneviratne SK. Long-term outcome after CT angiography in
7. Yeboah J, McClelland RL, Polonsky TS, Burke GL, Sibley CT, patients with possible acute coronary syndrome. Radiology. 2014;
O’Leary D, Carr JJ, Goff DC, Greenland P, Herrington DM. 132680.
21 Coronary Computed Tomographic Angiography for Detection of Coronary Artery Disease 389

18. Udelson JE, Beshansky JR, Ballin DS, Feldman JA, Griffith JL, Dunning A, Hadamitzky M, Hausleiter J, Kaufmann P, Lin F,
Handler J, Heller GV, Hendel RC, Pope JH, Ruthazer R, Spiegler Maffei E, Min JK, Shaw LJ, Chow BJ. Prognostic assessment of
EJ, Woolard RH, Selker HP. Myocardial perfusion imaging for coronary artery bypass patients with 64-slice computed tomography
evaluation and triage of patients with suspected acute cardiac angiography: anatomical information is incremental to clinical risk
ischemia: a randomized controlled trial. JAMA. 2002;288: prediction. J Am Coll Cardiol. 2011;58:2389–95.
2693–700. 30. Hadamitzky M, Achenbach S, Al-Mallah M, Berman D, Budoff M,
19. Patel MR, Peterson ED, Dai D, Brennan JM, Redberg RF, Anderson Cademartiri F, Callister T, Chang HJ, Cheng V, Chinnaiyan K,
HV, Brindis RG, Douglas PS. Low diagnostic yield of elective cor- Chow BJ, Cury R, Delago A, Dunning A, Feuchtner G, Gomez M,
onary angiography. N Engl J Med. 2010;362:886–95. Kaufmann P, Kim YJ, Leipsic J, Lin FY, Maffei E, Min JK, Raff G,
20. Min JK, Leipsic J, Pencina MJ, Berman DS, Koo BK, van Mieghem Shaw LJ, Villines TC, Hausleiter J, CONFIRM Investigators.
C, Erglis A, Lin FY, Dunning AM, Apruzzese P, Budoff MJ, Cole JH, Optimized prognostic score for coronary computed tomographic
Jaffer FA, Leon MB, Malpeso J, Mancini GB, Park SJ, Schwartz RS, angiography: results from the CONFIRM registry (COronary CT
Shaw LJ, Mauri L. Diagnostic accuracy of fractional flow reserve Angiography EvaluatioN For Clinical Outcomes: an InteRnational
from anatomic CT angiography. JAMA. 2012;308:1237–45. Multicenter Registry). J Am Coll Cardiol. 2013;62:468–76.
21. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert E, 31. Lin FY, Shaw LJ, Dunning AM, Labounty TM, Choi JH, Weinsaft
Scherer M, Bellinger R, Martin A, Benton R, Delago A, Min JK. JW, Koduru S, Gomez MJ, Delago AJ, Callister TQ, Berman DS,
Diagnostic performance of 64-multidetector row coronary com- Min JK. Mortality risk in symptomatic patients with nonobstructive
puted tomographic angiography for evaluation of coronary artery coronary artery disease: a prospective 2-center study of 2,583
stenosis in individuals without known coronary artery disease: patients undergoing 64-detector row coronary computed tomo-
results from the prospective multicenter ACCURACY (Assessment graphic angiography. J Am Coll Cardiol. 2011;58:510–9.
by Coronary Computed Tomographic Angiography of Individuals 32. Min JK, Dunning A, Lin FY, Achenbach S, Al-Mallah MH, Berman
Undergoing Invasive Coronary Angiography) trial. J Am Coll DS, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V,
Cardiol. 2008;52:1724–32. Chinnaiyan KM, Chow B, Delago A, Hadamitzky M, Hausleiter J,
22. Miller JM, Rochitte CE, Dewey M, Arbab-Zadeh A, Niinuma H, Karlsberg RP, Kaufmann P, Maffei E, Nasir K, Pencina MJ, Raff
Gottlieb I, Paul N, Clouse ME, Shapiro EP, Hoe J, Lardo AC, Bush GL, Shaw LJ, Villines TC. Rationale and design of the CONFIRM
DE, de Roos A, Cox C, Brinker J, Lima JA. Diagnostic performance (COronary CT Angiography EvaluatioN For Clinical Outcomes: an
of coronary angiography by 64-row CT. N Engl J Med. 2008;359: InteRnational Multicenter) Registry. J Cardiovasc Comput Tomogr.
2324–36. 2011;5:84–92.
23. Meijboom WB, van Mieghem CA, Mollet NR, Pugliese F, Weustink 33. Leipsic J, Taylor CM, Gransar H, Shaw LJ, Ahmadi A, Thompson
AC, van Pelt N, Cademartiri F, Nieman K, Boersma E, de Jaegere A, Humphries K, Berman DS, Hausleiter J, Achenbach S,
P, Krestin GP, de Feyter PJ. 64-slice computed tomography Al-Mallah M, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ,
coronary angiography in patients with high, intermediate, or low Chow BJ, Cury RC, Delago AJ, Dunning AL, Feuchtner GM,
pretest probability of significant coronary artery disease. J Am Coll Hadamitzky M, Kaufmann PA, Lin FY, Chinnaiyan KM, Maffei E,
Cardiol. 2007;50:1469–75. Raff GL, Villines TC, Gomez MJ, Min JK. Sex-based prognostic
24. Janne d’Othee B, Siebert U, Cury R, Jadvar H, Dunn EJ, Hoffmann implications of nonobstructive coronary artery disease: results from
U. A systematic review on diagnostic accuracy of CT-based detec- the International Multicenter CONFIRM Study. Radiology.
tion of significant coronary artery disease. Eur J Radiol. 2008;65: 2014:140269.
449–61. 34. Hulten E, Villines TC, Cheezum MK, Berman DS, Dunning A,
25. Shaw LJ, Hage FG, Berman DS, Hachamovitch R, Iskandrian Achenbach S, Al-Mallah M, Budoff MJ, Cademartiri F, Callister
A. Prognosis in the era of comparative effectiveness research: TQ, Chang HJ, Cheng VY, Chinnaiyan K, Chow BJ, Cury RC,
where is nuclear cardiology now and where should it be? J Nucl Delago A, Feuchtner G, Hadamitzky M, Hausleiter J, Kaufmann
Cardiol. 2012;19:1026–43. PA, Karlsberg RP, Kim YJ, Leipsic J, Lin FY, Maffei E, Plank F,
26. Motoyama S, Kondo T, Sarai M, Sugiura A, Harigaya H, Sato T, Raff GL, Labounty TM, Shaw LJ, Min JK, CONFIRM Investigators.
Inoue K, Okumura M, Ishii J, Anno H, Virmani R, Ozaki Y, Hishida Usefulness of coronary computed tomography angiography to
H, Narula J. Multislice computed tomographic characteristics of predict mortality and myocardial infarction among Caucasian,
coronary lesions in acute coronary syndromes. J Am Coll Cardiol. African and East Asian ethnicities (from the CONFIRM [Coronary
2007;50:319–26. CT Angiography Evaluation for Clinical Outcomes: an International
27. Motoyama S, Sarai M, Harigaya H, Anno H, Inoue K, Hara T, Multicenter] Registry). Am J Cardiol. 2013;111:479–85.
Naruse H, Ishii J, Hishida H, Wong ND, Virmani R, Kondo T, Ozaki 35. Min JK, Labounty TM, Gomez MJ, Achenbach S, Al-Mallah M,
Y, Narula J. Computed tomographic angiography characteristics of Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V,
atherosclerotic plaques subsequently resulting in acute coronary Chinnaiyan KM, Chow B, Cury R, Delago A, Dunning A, Feuchtner
syndrome. J Am Coll Cardiol. 2009;54:49–57. G, Hadamitzky M, Hausleiter J, Kaufmann P, Kim YJ, Leipsic J,
28. Min JK, Dunning A, Lin FY, Achenbach S, Al-Mallah M, Budoff Lin FY, Maffei E, Raff G, Shaw LJ, Villines TC, Berman
MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V, Chinnaiyan DS. Incremental prognostic value of coronary computed
K, Chow BJ, Delago A, Hadamitzky M, Hausleiter J, Kaufmann P, tomographic angiography over coronary artery calcium score for
Maffei E, Raff G, Shaw LJ, Villines T, Berman DS, CONFIRM risk prediction of major adverse cardiac events in asymptomatic
Investigators. Age- and sex-related differences in all-cause diabetic individuals. Atherosclerosis. 2014;232:298–304.
mortality risk based on coronary computed tomography 36. Rana JS, Dunning A, Achenbach S, Al-Mallah M, Budoff MJ,
angiography findings results from the International Multicenter Cademartiri F, Callister TQ, Chang HJ, Cheng VY, Chinnaiyan K,
CONFIRM (Coronary CT Angiography Evaluation for Clinical Chow BJ, Cury R, Delago A, Feuchtner G, Hadamitzky M, Hausleiter
Outcomes: an International Multicenter Registry) of 23,854 patients J, Kaufmann P, Karlsberg RP, Kim YJ, Leipsic J, Labounty TM, Lin
without known coronary artery disease. J Am Coll Cardiol. FY, Maffei E, Raff G, Villines TC, Shaw LJ, Berman DS, Min
2011;58:849–60. JK. Differences in prevalence, extent, severity, and prognosis of coro-
29. Small GR, Yam Y, Chen L, Ahmed O, Al-Mallah M, Berman DS, nary artery disease among patients with and without diabetes under-
Cheng VY, Chinnaiyan K, Raff G, Villines TC, Achenbach S, going coronary computed tomography angiography: results from
Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Delago A, 10,110 individuals from the CONFIRM (COronary CT Angiography
390 L.J. Shaw

EvaluatioN For Clinical Outcomes): an InteRnational Multicenter angiography: results from CONFIRM (COronary CT Angiography
Registry. Diabetes Care. 2012;35:1787–94. EvaluatioN For Clinical Outcomes: an InteRnational Multicenter
37. Chow BJ, Ahmed O, Small G, Alghamdi AA, Yam Y, Chen L, Registry). Eur Heart J. 2012;33:3088–97.
Wells GA. Prognostic value of CT angiography in coronary bypass 44. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP,
patients. JACC Cardiovasc Imaging. 2011;4:496–502. Douglas PS, Foody JM, Gerber TC, Hinderliter AL, King 3rd SB, Kligfield
38. Otaki Y, Gransar H, Berman DS, Cheng VY, Dey D, Lin FY, PD, Krumholz HM, Kwong RY, Lim MJ, Linderbaum JA, Mack MJ,
Achenbach S, Al-Mallah M, Budoff MJ, Cademartiri F, Callister Munger MA, Prager RL, Sabik JF, Shaw LJ, Sikkema JD, Smith Jr CR,
TQ, Chang HJ, Chinnaiyan K, Chow BJ, Delago A, Hadamitzky M, Smith Jr SC, Spertus JA, Williams SV, American College of Cardiology
Hausleiter J, Kaufmann P, Maffei E, Raff G, Shaw LJ, Villines TC, Foundation, American Heart Association Task Force on Practice Group,
Dunning A, Min JK. Impact of family history of coronary artery American College of Physicians, American Association for Thoracic
disease in young individuals (from the CONFIRM registry). Am Surgery, Preventive Cardiovascular Nurses Association, Society for
J Cardiol. 2013;111:1081–6. Cardiovascular Angiography and Interventions, and Society of Thoracic
39. Hadamitzky M, Taubert S, Deseive S, Byrne RA, Martinoff S, Surgeons. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for
Schomig A, Hausleiter J. Prognostic value of coronary computed the diagnosis and management of patients with stable ischemic heart dis-
tomography angiography during 5 years of follow-up in patients with ease: a report of the American College of Cardiology Foundation/American
suspected coronary artery disease. Eur Heart J. 2013;34:3277–85. Heart Association Task Force on Practice Guidelines, and the American
40. Ostrom MP, Gopal A, Ahmadi N, Nasir K, Yang E, Kakadiaris I, College of Physicians, American Association for Thoracic Surgery,
Flores F, Mao SS, Budoff MJ. Mortality incidence and the severity Preventive Cardiovascular Nurses Association, Society for Cardiovascular
of coronary atherosclerosis assessed by computed tomography Angiography and Interventions, and Society of Thoracic Surgeons. J Am
angiography. J Am Coll Cardiol. 2008;52:1335–43. Coll Cardiol. 2012;60:e44–164.
41. Andreini D, Pontone G, Mushtaq S, Bartorelli AL, Bertella E, 45. American College of Radiology Imaging Network. Rescue: an
Antonioli L, Formenti A, Cortinovis S, Veglia F, Annoni A, Agostoni ACRIN cardiovascular clinical trial. A study for patients with stable
P, Montorsi P, Ballerini G, Fiorentini C, Pepi M. A long-term prog- angina-comparing two methods of evaluating coronary artery dis-
nostic value of coronary CT angiography in suspected coronary ease [Internet] Accessed 11 Nov 2014. Available at: www.rescue-
artery disease. JACC Cardiovasc Imaging. 2012;5:690–701. trial.org.
42. Metz LD, Beattie M, Hom R, Redberg RF, Grady D, Fleischmann 46. PROMISE: prospective multicenter imagining study for evaluation
KE. The prognostic value of normal exercise myocardial perfusion of chest pain. [Internet] Accessed 11 Nov 2014. Available at:
imaging and exercise echocardiography: a meta-analysis. J Am https://www.promisetrial.org/.
Coll Cardiol. 2007;49:227–37. 47. ISCHMIA Study. [Internet]. Available at: https://www.ischemi-
43. Min JK, Berman DS, Dunning A, Achenbach S, Al-Mallah M, atrial.org/. Accessed 11 Nov 2014.
Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Cheng V, 48. Douglas PS, Hoffmann U. Anatomical versus functional testing for
Chinnaiyan K, Chow BJ, Cury R, Delago A, Feuchtner G, coronary artery disease. The New England Journal of Medicine.
Hadamitzky M, Hausleiter J, Kaufmann P, Karlsberg RP, Kim YJ, 2015;373:91.
Leipsic J, Lin FY, Maffei E, Plank F, Raff G, Villines T, Labounty 49. Investigators S-H. CT coronary angiography in patients with sus-
TM, Shaw LJ. All-cause mortality benefit of coronary pected angina due to coronary heart disease (SCOT-HEART): an
revascularization vs. medical therapy in patients without known open-label, parallel-group, multicentre trial. Lancet. 2015;
coronary artery disease undergoing coronary computed tomographic 385:2383–91.
 Cardiothoracic Surgery Applications:
Virtual CT Imaging Approaches 22
to Procedural Planning

Jerold S. Shinbane, Craig J. Baker, Mark J. Cunningham,

and Vaughn A. Starnes

Abstract
Cardiovascular computed tomographic angiography (CCTA) has led to a paradigm shift in
planning and performance of cardiothoracic surgical procedures, providing information
essential to decisions regarding surgical intervention. As the operating room and interven-
tional cardiology laboratory have evolved, merging into a hybrid space, CCTA has assumed
an essential role in determination of the optimal therapeutic modality and path of approach
for percutaneous, minimally invasive robotic and open surgical approaches in this setting.
CCTA has particular significance to planning of reoperation for coronary artery disease,
valvular heart disease, pericardial disease, congenital heart disease, cardiac masses, and
advanced heart failure. Communication of the data beyond the written report can be
achieved through images relevant for orientation and interventional approach. Review of
these virtual views with the multidisciplinary team is important for maximal application
and impact of this technology.

Keywords
Anomalous Coronary Arteries • Aortic Surgery • Cardiovascular Computed Tomographic
Angiography • Cardiothoracic Surgery • Computed Tomography • Congenital Heart Disease
• Coronary Artery Bypass Graft Surgery • Minimally Invasive Robotic Surgery •
Percutaneous Pulmonary Valve Replacement • Transcatheter Aortic Valve Implantation

Introduction
Electronic supplementary material The online version of this
chapter (doi:10.1007/978-3-319-28219-0_22) contains supplementary
material, which is available to authorized users. Cardiovascular computed tomographic angiography (CCTA)
has led to a paradigm shift in planning and performance of
J.S. Shinbane, MD, FACC, FHRS, FSCCT (*) cardiothoracic surgical procedures, providing information
Division of Cardiovascular Medicine,
essential to decisions regarding proceeding with surgical
Department of Internal Medicine,
Keck School of Medicine of the University of intervention, facilitation of pre-surgical planning, and assess-
Southern California, 1520 San Pablo Suite 300, ment for surgical efficacy and sequelae. CCTA provides
Los Angeles, CA 90033, USA a digitalized and individualized “Netter” illustration of the
e-mail: [email protected]
relationships between thoracic skeletal, vascular, visceral,
C.J. Baker, MD, FACS • M.J. Cunningham, MD and cardiac structures (Fig. 22.1, Video 1). Full field 3-D
Department of Surgery, Keck School of Medicine of the University
reconstructions utilizing editing software enable visualiza-
of Southern California, Los Angeles, CA USA
tion of multidimensional planes. Assessment of these views
V.A. Starnes, MD
is important for planning surgical access to target structures
Cardiovascular Thoracic Institute, Department of Surgery,
Keck School of Medicine of the University of Southern California, while avoiding important vascular and visceral thoracic struc-
Los Angeles, CA USA tures which may be in close proximity to the incisional plane.

© Springer International Publishing 2016 391

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_22
392 J.S. Shinbane et al.

mic cardiac arrest, initiation of peripheral cardiopulmonary

bypass, and peripheral vascular dissection and exposure prior
to midline sternotomy [3, 4]. Skeletal defects, traumatic
injury, metastatic disease, abscess, and osteomyelitis in the
sternum can also be identified (Figs. 22.4 and 22.5).
In the setting of initial surgery as well as re-operation for
obstructive coronary artery disease, the use of CCTA to define
native coronary anatomy has limitations due to calcification
of native coronary arteries and inability to define collateral
flow; therefore invasive coronary arteriography remains the
gold standard. CCTA can be useful in assessing graft location
and graft patency (Fig. 22.6). CCTA may be useful prior to
recurrent coronary artery bypass graft surgery in situations
where cardiac catheterization was unable to completely
define graft anatomy, particularly as to whether a graft was
occluded versus unable to be cannulated at cardiac catheter-
ization. CCTA in unoperated as well as previously operated
Fig. 22.1 A 3-D reconstruction demonstrating the relationships settings can define the location and patency of the left and
between thoracic skeletal, vascular, visceral, and cardiac structures right internal mammary arteries (Fig. 22.7). Depending on
the field of view, CCTA can assess for subclavian artery ste-
The operating room and interventional cardiology labora- noses. Surgical clip artifacts may make assessment of grafts
tory have evolved, merging into a hybrid space utilized by a more challenging, particularly at the anastomosis site with the
multidisciplinary team of surgeons, interventional cardiolo- native coronary artery (Fig. 22.8). Aortic characteristics, such
gists and imagers. CCTA plays an essential role in decisions as profound calcification/porcelain aorta, are important for
and guidance for determination of the optimal therapeutic surgical approaches requiring cross-clamping of the aorta or
modality and path of approach for percutaneous, minimally implantation of saphenous vein grafts into the aorta.
invasive robotic and open surgical approaches in this setting.
Communication of the data beyond the written report can be
achieved through images relevant for orientation and inter- Imaging Related to Surgery for Valvular
ventional approach. Review of these virtual views with the Disease
multidisciplinary team is important for maximal application
and impact of this technology. CCTA for Surgical Versus Percutaneous
Approach to Aortic Valve Disease

Imaging Related to Surgery for Coronary CCTA has become essential to decision-making and pre-
Artery Disease planning related to transcatheter aortic valve implantation
(TAVI), minimally invasive robotic or open surgical
CCTA has particular significance to planning of re-operation approaches for aortic valve replacement. Percutaneous
for coronary artery disease, as the number of prior operations approaches employ TAVI balloon-expandable and self-
incrementally increases risk. At re-operation, the majority of expanding valves [5–7]. CCTA provides data for decisions as
adverse events occur during sternotomy or pre-bypass dissec- to the feasibility of versus contraindication to TAVI access
tion due to injury to bypass grafts and great vessels [1, 2]. routes for percutaneous valve deployment including trans-
CCTA can visualize high risk sternotomy anatomy through femoral, transapical subclavian artery, or direct aortic
demonstration of structures coursing immediately posterior approaches [8, 9]. CCTA imaged anatomy limiting a trans-
to the sternum which may require special precautions femoral or aortic route include peripheral arterial diameter
(Figs. 22.2 and 22.3). High risk features on CCTA include the limitations based on catheter size, aortic tortuousity, high
right ventricle or aorta less than 1 cm from chest wall and risk atheromas, severe vascular calcification, chronic dissec-
coronary artery bypass grafts coursing across the midline less tions and aneurysms. CCTA related factors and potential
than 1 cm from the sternum [3]. Pre-operative CCTA assess- limitations for consideration of a transapical approach to
ment of the relationship of cardiovascular structures to the TAVI include the morphology and location of the left ven-
sternum has been used to plan alternate approaches in patients tricular apex, alignment of the left ventricular axis to the left
with high risk sternotomy anatomy, including: cancellation of ventricular outflow tract, significant septal hypertrophy and
surgery, non-sternotomy incisional approach, deep hypother- presence of ventricular thrombi.
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 393

a b

Fig. 22.2 Anomalous coronary arteries coursing in close proximity to partially edited to demonstrate the anomalous coronary circulation
the sternum. Panel (a) A 3-D volume rendered view demonstrating the (arrow). Panel (c) A 3-D volume rendered view demonstrating the rela-
sternum. Panel (b) A 3-D volume rendered view with the sternum tionship of the anomalous coronary arteries (arrows) to the sternum

Aortic annulus characteristics can also limit use of TAVI maximum and minimum diameter, area, and circumference
and therefore require operative approaches in patients who at the attachments of all three aortic cusps, “hinge points” in
are otherwise candidates for surgery. CCTA is the gold stan- a “virtual ring”, are essential for accurate assessment and
dard for annular geometry, measurements and physiology for provide virtual orientation for the TAVI team. The optimal
assessment of valve sizing and potential contraindication to fluoroscopic view for coaxial deployment should be noted by
a TAVI approach based on annulus size and morphology the RAO/LAO and cranial/caudal viewing angle of the “vir-
(Fig. 22.9). The annulus is often ovoid rather than circular in tual ring” created by these “hinge points” [9, 11].
shape, and can have variation in cusp length, height and rela- Detailed CCTA annular characterization and measure-
tion to the coronary artery ostia. Annular dynamic morpho- ments are essential to avoid undersizing or oversizing of the
logic changes occur throughout the cardiac cycle with valve relative to the annulus and avoidance of issues related
assessment for the largest diameter preferable [10]. Potential to the coronary artery ostia. Valve undersizing can lead to
annular eccentricity and elasticity therefore make detailed valve embolization or perivalvular leak. CCTA characteris-
coaxial characterization and measurement of the annulus tics, including the relationship of valve diameter relative to
essential for decisions as to a percutaneous versus surgical average annular diameter, degree of aortic root calcification,
approach and appropriate sizing of valves when TAVI is an angulation between the left ventricular outflow tract and the
option. In plane aligned aortic annular measurements of ascending aorta, and eccentricity of the annulus, are factors
394 J.S. Shinbane et al.

potentially predictive of post-procedure regurgitation [12– Relationships and characteristics of the annulus in rela-
14]. CCTA aortic annular sizing algorithms developed to tion to the coronary artery ostia must be taken into account
modestly oversize the implanted valve have led to reduction with CCTA analysis. Definition of the quantitative relation-
of perivalvular regurgitation [15]. Differences in individual ship between the aortic annulus, aortic sinuses, sinotubular
TAVI device characteristics and available sizes are also junction and the coronary artery ostia are important in order
important to decisions based on CCTA dimensions in order to avoid coronary artery compromise due to the device or
to avoid significant oversizing [16]. Valve oversizing can atherosclerotic plaque with valve deployment. If the annular
lead to annular rupture. Additionally, moderate to severe to ostial height is too small, the ostia could be covered by the
sub-annular left ventricular outflow tract calcium predicts device. The extent and morphology of annular and sub-annu-
rupture [17]. lar calcification is important, as this atherosclerotic plaque
can embolize into or partially or completely obstruct the
coronary artery ostium [18–22]. Given the possibility of
these complications, CCTA cardiovascular relationships to
the sternum need to be noted for TAVI candidates, as the
need for emergent conversion to an open sternotomy surgical
approach is a potential scenario. TAVI can also lead to con-
duction abnormalities including high grade atrioventricular
block. CCTA findings of deep valve placement relative to the
annulus, severe calcification of the landing site, and prosthe-
sis/patient mismatch have been associated with left bundle
branch block and high grade atrioventricular block
[23–28].
Multiple factors make CCTA assessment of the coro-
nary arteries challenging in severe to critical aortic steno-
sis patients. Given the advanced age of many patients being
considered for TAVI, as well as the underlying pathophysi-
ology of calcific aortic stenosis, significant calcification of
the coronary arteries is often present. From a CCTA image
acquisition standpoint, acute beta blockade and sublingual
Fig. 22.3 A 2-D axial view showing the right ventricle coursing nitroglycerin may be contraindicated as part of the CCTA
immediately posterior to the sternum imaging protocol in patients with severe to critical aortic

a b

Fig. 22.4 Sagittal views demonstrating traumatic injury to the chest. Panel (a) Demonstration of sternal fracture (arrow). Panel (b) Demonstration
of pneumopericardium (arrow)
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 395

can define the extent of infection through visualization of

abscesses, pseudo- aneurysms, fistulas, the relationship of the
coronary arteries to these structures, and presence of coronary
artery disease (Figs. 22.10, 22.11, 22.12, and 22.13, Video 2)
[30]. As these patients are sometimes critically ill, heart rate
control may be difficult, but images may still be diagnostic.
Prosthetic valve function can be viewed similarly to fluoro-
scopic views in order to assess mechanical valve motion as
well as the presence of thrombus/vegetation (Fig. 22.14).

CCTA for Surgical Versus Percutaneous

Approach to Pulmonary Valve Disease

With the advent of percutaneous pulmonary valve replace-

ment, surgical decision-making for pulmonary valve disease
Fig. 22.5 Sternal metastasis in a patient with aortic dissection must include assessment for the feasibility, risks and benefits
of each approach [31–34]. CCTA can be useful in imaging
many important decision-making factors including the size
and degree of calcification of the pulmonary annulus, the
presence of anomalous coronary arteries, and the 3-D rela-
tionship of the coronary arteries to the pulmonary annulus
(Fig. 22.15) [35]. These factors are important to avoid com-
plications such as compression of the coronary arteries with
valve deployment, pulmonary regurgitation due to undersiz-
ing of the valve relative to the annulus, or conduit/annulus
rupture due to oversizing of the valve relative to the annulus.
The close proximity of anomalous coronary arteries or
enlarged right heart structures to the sternum are important
to identify in case emergent open surgical intervention is
required.

CCTA for Surgical Versus Percutaneous

Approach to Mitral Valve Disease

Research and clinical approaches to mitral valve disease

include a spectrum of options including percutaneous clip-
Fig. 22.6 A 3-D view showing a left internal mammary artery graft to
the left anterior descending coronary artery (black arrow), saphenous
ping of valve leaflets, percutaneous mitral annuloplasty,
vein graft to an obtuse marginal branch (double black arrow), saphe- transcatheter mitral valve replacement, minimally invasive
nous vein graft to a diagonal artery (white arrow), and saphenous vein robotic mitral valve repair or replacement, and open ster-
graft to the posterior descending artery (double white arrow) notomy mitral valve repair or replacement. Anatomic defini-
tion of the valve leaflets, annulus, subvalvular apparatus,
stenosis, further limiting the ability to assess the coronary relationship of the coronary arteries and cardiac veins to the
arteries. In other aortic valve scenarios, such as chronic left atrioventricular groove, and presence or absence of cor-
severe aortic regurgitation, CCTA may be useful as an alter- onary artery disease are important components of CCTA
native to invasive cardiac catheterization prior to aortic valve analyses for decision-making and planning. Mitral annular
surgery in patients with low to intermediate risk of coronary size and geometry factors including valve tenting, height
artery disease [29]. and tethering of the mitral leaflets variability in number of
Endocarditis involving the aortic valve and aortic root can heads and insertions of the posterior papillary muscle, inter-
potentially lead to a higher risk of complications with inva- papillary muscle distance, mitral valve sphericity index,
sive cardiac catheterization due to large aortic vegetations, intercommissural and septolateral distance , and anterior
aortic pseudo-aneurysms, and aortic root abscesses. CCTA and posterior circumference of the mitral annulus can be
396 J.S. Shinbane et al.

Fig. 22.7 CCTA visualization of

the left (a) and right (b) internal a b
mammary arteries

assessed [36–38]. Mitral annular contour has a complex 3-D tionship of the coronary sinus / great cardiac vein, circum-
non-planar saddle-shaped morphology. More simplified, flex coronary artery and mitral annulus for novel
planar measurements may be important to annular sizing for percutaneous mitral annuloplasty procedures utilizing the
valve implantation [39]. cardiac vein system. There is great variability in these rela-
The presence of significant aorto-iliac disease limiting tionships, and segments where the circumflex coronary
peripheral cardiopulmonary bypass as well as the extent and artery courses between the coronary sinus/great cardiac
location of mitral calcification can limit minimally invasive vein and the annulus can potentially compress the circum-
surgical approaches to mitral valve disease. CCTA can be flex coronary artery [44–48].
useful to determine a right thoracotomy robotic versus ster-
notomy approach based on the degree of mitral valve calcifi-
cation as well as the degree of aorto-iliac disease [40, 41]. Imaging Related to Surgery for Congenital
CCTA is also useful as an alternative to coronary artery cath- Heart Disease
eterization in low to intermediate risk patients in preopera-
tive decisions for robotic mitral valve repair [42]. In congenital heart disease, the multitude of individual
Assessment of the 3-D spatial relationship of the circum- anomalies in the native state as well as palliative and cor-
flex coronary artery in the left atrioventricular groove and rective repairs in the operated state make the characteriza-
the mitral annulus are important to the placement of the tion of complete individualized anatomy in relation to the
sewing ring in mitral annuloplasty surgeries for mitral thorax important for hybrid lab interventional, minimally
regurgitation (Fig. 22.16) [43]. CCTA can assess the rela- robotic and open surgical approaches. Decisions regarding
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 397

Fig. 22.8 Surgical clip artifacts

(white arrows) with a clip
(double white arrow) obscuring
the anastomosis of the left
internal mammary artery graft to
the left anterior descending
coronary artery

Fig. 22.9 Panel (a) A 3-D view of

the aortic root demonstrating coaxial a b
2-D double oblique views of the
aortic annulus, sinuses of Valsalva,
sinotubular junction and ascending
aorta. Panel (b) A 2-D double
oblique maximal intensity projection
demonstrating the distance from the
left main coronary artery to the
aortic valve annulus

the use of CCTA versus CMR depend on multiple factors, Image definition of thoracic and abdominal situs, rota-
including the age of the patient, need for assessment of tional abnormalities of thoracic vasculature, atrial and ven-
coronary anatomy, and presence of pacemakers or ICDs. tricular septal defects, shunts and fistulas, and anomalous
CCTA is useful for determining anatomy and physiology large and small vessel anatomy can be achieved and defined
important to surgical planning, particularly in patients with in one 3-D data set (Figs. 22.17, 22.18, 22.19, 22.20, 22.21,
non-MR conditional pacemakers and implantable cardiac and 22.22, Videos 3, 4, 5 and 6). CCTA is useful for specific
defibrillators as CMR can be limited in use in these settings questions that other imaging modalities are unable to answer
[49–51]. The associated radiation with CCTA is a major as well as for creation of comprehensive roadmaps, particu-
issue, although techniques to minimize dose are being larly when the previous history of anatomy and previous sur-
advanced [52–55]. gical interventions are not known or well-defined. Innovations
398 J.S. Shinbane et al.

a b

c d

Fig. 22.10 Bicuspid aortic valve endocarditis with arterial emboli. the sinuses of Valsalva. Panel (c) A curved multiplanar reformatted
Due to high risk of invasive coronary artery angiography in this sce- view and corresponding 3-D reconstruction showing a patent left coro-
nario, CCTA was performed prior to aortic valve replacement. The nary artery circulation. Panel (d) A curved multiplanar reformatted
study demonstrated no evidence of aortic root abscess, aortic pseudoa- view and corresponding 3-D reconstruction showing a patent right
neurysm, or obstructive coronary artery disease. Panel (a) A 2-D double coronary artery. AoV aortic valve, Cx circumflex coronary artery, LAD
oblique view demonstrating a large, friable, vegetation on bicuspid aor- left anterior descending coronary artery, LM left main coronary artery,
tic valve leaflet. Panel (b) A 2-D double oblique image of the aortic root VEG vegetation, RCA right coronary artery
viewed in long axis showing the vegetation to be in close proximity to

in scanner hardware and software have lowered the radiation structed right ventricular outflow tract with pulmonary
doses allowing for imaging in infants and children with con- valve regurgitation, cardiovascular magnetic resonance
genital heart disease [54, 55, 57]. imaging (CMR) is a gold standard of measurement for
assessment of right ventricular size, right ventricular func-
tion, and pulmonary valve fractional regurgitation. Some
Post-surgical Sequelae: Tetralogy of Fallot, of these patients, though, have cardiac devices, potentially
Single Ventricle Physiology and Transposition limiting the use of CMR. In comparison to CMR, CCTA
of the Great Arteries assessment of right ventricular function and pulmonary
regurgitant fraction, calculated by the difference between
In complex congenital heart disease, such as tetralogy of biventricular systolic volume difference, can be achieved
Fallot, single ventricle physiology and transposition of the with the caveats that right ventricular volume can be over-
great arteries, CCTA can provide assessment of the unop- estimated and pulmonic regurgitant fraction underesti-
erated state as well as for sequelae of operative palliation mated using CMR as a gold standard [59]. CCTA can
or repair. In the pre-operative state, CCTA is useful for characterize the anatomy of the reconstructed pulmonary
characterizing anomalous coronary artery anatomy for sur- outflow tract and pulmonary vasculature for pulmonary
gical planning [58]. In the post-operative setting of recon- artery stenosis or enlargement/aneurysm (Videos 7 and 8).
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 399

Fig. 22.11 Multiplane views showing the relationship of an aortic pseudoaneurysm (black arrows) to the right coronary artery (white arrows) in
a patient with aortic valve endocarditis

For patients with surgical repair for single ventricle physi- sizing of ductus occlusion devices (Fig. 22.23). Options for
ology, opacification of the complete Fontan circuit can surgical versus percutaneous closure are dependent on patent
require specialized injection protocols, with venous injection ductus arteriosus size, morphology, and location and orifice
from two sites (upper and lower extremity) or delayed timing size of the aortic and pulmonary artery insertions. A percuta-
of imaging relative to injection in order to fully opacify the neous approach may be preferable for a ductal size of less
Fontan and pulmonary vasculature [60]. In surgically treated than 3 mm in diameter (coil occlusion) and 3–14 mm (coil or
transposition of the great arteries, CCTA can provide device occlusion) [69]. Ductal size of greater than 14 mm
assessment of stents and baffles, re-implanted coronary and those with complex morphology are associated with
arteries, and assessment of ventricular function [61–64]. increased risk of complications with percutaneous closure
Atrial and ventricular sepal defects can occur as single and surgical closure is usually performed, although in certain
anomalies or in association with additional complex anatomy. situations in high risk surgical patients, percutaneous closure
CCTA can characterize defects, providing such details as has been employed [70].
double-oblique assessment of coaxial defect size and rim
characteristics as well as providing preoperative assessment
for other cardiovascular anomalies which may need to be Anomalous Coronary Arteries
addressed at the time of surgical repair. In patients with
septal defects with identified complex additional anomalies, Specific morphologies of anomalous coronary arteries can
CCTA provides information important to surgical decision- lead to ischemia, infarction, and sudden cardiac death.
making and planning [56, 65–68]. Decisions regarding potential surgical therapy for correc-
tion depend on identification of high risk anatomy in the
appropriate clinical scenario. The CT imager should have
Patent Ductus Arteriosus an understanding of how these anatomic details affect surgi-
cal decision-making, planning and performance of proce-
In patients with patent ductus arteriosus, CCTA provides dures. CCTA can characterize detailed anatomy for surgical
important information for deciding between surgical decisions relating to anomalous coronary arteries. Anatomic
and percutaneous closure approach through precise charac- details include individual coronary artery presence or
terization of morphology and size and assessment for other absence, origin, ostial characteristics, course, termination,
associated cardiothoracic anomalies facilitating appropriate presence of coronary artery disease or aneurysm, and 3-D
400 J.S. Shinbane et al.

a b

c d

Fig. 22.12 Aortic valve endocarditis involving a mechanical valve artery, which subsequently courses into the pericardial sac with right
with paravalvular pseudoaneurysm/contained rupture. Panels (a–c) atrial hemopericardium/hematoma (white arrows) causing severe right
Multiple 2-D double oblique views demonstrate the aortic valve pseu- atrial compression. AoV aortic valve, LA left atrium, LAD left anterior
doaneurysm/contained rupture (white arrows) extending along the descending coronary artery, LM left main coronary artery, LV left ven-
superior aspect of the right atrioventricular groove. Panel (d) A 2-D tricle, PA pulmonary artery, RA right atrium, RCA right coronary artery,
double oblique view demonstrating the pseudoaneurysm/contained rup- RV right ventricle
ture (black arrows) causing narrowing of the proximal right coronary

relationship to other cardiovascular structures (Figs. 22.24, pathways for the anomalous artery to course back to its
22.25, 22.26, 22.27, 22.28, 22.29, 22.30, 22.31, 22.32, usual myocardial distribution: pre- pulmonic, inter-arterial,
22.33, 22.34, 22.35, 22.36, 22.37, and 22.38, Videos 9 trans-septal, or retro-aortic. The termination of an anoma-
and 10). In regard to the origin, the coronary artery can arise lous coronary artery can be into a capillary distribution
from the aortic sinuses, other locations on the aorta or other usual for a given coronary artery, the capillary distribution
vascular structures. Viewing the aortic sinuses as a clock in another myocardial segment, a cardiac chamber, or
face in the axial plane, the normal coronary artery origins another arterial or venous vascular structure. The lumen can
are at approximately 11 o’clock for right coronary artery have no evidence of coronary atherosclerosis, non-
and 4 o’clock for left main. Ostial morphology can include obstructive coronary atherosclerosis, obstructive coronary
a separate ostium, a shared ostium with another coronary artery disease, or aneurysmal dilatation.
artery, or an ostium off of another coronary artery. Ostial High risk features for cardiovascular events include
morphologies include presence of a slit-like ostium, and for absence of a coronary artery with inadequate compensatory
retrospectively gated studies, dynamic ostial compression arterial supply to a myocardial distribution, coronary artery
due to adjacent vascular structures. For coronary arteries take-off from the contralateral sinus with a slit-like ostium
arising from the contralateral sinus, there are four main and inter- arterial course, or an anomalous coronary artery
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 401

a b c

d e f

Fig. 22.13 Mechanical aortic valve endocarditis (same case as Fig. 22.12). lar groove, causing narrowing of the proximal right coronary artery. The
Serial virtual sternotomy 3-D reconstructions demonstrating the anatomy pseudoaneurysm/contained rupture subsequently courses into the pericar-
from anterior to posterior (a–f). The pseudoaneurysm/contained rupture dial sac with right atrial hemopericardium/ hematoma (black arrows). RA
(white arrows) extends along the superior aspect of the right atrioventricu- Right atrium, RCA right coronary artery, RV right ventricle

on the location and characteristics of the anomalous coronary

artery ostium. For an intramural aortic course with a slit-like
ostium above the sinotubular junction, the coronary artery can
be unroofed, whereas, below the sinotubular junction the
artery can be fenestrated. For a separate ostium without an
intramural aortic course, the artery can be reimplanted. For a
shared ostium without an intramural course, unroofing or
reimplantation would not be feasible, and therefore the pul-
monary artery can be translocated. In anomalous coronary
arteries with obstructive coronary artery disease, coronary
artery bypass grafting can be performed. This is not feasible
in the other scenarios as there would be competitive flow due
to the lack of coronary artery disease. In regard to abnormal
termination of a coronary artery into a venous structure, either
Fig. 22.14 Images demonstrating an immobile thrombus on the ante-
percutaneous or surgical occlusion can be performed depend-
rior leaflet of a mechanical prosthetic mitral valve which caused the ing on the caliber and tortuosity of the vessel.
leaflet to be immobile

arising from another structure such as the pulmonary artery. CCTA Imaging Related to Surgery
Pre-pulmonic, intra-septal and retro-aortic courses are usually for Advanced Heart Failure
low risk morphologies [35, 71]. For high risk anatomy in the
appropriate clinical situation, detailed characterization of the In the setting of coronary artery disease associated with
anomalous coronary anatomy defines the available surgical severe ischemic cardiomyopathy, challenging decisions
approaches including reimplantation of a coronary artery, relate to transplant versus high risk coronary artery bypass
unroofing of a coronary artery, bypass of a coronary artery, or surgery, often with additional decisions as to valvular repair
translocation of other cardiovascular structures impeding flow or replacement and ventricular aneurysmectomy. Assessment
to a coronary artery [69, 72]. Scenarios of bypass of a coro- of myocardial viability has become important to the pre-
nary artery require significant stenosis of the artery as other- procedure decision-making process. CMR has played an
wise competitive flow can lead to poor maturation or closure important role due to the ability to assess for infarct related
of the bypass graft. The surgical approach to a coronary artery fibrosis as well as regional contractility (Fig. 22.39) [73–76].
off of the pulmonary artery is reimplantation of the coronary These images can also be used for decision-making regard-
artery. Surgical approaches to an interarterial course depend ing viability and ventricular dimensions for planning of
402 J.S. Shinbane et al.

Fig. 22.15 Repaired Tetralogy of Fallot with a retroaortic left main approximately the 7 o’clock location on the aortic clock face in the
and duplication of arterial supply to the left anterior descending coro- axial view. The right coronary artery origin is likewise rotated clock-
nary artery distribution from left and right coronary arteries in the set- wise, with the ostium at the 2 o’clock location. Percutaneous interven-
ting of stenosis of the pulmonary valve conduit. 3-D reconstructions tion for repair of the homograft stenosis was inadvisable due to the
(upper panels) demonstrate a long left main arising from the left coro- close proximity of the right coronary artery to the pulmonary conduit.
nary sinus which courses retroaortic between the aorta and the left Given the close proximity of cardiovascular structures to the sternum,
atrium and subsequently gives off a left anterior descending coronary the patient was placed on cardiopulmonary bypass via right groin ves-
artery and circumflex coronary artery. The right coronary sinus gives sels prior to redo sternotomy in order to decompress the right ventricle.
off a single short ostium which subsequently gives off a right coronary Revision of the right ventricular outflow tract, and pulmonary valve
artery that traverses anteriorly between the aorta and a heavily calcified replacement were performed. During conduit/homograft resection, the
pulmonary conduit, and a branch which courses within the vascular dis- posterior layer of the conduit was left intact in order to avoid injury to
tribution of the left ventricular anterior wall and septum. There is there- the anomalous right coronary artery. Ao aorta, CX circumflex coronary
fore duplication of arterial supply to the left ventricular anterior wall artery, LAD left anterior descending coronary artery, LM left main coro-
distribution. 2-D thick maximum intensity projection views (lower pan- nary artery, PA pulmonary artery, RCA right coronary artery, RV right
els) show the coronary sinuses are rotated clockwise. Consequently, the ventricle (Reprinted from Shinbane et al. [35] with permission from
left main coronary artery originates more posterior than usual, at SAGE Publications)

revascularization. More recently, CCTA delayed enhance- nique requires re-imaging 10–15 min after administration of
ment imaging has been shown to reliably demonstrate fibro- iodinated contrast and therefore requires additional radia-
sis associated with myocardial infarction. In animal models, tion. The technique has been demonstrated to correlate with
delayed contrast imaging has been shown to correlate with thallium SPECT assessment of viability [78]. In the setting
acute and chronic infarct shape and transmurality including of acute myocardial infarction, CCTA delayed enhancement
assessment for necrosis in the acute setting [77]. This tech- correlates with CMR assessment of viability [79]. Delayed
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 403

a b c

Fig. 22.16 Distal right coronary artery fistula to the left ventricle at (arrow). Panel (c) A 2-D double oblique view of the fistulous connec-
level of mitral annulus in patient with a previous history of mitral valve tion of the aneurysmal distal right coronary artery to the left ventricle at
surgery. Panel (a) 3-D view demonstrating the distal the aneurysmal the level of the mitral annulus (arrow). LV left ventricle, RV right ven-
distal right coronary artery (arrow). Panel (b) Curved multiplanar refor- tricle, LA left atrium, LV left ventricle, RCA right coronary artery
matted view of the distal the aneurysmal distal right coronary artery

a b

Fig. 22.17 Presurgical assessment for repair of atrial septal defect. (a) 2-D axial view showing a large secundum atrial septal defect. (b) Curved
multiplanar reformat demonstrating no evidence of obstructive coronary artery disease in the right coronary artery segment shown

enhancement imaging can also be performed immediately with angiographic and clinical assessment of reperfusion
after cardiac catheterization without contrast reinjection with percutaneous coronary intervention [80–84]. As tech-
(Fig. 22.40). In preliminary studies in this setting, the degree niques evolve, CCTA delayed enhancement imaging may
of CCTA delayed enhancement was associated with increased ultimately serve in a similar capacity to CMR for preopera-
subsequent heart failure admissions, correlated with low tive decision-making and planning.
dose dobutamine assessment of viability, was an indepen- Ventricular assist devices have become an integral part of
dent predictor of future cardiovascular events, and correlated advanced heart failure management as bridges to cardiac
404 J.S. Shinbane et al.

a c

Fig. 22.18 A restrictive apical muscular ventricular septal defect with Panel (a) A 3-D coronal reconstruction demonstrating the level of the
a circuitous course. The defect is oriented anteroposterior on the left level of the ventricular septal defect (arrow). Panel (b) A 3-D axial
ventricular side septum but courses laterally on the right ventricular reconstruction demonstrating the ventricular septal defect (arrow).
side. The presence of prominent right ventricular apical muscle bands Panel (c) A 2-D double oblique view of the ventricular septal defect
also contributes to the circuitous course of the ventricular septal defect. (arrow)

a b

Fig. 22.19 Restrictive mid anteroseptal ventricular septal defect due to demonstrating the ventricular septal defect (arrow). Panel (b) A 2-D
old anterior myocardial infarction with myocardial wall thinning and double oblique view of the ventricular septal defect (arrow). LV left
contrast evidence of left to right flow. Panel (a) A 3-D reconstruction ventricle, RV right ventricle
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 405

a b

Fig. 22.20 CCTA demonstrating D Transposition of great arteries, sta- ventricles. The systemic ventricle (morphologic right ventricle) is in
tus post previous interatrial baffle, with additional finding of patent duc- close proximity to the sternum. Panel (d) Virtual endovascular view of
tus arteriosus. Panel (a) A 3-D reconstruction. Panel (b) A 2-D axial the patent baffle as it enters the left atrium. Ao aorta, LV left ventricle,
view demonstrating the aorta to be anterior and slightly rightward of the PA pulmonary artery, PDA patent ductus arteriosus, RLPV right lower
enlarged main pulmonary artery. Panel (c) A 2-D axial view demon- pulmonary vein, RUPV right upper pulmonary vein, RV right ventricle
strating the anatomic positions and physiologic relationships of the

a b c

Fig. 22.21 CCTA showing D transposition of the great arteries, status tion of the right coronary artery which arises posteriorly on the aortic
post interatrial baffle. Panel (a) A 3-D reconstruction coronal view with sinus and supplies the pulmonary ventricle (morphologic left ventricle).
skeletal structure. Panel (b) A 3-D reconstruction coronal view with Ao aorta, LAD left anterior descending coronary artery, PA pulmonary
skeletal structure removed. Panel (c) A 3-D reconstruction coronal view artery, RCA right coronary artery, RV right ventricle
highlighting the coronary artery anatomy. There is mirror image loca-
406 J.S. Shinbane et al.

a b c

Fig. 22.22 Unoperated congenitally corrected transposition of the strates poststenotic dilatation (double white arrows on a). Panel (c) 3-D
great arteries, dextrocardia, nonrestrictive ventricular septal defect, pul- volume rendered CCTA views demonstrate that the left (black arrow)
monary stenosis and anomalous coronary arteries. Panels (a, b) Axial and right (white arrow) coronary arteries arise from the most anterior
(a) and coronal (b) CCTA demonstrates the aorta (black arrow) arising cusp of the aorta and follow their respective morphologic ventricles. Ao
anterior and leftward of the main pulmonary artery (white arrow). aorta, PV pulmonary valve, RPA right pulmonary artery (Reprinted
Pulmonary stenosis is present. On this diastolic image, the open pulmo- from Shinbane et al. [56] with permission from SAGE Publications)
nary valve represents insufficiency. The right pulmonary artery demon-

a b c

Fig. 22.23 CCTA demonstration of a tubular patent ductus arteriosus performed. Panel (a) A 3-D reconstruction in context of skeletal struc-
measuring 2.2 cm in length arising from a prominent aortic ductus tures. Panel (b) A 3-D reconstruction with skeletal structures removed.
diverticulum and communicating with the superior portion of the main Panel (c) A 3-D reconstruction with editing plane demonstrating the
pulmonary artery (arrow). Given the size and characteristics, a percuta- lumen of the patent ductus arteriosus
neous ductal occluder device closure rather than surgical closure was

transplant as well as destination devices for those patients assess for issues throughout the system, including: inflow
who are not candidates for transplant. CCTA can be helpful obstruction by papillary muscle, inflow cannula malposition,
in assessment of feasibility of ventricular assist device thrombus, air in the cannula, outflow cannula kinking or mal-
implantation in children and small adults, as well as to iden- position, and aortic root thrombus [85–89].
tify potential obstacles to sternotomy incision for placement In heart transplant patients, CCTA has been preliminarily
(Fig. 22.41, Video 11). In patients with implanted ventricular studied to assess coronary arteries for chronic allograft vascu-
assist devices, CCTA can identify components of the system lopathy. The high negative predictive value of CCTA may
to assess for etiologies of ventricular assist device malfunction potentially be useful in this setting [90–93]. Limitations in
(Fig. 22.42). In patients with pulsatile devices, electrocardio- assessment of coronary branch vessels less than 1.5 mm for
graphic-gating can be utilized, while in those continuous- chronic allograft vasculopathy, nephrotoxic effects of iodin-
flow devices peripheral pulse-gating can be used to assess for ated contrast, and issues of timing and frequency of assess-
etiologies of low output and low flow states [85]. CCTA can ment leading to potential cumulative effects of radiation in
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 407

Fig. 22.24 Normal coronary artery origins and anomalous coronary the four primary courses (black circles) for anomalous coronary arteries
artery courses. 3-D axial view reconstruction (left panel) demonstrates arising from the contralateral sinus. CX circumflex coronary artery,
normal coronary artery origins with the right coronary artery origin at LAD left anterior descending coronary artery, LM left main coronary
11 o’clock and the left main coronary artery origin at 3:30 on the aortic artery, RCA right coronary artery (Reprinted from Shinbane et al. [35]
clock face. Thick maximum intensity projection in the axial view shows with permission from SAGE Publications)

this immunosuppressed population, necessitates further arteries, pericardial studding or effusion, and presence of
investigation of the role of CCTA post-transplant [94, 95]. lymphadenopathy or other thoracic masses within the field of
view. CCTA can also provide coronary artery assessment for
obstructive coronary artery disease prior to surgery. All of
CCTA Imaging Related to Surgery for Cardiac these factors are important to decisions as to resectability and
Masses surgical approach once a histologic tissue diagnosis is made.

While definitive diagnosis of cardiac tumors requires patho-

logic examination of the mass histology, CCTA can be used to CCTA Imaging Related to Surgery
characterize masses and associated findings important to diag- for Pericardial Disease
nosis and pre-surgical work-up and planning (Fig. 22.43) [96,
97]. CCTA can define morphology including 3-D shape, single Assessment for constrictive pericarditis is challenging and
versus multiple masses, and wide-based versus narrow-based often involves multiple modalities of imaging including
connection to the myocardium. Tissue characteristics, includ- echocardiography as well as invasive cardiac catheterization
ing attenuation of the mass, homogeneity versus heterogeneity to assess hemodynamic elements. CCTA can be helpful in
of attenuation in different areas within the mass, presence and assessing pericardial thickness by cardiac region as well as
pattern of calcification, and presence and pattern of vascularity, by the degree of calcification [98–100]. Surgical complica-
can be defined with CCTA. Descriptive features of the location tions can occur due to vascular damage related to dissecting
of the mass in relation to cardiovascular and thoracic structure the pericardium away from the coronary arteries. CCTA can
should be noted, including: intracameral, intramyocardial epi- define the relationship between the pericardium and coro-
cardial or pericardial location of the mass, invasion or involve- nary arteries, including areas of pericardial thickening, peri-
ment of other cardiac or thoracic structures by the mass from cardial calcification, as well as tethering of coronary arteries
its primary location, relationship of the mass to the coronary on dynamic images (Fig. 22.44).
408 J.S. Shinbane et al.

Fig. 22.25 Left coronary artery arising from a shared ostium on the tion demonstrated proximal occlusion of the right coronary artery with
right coronary sinus with a prepulmonic course and single-vessel right left to right collaterals. In this case, medical management of the dis-
coronary artery coronary artery disease. 3-D reconstructions (upper and eased single vessel was chosen. AO aorta, CX circumflex coronary
lower left panels) demonstrate a left coronary artery arising from a artery, LAD left anterior descending coronary artery, LM left main coro-
separate ostium on the right coronary sinus with a prepulmonic course. nary artery, PA pulmonary artery, RCA right coronary artery (Reprinted
A curved multiplanar reformat (lower right panel) shows significant from Shinbane et al. [35] with permission from SAGE Publications)
atherosclerotic disease of the right coronary artery. Cardiac catheteriza-

Decisions regarding percutaneous versus surgical aneurysm, and aortic rupture. Details of a dissection flap
approaches to drain pericardial fluid collections can be entry and exit site, location and extent of true and false
facilitated by CT assessment of the location, extent, and lumen, dissection into branch vessels, involvement of the
tissue characteristics of the pericardial effusion [101]. A sinuses of Valsalva, dissection into the coronary arteries, and
percutaneous approach may be limited by the complexity dissection into the pericardium can be defined (Figs. 22.46
of the effusion due to loculation of the effusion or effusion and 22.47) [102–104]. CCTA can assess coronary artery
tissue attenuation consistent with blood, proteinaceous anatomy when cardiac catheterization is high risk or
material, or thrombus. Accessibility by a sub-xiphoid unachievable due to aortic pathology, such as severe athero-
approach can be determined by the relation of the effusion sclerotic disease with large atheromas, thrombi, aneurysms,
to skeletal and thoracic structures (Fig. 22.45). For poste- or dissections. Similarly, in emergency department settings,
rior effusions, particularly in the setting of post cardiotho- when rapid assessment for thoracic and coronary artery trau-
racic surgery, a sub-xiphoid approach may not be feasible, matic abnormalities are crucial and time dependent, CCTA
while a CT guided drainage may be achievable. may be useful [105–107]. CCTA provides assessment of vas-
cular dimensions for endograft sizing and placement impor-
tant to endovascular aneurysm repair [108]. The presence
CCTA Imaging for Aortic Surgery and degree of atherosclerosis, calcification, and thrombus
can be important to cross clamp decisions related to multiple
CCTA and CMR diagnosis of acute and chronic aortic dis- types of cardiothoracic procedures. CCTA can also be useful
ease is well-established. These technologies can visualize in the assessment of infected aortic aneurysms, with findings
dissection, intramural hematoma, penetrating ulcer, aortic including saccular structure, contiguous soft tissue masses,
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 409

Fig. 22.26 Left coronary artery branches arising from the right coro- shows the separate right sinus ostium giving off a conus branch cours-
nary sinus with a prepulmonic left anterior descending coronary artery ing anterior to the right ventricular outflow tract with the diminutive left
arising from a separate ostium with a subsequent intramyocardial anterior descending coronary artery coursing intramyocardially via a
course and a retroaortic circumflex arising off of the coronary artery. transseptal course as well as the retroaortic circumflex. Surgery was not
3-D reconstructions (upper panels) demonstrate the left anterior required due to lower risk anatomic features, and due to the lack of
descending coronary artery arising just anterior and cranial to the right obstructive coronary artery disease. AO aorta, CX circumflex coronary
coronary artery arising from a separate ostium off of the right coronary artery, LAD left anterior descending coronary artery, LA left atrium, LM
sinus. The circumflex coronary artery arises off of the right coronary left main coronary artery, RCA right coronary artery (Reprinted from
artery and courses retroaortic, terminating in obtuse marginal branches. Shinbane et al. [35] with permission from SAGE Publications)
2-D double oblique thick maximum intensity projection (lower panel)

contrast enhancement, fluid, gas, and adjoining bone destruc- necessarily be the CCTA reading physician, detailed
tion [109]. For other aortic abnormalities, such as coarctation knowledge of the images and workstation software capa-
of the aorta, CCTA is useful for decision-making related to bilities are essential in order to attain a 3-D understanding
percutaneous or surgical intervention. Characterization of of an individual patient’s pre-surgical cardiothoracic anat-
coarctation location, size, calcification, collateral circulation, omy. Viewing modalities and presentations intuitive to the
as well as associated congenital anomalies, can be achieved. surgical approach are being advanced with 3-D printing of
individualized heart models from CCTA data for surgical
Conclusions planning [110–114]. A close working relationship between
The spectrum of cardiothoracic surgical options continues the imager, interventional cardiologist and surgeon and
to expand. CCTA can facilitate surgical procedures and presentation of relevant pre- surgical images to the multi-
requires continued investigation to define optimal proce- disciplinary team are import to the comprehensive utiliza-
dural approaches to coronary artery, valvular, and aortic tion of data to define approaches to particular cardiovascular
pathology. Although the cardiothoracic surgeon may not disease processes.
410 J.S. Shinbane et al.

Fig. 22.27 Left coronary artery arising from a shared ostium on the mum intensity projection view (lower right panel) shows myocardial
right coronary sinus with a retroaortic course and myocardial bridging bridging of the left anterior descending coronary artery. Given the lower
of the left anterior descending coronary artery. 3-D reconstructions risk anatomy and lack of obstructive coronary artery disease, surgical
(upper panels) demonstrate anomalous origin of the left main coronary intervention was not required. CX circumflex coronary artery, LAD left
artery off of its own ostium of the right coronary sinus taking a retro- anterior descending coronary artery, LM left main coronary artery, RCA
grade aortic course between the aorta and the left atrium. A curved right coronary artery (Reprinted from Shinbane et al. [35] with permis-
multiplanar reformat (lower left panel) shows the separate ostia of the sion from SAGE Publications.)
left main and right coronary artery. A 2-D double oblique thick maxi-
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 411

Fig. 22.28 Right coronary artery arising with a high takeoff from a opened in an oblique fashion and incised following the track of the right
separate ostium on the left coronary sinus with an interarterial course. coronary artery as it coursed through the intramural portion of the aorta
3-D reconstructions (upper panels) demonstrate anomalous takeoff of for 1.5 cm, allowing correction of the slit like orifice and rerouting of
the right coronary artery from the superior portion of the left coronary the interarterial course without the need for sternotomy in an athlete.
sinus with an interarterial course between the aorta and the pulmonary AO aorta, CX circumflex coronary artery, LAD left anterior descending
artery. Two-D double oblique thick maximum intensity projection coronary artery, LM left main coronary artery, PA pulmonary artery,
views (lower panels) show the interarterial course and the slit-like ori- RCA right coronary artery, RVOT right ventricular outflow tract
fice of the right coronary artery. Due to symptoms of exertional syncope (Reprinted from Shinbane et al. [35] with permission from SAGE
and high risk anatomy, surgical treatment was recommended. A mini- Publications)
mally invasive unroofing of the artery was performed, with the aorta
412 J.S. Shinbane et al.

Fig. 22.29 Panel (a) Left main coronary artery arising from a separate mended. A minimally invasive approach through a small 2nd intercostal
ostium within the right coronary sinus with an interarterial course. 3-D space incision was used in order to avoid sternotomy. As the slit-like
reconstructions (upper panels) demonstrate an anomalous takeoff of the ostium had an extremely short course, re-implantation of the LM was
left main coronary artery from its own ostium within the right coronary performed. Panel (b) The 3D views show the minimally invasive surgical
sinus with an interarterial course between the aorta and the pulmonary approach (white dotted line) through a small second intercostal space
artery. 2-D double oblique thick maximum intensity projection views incision perpendicular to sternum. AO aorta, CX circumflex coronary
(lower panels) show the intraarterial course and left main coronary artery artery, LAD left anterior descending coronary artery, LM left main coro-
with a slit-like orifice. Due to symptoms of exertional chest pain, positive nary artery, PA pulmonary artery, RCA right coronary artery (Reprinted
cardiac enzymes and high risk anatomy, surgical treatment was recom- from Shinbane et al. [35] with permission from SAGE Publications)
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 413

Fig. 22.30 Left main coronary artery (LM) arising from a separate with cardiogenic shock, intraaortic balloon pump placement and car-
ostium within the right coronary sinus with an interarterial course and diac catheterization had been performed with subsequent CCTA to fur-
multivessel coronary artery disease. 3-D reconstructions (upper panels, ther characterize anomalous coronary anatomy. Given the presence of
lower left panel) demonstrate an anomalous takeoff of the LM from its multivessel coronary artery disease, standard coronary artery bypass
own ostium within the right coronary sinus with an interarterial course surgery was performed. AO aorta, LAD left anterior descending coro-
between the aorta and the pulmonary artery. 2-D double oblique thick nary artery, LM left main coronary artery, PA pulmonary artery, RCA
maximum intensity projection view (lower right panel) shows the intra- right coronary artery (Reprinted from Shinbane et al. [35] with permis-
arterial course of the LM with a slit-like orifice. Due to presentation sion from SAGE Publications)
414 J.S. Shinbane et al.

Fig. 22.31 Left coronary artery arising from a separate ostium on the sinuses. 2-D double oblique thick maximum intensity projection views
right coronary sinus with an interarterial course with previous surgical (right panel) show the ostium has been surgically widened and extended
unroofing. 3-D reconstruction (left panel) demonstrates the left coro- to the commissure between the left and the right coronary sinus. There
nary artery with the left main coronary artery originating from its own was no obstructive coronary artery disease within any of these vessels.
ostium off of the right coronary sinus. There has been previous unroof- No further intervention was necessary. AO aorta, LM left main coronary
ing of the interarterial left main course with surgical widening and artery, RCA right coronary artery (Reprinted from Shinbane et al. [35]
extension to the commissure between the left and right coronary with permission from SAGE Publications)
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 415

Fig. 22.33 Anomalous coronary artery termination with a serpiginous artery origins were normal. There was no evidence of obstructive coro-
coronary artery fistula from the proximal left anterior descending coro- nary artery disease. An incidental wide-mouthed saccular aneurysm of
nary artery to the main pulmonary artery. 3-D reconstructions (upper the descending thoracic aorta at the level of the left atrium is seen in the
panels) demonstrate an extremely serpiginous fistula extended from the lower right panel. Given the size and profound tortuosity of the fistula
proximal left anterior descending coronary artery to the main pulmo- in the setting of exertional chest pain, surgical ligation of the fistula via
nary artery. 2-D double oblique thick maximum intensity projection a median sternotomy approach was performed. CX circumflex coronary
views (lower panels) demonstrate the termination of the fistula into the artery, Diag diagonal branch, LAD left anterior descending coronary
left anterolateral aspect of the main pulmonary artery just distal to the artery, LM left main coronary artery, PA pulmonary artery, RCA right
pulmonic valve. The remainder of the left anterior descending artery coronary artery (Reprinted from Shinbane et al. [35] with permission
followed a normal course without evidence of stenosis. The coronary from SAGE Publications)

Fig. 22.32 Anomalous termination of a coronary artery with coronary posterior aspect of the right ventricular outflow tract. Portions of the
artery fistula from the first septal perforating branch of the left anterior right coronary artery coursed immediately posterior to the sternum. No
descending coronary artery to the right ventricular outflow tract with significant stenoses of the coronary arteries were present. Other findings
history of Tetralogy of Fallot repair. 3-D reconstructions (upper panels) included a prosthetic aortic valve with normal leaflet motion, a right-
show a large caliber and tortuous left main coronary artery with a poste- sided aortic arch and descending aorta, and evidence of a prior repair of
rior and cranial takeoff. A fistula from a septal branch of the left anterior a ventricular septal defect. Given these findings, a percutaneous left
descending coronary artery terminates in the right ventricular infundibu- anterior descending coronary artery to right ventricular outflow tract fis-
lum. After takeoff of the fistula, the left anterior descending coronary tula occlusion with a 4-mm vascular plug was performed. Diag diagonal
artery continues as a normal caliber vessel along the anterior interven- branch, LAD left anterior descending coronary artery, RVOT right ven-
tricular groove. 2-D double oblique thick maximum intensity projection tricular outflow tract (Reprinted from Shinbane et al. [35] with permis-
views (lower panels) demonstrate the termination of the fistula into the sion from SAGE Publications)
416 J.S. Shinbane et al.

a b c

Fig. 22.34 Arteriovenous fistula due to anomalous right coronary 2-D double oblique view demonstrating the abnormal termination of
artery termination into the coronary sinus. The right coronary artery is the right coronary artery with an arteriovenous connection to the coro-
dilated throughout its course with a maximum dimension of 1.6 × 1.6 cm nary sinus, with the connection approximately 7 mm cm distal to the
and serpiginous in morphology. Panel (a) A 3-D reconstruction with coronary sinus ostium. Surgical closure was performed. RCA right
skeletal structure. Panel (b) A 3-D reconstruction with skeletal structure coronary artery
removed. Panel (c) Posterior rotation of 3-D reconstruction. Panel (d) A
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 417

Fig. 22.35 Congenital atresia of the left main coronary artery. 3-D system with an underdeveloped left anterior descending coronary artery
reconstructions (upper and lower left panel) demonstrate absence of and circumflex. Cardiac catheterization demonstrated other small right-
left main coronary artery with a single coronary artery ostium off of the to-left collaterals to the diminutive left anterior descending coronary
right coronary sinus. This single ostium gives off a right coronary artery artery and circumflex. Surgical management was challenging since the
right coronary artery and immediately after the ostium gives off a vessel left anterior descending coronary artery and circumflex were underde-
which courses prepulmonic branching into a conus branch as well as veloped. Coronary artery bypass was performed off pump with a free
two large collateral branches supplying a diminutive left coronary sys- left internal mammary artery anastomosed distally to a diagonal branch
tem with an underdeveloped left anterior descending coronary artery and anastomosed proximally to the aorta. AO aorta, COLL collateral,
and circumflex. A 2-D double oblique thick maximum intensity projec- CX circumflex coronary artery, LAD left anterior descending coronary
tion view (lower right panel) shows lack of connection between the left artery, LA left atrium, LM left main coronary artery, RCA right coronary
anterior descending coronary artery and circumflex and the left coro- artery (Reprinted from Shinbane et al. [35] with permission from SAGE
nary sinus. This single ostium gave off the right coronary artery that Publications)
provided large collateral branches supplying a diminutive left coronary
418 J.S. Shinbane et al.

a b

Fig. 22.36 Anomalous coronary artery anatomy with a single coronary ostium arising from the right coronary sinus giving off a left main taking
a retroaortic course and a right coronary artery. (a) 3-D reconstruction of the coronary arteries. (b) Double-oblique maximal intensity projection

a
b

Fig. 22.37 Origin of the right coronary artery from the pulmonary left-to-right collateral arteries that formed due to increased flow.
artery in a 38-year-old man with chest pain and anomalous anatomy at Usually, the left main coronary artery is the more common anomalous
cardiac catheterization. Oblique coronal CCTA image (Panel a) and coronary artery originating from the pulmonary artery. The patient’s
volume rendered image (Panel b) show origin of the right coronary presentation in adulthood was also unusual. PA pulmonary artery
artery (arrows) from the main pulmonary artery. Note the dilated ves- (Reprinted from Shriki et al. [71]; Reproduced with permission from
sels in the septum (arrowheads in a), which likely represent dilated the Radiological Society of North America, RSNA®.)
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 419

a b

c d

Fig. 22.38 Takeuchi repair of anomalous left coronary artery from the with the pulmonary artery made more translucent demonstrating the
pulmonary artery with an aortopulmonary window with an intrapulmo- aortic baffle to the left coronary artery. Panels (c, d) 2-D double oblique
nary tunnel baffling aortic flow to the left coronary artery. Panel (a) A views demonstrating the baffling of aortic flow (black arrows) to the
3-D reconstruction demonstrating the relationship of the aorta and pul- left coronary artery tunneled through the pulmonary artery. Ao aorta, PA
monary artery to the coronary artery. Panel (b) A 3-D reconstruction pulmonary artery
420 J.S. Shinbane et al.

a b

c d

Fig. 22.39 Magnetic resonance imaging assessment in a patient with enhanced view. Panel (b) 2 chamber delayed gadolinium enhanced
ischemic cardiomyopathy showing transmural mid to distal anterior and view. The patient underwent coronary artery bypass graft surgery and
inferior wall myocardial infarctions (arrows) on delayed gadolinium ventricular aneurysmectomy. Panel (c) Pre-surgical steady state free
enhancement views with viability of basal segments of these walls and precession 4 chamber view. Panel (d) Post-surgical steady state free
of the lateral territory. Panel (a) 4 chamber delayed gadolinium precession 4 chamber view

Fig. 22.40 Delayed CT contrast enhancement imaging performed

immediately after cardiac catheterization without contrast reinjection
demonstrating inferior and inferolateral delayed enhancement (arrows)
on a short axis view
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 421

a b

c d

Fig. 22.41 CCTA for pre-surgical planning prior to left ventricular coronary artery in relation to the sternum. Panel (d) 2-D axial view
assist device placement. Panel (a) A 3-D reconstruction in the context demonstrating the location of a saphenous vein graft to the circumflex
of skeletal structure. Panel (b) A 3-D reconstruction with skeletal struc- coronary artery in relation to the sternum. Cx circumflex coronary
tures removed. Panel (c) 2-D axial view demonstrating the location of artery, LIMA left internal mammary artery, SVG saphenous vein graft
the left internal mammary artery graft to the left anterior descending
422 J.S. Shinbane et al.

a b

Fig. 22.42 Left ventricular assist device for advanced heart failure. duit from the pump (white arrow). Panel (b). 3-D reconstruction in con-
Panel (a) A 2-D double oblique thick maximum intensity projection text of skeletal structures demonstrating inflow conduit/valve (back
view demonstrating inflow conduit/valve (back arrow) to the pump, left arrow) to the pump, left ventricular assist device pump (black double
ventricular assist device pump (black double arrow), and outflow con- arrow), and outflow conduit from the pump (white arrow)

a b

Fig. 22.43 CCTA demonstrating a solitary low attenuation lobulated Panel (a) 3-D reconstruction demonstrating the left atrial mass (arrow).
left atrial mass measuring 2.4 cm (craniocaudal) with a narrow stalk Panel (b) 2-D double oblique view demonstrating characteristics of the
attached to the interatrial septum near the fossa ovalis. There were mass (arrow), including lobulation, a narrow stalk attached to the inter-
hyperlucent areas and heterogeneous enhancement with contrast as atrial septum near the fossa ovalis, and heterogeneity with hyperlucent
well as areas of calcification. There was no involvement of other car- areas and heterogeneous enhancement with contrast. Panel (c) 3-D
diac structures. Surgical excision was performed with histologic diag- reconstruction of the coronary arteries demonstrating no evidence of
nosis of left atrial myxoma with organizing thrombus formation. coronary artery disease
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 423

a b

Fig. 22.44 Panel (a) Oblique 2-D image demonstrating the relation- pericarditis. Panel (b) Calcific constrictive pericarditis (white arrow) in
ship of the right coronary artery (black arrow) to thickened pericardium a patient with rheumatic heard disease, mitral valve replacement, and a
(white arrow) prior to pericardiectomy in a patient with constrictive dual chamber pacemaker

Fig. 22.45 A large

circumferential effusion
(arrows) with tissue
attenuation, consistent
proteinaceous material, and
complexity of structure which
required open surgical
dissection
424 J.S. Shinbane et al.

a b

c d e

Fig. 22.46 A large aortic aneurysm which may impede invasive car- anterior descending coronary artery; Panel (c) Axial view; Panel (d)
diac catheterization, with multimodal views including Panel (a) 3-D Coronal view; Panel (e) Sagittal view
view; Panel (b) Curved multiplanar reformat view visualizing the left

a b

Fig. 22.47 Aortic dissection making cardiac catheterization challenging for assessment for coronary artery disease. Panel (a) 3-D view. Panel (b)
double oblique 2-D view of an aortic dissection
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 425

References computed tomography annulus area sizing algorithm on outcomes

of transcatheter aortic valve replacement: a prospective, multi-
center, controlled trial. J Am Coll Cardiol. 2013;62(5):431–8.
1. Roselli EE, Pettersson GB, Blackstone EH, Brizzio ME,
16. Dvir D, Webb JG, Piazza N, Blanke P, Barbanti M, Bleiziffer S,
Houghtaling PL, Hauck R, et al. Adverse events during reopera-
et al. Multicenter evaluation of transcatheter aortic valve replace-
tive cardiac surgery: frequency, characterization, and rescue.
ment using either SAPIEN XT or CoreValve: degree of device
J Thorac Cardiovasc Surg. 2008;135(2):316–23, 23 e1–6.
oversizing by computed-tomography and clinical outcomes.
2. Sabik 3rd JF, Blackstone EH, Houghtaling PL, Walts PA, Lytle
Catheteriz Cardiovasc Interv. 2015;86:508–15.
BW. Is reoperation still a risk factor in coronary artery bypass sur-
17. Barbanti M, Yang TH, Rodes Cabau J, Tamburino C, Wood DA,
gery? Ann Thorac Surg. 2005;80(5):1719–27.
Jilaihawi H, et al. Anatomical and procedural features associated
3. Kamdar AR, Meadows TA, Roselli EE, Gorodeski EZ, Curtin RJ,
with aortic root rupture during balloon-expandable transcatheter
Sabik JF, et al. Multidetector computed tomographic angiography
aortic valve replacement. Circulation. 2013;128(3):244–53.
in planning of reoperative cardiothoracic surgery. Ann Thorac
Surg. 2008;85(4):1239–45. 18. Tops LF, Wood DA, Delgado V, Schuijf JD, Mayo JR, Pasupati S,
4. Gasparovic H, Rybicki FJ, Millstine J, Unic D, Byrne JG, Yucel et al. Noninvasive evaluation of the aortic root with multislice
K, et al. Three dimensional computed tomographic imaging in computed tomography implications for transcatheter aortic valve
planning the surgical approach for redo cardiac surgery after coro- replacement. JACC Cardiovasc Imaging. 2008;1(3):321–30.
nary revascularization. Eur J CardioThorac Surg. 2005; 19. Akhtar M, Tuzcu EM, Kapadia SR, Svensson LG, Greenberg RK,
28(2):244–9. Roselli EE, et al. Aortic root morphology in patients undergoing
5. Mack MJ, Leon MB, Smith CR, Miller DC, Moses JW, Tuzcu EM, percutaneous aortic valve replacement: evidence of aortic root
et al. 5-year outcomes of transcatheter aortic valve replacement or remodeling. J Thorac Cardiovasc Surg. 2009;137(4):950–6.
surgical aortic valve replacement for high surgical risk patients 20. Wood DA, Tops LF, Mayo JR, Pasupati S, Schalij MJ, Humphries
with aortic stenosis (PARTNER 1): a randomised controlled trial. K, et al. Role of multislice computed tomography in transcatheter
Lancet. 2015;385(9986):2477–84. aortic valve replacement. Am J Cardiol. 2009;103(9):1295–301.
6. Kapadia SR, Leon MB, Makkar RR, Tuzcu EM, Svensson LG, 21. Masson JB, Kovac J, Schuler G, Ye J, Cheung A, Kapadia S, et al.
Kodali S, et al. 5-year outcomes of transcatheter aortic valve Transcatheter aortic valve implantation: review of the nature,
replacement compared with standard treatment for patients with management, and avoidance of procedural complications. JACC
inoperable aortic stenosis (PARTNER 1): a randomised controlled Cardiovasc Interv. 2009;2(9):811–20.
trial. Lancet. 2015;385(9986):2485–91. 22. Stabile E, Sorropago G, Cioppa A, Cota L, Agrusta M, Lucchetti
7. Chieffo A, Buchanan GL, Van Mieghem NM, Tchetche D, V, et al. Acute left main obstructions following TAVI.
Dumonteil N, Latib A, et al. Transcatheter aortic valve implanta- EuroIntervention. 2010;6(1):100–5.
tion with the Edwards SAPIEN versus the Medtronic CoreValve 23. Testa L, Latib A, De Marco F, De Carlo M, Agnifili M, Latini RA,
Revalving system devices: a multicenter collaborative study: the et al. Clinical impact of persistent left bundle-branch block after
PRAGMATIC Plus Initiative (Pooled-RotterdAm-Milano- transcatheter aortic valve implantation with CoreValve Revalving
Toulouse In Collaboration). J Am Coll Cardiol. 2013; System. Circulation. 2013;127(12):1300–7.
61(8):830–6. 24. Latsios G, Gerckens U, Buellesfeld L, Mueller R, John D,
8. Kurra V, Schoenhagen P, Roselli EE, Kapadia SR, Tuzcu EM, Yuecel S, et al. “Device landing zone” calcification, assessed by
Greenberg R, et al. Prevalence of significant peripheral artery dis- MSCT, as a predictive factor for pacemaker implantation after
ease in patients evaluated for percutaneous aortic valve insertion: TAVI. Catheter Cardiovasc Interv. 2010;76(3):431–9.
preprocedural assessment with multidetector computed tomogra- 25. Guetta V, Goldenberg G, Segev A, Dvir D, Kornowski R,
phy. J Thorac Cardiovasc Surg. 2009;137(5):1258–64. Finckelstein A, et al. Predictors and course of high-degree atrio-
9. Achenbach S, Delgado V, Hausleiter J, Schoenhagen P, Min JK, ventricular block after transcatheter aortic valve implantation
Leipsic JA. SCCT expert consensus document on computed using the CoreValve Revalving System. Am J Cardiol.
tomography imaging before transcatheter aortic valve implanta- 2011;108(11):1600–5.
tion (TAVI)/transcatheter aortic valve replacement (TAVR). 26. Freeman M, Webb JG, Willson AB, Wheeler M, Blanke P, Moss
J Cardiovasc Comput Tomogr. 2012;6(6):366–80. RR, et al. Multidetector CT predictors of prosthesis-patient mis-
10. Blanke P, Russe M, Leipsic J, Reinohl J, Ebersberger U, Suranyi match in transcatheter aortic valve replacement. J Cardiovasc
P, et al. Conformational pulsatile changes of the aortic annulus: Comput Tomogr. 2013;7(4):248–55.
impact on prosthesis sizing by computed tomography for trans- 27. Nazif TM, Dizon JM, Hahn RT, Xu K, Babaliaros V, Douglas PS,
catheter aortic valve replacement. JACC Cardiovasc Interv. et al. Predictors and clinical outcomes of permanent pacemaker
2012;5(9):984–94. implantation after transcatheter aortic valve replacement: the
11. Blanke P, Schoepf UJ, Leipsic JA. CT in transcatheter aortic valve PARTNER (Placement of AoRtic TraNscathetER Valves) trial and
replacement. Radiology. 2013;269(3):650–69. registry. JACC Cardiovasc Interv. 2015;8(1 Pt A):60–9.
12. Watanabe Y, Lefevre T, Arai T, Hayashida K, Bouvier E, 28. Binder RK, Webb JG, Toggweiler S, Freeman M, Barbanti M,
Hovasse T, et al. Can we predict post-procedural paravalvular leak Willson AB, et al. Impact of post-implant SAPIEN XT geometry
after Edwards Sapien transcatheter aortic valve implantation? and position on conduction disturbances, hemodynamic perfor-
Catheter Cardiovasc Interv. 2015;86(1):144–51. mance, and paravalvular regurgitation. JACC Cardiovasc Interv.
13. Azzalini L, Ghoshhajra BB, Elmariah S, Passeri JJ, Inglessis I, 2013;6(5):462–8.
Palacios IF, et al. The aortic valve calcium nodule score (AVCNS) 29. Scheffel H, Leschka S, Plass A, Vachenauer R, Gaemperli O,
independently predicts paravalvular regurgitation after transcath- Garzoli E, et al. Accuracy of 64-slice computed tomography for
eter aortic valve replacement (TAVR). J Cardiovasc Comput the preoperative detection of coronary artery disease in patients
Tomogr. 2014;8(2):131–40. with chronic aortic regurgitation. Am J Cardiol. 2007;
14. Anger T, Bauer V, Plachtzik C, Geisler T, Gawaz M, Oberhoff M, 100(4):701–6.
et al. Non-invasive and invasive predictors of paravalvular regur- 30. Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J,
gitation post CoreValve(R) stent prosthesis implantation in aortic Scheffel H, et al. Multislice computed tomography in infective
valves. J Interv Cardiol. 2014;27(3):275–83. endocarditis: comparison with transesophageal echocardiography
15. Binder RK, Webb JG, Willson AB, Urena M, Hansson NC, and intraoperative findings. J Am Coll Cardiol. 2009;53(5):
Norgaard BL, et al. The impact of integration of a multidetector 436–44.
426 J.S. Shinbane et al.

