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Netter’s
Cardiology
2nd edition

Edited by

MARSCHALL S. RUNGE, MD, PhD

GEORGE A. STOUFFER, MD
CAM PATTERSON, MD, MBA
Illustrations by Frank H. Netter, MD

CONTRIBUTING ILLUSTRATORS
Carlos A. G. Machado, MD
John A. Craig, MD
David J. Mascaro, MS
Enid Hatton
Steven Moon, MA
Kip Carter, MS, CMI
Tiffany S. DaVanzo, MA, CMI
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

NETTER’S CARDIOLOGY, SECOND EDITION ISBN: 978-1-4377-0637-6

ISBN (online): 978-1-4377-0638-3

Copyright © 2010 by Saunders, an imprint of Elsevier Inc.

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by
any means, electronic or mechanical, including photocopying, recording, or any information storage and
retrieval system, without permission in writing from the Publisher. Details on how to seek permission,
further information about the Publisher’s permissions policies and our arrangements with organizations
such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our
Web site: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).

Notices

Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration
of administration, and contraindications. It is the responsibility of practitioners, relying on their own
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To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.

Previous edition copyrighted 2004

Library of Congress Cataloging-in-Publication Data

Netter’s cardiology / edited by Marschall S. Runge, George A. Stouffer, Cam Patterson ; illustrations by
Frank H. Netter ; contributing illustrator, Carlos A. G. Machado.—2nd ed.
p. ; cm.
Other title: Cardiology
Includes bibliographical references and index.
ISBN 978-1-4377-0637-6
1. Cardiology. 2. Cardiovascular system—Diseases. I. Runge, Marschall S.
II. Stouffer, George A. III. Patterson, Cam. IV. Netter, Frank H. (Frank Henry), 1906-1991.
V. Title: Cardiology.
[DNLM: 1. Cardiovascular Diseases. 2. Diagnostic Techniques, Cardiovascular. WG 120 N474 2011]
RC667.N47 2011
616.1′2—dc22
2010005892

Netter Director: Anne Lenehan

Editor: Elyse O’Grady
Editorial Assistant: Julie Goolsby
Project Manager: David Saltzberg
Design Manager: Steven Stave
Illustrations Manager: Karen Giacomucci Working together to grow
Marketing Manager: Jason Oberacker libraries in developing countries
Printed in China www.elsevier.com | www.bookaid.org | www.sabre.org

Last digit is the print number: 9 8 7 6 5 4 3 2 1

About the Editors

Marschall S. Runge, MD, PhD, was born in Austin, Texas, clinical and basic science research. His basic science research is
and was graduated from Vanderbilt University with a BA in in the areas of regulation of smooth muscle cell growth, the role
General Biology and a PhD in Molecular Biology. He received of the smooth muscle cytoskeleton in regulating signaling path-
his medical degree from the Johns Hopkins School of Medicine ways, thrombin generation, and renal artery stenosis.
and trained in internal medicine at Johns Hopkins Hospital. He Cam Patterson, MD, MBA, was born in Mobile, Alabama.
was a cardiology fellow and junior faculty member at Massachu- He was a Harold Sterling Vanderbilt Scholar and studied Psy-
setts General Hospital. Dr. Runge’s next position was at Emory chology and English at Vanderbilt University, graduating
University, where he directed the Cardiology Fellowship Train- summa cum laude. He participated in the Honors Research
ing Program. He then moved to the University of Texas Medical Program at Vanderbilt and conducted research in behavioral
Branch in Galveston, where he was Chief of Cardiology and pharmacology during that time. Dr. Patterson attended Emory
Director of the Sealy Center for Molecular Cardiology. He University School of Medicine, graduating with induction in the
came to the University of North Carolina (UNC) in 2000 as Alpha Omega Alpha Honor Society, and completed his resi-
Chair of the Department of Medicine. He is currently the dency in Internal Medicine at Emory University Hospitals. He
Charles Addison and Elizabeth Ann Sanders Distinguished Pro- became the youngest-ever Chief Resident at Grady Memorial
fessor of Medicine and Chair of the Department of Medicine. Hospital at Emory University in 1992, supervising over 200
In addition, in 2004, Dr. Runge was appointed President of house officers in four hospitals. He completed 3 years of research
UNC Physicians and Vice Dean for Clinical Affairs. Dr. Runge fellowship under the guidance of Edgar Haber at the Harvard
is board-certified in internal medicine and cardiovascular dis- School of Public Health, developing an independent research
eases and has spoken and published widely on topics in clinical program in vascular biology and angiogenesis that was sup-
cardiology and vascular medicine. He maintains an active clini- ported by a National Institutes of Health fellowship. In 1996,
cal practice in cardiovascular diseases and medicine in addition he accepted his first faculty position at the University of Texas
to his teaching and administrative activities in the Department Medical Branch, and in 2000, Dr. Patterson was recruited to the
of Medicine and the UNC School of Medicine. University of North Carolina at Chapel Hill to become the
George A. Stouffer, MD, was born in Indiana, Pennsylva- founding director of the UNC McAllister Heart Institute. In
nia, and was graduated from Bucknell University and the Uni- 2005, he also became Chief of the Division of Cardiology at
versity of Maryland School of Medicine. He completed his UNC. Dr. Patterson is the Ernest and Hazel Craige Distin-
internal medicine residency, cardiology fellowship, and inter- guished Professor of Cardiovascular Medicine, and he has been
ventional cardiology fellowship at the University of Virginia. recognized at UNC with the Ruth and Phillip Hettleman Prize
During his cardiology fellowship, he completed a 2-year National for Artistic and Scholarly Achievement. He is an Established
Institutes of Health research fellowship in the laboratory of Gary Investigator of the American Heart Association and a Burroughs
Owens at the University of Virginia. He was on the faculty at the Wellcome Fund Clinical Scientist in Translational Research.
University of Texas Medical Branch from 1995 to 2000, where He is a member of several editorial boards, including Circulation
he became an associate professor and served as Co-Director of and Journal of Clinical Investigation, and is an elected member of
Clinical Trials in the Cardiology Division and as Associate the American Society of Clinical Investigation and the Associa-
Director of the Cardiac Catheterization Laboratory. He joined tion of University Cardiologists. Dr. Patterson maintains active
the faculty at the University of North Carolina in 2000 and cur- research programs in the areas of angiogenesis and vascular
rently serves as the Henry A. Foscue Distinguished Professor of development, cardiac hypertrophy, protein quality control, and
Medicine and Director of the Cardiac Catheterization Labora- translational genomics and metabolomics. He is also the direc-
tory. Dr. Stouffer’s main focus is clinical cardiology with an tor of the Cardiac Genetics Clinic. He received his MBA from
emphasis on interventional cardiology, but he is also involved in the UNC Kenan-Flagler School of Business in 2008.
Preface

The first edition of Netter’s Cardiology was an effort to present lead to patient harm. We also added boxes and algorithms that
to clinicians the ever-increasing amount of medical information provide in an easy-to-read format quick overviews of critical
on cardiovascular diseases in a concise and highly visual format. diagnostic and therapeutic information covered in the text. (See
The challenge that clinicians face in “keeping up” with the the sample algorithm on the following page.) References are
medical literature has continued to grow in the 5 years since the annotated in the second edition of Netter’s Cardiology to guide the
first edition of Netter’s Cardiology. This need to process the ever- reader to a more in-depth review, if considered necessary. As in
expanding medical information base and apply new findings to the first edition, the contributing authors have taken advantage
the optimal care of patients is acute in all areas of medicine, but of the genius of Frank Netter by carefully selecting the best of
perhaps it is most challenging in disciplines that require practi- his artwork to illustrate the most important clinical concepts
tioners to understand a broad spectrum of evidence-based medi- covered in each chapter. When Netter artwork was unavailable
cine, such as the field of cardiovascular diseases. The explosion or difficult to apply to illustrate modern clinical concepts, we
of medical knowledge is also a very real educational issue for again utilized the great artistic talents of Carlos A. G. Machado,
learners at all levels—students, residents, practicing physicians— MD, to create new artwork or to skillfully edit and update some
who must rapidly determine what is and is not important, orga- of Frank Netter’s drawings. The combination of Dr. Machado’s
nize the key information, and then apply these principles outstanding skills as a medical artist and his knowledge of the
effectively in clinical settings. medical concepts being illustrated was an invaluable asset.
For the second edition of Netter’s Cardiology, our goal was As in the first edition, we chose to use authors from the
to produce an improved text that keeps these issues in clear University of North Carolina School of Medicine at Chapel
focus and also addresses important clinical areas that were Hill or those with close ties to the university. This allowed us
not well covered in the first edition or in many other cardiol- to select authors who are clinical authorities, many of whom
ogy texts. To accomplish this expansion while maintaining a are also well known for their national and international contri-
concise text that could be used as a ready reference, we again butions. All have active clinical practices that require daily use
avoided exhaustive treatment of topics. We also have made of the information covered in their chapters, and all are well
every effort to present the essential information in a reader- aware of the approach to patient management utilized by their
friendly format that increases the reader’s ability to learn the peers at other institutions and in other practice settings. Many
key facts without getting lost in details that can obfuscate the of the contributing authors of the first edition have continued
learning process. on as second-edition authors and have provided updates. Each
After a careful review of reader comments about the first author, whether a previous contributor or not, was given
edition, we made some substantial changes to achieve our clearly defined guidelines that emphasized the need to distill
educational goals. Chapters were added and topics expanded to the large amount of complex information in his or her field and
address reader concerns about the lack of coverage of a number to present it concisely in a carefully prescribed format main-
of important topics commonly encountered in clinical practice. tained across all chapters. The result is a text that is truly clini-
Examples include these new chapters: Chest Radiography, cally useful and less of a compendium than is commonly the
Echocardiography, Stress Testing and Nuclear Imaging, Car- case in many medical texts.
diac Computed Tomography and Magnetic Resonance Imaging, We believe that the changes we have made in the second
Left and Right Heart Catheterization, Identifying the Patient at edition substantially improve Netter’s Cardiology and ensure that
High Risk for Acute Coronary Syndrome: Plaque Rupture and it will continue to be a highly useful resource for all physicians,
“Immediate Risk,” Cardiogenic Shock after Myocardial Infarc- both generalists and subspecialists, who need to remain current
tion, Stress-Induced Cardiomyopathy, Supraventricular Tachy- in cardiology—from trainees to experienced practitioners.
cardia, Sleep Disorders and the Cardiovascular System, Whether we have succeeded will obviously be determined by
Cardiovascular Toxicity of Noncardiac Medications, and Sudden our readers. Based on our experience with the revision of
Cardiac Death in Athletes. The chapter subheadings of “Opti- the first edition, we welcome the comments, suggestions, and
mum Treatment” and “Avoiding Treatment Errors” are new criticisms of readers that will help us improve future editions of
additions that address concerns about therapeutic errors that can this work.
vi Preface

Algorithms have been color coded for quick reference.

Algorithm for Evaluating Patients in Whom

Renal Artery Stenosis Is Suspected

Clinical findings associated with renal artery stenosis

Present Absent

Noninvasive evaluation Follow clinically

(duplex ultrasonography of renal Treat risk factors
arteries, magnetic resonance
angiography, or computed Orange  test
tomographic angiography)

Renal artery stenosis present Renal artery stenosis absent Blue  all other

Nuclear imaging Follow clinically

to estimate fractional Treat risk factors
flow to each kidney

Unilateral renal artery Unilateral renal artery Bilateral renal artery

stenosis and asymmetric stenosis and symmetric stenosis present
perfusion present perfusion present

Follow clinically Green  treatment options

Treat risk factors

Consider revascularization

Marschall S. Runge, MD, PhD Cam Patterson, MD, MBA

Charles Addison and Elizabeth Ann Sanders Ernest and Hazel Craige Distinguished Professor of Medicine
Distinguished Professor of Medicine Professor of Medicine, Pharmacology, and Cell
Professor and Chair, Department of Medicine and Developmental Biology
The University of North Carolina School of Medicine Chief, Division of Cardiology
Chapel Hill, North Carolina Director, UNC McAllister Heart Institute
Associate Chair for Research, Department of Medicine
George A. Stouffer, MD The University of North Carolina School of Medicine
Henry A. Foscue Distinguished Professor of Medicine Chapel Hill, North Carolina
Chief of Clinical Cardiology
Director, C.V. Richardson Cardiac
Catheterization Laboratory
Director, Interventional Cardiology
Division of Cardiology
The University of North Carolina School of Medicine
Chapel Hill, North Carolina
About the Artists

Frank H. Netter, MD of choice among medical and health professions students the
Frank H. Netter was born in 1906 in New York City. He world over.
studied art at the Art Student’s League and the National The Netter illustrations are appreciated not only for their
Academy of Design before entering medical school at New York aesthetic qualities but, more importantly, for their intellectual
University, where he received his MD degree in 1931. During content. As Dr. Netter wrote in 1949, “clarification of a subject
his student years, Dr. Netter’s notebook sketches attracted the is the aim and goal of illustration. No matter how beautifully
attention of the medical faculty and other physicians, allowing painted, how delicately and subtly rendered a subject may be, it
him to augment his income by illustrating articles and text- is of little value as a medical illustration if it does not serve to
books. He continued illustrating as a sideline after establishing make clear some medical point.” Dr. Netter’s planning, concep-
a surgical practice in 1933, but he ultimately opted to give up tion, point of view, and approach are what inform his paintings
his practice in favor of a full-time commitment to art. After and what makes them so intellectually valuable.
service in the United States Army during World War II, Dr. Frank H. Netter, MD, physician and artist, died in 1991.
Netter began his long collaboration with the CIBA Pharmaceu- Learn more about the physician–artist whose work has
tical Company (now Novartis Pharmaceuticals). This 45-year inspired the Netter Reference Collection: www.netterimages.
partnership resulted in the production of the extraordinary col- com/artist/netter.htm.
lection of medical art so familiar to physicians and other medical
professionals worldwide. Carlos A. G. Machado, MD
In 2005, Elsevier Inc. purchased the Netter Collection Carlos A. G. Machado was chosen by Novartis to be Dr. Net-
and all publications from Icon Learning Systems. Now ter’s successor. He continues to be the main artist who contrib-
over 50 publications featuring the art of Dr. Netter are avail- utes to the Netter Collection of Medical Illustrations.
able through Elsevier Inc. (in the United States: www. Self-taught in medical illustration, cardiologist Carlos A. G.
us.elsevierhealth.com/Netter; outside the United States: www. Machado has contributed meticulous updates to some of Dr.
elsevierhealth.com). Netter’s original plates and has created many paintings of his
Dr. Netter’s works are among the finest examples of the use own in the style of Netter as an extension of the Netter Collec-
of illustration in the teaching of medical concepts. The 13-book tion. Dr. Machado’s photorealistic expertise and his keen insight
Netter Collection of Medical Illustrations, which includes the into the physician–patient relationship inform his vivid and
greater part of the more than 20,000 paintings created by Dr. unforgettable visual style. His dedication to researching each
Netter, has become one of the most famous medical works ever topic and subject he paints places him among the premier
published. The Netter Atlas of Human Anatomy, first published medical illustrators at work today.
in 1989, presents the anatomic paintings from the Netter Col- Learn more about his background and see more of his art at:
lection. Now translated into 16 languages, it is the anatomy atlas www.netterimages.com/artist/machado.htm.
Acknowledgments

This second edition of Netter’s Cardiology benefited enormously Julie Goolsby at Elsevier were instrumental in helping us make
from the hard work and talent of many dedicated individuals. a very good first edition more comprehensive and more focused
First, we thank the contributing authors. All are current or in its second edition.
former faculty members at the University of North Carolina We are also indebted to Ms. Angela Clotfelter-Rego, whose
School of Medicine, Chapel Hill, or have close ties to the insti- superb organizational skills helped make this text a reality.
tution. Without their intellect, dedication, and drive for excel- Special thanks go to Carolyn Kruse for excellent editing and Dr.
lence, Netter’s Cardiology, 2nd edition, could not have been Deborah Montague for invaluable reviewing and updating of
published. We had a solid foundation on which to build the the pharmacologic information.
second edition, thanks to the hard work of the first-edition We would especially like to acknowledge our families: our
contributing authors, many of whom we were fortunate to have wives—Susan Runge, Meg Stouffer, and Kristine Patterson—
continue on to this edition. We are also grateful for the invalu- whose constant support, encouragement, and understanding
able editorial contribution that Dr. E. Magnus Ohman made to made completion of this text possible; our children—Thomas,
the first edition. Elizabeth, William, John, and Mason Runge; Mark, Jeanie,
Special recognition goes to John A. Craig, MD, and Carlos Joy, and Anna Stouffer; and Celia, Anna Alyse, and Graham
A. G. Machado, MD. They are uniquely talented physician– Patterson—who inspire us and remind us that there is life
artists who, through their work, brought to life important con- beyond the computer; and, finally, our parents—whose persis-
cepts in medicine in the new and updated figures included in tence, commitment, and work ethic got us started on this road
this text. Anne Lenehan, Elyse O’Grady, Marybeth Thiel, and many, many years ago.
Contributors

Marschall S. Runge, MD, PhD Sharon Ben-Or, MD

Charles Addison and Elizabeth Ann Sanders Distinguished Surgical Resident, Division of Cardiothoracic Surgery
Professor of Medicine University of North Carolina School of Medicine
Professor and Chair, Department of Medicine Chapel Hill, North Carolina
Division of Cardiology
University of North Carolina School of Medicine Christoph Bode, MD, PhD
Chapel Hill, North Carolina Professor of Medicine
Chairman of Medicine
George A. Stouffer, MD Department of Cardiology and Angiology
Henry A. Foscue Distinguished Professor of Medicine University of Freiburg
Chief of Clinical Cardiology Freiburg, Germany
Director, C.V. Richardson Cardiac Catheterization
Laboratory Mark E. Boulware, MD
Director, Interventional Cardiology Instructor of Medicine
Division of Cardiology Division of Cardiology
University of North Carolina School of Medicine University of North Carolina School of Medicine
Chapel Hill, North Carolina Chapel Hill, North Carolina

Michael E. Bowdish, MD
Cam Patterson, MD, MBA Assistant Professor of Surgery
Ernest and Hazel Craige Distinguished Professor Division of Cardiothoracic Surgery
of Medicine University of North Carolina School of Medicine
Professor of Medicine, Pharmacology, and Cell and Chapel Hill, North Carolina
Developmental Biology
Chief, Division of Cardiology Bruce R. Brodie, MD
Director, UNC McAllister Heart Institute Clinical Professor of Medicine
Associate Chair for Research, Department of Medicine University of North Carolina Teaching Service at
University of North Carolina School of Medicine Moses Cone Memorial Hospital
Chapel Hill, North Carolina Board Chairman, LeBauer Cardiovascular Research
Foundation
Charles Baggett, MD Greensboro, North Carolina
Instructor of Medicine
Division of Cardiology Scott H. Buck, MD
Texas A&M School of Medicine Associate Professor of Pediatrics
Scott and White Memorial Hospital Division of Pediatric Cardiology
Temple, Texas The North Carolina Children’s Heart Center
University of North Carolina School of Medicine
Chapel Hill, North Carolina
Frédérique Bailliard, MD, MS
Assistant Professor of Pediatrics Thomas Burchell, BSc, MBBS, MRCP
Medical Director, Children’s Intermediate Cardiac Cardiology Specialist Registrar
Care Unit Department of Cardiology
Director, Non-Invasive Pediatric Cardiac Imaging The London Chest Hospital
Division of Pediatric Cardiology London, England
The North Carolina Children’s Heart Center
University of North Carolina School of Medicine
Wayne E. Cascio, MD
Chapel Hill, North Carolina
Professor of Cardiovascular Science and Medicine
Vice-Chairman, Department of Cardiovascular Sciences
Thomas M. Bashore, MD Brody School of Medicine
Professor of Medicine Director of Research, East Carolina Heart Institute
Vice-Chief, Clinical Operations and Education East Carolina University
Duke University Medical Center Chief of Cardiology, Pitt County Memorial Hospital
Durham, North Carolina Greenville, North Carolina
xii Contributors

Nizar Chahin, MD Robert B. Devlin, PhD

Clinical Assistant Professor of Neurology Senior Scientist
Division of Neuromuscular Diseases Human Studies Division
University of North Carolina School of Medicine National Health and Environmental Effects Research
Chapel Hill, North Carolina Laboratory
U.S. Environmental Protection Agency
Patricia P. Chang, MD, MHS Research Triangle Park, North Carolina
Assistant Professor of Medicine
Adjunct Assistant Professor of Epidemiology Mary Anne Dooley, MD, MPH
Director, Heart Failure and Transplantation Program Associate Professor of Medicine
Division of Cardiology Division of Rheumatology, Allergy and Immunology
University of North Carolina School of Medicine Thurston Arthritis Research Center
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Christopher D. Chiles, MD
Assistant Professor of Medicine Allison G. Dupont, MD
Division of Cardiology Instructor of Medicine
Texas A&M School of Medicine Division of Cardiology
Scott and White Memorial Hospital University of North Carolina School of Medicine
Temple, Texas Chapel Hill, North Carolina

