Case Studies in Clinical Cardiac Electrophysiology , 1st
Edition
Visit the link below to download the full version of this book:
https://medipdf.com/product/case-studies-in-clinical-cardiac-electrophysiology-1
st-edition/
Click Download Now
CONTENTS iii
Case Studies in
Clinical Cardiac
Electrophysiology
John M. Miller, MD
Professor of Medicine, Indiana University School of Medicine
Director, Clinical Cardiac Electrophysiology
Indianapolis, Indiana
Mithilesh K. Das, MD
Professor of Clinical Medicine, Indiana University School of Medicine
Indianapolis, Indiana
Douglas P. Zipes, MD
Distinguished Professor Emeritus of Medicine, Pharmacology and Toxicology
Indiana University School of Medicine
Emeritus Director, Krannert Institute of Cardiology
Indianapolis, Indiana
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY ISBN: 978-0-323-18772-5
Copyright © 2018 by 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 website: 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 experience and knowledge of
their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient,
and to take all appropriate safety precautions.
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.
Library of Congress Cataloging-in-Publication Data
Names: Miller, John M. (John Michael), 1954- author. | Das, Mithilesh K.,
author. | Zipes, Douglas P., author.
Title: Case studies in clinical cardiac electrophysiology / John Miller,
Mithilesh Das, Douglas Zipes.
Description: Philadelphia, PA : Elsevier, [2018] | Includes bibliographical
references and index.
Identifiers: LCCN 2016053043 | ISBN 9780323187725 (hardcover : alk. paper)
Subjects: | MESH: Heart Diseases--diagnosis | Electrophysiologic
Techniques,
Cardiac--methods | Case Reports
Classification: LCC RC683.5.E5 | NLM WG 141.5.F9 | DDC 616.1/2075--dc23
LC record available at https://lccn.loc.gov/2016053043
Content Strategist: Maureen Iannuzzi
Senior Content Development Specialist: Janice Galliard
Publishing Services Manager: Catherine Jackson
Project Manager: Kate Mannix
Design Direction: Brian Salisbury
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Keenly aware of the time and energy diverted from our families that was required to
perform these procedures and assemble the recordings into a form accessible by readers, we
dedicate this volume to our beloved wives (Jeanne, Rekha, and Joan), who have allowed us
the privilege of putting this work together. We also dedicate this work to the readers, who we
hope will benefit from the lessons we have tried to convey, and finally to their patients, who
we hope will in turn benefit from their learning.
CONTENTS
Foreword
The practice of clinical cardiac electrophysiology is one of clinical exploration that starts
with integration of the patient’s symptoms and cardiac evaluation with electrocardio-
graphic interpretation. One of the most gratifying experiences for patient and physician is
when this process culminates in the electrophysiology laboratory with confirmation of the
diagnosis and implementation of effective therapy for the arrhythmia with catheter abla-
tion. Mastery of each component is needed, and the knowledge that is gained from each
step can be applied to the previous step to refine one’s diagnostic acumen. We became
much better electrocardiographers by applying the knowledge gained from the pioneering
work that defined cardiac activation patterns and arrhythmia mechanisms using cardiac
mapping and programmed electrical stimulation. Expertise in the last step, interventional
electrophysiology, is the most challenging to acquire. It requires assimilation of complex
patterns of cardiac activation, interpretation of spontaneous changes in patterns, and ap-
plication of maneuvers to confirm a diagnosis, and this confirmation is critical for guiding
catheter ablation.
Drs. Miller, Das, and Zipes have assembled a wonderful book that captures the spirit of
clinical exploration leading to effective therapy. They use cases to describe pathophysio-
logic concepts that start with fundamentals and proceed to complex concepts. From the
electrophysiology laboratory they incorporate findings ranging from those that are classic
to those that are only recently described and that require a nuanced interpretation and
understanding, but that are critical to arriving at the correct diagnosis. Examples include
the newest technologies that are now being applied for delineation of arrhythmia mecha-
nisms and substrate.