31. McElhinney DB, Hellenbrand WE, Zahn EM, Jones TK, using cardiac multidetector computed tomography: implications
Cheatham JP, Lock JE, et al. Short- and medium-term outcomes for percutaneous coronary sinus mitral annuloplasty. J Am Coll
after transcatheter pulmonary valve placement in the expanded Cardiol. 2006;48(10):1938–45.
multicenter US melody valve trial. Circulation. 46. Feldman T, Kar S, Rinaldi M, Fail P, Hermiller J, Smalling R,
2010;122(5):507–16. et al. Percutaneous mitral repair with the MitraClip system: safety
32. Zahn EM, Hellenbrand WE, Lock JE, McElhinney and midterm durability in the initial EVEREST (Endovascular
DB. Implantation of the melody transcatheter pulmonary valve in Valve Edge-to-Edge REpair Study) cohort. J Am Coll Cardiol.
patients with a dysfunctional right ventricular outflow tract con- 2009;54(8):686–94.
duit early results from the u.s. Clinical trial. J Am Coll Cardiol. 47. Feldman T, Young A. Percutaneous approaches to valve repair for
2009;54(18):1722–9. mitral regurgitation. J Am Coll Cardiol. 2014;63(20):2057–68.
33. Armstrong AK, Balzer DT, Cabalka AK, Gray RG, Javois AJ, 48. Attizzani GF, Ohno Y, Capodanno D, Cannata S, Dipasqua F,
Moore JW, et al. One-year follow-up of the Melody transcatheter Imme S, et al. Extended use of percutaneous edge-to-edge mitral
pulmonary valve multicenter post-approval study. JACC valve repair beyond EVEREST (Endovascular Valve Edge-to-
Cardiovasc Interv. 2014;7(11):1254–62. Edge Repair) criteria: 30-day and 12-month clinical and echocar-
34. Meadows JJ, Moore PM, Berman DP, Cheatham JP, Cheatham diographic outcomes from the GRASP (Getting Reduction of
SL, Porras D, et al. Use and performance of the Melody Mitral Insufficiency by Percutaneous Clip Implantation) registry.
Transcatheter Pulmonary Valve in native and postsurgical, non- JACC Cardiovasc Interv. 2015;8(1 Pt A):74–82.
conduit right ventricular outflow tracts. Circ Cardiovasc Interv. 49. Cook SC, Dyke 2nd PC, Raman SV. Management of adults with
2014;7(3):374–80. congenital heart disease with cardiovascular computed tomogra-
35. Shinbane JS, Shriki J, Fleischman F, Hindoyan A, Withey J, Lee phy. J Cardiovasc Comput Tomogr. 2008;2(1):12–22.
C, et al. Anomalous coronary arteries: cardiovascular computed 50. Shinbane JS, Colletti PM, Shellock FG. MR imaging in patients
tomographic angiography for surgical decisions and planning. with pacemakers and other devices: engineering the future. JACC
World J Pediatr Congenital Heart Surg. 2013;4(2):142–54. Cardiovasc Imaging. 2012;5(3):332–3.
36. Delgado V, Tops LF, Schuijf JD, de Roos A, Brugada J, Schalij 51. Shinbane JS, Colletti PM, Shellock FG. Magnetic resonance
MJ, et al. Assessment of mitral valve anatomy and geometry with imaging in patients with cardiac pacemakers: era of “MR
multislice computed tomography. JACC Cardiovasc Imaging. Conditional” designs. J Cardiovasc Magn Reson. 2011;13:63.
2009;2(5):556–65. 52. Hoffmann A, Engelfriet P, Mulder B. Radiation exposure during
37. Shudo Y, Matsumiya G, Sakaguchi T, Miyagawa S, Yoshikawa Y, follow-up of adults with congenital heart disease. Int J Cardiol.
Yamauchi T, et al. Assessment of changes in mitral valve configu- 2007;118(2):151–3.
ration with multidetector computed tomography: impact of papil- 53. Ben Saad M, Rohnean A, Sigal-Cinqualbre A, Adler G, Paul
lary muscle imbrication and ring annuloplasty. Circulation. JF. Evaluation of image quality and radiation dose of thoracic and
2010;122(11 Suppl):S29–36. coronary dual-source CT in 110 infants with congenital heart dis-
38. Gordic S, Nguyen-Kim TD, Manka R, Sundermann S, ease. Pediatr Radiol. 2009;39(7):668–76.
Frauenfelder T, Maisano F, et al. Sizing the mitral annulus in 54. Huang MP, Liang CH, Zhao ZJ, Liu H, Li JL, Zhang JE, et al.
healthy subjects and patients with mitral regurgitation: 2D versus Evaluation of image quality and radiation dose at prospective
3D measurements from cardiac CT. Int J Cardiovasc Imaging. ECG-triggered axial 256-slice multi-detector CT in infants with
2014;30(2):389–98. congenital heart disease. Pediatr Radiol. 2011;41(7):858–66.
39. Blanke P, Dvir D, Cheung A, Ye J, Levine RA, Precious B, et al. 55. Paul JF, Rohnean A, Elfassy E, Sigal-Cinqualbre A. Radiation
A simplified D-shaped model of the mitral annulus to facilitate dose for thoracic and coronary step-and-shoot CT using a 128-
CT-based sizing before transcatheter mitral valve implantation. slice dual-source machine in infants and small children with con-
J Cardiovasc Comput Tomogr. 2014;8(6):459–67. genital heart disease. Pediatr Radiol. 2011;41(2):244–9.
40. Moodley S, Schoenhagen P, Gillinov AM, Mihaljevic T, Flamm 56. Shinbane JS, Shriki J, Hindoyan A, Ghosh B, Chang P, Farvid A,
SD, Griffin BP, et al. Preoperative multidetector computed et al. Unoperated congenitally corrected transposition of the great
tomograpy angiography for planning of minimally invasive arteries, nonrestrictive ventricular septal defect, and pulmonary
robotic mitral valve surgery: impact on decision making. J Thorac stenosis in middle adulthood: do multiple wrongs make a right?
Cardiovasc Surg. 2013;146(2):262–8 e1. World J Pediatr Congenital Heart Surg. 2012;3(1):123–9.
41. Higgins J, Mayo J, Skarsgard P. Cardiac computed tomography 57. Ihlenburg S, Rompel O, Rueffer A, Purbojo A, Cesnjevar R,
facilitates operative planning in patients with mitral calcification. Dittrich S, et al. Dual source computed tomography in patients
Ann Thorac Surg. 2013;95(1):e9–11. with congenital heart disease. Thorac Cardiovasc Surg. 2014;
42. Morris MF, Suri RM, Akhtar NJ, Young PM, Gruden JF, Burkhart 62(3):203–10.
HM, et al. Computed tomography as an alternative to catheter 58. Vastel-Amzallag C, Le Bret E, Paul JF, Lambert V, Rohnean A, El
angiography prior to robotic mitral valve repair. Ann Thorac Surg. Fassy E, et al. Diagnostic accuracy of dual-source multislice com-
2013;95(4):1354–9. puted tomographic analysis for the preoperative detection of coro-
43. Ghersin N, Abadi S, Sabbag A, Lamash Y, Anderson RH, Wolfson nary artery anomalies in 100 patients with tetralogy of Fallot.
H, et al. The three-dimensional geometric relationship between J Thorac Cardiovasc Surg. 2011;142(1):120–6.
the mitral valvar annulus and the coronary arteries as seen from 59. Yamasaki Y, Nagao M, Yamamura K, Yonezawa M, Matsuo Y,
the perspective of the cardiac surgeon using cardiac computed Kawanami S, et al. Quantitative assessment of right ventricular
tomography. Eur J CardioThorac Surg. 2013;44(6):1123–30. function and pulmonary regurgitation in surgically repaired tetral-
44. Mao S, Shinbane JS, Girsky MJ, Child J, Carson S, Oudiz RJ, ogy of Fallot using 256-slice CT: comparison with 3-Tesla
et al. Coronary venous imaging with electron beam computed MRI. Eur Radiol. 2014;24(12):3289–99.
tomographic angiography: three-dimensional mapping and rela- 60. Park EA, Lee W, Chung SY, Yin YH, Chung JW, Park JH. Optimal
tionship with coronary arteries. Am Heart J. 2005;150(2): scan timing and intravenous route for contrast-enhanced com-
315–22. puted tomography in patients after Fontan operation. J Comput
45. Choure AJ, Garcia MJ, Hesse B, Sevensma M, Maly G, Greenberg Assist Tomogr. 2010;34(1):75–81.
NL, et al. In vivo analysis of the anatomical relationship of coro- 61. Cook SC, McCarthy M, Daniels CJ, Cheatham JP, Raman
nary sinus to mitral annulus and left circumflex coronary artery SV. Usefulness of multislice computed tomography angiography
22 Cardiothoracic Surgery Applications: Virtual CT Imaging Approaches to Procedural Planning 427

to evaluate intravascular stents and transcatheter occlusion devices 76. Selvanayagam JB, Kardos A, Francis JM, Wiesmann F, Petersen
in patients with d-transposition of the great arteries after mustard SE, Taggart DP, et al. Value of delayed-enhancement cardiovascu-
repair. Am J Cardiol. 2004;94(7):967–9. lar magnetic resonance imaging in predicting myocardial viability
62. Oztunc F, Baris S, Adaletli I, Onol NO, Olgun DC, Guzeltas A, after surgical revascularization. Circulation. 2004;110(12):
et al. Coronary events and anatomy after arterial switch operation 1535–41.
for transposition of the great arteries: detection by 16-row mul- 77. Lardo AC, Cordeiro MA, Silva C, Amado LC, George RT, Saliaris
tislice computed tomography angiography in pediatric patients. AP, et al. Contrast-enhanced multidetector computed tomography
Cardiovasc Intervent Radiol. 2009;32(2):206–12. viability imaging after myocardial infarction: characterization of
63. Ou P, Celermajer DS, Marini D, Agnoletti G, Vouhe P, Brunelle F, myocyte death, microvascular obstruction, and chronic scar.
et al. Safety and accuracy of 64-slice computed tomography coro- Circulation. 2006;113(3):394–404.
nary angiography in children after the arterial switch operation for 78. Chiou KR, Liu CP, Peng NJ, Huang WC, Hsiao SH, Huang YL,
transposition of the great arteries. JACC Cardiovasc Imaging. et al. Identification and viability assessment of infarcted myocar-
2008;1(3):331–9. dium with late enhancement multidetector computed tomography:
64. Raman SV, Cook SC, McCarthy B, Ferketich AK. Usefulness of comparison with thallium single photon emission computed
multidetector row computed tomography to quantify right ven- tomography and echocardiography. Am Heart J. 2008;155(4):
tricular size and function in adults with either tetralogy of Fallot or 738–45.
transposition of the great arteries. Am J Cardiol. 2005; 79. Mahnken AH, Koos R, Katoh M, Wildberger JE, Spuentrup E,
95(5):683–6. Buecker A, et al. Assessment of myocardial viability in reperfused
65. Quaife RA, Chen MY, Kim M, Klein AJ, Jehle A, Kay J, et al. acute myocardial infarction using 16-slice computed tomography
Pre-procedural planning for percutaneous atrial septal defect clo- in comparison to magnetic resonance imaging. J Am Coll Cardiol.
sure: transesophageal echocardiography compared with cardiac 2005;45(12):2042–7.
computed tomographic angiography. J Cardiovasc Comput 80. Sato A, Hiroe M, Nozato T, Hikita H, Ito Y, Ohigashi H, et al.
Tomogr. 2010;4(5):330–8. Early validation study of 64-slice multidetector computed tomog-
66. Kivisto S, Hanninen H, Holmstrom M. Partial anomalous pulmo- raphy for the assessment of myocardial viability and the predic-
nary venous return and atrial septal defect in adult patients tion of left ventricular remodelling after acute myocardial
detected with 128-slice multidetector computed tomography. infarction. Eur Heart J. 2008;29(4):490–8.
J Cardiothorac Surg. 2011;6:126. 81. Habis M, Capderou A, Ghostine S, Daoud B, Caussin C, Riou JY,
67. Rajiah P, Kanne JP. Computed tomography of septal defects. et al. Acute myocardial infarction early viability assessment by
J Cardiovasc Comput Tomogr. 2010;4(4):231–45. 64-slice computed tomography immediately after coronary angi-
68. Amat F, Le Bret E, Sigal-Cinqualbre A, Coblence M, Lambert V, ography: comparison with low-dose dobutamine echocardiogra-
Rohnean A, et al. Diagnostic accuracy of multidetector spiral phy. J Am Coll Cardiol. 2007;49(11):1178–85.
computed tomography for preoperative assessment of sinus veno- 82. Habis M, Capderou A, Sigal-Cinqualbre A, Ghostine S, Rahal S,
sus atrial septal defects in children. Interact Cardiovasc Thorac Riou JY, et al. Comparison of delayed enhancement patterns on
Surg. 2011;12(2):179–82. multislice computed tomography immediately after coronary
69. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, angiography and cardiac magnetic resonance imaging in acute
Dearani JA, et al. ACC/AHA 2008 Guidelines for the Management myocardial infarction. Heart. 2009;95(8):624–9.
of Adults with Congenital Heart Disease: a report of the American 83. Sato A, Nozato T, Hikita H, Akiyama D, Nishina H, Hoshi T, et al.
College of Cardiology/American Heart Association Task Force on Prognostic value of myocardial contrast delayed enhancement
Practice Guidelines (writing committee to develop guidelines on with 64-slice multidetector computed tomography after acute
the management of adults with congenital heart disease). myocardial infarction. J Am Coll Cardiol. 2012;59(8):730–8.
Circulation. 2008;118(23):e714–833. 84. Rodriguez-Granillo GA, Rosales MA, Baum S, Rennes P,
70. Garcia-Montes JA, Camacho-Castro A, Sandoval-Jones JP, Rodriguez-Pagani C, Curotto V, et al. Early assessment of myo-
Buendia-Hernandez A, Calderon-Colmenero J, Patino-Bahena E, cardial viability by the use of delayed enhancement computed
et al. Closure of large patent ductus arteriosus using the Amplatzer tomography after primary percutaneous coronary intervention.
Septal Occluder. Cardiol Young. 2015;25(3):491–5. JACC Cardiovasc Imaging. 2009;2(9):1072–81.
71. Shriki JE, Shinbane JS, Rashid MA, Hindoyan A, Withey JG, 85. Raman SV, Sahu A, Merchant AZ, Louis LB, Firstenberg MS, Sun
DeFrance A, et al. Identifying, characterizing, and classifying B. Noninvasive assessment of left ventricular assist devices with
congenital anomalies of the coronary arteries. Radiographics. cardiovascular computed tomography and impact on manage-
2012;32(2):453–68. ment. J Heart Lung Transpl. 2010;29(1):79–85.
72. Mainwaring RD, Reddy VM, Reinhartz O, Petrossian E, 86. Boruah PK, Baruah D, Mahr C, Gaglianello N, Shahir
MacDonald M, Nasirov T, et al. Anomalous aortic origin of a K. Intermittent left ventricular assist device inflow tract obstruc-
coronary artery: medium-term results after surgical repair in 50 tion by prolapsing papillary muscle detected by multi-detector
patients. Ann Thorac Surg. 2011;92(2):691–7. computed tomography (MDCT). Int J Cardiol. 2014;176(1):
73. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, et al. e13–4.
The use of contrast-enhanced magnetic resonance imaging to 87. Bolen MA, Popovic ZB, Gonzalez-Stawinski G, Schoenhagen
identify reversible myocardial dysfunction. N Engl J Med. P. Left ventricular assist device malposition interrogated by 4-D
2000;343(20):1445–53. cine computed tomography. J Cardiovasc Comput Tomogr.
74. Klein C, Nekolla SG, Bengel FM, Momose M, Sammer A, Haas 2011;5(3):186–8.
F, et al. Assessment of myocardial viability with contrast- 88. Sorensen EN, Hiivala NJ, Jeudy J, Rajagopal K, Griffith
enhanced magnetic resonance imaging: comparison with positron BP. Computed tomography correlates of inflow cannula malposi-
emission tomography. Circulation. 2002;105(2):162–7. tion in a continuous-flow ventricular-assist device. J Heart Lung
75. Kuhl HP, Beek AM, van der Weerdt AP, Hofman MB, Visser CA, Transpl. 2013;32(6):654–7.
Lammertsma AA, et al. Myocardial viability in chronic ischemic 89. Mishkin JD, Enriquez JR, Meyer DM, Bethea BT, Thibodeau JT,
heart disease: comparison of contrast-enhanced magnetic reso- Patel PC, et al. Utilization of cardiac computed tomography angi-
nance imaging with (18)F-fluorodeoxyglucose positron emission ography for the diagnosis of left ventricular assist device thrombo-
tomography. J Am Coll Cardiol. 2003;41(8):1341–8. sis. Circ Heart Fail. 2012;5(2):e27–9.
428 J.S. Shinbane et al.

90. von Ziegler F, Leber AW, Becker A, Kaczmarek I, Schonermarck 103. Yoshida S, Akiba H, Tamakawa M, Yama N, Hareyama M,
U, Raps C, et al. Detection of significant coronary artery stenosis Morishita K, et al. Thoracic involvement of type A aortic dissec-
with 64-slice computed tomography in heart transplant recipients: tion and intramural hematoma: diagnostic accuracy – comparison
a comparative study with conventional coronary angiography. Int of emergency helical CT and surgical findings. Radiology.
J Cardiovasc Imaging. 2009;25(1):91–100. 2003;228(2):430–5.
91. von Ziegler F, Rummler J, Kaczmarek I, Greif M, Schenzle J, 104. Yoshikai M, Ikeda K, Itoh M, Noguchi R. Detection of coronary
Helbig S, et al. Detection of significant coronary artery stenosis artery disease in acute aortic dissection: the efficacy of 64-row
with cardiac dual-source computed tomography angiography in multidetector computed tomography. J Card Surg. 2008;
heart transplant recipients. Transplant Int. 2012;25(10):1065–71. 23(3):277–9.
92. Barthelemy O, Toledano D, Varnous S, Fernandez F, Boutekadjirt 105. Smayra T, Noun R, Tohme-Noun C. Left anterior descending
R, Ricci F, et al. Multislice computed tomography to rule out coro- coronary artery dissection after blunt chest trauma: assessment by
nary allograft vasculopathy in heart transplant patients. J Heart multi-detector row computed tomography. J Thorac Cardiovasc
Lung Transpl. 2012;31(12):1262–8. Surg. 2007;133(3):811–2.
93. Wever-Pinzon O, Romero J, Kelesidis I, Wever-Pinzon J, 106. Sato Y, Matsumoto N, Komatsu S, Matsuo S, Kunimasa T, Yoda
Manrique C, Budge D, et al. Coronary computed tomography S, et al. Coronary artery dissection after blunt chest trauma: depic-
angiography for the detection of cardiac allograft vasculopathy: a tion at multidetector-row computed tomography. Int J Cardiol.
meta-analysis of prospective trials. J Am Coll Cardiol. 2007;118(1):108–10.
2014;63(19):1992–2004. 107. Scaglione M, Pinto A, Pinto F, Romano L, Ragozzino A, Grassi
94. Rohnean A, Houyel L, Sigal-Cinqualbre A, To NT, Elfassy E, R. Role of contrast-enhanced helical CT in the evaluation of acute
Paul JF. Heart transplant patient outcomes: 5-year mean follow-up thoracic aortic injuries after blunt chest trauma. Eur Radiol.
by coronary computed tomography angiography. Transplantation. 2001;11(12):2444–8.
2011;91(5):583–8. 108. Higashiura W, Sakaguchi S, Tabayashi N, Taniguchi S, Kichikawa
95. Kobashigawa J. Coronary computed tomography angiography: is K. Impact of 3-dimensional-computed tomography workstation
it time to replace the conventional coronary angiogram in heart for precise planning of endovascular aneurysm repair. Circulation
transplant patients? J Am Coll Cardiol. 2014;63(19):2005–6. J. 2008;72(12):2028–34.
96. Hoey ET, Mankad K, Puppala S, Gopalan D, Sivananthan 109. Lin MP, Chang SC, Wu RH, Chou CK, Tzeng WS. A comparison
MU. MRI and CT appearances of cardiac tumours in adults. Clin of computed tomography, magnetic resonance imaging, and digi-
Radiol. 2009;64(12):1214–30. tal subtraction angiography findings in the diagnosis of infected
97. Rajiah P, Kanne JP, Kalahasti V, Schoenhagen P. Computed aortic aneurysm. J Comput Assist Tomogr. 2008;32(4):
tomography of cardiac and pericardiac masses. J Cardiovasc 616–20.
Comput Tomogr. 2011;5(1):16–29. 110. Sodian R, Schmauss D, Markert M, Weber S, Nikolaou K,
98. Suh SY, Rha SW, Kim JW, Park CG, Seo HS, Oh DJ, et al. The Haeberle S, et al. Three-dimensional printing creates models for
usefulness of three-dimensional multidetector computed tomogra- surgical planning of aortic valve replacement after previous
phy to delineate pericardial calcification in constrictive pericardi- coronary bypass grafting. Ann Thorac Surg. 2008;85(6):
tis. Int J Cardiol. 2006;113(3):414–6. 2105–8.
99. von Erffa J, Daniel WG, Achenbach S. Three-dimensional visual- 111. Schmauss D, Schmitz C, Bigdeli AK, Weber S, Gerber N, Beiras-
ization of severe pericardial calcification in constrictive pericardi- Fernandez A, et al. Three-dimensional printing of models for pre-
tis using multidetector-row computed tomography. Eur Heart operative planning and simulation of transcatheter valve
J. 2006;27(3):275. replacement. Ann Thorac Surg. 2012;93(2):e31–3.
100. Kameda Y, Funabashi N, Kawakubo M, Uehara M, Hasegawa H, 112. Schmauss D, Gerber N, Sodian R. Three-dimensional printing of
Kobayashi Y, et al. Heart in an eggshell – eggshell appearance cal- models for surgical planning in patients with primary cardiac
cified constrictive pericarditis demonstrated by three-dimensional tumors. J Thorac Cardiovasc Surg. 2013;145(5):1407–8.
images of multislice computed tomography. Int J Cardiol. 113. Schmauss D, Juchem G, Weber S, Gerber N, Hagl C, Sodian
2007;120(2):269–72. R. Three-dimensional printing for perioperative planning of com-
101. Rifkin RD, Mernoff DB. Noninvasive evaluation of pericardial plex aortic arch surgery. Ann Thorac Surg. 2014;97(6):
effusion composition by computed tomography. Am Heart 2160–3.
J. 2005;149(6):1120–7. 114. Ma XJ, Tao L, Chen X, Li W, Peng ZY, Chen Y, et al. Clinical
102. Hayter RG, Rhea JT, Small A, Tafazoli FS, Novelline application of three-dimensional reconstruction and rapid proto-
RA. Suspected aortic dissection and other aortic disorders: multi- typing technology of multislice spiral computed tomography angi-
detector row CT in 373 cases in the emergency setting. Radiology. ography for the repair of ventricular septal defect of tetralogy of
2006;238(3):841–52. Fallot. Genet Molecul Res. 2015;14(1):1301–9.
 Computed Tomographic Angiography
in the Assessment of Congenital Heart 23
Disease and Coronary Artery Anomalies

Priya Pillutla and Stephen C. Cook

Abstract
Advances in medical and surgical care have significantly increased the numbers of children
and adults living with congenital heart disease (CHD). This chapter will discuss anatomical
and imaging considerations for the major CHD lesions. Additionally, the role of computed
tomography in the planning of percutaneous and surgical repairs will be addressed, as well
as the use of this modality to monitor for possible post-intervention complications. Finally,
clinically significant coronary anomalies will be reviewed.

Keywords
Congenital heart disease • Cardiac computed tomography • Coronary anomalies

Introduction Prior to the introduction of cardiovascular magnetic

resonance (CMR) imaging and cardiovascular computed
Congenital heart disease (CHD) is the most common con- tomographic angiography (CCTA), transthoracic echocar-
genital disorder in newborns [1–3]. Approximately 6 per diography (TTE) and cardiac catheterization were the
1000 live births in the United States are affected by complex primary imaging modalities in the diagnosis and evaluation
CHD and as many as 75 per 1000 live births have simple of the patient with complex CHD [9]. Advances in TTE
lesions such as ventricular septal defects [4]. Improved med- imaging and its widespread availability have allowed it to
ical and surgical care in addition to evolving percutaneous largely replace cardiac catheterization as the predominant
methods of intervention have decreased early and late mor- imaging modality for CHD in children in most centers and
tality. As a result, mortality in infants and children with CHD the use of diagnostic cardiac catheterization in CHD appears
dropped 31 % between 1987 and 2005 [5] and the adult pop- to have declined [10]. In the hands of a skilled technologist,
ulation has undergone rapid growth. As of 2000, there were TTE provides non-invasive information regarding complex
nearly equal numbers of adults and children with severe CHD while avoiding radiation and intravenous contrast
CHD [6]. Currently, it is estimated there are approximately exposure associated with serial cardiac catheterizations.
800,000 adults with CHD in the United States [7] with a It also can be performed rapidly, provides important
prevalence in the adult population of 3000 per million [8]. hemodynamic data and is relatively inexpensive.
Both TTE and catheterization have disadvantages with
regards to imaging the adult with CHD. Anatomic windows
P. Pillutla, MD (*) for ultrasound may be limited by chest wall deformities (e.g.,
Adult Congenital Heart Disease Program, pectus deformities, spinal abnormalities) and post-surgical
Harbor-UCLA Medical Center, 1124 W. Carson Street, RB2,
changes. Transesophageal echocardiography can circumvent
Torrance, CA 90502, USA
e-mail: [email protected] some of these pitfalls but it requires an experienced operator
and carries the risks of any invasive procedure including con-
S.C. Cook, MD, FACC
Adult Congenital Heart Disease Center, Heart Institute, scious sedation. Additionally, it has limited use in the assess-
Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA ment of anterior structures such as conduits.

© Springer International Publishing 2016 429

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_23
430 P. Pillutla and S.C. Cook

CMR allows for three-dimensional structural and func- in adult CHD may avoid many potential pitfalls. Prior to
tional assessment of the heart as well as delineation of extra- commencing a study, the following should be described if
cardiac structures without ionizing radiation. The benefits of possible: the diagnostic indication, the original anatomic
CMR in the evaluation of the adult CHD patient are diverse defects, operative repairs if any and post-surgical anatomic
including quantification of both left and right ventricular size and hemodynamic changes. Thus, the study can be tailored
and systolic function, shunt quantification, evaluation and for the individual patient to provide the appropriate extent of
quantification of valvar disease, and assessment of myocar- anatomic coverage, proper timing of contrast administration,
dial perfusion and fibrosis [11]. Despite these numerous selection of the best image acquisition protocol and special
applications and advantages, CMR has several limitations attention to the structures of interest.
including prolonged acquisition time, signal void artifact due
to prior transcatheter interventions [12], claustrophobia, high
acquisition costs and the inability to perform CMR in patients Cardiac Anatomy: A Sequential Approach
with implantable cardioverter defibrillators or pacemakers.
Concurrently, there have been numerous advances (e.g., CHD is highly variable in its complexity and anatomic
reduced scan times; higher spatial/temporal resolution) in arrangements. Attempts to adequately describe complicated
the field of cardiovascular CT [13]. Consequently, CCTA lesions have led to a nuanced taxonomy of eponyms,
provides a suitable alternative to CMR. It yields an accurate synonymous and near-synonymous terms. For instance, even
assessment of intra- and extra-cardiac anatomy for patients the basic terms of “left” and “right” can lead to confusion.
with both simple and complex CHD while overcoming the By convention, they refer to morphologic characteristics of a
limitations of CMR. Furthermore, CCTA can provide cardiac chamber rather than position within the chest.
accurate quantification of volume and function comparable To reduce clinical confusion and facilitate academic
to CMR although such protocols typically require higher study, various systematic schemata have been developed.
radiation doses [14]. In contrast to CMR, acquisition time is Van Praagh’s “segmental approach” [26] describes each of
brief. Therefore, this technique should be strongly considered the three main segments of cardiac anatomy (the atria,
in patients with poor echocardiographic windows and ventricles and great arteries) in series. This is analogous to
contraindications to CMR. the construction of a home, where each segment builds off
Unfortunately, CCTA is not without disadvantages. This the prior with the atria serving as the foundation. The
technique still requires exposure to ionizing radiation as well sequence is often abbreviated by a sequence of three letters
as nephrotoxic contrast. Importantly, patients with CHD (X, Y, Z) where the first letter describes visceral-atrial situs,
have many potential sources of ongoing radiation exposure the second ventricular looping and the third the relationships
that often begin in infancy and continue throughout life. of the great arteries. This analysis is often helpful, particularly
Serial chest radiography, nuclear scans, computed for the evaluation of those with complex CHD, as it provides
tomography scans and diagnostic/therapeutic catheterizations a systematic and standardized approach that can be applied
are frequently performed in the setting of prior corrective or to any patient.
palliative interventions [15]. Therefore, physicians who
perform and/or refer patients for this procedure should be
familiar with radiation exposure and techniques available to Atrial Situs
reduce radiation exposure at the time of CCTA examination.
Fortunately, there are now a number of low-radiation Atrial situs most often follows the positioning of the unpaired
protocols that can be employed to significantly reduce the abdominal viscera. For instance, the normal arrangement is
radiation exposure including reduction of tube voltage (for situs solitus (S, _, _), in which the morphologic right atrium,
example to 80 kVp when feasible), adequate heart rate systemic venous return and liver are on the right side of the
control, use of prospectively triggered scanning, iterative patient. The morphologic left atrium, pulmonary venous
reconstruction and spectral detectors [16–25]. return, stomach and spleen are on the left side. The
morphology of the atrial appendage provides important clues
regarding right or left-sidedness (See Fig. 23.1).
CT Imaging Protocol The mirror image of this arrangement (with the morpho-
logic right atrium and liver on the patient’s left and the mor-
Methodical pre-study planning is of critical importance in phologic left atrium, stomach and spleen on the patient’s
the patient with CHD. Repeating a study due to suboptimal right) is situs inversus (I, _, _). Cases of both atria having
technique exposes the patient to excessive contrast and characteristics of either the left or right atrium (atrial isomer-
radiation exposure. Furthermore, crucial structures may be ism) are described as situs ambiguus (A, _, _), also known as
missed on a “standard” study. Collaboration with a specialist the heterotaxy syndrome.
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 431

a b

Fig. 23.1 Oblique axial view (a) demonstrates the features of a demonstrates a broad-based triangular appendage (arrowhead) sugges-
morphologic left atrium (LA), including its finger-like appearance and tive of a right atrial appendage. RA right atrium
pectinate muscles (arrows). In contrast, the oblique coronal view (b)

a b

Fig. 23.2 Volume-rendered three-dimensional reconstructions (a, b) monary artery of the morphologic left lung (L) travels over its main
demonstrating pulmonary situs solitus. The pulmonary artery of the bronchus and posterior to the upper lobe bronchus
morphologic right lung travels anteriorly to the bronchus (R). The pul-

Bronchial morphology may further assist in determining the first branch of the left mainstem bronchus courses below
atrial situs as the two frequently correlate with one another. (hyparterial) the left pulmonary artery (See Fig. 23.2). This
Normally, the first branch of the right mainstem bronchus bronchial configuration indirectly suggests atrial situs
courses above (eparterial) the right pulmonary artery whereas solitis.
432 P. Pillutla and S.C. Cook

a b

Fig. 23.3 Atrioventricular and ventriculoarterial concordance. The nal view (b) demonstrates ventriculoarterial concordance between the
oblique coronal view (a) demonstrates atrioventricular concordance LV and the aorta (Ao)
between the left atrium (LA) and left ventricle (LV). The oblique coro-

Atrial Isomerism tricuspid valve attachments to the septum and free wall, and
absence of fibrous continuity between the tricuspid valve and
Atrial isomerism, commonly referred to as heterotaxy syn- semilunar valve. Additionally, the tricuspid valve is normally
drome, is the result of duplication of the structures typical located more apically within the right ventricle when com-
of either the left or right side of the body. This syndrome is pared to the mitral valve. In contrast, the morphologic left
associated with intestinal abnormalities, poorly functioning ventricle has a smooth septal surface and fibrous continuity
or absent splenic tissue, and complex CHD [27]. In right between the mitral and semilunar valves.
atrial isomerism, both atria have the broad based triangular
atrial appendages typical of the right atrium and receive
systemic venous return (superior vena cava or SVC, infe- Semilunar Valve Relationships
rior vena cava or IVC, and coronary sinus). This is typically
associated with bilateral trilobed lungs, a large liver which Van Praagh described six potential relationships of the aortic and
spans the abdomen and asplenia. Left atrial isomerism is pulmonary valves. Each variant is defined by the position of the
characterized by both atria having narrow based atrial aortic valve relative to the pulmonary valve. In the normal rela-
appendages and receiving the ipsilateral pulmonary veins. tionship, solitus (_, _, S), the aortic valve is rightward and poste-
This is associated with bilateral bilobed lungs, interruption rior of the pulmonary valve. If the aortic valve is leftward and
of the IVC, a midline liver and polysplenia. posterior, it is termed inversus (_, _, I). When the aortic valve is
rightward and anterior, it is termed D-malposition (_, _, D), and
when the aortic valve is leftward and anterior, it is L-malposition
Ventricular Looping (_, _, L). Uncommonly, the aortic valve can lie directly anterior
(_, _, A) or directly posterior (_, _, P) to the pulmonary valve.
The normal anatomic position of the morphologic right ven-
tricle is to the right and anterior of the left ventricle. This
arrangement is called “D-loop” (_, D, _) and results from Concordant/Discordant Relationships
rightward or dextro-looping of the primitive heart early in
fetal development. If the primitive heart developed in a left- Tynan and colleagues [28] proposed an alternate means of
ward (levo-) fashion, it can result in the left ventricle anterior describing complicated CHD. Their approach places greater
and rightward of the right ventricle or “L-loop” (_, L, _). emphasis on the connections between the different segments.
Features of the morphologic right ventricle include the Segments can be concordant (normally related) or discor-
presence of coarse trabeculae, a prominent moderator band, dant (See Fig. 23.3). For instance, if the right atrium connects
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 433

normally via a tricuspid valve to the right ventricle, there is anastomosis site or the pulmonary veins. CCTA, which is
atrioventricular concordance. If the right ventricle then well characterized in the evaluation of the pulmonary veins
gives rise to the pulmonary artery, there is ventriculoarterial prior to or following radiofrequency ablation [33] is ideally
concordance. In d-transposition of the great arteries (d-TGA), suited to evaluate the pulmonary venous anatomy in the adult
in which the right ventricle gives rise to the aorta, there is CHD patient with native disease as well as the post-operative
ventriculoarterial discordance. Atrioventricular connections patient to determine the presence/absence of stenosis after
may also be absent (e.g., tricuspid atresia) or doubly- prior palliative repair (See Fig. 23.4).
committed (connected to both ventricles, either equally or
unequally). Cor Triatriatum
Cor triatriatum is caused when there is stenosis of the com-
mon pulmonary vein [34]. Hence, the pulmonary veins enter
Congenital Heart Defects of Simple a “pulmonary venous” chamber which drains into the left
and Moderate Complexity atrium (cor triatriatum sinistrum) via an opening. It may
alternatively communicate with the right atrium. This orifice
Venous Abnormalities may be imperforate, restrictive, multiple, or large and nonre-
strictive. Cor triatiatrum dextrum is caused by persistence of
Systemic Venous Abnormalities the right valve of the sinus venosus and divides the right
Systemic venous anomalies include bilateral SVC (which atrium into three chambers; it is far less common. Commonly
may or may not be connected via a bridging innominate associated defects include atrial septal defect or patent fora-
vein), a unilateral left SVC (which most frequently drains men ovale, PAPVR and persistent left SVC.
into an enlarged coronary sinus, less commonly draining Without surgical correction, a highly restrictive commu-
directly to the left atrium) and interrupted IVC (often with nication between the pulmonary venous confluence and the
continuation via the azygous or hemiazygous veins). left atrium is associated with high mortality during infancy.
In contrast, the patient with mild or no obstruction may not
Pulmonary Venous Abnormalities present until later in adult life. CCTA provides excellent spa-
Abnormal pulmonary venous return is described as being tial resolution for defining pulmonary venous and pulmonary
total or partial. In total anomalous venous return (TAPVR), venous anatomy in this condition, both in the unrepaired and
all four pulmonary veins drain anomalously. There are four post-operative state.
variants of TAPVR: supracardiac, cardiac, infracardiac and
mixed. Supracardiac-type is the most common with the pul-
monary veins connecting to the systemic venous circulation Defects in Septation
via the SVC, innominate vein or azygos vein. Cardiac-type
describes the pulmonary veins draining to the coronary sinus Atrial Septal Defects
or a similar vein into the right atrium. In patients with the Atrial septal defects, or ASDs, are among the most com-
infracardiac-type, the pulmonary veins drain into the portal mon congenital heart defects. They are classified by their
or hepatic veins. Mixed is any combination of the above anatomic location. The two most common variants, secun-
venous abnormalities. If any of these lesions are associated dum and primum, are true defects within the atrial septum.
with any degree of obstruction, which is particularly com- The sinus venous defect is not a true defect in the atrial
mon in the infracardiac-type, severe pulmonary congestion septum but rather a deficiency in the wall separating the
may result. In this setting, surgical palliation is usually pulmonary veins from the right atrium. This results in a
required during the newborn period. left-to-right shunt similar to the primum and secundum
If at least one of the veins drains inappropriately, it is ASDs. The coronary sinus ASD shares a similar aberration
described as partial (PAPVR). There is a wide spectrum of and physiologic outcome. Here, there is a deficiency in the
anatomic malformations in PAPVR and many different types wall separating the coronary sinus from the left atrium (See
of connections between the systemic venous and pulmonary Fig. 23.5).
venous circulations have been reported [29–32]. PAPVR is Of these, ostium secundum defects or secundum ASDs,
often associated with a sinus venosus atrial septal defect are the most common variant. Ostium primum defects or pri-
(ASD). When the right-sided pulmonary veins drain anoma- mum ASDs are the next most common. As the primum por-
lously to the IVC (typically near the diaphragm) and in the tion of the atrial septum is contiguous with the atrioventricular
presence of right lung hypoplasia, this constellation is termed valves and intraventricular septum, primum ASDs are typi-
“scimitar syndrome” (from the resemblance of the curvilin- cally classified within the spectrum of atrioventricular septal
ear anomalous connection to a curved sword). defects (AVSDs or atrioventricular canal defects).
Late complications following surgical correction of either Sinus venous ASDs are uncommon and account for
TAPVR or PAPVR include stenosis of the SVC, the approximately 5–10 % of all ASDs [35]. They most often
434 P. Pillutla and S.C. Cook

a b

Fig. 23.4 Volume rendered three dimensional reconstructions demon- to the inferior vena cava (a). Note the normal return of the left pulmonary
strate anomalous return of the right superior pulmonary vein (RSPV) to veins to the left atrium (b). LA left atrium, LIPV left inferior pulmonary
the superior vena cava (SVC) and right inferior pulmonary vein (RIPV) vein, LSPV left superior pulmonary vein, RA right atrium

atrium. While these defects do not involve the atrial septum,

they are physiologically similar.
Because of increased right atrial compliance, shunt flow
across the ASD is left to right (in the presence of normal
pulmonary vascular resistance). Significant shunts lead to
volume overload and dilation of the right-sided cardiac
chambers. Thus, closure of an ASD is indicated (either surgi-
cally or percutaneously) if right atrial or right ventricular
enlargement are present, with or without symptoms [36]. In
the presence of severe pulmonary hypertension, the shunt
may reverse direction and flow from right to left (Eisenmenger
physiology). The etiology of pulmonary hypertension in
such patients is not clear and may not be solely due to a large
left to right shunt over many decades [35]. ASD closure may
be considered in patients with pulmonary hypertension pro-
Fig. 23.5 Atrial septal defects: A indicates the superior sinus venosus vided there is a net left-to-right shunt and evidence of sub-
atrial septal defect (ASD); B secundum ASD, C inferior sinus venosus
ASD, D ostium primum ASD or partial atrioventricular septal defect, E
systemic pulmonary arterial pressure or evidence of
secundum ASD without posterior septal rim, and F coronary sinus pulmonary arterial vasoreactivity [36].
ASD. SVC superior vena cava, IVC inferior vena cava (Reprinted from Prior to the advent of atrial septal occlusion devices per-
Webb et al. [35] with permission of Wolters Kluwer) formed in the cardiac catheterization laboratory [37], the treat-
ment of choice had largely been surgical management. Currently,
occur at the junction of the SVC and the right atrium. A many secundum defects can now be managed percutaneously
defect in this area creates a connection between the right with fewer complications and shorter inpatient hospital stays
upper pulmonary veins and the right atrium. Less commonly, when compared with conventional surgical management [38].
they can involve the junction of the IVC and the right lower The success of percutaneous closure is determined by the pres-
pulmonary veins. Coronary sinus defects are more rare and ence of adequate rims of atrial tissue to secure the device.
often described as an “unroofing” of the coronary sinus, The spatial resolution of multi-detector CT provides an
allowing drainage from the coronary sinus into the left excellent modality for pre-procedural planning in ASD
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 435

a b

Fig. 23.6 Oblique axial (a) and sagittal (b) views demonstrate the interventional assessment to determine suitability for transcatheter clo-
anatomy of the atrial septal defect (*) as well as anatomic information sure. (I) inferior rim, LA left atrium, (R) retroaortic rim, (S) superior
regarding surrounding rims that are often helpful in the pre- rim, SVC superior vena cava

closure, particularly if a percutaneous approach is planned and extends from under the aortic valve towards the septal
[39]. Complete CT assessment prior to percutaneous closure leaflet of the tricuspid valve; defects that cross into the mus-
of a secundum ASD should include assessment of pulmo- cular, inlet or outlet septum are termed perimembranous.
nary venous anatomy and exclusion of anomalous pulmo- Outlet or supracristal (other terms include infundibular,
nary venous return, the dimensions of the defect, presence of conal, subpulmonary or doubly committed subarterial)
any fenstrations and characterization of the superior, inferior defects are in the smooth-walled septum, in continuity with
and retroaortic rims (See Fig. 23.6). Rims may be deficient the crista supraventricularis and the pulmonary valve.
or absent and are a key factor in choosing the appropriate The natural history and presentation of VSDs are vari-
closure strategy. Sinus venosus and primum ASDs should be able. Small defects located in the muscular septum may
specifically excluded. Additionally, depending upon the age undergo spontaneous closure. Occasionally, aneurysmal tis-
of the patient, characterization of the coronary arteries may sue from the tricuspid valve may result in spontaneous clo-
be necessary. sure of a perimembranous VSD. Small, restrictive defects
CCTA may be useful in the post-procedure patient, par- may be of little hemodynamic consequence. However, large
ticularly if a percutaneous closure was performed. The study nonrestrictive defects expose the right ventricle and
should include characterization of device seating, assessment pulmonary artery bed to the systemic pressure of the left
to exclude tissue erosion from the device, impingement on ventricle. Over time, due to increased pulmonary blood flow,
surrounding structures such as the atrioventricular or semilu- pulmonary vascular resistance will rise and ultimately lead
nar valves, pulmonary venous obstruction, and pericardial to a reversal of the shunt (right-to-left) consistent with
effusion [40]. A residual shunt should also be excluded. Eisenmenger physiology. Thus early surgical intervention is
indicated for defects causing a significant left-to-right shunt
Ventricular Septal Defects and evidence of left-sided volume overload [36] in order to
As with ASDs, ventricular septal defects (VSDs) are among avoid progressive and irreversible changes of pulmonary
the most common CHD lesions. They too are described by vascular disease. Other considerations for surgical referral
their position within the septum. The ventricular septum is include secondary phenomena such as infective endocarditis
divided into four regions: inlet, membranous, outlet and or aortic regurgitation (often seen in the setting of a suprac-
muscular. The inlet septum separates the mitral and tricuspid ristal VSD).
valves. The muscular septum extends from the inlet towards Ongoing advances in transcatheter techniques now pro-
the apex of the heart. The membranous septum itself is small vide an alternative method to address defects located in the
436 P. Pillutla and S.C. Cook

of equal size. Here, the common AV valve is symmetrically

located over both ventricles. An unbalanced AVSD occurs
when one of the ventricles is significantly smaller than the
other. AVSDs are characterized by anterior displacement of
the left ventricular outflow tract (LVOT), causing it to
elongate and narrow. This “gooseneck” deformity can cause
significant LVOT obstruction and may be worsened by
abnormal attachments from the AV valves.
Thus, notable morphological features of AVSDs which
may be seen on CT include the following: insertion of the AV
valve leaflets at the same level at the crux of the heart (rather
than the normal apical displacement of the tricuspid valve);
any deficiency in the AV septum; anterior displacement and
elongation of the LVOT and abnormal AV valves. The left
AV valve is often cleft.
Most adult patients with this diagnosis will have
undergone prior surgical palliation in infancy. Late
complications associated with AVSDs include left or right
AV valve regurgitation associated with a cleft or otherwise
structurally abnormal valve, residual atrial or ventricular
Fig. 23.7 An oblique axial image demonstrates a restrictive, muscular level shunt and LVOT obstruction.
ventricular septal defect (VSD; *)

Aortic Abnormalities
perimembranous and muscular portions of the interventricu-
lar septum in select cases [41, 42]. This technique has been Patent Ductus Arteriosus
demonstrated to be safe and effective when performed in The ductus arteriosus is a fetal vascular channel connecting
experienced centers. The most significant late-onset compli- the main pulmonary trunk to the descending aorta and which
cation in the perimembranous closure group is complete is essential for fetal circulation. Before birth, the ductus
atrioventricular block, which requires careful serial arteriosus allows much of the oxygenated blood from the
follow-up. placenta to bypass the pulmonary vascular bed and supply
Following either surgical or percutaneous device closure, the systemic circulation via the descending aorta. It typically
CCTA has utility in assessing the adequacy of closure via the closes spontaneously within a week following birth. Beyond
detection of residual defects (See Fig. 23.7). It is also useful this time, if the vessel remains patent, a shunt (patent ductus
in the pre-catheterization assessment to evaluate defect size arteriosus or PDA) now exists between the systemic and
as well as relationship of the defect to surrounding anatomic pulmonary vascular beds.
structures to determine suitability for percutaneous closure. This may be beneficial in certain congenital heart condi-
tions such as pulmonary atresia or hypoplastic left heart syn-
Atrioventricular Septal Defects drome, for which the PDA can provide a stable source of
Atrioventricular septal defects (AVSD) include a range of blood flow to either the pulmonary or systemic circulation. In
anomalies which share defects within the atrioventricular an otherwise normal circulation, a PDA may have serious
(AV) septum and, often, defects of the AV valves [43]. Up to sequelae that are mainly determined by the size of the size of
45 % of patients with Down syndrome have CHD and, of the ductus. As pulmonary vascular resistance falls following
these, approximately 45 % have an AVSD [44]. birth, the left-to-right shunt increases. Though a small PDA is
A number of terms are used to further classify the various often of little hemodynamic consequence, a large PDA can
anatomic features and “balance” of the ventricles associated expose the pulmonary vascular bed to excess pulmonary
with the AVSD. A complete AVSD has a single defect with a blood flow, eventually causing increased pulmonary vascular
primum ASD and inlet VSD along with a common AV valve. resistance and pulmonary hypertension. Pulmonary hyperten-
A partial AVSD always includes a primum ASD and there sion may persist even after the duct is closed.
are two distinct AV valves. A transitional AVSD is a partial While surgical ligation of a ductus is a straightforward
AVSD accompanied by a small inlet VSD; there are often surgical procedure, catheter-based techniques have now
anomalous chordal attachments to the ventricular septum. A become the procedure of choice for the majority of PDAs
balanced AVSD occurs when the left and right ventricles are [45]. Pre-intervention CCTA is useful to characterize the
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 437

distal to the origin of the left subclavian artery at the insertion

of the ductus arteriosus. This “juxtaductal” tissue of the aorta
has characteristics similar to ductal tissue leading to further
constriction in the post-natal period. This single theory does
not fully explain the pathophysiology since there also exists
a diffuse form of CoA characterized by hypoplasia of the
transverse arch.
This malformation may occur in isolation (simple CoA)
or in conjunction with other abnormalities (complex CoA).
Complex CoA is often associated with a bicuspid aortic
valve, subaortic stenosis, VSDs, mitral valve abnormalities
such as parachute mitral valve, intracranial aneurysms or
Turner syndrome.
When discovered in infancy, CoA is most often repaired
surgically. Current surgical techniques include resection of
the CoA with end-to-end anastomosis, subclavian flap
aortoplasty, patch aortoplasty and interposition jump graft.
Each technique has specific advantages, disadvantages and
associated long-term complications. Native lesions identified
in the adolescent or young adult are sometimes treated with
balloon angioplasty but there may be residual stenosis,
Fig. 23.8 Oblique sagittal view demonstrates a small patent ductus
ateriosus (arrow). Ao Aorta, MPA main pulmonary artery restenosis or aneurysm formation at the intervention site
[50]. Stent implantation is a favorable approach for select
patients with both native CoA and recoarctation and there are
size, shape and course of the duct as well as its diameter at long-term studies demonstrating acceptable safety and effi-
the pulmonary and aortic ends. These factors help determine cacy [36, 51–55].
the type of occluder device chosen at the time of intervention Complications in the patient with unoperated CoA are
(See Fig. 23.8). numerous and include systemic arterial hypertension,
accelerated coronary artery disease, stroke, aortic dissection
Aortopulmonary Window or rupture, congestive heart failure or intracranial hemorrhage
The aortopulmonary (AP) window is a rare congenital defect [56]. Late complications in operated CoA include
defined as a direct communication between the pulmonary recoarctation, aortic dilation and aortic dissection. Thus, life-
artery and the ascending aorta. While physiologically similar long followup and late postoperative imaging via CCTA or
to a large PDA, most cases of AP window have a defect in CMR are imperative for the patient with CoA, even in the
the proximal portion of the AP septum, between the semilu- setting of an acceptable surgical or percutaneous result.
nar valves and the pulmonary bifurcation. Nearly half of CCTA offers significant advantages in the assessment
affected patients have associated defects including aortic ori- of the patient with CoA who has previously undergone
gin of the right pulmonary artery, interrupted aortic arch, transcatheter therapy, particularly stenting. Many trans-
tetralogy of Fallot or coronary anomalies [46–49]. catheter devices including stents create significant signal
Surgical closure is indicated for nearly all patients with void artifact precluding an accurate assessment of the
AP window. A small AP window may present in adulthood anatomy of interest on CMR. In contrast, CCTA provides
with a continuous murmur and left heart enlargement. If the an accurate assessment of the lumen of the stented seg-
AP window is large and nonrestrictive, however, the patient ment and surrounding anatomic structures without signifi-
will present with pulmonary hypertension, cyanosis and cant artifact.
Eisenmenger physiology. In the patient with an unoperated The CCTA exam in a patient with native CoA or recoarc-
AP window, CCTA should inspect and confirm not only the tation should include the dimensions and anatomy (such as
presence of a window but also associated lesions. For those aneurysm and dissection) of the CoA segment, precise mea-
with repaired AP windows, serial late CCTA should evaluate surements of the entire aortic arch (which may be hypoplas-
the aortic and pulmonary artery architecture. tic) and description of collateral vessels bypassing the region
of stenosis [57]. Because of the risk of accelerated coronary
Coarctation of the Aorta/Interrupted Aortic Arch artery disease, special attention should be paid to the coro-
Coarctation of the aorta (CoA) is defined as a focal narrowing nary arteries. Finally, associated congenital cardiac lesions
of the aorta. Most commonly the area of narrowing is just including other forms of left ventricular outflow tract
438 P. Pillutla and S.C. Cook

obstruction (bicuspid aortic valve, subaortic stenosis) and permits for comprehensive imaging of the aorta in addition
mitral valve anomalies should be excluded. to the aortic valve. Complementary three-dimensional
Interruption of the aorta is defined as a complete separation volume-rendered reconstructions performed with off-line
between the ascending and descending aorta. There are analysis may provide important information about aortic
multiple branching patterns but the morphology can be dimensions that can guide management.
generally classified as Type A (interruption distal to the left
subclavian artery), Type B (between the carotid and Subvalvar Aortic Stenosis
subclavian arteries) or Type C (between the carotid arteries) Subvalvar aortic stenosis (subAS) is most frequently caused
[58]. Aortic interruptions may be associated with other by a fibrous membrane or ring of tissue although it can also
congenital anomalies including transposition of the great assume a diffusely hypoplastic or focal tunnel-type obstruc-
arteries, conotruncal anomalies with a VSD or subaortic tion. Although it can occur in isolation, more than half of cases
stenosis. Surgical therapy is required to restore continuity of are associated with another congenital defect such as VSD,
the aorta and concomitant defects. Late complications CoA, Shone’s complex, PDA, persistent left SVC or valvar
primarily involve restenosis at the site of prior surgical repair. aortic stenosis [63, 64]. There is also an association with mitral
CCTA may be used in this population for characterization of valve abnormalities [65, 66]. The degree of stenosis may
the aorta, arch anatomy and other cardiac defects as well as remain stable but most tend progress over time. Additionally,
evaluation of post-operative complications and/or to assess subAS may be associated with aortic regurgitation. In contrast
the efficacy of prior interventions. to valvar aortic stenosis, this lesion is not amenable to cathe-
ter-based interventions and the management is surgical when
indicated. Unfortunately, there is a significant risk of recur-
Congenital Valvar Disease rence despite surgical intervention. Thus, a history of subAS
or associated defects should prompt close inspection of the left
Bicuspid Aortic Valve/Valvar Aortic Stenosis ventricular outflow tract in patients undergoing CCTA exami-
A bicuspid aortic valve (BAV) is one of the most common nations (See Fig. 23.9).
congenital heart abnormalities, affecting slightly more than
1 % of the general population [4]. The term “bicuspid” is a Supravalvar Aortic Stenosis
misnomer. The valve apparatus is typically composed of Supravalvar aortic stenosis (supraAS) is defined as stenosis
three cusps but two of the cusps are fused. The resulting immediately above the sinuses of Valsalva. This is an uncom-
valve is functionally bicuspid. Most commonly this fusion is mon occurrence in the general population but affects 30–50 %
along the left and right coronary cusps. Most congenitally of individuals with Williams Syndrome (7q11.23 deletion
malformed aortic valves are bicuspid but the aortic valve can syndrome) [67, 68]. Features of Williams syndrome include
be unicuspid, quadricuspid or simply dysplastic. The aortic supraAS, peripheral pulmonary stenosis, a characteristic
annulus may be hypoplastic. Rheumatic heart disease facial appearance, developmental delay and often a particu-
accounts for a significant proportion of acquired aortic valve larly cheerful and outgoing personality. Associated lesions
stenosis in the pediatric population. include aortic valve abnormalities, Shone’s complex and cor-
BAV can lead to aortic stenosis, aortic regurgitation or onary artery abnormalities. Individuals with supraAS are
mixed valvar disease with both stenosis and regurgitation. thought to be at risk of premature atherosclerosis due to con-
Importantly, BAV is associated with abnormalities in the tinuous exposure of the coronary arteries to supranormal
aortic media which can cause dilation of the proximal pressures. The treatment of choice, due to the proximity to the
ascending aorta and which are unrelated to the severity of coronary arteries, is surgical. CCTA may assist in the initial
valve disease [59]. Thus, BAV is a disease both of the aortic diagnosis of this defect and may furthermore provide insight
valve and of the aorta. BAV is also associated with an into the coronary artery anatomy and late outcomes in this
increased risk of coarctation, interrupted aortic arch [60] and population that have not yet been well established.
coronary artery anomalies [61].
Transthoracic echocardiography is the primary non- Pulmonary Stenosis
invasive modality in the evaluation of aortic valvar disease. Congenital pulmonary valvar stenosis (PS) is most often an
This technique provides an assessment of the valve (degree isolated defect, but it may also occur in combination with
of stenosis/regurgitation), ventricular size/function and the subvalvar stenosis. A wide variety of malformations of the
proximal ascending aorta and arch. In patients with poor valve can be present including the classical form (a dome-
acoustic windows (e.g., obesity, pulmonary disease, chest shaped valve), a hypoplastic valve annulus, thickened or
wall deformities), CCTA provides an alternate method to fused leaflets or even a dysplastic, myxomatous valve [69].
assess valve morphology and dimensions. CCTA estimates In cases of significant PS, the right ventricle and right ven-
of valve area correlate highly with TEE dimensions [62]. tricular outflow tract become hypertrophied and there is
Importantly, particularly in the patient with BAV, CCTA often dynamic subvalvar obstruction. Additionally, severe PS
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 439

a b

Fig. 23.9 Oblique axial (a) and sagittal (b) views demonstrating a discrete subaortic membrane (arrowhead) in a patient with a bicuspid aortic
valve and coarctation of the aorta. Note the calcification of the anterior mitral valve leaflet (arrow). Ao aorta, LV left ventricle

is typically accompanied by poststenotic dilation of the main VSD, right ventricular outflow tract obstruction (RVOTO),
pulmonary artery. Valvar PS is encountered more frequently overriding aorta and right ventricular hypertrophy secondary
in individuals with Noonan syndrome [70–72]. to RVOTO. Anterior and superior displacement of the outlet
Severe or critical PS diagnosed at any age is generally (infundibular) septum is the defining feature and accounts
treated with balloon valvuloplasty. However, in complex for the first three components of this defect. Right ventricular
cases (such as those with a hypoplastic pulmonary valve hypertrophy is a consequence of RVOTO. The degree of
annulus, severe pulmonary insufficiency or subvalvar/supra- RVOTO varies and may include dysplastic pulmonary valve
valvar PS), surgery is usually the treatment of choice. Surgery leaflets as well as subpulmonary or pulmonary arterial
is also reserved for patients with dysplastic valves that often involvement.
do not respond to transcatheter therapy. An important late TOF can be “syndromic” (associated with additional non-
complication following either balloon valvuloplasty or surgi- cardiac congenital anomalies) or “nonsyndromic.” Important
cal valvotomy is pulmonary regurgitation. syndromes associated with TOF include DiGeorge syndrome
The anterior position of the pulmonary valve and the right (22q11.2 microdeletion), Down syndrome (Trisomy 21),
ventricular outflow tract may preclude complete evaluation Edward syndrome (Trisomy 18) and Patau syndrome
with echocardiography, particularly in the patient with prior (Trisomy 13). TOF may be associated with other congenital
surgery. CCTA is well suited to image this patient population cardiac abnormalities including ASDs, left SVC to coronary
for delineation of the right ventricular outflow tract, pulmo- sinus or a right aortic arch. Approximately 5–10 % will have
nary valve annulus and distal structures including the branch coronary anomalies [73–75] including the left anterior
pulmonary arteries. Pre-interventional assessment of pulmo- descending artery arising from the right coronary artery, cir-
nary valve anatomy and dimensions may help predict suit- cumflex artery arising from the right coronary artery, a large
ability for balloon valvuloplasty. Lastly, CCTA can provide conus branch or a single coronary artery system.
quantification of right ventricular size and function in The complete intracardiac repair of TOF includes relief of
patients following transcatheter or surgical intervention who RVOTO and patch closure of the VSD. Operative repair of
have residual PS or regurgitation. RVOTO may occur via a variety of techniques. Patients with
a restrictive pulmonary valve annulus may require a longitu-
dinal incision of the pulmonary valve with subsequent patch
Other Lesions augmentation (transannular patch) and augmentation of the
pulmonary arteries when indicated. In more severe forms
Tetralogy of Fallot (pulmonary atresia), a right ventricular-to-pulmonary artery
Tetralogy of Fallot (TOF) is the most common cause of cya- conduit is performed to establish continuity between the
notic CHD. It is comprised of the following: malalignment right ventricle and pulmonary arteries.
440 P. Pillutla and S.C. Cook

a b

Fig. 23.10 The oblique coronal (a) and sagittal (b) views demonstrate tricle (RV) when compared to the size of the left ventricle (LV). Prior
the long-term complications associated with tetralogy of Fallot. palliative procedures often result in branch pulmonary artery stenosis
Lifelong pulmonary insufficiency is a consequence associated with often requiring transcatheter therapy (arrows). RA right atrium
prior surgical palliations (arrowhead) that results in a dilated right ven-

Following these repairs, there may be significant residual Lastly, progressive aortic root dilation is frequently
pulmonary regurgitation. This is often well tolerated until ado- demonstrated in the adult tetralogy of Fallot population
lescence and young adulthood, when progressive right ven- despite adequate surgical repair [79]. This process may be
tricular enlargement and systolic dysfunction may cause due to an inherent aortopathy rather than a sequelae of the
dyspnea on exertion, chest pain, ventricular arrhythmias or intracardiac defects [80]. Therefore, CCTA assessment of
even sudden cardiac death. Therefore, symptomatic patients the adolescent or adult patient with TOF should include
with these findings should be considered for surgical pulmo- close inspection of the aortic anatomy at the time of
nary valve replacement. Novel transcatheter pulmonary valve examination. It can be helpful to index the aortic root size
implantation techniques are currently being used (such as the to body surface area and age using standard nomograms
Melody® Transcatheter Pulmonary Valve, Medtronic, Fridley, [81, 82].
MN and Edwards SAPIEN Pulmonic Transcatheter Heart
Valve, Edwards LifeSciences LLC, Irvine, CA) to address pul-
monary valve disease while avoiding the risks associated with Congenital Heart Defects of Great
multiple re-operations in this complex group of patients [76]. Complexity
Non-invasive imaging studies obtained routinely or in
anticipation of pulmonary valve replacement should assess Double Outlet Right Ventricle
right and left ventricular volumes and function, anatomy and
size of the right ventricular outflow tract, presence/absence Double outlet right ventricle (DORV) is a type of ventriculo-
of residual VSD and anatomy of the proximal and distal arterial discordance in which both great arteries arise 50 %
branch pulmonary arteries (See Fig. 23.10). The distance or more from the right ventricle. DORV is not a single con-
between the coronary arteries and the sternum should be genital defect, but rather a continuum of defects best under-
examined and, care should be taken to examine the course of stood by the relationship by the relationship between the
the left anterior descending artery as it may cross over the great vessels and the position of the VSD. The location of the
right ventricular outflow tract. Finally, CCTA plays an VSD further corresponds with each specific physiologic
important role in pre-procedure planning for transcatheter subtype [83].
interventions. Particular attention should be paid to conduit The location of the VSD may be subaortic, subpulmonic,
or right ventricular outflow tract dimensions and the distance doubly-committed (a single defect lying inferior to both the
between the coronary arteries and the RVOT as cases of cata- aorta and pulmonary artery) or remote from the great arteries
strophic coronary artery compression during transcatheter (in other words noncommitted). The relationship of the great
valve implantation have been reported [77, 78]. arteries is defined by the position of the aorta relative to the
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 441

a b

Fig. 23.11 An oblique saggital view (a) and oblique axial view (b) discordance between the right ventricle (RV) and the aorta (AO). The
demonstrate the the key anatomic findings in d-transposition of the oblique axial view displays the anterior-posterior relationship of the
great arteries. The oblique saggital view demonstrates ventriculoarterial great arteries. MPA main pulmonary artery, AoV aortic valve

pulmonary artery. Although normal relationships may exist, Glenn shunt) partially unloads the right ventricle. Systemic
typically the aorta lies rightward and posterior to the pulmo- venous return from the SVC will be via the Glenn to the
nary artery. Alternatively, the aorta may lie side by side or pulmonary artery; the right ventricle will pump only IVC
rightward and anterior to the pulmonary artery with the sub- systemic venous return to the lungs.
pulmonic variant (d-TGA physiology) of DORV. Late outcomes of DORV are variable and are chiefly deter-
PS is commonly observed in DORV, occurring in over mined by the underlying anatomy and type of surgical pallia-
50 % of cases [84–86]. Other associated anomalies include tion. Complications include obstruction of the right
secundum ASDs, relative hypoplasia of the left ventricle, ventricular-to-pulmonary artery conduit, stenosis of interven-
mitral valve anomalies (atrioventricular attachments to the tricular tunnels, subaortic stenosis, and neo-aortic valve regur-
septum), a persistent left SVC, and coronary artery anoma- gitation or neo-aortic root dilation (in patients undergoing
lies. CoA or arch hypoplasia commonly occurs in the subpul- arterial switch). CCTA is suitable in the pre-operative assess-
monary variant of DORV (Taussig-Bing anomaly). Although ment of this lesion as it accurately describes the three-dimen-
these associated defects are relatively uncommon, when pres- sional relationship of the VSD to surrounding structures such
ent, they create a significant impact on the physiology of the as the great arteries and coronary arteries. Furthermore, it pro-
underlying defect as well as surgical management options. vides an accurate assessment of post-operative anatomic
Given the variety of anatomic relationships and associ- changes particularly to conduits and the neo-aorta.
ated features, surgical palliative approaches to repair of
DORV are diverse. Repairs often include closure of the VSD
such that blood flow is routed (“tunneled”) to restore conti- D-Transposition of the Great Arteries
nuity between the left ventricle and the aorta (subaortic
DORV). An arterial switch procedure may be performed to D-Transposition of the great arteries (TGA) is one of the
restore left ventricular-aortic continuity in patients with most common severe congenital cardiac anomalies and is
DORV with subpulmonary VSD. Associated features such often lethal to affected infants if intervention is not per-
as ASDs and atrioventricular valve chordae are addressed formed. Although TGA may accompany other complex
simultaneously. In some cases, biventricular repair is not CHD (for example DORV), this term is most commonly
always possible, and a single ventricle palliation is per- used to describe isolated ventriculoarterial discordance. In
formed (e.g., staged Fontan procedure). Occasionally a “one other words, the right ventricle gives rise to the aorta and
and one-half ventricle” repair may be chosen. In this sce- coronary arteries and the left ventricle gives rise to the pul-
nario, a cavopulmonary anastomosis (usually a bidirectional monary artery (See Fig. 23.11).
442 P. Pillutla and S.C. Cook

a b

Fig. 23.12 An oblique saggital view (a) demonstrates the anatomic Although pacing leads and contrast opacification in the systemic right
appearance of the pulmonary venous baffle (arrows) in this patient with ventricle impair image quality, systemic venous baffle obstruction can
d-transposition of the great arteries and an atrial switch (Mustard proce- still be seen (arrowhead). Secondary findings such as a prominent azy-
dure). The coronal view (b) reveals the systemic venous baffle. gous vein may suggest the presence of this anomaly

The name d-TGA arises from the most common anatomic Before the advent of improved coronary artery surgical
relationship of the aortic and pulmonary valves resulting in techniques, redirecting blood at the atrial level was associ-
this anatomic relationship. The aorta is transposed with pul- ated with lower mortality than attempting to switch the aorta
monary artery such that the aorta is anterior and rightward of and pulmonary arteries to their typical anatomic positions.
the pulmonary artery. Recall that, the prefixes d- and l- The Mustard and the Senning procedures “baffle” pulmo-
describe only the anatomic position of the aortic and pulmo- nary venous return to the right ventricle and systemic venous
nary valves and not the arrangement of the remaining return to the left ventricle. This allows oxygen-rich blood to
segmental cardiac anatomy. Associated defects include reach the systemic circulation via the morphologic right ven-
VSD, left ventricular outflow tract obstruction, CoA and tricle and oxygen-poor blood to reach the lungs via the mor-
coronary artery abnormalities. phologic left ventricle.
The physiology of d-TGA is often described as two circula- While the redirection of atrial blood flow restores a nor-
tions “in parallel” in contrast to the normal circulation, which mal circulation, there are negative late sequelae. The supe-
occurs “in series.” The systemic venous return passes from the rior and inferior systemic venous baffles that redirect venous
right atrium into the right ventricle, then to the aorta and sys- return from the SVC and IVC (respectively) to the morpho-
temic arterial circulation without ever reaching the lungs. logic left ventricle can develop baffle leaks or stenosis.
Similarly, the pulmonary venous return enters the left atrium Similarly, the pulmonary venous baffle may develop stenosis
and left ventricle only to return to the pulmonary arterial bed. as well. Finally, the morphologic right ventricle is not well
Without a substantial mixing lesion, this parallel circula- suited to tolerate lifelong systemic blood pressure. This ulti-
tion is not sustainable and can quickly result in death. mately leads to hypertrophy, dilation and failure.
Continuous prostaglandin infusion can maintain patency of In the patient with a Mustard or Senning palliation, CCTA
the ductus arteriosus and facilitate mixing. In the absence of is valuable to assess not only the complex anatomy and asso-
a significant ASD or VSD, a balloon atrial septostomy may ciated post-operative changes encountered with this popula-
be necessary to stabilize an infant until definitive surgical tion, but also the late onset complications such as baffle
repair can be performed. Prior to the availability of balloon obstruction and residual hemodynamic lesions (See
septostomy, a surgical excision of atrial tissue without car- Fig. 23.12). Although CMR is frequently performed to assess
dio-pulmonary bypass was performed (the Blalock-Hanlon quantification of RV volumes and function, CCTA may be
procedure). utilized to quantify this data in this population as well.
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 443

a b

Fig. 23.13 The oblique saggital (a) and coronal (b) images display the tion with the aorta (Ao). Further, there is dilation of the main pulmonary
underlying anatomy and demonstrate ventriculoarterial discordance in artery (MPA) segment, suggesting right ventricular outflow tract
this patient with congenitally corrected transposition of the great arter- (RVOT) obstruction. RVOT obstruction is often associated with a large
ies (CCTGA). Here, the systemic right ventricle (RV) is in communica- ventricular septal defect. LV left ventricle, SVC superior vena cava

Contemporary surgical repair of d-TGA is the arterial the right atrium through the mitral valve and morphologic
switch procedure, in which the aorta and pulmonary left ventricle, ultimately reaching the pulmonary arterial bed
arteries are switched to restore ventriculoarterial via the pulmonary valve. Similarly, pulmonary venous return
concordance. This requires excision and mobilization of courses from the left atrium through the tricuspid valve into
the proximal coronary arteries and surrounding “buttons” a morphologic right ventricle and ultimately the systemic
of aortic tissue along with the Lecompte maneuver to bring circulation via the aortic valve. In other words, “two wrongs
the pulmonary artery to the anterior position. Late sequelae make a right.” Other terms for this condition include “l-TGA”
following the arterial switch include coronary artery or ventricular inversion.
abnormalities, myocardial ischemia, stenosis at the great Patients with CCTGA usually have a normal (levocardia)
artery anastomoses or arrhythmias. There may also be neo- or midline (mesocardia) position of the heart within the
aortic root dilation and neo-aortic valve regurgitation chest. However, 20 % of patients have dextrocardia, in which
[87–90]. the heart is on the right side of the chest and 5 % will have
In the patient who has undergone an arterial switch proce- situs inversus [92–95].
dure, CCTA is an ideal modality for assessment of the coro- Over 90 % have associated lesions, most commonly VSD,
nary arteries [91]. It also is extremely useful for examining left ventricular outflow tract obstruction or abnormalities of
the great artery anastomoses and neoaorta. In particular, one the systemic atrioventricular valve (morphologic tricuspid
should carefully inspect the pulmonary arteries to exclude valve) such as Ebstein-type malformations.
the presence of branch pulmonary artery stenosis as a result The most common late complications associated with
of the Lecompte maneuver. this condition are systemic atrioventricular valve regurgi-
tation and systemic (morphologic right) ventricular dys-
function and arrhythmias third degree atrioventricular
Congenitally Corrected Transposition (AV) block is particularly frequent [96, 97]. CCTA is
of the Great Arteries helpful for defining the underlying anatomy and associ-
ated defects for patients with CCTGA (See Fig. 23.13). It
In congenitally corrected transposition of the great arteries also is an ideal tool for assessment of coronary venous
(CCTGA), both atrioventricular and ventriculoarterial dis- anatomy to facilitate lead placement at the time of pace-
cordance are present. Systemic venous return courses from maker implantation.
444 P. Pillutla and S.C. Cook

Truncus Arteriosus Despite the wide variation in single ventricle pathology, the
types of surgical palliations ultimately share a similar
In truncus arteriosus, a single great artery (rather than two, physiologic goal.
aorta and pulmonary artery) arises from the base of the heart. As its name suggests, tricuspid atresia is defined by the
This single artery then gives rise to the coronary arteries, pul- absence of a tricuspid valve. Initially, blood returning to the
monary arteries and aorta. The truncal valve is usually right atrium passes through an ASD to the left heart and
trileaflet (69 %) but regurgitation is not uncommon. The mixes with pulmonary venous return. The right ventricle is
classification scheme presented here, Collett and Edwards, usually atretic or hypoplastic; it receives blood from the left
defines truncus arteriosus by the relationship of the pulmo- ventricle via a VSD. If there is ventriculoarterial concordance,
nary arteries [98]. A Type I truncus has a short common pul- the pulmonary arteries are often small and rely upon the duct
monary arterial trunk which gives rise to both pulmonary for pulmonary blood flow. Alternatively, if there is
arteries. Type II is defined by the absence of a main pulmo- ventriculoarterial discordance, the aorta arises from the
nary artery segment. The left and right branch pulmonary rudimentary right ventricle, and, upon occasion, there may
arteries arise in close proximity to one another from the be aortic obstruction requiring ductal patency.
ascending truncal artery. In type III, there is no main pulmo- Hypoplastic left heart syndrome (HLHS) describes a
nary artery segment, and the left and right pulmonary arteries spectrum of left-sided abnormalities that are insufficient to
arise separately at a distance from one another. Type IV is meet the demands of the systemic circulation. They are
defined by the absence of pulmonary arteries. Here, the lungs further qualified by stenosis or atresia of mitral and aortic
are supplied by aortopulmonary collateral vessels. This type valves. In other words: there may be mitral stenosis and
is more accurately classified as pulmonary atresia and is no aortic stenosis (MS/AS), mitral stenosis and aortic atresia
longer considered within the spectrum of truncus arteriosus. (MS/AA) or mitral atresia and aortic atresia (MA/AA) [99].
Truncus arteriosus is usually an isolated phenomenon but If the ascending aorta is severely atretic, the carotid and
has been reported in patients with DiGeorge syndrome coronary arteries rely upon retrograde ductal blood flow for
(22q.11.2 microdeletion). Associated conditions include aor- adequate perfusion.
tic arch anomalies including right aortic arch, coarctation of In most cases of single ventricle physiology, either the
the aorta and interruption of the aorta. Other commonly systemic or pulmonary bed relies upon patency of the ductal
associated defects include PDA, absence of a pulmonary artery. If the ductal artery constricts or becomes stenotic, the
artery and persistent left SVC. results can be catastrophic. Ductal patency can be maintained
This defect usually presents in the newborn period and, with a continuous infusion of prostaglandin and more
when diagnosed sufficiently early (before the development recently stents may be delivered via cardiac catheterization.
of severe pulmonary vascular disease), is treated by surgical Often a surgical shunt must be created to maintain a more
palliation. Surgical repair of truncus typically utilizes a stable blood supply.
conduit from the right ventricle to either the main pulmonary Modern congenital heart surgery can be traced to 1944
artery segment (Type I) or the branch pulmonary arteries with the creation of a systemic to pulmonary shunt conceived
(Types II and III). The long-term survival following initial of by Helen Taussig and performed by Alfred Blalock with
successful repair continues to improve and therefore the assistance from Vivian Thomas [100]. The original or classic
number of adolescents and adults with this complex lesion Blalock-Taussig shunt (BT shunt) is a direct anastomosis of
will continue to grow. For this reason, it is imperative to the subclavian artery to the ipsilateral pulmonary artery.
recognize late complications associated with this defect. Adaptations in this surgical technique led to the development
CCTA evaluation should include close inspection of the right of the modified BT shunt in which an artificial (e.g., Gore-
ventricle-pulmonary artery conduit to determine the Tex) graft connects the subclavian artery to the pulmonary
presence/absence of stenosis or calcification, anatomy of the artery without disrupting the integrity of the subclavian
proximal and distal branch pulmonary arteries, neo-aortic artery from the affected arm (See Fig. 23.14) [101]. Other
root dilatation, and ventricular volumes and function. systemic to pulmonary arterial shunts include the Waterston
shunt (ascending aorta to right pulmonary artery), the Potts
Single Ventricle Lesions shunt (descending aorta to left pulmonary artery), and the
Among the most complex congenital heart lesions are those Cooley shunt (proximal ascending aorta to right pulmonary
with severe hypoplasia or atresia of the left or right ventricle. artery within the pericardium). An alternative strategy used
Consequently, these patients are reliant on a single ventricle sometimes for the palliation of hypoplastic left heart
to perfuse both the pulmonary and systemic vascular beds. syndrome is the Sano shunt, a conduit located between the
The full spectrum of single ventricle lesions is beyond the right ventricle and the pulmonary artery. Contemporary
scope of this text. Nonetheless, the most important variations central shunts utilize an artificial graft between the ascend-
are tricuspid atresia and hypoplastic left heart syndrome. ing aorta and the main pulmonary artery.
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 445

Fig. 23.14 Aortopulmonary a b

shunts. (a) The classic
Blalock-Taussig shunt, (b) a
modified Blalock-Taussig
shunt, (c) a Waterston shunt,
and (d) the Potts shunt
(Reprinted from Khairy et al.
[101] with permission of
Wolters Kluwer)

c d

Although they are stable sources of pulmonary blood pulmonary artery (MPA) or the proximal branch left and
flow, systemic to pulmonary arterial shunts often lead to dis- right branch pulmonary arteries. Unfortunately, banding can
tortion of the pulmonary artery architecture because blood cause negative sequelae, particularly if the band was placed
flow is often directed towards one pulmonary artery. As pul- on a young patient who later outgrows the size of the band.
monary vascular resistance decreases with age, congestive Occasionally, the band may migrate distally, occluding one
heart failure may develop as a result of excessive pulmonary pulmonary artery and resulting in unopposed pulmonary
blood flow. Pulmonary hypertension may develop. Most arterial flow to the opposite branch. Post-stenotic dilation
importantly, these shunts can become kinked, occluded, nar- may result if the band that is placed too tightly. Structures
rowed or thrombosed, compromising pulmonary blood proximal to this band gradient are also exposed to increased
supply. afterload, and, as a result, pulmonary valve regurgitation,
In some circumstances, complete repair is not immedi- right ventricular enlargement and dysfunction and tricuspid
ately feasible or must be delayed. Here, surgical banding of valve insufficiency may ensue.
the pulmonary arteries is often utilized as an initial pallia- As patients grow and pulmonary vascular resistance
tion. Restricting the diameter of the pulmonary arteries can drops, BT shunts typically can no longer provide adequate
protect the pulmonary vascular bed from excessive blood pulmonary blood flow. The Glenn shunt (bidirectional) is an
flow. Surgical bands can be placed around either the main end-to-side anastomosis of the SVC to the undivided
446 P. Pillutla and S.C. Cook

a b

Fig. 23.15 Oblique sagittal (a) and axial (b) views demonstrate the a “steal phenomenon,” resulting in poor contrast opacification. Further,
challenges of accurately defining Fontan anatomy. Despite an accurate incomplete opacification of the IVC diminishes diagnostic accuracy to
timing bolus, this is a low cardiac output state leading to accumulation assess for thombus in this segment of the cavopulmonary anastomosis.
of contrast in the superior vena cava (SVC) and poor opacification of AAo ascending aorta, LPA left pulmonary artery, RPA right pulmonary
desired anatomic structures. In addition, collaterals (arrows) may create artery

pulmonary artery. It is most often performed as the second CCTA imaging may be promising in the assessment of the
stage in a series of staged palliations for single ventricle single ventricle patient to assess late-onset complications
physiology. The third stage, the Fontan procedure, is the including thrombus within the Fontan, fenestrations, collat-
final palliative procedure which connects the IVC directly to erals and single ventricle function [106]. However, there are
the pulmonary artery. The Glenn and Fontan shunts cannot important limitations of this technique. The issues of low-
be safely performed in infancy as pulmonary vascular resis- cardiac output, frequent collaterals and asymmetric blood
tance must first fall substantially, allowing a small gradient flow between the left and right lungs resulting from prior
between systemic venous pressure and pulmonary arterial cavopulmonary anastomoses create technical challenges for
pressure to drive forward flow. an accurate gated CCTA examination (See Fig. 23.15).
The Fontan procedure has undergone significant evolu- Simultaneous contrast injection from both an upper and
tion since its inception in 1971 [102]. Earlier techniques uti- lower extremity will allow dense and homogenous opacifica-
lized an atriopulmonary (right atrial appendage-to-pulmonary tion of the entire circulation but can be technically challeng-
artery) anastomosis. Late-onset complications including ing [107]. Due to these limitations, CMR is often the imaging
atrial arrhythmias, compression of the pulmonary veins and modality of choice unless otherwise contraindicated.
thrombus (as a result of severe atrial enlargement) prompted
surgical revisions of this technique. Surgical techniques cur-
rently in use utilize conduits made of artificial or pericardial Summary
tissue to direct systemic venous return directly to the pulmo-
nary arteries via either intracardiac (lateral tunnel Fontan) or Adults with CHD represent a large and diverse group of
extracardiac (extracardiac Fontan) routes. Occasionally, a patients with both simple and complex disease. Physicians
fenestration is placed within the Fontan itself to serve as a who care for patients with CHD challenged by the unique
“pop-off” for elevated systemic venous return (but at the cost needs of this rapidly growing population, including the need
of cyanosis). If pulmonary vascular resistance remains low for frequent non-invasive cardiovascular imaging. Although
post-operatively, such fenestrations can be later closed per- CMR has historically been recognized as the non-invasive
cutaneously. Collaterals (aortopulmonary or systemic imaging tool of choice in this patient population, advances in
venous) are frequent in this population [103–105]. CCTA have allowed it to become an extremely powerful
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 447

imaging modality as well. Due to the complexity of CHD, in athletes [114, 116]. Outcomes in milder forms of coronary
imaging specialists should understand the importance of anomalies (i.e. “normal variants”) are less well defined.
proper patient and protocol selection for CCTA and, ideally, Coronary artery anomalies may also occur in concert with
collaborate with adult congenital specialists to help plan and congenital heart defects (discussed later in this chapter).
successfully execute the CCTA examination.