Eugene H. Chung, MD
Carla S. Dupree, MD, PhD
Assistant Professor of Medicine
Associate Professor of Medicine
Section of Cardiac Electrophysiology
Medical Director, University of North Carolina Hospitals
Division of Cardiology
Heart Center at Meadowmont
University of North Carolina School of Medicine
Division of Cardiology
Chapel Hill, North Carolina
Heart Failure Program
University of North Carolina School of Medicine
David R. Clemmons, MD
Chapel Hill, North Carolina
Professor of Medicine
Director, Diabetes Center for Excellence
Joseph J. Eron, MD
Division of Endocrinology and Metabolism
Professor of Medicine
University of North Carolina School of Medicine
Director, Clinical Core, UNC Center for AIDS Research
Chapel Hill, North Carolina
Division of Infectious Disease
University of North Carolina School of Medicine
Romulo E. Colindres, MD
Chapel Hill, North Carolina
Professor of Medicine
Division of Nephrology and Hypertension
University of North Carolina School of Medicine Gina T. Eubanks, BA
Chapel Hill, North Carolina Supervisor, Research Project Coordinator
Division of Cardiovascular Medicine
John L. Cotton, MD Emory University
Associate Professor of Pediatrics Atlanta, Georgia
Director, Pediatric Echocardiography Laboratory
Division of Pediatric Cardiology Mark A. Farber, MD
The North Carolina Children’s Heart Center Associate Professor of Surgery and Interventional Radiology
University of North Carolina School of Medicine Director, UNC Endovascular Institute
Chapel Hill, North Carolina Division of Vascular Surgery
University of North Carolina School of Medicine
Gregory J. Dehmer, MD Chapel Hill, North Carolina
Professor of Medicine
Texas A&M University College of Medicine Elizabeth Boger Foreman, MD
Director, Cardiology Division Resident, Department of Neurology
Scott & White Healthcare University of North Carolina School of Medicine
Temple, Texas Chapel Hill, North Carolina
 Contributors xiii

Elman G. Frantz, MD Milan J. Hazucha, PhD

Associate Professor of Pediatrics Research Professor of Medicine
Director, Pediatric Cardiac Catheterization Laboratory Division of Pulmonary and Critical Care Medicine
The North Carolina Children’s Heart Center Center for Environmental Medicine, Asthma and Lung
University of North Carolina School of Medicine Biology
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Markus Frey, MD
Assistant Professor of Medicine G. William Henry, MD
Department of Cardiology and Angiology Professor of Pediatrics
University of Freiburg Division of Pediatric Cardiology
Freiburg, Germany The North Carolina Children’s Heart Center
University of North Carolina School of Medicine
Anil K. Gehi, MD Chapel Hill, North Carolina
Assistant Professor of Medicine
Section of Cardiac Electrophysiology Alan L. Hinderliter, MD
Division of Cardiology Associate Professor of Medicine
University of North Carolina School of Medicine Division of Cardiology
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Leonard S. Gettes, MD
Distinguished Professor of Medicine–Emeritus
Parag Kale, MD
Division of Cardiology
Department of Heart Transplantation, Northern California
University of North Carolina School of Medicine
Kaiser Permanente
Chapel Hill, North Carolina
Affiliated Assistant Professor of Medicine
Division of Cardiology
Ajmal Masood Gilani, MD
Stanford University School of Medicine
Neurologist
Santa Clara, California
Johnson Neurology
Clayton, North Carolina
Blair A. Keagy, MD
Professor of Surgery
Lee R. Goldberg, MD
Chief, Division of Vascular Surgery
Cardiologist
University of North Carolina School of Medicine
Tucson Heart Hospital
Chapel Hill, North Carolina
Tucson Medical Center
Tucson, Arizona
Eileen A. Kelly, MD
Thomas R. Griggs, MD Director, Women’s Heart Program
Professor of Medicine and Pathology and Laboratory NorthShore University HealthSystem
Medicine Glenview, Illinois
Division of Cardiology Clinical Assistant Professor
University of North Carolina School of Medicine University of Chicago Pritzker School of Medicine
Chapel Hill, North Carolina Chicago, Illinois

Eileen M. Handberg, PhD J. Larry Klein, MD

Associate Professor of Medicine Professor of Medicine and Radiology
Director, Clinical Programs Director, Advanced Cardiac Imaging
Division of Cardiovascular Medicine Division of Cardiology
University of Florida University of North Carolina School of Medicine
Gainesville, Florida Chapel Hill, North Carolina

Emily E. Hass, MD Daniel J. Lenihan, MD

Instructor of Medicine Professor of Medicine
Section of Cardiac Electrophysiology Director, Clinical Research
Division of Cardiology Division of Cardiovascular Medicine
University of North Carolina School of Medicine Vanderbilt University
Chapel Hill, North Carolina Nashville, Tennessee
xiv Contributors

Fong T. Leong, PhD, MRCP Paula F. Miller, MD

Instructor of Medicine Clinical Associate Professor of Medicine
Section of Cardiac Electrophysiology Director, Cardiac Rehabilitation
Division of Cardiology Director, Women’s Heart Program
University of North Carolina School of Medicine Division of Cardiology
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina

James P. Loehr, MD Peter Mills, BM, Bch, BSc, FRCP

Associate Professor of Pediatrics Consultant Cardiologist
Division of Pediatric Cardiology Department of Cardiology
The North Carolina Children’s Heart Center The London Chest Hospital
University of North Carolina School of Medicine London, England
Chapel Hill, North Carolina
Timothy A. Mixon, MD
Tift Mann, MD Assistant Professor of Medicine
Interventional Cardiologist Texas A&M University College of Medicine
Director, Wake Heart Research Cardiology Division
Wake Heart Center Scott & White Healthcare
Raleigh, North Carolina Temple, Texas

Martin Moser, MD
Anthony Mathur, MB, BChir, FRCP, PhD Assistant Professor of Medicine
Consultant Cardiologist Department of Cardiology and Angiology
Department of Cardiology University of Freiburg
The London Chest Hospital Freiburg, Germany
London, England
J. Paul Mounsey, MD, PhD
Professor of Medicine
Matthew A. Mauro, MD Director, Cardiac Electrophysiology Service
Ernest H. Wood Professor of Radiology and Surgery Division of Cardiology
Professor and Chair, Department of Radiology University of North Carolina School of Medicine
University of North Carolina School of Medicine Chapel Hill, North Carolina
Chapel Hill, North Carolina
Timothy C. Nichols, MD
Professor of Medicine and Pathology and Laboratory
Robert Mendes, MD
Medicine
Assistant Professor of Surgery
Director, Francis Owen Blood Research Laboratory
Division of Vascular Surgery
Division of Cardiology
University of North Carolina School of Medicine
University of North Carolina School of Medicine
Chapel Hill, North Carolina
Chapel Hill, North Carolina

Venu Menon, MD E. Magnus Ohman, MD, FRCPI

Staff Cardiologist Professor of Medicine
Director, Coronary Care Unit Associate Director, Duke Heart Center—Cardiology Clinics
Cleveland Clinic Director, Program for Advanced Coronary Disease
Cleveland, Ohio Duke Clinical Research Institute
Duke University Medical Center
Durham, North Carolina
Michael R. Mill, MD
Professor of Surgery José Ortiz, MD
Chief, Division of Cardiothoracic Surgery Section Chief, Cardiology
Director, Heart-Lung Transplant Program Louis Stokes Cleveland VA Medical Center
Director, UNC Comprehensive Transplant Center Assistant Professor of Medicine
Program Director, Cardiothoracic Surgery Residency Division of Cardiology
Program Case Western Reserve University and University Hospitals
University of North Carolina School of Medicine Case Medical Center
Chapel Hill, North Carolina Cleveland, Ohio
 Contributors xv

Kristine B. Patterson, MD Brett C. Sheridan, MD

Assistant Professor of Medicine Associate Professor of Surgery
Division of Infectious Disease Director, Heart Transplant Program
University of North Carolina School of Medicine Division of Cardiothoracic Surgery
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Blair Robinson, MD
Associate Professor of Pediatrics Ross J. Simpson, Jr., MD, PhD
Division of Pediatric Cardiology Professor of Medicine
The North Carolina Children’s Heart Center Director, Lipid and Prevention Clinics
University of North Carolina School of Medicine Division of Cardiology
Chapel Hill, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Hanna K. Sanoff, MD
Assistant Professor of Medicine Sidney C. Smith, Jr., MD
Division of Hematology and Oncology Professor of Medicine
Lineberger Comprehensive Cancer Center Division of Cardiology
University of North Carolina School of Medicine University of North Carolina School of Medicine
Chapel Hill, North Carolina Chapel Hill, North Carolina
Richard S. Schofield, MD Mark A. Socinski, MD
Professor of Medicine Professor of Medicine
Division of Cardiovascular Medicine Division of Hematology and Oncology
University of Florida Multidisciplinary Thoracic Oncology Program
Chief, Cardiology Section Lineberger Comprehensive Cancer Center
North Florida/South Georgia Veterans Health System University of North Carolina School of Medicine
Gainesville, Florida Chapel Hill, North Carolina
Kimberly A. Selzman, MD, MPH
Joseph Stavas, MD
Assistant Professor of Medicine
Associate Professor of Radiology
Director of Electrophysiology
University of North Carolina School of Medicine
George E. Wahlen Department of Veterans Affairs Medical
Chapel Hill, North Carolina
Center
Salt Lake City, Utah
Steven R. Steinhubl, MD
Jay D. Sengupta, MD Cardiologist
Instructor of Medicine Vice-President Global Medical, Thrombosis
Cleveland Clinic The Medicines Company
Cleveland, Ohio Zurich, Switzerland
Adjunct Faculty
Richard G. Sheahan, MD Geisinger Center for Health Research
Consultant Cardiologist/Electrophysiologist Danville, Pennsylvania
Beaumont Hospital and Royal College of Surgeons in Ireland
Dublin, Ireland Robert D. Stewart, MD, MPH
Assistant Professor of Surgery
Arif Sheikh, MD Division of Cardiothoracic Surgery
Assistant Professor of Radiology University of North Carolina School of Medicine
Director, Cardiovascular Nuclear Medicine and Targeted Chapel Hill, North Carolina
Radionuclide Therapy
Section of Nuclear Medicine and Division of General Susan Lyon Stone, MS
Medicine Environmental Health Scientist
University of North Carolina School of Medicine Human Studies Division
Chapel Hill, North Carolina U.S. Environmental Protection Agency
Research Triangle Park, North Carolina
David S. Sheps, MD, MSPH
Professor of Medicine Luis A. Tamara, MD
Division of Cardiovascular Medicine Staff Nuclear Medicine Physician
Emory University Division of Nuclear Medicine
Staff Cardiologist, Atlanta Veterans Health System Veterans Administration Medical Center
Atlanta, Georgia Bay Pines, Florida
xvi Contributors

Walter A. Tan, MD, MS Richard A. Walsh, MD

Associate Professor of Medicine John H. Hord Professor of Medicine
Clinical Associate Professor of Surgery Professor and Chairman, Department of Medicine
Director of Stroke Interventions Physician-in-Chief, University Hospitals Health System
Associate Director, Cardiac Catheterization Laboratories Case Western Reserve University and University Hospitals
Department of Cardiovascular Sciences Case Medical Center
The Brody School of Medicine Cleveland, Ohio
East Carolina University
Greenville, North Carolina Park W. Willis IV, MD
Sarah Graham Kenan Distinguished Professor of Medicine
David A. Tate, MD and Pediatrics
Associate Professor of Medicine Director, Cardiac Ultrasound Laboratories
Division of Cardiology Division of Cardiology
University of North Carolina School of Medicine University of North Carolina School of Medicine
Chapel Hill, North Carolina Chapel Hill, North Carolina

Georgeta Vaidean, MD, MPH, PhD Willis Wu, MD

Associate Professor of Epidemiology and Health Outcomes Instructor of Medicine
Touro College of Pharmacy Department of Cardiovascular Medicine
New York, New York Cleveland Clinic
Cleveland, Ohio
Bradley V. Vaughn, MD
Professor of Neurology and Biomedical Engineering Eric H. Yang, MD
Vice-Chair, Department of Neurology Assistant Professor of Medicine
Chief, Division of Sleep and Epilepsy Division of Cardiology
University of North Carolina School of Medicine University of North Carolina School of Medicine
Chapel Hill, North Carolina Chapel Hill, North Carolina

John Paul Vavalle, MD Andrew O. Zurick III, MD

Instructor of Medicine Instructor of Medicine
Duke University Medical Center Division of Cardiology
Durham, North Carolina University of North Carolina School of Medicine
Chapel Hill, North Carolina
Kinga Vereczkey-Porter, MD
Clinical Assistant Professor of Medicine
Division of Rheumatology, Allergy and Immunology
Thurston Arthritis Research Center
University of North Carolina School of Medicine
Chapel Hill, North Carolina
The History and Physical Examination
Marschall S. Runge, E. Magnus Ohman, and George A. Stouffer 1
T he ability to determine whether disease is present or
absent—and how that patient should be treated—is the
ultimate goal for clinicians evaluating patients with suspected
The History
A wealth of information is available to clinicians who carefully
heart disease. Despite the number of diagnostic tests available, assess the patient’s history. Key components are assessment
never has the importance of a careful history and physical exami- of the chief complaint; careful questioning for related, often
nation been greater. Opportunities for error in judgment are subtle symptoms that may further define the chief complaint;
abundant, and screening patients for coronary risk using a broad and determination of other factors that help categorize the
and unfocused panel of laboratory and noninvasive tests can lead likelihood of disease. Major symptoms of heart patients
to incorrect diagnoses and unnecessary testing. Selection of the include chest discomfort, dyspnea, palpitations, and syncope or
most appropriate test and therapeutic approach for each patient presyncope.
is based on a skillfully performed history and physical examina-
tion. Furthermore, interpretation of any test results is based on
Chest Discomfort
the prior probability of disease, which again is based on the
history and physical. While entire texts have been written on Determining whether chest discomfort results from a cardiac
cardiac history and physical examination, this chapter specifi- cause is often a challenge. The most common cause of chest
cally focuses on features of the cardiac history and the cardio- discomfort is myocardial ischemia, which produces angina pec-
vascular physical examination that help discern the presence or toris. Many causes of angina exist, and the differential diagnosis
absence of heart disease. for chest discomfort is extensive (Box 1-1). Angina that is repro-
ducible and constant in frequency and severity is often referred
to as stable angina. For the purposes of this chapter, stable angina
The Concept of Prior Probability is a condition that occurs when CAD is present and coronary
The history and physical examination should allow the clinician blood flow cannot be increased to accommodate for increased
to establish the prior probability of heart disease—that is, the myocardial demand. However, as discussed in Chapters 12
likelihood that the symptoms reported by the patient result from through 14, there are many causes of myocardial ischemia,
heart disease. A reasonable goal is to establish a patient’s risk of including fixed coronary artery stenoses and endothelial dys-
heart disease as “low,” “intermediate,” or “high.” One demon- function, which leads to reduced vasodilatory capacity.
stration of this principle in clinical medicine is the assessment A description of chest discomfort can help establish whether
of patients with chest pain, in which the power of exercise stress the pain is angina or of another origin. First, characterization
testing to accurately diagnose coronary heart disease (CHD) of the quality and location of the discomfort is essential (Fig.
depends on the prior probability of disease. In patients with a 1-1). Chest discomfort because of myocardial ischemia may be
very low risk of CHD based on clinical findings, exercise stress described as pain, a tightness, a heaviness, or simply an uncom-
testing resulted in a large number of false-positive test results. fortable and difficult-to-describe feeling. The discomfort can be
Because up to 15% of exercise stress tests produce positive localized to the mid-chest or epigastric area or may be charac-
results in individuals without CHD, use of this test in a low-risk terized as pain in related areas, including the left arm, both arms,
population can result in an adverse ratio of false-positive to the jaw, or the back. The radiation of chest discomfort to any
true-positive test results and unnecessary cardiac catheteriza- of these areas increases the likelihood of the discomfort being
tions. Conversely, in patients with a very high risk of CHD angina. Second, the duration of discomfort is important, because
based on clinical findings, exercise stress testing can result in chest discomfort due to cardiac causes generally lasts minutes.
false-negative test results—an equally undesirable outcome, Therefore, pain of very short duration (“seconds” or “moments”),
because patients with significant coronary artery disease (CAD) regardless of how typical it may be of angina, is less likely to be
and their physicians may be falsely reassured that no further of cardiac origin. Likewise, pain that lasts for hours, on many
evaluation or treatment is necessary. occasions, in the absence of objective evidence of myocardial
Emphasis is increasing on quantifying prior probability to an infarction (MI), is not likely to be of coronary origin. Third, the
even greater degree using various mathematical models. This is presence of accompanying symptoms should be considered.
a useful approach in teaching and may be clinically feasible in Chest discomfort may be accompanied by other symptoms
some diseases. However, for the majority of patients with sus- (including dyspnea, diaphoresis, or nausea), any of which
pected heart disease, categorizing risk as low, intermediate, and increase the likelihood that the pain is cardiac in origin. However,
high is appropriate, reproducible, and feasible in a busy clinical the presence of accompanying symptoms is not needed to define
practice. Therefore, obtaining the history and physical examina- the discomfort as angina. Fourth, factors that precipitate or
tion represents a key step before any testing, to minimize use of relieve the discomfort should be evaluated. Angina typically
inappropriate diagnostic procedures. occurs during physical exertion, during emotional stress, or in
4 SECTION I • Introduction

Box 1-1 Differential Diagnosis of Chest Discomfort involving platelet aggregation and clinically termed “unstable
angina” or “acute coronary syndrome” (see Chapters 13 and 14).
Cardiovascular Patients with heart disease need not present with chest pain
Ischemic at all. Anginal equivalents include dyspnea during exertion,
• Hyperthyroidism
abdominal discomfort, fatigue, or decreased exercise tolerance.
• Tachycardia (e.g., atrial fibrillation)
• Coronary spasm
Clinicians must be alert to and specifically ask about these symp-
• Coronary atherosclerosis (angina pectoris) toms. Often, a patient’s family member or spouse notices subtle
• Acute coronary syndrome changes in endurance in the patient or that the individual no
• Aortic stenosis longer performs functions that require substantial physical
• Hypertrophic cardiomyopathy effort. Sometimes patients may be unable to exert themselves
• Aortic regurgitation due to comorbidities. For instance, the symptoms of myocardial
• Mitral regurgitation
ischemia may be absent in patients with severe peripheral vas-
• Severe systemic hypertension
• Severe right ventricular/pulmonary hypertension cular disease who have limiting claudication. One should also
• Severe anemia/hypoxia be attuned to subtle or absent symptoms in individuals with
Nonischemic diabetes mellitus (including type 1 and type 2 diabetes), a “coro-
• Aortic dissection nary risk equivalent” as defined by the Framingham Risk
• Pericarditis Calculator.
• Mitral valve prolapse syndrome: autonomic dysfunction When considering the likelihood that CHD accounts for a
Gastrointestinal patient presenting with chest discomfort or any of the afore-
• Gastroesophageal reflux disease
mentioned variants, assessment of the cardiac risk factor profile
• Esophageal spasm is important. The Framingham Study first codified the concept
• Esophageal rupture of cardiac risk factors, and over time, quantification of risk using
• Hiatal hernia these factors has become an increasingly useful tool in clinical
• Cholecystitis medicine. Cardiac risk factors determined by the Framingham
Pulmonary Study include a history of cigarette smoking, diabetes mellitus,
• Pulmonary embolus hypertension, or hypercholesterolemia; a family history of CHD
• Pneumothorax (including MI, sudden cardiac death, and first-degree relatives
• Pneumonia having undergone coronary revascularization); age; and sex
• Chronic obstructive pulmonary disease (male). Although an attempt has been made to rank these risk
• Pleurisy factors, all are important, with a history of diabetes mellitus
Neuromusculoskeletal being perhaps the single most important factor. Subsequently,
• Thoracic outlet syndrome a much longer list of potential predictors of cardiac risk has been
• Degenerative joint disease of the cervical or thoracic made (Box 1-3). An excellent, easy-to-use model for predicting
spine risk is the Framingham Risk Calculator, as described in the
• Costochondritis Adult Treatment Panel III guidelines from the National Heart,
• Herpes zoster Lung and Blood Institute (see “Evidence” section).
Psychogenic Symptoms suggestive of vascular disease require special
• Anxiety attention. Peripheral vascular disease may mask CHD, because
• Depression the individual may not be able to exercise sufficiently to provoke
• Cardiac psychosis angina. A history of stroke, transient ischemic attack, or athero-
• Self-gain embolism in any vascular distribution is usually evidence of
significant vascular disease. Sexual dysfunction in men is not an
other circumstances of increased myocardial oxygen demand. uncommon presentation of peripheral vascular disease. The
When exercise precipitates chest discomfort, relief after cessa- presence of Raynaud’s-type symptoms should also be elicited,
tion of exercise substantiates the diagnosis of angina. Sublingual because such symptoms suggest abnormal vascular tone and
nitroglycerin also relieves angina, generally over a period of function, and increase the risk that CHD is present.
minutes. Instant relief or relief after longer periods lessens the Determining whether the patient has stable or unstable
likelihood that the chest discomfort was angina. angina is as important as making the diagnosis of angina. Stable
Although the presence of symptoms during exertion is angina is important to evaluate and treat, but does not neces-
important in assessing CHD risk, individuals, especially seden- sitate emergent intervention. Unstable angina, or acute coro-
tary ones, may have angina-like symptoms that are not related nary syndrome, however, carries a significant risk of MI or death
to exertion. These include postprandial and nocturnal angina or in the immediate future. The types of symptoms reported by
angina that occurs while the individual is at rest. As described patients with stable and unstable angina differ little, and the risk
herein, “rest-induced angina,” or the new onset of angina, con- factors for both are identical. Indeed, the severity of symptoms
notes a pathophysiology different from effort-induced angina. is not necessarily greater in patients with unstable angina, just
Angina can also occur in persons with fixed CAD and increased as a lack of chest discomfort does not rule out significant CHD.
myocardial oxygen demand due to anemia, hyperthyroidism, or The important distinction between stable and unstable coronary
similar conditions (Box 1-2). Angina occurring at rest, or with syndromes rests in whether the onset is new or recent and/or
minimal exertion, may denote a different pathophysiology, one progressive (e.g., occurring more frequently or with less
 CHAPTER 1 • The History and Physical Examination 5

