ECG Masters’ Collection

Favorite ECGs from Master Teachers Around the World

ECG Masters’ Collection
Favorite ECGs from Master Teachers Around the World

ECG Masters’
Editors:
Mohammad Shenasa, MD • Mark E. Josephson, MD • N. A. Mark Estes III, MD
Ezra A. Amsterdam, MD • Melvin Scheinman, MD

Collection
230 exceptional electrocardiogram case studies curated from the libraries of 60
internationally recognized master teachers of ECG interpretation are brought together
in this one-of-a-kind resource for student and teacher alike.
Organized by disease type, ECG case studies are presented in a clinical context fol-
lowed by questions and discussion. Medical students, residents, fellows, physicians
— anyone who is involved in caring for patients with various cardiovascular diseases
and other systemic pathologies — will find this unique collection with a global
perspective useful and practical in developing the skills necessary to reading ECGs.
Favorite ECGs from
Key Topics
Master Teachers
n  onduction Disturbances: Sinus Node Disease/Sick Sinus Syndrome, AV Conduction
C
Disturbances, AV Blocks, Bundle Branch Blocks, and Fascicular Blocks
Around the World
n  iscellaneous Phenomena: Concealed Conduction, Superabnormalities, Aberrancy
M

n
Conduction, Premature Atrial and Ventricular Contractions (PACs and PVCs)
Preexcitation Syndromes
Editors:
n Early Repolarization Mohammad Shenasa
Long and Short QT Syndromes
Mark E. Josephson
n

n Brugada Syndrome
n

n
Narrow QRS Complex Arrhythmias
Wide Complex Arrhythmias
N. A. Mark Estes III
n Ischemia and Infarction
Shenasa
Ezra A. Amsterdam
Electrolyte Disturbances, Pharmacological and Recreational Agents
Melvin Scheinman
n

n Paced Rhythms and Device Troubleshooting

Josephson
n Heart Failure, LVH, and Cardiomyopathies Estes
n Congenital Heart Diseases Amsterdam
Special Considerations: Age, Race, Gender, and Athletes Scheinman
n
Forewords by
n Syncope and ECG Troubleshooting
Francis E. Marchlinski
and Samuel Lévy
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edition for use by the first buyer.
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 ECG Masters’ Collection
Favorite ECGs from Master Teachers
Around the World

Mohammad Shenasa, MD
Mark E. Josephson, MD
N. A. Mark Estes III, MD
Ezra A. Amsterdam, MD
Melvin Scheinman, MD

Minneapolis, Minnesota
© 2017 Mohammad Shenasa, Mark E. Josephson, N. A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman

Cardiotext Publishing, LLC

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This book is intended for educational purposes and to further general scientific and medical knowledge, research,
and understanding of the conditions and associated treatments discussed herein. This book is not intended to
serve as and should not be relied upon as recommending or promoting any specific diagnosis or method of
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Due to ongoing research, discoveries, modifications to medicines, equipment and devices, and changes in
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Library of Congress Control Number: 2017937042

ISBN: 978-1-942909-08-8

eISBN: 978-1-942909-18-7

Printed in The United States of America

 Dedication

We dedicate this book in memory of Mark E. Josephson, MD (January 27, 1943 – January 11, 2017),
who inspired and mentored many of us. He gave the electrogram a new look - “ECG as a mapping
tool.” He is also the senior editor on this book.
 Contents

Contributors............................................................................................................................vii
Forewords................................................................................................................................xv
Dr. Francis Marchlinski
Dr. Samuel Lévy
Preface....................................................................................................................................xix
Abbreviations.........................................................................................................................xxi
Video Legends......................................................................................................................xxiii
Section 1 Introduction to the Interpretation of the Electrocardiogram���������������������������1
Section 2 Conduction Disturbances: Sinus Node Disease/Sick Sinus Syndrome,
AV Conduction Disturbances, AV Blocks, Bundle Branch Blocks, and
Fascicular Blocks....................................................................................................3
Section 3 Miscellaneous Phenomena: Concealed Conduction, Superabnormalities,
Aberrancy Conduction, Premature Atrial and Ventricular
Contractions (PACs and PVCs).............................................................................41
Section 4 Preexcitation Syndromes....................................................................................77
Section 5 Early Repolarization (ECG Pattern and the Syndrome)................................... 135
Section 6 Long and Short QT Syndromes......................................................................... 153
A. Long QT Syndrome...................................................................................... 153
B. Short QT Syndrome..................................................................................... 173
C. Torsades de Pointes..................................................................................... 175
D. Other Proarrhythmias.................................................................................. 193
Section 7 Brugada Syndrome............................................................................................ 197
Section 8 Narrow QRS Complex Arrhythmias..................................................................227
A. Inappropriate Sinus Tachycardia.................................................................227
B. Sinus Node Reentrant Tachycardia.............................................................229
C. Atrial Tachycardia/Atrial Flutter..................................................................231
D. Atrioventricular Nodal Reentrant Tachycardia...........................................255
E. Atrioventricular Reentrant Tachycardia......................................................283
F. Atrial Fibrillation..........................................................................................287
G. Junctional Rhythms.....................................................................................295

v
Section 9 Wide Complex Arrhythmias..............................................................................297
A. Ventricular Tachycardia/Fibrillation............................................................297
B. Supraventricular Tachycardia (SVT) with Bundle Branch Block (BBB).......355
C. Preexcited Tachycardia................................................................................ 371
D. Idioventricular Rhythm................................................................................373
Section 10 Ischemia and Infarction.....................................................................................375
Section 11 Electrolyte Disturbances, Pharmacological and Recreational Agents........... 413
Section 12 Paced Rhythms and Device Troubleshooting..................................................425
Section 13 Heart Failure, LVH, and Cardiomyopathies......................................................459
A. Arrhythmogenic Right Ventricular
Dysplasia/Cardiomyopathy (ARVD/C)..........................................................459
B. Hypertrophic Cardiomyopathy (HCM)........................................................479
C. Dilated Cardiomyopathy (DCM)..................................................................495
D. Chagas Cardiomyopathy.............................................................................501
E. Takotsubo (Stress) Cardiomyopathy............................................................ 511
F. Non-Compaction Cardiomyopathy.............................................................523
G. Pericarditis....................................................................................................525
H. Other Cardiomyopathies.............................................................................529
Section 14 Congenital Heart Diseases................................................................................533
Section 15 Special Considerations: Age, Race, Gender, and Athletes..............................583
Section 16 Syncope and ECG Troubleshooting..................................................................593
Appendix...............................................................................................................................621

vi u Contents
 Contributors

Editors Contributors
Mohammad Shenasa, MD, FACC, FHRS, Ahmed Abdel Aziz, MD, PhD
FAHA, FESC Professor, Critical Care Medicine Department,
Attending Physician, Department of Cairo University Hospitals, Cairo, Egypt
Cardiovascular Services, O’Conner Hospital;
Heart & Rhythm Medical Group, San Jose, Simon Abou Jaoude, MD
California Cardiology Department, Hotel-Dieu de France,
Saint Joseph University, Beirut, Lebanon
Mark E. Josephson, MD, FACC, FHRS, FAHA
Director, Harvard-Thorndike Electrophysiology Baris Akdemir, MD
Institute and Arrhythmia Service; Cardiac Electrophysiology Fellow, Cardiology,
Chief Emeritus, Division of Cardiovascular University of Minnesota, Minneapolis,
Medicine, Beth Israel Deaconess Medical Minnesota
Center; Herman C. Dana Professor of Medicine,
Jason Andrade, BSc, MD, FRCPC, FHRS
Harvard Medical School, Boston,
Clinical Assistant Professor, Department of
Massachusetts
Medicine, University of British Columbia,
N. A. Mark Estes III, MD, FACC, FHRS, Vancouver, British Columbia, Canada; Adjunct
FAHA, FESC Professor, Université de Montréal, Clinical
Professor of Medicine, Tufts University School Electrophysiology Service, Montreal Heart
of Medicine; Director, New England Cardiac Institute, Montreal, Quebec, Canada
Arrhythmia Center, Tufts Medical Center,
Samuel J. Asirvatham, MD, FACC, FHRS
Boston, Massachusetts
Consultant, Department of Cardiovascular
Ezra A. Amsterdam, MD Medicine, Division of Pediatric Cardiology,
Distinguished Professor, Associate Chief Department of Physiology and Biomedical
(academic affairs), Division of Cardiovascular Engineering; Professor of Medicine and
Medicine, University of California, Davis, Pediatrics, Mayo Clinic College of Medicine;
Medical Center, Sacramento, California Program Director, EP Fellowship Program,
Mayo Clinic, Rochester, Minnesota
Melvin Scheinman, MD, FACC, FHRS
Professor of Medicine, Walter H. Shorenstein Nitish Badhwar, MD, FACC, FHRS
Endowed Chair in Cardiology; Chief of Director, Cardiac Electrophysiology Training
Cardiology Genetics Arrhythmia Program, Program, Professor of Medicine, University of
University of California, San Francisco, California, San Francisco, San Francisco,
San Francisco, California California

vii
Adrian Baranchuk, MD, FACC, FRCPC, FCCS Catalin A. Buzea, MD, PhD
Professor of Medicine (Tenure), Head, Heart Cardiology Consultant, Cardiology
Rhythm Service, Queen’s University, Kingston, Department, Colentina University Hospital;
Ontario, Canada Associate Professor, “Carol Davila” University of
Medicine, Bucharest, Romania
Raimundo Barbosa-Barros, MD
Chief of Coronary Center, Messejana Hospital David J. Callans, MD, FHRS
Dr. Carlos Alberto Studart Gomes, Fortaleza, Professor of Medicine, Perelman School of
Ceará, Brazil Medicine; Associate Director of
Electrophysiology, University of Pennsylvania
Antoni Bayés de Luna, MD, PhD, FESC, FACC Health System, Philadelphia, Pennsylvania
Senior Investigator, Catalan Institute of
Cardiovascular Sciences, St. Pau Hospital, Francesc Carreras Costa, MD
Barcelona, Spain Cardiology Department, Hospital Santa Creu
i Sant Pau, Universitat Autónoma de Barcelona,
Bernard Belhassen, MD, FHRS Barcelona, Spain
Department of Cardiology, Tel-Aviv Sourasky
Medical Center; Sackler Faculty of Medicine, Lily Chen, MD
Tel-Aviv University, Tel-Aviv, Israel Resident of Internal Medicine, University
of California, Davis, Medical Center,
David G. Benditt, MD, FACC, FHRS, FRCPC, Sacramento, California
FESC
Cardiac Arrhythmia Center, Cardiovascular Alan Cheng, MD, FACC, FHRS, FAHA
Division, University of Minnesota Medical Associate Professor of Medicine, Associate
School, Minneapolis, Minnesota Professor of Pediatrics, Johns Hopkins
University School of Medicine, Baltimore,
Dan Blendea, MD, PhD, FHRS Maryland
Cardiac Arrhythmia Service, Department of
Medicine, Massachusetts General Hospital, Paolo China, MD
Boston, Massachusetts Unit of Electrophysiology and Cardiac Pacing,
Ospedale Dell’Angelo, Venice, Italy
Pedro Brugada, MD, PhD
Chairman, Cardiovascular Division, UZ Xavier Copie, MD
Brussel, Brussels, Belgium Cardiologist, Arrhythmia Department, Centre
Cardiologique du Nord, Saint-Denis, France
Jonathan Bui, MD
Research Assistant, Division of Cardiovascular Jane E. Crosson, MD
Medicine, University of California, Davis, Associate Professor, Pediatrics, Johns Hopkins
Medical Center, Sacramento, California Hospital, Baltimore, Maryland