Selected Lesions
Coronary Artery Anomalies
Abnormal Coronary Origins: ALCAPA
Incidence and Definitions and ARCAPA
Anomalous origin of the left coronary from the pulmonary
Congenital coronary anomalies affect between 0.2 and 5.6 % artery (ALCAPA, also called the Bland-White-Garland syn-
of the general population [108–112]. The incidence varies con- drome) is a serious anomaly in which the left coronary artery
siderably between studies due to a number of factors including arises from the pulmonary artery [117] (See Fig. 23.16).
referral bias, fewer autopsies being performed and absence of During fetal life, due to elevated pulmonary vascular resis-
strict diagnostic criteria. In addition, coronary anomalies can tance, myocardial perfusion is thought to be normal.
vary widely in severity. The presenting symptom for some However, upon birth, the pulmonary vascular resistance
anomalies may be sudden cardiac death; others may be entirely begins to fall, leading to insufficient perfusion of the left
benign and never diagnosed. Some authors have reported that ventricle. Typically there is vigorous collateral formation
coronary anomalies may cause anywhere between 12 and 19 % from the right coronary artery but despite this, the majority
of deaths among young athletes [113–115]. present in infancy with symptoms of congestive heart failure.
In the normal coronary circulation, the left main coronary Others may never have symptoms and there are reports of
artery arises from the left ostium (located centrally within patients reaching adulthood [118–121] though it appears to
the left sinus of Valsalva) and gives rise to the left anterior still confer a risk of sudden cardiac death.
descending artery and circumflex artery. The left anterior Anomalous origin of the right coronary artery from the
descending artery courses along the anterior interventricular pulmonary artery (ARCAPA) is a much rarer anomaly which
groove, gives off septal perforators and supplies most of the also has been associated with sudden cardiac death [122].
septum, anterior wall and apex while the circumflex artery
wraps posteriorly around the left atrioventricular groove. Coronary Artery Origin from the Improper Sinus
The right coronary artery arises from the right ostium (cen- Including Single Coronary Arteries
trally located within the right sinus of Valsalva), giving off Coronary arteries may be seen to arise anomalously from the
the marginal branch to the right ventricle and then curving incorrect sinus, with an incidence of 0.92 % for origin of the
posteriorly in the atrioventricular groove. Angelini and right coronary artery from the left sinus and 0.15 % for left
colleagues [116] suggest, in the context of known normal coronary artery from the right sinus [123]. Single coronary
coronary anatomy, the following definitions: normal (seen in arteries are even rarer, occurring in approximately 0.024–
>1 % of the general population), normal variant (uncommon 0.066 % of the population [108, 124, 125]. Although single
variant but seen in >1 % of the population) and anomaly coronary arteries are an isolated finding in the majority of
(observed in <1 % of the population). cases, they may be associated with other cardiac defects or
cause sudden cardiac death [125, 126].
In broad terms, coronary arteries arising from the incor-
Clinical Significance rect sinus (including single coronary arteries) may take a
number of routes including retrocardiac, retroaortic, infra-
Congenital coronary anomalies have been reported as the septal (supracristal), pre-pulmonary (crossing the right ven-
cause of chest pain, arrhythmias, myocardial infarction and tricular outflow tract) or intra-aortic (between the aorta and
sudden cardiac death. Yamanaka and colleagues [108], in a pulmonary artery) [123] (See Figs. 23.17, 23.18, 23.19 and
survey of 126,595 angiograms, classified 80 % of anomalies 23.20). Of these, the intra-aortic course has been most
as “benign” and 20 % as being potentially responsible for consistently implicated as a possible cause of sudden cardiac
serious sequelae. The literature has consistently reported an death. The ostium of the anomalously placed artery may be
association between certain coronary anomalies (such as slit-like, possibly predisposing to compression between the
anomalous left coronary artery from the pulmonary artery or great arteries [127–129]. Sudden cardiac death, when it
origin of the left coronary artery from the right sinus of occurs, is often precipitated by effort [129], which likely
Valsalva) and adverse clinical outcomes. Such coronary explains the increased incidence in athletes [113, 115,
variants may account for up to 15 % of sudden cardiac deaths 130–133].
448 P. Pillutla and S.C. Cook

a b

Fig. 23.16 A 2 month old infant presented with failure to thrive. Axial (though its origin is posteriorly displaced) and the right coronary artery
views (a) and (b) demonstrating the LAD arising from the pulmonary is dilated. AO aorta, PA pulmonary artery, LAD left anterior descending
artery (anomalous left coronary artery arising from the pulmonary artery, RCA right coronary artery, LCX left circumflex artery
artery or ALCAPA) (Note that the LCX arises normally from the aorta

as dual origin of the left anterior descending and left circum-

flex arteries) and geographical variations of the coronary
ostia within the appropriate sinus (See Fig. 23.21).

Coronary Anomalies in Congenital Heart Disease

Multiple coronary anomalies have been reported in patients
with d-transposition of the great arteries (d-TGA) [134].
Most frequently, the left coronary artery arises from the
“anterior facing” sinus and the right coronary artery arises
from the “posterior facing” sinus. As in normal hearts,
there may be single coronary arteries, multiple coronary
ostia or coronary arteries arising from an improper cusp. In
patients who have undergone the arterial switch procedure
(in which the coronary arteries are re-implanted into the
neo-aorta), coronary events are not infrequent with a preva-
lence of 2–11 % [135–140]. Thus, it is critically important
to evaluate on CCTA the coronary arterial origins and
course to exclude kinking, compression and intimal thick-
ening [135, 141, 142].
Patients with tetralogy of Fallot also commonly have cor-
onary anomalies including single coronary arteries in 5 %,
Fig. 23.17 This three-dimensional reconstruction demonstrates a sin-
gle coronary artery, arising from the right coronary cusp. RCC right coronary arteries with anomalous origins in 5 % and a large
coronary cusp, LAD left anterior descending artery, RCA right coronary conus artery in anywhere from 20 to 40 % [73, 74, 143]. Of
artery particular concern is the variant in which the left anterior
descending artery arises from the right coronary artery,
Normal Variants and Minor Coronary Anomalies crossing the right ventricular outflow tract in the process.
Other coronary variants with minor or no significant clinical This can pose difficulties during surgery as the left anterior
sequelae include intramural course (also known as artery will be at risk when the chest is opened. Careful
“myocardial bridging”), “absent” left main (better described assessment for coronary anomalies in this population can
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 449

a b

Fig. 23.18 (a, b) (a) Shown in this three-dimensional reconstruction is origin (arrow) of the right coronary artery. LCC left coronary cusp,
an anomalous right coronary artery originating from the left coronary LAD left coronary artery, RCA right coronary artery
cusp. (b) Curved multi-planar reconstruction demonstrates the slit-like

a b

Fig. 23.19 (a, b) Three-dimensional reconstructions demonstrates a artery travels behind the aorta. AO aorta, PA pulmonary artery, LCX left
single coronary artery variant in which the left anterior descending circumflex artery, LAD left coronary artery, RCA right coronary artery
artery courses anterior to the pulmonary artery and the circumflex

help guide surgical repair [144] and should therefore be coronary ostia arise from the “facing” sinus. As the coro-
excluded prior to any intervention to the right ventricular nary arteries not infrequently arise from the improper sinus,
outflow tract. it may be helpful to describe both the origin of the anoma-
Congenitally corrected transposition (l-TGA) typically lous artery in addition to the territory supplied. The left
follows a similar pattern to d-TGA, in which the two main coronary artery will, as in normal individuals, supply the
450 P. Pillutla and S.C. Cook

a b

Fig. 23.20 (a, b) (a) Three-dimensional reconstruction shows an tion demonstrates the intraarterial course in addition to the slit-like ori-
anomalous right coronary artery arising from the left coronary cusp, fice of the right coronary artery (arrow). AO aorta, PA pulmonary artery,
following an intra-arterial course. (b) Curved multiplanar reconstruc- RCA right coronary artery, LAD left anterior descending artery

References
1. Tennant PW, Pearce MS, Bythell M, Rankin J. 20-year survival of
children born with congenital anomalies: a population-based
study. The Lancet. 1920;375(9715):649–56.
2. Bird TM, Hobbs CA, Cleves MA, Tilford JM, Robbins
JM. National rates of birth defects among hospitalized newborns.
Birth Defects Res A Clin Mol Teratol. 2006;76(11):762–9.
3. Canfield MA, Honein MA, Yuskiv N, Xing J, Mai CT, Collins JS,
et al. National estimates and race/ethnic-specific variation of
selected birth defects in the United States, 1999–2001. Birth
Defects Res A Clin Mol Teratol. 2006;76(11):747–56.
4. Hoffman JI, Kaplan S. The incidence of congenital heart disease.
J Am Coll Cardiol. 2002;39(12):1890–900.
5. Khairy P, Ionescu-Ittu R, Mackie AS, Abrahamowicz M, Pilote L,
Marelli AJ. Changing mortality in congenital heart disease. J Am
Coll Cardiol. 2010;56(14):1149–57.
6. Marelli AJ, Mackie AS, Iwaki H, Rahme E, Pilote L. Congenital
heart disease in the general population: changing prevalence and
age distribution. Circulation. 2007;115:163–72.
7. Warnes CA, Liberthson R, Danielson GK, Dore A, Harris L,
Hoffman JI, et al. Task force 1: the changing profile of congenital
heart disease in adult life. J Am Coll Cardiol. 2001;37(5):1170–5.
8. van der Bom T, Bouma BJ, Meijboom FJ, Zwinderman AH,
Mulder BJ. The prevalence of adult congenital heart disease,
Fig. 23.21 Three-dimensional reconstruction demonstrates dual ostia results from a systematic review and evidence based calculation.
for the left coronary artery and left circumflex artery (“absent left Am Heart J. 2012;164(4):568–75.
main”), a benign variant. RCA right coronary artery, LAD left anterior 9. Ho VB. ACR appropriateness criteria on suspected congenital
descending artery, LCX left circumflex artery heart disease in adults. J Am Coll Radiol. 2008;5(2):97–104.
10. Han BK, Lesser AM, Vezmar M, Rosenthal K, Rutten-Ramos
SLJ, Caye D, et al. Cardiovascular imaging trends in congenital
morphologic left ventricle but arises from the “right facing” heart disease: a single center experience. J Cardiovasc Comput
sinus. The right coronary artery will supply the morpho- Tomogr. 2013;7(6):361–6.
11. Knauth Meadows A, Ordovas K, Higgins CB, Reddy GP. Magnetic
logic (systemic) right ventricle but arises from the “left fac-
resonance imaging in the adult with congenital heart disease.
ing” sinus [145]. Semin Roentgenol. 2008;43(3):246–58.
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 451

12. Cook SC, Raman SV. Multidetector computed tomography in the 29. Van Meter JC, LeBlanc JG, Culpepper 3rd WS, Ochsner JL. Partial
adolescent and young adult with congenital heart disease. anomalous pulmonary venous return. Circulation. 1990;82(5
J Cardiovasc Comput Tomogr. 2008;2(1):36–49. Suppl):IV195–8.
13. Otero HJ, Steigner ML, Rybicki FJ. The “post-64” era of coronary 30. Broy C, Bennett S. Partial anomalous pulmonary venous return.
CT angiography: understanding new technology from physical Mil Med. 2008;173(6):523–4.
principles. Radiol Clin North Am. 2009;47(1):79–90. 31. Shumacker HB. Partial anomalous pulmonary venous return.
14. Raman SV, Cook SC, McCarthy B, Ferketich AK. Usefulness of Chest J. 1966;49(3):309–16.
multidetector row computed tomography to quantify right ven- 32. Gustafson RA, Warden HE, Murray GF, Hill RC, Rozar GE. Partial
tricular size and function in adults with either tetralogy of Fallot or anomalous pulmonary venous connection to the right side of the
transposition of the great arteries. Am J Cardiol. 2005;95(5): heart. J Thorac Cardiovasc Surg. 1989;98(5 Pt 2):861–8.
683–6. 33. Lacomis JM, Wigginton W, Fuhrman C, Schwartzman D,
15. Hoffmann A, Engelfriet P, Mulder B. Radiation exposure during Armfield DR, Pealer KM. Multi-detector row CT of the left atrium
follow-up of adults with congenital heart disease. Int J Cardiol. and pulmonary veins before radio-frequency catheter ablation for
2007;118(2):151–3. atrial fibrillation. Radiographics. 2003;23(suppl_1):S35–48.
16. Neefjes LA, Dharampal AS, Rossi A, Nieman K, Weustink AC, 34. Brown David W, Geva T. Anomalies of the pulmonary veins. In:
Dijkshoorn ML, et al. Image quality and radiation exposure using Allen Hugh D, Driscoll DJ, Shaddy Robert E, Feltes Timothy F,
different low-dose scan protocols in dual-source CT coronary editors. Moss and Adams’ heart disease in infants, children and
angiography: randomized study. Radiology. 2011;261(3):779–86. adolescents. 8th ed. Philadelphia: Lippincott Williams & Wilkins;
17. Khan A, Khosa F, Nasir K, Yassin A, Clouse ME. Comparison of 2013. p. 809–39.
radiation dose and image quality: 320-MDCT versus 64-MDCT 35. Webb G, Gatzoulis MA. Atrial septal defects in the adult recent
coronary angiography. AJR Am J Roentgenol. 2011;197(1):163. progress and overview. Circulation. 2006;114(15):1645–53.
18. Stolzmann P, Goetti R, Baumueller S, Plass A, Falk V, Scheffel H, 36. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM,
et al. Prospective and retrospective ECG-gating for CT coronary Dearani JA, et al. ACC/AHA 2008 guidelines for the management
angiography perform similarly accurate at low heart rates. Eur of adults with congenital heart disease: a Report of the American
J Radiol. 2011;79(1):85–91. College of Cardiology/American Heart Association Task Force on
19. Hosch W, Heye T, Schulz F, Lehrke S, Schlieter M, Giannitsis E, Practice Guidelines (Writing Committee to Develop Guidelines
et al. Image quality and radiation dose in 256-slice cardiac com- on the Management of Adults With Congenital Heart Disease)
puted tomography: comparison of prospective versus retrospec- Developed in Collaboration With the American Society of
tive image acquisition protocols. Eur J Radiol. 2011;80(1): Echocardiography, Heart Rhythm Society, International Society
127–35. for Adult Congenital Heart Disease, Society for Cardiovascular
20. Choi TY, Malpeso J, Li D, Sourayanezhad S, Budoff MJ. Radiation Angiography and Interventions, and Society of Thoracic Surgeons.
dose reduction with increasing utilization of prospective gating in J Am Coll Cardiol. 2008;52(23):e143–263.
64-multidetector cardiac computed tomography angiography. 37. King TD, Thompson SL, Steiner C, Mills NL. Secundum atrial
J Cardiovasc Comput Tomogr. 2011;5(4):264–70. septal defect: nonoperative closure during cardiac catheterization.
21. LaBounty TM, Leipsic J, Poulter R, Wood D, Johnson M, Srichai JAMA. 1976;235(23):2506–9.
MB, et al. Coronary CT angiography of patients with a normal 38. Du ZD, Hijazi ZM, Kleinman CS, Silverman NH, Larntz K.
body mass index using 80 kVp versus 100 kVp: a prospective, Comparison between transcatheter and surgical closure of secundum
multicenter, multivendor randomized trial. Am J Roentgenol. atrial septal defect in children and adults: results of a multicenter
2011;197(5):W860–7. nonrandomized trial. J Am Coll Cardiol. 2002;39(11):1836–44.
22. Leipsic J, LaBounty TM, Mancini GJ, Heilbron B, Taylor C, 39. Gade CL, Bergman G, Naidu S, Weinsaft JW, Callister TQ, Min
Johnson MA, et al. A prospective randomized controlled trial to JK. Comprehensive evaluation of atrial septal defects in individuals
assess the diagnostic performance of reduced tube voltage for undergoing percutaneous repair by 64-detector row computed
coronary CT angiography. Am J Roentgenol. 2011;196(4): tomography. Int J Cardiovasc Imaging. 2007;23(3):397–404.
801–6. 40. Zaidi AN, Cheatham JP, Raman SV, Cook SC. Multislice com-
23. Zhang C, Zhang Z, Yan Z, Xu L, Yu W, Wang R. 320-row CT puted tomographic findings in symptomatic patients after
coronary angiography: effect of 100-kV tube voltages on image amplatzer septal occluder device implantation. J Interv Cardiol.
quality, contrast volume, and radiation dose. Int J Cardiovasc 2009;22(1):92–7.
Imaging. 2011;27(7):1059–68. 41. Butera G, Carminati M, Chessa M, Piazza L, Micheletti A, Negura
24. Oda S, Utsunomiya D, Funama Y, Awai K, Katahira K, Nakaura DG, et al. Transcatheter closure of perimembranous ventricular
T, et al. A low tube voltage technique reduces the radiation dose at septal defects: early and long-term results. J Am Coll Cardiol.
retrospective ECG-gated cardiac computed tomography for ana- 2007;50(12):1189–95.
tomical and functional analyses. Acad Rradiol. 2011;18(8): 42. Holzer R, Balzer D, Cao QL, Lock K, Hijazi ZM. Device closure
991–9. of muscular ventricular septal defects using the amplatzer
25. Ghadri JR, Küest SM, Goetti R, Fiechter M, Pazhenkottil AP, muscular ventricular septal defect occluder: immediate and
Nkoulou RN, et al. Image quality and radiation dose comparison mid-term results of a US registry. J Am Coll Cardiol. 2004;
of prospectively triggered low-dose CCTA: 128-slice dual-source 43(7):1257–63.
high-pitch spiral versus 64-slice single-source sequential acquisi- 43. Craig B. Atrioventricular septal defect: from fetus to adult. Heart.
tion. Int J Cardiovasc Imaging. 2012;28(5):1217–25. 2006;92(12):1879–85.
26. Van Praagh R. Terminology of congenital heart disease. Glossary 44. Freeman SB, Taft LF, Dooley KJ, Allran K, Sherman SL, Hassold
and commentary. Circulation. 1977;56(2):139–43. TJ, et al. Population-based study of congenital heart defects in
27. Applegate KE, Goske MJ, Pierce G, Murphy D. Situs revisited: Down syndrome. Am J Med Genet. 1998;80(3):213–7.
imaging of the heterotaxy syndrome 1. Radiographics. 1999;19(4): 45. Grifka R, Transcatheter PDA. Closure: equipment and technique.
837–52. J Interv Cardiol. 2001;14(1):97–107.
28. Tynan MJ, Becker AE, Macartney FJ, Jimenez MQ, Shinebourne 46. Mori K, Ando M, Takao A, Ishikawa S, Imai Y. Distal type of
EA, Anderson RH. Nomenclature and classification of congenital aortopulmonary window. Report of 4 cases. Br Heart J. 1978;
heart disease. Br Heart J. 1979;41(5):544–53. 40(6):681–9.
452 P. Pillutla and S.C. Cook

47. Berry TE, Bharati S, Muster AJ, Idriss FS, Santucci B, Lev M, 66. Marasini M, Zannini L, Ussia GP, Pinto R, Moretti R, Lerzo F,
et al. Distal aortopulmonary septal defect, aortic origin of the right et al. Discrete subaortic stenosis: incidence, morphology and
pulmonary artery, intact ventricular septum, patent ductus surgical impact of associated subaortic anomalies. Ann Thorac
arteriosus and hypoplasia of the aortic isthmus: a newly recog- Surg. 2003;75(6):1763–8.
nized syndrome. Am J Cardiol. 1982;49(1):108–16. 67. Williams JCP, Barratt-Boyes BG, Lowe JB. Supravalvular aortic
48. Bertolini A, Dalmonte P, Bava GL, Moretti R, Cervo G, Marasini stenosis. Circulation. 1961;24(6):1311–8.
M. Aortopulmonary septal defects. A review of the literature and 68. Beuren AJ, Schulze C, Eberle P, Harmjanz D, Apitz J. The syn-
report of ten cases. J Cardiovasc Surg (Torino). 1994;35(3): drome of supravalvular aortic stenosis, peripheral pulmonary ste-
207–13. nosis, mental retardation and similar facial appearance. Am
49. Blieden LC, Moller JH. Aorticopulmonary septal defect. An expe- J Cardiol. 1964;13(4):471–83.
rience with 17 patients. Br Heart J. 1974;36(7):630. 69. Gikonyo BM, Lucas RV, Edwards JE. Anatomic features of con-
50. Rao PS. Coarctation of the aorta. Curr Cardiol Rep. 2005;7(6): genital pulmonary valvar stenosis. Pediatr Cardiol. 1987;8(2):
425–34. 109–16.
51. Hamdan MA, Maheshwari S, Fahey JT, Hellenbrand WE. 70. Noonan JA. Hypertelorism with Turner phenotype: a new syn-
Endovascular stents for coarctation of the aorta: initial results and drome with associated congenital heart disease. American Journal
immediate-term follow-up. J Am Coll Cardiol. 2001;38(5): of Diseases of Children. 1968;116(4):373–80.
1518–23. 71. Mendez HM, Opitz JM, Reynolds JF. Noonan syndrome: a review.
52. Chessa M, Carrozza M, Butera G, Pizza L, Negura DG, Bussadori Am J Med Genet. 1985;21(3):493–506.
C, et al. Results and mid-long-term follow-up of stent implantation 72. Burch M, Sharland M, Shinebourne E, Smith G, Patton M,
for native and recurrent coarctation of the aorta. Eur Heart McKenna W. Cardiologic abnormalities in Noonan syndrome:
J. 2014;26(24):2728–32. phenotypic diagnosis and echocardiographic assessment of 118
53. Forbes TJ, Moore P, Pedra CA, Zahn EM, Nykanen D, Amin Z, patients. J Am Coll Cardiol. 1993;22(4):1189–92.
et al. Intermediate follow-up following intravascular stenting for 73. Dabizzi RP, Caprioli G, Aiazzi L, Castelli C, Baldrighi G,
treatment of coarctation of the aorta. Catheter Cardiovasc Interv. Parenzan L, et al. Distribution and anomalies of coronary arteries
2007;70(4):569–77. in tetralogy of fallot. Circulation. 1980;61(1):95–102.
54. Forbes TJ, Garekar S, Amin Z, Zahn EM, Nykanen D, Moore P, 74. Fellows KE, Freed MD, Keane JF, Praagh R, Bernhard WF,
et al. Procedural results and acute complications in stenting native Castaneda AC. Results of routine preoperative coronary angiogra-
and recurrent coarctation of the aorta in patients over 4 years of phy in tetralogy of Fallot. Circulation. 1975;51(3):561–6.
age: a multi-institutional study. Catheter Cardiovasc Interv. 2007; 75. Hurwitz RA, Smith W, King H, Girod DA, Caldwell RL. Tetralogy
70(2):276–85. of Fallot with abnormal coronary artery: 1967 to 1977. J Thorac
55. Forbes TJ, Kim DW, Du W, Turner DR, Holzer R, Amin Z, et al. Cardiovasc Surg. 1980;80(1):129–34.
Comparison of surgical, stent, and balloon angioplasty treatment 76. Lurz P, Bonhoeffer P, Taylor AM. Percutaneous pulmonary valve
of native coarctation of the aorta: an observational study by the implantation: an update. Expert Rev Cardiovasc Ther. 2009;7(7):
CCISC (Congenital Cardiovascular Interventional Study 823–33.
Consortium). J Am Coll Cardiol. 2011;58(25):2664–74. 77. Wittwer ED, Pulido JN, Gillespie SM, Cetta F, Dearani JA. Left
56. Cohen MARC, Fuster V, Steele PM, Driscoll D, McGoon main coronary artery compression following Melody pulmonary
DC. Coarctation of the aorta. Long-term follow-up and prediction valve implantation: use of Impella support as rescue therapy and
of outcome after surgical correction. Circulation. 1989;80(4): perioperative challenges with ECMO. Case Rep Crit Care 2014
840–5. (2014), Article ID 959704, 3 pages.
57. Sebastiá C, Quiroga S, Boyé R, Perez-Lafuente M, Castellà E, 78. Morray BH, McElhinney DB, Cheatham JP, Zahn EM, Berman DP,
Alvarez-Castells A. Aortic stenosis: spectrum of diseases depicted Sullivan PM, et al. Risk of coronary artery compression among
at multisection CT. Radiographics. 2003;23(Suppl_1):S79–91. patients referred for transcatheter pulmonary valve implantation a
58. Weinberg Paul M, Natarajan S, Rogers Lindsay S. Aortic arch and multicenter experience. Circ Cardiovasc Interv. 2013;6(5):535–42.
vascular anomalies. In: Allen Hugh D, Driscoll DJ, Shaddy Robert 79. Niwa K, Siu SC, Webb GD, Gatzoulis MA. Progressive aortic root
E, Feltes Timothy F, editors. Moss and Adams’ heart disease in dilatation in adults late after repair of tetralogy of fallot.
infants, children, and adolescents. 8th ed. Philadelphia: Lippincott Circulation. 2002;106(11):1374–8.
Williams & Wilkins; 2013. p. 758–98. 80. Tan JL, Davlouros PA, McCarthy KP, Gatzoulis MA, Ho SY.
59. Siu SC, Silversides CK. Bicuspid aortic valve disease. J Am Coll Intrinsic histological abnormalities of aortic root and ascending
Cardiol. 2010;55(25):2789–800. aorta in tetralogy of fallot: evidence of causative mechanism for
60. Duran AC, Frescura C, Sans-Coma V, Angelini A, Basso C, aortic dilatation and aortopathy. Circulation. 2005;112(7):961–8.
Thiene G. Bicuspid aortic valves in hearts with other congenital 81. Roman MJ, Devereux RB, Kramer-Fox R, O’Loughlin J. Two-
heart disease. J Heart Valve Dis. 1995;4(6):581–90. dimensional echocardiographic aortic root dimensions in normal
61. Roberts WC. The congenitally bicuspid aortic valve: a study of 85 children and adults. Am J Cardiol. 1989;64(8):507–12.
autopsy cases. Am J Cardiol. 1970;26(1):72–83. 82. Mongeon FP, Gurvitz MZ, Broberg CS, Aboulhosn J, Opotowsky
62. Feuchtner GM, Müeller S, Bonatti J, Schachner T, Velik-Salchner AR, Kay JD, et al. Aortic root dilatation in adults with surgically
C, Pachinger O, et al. Sixty-four slice CT evaluation of aortic ste- repaired tetralogy of Fallot: a multicenter cross-sectional study.
nosis using planimetry of the aortic valve area. Am J Roentgenol. Circulation. 2013;127(2):172–9.
2007;189(1):197–203. 83. Bashore TM. Adult congenital heart disease right ventricular out-
63. Newfeld EA, Muster AJ, Paul MH, Idriss FS, Riker WL. Discrete flow tract lesions. Circulation. 2007;115(14):1933–47.
subvalvular aortic stenosis in childhood: study of 51 patients. Am 84. Van Praagh R, Pérez-Trevino C, Reynolds JL, Moes CAF, Keith
J Cardiol. 1976;38(1):53–61. JD, Roy DL, et al. Double outlet right ventricle {S, D, L} with
64. Kelly DT, Wulfsberc E, ROWE RD. Discrete subaortic stenosis. subaortic ventricular septal defect and pulmonary stenosis: report
Circulation. 1972;46(2):309–22. of six cases. Am J Cardiol. 1975;35(1):42–53.
65. Cohen L, Bennani R, Hulin S, Malergue MC, Yemets I, Kalangos 85. Sondheimer HM, Freedom RM, Olley PM. Double outlet right
A, et al. Mitral valvar anomalies and discrete subaortic stenosis. ventricle: clinical spectrum and prognosis. Am J Cardiol. 1977;
Cardiol Young. 2002;12(02):138–46. 39(5):709–14.
23 Computed Tomographic Angiography in the Assessment of Congenital Heart Disease and Coronary Artery Anomalies 453

86. Zamora R, Moller JH, Edwards JE. Double-outlet right ventricle bidirectional Glenn procedures. J Am Coll Cardiol. 1993;
anatomic types and associated anomalies. Chest J. 1975;68(5): 22(1):207–15.
672–7. 105. McElhinney DB, Reddy VM, Hanley FL, Moore P. Systemic
87. Losay J, Touchot A, Serraf A, Litvinova A, Lambert V, Piot JD, venous collateral channels causing desaturation after bidirectional
et al. Late outcome after arterial switch operation for transposition cavopulmonary anastomosis: evaluation and management. J Am
of the great arteries. Circulation. 2001;104 Suppl 1:I-121. Coll Cardiol. 1997;30(3):817–24.
88. Kirklin JW, Blackstone EH, Tchervenkov CI, Castaneda 106. Spevak PJ, Johnson PT, Fishman EK. Surgically corrected con-
AR. Clinical outcomes after the arterial switch operation for genital heart disease: utility of 64-MDCT. Am J Roentgenol.
transposition. Patient, support, procedural, and institutional risk 2008;191(3):854–61.
factors. Congenital Heart Surgeons Society. Circulation. 1992; 107. Greenberg SB, Bhutta ST. A dual contrast injection technique for
86(5):1501–15. multidetector computed tomography angiography of Fontan
89. Prifti E, Crucean A, Bonacchi M, Bernabei M, Murzi B, Luisi SV, procedures. Int J Cardiovasc Imaging. 2008;24(3):345–8.
et al. Early and long term outcome of the arterial switch operation 108. Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595
for transposition of the great arteries: predictors and functional patients undergoing coronary arteriography. Cathet Cardiovasc
evaluation. Eur J Cardiothorac Surg. 2002;22(6):864–73. Diagn. 1990;21(1):28–40.
90. Schwartz ML, Gauvreau K, del Nido P, Mayer JE, Colan SD. 109. Click RL, Holmes DR, Vlietstra RE, Kosinski AS, Kronmal RA.
Long-term predictors of aortic root dilation and aortic regurgitation Anomalous coronary arteries: location, degree of atherosclerosis
after arterial switch operation. Circulation. 2004;110(11 Suppl 1): and effect on survival: a report from the Coronary Artery Surgery
II-128. Study. J Am Coll Cardiol. 1989;13(3):531–7.
91. Ou P, Celermajer DS, Marini D, Agnoletti G, Vouhé P, Brunelle F, 110. Baitaxe HA, Wixson D. The incidence of congenital anomalies of
et al. Safety and accuracy of 64-slice computed tomography the coronary arteries in the adult population 1. Radiology.
coronary angiography in children after the arterial switch operation 1977;122(1):47–52.
for transposition of the great arteries. JACC Cardiovasc Imaging. 111. Engel HJ, Torres C, Page HL. Major variations in anatomical
2008;1(3):331–9. origin of the coronary arteries: angiographic observations in 4,250
92. Allwork SP, Bentall HH, Becker AE, Cameron H, Gerlis LM, patients without associated congenital heart disease. Cathet
Wilkinson JL, et al. Congenitally corrected transposition of the Cardiovasc Diagn. 1975;1(2):157–69.
great arteries: morphologic study of 32 cases. Am J Cardiol. 112. Angelini P, Villason S, Chan AV, Diez JG. Normal and anomalous
1976;38(7):910–23. coronary arteries in humans. In: Angelini P, editor. Coronary
93. Schiebler GL, Edwards JE, Burchell HB, DuShane JW, Ongley artery anomalies: a comprehensive approach. Philadelphia:
PA, Wood EH. Congenital corrected transposition of the great Lippincott Williams & Wilkins; 1999. p. 27–150.
vessels: a study of 33 cases. Pediatrics. 1961;27(5):851–88. 113. Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson
94. Bjarke BB, Kidd BSL. Congenitally corrected transposition of the HG. Nontraumatic sports death in high school and college athletes.
great arteries a clinical study of 101 cases. Acta Paediatr. 1976; Med Sci Sports Exerc. 1995;27(5):641–7.
65(2):153–60. 114. Maron BJ, Thompson PD, Puffer JC, McGrew CA, Strong WB,
95. Van Praagh R, Papagiannis J, Grünenfelder J, Bartram U, Douglas PS, et al. Cardiovascular preparticipation screening of
Martanovic P. Pathologic anatomy of corrected transposition of competitive athletes a statement for health professionals from the
the great arteries: medical and surgical implications. Am Heart Sudden Death Committee (clinical cardiology) and Congenital
J. 1998;135(5):772–85. Cardiac Defects Committee (cardiovascular disease in the young).
96. Graham TP, Bernard YD, Mellen BG, Celermajer D, Baumgartner American Heart Association. Circulation. 1996;94(4):850–6.
H, Cetta F, et al. Long-term outcome in congenitally corrected 115. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE. Sports-
transposition of the great arteries: a multi-institutional study. J Am related and non-sports-related sudden cardiac death in young
Coll Cardiol. 2000;36(1):255–61. adults. Am Heart J. 1991;121(2):568–75.
97. Presbitero P, Somerville J, Rabajoli F, Stone S, Conte MR. 116. Angelini P, Velasco JA, Flamm S. Coronary anomalies incidence,
Corrected transposition of the great arteries without associated pathophysiology, and clinical relevance. Circulation. 2002;105(20):
defects in adult patients: clinical profile and follow up. Br Heart J. 2449–54.
1995;74(1):57–9. 117. Bland EF, White PD, Garland J. Congenital anomalies of the coro-
98. Collett RW, Edwards JE. Persistent truncus arteriosus; a classifica- nary arteries: report of an unusual case associated with cardiac
tion according to anatomic types. Surg Clin North Am. hypertrophy. Am Heart J. 1933;8(6):787–801.
1949;29(4):1245. 118. Fierens C, Budts W, Denef B, Van de Werf F. A 72 year old woman
99. Tchervenkov CI, Jacobs JP, Weinberg PM, Aiello VD, Béland MJ, with ALCAPA. Heart. 2000;83(1):e2.
Colan SD, et al. The nomenclature, definition and classification of 119. Kristensen T, Kofoed KF, Helqvist S, Helvind M, Søndergaard L.
hypoplastic left heart syndrome. Cardiol Young. 2006;16(04): Anomalous origin of the left coronary artery from the pulmonary
339–68. artery (ALCAPA) presenting with ventricular fibrillation in an
100. Blalock A, Taussig HB. The surgical treatment of malformations adult: a case report. J Cardiothorac Surg. 2008;3:33.
of the heart: in which there is pulmonary stenosis or pulmonary 120. Selzman CH, Zimmerman MA, Campbell DN. ALCAPA in an
atresia. JAMA. 1945;128(3):189–202. adult with preserved left ventricular function. J Card Surg.
101. Khairy P, Poirier N, Mercier LAE. Univentricular heart. 2003;18(1):25–8.
Circulation. 2007;115(6):800–12. 121. Kang WC, Chung WJ, Choi CH, Park KY, Jeong MJ, Ahn TH,
102. Fontan F, Baudet E. Surgical repair of tricuspid atresia. Thorax. et al. A rare case of anomalous left coronary artery from the
1971;26(3):240–8. pulmonary artery (ALCAPA) presenting congestive heart failure
103. Grosse-Wortmann L, Al-Otay A, Yoo SJ. Aortopulmonary collat- in an adult. Int J Cardiol. 2007;115(2):e63–7.
erals after bidirectional cavopulmonary connection or Fontan 122. Williams IA, Gersony WM, Hellenbrand WE. Anomalous right
completion quantification with MRI. Circ Cardiovasc Imaging. coronary artery arising from the pulmonary artery: a report of 7 cases
2009;2(3):219–25. and a review of the literature. Am Heart J. 2006;152(5):1004.e9.
104. Triedman JK, Bridges ND, Mayer JE, Lock JE. Prevalence and 123. Angelini P. Coronary artery anomalies: an entity in search of an
risk factors for aortopulmonary collateral vessels after Fontan and identity. Circulation. 2007;115:1296–305.
454 P. Pillutla and S.C. Cook

124. Lipton MJ, Barry WH, Obrez I, Silverman JF, Wexler L. Isolated 135. Legendre A, Losay J, Touchot-Kone A, Serraf A, Belli E, Piot JD,
single coronary artery: diagnosis, angiographic classification, and et al. Coronary events after arterial switch operation for transposi-
clinical significance 1. Radiology. 1979;130(1):39–47. tion of the great arteries. Circulation. 2003;108(10 Suppl 1):
125. Desmet W, Vanhaecke J, Vrolix M, Van de Werf F, Piessens J, II-186.
Willems J, et al. Isolated single coronary artery: a review of 50 000 136. Brown JW, Park HJ, Turrentine MW. Arterial switch operation:
consecutive coronary angiographies. Eur Heart J. 1992;13(12): factors impacting survival in the current era. Ann Thorac Surg.
1637–40. 2001;71(6):1978–84.
126. Sharbaugh AH, White RS. Single coronary artery: analysis of the 137. Yamaguchi M, Hosokawa Y, Imai Y, Kurosawa H, Yasui H,
anatomic variation, clinical importance, and report of five cases. Yagihara T, et al. Early and midterm results of the arterial switch
JAMA. 1974;230(2):243–6. operation for transposition of the great arteries in Japan. J Thorac
127. Kragel AH, Roberts WC. Anomalous origin of either the right or Cardiovasc Surg. 1990;100(2):261–9.
left main coronary artery from the aorta with subsequent coursing 138. Prêtre R, Tamisier D, Bonhoeffer P, Mauriat P, Pouard P, Sidi D,
between aorta and pulmonary trunk: analysis of 32 necropsy et al. Results of the arterial switch operation in neonates with
cases. Am J Cardiol. 1988;62(10):771–7. transposed great arteries. The Lancet. 2001;357(9271):1826–30.
128. Cheitlin MD, De Castro CM, McAllister HA. Sudden death as a 139. Von Bernuth G. 25 years after the first arterial switch procedure:
complication of anomalous left coronary origin from the anterior mid-term results. Thorac Cardiovasc Surg. 2000;48(04):228–32.
sinus of Valsalva A not-so-minor congenital anomaly. Circulation. 140. Mayer Jr JE, Sanders SP, Jonas RA, Castaneda AR, Wernovsky G.
1974;50(4):780–7. Coronary artery pattern and outcome of arterial switch operation
129. Frescura C, Basso C, Thiene G, Corrado D, Pennelli T, Angelini for transposition of the great arteries. Circulation. 1990;
A, et al. Anomalous origin of coronary arteries and risk of sudden 82(5 Suppl):IV139–45.
death: a study based on an autopsy population of congenital heart 141. Tanel RE, Wernovsky G, Landzberg MJ, Perry SB, Burke
disease. Hum Pathol. 1998;29(7):689–95. RP. Coronary artery abnormalities detected at cardiac catheteriza-
130. Basso C, Maron BJ, Corrado D, Thiene G. Clinical profile of con- tion following the arterial switch operation for transposition of the
genital coronary artery anomalies with origin from the wrong aor- great arteries. Am J Cardiol. 1995;76(3):153–7.
tic sinus leading to sudden death in young competitive athletes. 142. Hauser M, Bengel FM, Kühn A, Sauer U, Zylla S, Braun SL, et al.
J Am Coll Cardiol. 2000;35(6):1493–501. Myocardial blood flow and flow reserve after coronary reimplan-
131. Taylor AJ, Rogan KM, Virmani R. Sudden cardiac death associ- tation in patients after arterial switch and Ross operation.
ated with isolated congenital coronary artery anomalies. J Am Circulation. 2001;103(14):1875–80.
Coll Cardiol. 1992;20(3):640–7. 143. Meng CCL, Eckner FAO, Lev M. Coronary artery distribution in
132. Eckart RE, Scoville SL, Campbell CL, Shry EA, Stajduhar KC, tetralogy of Fallot. Arch Surg. 1965;90(3):363–6.
Potter RN, et al. Sudden death in young adults: a 25-year review 144. Humes RA, Driscoll DJ, Danielson GK, Puga FJ. Tetralogy of
of autopsies in military recruits. Ann Intern Med. 2004;141(11): Fallot with anomalous origin of left anterior descending coronary
829–34. artery. Surgical options. J Thorac Cardiovasc Surg. 1987;94(5):
133. Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, et al. 784–7.
Sudden unexpected death in persons < 40 years of age. Am 145. Scott LD, Paul MG. Congenital anomalies of the coronary vessels
J Cardiol. 1991;68(13):1388–92. and the aortic root. In: Allen Hugh D, Driscoll DJ, Shaddy Robert
134. Wernovsky G, Sanders SP. Coronary artery anatomy and E, Feltes Timothy F, editors. Moss and Adams’ heart disease in
transposition of the great arteries. Coron Artery Dis. 1993;4(2): infants, children and adolescents. 8th ed. Philadelphia: Lippincott
148–58. Williams & Wilkins; 2013. p. 746–57.
 CCTA Cardiac Electrophysiology
Applications: Substrate Identification, 24
Virtual Procedural Planning,
and Procedural Facilitation

Jerold S. Shinbane, Leslie A. Saxon, Rahul N. Doshi,

Philip M. Chang, and Matthew J. Budoff

Abstract
Cardiovascular computed tomographic angiography (CCTA) is a valuable adjunctive tool in
the diagnosis and treatment of electrophysiologic disease. This modality provides visualiza-
tion of anatomy important to arrhythmia substrate identification, as well as electrophysiol-
ogy procedural planning, facilitation, and follow-up. Atrial fibrillation ablation requires a
detailed understanding of an individual patient’s presence and degree of atrial myopathy
and 3-D characterization of the relationships between the left atrium, the surrounding car-
diac and extracardiac thoracic structures. Electroanatomic mapping with CCTA image inte-
gration has revolutionized catheter–based therapies by allowing for electrical mapping and
ablation to occur on a 3-D map of the patient’s individual atrial anatomy. CCTA imaging
has assumed an important role in decisions and planning of atrial appendage occlusion
device procedures. Ventricular arrhythmias are associated with a spectrum of cardiovascu-
lar structural abnormalities which can be identified by CCTA. Cardiomyopathic substrates
associated with ventricular arrhythmias can be identified, although fibrosis imaging is more
evolved with cardiovascular magnetic resonance imaging. CCTA can visualize the coronary
venous system providing roadmaps for lead placement when obstacles to standard
approaches are identified. The role of CCTA will expand due to continued development of
novel cardiac electrophysiology applications for arrhythmogenic substrate identification
and procedural facilitation.

Keywords
Ablation • Atrial Fibrillation • Anomalous Coronary Arteries • Cardiac Electrophysiology
• Cardiomyopathy • Cardiovascular Magnetic Resonance Imaging • Computed Tomography
• Congenital Heart Disease • Electrophysiology • Ventricular Tachycardia

Electronic supplementary material The online version of this

chapter (doi:10.1007/978-3-319-28219-0_24) contains supplementary
L.A. Saxon, MD, FACC, FHRS • R.N. Doshi, MD, FACC, FHRS
material, which is available to authorized users.
P.M. Chang, MD
Department of Medicine, Division of Cardiovascular Medicine,
J.S. Shinbane, MD, FACC, FHRS, FSCCT (*)
Department of Internal Medicine, Keck School of Medicine of the
Division of Cardiovascular Medicine, Department
University of Southern California, Los Angeles, CA, USA
of Internal Medicine, Keck School of Medicine of the University
of Southern California, 1520 San Pablo Suite 300, Los Angeles, M.J. Budoff, MD
CA 90033, USA David Geffen School of Medicine at UCLA, Los Angeles
e-mail: [email protected] Biomedical Research Institute, Torrance, CA, USA

© Springer International Publishing 2016 455

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_24
456 J.S. Shinbane et al.

Introduction attention to details of patient preparation and image acquisi-

tion and processing is important to optimizing CCTA studies
Cardiovascular computed tomographic angiography (CCTA) in patients who may have irregular rhythms due to premature
can comprehensively assess cardiovascular structure and atrial contractions, premature ventricular contractions, or
function relevant to the assessment, treatment, and follow-up other arrhythmias including atrial fibrillation and atrial flut-
of patients with electrophysiologically-related disease pro- ter. Medications to control heart rate and rhythm as well as
cesses. CCTA provides 3-D visualization of cardiac cham- pacemaker reprogramming to regularize rhythms may be
bers, coronary vessels, and thoracic vasculature, including useful. Acquisition protocols which compensate for irregular
structures particularly important to cardiac electrophysiol- beats through deletion of short R-R intervals and analysis of
ogy such as the coronary veins, pulmonary veins, and left mid-diastolic phases of the R-R interval with an absolute
atrium. This comprehensive technology is extremely useful rather than relative time from the preceding R wave can
for the identification and characterization of cardiovascular improve image quality [1].
substrates relevant to cardiac electrophysiology, and has The indication for the CCTA study is important to deci-
great relevance to treatment of arrhythmias through pre- sions regarding the correct field of view and target structures
procedure planning, procedural facilitation, and procedural requiring maximum contrast opacification. The contrast circu-
follow-up. lation time and the injection protocol are important factors to
take into account to achieve maximal opacification of the
region or regions of interest. Assessment of right ventricular
Technical Issues Related to Image function as well as coronary venous anatomy requires proto-
Acquisition in Patients with Arrhythmias cols providing adequate contrast enhancement to these struc-
tures, while still opacifying other cardiac structures and
There are a variety of approaches for imaging patients with coronary arterial anatomy. Multiphase injection protocols
arrhythmia issues based on indication for study, rate and with varying amounts of contrast, diluted contrast, and/or
rhythm at the time of study, presence of a pacemaker or ICD saline can be administered at variable speeds of delivery to
and programmed lower rate and mode, CT scanner, imaging optimally opacify structures for various electrophysiology
and injection protocol, and editing software. Particular indications (Fig. 24.1).

a b

Fig. 24.1 Axial views demonstrating a contrast injection timing proto- for contrast enhancement of the left ventricle, useful for coronary artery
col for contrast enhancement of the right ventricle and left ventricle, assessment without streak artifacts in the superior vena cava (b)
useful for assessment of right ventricular pathology (a), and a protocol
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 457

As patients having CCTA for arrhythmia applications being investigated. These potential mechanisms affecting
often undergo electrophysiology procedures which may arrhythmia initiation and perpetuation include premature
require fluoroscopy, techniques to limit radiation dose are atrial foci from the pulmonary veins and atria, autonomic
extremely important. Dose reductions can be achieved influences, rotors defined by atrial anatomic and electrophys-
through limitation of field of view to essential structures and iologic substrate, and reentrant atrial flutter and atrial tachy-
use of dose limiting imaging protocols. Prospective gating cardia circuits defined by regional electrophysiology, cardiac
techniques or retrospective gating with dose modulation can structure, and myocardial fibrosis. Given these multiple
be used in some circumstances, but these techniques can be mechanisms, a variety of approaches to ablation target atrial
more limited in the setting of irregular rhythms. anatomy and electrophysiology, including catheter-based
Gated imaging can be problematic in the setting of the segmental or complete circumferential electrical isolation of
rhythm irregularity and elevated heart rate, but is feasible in the pulmonary veins, ablation of ectopic atrial foci, long lin-
some scenarios. Problems with irregularity can lead to ear lesions providing pathways of preferential conduction,
“step ladder” artifact limiting the ability to obtain diagnos- ablation of autonomic input, antral lesions targeting anatomy
tic assessment of segments of the coronary arteries [2, 3]. related to rotors, and ablation of reentrant circuits.
This artifact can be minimized using volume scanners Percutaneous catheter-based approaches are used to access
which can image the field of view in a single heartbeat. the left atrium via either a single or double transseptal tech-
With retrospective gating, cardiac structures including each nique depending on the number and types of left atrial cath-
coronary artery segment can be analyzed in the most opti- eters employed.
mal phase, but at the cost of an increased radiation dose. The performance of atrial fibrillation ablation requires
Assessment of the coronary arteries with retrospective gat- definition of an individual patient’s presence and degree of
ing is achievable in patients in atrial fibrillation prior to atrial myopathy as well as characterization of the relation-
ablation [4]. With prospective gating, algorithms rejecting ships between the left atrium and the surrounding cardiac
beats outside of a specified range have been developed for and thoracic structures. A pre-procedure study serves multi-
patients with irregular rhythms [5, 6]. In the setting of atrial ple purposes, acting as a means to decide whether to proceed
fibrillation with higher average ventricular rate response, with ablation based on the degree of atrial myopathy, a road-
end-systole may be a more optimal phase of image recon- map for procedural planning, a 3-D data set for intra-proce-
struction than end diastole [7, 8]. dure electroanatomic mapping and ablation, and a template
In patients with pacemakers and ICDs and higher pro- for comparison to future potential studies assessing for com-
grammed pacing rates the pacing rate can be transiently plications such pulmonary vein stenosis. CCTA character-
programmed down to the optimal rate for imaging, such as ization of the left atrium and pulmonary veins is achieved
60 bpm, if the patient’s native underlying heart rate is below through multiple modalities of evaluation including multi-
this value and the patient’s underlying condition allows this plane 2-D views, volumetric quantification of the atria, 3-D
change in programming. Reprogramming pacing function reconstructions, and virtual endovascular atrial views.
to a non-rate responsive modes can be helpful as the breath
hold process can trigger a rate response with some devices.
The presence of pacemakers or ICDs can also lead to beam Left Atrial Myopathy: Left Atrial Size,
hardening artifacts which can impact image quality. Morphology and Function
Decisions as to the use of CCTA versus CMR in patients
with pacemakers and ICDs depend on device specifics. The Atrial morphology is complex and therefore characterization
application of CMR for patients with cardiac pacemakers and of the presence and degree of atrial myopathy based on volu-
ICDs has undergone evolution with the advent of MR condi- metric assessment of size and function is of paramount
tional devices which allow for the use of MR imaging under importance. Left atrial volume is an important predictor of
specified conditions [9–12]. Even in scenarios where CMR procedural success with atrial fibrillation ablation, as recur-
can be performed, imaging artifacts can be problematic. Novel rence of atrial fibrillation is associated with an increased left
algorithms to decrease artifact are being developed [13, 14]. atrial volume (Fig. 24.2) [15, 16].
CCTA left atrial indexed volume reference values have
been reported [17–19]. In patients in sinus rhythm at the
CCTA for Cardiovascular Diagnostic time of the CCTA, atrial ejection fraction can be calculated
Assessment and Procedural Facilitation with retrospective gating (Fig. 24.3) [20]. CCTA left atrial
for Atrial Arrhythmias volumes correlate with CMR volumes [21]. Preprocedure
assessment of left atrial size and pulmonary vein anatomy
Atrial Fibrillation Ablation and size are similar for CMR and CCTA, although cumula-
tive radiation dose is decreased with CMR for image guided
The potential mechanisms of initiation and perpetuation of ablation [22]. Variation in pulmonary vein anatomy branch-
atrial fibrillation are multiple, with their relative roles still ing patterns can be characterized [23]. Assessment of atrial
458 J.S. Shinbane et al.

a b

Fig. 24.2 Axial (a) and sagittal (b) views demonstrating profound atrial enlargement in a patient with atrial fibrillation. The left atrial volume was
greater than 450 cc

Fig. 24.3 Assessment of left

a b
atrial volume during atrial systole
(a) and diastole (b)

wall thickness can be performed at multiple relevant loca- rate of atrial fibrillation recurrence and therefore have
tions including at the pulmonary veins, left pulmonary potential implications for ablation approach to this anat-
vein/ left atrial appendage ridge and posterior left atrium omy (Fig. 24.4) [25, 26]. CCTA provides volumetric evi-
[24, 25]. Thicker left pulmonary vein/left atrial appendage dence of reverse remodeling with successful atrial
ridges as assessed by CCTA are associated with a higher fibrillation ablation [27]. Successful ablation is associated
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 459

fibrillation ablation for “lone” atrial fibrillation demon-

strated similar ablation results to those with comorbidities,
with the degree of fibrosis being the determining factor of
success [41]. Post contrast T1 assessment of diffuse fibrosis
correlates with decreased tissue voltage, and presence of
atrial fibrillation. It also predicts success of ablation [42].
CCTA first pass attenuation can identify areas of atrial low
voltage areas, but requires further investigation [43].

Left Atrial Anatomy Relevant to Atrial

Fibrillation Ablation

Pulmonary venous anatomy demonstrates great variability

regarding vein number, location, size, shape, and ostial
complexity. CCTA can visualize these pulmonary vein char-
acteristics and can define the relationship between veins as
Fig. 24.4 Endovascular view showing a prominent ridge (arrows) well as between the left upper pulmonary vein and left atrial
between the left atrial appendage and left upper pulmonary vein. LAA appendage (Figs. 24.5, 24.6, and 24.7, Video 1). Workstation
left atrial appendage, LUPV left upper pulmonary vein, LLPV left lower
pulmonary vein
software can be used to quantify characteristics of the pul-
monary vein ostia, including area, maximum diameter, min-
imum diameter, and eccentricity. Key to these measurements
is identification of the left atrial/pulmonary vein interface,
with changes in atrial morphology with reversal of spheri- determination of the long axis of the vein at the ostium, and
cal remodeling [28]. In patients with paroxysmal atrial recognition that the vein ostium is often an ovoid rather than
fibrillation, reverse remodeling with improvement of atrial circular shape (Fig. 24.8). Three-D reconstructions can
transport function has been demonstrated by CCTA with serve as a roadmaps for ablation as well as templates for
successful ablation [29]. post ablation changes [44, 45]. In relation to other modali-
In addition to atrial size and function, the visualization of ties, CCTA and CMR offer similar ability to assess pulmo-
atrial fibrosis is important to assessment for atrial myopathy. nary vein morphology [46]. CCTA in comparison to invasive
CMR has been the primary imaging modality for this assess- venography, intracardiac echo, and transesophageal echo
ment through characterization of focal fibrosis with late performed during the procedure was superior to all of these
gadolinium enhancement and diffuse fibrosis with T1 map- other modalities in identifying veins. CCTA and intracar-
ping. Challenges exist though as left atrial wall thickness is diac echo provided comparable assessment of pulmonary
at the limit of the spatial resolution of CMR. Atrial fibrosis vein diameter, while diameters were larger based on venog-
can be characterized by CMR delayed gadolinium enhance- raphy and smaller based on transesophageal echo [47, 48].
ment [30]. The degree of left atrial fibrosis has been associ- Pulmonary vein stenosis is a potential complication of
ated with sick sinus syndrome, history of stroke, and atrial fibrillation ablation [49, 50]. The reported incidence
decreased atrial pump function [31–33]. The degree of is dependent on imaging technique, definition of a signifi-
preablation late gadolinium enhancement fibrosis has been cant stenosis, and degree of surveillance [51]. As tech-
associated with arrhythmia recurrence [34–36]. Post abla- niques have evolved with recognition of the need to ablate
tion left atria have increased scar density compared to preab- in the atrium outside of the pulmonary veins, the incidence
lation native fibrosis [37]. Delayed gadolinium enhancement of pulmonary vein stenosis has significantly decreased.
can assess the adequacy of lesion sets associated with pul- Stenosis can occur when ablation lesions are applied
monary vein isolation. Identification of gaps in lesion sets directly to the pulmonary veins [52]. Imaging technologies
may be the substrate post ablation arrhythmias and therefore which can visualize the atrial/pulmonary vein interface are
serve as targets for subsequent ablation therapy [38]. The therefore important to ablation lesion application within
completeness of pulmonary vein isolation as well as poste- the atria rather than the pulmonary veins. CCTA integration
rior and septal wall debulking lesions as assessed by CMR with catheter-based mapping has also been shown to
are markers of greater ablation success, particularly in the decrease the incidence of pulmonary vein stenosis [53]. As
setting of higher pre- ablation scar burden [39, 40]. Patients pulmonary vein stenosis can preexist ablation due to either
diagnosed with “lone” atrial fibrillation have evidence of extrinsic compression by other thoracic structures or due to
atrial fibrosis on CMR and procedural outcome of atrial a congenital etiology, the preprocedure study serves as a
460 J.S. Shinbane et al.

Fig. 24.5 Characterization of the left atrium and pulmonary veins left upper pulmonary vein, LLPV left lower pulmonary vein, RUPV
demonstrated through 2-D axial views and 3-D volumetric reconstruc- right upper pulmonary vein, RMPV right middle pulmonary vein, and
tion, demonstrating 2 left-sided pulmonary veins and variant anatomy RLPV right lower pulmonary vein
with 3-right sided pulmonary veins. LAA left atrial appendage, LUPV

Fig. 24.6 Characterization of the left atrium and pulmonary veins demonstrated through double oblique thick MIP (left panel), and a 3-D endo-
cardial view demonstrating 3-right sided pulmonary veins (right panel)

template appropriate interpretation of pulmonary vein find- monary vein stenosis after atrial fibrillation ablation is
ings post ablation [54]. Although CCTA is superior for pul- necessary [55]. CCTA is useful for the recognition of the
monary vein identification, transesophageal echo can be a anatomic degree of pulmonary vein stenosis (Fig. 24.9)
complementary modality for assessment of the pathophysi- [56]. In scenarios with moderate stenosis, the functional
ologic significance of stenosis [52]. The incidence of pul- significance of the pulmonary vein stenosis can be assessed
monary vein stenosis is decreasing, but establishment of by transesophageal echo and lung perfusion via assessment
screening algorithms and guidelines to assess the true cur- with V/Q scan [57]. CCTA integration with fluoroscopy
rent incidence and time course of the development of pul- can also facilitate procedural performance of pulmonary
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 461

vein stenting [58]. The patency of pulmonary vein stents mistaken for the orifices of pulmonary veins. Definition of
can also be visualized with CCTA (Fig. 24.10). anatomy of the mitral isthmus is important as ablation lines
Atrial anatomy other than the pulmonary veins important are sometimes applied to this region. The 3-D relationship of
to facilitation of atrial fibrillation ablation can be defined by the circumflex coronary artery, coronary sinus/great cardiac
CCTA. Atrial septal characteristics important to transseptal vein in relation to the left atrium and mitral annulus can be
puncture include definition of the location and size of the defined by CCTA [60]. Given these anatomic relationships,
fossa ovalis, presence of a patent foramen ovale, and pres- there is the potential for coronary artery damage with the
ence and degree of lipomatous hypertrophy of the atrial sep- application of ablation lesions in this area, potentially lead-
tum (Fig. 24.11). Atrial masses and thrombi can be identified, ing to myocardial infarction with the need for emergent
which could contraindicate transseptal catheterization. stenting. Additionally, sinus node dysfunction may occur as
CCTA can display the location of and wall thickness of left a left sinus node artery can course in this space [61].
atrial diverticulae (Fig. 24.12, Video 2). CCTA has shown Bachmann’s bundle is an interatrial muscle band providing a
these structures to have thinner walls than atrial myocardium pathway of preferential conduction between the atria. This
with frequent location near pulmonary veins and atrial bundle and its vascular supply can be visualized with CCTA
appendage ostia [59]. Atrial diverticulae could potentially and could potentially be in the path of a left atrial ablation
complicate catheter placement and manipulation if they are roof line [62].

Thoracic Anatomy Relevant to Atrial

Fibrillation Ablation

Thoracic anatomy relevant to ablation includes the relation-

ship of the esophagus and aorta to the posterior left atrium
and pulmonary veins. Left atrial-esophageal fistula has been
reported as a fatal complication of atrial fibrillation ablation
[63]. The relationship between the thin wall of the posterior
left atrium, pulmonary veins, esophagus and aorta can be
visualized prior to ablation (Figs. 24.13 and 24.14). There is
variability of the course of the esophagus and degree of con-
tact between the posterior left atrium/pulmonary veins,
esophagus and aorta [64, 65]. Barium swallow at the time of
CT has been used to opacify the esophagus for electroana-
tomic image integration with ablation procedures [66].
Esophageal motility, change of the position of the esophagus
with respiration, and patient position, can change the spatial
Fig. 24.7 Characterization of the relationship between and ostial char- relationship of the esophagus to the posterior left atrium
acteristics of a right upper and right middle pulmonary vein on a 3-D from the CCTA to the procedure as well as during the abla-
endocardial view tion procedure [67, 68].Additionally a variable layer of a

Fig. 24.8 Identification the left atrial/pulmonary vein interface, determination of the long axis of the vein at the os, and en face visualization of
an ovoid pulmonary vein os.
462 J.S. Shinbane et al.

a b

Fig. 24.9 2-D (a) and 3-D (b) volume rendered images demonstrating significant pulmonary vein stenosis (arrow) of a left lower pulmonary vein
(Courtesy of Dr. Jeffrey Schussler, Baylor University Medical Center, Dallas, Texas)

Fig. 24.10 Curved

multiplanar views of
pulmonary vein stents
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 463

pericardial fat pad can be visualized around the pulmonary

veins and posterior left atrium with CT which could conceiv-
ably provide some insulation to the esophagus with applica-
tion of ablation lesions in the left atrium [64, 69]. CCTA
identification of the coronary venous system is important for
catheter placement, mapping, and for ablation lines [70]. The
relationship between the upper pulmonary veins and the
bronchi can be characterized by CCTA and is important to
understand in order to avoid the rare but possible complica-
tion of atrio-bronchial fistula with ablation [71–73]. The
phrenic nerve has been visualized with CCTA, which can be
important to avoid diaphragmatic paralysis with atrial fibril-
lation ablation [74]. Epicardial adipose tissue can be quanti-
fied and has been associated with atrial fibrillation [75].
Incidental thoracic findings visualized on CCTA have also
been demonstrated to influence decisions regarding proceed-
ing with atrial fibrillation ablation [76].

CCTA Image Integration for Procedural

Facilitation of Atrial Fibrillation Ablation

Electroanatomic mapping with CCTA image integration

has revolutionized catheter–based therapies by allowing
for electrical mapping and ablation to occur on a 3-D map
of the patient’s individual endocardial left atrial anatomy
(Figs. 24.15, 24.16, 24.17, and 24.18, Videos 3, 4, 5, 6). The
Fig. 24.11 3-D double oblique view demonstrating lipomatous hyper-
process involves importation of the unprocessed DICOM
trophy of ther inter-atrail septum (arrows) images into the electrophysiology mapping system, use of

a b

Fig. 24.12 2-D double oblique (a) and 3-D (b) views demonstrating an atrial diverticulum (arrows) located on the anterior superior portion of the
left atrium
464 J.S. Shinbane et al.

a b c

Fig. 24.13 3-D reconstructions (a and b) demonstrating the relationship of the aorta to the posterior left atrium and left lower pulmonary vein. A
double oblique view (c) demonstrating the relationship of the esophagus and aorta to the posterior left atrium and pulmonary veins

a b c

Fig. 24.14 3-D reconstructions (a and b) demonstrating the relation- gus and aorta to the posterior left atrium and pulmonary veins. In this
ship of the aorta to the posterior left atrium and left lower pulmonary case, the esophagus (arrow) is “sandwiched” between spine and aorta at
vein. A 2-D axial view (c) demonstrates the relationship of the esopha- the level of the left lower pulmonary vein.

edge detection software to delineate and edit down to relevant Electroanatomic mapping with image integration
cardiac and vascular structures including the left atrium and allows for arrhythmia activation and propagation, voltage
in some electrophysiology laboratories the aorta and esopha- maps, catheter position, and ablation lesion set location to
gus. Subsequently, a separate catheter-based anatomic map is be displayed on the 3-D CCTA reconstruction. Ablation
created using fiduciary landmark points in the left atrium fol- guided by integration of pre-procedure CCTA with real
lowed by registration of surface points defining the endocar- time catheter-based electroanatomic maps can increase
dial boundaries of the left atrium. The anatomic catheter-based the efficacy of and decrease complications associated
map is then integrated with the CCTA images with assessment with atrial fibrillation ablation. This technique has been
of markers of successful integration defined by an acceptable shown to be helpful in increasing restoration of sinus
catheter to endocardium distances which have been demon- rhythm and decreasing recurrence of atrial fibrillation
strated to be accurate [77, 78]. If registration is inadequate, compared to electroanatomic mapping alone [53, 80].
catheter based points are edited and new points registered to Clinical outcome though is still dependent on achieving
ensure that the atrial endocardial surface has been adequately successful pulmonary vein isolation [81]. The localization
mapped. Atrial size is important to integration techniques as of the ablation catheter tip on the endocardial left atrial
greater misregistration occurs with larger dimensions [79]. reconstruction can help to ensure that radiofrequency
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 465

a b

Fig. 24.15 Initial image processing for electroanatomic mapping with right ventricle (yellow) edited out, with the left atrium (purple) subse-
CCTA image integration showing segmentation of vascular structures quently rotated to demonstrate the posterior left atrium (b)
(a) with the aorta (green), pulmonary arteries (orange), right atrium and

a b

Fig. 24.16 Image processing for electroanatomic mapping with CCTA image integration with a catheter-based anatomic map of the left atrium
(a, upper image) and the 3-D volume rendered CT image of the left atrium (a, lower image) with integration of these images (b)
466 J.S. Shinbane et al.

applications are placed in the atrium and not in the pulmo-

nary veins or ostia to avoid pulmonary vein stenosis.
Subsequent to ablation, mapping using this system can be
performed to ensure electrical isolation of the pulmonary
veins.
Placement of uninterrupted ablation lines around pulmo-
nary veins and as long linear lesions within the atrium are
important to the performance of atrial fibrillation ablation,
as gaps within these lesion lines can lead to unsuccessful
procedures. Gaps within ablation lines can also serve as a
substrate for post-ablation atrial flutter reentry [82, 83].
Image integration allows for registration of the position of
ablation lesions, therefore facilitating placement of lesion
sets to create continuous lines.
CCTA or CMR image integration with catheter-based
intracardiac maps can be additionally merged with intracar-
diac echocardiography, providing real time visualization of
the esophagus, visualization of transseptal puncture, append-
age thrombi, ablation catheter contact and lesion depth, pul-
monary vein stenosis, and pericardial effusion (Figs. 24.19
and 24.20) [84–89]. Multimodal imaging with integration of
CCTA images and real-time fluoroscopy is also being pre-
liminarily investigated [90]. The integration of cone beam
Fig. 24.17 Electroanatomic mapping with image integration demon- CT obtained at the time of ablation with electroanatomic
strating an endocardial view of the left upper pulmonary vein after mapping has also been performed [91].
radiofrequency catheter isolation of the vein with encircling radiofre-
quency energy applications (red spheres)

a b

Fig. 24.18 Electroanatomic mapping with image integration demonstrating mapping of arrhythmia electrical activation (a) and arrhythmia wave-
front propagation (b)
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 467

Atrial Appendage Thrombus Assessment cles (Fig. 24.21). Contractile function of the appendage in
the setting of atrial myopathy and atrial fibrillation is
The recognition of atrial thrombi is extremely important depressed with concomitant decreased flow velocity. These
prior to consideration of atrial fibrillation ablation. The left factors make it difficult to analyze for thrombi, as filling
atrial appendage is a complicated potentially multi-lobed defects can be due to inadequate contrast filling of the
tube-like structure with an intricate array of pectinate mus- appendage [92–94].

Fig. 24.19 Components of electroanatomic mapping with CCTA and intracardiac echo image integration, with a catheter-based anatomic map
(upper left image), CCTA (lower left image), and intracardiac echo (right image)

Fig. 24.20 Electroanatomic mapping with CCTA and intracardiac echo image integration demonstrating an endocardial view after radiofre-
quency catheter pulmonary vein isolation with encircling radiofrequency energy applications (red spheres)
468 J.S. Shinbane et al.