Most commonly radiates to

left shoulder and/or ulnar
aspect of left arm and hand

May also radiate to neck,

jaw, teeth, back, abdomen,
or right arm

Common
descriptions
of pain

Viselike Constricting Crushing weight

and/or pressure
Fear Perspiration

Other Shortness
manifestations of breath Nausea,
of myocardial vomiting
ischemia

Weakness, collapse, coma

Chiefly retrosternal and intense

Figure 1-1 Pain of myocardial ischemia.

exertion). The initial presentation of angina is, by definition, Finally, it is important to distinguish those patients who
unstable angina; although for a high percentage of individuals have noncoronary causes of chest discomfort from those with
this may merely represent the first recognizable episode of CHD. Patients with gastroesophageal reflux disease (GERD)
angina. For those with unstable angina, the risk of MI in the often present with symptoms that are impossible to distinguish
near future is markedly increased. Likewise, when the patient from angina. In numerous studies, GERD is the most common
experiences angina in response to decreased levels of exertion diagnosis in patients who undergo diagnostic testing for angina
or when exertional angina has begun to occur at rest, these and are found not to have CHD. The characteristics of the pain
urgent circumstances require immediate therapy. The treat- can be identical. Because exercise can increase intra-abdominal
ment of stable angina and acute coronary syndrome is discussed pressure, GERD may be exacerbated with exercise, especially
in Chapters 12, 13, and 14. The Canadian Cardiovascular after meals. Symptoms from GERD can also be relieved with
Society Functional Classification of Angina Pectoris is a useful use of sublingual nitroglycerin. GERD can also result in
guide for everyday patient assessment (Box 1-4). Categorizing
patients according to their class of symptoms is rapid and precise
and can be used in follow-up. Class IV describes the typical Box 1-3 Cardiac Risk Factors
patient with acute coronary syndrome. • Diabetes
• Smoking
• Hypertension
Box 1-2 Conditions that Cause Increased • High cholesterol
• Hyperlipidemia
Myocardial Oxygen Demand
• Sedentary lifestyle
• Hyperthyroidism • High-fat diet
• Tachycardia of various etiologies • Stress
• Hypertension • “Metabolic syndrome”
• Pulmonary embolism • Family history of CHD (including history of MI, sudden
• Pregnancy cardiac death, and first-degree relatives who underwent
• Psychogenic coronary revascularization)
• Central nervous system stimulants • Age
• Exercise • Male sex
• Psychological stress • Obesity
• Fever
CHD, coronary heart disease; MI, myocardial infarction.
6 SECTION I • Introduction

Left-Sided Cardiac Heart Failure

Box 1-4 Canadian Cardiovascular Society
Classification of Angina Pectoris Cardiac auscultation for third heart sounds
(S3) and murmurs should be performed in
I Ordinary physical activity, for example, walking or standard positions, including that with the
climbing stairs, does not cause angina; angina occurs patient sitting forward.
with strenuous, rapid, or prolonged exertion at work
S1 Systolic S2 S3
or recreation.
murmur
II Slight limitation of ordinary activity; for example,
angina occurs when walking or stair climbing after
meals, in cold, in wind, under emotional stress, or
only during the few hours after awakening, when
walking more than two blocks on the level, or when
climbing more than one flight of ordinary stairs at a
normal pace and during normal conditions.
III Marked limitation of ordinary activity; for example, Chest auscultation reveals bilateral
angina occurs when walking one or two blocks on rales and pleural effusions (when
the level or when climbing one flight of stairs during CHF is chronic).
normal conditions and at a normal pace.
IV Inability to carry on any physical activity without
discomfort; angina syndrome may be present at rest.

From Campeau L. Grading of angina pectoris [letter]. Circulation.

1976;54:522–523.

early-morning awakening (as can unstable angina) but tends to

awaken individuals 2 to 4 hours after going to sleep, rather than Cyanosis of lips
and nail beds
1 to 2 hours before arising, as is the case with unstable angina.
may be present
Other causes (see Box 1-1) of angina-like pain can be benign, if the patient
or suggestive of other high-risk syndromes, such as aortic is hypoxic.
dissection or pulmonary embolus. Many of these “coronary
mimics” can be ruled out by patient history, but others, such
as valvular aortic stenosis, can be confirmed or excluded by
physical examination. The goal of taking the history is to alert
the clinician to entities that can be confirmed or excluded
by physical examination, or that necessitate further diagnostic
testing.

Patients with left-sided

Dyspnea, Edema, and Ascites CHF may be uncomfortable
lying down.
Dyspnea can accompany angina pectoris or it can be an
anginal equivalent. Dyspnea can also reflect congestive heart
Figure 1-2 Physical examination. CHF, congestive heart failure.
failure (CHF) or occur because of noncardiac causes. The key
to understanding the etiology of dyspnea is a clear patient
history, which is then confirmed by a targeted physical
examination. distinguish them. With LV systolic dysfunction, dyspnea tends
Dyspnea during exertion that quickly resolves at rest or to gradually worsen, and its exacerbation is more variable than
with use of nitroglycerin may be a result of myocardial ischemia. that of exertional dyspnea resulting from myocardial ischemia,
It is important to establish the amount of activity necessary although both are due to fluctuations in pulmonary arterial
to provoke dyspnea, the reproducibility of these symptoms, volume and left atrial filling pressures. Typically, patients with
and the duration of recovery. As with angina, dyspnea as LV systolic dysfunction do not recover immediately after exer-
an anginal equivalent or an accompanying symptom tends to cise cessation or use of sublingual nitroglycerin, and the dyspnea
occur at a given workload or stress level; dyspnea occurring may linger for longer periods. Orthopnea, the occurrence of
one day at low levels of exertion but not prompted by vigorous dyspnea when recumbent, or paroxysmal nocturnal edema pro-
exertion on another day is less likely to be an anginal vides further support for a presumptive diagnosis of LV systolic
equivalent. dysfunction. Patients with LV diastolic dysfunction tend to
In patients with CHF, dyspnea generally reflects increased present abruptly with severe dyspnea that resolves more rapidly
left ventricular (LV) filling pressures (Fig. 1-2). Although most in response to diuretic therapy than does dyspnea caused by LV
commonly LV systolic dysfunction is the cause of the dyspnea, systolic dysfunction. The New York Heart Association (NYHA)
dyspnea also occurs in individuals with preserved LV systolic Classification for CHF (Table 1-1) is extremely useful in fol-
function and severe diastolic dysfunction. These two entities lowing patients with CHF and provides a simple and rapid
present differently, however, and physical examination can means for longitudinal assessment. The NYHA Classification
 CHAPTER 1 • The History and Physical Examination 7

Table 1-1 Comparison of the ACC/AHA and the NYHA Classifications of Heart Failure
ACC/AHA Stage NYHA Functional Class

Stage Description Class Description

A Patients without structural heart disease No comparable
and without symptoms of heart failure functional class
but who are at high risk for the
development of heart failure
B Patients with structural heart disease that is I (Mild) No limitation of physical activity. Ordinary physical
strongly associated with the development activity does not cause undue fatigue, palpitation,
of heart failure but who have never or dyspnea.
shown signs or symptoms of heart failure
C Patients who have current or prior II (Mild) Slight limitation of physical activity. Comfortable at
symptoms of heart failure and underlying rest, but ordinary physical activity results in
structural heart disease fatigue, palpitation, or dyspnea.
III (Moderate) Marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity causes fatigue,
palpitation, or dyspnea.
D Patients with advanced structural heart IV (Severe) Unable to carry out any physical activity without
disease and symptoms of heart failure at discomfort. Symptoms of cardiac insufficiency at
rest despite maximal medical therapy rest. If any physical activity is undertaken,
discomfort is increased.

ACC/AHA, American College of Cardiology/American Heart Association; NYHA, New York Heart Association. NYHA data from the Criteria
Committee of the New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis. Boston:
Brown; 1964. ACC/AHA data from ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult.
Circulation. 2005:112:e154–e235.

also correlates well with prognosis. Patients who are NYHA RV failure as an etiology. In addition, for peripheral edema
class I have a low risk of death or hospital admission within the and ascites, it is important to ask questions directed toward
following year. In contrast, the annual mortality rate of those determining the presence of anemia, hypoproteinemia, or other
with NYHA class IV symptoms exceeds 30%.
As with chest discomfort, the differential diagnosis of dyspnea
is broad, encompassing many cardiac and noncardiac causes Box 1-5 Differential Diagnosis of Dyspnea
(Box 1-5). Congenital heart disease, with or without pulmonary
Pulmonary
hypertension, can cause exertional dyspnea. Patients with sig-
• Reactive airways disease (asthma)
nificant intra- or extracardiac shunts and irreversible pulmonary • Chronic obstructive pulmonary disease
hypertension (Eisenmenger’s syndrome) are dyspneic during • Emphysema
minimal exertion and often at rest. It is also possible to have • Pulmonary edema
dyspnea because of acquired valvular heart disease, usually from • Pulmonary hypertension
aortic or mitral valve stenosis or regurgitation. All of these • Lung transplant rejection
causes should be easily distinguished from CHD or CHF by • Infection
• Interstitial lung disease
physical examination. Primary pulmonary causes of dyspnea
• Pleural disease
must be considered, with chronic obstructive pulmonary • Pulmonary embolism
disease (COPD) and reactive airways disease (asthma) being • Respiratory muscle failure
most common. Again, a careful history for risk factors (e.g., • Exercise intolerance
cigarette smoking, industrial exposure, allergens) associated
Cardiac
with these entities and an accurate physical examination should
• Ischemic heart disease/angina pectoris
distinguish primary pulmonary causes from dyspnea due to
• Right-sided heart failure
CHD or CHF. • Aortic stenosis or regurgitation
Peripheral edema and ascites are physical examination find- • Arrhythmias
ings consistent with pulmonary hypertension and/or right ven- • Dilated cardiomyopathy
tricular (RV) failure. These findings are included in the history • Hypertrophic cardiomyopathy
because they may be part of the presentation. Although patients • Congestive heart failure
often comment on peripheral edema, with careful questioning • Mitral regurgitation or stenosis
• Mediastinal abnormalities
they may also identify increasing abdominal girth consistent
• Pericardial tuberculosis
with ascites. Important questions on lower extremity edema • Transposition of the great arteries
include determination of whether the edema is symmetric (uni-
lateral edema suggests alternate diagnoses) and whether the Other
edema improves or resolves with elevation of the lower extremi- • Blood transfusion reaction
ties. The finding of “no resolution overnight” argues against • Measles
8 SECTION I • Introduction

causes. The differential diagnosis of edema is broad and beyond Box 1-6 Differential Diagnosis for Syncope
the scope of this chapter.
Cardiogenic
• Mechanical
Palpitations and Syncope Outflow tract obstruction
Pulmonary hypertension
It is normal to be aware of the sensation of the heart beating, Congenital heart disease
particularly during or immediately after exertion or emotional Myocardial disease: low-output states
stress. Palpitations refer to an increased awareness of the heart • Electrical
beating. Patients use many different descriptions, including a Bradyarrhythmias
“pounding or racing of the heart,” the feeling that their heart is Tachyarrhythmias
“jumping” or “thumping” in their chest, the feeling that the • Neurocardiogenic
Vasovagal (vasodepression)
heart “skips beats” or “races,” or countless other descriptions.
Orthostatic hypotension
A history showing that palpitations have begun to occur during
or immediately after exertion, and not at other times, raises the Other
concern that these sensations reflect ventricular ectopy associ- • Peripheral neuropathy
ated with myocardial ischemia. It is more difficult to assess the • Medications
significance of palpitations occurring at other times. Supraven- • Primary autonomic insufficiency
• Intravascular volume depletion
tricular and ventricular ectopy may occur at any time and may
• Reflex
be benign or morbid. As discussed in Chapters 29, 30, and 31, • Cough
ventricular ectopy is worrisome in patients with a history of MI • Micturition
or cardiomyopathy. Lacking this information, clinicians should • Acute pain states
be most concerned if lightheadedness or presyncope accompa- • Carotid sinus hypersensitivity
nies palpitations.
Syncope generally indicates an increased risk for sudden
cardiac death and is usually a result of cardiovascular disease and
arrhythmias. If a syncopal episode is a presenting complaint, the technology today, even the most sophisticated patients expect
patient should be admitted for further assessment. In approxi- to be examined, to have their hearts listened to, and to be told
mately 85% of patients, the cause of syncope is cardiovascular. whether worrisome findings exist or the examination results
In patients with syncope, one must assess for CHD, cardiomy- were normal.
opathy, and congenital or valvular heart disease. In addition,
neurocardiogenic causes represent a relatively common and
General Inspection and Vital Signs
important possible etiology for syncope. Box 1-6 shows the dif-
ferential diagnosis for syncope. It is critical to determine whether Much useful information can be gained by an initial “head-to-
syncope really occurred. A witness to the episode and documen- toe” inspection and assessment of vital signs. For instance,
tation of an intervening period are very helpful. In addition, truncal obesity may signal the presence of type 2 diabetes or the
with true syncope, injuries related to the sudden loss of con- metabolic syndrome. Cyanosis of the lips and nail beds may
sciousness are common. However, an individual who reports indicate underlying cyanotic heart disease. Hairless, dry-skinned
recurrent syncope (witnessed or unwitnessed) but has never lower extremities or distal ulceration may indicate peripheral
injured himself or herself may not be experiencing syncope. vascular disease. Other findings are more specific (Fig. 1-3).
This is not to lessen the concern that a serious underlying Abnormalities of the digits are found in atrial septal defect;
medical condition exists but instead to reaffirm that the symp- typical findings of Down’s syndrome indicate an increased inci-
toms fall short of syncope, with its need for immediate dence of ventricular septal defect or more complex congenital
evaluation. heart disease; hyperextensible skin and lax joints are suggestive
of Ehlers-Danlos syndrome; and tall individuals with arachno-
dactyly, lax joints, pectus excavatum, and an increased arm
The Physical Examination length-to-height ratio may have Marfan’s syndrome. These rep-
There are several advantages to obtaining a patient’s history resent some of the more common morphologic phenotypes in
before the physical examination. First, the information gained individuals with heart disease. Vital signs can also be helpful.
in the history directs the clinician to pay special attention to Although normal vital signs do not rule out CHD, marked
aspects of the physical examination. For instance, a history con- hypertension may signal cardiac risk, whereas tachycardia,
sistent with CHD necessitates careful inspection for signs of tachypnea, and/or hypotension at rest suggest CHF.
vascular disease; a history suggestive of CHF should make the
clinician pay particular attention to the presence of a third heart
Important Components of the
sound. Second, the history allows the clinician to establish a
Cardiovascular Examination
rapport with patients, to assure patients that he or she is inter-
ested in their well-being, and that the physical examination is The clinician should focus efforts on those sites that offer a
an important part of a complete evaluation. In this light, the window into the heart and vasculature. Palpation and careful
therapeutic value of the physical examination to the patient inspection of the skin for secondary changes because of vascular
should not be underestimated. Despite the emphasis on disease or diabetes is important. Lips, nail beds, and fingertips
 CHAPTER 1 • The History and Physical Examination 9

Marfan’s syndrome Ehlers-Danlos syndrome

Upper body segment

Hyperextensibility of
thumbs and fingers Hyperextensibility
of elbows

Easy splitting of the

skin (so-called cigarette
paper scars) over
bony prominences, Hyperelasticity
hyperelastic auricles of skin
Lower body segment

Down’s syndrome
Typical facies seen in Down’s syndrome

Upward slanting
eyes contrasting
with ethnic group

Small mouth with

protruding tongue

Walker-Murdoch wrist sign.

Because of long fingers
and thin forearm, thumb
and little finger overlap
when patient grasps wrist. Wide gap between the “Simian“ crease
first and second toes on the palm

Figure 1-3 Physical examination: general inspection.

should be examined for cyanosis (including clubbing of over both carotids, over the femoral arteries, and in the abdomen.
the fingernails) and, when indicated, for signs of embolism. Abdominal auscultation should be performed, carefully listening
Examination of the retina using an ophthalmoscope can reveal for aortic or renal bruits, in the mid-abdominal area before
evidence of long-standing hypertension, diabetes, or atheroem- abdominal palpation, which can stimulate increased bowel
bolism, denoting underlying vascular disease. Careful examina- sounds. Distinguishing bruits from transmitted murmurs in the
tion of the chest, including auscultation, can help to differentiate carotid and abdominal areas can be challenging. When this is a
causes of dyspnea. The presence of dependent rales is consistent concern, carefully marching out from the heart using the stetho-
with left-sided heart failure. Pleural effusions can result from scope can be helpful. If the intensity of the murmur or bruit
long-standing LV dysfunction or noncardiac causes and can continually diminishes farther from the heart, it becomes more
be present with predominantly right-sided heart failure, likely that this sound originates from the heart, rather than from
representing transudation of ascites into the pleural space. a stenosis in the peripheral vasculature. Much information is
Hyperexpansion with or without wheezing suggests a primary available about the peripheral vascular examination, but by fol-
pulmonary cause of dyspnea, such as COPD or reactive airways lowing the simple steps outlined herein, the examiner can gather
disease. The presence of wheezing rather than rales does not the majority of the accessible clinical information.
rule out left-sided heart failure. It is not uncommon to hear Examination of the jugular venous pulsations is a commonly
wheezing with left-sided CHF. Most commonly, wheezing from forgotten step. Jugular venous pressure, which correlates with
left-sided CHF is primarily expiratory. Inspiratory and expira- right atrial pressure and RV diastolic pressure, should be esti-
tory wheezing, particularly with a prolonged inspiratory- mated initially with the patient lying with the upper trunk ele-
to-expiratory ratio, is more likely to be caused by intrinsic lung vated 30 degrees. In this position, at normal jugular venous
disease. pressure, no pulsations are visible. This correlates roughly to a
The vascular examination is an important component of a jugular venous pressure less than 6 to 10 cm. The absence of
complete evaluation. The quality of the pulses, in particular the jugular vein pulsations with the patient in this position can be
carotid and the femoral pulses, can identify underlying disease confirmed by occluding venous return by placing a fingertip
(Fig. 1-4). Diminished or absent distal pulses indicate peripheral parallel to the clavicle in the area of the sternocleidomastoid
vascular disease. The examiner should also auscultate for bruits muscle. The internal and external jugular veins should partially
10 SECTION I • Introduction

Examples of carotid pulses and the Examples of venous pulses and the
entities with which they are associated entities with which they are associated
Normal Normal
S1 S2 S1 S2 S1 S2
Phono Phono

Carotid Jugular a c
pulse v h
pulse x y
ECG ECG

Hypertrophic cardiomyopathy Tricuspid regurgitation

(Bisferiens pulse)
S1 S2 S1SM S2 S1 SM S2
Phono Phono
v S3 v S3
Jugular a a
Carotid pulse
pulse y y
ECG
ECG
Aortic regurgitation Pulmonary hypertension
(Corrigan’s pulse) secondary to mitral stenosis
Diastolic
S1 S2 murmur SM
Phono
Phono a S S
1 2
Jugular
Carotid pulse c v
pulse x y
ECG
ECG
Careful auscultation of the abdomen can reveal Cardiac apical impulse (palpation of the precordium)
bruits from vessels such as aorta and renal arteries. S1 S2 S1 S2 S1 S2
Hyperdynamic Diffuse and
Dilatation of the abdominal portion of
impulse sustained
the aorta can be recognized by palpation.
(hypertrophic (left ventricular
cardiomyopathy) dysfunction)
Diminished or absent peripheral pulses Normal
indicate peripheral vascular disease.