Haran Burri, MD Mohammad Dalili, MD

Assistant Professor, Cardiology Department, Rajaie Cardiovascular Medical and Research
University Hospital of Geneva, Geneva, Center, Iran University of Medical Sciences,
Switzerland Tehran, Iran

viii u Contributors
Andrei G. Dan, MD, PhD, FESC, FAHA, Andrew E. Epstein, MD, FACC, FHRS, FAHA
FEHRA Professor of Medicine, Electrophysiology
Head of Cardiology Department and Internal Section, Cardiovascular Division, University of
Medicine Clinic, Colentina University Hospital; Pennsylvania, Philadelphia, Pennsylvania
Professor, “Carol Davila” University of
Medicine, Bucharest, Romania Sabine Ernst, MD, PhD, FESC
Consultant Cardiologist, Reader in Cardiology,
Judith Daniels, RN, CRDS, CEPS Lead EP Researcher, Royal Brompton Hospital,
Registered Nurse, EP Lab, Milpark Hospital, National Heart and Lung Institute, Imperial
Johannesburg, Gauteng, South Africa College, London, United Kingdom

Luiz Carlos de Abreu, PhD Luis Alberto Escobar Robledo, MS

Chief, Design of Studies and Scientific Writing Fellow, Catalan Institute of Cardiovascular
Laboratory, ABC School of Medicine, Santo Sciences, St. Pau Hospital, Barcelona, Spain
André, São Paulo, Brazil; Program in Molecular
and Integrative Physiological Sciences (MIPS), Tamer S. Fahmy, MD, PhD
Department of Environmental Health, Harvard Associate Professor, Critical Care Medicine
T. H. Chan School of Public Health, Boston, Department, Cairo University Hospitals, Cairo,
Massachusetts Egypt

Arnaud Denis, MD Guy Fontaine, MD, PhD, HDR

Hôpital Cardiologique du Haut Lévèque, CHU Centre Hospitalier Pitié-Salpêtrière and
de Bordeaux, Université de Bordeaux and Université Pierre et Marie Curie, Department of
LYRIC Institute, Bordeaux, France Rhythmology, Paris, France

Nicolas Derval, MD Robert Frank, MD

Hôpital Cardiologique du Haut Lévèque, CHU Institut de Cardiologie, Hopital Pitié
de Bordeaux, Université de Bordeaux and Salpétrière, Paris, France
LYRIC Institute, Bordeaux, France
Javier García-Niebla, RN
Marc Dubuc, MD, FRCPC, FACC, FHRS Servicios Sanitarios del Area de Salud de El
Associate Professor of Medicine, Université de Hierro, Valle del Golfo Health Center, Canary
Montréal; Clinical Electrophysiology Service, Island, Spain
Montreal Heart Institute, Montreal, Quebec,
Diego Goldwasser, MD
Canada
Institut Cátala de Ciences Cardiovasculars, Sant
Kenneth A. Ellenbogen, MD, FHRS Pau Hospital; Cardiology Department, Hospital
Kontos Professor of Medicine, Chair, Division Quiron Barcelona, Barcelona, Spain
of Cardiology, Virginia Commonwealth
Judith A. Groeneweg, MD, PhD
University, Pauley Heart Center, Richmond,
University Medical Center Utrecht, The
Virginia
Netherlands

Contributors u ix
Majid Haghjoo, MD, FACC, FESC Heikki V. Huikuri, MD, PhD
Director, Department of Cardiac Professor, Medical Research Center Oulu,
Electrophysiology, Rajaie Cardiovascular Research Unit of Internal Medicine, University
Medical and Research Center, Tehran, Iran of Oulu and Oulu University Hospital, Oulu,
Finland
Michel Haïssaguerre, MD, PhD
Hôpital Cardiologique du Haut Lévèque, CHU James E. Ip, MD
de Bordeaux, Université de Bordeaux and Assistant Professor of Medicine, Division of
LYRIC Institute, Bordeaux, France Cardiology, Cardiac Electrophysiology
Laboratory, Cornell University Medical Center,
Frederick T. Han, MD, FACC, FHRS New York Presbyterian Hospital, New York,
Assistant Professor of Medicine, Division of New York
Cardiovascular Medicine, University of Utah
Health Sciences Center, Salt Lake City, Utah Pierre Jaïs, MD, PhD
Hôpital Cardiologique du Haut Lévèque, CHU
Richard N. Hauer, MD, PhD, FESC de Bordeaux, Université de Bordeaux and
Professor of Cardiology, Netherlands Heart LYRIC Institute, Bordeaux, France
Institute, University Medical Center Utrecht,
The Netherlands Mohammad-Ali Jazayeri, MD
Division of Cardiovascular Diseases, University
Shahriar Heidary, MD, FACC of Kansas Hospital & Medical Center, Kansas
Adjunct Clinical Instructor, Department of City, Kansas
Internal Medicine, Division of Cardiovascular
Medicine, Stanford University Medical School, Mohammad-Reza Jazayeri, MD
Stanford, California Heart, Lung & Vascular, Bellin Health, Green
Bay, Wisconsin
Hein Heidbuchel, MD, PhD, FESC, FEHRA
Professor and Chair, Department of Cardiology, Charles Jazra, MD, FACC, FESC
Antwerp University Hospital, Antwerp, Cardiology Department, Saint Joseph Hospital,
Belgium; Guest Professor, Cardiology, Hasselt Bauchrieh, Beirut, Lebanon
University, Hasselt, Belgium
Juhani Junttila, MD, PhD
Mélèze Hocini, MD Associate Professor, Medical Research Center
Hôpital Cardiologique du Haut Lévèque, CHU Oulu, Research Unit of Internal Medicine,
de Bordeaux, Université de Bordeaux and University of Oulu and Oulu University
LYRIC Institute, Bordeaux, France Hospital, Oulu, Finland

Henry H. Hsia, MD, FACC, FHRS Gautham Kalahasty, MD

Health Science Professor of Medicine, Program Director, Cardiology Fellowship
University of California, San Francisco; Program, Virginia Commonwealth University,
Chief, Arrhythmia Service, VA Medical Center, Pauley Heart Center, Richmond, Virginia
San Francisco, California

x u Contributors
Jonathan Kalman, MBBS, PhD, FRACP, FHRS Balaji Krishnan, MD
Professor of Medicine and Director of Cardiac Cardiac Arrhythmia Center, Cardiovascular
Arrhythmia Service, Department of Cardiology, Division, University of Minnesota Medical
Royal Melbourne Hospital and Department of School, Minneapolis, Minnesota
Medicine, University of Melbourne, Melbourne,
Australia Gilles Lascault, MD
Cardiologist, Arrhythmia Department, Centre
Demosthenes G. Katritsis, MD, PhD, FRCP, Cardiologique du Nord, Saint-Denis, France
FESC, FACC
Beth Israel Deaconess Medical Center, Harvard Robert Lemery, MD, FHRS, FESC, FRCPC
Medical School, Boston, Massachusetts Cardiac Electrophysiology, University of Ottawa
Heart Institute, Ottawa, Canada
George D. Katritsis, MBChB, BSc
Oxford University Clinical Academic Graduate Antoine Lepillier, MD
School, Radcliffe Hospital, Oxford, UK Cardiologist, Arrhythmia Department, Centre
Cardiologique du Nord, Saint-Denis, France
Tuomas Kenttä, PhD
Post doc researcher, Medical Research Center Bruce B. Lerman, MD
Oulu, Research Unit of Internal Medicine, H. Altschul Master Professor of Medicine;
University of Oulu and Oulu University Chief, Division of Cardiology; Director, Cardiac
Hospital, Oulu, Finland Electrophysiology Laboratory, Cornell
University Medical Center, New York
Bradley P. Knight, MD, FACC, FHRS Presbyterian Hospital, New York, New York
Medical Director, Center for Heart Rhythm
Disorders, Bluhm Cardiovascular Institute, Mohamed Magdy, MSc, L’AFSA, PhD, MD
Northwestern Memorial Hospital, Cooley Electrophysiology Fellow, Nancy CHU France;
Professor of Medicine, Lecturer, Cairo University Hospital,
Northwestern University, Feinberg School of Egypt; Head of EP Lab, Al Qassimi Hospital,
Medicine, Chicago, Illinois United Arab Emeriates

Pieter Koopman, MD Moussa Mansour, MD

Electrophysiologist, Heart Center Hasselt, Jessa Cardiac Arrhythmia Service, Department of
Hospital, Hasselt, Belgium Medicine, Massachusetts General Hospital,
Boston, Massachusetts
Peter R. Kowey, MD, FACC
Professor, Jefferson Medical College, Lankenau Frank I. Marcus, MD
Institute for Medical Research, Professor of Medicine, Section of Cardiology,
Philadelphia, Pennsylvania University of Arizona Medical Center, Tucson,
Arizona
Andrew D. Krahn, MD, FRCPC
Heart Rhythm Services, Department of Albert Massó van Roessel, MD
Medicine, Division of Cardiology, St. Paul’s Department of Medicine, Universitat
Hospital, University of British Columbia, Internacional de Catalunya, Barcelona, Spain
Vancouver, British Columbia, Canada

Contributors u xi
John M. Miller, MD, FHRS, FACC Inger Olson, MD
Professor of Medicine, Indiana University Clinical Associate Professor, Department of
School of Medicine; Director, Clinical Cardiac Pediatrics (Cardiology), Stanford University
Electrophysiology, Indiana University Health, School of Medicine, Stanford, California
Indianapolis, Indiana
Ali Oto, MD, FESC, FACC, FHRS, FISHNE
Fred Morady, MD Professor of Cardiology, Chairman, Department
McKay Professor of Cardiovascular Disease, of Cardiology, MHG, Memorial Ankara
Professor of Medicine, University of Michigan Hospital, Ankara, Turkey
Health System, Ann Arbor, Michigan
Santosh K. Padala, MD
Daniel J. Murphy, Jr., MD Cardiac Electrophysiology Fellow, Division of
Professor, Department of Pediatrics Cardiology, Virginia Commonwealth
(Cardiology) Stanford University School of University, Pauley Heart Center, Richmond,
Medicine, Stanford, California Virginia