Transesophageal echo is the gold standard for the assess-

ment of left atrial appendage thrombi. In patients with pre-
procedure non-gated CCTA prior to atrial fibrillation ablation,
the sensitivity is high for ruling out thrombus, especially in
lower risk patients (age <52 and CHADS2 score <1), but spec-
ificity, positive predictive value, and inter-observer consensus
remains more limited (Fig. 24.22) [95–101]. The degree of
pseudofilling defects correlate with the degree of left atrial
emptying abnormality in patients with chronic atrial fibrilla-
tion as assessed by CCTA volumetric analysis [102]. Delayed
CCTA images allow more time for left atrial appendage fill-
ing, improving detection of pseudofilling defects (Fig. 24.23)
[103–105]. These images can be performed with a more
restricted field of view to limit radiation exposure with delayed
imaging. Imaging in the prone position may decrease false
positive results [106]. The left atrial appendage/ascending
aorta Hounsfield Unit ratio is inversely related to the degree of
spontaneous echo contrast and presence of thrombi [107].
This ratio may be useful as there are limitations to the visual
assessment of the left atrial appendage for thrombus [99]. Fig. 24.22 Double oblique 2-D view demonstrating a filling defect
(arrow) in the tip of the left atrial appendage with a differential diagno-
Definition of the optimal left atrial appendage/ascending aorta
sis of incomplete filling of the appendage versus thrombus
Hounsfield Unit ratio is dependent on whether the ratio is

Fig. 24.21 Double oblique 2-D view (left panel) showing the complex views (right panels) show the shape of the left atrial appendage ostium
anatomy of the left atrial appendage (arrow) with a multi-lobed tube- and ridge separating it from the left upper pulmonary vein
like structure with an intricate array of pectinate muscles. Endocardial
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 469

a b

Fig. 24.23 2-D double oblique views of the left atrial appendage showing a filling defect (arrow) on first pass imaging (a) and complete opacifica-
tion (arrow) of the appendage on a delayed image (b)

assessed during standard left atrial opacification or delayed transseptal route, minimally invasive catheter-based epi-
images and whether the focus is on sensitivity and negative cardial occlusion, and minimally invasive or open surgical
predictive values or specificity and positive predictive value. appendectomy. CCTA can provide virtual procedural images
With these techniques the sensitivity and negative predictive defining the path and possible obstacles to transseptal, subxi-
value are excellent with some limitations to positive predictive phoid transcatheter, minimally invasive surgical or open sur-
value and specificity [99, 108–110]. gical approaches (Figs. 24.29 and 24.30). Stroke risk based
on left atrial appendage morphology requires further study
due to variability in results [116–122].
Left Atrial Appendage Occlusion Devices
for Stroke Prevention with Atrial Fibrillation/
Atrial Flutter CCTA in Other Supraventricular Tachycardias

Devices have been developed for left atrial appendage occlu- CCTA definition of atrial structures is important to the spec-
sion to decrease thromboembolic risk associated with atrial trum of supraventricular tachycardia ablation. CCTA has
fibrillation and atrial flutter [111, 112]. Classification sys- been used to define anatomic characteristics important to
tems defining left atrial appendage morphology are evolving ablation of cavotricuspid isthmus dependent atrial flutter.
as multiple shapes and geometries exist [113]. These mor- Visualization of characteristics including steep angulation of
phologies can be defined by the left atrial appendage ostial a thick-walled cavotricuspid isthmus and prominence of the
size, morphology and location, the length of the main body, Eustachian ridge distinguished challenging cases and deter-
the number, length, angulation and degree of trabeculation of mined successful approach to this anatomy [123]. CCTA
lobes, and the relationship of the appendage to other struc- with image integration and electroanatomic mapping is use-
tures (Figs. 24.24, 24.25, 24.26, 24.27, and 24.28, Videos 7, 8, ful for ablation of complex atrial tachycardia circuits [124].
9, 10, 11, 12). CCTA defined left atrial appendage morphol- For ablation of accessory pathways in Wolff-Parkinson-
ogy has become important to decisions to whether to proceed White syndrome, issues related to the coronary sinus/great
with closure, the choice of closure approach, and the specific cardiac vein have ramifications for mapping. The coronary
type of closure device [114, 115]. The methods for left atrial sinus/great cardiac vein has a variable location in relation to
appendage occlusion include endovascular occlusion via a the mitral annulus often coursing above the annulus rather
470 J.S. Shinbane et al.

a b c

d e

Fig. 24.24 Multimodal views demonstrating a “chicken-wing” mor- double oblique (b), endovascular (c), and 2-D double oblique aligned
phology left atrial appendage (arrows) with a long main lobe which along long axis (d) and short axis (e) of the appendage ostium
subsequently has an acute angulation. Views include: 3-D (a), 2-D

Fig. 24.25 Left lateral 3-D views demonstrating the relationship of a “chicken wing” morphology left atrial appendage to an aneurysmal pulmo-
nary artery. LAA left atrial appendage, PA main pulmonary artery

than at the annular level. In these anatomic scenarios, coronary coronary sinus to the circumflex coronary artery is important
sinus catheters record the atrial insertion of an accessory path- in order to avoid complications. CCTA can define areas of
way rather than providing a true annular signal [125]. CCTA crossing and overlap between these structures (Fig. 24.31) [60,
can define the individual relationship between the coronary 126]. CCTA can also define anatomic findings important to
sinus/great cardiac vein and the annulus important to interpre- catheter placement and mapping of certain accessory pathway
tation of coronary sinus lead electrograms. In regard to abla- substrates. The presence of a coronary sinus diverticulum or
tion in the coronary sinus, knowledge of the relationship of the isolated unroofed coronary sinus can be visualized [127, 128].
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 471

a b

Fig. 24.26 3-D (a) and 2-D double oblique (b) views demonstrating the morphology of the left atrial appendage to be “cauliflower” shaped
(arrow) with a single short lobe

a b

Fig. 24.27 3-D (a) and 2-D double oblique (b) views demonstrating the morphology of the left atrial appendage to be “cactus” shaped (arrow)
with a long main lobe followed by several branching lobes

Assessment of Anatomic Substrates abnormalities, often with the first manifestation of disease
Associated with Ventricular Arrhythmias being sudden death. Vascular and valvular anatomies
and Sudden Cardiac Death associated with sudden cardiac death due to hemodynamic
compromise or ventricular arrhythmias can be identified by
Ventricular arrhythmias are associated with a spectrum of CCTA, and include anomalous coronary arteries, severe
cardiovascular structural or primary electrophysiologic coronary artery disease, critical aortic stenosis, and aortic
472 J.S. Shinbane et al.

Fig. 24.28 Left lateral 3-D views demonstrating the anterior angulation of the left atrial appendage. LAA left atrial appendage, PA main pulmo-
nary artery

a b c

Fig. 24.29 Serial cranial to caudal 3-D axial views (a–c) demonstrating the anatomic relationship between a “chicken-wing” morphology left
atrial appendage and the main pulmonary artery. Ao aorta, LAA left atrial appendage, PA main pulmonary artery

aneurysm and dissection. High risk anomalous coronary visualization of the coronary arteries with CCTA may
artery anatomies include coronary artery off of the contralat- facilitate differentiation between ischemic and non-isch-
eral sinus with an interarterial course and slit-like ostium, emic cardiomyopathy [133–135].
coronary artery origin from the pulmonary artery, and left The visualization of myocardial fibrosis is important to
main coronary atresia, all of which can be visualized by the differential diagnosis and prognosis of cardiomyopathic
CCTA [129–132]. states. CMR delayed gadolinium enhancement has played a
Cardiomyopathic substrates associated with sudden primary role in fibrosis imaging. CMR delayed contrast
cardiac death due to hemodynamic compromise or ven- enhancement has the ability to visualize myocardial infarct
tricular arrhythmias can be identified by CCTA. Cine- scar and its anatomic relationship to viable myocardium
CCTA can characterize cardiomyopathic substrates [136–139]. In ischemic cardiomyopathy, delayed contrast
through reproducible volumetric measurement of ventricu- enhancement can be used to localize myocardial segments
lar volumes and ejection fraction, ventricular wall thick- with scar, determine the morphology, transmurality and
ness, and ventricular regional wall motion. Direct complexity of scar, and define the total percentage of myo-
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 473

a b c d

e f g h

Fig. 24.30 Serial caudal to cranial (a–h) 3-D axial views demonstrat- descending coronary artery, LA left atrium, LAA left atrial appendage,
ing a virtual subxiphoid approach to a “chicken-wing” morphology left LV left ventricle, and RV right ventricle
atrial appendage. Cx circumflex coronary artery, LAD left anterior

Fig. 24.31 The left-lateral view (left panel) and diaphragmatic view AIV anterior interventricular vein, CS coronary sinus, GV great cardiac
(right panel) of the heart. The left circumflex coronary artery and coro- vein, LA left atrium, LAV left atrial vein, LCX left circumflex coronary
nary veins are clearly displayed. The great cardiac vein is seen overly- artery, LV left ventricle, MV middle cardiac vein, MRV marginal vein,
ing the left circumflex coronary artery for a short (<30 mm) segment. PV posterior vein (Reprinted from Mao et al. [60] with permission from
The marginal vein is dominant, and the posterior vein is small in size. Elsevier)

cardium infarcted. The presence and degree of delayed con- arrhythmogenic right ventricular cardiomyopathy [155,
trast enhancement is associated with increased ventricular 156]. CMR derived 3-D location, transmurality, heterogene-
arrhythmias and worse prognosis in ischemic cardiomyopa- ity and complexity of the scar, presence of an anatomic isth-
thy [140–142], nonischemic dilated cardiomyopathy [142– mus, and relation of the fibrosis to the atrioventricular annuli
147], hypertrophic cardiomyopathy [148–154], and can assist in the planning and performance of ventricular
474 J.S. Shinbane et al.

tachycardia ablation. These imaging factors can help to

delineate whether an epicardial approach is required to reach
a ventricular tachycardia circuit, whether ablation lines
should be extended to an atrioventricular annulus, and where
the location of a potential critical isthmus areas for ablation
[157–162]. Integration of 3-D fibrosis reconstruction from
late gadolinium enhancement CMR with electroanatomic
catheter mapping in the EP laboratory can further facilitate
ventricular tachycardia ablation [157].
The presence of a non-MR conditional implantable
device continues to limit the application of CMR imaging.
Additional limitation is related to quality of image acquisi-
tion in patients with devices. In settings where delayed
gadolinium enhancement CMR has been utilized in patients
with ICDs, artifact can potentially limit image quality, but
techniques to minimize these artifacts are being investi-
gated [14]. CCTA delayed contrast enhancement imaging is
particularly useful in the assessment of patients with pre-
existing non-MR conditional cardiac devices. Delayed Fig. 24.32 CCTA axial view demonstrating fibrofatty replacement of
right ventricular myocardium, low-attenuation trabeculations, and right
enhancement imaging with CCTA can image fibrosis asso- ventricular free wall scalloping in arrhythmogenic right ventricular car-
ciated with myocardial infarction [163–165]. Lipomatous diomyopathy. A right ventricular defibrillation lead is present with
metaplasia of areas of chronic myocardial infarction can be beam hardening artifact.
identified with CT [166]. CCTA delayed contrast enhance-
ment can characterize dense areas of fibrosis in hypertro-
phic cardiomyopathy [167]. dia ablation [175]. Multiple techniques have been used to
The diagnosis of arrhythmogenic right ventricular cardio- integrate CCTA images into modalities for mapping and abla-
myopathy/dysplasia involves criteria including clinical and tion of ventricular tachycardia circuits. CCTA delayed con-
family history, electrophysiologic findings, and right ventric- trast enhancement imaging of infarct scar has been used to
ular structural, functional and tissue pathology abnormalities facilitate epicardial ablation of a ventricular tachycardia cir-
[168, 169]. Although CMR imaging has been the diagnostic cuit in the setting of an ICD [176]. Myocardial infarct scar
imaging modality of choice, CCTA can also visualize the related ventricular tachycardia circuits have been ablated in
anatomic features associated with arrhythmogenic right ven- sinus rhythm, facilitated by integration of single-photon
tricular cardiomyopathy/dysplasia, such as epicardial and emission CT, CCTA, and electroanatomic mapping [177].
myocardial fat, low-attenuation trabeculations, right ventricu- Facilitation of ventricular tachycardia ablation through fusion
lar free wall scalloping, right ventricular enlargement, and imaging of delayed enhancement CMR, CCTA and electro-
global and regional right ventricular wall motion abnormali- anatomic mapping for ablation of ventricular tachycardia has
ties (Fig. 24.32) [170, 171]. Biventricular involvement in been performed [178]. CCTA has also demonstrated evidence
arrhythmogenic right ventricular cardiomyopathy/dysplasia of microvascular obstruction after radiofrequency ablation of
by CCTA has also been seen [172]. ventricular tachycardia as evidenced by wall motion abnor-
malities, first pass hypoenhancement and delayed contrast
hyperenhancement correlating with CMR [179].
Ventricular Tachycardia Ablation For patients with congenital heart disease undergoing
supraventricular and ventricular tachycardia ablation, CMR
CCTA can be useful in the planning and performance of abla- also characterizes important anatomy for procedural plan-
tion for ventricular tachycardia. CT can define areas of wall ning. Important findings on CMR include ventricular septal
thinning which correlate with areas of low voltage and abnor- defects, ventricular thrombus, baffle pathways to the ventri-
mal ventricular activity important to ventricular tachycardia cles, and myocardial fibrosis. Pressure and volume overload
circuits [173]. CT defined areas of lipomatous metaplasia in from unrepaired and repaired congenital lesions as well as
regions of chronic myocardial infarction can be defined and atrial and ventricular surgical incisions lead to fibrosis and
may have relevance to critical sites of ventricular tachycardia therefore arrhythmia substrate [180–185]. Challenges of ven-
circuits [174]. The combined integration of CMR assessment tricular tachycardia ablation include mapping during ventric-
of fibrosis and CCTA derived wall thinning and location of ular arrhythmias with attendant risk of hemodynamic
the coronary arteries with electroanatomic mapping is feasi- instability. Characterization of critical isthmuses based on
ble and provides important features for ventricular tachycar- advanced cardiac imaging are useful to ablation of ventricular
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 475

tachycardia circuits while the patient is in sinus rhythm. CCTA for Device Therapies
Ventricular tachycardia incisional reentry isthmuses in oper-
ated congenital heart disease can be defined and ablated in CCTA can visualize the coronary venous system and may
sinus rhythm by spanning isthmuses between annuli and scar/ potentially play an important role in cardiac resynchroniza-
patch [186]. The combination of remote magnetic navigation, tion therapy (CRT) [60, 188]. CRT is used to optimize cardiac
3-D image integration, and electroanatomic mapping has function through resynchronization of ventricular contraction
facilitated safe and feasible ablation in patients with complex in patients with dilated ischemic and non-ischemic cardiomy-
congenital anomalies [187]. opathy, ventricular conduction abnormalities, and moderate
to severe heart failure. With CRT, a pacing lead is placed in a
branch vessel of the coronary venous system to achieve left
ventricular pacing. As opposed to the right atrial and right
ventricular leads, which can be actively fixated in many posi-
tions in their respective chambers with relative ease, place-
ment of the coronary venous lead can be challenging, as lead
position is limited by the individual confines and variation of
the existing coronary venous anatomy.
CCTA coronary venous imaging can provide roadmaps
for lead placement, with potential avoidance of a percuta-
neous approach in the setting of inadequate anatomy.
Detailed assessment of the coronary venous anatomy
includes coronary sinus diameter, 3-D location of branch
vessels relative to the left ventricle myocardial segments ,
branch vessel diameter and angulation off of the coronary
sinus/great cardiac vein (Figs. 24.33 and 24.34, Videos 13
and 14) [60]. CCTA can also visualize structures which
could complicate access to the coronary venous system,
such as a prominent Thebesian valve covering the coronary
sinus ostium (Fig. 24.35) [189]. Other abnormalities, such
as coronary sinus diverticulae, left superior vena cava to
coronary sinus connections, and unroofed coronary sinuses
can also be identified (Figs. 24.36 and 24.37). Visualization
of the phrenic nerve and its relation to the coronary venous
anatomy may be important to lead placement in order to
Fig. 24.33 3-D volume rendered image demonstrating visualization of
avoid diaphragmatic pacing (Fig. 24.38) [190]. CCTA is
the coronary venous system including the coronary sinus (double white
arrow), a middle cardiac vein (black arrow), and a posterolateral vein deemed appropriate for the assessment of coronary venous
(single white arrow) imaging for CRT [191–193].

Fig. 24.34 CCTA 3-D views demonstrating localization of the myocardial segment associated with the distal portion of the posterolateral vein
(arrows)
476 J.S. Shinbane et al.

Fig. 24.37 3-D volume rendered view demonstrating a left superior

vena cava with connection to an aneurysmal coronary sinus. A right-
sided superior vena cava was not present

Fig. 24.35 Axial images at the coronary sinus os level demonstrating

a prominent Thebesian valve. CS coronary sinus, RA right atrium, RV
right ventricle, and LV left ventricle (Reprinted from Shinbane et al.
[189] with permission from John Wiley and Sons)

Fig. 24.38 3-D volume rendered image showing visualization of the

course (a–e) of the left phrenic nerve (Reprinted from Matsumoto et al.
[190] with permission from Elsevier)

catheters [194]. CCTA fusion with fluoroscopy has been per-

formed preliminarily with accurate fusion of structures
Fig. 24.36 CCTA demonstrating a coronary sinus diverticulum
(arrow). CS coronary sinus, DV diverticulum, GV great cardiac vein, IV [195]. CCTA can be used to plan CRT approach when obsta-
inferior vena cava, LA left atrium, MV marginal vein, and RA right cles to standard approaches are identified. CCTA delineation
atrium of ostial abnormalities limiting access to the coronary sinus
ostium have permitted procedural planning and facilitation
Preliminary data suggest that pre-procedure knowledge of of alternate approaches to endovascular access rather than
the 3-D coronary venous anatomy can facilitate procedures proceeding to epicardial lead placement (Fig. 24.39) [196].
through decreased procedure time and utilization of guide CCTA defined assessment of the location of the coronary
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 477

a b

c d

Fig. 24.39 Double cannulation approach to coronary venous lead engaged in the coronary sinus ostium (black arrow) with a torque wire
placement in the setting of a prominent Thebesian valve. Panel (a): 2-D extending into the great cardiac vein (double black arrow) and 7-French
axial view (a) demonstrating a well-formed and prominent Thebesian steerable decapolar coronary sinus catheter from the right femoral vein
valve (black arrow) covering the coronary sinus ostium. Serial intrapro- (white arrow) (RAO view). Panel (d): 7-French multipurpose outer and
cedure fluoroscopy images showing the sequential stages of coronary inner sheath have been pulled back to the mid right atrium (black
sinus cannulation and coronary venous left ventricular lead placement. arrow). The torque wire from left subclavian approach (double black
Panel (b): placement of 7 French steerable decapolar coronary sinus arrow) and 7-French steerable decapolar coronary sinus catheter from
catheter (white arrow) from a right femoral vein into the coronary sinus the right femoral vein (white arrow) have been advanced further into
ostium (right anterior oblique [RAO] view). Panels (c and d): coaxial the great cardiac vein (RAO view) (Reprinted from Cao et al. [196] with
alignment of both 7-French multipurpose sheath with the inner sheath permission from John Wiley and Sons)
478 J.S. Shinbane et al.

a b

c d

Fig. 24.40 2-D (a) and 3-D (b–d) views demonstrating anterior rota- placement in a patient with coronary venous anatomy not amenable to
tion of the left ventricle and relation to skeletal structures useful to plan- a percutaneous approach to cardiac resynchronization therapy
ning a minimally invasive approach to epicardial left ventricular lead

sinus ostium in relation to the floor of the right atrium has cardium and can also demonstrate the presence of pericardial
been identified as a factor leading to challenging CRT coro- effusion [200–203].
nary venous lead placement with a high coronary sinus Non-response is an issue in approximately one third of
ostium [197]. In cases where the coronary venous anatomy is patients undergoing CRT. The correlation between CCTA
not amenable to a venous approach to left ventricular lead visualized sites of coronary venous branch veins and echo
placement, CCTA can facilitate planning of approach to derived area of latest mechanical activation has been asso-
epicardial lead placement (Fig. 24.40). Postprocedurally, ciated with acute response to CRT, with lack of response
CCTA is useful for 3-D assessment of pacemaker and ICD associated with disparity in location between these sites
lead placement. With CRT, postprocedure CT was more [204]. The CMR literature has shown that the amount and
accurate than fluoroscopy and chest x-ray for documentation location of myocardial infarct scar is important to CRT
of exact lead position [198, 199]. CCTA can detect lead per- response. The percent total scar derived from delayed gad-
foration as evidenced by a lead tip visualized beyond the epi- olinium enhancement imaging has predicted response to
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 479

CRT, with greater response in patients with less than 15 % designs. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn
percent total scar and poor response in patients with pos- Reson. 2011;13:63.
11. Shinbane JS, Colletti PM, Shellock FG. MR imaging in patients
terolateral scar [205–207]. CCTA delayed contrast enhance- with pacemakers and other devices: engineering the future. JACC
ment imaging for assessment of non-response requires Cardiovasc Imaging. 2012;5(3):332–3.
study. Comprehensive analysis of factors important to 12. Wilkoff BL, Bello D, Taborsky M, Vymazal J, Kanal E, Heuer H,
response to CRT including coronary venous anatomy, 3-D et al. Magnetic resonance imaging in patients with a pacemaker
system designed for the magnetic resonance environment. Heart
global and regional ventricular function, and delayed Rhythm Off J Heart Rhythm Soc. 2011;8(1):65–73.
enhancement require further assessment for CRT planning 13. Gupta A, Subhas N, Primak AN, Nittka M, Liu K. Metal arti-
and facilitation to maximize response. fact reduction: standard and advanced magnetic resonance and
computed tomography techniques. Radiol Clin North Am. 2015;
53(3):531–47.
Conclusions 14. Stevens SM, Tung R, Rashid S, Gima J, Cote S, Pavez G, et al.
CCTA provides extensive imaging data important to the Device artifact reduction for magnetic resonance imaging of
diagnosis and treatment of electrophysiologically-relevant patients with implantable cardioverter-defibrillators and ventricu-
cardiovascular disease. Advanced cardiac imaging has fur- lar tachycardia: late gadolinium enhancement correlation with
electroanatomic mapping. Heart Rhythm Off J Heart Rhythm Soc.
thered the field of cardiac electrophysiology and will con- 2014;11(2):289–98.
tinue to have an impact through application to a greater 15. Abecasis J, Dourado R, Ferreira A, Saraiva C, Cavaco D, Santos
spectrum of arrhythmogenic substrates as well as ablation KR, et al. Left atrial volume calculated by multi-detector com-
and device procedures. puted tomography may predict successful pulmonary vein isola-
tion in catheter ablation of atrial fibrillation. Europace Eur Pacing
Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac
Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol.
References 2009;11(10):1289–94.
16. Helms AS, West JJ, Patel A, Lipinski MJ, Mangrum JM, Mounsey
1. Matsutani H, Sano T, Kondo T, Morita H, Arai T, Sekine T, et al. JP, et al. Relation of left atrial volume from three-dimensional com-
ECG-edit function in multidetector-row computed tomography cor- puted tomography to atrial fibrillation recurrence following abla-
onary arteriography for patients with arrhythmias. Circ J Off J Jpn tion. Am J Cardiol. 2009;103(7):989–93.
Circ Soc. 2008;72(7):1071–8. 17. Lin FY, Devereux RB, Roman MJ, Meng J, Jow VM, Jacobs A,
2. Shinbane JS. Cardiovascular computed tomographic angiogra- et al. Cardiac chamber volumes, function, and mass as deter-
phy in patients with atrial fibrillation: challenges of anatomy, mined by 64-multidetector row computed tomography: mean val-
physiology, and electrophysiology. J Cardiovasc Comput Tomogr. ues among healthy adults free of hypertension and obesity. JACC
2008;2(3):181–2. Cardiovasc Imaging. 2008;1(6):782–6.
3. Tsiflikas I, Drosch T, Brodoefel H, Thomas C, Reimann A, Till A, 18. Mahabadi AA, Samy B, Seneviratne SK, Toepker MH, Bamberg F,
et al. Diagnostic accuracy and image quality of cardiac dual-source Hoffmann U, et al. Quantitative assessment of left atrial volume by
computed tomography in patients with arrhythmia. Int J Cardiol. electrocardiographic-gated contrast-enhanced multidetector com-
2010;143(1):79–85. puted tomography. J Cardiovasc Comput Tomogr. 2009;3(2):80–7.
4. Sohns C, Kruse S, Vollmann D, Luthje L, Dorenkamp M, Seegers 19. Christiaens L, Varroud-Vial N, Ardilouze P, Ragot S, Mergy J,
J, et al. Accuracy of 64-multidetector computed tomography coro- Bonnet B, et al. Real three-dimensional assessment of left atrial
nary angiography in patients with symptomatic atrial fibrillation and left atrial appendage volumes by 64-slice spiral computed
prior to pulmonary vein isolation. Eur Heart J Cardiovasc Imaging. tomography in individuals with or without cardiovascular disease.
2012;13(3):263–70. Int J Cardiol. 2010;140(2):189–96.
5. Lee AM, Engel LC, Shah B, Liew G, Sidhu MS, Kalra M, et al. 20. Wolf F, Ourednicek P, Loewe C, Richter B, Gossinger HD,
Coronary computed tomography angiography during arrhythmia: Gwechenberger M, et al. Evaluation of left atrial function by mul-
radiation dose reduction with prospectively ECG-triggered axial tidetector computed tomography before left atrial radiofrequency-
and retrospectively ECG-gated helical 128-slice dual-source CT. J catheter ablation: comparison of a manual and automated 3D
Cardiovasc Comput Tomogr. 2012;6(3):172–83.e2. volume segmentation method. Eur J Radiol. 2010;75(2):e141–6.
6. Sidhu MS, Venkatesh V, Hoffmann U, Ghoshhajra BB. Advanced 21. Agner BF, Kuhl JT, Linde JJ, Kofoed KF, Akeson P, Rasmussen
adaptive axial-sequential prospectively electrocardiogram-triggered BV, et al. Assessment of left atrial volume and function in patients
dual-source coronary computed tomographic angiography in a patient with permanent atrial fibrillation: comparison of cardiac magnetic
with atrial fibrillation. J Comput Assist Tomogr. 2011;35(6):747–8. resonance imaging, 320-slice multi-detector computed tomogra-
7. Rist C, Johnson TR, Muller-Starck J, Arnoldi E, Saam T, Becker A, phy, and transthoracic echocardiography. Eur Heart J Cardiovasc
et al. Noninvasive coronary angiography using dual-source com- Imaging. 2014;15(5):532–40.
puted tomography in patients with atrial fibrillation. Invest Radiol. 22. Pontone G, Andreini D, Bertella E, Petulla M, Russo E, Innocenti
2009;44(3):159–67. E, et al. Comparison of cardiac computed tomography versus car-
8. Oda S, Honda K, Yoshimura A, Katahira K, Noda K, Oshima S, diac magnetic resonance for characterization of left atrium anatomy
et al. 256-Slice coronary computed tomographic angiography in before radiofrequency catheter ablation of atrial fibrillation. Int
patients with atrial fibrillation: optimal reconstruction phase and J Cardiol. 2015;179:114–21.
image quality. Eur Radiol. 2016;26(1):55–63. 23. Kaseno K, Tada H, Koyama K, Jingu M, Hiramatsu S, Yokokawa M,
9. Shinbane JS, Colletti PM, Shellock FG. MR in patients with pace- et al. Prevalence and characterization of pulmonary vein variants in
makers and ICDs: defining the issues. J Cardiovasc Magn Reson patients with atrial fibrillation determined using 3-dimensional com-
Off J Soc Cardiovasc Magnetic Reson. 2007;9(1):5–13. puted tomography. Am J Cardiol. 2008;101(11):1638–42.
10. Shinbane JS, Colletti PM, Shellock FG. Magnetic resonance imag- 24. Dewland TA, Wintermark M, Vaysman A, Smith LM, Tong E,
ing in patients with cardiac pacemakers: era of “MR Conditional” Vittinghoff E, et al. Use of computed tomography to identify atrial
480 J.S. Shinbane et al.

fibrillation associated differences in left atrial wall thickness and 39. Segerson NM, Daccarett M, Badger TJ, Shabaan A, Akoum N,
density. Pacing Clin Electrophysiol PACE. 2013;36(1):55–62. Fish EN, et al. Magnetic resonance imaging-confirmed ablative
25. Suenari K, Nakano Y, Hirai Y, Ogi H, Oda N, Makita Y, et al. Left debulking of the left atrial posterior wall and septum for treatment
atrial thickness under the catheter ablation lines in patients with of persistent atrial fibrillation: rationale and initial experience.
paroxysmal atrial fibrillation: insights from 64-slice multidetector J Cardiovasc Electrophysiol. 2010;21(2):126–32.
computed tomography. Heart Vessels. 2013;28(3):360–8. 40. Akoum N, Daccarett M, McGann C, Segerson N, Vergara G,
26. Makita Y, Nakano Y, Oda N, Suenari K, Sairaku A, Kajihara K, Kuppahally S, et al. Atrial fibrosis helps select the appropri-
et al. Use of preprocedural multidetector computed tomography to ate patient and strategy in catheter ablation of atrial fibrilla-
decrease atrial fibrillation recurrence following extensive encircling tion: a DE-MRI guided approach. J Cardiovasc Electrophysiol.
circumferential pulmonary vein isolation. J Cardiol. 2012;60(3): 2011;22(1):16–22.
236–41. 41. Mahnkopf C, Badger TJ, Burgon NS, Daccarett M, Haslam
27. Hanazawa K, Kaitani K, Hayama Y, Onishi N, Tamaki Y, Miyake TS, Badger CT, et al. Evaluation of the left atrial substrate in
M, et al. Effect of radiofrequency catheter ablation of persistent patients with lone atrial fibrillation using delayed-enhanced
atrial fibrillation on the left atrial function: assessment by 320-row MRI: implications for disease progression and response to cath-
multislice computed tomography. Int J Cardiol. 2015;179:449–54. eter ablation. Heart Rhythm Off J Heart Rhythm Soc. 2010;7(10):
28. Bisbal F, Guiu E, Cabanas P, Calvo N, Berruezo A, Tolosana JM, 1475–81.
et al. Reversal of spherical remodelling of the left atrium after 42. Ling LH, McLellan AJ, Taylor AJ, Iles LM, Ellims AH, Kumar S,
pulmonary vein isolation: incidence and predictors. Europace Eur et al. Magnetic resonance post-contrast T1 mapping in the human
Pacing Arrhythmias Cardiac Electrophysiol J Working Groups atrium: validation and impact on clinical outcome after catheter
Cardiac Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc ablation for atrial fibrillation. Heart Rhythm Off J Heart Rhythm
Cardiol. 2014;16(6):840–7. Soc. 2014;11(9):1551–9.
29. Tsao HM, Hu WC, Wu MH, Tai CT, Chang SL, Lin YJ, et al. The 43. Ling Z, McManigle J, Zipunnikov V, Pashakhanloo F, Khurram
impact of catheter ablation on the dynamic function of the left atrium IM, Zimmerman SL, et al. The association of left atrial low-voltage
in patients with atrial fibrillation: insights from four-dimensional regions on electroanatomic mapping with low attenuation regions
computed tomographic images. J Cardiovasc Electrophysiol. on cardiac computed tomography perfusion imaging in patients
2010;21(3):270–7. with atrial fibrillation. Heart Rhythm Off J Heart Rhythm Soc.
30. Oakes RS, Badger TJ, Kholmovski EG, Akoum N, Burgon NS, 2015;12(5):857–64.
Fish EN, et al. Detection and quantification of left atrial structural 44. Scharf C, Sneider M, Case I, Chugh A, Lai SW, Pelosi Jr F, et al.
remodeling with delayed-enhancement magnetic resonance imag- Anatomy of the pulmonary veins in patients with atrial fibrilla-
ing in patients with atrial fibrillation. Circulation. 2009;119(13): tion and effects of segmental ostial ablation analyzed by computed
1758–67. tomography. J Cardiovasc Electrophysiol. 2003;14(2):150–5.
31. Akoum N, McGann C, Vergara G, Badger T, Ranjan R, Mahnkopf 45. Jongbloed MR, Dirksen MS, Bax JJ, Boersma E, Geleijns K, Lamb
C, et al. Atrial fibrosis quantified using late gadolinium enhance- HJ, et al. Atrial fibrillation: multi-detector row CT of pulmonary
ment MRI is associated with sinus node dysfunction requiring vein anatomy prior to radiofrequency catheter ablation–initial expe-
pacemaker implant. J Cardiovasc Electrophysiol. 2012;23(1): rience. Radiology. 2005;234(3):702–9.
44–50. 46. Hamdan A, Charalampos K, Roettgen R, Wellnhofer E, Gebker
32. Daccarett M, Badger TJ, Akoum N, Burgon NS, Mahnkopf C, R, Paetsch I, et al. Magnetic resonance imaging versus computed
Vergara G, et al. Association of left atrial fibrosis detected by tomography for characterization of pulmonary vein morphology
delayed-enhancement magnetic resonance imaging and the risk before radiofrequency catheter ablation of atrial fibrillation. Am
of stroke in patients with atrial fibrillation. J Am Coll Cardiol. J Cardiol. 2009;104(11):1540–6.
2011;57(7):831–8. 47. Wood MA, Wittkamp M, Henry D, Martin R, Nixon JV, Shepard
33. Habibi M, Lima JA, Khurram IM, Zimmerman SL, Zipunnikov V, RK, et al. A comparison of pulmonary vein ostial anatomy by
Fukumoto K, et al. Association of left atrial function and left atrial computerized tomography, echocardiography, and venography in
enhancement in patients with atrial fibrillation: cardiac magnetic patients with atrial fibrillation having radiofrequency catheter abla-
resonance study. Circ Cardiovasc Imaging. 2015;8(2), e002769. tion. Am J Cardiol. 2004;93(1):49–53.
34. Marrouche NF, Wilber D, Hindricks G, Jais P, Akoum N, 48. To AC, Gabriel RS, Park M, Lowe BS, Curtin RJ, Sigurdsson G,
Marchlinski F, et al. Association of atrial tissue fibrosis identified et al. Role of transesophageal echocardiography compared to com-
by delayed enhancement MRI and atrial fibrillation catheter abla- puted tomography in evaluation of pulmonary vein ablation for
tion: the DECAAF study. JAMA. 2014;311(5):498–506. atrial fibrillation (ROTEA study). J Am Soc Echocardiogr Off Publ
35. Akoum N, Wilber D, Hindricks G, Jais P, Cates J, Marchlinski Am Soc Echocardiogr. 2011;24(9):1046–55.
F, et al. MRI assessment of ablation-induced scarring in atrial 49. Robbins IM, Colvin EV, Doyle TP, Kemp WE, Loyd JE, McMahon
fibrillation: analysis from the DECAAF study. J Cardiovasc WS, et al. Pulmonary vein stenosis after catheter ablation of atrial
Electrophysiol. 2015;26(5):473–80. fibrillation. Circulation. 1998;98(17):1769–75.
36. McGann C, Akoum N, Patel A, Kholmovski E, Revelo P, Damal K, 50. Packer DL, Keelan P, Munger TM, Breen JF, Asirvatham S,
et al. Atrial fibrillation ablation outcome is predicted by left atrial Peterson LA, et al. Clinical presentation, investigation, and man-
remodeling on MRI. Circ Arrhythm Electrophysiol. 2014;7(1): agement of pulmonary vein stenosis complicating ablation for atrial
23–30. fibrillation. Circulation. 2005;111(5):546–54.
37. Fukumoto K, Habibi M, Gucuk Ipek E, Khurram IM, Zimmerman 51. Dong J, Vasamreddy CR, Jayam V, Dalal D, Dickfeld T, Eldadah
SL, Zipunnikov V, et al. Comparison of preexisting and ablation- Z, et al. Incidence and predictors of pulmonary vein stenosis fol-
induced late gadolinium enhancement on left atrial magnetic lowing catheter ablation of atrial fibrillation using the anatomic
resonance imaging. Heart Rhythm Off J Heart Rhythm Soc. pulmonary vein ablation approach: results from paired magnetic
2015;12(4):668–72. resonance imaging. J Cardiovasc Electrophysiol. 2005;16(8):
38. Badger TJ, Daccarett M, Akoum NW, Adjei-Poku YA, Burgon NS, 845–52.
Haslam TS, et al. Evaluation of left atrial lesions after initial and 52. Sigurdsson G, Troughton RW, Xu XF, Salazar HP, Wazni OM,
repeat atrial fibrillation ablation: lessons learned from delayed- Grimm RA, et al. Detection of pulmonary vein stenosis by trans-
enhancement MRI in repeat ablation procedures. Circ Arrhythm esophageal echocardiography: comparison with multidetector com-
Electrophysiol. 2010;3(3):249–59. puted tomography. Am Heart J. 2007;153(5):800–6.
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 481

53. Martinek M, Nesser HJ, Aichinger J, Boehm G, Purerfellner compared with segmentation from pre-acquired computed tomog-
H. Impact of integration of multislice computed tomography raphy scan-implications for ablation strategy. Europace Eur Pacing
imaging into three-dimensional electroanatomic mapping on clini- Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac
cal outcomes, safety, and efficacy using radiofrequency ablation Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol.
for atrial fibrillation. Pacing Clin Electrophysiol PACE. 2007; 2014;16(9):1304–8.
30(10):1215–23. 69. Jang SW, Kwon BJ, Choi MS, Kim DB, Shin WS, Cho EJ, et al.
54. Wongcharoen W, Tsao HM, Wu MH, Tai CT, Chang SL, Lin YJ, Computed tomographic analysis of the esophagus, left atrium, and
et al. Preexisting pulmonary vein stenosis in patients undergo- pulmonary veins: implications for catheter ablation of atrial fibril-
ing atrial fibrillation ablation: a report of five cases. J Cardiovasc lation. J Interv Cardiac Electrophysiol Int J Arrhythmias Pacing.
Electrophysiol. 2006;17(4):423–5. 2011;32(1):1–6.
55. Rostamian A, Narayan SM, Thomson L, Fishbein M, Siegel RJ. The 70. Lemola K, Mueller G, Desjardins B, Sneider M, Case I, Good E,
incidence, diagnosis, and management of pulmonary vein stenosis et al. Topographic analysis of the coronary sinus and major cardiac
as a complication of atrial fibrillation ablation. J Interv Cardiac veins by computed tomography. Heart Rhythm Off J Heart Rhythm
Electrophysiol Int J Arrhythmias Pacing. 2014;40(1):63–74. Soc. 2005;2(7):694–9.
56. Saad EB, Marrouche NF, Saad CP, Ha E, Bash D, White RD, 71. Wu MH, Wongcharoen W, Tsao HM, Tai CT, Chang SL, Lin
et al. Pulmonary vein stenosis after catheter ablation of atrial YJ, et al. Close relationship between the bronchi and pulmo-
fibrillation: emergence of a new clinical syndrome. Ann Intern nary veins: implications for the prevention of atriobronchial fis-
Med. 2003;138(8):634–8. tula after atrial fibrillation ablation. J Cardiovasc Electrophysiol.
57. Saad EB, Rossillo A, Saad CP, Martin DO, Bhargava M, Erciyes D, 2007;18(10):1056–9.
et al. Pulmonary vein stenosis after radiofrequency ablation of atrial 72. Li YG, Yang M, Li Y, Wang Q, Yu L, Sun J. Spatial relationship
fibrillation: functional characterization, evolution, and influence of between left atrial roof or superior pulmonary veins and bron-
the ablation strategy. Circulation. 2003;108(25):3102–7. chi or pulmonary arteries by dual-source computed tomogra-
58. Krishnaswamy A, Tuzcu EM, Kapadia SR. Integration of MDCT phy: implication for preventing injury of bronchi and pulmonary
and fluoroscopy using C-arm computed tomography to guide struc- arteries during atrial fibrillation ablation. Europace Eur Pacing
tural cardiac interventions in the cardiac catheterization labora- Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac
tory. Catheter Cardiovasc Interv Off J Soc Cardiac Angiogr Interv. Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol.
2015;85(1):139–47. 2011;13(6):809–14.
59. Peng LQ, Yu JQ, Yang ZG, Wu D, Xu JJ, Chu ZG, et al. Left atrial 73. Desai AK, Osahan DS, Undavia MB, Nair GB. Bronchial injury
diverticula in patients referred for radiofrequency ablation of atrial post-cryoablation for atrial fibrillation. Ann Am Thorac Soc.
fibrillation: assessment of prevalence and morphologic charac- 2015;12(7):1103–4.
teristics by dual-source computed tomography. Circ Arrhythm 74. Squara F, Desjardins B, Marchlinski FE, Supple GE. Prospective
Electrophysiol. 2012;5(2):345–50. 3-dimensional computed tomography segmentation of the pericar-
60. Mao S, Shinbane JS, Girsky MJ, Child J, Carson S, Oudiz RJ, et al. diac right phrenic nerve in the setting of atrial fibrillation ablation.
Coronary venous imaging with electron beam computed tomographic Circ Arrhythm Electrophysiol. 2014;7(3):561–2.
angiography: three-dimensional mapping and relationship with coro- 75. Opolski MP, Staruch AD, Kusmierczyk M, Witkowski A,
nary arteries. Am Heart J. 2005;150(2):315–22. Kwiecinska S, Kosek M, et al. Computed tomography angiogra-
61. Chugh A, Makkar A, Yen Ho S, Yokokawa M, Sundaram B, Pelosi phy for prediction of atrial fibrillation after coronary artery bypass
F, et al. Manifestations of coronary arterial injury during catheter grafting: proof of concept. J Cardiol. 2015;65(4):285–92.
ablation of atrial fibrillation and related arrhythmias. Heart Rhythm 76. Wissner E, Wellnitz CV, Srivathsan K, Scott LR, Altemose
Off J Heart Rhythm Soc. 2013;10(11):1638–45. GT. Value of multislice computed tomography angiography of the
62. Saremi F, Channual S, Krishnan S, Gurudevan SV, Narula J, thorax in preparation for catheter ablation for the treatment of atrial
Abolhoda A. Bachmann Bundle and its arterial supply: imag- fibrillation: the impact of unexpected cardiac and extracardiac find-
ing with multidetector CT–implications for interatrial conduction ings on patient care. Eur J Radiol. 2009;72(2):284–8.
abnormalities and arrhythmias. Radiology. 2008;248(2):447–57. 77. Kistler PM, Earley MJ, Harris S, Abrams D, Ellis S, Sporton SC,
63. Pappone C, Oral H, Santinelli V, Vicedomini G, Lang CC, et al. Validation of three-dimensional cardiac image integration:
Manguso F, et al. Atrio-esophageal fistula as a complication of per- use of integrated CT image into electroanatomic mapping sys-
cutaneous transcatheter ablation of atrial fibrillation. Circulation. tem to perform catheter ablation of atrial fibrillation. J Cardiovasc
2004;109(22):2724–6. Electrophysiol. 2006;17(4):341–8.
64. Lemola K, Sneider M, Desjardins B, Case I, Han J, Good E, et al. 78. Sra J, Krum D, Hare J, Okerlund D, Thompson H, Vass M, et al.
Computed tomographic analysis of the anatomy of the left atrium Feasibility and validation of registration of three-dimensional left
and the esophagus: implications for left atrial catheter ablation. atrial models derived from computed tomography with a noncon-
Circulation. 2004;110(24):3655–60. tact cardiac mapping system. Heart Rhythm Off J Heart Rhythm
65. Cury RC, Abbara S, Schmidt S, Malchano ZJ, Neuzil P, Weichet J, Soc. 2005;2(1):55–63.
et al. Relationship of the esophagus and aorta to the left atrium and 79. Heist EK, Chevalier J, Holmvang G, Singh JP, Ellinor PT, Milan
pulmonary veins: implications for catheter ablation of atrial fibrilla- DJ, et al. Factors affecting error in integration of electroanatomic
tion. Heart Rhythm Off J Heart Rhythm Soc. 2005;2(12):1317–23. mapping with CT and MR imaging during catheter ablation of
66. Piorkowski C, Hindricks G, Schreiber D, Tanner H, Weise W, Koch atrial fibrillation. J Interv Cardiac Electrophysiol Int J Arrhythmias
A, et al. Electroanatomic reconstruction of the left atrium, pulmo- Pacing. 2006;17(1):21–7.
nary veins, and esophagus compared with the “true anatomy” on 80. Kistler PM, Rajappan K, Jahngir M, Earley MJ, Harris S, Abrams
multislice computed tomography in patients undergoing catheter D, et al. The impact of CT image integration into an electroana-
ablation of atrial fibrillation. Heart Rhythm Off J Heart Rhythm tomic mapping system on clinical outcomes of catheter ablation
Soc. 2006;3(3):317–27. of atrial fibrillation. J Cardiovasc Electrophysiol. 2006;17(10):
67. Good E, Oral H, Lemola K, Han J, Tamirisa K, Igic P, et al. 1093–101.
Movement of the esophagus during left atrial catheter ablation for 81. Kistler PM, Rajappan K, Harris S, Earley MJ, Richmond L, Sporton
atrial fibrillation. J Am Coll Cardiol. 2005;46(11):2107–10. SC, et al. The impact of image integration on catheter ablation of
68. Gavin AR, Singleton CB, McGavigan AD. Assessment of atrial fibrillation using electroanatomic mapping: a prospective ran-
oesophageal position by direct visualization with luminal contrast domized study. Eur Heart J. 2008;29(24):3029–36.
482 J.S. Shinbane et al.

82. Haissaguerre M, Hocini M, Sanders P, Sacher F, Rotter M, 97. Shapiro MD, Neilan TG, Jassal DS, Samy B, Nasir K, Hoffmann U,
Takahashi Y, et al. Catheter ablation of long-lasting persistent et al. Multidetector computed tomography for the detection of left
atrial fibrillation: clinical outcome and mechanisms of subsequent atrial appendage thrombus: a comparative study with transesopha-
arrhythmias. J Cardiovasc Electrophysiol. 2005;16(11):1138–47. geal echocardiography. J Comput Assist Tomogr. 2007;31(6):905–9.
83. Chae S, Oral H, Good E, Dey S, Wimmer A, Crawford T, et al. Atrial 98. Hur J, Kim YJ, Nam JE, Choe KO, Choi EY, Shim CY, et al.
tachycardia after circumferential pulmonary vein ablation of atrial Thrombus in the left atrial appendage in stroke patients: detection
fibrillation: mechanistic insights, results of catheter ablation, and with cardiac CT angiography--a preliminary report. Radiology.
risk factors for recurrence. J Am Coll Cardiol. 2007;50(18):1781–7. 2008;249(1):81–7.
84. Aleong R, Heist EK, Ruskin JN, Mansour M. Integration of intra- 99. Patel A, Au E, Donegan K, Kim RJ, Lin FY, Stein KM, et al.
cardiac echocardiography with magnetic resonance imaging allows Multidetector row computed tomography for identification of left
visualization of the esophagus during catheter ablation of atrial atrial appendage filling defects in patients undergoing pulmonary
fibrillation. Heart Rhythm Off J Heart Rhythm Soc. 2008;5(7):1088. vein isolation for treatment of atrial fibrillation: comparison with
85. Jongbloed MR, Bax JJ, van der Wall EE, Schalij MJ. Thrombus in transesophageal echocardiography. Heart Rhythm Off J Heart
the left atrial appendage detected by intracardiac echocardiography. Rhythm Soc. 2008;5(2):253–60.
Int J Cardiovasc Imaging. 2004;20(2):113–6. 100. Tang RB, Dong JZ, Zhang ZQ, Li ZA, Liu XP, Kang JP, et al.
86. Lakkireddy D, Rangisetty U, Prasad S, Verma A, Biria M, Comparison of contrast enhanced 64-slice computed tomog-
Berenbom L, et al. Intracardiac echo-guided radiofrequency cath- raphy and transesophageal echocardiography in detection of
eter ablation of atrial fibrillation in patients with atrial septal defect left atrial thrombus in patients with atrial fibrillation. J Interv
or patent foramen ovale repair: a feasibility, safety, and efficacy Cardiac Electrophysiol Int J Arrhythmias Pacing. 2008;22(3):
study. J Cardiovasc Electrophysiol. 2008;19(11):1137–42. 199–203.
87. den Uijl DW, Tops LF, Tolosana JM, Schuijf JD, Trines SA, 101. Gottlieb I, Pinheiro A, Brinker JA, Corretti MC, Mayer SA,
Zeppenfeld K, et al. Real-time integration of intracardiac echocar- Bluemke DA, et al. Diagnostic accuracy of arterial phase 64-slice
diography and multislice computed tomography to guide radiofre- multidetector CT angiography for left atrial appendage thrombus
quency catheter ablation for atrial fibrillation. Heart Rhythm Off in patients undergoing atrial fibrillation ablation. J Cardiovasc
J Heart Rhythm Soc. 2008;5(10):1403–10. Electrophysiol. 2008;19(3):247–51.
88. Ren JF, Marchlinski FE, Callans DJ. Left atrial thrombus associated 102. Ishiyama M, Akaike G, Matsusako M, Ueda T, Makidono A,
with ablation for atrial fibrillation: identification with intracardiac Ohde S, et al. Severity of pseudofilling defect in the left atrial
echocardiography. J Am Coll Cardiol. 2004;43(10):1861–7. appendage on cardiac computed tomography is a simple predictor
89. Saliba W, Thomas J. Intracardiac echocardiography during of the degree of left atrial emptying dysfunction in patients with
catheter ablation of atrial fibrillation. Europace Eur Pacing chronic atrial fibrillation. J Comput Assist Tomogr. 2012;36(4):
Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac 450–4.
Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol. 103. Hur J, Kim YJ, Lee HJ, Ha JW, Heo JH, Choi EY, et al. Left atrial
2008;10 Suppl 3:iii42–7. appendage thrombi in stroke patients: detection with two-phase
90. Knecht S, Skali H, O’Neill MD, Wright M, Matsuo S, Chaudhry cardiac CT angiography versus transesophageal echocardiogra-
GM, et al. Computed tomography-fluoroscopy overlay evaluation phy. Radiology. 2009;251(3):683–90.
during catheter ablation of left atrial arrhythmia. Europace Eur 104. Sawit ST, Garcia-Alvarez A, Suri B, Gaztanaga J, Fernandez-
Pacing Arrhythmias Cardiac Electrophysiol J Working Groups Friera L, Mirelis JG, et al. Usefulness of cardiac computed
Cardiac Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc tomographic delayed contrast enhancement of the left atrial
Cardiol. 2008;10(8):931–8. appendage before pulmonary vein ablation. Am J Cardiol. 2012;
91. Ejima K, Shoda M, Yagishita D, Futagawa K, Yashiro B, Sato T, 109(5):677–84.
et al. Image integration of three-dimensional cone-beam computed 105. Romero J, Husain SA, Kelesidis I, Sanz J, Medina HM, Garcia
tomography angiogram into electroanatomical mapping system to MJ. Detection of left atrial appendage thrombus by cardiac
guide catheter ablation of atrial fibrillation. Europace Eur Pacing computed tomography in patients with atrial fibrillation: a meta-
Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac analysis. Circ Cardiovasc Imaging. 2013;6(2):185–94.
Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol. 106. Tani T, Yamakami S, Matsushita T, Okamoto M, Toyama J,
2010;12(1):45–51. Suzuki S, et al. Usefulness of electron beam tomography in the
92. Qamruddin S, Shinbane J, Shriki J, Naqvi TZ. Left atrial append- prone position for detecting atrial thrombi in chronic atrial fibril-
age: structure, function, imaging modalities and therapeutic lation. J Comput Assist Tomogr. 2003;27(1):78–84.
options. Expert Rev Cardiovasc Ther. 2010;8(1):65–75. 107. Kim YY, Klein AL, Halliburton SS, Popovic ZB, Kuzmiak SA,
93. Garcia MJ. Detection of left atrial appendage thrombus by car- Sola S, et al. Left atrial appendage filling defects identified by
diac computed tomography: a word of caution. JACC Cardiovasc multidetector computed tomography in patients undergoing
Imaging. 2009;2(1):77–9. radiofrequency pulmonary vein antral isolation: a compari-
94. Saremi F, Channual S, Gurudevan SV, Narula J, Abolhoda son with transesophageal echocardiography. Am Heart J. 2007;
A. Prevalence of left atrial appendage pseudothrombus fill- 154(6):1199–205.
ing defects in patients with atrial fibrillation undergoing coro- 108. Choi BH, Ko SM, Hwang HK, Song MG, Shin JK, Kang WS,
nary computed tomography angiography. J Cardiovasc Comput et al. Detection of left atrial thrombus in patients with mitral ste-
Tomogr. 2008;2(3):164–71. nosis and atrial fibrillation: retrospective comparison of two-phase
95. Martinez MW, Kirsch J, Williamson EE, Syed IS, Feng D, Ommen computed tomography, transoesophageal echocardiography and
S, et al. Utility of nongated multidetector computed tomography surgical findings. Eur Radiol. 2013;23(11):2944–53.
for detection of left atrial thrombus in patients undergoing cath- 109. Hur J, Pak HN, Kim YJ, Lee HJ, Chang HJ, Hong YJ, et al.
eter ablation of atrial fibrillation. JACC Cardiovasc Imaging. Dual-enhancement cardiac computed tomography for assess-
2009;2(1):69–76. ing left atrial thrombus and pulmonary veins before radiofre-
96. Achenbach S, Sacher D, Ropers D, Pohle K, Nixdorff U, quency catheter ablation for atrial fibrillation. Am J Cardiol.
Hoffmann U, et al. Electron beam computed tomography for the 2013;112(2):238–44.
detection of left atrial thrombi in patients with atrial fibrillation. 110. Budoff MJ, Shittu A, Hacioglu Y, Gang E, Li D, Bhatia H,
Heart. 2004;90(12):1477–8. et al. Comparison of transesophageal echocardiography versus
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 483

computed tomography for detection of left atrial appendage filling dimensional model in an electroanatomically reconstructed right
defect (thrombus). Am J Cardiol. 2014;113(1):173–7. atrium for ablation of biatrial tachycardia. Heart Rhythm Off
111. Meier B, Blaauw Y, Khattab AA, Lewalter T, Sievert H, Tondo J Heart Rhythm Soc. 2011;8(1):152–3.
C, et al. EHRA/EAPCI expert consensus statement on catheter- 125. Shinbane JS, Lesh MD, Stevenson WG, Klitzner TS, Natterson PD,
based left atrial appendage occlusion. Europace Eur Pacing Wiener I, et al. Anatomic and electrophysiologic relation between
Arrhythmias Cardiac Electrophysiol J Working Groups Cardiac the coronary sinus and mitral annulus: implications for abla-
Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc Cardiol. tion of left-sided accessory pathways. Am Heart J. 1998;135(1):
2014;16(10):1397–416. 93–8.
112. Masoudi FA, Calkins H, Kavinsky CJ, Drozda Jr JP, Gainsley P, 126. Gopal A, Shah A, Shareghi S, Bansal N, Nasir K, Gopal D,
Slotwiner DJ, et al. ACC/HRS/SCAI left atrial appendage occlu- et al. The role of cardiovascular computed tomographic angiog-
sion device societal overview: a professional societal overview raphy for coronary sinus mitral annuloplasty. J Invasive Cardiol.
from the American College of Cardiology, Heart Rhythm Society, 2010;22(2):67–73.
and Society for Cardiovascular Angiography and Interventions. 127. Morin DP, Parker H, Khatib S, Dinshaw H. Computed tomog-
J Am Coll Cardiol. 2015;2015. raphy of a coronary sinus diverticulum associated with Wolff-
113. Koplay M, Erol C, Paksoy Y, Kivrak AS, Ozbek S. An investi- Parkinson-White syndrome. Heart Rhythm Off J Heart Rhythm
gation of the anatomical variations of left atrial appendage by Soc. 2012;9(8):1338–9.
multidetector computed tomographic coronary angiography. Eur 128. Miyahara Y, Kataoka K, Kawada M. Isolated unroofed coronary
J Radiol. 2012;81(7):1575–80. sinus on three-dimensional computed tomographic imaging. Ann
114. van Rosendael PJ, Katsanos S, van den Brink OW, Scholte Thorac Surg. 2012;93(6):2072.
AJ, Trines SA, Bax JJ, et al. Geometry of left atrial appendage 129. Shinbane JS, Shriki J, Fleischman F, Hindoyan A, Withey
assessed with multidetector-row computed tomography: impli- J, Lee C, et al. Anomalous coronary arteries: cardiovascu-
cations for transcatheter closure devices. EuroInterv J EuroPCR lar computed tomographic angiography for surgical decisions
Collab Working Group Interv Cardiol Eur Soc Cardiol. and planning. World J Pediatr Congenit Heart Surg. 2013;4(2):
2014;10(3):364–71. 142–54.
115. Freixa X, Tzikas A, Basmadjian A, Garceau P, Ibrahim 130. Shriki JE, Shinbane JS, Rashid MA, Hindoyan A, Withey JG,
R. The chicken-wing morphology: an anatomical challenge DeFrance A, et al. Identifying, characterizing, and classifying
for left atrial appendage occlusion. J Interv Cardiol. 2013; congenital anomalies of the coronary arteries. Radiogr Rev Publ
26(5):509–14. Radiol Soc N Am Inc. 2012;32(2):453–68.
116. Di Biase L, Santangeli P, Anselmino M, Mohanty P, Salvetti I, Gili 131. Levisman J, Budoff M, Karlsberg R. Congenital atresia of the left
S, et al. Does the left atrial appendage morphology correlate with main coronary artery: cardiac CT. Cathete Cardiovasc Interv Off
the risk of stroke in patients with atrial fibrillation? Results from a J Soc Cardiac Angiogr Interv. 2009;74(3):465–7.
multicenter study. J Am Coll Cardiol. 2012;60(6):531–8. 132. Opolski MP, Pregowski J, Kruk M, Witkowski A, Kwiecinska
117. Fukushima K, Fukushima N, Kato K, Ejima K, Sato H, S, Lubienska E, et al. Prevalence and characteristics of coronary
Fukushima K, et al. Correlation between left atrial appendage anomalies originating from the opposite sinus of Valsalva in 8,522
morphology and flow velocity in patients with paroxysmal atrial patients referred for coronary computed tomography angiography.
fibrillation. Eur Heart J Cardiovasc Imaging. 2016;17(1):59–66. Am J Cardiol. 2013;111(9):1361–7.
118. Petersen M, Roehrich A, Balzer J, Shin DI, Meyer C, Kelm M, 133. Andreini D, Pontone G, Pepi M, Ballerini G, Bartorelli AL,
et al. Left atrial appendage morphology is closely associated Magini A, et al. Diagnostic accuracy of multidetector computed
with specific echocardiographic flow pattern in patients with tomography coronary angiography in patients with dilated cardio-
atrial fibrillation. Europace Eur Pacing Arrhythmias Cardiac myopathy. J Am Coll Cardiol. 2007;49(20):2044–50.
Electrophysiol J Working Groups Cardiac Pacing Arrhythmias 134. Andreini D, Pontone G, Bartorelli AL, Agostoni P, Mushtaq
Cardiac Cell Electrophysiol Eur Soc Cardiol. 2015;17(4):539–45. S, Bertella E, et al. Sixty-four-slice multidetector computed
119. Nedios S, Kornej J, Koutalas E, Bertagnolli L, Kosiuk J, Rolf S, tomography: an accurate imaging modality for the evaluation of
et al. Left atrial appendage morphology and thromboembolic risk coronary arteries in dilated cardiomyopathy of unknown etiology.
after catheter ablation for atrial fibrillation. Heart Rhythm Off Circ Cardiovasc Imaging. 2009;2(3):199–205.
J Heart Rhythm Soc. 2014;11(12):2239–46. 135. Bhatti S, Hakeem A, Yousuf MA, Al-Khalidi HR, Mazur W,
120. Kosiuk J, Nedios S, Kornej J, Koutalas E, Bertagnolli L, Rolf Shizukuda Y. Diagnostic performance of computed tomography
S, et al. Impact of left atrial appendage morphology on peri- angiography for differentiating ischemic vs nonischemic car-
interventional thromboembolic risk during catheter ablation diomyopathy. J Nucl Cardiol Off Publ Am Soc Nucl Cardiol.
of atrial fibrillation. Heart Rhythm Off J Heart Rhythm Soc. 2011;18(3):407–20.
2014;11(9):1522–7. 136. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O,
121. Anselmino M, Scaglione M, Di Biase L, Gili S, Santangeli P, et al. The use of contrast-enhanced magnetic resonance imag-
Corsinovi L, et al. Left atrial appendage morphology and silent ing to identify reversible myocardial dysfunction. N Engl J Med.
cerebral ischemia in patients with atrial fibrillation. Heart Rhythm 2000;343(20):1445–53.
Off J Heart Rhythm Soc. 2014;11(1):2–7. 137. Klein C, Nekolla SG, Bengel FM, Momose M, Sammer A, Haas F,
122. Lee JM, Seo J, Uhm JS, Kim YJ, Lee HJ, Kim JY, et al. Why is et al. Assessment of myocardial viability with contrast-enhanced
left atrial appendage morphology related to strokes? An analysis magnetic resonance imaging: comparison with positron emission
of the flow velocity and orifice size of the left atrial appendage. tomography. Circulation. 2002;105(2):162–7.
J Cardiovasc Electrophysiol. 2015;26(9):922–27. 138. Kuhl HP, Beek AM, van der Weerdt AP, Hofman MB, Visser CA,
123. Kajihara K, Nakano Y, Hirai Y, Ogi H, Oda N, Suenari K, et al. Lammertsma AA, et al. Myocardial viability in chronic ischemic
Variable procedural strategies adapted to anatomical charac- heart disease: comparison of contrast-enhanced magnetic reso-
teristics in catheter ablation of the cavotricuspid isthmus using nance imaging with (18)F-fluorodeoxyglucose positron emission
a preoperative multidetector computed tomography analysis. tomography. J Am Coll Cardiol. 2003;41(8):1341–8.
J Cardiovasc Electrophysiol. 2013;24(12):1344–51. 139. Selvanayagam JB, Kardos A, Francis JM, Wiesmann F, Petersen
124. Sommer P, Piorkowski C, Arya A, Hindricks G. Successful SE, Taggart DP, et al. Value of delayed-enhancement car-
integration of a computed tomography-based left atrial three- diovascular magnetic resonance imaging in predicting myo-
484 J.S. Shinbane et al.

cardial viability after surgical revascularization. Circulation. 154. Green JJ, Berger JS, Kramer CM, Salerno M. Prognostic value of
2004;110(12):1535–41. late gadolinium enhancement in clinical outcomes for hypertrophic
140. Bello D, Fieno DS, Kim RJ, Pereles FS, Passman R, Song G, et al. cardiomyopathy. JACC Cardiovasc Imaging. 2012;5(4):370–7.
Infarct morphology identifies patients with substrate for sustained 155. Casolo G, Di Cesare E, Molinari G, Knoll P, Midiri M, Fedele
ventricular tachycardia. J Am Coll Cardiol. 2005;45(7):1104–8. F, et al. Diagnostic work up of arrhythmogenic right ven-
141. Bello D, Einhorn A, Kaushal R, Kenchaiah S, Raney A, Fieno tricular cardiomyopathy by cardiovascular magnetic reso-
D, et al. Cardiac magnetic resonance imaging: infarct size is an nance (CMR). Consensus statement La Radiologia Medica.
independent predictor of mortality in patients with coronary artery 2004;108(1–2):39–55.
disease. Magn Reson Imaging. 2011;29(1):50–6. 156. Tandri H, Saranathan M, Rodriguez ER, Martinez C, Bomma C,
142. Gao P, Yee R, Gula L, Krahn AD, Skanes A, Leong-Sit P, et al. Nasir K, et al. Noninvasive detection of myocardial fibrosis in
Prediction of arrhythmic events in ischemic and dilated cardio- arrhythmogenic right ventricular cardiomyopathy using delayed-
myopathy patients referred for implantable cardiac defibrilla- enhancement magnetic resonance imaging. J Am Coll Cardiol.
tor: evaluation of multiple scar quantification measures for late 2005;45(1):98–103.
gadolinium enhancement magnetic resonance imaging. Circ 157. Dickfeld T, Tian J, Ahmad G, Jimenez A, Turgeman A, Kuk R,
Cardiovasc Imaging. 2012;5(4):448–56. et al. MRI-Guided ventricular tachycardia ablation: integration
143. Nazarian S, Bluemke DA, Lardo AC, Zviman MM, Watkins SP, of late gadolinium-enhanced 3D scar in patients with implant-
Dickfeld TL, et al. Magnetic resonance assessment of the sub- able cardioverter-defibrillators. Circ Arrhythm Electrophysiol.
strate for inducible ventricular tachycardia in nonischemic cardio- 2011;4(2):172–84.
myopathy. Circulation. 2005;112(18):2821–5. 158. Yokokawa M, Tada H, Koyama K, Naito S, Oshima S, Taniguchi
144. Assomull RG, Prasad SK, Lyne J, Smith G, Burman ED, K. Nontransmural scar detected by magnetic resonance imaging
Khan M, et al. Cardiovascular magnetic resonance, fibrosis, and origin of ventricular tachycardia in structural heart disease.
and prognosis in dilated cardiomyopathy. J Am Coll Cardiol. Pacing Clin Electrophysiol PACE. 2009;32 Suppl 1:S52–6.
2006;48(10):1977–85. 159. Ashikaga H, Sasano T, Dong J, Zviman MM, Evers R, Hopenfeld
145. Wu KC, Weiss RG, Thiemann DR, Kitagawa K, Schmidt B, et al. Magnetic resonance-based anatomical analysis of scar-
A, Dalal D, et al. Late gadolinium enhancement by cardio- related ventricular tachycardia: implications for catheter ablation.
vascular magnetic resonance heralds an adverse prognosis Circ Res. 2007;101(9):939–47.
in nonischemic cardiomyopathy. J Am Coll Cardiol. 2008; 160. Schmidt A, Azevedo CF, Cheng A, Gupta SN, Bluemke DA, Foo
51(25):2414–21. TK, et al. Infarct tissue heterogeneity by magnetic resonance imaging
146. Cho JR, Park S, Choi BW, Kang SM, Ha JW, Chung N, et al. identifies enhanced cardiac arrhythmia susceptibility in patients with
Delayed enhancement magnetic resonance imaging is a significant left ventricular dysfunction. Circulation. 2007;115(15):2006–14.
prognostic factor in patients with non-ischemic cardiomyopathy. 161. Bogun FM, Desjardins B, Good E, Gupta S, Crawford T, Oral
Circ J Off J Jpn Circ Soc. 2010;74(3):476–83. H, et al. Delayed-enhanced magnetic resonance imaging in non-
147. Lehrke S, Lossnitzer D, Schob M, Steen H, Merten C, Kemmling ischemic cardiomyopathy: utility for identifying the ventricular
H, et al. Use of cardiovascular magnetic resonance for risk stratifi- arrhythmia substrate. J Am Coll Cardiol. 2009;53(13):1138–45.
cation in chronic heart failure: prognostic value of late gadolinium 162. Heidary S, Patel H, Chung J, Yokota H, Gupta SN, Bennett MV,
enhancement in patients with non-ischaemic dilated cardiomy- et al. Quantitative tissue characterization of infarct core and bor-
opathy. Heart. 2011;97(9):727–32. der zone in patients with ischemic cardiomyopathy by magnetic
148. Matoh F, Satoh H, Shiraki K, Saitoh T, Urushida T, Katoh H, et al. resonance is associated with future cardiovascular events. J Am
Usefulness of delayed enhancement magnetic resonance imaging Coll Cardiol. 2010;55(24):2762–8.
to differentiate dilated phase of hypertrophic cardiomyopathy and 163. Mahnken AH, Koos R, Katoh M, Wildberger JE, Spuentrup E,
dilated cardiomyopathy. J Card Fail. 2007;13(5):372–9. Buecker A, et al. Assessment of myocardial viability in reperfused
149. Suk T, Edwards C, Hart H, Christiansen JP. Myocardial scar acute myocardial infarction using 16-slice computed tomography
detected by contrast-enhanced cardiac magnetic resonance in comparison to magnetic resonance imaging. J Am Coll Cardiol.
imaging is associated with ventricular tachycardia in hypertrophic 2005;45(12):2042–7.
cardiomyopathy patients. Heart Lung Circ. 2008;17(5):370–4. 164. Chiou KR, Liu CP, Peng NJ, Huang WC, Hsiao SH, Huang YL,
150. Adabag AS, Maron BJ, Appelbaum E, Harrigan CJ, Buros JL, et al. Identification and viability assessment of infarcted myocar-
Gibson CM, et al. Occurrence and frequency of arrhythmias in dium with late enhancement multidetector computed tomography:
hypertrophic cardiomyopathy in relation to delayed enhance- comparison with thallium single photon emission computed tomog-
ment on cardiovascular magnetic resonance. J Am Coll Cardiol. raphy and echocardiography. Am Heart J. 2008;155(4):738–45.
2008;51(14):1369–74. 165. Sato A, Hiroe M, Nozato T, Hikita H, Ito Y, Ohigashi H, et al. Early
151. Oka K, Tsujino T, Nakao S, Lee-Kawabata M, Ezumi A, Masai M, validation study of 64-slice multidetector computed tomography
et al. Symptomatic ventricular tachyarrhythmia is associated with for the assessment of myocardial viability and the prediction of
delayed gadolinium enhancement in cardiac magnetic resonance left ventricular remodelling after acute myocardial infarction. Eur
imaging and with elevated plasma brain natriuretic peptide level Heart J. 2008;29(4):490–8.
in hypertrophic cardiomyopathy. J Cardiol. 2008;52(2):146–53. 166. Shriki JE, Shinbane J, Lee C, Khan AR, Burns N, Hindoyan A,
152. Kwon DH, Smedira NG, Rodriguez ER, Tan C, Setser R, et al. Incidental myocardial infarct on conventional nongated CT:
Thamilarasan M, et al. Cardiac magnetic resonance detection of a review of the spectrum of findings with gated CT and cardiac
myocardial scarring in hypertrophic cardiomyopathy: correlation MRI correlation. AJR Am J Roentgenol. 2012;198(3):496–504.
with histopathology and prevalence of ventricular tachycardia. 167. Zhao L, Ma X, Feuchtner GM, Zhang C, Fan Z. Quantification of
J Am Coll Cardiol. 2009;54(3):242–9. myocardial delayed enhancement and wall thickness in hypertro-
153. Fluechter S, Kuschyk J, Wolpert C, Doesch C, Veltmann C, Haghi phic cardiomyopathy: multidetector computed tomography versus
D, et al. Extent of late gadolinium enhancement detected by car- magnetic resonance imaging. Eur J Radiol. 2014;83(10):1778–85.
diovascular magnetic resonance correlates with the inducibility 168. McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstrom-
of ventricular tachyarrhythmia in hypertrophic cardiomyopathy. Lundqvist C, Fontaine G, et al. Diagnosis of arrhythmogenic
J Cardiovasc Mag Reson Off J Soc Cardiovasc Magn Reson. right ventricular dysplasia/cardiomyopathy. Task Force of the
2010;12:30. Working Group Myocardial and Pericardial Disease of the
24 CCTA Cardiac Electrophysiology Applications: Substrate Identification, Virtual Procedural Planning, and Procedural Facilitation 485

European Society of Cardiology and of the Scientific Council on 182. Yap SC, Harris L, Downar E, Nanthakumar K, Silversides CK,
Cardiomyopathies of the International Society and Federation of Chauhan VS. Evolving electroanatomic substrate and intra-atrial
Cardiology. Br Heart J. 1994;71(3):215–8. reentrant tachycardia late after Fontan surgery. J Cardiovasc
169. Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke Electrophysiol. 2012;23(4):339–45.
DA, et al. Diagnosis of arrhythmogenic right ventricular cardio- 183. Valente AM, Gauvreau K, Assenza GE, Babu-Narayan SV,
myopathy/dysplasia: proposed modification of the task force cri- Schreier J, Gatzoulis MA, et al. Contemporary predictors of death
teria. Circulation. 2010;121(13):1533–41. and sustained ventricular tachycardia in patients with repaired
170. Wu YW, Tadamura E, Kanao S, Yamamuro M, Nishiyama K, tetralogy of Fallot enrolled in the INDICATOR cohort. Heart.
Kimura T, et al. Structural and functional assessment of arrhyth- 2014;100(3):247–53.
mogenic right ventricular dysplasia/cardiomyopathy by multi- 184. Oosterhof T, Mulder BJ, Vliegen HW, de Roos A. Corrected
slice computed tomography: comparison with cardiovascular tetralogy of Fallot: delayed enhancement in right ventricular out-
magnetic resonance. Int J Cardiol. 2007;115(3):e118–21. flow tract. Radiology. 2005;237(3):868–71.
171. Bomma C, Dalal D, Tandri H, Prakasa K, Nasir K, Roguin A, 185. Harris MA, Johnson TR, Weinberg PM, Fogel MA. Delayed-
et al. Evolving role of multidetector computed tomography in enhancement cardiovascular magnetic resonance identifies fibrous
evaluation of arrhythmogenic right ventricular dysplasia/cardio- tissue in children after surgery for congenital heart disease.
myopathy. Am J Cardiol. 2007;100(1):99–105. J Thorac Cardiovasc Surg. 2007;133(3):676–81.
172. Matsuo S, Sato Y, Nakae I, Masuda D, Yomota M, Ashihara T, 186. Zeppenfeld K, Schalij MJ, Bartelings MM, Tedrow UB, Koplan
et al. Left ventricular involvement in arrhythmogenic right ven- BA, Soejima K, et al. Catheter ablation of ventricular tachycar-
tricular cardiomyopathy demonstrated by multidetector-row com- dia after repair of congenital heart disease: electroanatomic iden-
puted tomography. Int J Cardiol. 2007;115(3):e129–31. tification of the critical right ventricular isthmus. Circulation.
173. Komatsu Y, Cochet H, Jadidi A, Sacher F, Shah A, Derval N, et al. 2007;116(20):2241–52.
Regional myocardial wall thinning at multidetector computed 187. Ueda A, Suman-Horduna I, Mantziari L, Gujic M, Marchese P, Ho
tomography correlates to arrhythmogenic substrate in postinfarc- SY, et al. Contemporary outcomes of supraventricular tachycardia
tion ventricular tachycardia: assessment of structural and electri- ablation in congenital heart disease: a single-center experience in
cal substrate. Circ Arrhythm Electrophysiol. 2013;6(2):342–50. 116 patients. Circ Arrhythm Electrophysiol. 2013;6(3):606–13.
174. Sasaki T, Calkins H, Miller CF, Zviman MM, Zipunnikov V, Arai 188. Jongbloed MR, Lamb HJ, Bax JJ, Schuijf JD, de Roos A, van der
T, et al. New insight into scar-related ventricular tachycardia cir- Wall EE, et al. Noninvasive visualization of the cardiac venous
cuits in ischemic cardiomyopathy: fat deposition after myocardial system using multislice computed tomography. J Am Coll Cardiol.
infarction on computed tomography–A pilot study. Heart Rhythm 2005;45(5):749–53.
Off J Heart Rhythm Soc. 2015;12(7):1508–18. 189. Shinbane JS, Girsky MJ, Mao S, Budoff MJ. Thebesian valve
175. Cochet H, Komatsu Y, Sacher F, Jadidi AS, Scherr D, Riffaud M, imaging with electron beam CT angiography: implications for
et al. Integration of merged delayed-enhanced magnetic resonance resynchronization therapy. Pacing Clin Electrophysiol PACE.
imaging and multidetector computed tomography for the guidance 2004;27(9):1331–2.
of ventricular tachycardia ablation: a pilot study. J Cardiovasc 190. Matsumoto Y, Krishnan S, Fowler SJ, Saremi F, Kondo T, Ahsan
Electrophysiol. 2013;24(4):419–26. C, et al. Detection of phrenic nerves and their relation to cardiac
176. Cesario DA, Shinbane JS, Cao M, Saxon LA, Cunningham M, anatomy using 64-slice multidetector computed tomography. Am
Essilfie G. Use of CT delayed enhancement imaging and a ven- J Cardiol. 2007;100(1):133–7.
tricular assist device in ablation of recurrent ventricular tachycar- 191. Carbonaro S, Villines TC, Hausleiter J, Devine PJ, Gerber TC,
dia. Innov Cardiac Rhythm Manag. 2010;1:54–8. Taylor AJ. International, multidisciplinary update of the 2006
177. Friehling M, Menon PG, Ludwig DR, Schwartzman D. Single- Appropriateness Criteria for cardiac computed tomography.
photon emission computed tomographic-multidetector computed J Cardiovasc Comput Tomogr. 2009;3(4):224–32.
tomographic fusion image integration: a potential aid to left ventricu- 192. Hendel RC, Patel MR, Kramer CM, Poon M, Hendel RC, Carr
lar substrate ablation. Europace Euro Pacing Arrhythmias Cardiac JC, et al. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR
Electrophysiol J Working Groups Cardiac Pacing Arrhythmias 2006 appropriateness criteria for cardiac computed tomography
Cardiac Cell Electrophysiol Eur Soc Cardiol. 2014;16(12): and cardiac magnetic resonance imaging: a report of the American
1860–3. College of Cardiology Foundation Quality Strategic Directions
178. Akutsu Y, Kaneko K, Kodama Y, Li HL, Suyama J, Watanabe Committee Appropriateness Criteria Working Group, American
N, et al. Stratified three-dimensional fusion imaging of delayed College of Radiology, Society of Cardiovascular Computed
enhancement magnetic resonance and multi-detector computed Tomography, Society for Cardiovascular Magnetic Resonance,
tomography to identify a ventricular tachycardia focus. Int American Society of Nuclear Cardiology, North American Society
J Cardiovasc Imaging. 2013;29(8):1705–6. for Cardiac Imaging, Society for Cardiovascular Angiography and
179. Estornell-Erill J, Ridocci-Soriano F, Quesada-Dorador A, Interventions, and Society of Interventional Radiology. J Am Coll
Federico-Zaragoza P, Fabregat-Andres O, Palanca-Gil V, et al. Cardiol. 2006;48(7):1475–97.
Images in cardiology. Microvascular obstruction after radiofre- 193. European Heart Rhythm A, European Society of C, Heart Rhythm
quency ablation of ventricular tachycardia: comprehensive evalu- S, Heart Failure Society of A, American Society of E, American
ation by magnetic resonance imaging and computed tomography. Heart A, et al. 2012 EHRA/HRS expert consensus statement on
J Am Coll Cardiol. 2010;56(13):e25. cardiac resynchronization therapy in heart failure: implant and
180. Rathod RH, Prakash A, Powell AJ, Geva T. Myocardial fibro- follow-up recommendations and management. Heart Rhythm: Off
sis identified by cardiac magnetic resonance late gadolinium J Heart Rhythm Soc. 2012;9(9):1524–76.
enhancement is associated with adverse ventricular mechanics 194. Girsky MJ, Shinbane JS, Ahmadi N, Mao S, Flores F, Budoff
and ventricular tachycardia late after Fontan operation. J Am Coll MJ. Prospective randomized trial of venous cardiac com-
Cardiol. 2010;55(16):1721–8. puted tomographic angiography for facilitation of cardiac
181. Teh AW, Medi C, Lee G, Rosso R, Sparks PB, Morton JB, et al. resynchronization therapy. Pacing Clin Electrophysiol PACE.
Long-term outcome following ablation of atrial flutter occurring 2010;33(10):1182–7.
late after atrial septal defect repair. Pacing Clin Electrophysiol 195. Auricchio A, Sorgente A, Soubelet E, Regoli F, Spinucci G, Vaillant
PACE. 2011;34(4):431–5. R, et al. Accuracy and usefulness of fusion imaging between
486 J.S. Shinbane et al.

three-dimensional coronary sinus and coronary veins computed 201. Yavari A, Khawaja ZO, Krishnamoorthy S, McWilliams
tomographic images with projection images obtained using fluoros- ET. Perforation of right ventricular free wall by pacemaker lead
copy. Europace Euro Pacing Arrhythmias Cardiac Electrophysiol detected by multidetector computed tomography. Europace Eur
J Working Groups Cardiac Pacing Arrhythmias Cardiac Cell Pacing Arrhythmias Cardiac Electrophysiol J Working Groups
Electrophysiol Eur Soc Cardiol. 2009;11(11):1483–90. Cardiac Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc
196. Cao M, Chang P, Garon B, Shinbane JS. Cardiac resynchroniza- Cardiol. 2009;11(2):252–4.
tion therapy: double cannulation approach to coronary venous 202. Kim YS, Oh S, Park KW, Ree Cho K, Choi YS. Uncomplicated
lead placement via a prominent thebesian valve. Pacing Clin right ventricular lead perforation diagnosed with computed
Electrophysiol PACE. 2013;36(3):e70–3. tomography after permanent pacemaker implantation. Clin
197. Da Costa A, Gate-Martinet A, Rouffiange P, Cerisier A, Nadrouss Cardiol. 2009;32(7):E54.
A, Bisch L, et al. Anatomical factors involved in difficult cardiac 203. der Maur AC, Hoffmann A, Brink T, Erne P. Cardiac computed
resynchronization therapy procedure: a non-invasive study using tomography for the diagnosis of right ventricular implantable car-
dual-source 64-multi-slice computed tomography. Europace Eur dioverter-defibrillator lead perforation. Eur Heart J. 2009;30(7):869.
Pacing Arrhythmias Cardiac Electrophysiol J Working Groups 204. Van de Veire NR, Marsan NA, Schuijf JD, Bleeker GB, Wijffels
Cardiac Pacing Arrhythmias Cardiac Cell Electrophysiol Eur Soc MC, van Erven L, et al. Noninvasive imaging of cardiac venous
Cardiol. 2012;14(6):833–40. anatomy with 64-slice multi-slice computed tomography and
198. Sommer A, Kronborg MB, Norgaard BL, Gerdes C, Mortensen noninvasive assessment of left ventricular dyssynchrony by
PT, Nielsen JC. Left and right ventricular lead positions are 3-dimensional tissue synchronization imaging in patients with
imprecisely determined by fluoroscopy in cardiac resynchroni- heart failure scheduled for cardiac resynchronization therapy. Am
zation therapy: a comparison with cardiac computed tomogra- J Cardiol. 2008;101(7):1023–9.
phy. Europace Eur Pacing Arrhythmias Cardiac Electrophysiol 205. White JA, Yee R, Yuan X, Krahn A, Skanes A, Parker M, et al.
J Working Groups Cardiac Pacing Arrhythmias Cardiac Cell Delayed enhancement magnetic resonance imaging predicts
Electrophysiol Eur Soc Cardiol. 2014;16(9):1334–41. response to cardiac resynchronization therapy in patients
199. Rickard J, Ingelmo C, Sraow D, Wilkoff BL, Grimm RA, with intraventricular dyssynchrony. J Am Coll Cardiol. 2006;
Schoenhagen P, et al. Chest radiography is a poor predictor of 48(10):1953–60.
left ventricular lead position in patients undergoing cardiac resyn- 206. Bleeker GB, Kaandorp TA, Lamb HJ, Boersma E, Steendijk P, de
chronization therapy: comparison with multidetector computed Roos A, et al. Effect of posterolateral scar tissue on clinical and
tomography. J Interv Cardiac Electrophysiol Int J Arrhythmias echocardiographic improvement after cardiac resynchronization
Pacing. 2011;32(1):59–65. therapy. Circulation. 2006;113(7):969–76.
200. Pang BJ, Lui EH, Joshi SB, Tacey MA, Alison J, Seneviratne SK, 207. Chalil S, Stegemann B, Muhyaldeen SA, Khadjooi K, Foley PW,
et al. Pacing and implantable cardioverter defibrillator lead per- Smith RE, et al. Effect of posterolateral left ventricular scar on
foration as assessed by multiplanar reformatted ECG-gated car- mortality and morbidity following cardiac resynchronization ther-
diac computed tomography and clinical correlates. Pacing Clin apy. Pacing Clin Electrophysiol PACE. 2007;30(10):1201–9.
Electrophysiol PACE. 2014;37(5):537–45.
 Cardiovascular CT: Interventional
Cardiology Applications 25
Jeffrey M. Schussler

Abstract
Interventional cardiologists should embrace cardiac CT as a helpful additional to their
armamentarium in the treatment of cardiovascular disease. CCTA can improve the discrimi-
nation of patients for whom invasive evaluation and treatment will be most helpful. It can
be used in lieu of invasive evaluation after coronary and cardiac intervention, and is now
mandatory in the evaluation of the structural heart disease patient.