Figure 1-4 Important components of cardiac examination. ECG, electrocardiogram.

fill. Although with normal jugular venous pressure examination have a hyperdynamic apical impulse. Thrills, palpable vibrations
of the waveforms is less important, the head of the examination from loud murmurs or bruits, can also be palpated.
table can be lowered until the jugular venous pulsations are The RV impulse, if identifiable, is located along the left
evident. When the jugular venous pulsations are visible at 30 sternal border. Many clinicians prefer to palpate the RV impulse
degrees, the examiner should note the waveforms. It is possible with the base of the hand, lifting the fingertips off the chest
to observe and time the a and v waves by simultaneously timing wall. In RV hypertrophy, a sustained impulse can be palpated,
the cardiac apical impulse or the carotid impulse on the contra- and the fingertips then can be placed at the LV impulse to
lateral side. An exaggerated a wave is consistent with increased confirm that the two are distinct. In patients with a sustained
atrial filling pressures because of tricuspid valve stenosis or RV impulse, the examiner should again look for prominent a
increased RV diastolic pressure. A large v wave generally indi- and v waves in the jugular venous pulsations.
cates tricuspid valve regurgitation, a finding easily confirmed by
auscultation.
Cardiac Auscultation
Finally, before cardiac auscultation it is important to palpate
the precordium. This is the easiest way to identify dextrocardia. Hearing and accurately describing heart sounds is arguably the
Characteristics of the cardiac impulse can also yield important most difficult part of the physical examination. For this reason
clues about underlying disease. Palpation of the precordium is and because of the commonplace use of echocardiography,
best performed from the patient’s right side with the patient many clinicians perform a cursory examination. The strongest
lying flat. The cardiac apical impulse is normally located in arguments for performing cardiac auscultation carefully are to
the fifth intercostal space along the midclavicular line. Most determine whether further diagnostic testing is necessary; to
examiners use the fingertips to palpate the apical impulse. It is correlate findings of echocardiography with the clinical exami-
often possible to palpate motion corresponding to a third or nation so that, in longitudinal follow-up, the clinician can deter-
fourth heart sound. Use of the fingertips offers fine detail on mine progression of disease without repeating echocardiography
the size and character of the apical impulse. A diffuse and sus- at each visit; and because the more a clinician makes these cor-
tained apical impulse is consistent with LV systolic dysfunction. relations, the better his or her skills in auscultation will become
Patients with hypertrophic cardiomyopathy, in contrast, often and the better his or her patients will be served. It should also
 CHAPTER 1 • The History and Physical Examination 11

be noted that, with normal general cardiac physical examination the heart sounds. Is a single sound present, or is the first heart
results, the absence of abnormal heart sounds, and a normal sound split? Is a sound heard before S1, indicating an S4? Next,
electrocardiogram, the use of echocardiography for evaluation listen to the second heart sound. Normally the first component
of valvular or congenital heart disease is not indicated. Further- (A2, the aortic valve closing sound) is louder than the second
more, if there are no symptoms of CHF or evidence of hemo- component (P2, the pulmonic valve closing sound). A louder
dynamic compromise, echocardiography is not indicated for second component may indicate increased pulmonary pressure.
assessment of LV function. Practice guidelines from cardiolo- A more subtle finding is a reversal of A2 and P2 timing that
gists and generalists agree on this point, as do third-party insur- occurs with left bundle branch block and in some other circum-
ers. It is neither appropriate nor feasible to replace a careful stances. Additionally, it is important to assess whether A2 and
cardiovascular examination using auscultation with more expen- P2 are normally split or whether they are widely split with no
sive testing. respiratory variation—a finding suggestive of an atrial septal
The major impact of echocardiography has been in quantita- defect. The examiner should then listen carefully for a third
tive assessment of cardiovascular hemodynamics—that is, the heart sound. An S3 is often best heard over the tricuspid or
severity of valvular and congenital heart disease. No longer is it mitral areas and is a low-frequency sound. It is heard best with
necessary for the clinician to make an absolute judgment on the bell and is often not heard with the diaphragm.
whether an invasive assessment (cardiac catheterization) is After characterizing these heart sounds, it is time to listen
needed to further define hemodynamic status or whether the carefully for murmurs. Murmurs are classified according to
condition is too advanced to allow surgical intervention based their intensity, their duration, their location, and their ausculta-
on history and physical examination. But instead of diminishing tory characteristics: crescendo, decrescendo, blowing, among
the role of cardiac auscultation, the advent of echocardiography others. It is also important to note the site where the murmur
has redefined it. Auscultation remains important as a screening is loudest and whether the murmur radiates to another area
technique for significant hemodynamic abnormalities, as an of the precordium or to the carotids. All of these features
independent technique to focus and verify the echocardio- contribute to determining the origin of the murmur, the likeli-
graphic study, and an important means by which the physician hood that it represents an acute or chronic process, and how it
can longitudinally follow patients with known disease. affects the diagnostic and therapeutic approaches. Most impor-
There are several keys to excellence in auscultation. tantly, it is necessary for clinicians to judge whether a murmur
Foremost is the ability to perform a complete general cardiac represents cardiac disease or is innocent. Innocent murmurs,
physical examination, as described. The findings help the exam- also termed “flow murmurs,” are common in children. More
iner focus on certain auscultatory features. Second, it is impor- than 60% of children have innocent murmurs. Innocent
tant to use a high-quality stethoscope. Largely dictated by murmurs become less common in adults; however, an innocent
individual preference, clinicians should select a stethoscope murmur can still be found into the fourth decade of life. Altera-
that has bell and diaphragm capacity both (for optimal apprecia- tions in hemodynamics induced by pregnancy, anemia, fever,
tion of low- and high-frequency sounds, respectively) and that hyperthyroidism, or any state of increased cardiac output can
fits the ears comfortably and is well insulated so that external produce an innocent murmur. These murmurs are generally
sounds are minimized. Third, it is important to perform auscul- midsystolic, heard over the tricuspid or pulmonic areas, and do
tation in a quiet environment. Particularly as skills in ausculta- not radiate extensively. They are often loudest in thin individu-
tion are developing, trying to hone these in the hall of a busy als. Innocent murmurs do not cause alterations in the carotid
emergency department or on rounds while others are speaking pulse and do not coexist with abnormal cardiac impulses or with
is time spent poorly. Additionally, taking the time to return other abnormalities, such as extra heart sounds (S3 and S4), in
to see a patient with interesting findings detected during aus- adults. In elderly individuals a common finding is a systolic
cultation, and repetition, are keys to becoming competent in murmur that shares auditory characteristics with the murmur of
auscultation. aortic stenosis; however, carotid upstrokes are normal. This
The patient should be examined while he or she is in several finding, aortic sclerosis, may necessitate confirmation by echo-
positions: while recumbent, while in the left lateral decubitus cardiography. It represents sclerosis of the aortic leaflets but
position, and while sitting forward. Every patient is different without significant hemodynamic consequence.
and, using all three positions, the examiner can optimize the The characteristics of the most common and hemodynami-
chance that soft heart sounds can be heard. Likewise, it is impor- cally important murmurs are shown in Figure 1-5. As noted, the
tant to listen carefully at the standard four positions on the chest murmur is defined not only by its auditory characteristics but
wall (Fig. 1-5), as well as over the apical impulse and RV impulse also by the company it keeps. Often the key to excellence in
(if present). It is also best to isolate different parts of the exami- auscultation is being thorough in all aspects of the cardiovascu-
nation in time. Regardless of the intensity of various sounds, lar examination.
it is best always to perform the examination steps in the same
chronologic order, so that the presence of a loud murmur,
Maneuvers
for instance, does not result in failure to listen to the other
heart sounds. No discussion of cardiac auscultation would be complete without
Listen for S1 (the first heart sound) first. As with jugular the use of maneuvers to accentuate auscultatory findings. As
venous pulsations, the heart sounds can be timed by simultane- shown in Figure 1-6, patient positioning can alter peripheral
ously palpating the cardiac apical impulse or the carotid upstroke. vascular resistance or venous return, accentuating murmurs that
Even the most experienced clinician occasionally needs to time are modulated by these changes. Murmurs associated with fixed
12 SECTION I • Introduction

Cardiac Auscultation: Precordial areas of auscultation

Aortic area Pulmonic area

1
Valves 2

Pulmonic valve 3 Tricuspid area

4
Aortic valve
5
Mitral area
Mitral valve 6
7
Tricuspid area

Diagrams of murmurs
Innocent murmur Innocent murmur Systolic murmur from Systolic murmur Murmur and ejection Holosystolic Systolic murmur (chronic
with widely split S2 increased pulmonic flow followed by widely click (pulmonary murmur mitral regurgitation) with
followed by fixed, widely split S2 hypertension) (acute mitral S3 and S4 (dilated
split S2 (atrial septal defect) regurgitation) cardiomyopathy)
S2 S1 S2
S1 A2 P2 A2 P A2 P2 S1 EC
S1 S2 S1 ES 2
S1 S4 S1 S2 S3

Holosystolic murmur Late systolic murmur Ejection sound followed by a Continuous murmur Diastolic murmur Long diastolic murmur
(IVSD or mitral or following midsystolic murmur that extends through (patent ductus arteriosus) (aortic or pulmonary following opening snap
tricuspid regurgitation) click (mitral prolapse) A2 with widely split S2 and regurgitation) (mitral stenosis)
the presence of S4 (moderate
pulmonary stenosis) S1 S2
S1 S2 S1 A2 P2 S1 S2
S1 A2 S1 S2 OS
P2
S4

Click EC

Figure 1-5 Cardiac auscultation: Correlation of murmurs and other adventitious sounds with underlying pathophysiology.
 CHAPTER 1 • The History and Physical Examination 13

Vascular resistance and venous return are altered by maneuvers used to modify auscultatory Isometric exercise
findings of many different etiologies. Mitral valve prolapse is used here to exemplify the Handgrip also increases peripheral vascular
use of some of these maneuvers. resistance and ventricular volume, retarding
S1 Midsystolic S2 the midsystolic click that moves near S2.
click S1 Click S2

Systolic
murmur Murmur

Ejection clicks, such as those of a stenotic aortic valve, can be differentiated from
nonejection clicks, such as the click commonly auscultated in mitral valve prolapse.
The "mobility" of the click as response to
changes in the left ventricular volume Standing
provoked by the maneuvers points to a Decreases ventricular
nonejection click, in this case of mitral volume
valve prolapse. Systolic click S
Squatting S 1 2
near S2
Increases peripheral vascular Valsalva’s
resistance and ventricular In the second stage of Valsalva’s maneuver
volume diminishment of venous return and
S1 Systolic click S decrease of ventricular volume occurs.
2
near S2 Accentuated The click is less intense and moves near S1.
systolic The murmur is less audible as well.
murmur S1 Click Murmur
S2

Figure 1-6 Maneuvers.

valvular lesions change little with changes in position or the cardiovascular disease, whether CHD, valvular heart disease, or
maneuvers illustrated in Figure 1-6. Thus, these maneuvers are congenital heart disease, thereby determining the need for
most useful for diagnosing entities in which hemodynamic further testing. In the continual quest for improved noninvasive
status affects murmurs. The two classic examples are the testing, it is likely that a clinician’s skill will continue to evolve
click and murmur of mitral valve prolapse, as shown, and as the interplay between history taking, physical examination,
the aortic outflow murmur of hypertrophic cardiomyopathy and diagnostic testing further develops.
(not shown).
Additional Resources
Future Directions
ACC/AHA Joint Guidelines. <http://www.americanheart.org/presenter.
Handheld echocardiography machines can be carried on the jhtml?identifier=3004542>; Accessed 22.02.10.
shoulder and have a small transducer that can obtain echocar- Guidelines outlining the current opinion of experts from the American College of
diographic images of sufficient quality to quantify murmurs and Cardiology and the American Heart Association for managing cardiovascular
assess LV dysfunction. Although these portable echocardio- diseases.
graphic machines have advantages and have been incorporated American Heart Association. Heart Profilers. Available at: <http://www.
in medical school curricula at many institutions, they have not americanheart.org/presenter.jhtml?identifier=3000416>; Accessed 22.02.10.
yet replaced the stethoscope, nor are they likely to do so. Provides individual specific information based on your risk profile.
The roles of cardiac history and physical examination
National Heart, Lung and Blood Institute. National Cholesterol Education
have changed. Before the noninvasive testing of today, astute Program. Available at: <http://hp2010.nhlbihin.net/atpiii/calculator.
clinicians were the arbiters of whether invasive diagnostic testing asp?usertype=prof>; Accessed 22.02.10.
was needed, based largely on examination findings alone. Today A website where you can enter patient-specific data to calculate the 10-year
it is believed that the role of the clinician is to use physical risk of a cardiac event based on Framingham data (Framingham Risk
examination findings to establish the prior probability of Calculator).
14 SECTION I • Introduction

Evidence
National Heart, Lung and Blood Institute. Third Report of the Expert
Diamond GA, Forrester JS. Analysis of probability as an aid in the Panel on Detection, Evaluation, and Treatment of High Blood Choles-
clinical diagnosis of coronary-artery disease. N Engl J Med. 1979; terol in Adults (Adult Treatment Panel III) and ATP III Update
300:1350–1358. 2004: Implications of Recent Clinical Trials for the ATP III Guidelines. Avail-
able at: <http://www.nhlbi.nih.gov/guidelines/cholesterol>; Accessed
A classic discussion of the importance of pre-test and post-test probabilities in 10.11.09.
interpreting any diagnostic testing.
An overview of the current recommendations regarding treatment of
Harvey WP. Cardiac Pearls [video recording]. Atlanta: Emory Medical elevated lipids.
Television Network; 1981.
This video recording is a timeless example of Dr. Harvey—a master clinician—
and his approach to the evaluation of patients with cardiovascular disease.
Hurst JW, Morris DC. Chest Pain. Armonk, NY: Futura Publishing;
2001.
Drs. Hurst and Morris provide a sophisticated summary on the evaluation of
patients with chest pain.
Coronary Atherosclerosis
Cam Patterson and Marschall S. Runge 2
C ardiovascular diseases (CVDs)—coronary artery disease
(CAD), hypertension, congestive heart failure, and
stroke—are the leading cause of death and disability in elderly
The concept that endothelial injury is an inciting event in
atherosclerosis is common to most theories of pathogenesis.
Endothelial injury is a component of the earliest stages of
individuals in the Western world. In the United States, atherosclerosis, the formation of lesions that can be detected
the CVD death toll is nearly 1 million each year, and only at autopsy, the fatty streak (Fig. 2-1A). Most of the well-
the estimated cost of CVD treatment was over $400 billion characterized risk factors for atherosclerosis (hypertension, dia-
for 2006, with the likelihood that the incidence of CVD will betes mellitus, cigarette smoking, hyperlipidemia, advanced age,
continue to increase as the population ages and because of the elevated plasma homocysteine concentrations) injure the endo-
marked increases in diabetes and obesity that are occurring thelium, initiating a chain of events, all attributes of atheroscle-
today. The U.S. Census Bureau projects that nearly one in rosis: smooth muscle cell (SMC) proliferation, inflammatory
four individuals will be 65 years of age or older by 2035, and cell recruitment, and lipid deposition within the blood vessel
adults older than 65 years are two and a half times more likely (Fig. 2-1B). Though still early in development, potential diag-
to have hypertension and four times more likely to have nostic and/or therapeutic approaches based upon inflammatory
coronary heart disease than are those in the 40- to 49-year age signaling pathways now known to be important in atherogenesis
group. Additionally, throughout all age groups, the incidence hold promise.
of obesity and diabetes has increased dramatically across the Endothelial injury and the subsequent events that occur in
United States. the vessel wall initiate the progression from stable to unstable
Although the prevalence of atherosclerotic disease continues atherosclerotic plaques, ultimately leading to the rupture of
to increase in developed countries, death rates from CVDs in unstable plaques, thrombosis of the vessel, and, in many cases,
the United States have decreased by more than a third in the MI (Fig. 2-2). Lesion development in the medium and small
past 2 decades. This effect is due to primary and secondary vessels of cerebral vessels leads to stroke, and in renal and mes-
prevention strategies and to improvements in care and rehabili- enteric vasculature contributes to diabetic complications.
tation of patients with atherosclerotic diseases. An abundance of evidence suggests that atherosclerotic
Despite this encouraging news, atherosclerotic diseases lesions, at least in part, result from an excessive inflammatory
remain an enormous challenge for the clinician, for several response. For example, although elevated low-density lipopro-
reasons. Many preventive strategies involve lifestyle changes tein cholesterol (LDL-C) is a risk factor for premature athero-
that test the compliance of even the most devoted patients. sclerosis, the LDL-C must undergo oxidative modification to
The disease itself progresses silently for decades before symp- cause damage to the arterial wall. Cytokines, growth factors, and
toms develop, and the initial clinical presentation of atheroscle- oxidative stress may also contribute to atherosclerosis by mecha-
rotic disease is often a catastrophic event, such as myocardial nisms that are independent of LDL-C oxidation. Any of these
infarction (MI), stroke, or sudden cardiac death (SCD). The mediators can rapidly react with and inactivate nitric oxide,
diagnosis of atherosclerotic disease, particularly through non­ enhancing proatherogenic mechanisms such as leukocyte adhe-
invasive methods, is imperfect, and clinical manifestations of sion to endothelium, impaired vasorelaxation, and platelet
atherosclerotic diseases are often subtle and easily mistaken for aggregation (Fig. 2-3).
causes that are more benign. Therefore, although the diagnosis Numerous adaptive changes in vascular structure occur
and treatment of atherosclerotic diseases remain of paramount with aging in healthy individuals. These changes include
importance, the promise of future advances rests in a more increases in arterial stiffening, aortic root size, and aortic wall
detailed understanding of atherosclerosis, leading to earlier thickness (which resembles the increased intimal medial thick-
diagnosis and prevention that is ultimately more effective. ness during early atherogenesis) and measurable abnormalities
in vascular function, such as enhanced arterial systolic and
pulse pressure. Collagen content is increased, but elastin content
Etiology and Pathogenesis
is decreased.
Atherosclerotic plaques lead to clinical events (angina, MI) by Throughout the spectrum of atherogenesis, SMCs play a
two mechanisms. First, with gradual enlargement, plaques may pivotal role. SMCs are not terminally differentiated and can
obstruct blood flow within epicardial vessels, resulting in isch- undergo phenotypic modulation, reverting to cells capable of
emia to the myocardial tissue dependent on the affected vessel’s proliferation, migration, and secretion of mediators involved
blood supply. Alternatively, plaques may become symptomatic in these processes. These modulated SMC phenotypes have
because of acute rupture or thrombosis, resulting in catastrophic potentially opposing functions because they can repair vascular
acute occlusion of a vessel, the hallmark of MI. Indeed, the two damage but can also contribute to vascular disease such as
mechanisms are apt to be linked, because less catastrophic (and hypertension and atherosclerosis. In arteries prone to develop
subclinical) episodes of plaque rupture are probably one of the atherosclerosis, and in the sites of plaque destabilization
mechanisms by which nonocclusive plaques enlarge to become and rupture, the terminal events in lesion progression—the
symptomatic. number of SMCs—is often decreased. Because SMCs are
16 SECTION I • Introduction

Circulating monocyte
Adventitia
Muscularis Circulating Monocyte adheres Monocyte
Fatty streak Internal LDL-C to endothelium migrates into
Foam cell elastic LDL-C migrates into subendothelium
(intracellular
cholesterol)
lamina subendothelium
LDL-C
Intima
Free (extracellular) Monocyte
cholesterol Endothelium Insoluble LDL-C transforms into
aggregates Monocyte Macrophage
Cytotoxicity chemoattraction differentiation macrophage
form

Uptake of
oxidized LDL-C
Oxidation by macrophage
Oxidized LDL-C

Denaturation
Free H2O2
Intimal LDL-C radicals Foam cell
Extracellular cholesterol and cholesterol-filled forms
O2 Cholesterol
macrophages (foam cells) accumulate in Free
Glycation released
subendothelial space. Subsequent structural cholesterol
modifications if LDL-C particles render them Cholesterol
more atherogenic. Oxidation of subendothelial Interaction with ester
LDL-C attracts monocytes, which enter proteoglycans Extracellular
subendothelium and change into macrophages. Macrophage cholesterol
Macrophages may take up oxidized LDL-C to form
foam cells.

Cholesterol accumulation continues at plaque margins

Peripheral
Monocyte
fatty streak Fibrous cap forms over core
Apo
Foam cell Fibrous cap B-100
Extracellular LDL-C
Fibrous cap
cholesterol
Core
LDL-C

LDL-C

Smooth muscle
involved in Oxidized
collagen synthesis LDL-C
Smooth muscle Collagen synthesis and
cell migration secretion form fibrous cap
Smooth muscle Central core of Macrophage
cell transformed free (extracellular) Smooth muscle
into foam cell migrates into intima Foam cell
Foam cell death cholesterol
Smooth muscle
Fibrous plaque larger than fatty streak and occupies releases cholesterol
transformed
more of arterial lumen. Thickened cap synthesized into intima
into foam cell
by modified smooth muscle cells. Central core
consists of extracellular cholesterol. Foam cells
surrounding core derived primarily from smooth
muscle cells. Fatty streaks may continue to form at
periphery of plaque.

Figure 2-1 Atherogenesis: (A) Fatty streak formation. (B) Fibrous plaque formation. LDL-C, low-density lipoprotein cholesterol.
 CHAPTER 2 • Coronary Atherosclerosis 17

Fatty streak at margin

Fibrin Platelet
Lumen
Thrombus Fibrinogen
Fibrous cap
Plaque rupture Erythrocyte
Intimal disruption
and thrombus
Fibrous cap

Total or partial occlusion of coronary

artery due to plaque rupture
and thrombosis can cause angina
or frank myocardial infarction.

Plaques likely to rupture are termed unstable. Rupture

usually occurs in lipid-rich and foam cell–rich
peripheral margins and may result in thrombosis and
arterial occlusion.