Robert J. Myerburg, MD Carlos Alberto Pastore, MD, PhD, FESC

Professor of Medicine and Physiology, Division Director, Clinical Unit of Electrocardiography,
of Cardiology, American Heart Association Heart Institute (InCor), Hospital das Clínicas
Chair in Cardiovascular Research, University of da Faculdade de Medicina da Universidade de
Miami Miller School of Medicine, Miami, São Paulo, São Paulo, Brazil
Florida
Olivier Paziaud, MD
Yuji Nakazato, MD, PhD, FESC Cardiologist, Arrhythmia Department, Centre
Professor, Department of Cardiology, Heart Cardiologique du Nord, Saint-Denis, France
Center, Juntendo University Urayasu Hospital,
Urayasu City, Chiba, Japan Horácio Gomes Pereira Filho, MD
Assistant Physician, Clinical Unit of
Amit Noheria, MBBS, SM Electrocardiography, Heart Institute (InCor),
Assistant Professor of Medicine, Cardiac Hospital das Clínicas da Faculdade de Medicina
Electrophysiology, Washington University da Universidade de São Paulo, São Paulo, Brazil
School of Medicine, St. Louis, Missouri
Andrés Ricardo Pérez-Riera, MD, PhD
I. W. P. Obel, MBChB, FCP(SA), FACC Post Graduate Advisor at Design of Studies and
Specialist Cardiologist/Electrophysiologist, Scientific Writing Laboratory, ABC School of
Milpark Hospital, Johannesburg, Gauteng, Medicine, Santo André, São Paulo, Brazil
South Africa
Femi Philip, MD
Sercan Okutucu, MD Division of Cardiovascular Medicine, Kaiser
Department of Cardiology, Cardiology Permanente, Medical Center, Sacramento,
Specialist, Memorial Ankara Hospital, Ankara, California
Turkey
Olivier Piot, MD
Cardiologist, Arrhythmia Department, Centre
Cardiologique du Nord, Saint-Denis, France

xii u Contributors
Philip Podrid, MD Scott Sakaguchi, MD, FHRS, FACC, FACP
Professor, Boston University School of Professor, Department of Internal Medicine,
Medicine; Lecturer in Medicine, Harvard University of Minnesota, Minneapolis,
Medical School, Boston, Massachusetts; Minnesota
Attending Physician, West Roxbury VA
Hospital, West Roxbury, Massachusetts Nelson Samesima, MD, PhD
Supervising Physician, Clinical Unit of
Guillem Pons-Lladó, MD Electrocardiography, Heart Institute (InCor),
Cardiology Department, Hospital Santa Creu Hospital das Clínicas da Faculdade de Medicina
i Sant Pau, Universitat Autònoma de Barcelona, da Universidade de São Paulo, São Paulo, Brazil
Barcelona, Spain
Luca Santini, MD, PhD
Sergio Richter, MD Cardiology Division, G.B. Grassi Hospital,
Associate Professor of Medicine and Ostia-Lido, Rome, Italy
Cardiology, Department of Electrophysiology,
Heart Center, University of Leipzig, Leipzig, Massimo Santini, MD, FESC, FACC
Germany Past-President, World Society of Arrhythmias,
Rome, Italy
Michael P. Riley, MD, PhD
Assistant Professor of Medicine, Peter J. Schwartz, MD, FACC, FHRS, FAHA,
Electrophysiology Section, Cardiovascular FESC
Division, University of Pennsylvania, Director, Center for Cardiac Arrhythmias of
Philadelphia, Pennsylvania Genetic Origin, IRCCS Istituto Auxologico
Italiano, Milan, Italy
Magdi M. Saba, MD, FHRS
Consultant Cardiac Electrophysiologist, Hossein Shenasa, MD, MS, FACC
St. George’s Hospital and University of London, Staff Cardiologist, Electrophysiologist, Heart &
London, England Rhythm Medical Group, San Jose Area
Hospitals, San Jose, California
Frédéric Sacher, MD, PhD
Hôpital Cardiologique du Haut Lévèque, CHU Mariah Smith
de Bordeaux, Université de Bordeaux and Heart & Rhythm Medical Group, San Jose,
LYRIC Institute, Bordeaux, France California

Mohammad Ali Sadr-Ameli, MD Christian Steinberg, MD, FRCPC

Rajaie Cardiovascular Medical and Research Heart Rhythm Services, Department of
Center, Iran University of Medical Sciences, Medicine, Division of Cardiology, St. Paul’s
Tehran, Iran Hospital, University of British Columbia,
Vancouver, British Columbia, Canada
Johan Saenen, MD, PhD
Staff Member, Department of Cardiology, Benjamin Stripe, MD
Antwerp University Hospital, Antwerp, Fellow of Division of Cardiovascular Medicine,
Belgium University of California, Davis, Medical Center,
Sacramento, California

Contributors u xiii
Sakis Themistoclakis, MD Edward P. Walsh, MD, FHRS
Director, Unit of Electrophysiology and Cardiac Chief, Cardiac Electrophysiology, Boston
Pacing, Ospedale Dell’Angelo, Venice, Italy Children’s Hospital, Boston, Massachusetts;
Professor of Pediatrics, Harvard Medical
Vassil Traykov, MD, FEHRA School, Boston Massachusetts
Head of Department of Electophysiology and
Pacing, Clinic of Cardiology, Tokuda Hospital, David E. Ward, MD, FACC
Sofia, Bulgaria Consultant Cardiologist and
Electrophysiologist, Retired, London, England
Zian H. Tseng, MD, MAS
Murray Davis Endowed Professor, Associate Christopher E. Woods, MD, PhD, FHRS
Professor of Medicine in Residence, Cardiac Medical Director, Cardiac Electrophysiology,
Electrophysiology Section, Cardiology Division, Palo Alto Medical Foundation, Burlingame,
University of California, San Francisco, California
San Francisco, California
Begüm Yetiş Sayın, MD
George F. Van Hare, MD Department of Cardiology, Cardiology
Division Chief, Pediatric Cardiology, Louis Specialist, Memorial Ankara Hospital, Ankara,
Larrick Ward Professor of Pediatrics, Turkey
Washington University School of Medicine,
St. Louis, Missouri Li Zhang, MD
Associate Professor, Jefferson Medical College,
Nishant Verma, MD, MPH Lankenau Institute for Medical Research,
Assistant Professor of Medicine-Cardiology, Philadelphia, Pennsylvania
Cardiac Electrophysiology, Bluhm
Cardiovascular Institute, Northwestern
Memorial Hospital, Feinberg School of
Medicine, Northwestern University, Chicago,
Illinois

xiv u Contributors
 Foreword

It is exciting to see the publication of this case-based collection of ECGs from “Masters” in
electrocardiography and electrophysiology. It is also a pleasure for me to contribute the foreword to
this important book. This collection should be read by both early trainees and experienced
electrocardiographers. There are pearls littered throughout and the explanations and interpretations
grounded in physiology and fundamental vector analysis. The clinical relevance is made obvious by
the case format. The outstanding group of Editors have done a superb job with the organization of
the text in dividing it into focused sections to maximize ease of review and educational value. The
ECG recordings are characteristically the best from the experts’ collections. The tracings show the
incredible value of this simple yet elegant tool for diagnosing and localizing arrhythmias and
recognizing signature ECG patterns associated with unique genetically determined and acquired
arrhythmogenic syndromes.
It is important for me to also pay a special tip of the hat to one of the Co-Editors, Dr. Mark
Josephson. Not only is he the father of modern cardiac electrophysiology, but Mark has also been
inspirational in his love of the 12-lead ECG and his desire to maximize its full potential. For more
than 40 years, he has mentored a long collection of trainees on the correct interpretation of the 12-lead
ECG. Such phrases as “burn it in your brain” for a unique ECG pattern that was critical to recognize
within a second of display are always remembered with a smile throughout one’s career. I was a
lucky trainee who has many critical ECG images “burned in my brain.” His participation in
this important text adds to the glow of the other stellar editors and ECG aficionados and provides the
‘Grand Cru’ stamp to this effort.
This book should serve as an important reference, and I guarantee it will be pulled from the shelf
for decades to come. It is a gem and should be enjoyed by even those with only a modest interest in
the 12-lead ECG and the care of patients with cardiac arrhythmias. The true fans of the ECG will be
awed by the experience.
Francis E. Marchlinski, MD, FACC, FHRS, FAHA
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania

xv
 Foreword

The father of electrocardiography is Willem Einthoven (1860–1927), who first recorded the first
human ECG in 1902 at the University of Leiden, the Netherlands, where he used to teach. He received
the Nobel Prize in 1924 for his major invention. Since then, the ECG has fascinated a number of
cardiologists by the number of information that can be derived. Some of these famous
electrocardiographers such as Alfred Pick and Richard Langendorf, have described a number of
phenomena such as “concealed conduction” or “tachycardia/bradycardia-dependent bundle branch
block,” which were found later on to be correct using invasive electrophysiology. My generation is
fortunate to have met some of them and to learn from them. It is refreshing that Mohammad Shenasa,
Mark E. Josephson, N. A. Mark Estes III, Ezra A. Amsterdam, and Melvin Scheinman, the Editors of
this ECG Masters’ collection, have emphasized that the ECG remains an invaluable tool for clinicians
despite the advances made in the field of arrhythmias. This contribution, with the participation of
experts from around the world, will be extremely useful to clinicians, fellows in cardiology, and all
those who are involved in the management of cardiac arrhythmia patients.
This book is not a simple collection of ECGs. It is, in fact, the report of clinical situations in which
the ECG guides the diagnosis, signals the choice of the appropriate tests, and leads to the appropriate
management. The cases presented are not rare or unusual. They represent clinical settings that
cardiologists and clinicians will encounter in their daily practice—and this, in my view, adds to the
educational value of this book. I found it very interesting and enjoyable to read the ECG tracings put
into their clinical context.
The field of cardiac arrhythmias has been enriched by the major advances made in the last four
decades in better understanding tachycardia mechanisms due to the advent of intracardiac recordings,
invasive clinical electrophysiology, ablation, and new mapping techniques. The authors of the cases
refer to these techniques to support their interpretation and document the concepts used in their
interpretation, adding, when necessary, references and suggested reading.
I have no doubt that the authors have succeeded in providing the reader with an interesting,
enjoyable, and useful collection of clinical situations in which the correct ECG interpretation has
played a major role.
Samuel Lévy, MD, FACC, FESC, FAHA
Aix -Marseille Université
Marseille School of Medicine, France

xvii
 Preface

Each year, several new books or new editions are published on electrocardiography. Since the invention
of the electrocardiogram (ECG) by Willem Einthoven almost 110 years ago, the ECG has become the
most commonly used test worldwide, and its use continues to increase. The medical community has
subsequently gained a wealth of knowledge from the ECG for the diagnosis of many cardiac and non-
cardiac conditions, ranging from acute ischemia and infarction on the one hand to arrhythmias on the
other. Furthermore, the ECG is the first step in evaluating patients arriving at the emergency department,
as the results are immediately available. Likewise, the ECG has been used as a screening test for athletes
and is also used to identify patients at a high-risk of arrhythmias and sudden cardiac death.
Despite the emergence of other imaging modalities, the ECG remains a benchmark diagnostic test
and is an integral part of a risk stratification algorithm in almost all guidelines of all disciplines of
medicine.
Since the success of our 2015 book, The ECG Handbook of Contemporary Challenges, many of our
colleagues and friends encouraged us to provide a case-based collection of ECGs. Thus, we have
invited the most renowned physicians from around the world who read and interpret ECGs (i.e.,
electrocardiographers) to provide their most insightful examples. We also asked them to include their
interpretation of the ECG findings with appropriate, up-to-date references. All tracings are well
annotated and described. In addition, we suggested providing questions for the readers relating to the
ECGs and a discussion that makes this book useful for trainees at all levels.
Although the main theme of this book is electrocardiography, other imaging techniques are
discussed to validate the authors’ interpretations. We are extremely grateful that all of our colleagues
have unanimously accepted our invitation and provided their best cases.
The cases in this book are arranged according to topics in electrocardiography and arrhythmias.
Areas of focus include ECGs of inherited arrhythmia syndromes, athletic ECGs, and ECGs in
congenital heart disease. The book also discusses new ECG criteria/markers and syndromes related
to recently discovered channelopathies such as Brugada syndrome, early repolarization syndrome, and
the like. We are confident that this collection of ECGs from masters of electrocardiography from
around the world will prove useful and of great educational value to clinicians in many areas of
medicine. We believe this unique collection is similar to receiving a master art collection from the
Louvre or the Metropolitan Museum of Art that should be on everyone’s shelf as an ECG museum.
Finally, we wish to thank the Cardiotext staff, namely Mike Crouchet and Carol Syverson, for their
professionalism and for providing the text and figures in a high-quality format.
The Editors

xix
 Abbreviations

ACS acute coronary syndrome

AF atrial fibrillation
AP accessory pathway
APC atrial premature contraction
APD action potential duration
ARVC/D arrhythmogenic right ventricular cardiomyopathy/dysplasia
AT atrial tachycardia
AVNRT atrioventricular nodal reentrant tachycardia
AVRT atrioventricular reentrant tachycardia