Keywords
CCTA • Coronary CTA • CTCA • Coronary angiography • Percutaneous coronary
intervention • PCI • Non-invasive Angiography

Introduction presence and amount of calcification, tortuosity, coronary

variants, and anomalies. It can also be used to guide strate-
With its high specificity, coronary computed tomographic gies for approaching chronic total occlusions. After percuta-
angiography (CCTA) can be an extremely helpful test in neous revascularization, CCTA has utility in evaluation of
determining which patients do not require cardiac catheter- stent patency, and after coronary artery bypass grafting
ization. Given this fact, it seems somewhat counterintuitive (CABG) to evaluate graft patency. In the arena of structural
that this technology would be embraced by interventional heart disease, it can be used for planning for transcatheter
cardiologists. One would theorize that a strong non-invasive aortic valve replacement, atrial septal defect closure, as well
angiography program would reduce volume and divert as planning of other cardiac interventional procedures. In
patients away from the catheterization lab. In fact, centers addition, given the climate of scrutiny regarding appropriate-
where CCTA is available do not appear to have led to a ness of interventions, CCTA can be used to reduce unneces-
reduction in invasive volumes [1]. sary diagnostic cardiac catheterization volume.
Prior to invasive catheterization, CCTA can also help
interventionalists plan percutaneous coronary intervention
(PCI) strategies by alerting them to the presence of left main, Invasive Cardiac Catheterization
ostial, or multivessel disease, length and severity of lesions,
Invasive cardiac catheterization, the “gold standard”
diagnostic technique for the evaluation of coronary artery
J.M. Schussler, MD, FACC, FSCAI, FSCCT, FACP disease (CAD), has been used for clinical evaluation of
Division of Cardiology, Department of Internal Medicine, coronary stenosis since the 1960s [2–4]. However, it has
Baylor University Medical Center, Dallas, TX/Jack and Jane
several well-known drawbacks. There is a certain degree of
Hamilton Heart and Vascular Hospital, 621 N. Hall St. Suite 400,
Dallas, TX 75226, USA inter-observer variation when describing degree of stenosis
[5]. Quantitative coronary angiography, which is not used
Division of Cardiology, Department of Medicine,
Texas A&M College of Medicine, Dallas, TX, USA routinely in clinical practice, is helpful but does not
e-mail: [email protected] eliminate this error [6, 7].

© Springer International Publishing 2016 487

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_25
488 J.M. Schussler

Invasive coronary angiography allows only for the defini- Accuracy is high enough to determine whether coronary
tion of the lumen of the coronary. The plaque protruding into arteries have high-grade lesions, and which have minimal
the lumen of the coronary artery remains non-visualized disease (Fig. 25.2), and can accurately exclude left main or
unless intravascular ultrasound is used [8, 9]. This may lead multi-vessel coronary disease prior to catheterization [28–
to under-identification of the presence of disease in patients 32]. This can mean the difference between planning an inter-
with minimal angiographic disease, and can contribute to vention on a single proximal vessel or on the expectation of
underestimation of plaque burden due to compensatory a difficult multiple vessel intervention [33, 34].
expansion of the coronary arteries [10–13]. These non-flow- CCTA may also allow for improved planning of
limiting stenoses can be the cause of future acute coronary antiplatelet loading prior to catheterization. If suspected
syndromes and myocardial infarction [14]. surgical disease is discovered on CCTA, a “loading dose” of
There is a small but inherent risk of complication associ- clopidogrel may be withheld, reducing a delay in surgical
ated with invasive evaluation of the coronary arteries. This is revascularization (Fig. 25.3). While still not standard of care,
due to the need to directly instrument the coronary arteries, as newer studies suggest that it may be feasible in the future to
well as the obligate arterial access. The risk of major compli- send patients directly to coronary artery bypass graft surgery
cations such as death are approximately 0.1 % [15, 16], with without invasive angiography, relying on CCTA alone to
a combined risk of all major complications, such as stroke, guide surgical decision-making [35]. Once lesions are found,
renal failure, or major bleeding, of ≤2 % [17, 18]. Minor CCTA can also act as a “preview” of the coronary anatomy
complications, such as local pain, ecchymosis, or hematoma for planning of stent placement, including stent sizing prior
at the access site, can be higher, and are frequently a source of to invasive coronary angiography (Fig. 25.4) [36].
delayed discharge and patient dissatisfaction [19].
Invasive coronary angiography is considered the “gold
standard” for definitive cardiac evaluation in patients with Visualization of Coronary Ostia
chest pain [20]. As it is such a powerful tool, invasive
angiography has even been suggested as the test of choice in Visualization of the ostia of the coronaries may help an
inpatients with chest pain [21]. Angiography has been shown interventionalist in several ways. Anomalous coronary
to be better able to detect the presence of atherosclerotic arteries are better seen with CT, and can be helpful in
coronary disease than functional tests, reduces early returns planning catheter selection prior to invasive angiography
to the emergency department, and has an overall higher level [37]. Even in cases where true anomalies are not present, it
of patient satisfaction [22]. Invasive angiography has even can be helpful to know that a patient has an “anterior takeoff”
been suggested as the screening test of choice in the primary of a right coronary or a “posterior takeoff” of a left main, as
prevention of CAD [23]. However, due to the aforemen- this may lead to use of specific types of catheters for the
tioned risks, it often is used as a second line study in patients engagement of that artery (Fig. 25.5). Coronary CT is
who have low-to-moderate presumed risk or after perform- superior to invasive angiography in evaluating location and
ing functional testing [24]. severity of ostial stenosis (Fig. 25.6), and does not induce
coronary spasm, which can mimic ostial disease [38].

CT Coronary Evaluation Prior to Invasive

Coronary Evaluation Chronic Total Occlusions

Determination of Coronary Atherosclerosis Since the bolus of contrast reaches the arteries simultaneously,
Prior to Invasive Evaluation or Intervention it is difficult to distinguish high-grade lesions from totally
occluded coronaries. Newer data suggest that when
While traditional invasive angiography may be highly occlusions are found, CCTA may be helpful in defining the
accurate, less than 40 % of those patients who have invasive length of stenosis, complexity of the plaque, and therefore
angiography ultimately are found to have significant coronary give insight into the potential ease or difficulty in undertaking
disease [25]. With its high specificity and negative predictive complex percutaneous revascularization of these lesions
value, CCTA has the ability to accurately evaluate those (Fig. 25.7) [39–42].
patients who have no significant coronary disease, obviating
the need for further evaluation [26].
In patients with chest pain who have no observable Left Main Disease
coronary disease by CCTA, there is a nearly 100 % chance
that they will not require further cardiac evaluation, and will The presence of severe left main disease is potentially danger-
have no cardiac events for several years (Fig. 25.1) [27]. ous if not known prior to diagnostic angiography. Placement
25 Cardiovascular CT: Interventional Cardiology Applications 489

a b

c d

Fig. 25.1 Normal CCTA in a patient with risk factors for coronary coronary artery (e) demonstrate no plaque in any of the arterial tree. Ao
disease and chest pain. A 3-D view (a) and maximum intensity aorta, LAA left atrial appendage, LAD left anterior descending, Dx
projection (b) of the coronary anatomy demonstrates a right dominant diagonal, LCx left circumflex, RCA right coronary artery, PA pulmonary
system without coronary anomalies. Individual curved reformatted artery, LV left ventricle, OM obtuse marginal, PDA posterior descend-
images of the left anterior descending (c), left circumflex (d), and right ing artery
490 J.M. Schussler

a b

Fig. 25.2 Patient with chest pain referred for CCTA. On CT images, a high-grade lesion is seen in the mid left anterior descending (a, arrow).
More moderate plaque is noted proximal to the lesion (a, arrowhead). The same lesions are seen on the follow-up invasive angiogram (b)

a b

Fig. 25.3 A CCTA demonstrating a high-grade non-calcified plaque risk for compromise of the left circumflex, ramus intermedius (RI), and
involving the ostium of the left anterior descending (LAD) and distal first diagonal branches. This was less apparent on invasive angiography.
left main (a, arrow). The invasive angiogram (b) is shown for A surgical consultation was obtained, and the patient went on to
comparison. Based on the findings of the CCTA scan, it was felt that the successful bypass of the LAD, diagonal, and RI
location of the plaque was unfavorable for PCI as there would be a high

of a catheter into a diseased left main coronary artery can plans can be made to use smaller diagnostic catheters, or even
cause dramatic reduction of coronary blood flow, and can even have an intra-aortic balloon pump stationed close at hand.
result in death during diagnostic angiography [43, 44]. In a Left main disease identified on the CCTA allows
situation where left main disease is discovered on the CCTA, preparation for the potential hemodynamic compromise of
25 Cardiovascular CT: Interventional Cardiology Applications 491

a b c

d e f

Fig. 25.4 CCTA of a patient with cardiac risk factors and chest pain. Invasive coronary angiogram confirmed the high grade lesion in the
A CCTA (a, b, arrows) demonstrated a high grade lesion in the proxi- right coronary artery. A stent was selected (e) to cover not only the high
mal right coronary artery. The severity is suggested by the complex grade area (arrow), but also the more moderate plaque proximal and
nature of the plaque, with both soft and calcific portions, as well as the distal to the most severe portions of the lesion (f) (Reprinted from
compensatory expansion of the artery within the most severe area (c). Bhella et al. [36]. With permission from Bhella et al., Baylor University
The length and the extent of plaque were evident from the CCTA (d). Medical Center Proceedings)

engaging a catheter in a severely diseased left main coro- significance of coronary disease [49, 50]. Functional assess-
nary artery. It is important to remember that CCTA cannot ment of coronary lesions, especially when combined with
provide hemodynamic information. It is prudent to proceed anatomic assessment, allows for improved discrimination of
to invasive evaluation if non-invasive angiography suggests flow limiting versus non-flow limiting stenosis [51]. Proving
significant left main stenosis (Fig. 25.8). Now that left main functional significance prior to PCI leads to enduring clini-
coronary intervention has become more commonplace, cal benefit [52, 53]. Newer techniques combining non-
CTCA is a useful tool in pre-PCI planning for left main invasive coronary angiography with either myocardial
coronary intervention. It allows for accurate sizing of ves- perfusion (CT-MPI) or fractional flow reserve (FFRCT)
sels, and gives additional insight into plaque burden, calcifi- may allow for both anatomic as well as functional evalua-
cation and geometry of the major epicardial branches tion using CT [54, 55].
[46–48].

Plaque Evaluation
Fractional Flow Reserve and Myocardial
Perfusion Using Computed Tomography Comparison of CTCA with Intravascular
Ultrasound
As with invasive angiography, CT coronary angiography
provides an anatomic assessment of coronary artery steno- CCTA, like intravascular ultrasound (IVUS), has the ability
ses. It is clear that CCTA is at least as good, if not better, to visualize plaque and to roughly quantify its amount [56–58].
than perfusion assessment in evaluating for the presence and It is well known that patients with minimal CAD may still
492 J.M. Schussler

a b

c d

Fig. 25.5 CCTA of a patient with an “anterior” takeoff of the right alous and has no impact on the function of the artery. The ostium, seen
coronary artery (RCA). The axial image (a) demonstrates the ostium of on the 3-D reconstructed image (b), has a normal round orifice. Three
the right coronary artery slightly higher and more anterior than nor- dimensional views (c) show the high-anterior takeoff in relation to the
mally seen. The location on the axial “clock-face” of the aortic root is cusp and the left main. The pulmonary outflow (d) does not impinge on
approximately “1 o’clock” rather than the normal “10 to 12 o’clock” the artery. This artery would be best catheterized using a modified
location of a typical RCA ostium. This RCA location is not truly anom- Amplatz-type catheter rather than a typical Judkins-right catheter

have events due to plaque which is not fully defined by inva- Coronary Remodeling
sive coronary angiography. These types of non-stenotic
plaques are detectable by CCTA, and there is ongoing Unless IVUS is used, Glagov remodeling of coronary
research in the evaluation of plaque-stability using CCTA atherosclerotic lesions can be appreciated on CCTA bet-
(Fig. 25.9) [59–62]. ter than with invasive angiography (Fig. 25.10) [63]. As
25 Cardiovascular CT: Interventional Cardiology Applications 493

a b

Fig. 25.6 Oblique reconstructed views of the right coronary artery diagnostic angiogram not to aggressively “seat” the catheter inside the
(RCA) demonstrate a focal, high-grade ostial lesion (a – arrow). artery. Foreknowledge of the anatomy allowed for planning of guide
Corresponding invasive angiogram (b – arrow) confirms location and selection, as well as pre-loading with dual antiplatelet therapy, as there
severity of this blockage. Given the CCTA, care was taken with the was no suggest of surgical disease

the plaque intrudes on the lumen of the artery, compensa- Post-bypass Evaluation
tory arterial expansion occurs, which is seen on CCTA,
but not by conventional angiography [64, 65]. Outward There is excellent data to support the use of CCTA in the
coronary remodeling is often a clue that the plaque is evaluation of CABG patients [72–74]. In some respects, the
unstable, or that the stenosis seen by CCTA is severe imaging of bypass grafts is easier than native arteries, as
(Fig. 25.11) [66, 67]. there is less movement of the grafts and greater contrast
between the contrast in the grafts and the surrounding tissue.
Visualization of graft patency is often more easily performed
using 3-D views rather than axial or even MPR views. For
Post Intervention Evaluation by CTCA many newer post-bypass studies, CCTA has become the test
of choice to evaluate graft patency rather than traditional
Post-PCI Evaluation invasive evaluation [75–79] (Fig. 25.13).
In post CABG patients, it is important to alert the
While technically more challenging, CCTA can be used for technologist that the study is to be performed with the
coronary evaluation after stent placement. Imaging through intention of looking at aorta-coronary bypass grafts, so that
stents, especially in smaller caliber arteries, can be problem- more of the ascending aorta is visualized. Slice thickness
atic due to a significant amount of beam hardening artifact may be increased to reduce radiation. Imaging can be
due to the scatter of x-rays by the metallic stents. It is impor- performed on conduits with metallic proximal connectors,
tant to use appropriate window and threshold levels to obtain but there may be some hardening artifact when many metallic
adequate images, and techniques are available to assist in clips are present [77, 80, 81].
reducing artifact. In-stent restenosis, a process that occurs Patients are sometimes referred for invasive catheterization
through smooth muscle cell migration and neointimal hyper- with a history of CABG surgery, without information
plasia, has also been successfully evaluated by CCTA regarding the types of grafts or which arteries were bypassed.
(Fig. 25.12) [68, 69]. Patients who have had ostial stents It can then be a challenging and time-consuming task to find
placed can be evaluated for geographic “miss” of stenoses, in all of the grafts at cardiac catheterization. CCTA can be
preparation for repeat coronary angiography or intervention helpful, not only by delineating which grafts are patent, but
[70, 71]. by providing a “roadmap” as to the number of grafts, their
494 J.M. Schussler

a b

c d

Fig. 25.7 A patient with multivessel coronary disease: A high-grade (c, d – arrow). Severity of stenosis is suggested by the paucity of con-
lesion is shown in the left anterior descending, demonstrated by invasive trast, compensatory expansion, and a large plaque burden in the artery.
angiography (a) and CCTA (b). The lesion has the same CCTA charac- Complete occlusions cannot be easily distinguished from very high-
teristics as a complete occlusion with bridging collaterals grade stenoses based on CCTA characteristics

origins, as well as the location of the anastomoses with native calcification that exists in the native coronary arteries of
vessels prior to invasive angiography. CABG patients [82, 83].
Even though evaluation of bypass grafts is relatively
straightforward with CCTA, it has to be kept in mind that in
most cases the clinical situation will warrant evaluating not Evaluation of the Non-coronary Cardiac
only the status of the patient’s bypass grafts, but also that of Surgery Patient
the native coronary arteries either distal to the bypass
insertion site or of those coronary arteries that did not receive There is growing literature to support a strategy of non-
a bypass graft. Frequently, evaluation of native arteries in invasive coronary angiography in patients with only low or
patients with bypass grafts tends to be difficult or even moderate risk for coronary disease, prior to non-coronary
impossible with CCTA because of the often pronounced cardiac surgery [84]. In patients with valvular disease, such
25 Cardiovascular CT: Interventional Cardiology Applications 495

a b

Fig. 25.8 A high-grade stenosis of the left main coronary artery seen was so dramatically abnormal that it prompted the operator to deliber-
by CCTA (a, b, arrowhead). The corresponding invasive coronary ately choose a smaller French-sized catheter than normal, and have an
angiogram is seen (c, arrowhead), demonstrating a severe angiographic intra-aortic balloon pump in the room prior to catheterization (Reprinted
stenosis. There was immediate “damping” of the pressure tracing upon from Schussler et al. [45]. With permission from Schussler et al.,
engagement of a 4-French diagnostic catheter. The noninvasive study Baylor University Medical Center Proceedings)

as aortic valve stenosis or regurgitation, it is feasible to additional structural information which is relevant to the
exclude concomitant coronary stenosis prior to aortic valve case [37, 88–90]. Technology is now at the point where
surgery or even TAVR [85–87]. With congenital heart dis- many decisions to proceed with cardiac surgery can pro-
ease, coronary anomalies, or cardiac masses, it may actu- ceed without any invasive tests being performed
ally be more advantageous to perform a CCTA, as it gives (Fig. 25.14).
496 J.M. Schussler

a b

Fig. 25.9 Essentially “normal” coronary angiogram in a 33-year-old subclinical plaque in younger patients, they may be prescribed statin
woman. A “luminal irregularity” (a, white arrowhead) in the left therapy long before they would otherwise have been treated, which may
anterior descending artery corresponds to a non-calcified plaque (b, change their long-term clinical course
black arrow) seen by CCTA. It is possible that by defining asymptomatic,
25 Cardiovascular CT: Interventional Cardiology Applications 497

a b

c d

Fig. 25.10 CCTA of a patient with unstable angina demonstrating a to demonstrate the severity of plaque burden as accurately, but
large plaque burden impinging on the lumen of the proximal LAD (a, intravascular ultrasound (IVUS) (d, asterisk) confirms the CCTA
arrow, asterisk). The area of highest plaque burden (b) shows findings. IVUS tends to more accurately correspond to CCTA findings,
compensatory arterial expansion (asterisk), compared to the artery as it shows both intraluminal plaque as well as plaque morphology in
proximal and distal to the plaque. Coronary angiography (c) is unable the wall of the artery
498 J.M. Schussler

a b d

Fig. 25.11 CCTA and invasive angiogram in a man with chest pain: artery when compared to more proximal reference sections. Invasive
The proximal LAD has a complex, high-grade stenosis (a, arrow). angiography (d, arrow) may not as accurately demonstrate the severity
Closer and cross-sectional views of the plaque (b, arrow; c) show that of plaque burden due to the compensatory expansion and lack of arterial
it is made up of soft and calcified plaque, and there is expansion of the wall visualization
25 Cardiovascular CT: Interventional Cardiology Applications 499

a b

c d

Fig. 25.12 A CCTA of a patient with previous stents placed in the left the LAD stent (b, arrow) and the LCx stent (c, arrow). The right
anterior descending (LAD) and left circumflex (LCx), now having chest coronary artery has only minimal disease (d). No further cardiac testing
pain. Three dimensional image (a) show the location of the stents was needed with this patient
(arrows). The curved reformatted CT images demonstrate patency of
500 J.M. Schussler

a b

c d e

f g

Fig. 25.13 Cardiac CTA (3D images) of a patient with patent coronary the diagonal (Dx) is patent, which is confirmed on MPR imaging (e) as
bypasses is seen in panels a and b. Three-dimensional imaging is quite well as invasive angiography (g). The SVG to the left anterior
adequate in visualizing patent saphenous vein grafts (SVG), and multi- descending (LAD) has a high grade lesion (d, arrowhead), which is
planar reformatted (MPR) images are unnecessary. A patient with seen on invasive angiography (f). An occluded SVG with previous stent
diseased coronary bypasses is seen using 3-D imaging (c). The graft to is seen on the 3D images (c, asterisk)
25 Cardiovascular CT: Interventional Cardiology Applications 501

a b c

d e f

Fig. 25.14 CCTA performed in a young patient who is to undergo atrial pulmonary veins (RSPV right superior pulmonary vein, RIPV right infe-
septal defect (ASD) closure. The 3-D and MIP views (a, b) show no sig- rior pulmonary vein), which can alter management from percutaneous to
nificant coronary disease. This was confirmed with review of the axial surgical closure. Axial view (e) shows relation of the pulmonary artery
and reformatted images (not pictured). Axial image of the heart (c) clearly (PA) to the aorta (Ao) as well as the clear conduit from the left atrium
shows enlargement of the right ventricle (RV) compared to the left ven- (LA) to the right atrium. An “internal” view of the ASD as seen from the
tricle (LV), which is a sign of the chronicity of the volume overload of the right atrium shows the location of the left sided pulmonary veins across
right heart from the ASD. The ASD is shown from an “internal” view (d, the left atrium (f) (Reprinted from Reese et al. [90]. With permission from
arrow). This also allows for the evaluation of the size and location of the Baylor Health Care System. ©Baylor Health Care System)
502 J.M. Schussler

Conclusion study comparing coronary angiography and exercise thallium scin-

Interventional cardiologists should embrace CCTA as a tigraphy. Clin Cardiol. 1993;16(12):879–82.
15. Kennedy JW, Baxley WA, Bunnel IL, Gensini GG, Messer JV,
helpful addition to their armamentarium to diagnose and Mudd JG, et al. Mortality related to cardiac catheterization and
treat cardiovascular disease. There are many situations in angiography. Cathet Cardiovasc Diagn. 1982;8(4):323–40.
which the use of CCTA is not only complementary, but an 16. Noto Jr TJ, Johnson LW, Krone R, Weaver WF, Clark DA, Kramer
improvement on its invasive counterpart in the evaluation Jr JR, et al. Cardiac catheterization 1990: a report of the Registry of
the Society for Cardiac Angiography and Interventions (SCA&I).
of the cardiac patient. It can be an enormous aid in the Cathet Cardiovasc Diagn. 1991;24(2):75–83.
planning of complex interventional procedures, and can 17. Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ,
give additional information which invasive angiography Eagle KA, et al. ACC/AHA guidelines for coronary angiogra-
cannot. Further reductions in radiation dosage, improve- phy. A report of the American College of Cardiology/American
Heart Association Task Force on practice guidelines (Committee
ments in resolution, and more rapid acquisition time will on Coronary Angiography). Developed in collaboration with the
increase the interventionalist’s usage of cardiac CT. Society for Cardiac Angiography and Interventions. J Am Coll
Cardiol. 1999;33(6):1756–824.
18. Heuser RR. Outpatient coronary angiography: indications, safety,
and complication rates. Herz. 1998;23(1):21–6.
19. Ammann P, Brunner-La Rocca HP, Angehrn W, Roelli H, Sagmeister
References M, Rickli H. Procedural complications following diagnostic coro-
nary angiography are related to the operator’s experience and the
1. Auseon AJ, Advani SS, Bush CA, Raman SV. Impact of 64-slice catheter size. Catheter Cardiovasc Interv. 2003;59(1):13–8.
multidetector computed tomography on other diagnostic studies 20. Patel MR, Bailey SR, Bonow RO, Chambers CE, Chan PS,
for coronary artery disease. Am J Med. 2009;122(4):387–91. Epub Dehmer GJ, et al. ACCF/SCAI/AATS/AHA/ASE/ASNC/HFSA/
2009/04/01. HRS/SCCM/SCCT/SCMR/STS 2012 appropriate use criteria
2. Selinger H. Selective coronary cine-angiography. W V Med J. for diagnostic catheterization: a report of the American College
1966;62(10):336–7. of Cardiology Foundation Appropriate Use Criteria Task Force,
3. Spellberg RD, Unger I. The percutaneous femoral artery approach to Society for Cardiovascular Angiography and Interventions,
selective coronary arteriography. Circulation. 1967;36(5):730–3. American Association for Thoracic Surgery, American Heart
4. Weidner W, MacAlpin R, Hanafee W, Kattus A. Percutaneous Association, American Society of Echocardiography, American
transaxillary selective coronary angiography. Radiology. Society of Nuclear Cardiology, Heart Failure Society of America,
1965;85(4):652–7. Heart Rhythm Society, Society of Critical Care Medicine, Society of
5. Banerjee S, Crook AM, Dawson JR, Timmis AD, Hemingway Cardiovascular Computed Tomography, Society for Cardiovascular
H. Magnitude and consequences of error in coronary angiogra- Magnetic Resonance, and Society of Thoracic Surgeons. J Am Coll
phy interpretation (the ACRE study). Am J Cardiol. 2000;85(3): Cardiol. 2012;59(22):1995–2027. Epub 2012/05/15.
309–14. 21. deFilippi CR, Rosanio S, Tocchi M, Parmar RJ, Potter MA, Uretsky
6. Goldberg RK, Kleiman NS, Minor ST, Abukhalil J, Raizner AE. BF, et al. Randomized comparison of a strategy of predischarge
Comparison of quantitative coronary angiography to visual esti- coronary angiography versus exercise testing in low-risk patients
mates of lesion severity pre and post PTCA. Am Heart J. 1990; in a chest pain unit: in-hospital and long-term outcomes. J Am Coll
119(1):178–84. Cardiol. 2001;37(8):2042–9.
7. Herrington DM, Siebes M, Walford GD. Sources of error in quanti- 22. Wyer PC. Predischarge coronary angiography was better than exer-
tative coronary angiography. Cathet Cardiovasc Diagn. 1993;29(4): cise testing for reducing hospital use after low-risk chest pain. ACP
314–21. J Club. 2002;136(1):8.
8. Nissen SE, Gurley JC. Application of intravascular ultrasound for 23. Gandelman G, Bodenheimer MM. Screening coronary arteriogra-
detection and quantitation of coronary atherosclerosis. Int J Card phy in the primary prevention of coronary artery disease. Heart Dis.
Imaging. 1991;6(3-4):165–77. 2003;5(5):335–44.
9. Topol EJ, Nissen SE. Our preoccupation with coronary luminol- 24. Patel MR, Dehmer GJ, Hirshfeld JW, Smith PK, Spertus
ogy. The dissociation between clinical and angiographic findings in JA. ACCF/SCAI/STS/AATS/AHA/ASNC, 2009 Appropriateness
ischemic heart disease. Circulation. 1995;92(8):2333–42. Criteria for Coronary Revascularization: a report by the American
10. Arnett EN, Isner JM, Redwood DR, Kent KM, Baker WP, College of Cardiology Foundation Appropriateness Criteria Task
Ackerstein H, et al. Coronary artery narrowing in coronary heart Force, Society for Cardiovascular Angiography and Interventions,
disease: comparison of cineangiographic and necropsy findings. Society of Thoracic Surgeons, American Association for Thoracic
Ann Intern Med. 1979;91(3):350–6. Surgery, American Heart Association, and the American Society
11. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis of Nuclear Cardiology Endorsed by the American Society of
GJ. Compensatory enlargement of human atherosclerotic coronary Echocardiography, the Heart Failure Society of America, and the
arteries. N Engl J Med. 1987;316(22):1371–5. Society of Cardiovascular Computed Tomography. J Am Coll
12. Stiel GM, Stiel LS, Schofer J, Donath K, Mathey DG. Impact of Cardiol. 2009;53(6):530–53. Epub 2009/02/07.
compensatory enlargement of atherosclerotic coronary arteries on 25. Patel MR, Peterson ED, Dai D, Brennan JM, Redberg RF, Anderson
angiographic assessment of coronary artery disease. Circulation. HV, et al. Low diagnostic yield of elective coronary angiography. N
1989;80(6):1603–9. Engl J Med. 2010;362(10):886–95. Epub 2010/03/12.
13. Yamashita T, Colombo A, Tobis JM. Limitations of coronary angi- 26. Ravipati G, Aronow WS, Lai H, Shao J, DeLuca AJ, Weiss MB,
ography compared with intravascular ultrasound: implications for et al. Comparison of sensitivity, specificity, positive predictive
coronary interventions. Prog Cardiovasc Dis. 1999;42(2):91–138. value, and negative predictive value of stress testing versus 64-mul-
14. Macieira-Coelho E, Cantinho G, da Costa BB, Garcia-Alves M, tislice coronary computed tomography angiography in predicting
Lacerda AP, Dionisio I, et al. Minimal residual coronary obstructions obstructive coronary artery disease diagnosed by coronary angiog-
in patients who suffered a first myocardial infarction. A prospective raphy. Am J Cardiol. 2008;101(6):774–5. Epub 2008/03/11.
25 Cardiovascular CT: Interventional Cardiology Applications 503

27. Fazel P, Peterman MA, Schussler JM. Three-year outcomes and 42. Li P, Gai LY, Yang X, Sun ZJ, Jin QH. Computed tomography
cost analysis in patients receiving 64-slice computed tomographic angiography-guided percutaneous coronary intervention in chronic
coronary angiography for chest pain. Am J Cardiol. 2009;104(4): total occlusion. J Zhejiang Univ Sci B. 2010;11(8):568–74. Epub
498–500. 2010/07/30.
28. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert 43. Curtis MJ, Traboulsi M, Knudtson ML, Lester WM. Left main
E, et al. Diagnostic performance of 64-multidetector row coro- coronary artery dissection during cardiac catheterization. Can
nary computed tomographic angiography for evaluation of coro- J Cardiol. 1992;8(7):725–8. Epub 1992/09/01.
nary artery stenosis in individuals without known coronary artery 44. Devlin G, Lazzam L, Schwartz L. Mortality related to diagnos-
disease: results from the prospective multicenter ACCURACY tic cardiac catheterization. The importance of left main coro-
(Assessment by Coronary Computed Tomographic Angiography nary disease and catheter induced trauma. Int J Card Imaging.
of Individuals Undergoing Invasive Coronary Angiography) trial. 1997;13(5):379–84. discussion 85-6. Epub 1997/11/14.
J Am Coll Cardiol. 2008;52(21):1724–32. Epub 2008/11/15. 45. Schussler JM, Dockery WD, Johnson KB, Rosenthal RL, Stoler
29. Meijboom WB, Meijs MF, Schuijf JD, Cramer MJ, Mollet NR, RC. Critical left main coronary artery stenosis diagnosed by com-
van Mieghem CA, et al. Diagnostic accuracy of 64-slice computed puted tomographic coronary angiography. Proc (Bayl Univ Med
tomography coronary angiography: a prospective, multicenter, Cent). 2005;18(5):407.
multivendor study. J Am Coll Cardiol. 2008;52(25):2135–44. Epub 46. Morice MC, Serruys PW, Kappetein AP, Feldman TE, Stahle E,
2008/12/20. Colombo A, et al. Five-year outcomes in patients with left main
30. Mowatt G, Cook JA, Hillis GS, Walker S, Fraser C, Jia X, et al. disease treated with either percutaneous coronary intervention or
64-Slice computed tomography angiography in the diagnosis and coronary artery bypass grafting in the synergy between percuta-
assessment of coronary artery disease: systematic review and meta- neous coronary intervention with taxus and cardiac surgery trial.
analysis. Heart. 2008;94(11):1386–93. Epub 2008/08/02. Circulation. 2014;129(23):2388–94. Epub 2014/04/05.
31. Stein JH, Uretz EF, Parrillo JE, Barron JT. Cost and appropriateness 47. Ko BS, Crossett M, Seneviratne SK. Pre-procedural combined cor-
of radionuclide exercise stress testing by cardiologists and non- onary angiography and stress myocardial perfusion imaging using
cardiologists. Am J Cardiol. 1996;77(2):139–42. Epub 1996/01/15. 320-detector CT in unprotected left main and ostial left anterior
32. Dharampal AS, Papadopoulou SL, Rossi A, Meijboom WB, descending artery intervention. Cardiovascular intervention and
Weustink A, Dijkshoorn M, et al. Diagnostic performance of com- therapeutics. 2014. Epub 2014/08/02.
puted tomography coronary angiography to detect and exclude 48. Gauss S, Pflederer T, Marwan M, Daniel WG, Achenbach S.
left main and/or three-vessel coronary artery disease. Eur Radiol. Analysis of left main coronary artery and branching geometry by
2013;23(11):2934–43. Epub 2013/07/03. coronary CT angiography. Int J Cardiol. 2011;146(3):469–70. Epub
33. Otsuka M, Bruining N, Van Pelt NC, Mollet NR, Ligthart JM, 2010/12/15.
Vourvouri E, et al. Quantification of coronary plaque by 64-slice 49. Budoff MJ, Rasouli ML, Shavelle DM, Gopal A, Gul KM, Mao SS,
computed tomography: a comparison with quantitative intracoronary et al. Cardiac CT angiography (CTA) and nuclear myocardial perfu-
ultrasound. Invest Radiol. 2008;43(5):314–21. Epub 2008/04/22. sion imaging (MPI)-a comparison in detecting significant coronary
34. Van Mieghem CA, Thury A, Meijboom WB, Cademartiri F, Mollet artery disease. Acad Radiol. 2007;14(3):252–7. Epub 2007/02/20.
NR, Weustink AC, et al. Detection and characterization of coronary 50. Gupta G, Anwar A, Brophey MD, Schussler JM. Complementary
bifurcation lesions with 64-slice computed tomography coronary utility of multislice computed tomographic coronary angiogra-
angiography. Eur Heart J. 2007;28(16):1968–76. Epub 2007/07/12. phy for detection of high-grade lesions in patients with negative
35. Kim SY, Lee HJ, Kim YJ, Hur J, Hong YJ, Yoo KJ, et al. stress myocardial perfusion imaging. Proc (Bayl Univ Med Cent).
Coronary computed tomography angiography for selecting coro- 2008;21(4):389–91. Epub 2008/11/05.
nary artery bypass graft surgery candidates. Ann Thorac Surg. 51. Tonino PA, De Bruyne B, Pijls NH, Siebert U, Ikeno F, van’ t
2013;95(4):1340–6. Epub 2013/03/07. Veer M, et al. Fractional flow reserve versus angiography for guid-
36. Bhella PS, Hassan Y, Schussler JM. Usefulness of 64-slice coro- ing percutaneous coronary intervention. N Engl J Med. 2009;
nary computed tomographic angiography in the planning of per- 360(3):213–24. Epub 2009/01/16.
cutaneous coronary intervention. Proc (Bayl Univ Med Cent). 52. Pijls NH, Fearon WF, Tonino PA, Siebert U, Ikeno F, Bornschein
2010;23(1):27–8. Epub 2010/02/17. B, et al. Fractional flow reserve versus angiography for guiding per-
37. Berbarie RF, Dockery WD, Johnson KB, Rosenthal RL, Stoler RC, cutaneous coronary intervention in patients with multivessel coro-
Schussler JM. Use of multislice computed tomographic coronary nary artery disease: 2-year follow-up of the FAME (Fractional Flow
angiography for the diagnosis of anomalous coronary arteries. Am Reserve Versus Angiography for Multivessel Evaluation) study.
J Cardiol. 2006;98(3):402–6. Epub 2006/07/25. J Am Coll Cardiol. 2010;56(3):177–84. Epub 2010/06/12.
38. Pflederer T, Marwan M, Ropers D, Daniel WG, Achenbach S. CT 53. Tonino PA, Fearon WF, De Bruyne B, Oldroyd KG, Leesar MA,
angiography unmasking catheter-induced spasm as a reason for Ver Lee PN, et al. Angiographic versus functional severity of cor-
left main coronary artery stenosis. J Cardiovasc Comput Tomogr. onary artery stenoses in the FAME study fractional flow reserve
2008;2(6):406–7. Epub 2008/12/17. versus angiography in multivessel evaluation. J Am Coll Cardiol.
39. Mollet NR, Hoye A, Lemos PA, Cademartiri F, Sianos G, 2010;55(25):2816–21. Epub 2010/06/29.
McFadden EP, et al. Value of preprocedure multislice computed 54. Choi AD, Joly JM, Chen MY, Weigold WG. Physiologic evalua-
tomographic coronary angiography to predict the outcome of per- tion of ischemia using cardiac CT: Current status of CT myocardial
cutaneous recanalization of chronic total occlusions. Am J Cardiol. perfusion and CT fractional flow reserve. J Cardiovasc Comput
2005;95(2):240–3. Epub 2005/01/12. Tomogr. 2014;8(4):272–81. Epub 2014/08/26.
40. Van Mieghem CA, van der Ent M, de Feyter PJ. Percutaneous 55. Ko BS, Cameron JD, Leung M, Meredith IT, Leong DP, Antonis
coronary intervention for chronic total occlusions: value of prepro- PR, et al. Combined CT coronary angiography and stress myo-
cedural multislice CT guidance. Heart. 2007;93(11):1492. Epub cardial perfusion imaging for hemodynamically significant
2007/10/16. stenoses in patients with suspected coronary artery disease: a com-
41. Singh S, Singh N, Gulati GS, Ramakrishnan S, Kumar G, Sharma parison with fractional flow reserve. JACC Cardiovasc Imaging.
S, et al. Dual-source computed tomography for chronic total 2012;5(11):1097–111. Epub 2012/11/17.
occlusion of coronary arteries. Catheter Cardiovasc Interv. 2014. 56. Andreini D, Pontone G, Bartorelli AL, Trabattoni D, Mushtaq S,
doi:10.1002/ccd.25516. Bertella E, et al. Comparison of feasibility and diagnostic accuracy
504 J.M. Schussler

of 64-slice multidetector computed tomographic coronary angi- 71. Dehghani P, Marcuzzi D, Cheema AN. Use of multislice CT coro-
ography versus invasive coronary angiography versus intravascu- nary angiography to assess degree of left main stent overhang into
lar ultrasound for evaluation of in-stent restenosis. Am J Cardiol. the aorta. Heart. 2009;95(9):708. Epub 2009/04/16.
2009;103(10):1349–58. Epub 2009/05/12. 72. Jabara R, Chronos N, Klein L, Eisenberg S, Allen R, Bradford S,
57. Wijpkema JS, Tio RA, Zijlstra F. Quantification of coronary lesions et al. Comparison of multidetector 64-slice computed tomographic
by 64-slice computed tomography compared with quantitative angiography to coronary angiography to assess the patency of cor-
coronary angiography and intravascular ultrasound. J Am Coll onary artery bypass grafts. Am J Cardiol. 2007;99(11):1529–34.
Cardiol. 2006;47(4):891; author reply -2. Epub 2006/02/21. Epub 2007/05/29.
58. Hammer-Hansen S, Kofoed KF, Kelbaek H, Kristensen T, Kuhl 73. Chiurlia E, Menozzi M, Ratti C, Romagnoli R, Modena
JT, Thune JJ, et al. Volumetric evaluation of coronary plaque in MG. Follow-up of coronary artery bypass graft patency by mul-
patients presenting with acute myocardial infarction or stable tislice computed tomography. Am J Cardiol. 2005;95(9):1094–7.
angina pectoris-a multislice computerized tomography study. Am Epub 2005/04/22.
Heart J. 2009;157(3):481–7. Epub 2009/03/03. 74. Meyer TS, Martinoff S, Hadamitzky M, Will A, Kastrati A,
59. Inoue F, Sato Y, Matsumoto N, Tani S, Uchiyama T. Evaluation Schomig A, et al. Improved noninvasive assessment of coronary
of plaque texture by means of multislice computed tomography artery bypass grafts with 64-slice computed tomographic angi-
in patients with acute coronary syndrome and stable angina. Circ ography in an unselected patient population. J Am Coll Cardiol.
J. 2004;68(9):840–4. Epub 2004/08/27. 2007;49(9):946–50. Epub 2007/03/06.
60. Kunimasa T, Sato Y, Sugi K, Moroi M. Evaluation by multislice 75. Gao C, Liu Z, Li B, Xiao C, Wu Y, Wang G, et al. Comparison
computed tomography of atherosclerotic coronary artery plaques of graft patency for off-pump and conventional coronary arte-
in non-culprit, remote coronary arteries of patients with acute coro- rial bypass grafting using 64-slice multidetector spiral computed
nary syndrome. Circ J. 2005;69(11):1346–51. Epub 2005/10/26. tomography angiography. Interact Cardiovasc Thorac Surg.
61. Kunita E, Fujii T, Urabe Y, Tsujiyama S, Maeda K, Tasaki N, et al. 2009;8(3):325–9. Epub 2008/12/11.
Coronary plaque stabilization followed by color code plaque(TM) 76. Marini D, Agnoletti G, Brunelle F, Sidi D, Bonnet D, Ou P. Cardiac
analysis with 64-slice multidetector row computed tomography. CT angiography after coronary artery surgery in children using
Circ J. 2008. Epub 2008/12/17. 64-slice CT scan. Eur J Radiol. 2008. Epub 2008/07/16.
62. Yang QH, Chen YJ, Liu QQ, Dong M, Wen L, Song X, et al. 77. Schussler JM, White CH, Fontes MA, Master SA, Hamman BL.
Comparison of 320-row computed tomography coronary angiogra- Spyder proximal coronary vein graft patency over time: the SPPOT
phy with conventional angiography for the assessment of coronary study. Heart Surg Forum. 2009;12(1):E49–53. Epub 2009/02/24.
artery disease with different atherosclerotic plaque characteristics. 78. Schachner T, Feuchtner GM, Bonatti J, Bonaros N, Oehlinger A,
J Comput Assist Tomogr. 2012;36(6):646–53. Epub 2012/11/30. Gassner E, et al. Evaluation of robotic coronary surgery with intra-
63. Schwartz BG, Schussler JM, Rosenthal RL. Tumor-like coronary operative graft angiography and postoperative multislice computed
atheroma: a modern coronary evaluation with a historical perspec- tomography. Ann Thorac Surg. 2007;83(4):1361–7. Epub 2007/03/27.
tive. Texas Heart Institute journal / from the Texas Heart Institute 79. Gorantla R, Murthy JS, Muralidharan TR, Mandava R, Dev B,
of St Luke’s Episcopal Hospital, Texas Children's Hospital. Chandaga H, et al. Diagnostic accuracy of 64-slice multidetector
2011;38(3):275–8. Epub 2011/07/02. computed tomography in evaluation of post-coronary artery bypass
64. Funabashi N, Asano M, Komuro I. Non-calcified plaques of coro- grafts in correlation with invasive coronary angiography. Indian
nary arteries with obvious outward remodeling demonstrated by Heart J. 2012;64(3):254–60. Epub 2012/06/06.
multislice computed tomography. Int J Cardiol. 2006;109(2):264. 80. Peterman MA, Hamman BL, Schussler JM. 64-Slice CT angiogra-
Epub 2006/04/29. phy of saphenous vein graft anastomoses fashioned with interrupted
65. Tanaka M, Tomiyasu KI, Fukui M, Akabame S, Kobayashi-Takenaka nitinol clips. Ann Thorac Surg. 2007;83(3):1204. Epub 2007/02/20.
Y, Nakano K, et al. Evaluation of characteristics and degree of remod- 81. Schussler JM, Hamman BL. Multislice cardiac computed tomogra-
eling in coronary atherosclerotic lesions by 64-detector multislice com- phy of symmetry bypass connector. Heart. 2004;90(12):1480. Epub
puted tomography (MSCT). Atherosclerosis. 2008. Epub 2008/09/09. 2004/11/18.
66. Pedrazzini GB, D’Angeli I, Vassalli G, Faletra FF, Klersy C, 82. Malagutti P, Nieman K, Meijboom WB, van Mieghem CA, Pugliese
Pasotti E, et al. Assessment of coronary stenosis, plaque burden F, Cademartiri F, et al. Use of 64-slice CT in symptomatic patients
and remodeling by multidetector computed tomography in patients after coronary bypass surgery: evaluation of grafts and coronary
referred for suspected coronary artery disease. J Cardiovasc Med arteries. Eur Heart J. 2007;28(15):1879–85. Epub 2006/07/19.
(Hagerstown). 2011;12(2):122–30. Epub 2010/11/04. 83. Nazeri I, Shahabi P, Tehrai M, Sharif-Kashani B, Nazeri A.
67. Kroner ES, van Velzen JE, Boogers MJ, Siebelink HM, Schalij Assessment of patients after coronary artery bypass grafting
MJ, Kroft LJ, et al. Positive remodeling on coronary computed using 64-slice computed tomography. Am J Cardiol. 2009;103(5):
tomography as a marker for plaque vulnerability on virtual histol- 667–73. Epub 2009/02/24.
ogy intravascular ultrasound. Am J Cardiol. 2011;107(12):1725–9. 84. Berbarie RF, Aslam MK, Kuiper JJ, Matter GJ, Martin AW, Roberts
Epub 2011/04/13. WC, et al. Preoperative exclusion of significant coronary artery dis-
68. Hang CL, Lee YW, Guo GB, Youssef AA, Yip HK, Liu CF, et al. ease by 64-slice CT coronary angiography in a patient with a left
Evaluation of coronary artery stent patency by using 64-slice atrial myxoma. Proc (Bayl Univ Med Cent). 2006;19((2):121. Epub
multi-detector computed tomography and conventional coronary 2006/04/13.
angiography: a comparison with intravascular ultrasonography. Int 85. Gilard M, Cornily JC, Pennec PY, Joret C, Le Gal G, Mansourati
J Cardiol. 2013;166(1):90–5. Epub 2011/11/08. J, et al. Accuracy of multislice computed tomography in the pre-
69. Abdelkarim MJ, Ahmadi N, Gopal A, Hamirani Y, Karlsberg RP, operative assessment of coronary disease in patients with aortic
Budoff MJ. Noninvasive quantitative evaluation of coronary artery valve stenosis. J Am Coll Cardiol. 2006;47(10):2020–4. Epub
stent patency using 64-row multidetector computed tomography. 2006/05/16.
J Cardiovasc Comput Tomogr. 2010;4(1):29–37. Epub 2010/02/18. 86. Scheffel H, Leschka S, Plass A, Vachenauer R, Gaemperli O,
70. Rubinshtein R, Ben-Dov N, Halon DA, Lavi I, Finkelstein A, Lewis Garzoli E, et al. Accuracy of 64-slice computed tomography for the
BS, et al. Geographic miss with aorto-ostial coronary stent implan- preoperative detection of coronary artery disease in patients with
tation: insights from high-resolution coronary computed tomogra- chronic aortic regurgitation. Am J Cardiol. 2007;100(4):701–6.
phy angiography. EuroIntervention. 2014. Epub 2014/04/04. Epub 2007/08/19.
25 Cardiovascular CT: Interventional Cardiology Applications 505

87. Andreini D, Pontone G, Mushtaq S, Bartorelli AL, Ballerini G, 89. Tandon A, Allison RB, Grayburn PA, Hamman BL, Schussler
Bertella E, et al. Diagnostic accuracy of multidetector computed JM. Preoperative visualization of a muscular ventricular septal
tomography coronary angiography in 325 consecutive patients defect by 64-slice cardiac computed tomography. Proc (Bayl Univ
referred for transcatheter aortic valve replacement. Am Heart J. Med Cent). 2008;21(3):281. Epub 2008/07/17.
2014;168(3):332–9. Epub 2014/09/01. 90. Reese EA, Graybum PA, Hebeler RF, Rothstein JM, Schussler
88. Gibbs WN, Hamman BL, Roberts WC, Schussler JM. Diagnosis of JM. Preoperative visualization of an atrial septal defect by 64-slice
congenital unicuspid aortic valve by 64-slice cardiac computed tomog- cardiac computed tomography. Proc (Bayl Univ Med Cent).
raphy. Proc (Bayl Univ Med Cent). 2008;21((2):139. Epub 2008/04/03. 2009;22(3):234–5. Epub 2009/07/28.
 Cardiovascular Magnetic Resonance
Imaging: Overview of Clinical 26
Applications in the Context
of Cardiovascular CT

Jerold S. Shinbane, Jabi E. Shriki, Antreas Hindoyan,

and Patrick M. Colletti

Abstract
CMR can evaluate myocardial contractility, volumetry, strain, flow, perfusion, viability, and
vascular anatomy without ionizing radiation or iodinated contrast agents. Multiple pulse
sequences are acquired in different orientations to the heart and relevant vasculature, some
of which require gadolinium-based contrast agents. A strength of CMR is the ability to
determine tissue characteristics including edema, hemorrhage, iron content, inflammation,
and diffuse and focal fibrosis useful for the diagnosis of cardiomyopathic processes, peri-
cardial disease, and cardiac masses. CMR assessment of cardiovascular structure, function,
hemodynamics, extracardiac vasculature and thoracic structure, makes it a useful adjunct to
echocardiography in patients with congenital heart disease and valvular disease. Although
imaging of the coronary arteries is feasible with CMR, CCTA is the gold standard for non-
invasive coronary angiography providing detailed visualization of the entire coronary artery
tree. Decisions related to performing CMR versus CCTA require information patient profile
and strengths and limitations of each modality in relation to the posed clinical question.

Keywords
Anomalous Coronary Arteries • Cardiomyopathy • Cardiovascular Computed Tomographic
Angiography • Cardiovascular Magnetic Resonance Imaging • CMR • Computed
Tomography • Congenital Heart Disease • Gadolinium • T1 • T2

Introduction
Electronic supplementary material The online version of this
chapter (doi:10.1007/978-3-319-28219-0_26) contains supplementary
material, which is available to authorized users. Technologic advances in cardiovascular magnetic resonance
imaging (CMR) and cardiovascular computed tomography
J.S. Shinbane, MD, FACC, FHRS, FSCCT (*) angiography (CCTA) allow these modalities to comprehen-
Division of Cardiovascular Medicine, Department of Internal
sively visualize cardiovascular structures and function. The
Medicine, Keck School of Medicine of the University
of Southern California, 1520 San Pablo Suite 300, decision to perform CMR versus CCTA requires knowledge
Los Angeles, CA 90033, USA of the individual strengths and limitations of these imaging
e-mail: [email protected] techniques, the specific details of a patient’s medical history,
J.E. Shriki, MD and the clinical questions which need to be answered. In many
Department of Radiology, Puget VA Health System, clinical scenarios, echocardiography is performed as the initial
University of Washington, Seattle, WA, USA
e-mail: [email protected]
A. Hindoyan, MD P.M. Colletti, MD
Division of Cardiovascular Medicine, Department of Internal Department of Radiology, Keck School of Medicine of the
Medicine, Keck School of Medicine of the University of Southern University of Southern California, Los Angeles, CA, USA
California, Los Angeles, CA, USA e-mail: [email protected]

© Springer International Publishing 2016 507

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_26
508 J.S. Shinbane et al.

31
study to assess cardiovascular substrates, with CMR or CCTA P to depict the high energy phosphates, phosphocreatine and
performed when further cardiovascular characterization is ATP, and inorganic phosphate to evaluate intracellular pH.
necessary and a noninvasive approach is preferable. Given the In comparisons to CMR, the strengths of CCTA technolo-
rapid evolution of CMR, appropriateness criteria have been gies currently include a greater ability to characterize details
developed for specific cardiovascular indications [1, 2]. of coronary vasculature, shorter study times, and the ability
to image patients with non-MR conditional devices. As
opposed to data acquisition with CCTA as one axial imaging
Principles of CMR in Comparison to CCTA sequence leading to one comprehensive 3-D data cube, CMR
requires multiple views and MR imaging sequences. CT also
CT creates a 3-D spatial x-ray transmission electron density allows quantification of coronary artery calcium for risk
map of the tissues within an imaging slice or volume. With stratification. Both CCTA and CMR technologies are advanc-
the use of currently available multidetector and dual source ing rapidly, and therefore future applications may change
CT scanners, this may be performed within seconds with comparative strengths and limitations.
acquisition of a data cube with subsequent multiplanar and
3-D image analysis. CMR can evaluate myocardial contrac-
tility, volumetry, strain, flow, perfusion, viability, and vascu- Patient Selection and Preparation
lar anatomy without ionizing radiation or iodinated contrast
agents. Multiple pulse sequences are acquired in different While there is considerable effort focused on reducing the
orientations to the heart and relevant vasculature, some of radiation exposure with CCTA techniques, the lack of ionizing
which require gadolinium-based contrast agents. These radiation is an important strength of CMR. This issue is espe-
modalities include: steady state free precession for volumes cially important in young patients, who may be at increased
and function, T2 black blood imaging without and with fat long term risk of malignancy [3]. As opposed to iodinated
saturation for anatomy and edema, pre contrast T1 mapping contrast agents used in CCTA, which enhance vascular struc-
for diffuse fibrosis, T2* assessment of iron content, velocity- tures by increasing CT Hounsfield Units, gadolinium-based
encoded imaging for hemodynamics and flow, tagging for contrast agents are paramagnetic and change the magnetic
strain, MR contrast angiography, first pass perfusion, post properties of water in close proximity to the contrast agent.
contrast T1 mapping for diffuse fibrosis and delayed gado- The relative safety of gadolinium-based contrast agents is a
linium enhancement for inflammation and fibrosis. significant strength of MR. Iodinated contrast agents are associ-
CMR generally requires a system with components ated with a significant incidence of acute side effects including
including a cardiac specific multi-element receiver coil for allergic reaction, hypotension, bronchospasm, and pulmonary
coverage with preservation of resolution and for parallel edema along with acute and chronic nephropathy. Gadolinium-
(simultaneous) data acquisitions, cardiac triggering hardware based contrast agents though have been rarely associated with
and software, and a cardiac processing workstation with both worsening renal function and in patients with moderate to
appropriate software. Advances in acquisition efficiency severe renal dysfunction, particularly those on dialysis, neph-
may allow for non-gated real time cardiac imaging for rogenic systemic fibrosis, prompting guidelines for use of these
localization and for applications in investigational protocols. agents [4–6]. CMR techniques such as black blood imaging
and bright blood imaging allow for differentiation of vascula-
ture without the injection of a contrast agent.
Strengths and Limitations of CMR CMR imaging sequences and technology continue to rap-
Versus CCTA idly evolve with 3-D real time acquisition and increased field
strengths to 3 Tesla with attendant increased signal to noise
Strengths of CMR include evaluation of myocardial tissue ratio, but can be limited by field inhomogeneity and specific
characteristics, myocardial perfusion, ventricular function, absorption rate limits [7–9]. The effects, safety, and imaging
myocardial metabolism, viability, shunts, valvular function, characteristics of field strengths greater than 3 Tesla require
flow velocities, and peripheral vasculature without the need further investigation [10–12].
for iodinated contrast media or x-ray irradiation. Paramagnetic Patient size and body habitus are also important in deciding
contrast agents have greatly expanded the applications of which imaging modality to employ. Image quality can be compro-
CMR. The paramagnetic element gadolinium, when attached mised in patients with an increased body mass index with CCTA
to a chelating agent like DTPA, provides a means for contrast and may require increased radiation exposure for adequate imag-
enhancement, allowing assessment of perfusion and delayed ing [13]. This limitation is less significant with CMR, although
enhancement to detect acutely infarcted myocardium and there are limitations in MR access due to extreme patient size
chronic myocardial scar. CMR spectroscopy provides non- related to magnet bore diameter and table weight limits.
invasive assessment of myocardial metabolism, providing a Prior to CMR, patients require a complete history for
mechanistic understanding of myocardial function when using ferromagnetic prosthetic implants, devices, or depositions.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 509

a b c

d e f

Fig. 26.1 Artifact caused by pacemaker leads (arrows) on serial short axis delayed gadolinium enhancement images in the setting of an MR
conditional pacemaker. Panels (a–f) Serial slices base to mid ventricle

These may have relative or absolute contraindications to times on the order of seconds. The patient’s ability to lie still
MR imaging. It is important to ensure that patients with in a supine position and comply with breath hold commands
susceptible devices are not exposed to the MR environment. is important to both technologies, but can be more easily
Most prosthetic heart valves and annuloplasty rings can be achieved with CCTA given the short study times.
safely scanned, but specific details of compatibility need to Claustrophobia is a common consideration in imaging some
be assessed individually prior to patient study [14]. There patients, although, with appropriate premedication, this is
has been evolution in the scanning of patients with cardiac seldom a cause for premature termination of an examination
devices such as pacemakers and implantable cardiac defibril- [24, 25]. Larger bore magnets, open magnets, and visual
lators over time. Initially considered absolute contraindica- devices allowing patients to see out of the magnet may make
tions for MRI, some preliminary data suggested that imaging this even less of an issue in the future.
may not be absolutely contraindicated in this setting with During image acquisition, special attention needs to be
specification of certain device and scanning conditions [15, focused on electrocardiographic recording for monitoring and
16]. Detailed knowledge of patient, device, scanner, scanning gating, as the MR environment can interfere with sensing of
protocol, alternative imaging techniques and importance of the QRS complex. Attention to skin prep, lead placement, and
the clinical question are important factors in determination ECG vector can improve the ability to perform ECG gating,
of individualized risk versus benefit of performance of an which is especially important when stress imaging is being
MR study [17, 18]. Some cardiac device technologies have considered [26, 27]. Due to acoustic noise associated with
now been engineered to be MR conditional [18–23]. Even in scanning, auditory protection with ear plugs is necessary [28].
the setting of scanning patients with MR conditional devices,
artifacts caused by leads and generators can affect image
quality (Fig. 26.1). Coronary Artery Visualization
Although study times for CMR have decreased due to
advances in technology as well as efficiency of imaging cen- CMR techniques can visualize coronary arteries for the
ters in performing protocols, studies are still significantly assessment of coronary artery disease [29–33].
longer than those achieved with CCTA which have scanning Additionally, CMR can assess patency and stenoses of
510 J.S. Shinbane et al.

coronary artery bypass grafts [34]. Advances in technique Assessment for Ventricular Myopathy
have improved the ability to visualize coronary arteries
with respiratory gating, but there are issues of cardiac, Ischemic Cardiomyopathy
coronary artery, and respiratory motion as well as prob-
lems with assessment of small caliber vessels [35–37]. CMR can characterize cardiac structures and function by
Whole heart imaging with respiratory gating has improved reproducibly assessing right and left ventricular volumes,
the ability to visualize the coronary arteries [31–33]. ejection fraction, wall thickness, and wall motion [57–62].
Although imaging of the coronary arteries is feasible with The ability to comprehensively assess ejection fraction, wall
CMR, CCTA is the gold standard for noninvasive coro- motion, perfusion, and viability is a great strength of CMR in
nary angiography providing detailed visualization of the the characterization of myocardial substrates associated with
entire coronary artery tree. An additional strength of coronary artery disease. Multimodal assessment with compo-
CCTA is fractional flow reserve based on using computa- nents including coronary anatomy, ventricular function, per-
tional fluid dynamics to assess for the significance of cor- fusion with pharmacologic stress, and assessment of fibrosis
onary artery stenoses [38–42]. provides comprehensive evaluation of ischemic heart disease
Since myocardial infarction can occur due to plaque rup- with high accuracy and predictive value [30, 63–66].
ture and thrombosis in coronary arteries without obstructive The performance of rest and stress first pass imaging as
disease, there is a need for techniques to characterize plaques well as delayed enhancement imaging are practical strengths
potentially at higher risk for rupture [43, 44]. Both CCTA of CMR important to characterization of ischemia, myocar-
and CMR can assess tissue characteristics of coronary artery dial infarction, and ischemic cardiomyopathy (Figs. 26.2,
plaque, but identification of vulnerable plaques requires fur- 26.3, 26.4, 26.5, 26.6 and 26.7, Video 1). First-pass perfusion
ther study [45]. CMR can assess tissue characteristics of ves- images of the heart, acquired immediately after injection of
sel wall and atheromas through assessment of fibrous tissue, gadolinium can be obtained with CMR and are useful in evalu-
fat, and calcified lesion components, but requires continued ation of perfusion abnormalities at rest and during pharmaco-
investigation to identify characteristics of vulnerable plaques logic stress [67–70]. CMR perfusion correlates with invasive
[46, 47]. CMR can assess for vascular remodeling with fractional flow reserve and offers prognostic information
changes in wall thickness and lumen size [48]. Non-calcified important to risk stratification [68, 71–74]. Quantitative perfu-
plaque detection and quantification between CMR and CT sion analysis and 3-D myocardial perfusion providing whole
have been comparable, but CMR provides greater informa- heart coverage are being investigated [65, 75]. Preliminary
tion on tissue characteristics associated with plaques and comparison of a CCTA protocol including coronary angiog-
vascular injury [49, 50]. raphy and stress/rest perfusion versus CMR perfusion dem-
Anomalous coronary arteries can be diagnosed with onstrated similar accuracy using invasive catheterization with
CMR [29, 51]. In addition to definition of anatomy of fractional flow reserve as a gold standard [76].
anomalous coronary artery origin, CMR can also assess The advent of CCTA fractional flow reserve allows for the
functional significance through perfusion imaging [52]. assessment of hemodynamic significance of coronary artery
CCTA can more comprehensively assess the characteris- stenoses. CCTA fractional flow reserve can be obtained from
tics of anomalous coronary arteries including ostial loca- standard images using computational fluid dynamics to assess
tion and morphology, course, termination, and 3-D for significance of coronary artery stenoses. Specialized com-
relationship to thoracic vascular and nonvascular structure putational programs may be applied to good quality CCTA
[53, 54]. datasets to track the longitudinal enhanced coronary artery
CMR is also useful in the assessment and understanding attenuation in search of relative differential drop-off that may
of microvascular coronary artery disease. Phosphorus-31 be associated with reduced fractional flow reserve. In initial
nuclear magnetic resonance spectroscopy has provided a studies, the use of CCTA coupled with CT fractional flow
window into understanding myocardial metabolism through reserve has increased the diagnostic accuracy of studies over
assessment of myocardial high-energy phosphates. This tool traditional stress imaging modalities using invasive fractional
has allowed insight into mechanisms of chest pain in the flow reserve as a gold standard [38–42]. Further innovation,
absence of obstructive coronary artery disease [55]. Studies with evaluation for accuracy, reproducibility, standardization
have demonstrated direct evidence of metabolic abnormalities of acquisition and reporting, and practicality of performance
consistent with ischemia in women with chest pain without as part of CCTA analysis is ongoing [77].
obstructive coronary artery disease, and proven essential in With delayed enhancement images obtained approxi-
forwarding the understanding of microvascular coronary mately 10 min after gadolinium-based contrast administra-
artery disease [56]. tion, gadolinium clears from normal myocardium, but
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 511

Fig. 26.2 First pass myocardial perfusion study with serial short axis ment. Panel (c) Right and left ventricular chamber enhancement. Panel
images demonstrating the progression of gadolinium enhancement. (d) Ventricular myocardial enhancement
Panel (a) Pre-gadolinium. Panel (b) Right ventricular chamber enhance-

Fig. 26.3 First pass perfusion (left panel) and delayed gadolinium anterior, and anterolateral walls (left panel arrows) with matching areas
enhancement images (right panel) demonstrating decreased signal of delayed contrast enhancement (right panel arrows) consistent with
intensity in a subendocardial distribution involving the anteroseptal, an anterolateral myocardial infarction
512 J.S. Shinbane et al.

Fig. 26.6 Transmural inferolateral myocardial infarction (arrows) on a

Fig. 26.4 Delayed gadolinium enhancement view showing a myocar- delayed gadolinium enhancement short axis view
dial infarct (arrows) with extensive involvement of the mid anterior
wall and apex due to mid occlusion of a wraparound left anterior
descending coronary artery
subendocardial delayed enhancement and increasing degrees
of transmural extension depending on the extent of infarct
[81]. There may be areas of peri-infarct tissue heterogeneity
representing areas of viable myocardium and fibrosis. These
heterogeneous areas may increase the propensity for the
development of ventricular tachycardia [82]. Microvascular
obstruction is usually depicted as a subendocardial non-
enhancing area due to tissue necrosis which is completely
surrounded by delayed enhancement [83].
In ischemic cardiomyopathy, gadolinium delayed
enhancement images can assess for areas of viability prior to
potential revascularization. Specifically, in patients with
ischemic cardiomyopathy, delayed hyperenhancement
correlates with lack of viability defined by thallium single
photon emission computed tomography [84]. Soon after
acute myocardial infarction, gadolinium delayed
enhancement CMR provides assessment of infarct size
which correlates well with clinical infarct indices [85]. The
degree of wall thickening correlates with degree of
myocardial non-enhancement on delayed images after recent
myocardial infarction and predicts improvement in wall
thickening as assessed by follow-up examinations [86].
Fig. 26.5 Delayed gadolinium enhancement 2 chamber view demon- In addition to late gadolinium enhancement, techniques
strating transmural myocardial enhancement and wall thinning due to for assessment of tissue damage associated with acute
infarction involving the mid to distal left anterior descending coronary myocardial infarction include pre-contrast T1-mapping
artery distribution and T2 weighted imaging for edema. Pre-contrast T1 map-
enhances areas of fibrosis or inflammation [78]. Delayed ping may be helpful in assessment of the extent of myo-
enhancement imaging using iodinated contrast agent with cardial injury in acute myocardial infarction [87, 88]. Late
CCTA is also able to image fibrosis associated with myocar- gadolinium enhancement may underestimate the extent
dial infarction, but is currently less well established [79, 80]. of acute myocardial infarction compared to T2 weighted
Delayed gadolinium enhancement may be useful in sequences, particularly in patients with acute reperfusion
assessing a variety of cardiomyopathic processes. Myocardial [89]. Hypointensity on T2 weighted imaging is a marker of
infarction related delayed contrast enhancement typically hemorrhage and is associated with infarct extent, microvas-
occurs in the anatomic distribution of coronary arteries with cular obstruction, depression of ventricular function, and
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 513

a b

Fig. 26.7 Delayed contrast enhancement views showing wall thinning thinning and delayed gadolinium enhancement (arrows). Panel (b) 2
and delayed contrast enhancement associated with a myocardial infarct. chamber view demonstrating the apical wall thinning and delayed gad-
Panel (a) 4 chamber view demonstrating apical and mid septal wall olinium enhancement (arrows)

prognosis [90]. T2* imaging can provide identification and Mid-wall fibrosis can occur in dilated non-ischemic car-
quantification of post infarction and post reperfusion intra- diomyopathy, and has been associated with worse prognosis
myocardial hemorrhage and is associated with microvascu- and ventricular arrhythmias [92, 93]. The presence and
lar obstruction [91]. degree of gadolinium enhancement can predict remodeling
response to beta-blockers in both ischemic and non-ischemic
cardiomyopathy [93]. The presence of late gadolinium
Characterization of Non-ischemic enhancement is an independent predictor of malignant
Cardiomyopathic Processes arrhythmias and of increased overall mortality, heart failure
and hospitalization [94–96]. The extent of fibrosis can be
The same sequences used to characterize ischemic quantified in dilated non-ischemic cardiomyopathy, extent of
cardiomyopathy can be utilized in the assessment of non- fibrosis has been shown to be a predictor of malignant
ischemic cardiomyopathic processes. Delayed contrast arrhythmias and prognosis [97, 98].
enhancement may be useful in differentiating ischemic from Myocardial T1 mapping allows assessment of diffuse
non-ischemic dilated cardiomyopathy. A delayed myocardial fibrosis and can be performed with non-contrast
enhancement subendocardial to transmural infarct pattern in (native T1) and post-contrast (extracellular volume
the distribution of a coronary artery is more likely consistent measurement) sequences [99, 100]. Non-contrast (native T1)
with ischemic cardiomyopathy as opposed to other patterns studies demonstrate myocyte and interstitial disease. Post-
such as sub-epicardial and mid wall fibrosis [81]. contrast assessment of extracellular volume fraction is a
Interpretation of gadolinium delayed contrast enhance- marker of interstitial myocardial collagen content and is
ment has become more complex as it has been recognized elevated in fibrotic and infiltrative myocardial disease
to occur in a variety of cardiovascular disease processes processes. This novel modality has the potential for early
associated with fibrosis or inflammation. Interpretation of detection and disease monitoring for the clinical disease
delayed enhancement requires correlation of the individual staging of cardiomyopathic processes. In non-ischemic
patient’s medical history and the posed clinical question dilated cardiomyopathy, native T1 mapping can identify dif-
with the pattern of delayed enhancement. Assessment of the fuse fibrosis compared to normal myocardium [101]. Post-
sensitivity and specificity of delayed enhancement patterns contrast T1 mapping for the calculation of extracellular
for diagnoses of specific disease processes requires greater volume can be identified in severe dilated cardiomyopathy
investigation. and in some patients with early dilated cardiomyopathy [98].
514 J.S. Shinbane et al.

Preliminary assessment of extracellular volume by equilib- presence of apical delayed gadolinium enhancement [115].
rium contrast enhanced CCTA in cardiomyopathic processes The presence and extent of late gadolinium enhancement is
is being investigated [102, 103]. an independent predictor of prognosis in the apical variant of
hypertrophic cardiomyopathy [116, 117]. In children with
hypertrophic cardiomyopathy, the presence and extent of late
Hypertrophic Cardiomyopathy gadolinium enhancement is predictive of adverse events
similar to adults [118].
In hypertrophic cardiomyopathy, CMR and CCTA can be use- Delayed gadolinium enhancement has relevance for elec-
ful for defining phenotype, function, and potential etiology of trophysiology and interventional cardiology procedures in
ischemia. CMR can characterize regional wall thickness, hypertrophic cardiomyopathy patients. The extent of fibrosis
indexed ventricular mass, ejection fraction, fibrosis, valvular in hypertrophic cardiomyopathy is a predictor of inducibility
function and hemodynamic data including gradients (Video 2) of ventricular tachycardia during electrophysiology exams
[104–108]. Late gadolinium enhancement by CMR correlates [119]. Areas of late gadolinium enhancement correlate with
with the amount of myocardial fibrosis on histologic examina- areas of abnormal depolarization and repolarization and the
tion (Fig. 26.8) [109]. The presence of gadolinium enhance- origin of ventricular tachycardia in patients with hypertro-
ment in the substrate of hypertrophic cardiomyopathy provides phic cardiomyopathy and clinical ventricular tachycardia
prognostic risk information for all-cause and cardiac mortality [120]. Preoperative and follow-up studies may be useful in
[110]. Serial studies in patients with late gadolinium enhance- patients undergoing surgical myocardial resection or coro-
ment may demonstrate rapid progression [111, 112]. nary artery septal embolization [106, 121]. CMR can image
The presence and quantitative extent of late gadolinium location and extent of myocardial infarction created by ven-
enhancement in hypertrophic cardiomyopathy is predictive tricular septal ablation [122, 123]. Preliminary studies of
of the development of systolic dysfunction and sudden native T1 and post-contrast T1 mapping demonstrate that the
cardiac death events [113]. In comparison to non-ischemic presence of diffuse fibrosis can be detected non-invasively
dilated cardiomyopathy, the dilated phase of hypertrophic [101, 124, 125].
cardiomyopathy has a greater extent of delayed enhancement, CCTA can assess regional wall thickness comparable to
predominantly in the septal and anterior walls [114]. In CMR. CCTA delayed enhancement imaging can detect dense
apical hypertrophic cardiomyopathy, echocardiographic areas of fibrosis in hypertrophic cardiomyopathy, but can
assessment of the apex can be challenging. CMR can iden- underestimate total delayed enhancement [126]. Angina in
tify apical variants including an apical pouch as well as the hypertrophic cardiomyopathy can be due to multiple etiolo-
gies. Stress imaging can be associated with false positive
findings for epicardial coronary artery disease. CCTA is
therefore useful in the assessment for epicardial coronary
artery disease in hypertrophic cardiomyopathy [127].