The authors are renowned teachers who apply their wealth of experience in communi-
cating complex scenarios and concepts to make the cases accessible for the complete range
of students of clinical electrophysiology, from the trainee to the advanced practitioner.
The cases clarify concepts and provide fundamentals for the new student, but also provide
insights that will expand the knowledge of experienced clinicians. Dr Miller’s hand is
evident throughout in the superb graphics, for which he is widely known among teachers
of cardiology.
One of the amazing aspects of biology, medicine, and certainly extending to cardiac
electrophysiology, is the variability that one encounters from patient to patient. After
years in the field, one still encounters new arrhythmia problems. A solid basis in under-
standing mapping and diagnostic maneuvers is required for solving new puzzles in the
electrophysiology laboratory, and this learning is acquired from the study of cases. You
can never analyze too many cases. I congratulate the authors of Case Studies in Clinical
Cardiac Electrophysiology on a wonderful book.
William G. Stevenson, MD
Director, Cardiac Arrhythmia Program
Cardiovascular Division
Brigham and Women's Hospital
Professor of Medicine, Harvard Medical School
Boston, Massachusetts
vii
CONTENTS
Preface
The understanding and care of patients with heart rhythm disturbances (clinical cardiac
electrophysiology [EP]) has evolved in the last three decades from simple diagnostic stud-
ies of the conduction system using a few electrodes, to complex diagnostic and therapeutic
procedures involving recording and stimulation from a large number of electrodes, for the
purpose of finding and ablating arrhythmogenic tissue. With this dramatic change in the
character of EP studies has come the critical need for careful analysis and thorough under-
standing of the meaning of recordings that are made and results of stimulation in order to
achieve optimal results from ablation. At the same time, EP training programs have come
under increasing pressure to perform more procedures in a shorter amount of time, result-
ing in compromising time for careful and methodical study of and learning from these
procedures that are rich with teaching material. Although many excellent texts in our field
explain the principles of recording and stimulation in treatment of arrhythmias, for ex-
ample, Clinical Arrhythmology and Electrophysiology, few are structured to show their
practical application in a case-study format. In light of this, the purpose of this volume is
to take the reader through a representative series of EP procedures from start to finish,
evaluating results of diagnostic pacing maneuvers, sampling and comparing characteristics
of electrograms, and selection of appropriate sites for ablation. It is our hope that readers
will benefit from this mode of presentation, highlighting some of the limitations of tech-
niques that are used on a daily basis, with the aim of improving the efficacy and safety of
procedures they perform on their patients.
Acknowledgments
We gratefully acknowledge the role played by our nursing and technical staff with whom
we performed the procedures reviewed in this work, as well as electrophysiology fellows,
whose patience in keeping catheters in place during long procedures contributed greatly to
the quality of the figures. We also acknowledge our patients, who provide a constant source
for learning.
ix
PA RT 1 Sinus Node, AV Node, and His-Purkinje System
Sinus Node and Atrioventricular
Conduction Disease 1
Case Presentation
A 56-year-old man experienced syncope while walking at work. Coworkers called emer-
gency medical services (EMS). Upon the arrival of EMS, he was awake and feeling normal
but was convinced to go to the emergency room (ER). The patient had a history of anterior
wall myocardial infarction (MI), percutaneous coronary intervention (PCI), to left anterior
descending coronary artery (LAD) several years before, and a negative stress test within the
last 6 months. Examination results were normal except for obesity. ECG showed sinus
rhythm, long PR, right bundle branch block (RBBB), left anterior fascicular block (LAFB),
and anterior scar. Echocardiogram revealed ejection fraction (EF) 40% and anterior hypo-
kinesis. The patient was referred for electrophysiology (EP) study.