Figure 2-2 Atherogenesis: Unstable plaque formation.

important in maintaining plaque stability (most of the intersti- and other similar approaches are less likely to offer therapeutic
tial collagen fiber deposition important for tensile strength of effectiveness (see Chapter 72).
the fibrous cap is secreted by SMCs), the paucity of SMCs
increases the likelihood of plaque rupture. Therefore, it is likely
that SMC proliferation is deleterious in the early stages of ath-
Clinical Presentation
erosclerotic lesion formation, whereas loss of SMCs (and Understanding the symptoms of myocardial ischemia is essen-
decreased capacity for proliferation) in later stages increases the tial in the context of atherosclerosis, and the brief descriptions
likelihood of plaque destabilization and clinical outcomes such provided represent an overview. These topics are discussed in
as MI and stroke. more detail in Chapters 1, 12, 13, and 14. There are three classic
A large body of data now implicates both circulating and clinical presentations of coronary atherosclerosis. The first is
resident stem cells in the pathogenesis of and protection against angina pectoris, the characteristic ischemia-induced chest pain.
atherosclerosis. Although the biology and contribution of stem The chest pain of angina is typically retrosternal, with radiation
cells to progression and regression of atherosclerosis remains to the arms and neck, and is often accompanied by dyspnea (Fig.
incompletely understood, some data suggest that depletion of 2-4). Angina may occur predictably with exertion (stable angina)
stem cells during the process of aging serves as a trigger for or, more ominously, at rest or in an accelerating pattern (unsta-
progression of atherosclerotic lesions. ble angina). The symptoms of stable angina are often subtle and
Advances in molecular biologic and genetic approaches difficult to distinguish from other causes of chest discomfort.
promise a more detailed understanding of atherosclerosis and This is particularly true in women, in whom the typical symp-
improved diagnostic and therapeutic methods. In the past 2 toms described herein are less commonly present.
decades, an explosion of information based on identification of If not treated promptly, unstable angina may be a harbinger
genes and proteins involved in experimental atherosclerosis has of MI, the second classic presentation of atherosclerosis. Patients
resulted in better understanding of the biology of atherosclero- with MI frequently, but not exclusively, present with chest pain;
sis. Unfortunately, these advances have generally not translated however, unlike anginal pain, the pain of MI is typically unre-
into better diagnostic testing. In addition, because with rare mitting and more severe and may be accompanied by autonomic
exceptions atherosclerosis is a multigenic disease, gene therapy symptoms, such as nausea and vomiting. Arrhythmias may ensue
18 SECTION I • Introduction

Risk Factors in Coronary Artery Disease

Insulin
Hypertension
Hypercholesterolemia ( LDL-C) ( hydrostatic pressure) Cigarette smoking Diabetes mellitus ( glucose)

Plaque formation Plaque instability and rupture

Interaction of risk factors in atherogenesis

Hypertension enhances LDL-C
LDL-C infiltration via increased
hydrostatic pressure and
endothelial disruption
Cigarette smoking increases
LDL-C oxidation and arterial
wall inflammation

Subendothelial Inflammation
infiltration
of LDL-C
Foam cell
Oxidized formation
LDL-C

Diabetes Subendothelial
mellitus LDL-C Increased
blood pressure
Glycosylated stimulates smooth
Elevated glucose levels muscle migration
promote glycosylation of LDL-C LDL-C
into intima

Figure 2-3 Classical risk factors in coronary artery disease: Relationship to excessive inflammatory responses. LDL-C, low-density
lipoprotein cholesterol.

from ischemia-induced electrical instability of the myocardium. access to automatic external defibrillation devices, and to
In severe cases, symptoms of heart failure because of acute left improve emergency medical access improve survival in out-of-
or right ventricular dysfunction may also be present. Ventricular hospital SCD. Resuscitation after SCD is more effective in
dysfunction is an ominous sign in patients with MI and merits patients admitted to the hospital, largely because of continuous
prompt attention. electrocardiographic monitoring and the development of coro-
The third presentation of atherosclerosis is SCD due to ven- nary care units that provide advanced care for patients who
tricular fibrillation, which is the first clinical manifestation experienced MI.
of coronary atherosclerosis in about 25% of patients with It should be noted that more than 50% of patients with
the disease (see Chapter 30). The only hope of survival for myocardial ischemia present with atypical symptoms ranging
patients who present with SCD is prompt administration of from “anginal equivalents” to nonspecific symptoms in the
cardiopulmonary resuscitation and ventricular defibrillation. setting of acute MI. For this reason, a high index of clinical
Several studies have demonstrated that community-based suspicion should endorse further diagnostic testing in individu-
efforts to train the public in resuscitation techniques, to provide als with atypical symptoms.
 CHAPTER 2 • Coronary Atherosclerosis 19

Typical anginal pain is frequently exertional and subsides

predictably within a few minutes of rest. The pain may also be
exacerbated by emotional stress and drug use, including tobacco
and cocaine. It is often described as aching, pressure, heaviness,
or squeezing. The diagnosis is further complicated by the
number of other causes of chest discomfort, many of which are
also medical emergencies. Other CVDs, including aortic dissec-
tion and acute pericarditis, may produce chest pain. More
common cardiac, noncoronary causes of ischemic chest pain
are systemic hypertension and endothelial dysfunction or syn-
drome X. Individuals with marked hypertension may experience
exertional chest pain as a result of subendocardial ischemia,
which often occurs in the absence of angiographically significant
coronary stenosis. Similarly, patients with syndrome X experi-
ence effort-induced chest pain, probably due to subendocardial
ischemia from the inability of the coronary arteries to undergo
vasodilation normally. Based on the biology of atherosclerosis,
as discussed above, it is no surprise that considerable overlap
exists between patients with hypertension and/or endothelial
dysfunction and those with significant atherosclerotic lesions.
Pulmonary causes of chest pain include pulmonary embolism
and pulmonary hypertension, the latter of which may be exer-
tional and difficult to distinguish from myocardial ischemia
based on symptoms alone. Gastrointestinal diseases are very
common and frequently difficult to distinguish from angina
pectoris based on medical history; gastroesophageal reflux and
esophageal spasm frequently cause chest discomfort similar to
angina, as can gastritis and peptic ulcer disease. Musculoskeletal
conditions, such as muscle strains and arthritis, may produce
Common precipitating factors in angina Characteristic distribution angina-like symptoms. Finally, the distribution of herpes zoster
pectoris: Heavy meal, exertion, cold, of pain in angina pectoris pain may suggest angina pectoris to the clinician, particularly
smoking if the typical herpes zoster rash has not yet appeared. Thus,
the nonspecific nature of angina pectoris symptoms, plus the
broad overlap with other common disorders, contributes to the
difficulties in the diagnosis of CAD based on signs and symp-
Figure 2-4 Angina pectoris. toms alone.

Differential Diagnosis Diagnostic Approach

Identification of patients with coronary atherosclerosis is one of The suspicion of coronary atherosclerosis is raised by a careful
the classic dilemmas in clinical decision making for three history and physical examination—in particular, the solicitation
reasons. First, as much as 70% luminal obstruction by an of symptoms of angina pectoris and the consideration of poten-
atherosclerotic lesion is necessary to cause hemodynamically tial risk factors for the development of atherosclerosis. Lacking
significant obstruction that results in myocardial ischemia and definitive noninvasive diagnostic testing for coronary athero-
the symptoms of angina. Second, many lesions that rupture or sclerosis, the importance of the history and physical examination
undergo thrombosis and lead to MI are nonobstructive, and cannot be overstated.
neither the identification of suspect lesions by angiography or A host of diagnostic methods are available for the clinician
the early warning symptoms of angina necessarily forewarn of evaluating a patient for CAD. The first step in the evaluation of
dramatic clinical presentations such as unstable angina or MI. patients suspected of having coronary atherosclerosis is 12-lead
Third, the symptoms of angina pectoris, and even MI, can be electrocardiography. In patients with MI the characteristic
especially subtle and difficult to distinguish from other causes abnormality detected is ST-segment elevation, whereas patients
of chest discomfort, even for an experienced clinician. More- with angina may have evidence of prior myocardial injury (Q
over, often cardiac symptoms are not recognized by the patient waves) or ST-segment depression, or a normal ECG. Other
before an acute presentation. The failure to identify the symp- abnormalities may also occur, and ST-segment changes may
toms of myocardial ischemia is one of the most common, and disappear when ischemic symptoms resolve. Electrocardiogra-
the most costly, clinical errors. For all these reasons, there is phy is a relatively specific but not highly sensitive indicator of
much interest in advanced diagnostic testing for cardiovascular CAD, and a normal ECG never excludes coronary disease under
risk, as discussed in detail in Chapters 3 to 10. any circumstances. When MI is suspected, cardiac markers
20 SECTION I • Introduction

Beam sweep Sheath

Ultrasound
probe

Rotating mirror
Transducer
Rotating beam transducer
Adventitia
Beam
Media
Simultaneous
Intima transducer beam
Normal artery
Differences in acoustic sensitivity
allow discrimination of vessel
wall components
Phased array transducer Multiple
transducer array
Guide wire

Serial sections

Ultrasound study of Concentric atheromatous Section of artery with Plaque with bright,
normal coronary artery narrowing of lumen large atheromatous plaque calcific echodensity

Figure 2-5 Intravascular ultrasonography.

(creatine kinase-MB and troponin T or I) should be monitored for atherosclerosis and, although the risks of angiography in
for evidence of myocardial injury. otherwise healthy patients are very low, postprocedure compli-
Additional studies to test for atherosclerosis fall in two cations occur in a small percentage of patients. Coronary arte-
groups: functional studies and anatomic studies. Among the riography provides detailed information about the size and
functional studies, the most straightforward is the exercise extent of atherosclerotic lesions. Further definition of lesion
treadmill test, which detects ST depression during exercise as a characteristics can be performed using intravascular ultrasound
marker for obstructive CAD. Though simple to perform and (Fig. 2-5) or other imaging methods; however, these additional
relatively specific, the sensitivity of exercise treadmill tests falls studies are more commonly used for research than for clinical
in the 70% to 80% range at best. The sensitivity of provocative purposes. In addition to its invasive nature, the other disadvan-
studies such as the treadmill test can be greatly enhanced by tage of coronary arteriography is that functional information
adding radionuclide scintigraphy, echocardiography, or PET regarding the extent of ischemia from a given lesion is not pro-
(particularly when knowledge of myocardial viability is impor- vided; this may not matter in the case of severe stenoses, but in
tant). Functional studies have the advantage of being noninva- moderate stenoses (50% to 70%), it can be important. Recent
sive and, although their sensitivities in detection of significant advances in imaging have led to the expanded utilization of
CAD are improving, they do not equal the sensitivity of coro- noninvasive CT angiography; best employed for the detection
nary angiography. Typically, the predictive accuracy of any non- of proximal coronary artery stenosis, this technology may ulti-
invasive test is best with severe multivessel CAD; the predictive mately obviate the need for routine coronary angiography in
accuracy of these tests in single-vessel CAD is in the range of many circumstances.
65% to 75%. Therefore, if clinical suspicion is high and a defini-
tive diagnosis is needed, anatomic evaluation (coronary angiog-
raphy) should be considered even in individuals with negative Management and Therapy
noninvasive evaluation results.
Optimum Treatment
The definitive anatomic test for CAD is coronary arteriog-
raphy, which is the gold standard for diagnosis of coronary The management of patients with coronary atherosclerosis
atherosclerosis. It is also the most invasive diagnostic procedure depends on the initial presentation of the disease. For patients
 CHAPTER 2 • Coronary Atherosclerosis 21

presenting with acute MI, thrombolysis or acute percutaneous events in SMCs within lesions, have been in development for
revascularization should be considered, if appropriate, com- several years, but little progress has been made in clinical appli-
bined with pharmacologic therapies, as described in detail in cation. Antioxidant strategies are under consideration to arrest
Chapters 13 and 14. Patients with stable angina pectoris are or reverse atherosclerotic lesions, given the pleiotropic effects
generally treated with aspirin, β-blocker therapy, and nitrates as of oxidants on cellular events that accelerate the atherosclerotic
needed for symptoms (Chapter 12). Percutaneous coronary process. Although the use of antioxidant vitamins has not been
intervention is an increasingly important therapy, even in stable beneficial, more effective antioxidant strategies may be neces-
coronary syndromes (Chapters 12 and 15). Coronary artery sary to reverse or prevent the progression of lesion formation
bypass surgery may be needed for patients with refractory and may optimally be targeted to patients with markers of high
angina or those with extensive coronary disease that is not levels of oxidative stress as detected noninvasively. Similarly,
amenable to percutaneous revascularization (Chapter 16). In there is significant interest in therapies that diminish inflamma-
selected subsets—multivessel CAD in diabetic persons or in tion, but prospective randomized studies have yet to be
individuals with impaired left ventricular systolic function— completed.
coronary artery bypass surgery is effective. Until the latter part of the 1950s, only palliative therapies
Although well-validated therapies for the consequences of were widely available to patients with atherosclerosis and its
coronary atherosclerotic disease exist, specific therapies aimed complications. Although huge strides have been taken in the
at treating or preventing atherosclerosis itself are lacking. Risk approach to this disease, much progress remains to be made.
factor modification largely prevents progression of atheroscle- First, specific serum markers of atherosclerosis would be hugely
rotic lesions that have formed (and lessens the formation of beneficial, not only for diagnosis, but as a screening tool for
new lesions), but there is scant evidence that lesions can sub- testing large populations at risk for atherosclerosis. The use of
stantially regress, even with aggressive risk factor modification. inflammatory markers, such as C-reactive protein levels, is an
Lipid-lowering agents—statins in particular—are thought to important step in this direction, but more sensitive and specific
stabilize lesions through various mechanisms, ultimately decreas- tests are needed. Second, improvements in the ability to analyze
ing the likelihood of plaque rupture, acute coronary syndrome, coronary artery anatomy noninvasively are needed; recent
or cardiac death. Numerous studies have demonstrated risk improvements in CT and MRI technologies are especially
reduction in individuals treated with statins. Similarly, aspirin promising. Finally, development of specific therapies that can
therapy may prevent complications related to atherosclerosis by reverse or prevent atherosclerotic lesion development remains
inhibiting platelet function, but aspirin probably has little effect a hope for the future. Gene therapy remains promising if
on atherosclerotic lesions. appropriate targets can be identified and safety issues resolved.
However, newer studies documenting the involvement of many
redundant signaling pathways in atherogenesis, along with
Avoiding Treatment Errors
improvements in targeted pharmacologic therapies, probably
The database of clinical trials in individuals at risk for acute indicate that pharmaceutical approaches will dominate future
cardiac events is growing exponentially. Guidelines are fre- therapies.
quently updated from the major international cardiovascular
societies, and practitioners are encouraged to consult them
regularly as treatment recommendations evolve. Of course, the Additional Resources
most common treatment error in patients with coronary athero- Choudhury RP, Fuster V, Fayad ZA. Molecular, cellular and functional
sclerosis is undertreatment. It is crucial that neither patients nor imaging of atherothrombosis. Nat Rev Drug Discov. 2004;3:913–925.
their health care providers underestimate cardiovascular risk, a An update of recent advances in molecular imaging of early and late stages of
significant proportion of which is modifiable. atherosclerotic disease.
Fuster V, Moreno P, Fayad ZA, et al. Atherothrombosis and high-risk
Future Directions plaque. Part I: Evolving concepts. J Am Coll Cardiol. 2005;46:937–954.
Provides a concise overview of the pathogenesis of unstable plaques.
For the immediate future, investigators of the pathogenesis of
coronary atherosclerosis will probably focus on the interplay
between genetic and environmental factors. Current approaches Evidence
include (1) identifying families of genes (using DNA gene chip
or microarray technologies), proteins, or metabolic factors Bhatt DL, Steg PG, Ohman EM, et al. International prevalence, recog-
that may predispose individuals to atherosclerosis development; nition, and treatment of cardiovascular risk factors in outpatients with
(2) defining genetic-environmental interactions that accelerate atherothrombosis. JAMA. 2006;295:180–189.
atherosclerosis; and (3) elucidating key cellular events in athero- Provides a systematic overview for diagnosis and management of patients with
genesis using genetic approaches, from initiation of gene expres- known atherothrombotic disease.
sion to how vascular and myocardial cells deal with degraded Drouet J. Atherothrombosis as a systemic disease. Cerebrovasc Dis.
proteins and other cellular components. 2002;13(Suppl 1):1–6.
Several new approaches are under consideration as therapeu- An update for the management of cerebrovascular disease.
tic methods for patients with atherosclerosis. Gene therapy
approaches, particularly those designed to inhibit cell cycle
Use of Diagnostic Testing
Thomas Burchell, Anthony Mathur, and Peter Mills 3
T he physician confronted with a patient with suspected
cardiovascular disease has a multitude of tests available
to provide diagnostic and prognostic information. Chapters 4
24- to 72-hour monitor, a patient-activated event monitor worn
for 1 to 4 weeks, or a subcutaneous Reveal device (up to 2 years).
Continuous ST-segment monitoring also collects prognostic
through 10 describe the various modalities for diagnosing car- data on patients who have had a coronary event.
diovascular diseases. This chapter focuses on the selection of the Exercise ECG is a relatively inexpensive investigation used
most appropriate tests for individual patients. in the diagnosis and management of coronary artery disease
Generally, the available cardiovascular diagnostic tests can be (CAD). However, with a sensitivity of approximately 67% and
divided into two categories: Tests that assess anatomy and tests a specificity of 84% for the detection of significant CAD in an
that assess function. These categories are merging, as tests once optimal setting (and much lower accuracy reported in other
used solely for anatomic purposes are modified to also assess settings), the main value of exercise ECG lies in excluding CAD
function. The choice of test depends not only on the question in patients who have a moderate or low pre-test probability of
being asked but also on the cost-effectiveness and predictive significant coronary stenoses. The risk of false-negative results
value of the test and the relative value of anatomic versus func- in patients with a high pre-test probability of CAD is relatively
tional information. An anatomic assessment (using a test vali- high; these patients should be referred for a more sensitive test
dated by comparison with coronary angiography) may be useful such as coronary angiography.
in some settings, but it does not eliminate the need for a func-
tional assessment, which may be even more predictive of a
Biochemical Markers
patient’s prognosis and need for further intervention.
New imaging techniques must be carefully evaluated for Serum troponin T and I are highly sensitive and specific markers
accuracy, ability to provide the needed information, and cost- for myocardial injury that are widely accepted as the standard
effectiveness compared with existing methods of obtaining biomarkers for the diagnosis of MI. Elevated troponin levels
similar information. It should be noted that the initial descrip- predict mortality in acute coronary syndromes as well as other
tion of the sensitivity and specificity of a diagnostic test may diseases, including heart failure, renal failure, and sepsis. In
overestimate what can be achieved in practice. Initial publica- acute MI, serum troponin levels rise after 2 to 3 hours, become
tions usually describe the assessment of a diagnostic test under detectable in the bloodstream at 6 to 12 hours, and remain
rigorous conditions by experienced operators in a highly selected elevated for up to 14 days. Caution interpreting positive tropo-
population. The true measure of a test is its ability to produce nin results should be used, however, because of the wide range
reliable information in a typical clinical environment. of nonischemic cardiac and noncardiac conditions that can cause
This chapter reviews the available tests that most frequently elevated serum concentrations. These conditions are numerous
provide diagnostic and prognostic information in the evaluation and include tachyarrythmia, myocarditis, direct current cardio-
of patients with suspected cardiovascular disease. As with all version, renal failure, sepsis, pulmonary embolism, and stroke.
diagnostic tests, the pre-test probability of disease must be con- The other main caution in interpretation is an understanding of
sidered carefully, both in choosing the most appropriate test and the details of the test used locally; the many commercially avail-
in its interpretation. able assays have different upper limits of normal.
Brain natriuretic peptide and its co-secreted N-terminal
fragment are useful in the diagnosis of acute heart failure in an
Diagnostic Tests emergency department and management of chronic heart failure
in a primary care setting. They may be useful to establish prog-
Electrocardiography
nosis in heart failure, in that both markers are typically higher
The resting ECG is the most frequently performed investiga- in patients with worse outcomes. Although they are highly sen-
tion in evaluating patients with cardiovascular disease (see sitive and therefore have very few false-negative results, they
Chapter 4). Electrocardiography is a highly versatile diagnostic unfortunately lack the specificity needed to exclude false-
test, providing information on a broad spectrum of clinical con- positive results and are often therefore used as a “rule out” test
ditions, ranging from metabolic disturbances (e.g., hypo- and for heart failure. Serum levels are elevated in patients with renal
hyperkalemia) and pharmacologic toxicity to ischemic heart failure, because both peptides are renally excreted. Results
disease (e.g., acute myocardial infarction [MI], unstable angina), should be interpreted in the clinical context, and positive results
arrhythmia, and pericardial disease (see Chapter 4). With such should invariably be followed by functional imaging such as an
versatility, this simple-to-perform test is cost effective. echocardiogram to formally assess cardiac function.
In the investigation of suspected or known arrhythmias,
Holter electrocardiographic monitoring augments the resting
Echocardiography
ECG by allowing correlation of patient symptoms to the rhythm
disturbance and the subsequent monitoring of the patient’s Echocardiography provides a versatile and cost-effective method
response to treatment. This can be in the form of a continuous for assessing cardiac anatomy and function (see Chapter 6). The
24 SECTION I • Introduction

Transducer element rotated to change plane of image Transducer advanced and

withdrawn to desired level

180˚
Transgastric

0˚ Upper esophagus

90˚
Mid esophagus
Posterior

Right Left

Anterior

Transducer probe flexed to change plane of image Positions and axes of image of esophageal probe

Figure 3-1 Transesophageal echocardiography.

greatest values of echocardiography are the capacity for simul- or necrosis in patients with CAD. The addition of pharmaco-
taneous assessment of valvular, pericardial, myocardial, and logic or exercise-induced stress to detect inducible ischemia
extracardiac abnormalities. Because complex image processing provides increased sensitivity and specificity compared with
is not needed, the results of the study are immediately available ECG exercise testing (Fig. 3-3, upper panel). In 21 studies, the
to the experienced echocardiographer. In addition, it is possible sensitivity of exercise stress echocardiography averaged 84%
to perform echocardiography on critically ill patients who (range 71% to 97%) and the specificity averaged 86% (range
cannot be moved, or in other circumstances when a portable 64% to 100%). The use of echocardiography can be limited
test is preferable. For these reasons, echocardiography is the by technical considerations, including an inability to obtain
preferred screening imaging test for further assessing suspected diagnostic images in some patients (an estimated 15%). Stress
myocardial dysfunction. Moreover, the use of Doppler echocar- echocardiography is indicated for individuals who have an inter-
diography (Doppler) to measure flow allows the measurement mediate prior probability of CAD and for individuals with
of peak velocity across valves, the mapping of regurgitant jets, abnormal ECGs or who are prescribed medications that can
the estimation of pulmonary artery pressures, and the detection cause ECG abnormalities with stress (such as digoxin). In either
of shunts (e.g., ventricular and atrial septal defects). The severity of these cases the predictive value of exercise ECG is substan-
of valvular heart disease and its contribution to the clinical tially reduced, justifying the use of an imaging technique
presentation can be determined immediately. For patients with during stress.
chest pain, congestive heart failure, or arrhythmias, echocar-
diography provides a rapid means of determining underlying
Contrast Echocardiography
cardiovascular function.
Transesophageal echocardiography adds to the sensitivity Injection into the circulation of contrast agents that reflect
of transthoracic echocardiography, because views of the heart ultrasound (either agitated saline or microspheres) helps dem-
are not impeded by artifact related to the lungs or chest wall onstrate intracardiac shunts, improves resolution of cardiac
(Figs. 3-1 and 3-2). In addition, transesophageal echocardiogra- structures, and enhances spectral Doppler signals of flow-
phy allows visualization of structures that are usually not well through heart valves (see Fig. 3-3, lower panel). Although con-
seen by transthoracic echocardiography (e.g., the left atrial trast echocardiography is not indicated for all patients, it can
appendage). The development of transesophageal echocardiog- allow quantification of the severity of an intracardiac shunt,
raphy has also been an important advance in the management thereby indicating whether invasive testing (cardiac catheteriza-
of patients who are undergoing cardiothoracic surgery, provid- tion) or surgery is needed. It can also improve border detection
ing information on left ventricular (LV) function and the success within the left ventricle allowing more accurate assessment of
of valvular repair. In addition, transesophageal echocardiogra- LV function.
phy may allow a more accurate determination of valvular dys-
function and assessment for bacterial endocarditis, intracardiac
Tissue Doppler
thromboses, or both.
In addition to its usefulness in assessing valvular heart The processing of Doppler signals reflected by the myocardium
disease, echocardiography provides information on regional gives two-dimensional directional information that allows better
wall motion abnormalities suggestive of myocardial ischemia visualization of the endocardium and assessment of ventricular
 CHAPTER 3 • Use of Diagnostic Testing 25

Upper esophageal position

Long axis of probe rotated to alter axis of image right and left
R. atrial appendage
Longitudinal plane 90˚
R. coronary cusp
180˚
R. atrium Noncoronary cusp
Axis
Superior vena cava L. coronary cusp
0˚ Interatrial septum
Transverse R. atrium
plane 0˚ L. atrium L. atrium
Longitudinal view Transverse view

Biplane studies carried out in longitudinal and transverse planes.