BB bundle branch
BBB bundle branch block
BS Brugada syndrome

CAD coronary artery disease

CHF congestive heart failure
CL cycle length

DDD dual-chamber pacing

EADs early afterdepolarizations

ECG electrocardiogram
EF ejection fraction

HCM hypertrophic cardiomyopathy

HPS His-Purkinje system
HR heart rate

ICD implantable cardioverter-defibrillator

LA left atrial
LAD left axis deviation
LAFB left anterior fascicular block
LBB left bundle branch
LBBB left bundle branch block
LQTS long QT syndrome

xxi
LV left ventricle
LVEF left ventricular ejection fraction
LVH left ventricular hypertrophy
LVOT left ventricular outflow tract

MI myocardial infarction
MRI magnetic resonance imaging

OD once daily
ORT orthodromic reciprocating tachycardia

PABs premature atrial beats

PAC premature atrial contraction
PJRT permanent form of junctional reciprocating tachycardia
PV pulmonary vein
PVC premature ventricular contraction
PVI pulmonary vein isolation

RA right atrial
RBB right bundle branch
RBBB right bundle branch block
RV right ventricle
RVA right ventricular apex
RVH right ventricular hypertrophy
RVOT right ventricular outflow tract

SCD sudden cardiac death

SQTS short QT syndrome
SR sinus rhythm
SVT supraventricular tachycardia

TdP torsades de pointes

VF ventricular fibrillation
VT ventricular tachycardia

WCT wide complex tachycardia

WPW Wolff–Parkinson–White syndrome

xxii u Abbreviations
 Video Legends

Video 13B.5.1 Short axis shows concentric LVH

Video 13B.5.2  ong axis 3-chamber view shows concentric LVH and pronounced apical
L
hypertrophy consistent with apical hypertrophic cardiomyopathy

Video 13B.6.1 Short axis of mild left ventricular hypertrophy

Video 13B.6.2 Long axis 3-chamber view of hypertrophic cardiomyopathy

Video 13E.3.1  pical, three-chamber view echocardiogram showing akinesis in the mid to distal
A
anteroseptum and apex

Video 13E.3.2 Enlarged view of Video 13E.3.1

Video 13E.3.3 Coronary angiogram

Video 13E.3.4 Right coronary

Video 13E.3.5 Left coronary

Video 15.6.1 Echocardiogram showing LVEF of 74% with mild concentric LVH

Video 15.6.2 MRI, 4-chamber view

xxiii
 SECTION 1
Introduction to the Interpretation of the Electrocardiogram

CASE
Mohammad Shenasa, MD 1.1

The first and most important step in ECG interpretation is the differentiation between “normal”
and “abnormal.”
The second step consists of differentiation between the various abnormal ECG patterns and
their correlation with known pathologic conditions. In particular, the recent discoveries with small
subtle significant markers for adverse events such as early repolarization, Brugada-type ECGs, and
other channelopathies.
Information about the ECG in disease is much more complex than knowledge of normal
variation. Yet, it is in the differentiation between normal and abnormal that difficulties in ECG
interpretation frequently arise.
Below are two examples of normal ECGs.
Heart rate: 64 bpm
PR interval: 154 ms
QRS duration: 98 ms
QT/QTc: 406/415 ms
Normal ST-T wave patterns

Figure 1.1.1

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World © 2017 Mohammad Shenasa, Mark E. Josephson,
N. A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-08-8. 1
Heart rate: 80 bpm
PR interval: 148 ms
QRS duration: 92 ms
QT/QTc: 364/420 ms

Figure 1.1.2

It is important to have a systematic approach when analyzing and interpreting ECGs.

1. Baseline findings in sinus rhythm.
2. Observations during tachycardias.
3. Analysis of the changes of the cardiographic morphologies (transient changes).
4. Mode of spontaneous initiation and termination.
5. Maneuvers during tachycardias.
In a stepwise approach to ECG or rhythm analysis, one should determine the rate of the
tachycardia (fast or slow), the QRS duration (wide or narrow) and morphology, and the relationship
of the P wave to the QRS, whether it is before, during, or after and if there is a one-to-one
relationship between the P wave and the QRS.
Other important points regarding interpretation of the ECG:
1. Determine the origin and initiation of cardiac arrhythmias.
2. Look for myocardial ischemia and infarction.
3. Evidence of electrolyte imbalance and reversible causes.
4. Systemic and myocardial disorders.
5. Measure; do not eyeball the intervals.
6. Focus on zone of transition.

References
1. Wellens HJ, Gorgels AP. The electrocardiogram 102 years after Einthoven. Circulation. 2004;109(5):562–564.
2. Yong CM, Froelicher V, Wagner G. The electrocardiogram at a crossroads. Circulation. 2013;128(1):79–82.
3. Stern S. Electrocardiogram: Still the cardiologist’s best friend. Circulation. 2006;113(19):e753–e756.

2 u Case 1.1
 SECTION 2
Conduction Disturbances: Sinus Node Disease/Sick Sinus Syndrome,
AV Conduction Disturbances, AV Blocks, Bundle Branch Blocks,
and Fascicular Blocks

CASE
2.1
Amit Noheria, MBBS, SM
Samuel J. Asirvatham, MD

Patient History
A 36-year-old male with congenitally corrected transposition of great arteries (CC-TGA) presents
with fatigue.

Questions
1. What can you say about antegrade and retrograde AV conduction from ECGs in Figure 2.1.1
and 2.1.2?
2. What relevance does this have for decisions on pacemaker implantation?

Figure 2.1.1

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World © 2017 Mohammad Shenasa, Mark E. Josephson,
N. A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-08-8. 3
Figure 2.1.2

Discussion, Interpretation, and Answer

Levo-looping of the embryonic bulboventricle from the developing heart tube results in
morphologic ventricular inversion—morphologic right ventricle positioned on the left side and the
morphologic left ventricle and the left bundle branches on the right. L-looping frequently occurs
with double switch—atrioventricular and ventriculoarterial—in context of normally positioned atria
(situs solitus) and transposition of great arteries, and is often referred to as CC-TGA. CC-TGA can
be associated with membranous ventricular septal defect (VSD), pulmonary stenosis, and Ebstein’s
anomaly of the morphologic tricuspid valve.
With situs solitus, the sinus node anatomy and atrial activation may be normal with a normal
P-wave axis and morphology, as is seen in this case. L-looping can, however, occur in patients with situs
inversus or situs ambiguus (heterotaxy syndromes with asplenia or polysplenia) that might impact the
location of the sinus node and P-wave axis. The ventricular septal activation in CC-TGA occurs from
the morphologic left bundle branch from right to left. As seen in the junctional escape complexes in
Figure 2.1.3, conducted QRS complexes in CC-TGA are characterized by Q waves in leads V1–V2 and
inferior leads (red arrows), and absence of “septal Q waves” in the left lateral leads (blue arrows).

4 u Section 2: Conduction Disturbances: Sinus Node Disease

Figure 2.1.3

One-third of patients with CC-TGA develop complete AV block. The AV conduction system in
CC-TGA (and double-inlet left ventricle) is characterized by an anteriorly displaced AV node outside
the triangle of Koch at the base of the right atrial appendage.1,2 This gives rise to an anteriorly
displaced AV bundle (bundle of His) that goes around the lateral/superior aspect of the valve of the
transposed pulmonary artery that arises in juxtaposition to the mitral valve of the morphologic left
ventricle (subpulmonary). This AV bundle continues and splits into the left and right bundle
branches along the superior aspect of a membranous VSD that is often present. The normally
located AV node in the triangle of Koch typically does not connect to the ventricle on account of
malalignment of the atrial and ventricular septae. However, in certain patients this can function as
the second AV nodal connection to a separate distinct bundle of His that courses along the inferior
margin of the VSD.1,3
Figure 2.1.1 shows sinus rhythm (Figure 2.1.3, vertical black arrows) with complete AV nodal
conduction block. There is escape junctional rhythm with narrow complexes (black horizontal
arrows, ~1900 ms or 32 bpm). The junctional rhythm is intermittently interrupted by wide QRS
complexes (asterisks). The wide QRS complexes have a slurred onset and suggesting an “extra-
fascicular” myocardial origin. The positive precordial concordance (upright QRS in leads V1 and
V4 –V6) and the left frontal place axis localize the wide complexes to the posterior paraseptal region
along the left-side AV annulus. As both wide QRS complexes in this tracing have a short, fixed
preceding PR interval, it is quite likely these ventricular activations occur over a left posterior
paraseptal accessory AV pathway. Only two P waves conduct over this accessory pathway (asterisks),
and the others are blocked. The accessory pathway has weak antegrade conduction properties and is
low risk for sudden death from rapid conduction of atrial fibrillation. Another observation in this
ECG is the ventriculophasic sinus arrhythmia shown by the changing PP interval (orange double-
headed arrows, L—long, S—short).
The level of AV block is thought to most commonly occur at the level of the AV bundle. The
narrow escape complexes, albeit with a left axis (rS in lead II) would suggest either AV block at the

Case 2.1 u 5
level of the anterior AV node with junctional escape complexes with a left axis on account of variant
ventricular anatomy, remodeling, or intraventricular conduction abnormalities, or alternatively
block at the anterior AV bundle but escape complexes from a preserved posterior AV conduction
system (expected to have left superior axis due to the relatively posterior location).
All the junctional escape complexes in Figure 2.1.1 time coincidentally with or immediately
after sinus P waves. This precludes any assessment of retrograde VA conduction, as the atrial tissue
is refractory and unexcitable after sinus activation. The first QRS complex in Figure 2.1.2, however,
allows assessment of retrograde conduction. This QRS complex is followed by a retrograde P wave
with a short RP interval (Figure 2.1.4, arrow). This P wave is negative in inferior leads (II > III),
isoelectric in lead I, positive in lead V1, and would localize to the left posteroseptal region,
consistent with the location of the atrioventricular accessory pathway. The subsequent QRS
complex is followed by P-wave fusion between sinus rhythm and retrograde atrial activation
(asterisk). Following pacemaker implantation, the brisk retrograde conduction can lead to
pacemaker syndrome or pacemaker-mediated tachycardia.

