Ebook The ESC textbook of cardiovascular medicine: Part 1

The ESC Textbook of

Cardiovascular
Medicine

A JOHN CAMM
THOMAS F. LÜSCHER
PATRICK W. SERRUYS
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List of Contributors

Editors:
A John Camm MD FESC FRCP
FACC FAHA FCGC
Professor of Clinical Cardiology,
Chairman of the Division of Cardiac and
Vascular Sciences, St George’s
University of London, London, UK
Thomas F Lüscher MD FRCP
Professor and Head of Cardiology,
University Hospital, Zurich, Switzerland
Patrick W Serruys MD PhD FESC
FACC
Professor of Medicine and Interventional
Cardiology, Head of the Department of
Interventional Cardiology, Thoraxcenter,
Erasmus Medical Centre, Rotterdam,
The Netherlands

Bert Andersson MD PhD
Department of Cardiology, Sahlgrenska
University Hospital, Gothenburg, Sweden
Annalisa Angelini MD
Department of Cardiovascular Pathology,
Universita di Padova, Via A. Gabelli 61,
Padova, Italy
Stefan Anker MD PhD
Clinical Research Fellow, Department of
Cardiac Medicine, National Heart and Lung
Institute, London, UK
Velislav N Batchvarov MD
Department of Cardiac and Vascular
Sciences, St George’s Medical School,
London, UK
Iris Baumgartner MD
Swiss Cardiovascular Center, Division of
Angiology, University Hospital, 3010-Bern,
Switzerland

Authors:
Stephan Achenbach MD FESC
Department of Internal Medicine, University
of Erlangen, Erlangen, Germany

Antoni Bayés de Luna MD
Director of Cardiology Department,
Hospital Santa Creu i Sant Pau, Barcelona,
Spain

Etienne Aliot MD FESC FACC
Department of Cardiology, University of
Nancy, Vandoeuvre-les-Nancy, France

Giancarlo Biamino MD
Department of Clinical and Interventional
Angiology, Heartcenter Leipzig, Leipzig,
Germany

Maurits A Allessie MD PhD
Physiology Department, Maastricht
University, Cardiovascular Research
Institute Maastricht, Maastricht, The
Netherlands

Jean-Jacques Blanc MD FESC
Département de Cardiologie, Hôpital de la
Cavale Blanche, Brest, France
Carina Blomström-Lundqvist MD PhD
FESC FACC

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Department of Cardiology, University
Hospital in Uppsala, Uppsala, Sweden
Giacomo G Boccuzzi MD
Unità di Cardiologia Invasiva, Ospedale San
Giovanni Bosco, Torino, Italy
Eric Boersma MSc PhD FESC

Associate Professor of Clinical
Cardiovascular Epidemiology, Department
of Cardiology, Erasmus Medical Center,
Rotterdam, The Netherlands

Pathophysiology, Imperial College of
Science, Technology and Medicine,
Hammersmith Hospital, London, UK
Alessandro Capucci MD
Centro Studi, Associazione Cardiologi
Ospedalieri, FIRE Study Investigators,
Firenze, Italy
Raffaele De Caterina MD PhD
Director of University Cardiology Division,
Università degli Studi di Chieti G
D’Annunzio, Chieti, Italy

Henri Bounameaux MD
Professor of Medicine and Director of
Division of Angiology and Homeostasis,
University Hospital of Geneva, Geneva,
Switzerland

Christian de Chillou MD PhD
Department of Cardiology, University of
Nancy, Hopital de Brabois, Vandoeuvre-lesNancy, France

Günter Breithardt MD FESC FACC
Professor of Medicine, Department of
Cardiology and Angiology, University of

Münster, Münster, Germany

Francesco Cosentino MD PhD
Division of Cardiology, 2nd Faculty of
Medicine, La Sapienza University, Ospedale
Sant’ Andrea, Rome, Italy

Michele Brignole MD FESC
Chief of Department of Cardiology,
Department of Cardiology, Ospedali de
Tigullion, Lavagna, Italy,

Filippo Crea MD PhD FESC FACC
Professor of Cardiology, Director, Institute
of Cardiology, Catholic University of the
Sacred Heart, Rome, Italy

Pedro Brugada MD PhD
Cardiovascular Center, Onze Lieve Vrouw
Hospital, Aalst, Belgium

Harry JGM Crijns MD PhD FESC
Department of Cardiology, University
Hospital Maastricht, Maastricht, The
Netherlands

Dirk Brutsaert MD
Laboratory of Physiology, University of
Antwerp, Antwerp, Belgium
Harry R Büller MD PhD