Omniplane transducer may rotate plane of examination through 180˚.

Midesophagus position
Tricuspid valve
Mitral valve L. ventricle R. atrium R. ventricle
Long-axis plane
L. atrium Left ventricle

Mitral valve

180˚
Interatrial septum
Four-chamber
plane Left atrium

Longitudinal view Transverse view

Transducer in mid esophagus allows series of longitudinal, transverse,
and oblique sections, depending on position of axis and plane of image
Transgastric position

Longitudinal plane (long-axis view) R. ventricle L. ventricle Anteroseptal wall Interoposterior wall
L. ventrical
Short-axis plane

0˚ 180˚ Aorta

90˚
Short-axis view Long-axis view
Anteflexion alters axis
of image up and down
Transducer head in proximal stomach for short-axis and long-axis planes

Figure 3-2 Transesophageal echocardiography: Positions.

wall motion. Tissue Doppler is helpful for the assessment of can be performed using either modified transthoracic or trans-
regional wall abnormalities at rest or with stress as well as being esophageal probes. It can provide high-quality images of struc-
a useful adjunct in assessing diastolic dysfunction. Though not tural abnormalities, valves, and shunts that can be especially
needed in every study, tissue Doppler can be extremely useful useful in congenital abnormalities. It is technically difficult to
in difficult-to-image individuals. perform and is mainly used in specialist centers for LV function
analysis and preoperative visualization of the mitral valve.
Three-dimensional Echocardiography
Radionuclide Testing
This relatively new extension to echocardiography technology
allows the visualization of cardiac structures in three dimensions Radionuclide imaging assesses LV function and detects induc-
over time. Three-dimensional echocardiography (3D echo) ible ischemia secondary to CAD. As described in Chapter 7,
26 SECTION I • Introduction

Exercise echocardiography
Left ventricle
Anteroseptal wall Left ventricle Left ventricle Anteroseptal wall
Right ventricle
Anteroseptal wall
Aortic valve
Left atrium
Inferoposterior wall

Anterior leaflet Inferoposterior wall

mitral valve
Resting echocardiogram Baseline stress echocardio-
gram long axis
Diastolic postexercise echocardio-
gram, long axis

Left ventricle Anteroseptal wall

Exercise performed to elicit ischemic
signs and postexercise echocardiogram
used to evaluate ventricular function,
wall motion, and thickness. Often
correlated with stress echocardiography Inferoposterior wall

Systolic postexercise echocardio-

gram, long axis

Contrast echocardiography

Right atrium Left atrium

Peripheral venous contrast
agent confined to right side
of heart in normal patient

Injection
Contrast echocardiogram of bolus
shows right-to-left shunt
through atrial septal defect Peripheral venous injection of solution
Right ventricle Left ventricle contains acoustically dense microbubbles,
affording contrast agent that delineates
Bubble study in atrial septal defect intracardiac structures and identifies shunts.
Microbubble solution

Figure 3-3 Exercise and contrast echocardiography.

quantitative assessment of right and left ventricular ejection advantage of stress MPI is that the number of patients
fractions (EFs) is highly accurate with this technique and can be for whom this imaging technique cannot be used is small. In
related to long-term prognosis. addition, stress radionuclide MPI has a proven role in predicting
Stress (exercise or pharmacologic) radionuclide myocardial future cardiac events and, importantly, is able to predict a low
perfusion imaging (MPI) in patients with suspected CAD yields mortality and subsequent infarction rate in patients with
a sensitivity of approximately 85% to 90%. When gated SPECT a totally normal scan. The use of certain radioactive tracers
is used, the specificity for excluding CAD is approximately 90%. (such as thallium) leads to a high false-positive rate; therefore,
Thus, radionuclide imaging is more specific and sensitive in technical considerations are paramount when performing and
detecting significant CAD than is exercise ECG testing and interpreting such scans. In general, the indications for stress
(like exercise echocardiography) has particular value when the MPI are similar to those for stress echocardiography: an inter-
resting ECG is abnormal and when patients are unable to mediate prior probability of disease, an abnormal baseline ECG,
achieve more than 85% of their maximum predicted heart rate or both. Both tests are also useful for patients who cannot exer-
because of locomotor or other reasons. The accuracy for cise adequately, because pharmacologic agents can be used to
diagnosing CAD is probably similar to the accuracy of stress induce stress.
echocardiography, and the choice often depends on study PET, on its own or in combination with cardiac CT
availability and frequency of use at a given center. One (PET-CT), is still used mainly as a research technique. It
 CHAPTER 3 • Use of Diagnostic Testing 27

Rest PET Scintigraphy

13NH 18FDG
3 MBF Glucose

Plane 1

Plane 2 Cardiac MRI in the four-chamber long-axis view

demonstrating midventricular variant of
hypertrophic cardiomyopathy

Plane 3

Plane 4

Before Revascularization
This is an example of a mismatch pattern on PET. The pattern was found
in a patient who had a significant anterior perfusion abnormality on
13NH imaging for assessment of MBF, but who demonstrated significant
3
uptake of 18FDG in the anterior wall. This pattern is indicative of
Hyperenhanced cardiac MRI used to detect
hypoperfused but metabolically active hibernating myocardium.
myocardial viability in a patient with subtotally
occluded left anterior descending and RCA and an
Image courtesy of Heinrich R. Schelbert, MD, PhD, FACC. ejection fraction of 30%. Myocardial scarring
shows up as bright contrast in this technique, and
this study shows normal myocardial viability
Figure 3-4 Cardiac positron emission tomography (PET). 18FDG, despite the presence of multivessel coronary artery
18-fluorine labeled 2-deoxy-2-fluoro-D-glucose; MBF, disease and left ventricular dysfunction.
myocardial blood flow.
Figure 3-5 Cardiac magnetic resonance imaging (MRI). RCA,
does, however, have validated clinical applications; quantitative right coronary artery.
assessment of perfusion using rubidium-82 or 13NH3 has a sen-
Magnetic Resonance Imaging
sitivity of 92% and a specificity of 90% for the detection of
significant proximal CAD. The other main clinical use is the MRI is a relatively safe and extremely sensitive imaging modal-
assessment of myocardial viability before planned revasculariza- ity that is superior to other noninvasive investigations in diag-
tion, using 18-fluorine labeled 2-deoxy-2-fluoro-D-glucose nosing congenital heart disease, diseases of the aorta, anomalous
(18FDG; Fig. 3-4). Mainstream clinical use of PET is limited by coronary arteries, and right ventricular dysplasia (Fig. 3-5). It is
availability, technical complexity, and high cost. also now the accepted gold standard test for assessing left and
Radionuclide imaging carries a relatively high radiation right ventricular volumes, regional and global function as
burden and in many centers is being replaced with either stress measured by EF, with a reproducibility of ±2.5% under
echocardiography or stress cardiac MRI, which do not use ion- experimental conditions. The role of MRI has been further
izing radiation (see below). extended to evaluation of myocardial perfusion both at rest and
28 SECTION I • Introduction

A B C
This is a multiplanar reconstruction (MPR) of a 64-slice cardiac CT scan
showing the right coronary artery projected in (A) axial, (B) coronal, and
(C) saggital views. It shows multiple calcified plaques (arrows) but the
lumen of the artery is unobstructed.

Figure 3-7 Computed tomography (CT) coronary angiography.

This is a short-axis late gadolinium enhanced cardiac magnetic

resonance image taken at the level of the mid ventricle. It shows an area
probability of CAD, coronary angiography should be consid-
of increased signal intensity in the lateral wall, indicating a previous ered as an initial diagnostic step.
subendocardial myocardial infarction.

Image courtesy of Dr. Mark A. Westwood and Dr. L. Geri Davies, the Computed Tomography
London Chest Hospital, UK.
With the advent of multislice and dual-source CT scanners, the
Figure 3-6 Magnetic resonance viability imaging.
improvement in both spatial and temporal resolution has allowed
this imaging modality to effectively visualize the heart, signifi-
under pharmacologic stress using gadolinium-based contrast cantly reducing the movement artifacts seen previously. This
agents. MRI can be useful in assessing myocardial viability specifically allows imaging of the coronary arteries (Fig. 3-7)
before planned revascularization, because it can accurately visu- and significant stenoses within them and can be used in certain
alize wall thickness throughout the left ventricle, allowing an circumstances instead of coronary angiography. The positive
assessment of whether normal wall thickening occurs with and negative predictive values of CT angiography are approxi-
systole. It is now also possible to assess viability in areas of previ- mately 82% and 93%, respectively, as compared with coronary
ous infarction using late gadolinium enhancement (Fig. 3-6), angiography. It is therefore a useful test to rule out significant
which accurately delineates scar from normal myocardium, even CAD in patients with low or intermediate pre-test probability,
in areas of the left ventricle where the wall is thinned. who have a contraindication to conventional coronary angiog-
Advances in MRI contrast agents and imaging technology raphy. The relatively large radiation dose (approximately 10 to
have led to the development of “coronary magnetic resonance 15 mSv), though decreasing with technologic advances, does
angiography” capable of imaging the major coronary arteries; however mean some clinicians would prefer to use alternative
however, this is unlikely to outperform either standard coronary tests such as stress echocardiography or stress MRI, which do
angiography or CT coronary angiography because of the physi- not use ionizing radiation.
cal limitations in temporal resolution. The use of MRI is limited
because of the cost and availability of scanners capable of gating
Cardiac Catheterization
the image to the ECG (which is necessary to resolve cardiac
structure) and because an increasing number of patients have Cardiac catheterization, considered the gold standard investiga-
permanent pacemakers or implantable defibrillators that are tion for patients with CAD, allows the assessment of both
currently absolute contraindications for MRI. coronary artery anatomy and LV function with very high spatial
Thus, for obtaining anatomic information, most cardiolo- and temporal resolution (Fig. 3-8). Historically, cardiac cathe-
gists advocate transthoracic echocardiography as a first step, terization provided the only means of measuring hemodynamic
followed by either transesophageal echocardiography or MRI if parameters (e.g., pressure and oxygen saturation) within various
better definition of the cardiac structures is needed. For assess- heart chambers to assess cardiac anatomy and physiology.
ment of CAD, stress ECG would be used as a screening test Most of these techniques have been superseded by noninvasive
only in individuals with a low pre-test probability of disease and tests already described. There are difficult situations, such as
a normal baseline ECG. Perfusion MRI, CT coronary angiog- the assessment of some valvular lesions or the differentiation
raphy, stress echocardiography, or MPI should be used for indi- of pericardial constriction from myocardial restriction (see
viduals who have an intermediate prior probability of disease, Chapters 10, 20, and 43), that still often require cardiac
an abnormal baseline ECG, or both, or who are taking medica- catheterization.
tions that could nonspecifically alter the ECG during exercise. Today, the most common use of cardiac catheterization is in
Patients who are unable to exercise are also well suited for conjunction with coronary angiography for anatomic delinea-
pharmacologic stress testing with echocardiographic, MRI, or tion of CAD and LV function in anticipation of revasculariza-
nuclear imaging. For most individuals with a high pre-test tion (Chapters 9 and 10). Because of its invasive nature, coronary
 CHAPTER 3 • Use of Diagnostic Testing 29

Catheter
introduced
into brachial
or
femoral artery
and passed
retrograde via
aorta to
L. ventricle

Seldinger technique for catheterization of femoral artery

Needle introduced
into artery Needle withdrawn

Catheter wire passed

through needle Catheter introduced
over wire

Figure 3-8 Left-sided heart catheterization.

angiography carries a 0.1% risk of a major adverse cardiovascu- physiologic as well as anatomic grounds. Thus, in an individual
lar event in most laboratories; for this reason, it is often per- with compelling symptoms, a noninvasive test diagnostic of
formed after a positive or equivocal noninvasive test. However, myocardial ischemia, or both, but with only moderate stenoses
the sensitivities and specificities of stress echocardiography, by coronary angiography, intravascular ultrasound and/or
MPI, and stress cardiac MRI are such that a patient with a high Doppler flow measurements may be indicated to ascertain
pre-test probability of CAD would be at risk for a false-negative whether a moderate stenosis by angiography is functionally
noninvasive test. For these individuals, coronary angiography important and a candidate lesion for revascularization.
should be the initial diagnostic test. Coronary angiography
is required before revascularization, by either percutaneous
Electrophysiology Studies
approaches or bypass surgery.
Based on the direct access to the coronary arteries provided Although resting ECG and Holter monitoring often provide
by coronary angiography, new techniques have been developed diagnostic information on the conditions of patients presenting
to provide increased accuracy in the diagnosis of coronary with palpitations or syncope, electrophysiology studies have a
heart disease. Intravascular ultrasound provides high-resolution role in diagnosing the conditions of patients in which a cardiac
images of the coronary arterial wall and has greater sensitivity etiology is unclear. Invasive stimulation studies are used to diag-
in identifying the extent of coronary atheroma than does coro- nose both ventricular and supraventricular arrhythmias and to
nary angiography alone (see Chapter 9). In particular, intravas- test the integrity of the conduction system in patients with
cular ultrasound emphasizes the importance of the “burden” of syncopal episodes (see Chapter 33).
plaque that extends toward the adventitia rather than encroach-
ing on the lumen. Functional information about the physiologic
Avoiding Diagnostic
impact of a coronary stenosis is obtainable through measure-
ments of blood flow and pressure drop across these lesions with
Testing Errors
miniaturized pressure and Doppler transducers on the ends of Whichever test(s) you use in your diagnostic workup, it is not
guide wires. These measurements correlate with long-term uncommon to get unexpected or surprising results. This can
prognosis and thus provide a means of targeting therapy on cause confusion, especially if the result does not fit the clinical
30 SECTION I • Introduction

picture. There is obviously the possibility that the result is article: a report of the American College of Cardiology/American
incorrect, being either false positive or false negative, as dis- Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE
Committee to Update the 1997 Guidelines for the Clinical Application of
cussed. There is also the possibility of detecting bystander
Echocardiography). Circulation. 2003;108(9):1146–1162.
disease that may be unrelated to the disease process being inves-
tigated (e.g., features of hypertrophic cardiomyopathy being Chow BJ, Larose E, Bilodeau S, et al. The ‘what, when, where, who and
how?’ of cardiac computed tomography in 2009: guidelines for the clinician.
identified on a viability/perfusion cardiac MRI scan for coronary Can J Cardiol. 2009;25:135–139.
disease). It may, however, still not explain the findings, in which
Review article describing indications, contraindications, advantages, and pitfalls of
case it is essential to revisit the history and clinical examination,
cardiac computed tomography.
because these can provide a wealth of useful information. It
must be remembered that tests are always an adjunct to clinical Gibbons RJ, Araoz PA, Williamson EE. The year in cardiac imaging. J Am
Coll Cardiol. 2009;53(1):54–70.
history and examination, and sometimes the addition of more
complex cardiac investigations does not lead to an improvement Comprehensive review and comment about recent advances in all aspects of cardiac
in diagnostic capability. imaging.
Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update
for exercise testing: summary article. A report of the American College of
Future Directions Cardiology/American Heart Association Task Force on Practice Guidelines
(Committee to Update the 1997 Exercise Testing Guidelines). J Am Coll
The near future in cardiac testing lies with improvements in Cardiol. 2002;40(8):1531–1540.
current technology, allowing safer, more accurate tests to guide
the physician in patient care. Cardiac CT, with more sources
Evidence
and slices, will allow increases in temporal and spatial resolution,
respectively, while reducing the overall radiation dose. This Beller GA, Zaret BL. Contributions of nuclear cardiology to diagnosis
should improve the accuracy of assessing coronary disease and prognosis of patients with coronary artery disease. Circulation.
and potentially allow plaque characterization. Cardiac MRI 2000;101:1465–1478.
will become more widespread as the number of scanners Review article describing nuclear techniques in assessing myocardial ischemia.
increases and the body of evidence builds further. This modality Camici PG. Positron emission tomography and myocardial imaging.
will more than likely replace the common use of radionuclide Heart. 2000;83:475–480.
imaging for assessment of LV function and myocardial perfu-
Review article describing the advantages of and uses for myocardial PET
sion. The potential for coronary visualization exists and will imaging.
undoubtedly continue to be refined for clinical use. There is
Jerosch-Herold M, Muehling O. Stress perfusion magnetic resonance
further promising work in MRI spectroscopy coils, allowing the imaging of the heart. Top Magn Reson Imaging. 2008;19:33–42.
assessment of metabolic function as well as perfusion and viabil-
Comprehensive review of stress cardiac MRI perfusion imaging.
ity. Pacemakers and implantable cardiac defibrillators will prob-
ably be made MRI “safe,” allowing the scanning of this important Meijboom WB, van Mieghem CA, Mollet NR, et al. 64-slice computed
patient group. tomography coronary angiography in patients with high, intermediate,
or low pretest probability of significant coronary artery disease. J Am
With the advent of more powerful computers, real-time 3D
Coll Cardiol. 2007;50:1469–1475.
echo will become widely available; the exact indications for its
Study assessing the usefulness of 64-slice CT coronary angiography to detect
use, however, are yet to be determined, since it lacks large vali-
or rule out coronary artery disease (CAD) in patients with various estimated
dation studies. New testing modalities will undoubtedly appear, pre-test probabilities of CAD compared to the gold standard of invasive coronary
but the reader is cautioned to wait until these are validated for angiography.
the clinical question being asked before being tempted to adopt
Sekhri N, Feder GS, Junghans C, et al. Incremental prognostic value
them into clinical practice. of the exercise electrocardiogram in the initial assessment of patients
with suspected angina: cohort study. BMJ. 2008;13;337:a2240.
Additional Resources
Multicenter cohort study assessing the relative and prognostic benefits of per-
Berman DS, Hachamovitch R, Shaw LJ, et al. Roles of nuclear cardiology, forming an exercise ECG in addition to a clinical history and resting ECG in
cardiac computed tomography, and cardiac magnetic resonance: assessment patients attending the Rapid Access Chest Pain Clinic in the United Kingdom.
of patients with suspected coronary artery disease. J Nucl Med. 2006; Concluded that the addition of an exercise ECG added little prognostic value
47(1):74–82. above clinical history and resting ECG.
Review article discussing the relative merits of these three myocardial perfusion
modalities.
Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003
guideline update for the clinical application of echocardiography: summary
Electrocardiography
Leonard S. Gettes 4
I t is now more than 100 years since the Dutch physiologist
Willem Einthoven recorded the first ECG from humans.
Although the number of recording leads has increased from 3
alteration of the ECG waveform. However, when they are
placed within the body torso, as is the case during exercise
testing and when patients are monitored in critical care areas,
to at least 12 and the recording instruments have evolved into the waveform recorded by the limb leads will be affected.
sophisticated automated digital recorders capable of recording,
measuring, and interpreting the electrocardiographic waveform,
the basic principles underlying the ECG are unchanged. The
Electrocardiographic Waveform
electrocardiograph is basically a voltmeter that records, from The ECG waveform consists of a P wave, a PR interval, the
the body surface, the uncanceled voltage gradients created as QRS complex, an ST segment, and T and U waves. The rela-
myocardial cells sequentially depolarize and repolarize. tionship of these waveform components to the underlying action
The ECG is the most commonly used technique to detect potentials of the various cardiac tissues is shown in Figure 4-2A,
and diagnose heart disease and to monitor therapies that influ- as is an example of a normal 12-lead ECG in Figure 4-2B. The
ence the heart’s electrical activity. It is noninvasive, virtually P wave reflects depolarization of the atria, the QRS complex
risk free, and relatively inexpensive. Since its introduction, reflects depolarization of the ventricles, and the ST segment and
a large database has been assembled correlating the ECG T wave reflect repolarization of the ventricles. The U wave
waveform recorded from the body surface to the underlying occurs after the T wave and is thought to be an electromechani-
electrical activity of individual cardiac cells on the one hand, cal event coupled to ventricular relaxation.
and to the clinical presentation of the patient on the other, Depolarization of the sinus node occurs before the onset
thereby providing insight into the electrical behavior of the of the P wave, but its voltage signal is too small to be recorded
heart and its modification by physiologic, pharmacologic, and on the body surface by clinically used electrocardiographic
pathologic events. machines and the event is electrocardiographically silent. Simi-
larly, the electrical activity of the atrioventricular (AV) junction
and the His-Purkinje system, which occur during the PR inter-
Leads val, is electrocardiographically silent.
Twelve leads are routinely used to record the body surface
ECG: three bipolar limb leads labeled I, II, and III; three aug-
P Wave
mented limb leads labeled aVR, aVL, and aVF; and six unipolar
chest leads labeled V1 through V6 (Fig. 4-1). In the bipolar limb The P wave is caused by the voltage gradients created as the
leads, the negative pole for each of the leads is different, whereas atrial cells sequentially depolarize. The shape and duration of
in the unipolar chest leads, the negative pole is constant and the P wave are determined by the sequence of atrial depolariza-
created by the three limb leads. This is referred to as Wilson’s tion and the time required to depolarize the cells of both atria.
central terminal. The positive chest lead is, in effect, an exploring The sinus node is located at the junction of the superior vena
lead that can be placed anywhere. In children, the routine ECG cava and the right atrium, and the direction of atrial depolariza-
often includes leads placed on the right side of the chest in posi- tion, from right to left, from superior to inferior, and from
tions referred to as V3R and V4R. Similar right-sided chest leads anterior to posterior reflects this geography. This results in a
are often used in adults to diagnose right ventricular infarction, P wave that is characteristically upright or positive in leads I, II,
and one or more leads placed on the back are sometimes used V5, and V6 and inverted or negative in lead aVR. In lead V1, the
to diagnose posterior wall infarction. P wave may be upright, biphasic, or inverted. The amplitude
The chest leads are relatively close to the heart and are influ- and duration of the normal sinus P wave may be affected by
enced by the electrical activity directly under the recording atrial hypertrophy and dilation and by slowing of interatrial and
electrode. This is in contrast to the limb leads in which the intra-atrial conduction.
electrodes are placed outside of the body torso. Changes in the Impulses arising from an ectopic atrial focus are associated
position of an individual chest lead or the relationship between with P waves whose shape depends on the location of the focus.
the chest leads and the heart may cause significant changes If the abnormal focus is in close proximity to the sinus node,
in the ECG pattern. For instance, if the patient is in a sitting the sequence of atrial activation will be normal or nearly normal,
rather than a supine position, the relationship of the various and the P wave will resemble the normal sinus P wave. The
chest leads to the heart will change and the ECG waveform more distant the ectopic focus is from the sinus node, the more
recorded by the chest leads may be altered. Similarly, if a chest abnormal will be the sequence of atrial activation and the P-wave
lead is placed an interspace too high or too low, the ECG wave- configuration. For instance, impulses originating in the inferior
form recorded by that lead will change. For this reason, when portion of the atrium or within the AV node will depolarize the
serial ECGs are recorded, it is important that lead placement atria in a retrograde, superiorly oriented direction and will be
be consistent and reproducible. In contrast, limb leads may be associated with the P waves that are inverted in leads II, III, and
placed anywhere on the various limbs with little significant aVF and upright in lead aVR (Fig. 4-3).
32 SECTION I • Introduction

Limb leads

Lead I Lead II Lead III

Augmented limb leads

Lead aVR Lead aVL Lead aVF

Precordial leads

When current flows toward red

V6
arrowheads, upward deflection
occurs in ECG
V5
When current flows away from red
V4 arrowheads, downward deflection
V1 V2 V3 occurs in ECG

When current flows perpendicular

to red arrows, no deflection or
biphasic deflection occurs

Figure 4-1 Electrocardiographic leads and reference lines. ECG, electrocardiogram.