Figure 2.1.4

This patient had CC-TGA without evidence of VSD or pulmonary stenosis. The systemic
ventricle (morphologic right ventricle) was hypertrophied and had reduction in systolic function
(ejection fraction 30%). He received an atrial-biventricular cardiac resynchronization therapy
pacemaker (he declined defibrillator implantation). On electrophysiology study, he had a left-sided
posteroseptal accessory pathway with good retrograde conduction properties (effective refractory
period 270 ms) that was successfully ablated.

References
1. Anderson RH, Becker AE, Arnold R, et al. The conducting tissues in congenitally corrected transposition.
Circulation. 1974;50(5):911–923.
2. Anderson RH, Arnold R, Thapar MK, et al. Cardiac specialized tissue in hearts with an apparently single ventricular
chamber (double inlet left ventricle). Am. J. Cardiol. 1974;33(1):95–106.
3. Hosseinpour AR, McCarthy KP, Griselli M, et al. Congenitally corrected transposition: Size of the pulmonary trunk
and septal malalignment. Ann. Thorac. Surg. 2004;77(6):2163–2166.

6 u Section 2: Conduction Disturbances: Sinus Node Disease

Antoni Bayés de Luna, MD CASE
2.2
Luis Alberto Escobar Robledo, MS
Albert Massó van Roessel, MD

Patient History
A 65-year-old patient with chronic obstructive pulmonary disease (COPD) that present in a long
strip recording of lead II evident brusque changes of P wave (Figure 2.2.1).

Figure 2.2.1 Continuous lead II. Observe the abrupt and repeated change in P-wave morphology and polarity not related to the
respiration in a patient with chronic obstructive pulmonary disease (COPD). Two types of P-wave morphology are observed: peaked P wave
and flat P wave.

Question
How might these changes be explained?
These ECG changes of P wave may be due to:
1. Changes with respiration
2. Fusion beats between sinus and ectopic rhythm
3. Artifacts
4. Sinus rhythm with atrial aberrancy

Discussion, Interpretation, and Answer

The correct answer is 4.
These changes are due to atrial aberrancy. This concept was coined more than 40 years ago by
Chung in 19721 as “the bizarre configuration of the P wave of a sinus beat immediately after an
atrial, AV, or ventricular premature complexes, and is equivalent in the atria to the concept of
ventricular aberrancy”.

Case 2.2 u 7
 The concept of atrial aberrancy also encompasses brusque changes of P-wave morphology that
may appear in either the same or separate ECG strip, and may or may not be related to the changes
in heart rate.2,3 These changes in morphology (aberrancy) are due to transient changes in the way of
transmission of the sinus impulses in the atria. This can sometimes be due to transient interatrial
block; however, in this case where there is no ECG pattern of interatrial block,4–7 it may be due to
changes in the transmission of stimulus probably through right atrium. These changes may appear
in the same recording, (Figure 2.2.1), in different days (Figure 2.2.2), or immediately after an atrial
or ventricular premature beat (Figures 2.2.3–2.2.5). In the setting of Chung,1 aberrant atrial
conduction is an infrequent ECG finding that usually occurs in the elderly with organic heart
disease, especially ischemic heart disease. It can also be in chronic cor pulmonale.2 The clinical
significance is uncertain, but usually occurs in patients with heart disease and atrial involvement.
The current case has the following characteristics:
The P-wave changes are not an artifact, are not related with respiration, and are not fusion beats.
1. The recording starts with 3 flat P wave followed by 13-peaked P wave, 17-flat P wave, and finally
3 peaked waves. This is not a respiratory cycle.
2. The changes from one morphology to another are sudden or with only one complex (the third of
second strip) that may correspond to a minor degree of aberrancy. Therefore, there are no fusion
beats.
The type of aberrancy of Figure 2.2.2 may explain that patients with important subacute cor
pulmonale and pathological P wave of right atrium enlargement (Figure 2.2.2A) may present
transient or permanent disappearance of the ECG criteria of the right atrial enlargement
(Figure 2.2.2A, 2.2.2B, and 2.2.2C).

Figure 2.2.2 A. A 45-year-old patient with subacute cor pulmonale. Note the right axis of P wave (ÂP) around + 80º (right) few days
later (B), the ÂP was left, returning to the right in a third ECG (C) recorded at 15 days. This example shows that criteria of right atrial
enlargement may be concealed due to atrial aberrancy.

8 u Section 2: Conduction Disturbances: Sinus Node Disease

 Finally, in Figures 2.2.3 to 2.2.5, we can see different changes of the P wave that appear after an
premature atrial complex (PAC) or an premature ventricular complex (PVC). These bizarre P waves
are not an artifact or an escape beat. They most likely correspond to atrial aberrancy due to them
being recorded at different times with the same morphology. Figure 2.2.3 shows that after a PAC
there is a change in the refractory period of the atria, and the next impulse (x) is partially blocked in
the same part of the right atrium and presents a very different pattern (more peaked) than the
other ones.

Figure 2.2.3 A P wave that appeared after a PAC that has different morphology from previous and successive ones. It is not an artifact
or escape complex because it was recorded many times with the same PR, and is most likely explained by atrial aberrancy.

Figure 2.2.4 also shows a transient change of P wave after a PAC. The P wave changes from a
pattern of advanced interatrial block (aIAB) to another of partial interatrial block (pIAB) (from ± to
bimodal (x)) that occur is due to the refractory period of the upper part of atria being shortened due
to PAC. The next P wave may be conducted with lower degree of interatrial block (IAB) (transient or
second-degree A-IAB).

Figure 2.2.4 In the presence of an A-IAB pattern (first P ± in VF) after a PAC there is a pause followed by transient P-IAB pattern that is
followed again by a pattern of A-IAB.

In other occasions (Figure 2.2.5) the presence of A-IAB (P ± in II) after one PVC appears as a
pause followed by a peaked P wave that has a normal PR interval and is not an artifact. This
presumably corresponds to an atrial aberrancy (right atrium).

Figure 2.2.5 In a case of A-IAB after two sinus beats with ± morphology of P wave, a PVC appears which is followed by a P wave with
normal P-R conduction and different morphology, only positive (peaked P). This is due to atrial aberrancy.

Case 2.2 u 9
Conclusion
• Carefully watching the P wave is a useful way to perform the correct diagnosis. Cases with atrial
aberrancy that appears transiently explain that the diagnosis of RAE may be temporally masked6
(Figure 2.2.2).
• Cases of atrial aberrancy usually appear in the elderly with organic heart disease and atrial
involvement.

References
1. Chung E. Aberrant atrial conduction. Unrecognized electrocardiographic entity. Br. Heart J. 1972;34:341–346.
2. Júlia J, Bayés de Luna A, Candell J, et al. Aberrancia auricular: A proposito de 21 casos. Rev. Esp. Cardiol.
1978;31(2):207.
3. Bayés de Luna A. Bloqueo a nivel auricular. Rev. Esp. Cardiol. 1979;32(1):5–10.
4. Bayés de Luna A, Fort de Ribot R, Trilla E, et al. Electrocardiographic and vectorcardiographic study of interatrial
conduction disturbances with left atrial retrograde activation. J. Electrocardiol. 1985;18(1):1–13.
5. Bayés de Luna A, Platonov P, García-Cosio F, et al. Interatrial blocks. A separate entity from left atrial enlargement:
A consensus report. J. Electrocardiol. 2012;45:445–451.
6. Bayés de Luna A. Clinical electrocardiography. Sussex, U.K.: Wiley-Blackwell. 2012;103.
7. Bayés de Luna A, Massó-van Roessel A, Escobar Robledo LA. The diagnosis and clinical implications of interatrial
block. Eur. Cardiol. Rev. 2015;10(1):54–59.

10 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
Bernard Belhassen, MD 2.3
Patient History
The following electrocardiogram (ECG) tracings were recorded during electrophysiology studies
performed without sedation in a 71-year-old male with obstructive hypertrophic cardiomyopathy
and recurrent syncope.

Figure 2.3.1

Discussion
Baseline ECG shows sinus rhythm with normal PR and QRS duration. The His potential has normal
configuration; AH is prolonged at 150 ms and HV normal (50 ms). Incremental atrial pacing showed
supra-Hissian block with Wenckebach sequence at 100/minute.
Catheter-induced atrial fibrillation (AF) then occurred. Heart rate initially ranged from 50 to
85/minute then atrioventricular (AV) block lasting 3 seconds occurred (Figure 2.3.1). This event was

Case 2.3 u 11
reproducibly documented and not related to any significant change in the patient’s respiratory
status. After AF spontaneously converted after #5 minute, short bursts of rapid atrial pacing
reproducibly induced transient AV block on very late sinus beats (Figure 2.3.2).
Despite the fact the His potential could not be recorded during AV block, the assumption was a
phase 4 dependent block located at the proximal His area. A similar case was previously reported.1

Figure 2.3.2

Reference
1. Belhassen B, Danon L, Shoshani D, et al. Paroxysmal atrioventricular block triggered by orthostatic hypotension.
Am. Heart J. 1986;112:1107–1109.

12 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
2.4
Andrei G. Dan, MD, PhD
Catalin A. Buzea, MD, PhD

Patient History
An 86-year-old female with history of hypertension and hypercholesterolemia is admitted for
orthostatic syncope preceded by dizziness. The patient has left hemiparesis after an ischemic
stroke. She is under treatment with perindopril, indapamide, rosuvastatin, and clopidogrel.

Questions
1. What is the underlying rhythm?
2. Could help this tracing in explaining the etiology of syncope?

Figure 2.4.1 Sinus rhythm with second-degree atrioventricular block with Luciani periods (standard leads).

Figure 2.4.2 Sinus rhythm with second-degree AV atrioventricular with Luciani periods (precordial leads). The second QRS complex has
different morphology suggesting aberrancy.

Case 2.4 u 13
Discussion, Interpretation, and Answers
The two tracings are simultaneous depicting standard and precordial leads. The atrial rhythm is
sinus (positive P wave in II, III, and aVF). The PP is regular (red marks) and the rhythm is sinus
tachycardia at 107 bpm. There is a group beating. The first QRS of the group (A) has right bundle
branch block morphology with the leftward axis and clockwise rotation in the horizontal plan
suggesting anterosuperior haemiblock. The second QRS complex (B) is slightly modified suggesting
increased right intraventricular delay. The reason for this could be phase 3 aberrancy because it
follows a long-short cycle (similar to Ashman phenomenon in atrial fibrillation). The PR interval
(green marks) of the first QRS is 160 ms, the second is 200 ms and the third P is not followed by a
QRS complex. This is highly suggestive for a Mobitz type I, second-degree atrioventricular block.
Therefore, a bifascicular block is accompanied by a second-degree atrioventricular block; the last
one could be localized at the atrioventricular node level (indicating a multilevel block) or less likely
at the level of posteroinferior fascicle of the left bundle branch (indicating an incomplete
trifascicular block). For this patient, the ischemic etiology is more probable than a degenerative one
because of his risk factors and history. There is a risk for progression to more advanced block and
there is a high index of suspicion that the patient suffered an arrhythmic syncope. A pacemaker
implantation is advisable.

14 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
2.5
Andrei G. Dan, MD, PhD
Catalin A. Buzea, MD, PhD

Patient History
An 81-year-old patient is admitted in the neurology department for altered peripheral sensitivity. She
is under treatment with valproate for epilepsy and described several episodes of lightheadedness.
Two consecutive electrocardiogram (ECG) tracings were obtained during her hospitalization.