Professor and Chair, Department of
Vascular Medicine, University of
Amsterdam, Amsterdam, The Netherlands

Jean Dallongeville MD PhD
Head of Laboratory, Arteriosclerosis
Department, Pasteur Institute, Lille, France
Werner G Daniel MD FESC FACC
Professor of Internal Medicine, Medical
Clinic II/Cardiology, University Clinic
Erlangen, Erlangen, Germany

José A Cabrera MD PhD
Director of Arrhythmia Unit, Department of
Cardiology, Fundacion Jimenez Diaz,
Madrid, Spain

John E Deanfield MD FRCP
Professor of Cardiology, Great Ormond
Street Hospital, London, UK

Paolo G Camici MD FESC FACC FAHA
FRCP
Professor of Cardiovascular

Maria Cristina Digilio MD
Chief of Dysmorphology, Medical Genetics,
Bambino Gesu Hospital, Rome, Italy

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Robert Dion MD PhD
Professor and Head of Department of
Cardiothoracic Surgery, Leiden University
Medical Centre, Leiden,
The Netherlands
Lars Eckardt MD
Klinik und Poliklinik C,
Universitätsklinikum
(Kardiologie/Angiologie), Münster,
Germany
Raimund Erbel MD
Professor of Cardiology, Department of
Cardiology, West German Heart Centre,
University Duisburg-Essen
Robert Fagard MD PhD
Professor of Medicine, Hypertension
Department, University of Leuven, Leuven,
Belgium
Erling Falk MD PhD
Professor of Cardiovascular Pathology,
Department of Cardiology, University of
Aarhus, Aarhus, Denmark
Jerónimo Farré MD PhD FESC
Professor and Chair, Department of
Cardiology, Fundacion Jimenez Diaz,
Madrid, Spain
Pim J de Feyter MD PhD
Cardiologist, Erasmus Medical Centre,

Rotterdam, The Netherlands
Frank A Flachskampf MD FESC FACC
Professor of Internal Medicine, Medical
Clinic II/Cardiology, University Clinic
Erlangen, Erlangen, Germany
Keith AA Fox MD FRCP FESC
Professor of Cardiology and Head of
Medical and Radiological Sciences,
Department of Cardiological Research,
University of Edinburgh, Edinburgh, UK
Kim Fox MD FRCP FESC
Professor of Clinical Cardiology,

Department of Cardiology, Royal Brompton
Hospital, London, UK
Pietro Francia MD
Division of Cardiology, 2nd Faculty of
Medicine, University La Sapienza, Ospedale
Sant’ Andrea, Rome, Italy
Nazzareno Galiè MD
Institute of Cardiology, University of
Bologna, Bologna, Italy
Roy Gardner MD
Department of Cardiology, Western
Infirmary, Glasgow, UK
Stephan Gielen MD
Senior Resident, Department of Cardiology,
University of Leipzig, Leipzig, Germany
Christianne JM de Groot MD PhD
Gynaecologist/Obstetrician, Department of

Obstetrics and Gynaecology, Erasmus
Medical Centre, Rotterdam, The
Netherlands
Rainer Hambrecht MD
Department of Cardiology, University of
Leipzig, Heart
Centre, Leipzig, Germany
Christian W Hamm MD
Professor of Medicine and Medical Director,
Abt. Für Kardiologie, Kerckhoff Clinic &
Max-Planck-Institute, Bad Nauheim,
Germany
Liv Hatle MD
Norwegian University of Technology and
Science, Trondheim, Norway
Axel Haverich MD
Hannover School of Medicine, Department
of Cardiology, Hannover, Germany
Christopher Heeschen MD
Professor for Oncology and Transplantation
Medicine, Experimental Surgery,
Department of Surgery, LudwigMaximilians-University, Munich, Germany

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Otto M Hess MD
Department of Cardiology,
Universitätsklinik Inselspital, Bern,
Switzerland

Aroon Hingorani MA PhD FRCP
Senior Fellow and Reader in Clinical
Pharmacology, Centre for Clinical
Pharmacology, Department of Medicine,
University College London, London, UK

Michel Komajda MD FESC
Département de Cardiologie, Pitié
Salpêtrière Hospital, Paris, France
Paul Kotwinski MD
Medical Genetics, Bambino Gesu Hospital,
Rome, Italy
Gaetano A Lanza MD FESC
Università Cattolica di Roma, Istituto di
Cardiologia, Rome, Italy

Vibeke E Hjortdal MD DMSc PhD
Professor of Congenital Heart Surgery,
Department of Thoracic and Cardiovascular
Surgery, University Hospital of Aarhus,
Aarhus, Denmark