PR Interval QRS Complex

The PR interval extends from the onset of the P wave to the The QRS complex reflects ventricular depolarization. The
onset of the QRS complex and includes the P wave and the PR interventricular septum is the first portion of the ventricle to
segment (the segment from the end of the P wave to the onset be depolarized. Thereafter, the impulse spreads through the
of the QRS), which consists of atrial repolarization and depo- His-Purkinje system and then depolarizes the ventricles simul-
larization of the AV node and His-Purkinje system. The PR taneously, from apex to base and from endocardium to epicar-
interval is prolonged by factors that slow AV nodal conduction, dium. Because the left ventricle is three times the size of
such as a decrease in sympathetic tone or an increase in vagal the right, its depolarization overshadows and largely obscures
tone, by drugs that have these effects such as digitalis and right ventricular depolarization. The QRS complex reflects
the β-adrenergic blocking agents, and by a variety of inflamma- this left ventricular dominance, and for this reason, the QRS
tory, infiltrative, and degenerative diseases that affect the AV complex is usually upright or positive in leads I, V5, and V6, the
junction. The PR interval is shortened when impulses bypass left-sided and more posterior leads, and negative or inverted
the AV node and reach the ventricles via an AV nodal bypass in aVR and V1, the right-sided and more anterior leads. It
tract to cause ventricular preexcitation (Wolff-Parkinson-White is only in situations such as right bundle branch block and sig-
syndrome). nificant right ventricular hypertrophy that the electrical activity
 CHAPTER 4 • Electrocardiography 33

Action potentials
SA node
Normal ECG
Atrial muscle
AV node I aVR V4
V1
Common
bundle
Bundle
branches II aVL V5
Purkinje V2
fibers
Ventricular
muscle
B III aVF V3 V6

Example of a normal ECG recorded from a 24-year-old woman. Note that

T the P wave is upright in leads I and II and inverted in aVR. The QRS
P
U complex gradually changes from negative to V1 to positive V6. Note that the
QRS polarity of the T wave is similar to that of the QRS complex.
0.2 0.4 0.6
A Seconds

Figure 4-2 (A) Relation of action potential from the various cardiac regions to the body surface electrocardiogram (ECG). (B) Normal
ECG.

associated with right ventricular depolarization is identified on sequence of activation. Such slowing may be caused by cardioac-
the ECG. tive drugs, an increase in extracellular potassium concentration,
The QRS complex is altered in both shape and duration by and diffuse fibrosis or scarring as may occur in patients with
abnormalities in the sequence of ventricular activation. These severe cardiomyopathies.
include the bundle branch blocks (Fig. 4-4A), the fascicular The electrocardiographic criteria for the diagnosis of
blocks, ventricular preexcitation (Fig. 4-4B), nonspecific intra- intraventricular conduction disturbances have been published.
ventricular conduction disturbances, and ectopic ventricular Important features include the following:
beats (Fig. 4-4C). The increase in QRS duration may range
from a few milliseconds, as in the case of fascicular blocks, to 1. The fascicular blocks, by altering the initial portion of
more than 40 milliseconds, as with bundle branch blocks. The the QRS complex as well as the electrical axis in the frontal
fascicular blocks reflect conduction slowing in one fascicle of plane, may obscure the diagnosis of a prior myocardial infarc-
the left bundle and are characterized by a shift in electrical axis tion (MI) while causing other changes that can simulate an
and subtle changes in the initial portion of the QRS complex. infarction.
The bundle branch blocks are caused by conduction slowing 2. Right bundle branch block does not affect the initial portion
or block in the right or left bundle branch, usually caused by of the QRS complex, because activation of the interventricu-
fibrosis, calcification, or congenital abnormalities involving lar septum and the left ventricle are unaffected. Thus, the
the conducting system. They are associated with more pro- electrocardiographic changes of a prior MI or left ventricular
nounced abnormalities in the sequence of ventricular activation hypertrophy can still be appreciated.
than are the fascicular blocks and thus with more significant 3. Left bundle branch block and ventricular preexcitation
changes in the QRS configuration. Intraventricular conduction do affect the initial portion of the QRS complex. Thus, the
abnormalities may also occur without a change in QRS configu- ECG changes associated with a prior MI and hypertrophy
ration and reflect slow conduction without a change in the can be obscured or, as frequently occurs with ventricular
preexcitation, can be mimicked.
4. Abnormalities in the sequence of depolarization are always
associated with abnormalities in the sequence of repolariza-
I
aVR tion. This results in secondary changes in the ST segment
V1 V4 and T wave. This is particularly prominent in the setting
of left bundle branch block and ventricular preexcitation
II aVL (see Figs. 4-4A and B).
V5 5. Changes in intraventricular conduction may be rate depen-
V2
dent and present only when the rate is above a critical
III level or after an early atrial premature beat. In this situation
aVF V6
V3 it is referred to as rate-dependent aberrant ventricular
conduction.
Electrocardiogram showing an ectopic atrial rhythm. It was recorded
from a 59-year-old man. The polarity of the P wave is abnormal. It is 6. The shape and duration of the QRS complex of ectopic
inverted in leads II, III, and aVF and upright in lead aVR. ventricular beats will be influenced by the site of the ectopic
focus just as the shape and duration of atrial ectopic beats are
Figure 4-3 Ectopic atrial rhythm. influenced by their site of origin.
Another Random Scribd Document
with Unrelated Content
is not yet much promise of leaf and flower, but the catkins hang
upon the trees and the hedges are turning green, and the days are
long and the evenings are light. I think that Easter Monday is the
greatest holiday of the year to East London.
It has replaced the old May-day. Formerly, when by the old style
May-day fell on what is now the 14th, it came very happily at the
real commencement of the English spring. We are liable to east
winds and to cold and frost till about the middle of May, after which
it is seldom that the east wind returns. On that day the whole City
turned out to welcome summer. Think what they had gone through;
the streets unpaved, mere morasses of mud and melting snow; the
houses with their unglazed windows boarded up with shutters; the
long evenings spent crouching round the fire or in bed; no fresh
meat, no vegetables, only salted meat and birds, and, to finish with,
the forty days of fasting on dried fish, mostly so stale that it would
not now be allowed to be offered for sale. And here was summer
coming again! Out of the City gates poured the young men and the
maidens to gather the branches and blossoms of the white-thorn, to
come back laden with the greenery and to dance and sing around
the May-pole.
May-day has long ceased to be a popular festival. The Puritans
killed it. Yet there still linger some of the old signs of rejoicing. To
this day the carmen deck their horses with ribbons and artificial
flowers on May-day. Until quite recently there were one or two May-
day processions still to be seen in the streets. The chimney-sweeps
kept up the custom longest. They came out in force, dressed up with
fantastic hats and colored ribbons. In the midst was a moving arbor
of green branches and flowers, called Jack in the Green. Beside him
ran and danced a girl in gay colors, who was Maid Marian. Before
him went a fife and drum or a fiddler, and they stopped at certain
points to dance round Jack in the Green. Another procession,
discontinued before that of the chimney-sweeps, was that of the
milkmaids. The dairy women, dressed in bright colors and having
flowers in their hair or in their hats, led along a milch cow covered
with garlands. After the cow came a man inside a frame which bore
a kind of trophy consisting of silver dishes and silver goblets, lent for
the occasion and set in flowers. Of course they had a fiddler, always
represented in the pictures as one-legged, but perhaps the absence
of a leg was not an essential.
May-day is gone. Its place is taken, and more than taken, by
Easter Monday. It is the fourth and last day of the longest holiday in
the whole year. From Good Friday to Monday, both inclusive, no
work is done, no workshops are opened. The first day, the Day of
Tenebræ, the day of fasting and humiliation, is observed by East
London as a day of great joy; it is a day on which the men seek their
amusements without the women; on this day there are sports, with
wrestling and boxing, with foot-ball and athletics; the women, I
think, mostly stay at home. On the Saturday little is done but to rest,
yet there are railway excursions; many places of amusement, such
as the Crystal Palace and the Aquarium (they offer a long round of
shows lasting all through the day), are open. Easter Sunday is
exactly like any other Sunday. But Monday—Monday is the holiday
for all alike, men, women, and children. Poor and miserable must
that man be who cannot find something for Easter Monday.
There used to be the Epping Hunt. This absurd burlesque of a
hunt was the last survival of the right claimed by the citizens of
London to hunt in the forests of Middlesex. On Easter Monday the
“hunt” assembled; it consisted of many hundreds of gallant
huntsmen mounted on animals of every description, including the
common donkey; there were also hundreds of vehicles of every kind
bringing people out to see the hunting of the stag. It was a real stag
and a real hunt. That is to say, the stag was brought in a cart and
turned out, the horsemen forming an avenue for him to run, while
the hounds waited for him. There was a plunge, a shout; the stag
broke through the horsemen and ran off into the cover of the forest,
followed by the whole mob at full gallop; the hounds seem to have
been for the most part behind the horses, which was certainly safer
for them. The stag was not killed, but was captured and taken away
in the cart that brought him. The Epping Hunt is no longer
celebrated, nor is Epping Forest any longer one of the haunts of
Easter Monday.

Hampstead Heath, Looking “Hendon Way.”

 Five miles from St. Paul’s cathedral lies a broad heath on the
plateau of a hill. This is Hampstead Heath. Two hundred years ago,
on the edge of the heath was a Spa, with a fashionable assembly-
room and a tavern. The Spa decayed, and the place became the
residence of a few wealthy merchants, each with his stately garden.
Some of these houses and these gardens survive to this day; most
of them are built over, and Hampstead is now a suburb of eighty
thousand people, standing on the slope and top of a long hill rising
to the height of nearly five hundred feet. The heath, however, has
never been built upon. It is a strangely beautiful place; not a park,
not a garden, not anything artificial, simply a wild heath covered
with old and twisted gorse bushes, with fern and bramble, and in
spring lovely with the white-thorn and the blackthorn and the
blossoms of the wild crab-apple, Britain’s only native fruit. The heath
is cut up into miniature slopes and tiny valleys; a high causeway
runs right across it; the place is so high that there is a noble view of
the country beyond, while at rare intervals, when the air is clear, the
whole valley of the Thames lies at the spectator’s feet, and London,
with her thousand spires and towers is clearly visible, with St. Paul’s
towering over the whole.
The heath is the favorite resort of the holiday makers of Easter
Monday; a kind of fair is permitted on one side, with booths and the
customary bawling. There are never any shows on Hampstead Heath
—I know not why. The booths are for rifle galleries, for tea and
coffee and ices, for cakes and ginger-beer, for crafty varieties in the
game of dropping rings or pretty trifles for bowls and skittles, and
for “shying” sticks at cocoanuts. No stalls are allowed for the sale of
strong drink. Here the people assemble in the morning, beginning
about ten, and continue to arrive all day long, dispersing only when
the sun goes down and the evening becomes too cold for strolling
about. They may be numbered by the hundred thousand. Here are
the factory girls, going about in little companies, adorned with
crimson and blue feathers; they run about laughing and shrieking in
the simple joy of life and the exhilarating presence of the crowd;
they do not associate with the lads, who dress up their hats with
paper ribbon and hurl jokes, lacking in originality as in delicacy, at
the girls as they run past. There are a great many children; the
policemen in the evening bring the lost ones, disconsolate, to the
station. Some of them have come with their parents; some of them,
provided with a penny each, have come alone; it is wonderful to see
what little mites run about the heath, hand in hand, without any
parents or guardians. There are young married couples carrying the
baby. All the people alike crowd into the booths and take their
chance at what is going on; they “shy” at the cocoanuts as if it were
a new game invented for that day, they dance in the grass to the
inspiring strains of a concertina, they swing uproariously in the high
wooden carriages, they are whirled breathlessly round and round on
the steam-conducted wooden cavalry, and all the time with shouting
and with laughing incessant. For, you see, the supreme joy, the true
foundation of all this happiness, is the fact that they are all out again
in the open, that the winter is over and gone, and that they can
once more come out all together, as they love, in a vast multitude.
To be out in the open, whether on the seashore or on Hampstead
Heath, in a great crowd, is itself happiness enough. There is more
than the joy of being in a crowd; there is also the joy of being once
more on the green turf. Deep down, again, in the hearts of these
townbred cockneys there lies, ineradicable, the love of the green
fields and the country air. So some of them leave the crowd and
wander on the less frequented part of the heath. They look for
flowers, and pick what they can find; the season is not generally so
far advanced as to tempt them with branches of hawthorn, nor are
the fields yet covered with buttercups; the buds are swelling, the
grass puts on a brighter green, but the spring as yet is all in
promise. There are other country places of resort, but Hampstead is
the favorite.
For those who do not go out of London on Easter Monday there
are more quiet recreations. On that day Canon Barnett opens his
annual exhibition of loan pictures at his schools beside his church at
Whitechapel; to the people of his quarter he offers every year an
exhibition of pictures which is really one of the best of the yearly
shows, though the West End knows nothing about it, and there is no
private view attended by the fashionable folk, who go to see each
other. There is a catalogue; it is designed as a guide and an aid to
the reader; it is therefore descriptive; in the evening ladies go round
with small parties and give little talks upon the pictures, explaining
what the artist meant and how his design has been carried out. Such
a party I once watched before Burne-Jones’s picture of “The Briar
Rose.” The people gazed; they saw the brilliant coloring, the briar-
rose everywhere, the sleeping knights, the courtyard—all. Then the
guide began, and their faces lit up with pleasure and understanding,
and all went home that evening richer for the contemplation and the
comprehension of one great work of art.
At the People’s Palace there are concerts morning and evening;
perhaps also there is some exhibition or attraction of another kind;
there are other loan exhibitions possible besides those of art.
Some of the people, but not many, go off westward and wander
about the halls of the British Museum. I do not know why they go
there, because ancient Egypt is to them no more than modern
Mexico, and the Etruscan vases are no more interesting than the
“Souvenir of Margate,” which costs a penny. But they do go; they
roam from room to room with listless indifference, seeing nothing. In
the same spirit of curiosity, baffled yet satisfied, they go to the South
Kensington Museum and gaze upon its treasures of art; or they go to
the National Portrait Gallery, finding in Queen Anne Boleyn a striking
likeness to their own Maria, but otherwise not profiting in any
discoverable manner by the contents of the gallery. And some of
them go to the National Gallery, where there are pictures which tell
stories. Or some get as far as Kew Gardens, tempted by the
reputation of the houses which provide tea and shrimps and water-
cresses outside the gardens, as much as by the Palm House and the
Orchid Houses within.
The streets on Easter Monday present a curious Sunday-like
appearance, with shops shut and no vehicles except the omnibus,
but in the evening the theater and the music-hall are open, and they
are crammed with people.
Therefore, though Easter Monday is the greatest of the people’s
holidays, it is so chiefly because it is the first, and because, like the
May-day of old, it stands for the end of the long, dark winter and the
first promise of the spring. Even in the streets, the streets of dreary
monotony, the East Londoners feel their blood stir and their pulses
quicken when the April day draws out and once more there comes
an evening light enough and long enough to take them out by tram
beyond the bricks.
The holiday of early summer is Whit-Monday, which is also a
movable feast, and falls seven weeks after Easter, so that it is due
on some day between May 12th and June 12th. I have already
observed that the cold east wind, which retards our spring, generally
ceases before the middle of May, though in our climate nothing is
certain—not even hot weather in July and August. When it falls
reasonably late, say in the first week of June, there is some
probability that the day will be warm, even though there may be
showers; that the woods will be resonant with warblers, the fields
golden with buttercups, the hedges bright with spring flowers, the
bushes white and pink with May blossom, and the orchards glorious
with the pink of the apple and the creamy white of the cherry and
the pear. On this day the East Londoner goes farther afield; he is not
content with Hampstead Heath, and he will not remain under cover
at the Crystal Palace. Trains convey him out of London. He goes
down to Southend, at the mouth of the Thames; there, at low tide,
he can gaze upon a vast expanse of mud or he can walk down a pier
a mile and a half long, or, if it is high tide, he may delight in the
dancing waters with innumerable boats and yachts. Above all, at
Southend he will find all the delights that endear the seaside to him;
there is the tea with shrimps—countless shrimps, quarts and gallons
of shrimps; he is among his own kind; there is no one to scoff when,
to the music of the concertina, he takes out his companion to dance
in the road; he sings his music-hall ditties unchecked; he bawls the
cry of the day, and it is counted unto him for infinite humor.
Southend on Whit-Monday is a place for the comic man and the
comic artist; it is also the place for the humorist.