Amyloidosis

Amyloid infiltrative cardiomyopathy occurs due to myocar-

dial amyloid deposition associated with a spectrum of dis-
ease processes including hematologic, chronic inflammatory,
hereditary and senescent etiologies. CMR delayed gadolinium
enhancement can detect amyloid accumulation in the intersti-
tium reflective of amyloid burden (Figs. 26.9 and 26.10) [128,
129]. Diffuse myocardial amyloid is a predictor of mortality
[130]. In systemic amyloid, the presence of delayed enhance-
ment is associated with worse prognosis [131, 132]. Patterns
of delayed gadolinium enhancement may differ depending on
etiology, with a transmural pattern more likely to be associ-
ated with transthyretin-related amyloidosis than light-chain
amyloidosis [133]. Assessment of diffuse amyloid can be
Fig. 26.8 Short axis delayed gadolinium enhancement view demon- challenging as it may be associated with inability to null myo-
strating contrast enhancement in hypertrophic cardiomyopathy cardium. The pre contrast assessment myocardium nulling is
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 515

important in amyloid, as there may be limited ability to null Anderson-Fabry Disease

myocardium before contrast infusion in diffuse amyloid. This
is important to the interpretation of inability to null myocar- Anderson-Fabry disease is an X-linked storage disease
dium on post contrast imaging [134]. due to abnormal sphingolipid metabolism which can lead
to significant ventricular myocardial thickening and can
therefore mimic hypertrophic cardiomyopathy and cardiac
amyloidosis. CMR can visualize involvement through use
of delayed gadolinium enhancement imaging in storage
diseases such as Anderson-Fabry disease [135]. Native
T1 mapping can demonstrate abnormalities before left
ventricular wall thickening has occurred and correlates
with early systolic and diastolic abnormalities as defined
by echocardiography [136]. In disease follow-up, CMR
has documented decreased left ventricular mass and wall
thickness and reduced myocardial T2 relaxation times
with therapy [137].

Sarcoidosis

Cardiac sarcoidosis can occur as part of systemic involvement

or can exist with solely cardiac involvement. Gadolinium
enhanced CMR can identify inflammation and fibrosis asso-
ciated with cardiac sarcoidosis (Fig. 26.11) [138]. CMR
delayed contrast enhancement in patients with systemic sar-
coid has been associated with a higher rate of sudden car-
diac death and ventricular tachyarrhythmias [139–141]. A
decrease in delayed contrast enhancement has been reported
with steroid therapy [142]. A significant degree of delayed
Fig. 26.9 Short axis delayed gadolinium contrast view demonstrating gadolinium enhancement has also been associated with a
diffuse, patchy delayed enhancement (arrows) associated with familial lack of ventricular functional improvement and poor out-
ATTR cardiac amyloidosis
comes with steroid therapy [143].

Fig. 26.11 Short axis delayed gadolinium enhancement view demon-

Fig. 26.10 Short axis delayed gadolinium image demonstrating strating cardiac sarcoidosis with involvement of the right ventricular
enhancement (arrows) due senile systemic ATTR amyloidosis aspect of the basal septum (arrow)
516 J.S. Shinbane et al.

CMR can be useful for assessment of prognosis in the

setting of myocarditis. In children with myocarditis, the
presence of late gadolinium enhancement in children pre-
dicted poor outcome [153]. In patients with clinical suspi-
cion of myocarditis, a normal CMR predicted good
prognosis which is independent of symptoms and other
clinical findings [154]. In acute myocarditis, CMR evi-
dence of edema was indicative of reversibility [155]. Data
on CCTA comparison to CMR are limited, but preliminar-
ily have demonstrated that in acute myocarditis, delayed
contrast enhancement CT correlated with CMR enhance-
ment [156–158].
CMR can detect early changes in autoimmune pro-
Fig. 26.12 Short axis delayed gadolinium enhancement images cesses causing myocarditis, including early changes of
demonstrate subepicardial enhancement associated with acute edema and subclinical perimyocardial involvement
myocarditis through delayed gadolinium enhancement [159, 160].
Combined CMR modalities of T2-weighted and early and
late enhancement are preliminarily being assessed for car-
Myocarditis diac involvement in systemic lupus erythematosus [161].
In contrast, CCTA can be used to assess for coronary artery
CMR has become an important modality for the diagno- involvement with systemic lupus erythematosis due to vas-
sis and characterization of acute and chronic myocarditis. culitis [162].
The Lake Louise Consensus Criteria have been created Myocarditis and cardiomyopathy can occur due to viral,
based on early and delayed gadolinium enhancement and bacterial, fungal, or parasitic infection. Gadolinium
edema imaging (Fig. 26.12) [144]. Delayed gadolinium enhancement associated with the inflammatory process in
enhancement can be seen in acute and chronic myocarditis. Chagas disease has also been reported [163]. In Chagas
A combined approach with early and delayed gadolinium disease, the extent of myocardial fibrosis correlates with
enhancement and edema imaging can be useful for diag- disease severity, and delayed enhancement imaging can
nosis and characterization of acute myocarditis and dif- detect involvement in the early subclinical phase of disease
ferentiation from acute myocardial infarction [145–147]. [164].
Additional findings of pericardial effusion and or pericar- Endocardial fibrosis is a rare form of restrictive cardiomy-
dial delayed enhancement can be seen associated with peri- opathy, which is challenging from the etiologic, diagnostic
myocarditis. Acute myocarditis findings may vary in regard and therapeutic standpoints with multiple potential associa-
to delayed gadolinium enhancement presence and pattern tions including ischemic, congenital, hematologic, autoim-
with variable correlation with histologic findings charac- mune and infectious disease processes [165–169]. This
terized by biopsy [148]. Late gadolinium enhancement is processes can occur in complex and potentially multifacto-
also useful in the diagnosis and characterization of chronic rial scenarios. CMR is helpful in the diagnosis of subendo-
myocarditis. cardial fibrosis due to the ability to differentiate tissue
T1 imaging is being assessed along with multiple other characteristics including normal myocardium, fibrosis,
CMR indices. In patients with severe subacute myocardi- edema, and thrombi (Fig. 26.13).
tis, late gadolinium enhancement coupled with T1 post-
contrast imaging had better diagnostic accuracy than
standard Lake Louise indices for myocarditis [149]. Hemochromatosis
Studies preliminarily assessing the relative value of T1 and
T2 for differentiation of acute versus chronic myocarditis CMR properties associated with myocardial iron content can
have demonstrated variable results as to the superiority of be useful for the assessment in primary hereditary causes of
T1 versus T2 imaging sequences [150–152]. iron overload as well as secondary transfusion- dependent
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 517

Fig. 26.13 Restrictive

cardiomyopathy with
endomyocardial fibrosis in a patient
with a history of parasitic infection
in the setting of rheumatoid
arthritis. A 4 chamber delayed
gadolinium enhancement image
shows endomyocardial fibrosis
which is most prominent in the mid
to apical left ventricle (white
arrows). A large wall-contoured
mural thrombus is present at the
left ventricular apex (black arrow).
Additionally, biatrial enlargement
is present. LA left atrium, LV left
ventricle, RA right atrium, RV right
ventricle

anemias. T2* relaxation times are useful for quantification has been reported [177–179]. CMR can be useful to detect
myocardial iron overload, serial surveillance for iron over- early structural and functional abnormalities in myotonic
load, and assessment of response to treatment [170–172]. muscular dystrophy [180]. In myotonic muscular dystrophy,
the presence of delayed gadolinium enhancement had a high
prevalence in patients without evidence of ECG, arrhythmia
Muscular Dystrophies monitoring or echo abnormalities [181]. Additionally, post-
contrast myocardial T1 abnormalities have been seen in
CMR can detect evidence of cardiac involvement in myotonic muscular dystrophy compared to control subjects
Duchenne muscular dystrophy. In young patients with [182].
Duchenne muscular dystrophy, abnormal strain patterns
occur and increase with age [173]. Abnormal post contrast
T1 findings can be seen, even in some patients with normal Takotsubo (Stress-Mediated) Cardiomyopathy
left ventricular ejection fraction and no evidence of delayed
gadolinium enhancement. Therefore, post contrast T1 CMR can be useful in differentiating Takotsubo (stress-
sequences could potentially be useful for detection of early mediated) cardiomyopathy from other etiologies in patients
cardiac involvement [174]. In Duchenne muscular dystro- presenting with ECG changes, cardiac enzyme elevation,
phy carriers, increased ventricular volumes, myocardial and regional wall motion abnormalities with no evidence of
mass reduction, regional myocardial thinning, depression of obstructive epicardial coronary artery disease. Areas of mid
ejection fraction, and late gadolinium enhancement are to apical reversible wall motion abnormities correlate with
common [175, 176]. In other muscular dystrophies such as evidence of edema on T2 weighted imaging and typically
Becker-Kiener and limb-girdle muscular dystrophy, occur without delayed contrast enhancement [183]. Late
depressed ejection fraction late gadolinium enhancement gadolinium enhancement has been reported, in the subacute
518 J.S. Shinbane et al.

phase of Takotsubo cardiomyopathy and was associated with should be considered in patients suspected of having ARVC
greater severity and longer recovery than in those patients prior to device placement.
without enhancement [184, 185]. The initial focus of CMR identification of ARVC/D
related to characterization of intramyocardial fat, but this

Arrhythmogenic Right Ventricular

Cardiomyopathy/Dysplasia (ARVC/D)

ARVC/D is associated with ventricular arrhythmias and

sudden cardiac death [186, 187]. Diagnosis is challenging
and involves multiple possible factors, including clinical
symptoms, family history, ECG and electrophysiologic
findings, ventricular anatomy and function, and ventricular
tissue characteristics [188, 189]. Imaging for abnormalities
associated with ARVC/D can be missed with multiple
imaging modalities. CMR has become the diagnostic
modality most commonly used to assess for ARVC/D, as
CMR can differentiate tissue characteristics, as well as pro-
vide assessment of right ventricular size, shape, and func-
tion (Fig. 26.14, Video 3). It is also important to note that
the differential diagnosis of right ventricular enlargement
and wall motion abnormalities includes right ventricular
cardiomyopathy due to pressure or volume overload due to
shunts, aortic valve, left ventricular, mitral valve, pulmo-
nary vein, pulmonary artery, pulmonary valve, and tricus-
pid valve abnormalities. CMR can comprehensively and
systematically assess for these etiologies of right ventricu- Fig. 26.14 Short axis delayed contrast enhancement view of arrhyth-
mogenic right ventricular cardiomyopathy/dysplasia with right ven-
lar cardiomyopathy in order to differentiate them from
tricular enlargement and evidence of left ventricular involvement
ARVC/D. As CMR may be problematic in patients with demonstrated by late gadolinium enhancement of the left ventricular
non-MR conditional devices, comprehensive diagnosis myocardium (arrows). LV left ventricle, RV right ventricle

Fig. 26.15 Short axis, delayed enhancement views show deep trabec- signal, which would normally suppress or darken myocardium. In this
ulation in a case of ventricular non-compaction. Delayed enhancement case, there is bright signal from contrast in the blood pool interdigitat-
images were obtained with an inversion time chosen to null myocardial ing into the bands of non-compacted myocardium
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 519

finding may also be present in normal subjects [190]. may correlate with the occurrence of clinical sustained
Initially, there was over-diagnosis of ARVC/D, partially ventricular tachycardia [205]. Delayed gadolinium
due to focus on fat involvement and thinning of the right enhancement can occur and patterns can be heterogeneous.
ventricle [191]. Subsequent focus has shifted to right ven- The presence and extent of late gadolinium enhancement has
tricular size, shape, and function, with assessment for been associated with severity of disease [206, 207]. CCTA
global and regional right ventricular wall motion abnormal- can also accurately assess the degree of non-compacted to
ities, scalloping of the ventricle, increased trabeculation, compacted myocardium [208, 209].
and delayed enhancement [192, 193]. Delayed enhance-
ment due to fibrofatty infiltrates in ARVC/D can be chal-
lenging to visualize though due to the thin wall of the right Assessment of Atrial Myopathy
ventricle [194]. Delayed enhancement can be seen in the
left ventricle in ARVC/D. The revised 2010 ARVC/D Task Similar to ventricular myopathy, atrial myopathy as evi-
Force criteria include major and minor CMR criteria related denced by atrial enlargement, depression of atrial func-
to right ventricular size and regional wall motion [189]. tion, and focal and diffuse fibrosis, can be characterized by
CMR involvement as defined by ARVC/D Task Force crite- CMR. Imaging challenges exist though, due to the complex
ria as well as fatty infiltration, delayed enhancement and shape and thin walls of the atria. Normal ranges for right
left ventricular involvement in conjunction with electrocar- and left atrial volume by CMR have been determined [210,
diographic abnormalities on ECG and Holter in ARVC/D 211] Assessment of atrial function can be achieved based on
mutation carriers was associated with the development of volumetric assessment and strain imaging [212–214]. CCTA
sustained ventricular arrhythmias [195]. and CMR atrial volumes are comparable in persistent atrial
CMR is useful in identifying mimics of ARVC/D and fibrillation [215]. Atrial myopathy as evidenced by atrial
alternative etiologies of cardiomyopathy [196, 197] CMR delayed gadolinium enhancement is associated with older
findings can help to differentiate such disease processes as age, history of atrial fibrillation and structural heart disease
Brugada syndrome and cardiac sarcoidosis from ARVC/D. [216]. The degree of delayed contrast enhancement associ-
CMR assessment for structural changes associated with ated with decreased left atrial function and is an independent
Brugada syndrome has only demonstrated subtle anatomic factor associated with previous occurrence of stroke [217,
findings in comparison to normal volunteers, therefore CMR 218]. Delayed gadolinium atrial enhancement can also be
may be useful in differentiating ARVC/D from Brugada visualized in infiltrative processes involving the atrial such
syndrome [198, 199]. Some CMR features may be use- as amyloid [219].
ful in differentiating ARVC/D from sarcoidosis. ARVC/D Assessment of structure and function is important to the
demonstrates greater right ventricular volumes and lower treatment of supraventricular arrhythmias, as sequelae of
right ventricular ejection fraction, while sarcoid patients atrial myopathy include atrial tachycardia, atrial flutter,
have septal delayed gadolinium enhancement and a greater and atrial fibrillation. CCTA and CMR provide similar
degree of left ventricular involvement as differentiating fea- assessment of pulmonary veins before atrial fibrillation
tures [200]. ablation [220]. In addition to atrial volumes and function,
CMR can characterize pulmonary vein location, shape,
complexity, and variation to help in the pre-operative plan-
Ventricular Non-compaction ning, procedural facilitation, and postoperative follow-up
for atrial fibrillation ablation procedures [221–226]. Large
CMR also provides excellent imaging of intraventricular pulmonary vein size by CMR correlates with recurrence of
ventricular structures such as trabeculae and is helpful in the atrial fibrillation after pulmonary vein isolation [227].
diagnosis of ventricular non-compaction (Fig. 26.15). Similar to CCTA, the integration of real time catheter-
Familial and sporadic cases occur, with clinical manifestations based electro- anatomic maps and 3-D CMR angiography
including congestive heart failure, ventricular arrhythmias images obtained pre-procedure facilitates the performance
and thromboembolic events [201]. Criteria including of ablation procedures (Fig. 26.16) [228–230]. Integration
percentage of non-compacted left ventricular myocardial of intracardiac echo and CMR images can allow for map-
mass, the ratio of non-compacted to compacted myocardium, ping and ablation with real time localization of esophageal
and location of non-compaction are useful in differentiating position and catheter tissue contact (Fig. 26.17) [231].
ventricular non-compaction from other conditions including Similar to cardiovascular CCTA, CMR has been used to
hypertrophic cardiomyopathy, dilated cardiomyopathy, diagnose and provide surveillance for pulmonary vein ste-
hypertensive heart disease, and hypertrophy associated with nosis, a potential complication of atrial fibrillation abla-
aortic stenosis [202–204]. The degree of non-compaction tion [232–235].
520 J.S. Shinbane et al.

Delayed gadolinium enhancement can assess preabla- [237]. The greater the scar created by ablation the lower the
tion scar due to atrial myopathy and post procedure scar recurrence rate [238]. Acute ablation lesions can display
created by ablation lesions. In comparison to myopathy hyperenhancement as well as areas of no reflow phenom-
related fibrosis, ablation scar has greater density [236]. The ena. Areas of initial no reflow were better predictors of scar
greater the preablation delayed gadolinium enhancement due at 3 months and lack of arrhythmia recurrence compared to
to atrial myopathy, the greater the recurrence postablation acutely hyperenhanced areas [239]. In preliminary studies,
diffuse atrial fibrosis assessment though T1 mapping cor-
related with catheter–based tissue mapping voltage, atrial
fibrillation and atrial fibrillation arrhythmia recurrence
[240, 241].
An important component of imaging related to atrial
myopathy and atrial fibrillation therapies is evaluation of the
left atrial appendage for atrial thrombi. Left atrial appendage
size, morphology and function can be assessed with CMR
[242, 243]. Although CMR can identify atrial appendage
thrombi, the technology can misidentify poor contrast filling
of the appendage as thrombus and can overestimate the size
of thrombi [244, 245]. CMR studies show low diagnostic
accuracy for detection of atrial thrombi related to limitations
in spatial resolution [246]. CCTA has excellent negative pre-
dictive value, but limited positive predictive value and there-
fore transesophageal echo remains the gold standard for
assessment of atrial appendage thrombi [247]. In regard to
left atrial appendage occlusion procedures for prophylaxis
against stroke, CMR has been shown to be useful for the
planning and follow-up. CMR can quantify the left atrial
appendage with appendage ostial diameter and appendage
long-axis diameter, and can assess for appendage occlusion
after device placement [248]. CCTA provides superior image
Fig. 26.16 Endovascular view of the left upper and left lower pulmo-
resolution for detailed assessment of the multiple morpholo-
nary veins obtained from reconstruction of a MR angiogram (lower
right panel) for use with integration with electroanatomic mapping to gies of the appendage for planning of atrial appendage occlu-
facilitate atrial fibrillation ablation sion techniques [249, 250].

Fig. 26.17 Volume rendered MR angiography integration with intracardiac echo images for atrial fibrillation ablation
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 521

Congenital and Acquired Valvular Heart CCTA and CMR provide the ability to assess valve mor-
Disease phology to differentiate bicuspid valves from tricuspid
valves. These modalities can also identify associated find-
Echocardiography is the first line modality for assessment of ings including aortopathy, coarctation, or patent ductus arte-
valvular heart disease. As adjuncts to transthoracic and trans- riosus. CMR [265–269].
esophageal echocardiography, both CMR and CT have com- The spectrum of issues related to prosthetic valves, includ-
plementary roles in order to define anatomy and pathophysiology ing pannus, thrombus, paravalvular leak, abscess, mycotic
challenging to visualize or quantitate with echocardiography. aneurysm and pseudoaneurysm can be visualized with both
The strengths of CT relate predominantly to anatomy, while CMR and CCTA, with choice depending on relative concerns
CMR is helpful with tissue characteristics, anatomy, and physi- about image quality related to the specific type of valve. In
ology. Transesophageal echocardiography remains the gold prosthetic valve assessment, retrospectively gated CT can be
standard for the diagnosis of endocarditis, as with transthoracic used to assess mechanical valve motion and can be helpful to
echo, CMR and CCTA, small and hypermobile vegetations and identify and characterize restricted motion due to pannus or
leaflet perforations can be missed. Image quality issues exist thrombus. In mechanical valve models, CT can identify lim-
with all modalities due to artifacts associated with mechanical ited mechanical leaflet closure similar to fluoroscopy and can
and bioprosthetic valves. Issues particular to CMR include assess for abnormal leaflet motion including frozen leaflets
contraindications to imaging ball and cage valves, dephasing [270]. CT can visualize pannus formation with some limita-
artifacts, and signal void with imaging of calcium. Issues par- tion due to beam hardening artifact [271–273]. CCTA can be
ticular to CT relate to beam hardening artifacts. Tomographic potentially performed as a replacement for invasive coronary
imaging with CMR and CCTA allows assessment of adjacent angiography in order to decrease embolic risk from thrombus
structures for fistulas, abscesses, aneurysms, pseudoaneu- or vegetation, before prosthetic valve reoperation. In patients
rysms, and stigmata of embolic phenomena [251–253]. The with previously known coronary artery disease and in some
use of 18F fluorodeoxyglucose PET/CT in the setting of pros- patients with no previous known coronary artery disease
thetic valve endocarditis has preliminarily demonstrated though imaging may be non-diagnostic [274].
increased sensitivity compared with echocardiography, CMR, A strength of CMR is assessment of the physiology of
and CCTA [254]. regurgitant valvular disease through steady state free
precession functional imaging, ventricular volumes, and
regurgitant fraction with velocity encoded imaging
Aortic Valve (Fig. 26.18, Video 4) [275]. CMR aortic regurgitant orifice
correlates with regurgitant volume and regurgitant fraction
In the assessment of aortic valve stenosis, CMR can be used
to quantitate effective aortic valve orifice area, which is com-
parable to transthoracic and transesophageal echo [255–257].
Transvalvular mean pressure gradients though can be under-
estimated compared to transthoracic echocardiography [258].
In the setting of cardiomyopathy associated with severe aortic
stenosis, late gadolinium enhancement can be visualized cor-
relating with abnormalities of diastolic and systolic dysfunc-
tion [259, 260]. The degree of fibrosis provides prognostic
assessment of all cause mortality and correlates inversely
with the degree of functional improvement after aortic valve
replacement and [261].
In assessment and planning for transcatheter aortic valve
implantation (TAVI), CCTA is the gold standard for charac-
terization of preprocedure anatomy [262]. CMR can be used,
with some limitations due to signal void associated with cal-
cium. It is helpful for post procedure assessment of aortic
regurgitation. In comparison to CCTA, CMR can quantitate
aortic anatomy for TAVI, but is limited when prosthetic
valves are present due to ferromagnetic artifact associated
with struts [263]. CMR can also document reverse remodel-
ing including decrease in late gadolinium enhancement post
TAVI [264]. Fig. 26.18 Mild aortic regurgitation with an eccentric jet
522 J.S. Shinbane et al.

by CMR phase velocity mapping [276]. Two-D echo may demonstrated decreases in left ventricular volumes, mitral
have difficulties with eccentric jets compared to CMR and annular diameter, myocardial mass, and left atrial size [292].
3-D echo [277]. CCTA can provide more limited information In prosthetic valve mitral regurgitation, CMR can assess jet
regarding aortic regurgitation. Preliminarily, CCTA assess- size and density for assessment of severe MR with trans-
ment of regurgitant orifice area correlated with degree of aor- esophageal echo as a reference [293].
tic regurgitation by CMR [278]. CCTA volumetric assessment CCTA can assess mitral valve, mitral annular and subval-
of aortic regurgitation is extrapolated from right and left ven- vular morphology, valve function, and definition of the coro-
tricular stroke volume and must occur in isolation from other nary artery and coronary venous 3-D anatomy in the region
valvular lesions for assessment [279]. of the mitral annulus [294–298]. Planimetry of the mitral
CMR is useful for assessment of aortic valve regurgita- valve area can be performed in patients with mitral stenosis
tion after TAVI. CMR assessment of aortic valve regurgitant [299]. CCTA can also provide volumetric assessment of ven-
volume and regurgitant fraction after TAVI demonstrates tricular function and myocardial mass in the setting of mitral
that echocardiography can underestimate the degree of aor- regurgitation comparable to CMR [300].
tic regurgitation [280–283]. After TAVI, CMR can more
accurately classify the degree of paravalvular leak and can
provide greater prognostic significance than transthoracic Pulmonary Valve
echo [284]. CMR assessment of aortic regurgitation effect
on ventricular remodeling after TAVI shows that mild to CMR is useful for assessment of pulmonary valve regurgita-
moderate aortic regurgitation is common. Degrees of aortic tion or stenosis as well as the effect of these valvular abnor-
regurgitation beyond mild lead to prevention of positive malities on the right ventricle and pulmonary arteries. These
remodeling with TAVI. For prediction of post TAVI aortic factors are particularly important in the assessment, treat-
regurgitation, both CMR and CCTA demonstrate that larger ment and follow-up of patients with abnormalities of the pul-
annuli are associated with post procedure regurgitation monary valve and right ventricular outflow tract such as
[285]. For assessment of TAVI perivalvular leak, CCTA is those with tetralogy of Fallot (Fig. 26.19). CMR can provide
helpful as an adjunct to echo for procedural planning. For assessment of valve morphology and motion, right ventricu-
surgically placed valves, it can be challenging to differenti- lar morphology, volumes, and function, velocity encoded
ate paravalvular leak from residual surgical suture material imaging for calculation of fractional regurgitation, and angi-
on CCTA. ographic assessment of the pulmonary arteries [301–303].
CMR also has been utilized for the follow-up of percutane-
ous pulmonary valve replacement [304].
Mitral Valve

The mitral valve has complex morphology and motion. Due Tricuspid Valve
to its saddle shape and subvalvular apparatus, volumetric
assessment of mitral regurgitation is challenging with all The tricuspid valve has complex anatomy making assess-
modalities. Mitral regurgitant fraction can be extrapolated ment with CMR challenging. There are limited CMR data
from CMR phase contrast velocity mapping of aortic outflow related to assessment of annular dimensions, valve geometry,
volume and left ventricular stroke volume [286, 287]. CMR and the effect of tricuspid regurgitation on right ventricular
measurement of anatomic regurgitant orifice correlated with function [305–307]. CCTA has additional issues related to
CMR regurgitant fraction and volume as well as with cardiac the heterogeneity of contrast in the right atrium and right
catheterization regurgitant fraction and volume [288]. With ventricle. Preliminary study of tricuspid annular geometry
mitral valve prolapse, CMR assessment and quantification of using CCTA is being performed [308].
valvular characteristics of anterior leaflet length, posterior
leaflet displacement, posterior leaflet thickness, and the pres-
ence of flail leaflet were predictors of the degree of mitral Congenital Heart Disease
regurgitation [289]. Negative remodeling with CMR delayed
gadolinium enhancement can be seen in primary mitral The ability of CMR to provide comprehensive assessment of
regurgitation [290]. In ischemic mitral regurgitation, the cardiovascular structure and function, as well as an extra-
degree of basal fibrosis on CMR was a predictor of postop- cardiac vasculature and thoracic structure, makes it useful in
erative ejection fraction and adverse outcome [291]. For per- the diagnosis, facilitation of treatment, and follow-up of
cutaneous mitral valve clip repair for mitral regurgitation, patients with congenital heart disease [309–312]. CMR can
CMR performed pre and post procedure was feasible and assess simple and complex congenital heart disease in the
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 523

a b

c d

Fig. 26.19 Reconstructed right ventricular outflow tract in the setting tract and pulmonary arteries. The branch pulmonary arteries are patent
of repaired tetralogy of Fallot. Panel (a): MR angiogram showing the and without evidence of stenoses. Panel (d): Coaxial view of the pulmo-
patch reconstruction of the right ventricular outflow tract. Panel (b): nary valve with severe regurgitation (regurgitant fraction of 48 %). LV
Delayed gadolinium short axial view demonstrating enhancement of left ventricle, LPA left pulmonary artery, PV pulmonary valve, RPA
the patch reconstruction of the right ventricular outflow tract. Panel (c): right pulmonary artery, RV right ventricle, RVOT right ventricular out-
MR angiogram showing the reconstructed right ventricular outflow flow tract

native state or after interventional or surgical treatment. As as well as post procedural follow-up [313–315]. Cardiac
many congenital heart disease patients have implanted car- shunts can be accurately assessed over the spectrum of pul-
diac devices or other surgical prosthetic materials, CMR monary to systemic shunt ratios [310]. Delayed enhance-
imaging challenges exist which may contraindicate imaging ment imaging can be used to assess the location and degree
or lead to artifacts limiting interpretation. Artifacts associ- of fibrosis associated with cardiomyopathy or surgical
ated with sternotomy wires can affect imaging of structures patches (Fig. 26.20) [316]. Novel approaches providing
adjacent to the sternum. faster imaging sequences performed without breath hold
CMR is useful in pre-procedure planning for interven- in a more operator-independent manner should increase
tional and surgical approaches to congenital heart disease the utility of CMR for the assessment of congenital heart
524 J.S. Shinbane et al.

slices or axial slices with better reproducibility seen with

use of axial slices after operation for tetralogy of Fallot
[325]. After surgical repair, phase contrast velocity CMR
can assess for differential regurgitant fraction of right and
left pulmonary arteries [326, 327]. Differences in measure-
ment of pulmonary regurgitation depend on whether expi-
ratory breath hold, inspiratory breath hold, or imaging
without breath-hold is performed. Expiratory breath hold
led to the lowest level of pulmonary regurgitation possibly
due to changes in airway pressure [328]. Transthoracic
echocardiogram is limited compared to CMR for assess-
ment of pulmonic regurgitation in patients with repaired
tetralogy of Fallot [329].
Late gadolinium enhancement can be utilized to visualize
biventricular fibrosis after tetralogy of Fallot repair and has
correlated with ventricular dysfunction, poor exercise toler-
ance and elevation of neurohormonal factors [330].
Restrictive right ventricular physiology has been associated
with the degree of late gadolinium enhancement of the oper-
Fig. 26.20 A short axis delayed gadolinium view showing enhance- ated right ventricular outflow tract [331]. Biventricular nega-
ment of a ventricular septal defect patch (arrow) associated with repair
tive remodeling has been seen with assessment of diffuse
of tetralogy of Fallot. LV left ventricle, RV right ventricle
fibrosis with T1 post contrast imaging [332].
The strengths of CCTA for assessment of tetralogy of
disease. Real time cardiac catheterization guided by mag- Fallot include detailed assessment of pulmonary vascular
netic resonance in compatible lab settings is being investi- anatomy and assessment of coronary artery anatomy in
gated for use in the assessment and treatment of congenital relation to other structures for anomalous course prior to
heart disease [317, 318]. surgery [333–335]. Although radiation exposure is a concern
particularly in the pediatric population, dose sparing proto-
cols can allow for sub-millisievert exposures [336].
Tetralogy of Fallot Preliminary study has demonstrated assessment of right ven-
tricular volumes and ejection fraction comparable to CMR
CMR can be used for diagnosis of cardiovascular findings in [337]. CCTA can be used for rapid prototyping of models for
tetralogy of Fallot. All routes of pulmonary blood flow in assessment and planning of patch repair of ventricular septal
patients with pulmonary stenosis or pulmonary atresia defects in tetralogy of Fallot [333].
including pulmonary artery flow and aorto pulmonary col-
laterals are important for surgical decisions and planning
[319, 320]. CMR can provide characterization of these fac- Single Ventricle Physiology
tors similarly to invasive angiography [321].
In follow-up of right ventricular outflow reconstruction There are a spectrum of congenital syndromes with single
in tetralogy of Fallot, quantitation of pulmonary fractional ventricle physiology with surgical interventions including
regurgitation and right ventricular volumes are important creation of Fontan circulation and a host of other cavo- pul-
for decisions to intervene with interventional cardiology or monary surgeries. MR angiography can define these cir-
surgical approaches [322]. Ventricular dysfunction late cuits, assess for baffle and conduit stenoses or leaks, and
after surgical repair of tetralogy of Fallot is associated with identify additional anomalous circulation (Fig. 26.21,
worse prognosis [323]. Definition of right ventricle and Video 5). CMR provides quantification of cavo-pulmonary
outflow tract anatomy and geometry is potentially more flow through phase contrast velocity mapping assessment of
challenging after surgical reconstruction due to artifacts. flow in the superior and inferior vena cava and left and right
CMR can assess right ventricular indexed volumes and pulmonary arteries [338]. Time resolved 3-D magnetic reso-
phase contrast velocity encoded imaging can quantify pul- nance can assess vascular anatomy and flow dynamics of
monary regurgitant fraction in repaired tetralogy of Fallot cavo-pulmonary circuits including Fontan circulation [339].
[324]. Ventricular volumes can be measured by short axis In contradistinction, CCTA can be challenging to use for
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 525

a b c

Fig. 26.21 MR angiography views of pulmonary atresia and hypoplas- atrium to the left pulmonary artery via the right atrial appendage is pat-
tic right ventricle, status post Fontan. Panel (a): The superior vena cava ent. Panel (c): There is a normal connection of the inferior vena cava to
connection to the right pulmonary artery (arrow) is patent. The right the right atrium. IVC inferior vena cava, LPA left pulmonary artery, RA
atrium is severely enlarged. Panel (b): The anastomosis of the right right atrium, RAA right atrial appendage, RPA right pulmonary artery

opacification of the Fontan circulation with upper extremity transposition of the great arteries, assessment of ventricular
venous contrast injection and may require specialized injec- structure and function related to pulmonary artery banding
tion protocols including delayed contrast imaging or simul- (Figs. 26.22 and 26.23), and evaluation and follow-up of
taneous upper and lower extremity venous contrast injection arterial switch procedures.
[340, 341]. Assessment of function of the morphologic right ventri-
CMR indexed end-diastolic ventricular volume is a pre- cle in the systemic position is important for surgical deci-
dictor of outcome in patients with Fontan anatomy [342]. sions in transposition of the great arteries. In the setting of
Assessment of superior and inferior vena cava flow in Fontan D-transposition of the great arteries status post atrial
patients in the context of quantification of geometry has been switch, the extent of late gadolinium enhancement of the
used to assess fluid dynamic power loss in Fontan circuits morphologic right ventricle in the systemic position is
[343–345]. In late Fontan survivors, ventricular delayed gad- associated with decreased ejection fraction and is a predic-
olinium enhancement has been identified with its extent tor of adverse outcome [347]. In young adults status post
associated with ventricular enlargement and dysfunction, previous atrial switch, CMR demonstrated no evidence of
increased ventricular mass and non-sustained ventricular inducible ischemia [348]. In congenitally corrected trans-
tachycardia [346]. position of the great arteries or surgically palliated
D-transposition of the great arteries with atrial switch,
dobutamine CMR can be used to assess for follow-up for
Transposition of the Great Arteries dysfunction due to right ventricular pressure overload
[349]. Additionally, as the morphologic left ventricle is in
In the setting of transposition of the great arteries, CCTA the pulmonary position, CMR can assess ventricular wall
and CMR are helpful in 3-D definition of the anatomic and thickness, volumes, ejection fraction, and response to pul-
physiologic relationships of the pulmonary arteries, aorta, monary artery banding for potential arterial switch opera-
cardiac chambers, valves, and thoracic visceral and skeletal tions. CMR can also define issues related to surgical baffles
structures. In the assessment and reporting the findings, it is [350, 351]. Additional congenital anomalies in the setting
essential to define the atrioventricular valves and cardiac of transposition of the great arteries can also be identified
chambers by morphology and physiologic function. A with CMR (Fig. 26.24) [352].
spectrum of uses in the setting of native and operated trans- CCTA is also useful in the diagnosis, procedural and sur-
position syndromes exist, including initial diagnosis and gical planning and follow-up of congenital heart disease
characterization, planning of atrial switch procedures for D related to transposition of the great arteries. Large and small
526 J.S. Shinbane et al.

a b

c d

Fig. 26.22 Transposition of the great arteries (D-type), status post pre- the pulmonary artery banding, there is hypertrophy of the previously
vious atrial baffle procedure in childhood, with subsequent pulmonary thin morphologic left ventricular myocardium in the venous position
artery banding in preparation for an arterial switch operation. Panel (a): (arrow). Panel (d): After arterial switch, the neoaorta is located poste-
An axial view demonstrates the anterior position of the aorta. Panel (b): rior to the main pulmonary artery. Ao aorta
MR angiogram status post pulmonary artery banding. Panel (c): Due to

Fig. 26.24 Multiple views of unrepaired congenitally corrected trans- cle). Panel (c): A 4 chamber view demonstrating continuity between the
position of the great arteries with additional anomalies including a left- morphologic left ventricle and main pulmonary artery. Panel (d): A
sided superior vena cava and partial anomalous pulmonary venous long axis view demonstrating continuity between the morphologic right
return. Panel (a): An axial view demonstrating the anterior and leftward ventricle and aorta. Panel (e): MR angiogram demonstrating bilateral
position of the aorta in relation to the pulmonary artery (L-transposed superior vena cavae. The right upper pulmonary vein drains anoma-
great arteries). Panel (b): A 4 chamber view demonstrating the right lously into the right superior vena cava. Ao aorta, AV atrioventricular,
atrium leading to the morphologic left ventricle (pulmonary ventricle) LA left atrium, LV left ventricle, PA pulmonary artery, RA right atrium,
and left atrium leading to morphologic right ventricle (systemic ventri- RV right ventricle, SVC superior vena cava
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 527

vessel anatomy can be characterized, particularly assessment

of coronary artery anomalies in relation to other cardiotho-
racic structure in the presurgical and postoperative states.
CCTA is useful for evaluation of baffles associated with
atrial switch procedures [353]. After arterial switch, CCTA
is assess reimplanted coronary arteries for coronary artery
stenoses and for anomalous courses with potential coronary
artery compression [354].

Ebstein Anomaly

CMR and CCTA can be useful adjuncts to echocardiography

for the evaluation of Ebstein anomaly (Fig. 26.25, Video 6).
CMR measurement of right to left heart volumes and quanti-
fication of functional and atrialized right ventricular volumes
and total right/left volume index can help to determine the
severity of Ebstein anomaly [355–357]. CCTA can identify
Fig. 26.23 MR angiogram demonstrating narrowing of the main pul- other cardiothoracic findings of large and small vessels
monary artery (arrows) due to surgical banding in the setting of including anomalous coronary arteries [358].
D-transposition of the great arteries

a b

c d e
528 J.S. Shinbane et al.

Septal Defects [361]. Three-D MRA can characterize partial anomalous

pulmonary venous return associated with atrial septal defects
For planning and follow-up of percutaneous closure of [320, 362, 363].
secundum atrial septal defects, CMR can assess atrial septal CCTA can be useful for preprocedure interventional and
margins, maximal and minimal defect dimensions compara- surgical planning as well as assessment of percutaneous clo-
ble to transesophageal echo (Figs. 26.26 and 26.27) [314, sure for atrial septal defect sizing and characteristics includ-
359]. Additional data include coaxial velocity encoded CMR ing complex and multiple defects, assessment of coronary
atrial septal defect flow, size and shape [360]. In assessment arteries and assessment of partial anomalous pulmonary
of Qp/Qs, CMR is comparable to cardiac catheterization venous return associated with atria septal defects [364–366].
Post-intervention assessment includes percutaneous closure
device location for diagnosis of malposition or extension
into systemic or pulmonary veins and assessment of right
ventricular remodeling after closure [367, 368].
For ventricular septal defects, CMR and CCTA can provide
pre-procedure interventional and surgical planning through
definition of size, location, 3-D relationships to other struc-
tures, and identification of other cardiovascular anomalies
[369]. CMR and CCTA imaging can be integrated with fluo-
roscopy for guidance of percutaneous closure interventions
[370]. CMR can provide assessment of Qp:Qs, characteriza-
tion of location and extent of myocardial infarct scar associ-
ated post-infarct ventricular septal defects, and can quantify
sequelae of complex surgeries such as atrioventricular septal
defect closure with flow dynamic characteristics of AV valve
regurgitation after repair [371]. Multimodality imaging with
CCTA and CMR can be useful adjuncts in complex scenarios
(Fig. 26.28, Videos 7 and 8) [372].

Fig. 26.25 CMR view of Ebstein anomaly. An axial steady state free
precession view demonstrating apical displacement of the tricuspid Cardiac Masses
leaflets, therefore dividing the right ventricle into functional and atrial-
ized portions. Apical displacement of the septal leaflet and posterior
CMR is helpful in the evaluation of cardiac masses due to the
leaflet is shown (arrow). ARV atrialized right ventricle, FRV functional
right ventricle, TV PL tricuspid valve posterior leaflet, TV SL tricuspid ability to comprehensively assess tissue characteristics, as
valve septal leaflet well as involvement of a mass in relation to surrounding

Fig. 26.26 CMR 4 chamber images demonstrating a large secundum atrial septal defect, with right ventricular enlargement and hypertrophy and
right atrial enlargement
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 529

a b

Fig. 26.27 Eisenmenger syndrome due to a large secundum atrial septal (b): An axial view demonstrates significant pulmonary artery enlargement due
defect. Panel (a): A 4 chamber view shows the secundum atrial septal defect to pulmonary hypertension. Ao aorta, ASD atrial septal defect, LA left atrium,
(arrows), right atrial enlargement, and right ventricular enlargement. Panel LV left ventricle, PA pulmonary artery, RA right atrium, RV right ventricle

cardiac and thoracic structures. Anatomic definition of masses [389]. CCTA can be particularly useful in assessing the
include: number of masses, shape, morphology of the con- relationship of the coronary arteries to cardiac and extra-
nection to the heart, intracameral, subendocardial, myocar- cardiac masses.
dial, epicardial, pericardial, or extracardiac location, and
presence of invasion of the mass into structures (Figs. 26.29,
26.30, 26.31 and 26.32, Video 9). CMR is especially useful in Assessment of Pericardial Disease
assessment of the tissue of masses based on T1 and T2 char-
acteristics as well as the presence, degree and location of per- Pericardial disease includes a spectrum of processes due to
fusion and delayed gadolinium enhancement [373]. Mass infectious, inflammatory, malignant, ischemic, and trau-
location, tissue characteristics, and presence of pericardial or matic etiologies. Echocardiography is an important imag-
pleural involvement are important factors for evaluating and ing modality for initial assessment of the presence and
staging benign or malignant cardiac neoplasms when findings hemodynamic effects of pericardial effusion and pericar-
are compared to actual histologic examination [374]. dial thickening. Tomographic processes including CMR
Benign tumors, primary malignant tumors, and meta- and CCTA can provide additional assessment through
static malignant tumors, have been identified with CMR, biventricular morphology and function related to pericar-
including fibromas, lipomas, myxomas, mesotheliomas, dial disease processes, regional assessment of pericardial
sarcomas, lymphomas, melanomas, and metastatic carcino- fluid and pericardial thickening. The strength of CMR
mas [375–385]. Tumor mimics can also be identified includes the ability to define tissue characteristics related
including lipomatous hypertrophy of the interatrial septum, to T1 and T2 weighting, delayed gadolinium assessment of
prominent crista terminalis, Chiari network, and thrombus pericardial inflammation (Fig. 26.33), and tagging to
[377, 386, 387]. Although CMR is useful, histologic tissue assess for areas of adhesion [390–392]. CCTA provides
analysis remains the gold standard for diagnosis [388]. Due more limited tissue characterization, but is useful for
to its excellent spatial resolution, CCTA can provide assess- assessing the degree and location of pericardial calcifica-
ment of cardiac mass morphology, location, with some tion, Hounsfield density estimation of the hematocrit of
ability tissue characterization based on Hounsfield Units effusion, pericardial fat, relationship of calcified pericar-
and contrast enhancement. It is useful in situations in which dium to the coronary arteries, and assessment for other
application of CMR is challenging or contraindicated thoracic disease [393].
530 J.S. Shinbane et al.

Fig. 26.28 Unoperated congenital heart disease with Eisenmenger volume and pressure overload. A severe regurgitant jet of pulmonary
syndrome due to a double outlet right ventricle with a large ventricular regurgitation is preferentially directed towards the right ventricle. Panel
septal defect. Panel (a): Serial short axis steady state free precession (b): A steady state free precession view shows a patent ductus arterio-
views from apex to base show the double outlet right ventricle with a sus. Ao aorta, LV left ventricle, PA pulmonary artery, PDA patent ductus
large ventricular septal defect. There is moderate dilatation and hyper- arteriosus, PR pulmonary regurgitation, RV right ventricle, VSD ven-
trophy of right ventricle and a D-shaped septum due to right ventricular tricular septal defect

Vascular Disease lipid core, fibrosis, calcium, and dynamic contrast enhance-
ment via k-trans measurement. In addition to congenital aor-
CMR and MR angiography are reliable for the detection tic lesions such as coarctation of the aorta (Fig. 26.34) and
of aortic aneurysm and aortic dissection. Gated CMR is Marfan syndrome, CMR can diagnose acquired vascular and
particularly helpful for evaluation of the aortic root for valvular heart disease including aneurysm, dissection,
aneurysm, dissection, and aortic valve function. Contrast and wall abnormalities such as penetrating ulcers, calcifica-
enhanced black blood MR is particularly helpful for tion, or thrombus with ability to assess all aortic segments
evaluating aortic plaque, ulceration and intramural (Fig. 26.35, Video 10) [394–396]. CMR and CCTA may be
hemorrhage. particularly useful in assessment of aortic grafts particularly
Carotid MRA is generally effective in diagnosing steno- for endoleak with some studies favoring CMR, although
sis. Carotid plaque MR evaluation can measure wall thick- CCTA can be useful when calcified plaque is present [397–
ness and volume and analyze plaque components including 399]. Clinically useful abdominal aorta and branch images
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 531

Fig. 26.29 A large, broad-based mass is present arising from the

right ventricle (white arrows). There is also an enhancing mass
in the right atrium (arrowhead). A right lower lobe enhancing lung
mass is present (black arrow), likely representing a metastasis.
A right pleural effusion is also present. The diagnosis was
metastatic angiosarcoma

a b c

d e

Fig. 26.30 A CMR study from a patient with a left atrial mass (arrows) onstrated heterogeneous enhancement immediately post contrast. Panel
with characteristics most consistent with myxoma. Panel (a): Within (e): There was heterogeneous enhancement on delayed contrast images.
the left atrium there was a 3.3 × 1.8 × 2.4 cm intracameral mass along There was no evidence of myocardial invasion, pericardial effusion or
the interatrial septum at the fossa ovalis. Panel (b): The mass was pleural effusions. The diagnosis of left atrial myxoma with organized
hyperintense on the T2-weighted images. Panel (c): The mass was thrombus formation was confirmed based on the surgical histological
isointense to muscle on T1-weighted images. Panel (d): The mass dem- evaluation
532 J.S. Shinbane et al.

Fig. 26.31 Large atrial myxoma which obstructs the mitral valve during atrial systole

a c

Fig. 26.32 Chronic myocardial infarction with an apical aneurysm and an apical thrombus (arrows). Panel (a): Short axis first pass perfusion
image. Panel (b): Short axis functional image. Panel (c): Delayed gadolinium enhancement 4 chamber view
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 533

CCTA. In addition to arterial system abnormalities, CMR

and CCTA can identify congenital and acquired abnormali-
ties of the systemic veins such as left-sided superior vena
cava with a connection to an aneurysmal coronary sinus,
interrupted inferior vena cava, and superior vena cava
compression.

Summary

Both CCTA and CMR are robust imaging modalities for

characterization of cardiovascular substrates. Decisions
related to performing CMR versus CCTA require informa-
tion including patient age, allergy history, clinical stability
to be in the MR environment for the amount of time neces-
sary for study, history of claustrophobia, history of ferro-
magnetic devices, implant or deposits, devices, renal
function, cardiac rhythm and rate, strengths and limitations
of other imaging modalities, and the posed clinical ques-
tion. CMR provides assessment for the diagnosis and treat-
ment of cardiovascular disease, including cardiovascular
Fig. 26.33 A 4 chamber view demonstrating pericardial delayed gado-
linium enhancement (arrows) associated with pericarditis structure, function, tissue characterization, myocardial per-
fusion, and metabolism. Applications include the assess-
ment of coronary artery disease, cardiomyopathic
are readily obtained with either MRA or CCTA. Either may substrates, congenital heart disease, thoracic vasculature,
be performed for the evaluation of vascular anomalies and valvular function, masses, pericardial disease and assess-
renal artery stenosis. CCTA may be preferred due to superior ment of aortic and branch vessel anatomy. Advances in
resolution and reliability. Clinically useful extremity vessel technology will continue to lead to novel clinical and
images are also readily obtained with either MRA or research applications.
534 J.S. Shinbane et al.

Fig. 26.34 Serial sagittal slices demonstrating coarctation of the aorta

26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 535

Interventions, Society of Cardiovascular Computed Tomography,

Society for Cardiovascular Magnetic Resonance, and Society of
Thoracic Surgeons. J Am Coll Cardiol. 2014;63(4):380–406.
3. Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of can-
cer associated with radiation exposure from 64-slice computed
tomography coronary angiography. JAMA. 2007;298(3):317–23.
4. Ergun I, Keven K, Uruc I, Ekmekci Y, Canbakan B, Erden I, et al.
The safety of gadolinium in patients with stage 3 and 4 renal fail-
ure. Nephrol Dial Transpl Off Publ Eur Dial Transpl Assoc Eur
Renal Assoc. 2006;21(3):697–700.
5. Sadowski EA, Bennett LK, Chan MR, Wentland AL, Garrett AL,
Garrett RW, et al. Nephrogenic systemic fibrosis: risk factors and
incidence estimation. Radiology. 2007;243(1):148–57.
6. Thomsen HS, Morcos SK, Almen T, Bellin MF, Bertolotto M,
Bongartz G, et al. Nephrogenic systemic fibrosis and gadolinium-
based contrast media: updated ESUR Contrast Medium Safety
Committee guidelines. Eur Radiol. 2013;23(2):307–18.
7. Nayak KS, Cunningham CH, Santos JM, Pauly JM. Real-time car-
diac MRI at 3 tesla. Magn Reson Med. 2004;51(4):655–60.
8. McGee KP, Debbins JP, Boskamp EB, Blawat L, Angelos L, King
KF. Cardiac magnetic resonance parallel imaging at 3.0 Tesla:
technical feasibility and advantages. J Magn Reson Imaging
JMRI. 2004;19(3):291–7.
9. Gharib AM, Elagha A, Pettigrew RI. Cardiac magnetic resonance
at high field: promises and problems. Curr Probl Diagn Radiol.
2008;37(2):49–56.
10. Suttie JJ, Delabarre L, Pitcher A, van de Moortele PF, Dass S,
Snyder CJ, et al. 7 Tesla (T) human cardiovascular magnetic reso-
nance imaging using FLASH and SSFP to assess cardiac function:
validation against 1.5 T and 3 T. NMR Biomed. 2012;25(1):27–34.
11. von Knobelsdorff-Brenkenhoff F, Tkachenko V, Winter L, Rieger
J, Thalhammer C, Hezel F, et al. Assessment of the right ventricle
with cardiovascular magnetic resonance at 7 Tesla. J Cardiovasc
Magn Reson Off J Soc Cardiovasc Magn Reson. 2013;15:23.
12. Klix S, Els A, Paul K, Graessl A, Oezerdem C, Weinberger O,
et al. On the subjective acceptance during cardiovascular magnetic
resonance imaging at 7.0 Tesla. PLoS One. 2015;10(1), e0117095.
13. Raff GL, Gallagher MJ, O’Neill WW, Goldstein JA. Diagnostic
Fig. 26.35 MR angiogram demonstrates multifocal plaques, bilateral
accuracy of noninvasive coronary angiography using 64-slice spi-
renal artery stenosis (upper arrows), and a saccular aneurysm of infra-
ral computed tomography. J Am Coll Cardiol. 2005;46(3):552–7.
renal aorta (lower arrow)
14. Shellock FG. Prosthetic heart valves and annuloplasty rings:
assessment of magnetic field interactions, heating, and artifacts at
1.5 Tesla. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn
References Reson. 2001;3(4):317–24.
15. Martin ET, Coman JA, Shellock FG, Pulling CC, Fair R, Jenkins
1. Hendel RC, Patel MR, Kramer CM, Poon M, Hendel RC, Carr JC, K. Magnetic resonance imaging and cardiac pacemaker safety at
et al. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 1.5-Tesla. J Am Coll Cardiol. 2004;43(7):1315–24.
appropriateness criteria for cardiac computed tomography and 16. Gimbel JR. Magnetic resonance imaging of implantable cardiac
cardiac magnetic resonance imaging: a report of the American rhythm devices at 3.0 tesla. Pacing Clin Electrophysiol PACE.
College of Cardiology Foundation Quality Strategic Directions 2008;31(7):795–801.
Committee Appropriateness Criteria Working Group, American 17. Shinbane JS, Colletti PM, Shellock FG. MR in patients with pace-
College of Radiology, Society of Cardiovascular Computed makers and ICDs: defining the issues. J Cardiovasc Magn Reson
Tomography, Society for Cardiovascular Magnetic Resonance, Off J Soc Cardiovasc Magn Reson. 2007;9(1):5–13.
American Society of Nuclear Cardiology, North American Society 18. Shinbane JS, Colletti PM, Shellock FG. Magnetic resonance
for Cardiac Imaging, Society for Cardiovascular Angiography and imaging in patients with cardiac pacemakers: era of “MR
Interventions, and Society of Interventional Radiology. J Am Coll Conditional” designs. J Cardiovasc Magn Reson Off J Soc
Cardiol. 2006;48(7):1475–97. Cardiovasc Magn Reson. 2011;13:63.
2. Wolk MJ, Bailey SR, Doherty JU, Douglas PS, Hendel RC, 19. Wilkoff BL, Bello D, Taborsky M, Vymazal J, Kanal E, Heuer H,
Kramer CM, et al. ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/ et al. Magnetic resonance imaging in patients with a pacemaker
SCCT/SCMR/STS 2013 multimodality appropriate use criteria system designed for the magnetic resonance environment. Heart
for the detection and risk assessment of stable ischemic heart dis- Rhythm Off J Heart Rhythm Soc. 2011;8(1):65–73.
ease: a report of the American College of Cardiology Foundation 20. Bailey WM, Rosenthal L, Fananapazir L, Gleva M, Mazur A,
Appropriate Use Criteria Task Force, American Heart Association, Rinaldi CA, et al. Clinical safety of the ProMRI pacemaker sys-
American Society of Echocardiography, American Society of tem in patients subjected to head and lower lumbar 1.5-T magnetic
Nuclear Cardiology, Heart Failure Society of America, Heart resonance imaging scanning conditions. Heart Rhythm Off J Heart
Rhythm Society, Society for Cardiovascular Angiography and Rhythm Soc. 2015;12(6):1183–91.
536 J.S. Shinbane et al.

21. Gold MR, Sommer T, Schwitter J, Al Fagih A, Albert T, Merkely 38. Norgaard BL, Leipsic J, Gaur S, Seneviratne S, Ko BS, Ito H,
B, et al. Full-body MRI in patients with an implantable cardio- et al. Diagnostic performance of noninvasive fractional flow
verter-defibrillator: primary results of a randomized study. J Am reserve derived from coronary computed tomography angiogra-
Coll Cardiol. 2015;65(24):2581–8. phy in suspected coronary artery disease: the NXT trial (Analysis
22. Shinbane JS, Colletti PM, Shellock FG. MR imaging in patients of Coronary Blood Flow Using CT Angiography: Next Steps).
with pacemakers and other devices: engineering the future. JACC J Am Coll Cardiol. 2014;63(12):1145–55.
Cardiovasc Imaging. 2012;5(3):332–3. 39. Min JK, Leipsic J, Pencina MJ, Berman DS, Koo BK, van
23. Colletti PM, Shinbane JS, Shellock FG. “MR-conditional” pace- Mieghem C, et al. Diagnostic accuracy of fractional flow reserve
makers: the radiologist’s role in multidisciplinary management. from anatomic CT angiography. JAMA. 2012;308(12):1237–45.
AJR Am J Roentgenol. 2011;197(3):W457–9. 40. Nakazato R, Park HB, Berman DS, Gransar H, Koo BK, Erglis A,
24. Francis JM, Pennell DJ. Treatment of claustrophobia for cardio- et al. Noninvasive fractional flow reserve derived from computed
vascular magnetic resonance: use and effectiveness of mild seda- tomography angiography for coronary lesions of intermediate ste-
tion. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson. nosis severity: results from the DeFACTO study. Circ Cardiovasc
2000;2(2):139–41. Imaging. 2013;6(6):881–9.
25. Eshed I, Althoff CE, Hamm B, Hermann KG. Claustrophobia and 41. Koo BK, Erglis A, Doh JH, Daniels DV, Jegere S, Kim HS, et al.
premature termination of magnetic resonance imaging examina- Diagnosis of ischemia-causing coronary stenoses by noninvasive
tions. J Magn Reson Imaging JMRI. 2007;26(2):401–4. fractional flow reserve computed from coronary computed tomo-
26. Chia JM, Fischer SE, Wickline SA, Lorenz CH. Performance of graphic angiograms. Results from the prospective multicenter
QRS detection for cardiac magnetic resonance imaging with a DISCOVER-FLOW (Diagnosis of Ischemia-Causing Stenoses
novel vectorcardiographic triggering method. J Magn Reson Obtained Via Noninvasive Fractional Flow Reserve) study. J Am
Imaging JMRI. 2000;12(5):678–88. Coll Cardiol. 2011;58(19):1989–97.
27. Dimick RN, Hedlund LW, Herfkens RJ, Fram EK, Utz 42. Wong DT, Ko BS, Cameron JD, Leong DP, Leung MC, Malaiapan
J. Optimizing electrocardiograph electrode placement for cardiac- Y, et al. Comparison of diagnostic accuracy of combined assess-
gated magnetic resonance imaging. Invest Radiol. 1987; ment using adenosine stress computed tomography perfusion + com-
22(1):17–22. puted tomography angiography with transluminal attenuation
28. Counter SA, Olofsson A, Grahn HF, Borg E. MRI acoustic noise: gradient + computed tomography angiography against invasive frac-
sound pressure and frequency analysis. J Magn Reson Imaging tional flow reserve. J Am Coll Cardiol. 2014;63(18):1904–12.
JMRI. 1997;7(3):606–11. 43. Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger
29. Budoff MJ, Achenbach S, Duerinckx A. Clinical utility of com- J, et al. From vulnerable plaque to vulnerable patient: a call for
puted tomography and magnetic resonance techniques for nonin- new definitions and risk assessment strategies: part I. Circulation.
vasive coronary angiography. J Am Coll Cardiol. 2003; 2003;108(14):1664–72.
42(11):1867–78. 44. Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger
30. Plein S, Greenwood JP, Ridgway JP, Cranny G, Ball SG, J, et al. From vulnerable plaque to vulnerable patient: a call for
Sivananthan MU. Assessment of non-ST-segment elevation acute new definitions and risk assessment strategies: part II. Circulation.
coronary syndromes with cardiac magnetic resonance imaging. 2003;108(15):1772–8.
J Am Coll Cardiol. 2004;44(11):2173–81. 45. Yeon SB, Sabir A, Clouse M, Martinezclark PO, Peters DC,
31. Yang Q, Li K, Liu X, Bi X, Liu Z, An J, et al. Contrast-enhanced Hauser TH, et al. Delayed-enhancement cardiovascular magnetic
whole-heart coronary magnetic resonance angiography at 3.0-T: a resonance coronary artery wall imaging: comparison with mul-
comparative study with X-ray angiography in a single center. tislice computed tomography and quantitative coronary angiogra-
J Am Coll Cardiol. 2009;54(1):69–76. phy. J Am Coll Cardiol. 2007;50(5):441–7.
32. Liu Z, Yang Q, Zhao Y, Jin L, Jerecic R, Xu D, et al. Use of coro- 46. Nikolaou K, Becker CR, Muders M, Babaryka G, Scheidler J,
nary anatomy and late enhancement information both derived Flohr T, et al. Multidetector-row computed tomography and mag-
from contrast-enhanced whole-heart coronary MRA at 3 T for the netic resonance imaging of atherosclerotic lesions in human
assessment of ischemic left ventricular dysfunction. Clin Imaging. ex vivo coronary arteries. Atherosclerosis. 2004;174(2):243–52.
2011;35(3):222–4. 47. Fayad ZA, Fuster V, Nikolaou K, Becker C. Computed tomogra-
33. Yang Q, Li K, Liu X, Du X, Bi X, Huang F, et al. 3.0T whole-heart phy and magnetic resonance imaging for noninvasive coronary
coronary magnetic resonance angiography performed with angiography and plaque imaging: current and potential future con-
32-channel cardiac coils: a single-center experience. Circ cepts. Circulation. 2002;106(15):2026–34.
Cardiovasc Imaging. 2012;5(5):573–9. 48. Kim WY, Stuber M, Bornert P, Kissinger KV, Manning WJ,
34. Stauder NI, Klumpp B, Stauder H, Blumenstock G, Fenchel M, Botnar RM. Three-dimensional black-blood cardiac magnetic
Kuttner A, et al. Assessment of coronary artery bypass grafts by resonance coronary vessel wall imaging detects positive arterial
magnetic resonance imaging. Br J Radiol. 2007;80(960): remodeling in patients with nonsignificant coronary artery dis-
975–83. ease. Circulation. 2002;106(3):296–9.
35. Achenbach S, Kessler W, Moshage WE, Ropers D, Zink D, 49. Viles-Gonzalez JF, Poon M, Sanz J, Rius T, Nikolaou K, Fayad
Kroeker R, et al. Visualization of the coronary arteries in three- ZA, et al. In vivo 16-slice, multidetector-row computed tomogra-
dimensional reconstructions using respiratory gated magnetic phy for the assessment of experimental atherosclerosis: compari-
resonance imaging. Coron Artery Dis. 1997;8(7):441–8. son with magnetic resonance imaging and histopathology.
36. Kessler W, Achenbach S, Moshage W, Zink D, Kroeker R, Nitz W, Circulation. 2004;110(11):1467–72.
et al. Usefulness of respiratory gated magnetic resonance coronary 50. Kuo YS, Kelle S, Lee C, Hinojar R, Nagel E, Botnar R, et al.
angiography in assessing narrowings > or = 50 % in diameter in Contrast-enhanced cardiovascular magnetic resonance imaging of
native coronary arteries and in aortocoronary bypass conduits. Am coronary vessel wall: state of art. Expert Rev Cardiovasc Ther.
J Cardiol. 1997;80(8):989–93. 2014;12(2):255–63.
37. So NM, Lam WW, Li D, Chan AK, Sanderson JE, Metreweli 51. Post JC, van Rossum AC, Bronzwaer JG, de Cock CC, Hofman
C. Magnetic resonance coronary angiography with 3D TrueFISP: MB, Valk J, et al. Magnetic resonance angiography of anomalous
breath-hold versus respiratory gated imaging. Br J Radiol. coronary arteries. A new gold standard for delineating the proxi-
2005;78(926):116–21. mal course? Circulation. 1995;92(11):3163–71.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 537

52. Bunce NH, Rahman SL, Keegan J, Gatehouse PD, Lorenz CH, 66. Heer T, Reiter S, Hofling B, Pilz G. Diagnostic performance of
Pennell DJ. Anomalous coronary arteries: anatomic and func- non-contrast-enhanced whole-heart magnetic resonance coronary
tional assessment by coronary and perfusion cardiovascular mag- angiography in combination with adenosine stress perfusion
netic resonance in three sisters. J Cardiovasc Magn Reson Off cardiac magnetic resonance imaging. Am Heart J. 2013;
J Soc Cardiovasc Magn Reson. 2001;3(4):361–9. 166(6):999–1009.
53. Sato Y, Matsumoto N, Komatsu S, Kunimasa T, Yoda S, Tani S, 67. Cheng AS, Pegg TJ, Karamitsos TD, Searle N, Jerosch-Herold M,
et al. Anomalous origin of the right coronary artery: depiction at Choudhury RP, et al. Cardiovascular magnetic resonance perfusion
whole-heart coronary magnetic resonance angiography. Int imaging at 3-tesla for the detection of coronary artery disease: a
J Cardiol. 2008;127(2):274–5. comparison with 1.5-tesla. J Am Coll Cardiol. 2007;
54. Shinbane JS, Shriki J, Fleischman F, Hindoyan A, Withey J, Lee 49(25):2440–9.
C, et al. Anomalous coronary arteries: cardiovascular computed 68. Jahnke C, Nagel E, Gebker R, Kokocinski T, Kelle S, Manka R,
tomographic angiography for surgical decisions and planning. et al. Prognostic value of cardiac magnetic resonance stress tests:
World J Pediatr Congenit Heart Surg. 2013;4(2):142–54. adenosine stress perfusion and dobutamine stress wall motion
55. Buchthal SD, den Hollander JA, Merz CN, Rogers WJ, Pepine CJ, imaging. Circulation. 2007;115(13):1769–76.
Reichek N, et al. Abnormal myocardial phosphorus-31 nuclear 69. Dall’Armellina E, Morgan TM, Mandapaka S, Ntim W, Carr JJ,
magnetic resonance spectroscopy in women with chest pain but Hamilton CA, et al. Prediction of cardiac events in patients with
normal coronary angiograms. N Engl J Med. 2000; reduced left ventricular ejection fraction with dobutamine
342(12):829–35. cardiovascular magnetic resonance assessment of wall motion
56. Johnson BD, Shaw LJ, Buchthal SD, Bairey Merz CN, Kim HW, score index. J Am Coll Cardiol. 2008;52(4):279–86.
Scott KN, et al. Prognosis in women with myocardial ischemia in 70. Kuijpers D, Ho KY, van Dijkman PR, Vliegenthart R, Oudkerk
the absence of obstructive coronary disease: results from the M. Dobutamine cardiovascular magnetic resonance for the
National Institutes of Health-National Heart, Lung, and Blood detection of myocardial ischemia with the use of myocardial tag-
Institute-Sponsored Women’s Ischemia Syndrome Evaluation ging. Circulation. 2003;107(12):1592–7.
(WISE). Circulation. 2004;109(24):2993–9. 71. Costa MA, Shoemaker S, Futamatsu H, Klassen C, Angiolillo DJ,
57. Cranney GB, Lotan CS, Dean L, Baxley W, Bouchard A, Pohost Nguyen M, et al. Quantitative magnetic resonance perfusion
GM. Left ventricular volume measurement using cardiac axis imaging detects anatomic and physiologic coronary artery disease
nuclear magnetic resonance imaging. Validation by calibrated as measured by coronary angiography and fractional flow reserve.
ventricular angiography. Circulation. 1990;82(1):154–63. J Am Coll Cardiol. 2007;50(6):514–22.
58. Rumberger JA, Behrenbeck T, Bell MR, Breen JF, Johnston DL, 72. Shah R, Heydari B, Coelho-Filho O, Murthy VL, Abbasi S, Feng
Holmes Jr DR, et al. Determination of ventricular ejection JH, et al. Stress cardiac magnetic resonance imaging provides
fraction: a comparison of available imaging methods. The effective cardiac risk reclassification in patients with known or
Cardiovascular Imaging Working Group. Mayo Clin Proc. suspected stable coronary artery disease. Circulation.
1997;72(9):860–70. 2013;128(6):605–14.
59. Scharhag J, Schneider G, Urhausen A, Rochette V, Kramann B, 73. Lipinski MJ, McVey CM, Berger JS, Kramer CM, Salerno
Kindermann W. Athlete’s heart: right and left ventricular mass and M. Prognostic value of stress cardiac magnetic resonance imaging
function in male endurance athletes and untrained individuals in patients with known or suspected coronary artery disease: a
determined by magnetic resonance imaging. J Am Coll Cardiol. systematic review and meta-analysis. J Am Coll Cardiol.
2002;40(10):1856–63. 2013;62(9):826–38.
60. Rominger MB, Bachmann GF, Geuer M, Puzik M, Boedeker 74. Miller CD, Case LD, Little WC, Mahler SA, Burke GL, Harper
RH, Ricken WW, et al. Accuracy of right and left ventricular EN, et al. Stress CMR reduces revascularization, hospital
heart volume and left ventricular muscle mass determination readmission, and recurrent cardiac testing in intermediate-risk
with cine MRI in breath holding technique. RoFo. 1999; patients with acute chest pain. JACC Cardiovasc Imaging.
170(1):54–60. 2013;6(7):785–94.
61. Ioannidis JP, Trikalinos TA, Danias PG. Electrocardiogram-gated 75. Jogiya R, Morton G, De Silva K, Reyes E, Hachamovitch R,
single-photon emission computed tomography versus cardiac Kozerke S, et al. Ischemic burden by 3-dimensional myocardial
magnetic resonance imaging for the assessment of left ventricular perfusion cardiovascular magnetic resonance: comparison with
volumes and ejection fraction: a meta-analysis. J Am Coll Cardiol. myocardial perfusion scintigraphy. Circ Cardiovasc Imaging.
2002;39(12):2059–68. 2014;7(4):647–54.
62. Grothues F, Moon JC, Bellenger NG, Smith GS, Klein HU, 76. Bettencourt N, Chiribiri A, Schuster A, Ferreira N, Sampaio F,
Pennell DJ. Interstudy reproducibility of right ventricular volumes, Pires-Morais G, et al. Direct comparison of cardiac magnetic
function, and mass with cardiovascular magnetic resonance. Am resonance and multidetector computed tomography stress-rest
Heart J. 2004;147(2):218–23. perfusion imaging for detection of coronary artery disease. J Am
63. Bodi V, Sanchis J, Nunez J, Mainar L, Lopez-Lereu MP, Coll Cardiol. 2013;61(10):1099–107.
Monmeneu JV, et al. Prognostic value of a comprehensive cardiac 77. Morris PD, van de Vosse FN, Lawford PV, Hose DR, Gunn JP.
magnetic resonance assessment soon after a first ST-segment “Virtual” (computed) fractional flow reserve: current challenges
elevation myocardial infarction. JACC Cardiovasc Imaging. and limitations. JACC Cardiovasc Interv. 2015;8(8):1009–17.
2009;2(7):835–42. 78. Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O,
64. Eitel I, de Waha S, Wohrle J, Fuernau G, Lurz P, Pauschinger M, et al. Relationship of MRI delayed contrast enhancement to
et al. Comprehensive prognosis assessment by CMR imaging after irreversible injury, infarct age, and contractile function.
ST-segment elevation myocardial infarction. J Am Coll Cardiol. Circulation. 1999;100(19):1992–2002.
2014;64(12):1217–26. 79. Gerber BL, Belge B, Legros GJ, Lim P, Poncelet A, Pasquet A,
65. Mordini FE, Haddad T, Hsu LY, Kellman P, Lowrey TB, Aletras et al. Characterization of acute and chronic myocardial infarcts by
AH, et al. Diagnostic accuracy of stress perfusion CMR in multidetector computed tomography: comparison with contrast-
comparison with quantitative coronary angiography: fully enhanced magnetic resonance. Circulation. 2006;113(6):823–33.
quantitative, semiquantitative, and qualitative assessment. JACC 80. Sato A, Nozato T, Hikita H, Akiyama D, Nishina H, Hoshi T, et al.
Cardiovasc Imaging. 2014;7(1):14–22. Prognostic value of myocardial contrast delayed enhancement
538 J.S. Shinbane et al.

with 64-slice multidetector computed tomography after acute 94. Perazzolo Marra M, De Lazzari M, Zorzi A, Migliore F, Zilio F,
myocardial infarction. J Am Coll Cardiol. 2012;59(8):730–8. Calore C, et al. Impact of the presence and amount of myocardial
81. McCrohon JA, Moon JC, Prasad SK, McKenna WJ, Lorenz CH, fibrosis by cardiac magnetic resonance on arrhythmic outcome
Coats AJ, et al. Differentiation of heart failure related to dilated and sudden cardiac death in nonischemic dilated cardiomyopathy.
cardiomyopathy and coronary artery disease using gadolinium- Heart Rhythm Off J Heart Rhythm Soc. 2014;11(5):856–63.
enhanced cardiovascular magnetic resonance. Circulation. 95. Kuruvilla S, Adenaw N, Katwal AB, Lipinski MJ, Kramer CM,
2003;108(1):54–9. Salerno M. Late gadolinium enhancement on cardiac magnetic
82. Schmidt A, Azevedo CF, Cheng A, Gupta SN, Bluemke DA, Foo resonance predicts adverse cardiovascular outcomes in
TK, et al. Infarct tissue heterogeneity by magnetic resonance nonischemic cardiomyopathy: a systematic review and meta-
imaging identifies enhanced cardiac arrhythmia susceptibility in analysis. Circ Cardiovasc Imaging. 2014;7(2):250–8.
patients with left ventricular dysfunction. Circulation. 96. Wu KC, Weiss RG, Thiemann DR, Kitagawa K, Schmidt A, Dalal
2007;115(15):2006–14. D, et al. Late gadolinium enhancement by cardiovascular magnetic
83. Lardo AC, Cordeiro MA, Silva C, Amado LC, George RT, Saliaris resonance heralds an adverse prognosis in nonischemic
AP, et al. Contrast-enhanced multidetector computed tomography cardiomyopathy. J Am Coll Cardiol. 2008;51(25):2414–21.
viability imaging after myocardial infarction: characterization of 97. Neilan TG, Coelho-Filho OR, Danik SB, Shah RV, Dodson JA,
myocyte death, microvascular obstruction, and chronic scar. Verdini DJ, et al. CMR quantification of myocardial scar provides
Circulation. 2006;113(3):394–404. additive prognostic information in nonischemic cardiomyopathy.
84. Ansari M, Araoz PA, Gerard SK, Watzinger N, Lund GK, Massie JACC Cardiovasc Imaging. 2013;6(9):944–54.
BM, et al. Comparison of late enhancement cardiovascular 98. aus dem Siepen F, Buss SJ, Messroghli D, Andre F, Lossnitzer D,
magnetic resonance and thallium SPECT in patients with coronary Seitz S, et al. T1 mapping in dilated cardiomyopathy with cardiac
disease and left ventricular dysfunction. J Cardiovasc Magn Reson magnetic resonance: quantification of diffuse myocardial fibrosis
Off J Soc Cardiovasc Magn Reson. 2004;6(2):549–56. and comparison with endomyocardial biopsy. Eur Heart
85. Ingkanisorn WP, Rhoads KL, Aletras AH, Kellman P, Arai J Cardiovasc Imaging. 2015;16(2):210–6.
AE. Gadolinium delayed enhancement cardiovascular magnetic 99. Moon JC, Messroghli DR, Kellman P, Piechnik SK, Robson MD,
resonance correlates with clinical measures of myocardial infarc- Ugander M, et al. Myocardial T1 mapping and extracellular
tion. J Am Coll Cardiol. 2004;43(12):2253–9. volume quantification: a Society for Cardiovascular Magnetic
86. Ichikawa Y, Sakuma H, Suzawa N, Kitagawa K, Makino K, Resonance (SCMR) and CMR Working Group of the European
Hirano T, et al. Late gadolinium-enhanced magnetic resonance Society of Cardiology consensus statement. J Cardiovasc Magn
imaging in acute and chronic myocardial infarction. Improved Reson Off J Soc Cardiovasc Magn Reson. 2013;15:92.
prediction of regional myocardial contraction in the chronic state 100. Iles L, Pfluger H, Phrommintikul A, Cherayath J, Aksit P, Gupta
by measuring thickness of nonenhanced myocardium. J Am Coll SN, et al. Evaluation of diffuse myocardial fibrosis in heart failure
Cardiol. 2005;45(6):901–9. with cardiac magnetic resonance contrast-enhanced T1 mapping.
87. Stork A, Muellerleile K, Bansmann PM, Graessner J, Kaul M, J Am Coll Cardiol. 2008;52(19):1574–80.
Kemper J, et al. Value of T2-weighted, first-pass and delayed 101. Puntmann VO, Voigt T, Chen Z, Mayr M, Karim R, Rhode K,
enhancement, and cine CMR to differentiate between acute and et al. Native T1 mapping in differentiation of normal myocardium
chronic myocardial infarction. Eur Radiol. 2007;17(3):610–7. from diffuse disease in hypertrophic and dilated cardiomyopathy.
88. Dall’Armellina E, Piechnik SK, Ferreira VM, Si QL, Robson MD, JACC Cardiovasc Imaging. 2013;6(4):475–84.
Francis JM, et al. Cardiovascular magnetic resonance by non 102. Treibel TA, Bandula S, Fontana M, White SK, Gilbertson JA,
contrast T1-mapping allows assessment of severity of injury in Herrey AS, et al. Extracellular volume quantification by dynamic
acute myocardial infarction. J Cardiovasc Magn Reson Off J Soc equilibrium cardiac computed tomography in cardiac amyloidosis.
Cardiovasc Magn Reson. 2012;14:15. J Cardiovasc Comput Tomogr. 2015;9:585–92.
89. Ubachs JF, Engblom H, Erlinge D, Jovinge S, Hedstrom E, 103. Saeed M, Hetts SW, Jablonowski R, Wilson MW. Magnetic reso-
Carlsson M, et al. Cardiovascular magnetic resonance of the nance imaging and multi-detector computed tomography assess-
myocardium at risk in acute reperfused myocardial infarction: ment of extracellular compartment in ischemic and non-ischemic
comparison of T2-weighted imaging versus the circumferential myocardial pathologies. World J Cardiol. 2014;6(11):1192–208.
endocardial extent of late gadolinium enhancement with 104. Dong SJ, MacGregor JH, Crawley AP, McVeigh E, Belenkie I,
transmural projection. J Cardiovasc Magn Reson Off J Soc Smith ER, et al. Left ventricular wall thickness and regional
Cardiovasc Magn Reson. 2010;12:18. systolic function in patients with hypertrophic cardiomyopathy. A
90. Eitel I, Kubusch K, Strohm O, Desch S, Mikami Y, de Waha S, three-dimensional tagged magnetic resonance imaging study.
et al. Prognostic value and determinants of a hypointense infarct Circulation. 1994;90(3):1200–9.
core in T2-weighted cardiac magnetic resonance in acute 105. Devlin AM, Moore NR, Ostman-Smith I. A comparison of MRI
reperfused ST-elevation-myocardial infarction. Circ Cardiovasc and echocardiography in hypertrophic cardiomyopathy. Br
Imaging. 2011;4(4):354–62. J Radiol. 1999;72(855):258–64.
91. O’Regan DP, Ahmed R, Karunanithy N, Neuwirth C, Tan Y, 106. Schulz-Menger J, Strohm O, Waigand J, Uhlich F, Dietz R,
Durighel G, et al. Reperfusion hemorrhage following acute Friedrich MG. The value of magnetic resonance imaging of the
myocardial infarction: assessment with T2* mapping and effect left ventricular outflow tract in patients with hypertrophic
on measuring the area at risk. Radiology. 2009;250(3):916–22. obstructive cardiomyopathy after septal artery embolization.
92. Assomull RG, Prasad SK, Lyne J, Smith G, Burman ED, Khan M, Circulation. 2000;101(15):1764–6.
et al. Cardiovascular magnetic resonance, fibrosis, and prognosis 107. Teraoka K, Hirano M, Ookubo H, Sasaki K, Katsuyama H, Amino
in dilated cardiomyopathy. J Am Coll Cardiol. 2006; M, et al. Delayed contrast enhancement of MRI in hypertrophic
48(10):1977–85. cardiomyopathy. Magn Reson Imaging. 2004;22(2):155–61.
93. Bello D, Shah DJ, Farah GM, Di Luzio S, Parker M, Johnson MR, 108. Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC,
et al. Gadolinium cardiovascular magnetic resonance predicts Pennell DJ. Toward clinical risk assessment in hypertrophic
reversible myocardial dysfunction and remodeling in patients with cardiomyopathy with gadolinium cardiovascular magnetic
heart failure undergoing beta-blocker therapy. Circulation. resonance. J Am Coll Cardiol. 2003;41(9):1561–7.
2003;108(16):1945–53.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 539