Baseline ECG
I aVR V1 V4
II aVL V2 V5 Figure 1-1
III aVF V3 V6
II
The ECG in Fig. 1-1 shows sinus rhythm with a prolonged P wave (left atrial abnormality),
slightly prolonged PR interval, RBBB and left anterior fascicular block, and an extensive
anterior infarction. On the basis of this, there are many possible causes of syncope—atrial
arrhythmias (atrial flutter and fibrillation, other reentrant atrial tachycardias), heart block
(either in AV node or His-Purkinje system), or ventricular arrhythmia (ventricular tachy-
cardia or fibrillation). There is nothing in the ECG to favor one cause of syncope over
another, and because treatment strategies are very different depending on the cause
(medications or ablation for atrial arrhythmias; pacemaker for heart block; implantable
defibrillator for ventricular arrhythmias), further investigation is needed.
1
2 CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
Evaluation
Baseline Intracardiac Recordings
1
2
V1
V6
HRA
Figure 1-2 A V
H
Hisprox
Hismid
Hisdist
RBB
AH 85 ms HV 85 ms
RV
200 ms
Intracardiac recordings during sinus rhythm (Fig. 1-2) show atrial (A), His (H), and
ventricular (V) recordings as noted. This confirms the presence of His-Purkinje disease,
with an HV interval of 85 ms—prolonged (normal, 40 to 55 ms), but not enough to
implicate His-Purkinje dysfunction as a cause of heart block. Surprisingly, though the PR
interval is somewhat prolonged, the AH interval is normal (85 ms [normal, 60 to 125 ms]).
Usually, prolongation of the PR interval is caused by the AV nodal (AH) component, be-
cause to prolong the PR even 60 ms from His-Purkinje disease would require a lengthening
of the HV to a degree (that is, from 40 ms to 100 ms) that 1:1 conduction would be unlikely.
Note also that there is a delay between the distal His recording and right bundle branch
(RBB)—there is usually ,10 ms between these—and that the RBBB is further caused by
delay or block between the RBB and RV apical electrogram, with a QRS onset (dashed blue
line) to RV electrogram of 75 ms (normal, 10 to 35 ms).
Sinus Rhythm And Ventricular Pacing
1
2
3
V1
V6
Figure 1-3
HRA A V V A
H
Hisprox
H
Hismid
Hisdist
RV
200 ms S S
CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 3
The left side of Fig. 1-3 shows a sinus rhythm complex as in the previous figure for refer-
ence, whereas the 2 complexes on the right are during pacing from the right ventricular
apical region. Note that there is retrograde conduction to the atria, with the His bundle
activated from distal to proximal as expected. Usually, the timing of the His potential is
before the local ventricular electrogram in the His recoding, because conduction proceeds
more rapidly up the RBB to the His than does muscle-to-muscle propagation from apex to
base. Because there is RBBB in this case, the impulse cannot ascend the RBB as it normally
would and instead must traverse the interventricular septum, enter the left bundle branch,
and then activate the His retrogradely. These findings just confirm the His-Purkinje disease
but give no further insight as to the cause of syncope.
Retrograde His-Purkinje Conduction
Normal RBBB
I I
II II
V1 V1
H H
HBp HBp
HBm HBm
HBd HBd
Figure 1-4
RVA V RVA V
LBB LBB
RBB RBB
As illustrated in Fig. 1-4, in patients with normal His-Purkinje function (at left), pacing
from the right ventricular apex (red circle) results in retrograde conduction over the RBB
(white line) that is more rapid than muscle-to-muscle conduction (wavy line in septum),
resulting in a His potential (H) inscribed before the larger local ventricular recording (V).
At right, in the presence of anterograde RBBB, the paced wavefront cannot ascend the
blocked right bundle and instead crosses the interventricular septum (wavy horizontal line)
to engage the left bundle, and then proceeds rapidly to the His that now appears after the
local ventricular recording (that is again generated after muscle-to-muscle spread).
4 CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
Atrial Pacing
1
V1
V6
Figure 1-5 HRA
S S S S S
AH 90 ms
Hisprox
A
HV
Hismid
Hisdist
HV 85 ms
RV 400 ms
Rapid pacing can often reveal abnormalities of AV conduction that were not very evident
at rest. In Fig. 1-5, pacing the atrium (S) slightly faster than the sinus rate shows minimal
change in either AH (90 ms) or HV (85 ms) intervals. It is useful to display multiple elec-
trode pairs of His recordings because the signal amplitude may vary enough between
complexes that the His potential may be poorly visible or even absent in one electrode pair
(Hisdist in this case), whereas it is readily visible in other electrode pairs.