The Shooting-Gallery.
 One must not be hard upon the Whit-Monday holiday-maker. He is
at least good-humored; there is less drunkenness than one would
expect; there is very little fighting, but there is noise—yes, there is a
good deal of noise. These children of nature, if they feel happy,
instinctively laugh and shout to proclaim their happiness. They would
like the bystanders to share it with them; they cannot understand
the calm, cold and unsympathetic faces which gaze upon them as
they go bawling on their way. They would like a friendly chorus, a
fraternal hand upon the shoulder, an invitation to a drink. Let us put
ourselves in their place and have patience with them.
I have already mentioned Epping Forest in connection with the
cockney hunt of Easter Monday. But to be seen in the true splendor
of its beauty Epping Forest must be visited in early June. It is the
East Londoner’s forest; fifty years ago he had two; on the east of
Epping Forest lay another and a larger, called Hainault Forest. It was
disforested and cleared and laid out in farms in the year 1850.
Epping, however, remains. It is about sixteen miles north of the
river; encroachments have eaten into its borders, and almost into its
very heart. For a long time no one paid any attention. Suddenly,
however, it was discovered that the forest, which had once covered
twelve thousand acres, now covered only three thousand. Three
fourths had been simply stolen. Then the City of London woke up,
appointed a verderer and rangers, drew a map of what was left, and
sternly forbade any more encroachments. What is left is a very
beautiful wild forest; deer roam about its glades; for the greater part
of the year it is quite a lonely place, only receiving visitors on
Saturday afternoons and Sundays. It is a narrow, cigar-shaped wood
about a mile broad and eight miles long. There are outlying bits on
the north and on the south. The ancient continuity of the forest is
gone, but there are tangles of real wood and coppice here and
there; the central point of the forest, that which attracts most
people, is a small bit of wild wood lying on a hill. Here the ground is
rough and broken; everywhere are oaks, elms, beeches, and
hornbeams, with a veritable jungle of wild roses, sloes, thorns, and
brambles. The woods are filled with singing birds; the ground is
covered with wild flowers. Imagine the joy of the East Londoner on
Whit-Monday when he plunges up to his knees in the buttercups, the
wild anemones, and the flowering grasses, while the lark sings
overhead, and thrush and blackbird call from the woods around him,
and the sun warms him and the sweet air refreshes him. Such an
one I followed once and watched. He was a young fellow of twenty-
one or so, with his wife, a girl of nineteen, behind him. He had taken
the pipe out of his mouth; instinctively he felt that the pipe was out
of place; he threw himself down upon the grass and clasped his
hands under his head. “Gawspel truth, old gal!” he cried, out of the
fullness of his heart. “It’s fine! It’s fine!”
It was fine, and it was Whit-Monday, and a hundred thousand
others like unto this young fellow and his bride were wandering
about the forest that day.
There are not many students of archæology in East London, which
is a pity, since there are many points of interest within their reach.
All round the forest, for instance, and within the forest there are
treasures. To begin with, there are two ancient British camps still in
good preservation; there is a most picturesque deserted church,
called old Chingford church; there is the ancient Saxon church,
whose walls are oaken trunks, put up to commemorate the halt of
those who carried St. Cuthbert’s bones; there is Waltham Abbey,
where King Harold lies buried; and if you take a little walk to the
east you will find yourself at Chigwell, and you may dine at the inn
where, in the Gordon troubles, as presented in “Barnaby Rudge,” the
landlord found a trifle of glass broken. But the joy in things ancient
has not yet been found out by the London workman. Now and again
he is a lover of birds or a student of flowers; for such an one Epping
is a haunt of which he can never tire, for it is the only place near
London where he can watch heron, hawk, kingfisher, and the wild
water-fowl.
Or the people go farther afield by cheap excursion trains. Their
coming is not welcomed by the inhabitants of the towns which are
their destination. They go to Brighton or to Hastings; they sit in long
rows, side by side, upon the shingle idly watching the waves; they
go to Portsmouth and sit on Southsea beach watching the ships.
They even get across to the Isle of Wight. Last year I was at a little
town in that island called Yarmouth. I there made the acquaintance
of an ancient mariner who was employed by Lloyd’s to take the
names of all the ships which passed into the Solent, here a narrow
strait. He told me in conversation that I ought to see their church,
which is old and beautiful. I replied that I had attempted to do so,
but found the door shut. Upon which he gave me the following
remarkable reason for this apparent want of hospitality. I quote his
words to show the local opinion of the tripper. “You see,” he said,
“it’s all along of they London trippers. One Whit-Monday they came
here and they found the church doors open and in they went,
nosebags and cigarettes and all. Then the parson he came along,
and he looked in. ‘Well,’ says the parson, ‘Dash my wig!’ he says.
‘Get up off of them seats,’ he says, ‘and take your ’ats off your ’eads,’
he says, ‘and take they stinkin’ bits o’ paper out of your mouths,’ he
says, ‘and get out of the bloomin’ church,’ he says. And he puts the
key in his own pocket, and that’s why you can’t get into the church.”
The remarkable language attributed to the parson on this occasion
illustrates the depth of local feeling about East London out on a
holiday.
The August bank-holiday is a repetition of Whit-Monday, without
the freshness of that early summer day. By the end of July the
foliage of the trees has become dark and heavy; the best of the
flowers are over in field as well as garden; the sadness of autumn is
beginning. All through the summer, especially on Saturdays and
Sundays, the excursion trains are running in all directions, but
especially to the seaside; the excursion steamers run to Southend,
Walton, Margate, and Ramsgate. For those who stay at home there
are the East-End parks, Victoria Park, West Ham Park, Finsbury Park,
Clissold Park, Wanstead Park. They are thronged with people
strolling or sitting quietly along the walks. All these parks are alike in
their main features; they are laid out in walks and avenues planted
with trees; they contain broad tracts of green turf; there is an
inclosure for cricket; sometimes there is a gymnasium, and there is
an ornamental water, generally very pretty, with rustic bridges,
swans, and boats let out for hire. Where there is no park, as at
Wapping and Poplar by the riverside, there are recreation grounds.
In all of them a band of music plays on stated evenings.
 On Margate Sands.

This restoration of the garden to the people is a great feature of

modern attempts at civilization; it seems terrible that there should
be no place anywhere for children to play except the streets, or for
the old people to sit except in the public house. London is now
dotted with parks, chiefly small and covered with gardens. Nearly all
the churchyards have been converted into gardens; the headstones
are ranged along the walls; they might just as well be taken away;
one or two “altar tombs” are left. The rest of the ground is planted
with flowering shrubs—lilac, laburnum, ribes, the Pyrus Japonica,
and the like; the walks are asphalted, and seats are provided. Nearly
all the year round one may see the old people walking about the
paths or sitting in the sun; part of the ground is given to the
children. It is difficult, indeed, to exaggerate the boon conferred
upon a crowded city by these breathing-places, where one can be
quiet. The summer amusements of the people, you will observe, are
not all made up of noisy crowds and musical trippers; add the
summer evening walk in the park and, all the year round, the rest in
the garden that is a disused burial-ground.
For the children there is the day in the country. Every summer day
long caravans of wagons filled with children, singing and shouting as
they go, drive along the roads to the nearest country place, or
excursion trains crammed with children are carried off to the nearest
seaside places. They run about on the seashore, they bathe, they sit
down to a tea of cake and buns, and they are taken home at night
tired out but singing and shouting to the end. This summer “day
out” is the one great holiday for the children; they scheme to get put
on the lists of more than one excursion; they look forward to it; they
count upon it. Every year vigorous appeals are made in the papers
for help to send the children away upon their annual holiday; these
appeals are of course pitched extravagantly high; they talk a
conventional jargon about the little ones who grow up without ever
gazing upon a green leaf or a tree. Rubbish! There is not a street
anywhere in London where a garden, if it is only a disused burial-
ground, is not accessible if the children choose to go there. Mostly
the very little ones prefer the dirt pies in the gutter, but even for
them the wagonette comes now and then to carry them off for the
whole day to the grass of Victoria Park. Still, it is a very great thing
that they should, once at least in the year, be carried away into real
country and have a glimpse of meadows, woods, and cows and
sheep.
When they grow older they are still better off. It is quite common
now for young men who carry on the Settlements and the boys’
clubs to get the lads under their care to save up week by week until
they have amassed the sum of five shillings. On this capital, with
management, they are enabled to get a week’s holiday by the
seaside. It is a glorious time for them. A convenient place is found; it
must be on the seashore; it should be quite free from any town or
village; there must be no temptations of any kind; the lads are there
to breathe fresh air and life, quite cut off from any suggestion of
town life. They sleep, every boy in his own rug, on dry, clean straw
in a barn, which is also their refectory, their lecture-hall, their
concert and their singing-room. On the seashore there are boats for
them; they row and sail and they go deep-sea fishing; they bathe
every day, and they have swimming matches; on the sands they run
races; in the evening they sing, they box, they look at dissolving
views, and they lie down on the straw to rest. Their food is plain; it
consists principally of boiled beef and potatoes, with cocoa and
coffee and bread and butter. Of course this magnificent holiday
demands a head and leader and obedience. But there is hardly ever
any hitch or breakdown or row among the lads.
The hopping, considered as an amusement, should be placed
next, but we have already shown the place it takes in the year of the
factory girl. It is indeed amusement to all concerned, especially if the
weather be fine; it is amusement with profit; the hoppers come
home with a pocket full of money; they have left their pasty cheeks
in the country, and they bring back rosy cheeks and freckled noses
and sunburned hands, with the highest spirits possible. The hopping,
I confess, is not always idyllic. Last autumn it was reported that
Maidstone Gaol was filled with hoppers charged with being
disorderly; their camps might be conducted with more care for
cleanliness; London roughs should not be allowed to come down on
Sunday and mar this Arcadia. But the complainant, a well-known
clergyman of the district, spoke with moderated condemnation. A
more careful classification of the families in each encampment, he
thinks; some check on the Sunday drink, which now flows at the
sweet will of the people; some hindrance to the incursion of the
Sunday rough; a more careful system of inspection—these things
would go far to remove all reproach from the hopping. Meantime, as
a proof of the substantial results of the work the roadway outside
the principal station for their return was this year observed to be
strewn with the old boots discarded by the hoppers when they
bought new ones on their way home.
The river Lea, which, according to some, is the natural boundary
of East London,—but it has leaped across that boundary,—is part of
the summer amusements. The stream at its mouth, where it is a
tributary to the Thames, is a black and murky river indeed. Higher
up above the works it is a pleasant little river, winding along at
leisure through a broad, marshy valley. The ground is soft and easy
to be worked, the incline is so gradual that it might easily and at
small expense be made an ornamental stream, moderately broad
and able to carry racing boats, flowing beside gardens and under
summer-houses and between orchards from its source to its mouth.
Instead of this, it has been mercilessly divided into “cuts,” channels,
and mill-streams running off at wide angles, joining again lower
down, separating again into other cuts and channels, again to unite.
On its way it receives the refuse of mills, the refuse of towns; it
passes Ware and Ryehouse, Tottenham, Clapton, and Hackney; its
course unfortunately lies for the most part through a broad level of
soft earth—marshy and low—which permits these cuttings and
humiliations. It is accused of being a sewer; young men row upon it;
boys bathe in it, but with remonstrance and complaint. The stream
is, it must be confessed, in its lower reaches, offensive. Sore throats
are caught beside its banks; sometimes people write indignantly
about it to the papers. There is a little fuss, summer passes, in the
winter no one goes near the river Lea, things are forgotten, and all
goes on as before.
It is not possible for a river to flow for thirty miles without having
lovely stretches and picturesque corners. The Lea, with all its
drawbacks, does possess these inevitable lapses into beauty. But in
these pages we cannot stop to point them out. Where the Lea is
beautiful it is outside the widest limits assignable to East London.
Where the Lea is ugly, dirty, and disreputable, it used to form the
eastern boundary to East London.
In the brief sketch of the summer amusements I have said
nothing of the bicycle. Now, all the roads outside London are on
Saturday and Sunday dotted with the frequent bicycle. It goes out in
companies of twenty and thirty; it goes out by twos and threes; it
goes out singly. On one Sunday twenty-five thousand bicycles were
counted crossing one bridge over the Thames and making for the
country beyond. And it seems that there are none so poor as not to
afford a bicycle. The secret is, I believe, that a second-hand bicycle,
or a bicycle of the last fashion but one, or a damaged bicycle, may
be purchased of its owner for a mere trifle, and these lads learn very
quickly how to repair the machine themselves.
But the summer all too quickly draws to an end. By the middle of
September twilight falls before seven. There are no more evening
spins ten miles out and back again; by the end of October twilight
falls at five; then there are no more Saturday afternoons on the
road. The weather breaks, the roads are heavy, the bicycle is laid
aside for the next four months, perhaps for more, because the cold
east wind of early spring does not make the roads pleasant except
for the hardiest and the strongest. The winter amusements begin.
For the factory girls and the dockers we have seen what they are:
the street first and foremost; always the street, imperfectly lit, the
pavement crowded; always the street, in which the girls march up
and down three or four abreast. Their laugh is loud, but it is not
forced; their jokes and their badinage with the lads are
commonplace and coarse, but they pass for wit; they enjoy the
quick pulse when all the world is young; they are as happy as any
girls in any other class; they need not our pity; youth, if it has
enough to eat and its evening of amusement, is always happy.
They have, then, the boulevard without the café, the street with
the public house and the invitation from youth, prodigal of its pence,
to step in and have a drink. In addition, they have the music-hall
and the theater. For some there is the club; but only a few,
comparatively, can be persuaded to go into the club for an hour or
two every evening. Most of them have no desire for a quiet place;
they are obliged to be quiet in the factory; at night they like to make
up for the day’s long silence.
So with their companions, the casual hands, the factory lads, the
Hooligans, the children of the kerb, they rejoice in the days of their
youth.
Let us mount the social scale; we come to the craftsman in steady
work, to the small clerk, to the small shopkeeper. Not that these are
of equal rank. The working-man consorts with other working-men;
the small clerk calls himself a gentleman; the small shopkeeper is a
master. What have they for amusements? The small shopkeeper
seems to get along altogether without any amusement. He keeps his
“place” open till late in the evening; he shuts it, takes his supper,
and goes to bed. His social ambitions are limited by the distinctions
to be acquired in his chapel; he reads a halfpenny journal for all his
literature.
As for what is offered to those who will accept these gifts, there
are lectures first and foremost; there are the lectures offered every
winter at Toynbee Hall. These lectures are not, if you please, given
by the “man in the street”; the lecturers are the most distinguished
men in their own lines to be found; there is no talking “down” to the
Whitechapel audience; those serious faces show that they are here
to be taught, if the lecturer has anything to tell them, or to receive
suggestions and advice; they are all of the working-class; they are
far more appreciative than the audiences of the West End; they read
and think; they have been trained and encouraged to read and think
by Canon Barnett for many years; they are very much in earnest,
and they do not come with vacuous minds; as Emerson said of the
traveler so we may say of a man who listens to a lecture—he takes
away what he brought with him. About the Settlements and the gifts
which they offer, with full hands, to the people, I speak in the next
chapter.

Toynbee Hall and St. Jude’s Church.

What Barnett and Toynbee Hall have done for the intellectual side
the People’s Palace has done for the musical side. Its cheap concerts
have led the people, naturally inclined to music, insensibly into ways
of good taste; the palace was fortunate, at first, in getting a musical
director who knew how to lead the people on; one of the most
gratifying successes of this institution has been its music. They have
now their own orchestra, vocal and instrumental. At the same place
are held exhibitions, from time to time, of East London industries, of
pictures, of arts and crafts of all kinds. Here is the finest gymnasium
in London, and here are many clubs—for foot-ball, cricket, and
games of all kinds.
One omission in the amusements of London must be noted. There
are no public dancing-halls. I see no reason at all why a public
dancing-hall should not be carried on with as much attention to
good behavior as a private dance, or a theater, or any other place
where people assemble together. It requires only the coöperation of
the people themselves, without the aid of the police. Meantime,
there is no form of exercise, to my mind, so delightful to the young
and so healthful as dancing; nothing that more satisfies the
restlessness of youth than the rapid and rhythmic movement of the
limbs in the dance. Nature makes the young long to jump about;
education should take in hand their jumping and make it part of the
orderly recreation which we are substituting for the old brutal sports.
Dancing was tried at the People’s Palace; it was a great success; the
balls given in the Queen’s Hall were crowded, and the people were
as orderly as could be desired. But, indeed, the whole feeling of the
assembly was in favor of order.
The theater and the music-hall claim, and claim successfully, their
supporters; concerning the former one has only to recognize that it
may be a school of good manners, as well as of good sentiments,
and that it is also an institution capable of ruining a whole
generation. The pieces given at the theaters of East London are, so
far as I have observed, chiefly melodramas. The music-halls are
places frankly of amusement, and for the most part, I believe, vulgar
enough, but not otherwise mischievous.
And there is the public billiard-room, with all that it means—the
betting man, the professional player, the proximity to the bar, the
beer and the tobacco, and the talk. It attracts the young clerk more
readily than the young craftsman. It is his first step downward. If it
does not plunge him beneath the waves after the fashion that we
have witnessed, it will keep him where he is and what he is—a
writing machine, a machine on hire at a wage not so very much
better than a typewriting instrument, all his life. Let us rather
contemplate the thousands of lads who attend the classes at the
palace, the polytechnics, and the Settlements; let us rather think of
those who crowd into the concerts, sit as students at the lectures
and listen and look on while the guide leads them round the
exhibitions.
In this long list of amusements I must have omitted some,
perhaps many. For instance, I have not spoken of reading or of
literature. The craftsman of East London has not yet begun to read
books; at present he only reads the paper; his children read the
penny dreadfuls, and are beginning to read books.
Considering that Sunday afternoon is especially the time of rest,
we must not forget one form of recreation peculiar to that time. It
takes the form of an address given in some chapel. There is
generally a short service, with prayer and the singing of a hymn; the
people who attend and crowd the chapel seem to like this addition
to the address which follows. It is intended to be of a kind likely to
interest and to instruct; the first duty of the lecturer is to choose a
subject which does both; I have myself on more than one occasion
attempted to address working-men on the Sunday afternoon; I have
found them easy to interest and quick to take up points. As at
Toynbee Hall, one must not talk “down” to them. Indeed, the men
who come to such lectures are the most intelligent and the best
educated of the whole population. It is pleasant and restful for
them; the chapel is warm; the singing is not disagreeable, even
though in their own homes psalmody is not commonly practised; to
be called away on a dark and gloomy November afternoon and led
gently into another world, with new scenery and other conditions, is
that complete change which is the best rest of all. The lecturer need
not be afraid of tiring his audience; he may go on as long as he
pleases; when he leaves off they will crowd round him and beg him
to come again.
 Many other omissions I have made purposely. There are the
drinking and the gambling clubs, the betting clubs, haunts, and
dens, if one choose to consult the police and to hunt them up, which
would enable one to finish this chapter with a lurid picture. Where
there are so many men and women there will always be found a
percentage of the bad, the worse, and the worst. It is the hopeful
point about East London that wherever the better things are offered
they are accepted by the better sort; not by a few here and a few
there, but by thousands who are worthy of the better things.
 XII
THE HELPING HAND
 XII

THE HELPING HAND

T HE work that lies before us in every city waiting for the Helping
Hand—the human wreckage, bankruptcy, age, sickness, poverty,
which must always be forming anew however we may meet it and
find alleviation—will certainly not decrease as the years roll on. The
point for us to consider here is not the volume and variety of the
forces which cause this wreckage, but the attempts which are now
being made to find this alleviation and, if possible, a remedy.
The Helping Hand has a history, and it is very simple:
1. First of all it threw a penny to the beggar because he was a
beggar.
2. Secondly, it offered free meals and free quarters in every
monastic house to every beggar because he was a beggar.
3. It continued to give the penny and the free meals and the
lodging to the beggar because he was a beggar, but it ordered the
beggar to go back to work.
4. It arrested, imprisoned, branded, and flogged the beggar
because he was a beggar. It continued also to give him a penny for
the same reason.
5. It founded almshouses for some of the aged poor; those who
could not get in continued to receive their penny and their flogging
because they were beggars.
 6. It founded workhouses, Bridewell, and houses of correction for
the beggar. And it continued to give that penny to the beggar
because he was a beggar.
7. It built houses for the reception of the poor who could no
longer work, infirmaries for the sick, orphanages and homes for poor
children, casual wards for the homeless. It made begging an offense
in the eyes of the law. Yet it continued to give the beggar a penny
because he was a beggar.
8. It discovered that a multitude of rogues and people who will
not work trade upon the charity and the pity of people, sending
around letters asking for help. It therefore established an
association, with branches everywhere, to expose the fraudulent. Yet
it continued to give the beggar a penny because he was a beggar.
In other words, the Helping Hand has never been able to refrain
from giving that penny which encourages the “masterless” man, and
the man who will not work, and the fraudulent, and the writer of the
begging letter. Could the Helping Hand be persuaded to refuse that
penny for a single fortnight, to turn a deaf ear resolutely to the
starving family on the road, to the starving children on the
pavement, to the starving woman who stands silent, mournful,
appealing with mute looks of misery, only for a single fortnight, the
existence of the beggar would come to a sudden end. This the
Helping Hand can never be persuaded to do. Therefore we have with
us not only the real misery caused by fate, by fortune, by the natural
consequences of folly and weakness and crime, but also the
pretended misery of those who live upon the pity of the world and
trade on that strange self-indulgence which gives the dole to remove
an unpleasant object out of sight and to awaken the glow which
follows with the sense of charity.
I leave aside in this place the casual dole—the penny to the
beggar because he is a beggar; it is illustrated for all time by the
partition of the cloak between St. Martin and the beggar. The saint,
then a gallant cavalryman, did not stop—or stoop—to inquire into
the merits of the case; here was a beggar. Was he really starving?
could he work? were his sufferings pretended? was he really cold?
did he deserve any help at all? Was he, on the contrary, well fed and
nourished, money in purse, food in wallet, a sufficiency of clothes on
his back, a fire and a pot over it at home, with a well-fed family and
a wife on the same “lay” at the other gate of the city? Let us leave
the Bishop of Ligugé as a type for all the centuries of the unthinking
charity which gives the penny to the beggar because he is a beggar.
Let us turn to other and later developments. The Helping Hand
has founded and endowed and now maintains by voluntary
contributions hospitals of every kind for the sick; by rates and taxes,
workhouses for the poor, schools for the children. Yet there has
passed—there is now passing—over the work of charity a great and
most remarkable revolution; it is a revolution characteristic of a time
in which every theory of social life, social conditions, and social
responsibilities has been completely changed. The old duties remain
still; schools and hospitals have been multiplied; if almshouses have
not increased, the workhouse system has become better organized.
But we have become aware of other duties, of new responsibilities.
It is now understood that it is not enough to put the children to
school from one to fourteen; they must be looked after when they
leave school; it is not enough to provide for the diseases of the
body; we must make provision for the diseases, and the cause of the
diseases, of the mind. The Helping Hand is at work in these days for
the arrest of degeneracy; for the opening up of art, literature, music,
science, culture of all kinds, to the better sort among the working-
classes; for the wider extension of the area and the depth of culture;
for the creation of that kind of public opinion which, more than
anything else, makes for public order and the maintenance of law;
for the care and safeguarding of young people at the perilous time
of emancipation from school; for the rescue of those who can be
rescued; for the cleansing of the slums; for the restoration to the
world of those who, as we have seen, have dropped out; and for the
prevention of pauperizing by ill-considered schemes of ill-informed
benevolence.
 These are general
terms. In order to
carry out its work in
detail, the Helping
Hand looks after the
children in their
homes, while the
Board-school looks
after their teaching; it
provides cases for the
hospital, and aids the
parish authorities
during sickness in the
home; it introduces
the social side into
the lives of the better
sort; it devises
attractions for the
young people who
stand at the parting
of the ways, where
temptation is strong
and the primrose
path is bright with
flowers; it teaches
the lads a trade, and
the girls a love for
the quiet life; it
wages war with the
public house and the
The New Whitechapel Art Gallery. street; it endeavors
(The building to the right is a free library.) to bring back the
lowest strata to a
sense of religion
which they have come to think the peculiar and rather
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