109. Moravsky G, Ofek E, Rakowski H, Butany J, Williams L, Ralph- 124. Hussain T, Dragulescu A, Benson L, Yoo SJ, Meng H, Windram J,
Edwards A, et al. Myocardial fibrosis in hypertrophic et al. Quantification and significance of diffuse myocardial fibrosis
cardiomyopathy: accurate reflection of histopathological findings and diastolic dysfunction in childhood hypertrophic cardiomyopa-
by CMR. JACC Cardiovasc Imaging. 2013;6(5):587–96. thy. Pediatr Cardiol. 2015;36(5):970–8.
110. Bruder O, Wagner A, Jensen CJ, Schneider S, Ong P, Kispert EM, 125. Ellims AH, Iles LM, Ling LH, Hare JL, Kaye DM, Taylor
et al. Myocardial scar visualized by cardiovascular magnetic AJ. Diffuse myocardial fibrosis in hypertrophic cardiomyopathy
resonance imaging predicts major adverse events in patients with can be identified by cardiovascular magnetic resonance, and is
hypertrophic cardiomyopathy. J Am Coll Cardiol. 2010; associated with left ventricular diastolic dysfunction. J Cardiovasc
56(11):875–87. Magn Reson Off J Soc Cardiovasc Magn Reson. 2012;14:76.
111. Choi HM, Kim KH, Lee JM, Yoon YE, Lee SP, Park EA, et al. 126. Zhao L, Ma X, Feuchtner GM, Zhang C, Fan Z. Quantification of
Myocardial fibrosis progression on cardiac magnetic resonance in myocardial delayed enhancement and wall thickness in
hypertrophic cardiomyopathy. Heart. 2015;101(11):870–6. hypertrophic cardiomyopathy: multidetector computed
112. Todiere G, Aquaro GD, Piaggi P, Formisano F, Barison A, Masci tomography versus magnetic resonance imaging. Eur J Radiol.
PG, et al. Progression of myocardial fibrosis assessed with cardiac 2014;83(10):1778–85.
magnetic resonance in hypertrophic cardiomyopathy. J Am Coll 127. Shariat M, Thavendiranathan P, Nguyen E, Wintersperger B, Paul
Cardiol. 2012;60(10):922–9. N, Rakowski H, et al. Utility of coronary CT angiography in
113. Chan RH, Maron BJ, Olivotto I, Pencina MJ, Assenza GE, Haas T, outpatients with hypertrophic cardiomyopathy presenting with
et al. Prognostic value of quantitative contrast-enhanced angina symptoms. J Cardiovasc Comput Tomogr. 2014;
cardiovascular magnetic resonance for the evaluation of sudden 8(6):429–37.
death risk in patients with hypertrophic cardiomyopathy. 128. Maceira AM, Joshi J, Prasad SK, Moon JC, Perugini E, Harding I,
Circulation. 2014;130(6):484–95. et al. Cardiovascular magnetic resonance in cardiac amyloidosis.
114. Matoh F, Satoh H, Shiraki K, Saitoh T, Urushida T, Katoh H, et al. Circulation. 2005;111(2):186–93.
Usefulness of delayed enhancement magnetic resonance imaging 129. Maceira AM, Prasad SK, Hawkins PN, Roughton M, Pennell
to differentiate dilated phase of hypertrophic cardiomyopathy and DJ. Cardiovascular magnetic resonance and prognosis in cardiac
dilated cardiomyopathy. J Card Fail. 2007;13(5):372–9. amyloidosis. J Cardiovasc Magn Reson Off J Soc Cardiovasc
115. Kebed KY, Al Adham RI, Bishu K, Askew JW, Klarich KW, Magn Reson. 2008;10:54.
Araoz PA, et al. Evaluation of apical subtype of hypertrophic 130. White JA, Kim HW, Shah D, Fine N, Kim KY, Wendell DC, et al.
cardiomyopathy using cardiac magnetic resonance imaging with CMR imaging with rapid visual T1 assessment predicts mortality
gadolinium enhancement. Am J Cardiol. 2014;114(5):777–82. in patients suspected of cardiac amyloidosis. JACC Cardiovasc
116. Hen Y, Iguchi N, Utanohara Y, Takada K, Machida H, Takayama Imaging. 2014;7(2):143–56.
M, et al. Prognostic value of late gadolinium enhancement on 131. Syed IS, Glockner JF, Feng D, Araoz PA, Martinez MW, Edwards
cardiac magnetic resonance imaging in Japanese hypertrophic WD, et al. Role of cardiac magnetic resonance imaging in the
cardiomyopathy patients. Circulation J Off J Jpn Circulation Soc. detection of cardiac amyloidosis. JACC Cardiovasc Imaging.
2014;78(4):929–37. 2010;3(2):155–64.
117. Hanneman K, Crean AM, Williams L, Moshonov H, James S, 132. Austin BA, Tang WH, Rodriguez ER, Tan C, Flamm SD, Taylor
Jimenez-Juan L, et al. Cardiac magnetic resonance imaging DO, et al. Delayed hyper-enhancement magnetic resonance
findings predict major adverse events in apical hypertrophic imaging provides incremental diagnostic and prognostic utility in
cardiomyopathy. J Thorac Imaging. 2014;29(6):331–9. suspected cardiac amyloidosis. JACC Cardiovasc Imaging.
118. Chaowu Y, Shihua Z, Jian L, Li L, Wei F. Cardiovascular magnetic 2009;2(12):1369–77.
resonance characteristics in children with hypertrophic 133. Vogelsberg H, Mahrholdt H, Deluigi CC, Yilmaz A, Kispert EM,
cardiomyopathy. Circ Heart Fail. 2013;6(5):1013–20. Greulich S, et al. Cardiovascular magnetic resonance in clinically
119. Fluechter S, Kuschyk J, Wolpert C, Doesch C, Veltmann C, Haghi D, suspected cardiac amyloidosis: noninvasive imaging compared to
et al. Extent of late gadolinium enhancement detected by cardiovas- endomyocardial biopsy. J Am Coll Cardiol. 2008;51(10):
cular magnetic resonance correlates with the inducibility of ventricu- 1022–30.
lar tachyarrhythmia in hypertrophic cardiomyopathy. J Cardiovasc 134. Dungu JN, Valencia O, Pinney JH, Gibbs SD, Rowczenio D,
Magn Reson Off J Soc Cardiovasc Magn Reson. 2010;12:30. Gilbertson JA, et al. CMR-based differentiation of AL and ATTR
120. Sakamoto N, Kawamura Y, Sato N, Nimura A, Matsuki M, cardiac amyloidosis. JACC Cardiovasc Imaging. 2014;7(2):
Yamauchi A, et al. Late gadolinium enhancement on cardiac 133–42.
magnetic resonance represents the depolarizing and repolarizing 135. Moon JC, Sachdev B, Elkington AG, McKenna WJ, Mehta A,
electrically damaged foci causing malignant ventricular Pennell DJ, et al. Gadolinium enhanced cardiovascular magnetic
arrhythmia in hypertrophic cardiomyopathy. Heart Rhythm Off resonance in Anderson-Fabry disease. Evidence for a disease
J Heart Rhythm Soc. 2015;12(6):1276–84. specific abnormality of the myocardial interstitium. Eur Heart
121. White RD, Obuchowski NA, Gunawardena S, Lipchik EO, Lever J. 2003;24(23):2151–5.
HM, Van Dyke CW, et al. Left ventricular outflow tract obstruction 136. Pica S, Sado DM, Maestrini V, Fontana M, White SK, Treibel T,
in hypertrophic cardiomyopathy: presurgical and postsurgical et al. Reproducibility of native myocardial T1 mapping in the
evaluation by computed tomography magnetic resonance imaging. assessment of Fabry disease and its role in early detection of
Am J Card Imaging. 1996;10(1):1–13. cardiac involvement by cardiovascular magnetic resonance.
122. Yuan J, Qiao S, Zhang Y, You S, Duan F, Hu F, et al. Follow-up by J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson.
cardiac magnetic resonance imaging in patients with hypertrophic 2014;16:99.
cardiomyopathy who underwent percutaneous ventricular septal 137. Imbriaco M, Pisani A, Spinelli L, Cuocolo A, Messalli G, Capuano
ablation. Am J Cardiol. 2010;106(10):1487–91. E, et al. Effects of enzyme-replacement therapy in patients with
123. Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Anderson-Fabry disease: a prospective long-term cardiac magnetic
Breen JF, et al. Comparison of surgical septal myectomy and resonance imaging study. Heart. 2009;95(13):1103–7.
alcohol septal ablation with cardiac magnetic resonance imaging 138. Smedema JP, Snoep G, van Kroonenburgh MP, van Geuns RJ,
in patients with hypertrophic obstructive cardiomyopathy. J Am Dassen WR, Gorgels AP, et al. Evaluation of the accuracy of
Coll Cardiol. 2007;49(3):350–7. gadolinium-enhanced cardiovascular magnetic resonance in the
540 J.S. Shinbane et al.

diagnosis of cardiac sarcoidosis. J Am Coll Cardiol. 153. Sachdeva S, Song X, Dham N, Heath DM, DeBiasi RL. Analysis
2005;45(10):1683–90. of clinical parameters and cardiac magnetic resonance imaging as
139. Nadel J, Lancefield T, Voskoboinik A, Taylor AJ. Late gadolinium predictors of outcome in pediatric myocarditis. Am J Cardiol.
enhancement identified with cardiac magnetic resonance imaging 2015;115(4):499–504.
in sarcoidosis patients is associated with long-term ventricular 154. Schumm J, Greulich S, Wagner A, Grun S, Ong P, Bentz K, et al.
arrhythmia and sudden cardiac death. Eur Heart J Cardiovasc Cardiovascular magnetic resonance risk stratification in patients
Imaging. 2015;16(6):634–41. with clinically suspected myocarditis. J Cardiovasc Magn Reson
140. Crawford T, Mueller G, Sarsam S, Prasitdumrong H, Chaiyen N, Off J Soc Cardiovasc Magn Reson. 2014;16:14.
Gu X, et al. Magnetic resonance imaging for identifying patients 155. Vermes E, Childs H, Faris P, Friedrich MG. Predictive value of
with cardiac sarcoidosis and preserved or mildly reduced left CMR criteria for LV functional improvement in patients with
ventricular function at risk of ventricular arrhythmias. Circ acute myocarditis. Eur Heart J Cardiovasc Imaging.
Arrhythm Electrophysiol. 2014;7(6):1109–15. 2014;15(10):1140–4.
141. Greulich S, Deluigi CC, Gloekler S, Wahl A, Zurn C, Kramer U, 156. Dambrin G, Laissy JP, Serfaty JM, Caussin C, Lancelin B, Paul
et al. CMR imaging predicts death and other adverse events in JF. Diagnostic value of ECG-gated multidetector computed
suspected cardiac sarcoidosis. JACC Cardiovasc Imaging. tomography in the early phase of suspected acute myocarditis. A
2013;6(4):501–11. preliminary comparative study with cardiac MRI. Eur Radiol.
142. Shimada T, Shimada K, Sakane T, Ochiai K, Tsukihashi H, Fukui 2007;17(2):331–8.
M, et al. Diagnosis of cardiac sarcoidosis and evaluation of the 157. Boussel L, Gamondes D, Staat P, Elicker BM, Revel D, Douek
effects of steroid therapy by gadolinium-DTPA-enhanced mag- P. Acute chest pain with normal coronary angiogram: role of
netic resonance imaging. Am J Med. 2001;110(7):520–7. contrast-enhanced multidetector computed tomography in the
143. Ise T, Hasegawa T, Morita Y, Yamada N, Funada A, Takahama H, differential diagnosis between myocarditis and myocardial
et al. Extensive late gadolinium enhancement on cardiovascular infarction. J Comput Assist Tomogr. 2008;32(2):228–32.
magnetic resonance predicts adverse outcomes and lack of 158. Axsom K, Lin F, Weinsaft JW, Min JK. Evaluation of myocarditis
improvement in LV function after steroid therapy in cardiac sar- with delayed-enhancement computed tomography. J Cardiovasc
coidosis. Heart. 2014;100(15):1165–72. Comput Tomogr. 2009;3(6):409–11.
144. Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, 159. Puntmann VO, D’Cruz D, Smith Z, Pastor A, Choong P, Voigt T,
Alakija P, Cooper LT, et al. Cardiovascular magnetic resonance in et al. Native myocardial T1 mapping by cardiovascular magnetic
myocarditis: a JACC White Paper. J Am Coll Cardiol. resonance imaging in subclinical cardiomyopathy in patients with
2009;53(17):1475–87. systemic lupus erythematosus. Circ Cardiovasc Imaging.
145. Abdel-Aty H, Boye P, Zagrosek A, Wassmuth R, Kumar A, 2013;6(2):295–301.
Messroghli D, et al. Diagnostic performance of cardiovascular 160. Hoey ET, Gulati GS, Ganeshan A, Watkin RW, Simpson H,
magnetic resonance in patients with suspected acute myocarditis: Sharma S. Cardiovascular MRI for assessment of infectious and
comparison of different approaches. J Am Coll Cardiol. inflammatory conditions of the heart. AJR Am J Roentgenol.
2005;45(11):1815–22. 2011;197(1):103–12.
146. Laissy JP, Hyafil F, Feldman LJ, Juliard JM, Schouman-Claeys E, 161. Abdel-Aty H, Siegle N, Natusch A, Gromnica-Ihle E, Wassmuth
Steg PG, et al. Differentiating acute myocardial infarction from R, Dietz R, et al. Myocardial tissue characterization in systemic
myocarditis: diagnostic value of early- and delayed-perfusion car- lupus erythematosus: value of a comprehensive cardiovascular
diac MR imaging. Radiology. 2005;237(1):75–82. magnetic resonance approach. Lupus. 2008;17(6):561–7.
147. Monney PA, Sekhri N, Burchell T, Knight C, Davies C, Deaner A, 162. Shriki J, Shinbane JS, Azadi N, Su TI, Hirschbein J, Quismorio Jr
et al. Acute myocarditis presenting as acute coronary syndrome: FP, et al. Systemic lupus erythematosus coronary vasculitis
role of early cardiac magnetic resonance in its diagnosis. Heart. demonstrated on cardiac computed tomography. Curr Probl Diagn
2011;97(16):1312–8. Radiol. 2014;43(5):294–7.
148. Francone M, Chimenti C, Galea N, Scopelliti F, Verardo R, Galea 163. Bocchi EA, Kalil R, Bacal F, de Lourdes HM, Meneghetti C,
R, et al. CMR sensitivity varies with clinical presentation and Magalhaes A, et al. Magnetic resonance imaging in chronic
extent of cell necrosis in biopsy-proven acute myocarditis. JACC Chagas’ disease: correlation with endomyocardial biopsy findings
Cardiovasc Imaging. 2014;7(3):254–63. and Gallium-67 cardiac uptake. Echocardiography. 1998;15(3):
149. Radunski UK, Lund GK, Stehning C, Schnackenburg B, Bohnen 279–88.
S, Adam G, et al. CMR in patients with severe myocarditis: 164. Rochitte CE, Oliveira PF, Andrade JM, Ianni BM, Parga JR, Avila
diagnostic value of quantitative tissue markers including LF, et al. Myocardial delayed enhancement by magnetic resonance
extracellular volume imaging. JACC Cardiovasc Imaging. imaging in patients with Chagas’ disease: a marker of disease
2014;7(7):667–75. severity. J Am Coll Cardiol. 2005;46(8):1553–8.
150. Ferreira VM, Piechnik SK, Dall’Armellina E, Karamitsos TD, 165. Bukhman G, Ziegler J, Parry E. Endomyocardial fibrosis: still a
Francis JM, Ntusi N, et al. T(1) mapping for the diagnosis of acute mystery after 60 years. PLoS Negl Trop Dis. 2008;2(2), e97.
myocarditis using CMR: comparison to T2-weighted and late 166. Kobayashi Y, Giles JT, Hirano M, Yokoe I, Nakajima Y, Bathon
gadolinium enhanced imaging. JACC Cardiovasc Imaging. JM, et al. Assessment of myocardial abnormalities in rheumatoid
2013;6(10):1048–58. arthritis using a comprehensive cardiac magnetic resonance
151. Hinojar R, Foote L, Arroyo Ucar E, Jackson T, Jabbour A, Yu CY, approach: a pilot study. Arthritis Res Ther. 2010;12(5):R171.
et al. Native T1 in discrimination of acute and convalescent stages 167. Francone M, Iacucci I, Mangia M, Carbone I. Endomyocardial dis-
in patients with clinical diagnosis of myocarditis: a proposed ease related to idiopathic hypereosinophilic syndrome: a cardiac
diagnostic algorithm using CMR. JACC Cardiovasc Imaging. magnetic resonance evaluation. Pediatr Cardiol. 2010;31(6):921–2.
2015;8(1):37–46. 168. Alter P, Maisch B. Endomyocardial fibrosis in Churg-Strauss syn-
152. Bohnen S, Radunski UK, Lund GK, Kandolf R, Stehning C, drome assessed by cardiac magnetic resonance imaging. Int
Schnackenburg B, et al. Performance of t1 and t2 mapping cardio- J Cardiol. 2006;108(1):112–3.
vascular magnetic resonance to detect active myocarditis in 169. Syed IS, Martinez MW, Feng DL, Glockner JF. Cardiac magnetic
patients with recent-onset heart failure. Circ Cardiovasc Imaging. resonance imaging of eosinophilic endomyocardial disease. Int
2015;8(6):e003073. J Cardiol. 2008;126(3):e50–2.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 541

170. Wood JC, Origa R, Agus A, Matta G, Coates TD, Galanello 186. Corrado D, Thiene G, Nava A, Rossi L, Pennelli N. Sudden death
R. Onset of cardiac iron loading in pediatric patients with in young competitive athletes: clinicopathologic correlations in 22
thalassemia major. Haematologica. 2008;93(6):917–20. cases. Am J Med. 1990;89(5):588–96.
171. Carpenter JP, He T, Kirk P, Roughton M, Anderson LJ, de Noronha 187. Tabib A, Loire R, Chalabreysse L, Meyronnet D, Miras A,
SV, et al. On T2* magnetic resonance and cardiac iron. Circulation. Malicier D, et al. Circumstances of death and gross and
2011;123(14):1519–28. microscopic observations in a series of 200 cases of sudden death
172. Wood JC. Use of magnetic resonance imaging to monitor iron associated with arrhythmogenic right ventricular cardiomyopathy
overload. Hematol Oncol Clin North Am. 2014;28(4):747–64, vii. and/or dysplasia. Circulation. 2003;108(24):3000–5.
173. Hor KN, Wansapura J, Markham LW, Mazur W, Cripe LH, Fleck 188. McKenna WJ, Thiene G, Nava A, Fontaliran F, Blomstrom-
R, et al. Circumferential strain analysis identifies strata of Lundqvist C, Fontaine G, et al. Diagnosis of arrhythmogenic right
cardiomyopathy in Duchenne muscular dystrophy: a cardiac ventricular dysplasia/cardiomyopathy. Task Force of the Working
magnetic resonance tagging study. J Am Coll Cardiol. Group Myocardial and Pericardial Disease of the European
2009;53(14):1204–10. Society of Cardiology and of the Scientific Council on
174. Soslow JH, Damon BM, Saville BR, Lu Z, Burnette WB, Lawson Cardiomyopathies of the International Society and Federation of
MA, et al. Evaluation of post-contrast myocardial t1 in duchenne Cardiology. Br Heart J. 1994;71(3):215–8.
muscular dystrophy using cardiac magnetic resonance imaging. 189. Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke
Pediatr Cardiol. 2015;36(1):49–56. DA, et al. Diagnosis of arrhythmogenic right ventricular
175. Lang SM, Shugh S, Mazur W, Sticka JJ, Rattan MS, Jefferies JL, cardiomyopathy/dysplasia: proposed modification of the task
et al. Myocardial fibrosis and left ventricular dysfunction in force criteria. Circulation. 2010;121(13):1533–41.
Duchenne muscular dystrophy carriers using cardiac magnetic 190. di Cesare E. MRI assessment of right ventricular dysplasia. Eur
resonance imaging. Pediatr Cardiol. 2015;36(7):1495–501. Radiol. 2003;13(6):1387–93.
176. Schelhorn J, Schoenecker A, Neudorf U, Schemuth H, Nensa F, 191. Bomma C, Rutberg J, Tandri H, Nasir K, Roguin A, Tichnell C,
Nassenstein K, et al. Cardiac pathologies in female carriers of et al. Misdiagnosis of arrhythmogenic right ventricular dysplasia/
Duchenne muscular dystrophy assessed by cardiovascular mag- cardiomyopathy. J Cardiovasc Electrophysiol. 2004;15(3):300–6.
netic resonance imaging. Eur Radiol. 2015;25(10):3066–72. 192. Casolo G, Di Cesare E, Molinari G, Knoll P, Midiri M, Fedele F,
177. Wahbi K, Meune C, el Hamouda H, Stojkovic T, Laforet P, Becane et al. Diagnostic work up of arrhythmogenic right ventricular cardio-
HM, et al. Cardiac assessment of limb-girdle muscular dystrophy myopathy by cardiovascular magnetic resonance (CMR). Consensus
2I patients: an echography, Holter ECG and magnetic resonance statement La Radiologia Medica. 2004;108(1–2):39–55.
imaging study. Neuromuscul Disord NMD. 2008;18(8):650–5. 193. Bluemke DA, Krupinski EA, Ovitt T, Gear K, Unger E, Axel L,
178. Yilmaz A, Gdynia HJ, Baccouche H, Mahrholdt H, Meinhardt G, et al. MR imaging of arrhythmogenic right ventricular
Basso C, et al. Cardiac involvement in patients with Becker cardiomyopathy: morphologic findings and interobserver
muscular dystrophy: new diagnostic and pathophysiological reliability. Cardiology. 2003;99(3):153–62.
insights by a CMR approach. J Cardiovasc Magn Reson Off J Soc 194. Tandri H, Saranathan M, Rodriguez ER, Martinez C, Bomma C,
Cardiovasc Magn Reson. 2008;10:50. Nasir K, et al. Noninvasive detection of myocardial fibrosis in
179. Yilmaz A, Gdynia HJ, Mahrholdt H, Sechtem U. Cardiovascular arrhythmogenic right ventricular cardiomyopathy using delayed-
magnetic resonance reveals similar damage to the heart of patients enhancement magnetic resonance imaging. J Am Coll Cardiol.
with Becker and limb-girdle muscular dystrophy but no cardiac 2005;45(1):98–103.
symptoms. J Magn Reson Imaging JMRI. 2009;30(4):876–7. 195. te Riele AS, Bhonsale A, James CA, Rastegar N, Murray B, Burt
180. Hermans MC, Faber CG, Bekkers SC, de Die-Smulders CE, JR, et al. Incremental value of cardiac magnetic resonance imaging
Gerrits MM, Merkies IS, et al. Structural and functional cardiac in arrhythmic risk stratification of arrhythmogenic right ventricular
changes in myotonic dystrophy type 1: a cardiovascular magnetic dysplasia/cardiomyopathy-associated desmosomal mutation
resonance study. J Cardiovasc Magn Reson Off J Soc Cardiovasc carriers. J Am Coll Cardiol. 2013;62(19):1761–9.
Magn Reson. 2012;14:48. 196. Quarta G, Husain SI, Flett AS, Sado DM, Chao CY, Tome Esteban
181. Petri H, Ahtarovski KA, Vejlstrup N, Vissing J, Witting N, Kober MT, et al. Arrhythmogenic right ventricular cardiomyopathy
L, et al. Myocardial fibrosis in patients with myotonic dystrophy mimics: role of cardiovascular magnetic resonance. J Cardiovasc
type 1: a cardiovascular magnetic resonance study. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson. 2013;15:16.
Magn Reson Off J Soc Cardiovasc Magn Reson. 2014;16(1):59. 197. Liu T, Pursnani A, Sharma UC, Vorasettakarnkij Y, Verdini D,
182. Turkbey EB, Gai N, Lima JA, van der Geest RJ, Wagner KR, Deeprasertkul P, et al. Effect of the 2010 task force criteria on
Tomaselli GF, et al. Assessment of cardiac involvement in reclassification of cardiovascular magnetic resonance criteria for
myotonic muscular dystrophy by T1 mapping on magnetic arrhythmogenic right ventricular cardiomyopathy. J Cardiovasc
resonance imaging. Heart Rhythm Off J Heart Rhythm Soc. Magn Reson Off J Soc Cardiovasc Magn Reson. 2014;16:47.
2012;9(10):1691–7. 198. Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R,
183. Iacucci I, Carbone I, Cannavale G, Conti B, Iampieri I, Rosati R, Brugada P, et al. Proposed diagnostic criteria for the Brugada
et al. Myocardial oedema as the sole marker of acute injury in syndrome: consensus report. Circulation. 2002;106(19):2514–9.
Takotsubo cardiomyopathy: a cardiovascular magnetic resonance 199. Papavassiliu T, Wolpert C, Fluchter S, Schimpf R, Neff W, Haase
(CMR) study. Radiol Med. 2013;118(8):1309–23. KK, et al. Magnetic resonance imaging findings in patients with
184. Avegliano G, Huguet M, Costabel JP, Ronderos R, Bijnens B, Brugada syndrome. J Cardiovasc Electrophysiol. 2004;15(10):
Kuschnir P, et al. Morphologic pattern of late gadolinium 1133–8.
enhancement in Takotsubo cardiomyopathy detected by early 200. Steckman DA, Schneider PM, Schuller JL, Aleong RG, Nguyen
cardiovascular magnetic resonance. Clin Cardiol. 2011; DT, Sinagra G, et al. Utility of cardiac magnetic resonance imaging
34(3):178–82. to differentiate cardiac sarcoidosis from arrhythmogenic right ven-
185. Naruse Y, Sato A, Kasahara K, Makino K, Sano M, Takeuchi Y, tricular cardiomyopathy. Am J Cardiol. 2012;110(4):575–9.
et al. The clinical impact of late gadolinium enhancement in 201. Carrilho-Ferreira P, Almeida AG, Pinto FJ. Non-compaction car-
Takotsubo cardiomyopathy: serial analysis of cardiovascular diomyopathy: prevalence, prognosis, pathoetiology, genetics, and
magnetic resonance images. J Cardiovasc Magn Reson Off J Soc risk of cardioembolism. Curr Heart Fail Rep. 2014;11(4):
Cardiovasc Magn Reson. 2011;13:67. 393–403.
542 J.S. Shinbane et al.

202. Petersen SE, Selvanayagam JB, Wiesmann F, Robson MD, Francis magnetic resonance imaging in a general cardiology population.
JM, Anderson RH, et al. Left ventricular non-compaction: insights J Cardiovasc Electrophysiol. 2015;26(5):484–92.
from cardiovascular magnetic resonance imaging. J Am Coll 217. Habibi M, Lima JA, Khurram IM, Zimmerman SL, Zipunnikov V,
Cardiol. 2005;46(1):101–5. Fukumoto K, et al. Association of left atrial function and left atrial
203. Cheng H, Zhao S, Jiang S, Lu M, Yan C, Ling J, et al. Comparison enhancement in patients with atrial fibrillation: cardiac magnetic
of cardiac magnetic resonance imaging features of isolated left resonance study. Circ Cardiovasc Imaging. 2015;8(2), e002769.
ventricular non-compaction in adults versus dilated 218. Daccarett M, Badger TJ, Akoum N, Burgon NS, Mahnkopf C,
cardiomyopathy in adults. Clin Radiol. 2011;66(9):853–60. Vergara G, et al. Association of left atrial fibrosis detected by
204. Grothoff M, Pachowsky M, Hoffmann J, Posch M, Klaassen S, delayed-enhancement magnetic resonance imaging and the risk of
Lehmkuhl L, et al. Value of cardiovascular MR in diagnosing left stroke in patients with atrial fibrillation. J Am Coll Cardiol.
ventricular non-compaction cardiomyopathy and in discriminat- 2011;57(7):831–8.
ing between other cardiomyopathies. Eur Radiol. 2012;22(12): 219. Kwong RY, Heydari B, Abbasi S, Steel K, Al-Mallah M, Wu H,
2699–709. et al. Characterization of cardiac amyloidosis by atrial late
205. Choudhary P, Hsu CJ, Grieve S, Smillie C, Singarayar S, gadolinium enhancement using contrast-enhanced cardiac
Semsarian C, et al. Improving the diagnosis of LV non-compaction magnetic resonance imaging and correlation with left atrial
with cardiac magnetic resonance imaging. Int J Cardiol. conduit and contractile function. Am J Cardiol. 2015;116:622–9.
2015;181:430–6. 220. Hamdan A, Charalampos K, Roettgen R, Wellnhofer E, Gebker R,
206. Wan J, Zhao S, Cheng H, Lu M, Jiang S, Yin G, et al. Varied dis- Paetsch I, et al. Magnetic resonance imaging versus computed
tributions of late gadolinium enhancement found among patients tomography for characterization of pulmonary vein morphology
meeting cardiovascular magnetic resonance criteria for isolated before radiofrequency catheter ablation of atrial fibrillation. Am
left ventricular non-compaction. J Cardiovasc Magn Reson Off J Cardiol. 2009;104(11):1540–6.
J Soc Cardiovasc Magn Reson. 2013;15:20. 221. Hauser TH, McClennen S, Katsimaglis G, Josephson ME,
207. Nucifora G, Aquaro GD, Pingitore A, Masci PG, Lombardi Manning WJ, Yeon SB. Assessment of left atrial volume by
M. Myocardial fibrosis in isolated left ventricular non-compaction contrast enhanced magnetic resonance angiography. J Cardiovasc
and its relation to disease severity. Eur J Heart Fail. 2011; Magn Reson Off J Soc Cardiovasc Magn Reson. 2004;
13(2):170–6. 6(2):491–7.
208. Melendez-Ramirez G, Castillo-Castellon F, Espinola-Zavaleta N, 222. Lickfett L, Kato R, Tandri H, Jayam V, Vasamreddy CR, Dickfeld
Meave A, Kimura-Hayama ET. Left ventricular noncompaction: a T, et al. Characterization of a new pulmonary vein variant using
proposal of new diagnostic criteria by multidetector computed magnetic resonance angiography: incidence, imaging, and
tomography. J Cardiovasc Comput Tomogr. 2012;6(5):346–54. interventional implications of the “right top pulmonary vein”.
209. Sidhu MS, Uthamalingam S, Ahmed W, Engel LC, Vorasettakarnkij J Cardiovasc Electrophysiol. 2004;15(5):538–43.
Y, Lee AM, et al. Defining left ventricular noncompaction using car- 223. Kato R, Lickfett L, Meininger G, Dickfeld T, Wu R, Juang G,
diac computed tomography. J Thorac Imaging. 2014;29(1):60–6. et al. Pulmonary vein anatomy in patients undergoing catheter
210. Maceira AM, Cosin-Sales J, Roughton M, Prasad SK, Pennell ablation of atrial fibrillation: lessons learned by use of magnetic
DJ. Reference left atrial dimensions and volumes by steady state resonance imaging. Circulation. 2003;107(15):2004–10.
free precession cardiovascular magnetic resonance. J Cardiovasc 224. Mansour M, Holmvang G, Sosnovik D, Migrino R, Abbara S,
Magn Reson Off J Soc Cardiovasc Magn Reson. 2010;12:65. Ruskin J, et al. Assessment of pulmonary vein anatomic variability
211. Maceira AM, Cosin-Sales J, Roughton M, Prasad SK, Pennell by magnetic resonance imaging: implications for catheter ablation
DJ. Reference right atrial dimensions and volume estimation by techniques for atrial fibrillation. J Cardiovasc Electrophysiol.
steady state free precession cardiovascular magnetic resonance. 2004;15(4):387–93.
J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson. 225. Nori D, Raff G, Gupta V, Gentry R, Boura J, Haines DE. Cardiac
2013;15:29. magnetic resonance imaging assessment of regional and global
212. Jahnke C, Fischer J, Mirelis JG, Kriatselis C, Gerds-Li JH, Gebker left atrial function before and after catheter ablation for atrial
R, et al. Cardiovascular magnetic resonance imaging for accurate fibrillation. J Interv Card Electrophysiol. 2009;26(2):109–17.
sizing of the left atrium: predictability of pulmonary vein isolation 226. Mahabadi AA, Samy B, Seneviratne SK, Toepker MH, Bamberg F,
success in patients with atrial fibrillation. J Magn Reson Imaging Hoffmann U, et al. Quantitative assessment of left atrial volume by
JMRI. 2011;33(2):455–63. electrocardiographic-gated contrast-enhanced multidetector com-
213. Kowallick JT, Morton G, Lamata P, Jogiya R, Kutty S, Hasenfuss puted tomography. J Cardiovasc Comput Tomogr. 2009;3(2):80–7.
G, et al. Quantification of atrial dynamics using cardiovascular 227. Hauser TH, Essebag V, Baldessin F, McClennen S, Yeon SB,
magnetic resonance: inter-study reproducibility. J Cardiovasc Manning WJ, et al. Prognostic value of pulmonary vein size in
Magn Reson Off J Soc Cardiovasc Magn Reson. 2015;17:36. prediction of atrial fibrillation recurrence after pulmonary vein
214. Vardoulis O, Monney P, Bermano A, Vaxman A, Gotsman C, isolation: a cardiovascular magnetic resonance study. J Cardiovasc
Schwitter J, et al. Single breath-hold 3D measurement of left atrial Magn Reson Off J Soc Cardiovasc Magn Reson. 2015;17:49.
volume using compressed sensing cardiovascular magnetic 228. Dickfeld T, Calkins H, Zviman M, Kato R, Meininger G, Lickfett
resonance and a non-model-based reconstruction approach. L, et al. Anatomic stereotactic catheter ablation on three-
J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson. dimensional magnetic resonance images in real time. Circulation.
2015;17:47. 2003;108(19):2407–13.
215. Agner BF, Kuhl JT, Linde JJ, Kofoed KF, Akeson P, Rasmussen 229. Dickfeld T, Calkins H, Zviman M, Meininger G, Lickfett L,
BV, et al. Assessment of left atrial volume and function in patients Roguin A, et al. Stereotactic magnetic resonance guidance for
with permanent atrial fibrillation: comparison of cardiac magnetic anatomically targeted ablations of the fossa ovalis and the left
resonance imaging, 320-slice multi-detector computed atrium. J Interv Card Electrophysiol. 2004;11(2):105–15.
tomography, and transthoracic echocardiography. Eur Heart 230. Bertaglia E, Brandolino G, Zoppo F, Zerbo F, Pascotto
J Cardiovasc Imaging. 2014;15(5):532–40. P. Integration of three-dimensional left atrial magnetic resonance
216. Cochet H, Mouries A, Nivet H, Sacher F, Derval N, Denis A, et al. images into a real-time electroanatomic mapping system:
Age, atrial fibrillation, and structural heart disease are the main validation of a registration method. Pacing Clin Electrophysiol
determinants of left atrial fibrosis detected by delayed-enhanced PACE. 2008;31(3):273–82.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 543

231. Aleong R, Heist EK, Ruskin JN, Mansour M. Integration of intra- 247. Budoff MJ, Shittu A, Hacioglu Y, Gang E, Li D, Bhatia H, et al.
cardiac echocardiography with magnetic resonance imaging Comparison of transesophageal echocardiography versus
allows visualization of the esophagus during catheter ablation of computed tomography for detection of left atrial appendage filling
atrial fibrillation. Heart Rhythm Off J Heart Rhythm Soc. defect (thrombus). Am J Cardiol. 2014;113(1):173–7.
2008;5(7):1088. 248. Mohrs OK, Schraeder R, Petersen SE, Scherer D, Nowak B,
232. Robbins IM, Colvin EV, Doyle TP, Kemp WE, Loyd JE, McMahon Kauczor HU, et al. Percutaneous left atrial appendage transcatheter
WS, et al. Pulmonary vein stenosis after catheter ablation of atrial occlusion (PLAATO): planning and follow-up using contrast-
fibrillation. Circulation. 1998;98(17):1769–75. enhanced MRI. AJR Am J Roentgenol. 2006;186(2):361–4.
233. Taylor GW, Kay GN, Zheng X, Bishop S, Ideker RE. Pathological 249. van Rosendael PJ, Katsanos S, van den Brink OW, Scholte AJ,
effects of extensive radiofrequency energy applications in the Trines SA, Bax JJ, et al. Geometry of left atrial appendage
pulmonary veins in dogs. Circulation. 2000;101(14):1736–42. assessed with multidetector-row computed tomography:
234. Dill T, Neumann T, Ekinci O, Breidenbach C, John A, Erdogan A, implications for transcatheter closure devices. EuroIntervention.
et al. Pulmonary vein diameter reduction after radiofrequency 2014;10(3):364–71.
catheter ablation for paroxysmal atrial fibrillation evaluated by 250. Poulter RS, Tang J, Jue J, Ibrahim R, Nicolaou S, Mayo J, et al.
contrast-enhanced three-dimensional magnetic resonance Cardiac computed tomography follow-up of left atrial appendage
imaging. Circulation. 2003;107(6):845–50. exclusion using the Amplatzer Cardiac Plug device. Can J Cardiol.
235. Arentz T, Jander N, von Rosenthal J, Blum T, Furmaier R, 2012;28(1):119.e1–3.
Gornandt L, et al. Incidence of pulmonary vein stenosis 2 years 251. Thadani SR, Dyverfeldt P, Gin A, Chitsaz S, Rao RK, Hope
after radiofrequency catheter ablation of refractory atrial MD. Comprehensive evaluation of culture-negative endocarditis
fibrillation. Eur Heart J. 2003;24(10):963–9. with use of cardiac and 4-dimensional-flow magnetic resonance
236. Fukumoto K, Habibi M, Gucuk Ipek E, Khurram IM, Zimmerman imaging. Tex Heart Inst J. 2014;41(3):351–2.
SL, Zipunnikov V, et al. Comparison of preexisting and ablation- 252. Harris KM, Ang E, Lesser JR, Sonnesyn SW. Cardiac magnetic
induced late gadolinium enhancement on left atrial magnetic resonance imaging for detection of an abscess associated with
resonance imaging. Heart Rhythm Off J Heart Rhythm Soc. prosthetic valve endocarditis: a case report. Heart Surg Forum.
2015;12(4):668–72. 2007;10(3):E186–7.
237. Oakes RS, Badger TJ, Kholmovski EG, Akoum N, Burgon NS, 253. Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J,
Fish EN, et al. Detection and quantification of left atrial structural Scheffel H, et al. Multislice computed tomography in infective
remodeling with delayed-enhancement magnetic resonance endocarditis: comparison with transesophageal echocardiography
imaging in patients with atrial fibrillation. Circulation. and intraoperative findings. J Am Coll Cardiol. 2009;53(5):
2009;119(13):1758–67. 436–44.
238. Peters DC, Wylie JV, Hauser TH, Nezafat R, Han Y, Woo JJ, et al. 254. Saby L, Laas O, Habib G, Cammilleri S, Mancini J, Tessonnier L,
Recurrence of atrial fibrillation correlates with the extent of post- et al. Positron emission tomography/computed tomography for
procedural late gadolinium enhancement: a pilot study. JACC diagnosis of prosthetic valve endocarditis: increased valvular
Cardiovasc Imaging. 2009;2(3):308–16. 18 F-fluorodeoxyglucose uptake as a novel major criterion. J Am
239. McGann C, Kholmovski E, Blauer J, Vijayakumar S, Haslam T, Coll Cardiol. 2013;61(23):2374–82.
Cates J, et al. Dark regions of no-reflow on late gadolinium 255. John AS, Dill T, Brandt RR, Rau M, Ricken W, Bachmann G,
enhancement magnetic resonance imaging result in scar formation et al. Magnetic resonance to assess the aortic valve area in aortic
after atrial fibrillation ablation. J Am Coll Cardiol. 2011; stenosis: how does it compare to current diagnostic standards?
58(2):177–85. J Am Coll Cardiol. 2003;42(3):519–26.
240. Beinart R, Khurram IM, Liu S, Yarmohammadi H, Halperin HR, 256. Malyar NM, Schlosser T, Barkhausen J, Gutersohn A, Buck T,
Bluemke DA, et al. Cardiac magnetic resonance T1 mapping of Bartel T, et al. Assessment of aortic valve area in aortic stenosis
left atrial myocardium. Heart Rhythm Off J Heart Rhythm Soc. using cardiac magnetic resonance tomography: comparison with
2013;10(9):1325–31. echocardiography. Cardiology. 2008;109(2):126–34.
241. Ling LH, McLellan AJ, Taylor AJ, Iles LM, Ellims AH, Kumar S, 257. Garcia J, Kadem L, Larose E, Clavel MA, Pibarot P. Comparison
et al. Magnetic resonance post-contrast T1 mapping in the human between cardiovascular magnetic resonance and transthoracic
atrium: validation and impact on clinical outcome after catheter Doppler echocardiography for the estimation of effective orifice
ablation for atrial fibrillation. Heart Rhythm Off J Heart Rhythm area in aortic stenosis. J Cardiovasc Magn Reson Off J Soc
Soc. 2014;11(9):1551–9. Cardiovasc Magn Reson. 2011;13:25.
242. Heist EK, Refaat M, Danik SB, Holmvang G, Ruskin JN, Mansour 258. Garcia J, Capoulade R, Le Ven F, Gaillard E, Kadem L, Pibarot P,
M. Analysis of the left atrial appendage by magnetic resonance et al. Discrepancies between cardiovascular magnetic resonance
angiography in patients with atrial fibrillation. Heart Rhythm Off and Doppler echocardiography in the measurement of transvalvular
J Heart Rhythm Soc. 2006;3(11):1313–8. gradient in aortic stenosis: the effect of flow vorticity. J Cardiovasc
243. Muellerleile K, Sultan A, Groth M, Steven D, Hoffmann B, Adam Magn Reson Off J Soc Cardiovasc Magn Reson. 2013;15:84.
G, et al. Velocity encoded cardiovascular magnetic resonance to 259. Hoffmann R, Altiok E, Friedman Z, Becker M, Frick
assess left atrial appendage emptying. J Cardiovasc Magn Reson M. Myocardial deformation imaging by two-dimensional speckle-
Off J Soc Cardiovasc Magn Reson. 2012;14:39. tracking echocardiography in comparison to late gadolinium
244. Ohyama H, Hosomi N, Takahashi T, Mizushige K, Osaka K, enhancement cardiac magnetic resonance for analysis of
Kohno M, et al. Comparison of magnetic resonance imaging and myocardial fibrosis in severe aortic stenosis. Am J Cardiol.
transesophageal echocardiography in detection of thrombus in the 2014;114(7):1083–8.
left atrial appendage. Stroke J Cereb Circ. 2003;34(10):2436–9. 260. Lee SP, Park SJ, Kim YJ, Chang SA, Park EA, Kim HK, et al.
245. Ohyama H, Mizushige K, Hosomi N. Magnetic resonance imag- Early detection of subclinical ventricular deterioration in aortic
ing of left atrial thrombus. Heart. 2002;88(3):233. stenosis with cardiovascular magnetic resonance and
246. Mohrs OK, Nowak B, Petersen SE, Welsner M, Rubel C, echocardiography. J Cardiovasc Magn Reson Off J Soc Cardiovasc
Magedanz A, et al. Thrombus detection in the left atrial appendage Magn Reson. 2013;15:72.
using contrast-enhanced MRI: a pilot study. AJR Am J Roentgenol. 261. Azevedo CF, Nigri M, Higuchi ML, Pomerantzeff PM, Spina GS,
2006;186(1):198–205. Sampaio RO, et al. Prognostic significance of myocardial fibrosis
544 J.S. Shinbane et al.

quantification by histopathology and magnetic resonance imaging 275. Gelfand EV, Hughes S, Hauser TH, Yeon SB, Goepfert L,
in patients with severe aortic valve disease. J Am Coll Cardiol. Kissinger KV, et al. Severity of mitral and aortic regurgitation as
2010;56(4):278–87. assessed by cardiovascular magnetic resonance: optimizing
262. Holmes Jr DR, Mack MJ, Kaul S, Agnihotri A, Alexander KP, correlation with Doppler echocardiography. J Cardiovasc Magn
Bailey SR, et al. 2012 ACCF/AATS/SCAI/STS expert consensus Reson Off J Soc Cardiovasc Magn Reson. 2006;8(3):503–7.
document on transcatheter aortic valve replacement. J Am Coll 276. Debl K, Djavidani B, Buchner S, Heinicke N, Fredersdorf S,
Cardiol. 2012;59(13):1200–54. Haimerl J, et al. Assessment of the anatomic regurgitant orifice in
263. Crouch G, Bennetts J, Sinhal A, Tully PJ, Leong DP, Bradbrook aortic regurgitation: a clinical magnetic resonance imaging study.
C, et al. Early effects of transcatheter aortic valve implantation Heart. 2008;94(3), e8.
and aortic valve replacement on myocardial function and aortic 277. Ewe SH, Delgado V, van der Geest R, Westenberg JJ, Haeck ML,
valve hemodynamics: insights from cardiovascular magnetic Witkowski TG, et al. Accuracy of three-dimensional versus two-
resonance imaging. J Thorac Cardiovasc Surg. 2015;149(2): dimensional echocardiography for quantification of aortic
462–70. regurgitation and validation by three-dimensional three-directional
264. Fairbairn TA, Steadman CD, Mather AN, Motwani M, Blackman velocity-encoded magnetic resonance imaging. Am J Cardiol.
DJ, Plein S, et al. Assessment of valve haemodynamics, reverse 2013;112(4):560–6.
ventricular remodelling and myocardial fibrosis following 278. Ko SM, Park JH, Shin JK, Kim JS. Assessment of the regurgitant
transcatheter aortic valve implantation compared to surgical aortic orifice area in aortic regurgitation with dual-source CT:
valve replacement: a cardiovascular magnetic resonance study. Comparison with cardiovascular magnetic resonance. J Cardiovasc
Heart. 2013;99(16):1185–91. Comput Tomogr. 2015;9(4):345–53.
265. Rossi A, van der Linde D, Yap SC, Lapinskas T, Kirschbaum S, 279. Feuchtner GM, Spoeck A, Lessick J, Dichtl W, Plass A, Leschka
Springeling T, et al. Ascending aorta dilatation in patients with S, et al. Quantification of aortic regurgitant fraction and volume
bicuspid aortic valve stenosis: a prospective CMR study. Eur with multi-detector computed tomography comparison with
Radiol. 2013;23(3):642–9. echocardiography. Acad Radiol. 2011;18(3):334–42.
266. Malaisrie SC, Carr J, Mikati I, Rigolin V, Yip BK, Lapin B, et al. 280. Frick M, Meyer CG, Kirschfink A, Altiok E, Lehrke M, Brehmer K,
Cardiac magnetic resonance imaging is more diagnostic than et al. Evaluation of aortic regurgitation after transcatheter aortic valve
2-dimensional echocardiography in determining the presence of implantation: aortic root angiography in comparison to cardiac mag-
bicuspid aortic valve. J Thorac Cardiovasc Surg. 2012;144(2): netic resonance. EuroIntervention. 2015;10(11): Epub ahead of print.
370–6. 281. Sherif MA, Abdel-Wahab M, Beurich HW, Stocker B, Zachow D,
267. Buchner S, Hulsmann M, Poschenrieder F, Hamer OW, Fellner C, Geist V, et al. Haemodynamic evaluation of aortic regurgitation
Kobuch R, et al. Variable phenotypes of bicuspid aortic valve after transcatheter aortic valve implantation using cardiovascular
disease: classification by cardiovascular magnetic resonance. magnetic resonance. EuroIntervention. 2011;7(1):57–63.
Heart. 2010;96(15):1233–40. 282. Merten C, Beurich HW, Zachow D, Mostafa AE, Geist V, Toelg R,
268. Murphy DJ, McEvoy SH, Iyengar S, Feuchtner G, Cury RC, et al. Aortic regurgitation and left ventricular remodeling after trans-
Roobottom C, et al. Bicuspid aortic valves: diagnostic accuracy of catheter aortic valve implantation: a serial cardiac magnetic reso-
standard axial 64-slice chest CT compared to aortic valve image nance imaging study. Circ Cardiovasc Interv. 2013;6(4):476–83.
plane ECG-gated cardiac CT. Eur J Radiol. 2014;83(8): 283. Ribeiro HB, Le Ven F, Larose E, Dahou A, Nombela-Franco L,
1396–401. Urena M, et al. Cardiac magnetic resonance versus transthoracic
269. Alkadhi H, Leschka S, Trindade PT, Feuchtner G, Stolzmann P, echocardiography for the assessment and quantification of aortic
Plass A, et al. Cardiac CT for the differentiation of bicuspid and regurgitation in patients undergoing transcatheter aortic valve
tricuspid aortic valves: comparison with echocardiography and implantation. Heart. 2014;100(24):1924–32.
surgery. AJR Am J Roentgenol. 2010;195(4):900–8. 284. Hartlage GR, Babaliaros VC, Thourani VH, Hayek S, Chrysohoou
270. Sucha D, Symersky P, Vonken EJ, Provoost E, Chamuleau SA, C, Ghasemzadeh N, et al. The role of cardiovascular magnetic
Budde RP. Multidetector-row computed tomography allows resonance in stratifying paravalvular leak severity after
accurate measurement of mechanical prosthetic heart valve leaflet transcatheter aortic valve replacement: an observational outcome
closing angles compared with fluoroscopy. J Comput Assist study. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn
Tomogr. 2014;38(3):451–6. Reson. 2014;16:93.
271. Symersky P, Budde RP, de Mol BA, Prokop M. Comparison of 285. Jabbour A, Ismail TF, Moat N, Gulati A, Roussin I, Alpendurada
multidetector-row computed tomography to echocardiography F, et al. Multimodality imaging in transcatheter aortic valve
and fluoroscopy for evaluation of patients with mechanical implantation and post-procedural aortic regurgitation: comparison
prosthetic valve obstruction. Am J Cardiol. 2009;104(8): among cardiovascular magnetic resonance, cardiac computed
1128–34. tomography, and echocardiography. J Am Coll Cardiol.
272. Tsai IC, Lin YK, Chang Y, Fu YC, Wang CC, Hsieh SR, et al. 2011;58(21):2165–73.
Correctness of multi-detector-row computed tomography for 286. Chan KM, Wage R, Symmonds K, Rahman-Haley S, Mohiaddin
diagnosing mechanical prosthetic heart valve disorders using RH, Firmin DN, et al. Towards comprehensive assessment of
operative findings as a gold standard. Eur Radiol. mitral regurgitation using cardiovascular magnetic resonance.
2009;19(4):857–67. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson.
273. Ueda T, Teshima H, Fukunaga S, Aoyagi S, Tanaka H. Evaluation 2008;10:61.
of prosthetic valve obstruction on electrocardiographically gated 287. Shanks M, Siebelink HM, Delgado V, van de Veire NR, Ng AC,
multidetector-row computed tomography – identification of Sieders A, et al. Quantitative assessment of mitral regurgitation:
subprosthetic pannus in the aortic position. Circ J Off J Jpn Circ comparison between three-dimensional transesophageal
Soc. 2013;77(2):418–23. echocardiography and magnetic resonance imaging. Circ
274. Tanis W, Sucha D, Laufer W, Habets J, van Herwerden LA, Cardiovasc Imaging. 2010;3(6):694–700.
Symersky P, et al. Multidetector-row computed tomography for 288. Buchner S, Debl K, Poschenrieder F, Feuerbach S, Riegger GA,
prosthetic heart valve dysfunction: is concomitant non-invasive Luchner A, et al. Cardiovascular magnetic resonance for direct
coronary angiography possible before redo-surgery? Eur Radiol. assessment of anatomic regurgitant orifice in mitral regurgitation.
2015;25(6):1623–30. Circ Cardiovasc Imaging. 2008;1(2):148–55.
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 545

289. Delling FN, Kang LL, Yeon SB, Kissinger KV, Goddu B, Manning pulmonary regurgitation and pulmonary artery aneurysm. Tex
WJ, et al. CMR predictors of mitral regurgitation in mitral valve Heart Inst J. 2014;41(3):349–50.
prolapse. JACC Cardiovasc Imaging. 2010;3(10):1037–45. 304. Secchi F, Resta EC, Cannao PM, Tresoldi S, Butera G, Carminati
290. Van De Heyning CM, Magne J, Pierard LA, Bruyere PJ, Davin L, M, et al. Four-year cardiac magnetic resonance (CMR) follow-up
De Maeyer C, et al. Late gadolinium enhancement CMR in of patients treated with percutaneous pulmonary valve stent
primary mitral regurgitation. Eur J Clin Invest. 2014; implantation. Eur Radiol. 2015;25:3606–13.
44(9):840–7. 305. Cho IJ, Oh J, Chang HJ, Park J, Kang KW, Kim YJ, et al. Tricuspid
291. Takeda K, Matsumiya G, Hamada S, Sakaguchi T, Miyagawa S, regurgitation duration correlates with cardiovascular magnetic
Yamauchi T, et al. Left ventricular basal myocardial scarring resonance-derived right ventricular ejection fraction and predict
detected by delayed enhancement magnetic resonance imaging prognosis in patients with pulmonary arterial hypertension. Eur
predicts outcomes after surgical therapies for patients with Heart J Cardiovasc Imaging. 2014;15(1):18–23.
ischemic mitral regurgitation and left ventricular dysfunction. 306. Maffessanti F, Gripari P, Pontone G, Andreini D, Bertella E,
Circ J Off J Jpn Circ Soc. 2011;75(1):148–56. Mushtaq S, et al. Three-dimensional dynamic assessment of tricus-
292. Krumm P, Zuern CS, Wurster TH, Mangold S, Klumpp BD, pid and mitral annuli using cardiovascular magnetic resonance. Eur
Henning A, et al. Cardiac magnetic resonance imaging in patients Heart J Cardiovasc Imaging. 2013;14(10):986–95.
undergoing percutaneous mitral valve repair with the MitraClip 307. Kim HK, Kim YJ, Park EA, Bae JS, Lee W, Kim KH, et al.
system. Clin Res Cardiol Off J German Cardiac Soc. Assessment of haemodynamic effects of surgical correction for
2014;103(5):397–404. severe functional tricuspid regurgitation: cardiac magnetic
293. Simprini LA, Afroz A, Cooper MA, Klem I, Jensen C, Kim RJ, resonance imaging study. Eur Heart J. 2010;31(12):1520–8.
et al. Routine cine-CMR for prosthesis-associated mitral 308. van Rosendael PJ, Joyce E, Katsanos S, Debonnaire P, Kamperidis
regurgitation: a multicenter comparison to echocardiography. V, van der Kley F, et al. Tricuspid valve remodelling in functional
J Heart Valve Dis. 2014;23(5):575–82. tricuspid regurgitation: multidetector row computed tomography
294. Feuchtner GM, Alkadhi H, Karlo C, Sarwar A, Meier A, Dichtl W, insights. Eur Heart J Cardiovasc Imaging. 2016;17:96–105.
et al. Cardiac CT angiography for the diagnosis of mitral valve 309. Fratz S, Hess J, Schuhbaeck A, Buchner C, Hendrich E, Martinoff
prolapse: comparison with echocardiography1. Radiology. S, et al. Routine clinical cardiovascular magnetic resonance in
2010;254(2):374–83. paediatric and adult congenital heart disease: patients, protocols,
295. Koo HJ, Yang DH, Oh SY, Kang JW, Kim DH, Song JK, et al. questions asked and contributions made. J Cardiovasc Magn
Demonstration of mitral valve prolapse with CT for planning of Reson Off J Soc Cardiovasc Magn Reson. 2008;10:46.
mitral valve repair. Radiographics Rev Publ Radiol Soc North Am 310. Arheden H, Holmqvist C, Thilen U, Hanseus K, Bjorkhem G,
Inc. 2014;34(6):1537–52. Pahlm O, et al. Left-to-right cardiac shunts: comparison of
296. Smith T, Gurudevan S, Cheng V, Trento A, Derobertis M, measurements obtained with MR velocity mapping and with
Thomson L, et al. Assessment of the morphological features of radionuclide angiography. Radiology. 1999;211(2):453–8.
degenerative mitral valve disease using 64-slice multi detector 311. Sorensen TS, Korperich H, Greil GF, Eichhorn J, Barth P, Meyer
computed tomography. J Cardiovasc Comput Tomogr. 2012; H, et al. Operator-independent isotropic three-dimensional
6(6):415–21. magnetic resonance imaging for morphology in congenital heart
297. Choure AJ, Garcia MJ, Hesse B, Sevensma M, Maly G, Greenberg disease: a validation study. Circulation. 2004;110(2):163–9.
NL, et al. In vivo analysis of the anatomical relationship of 312. Kilner PJ, Geva T, Kaemmerer H, Trindade PT, Schwitter J, Webb
coronary sinus to mitral annulus and left circumflex coronary GD. Recommendations for cardiovascular magnetic resonance in
artery using cardiac multidetector computed tomography: adults with congenital heart disease from the respective working
implications for percutaneous coronary sinus mitral annuloplasty. groups of the European Society of Cardiology. Eur Heart
J Am Coll Cardiol. 2006;48(10):1938–45. J. 2010;31(7):794–805.
298. Mao S, Shinbane JS, Girsky MJ, Child J, Carson S, Oudiz 313. Haramati LB, Glickstein JS, Issenberg HJ, Haramati N, Crooke
RJ, et al. Coronary venous imaging with electron beam GA. MR imaging and CT of vascular anomalies and connections
computed tomographic angiography: three-dimensional map- in patients with congenital heart disease: significance in surgical
ping and relationship with coronary arteries. Am Heart J. planning. Radiographics Rev Publ Radiol Soc North Am Inc.
2005;150(2):315–22. 2002;22(2):337–47; discussion 48–9.
299. Messika-Zeitoun D, Serfaty JM, Laissy JP, Berhili M, Brochet E, 314. Durongpisitkul K, Tang NL, Soongswang J, Laohaprasitiporn D,
Iung B, et al. Assessment of the mitral valve area in patients with Nanal A. Predictors of successful transcatheter closure of atrial
mitral stenosis by multislice computed tomography. J Am Coll septal defect by cardiac magnetic resonance imaging. Pediatr
Cardiol. 2006;48(2):411–3. Cardiol. 2004;25(2):124–30.
300. Guo YK, Yang ZG, Ning G, Rao L, Dong L, Pen Y, et al. Sixty- 315. Taylor AM, Dymarkowski S, Hamaekers P, Razavi R, Gewillig M,
four-slice multidetector computed tomography for preoperative Mertens L, et al. MR coronary angiography and late-enhancement
evaluation of left ventricular function and mass in patients with myocardial MR in children who underwent arterial switch surgery
mitral regurgitation: comparison with magnetic resonance for transposition of great arteries. Radiology. 2005;234(2):542–7.
imaging and echocardiography. Eur Radiol. 2009;19(9):2107–16. 316. Harris MA, Johnson TR, Weinberg PM, Fogel MA. Delayed-
301. Lewis MJ, O’Connor DS, Rozenshtien A, Ye S, Einstein AJ, enhancement cardiovascular magnetic resonance identifies fibrous
Ginns JM, et al. Usefulness of magnetic resonance imaging to tissue in children after surgery for congenital heart disease.
guide referral for pulmonary valve replacement in repaired J Thorac Cardiovasc Surg. 2007;133(3):676–81.
tetralogy of Fallot. Am J Cardiol. 2014;114(9):1406–11. 317. Geva T, Marshall AC. Magnetic resonance imaging-guided cath-
302. Vliegen HW, van Straten A, de Roos A, Roest AA, Schoof PH, eter interventions in congenital heart disease. Circulation.
Zwinderman AH, et al. Magnetic resonance imaging to assess the 2006;113(8):1051–2.
hemodynamic effects of pulmonary valve replacement in adults 318. Tzifa A, Krombach GA, Kramer N, Kruger S, Schutte A, von
late after repair of tetralogy of fallot. Circulation. Walter M, et al. Magnetic resonance-guided cardiac interventions
2002;106(13):1703–7. using magnetic resonance-compatible devices: a preclinical study
303. Shah R, Shriki J, Shinbane JS. Cardiovascular magnetic resonance and first-in-man congenital interventions. Circ Cardiovasc Interv.
depiction of quadricuspid pulmonary valve with associated 2010;3(6):585–92.
546 J.S. Shinbane et al.

319. Geva T, Greil GF, Marshall AC, Landzberg M, Powell 333. Ma XJ, Tao L, Chen X, Li W, Peng ZY, Chen Y, et al. Clinical
AJ. Gadolinium-enhanced 3-dimensional magnetic resonance application of three-dimensional reconstruction and rapid
angiography of pulmonary blood supply in patients with complex prototyping technology of multislice spiral computed tomography
pulmonary stenosis or atresia: comparison with x-ray angiography. angiography for the repair of ventricular septal defect of tetralogy
Circulation. 2002;106(4):473–8. of Fallot. Genet Mol Res GMR. 2015;14(1):1301–9.
320. Prasad SK, Soukias N, Hornung T, Khan M, Pennell DJ, Gatzoulis 334. Lin MT, Wang JK, Chen YS, Lee WJ, Chiu HH, Chen CA, et al.
MA, et al. Role of magnetic resonance angiography in the Detection of pulmonary arterial morphology in tetralogy of Fallot
diagnosis of major aortopulmonary collateral arteries and partial with pulmonary atresia by computed tomography: 12 years of
anomalous pulmonary venous drainage. Circulation. 2004; experience. Eur J Pediatr. 2012;171(3):579–86.
109(2):207–14. 335. Vastel-Amzallag C, Le Bret E, Paul JF, Lambert V, Rohnean A, El
321. Bernardes RJ, Marchiori E, Bernardes PM, Monzo Gonzaga MB, Fassy E, et al. Diagnostic accuracy of dual-source multislice
Simoes LC. A comparison of magnetic resonance angiography computed tomographic analysis for the preoperative detection of
with conventional angiography in the diagnosis of tetralogy of coronary artery anomalies in 100 patients with tetralogy of Fallot.
Fallot. Cardiol Young. 2006;16(3):281–8. J Thorac Cardiovasc Surg. 2011;142(1):120–6.
322. Oosterhof T, van Straten A, Vliegen HW, Meijboom FJ, van Dijk 336. Bardo DM, Asamato J, Mackay CS, Minette M. Low-dose coro-
AP, Spijkerboer AM, et al. Preoperative thresholds for pulmonary nary artery computed tomography angiogram of an infant with
valve replacement in patients with corrected tetralogy of Fallot tetralogy of fallot using a 256-slice multidetector computed
using cardiovascular magnetic resonance. Circulation. 2007; tomography scanner. Pediatr Cardiol. 2009;30(6):824–6.
116(5):545–51. 337. Raman SV, Cook SC, McCarthy B, Ferketich AK. Usefulness of
323. Ghai A, Silversides C, Harris L, Webb GD, Siu SC, Therrien multidetector row computed tomography to quantify right
J. Left ventricular dysfunction is a risk factor for sudden cardiac ventricular size and function in adults with either tetralogy of
death in adults late after repair of tetralogy of Fallot. J Am Coll Fallot or transposition of the great arteries. Am J Cardiol.
Cardiol. 2002;40(9):1675–80. 2005;95(5):683–6.
324. Rebergen SA, Chin JG, Ottenkamp J, van der Wall EE, de Roos 338. Whitehead KK, Sundareswaran KS, Parks WJ, Harris MA,
A. Pulmonary regurgitation in the late postoperative follow-up of Yoganathan AP, Fogel MA. Blood flow distribution in a large
tetralogy of Fallot. Volumetric quantitation by nuclear magnetic series of patients having the Fontan operation: a cardiac magnetic
resonance velocity mapping. Circulation. 1993;88(5 Pt 1): resonance velocity mapping study. J Thorac Cardiovasc Surg.
2257–66. 2009;138(1):96–102.
325. Fratz S, Schuhbaeck A, Buchner C, Busch R, Meierhofer C, 339. Goo HW, Yang DH, Park IS, Ko JK, Kim YH, Seo DM, et al.
Martinoff S, et al. Comparison of accuracy of axial slices versus Time-resolved three-dimensional contrast-enhanced magnetic
short-axis slices for measuring ventricular volumes by cardiac resonance angiography in patients who have undergone a Fontan
magnetic resonance in patients with corrected tetralogy of fallot. operation or bidirectional cavopulmonary connection: initial
Am J Cardiol. 2009;103(12):1764–9. experience. J Magn Reson Imaging JMRI. 2007;25(4):727–36.
326. Kang IS, Redington AN, Benson LN, Macgowan C, Valsangiacomo 340. Park EA, Lee W, Chung SY, Yin YH, Chung JW, Park JH. Optimal
ER, Roman K, et al. Differential regurgitation in branch pulmonary scan timing and intravenous route for contrast-enhanced computed
arteries after repair of tetralogy of Fallot: a phase-contrast cine tomography in patients after Fontan operation. J Comput Assist
magnetic resonance study. Circulation. 2003;107(23):2938–43. Tomogr. 2010;34(1):75–81.
327. Lee C, Lee CH, Kwak JG, Kim SH, Shim WS, Lee SY, et al. 341. Greenberg SB, Bhutta ST. A dual contrast injection technique for
Factors associated with right ventricular dilatation and dysfunction multidetector computed tomography angiography of Fontan
in patients with chronic pulmonary regurgitation after repair of procedures. Int J Cardiovasc Imaging. 2008;24(3):345–8.
tetralogy of Fallot: analysis of magnetic resonance imaging data 342. Rathod RH, Prakash A, Kim YY, Germanakis IE, Powell AJ,
from 218 patients. J Thorac Cardiovasc Surg. 2014; Gauvreau K, et al. Cardiac magnetic resonance parameters predict
148(6):2589–95. transplantation-free survival in patients with fontan circulation.
328. Johansson B, Babu-Narayan SV, Kilner PJ. The effects of breath- Circ Cardiovasc Imaging. 2014;7(3):502–9.
holding on pulmonary regurgitation measured by cardiovascular 343. Ovroutski S, Nordmeyer S, Miera O, Ewert P, Klimes K, Kuhne T,
magnetic resonance velocity mapping. J Cardiovasc Magn Reson et al. Caval flow reflects Fontan hemodynamics: quantification by
Off J Soc Cardiovasc Magn Reson. 2009;11:1. magnetic resonance imaging. Clin Res Cardiol Off J German
329. Mercer-Rosa L, Yang W, Kutty S, Rychik J, Fogel M, Goldmuntz Cardiac Soc. 2012;101(2):133–8.
E. Quantifying pulmonary regurgitation and right ventricular 344. Restrepo M, Mirabella L, Tang E, Haggerty CM, Khiabani RH,
function in surgically repaired tetralogy of Fallot: a comparative Fynn-Thompson F, et al. Fontan pathway growth: a quantitative
analysis of echocardiography and magnetic resonance imaging. evaluation of lateral tunnel and extracardiac cavopulmonary
Circ Cardiovasc Imaging. 2012;5(5):637–43. connections using serial cardiac magnetic resonance. Ann Thorac
330. Babu-Narayan SV, Kilner PJ, Li W, Moon JC, Goktekin O, Surg. 2014;97(3):916–22.
Davlouros PA, et al. Ventricular fibrosis suggested by 345. Haggerty CM, Restrepo M, Tang E, de Zelicourt DA,
cardiovascular magnetic resonance in adults with repaired Sundareswaran KS, Mirabella L, et al. Fontan hemodynamics
tetralogy of fallot and its relationship to adverse markers of clini- from 100 patient-specific cardiac magnetic resonance studies: a
cal outcome. Circulation. 2006;113(3):405–13. computational fluid dynamics analysis. J Thorac Cardiovasc Surg.
331. Munkhammar P, Carlsson M, Arheden H, Pesonen E. Restrictive 2014;148(4):1481–9.
right ventricular physiology after tetralogy of Fallot repair is 346. Rathod RH, Prakash A, Powell AJ, Geva T. Myocardial fibrosis
associated with fibrosis of the right ventricular outflow tract identified by cardiac magnetic resonance late gadolinium
visualized on cardiac magnetic resonance imaging. Eur Heart enhancement is associated with adverse ventricular mechanics
J Cardiovasc Imaging. 2013;14(10):978–85. and ventricular tachycardia late after Fontan operation. J Am Coll
332. Kozak MF, Redington A, Yoo SJ, Seed M, Greiser A, Grosse- Cardiol. 2010;55(16):1721–8.
Wortmann L. Diffuse myocardial fibrosis following tetralogy of 347. Rydman R, Gatzoulis MA, Ho SY, Ernst S, Swan L, Li W, et al.
Fallot repair: a T1 mapping cardiac magnetic resonance study. Systemic right ventricular fibrosis detected by cardiovascular
Pediatr Radiol. 2014;44(4):403–9. magnetic resonance is associated with clinical outcome, mainly
26 Cardiovascular Magnetic Resonance Imaging: Overview of Clinical Applications in the Context of Cardiovascular CT 547

new-onset atrial arrhythmia, in patients after atrial redirection sur- patients evaluated for possible transcatheter closure. Circ
gery for transposition of the great arteries. Circ Cardiovasc Cardiovasc Imaging. 2008;1(1):31–40.
Imaging. 2015;8(5):e002628. 361. Weber C, Weber M, Ekinci O, Neumann T, Deetjen A, Rolf A,
348. Tobler D, Motwani M, Wald RM, Roche SL, Verocai F, Iwanochko et al. Atrial septal defects type II: noninvasive evaluation of
RM, et al. Evaluation of a comprehensive cardiovascular magnetic patients before implantation of an Amplatzer Septal Occluder and
resonance protocol in young adults late after the arterial switch on follow-up by magnetic resonance imaging compared with TEE
operation for d-transposition of the great arteries. J Cardiovasc and invasive measurement. Eur Radiol. 2008;18(11):2406–13.
Magn Reson Off J Soc Cardiovasc Magn Reson. 2014;16:98. 362. Riesenkampff EM, Schmitt B, Schnackenburg B, Huebler M,
349. Tulevski II, van der Wall EE, Groenink M, Dodge-Khatami A, Alexi-Meskishvili V, Hetzer R, et al. Partial anomalous pulmonary
Hirsch A, Stoker J, et al. Usefulness of magnetic resonance venous drainage in young pediatric patients: the role of magnetic
imaging dobutamine stress in asymptomatic and minimally resonance imaging. Pediatr Cardiol. 2009;30(4):458–64.
symptomatic patients with decreased cardiac reserve from 363. Ferrari VA, Scott CH, Holland GA, Axel L, Sutton MS. Ultrafast
congenital heart disease (complete and corrected transposition of three-dimensional contrast-enhanced magnetic resonance angiog-
the great arteries and subpulmonic obstruction). Am J Cardiol. raphy and imaging in the diagnosis of partial anomalous pulmo-
2002;89(9):1077–81. nary venous drainage. J Am Coll Cardiol. 2001;37(4):1120–8.
350. Fogel MA, Hubbard A, Weinberg PM. Mid-term follow-up of 364. Tada N, Takizawa K, Mizutani Y, Suzuki S, Sakurai M, Arai T,
patients with transposition of the great arteries after atrial inversion et al. Multiple atrial septal defects in multidetector-row computed
operation using two- and three-dimensional magnetic resonance tomography. JACC Cardiovasc Interv. 2014;7(6):e61–2.
imaging. Pediatr Radiol. 2002;32(6):440–6. 365. Kivisto S, Hanninen H, Holmstrom M. Partial anomalous pulmo-
351. Johansson B, Babu-Narayan SV, Kilner PJ, Cannell TM, nary venous return and atrial septal defect in adult patients
Mohiaddin RH. 3-dimensional time-resolved contrast-enhanced detected with 128-slice multidetector computed tomography.
magnetic resonance angiography for evaluation late after the J Cardiothorac Surg. 2011;6:126.
mustard operation for transposition. Cardiol Young. 366. Amat F, Le Bret E, Sigal-Cinqualbre A, Coblence M, Lambert V,
2010;20(1):1–7. Rohnean A, et al. Diagnostic accuracy of multidetector spiral
352. Shinbane JS, Shriki J, Hindoyan A, Ghosh B, Chang P, Farvid A, computed tomography for preoperative assessment of sinus veno-
et al. Unoperated congenitally corrected transposition of the great sus atrial septal defects in children. Interact Cardiovasc Thorac
arteries, nonrestrictive ventricular septal defect, and pulmonary Surg. 2011;12(2):179–82.
stenosis in middle adulthood: do multiple wrongs make a right? 367. Berbarie RF, Anwar A, Dockery WD, Grayburn PA, Hamman BL,
World J Pediatr Congenit Heart Surg. 2012;3(1):123–9. Vallabhan RC, et al. Measurement of right ventricular volumes
353. Cook SC, McCarthy M, Daniels CJ, Cheatham JP, Raman before and after atrial septal defect closure using multislice com-
SV. Usefulness of multislice computed tomography angiography puted tomography. Am J Cardiol. 2007;99(10):1458–61.
to evaluate intravascular stents and transcatheter occlusion devices 368. Marini D, Ou P, Boudjemline Y, Kenny D, Bonnet D, Agnoletti
in patients with d-transposition of the great arteries after mustard G. Midterm results of percutaneous closure of very large atrial
repair. Am J Cardiol. 2004;94(7):967–9. septal defects in children: role of multislice computed tomogra-
354. Ou P, Mousseaux E, Azarine A, Dupont P, Agnoletti G, Vouhe P, phy. EuroIntervention. 2012;7(12):1428–34.
et al. Detection of coronary complications after the arterial switch 369. Artis NJ, Thomson J, Plein S, Greenwood JP. Percutaneous clo-
operation for transposition of the great arteries: first experience sure of postinfarction ventricular septal defect: cardiac magnetic
with multislice computed tomography in children. J Thorac resonance-guided case selection and postprocedure evaluation.
Cardiovasc Surg. 2006;131(3):639–43. Can J Cardiol. 2011;27(6):869.e3–5.
355. Yalonetsky S, Tobler D, Greutmann M, Crean AM, Wintersperger 370. Ratnayaka K, Raman VK, Faranesh AZ, Sonmez M, Kim JH,
BJ, Nguyen ET, et al. Cardiac magnetic resonance imaging and Gutierrez LF, et al. Antegrade percutaneous closure of membra-
the assessment of ebstein anomaly in adults. Am J Cardiol. nous ventricular septal defect using X-ray fused with magnetic
2011;107(5):767–73. resonance imaging. JACC Cardiovasc Interv. 2009;2(3):224–30.
356. Hosch O, Sohns JM, Nguyen TT, Lauerer P, Rosenberg C, 371. Calkoen EE, Westenberg JJ, Kroft LJ, Blom NA, Hazekamp MG,
Kowallick JT, et al. The total right/left-volume index: a new and Rijlaarsdam ME, et al. Characterization and quantification of
simplified cardiac magnetic resonance measure to evaluate the dynamic eccentric regurgitation of the left atrioventricular valve after
severity of Ebstein anomaly of the tricuspid valve: a comparison atrioventricular septal defect correction with 4D Flow cardiovascular
with heart failure markers from various modalities. Circ magnetic resonance and retrospective valve tracking. J Cardiovasc
Cardiovasc Imaging. 2014;7(4):601–9. Magn Reson Off J Soc Cardiovasc Magn Reson. 2015;17:18.
357. Hosch O, Ngyuen TT, Lauerer P, Schuster A, Kutty S, Staab W, 372. Schueler R, Sinning JM, Zimmer S, Nickenig G, Hammerstingl
et al. BNP and haematological parameters are markers of severity C. Multimodality imaging for interventional planning and device
of Ebstein’s anomaly: correlation with CMR and cardiopulmonary closure of an atypical ventricular septal defect occurring late after
exercise testing. Eur Heart J Cardiovasc Imaging. 2015; myocardial infarction. Eur Heart J. 2014;35(15):1007.
16(6):670–5. 373. Grizzard JD, Ang GB. Magnetic resonance imaging of pericardial
358. Aggarwala G, Thompson B, van Beek E, Jagasia D. Multislice disease and cardiac masses. Magn Reson Imaging Clin N Am.
computed tomography angiography of Ebstein anomaly and 2007;15(4):579–607, vi.
anomalous coronary artery. J Cardiovasc Comput Tomogr. 374. Hoffmann U, Globits S, Schima W, Loewe C, Puig S, Oberhuber
2007;1(3):168–9. G, et al. Usefulness of magnetic resonance imaging of cardiac and
359. Teo KS, Disney PJ, Dundon BK, Worthley MI, Brown MA, paracardiac masses. Am J Cardiol. 2003;92(7):890–5.
Sanders P, et al. Assessment of atrial septal defects in adults 375. Brechtel K, Reddy GP, Higgins CB. Cardiac fibroma in an infant:
comparing cardiovascular magnetic resonance with magnetic resonance imaging characteristics. J Cardiovasc Magn
transoesophageal echocardiography. J Cardiovasc Magn Reson Reson Off J Soc Cardiovasc Magn Reson. 1999;1(2):159–61.
Off J Soc Cardiovasc Magn Reson. 2010;12:44. 376. Kamiya H, Ohno M, Iwata H, Ohsugi S, Sawada K, Koike A, et al.
360. Thomson LE, Crowley AL, Heitner JF, Cawley PJ, Weinsaft JW, Cardiac lipoma in the interventricular septum: evaluation by com-
Kim HW, et al. Direct en face imaging of secundum atrial septal puted tomography and magnetic resonance imaging. Am Heart
defects by velocity-encoded cardiovascular magnetic resonance in J. 1990;119(5):1215–7.
548 J.S. Shinbane et al.