Atrial Pacing
V1
V6
Figure 1-6 420 ms 400 ms 380 ms
HRA S S S S S S S S S S
AH (ms): 140 145 170 185 230 -- 115 130 190 230
Hisprox
H H H H H ∗ H H H H
Hismid
HV (ms): 100 110 112 115 115 90 115 --
Hisdist
RV
400 ms
More rapid pacing starts to reveal some abnormalities. As the pacing rate increases (cycle
length decreases), the AH is expected to prolong but the HV interval usually remains con-
stant. In Fig. 1-6, the AH (in blue) does prolong, but so does the HV interval (in green). The
asterisk denotes where AV nodal block occurs (no subsequent His potential), but three
cycles after this, there is a His potential not followed by a QRS (infra-His block; green dash)
CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 5
and the HV intervals on the prior two cycles had prolonged (thus, infra-His Wenckebach).
This is distinctly abnormal and likely warrants pacemaker implantation. However, this may
not be the reason that syncope had occurred (there may be other abnormalities that have
not yet been uncovered during the study).
Atrial Pacing
V1
V6
HRA Figure 1-7
S S S 4.15 sec sinus pause
Hisprox
Hismid
Hisdist
RV
1 sec
In Fig. 1-7, pacing is repeated for 1 min at the same cycle length as shown in the
prior figure to stress the sinus node. Upon cessation of pacing, a prolonged sinus pause
(4.15 seconds) is observed; a junctional escape complex occurs after 3 seconds. This is
another potential cause of syncope (sinus node dysfunction).
6 CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
Ventricular Pacing
∗
1
V1
V6
Sinus Sinus
Figure 1-8 HRA
A A A
Hisprox
Hismid
H
H H H
Hisdist
RV S S S S S S
400 ms
Turning to the ventricles (Fig. 1-8), slow ventricular pacing again shows that there is retro-
grade conduction; the first and last atrial complexes are sinus in origin (HRA before His
atrial recordings) but the middle three complexes are retrogradely conducted. The first two
of these (blue arrows) are over the fast pathway, but after the fourth ventricular stimulus,
the ventriculoatrial interval suddenly increases, signifying a switch to a slow pathway (red
arrow). Immediately after this, there is a QRS complex that is not fully paced (asterisk); this
is because of fusion between the paced wavefront and one over the normal conduction
system (see His potential). This is the result of an atypical AV nodal echo (retrograde slow
pathway, anterograde fast—blue arrow). This is a common finding and, unless accompa-
nied by sustained atypical AV nodal reentrant SVT, has no relevance for the diagnosis of
syncope.
Ventricular Stimulation
V1
V6
Figure 1-9
HRA
SA SA
Hisprox
Hismid
H H H
Hisdist
RV S
1 400 ms S1 S2 S3 S4
CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 7
The last part of the syncope evaluation consists of programmed ventricular stimulation. As
shown in Fig. 1-9, standard stimulation (here, with triple extrastimuli, S2 to S4) initiates a
rapid, hemodynamically unstable ventricular tachycardia (CL 250 ms) that stopped spon-
taneously after 15 seconds. Given the presence of a prior MI and “serious” syncope, this
arrhythmia was deemed a reasonable candidate for the cause of his syncope. He received a
dual-chamber ICD later that day. Note that a His potential is seen on occasion but not with
every complex—excluding bundle branch reentry as a possible cause of the tachycardia
(SA 5 atrial stimulus).
Summary
n This man had syncope in the presence of structural heart disease—which always needs
further evaluation.
n Multiple potential causes of syncope may be present in the same patient; in this case,
n Sinus node dysfunction
n His-Purkinje dysfunction
n Ventricular tachycardia
n Judgment must be used to determine which possible cause(s) of syncope should be
treated and how.