Questions
1. What could explain the progression to the second tracing?
2. What is the nature of the premature beats (red star)?

Figure 2.5.1 Normal sinus rhythm with right bundle branch block and left anterior fascicular block.

Case 2.5 u 15
Figure 2.5.2 Complete atrioventricular block in same patient with supernormality phenomenon.

Discussion, Interpretation, and Answers

There is normal sinus rhythm in the first tracing. QRS morphology indicates right bundle branch
block morphology with secondary type repolarization abnormalities. The QRS axis is leftward
(−60º) indicating left anterosuperior hemiblock. The PR interval is 210 ms (longer than normal for
the rate). The above mentioned findings indicate bifascicular block and first-degree atrioventricular
block. The conduction abnormality could be at two levels or indicating incomplete trifascicular
block.
In the second tracing, the atrial rhythm is sinus (93 bpm) and the ventricular rhythm is slow
(36 bpm). There is no relation between the atrial and ventricular rhythm (variable PR interval,
atrioventricular dissociation). This is indicative for complete atrioventricular block. As the QRS
morphology is similar with that observed in the first tracing, the subsidiary pacemaker is situated at
the left inferoposterior left branch level. Some atrial impulses (red star) are slightly delayed and are
conducted to the ventricle giving the false impression of extrasystoles. These beats could represent
“supernormal” conduction as this conduction is unexpected. Several explanations exist for
supernormal conduction including gap phenomenon, supernormal excitability and concealed
conduction.1 The patient has indication for pacemaker implantation.

Reference
1. Bayés de Luna A. Clinical Electrocardiography: A Textbook. 4th ed. Sussex, U.K.: Wiley-Blackwell. 2012.

16 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
2.6
Andrew E. Epstein, MD
Michael P. Riley, MD, PhD

Patient History
An 86-year-old asymptomatic male referred for pacemaker implantation for progressive
atrioventricular (AV) block.

Figure 2.6.1

Discussion
There is marked first-degree AV block. Sinus rhythm is confirmed by a normal P-wave axis and
premature ventricular complexes that do not reset the sinus rate but do have concealed retrograde
conduction leading to AV block of the subsequent sinus beat. A pacemaker was not implanted.

Case 2.6 u 17
CASE
2.7 N. A. Mark Estes III, MD

Patient History
ECG of an 82-year-old asymptomatic male with pulmonary sarcoidosis for 50 years.

Questions
1. What is the ECG abnormality?
2. What are the common ECG manifestations of cardiac sarcoidosis?

Figure 2.7.1

Discussion
This ECG demonstrates left bundle branch block with a QRS duration of 176 ms and first-degree
atrioventricular block (PR 248 ms). Infra-Hisian conduction system disease is the most common
ECG manifestation of cardiac sarcoidosis, which has a tendency to involve the basal portion of the
intraventricular septum and manifest with conduction system involvement.

18 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
N. A. Mark Estes III, MD 2.8
Patient History
ECG of a 50-year-old male with no prior cardiac history resuscitated from cardiac arrest due to
sustained ventricular tachycardia.
Echocardiogram demonstrated a left ventricular ejection fraction of 25% with anteroseptal and
inferior left ventricular hypokinesis. Coronary angiography demonstrated no obstructive disease.

Questions
1. What is the ECG abnormality?
2. What cardiovascular condition is likely to cause these ECG abnormality and cardiac arrest?

Figure 2.8.1

Discussion
The ECG demonstrates right bundle branch block (RBBB) (QRS 144 ms) and first-degree
atrioventricular (AV) block (PR 264 ms). Multiple premature ventricular contractions with a left
bundle branch block morphology are present. The ECG shows a RBBB with a left axis/left anterior
hemiblock with a first-degree AV block. With the extensive conduction system disease, impaired left
ventricular function, multiple regional wall motion abnormalities, and sustained ventricular
tachycardia, cardiac sarcoidosis would be at the top of the differential diagnosis. This was confirmed
by cardiac magnetic resonance imaging and positron emission tomography scan. Pulmonary
sarcoidosis was diagnosed by pulmonary function tests and a chest computed tomography.

Case 2.8 u 19
CASE
2.9
Mohammad-Ali Jazayeri, MD
Mohammad-Reza Jazayeri, MD

Patient History
Two cases form the basis for this scenario. The first case is from a 69-year-old female who presented
with bradycardia and two month history of exertional dyspnea. She denied any syncope or
presyncope. Figure 2.9.1 top is her 12-lead ECG at the time of presentation showing 2:1 AV block,
persistent PP alternans, PR interval of 200 ms, and complete right bundle branch block (RBBB). An
echocardiogram showed her left ventricle with mild asymmetric hypertrophy, normal systolic
function, and mild to moderate diastolic dysfunction. The second case is an 81-year-old gentleman
diagnosed with severe aortic stenosis who underwent a transcatheter aortic valve insertion (TAVI)
with a 29-mm Medtronic Corevalve system (MCS) without any complication except for a transient
Mobitz type I, second-degree AV block at the conclusion of the procedure. Figure 2.9.1 bottom is a
three-day postoperative telemetry tracing.

Figure 2.9.1 Second-degree AV block with 2:1 and 3:2 conduction. The top panel depicts sinus rhythm (SR) with 2:1 AV conduction and
right bundle branch block (RBBB). Of note, there is PP alternans with the intervals being shorter (760 ms) when a QRS complex is present
in between. The bottom panel is a rhythm strip (ECG leads II and V1) showing grouped beating of Wenckebach periodicity during SR
(arrows) at a cycle length of 800 ms. Lead II shows persistent left axis deviation. Note that during each group, the first P is conducted with
a PR interval of 360 ms and RBBB (#1, 3, 5). The second P wave is conducted with a longer PR interval of 560 ms and left BBB. The third P
is completely blocked.

20 u Section 2: Conduction Disturbances: Sinus Node Disease

 Question
What is the most appropriate action to be taken for these two patients?
1. Permanent pacemaker implantation (PPI) for both patients
2. Electrophysiologic study (EPS) in case 1 and PPI for case 2
3. EPS for both patients
4. None of the above

Discussion
Case 1 underwent EPS to determine the site of her AV block before committing her to PPI. Her
baseline rhythm was sinus with a cycle length (CL) of 905 ms and 1:1 AV conduction, AH interval of
97 ms, and HV interval of 70 ms. During rapid atrial pacing, 1:1 AV conduction was present at a CL
of 820 ms. with block commencing in the AV node at CL of 810 ms. The patient was then started on
procainamide infusion at 100 mg/min. After infusion of 350 mg of procainamide, her HV interval
progressively prolonged to 105 ms and she started to have 2:1 AV block below the HB recording site,
which progressed to third-degree AV block (Figure 2.9.2). Case 2 underwent PPI because there was a
progressive worsening of the His-Purkinje system (HPS) conduction over 7 days postoperatively and
he clearly demonstrated the ECG signs of “bilateral bundle branch block (BBBB).” Figure 2.9.3 shows
preoperative progression of the HPS conduction abnormality over a period of one month, which
resulted in complete RBBB with a left axis deviation.

Figure 2.9.2 Spontaneous and drug-induced advanced AV block. Panel A shows sinus rhythm with a cycle length of 760 ms and 1:1
AV conduction on the left (first five beats), which spontaneously converts to 2:1 AV block. Of note, the PR remains unchanged after the
conversion, which favors the His-Purkinje system (HPS) as being the site of block. Panel B is obtained during an electrophysiological study,
when the patient after being given intravenous procainamide developed third-degree AV block. This observation further confirms the HPS
involvement as the site of block in this patient. It should be mentioned that the paper speed is different in panels A and B.

Case 2.9 u 21
Figure 2.9.3 Preoperative and postoperative ECGs. The ECGs are arranged in a chronological order. Panels A to C are preoperative
ECGs showing gradual progression of the His-Purkinje system conduction disturbances from left axis deviation (LAD) in panel A to right
ventricular conduction delay in addition to LAD shown in panel B to right bundle branch block and left anterior fascicular block in panel
C, which occurred over a one-month period. Panel D is a 7-day postoperative ECG showing left bundle branch block with marked PR
prolongation of 402 ms.

Discussion
The critical issue presented in these cases is whether or not these two patients had advanced
conduction abnormalities in the HPS and, therefore, were susceptible to third-degree AV block.
A 2:1 AV block is a form of second-degree AV block and may be localized to the AV node or the
HPS. A normal PR interval of the conducted beats favors the HPS as being the site of block.
However, a prolonged PR interval would not be helpful in localizing the site of block. Coexistence of
2:1 AV block with BBB does not necessarily translate into the site of block being in the HPS as in
15%–20% of these patients the site of 2:1 block is the AV node.1 Exercise stress testing may
differentiate the site of block by worsening the degree of AV block when the HPS is the site or by
improving the AV conduction when the AV node is the culprit. Pharmacological stress testing of
the HPS with intravenous administration of a class IA antiarrhythmic agent during EPS is another
technique to identify a group of patients who maybe at risk of complete AV block and in need of
PPI.2,3 Of note, the PP alternans seen in Figure 2.9.1A is a phenomenon known as “ventriculophasic
sinus arrhythmia” occurring in patients with heart block, in which the PP intervals with a QRS
complex sandwiched in between is shorter than those with no QRS complex in between.4,5
BBBB is an old terminology, in which the occurrence of third-degree AV block maybe eminent.6
A large number (up to 80%) of complete AV block have been attributed to BBBB.7 Different degrees
of conduction delay in bundle branches may electrocardiographically manifest as “bifascicular
block” or “alternating bundle branch block.” The latter situation is an intriguing phenomenon, in

22 u Section 2: Conduction Disturbances: Sinus Node Disease

which properly timed 3:1 conduction in one BB with a shorter propagation time, and 3:2 conduction
in the contralateral BB with a longer propagation time would manifest as a grouped beating pattern
which mimics Wenckebach periodicity but in the HPS (Figure 2.9.1B). In the setting of an acute
insult to the conduction system such as acute myocardial infarction or iatrogenic injury during
surgical procedures and valve replacement/implantation, the conduction abnormalities may be
completely or partially reversible. On the contrary, however, during chronic and degenerative
disease processes, the conduction disturbances are usually permanent and progressive.
Over the past decade, TAVI has emerged as a valuable and effective strategy to replace the aortic
valve in elderly patients with severe aortic valve stenosis who are high-risk surgical candidates. This
technique, however, has been associated with high incidence of postoperative AV conduction
disturbances. Obviously, understanding the anatomy of the conduction system and its close
proximity to the aortic valve apparatus is essential for prevention of AV block or prediction of a
need for PPI. The bundle of His (BH) and its left bundle branch are located in the central fibrous
body, adjacent to the non-coronary cusp of the aortic valve. The AV node/BH junction and the
uppermost portion of the RBBB are also in the vicinity of this region. Currently, there are two
prototypical transcatheter aortic valves available in the market: the self-expanding MCS and
balloon-expandable Edwards SAPIEN valve (ESV). The reported incidence of new left BBB, third-
degree AV block, and PPI has been 29%–65%, 15%–44%, and 9%–49%, respectively for MCS and
6%–18%, 0%–27%, and 0%–27%, respectively for ESV.8 The higher incidence of conduction
disturbances has been attributed to a deeper insertion and perhaps further radial forces of
expansion exerted by the MCS stent cage to the neighboring conduction system, particularly the
LBB.9 Consequently, in the presence of preexisting RBBB, newly developed LBBB may ultimately
lead to third-degree AV block.