Christophe Leclercq MD PhD
Department de Cardiologie, Centre Cardiopneumologique, Centre Hospitalier
Universitaire Pontchaillou, Rennes, France

Stefan H Hohnloser MD
Professor of Medicine, Department of
Cardiology, JW Goethe University,
Frankfurt, Germany

Cecilia Linde MD PhD FESC
Head of Cardiology, Department of
Cardiology, Karolinska Hospital,
Stockholm, Sweden

Stephen Humphries MD
Cardiovascular Genetics, British Heart
Foundation Laboratories, Royal Free and
University College Medical School, London,
UK

Gregory YH Lip MD FRCP DFM FACC
FESC
Professor of Cardiovascular Medicine and
Director of Haemostasis Thrombosis and
Vascular Biology Unit, University
Department of Medicine, City Hospital,
Birmingham, UK

Bernard Iung MD
Professor of Cardiology, Cardiology
Department, Bichat Hospital, Paris, France
Pierre Jaïs MD
Service du Professeur Clémenty, Hôpital du
Haut Levêque, Bordeaux, France

Raymond MacAllister MA MD FRCP
Reader in Clinical Pharmacology, Centre for
Clinical Pharmacology, Department of

Medicine, University College London,
London, UK

Lukas Kappenberger MD
Médecin Chef, Division de Cardiologie,
Centre Hospitalier Universitaire Vaudois
Lausanne, Lausanne, Switzerland

Felix Mahler MD
Professor of Angiology, Cardiovascular
Department, University Hospital Bern, Bern,
Switzerland

Philipp A Kaufmann MD
Nuclear Medicine and Cardiology,
University Hospital Zürich, Zurich,
Switzerland

Bernhard Maisch MD FESC FACC
Professor and Director of Internal Medicine
and Cardiology, Phillips University,
Marburg, Germany

Sverre E Kjeldsen MD PhD FAHA
Chief Physician and Professor, Department
of Cardiology, Ullevaal University Hospital,
Oslo, Norway

Marek Malik PhD MD DSc DScMed
FACC FESC

Department of Cardiac and Vascular

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Sciences, St George’s Hospital Medical
School, London, UK
Guiseppe Mancia MD PhD
Professor of Dipartimento di Medicina,
Universita Milano-Bicocca in Ospedale San
Gerardo Monza, Monza, Italy
Bruno Marino MD
Professor of Pediatrics and Chief of
Pediatric Oncology, Department of
Pediatrics, University La Sapienza, Rome,
Italy
Carlo Di Mario MD
Consultant Cardiologist, Catheterization
Laboratory, Royal Brompton Hospital,
London, UK
William McKenna MD FACC FESC
Department of Cardiology, The Heart
Hospital, London, UK
John McMurray BSc (Hons) MBChB
(Hons) MD FRCP FESC FACC
Professor of Medical Cardiology,
Department of Cardiology, Western
Infirmary, Glasgow, UK
Raad H Mohiaddin MD PhD FRCR
FRCP FESC

Consultant and Reader in Cardiovascular
Imaging Royal Brompton Hospita and
Imperial College London

S Bertil Olsson MD PhD FESC FAHA
MRPhS
Professor, Department of Cardiology,
University Hospital Lund, Lund, Sweden
Dudley J Pennell MD FRCP FACC FESC
Director of Cardiovascular Magnetic
Resonance Unit, Royal Brompton Hospital,
London, UK
John Pepper MA MChir FRCS
Professor of Cardiothoracic Surgery,
Cardiac Department, Royal Brompton
Hospital, London, UK
Joep Perk MD FESC
Consultant, Department of Internal
Medicine, Public Health Department,
Oskarshamn, Sweden
Luc Pierard MD PhD FESC FACC
Professor of Medicine and Head of
Department of Cardiology, Service de
Cardiologie, University Hospital SartTilman, Université de Liège, Liège, Belgium
Patrizia Presbitero MD
Chief of Interventional Cardiology
Department, Istituto Clinico Humanitas,
Rozzano, Italy
Silvia G Priori MD PhD
Associate Professor of Cardiology,

University of Pavia, Pavia, Italy

John Morgan MA MD FRCP
Consultant Cardiologist, Wessex
Cardiothoracic Centre, Southampton
University Hospital, Southampton, UK

Henry Purcell MB PhD
Senior Fellow in Cardiology, Department of
Cardiology, Royal Brompton Hospital,
London, UK

Carlo Napolitano MD PhD
Senior Research Associate, Molecular
Cardiology, Fondazione Salvatore Maugeri,
Pavia, Italy

Henrik M Reims MD
Department of Cardiology, Ullevaal
University Hospital, Oslo, Norway