377. Salanitri JC, Pereles FS. Cardiac lipoma and lipomatous hypertro- cardiovascular magnetic resonance imaging: a multicenter experi-
phy of the interatrial septum: cardiac magnetic resonance imaging ence. J Am Coll Cardiol. 2011;58(10):1044–54.
findings. J Comput Assist Tomogr. 2004;28(6):852–6. 389. Rajiah P, Kanne JP, Kalahasti V, Schoenhagen P. Computed
378. Matsuoka H, Hamada M, Honda T, Kawakami H, Abe M, tomography of cardiac and pericardiac masses. J Cardiovasc
Shigematsu Y, et al. Morphologic and histologic characterization Comput Tomogr. 2011;5(1):16–29.
of cardiac myxomas by magnetic resonance imaging. Angiology. 390. Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B,
1996;47(7):693–8. et al. American Society of Echocardiography clinical recommen-
379. Watanabe AT, Teitelbaum GP, Henderson RW, Bradley Jr dations for multimodality cardiovascular imaging of patients with
WG. Magnetic resonance imaging of cardiac sarcomas. J Thorac pericardial disease: endorsed by the Society for Cardiovascular
Imaging. 1989;4(2):90–2. Magnetic Resonance and Society of Cardiovascular Computed
380. Inoko M, Iga K, Kyo K, Kondo H, Tamura T, Izumi C, et al. Tomography. J Am Soc Echocardiography Off Publ Am Soc
Primary cardiac angiosarcoma detected by magnetic resonance Echocardiography. 2013;26(9):965–1012.e15.
imaging but not by computed tomography. Intern Med. 391. Bogaert J, Francone M. Cardiovascular magnetic resonance in
2001;40(5):391–5. pericardial diseases. J Cardiovasc Magn Reson Off J Soc
381. Tahara T, Takase B, Yamagishi T, Takayama E, Miyazaki K, Cardiovasc Magn Reson. 2009;11:14.
Arakawa K, et al. A case report on primary cardiac non-Hodgkin’s 392. Taylor AM, Dymarkowski S, Verbeken EK, Bogaert J. Detection
lymphoma: an approach by magnetic resonance and thallium-201 of pericardial inflammation with late-enhancement cardiac mag-
imaging. J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn netic resonance imaging: initial results. Eur Radiol.
Reson. 1999;1(2):163–7. 2006;16(3):569–74.
382. Schrem SS, Colvin SB, Weinreb JC, Glassman E, Kronzon 393. Rifkin RD, Mernoff DB. Noninvasive evaluation of pericardial
I. Metastatic cardiac liposarcoma: diagnosis by transesophageal effusion composition by computed tomography. Am Heart
echocardiography and magnetic resonance imaging. J Am Soc J. 2005;149(6):1120–7.
Echocardiography Off Publ Am Soc Echocardiography. 394. Muzzarelli S, Meadows AK, Ordovas KG, Higgins CB, Meadows
1990;3(2):149–53. JJ. Usefulness of cardiovascular magnetic resonance imaging to
383. Mousseaux E, Meunier P, Azancott S, Dubayle P, Gaux JC. Cardiac predict the need for intervention in patients with coarctation of the
metastatic melanoma investigated by magnetic resonance imag- aorta. Am J Cardiol. 2012;109(6):861–5.
ing. Magn Reson Imaging. 1998;16(1):91–5. 395. Dormand H, Mohiaddin RH. Cardiovascular magnetic resonance
384. Testempassi E, Takeuchi H, Fukuda Y, Harada J, Tada S. Cardiac in Marfan syndrome. J Cardiovasc Magn Reson Off J Soc
metastasis of colon adenocarcinoma diagnosed by magnetic reso- Cardiovasc Magn Reson. 2013;15:33.
nance imaging. Acta Cardiol. 1994;49(2):191–6. 396. Hartnell GG. Imaging of aortic aneurysms and dissection: CT and
385. Weinsaft JW, Kim HW, Shah DJ, Klem I, Crowley AL, Brosnan R, MRI. J Thorac Imaging. 2001;16(1):35–46.
et al. Detection of left ventricular thrombus by delayed- 397. Cantisani V, Ricci P, Grazhdani H, Napoli A, Fanelli F, Catalano
enhancement cardiovascular magnetic resonance prevalence and C, et al. Prospective comparative analysis of colour-Doppler ultra-
markers in patients with systolic dysfunction. J Am Coll Cardiol. sound, contrast-enhanced ultrasound, computed tomography and
2008;52(2):148–57. magnetic resonance in detecting endoleak after endovascular
386. Gaudio C, Di Michele S, Cera M, Nguyen BL, Pannarale G, abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg Off
Alessandri N. Prominent crista terminalis mimicking a right atrial J Eur Soc Vasc Surg. 2011;41(2):186–92.
mixoma: cardiac magnetic resonance aspects. Eur Rev Med 398. Dudeck O, Schnapauff D, Herzog L, Lowenthal D, Bulla K, Bulla
Pharmacol Sci. 2004;8(4):165–8. B, et al. Can early computed tomography angiography after endo-
387. Hong YJ, Hur J, Kim YJ, Lee HJ, Nam JE, Kim HY, et al. The vascular aortic aneurysm repair predict the need for reintervention
usefulness of delayed contrast-enhanced cardiovascular magnetic in patients with type II endoleak? Cardiovasc Intervent Radiol.
resonance imaging in differentiating cardiac tumors from thrombi 2015;38(1):45–52.
in stroke patients. Int J Cardiovasc Imaging. 2011;27 Suppl 399. Muller-Wille R, Borgmann T, Wohlgemuth WA, Zeman F, Pfister
1:89–95. K, Jung EM, et al. Dual-energy computed tomography after endo-
388. Beroukhim RS, Prakash A, Buechel ER, Cava JR, Dorfman AL, vascular aortic aneurysm repair: the role of hard plaque imaging
Festa P, et al. Characterization of cardiac tumors in children by for endoleak detection. Eur Radiol. 2014;24(10):2449–57.
 Cardiovascular CT in the Emergency
Department 27
Asim Rizvi and James K. Min

Abstract
Acute-onset chest pain is one of the most common presentations in the emergency depart-
ment (ED) and despite a thorough, time intensive, and costly ED evaluation utilizing the
standard strategy, there is a non-negligible clinical risk of missed acute coronary syndrome
(ACS) with 2–5 % of these patients being discharged inappropriately. The resultant conse-
quences are, increased risk of short and long term mortality. This chapter discusses the
current role of cardiac computed tomography in the evaluation of patients with acute chest
pain in the ED and evaluates the current evidence supporting accuracy and safety of cardiac
computed tomography, as well as it’s ability to reduce ED cost.

Keywords
Acute coronary syndrome • Cardiac • Chest pain • Emergency department • Coronary
computed tomography angiography

Current State of the Literature Such an approach is costly, time-consuming and puts
additional strain on already limited resources.
Acute chest pain is one of the most frequent reasons for
patient visits to the emergency department (ED) in the United
States and a large amount of expense and time is spent in the Diagnosis of ACS
workup of these patients. It is estimated that as many as 6
million people per year visit the ED with chest pain [1]; The term ACS describes clinical manifestations of acute
however, only a small minority of these patients ultimately myocardial ischemia induced by coronary artery disease
receive a diagnosis of acute coronary syndrome (ACS) as the (CAD). The American Heart Association (AHA) differenti-
etiology of their chest pain [2]. Although most of these ates among ACS that involve myocardial infarction (MI)
patients do not have a life-threatening underlying condition, with acute ST segment elevation (STEMI), MI without ST
a large proportion of these patients undergo routine evaluation segment elevation (non-STEMI), and unstable angina (UA)
of acute chest pain that includes hospital admission or obser- [3–5]. The diagnosis of STEMI is clear by ECG alone, but
vation unit stay to rule out ACS with the use of serial electro- diagnosis of non-STEMI and UA is more challenging and
cardiography (ECG) and cardiac biomarker assessment. requires additional data to risk stratify patients appropriately
[6]. The third universal definition of MI, published in 2012,
states that the diagnostic criteria for MI require a rise and/or
fall of cardiac biomarkers (preferably troponins) with at least
A. Rizvi, MD • J.K. Min, MD, FACC (*) one value above the 99th percentile of the upper reference
Dalio Institute of Cardiovascular Imaging,
limit. In addition, patient should have symptoms of ischemia
NewYork-Presbyterian Hospital and Weill Cornell Medical College,
413 E. 69th Street Suite 108, New York, NY 10021, USA with new ECG changes and imaging evidence of a new loss
e-mail: [email protected] of viable myocardium or new regional wall motion

© Springer International Publishing 2016 549

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0_27
550 A. Rizvi and J.K. Min

abnormality, or the identification of an intracoronary throm- a new and promising imaging modality for the detection and
bus by angiography or autopsy [7]. However, the initial stan- assessment of coronary stenosis and atherosclerotic plaque,
dard ED evaluation of patients with acute chest pain [8] does and has become integral in the assessment of patients with
not often provide a firm diagnosis for appropriate triage deci- suspected ACS. Several single-center and multicenter studies
sion and to safely rule out ACS based on negative cardiac have demonstrated the feasibility, safety, and accuracy of
troponin and ECG. cardiac CT in the ED to exclude the presence of CAD [9,
17–30]. Most patients with ACS have significant coronary
stenosis, and ACS is rare in the absence of coronary
Risk Assessment in the Emergency Department atherosclerosis [31, 32]. Therefore, the detection of
obstructive CAD may be effective in identifying patients
Patients with acute chest pain are generally stratified into with ACS and the exclusion of coronary atherosclerosis may
high, intermediate, or low risk categories during their early be helpful in ruling out ACS.
clinical assessment in the ED. This risk assessment work-up Given the excellent predictive value, CCTA allows for
traditionally includes patient’s history of prior cardiovascular improved risk stratification of patients and appropriate triage,
events, repeated physical examinations, and serial and can be considered an alternative to standard ED
electrocardiographic and biochemical marker measurements evaluation of acute chest pain patients. Furthermore, CCTA
[9–11]. Patients who are at high-risk of ACS or have STEMI has been shown to reduce length of stay in the hospital. A
based on ECG findings should be admitted and treated meta-analysis comparing CCTA to standard care triage of
promptly as per guidelines [8]. Patients who are at low to acute chest pain in a total of 3266 low-to intermediate risk
intermediate risk carry a 5–20 % risk of an ACS and the patients presenting to the ED noted that only 1.3 % overall
current standard of care for these patients includes serial MIs occurred mostly during the index hospitalization. In
ECG and cardiac troponin measurements followed by stress addition, length of stay in the hospital was significantly
testing with or without imaging to exclude myocardial reduced with CCTA compared to standard care strategy. It
ischemia [8]. This approach leads to prolonged hospital stay was also found that CCTA significantly increased invasive
and significant cost burden and eventually only 2–8 % of this coronary angiography (8.4 % versus 6.3 %) and
patient group is diagnosed with ACS [12]. revascularization (4.6 % versus 2.6 %). This meta-analysis
Multiple risk stratification models based upon included three major multicenter trials, CT-STAT [28],
multivariable regression techniques have been created in ACRIN-PA [30], and ROMICAT II [29], which have been
order to help clinicians in therapeutic decision making and pivotal in demonstrating the safe use of CCTA for early
includes the Thrombolysis in Myocardial Infarction (TIMI) triage of patients in the ED [33]. In each of these trials,
risk score, Global Registry of Acute Coronary Events patients with no ECG changes and a negative initial troponin
(GRACE) risk score, and the Platelet Glycoprotein IIb/IIIa in were randomized to either CCTA or standard treatment with
Unstable Angina: Receptor Suppression Using Integrillin serial cardiac markers and ECGs.
Therapy (PURSUIT) risk model [13–15]. The TIMI risk The CT-STAT (Coronary Computed Tomographic
score is a simple and easily applied scoring system that has Angiography for Systematic Triage of Acute Chest Pain
been validated for patients who present to the ED, and aids in Patients to Treatment) is a multicenter trial of low risk ED
assessing the likelihood of developing an adverse cardiac patients that prospectively included 699 patients who were
outcome (death, reinfarction, or recurrent severe ischemia either randomly allocated to CCTA (n =361) versus
requiring revascularization) within 14 days of presentation in myocardial perfusion imaging (MPI) (n = 338). The
patients presenting with UA and NSTEMI [14]. investigators sought to compare the efficiency, cost, and
Despite these clinical risk scores, uncertainty often exists safety of using CCTA in the evaluation of patients with acute
as to the etiology of a patient’s symptoms and the potential chest pain and low risk of ACS [28]. The primary outcome of
adverse prognosis associated with them. This uncertainty the study was time to diagnosis. The investigators also
emphasizes the need for diagnostic strategies that facilitate showed a cost reduction in patients randomized to
rapid and reliable early triage of patients who are at low-to- CCTA. Those in the CCTA arm had a 54 % reduction in time
intermediate risk for ACS [16]. to diagnosis and 38 % reduction in costs. There was no
difference in major adverse cardiac events (MACE) between
the two study groups [28].
Supporting Evidence for Cardiac CT Use The ACRIN-PA (American College of Radiology
in the Emergency Department Imaging Network- Pennsylvania) multicenter trial was
designed to evaluate the safety of CCTA strategy, defined as
With improvements in imaging capabilities, coronary the absence of MI or cardiac death during 30-day follow-up,
computed tomography angiography (CCTA) has emerged as in low-to-intermediate risk patients in the ED [30]. This trial
27 Cardiovascular CT in the Emergency Department 551

included 1370 patients randomized in a 2:1 ratio to CCTA known heart disease—acute symptoms with suspicion of
versus standard of care. The trial concluded that utilization ACS (urgent presentation) (Appropriate, score 7)” in patients
of CCTA early in the ED was safe and of the 640 patients with the following [35]:
with negative CCTA examinations, none of them died or
had a myocardial infarction within 30 days of presentation. • Normal ECG and cardiac biomarkers and low pretest
They also found that early CCTA led to a shorter mean probability of CAD
hospital stay (18 versus 24.8 h) and subsequently more fre- • Normal ECG and cardiac biomarkers and intermediate
quent ED discharge when compared to standard of care pretest probability of CAD
(50 % versus 23 %) [30]. • ECG uninterpretable and low pretest probability of CAD
The ROMICAT II (Rule Out Myocardial Infarction Using • ECG uninterpretable and intermediate pretest probability
Computer Assisted Tomography) trial is a multicenter of CAD
comparative effectiveness trial that randomized patients to • Non-diagnostic ECG or equivocal cardiac biomarkers and
early implementation of CCTA versus standard ED evaluation low pretest probability of CAD
in 1000 low-to-intermediate risk patients recruited from nine • Non-diagnostic ECG or equivocal cardiac biomarkers and
centers in the United States with suspected ACS [29]. The intermediate pretest probability of CAD
primary endpoint was length of stay. Approximately 8 % of
the study patients developed ACS. The study showed that
early CCTA utilization decreased the mean length of stay in Evolution of Coronary CT Angiography
the hospital by 7.6 h compared to standard ED evaluation Technology
and patients were more often discharged directly from the
ED (47 vs. 12 %). Additionally, there were no missed cardiac Since the introduction of CT as a tool for medical imaging,
events within 72 h, making CCTA a viable alternative for there has been a desire to apply this technology for imaging
low-intermediate risk patients in the ED. However, increased of the heart. Electron-beam CT (EBCT) had been proposed
diagnostic testing and higher radiation exposure was earlier to the introduction of multi-detector row CT
observed in the CCTA group. While there was a reduction in (MDCT) scanners, for the evaluation of patients arriving in
ED costs with an early CCTA strategy, there was no overall the ED with acute chest pain. EBCT had better temporal
reduction in the cost of care during index hospitalization or but inferior spatial resolution as compared to MDCT, and
28-day follow-up [29]. this approach relied on the total coronary calcium score,
In aggregate, these studies support the use of CCTA as an called the Agatston score [36] as a measure of overall
efficient and safe alternative to the more traditional triaging plaque burden, and showed high sensitivity but low speci-
methods for low and low-to-intermediate risk patients as an ficity for the detection of obstructive CAD. Technologic
option to exclude obstructive CAD as the etiology of chest development continued to 16-detector row and subse-
pain, while allowing for a faster ED discharge and ED cost quently the 64-detector row MDCT scanners in 2002 and
savings. However, such use of CCTA has been associated 2005, respectively, which were used to obtain ECG-
with increases in downstream invasive coronary angiography synchronized images of the heart at high spatial and tempo-
(ICA) and coronary revascularization, and the benefit of this ral resolution [37], to quantify coronary artery calcium
approach requires further study. [38], and to detect coronary artery stenosis [37, 39]. These
scanners were capable of image acquisition with high spa-
tial resolution (0.5–0.8 mm isotropic resolution), high tem-
Appropriate Use and Guidelines poral resolution (350–400 ms), and sufficient Z-axis
coverage (20–40 mm). Scan times with these scanners were
The use of CCTA in patients presenting to the ED with acute less than 10 s when only the heart is evaluated and less than
chest pain and low-to-intermediate risk of ACS is supported 20 s when the entire thorax is imaged with ECG synchroni-
by the current literature, as previously discussed. The Society zation. The field of CCTA has continued to improve since
of Cardiovascular Computed Tomography (SCCT) has 2005 with the introduction of MDCT scanners capable of
recently published guidelines for the use of CCTA in the even greater spatial resolution (up to 0.23 mm in-plane
diagnosis of acute chest pain in patients with suspected ACS resolution), higher temporal resolution (via dual-source
in the ED [34]. A summary of these guidelines is presented and high-pitch helical technology), and increased volume
in Tables 27.1 and 27.2. coverage (through 256- or 320-detector arrays). Broader
The ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/ 256- or 320- detector arrays allow complete volume cover-
SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac age of the heart in a single heartbeat, thus reducing limita-
Computed Tomography lists the use of CCTA as appropriate tions concerning arrhythmia, and high and variable heart
for “detection of CAD in symptomatic patients without rates [37, 38, 40].
552 A. Rizvi and J.K. Min

Table 27.1 Society of cardiovascular computed tomography (SCCT) guidelines on the use of CCTA for patients presenting with acute chest pain
in the ED [34]
I. Site Requirements
Equipment
Required equipment:
≥64 detector rows scanner that is equipped with coronary artery-specific capabilities
Advanced cardiac life support (ACLS) equipment to be present in the patient preparation and scanner areas
Image interpretation platforms with three-dimensional post-processing software
Prior year CCTA, with a minimum volume of 300 scans per year
CT laboratory accreditation
Recommended equipment:
Scanner that is equipped to perform prospectively triggered axial scanning protocols in appropriate patients should be available for radiation
dose reduction
Quality assurance program goals:
Achieving a diagnostic-quality scan rate of ≥95 %
Quarterly median radiation dose rate within target reference level, established by the SCCT guidelines on radiation dose and dose-
optimization strategies in cardiovascular CT
Quarterly review of CCTA interpretation compared with invasive angiography, achieving at least 75 % per-patient accuracy
Staffing requirements:
At least one technologist is required with prior volume experience of at least 100 CCTA scans
Current ACLS certification is required for technologists performing scans without the immediate proximity of an ACLS-certified nurse
For beta-blocker premedication of patients, properly trained ACLS-certified nursing staff is required
For prompt response to urgent or emergent complications, rapid response team and/or ACLS-certified physician must be available
Scanner operation and availability, and staffing-service hours must satisfy ED minimum requirements
II. Interpreting Physician Requirements
Requirements:
At least one physician with a minimum of 2 years of clinical experience and/or at least 300 prior CCTA scan interpretations
All other interpreting physicians must attain and maintain level-2 or the equivalent CCTA certification
Interpreting physicians must be promptly available in person or by phone for consultation about patient preparation and scan protocol
Interpreting physicians must be trained in the best-practice protocol selection of the scanners in use
A qualified physician must interpret all non-cardiac anatomy on all scans
Recommendations:
Certification Board of Cardiovascular Computed Tomography certification or American College of Radiology Board certification or dedicated
fellowship training in advanced cardiac imaging
III. Patient Selection
Appropriate indications:
Patients with acute chest pain with clinically suspected coronary ischemia
ECG negative or indeterminate for myocardial ischemia
Low to intermediate pretest likelihood by risk stratification tools (e.g., Thrombolysis in Myocardial Infarction [TIMI] grade of low [0–2] or
intermediate [3–4])
Equivocal or inadequate previous functional testing during index ED hospitalization or within the previous 6 months
Uncertain indications:
High clinical likelihood of ACS by clinical assessment and standard risk criteria (e.g., TIMI grade >4)
Previously known CAD (prior myocardial infarction, prior ischemia, prior revascularization, coronary artery calcium score >400)
Relative contraindications:
In case of history of allergic reaction to iodinated contrast without history of anaphylaxis or allergic reaction after adequate steroid/
antihistamine preparation, alternative testing should be preferred
Glomerular filtration rate (GFR) <60
Previous substantial volume of contrast within 24 h
Factors leading to potentially non-diagnostic scans (vary with scanner technology and site capabilities)
Heart rate is greater than the site maximum for reliable diagnostic scans after beta-blockers
Contraindications to beta-blockers and inadequate heart rate control
Atrial fibrillation or other markedly irregular rhythm
Body mass index >39 kg/m2
Absolute contraindications:
ACS: definite
GFR <30 unless on chronic dialysis or evidence of acute tubular necrosis
Previous anaphylaxis after iodinated contrast administration
Previous episode of contrast allergy after adequate steroid/antihistamine preparation
Inability to cooperate, including inability to raise arms
Pregnancy or uncertain pregnancy status in premenopausal women
Patient preparation, scan protocol, and reporting should follow the SCCT guidelines. In addition, interpretation of the CCTA should be tailored
according to the needs of the ED
27 Cardiovascular CT in the Emergency Department 553

Table 27.2 An example of management recommendations [34] Detection of Coronary Plaque by CCTA
Sample management recommendations to emergency department
physicians CCTA is a contrast-enhanced CT scan used for non-invasive
Stenosis 0–25 % (ACS unlikely): evaluation of the coronary arteries. The prognostic value and
Reasonable to discharge the patient cost-effectiveness of CCTA have been described by many
Follow-up at physician’s discretion
studies [43–55]. As opposed to non-contrast coronary cal-
Stenosis 26–49 % (ACS unlikely):
Reasonable to discharge the patient cium scoring, contrast-enhanced CCTA can identify calci-
Outpatient follow-up is recommended for preventive measures fied, non-calcified, and partially calcified (calcified and
Stenosis 50–69 % (ACS possible): non-calcified) lesions of the coronary arteries. There is sup-
Further evaluation of the patient is indicated before discharge porting evidence that the manual quantification of the coro-
Stenosis >70 % (ACS likely): nary plaque volumes by CCTA for non-calcified and partially
Admit the patient for further evaluation
calcified plaques correlate closely with invasive intravascu-
lar ultrasound [56–59]. The detection of non-calcified plaque
is more challenging compared to calcified plaque detection,
and optimal image quality is required that can be achievable
Coronary Artery Calcium Quantification by using 64-slice scanners.
Beyond high-grade coronary stenoses, specific coronary
Prior to discussion of CCTA in the evaluation of acute chest plaque features are linked with ACS and other adverse
pain patients presenting to the ED, the role of non-contrast cardiovascular events. Studies have shown that potentially
coronary artery calcium (CAC) scanning is worthy to men- vulnerable plaques have distinct features that include large
tion. CAC scan is relatively cheaper and faster to conduct plaque volume, large necrotic core size, attenuated fibrous
and interpret. Due to the strong correlation of CAC to overall caps, and positive arterial remodeling (growth of
coronary artery atherosclerotic disease burden, there has atherosclerotic plaque into the vessel wall rather than the
been interest to use CAC scan in low-to-intermediate risk vessel lumen) [60, 61]. Furthermore, the presence of “spotty”
patients and to exclude CAD in patients with CAC score of plaque calcifications has been associated with acute
zero. An American College of Cardiology Foundation/ MI. CCTA can assess some of these “adverse” features of
American Heart Association consensus statement endorsed potentially vulnerable plaques [62]. Therefore, CCTA
the use of CAC testing for low-risk symptomatic patients as assessment of plaque may prove prognostically useful when
a “filter” for further cardiovascular testing. It is recommended including identification of adverse plaque features. The
that CAC scoring may be used in a binary fashion such that “adverse” plaque features associated with ACS and other
CAC of zero excludes CAD and no further testing is adverse cardiovascular events to date include low attenuation
performed as compared to CAC >0, for which additional plaque, positive remodeling, spotty calcifications, and the
functional stress testing for obstructive CAD can be “napkin-ring sign”. Studies have demonstrated the
considered [41]. characteristics of coronary plaque in patients presenting with
In contrast, a recent analysis from the CONFIRM regis- ACS [63–66]. Patients with ACS had greater portions of
try demonstrated that CCTA findings were superior to non-calcified plaque, had larger plaque volumes, presented
CAC scoring for adverse cardiovascular outcomes in more often with “spotty” calcifications, and included plaques
10,037 low-to-intermediate risk patients, albeit stable with greater positive remodeling and lower CT attenuation
rather than acute in presentation, undergoing both CAC than patients with stable angina [63, 64, 66]. Furthermore,
and CCTA. CCTA occasionally demonstrated significant the presence of a napkin-ring sign has also been shown to be
luminal stenosis of ≥50 % in patients with zero CAC score a sign of high-risk coronary plaque [64, 67, 68].
(3.5 % incidence). The investigators concluded that in Beyond these plaque features that require generally
symptomatic patients with a CAC score of 0, obstructive arduous measurements, prior investigations have also
CAD is possible and is associated with increased cardio- shown that major adverse cardiac events (MACE) were
vascular events [42]. associated with more easily identifiable characteristics,
The major disadvantage of CAC scan is the inability to including a higher amount of non-calcified plaque in non-
visualize non-calcified plaque, which may be present in a obstructive CAD. Conversely, the amount of calcified
large proportion of patients. Moreover, non-calcified plaque was not significantly associated with an increased
plaque carries with it important prognostic value that can risk for MACE [51].
be readily assessed by CCTA but not by CAC scan.
Therefore, CAC scan is not widely considered a first-line
test because of its inability to rule out stenosis by non- Non-coronary CCTA Findings
calcified plaque and low specificity for obstructive CAD,
and CCTA may be a preferable option for most patients A multitude of additional information proffered by CCTA
with acute chest pain. may be of benefit in the acute and long-term assessment of
554 A. Rizvi and J.K. Min

the ED patients. This includes evaluation of non-coronary The ability of CCTA to rapidly exclude obstructive CAD
cardiac findings, including left ventricle volume and ejection among ED patients helps in identifying patients who can be
fraction; left ventricular mass; right heart dimensions and safely and rapidly discharged from the ED relative to standard
function; and great vessel pathology; as well as non-cardiac of care [33, 84]. The American College of Cardiology (ACC)/
thoracic pathology of a patient’s chest pain [69–75]. American Heart Association (AHA) guidelines have incorpo-
Furthermore, identification of pulmonary nodules as a non- rated CCTA among current noninvasive tests for use in low-to-
cardiac incidental finding can improve follow-up related to intermediate risk patients with suspected ACS. However,
potentially adverse findings [76–79]. current literature still lacks a standardized approach to guide
The assessment of non-cardiac thoracic pathology by ED patient management based on cardiac CT findings.
utilizing CCTA may include aortic dissection, pulmonary
embolism, pneumonia, pericardial disease, abscesses,
effusions, and cancer [45, 80, 81]. In this regard, some Radiation Risk
investigators have considered whether acute chest pain needs
to be evaluated with a “triple rule-out” protocol which Although CCTA has evolved as a useful diagnostic imaging
effectively increases the Z-axis coverage of the CT scan, and modality in the assessment of CAD, the potential risks due to
allows for exclusion of ACS, aortic dissection, and pulmo- ionizing radiation exposure associated with CCTA have
nary embolus in a single scan; but there is no clear clinical raised concerns, particularly with regard to potential long-
benefit to this extended approach which has the disadvantage term risks of radiation-induced malignancy, and has led to
of significantly increased radiation dose, higher imaging the “As Low As Reasonably Achievable (ALARA)” principle
costs, and longer interpretation and reporting time. Thus, of radiation protection [85]. In spite of the fact that the
routine use of a “triple rule-out” protocol is not currently increased risk of malignancy from CCTA remains
recommended [34]. controversial, the ALARA principle prevails in clinical
practice. The clinical usefulness of CCTA for the rapid
evaluation of chest pain in the ED must be weighed against
Diagnostic Accuracy of CCTA the radiation exposure. Improvements in CCTA technology,
including prospective ECG triggering, tube voltage reduction
Prospective multicenter diagnostic performance have to 100 kV or less in non-obese patients, use of iterative image
demonstrated the ability of CCTA to accurately detect reconstruction, and high-pitch helical acquisition, have
coronary stenosis when compared to invasive coronary allowed for substantial reduction of radiation doses by CCTA
angiography (ICA) as a reference standard. In the to <1 mSv. These 1 mSv scans, though theoretically
ACCURACY (Assessment by Coronary Computed attractive, are still not routine due to certain challenges such
Tomographic Angiography of Individuals Undergoing as higher heart rates and arrhythmias, and large body habitus.
Invasive Coronary Angiography) trial [18], 230 patients
underwent both CCTA and ICA for non-emergent typical or
atypical chest pain. The study investigators demonstrated Indications
CCTA to have a sensitivity of 95 %, specificity of 83 %,
positive predictive value of 64 %, and negative predictive The use of cardiac CT to rule out ACS, especially in low-to-
value of 99 % for prediction of obstructive CAD with >50 % intermediate risk patients, is supported by the recent SCCT
stenosis by ICA. The high negative predictive value of 99 % guidelines [34], which recommends CCTA in the setting of
at both the patient and the vessel level demonstrated that acute chest pain in patients with low-to-intermediate
cardiac CT is an effective non-invasive alternative to ICA to likelihood of ACS with negative initial electrocardiographic
rule out obstructive CAD [18]. Furthermore, a meta-analysis and biochemical markers, and TIMI grade ≤4. The indica-
of 40 ACCURACY studies concluded that in comparison tions according to these guidelines are as follows [34]:
with ICA, the sensitivity and specificity of CCTA to detect
≥50 % stenosis were 99 % and 89 %, respectively at per Appropriate Indications
patient level, and 90 % and 97 %, respectively at per segment • Patients with acute chest pain with clinically suspected
level [82]. Particularly germane to the topic at hand, CCTA coronary ischemia
in low-to-intermediate risk patients suspected to have ACS • ECG negative or indeterminate for myocardial ischemia
retains its very high sensitivity (92 %) and negative predictive • Low-to-intermediate pretest likelihood by risk stratifica-
value (99 %), with MACE at 30 days, 6 months, or at 1 year tion tools (e.g., TIMI grade of low [0–2] or intermediate
equal to zero or minimal in patients who were discharged [3–4])
with a normal CCTA or when CCTA demonstrated mild non- • Equivocal or inadequate previous functional testing during
obstructive disease [25, 26, 83]. index ED hospitalization or within the previous 6 months
27 Cardiovascular CT in the Emergency Department 555

Uncertain Indications – Contraindications to beta-blockers and inadequate

• High clinical likelihood of ACS by clinical assessment heart rate control
and standard risk criteria (e.g., TIMI grade >4) – Atrial fibrillation or other markedly irregular rhythm
• Previously known CAD (prior MI, prior ischemia, prior – Body mass index >39 kg/m2
revascularization, coronary artery calcium score >400)

Moreover, the ACCF/SCCT/ACR/AHA/ASE/ASNC/ Summary of Strengths

NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for
Cardiac Computed Tomography lists the use of CCTA as CCTA is unique from prior forms of imaging in that it does
appropriate for “detection of CAD in symptomatic patients not require stress provocation to determine burden of
without known heart disease—acute symptoms with CAD. Multiple single-center and multicenter trials have
suspicion of ACS (urgent presentation) (Appropriate, score established CCTA as a noninvasive diagnostic test with
7)” [35], as previously discussed. excellent sensitivity (97.2 %) and good specificity (87.4 %)
for the detection of obstructive CAD with >50 % stenosis
[17, 18]. The major strength of CCTA is its high negative
Contraindications predictive value for stenosis (99 %). In addition, CCTA is
highly sensitive (90 %) and specific (92 %) for the detection
CCTA is contraindicated in patients with severe renal of calcified and non-calcified coronary atherosclerotic plaque
impairment because of the high risk of contrast-induced [57, 59, 86].
nephropathy (CIN). In addition, pregnancy is a contraindi-
cation due to radiation exposure. Prior contrast reactions
are a relative contraindication; such patients can frequently Summary of Limitations
be pre-treated with the use of a steroid and anti-histamine
medications one day prior to the CT examination. The A significant limitation of the CCTA is its lower specificity
absolute and relative contraindications to CCTA according that may be attributable to a spatial resolution of about
to SCCT recently published guidelines include the 0.5 mm. This non-ideal specificity of CCTA is concerning
following [34]: and could lead to increased downstream testing and, possibly,
ICA with revascularization, thus warranting further improve-
Absolute Contraindications ments in CCTA technology. Another important limitation is
• ACS: definite that patients with extensive coronary calcification may have
• GFR <30 unless on chronic dialysis or evidence of acute non-diagnostic scans because of calcium “blooming” and
tubular necrosis “beam hardening” artifacts. Cardiac dysrhythmias and inad-
• Previous anaphylaxis after iodinated contrast equate heart rate control during imaging are other factors
administration leading to sub-optimal scans for diagnostic purposes.
• Previous episode of contrast allergy after adequate ste- Moreover, assessment of CAD by cardiac CT requires ion-
roid/antihistamine preparation izing radiation exposure and administration of contrast dye,
• Inability to cooperate, including inability to raise arms compared to other modalities (e.g., exercise treadmill, rest
• Pregnancy or uncertain pregnancy status in premenopausal echocardiography, exercise or pharmacologic stress echocar-
women diography, rest or stress cardiac magnetic resonance imag-
ing). Patients with significant contrast dye allergies or renal
insufficiency are not candidates for CCTA. Morbid obesity
Relative Contraindications can compromise image quality and thus reduce diagnostic
• Alternative testing should be preferred in these cases: his- accuracy or require higher doses of radiation. Higher heart
tory of allergic reaction to iodinated contrast without his- rates and arrhythmias can cause misregistration artifacts,
tory of anaphylaxis or allergic reaction after adequate leading to poor visualization of the coronary arteries.
steroid/antihistamine preparation
• Glomerular filtration rate (GFR) <60
• Previous substantial volume of contrast within 24 h (this Future Directions
will vary with the GFR)
• Factors leading to potentially nondiagnostic scans (vary Chest pain is so commonly encountered in the practice of
with scanner technology and site capabilities) medicine and future advancements in CCTA technology are
– Heart rate is greater than the site maximum for reliable expected to improve the overall accuracy of CT-determined
diagnostic scans after beta-blockers stenosis in comparison with reference standard fractional
556 A. Rizvi and J.K. Min

flow reserve (FFR) measurements during ICA. Currently, report of the American College of Cardiology Foundation/
investigators are interested in changing the face of how ACS American Heart Association Task Force on Practice Guidelines
developed in collaboration with the American Academy of Family
is diagnosed and managed by improving the specificity of Physicians, Society for Cardiovascular Angiography and
qualitative determination of coronary stenosis by fractional Interventions, and the Society of Thoracic Surgeons. J Am Coll
flow reserve derived from CT, or FFRCT, a novel non-invasive Cardiol. 2011;57(19):e215–367.
method that applies computational fluid dynamics for the 9. Goldstein JA, Gallagher MJ, O’Neill WW, Ross MA, O’Neil BJ,
Raff GL. A randomized controlled trial of multi-slice coronary
calculation of FFR from typically acquired CCTA studies. computed tomography for evaluation of acute chest pain. J Am Coll
This technique has been demonstrated to have higher Cardiol. 2007;49(8):863–71.
diagnostic performance for ischemia-causing lesions than 10. Tosteson AN, Goldman L, Udvarhelyi IS, Lee TH. Cost-
any other functional imaging method [87]. Importantly, effectiveness of a coronary care unit versus an intermediate care
unit for emergency department patients with chest pain. Circulation.
given its ability to obviate the requirement for use of 1996;94(2):143–50.
adenosine or for additional scanning, this technique offers 11. Goodacre S, Calvert N. Cost effectiveness of diagnostic strategies
the added safety to not require increased radiation doses. In for patients with acute, undifferentiated chest pain. Emerg Med
the future, it is expected that the maturation of dual-energy J. 2003;20(5):429–33.
12. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD,
CT may further improves stenosis assessment and diagnostic Borden WB, et al. Heart disease and stroke statistics – 2012 update:
accuracy in patients with heavy coronary calcifications, and a report from the American Heart Association. Circulation.
may allow for further radiation reduction. In aggregate, 2012;125(1):e2–220.
noninvasive coronary imaging by CT is likely here to stay. 13. Granger CB, Goldberg RJ, Dabbous O, Pieper KS, Eagle KA,
Cannon CP, et al. Predictors of hospital mortality in the global
registry of acute coronary events. Arch Intern Med. 2003;163(19):
2345–53.
14. Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T,
References Papuchis G, et al. The TIMI risk score for unstable angina/non-ST
elevation MI: a method for prognostication and therapeutic decision
1. Niska R, Bhuiya F, Xu J. National Hospital Ambulatory Medical making. JAMA. 2000;284(7):835–42.
Care Survey: 2007 emergency department summary. Natl Health 15. Invasive compared with non-invasive treatment in unstable coro-
Stat Rep. 2007;2010(26):1–31. nary-artery disease: FRISC II prospective randomised multicentre
2. Graff LG, Dallara J, Ross MA, Joseph AJ, Itzcovitz J, Andelman study. FRagmin and Fast Revascularisation during InStability in
RP, et al. Impact on the care of the emergency department chest Coronary artery disease Investigators. Lancet. 1999;354(9180):
pain patient from the chest pain evaluation registry (CHEPER) 708–15.
study. Am J Cardiol. 1997;80(5):563–8. 16. Pollack Jr CV, Sites FD, Shofer FS, Sease KL, Hollander JE.
3. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Application of the TIMI risk score for unstable angina and non-ST
Hochman JS, et al. ACC/AHA 2002 guideline update for the manage- elevation acute coronary syndrome to an unselected emergency
ment of patients with unstable angina and non-ST-segment elevation department chest pain population. Acad Emerg Med. 2006;13(1):
myocardial infarction – summary article: a report of the American 13–8.
College of Cardiology/American Heart Association task force on 17. Miller JM, Rochitte CE, Dewey M, Arbab-Zadeh A, Niinuma H,
practice guidelines (Committee on the Management of Patients With Gottlieb I, et al. Diagnostic performance of coronary angiography
Unstable Angina). J Am Coll Cardiol. 2002;40(7):1366–74. by 64-row CT. N Engl J Med. 2008;359(22):2324–36.
4. Luepker RV, Apple FS, Christenson RH, Crow RS, Fortmann SP, 18. Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert E,
Goff D, et al. Case definitions for acute coronary heart disease in et al. Diagnostic performance of 64-multidetector row coronary
epidemiology and clinical research studies: a statement from the computed tomographic angiography for evaluation of coronary
AHA Council on Epidemiology and Prevention; AHA Statistics artery stenosis in individuals without known coronary artery
Committee; World Heart Federation Council on Epidemiology and disease: results from the prospective multicenter ACCURACY
Prevention; the European Society of Cardiology Working Group on (Assessment by Coronary Computed Tomographic Angiography of
Epidemiology and Prevention; Centers for Disease Control and Individuals Undergoing Invasive Coronary Angiography) trial.
Prevention; and the National Heart, Lung, and Blood Institute. J Am Coll Cardiol. 2008;52(21):1724–32.
Circulation. 2003;108(20):2543–9. 19. Johnson TR, Nikolaou K, Wintersperger BJ, Knez A, Boekstegers
5. Ornato JP, American College of Cardiology/American Heart P, Reiser MF, et al. ECG-gated 64-MDCT angiography in the
A. Management of patients with unstable angina and non-ST- differential diagnosis of acute chest pain. AJR Am J Roentgenol.
segment elevation myocardial infarction: update ACC/AHA 2007;188(1):76–82.
guidelines. Am J Emerg Med. 2003;21(4):346–51. 20. Gallagher MJ, Ross MA, Raff GL, Goldstein JA, O’Neill WW,
6. Kaul P, Newby LK, Fu Y, Hasselblad V, Mahaffey KW, Christenson O’Neil B. The diagnostic accuracy of 64-slice computed
RH, et al. Troponin T and quantitative ST-segment depression offer tomography coronary angiography compared with stress nuclear
complementary prognostic information in the risk stratification of imaging in emergency department low-risk chest pain patients. Ann
acute coronary syndrome patients. J Am Coll Cardiol. 2003; Emerg Med. 2007;49(2):125–36.
41(3):371–80. 21. Rubinshtein R, Halon DA, Gaspar T, Jaffe R, Karkabi B, Flugelman
7. Vafaie M, Katus HA. Myocardial infarction. New universal defini- MY, et al. Usefulness of 64-slice cardiac computed tomographic
tion and its implementation in clinical practice. Herz. 2013; angiography for diagnosing acute coronary syndromes and
38(8):821–7. predicting clinical outcome in emergency department patients with
8. Wright RS, Anderson JL, Adams CD, Bridges CR, Casey Jr DE, chest pain of uncertain origin. Circulation. 2007;115(13):1762–8.
Ettinger SM, et al. 2011 ACCF/AHA focused update incorporated 22. Johnson TR, Nikolaou K, Becker A, Leber AW, Rist C,
into the ACC/AHA 2007 guidelines for the management of patients Wintersperger BJ, et al. Dual-source CT for chest pain assessment.
with unstable angina/non-ST-elevation myocardial infarction: a Eur Radiol. 2008;18(4):773–80.
27 Cardiovascular CT in the Emergency Department 557

23. Takakuwa KM, Halpern EJ. Evaluation of a “triple rule-out” 36. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte Jr
coronary CT angiography protocol: use of 64-Section CT in low-to- M, Detrano R. Quantification of coronary artery calcium using
moderate risk emergency department patients suspected of having ultrafast computed tomography. J Am Coll Cardiol. 1990;15(4):
acute coronary syndrome. Radiology. 2008;248(2):438–46. 827–32.
24. Ueno K, Anzai T, Jinzaki M, Yamada M, Kohno T, Kawamura A, 37. Ohnesorge B, Flohr T, Becker C, Kopp AF, Schoepf UJ, Baum U,
et al. Diagnostic capacity of 64-slice multidetector computed et al. Cardiac imaging by means of electrocardiographically gated
tomography for acute coronary syndrome in patients presenting multisection spiral CT: initial experience. Radiology. 2000;
with acute chest pain. Cardiology. 2009;112(3):211–8. 217(2):564–71.
25. Hollander JE, Chang AM, Shofer FS, McCusker CM, Baxt WG, 38. Kopp AF, Ohnesorge B, Becker C, Schroder S, Heuschmid M,
Litt HI. Coronary computed tomographic angiography for rapid Kuttner A, et al. Reproducibility and accuracy of coronary calcium
discharge of low-risk patients with potential acute coronary measurements with multi-detector row versus electron-beam
syndromes. Ann Emerg Med. 2009;53(3):295–304. CT. Radiology. 2002;225(1):113–9.
26. Hollander JE, Chang AM, Shofer FS, Collin MJ, Walsh KM, 39. Achenbach S, Ulzheimer S, Baum U, Kachelriess M, Ropers D,
McCusker CM, et al. One-year outcomes following coronary Giesler T, et al. Noninvasive coronary angiography by retrospectively
computerized tomographic angiography for evaluation of ECG-gated multislice spiral CT. Circulation. 2000;102(23):2823–8.
emergency department patients with potential acute coronary 40. Laudon DA, Vukov LF, Breen JF, Rumberger JA, Wollan PC,
syndrome. Acad Emerg Med. 2009;16(8):693–8. Sheedy 2nd PF. Use of electron-beam computed tomography in the
27. Hansen M, Ginns J, Seneviratne S, Slaughter R, Premaranthe M, evaluation of chest pain patients in the emergency department. Ann
Samardhi H, et al. The value of dual-source 64-slice CT coronary Emerg Med. 1999;33(1):15–21.
angiography in the assessment of patients presenting to an acute 41. Greenland P, Bonow RO, Brundage BH, Budoff MJ, Eisenberg MJ,
chest pain service. Heart Lung Circ. 2010;19(4):213–8. Grundy SM, et al. ACCF/AHA 2007 clinical expert consensus
28. Goldstein JA, Chinnaiyan KM, Abidov A, Achenbach S, Berman document on coronary artery calcium scoring by computed
DS, Hayes SW, et al. The CT-STAT (Coronary Computed tomography in global cardiovascular risk assessment and in
Tomographic Angiography for Systematic Triage of Acute Chest evaluation of patients with chest pain: a report of the American
Pain Patients to Treatment) trial. J Am Coll Cardiol. 2011; College of Cardiology Foundation Clinical Expert Consensus Task
58(14):1414–22. Force (ACCF/AHA Writing Committee to Update the 2000 Expert
29. Hoffmann U, Truong QA, Schoenfeld DA, Chou ET, Woodard PK, Consensus Document on Electron Beam Computed Tomography)
Nagurney JT, et al. Coronary CT angiography versus standard developed in collaboration with the Society of Atherosclerosis
evaluation in acute chest pain. N Engl J Med. 2012;367(4): Imaging and Prevention and the Society of Cardiovascular
299–308. Computed Tomography. J Am Coll Cardiol. 2007;49(3):378–402.
30. Litt HI, Gatsonis C, Snyder B, Singh H, Miller CD, Entrikin DW, 42. Villines TC, Hulten EA, Shaw LJ, Goyal M, Dunning A, Achenbach
et al. CT angiography for safe discharge of patients with possible S, et al. Prevalence and severity of coronary artery disease and
acute coronary syndromes. N Engl J Med. 2012;366(15): adverse events among symptomatic patients with coronary artery
1393–403. calcification scores of zero undergoing coronary computed
31. Diver DJ, Bier JD, Ferreira PE, Sharaf BL, McCabe C, Thompson tomography angiography: results from the CONFIRM (Coronary
B, et al. Clinical and arteriographic characterization of patients with CT Angiography Evaluation for Clinical Outcomes: An
unstable angina without critical coronary arterial narrowing (from International Multicenter) registry. J Am Coll Cardiol. 2011;
the TIMI-IIIA Trial). Am J Cardiol. 1994;74(6):531–7. 58(24):2533–40.
32. Roe MT, Harrington RA, Prosper DM, Pieper KS, Bhatt DL, Lincoff 43. Motoyama S, Sarai M, Harigaya H, Anno H, Inoue K, Hara T, et al.
AM, et al. Clinical and therapeutic profile of patients presenting Computed tomographic angiography characteristics of
with acute coronary syndromes who do not have significant coro- atherosclerotic plaques subsequently resulting in acute coronary
nary artery disease. The Platelet Glycoprotein IIb/IIIa in Unstable syndrome. J Am Coll Cardiol. 2009;54(1):49–57.
Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) 44. Nance Jr JW, Schlett CL, Schoepf UJ, Oberoi S, Leisy HB, Barraza
Trial Investigators. Circulation. 2000;102(10):1101–6. Jr JM, et al. Incremental prognostic value of different components
33. Hulten E, Pickett C, Bittencourt MS, Villines TC, Petrillo S, Di of coronary atherosclerotic plaque at cardiac CT angiography
Carli MF, et al. Outcomes after coronary computed tomography beyond coronary calcification in patients with acute chest pain.
angiography in the emergency department: a systematic review and Radiology. 2012;264(3):679–90.
meta-analysis of randomized, controlled trials. J Am Coll Cardiol. 45. Min JK, Shaw LJ, Devereux RB, Okin PM, Weinsaft JW, Russo DJ,
2013;61(8):880–92. et al. Prognostic value of multidetector coronary computed
34. Raff GL, Chinnaiyan KM, Cury RC, Garcia MT, Hecht HS, tomographic angiography for prediction of all-cause mortality.
Hollander JE, et al. SCCT guidelines on the use of coronary J Am Coll Cardiol. 2007;50(12):1161–70.
computed tomographic angiography for patients presenting with 46. Gaemperli O, Valenta I, Schepis T, Husmann L, Scheffel H,
acute chest pain to the emergency department: a report of the Desbiolles L, et al. Coronary 64-slice CT angiography predicts
Society of Cardiovascular Computed Tomography Guidelines outcome in patients with known or suspected coronary artery
Committee. J Cardiovasc Comput Tomogr. 2014;8(4):254–71. disease. Eur Radiol. 2008;18(6):1162–73.
35. Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O’Gara P, 47. Hadamitzky M, Freissmuth B, Meyer T, Hein F, Kastrati A,
et al. ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR Martinoff S, et al. Prognostic value of coronary computed
2010 appropriate use criteria for cardiac computed tomography. A tomographic angiography for prediction of cardiac events in
report of the American College of Cardiology Foundation patients with suspected coronary artery disease. JACC Cardiovasc
Appropriate Use Criteria Task Force, the Society of Cardiovascular Imaging. 2009;2(4):404–11.
Computed Tomography, the American College of Radiology, the 48. Carrigan TP, Nair D, Schoenhagen P, Curtin RJ, Popovic ZB,
American Heart Association, the American Society of Halliburton S, et al. Prognostic utility of 64-slice computed
Echocardiography, the American Society of Nuclear Cardiology, tomography in patients with suspected but no documented coronary
the North American Society for Cardiovascular Imaging, the artery disease. Eur Heart J. 2009;30(3):362–71.
Society for Cardiovascular Angiography and Interventions, and the 49. Chow BJ, Wells GA, Chen L, Yam Y, Galiwango P, Abraham A,
Society for Cardiovascular Magnetic Resonance. J Cardiovasc et al. Prognostic value of 64-slice cardiac computed tomography
Comput Tomogr. 2010;4(6):407.e1–33. severity of coronary artery disease, coronary atherosclerosis, and
558 A. Rizvi and J.K. Min

left ventricular ejection fraction. J Am Coll Cardiol. 2010; 65. Hoffmann U, Moselewski F, Nieman K, Jang IK, Ferencik M,
55(10):1017–28. Rahman AM, et al. Noninvasive assessment of plaque morphology
50. Kristensen TS, Kofoed KF, Kuhl JT, Nielsen WB, Nielsen MB, and composition in culprit and stable lesions in acute coronary
Kelbaek H. Prognostic implications of nonobstructive coronary syndrome and stable lesions in stable angina by multidetector
plaques in patients with non-ST-segment elevation myocardial computed tomography. J Am Coll Cardiol. 2006;47(8):1655–62.
infarction: a multidetector computed tomography study. J Am Coll 66. Ferencik M, Schlett CL, Ghoshhajra BB, Kriegel MF, Joshi SB,
Cardiol. 2011;58(5):502–9. Maurovich-Horvat P, et al. A computed tomography-based coronary
51. Russo V, Zavalloni A, Bacchi Reggiani ML, Buttazzi K, Gostoli V, lesion score to predict acute coronary syndrome among patients
Bartolini S, et al. Incremental prognostic value of coronary CT with acute chest pain and significant coronary stenosis on coronary
angiography in patients with suspected coronary artery disease. computed tomographic angiogram. Am J Cardiol. 2012;110(2):
Circ Cardiovasc Imaging. 2010;3(4):351–9. 183–9.
52. Min JK, Feignoux J, Treutenaere J, Laperche T, Sablayrolles J. The 67. Maurovich-Horvat P, Hoffmann U, Vorpahl M, Nakano M, Virmani
prognostic value of multidetector coronary CT angiography for the R, Alkadhi H. The napkin-ring sign: CT signature of high-risk
prediction of major adverse cardiovascular events: a multicenter coronary plaques? JACC Cardiovasc Imaging. 2010;3(4):440–4.
observational cohort study. Int J Cardiovasc Imaging. 2010;26(6): 68. Narula J, Achenbach S. Napkin-ring necrotic cores: defining cir-
721–8. cumferential extent of necrotic cores in unstable plaques. JACC
53. Petretta M, Daniele S, Acampa W, Imbriaco M, Pellegrino T, Cardiovasc Imaging. 2009;2(12):1436–8.
Messalli G, et al. Prognostic value of coronary artery calcium score 69. Lin FY, Devereux RB, Roman MJ, Meng J, Jow VM, Jacobs A,
and coronary CT angiography in patients with intermediate risk of et al. Cardiac chamber volumes, function, and mass as determined
coronary artery disease. Int J Cardiovasc Imaging. 2012;28(6): by 64-multidetector row computed tomography: mean values
1547–56. among healthy adults free of hypertension and obesity. JACC
54. Alexanderson E, Canseco-Leon N, Inarra F, Meave A, Dey D. Cardiovasc Imaging. 2008;1(6):782–6.
Prognostic value of cardiovascular CT: is coronary artery calcium 70. Raman SV, Shah M, McCarthy B, Garcia A, Ferketich AK. Multi-
screening enough? The added value of CCTA. J Nucl Cardiol. detector row cardiac computed tomography accurately quantifies
2012;19(3):601–8. right and left ventricular size and function compared with cardiac
55. American College of Cardiology Foundation Task Force on Expert magnetic resonance. Am Heart J. 2006;151(3):736–44.
Consensus D, Mark DB, Berman DS, Budoff MJ, Carr JJ, Gerber 71. Yamamuro M, Tadamura E, Kubo S, Toyoda H, Nishina T, Ohba M,
TC, et al. ACCF/ACR/AHA/NASCI/SAIP/SCAI/SCCT 2010 et al. Cardiac functional analysis with multi-detector row CT and
expert consensus document on coronary computed tomographic segmental reconstruction algorithm: comparison with echocardiog-
angiography: a report of the American College of Cardiology raphy, SPECT, and MR imaging. Radiology. 2005;234(2):381–90.
Foundation Task Force on Expert Consensus Documents. J Am 72. Henneman MM, Schuijf JD, Jukema JW, Holman ER, Lamb HJ, de
Coll Cardiol. 2010;55(23):2663–99. Roos A, et al. Assessment of global and regional left ventricular
56. Schepis T, Marwan M, Pflederer T, Seltmann M, Ropers D, Daniel function and volumes with 64-slice MSCT: a comparison with 2D
WG, et al. Quantification of non-calcified coronary atherosclerotic echocardiography. J Nucl Cardiol. 2006;13(4):480–7.
plaques with dual-source computed tomography: comparison with 73. Gilkeson RC, Markowitz AH, Balgude A, Sachs PB. MDCT evalu-
intravascular ultrasound. Heart. 2010;96(8):610–5. ation of aortic valvular disease. AJR Am J Roentgenol. 2006;
57. Leber AW, Becker A, Knez A, von Ziegler F, Sirol M, Nikolaou K, 186(2):350–60.
et al. Accuracy of 64-slice computed tomography to classify and 74. Gilard M, Cornily JC, Pennec PY, Joret C, Le Gal G, Mansourati J,
quantify plaque volumes in the proximal coronary system: a et al. Accuracy of multislice computed tomography in the preopera-
comparative study using intravascular ultrasound. J Am Coll tive assessment of coronary disease in patients with aortic valve
Cardiol. 2006;47(3):672–7. stenosis. J Am Coll Cardiol. 2006;47(10):2020–4.
58. Leber AW, Knez A, Becker A, Becker C, von Ziegler F, Nikolaou 75. Jongbloed MR, Lamb HJ, Bax JJ, Schuijf JD, de Roos A, van der
K, et al. Accuracy of multidetector spiral computed tomography in Wall EE, et al. Noninvasive visualization of the cardiac venous sys-
identifying and differentiating the composition of coronary tem using multislice computed tomography. J Am Coll Cardiol.
atherosclerotic plaques: a comparative study with intracoronary 2005;45(5):749–53.
ultrasound. J Am Coll Cardiol. 2004;43(7):1241–7. 76. Lehman SJ, Abbara S, Cury RC, Nagurney JT, Hsu J, Goela A,
59. Petranovic M, Soni A, Bezzera H, Loureiro R, Sarwar A, Raffel C, et al. Significance of cardiac computed tomography incidental find-
et al. Assessment of nonstenotic coronary lesions by 64-slice ings in acute chest pain. Am J Med. 2009;122(6):543–9.
multidetector computed tomography in comparison to intravascular 77. Machaalany J, Yam Y, Ruddy TD, Abraham A, Chen L, Beanlands
ultrasound: evaluation of nonculprit coronary lesions. J Cardiovasc RS, et al. Potential clinical and economic consequences of noncar-
Comput Tomogr. 2009;3(1):24–31. diac incidental findings on cardiac computed tomography. J Am
60. Narula J, Strauss HW. The popcorn plaques. Nat Med. 2007; Coll Cardiol. 2009;54(16):1533–41.
13(5):532–4. 78. Lee CI, Tsai EB, Sigal BM, Plevritis SK, Garber AM, Rubin GD.
61. Narula J, Garg P, Achenbach S, Motoyama S, Virmani R, Strauss Incidental extracardiac findings at coronary CT: clinical and eco-
HW. Arithmetic of vulnerable plaques for noninvasive imaging. Nat nomic impact. AJR Am J Roentgenol. 2010;194(6):1531–8.
Clin Pract Cardiovasc Med. 2008;5 Suppl 2:S2–10. 79. Koonce J, Schoepf JU, Nguyen SA, Northam MC, Ravenel JG.
62. Maurovich-Horvat P, Ferencik M, Voros S, Merkely B, Hoffmann Extra-cardiac findings at cardiac CT: experience with 1,764
U. Comprehensive plaque assessment by coronary CT angiography. patients. Eur Radiol. 2009;19(3):570–6.
Nat Rev Cardiol. 2014;11(7):390–402. 80. Kim TJ, Han DH, Jin KN, Won LK. Lung cancer detected at car-
63. Motoyama S, Kondo T, Sarai M, Sugiura A, Harigaya H, Sato T, diac CT: prevalence, clinicoradiologic features, and importance of
et al. Multislice computed tomographic characteristics of coronary full-field-of-view images. Radiology. 2010;255(2):369–76.
lesions in acute coronary syndromes. J Am Coll Cardiol. 2007; 81. Ostrom MP, Gopal A, Ahmadi N, Nasir K, Yang E, Kakadiaris I,
50(4):319–26. et al. Mortality incidence and the severity of coronary atherosclero-
64. Pflederer T, Marwan M, Schepis T, Ropers D, Seltmann M, sis assessed by computed tomography angiography. J Am Coll
Muschiol G, et al. Characterization of culprit lesions in acute Cardiol. 2008;52(16):1335–43.
coronary syndromes using coronary dual-source CT angiography. 82. Mowatt G, Cook JA, Hillis GS, Walker S, Fraser C, Jia X, et al.
Atherosclerosis. 2010;211(2):437–44. 64-Slice computed tomography angiography in the diagnosis and
27 Cardiovascular CT in the Emergency Department 559

assessment of coronary artery disease: systematic review and meta- computed tomographic angiography: a report of the Society of
analysis. Heart. 2008;94(11):1386–93. Cardiovascular Computed Tomography Guidelines Committee.
83. Hoffmann U, Bamberg F, Chae CU, Nichols JH, Rogers IS, J Cardiovasc Comput Tomogr. 2009;3(3):190–204.
Seneviratne SK, et al. Coronary computed tomography angiogra- 86. Achenbach S, Moselewski F, Ropers D, Ferencik M, Hoffmann U,
phy for early triage of patients with acute chest pain: the ROMICAT MacNeill B, et al. Detection of calcified and noncalcified coro-
(Rule Out Myocardial Infarction using Computer Assisted nary atherosclerotic plaque by contrast-enhanced, submillimeter
Tomography) trial. J Am Coll Cardiol. 2009;53(18):1642–50. multidetector spiral computed tomography: a segment-based
84. Cheezum MK, Bittencourt MS, Hulten EA, Scirica BM, Villines comparison with intravascular ultrasound. Circulation. 2004;
TC, Blankstein R. Coronary computed tomographic angiography in 109(1):14–7.
the emergency room: state of the art. Expert Rev Cardiovasc Ther. 87. Min JK, Leipsic J, Pencina MJ, Berman DS, Koo BK, van
2014;12(2):241–53. Mieghem C, et al. Diagnostic accuracy of fractional flow reserve
85. Abbara S, Arbab-Zadeh A, Callister TQ, Desai MY, Mamuya W, from anatomic CT angiography. JAMA. 2012;308(12):
Thomson L, et al. SCCT guidelines for performance of coronary 1237–45.
 Index

A Cardiothoracic surgery, 391–424

Ablation, 433, 457–470, 474–475, 479, 514, 519, 520 Cardiovascular computed tomographic angiography (CCTA), 30, 47,
Acute coronary syndrome (ACS), 108, 168, 169, 171, 173, 326, 355, 105, 133, 179, 199, 275, 341, 350, 381, 456, 487, 507, 546
356, 358, 363, 364, 384–387, 488, 549–556 Cardiovascular magnetic resonance (CMR) imaging, 230, 398, 429,
All-cause mortality, 105–108, 361, 386 474, 507–535
Angiography, 6, 29, 33, 63, 104, 123, 133, 154, 157, 179, 191, 212, Carotid CT angiography, 319–335
232, 241, 257, 275, 297, 319, 340, 354, 381, 398, 429, Chest pain, 108, 115, 168, 171, 173, 212, 213, 225, 236, 237, 285,
456, 487, 507, 546 292, 326, 340, 363–365, 376, 382–386, 412, 415, 418, 440, 447,
Angiosarcoma, 278, 281, 289, 290, 531 488, 489, 491, 498, 499, 510, 549–555
Anomalous coronary arteries, 61, 62, 171–173, 393, 395, 398–401, Chronic kidney disease (CKD), 125
406, 407, 415, 418, 472, 488, 510, 527 Computed tomography angiography (CTA), 9, 18, 19, 114, 115, 137,
Aorta CT angiography, 319–335 161, 163, 166, 167, 179, 191–209, 302, 303, 316, 319–322,
Aortic annulus (AA), 50, 54, 244, 257–267, 393, 394, 397, 438 325–330, 332–335
Aortic dissection, 173, 321–323, 325, 326, 395, 424, 437, 530, 554 Computed tomography (CT), 3, 25, 36, 48, 103, 121, 134, 147, 157,
Aortic regurgitation (AR), 246, 250, 251, 395, 435, 438, 521, 522 179, 191, 212, 221, 241, 257, 275, 319, 337, 350, 384, 391, 456,
Aortic stenosis (AS), 59, 243–246, 250, 251, 255–257, 394, 395, 437, 487, 508, 545
438, 441, 444, 462, 472, 519, 521 Computed tomography (CT) perfusion, 185, 330, 357, 368
Aortic surgery, 408–409 Congenital heart disease (CHD), 14, 140, 142, 247, 277, 338–340,
Aortic valvular calcifications (AVC), 256, 265, 267 342, 343, 366, 396–398, 429–448, 475, 495, 522–525,
Arrhythmogenic right ventricular cardiomyopathy (ARVC), 222, 223, 532, 533
235, 470, 514–515 Contrast, 3, 29, 35, 48, 121, 134, 154, 160, 180, 191, 212, 222, 241,
Atherosclerosis, 3, 5, 7, 20, 101, 103–106, 108–112, 121–125, 264, 275, 296, 319, 341, 353, 402, 429, 456, 488, 508, 548
127–129, 157, 179, 212, 214, 229, 246, 307, 308, 310, Convolution kernel, 149, 151
320, 334, 355, 361, 362 Coronary angiography, 10, 13, 16, 18, 20, 21, 31, 33, 43, 63, 123, 140,
Atrial fibrillation, 12, 18, 19, 135, 150, 152, 192, 204, 251, 278, 285, 157, 161, 163–165, 167–171, 174, 179, 180, 183, 184, 212, 214,
455–469, 519, 520, 552, 555 217, 241, 243, 245, 248, 354, 355, 357, 363, 366–371, 385, 387,
487, 488, 491–494, 510, 521, 550, 551, 554
Coronary anomalies, 63, 172, 437, 439, 447–450, 489, 495
B Coronary artery bypass graft surgery, 51, 63, 212, 392, 421, 488
Bioprosthetic valves, 521 Coronary artery calcium (CAC), 5, 13, 62, 64, 102–110, 121,
Bypass grafts, 48, 51, 63, 139, 140, 155, 179–183, 212, 271, 304, 313, 127–128, 139, 140, 229, 353, 369, 382, 383, 508,
314, 362, 372, 392, 401, 421, 487, 488, 493, 494, 510 551–553, 555
Coronary artery calcium scanning, 13, 102, 103, 139, 355
Coronary artery disease, 3, 27, 48, 101, 121, 133, 147, 157, 179, 212,
C 222, 312, 349, 381, 437, 472, 487, 509, 545
Calcium scoring, 5, 7, 9, 39, 102–109, 115, 122, 124, 126, 128, 137, Coronary artery ostium, 394, 401, 417
139, 140, 217, 218, 242, 245, 551–553, 555 Coronary calcium, 5, 7, 10, 19–20, 101–103, 105, 106, 111, 171, 265,
Cardiac, 3, 25, 33, 48, 101, 121, 133, 147, 157, 180, 191, 212, 361, 368, 551, 553
222, 241, 257, 275, 297, 319, 349, 382, 391, 429, 455, Coronary computed tomography angiography (CCTA), 179, 550
487, 508, 545 CT angiography acquisition and protocol, 321
Cardiac computed tomography (CCT), 4–5, 7, 16–18, 20, 25–29, 31, CT coronary angiography (CTCA), 10, 13, 21, 140, 171, 212, 243,
35, 38, 39, 43–44, 121, 147–151, 154, 157, 171, 180, 191–195, 245, 365, 366, 491–493
199–207, 209, 222, 223, 225–229, 242, 246, 248, 277, 284, 298, CT radiation metrics, 34
337, 349–372, 498, 550–551, 554, 555 Curved multiplanar reformatted, 50, 52, 62, 63, 65, 142, 144, 324,
Cardiac electrophysiology, 455–478 398, 403, 408, 410, 424
Cardiac mass, 48, 275–292, 407, 495, 528–529
Cardiac metastases, 287, 288
Cardiac structure, 16, 133, 191–209, 391, 392, 422, 430, 456, 457, 510 D
Cardiac valve, 121, 127, 209, 241, 242 Delayed enhanced MDCT (DE-MDCT), 214
Cardiomyopathy, 115, 192, 214, 218, 222–224, 231–236, 246, 278, Detector coverage, 27, 320
363, 373, 401, 421, 474, 475, 510, 512–517, 521, 523 Diastolic function, 195, 199, 204

© Springer International Publishing 2016 561

M.J. Budoff, J.S. Shinbane (eds.), Cardiac CT Imaging: Diagnosis of Cardiovascular Disease,
DOI 10.1007/978-3-319-28219-0
562 Index

Dilated cardiomyopathy, 223, 232, 237, 246, 278, 474, 513, 514, 519 O
Dose modulation, 10, 18–21, 40, 41, 44, 321, 457 Orientation, 47–97, 161, 163, 172, 223, 324, 392, 393
Double-oblique, 159, 251, 399, 418 Orthogonal views, 209

E P
Effectiveness research, 381, 382, 384, 387 Paravalvular regurgitation (PAR), 259, 260, 265
Electrophysiology, 455–479, 514 Percutaneous coronary intervention (PCI), 167, 173, 179, 212, 304,
Emergency department (ED), 115, 363, 364, 382–385, 488, 549–556 362, 363, 369, 370, 372, 403, 487, 490, 491
Epicardial adipose tissue (EAT), 127, 463 Percutaneous pulmonary valve replacement, 395, 522
Pericardial, 48, 59, 199, 204, 207, 221–237, 277–279, 286, 287, 289,
322, 338, 342, 343, 400, 401, 407–408, 435, 446, 463, 466, 478,
G 516, 529–531, 533, 554
Gadolinium, 216, 225, 230, 233, 236, 284, 287, 316, 325, 328, 330, Peripheral angiogram, 317
333, 334, 421, 459, 474, 478, 508–525, 529, 532, 533 Peripheral CT, 154, 297–304, 309, 316
Peripheral CT angiogram, 154, 297–304, 309, 316
Peripheral vascular CT angiography, 297–298, 303
H Peripheral vascular disease, 111, 245, 303
Human immunodeficiency virus (HIV), 111, 127–129, 278, 342, 343 PET-MPI, 350, 353, 354, 368, 369, 372–374
Pitch, 6–9, 12, 13, 17, 19, 20, 27–30, 36–37, 42–43, 134–136,
149–152, 160, 162, 185, 320, 326, 551, 554
I Plaque, 3, 30, 53, 101, 121, 139, 148, 157, 199, 212, 229, 268, 299,
Image acquisition, 6–8, 13–16, 19, 30, 62, 64, 133–144, 160, 327, 355, 384, 394, 488, 510, 546
162, 171, 212, 222, 223, 232, 275, 321, 329, 394, 430, 456–457, Positron emission tomography (PET), 191, 212, 351, 353–355, 369,
474, 477, 509, 551 370, 374, 375
Primary prevention, 105–108, 110, 112, 488
Progression, 103, 114, 121–129, 179, 181, 237, 244, 255, 271, 325,
L 361, 511, 514
Left ventricle (LV), 4, 5, 9, 14, 49, 54, 55, 58, 60, 135, 191–193, Protocols, 7–9, 14, 15, 18, 19, 38, 39, 42, 102, 123, 136, 139,
195, 200, 212, 224, 229, 235, 249, 257, 264, 275, 277, 278, 157–161, 171, 181, 185–182, 199, 222, 237, 243, 248, 277, 284,
281, 338, 340, 400, 403–406, 432, 435, 436, 439–444, 447, 296, 321, 322, 325, 327–329, 351, 363, 373, 399, 430, 456, 457,
450, 456, 473, 475, 476, 478, 489, 501, 517, 519, 523, 525, 508, 509, 524
526, 529, 530, 554 Pulmonary arterial hypertension (PAH), 54, 55, 337–339, 341–343
Pulmonary artery, 16, 48, 139, 172, 191, 223, 242, 276, 337, 398, 431,
465, 489, 518,
M
Magnetic resonance imaging (MRI), 12, 193, 199, 204, 212, 214, 216,
222, 223, 227, 229–234, 236, 241, 242, 247, 281, 303, 307, 310, Q
314, 316, 319, 321, 322, 330, 333, 341, 509 Quality research, 381–383, 385
Maximum intensity projection (MIP), 62, 142, 154, 155, 159, 161,
163–165, 202, 207, 245, 257, 300–302, 311, 323, 328–330, 333,
402, 407, 409–415, 417, 422, 460, 489, 501 R
MDCT myocardial viability, 212, 214–217 Radiation, 3, 25, 33, 53, 104, 129, 134, 149, 160, 181, 199, 212, 241,
Mechanical prosthetic valves, 251, 401 277, 321, 350, 381, 397, 429, 457, 493, 508, 547
Mesenteric CT angiography, 319–335 Randomized trials, 115, 124, 128, 129, 256, 361, 364,
Methodology, 10, 12–14, 21, 39, 40, 102–104, 133–144, 340 382, 384–386
Minimally invasive robotic surgery, 392, 395 Reconstruction, 3, 25, 39, 47, 104, 147, 159, 180, 192, 215, 223, 245,
Mitral regurgitation, 224, 233, 241, 246–247, 396, 522 270, 298, 319, 351, 391, 430, 457, 492, 520, 550
Mitral stenosis, 243, 246, 248, 264, 278, 444, 522 Renal CT angiography, 327
Multicenter trial, 341, 357, 358, 363, 381–383, 550, 555 Restrictive cardiomyopathy, 223, 231, 234, 516, 517
Multidetector CT (MDCT), 6–10, 12–21, 102, 104, 123, 134, 136, Retrospective and prospective ECG gating, 8, 10, 27, 135, 149, 160,
181, 182, 191, 192, 199, 204, 205, 212–218, 246–249, 257–264, 199, 204, 222, 243, 248, 251, 275
270, 271, 322, 326–328, 333, 334, 551 Right heart catheterization, 338–340
Myocardial, 4, 30, 48, 106, 121, 141, 164, 181, 191, 212, 222, 275, Right ventricle, 4, 48, 158, 192, 222, 242, 276, 337, 392, 430, 456,
308, 350, 382, 400, 430, 457, 488, 508, 545 501, 507
Myocardial fibrosis, 212, 214–217, 233, 278, 472, 474, 513, Risk factors, 20, 35, 101–112, 122, 125, 127, 139, 140, 214, 268, 270,
514, 516, 517 309, 334, 360–362, 365, 489, 491
Myocardial perfusion imaging (MPI), 173, 174, 214, 351, 362, 363, Risk prediction, 110, 111
368, 370, 550, 560
Myxoma, 193, 277, 278, 281, 286–287, 289, 291, 292, 422,
438, 529, 531, 532 S
Scanning parameters, 37, 39
Scan protocols, 38, 248, 322, 325
N Scan speed, 9, 25, 27, 320
Non-invasive angiography, 6, 487, 491 Serial CT imaging, 72
Index 563

Single photon emission computed tomography (SPECT), 161, 167, Takotsubo cardiomyopathy, 236, 517–518
191, 199, 204, 212, 214, 351–355, 357, 359, 363, 364, 368–376, Temporal resolution, 6–8, 10–13, 16–17, 21, 25–29, 31, 43, 134, 147,
402, 512 149, 152, 153, 157, 174, 181, 212, 222, 242, 246–248, 257, 268,
Sinus of Valsalva (SOV), 50, 61, 265, 266, 447, 448 299, 320, 321, 334, 430, 551
Spatial resolution, 3, 5, 6, 9, 14–17, 21, 25, 26, 29, 44, 134, 141, Thrombus, 4, 53, 56, 169, 193, 194, 223, 236, 246, 247, 251, 276–278,
147–149, 153, 154, 157, 161, 164, 214, 217, 222, 223, 227, 229, 280, 281, 283–286, 301, 304, 310, 319, 323–326, 331, 340–342,
242, 251, 297, 310, 314, 316, 326, 327, 330, 333, 334, 398, 433, 392, 395, 401, 406, 408, 422, 446, 467–469, 474, 517, 520, 521,
434, 459, 520, 529, 551, 555 529–532, 550
SPECT-MPI, 351–355, 359, 362–364, 368–369, 373, 374 Trans-aortic valve replacement (TAVR), 242, 244–246, 251, 267, 495
Statins, 108, 113, 122–126, 128, 368, 382 Transcatheter aortic valve implantation (TAVI), 255–268, 392–394,
Stenosis, 6, 57, 104, 123, 140, 154, 157, 179, 209, 212, 241, 255, 278, 521, 522
298, 321, 337, 353, 384, 392, 433, 457, 487, 505 Transesophageal echocardiography (TEE), 242, 248, 255, 258–260,
Stents, 3, 113, 151, 183–182, 212, 213, 299, 302–304, 310–314, 323, 325, 284, 322, 429, 438, 521
326, 332, 354, 370, 399, 437, 444, 488, 491, 493, 499, 500
Stress CT perfusion, 368
Systemic arterial disease, 303, 314–315 V
Systolic function, 195, 223, 231, 234, 338, 343, 430 Vascular CT angiography, 297–298, 303–305
Ventricular tachycardia, 474–475, 512, 514, 519, 525
Volume-rendered, 9, 52–53, 62, 66, 141, 142, 154–155, 159, 202, 207,
T 224, 228, 244, 248, 257, 303, 305, 306, 310, 312–314, 321,
T1, 459, 508, 512–517, 520, 524, 529, 531 324–327, 329, 331, 332, 393, 418, 431, 434, 438, 462, 465, 475,
T2, 225, 508, 512, 513, 515–517, 529, 531 476, 520