References
1. Barold SS, Hayes DL. Second-degree atrioventricular block: A reappraisal. Mayo Clin Proc. 2001;76(1):44–57.
2. Twidale N, Heddle WF, Tonkin AM. Procainamide administration during electrophysiology study-utility as a
provocative test for intermittent atrioventricular block. Pacing Clin. Electrophysiol. 1988;11:1388–397.
3. Englund A, Bergfeldt L, Rosenqvist M. Pharmacological stress testing of the His-Purkinje system in patients with
bifascicular block. Pacing Clin. Electrophysiol. 1998;21:1979–1987.
4. Rosenbaum MB, Lepeschkin E. The effect of ventricular systole on auricular rhythm in auriculoventricular block.
Circulation. 1955;11:240–261.
5. Schamroth L. Ventriculophasic atrial extrasystoles associated with complete artrioventricular block. Am. J. Cardiol.
1968;21:593–596.
6. Rosenbaum MB, Lepeschkin E. Bilateral bundle branch block. Am. Heart J. 1955;50:38–61.
7. Lopez JF. Electrocardiographic findings in patients with complete atrioventricular block. Br Heart J. 1968;30:20–28.
8. Nuis RJ, Van Mieghem NM, Schultz CJ, et al. Timing and potential mechanisms of new conduction abnormalities
during the implantation of the Medtronic CoreValve System in patients with aortic stenosis. Eur. Heart J.
2011;32:2067–2074.
9. Fraccaro C, Buja G, Tarantini G, et al. Incidence, predictors, and outcome of conduction disorders after
transcatheter self expandable aortic valve implantation. Am. J. Cardiol. 2011;107:747–754.

Case 2.9 u 23
CASE
2.10
Nishant Verma, MD, MPH
Bradley P. Knight, MD

Patient History
A two-lead rhythm strip was recorded in an elderly male admitted to the hospital for acute
abdominal pain (Figure 2.10.1). You are consulted for bradycardia. What is the mechanism of
the transient bradycardia and resolution of the intraventricular conduction delay?

Figure 2.10.1 Lead rhythm strip showing transient bradycardia and QRS narrowing.

Discussion
The rhythm strip shows sinus rhythm at a rate of approximately 90 bpm and a bundle branch block
(BBB), followed by seven beats of bradycardia at a rate that is about half the initial rate and is
associated with transient resolution of the BBB. At first glance, it appears that the patient has sinus
node disease. However, there are a series of premature atrial contractions (PACs) denoted by the
arrows. The first one conducts with an IVCD; thereafter, they occur in a bigeminal pattern with AV
block. Note that the fifth QRS complex is preceded by a PAC that deforms the T-wave. The sixth
QRS complex is followed by a PAC that blocks in the AV node and sets up a bigeminal pattern of
blocked PACs resulting in ventricular bradycardia. The bradycardia is associated with transient
resolution of the BBB. Clues that the bradycardia is caused by atrial bigeminy with blocked PACs
rather than sudden sinus node dysfunction are the subtle presence of the blocked PACs as well as
the PAC that conducts before the fifth QRS complex.

24 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
2.11
Gilles Lascault, MD
Olivier Piot, MD

Patient History
A 48-year-old female patient was hospitalized in a state of emergency for recurrent presyncopal
episodes during the last 24 hours. The history of the patient revealed nothing except she had
complained for several weeks of scapular and spinal unexplained pain relieved by anti-
inflammatory drugs. She had no fever, no tick bites, no cutaneous eruption (such as erythema
migrans rash). She did not walk in the woods and forests. At admission clinical examination,
echocardiogram and standard blood tests were normal (including c-reactive protein). Cardiac
magnetic resonance imaging and positron emission tomography scan showed no cardiac
abnormalities.
The ECG (Figure 2.11.1) at admission showed high degree block. The basal PR interval is
increased and the blocked P wave is preceded by a progressive increase in PR interval (type I block).
There is a complete right bundle branch block (QRS duration around 140 ms) with a normal QRS
axis. An electrophysiology study was done and confirmed an atrioventricular (AV) nodal block and
a normal HV interval (40 ms). During hospitalization heart rhythm was continuously monitored.
After 4 days, atrio-ventricular and intra-ventricular AV conduction disturbances had progressively
vanished along with the symptoms (Figure 2.11.2). No pacemaker implantation was indicated. Blood
tests were eventually positive for recent infection by Borrelia burgdorferi (IgM positive), confirming
the diagnosis of Lyme disease. An appropriate antibiotic treatment was then started.

Figure 2.11.1 AVB Lyme 1.

Case 2.11 u 25
Figure 2.11.2 AVB Lyme 2.

Discussion
Acute AV block can occur during adulthood and has various causes. Among the different causes,
Lyme disease must be systematically suspected and blood tests performed. This diagnosis is
important since the conduction disturbances are reversible after days or weeks. It may be difficult,
as in the present patient, to suspect Lyme disease.

Question
Before atrioventricular conduction disturbances, when is it appropriate to suspect Lyme disease?

Answer
In the presence of atrioventricular block (first-, second-, or third-degree), it is important to carefully
analyze the history of the patient. It is easy to suspect Lyme disease when the patient is at risk of
exposure to infected ticks, or has had a tick bite followed by erythema migrans rash and secondarily
by cardiac, musculo-skeletal or neurological manifestations. This sequence may not be present.
Lyme disease has to be suspected when there is no evidence of (many) other causes of AV block.
Lyme disease must be considered before the sudden appearance of AV conduction disturbances of
unknown origin in a young and previously healthy patient. The final diagnosis relies on a positive
Lyme antibody test.

Reference
1. Krause PJ, Bockenstedt LK. Lyme disease and the Heart. Circulation. 2013;127:e451–e454.

26 u Section 2: Conduction Disturbances: Sinus Node Disease

 CASE
Fred Morady, MD 2.12
Patient History
This ECG (Figure 2.12.1) was recorded during preoperative evaluation of a 53-year-old female
scheduled to undergo shoulder surgery. She had a septal myocardial infarction 2 years earlier.

Figure 2.12.1

Question
What is the explanation for variability in the PR intervals and QRS complexes?

Explanation
There are two different PR intervals (200 and 360 ms) that alternate. The QRS complexes also
alternate, with a right bundle branch block configuration always associated with the longer of the
two PR intervals. The most plausible explanation for the varying PR intervals is that there are dual
atrioventricular nodal pathways, with atrioventricular conduction occurring on an alternating basis
through the fast and slow pathways. Because of the longer AH interval when there is conduction
through the slow pathway, the HH interval preceding the QRS complex that occurs at the end of the
longer PR interval is also longer. This results in phase 4 block in the right bundle. Phase 4 block is a
pathologic, not a physiologic phenomenon. It probably occurred in this patient because of the prior
septal infarction, with some degree of involvement of the right bundle.

Case 2.12 u 27
CASE
2.13 Fred Morady, MD

Patient History
This electrocardiogram (Figure 2.13.1) was recorded in a 76-year-old male who was hospitalized for
treatment of prostate cancer.

Question
What is the mechanism of the atrioventricular (AV) block?

Figure 2.13.1

Explanation
There is sinus rhythm at 75 bpm, initially with 1:1 AV conduction and a left bundle branch block.
A premature atrial complex (PAC) that is not conducted to the ventricles occurs and is followed by
2:1 AV block. The 2:1 AV block is caused by functional infranodal block. The PAC was blocked in
the AV node, which created a “long–short” sequence in the bundle of His (see ladder diagram,
Figure 2.13.2). The long diastolic interval resulted in prolongation of refractoriness in the His
bundle, which lead to infranodal AV block with the next sinus beat. The ongoing 2:1 AV block is
caused by perpetuation of the “long–short” sequence in the His bundle, as depicted in Figure 2.13.2.
Note that the QRS complexes become narrow during the 2:1 AV block. This indicates that the left

28 u Section 2: Conduction Disturbances: Sinus Node Disease

bundle branch block was caused by phase 3 block in the left bundle that resolved with the
bradycardia.
This type of block can occur when the refractory period of the His bundle is mildly longer than
that of the AV node and is not necessarily an indication for pacemaker implantation in an individual
who is asymptomatic.

Figure 2.13.2

Case 2.13 u 29
CASE
2.14 Fred Morady, MD

Question
What is the most likely mechanism of the atrioventricular (AV) block on this 6-lead
electrocardiogram (Figure 2.14.1)?

Figure 2.14.1

Explanation
The first two complexes the ECG are sinus rhythm with a normal PR interval and with a narrow
QRS complex. There is an atrial premature depolarization that is followed by complete AV block
during the remaining portion of the recording. This is a typical example of paroxysmal AV block.
Paroxysmal AV block is third-degree AV block that occurs suddenly and unexpectedly following
a period of normal AV conduction. The AV block is often initiated by a premature atrial or
ventricular depolarization and usually resumes only after an escape beat.
In this ECG, there are two sinus beats followed by a conducted premature atrial depolarization.
The premature atrial depolarization results in lengthening of the subsequent PP interval by
approximately 200 ms. In patients susceptible to paroxysmal AV block, lengthening of the PP
interval allows hypopolarization due to spontaneous diastolic depolarization in the His-Purkinje

30 u Section 2: Conduction Disturbances: Sinus Node Disease

system, causing phase 4 block. Although not shown on this ECG, the patient eventually had an
escape beat which resulted in resumption of 1:1 AV conduction. The escape beat depolarizes the
His-Purkinje system and “resets” normal AV conduction.
It is noteworthy that the sinus cycle length during the AV block is not longer than when there
was AV conduction. This rules out vagally-mediated AV block.

Reference
1. Rosenbaum MB, Elizari MV, Levi RJ, et al. Paroxysmal atrioventricular block and spontaneous diastolic
depolarization. Chest. 1973;63:678–688.

Case 2.14 u 31
CASE
2.15 Yuji Nakazato, MD, PhD

Patient History
This 34-year-old female arrived to the hospital with palpitations. She had a history of atrial septal
defect closure at 12 years old and myocarditis at 30 years old. A Holter ECG was recorded for the
evaluation of arrhythmias.

Question
How can you explain the findings (arrow and star) on Figure 2.15.2?

Figure 2.15.1

32 u Section 2: Conduction Disturbances: Sinus Node Disease

Figure 2.15.2

Case 2.15 u 33
Figure 2.15.3

34 u Section 2: Conduction Disturbances: Sinus Node Disease

Figure 2.15.4

Discussion
In Figure 2.15.1, Mobitz type II atrioventricular (AV) block is observed on the Holter ECG. The
rhythm strip of leads V1 and V2 are demonstrated in Figure 2.15.2. As the arrow indicated in the
upper panel, premature atrial contraction (PAC) without ventricular conduction followed by
junctional escape is clearly observed. In the lower panel, the arrow indicates His extrasystole just
preceding QRS (same as sinus rhythm which) conducted to the ventricle faster than atrium. For
reference, standard 12 leads ECG are presented in Figure 2.15.3. According to this behavior,
extrasystole of His bundle was strongly suspected. Confirmation of the diagnosis was made by a
recording of His bundle electrogram (Figure 2.15.4). The electrogram of His extrasystole
(He: arrow) and following retrograde conduction to the atrium are clearly demonstrated.
Nonconducted PAC with a long coupling interval is often mistaken as true AV block. Therefore,
this phenomenon is called pseudo AV block. If AV block-like findings were shown on a surface ECG,
extrasystole of the His bundle should not be forgotten.