Christoph A Nienaber MD
Head of Department of Cardiology and
Vascular Medicine, Universitats Klinikum
Rostock, Rostock, Germany

Arsen D Ristic MD FESC
Department of Cardiology, Belgrade
University Medical School and Institute for
Cardiovascular Diseases of the Clinical

Center of Serbia, Belgrade, Serbia and
Montenegro

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Jos Roelandt MD PhD FESC FACC
FAHA
Professor of Cardiology, Department of
Cardiology, Erasmus Medical Center,
Rotterdam, The Netherlands
Marco Roffi MD
Head of Cardiology, University Hospital
Zürich, Zürich, Switzerland
Jolien W Roos-Hesselink PhD MD
Cardiologist, Department of Cardiology,
Erasmus Medical Centre, Rotterdam, The
Netherlands
Annika Rosengren MD
Deparment of Medicine, Sahlgrenska
University ospital/Ostra, Goteborg, Sweden
Lars Ryden MD FRCP DESC FACC
Professor of Cardiology, Department of
Cardiology, Karolinska Hospital,
Stockholm, Sweden
Hugo Saner MD
Head of Cardiovascuar Prevention and
Rehabilitation Inselspital, Swiss
Cardiovascular Center Bern, Bern,
Switzerland

Heinz-Peter Schultheiss MD
Professor and Director Cardiology and
Pulmonology, University Hospital Benjamin
Franklin, Berlin, Germany
Peter J Schwartz MD
Professor of Department of Cardiology,
Policlinico S. Metteo IRCCS, Pavia, Italy
Udo P Sechtem MD
Professor and Head, Department of
Cardiology, Robert Bosch Medical Centre,
Stuttgart, Germany
Co-chairman of Cardiology, Department of
Cardiology,
University Hospital Bern, Bern, Switzerland
Mary N Sheppard MD FRCPath
Department of Histopathology, Royal
Brompton Hospital, London, UK
Gerald Simonneau MD
Service de Pneumologie, Hôpital Antoine
Béclère, Clamart, France
Jordi Soler-Soler MD FESC FACC
Professor of Cardiology, Department of
Cardiology, University Hospital, Barcelona,
Spain

Irina Savelieva MD
Division of Cardiac and Vascular Sciences,
St George’s Hospital Medical School,
London, UK

Richard Sutton DScMed FRCP FESC
Consultant Cardiologist, Royal Brompton
Hospital, London, UK

Dierk Scheinert MD
Department of Clinical and Interventional
Angiology, Heartcenter Leipzig, Leipzig,
Germany

Karl Swedberg MD PhD
Professor of Medicine, Department of
Medicine, Sahlgrenska University
Hospital/Östra, Gothenburg, Sweden

Sebastian M Schellong MD
Head of Division of Angiology, Division of
Vascular Medicine, University Hospital Carl
Gustav Carus, Dresden, Germany

William D Toff BSc MD MRCP
Senior Lecturer in Cardiology, University of
Leicester, Leicester, UK

Andrej Schmidt MD
Department of Clinical and Interventional
Angiology, Heartcenter Leipzig, Leipzig,
Germany

Marko Turina MD

Professor of Surgery, University Hospital,
Zurich, Switzerland
S Richard Underwood MD FRCP FRCR
FESC FACC

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Professor of Cardiac Imaging, National
Heart and Lung Institute, Imperial College,
Royal Brompton Hospital, London, UK
Alec Vahanian MD
Head of Department, Cardiology
Department, Hôpital Bichat, Paris, France
Patrick Vallance PhD FRCP
Professor, Centre for Clinical
Pharmacology, The Rayne Institute,
London, UK
Hein JJ Wellens MD PhD FESC FACC
Interuniversity Institute of Cardiology,
Maastricht, The Netherlands
Frans Van de Werf MD PhD FESC
FACC FAHA
Professor and Head of Department of
Cardiology, Gasthuisberg University
Hospital, Leuven, Belgium
William Wijns MD PhD
Cardiovascular Centre, Onze-Lieve-Vrouw
Ziekenhuis, Aalst, Belgium
Robert Yates MBBCh FRCP

Consultant Fetal and Paediatric Cardiologist,
Cardiothoracic Department, Great Ormond
Street Hospital for Children, London, UK
Felix Zijlstra MD PhD
Director of Coronary Care Unit and
Catheterization Laboratory, Cardiology
Department, Academic Hospital Groningen,
Groningen, The Netherlands