Reference
1. Damato AN, Lau SH, Bobb G. Cardiac arrhythmia simulated by concealed bundle of His extrasystole in the dog. Cir
Res. 1971;28:316.

Case 2.15 u 35
CASE
2.16 Philip Podrid, MD

Patient History
A 58-year-old male presents with a history of substernal chest pressure radiating to his arms
and jaw. It is associated with shortness of breath. Upon presentation to the emergency
department an electrocardiogram is obtained.

Questions
1. What is the underlying abnormality of the QRS complexes?
2. What accounts for the long RR intervals?

Figure 2.16.1

Diagnosis
Acute inferior wall ST segment elevation myocardial infarction (STEMI), second-degree AV block
(Mobitz type II), sinus node exit block.

36 u Section 2: Conduction Disturbances: Sinus Node Disease

Discussion
The rhythm is irregular as a result of short RR intervals which are the same and long RR intervals
(↔,┌┐) which are the same. The rhythm is regularly irregular. The short RR intervals have a rate of
90 bpm. The QRS complex duration is normal (0.08 seconds) and there is a normal morphology and
axis between 0° and +90° (positive QRS complex in leads I and aVF). There is a tall R wave in lead V2
(←) which is termed early transition or counterclockwise rotation. This is due to a shift of the
electrical axis in the horizontal plan. This is established by imagining the heart as if viewed from
under the diaphragm. With counterclockwise rotation the left ventricular forces are shifted
anteriorly and become prominent in the anterior precordial leads, especially V2. The QT/QTc
intervals are normal (360/440 ms). There is J point and ST segment elevation seen in leads II, III,
and aVF (↓) consistent with an acute inferior wall STEMI. There are Q waves in these leads,
indicating that there is already infarcted tissue. There is ST segment depression in leads I and aVL
(↑) which represent reciprocal changes associated with the STEMI. There is also ST segment
depression in leads V2–V3 (^) which suggests posterior wall involvement with the inferior wall
infarction, although these might also be reciprocal changes. There is a P wave before each QRS
complex (+) with a stable PR interval (0.28 seconds). The P waves are positive in leads I, II, aVF, and
V4 –V6. Following QRS complexes 6–8 there are P waves (*) that are not conducted, accounting for
the long RR intervals (┌┐). The PP intervals are constant (└┘) with a rate of 90 bpm. There is an
underlying normal sinus rhythm. The presence of an occasional non conducted P wave defines a
second-degree AV block. The second-degree AV block presents with a pattern of 2:1 AV conduction
or block. This may be either a Mobitz type I or II. Since all the PR intervals are the same when there
are several sequential P waves that are conducted, this represents Mobitz type II. There first two
long RR intervals (↔) are not the result of a non conducted P wave as there is no P wave seen during
these long intervals. Therefore this is not second-degree AV block, Mobitz type II but rather is a
sinus node pause. As the PP interval around the pause is equal to two sinus intervals (└┘) this is a
sinus node exit block.

Case 2.16 u 37
CASE
2.17 Vassil Traykov, MD

Patient History
A 75-year-old hypertensive male with no significant structural heart disease reported recurrent
syncope without prodromal symptoms.
During one of the episodes the patient suffered a mild facial trauma due to syncope. His medical
treatment included angiotensin receptor blocker, diuretic, and a beta-blocker. The patient was
referred to a general cardiologist who recorded the ECG shown on Figure 2.17.1. This recording
shows right bundle branch block (RBBB) and left anterior fascicular block (LAFB) alternating with
RBBB and left posterior fascicular block. PR interval is borderline at 200 ms, slightly longer with
RBBB LAFB configuration. Beta-blocker therapy was discontinued and the patient was sent for
pacemaker implantation. When the patient was admitted to the clinic for the procedure, the
conduction disturbance had progressed with a block in the left anterior fascicle resulting in 2:1
atrioventricular block shown on Figure 2.17.2. Red arrows denote the P waves and blue lines show
blocked P waves.

Figure 2.17.1

38 u Section 2: Conduction Disturbances: Sinus Node Disease

Figure 2.17.2

Case 2.17 u 39
 SECTION 3
Miscellaneous Phenomena: Concealed Conduction,
Superabnormalities, Aberrancy Conduction, Premature Atrial and
Ventricular Contractions (PACs and PVCs)

CASE
David J. Callans, MD 3.1
Patient History
A 67-year-old male with no structural heart disease, complained of palpitations caused by
premature ventricular complexes.

Figure 3.1.1

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World © 2017 Mohammad Shenasa, Mark E. Josephson,
N. A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-08-8. 41
Discussion
In the electrophysiology (EP) lab, activation mapping from the anterior intraventricular vein (AIV)
was slightly earlier than the endocardium just anterior to the aorta (−20 vs. −13 ms from QRS
onset). Pacemapping from the AIV had a qS morphology in lead I, consistent with epicardial
stimulation; pacemapping from the LV endocardium had a dominant R wave in lead I. Neither site
matched the premature ventricular contraction (PVC) morphology (rS) in lead I, as the PVC seemed
to be “in between” the pacemaps. In fact, endocardial ablation resulted in late disappearance of the
PVCs, followed by a reduction in frequency but not elimination. Afterwards, ablation from the AIV
resulted in elimination of the PVCs suggesting a site of origin “in between” the two sites.

42 u Section 3: Miscellaneous Phenomena: Concealed Conduction

 CASE
Mohammad Dalili, MD 3.2

Figure 3.2.1

Nonconducted atrial premature contraction (APC; red arrows). Note the pause that is less than
compensatory.

Comments
The APC has to get into the sinus node; it resets the node and then the sinus node fires and
activates the atrium. The time it takes for the next P wave to appear allows for a junctional escape
(yellow arrows)—note the shorter PR interval after the pause.

Case 3.2 u 43
CASE
3.3
Arnaud Denis, MD
Pierre Jaïs, MD, PhD

Patient History
A 63-year-old female was referred to our institution for dyspnea (NYHA II) without any other
symptom. Transthoracic echocardiography revealed a moderately reduced left ventricular ejection
fraction (40%).
Figure 3.3.1 – Figure 3.3.4 are presented with Lewis diagrams (abbreviations—A: atrium, AVN:
atrioventricular node, HPS: His-Purkinje system, and V: ventricle).

Figure 3.3.1

44 u Section 3: Miscellaneous Phenomena: Concealed Conduction

 Heart rate is 75 bpm with narrow QRS complexes. There is no P wave just before the QRS.
A sinus P wave (positive in leads I, II, III, aVF and negative in leads V1 and aVR, solid arrow) is
present just after each QRS and is fused with the ST segment and the beginning of the T wave.
Two hypotheses can be offered:
1. The P wave is conducted to the ventricle with a PR interval of 600 ms through a slow pathway. In
this hypothesis, the fast pathway is blocked antegrade because of a concealed retrograde
conduction coming from the previous beat.
2. Isorhythmic dissociation may be present; that is, a junctional rhythm that is a little bit faster
than the sinus rate. In that case, there is no relationship between the sinus P wave and QRS.

Figure 3.3.2

Sinus rhythm is stable at 75 bpm. The ventricular rhythm is irregular, and there are more QRS
complexes than P waves.
1. The first P wave is conducted to the ventricle with a normal PR interval (160 ms), the second with
a PR interval of 340 ms, and the third one with PR interval of 180 ms. The variation of the PR
interval can be explain by dual AV nodal physiology properties or concealed junctional ectopies.

Case 3.3 u 45
2. Same sequences described in Figure 3.3.1. The coexistence of P wave conducted to the ventricle
with normal, prolonged or very prolonged PR interval support the hypothesis of dual AV nodal
physiology. Two narrow QRS complexes (with the same morphology as the normal sinus QRS)
are apparently not preceded by P waves (solid arrow). These QRS complexes can be explained by
dual AV nodal physiology properties (double ventricular response due to a single atrial
depolarization through both AV nodal pathways) or junctional ectopy conducted to the ventricle
but not to the atrium. All of these ECG patterns cannot be explained by junctional ectopies,
especially when the P wave is conducted to the ventricle with a very prolonged PR interval.
All ECG patterns are explained by the presence of dual AV nodal pathways capable of
conduction through the fast pathway, the slow pathway or both at the same time. There is always a
concealed retrograde conduction that explains the variation of the PR interval and the self-
perpetuation of the mechanism.

Figure 3.3.3

46 u Section 3: Miscellaneous Phenomena: Concealed Conduction

1. The first P wave is conducted to the ventricle through the slow pathway with a very prolonged PR
interval. Then, the second P wave blocks in the AV node. The third P wave is conducted only
through the fast pathway, resulting in a normal PR interval.
2. Double ventricular response to a single P wave occurs through both fast and slow pathways. The
second QRS complex that is conducted through the slow pathway is conducted to the ventricle
with a complete right bundle branch block (RBBB) and left anterior fascicular aberrancy. This is
followed by an atrial ectopy (dotted arrow) that conducts to the ventricle through the fast
pathway.
3. Double ventricular response occurs as described in step 2. The following sinus P wave (solid
arrow) is fused with the previous T wave and is conducted through the fast pathway with an
RBBB and through the slow pathway without ventricular aberrancy.
4. The following P wave is conducted to the ventricle through the slow pathway as described in
Figure 3.3.1. Indeed, the fast pathway is blocked anterogradely by the concealed retrograde
conduction through the fast pathway, which is coming from the previous beat.

Figure 3.3.4

Case 3.3 u 47
This is the ECG immediately after a slow pathway ablation, which shows sinus P-wave conduction
through only the fast pathway (with a normal PR).
All ECG patterns are explained by the presence of dual AV nodal pathways. P-waves can be
conducted to the ventricle either through the fast pathway, the slow pathway (which is very slow), or
both pathways at the same time. The patient’s symptoms can be explained by a pseudo pacemaker
syndrome that was due to the loss of AV synchrony. A slow pathway ablation was performed with an
endpoint of complete slow pathway elimination. Patient was asymptomatic after ablation and her
left ventricular ejection fraction was normalized 2 months after the ablation, supported the
hypothesis of rhythmic cardiomyopathy.

48 u Section 3: Miscellaneous Phenomena: Concealed Conduction

 CASE
3.4
Arnaud Denis, MD
Frédéric Sacher, MD, PhD

Patient History
A 55-year-old male without medical history presented with recurrent episodes of palpitation.
Twelve-lead ECGs during palpitations are presented below.

Question
What is the mechanism (1) of the palpitation, (2) of the blocked P wave, and (3) of the wide QRS?
Does the patient need an antiarrhythmic drug and/or a pacemaker implantation?
ECGs are presented with Lewis diagrams (abbreviations: A: atrium, AVN: atrio-ventricular
node, HPS: His-Purkinje system, and V: ventricle).

Figure 3.4.1

Case 3.4 u 49