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Foreword

Cardiovascular disease has become the foremost cause of death and permanent disability
in western countries, and is set to become the foremost cause of death and permanent
disability worldwide by the year 2020. We are confronting a pandemic that will be a
heavy burden on the population and that will cause much human suffering. The burden
on health systems is also considerable in terms of healthcare expenditure, which looks set
to continue growing. Cardiovascular disease is becoming increasingly common, in
particular all types of atherothrombosis. This is driven by the rapid increase in the
prevalence of risk factors among the world’s population, such as the increasing frequency
of obesity, type 2 diabetes, smoking, physical inactivity and psychological stress
combined with a gradual increase in consumption of energy-dense foods and lower
consumption of fruit and vegetables. In this context, the burden of cardiovascular disease
will continue to increase with a gradual increase in life expectancy in the population.
Despite major progress in this field over the last 50 years, there is still much to learn
about the progression of cardiovascular disease, particularly in understanding the
mechanism of disease, the pathophysiology and evolution of diagnostic methods. The
explosion of imaging techniques combined with ever more refined biological assays,

particularly those based on genomics and proteomics, have all helped to make the
diagnosis of cardiovascular diseases considerably more accurate and rapid. This
exponential progress is the result of very active research and heavy investment in this
field. This exciting progress has been translated from basic research into clinical
management, thanks to active clinical research in cardiovascular disease. A large number
of clinical trials, surveys and registries have helped us to understand both the impact of
cardiovascular disease on the population and the impact of new strategies for diagnosis
and management. European cardiologists have played an active part in advancing
research in cardiovascular disease in basic, clinical and population sciences. The overall
result is an improvement in diagnostic and therapeutic potential, as well as better
prevention measures. Patients now benefit from a greater diversity of therapeutic options
than ever before. The dissemination of this increased knowledge base is of paramount
importance because physicians need to be aware of the best evidence concerning the most
suitable treatment strategies for a particular disease. They need to implement this
information in their daily routine practice, and keep abreast of changes and improvements
in the management of cardiovascular disease. The ESC mission statement is to improve
the quality of life of the European population by reducing the burden of cardiovascular
disease. To fulfil its mission, the ESC has taken on the responsibility of training
cardiologists and disseminating knowledge through congress activity, writing and
publication of guidelines and, now, publication of The ESC Textbook of Cardiovascular
Medicine. This is the first textbook to be proposed by an international society of

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cardiology. More specifically, the goals of the textbook are to address the knowledge
requirements specified in the ESC Core Syllabus, to be consistent with ESC Guidelines
and best practice and to produce a clinically focused resource for cardiologists and
trainees. In all, The ESC Textbook of Cardiovascular Medicine is set to become the new
benchmark for cardiologists in Europe and beyond. The textbook is available in

traditional printed format, as well as an online edition complete with CME-accredited
self-assessment programmes. The online edition will be regularly updated, and it is hoped
that translations will be available in the future. A large number of prominent European
cardiologists have contributed to this comprehensive textbook that covers all aspects of
cardiovascular disease from diagnosis to management and prevention. As a teaching text,
this textbook covers knowledge that every general cardiologist needs to know and keep
current, but does not address all the information needs of subspecialists. The concise and
practical style was deliberately chosen to make this textbook easy to use. We would like
to take this opportunity to thank all those who have contributed so generously their
experience, and time, in order to produce this work, most particularly the authors and the
co-editors. The wealth of their experience will be invaluable in bringing the most
pertinent information to our colleagues throughout Europe and around the world. We are
confident that this textbook will enjoy wide recognition, and hope that it will become a
reference work for cardiologists around the globe.
Jean-Pierre Bassand President European Society of Cardiology 2002–2004
Michael Tendera President European Society of Cardiology 2004-2006

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Preface

The goal of every good medical textbook is to teach excellence in medicine. This is the
main purpose of this new ESC Textbook of Cardiovascular Medicine. This book
specifically attempts to draw together all up-to-date strands of relevant information and
use all appropriate modern educational methods to ensure good and comprehensive
learning. It is not merely a treatise on theory but a practical compendium on cardiac and
vascular disease. Yogi Berra, the great Yankee baseball player, once said ‘theory and
practice are in theory the same, but in practice they are not!’ It is the editors’ intention to
harmonize theory and practice in this new teaching text. The ESC Textbook of

Cardiovascular Medicine is the first ever cardiovascular textbook to be published in
partnership with an international medical society, and is set to become the standard text
in Europe and beyond. Initiated by the ESC Board and strongly supported by the
President, it represents a major undertaking and long-term commitment from the ESC.
Everything a trainee or practising cardiologist needs to know
As a teaching or training text structured around the ESC Core Syllabus, The ESC
Textbook of Cardiovascular Medicine contains the knowledge that every general
cardiologist should strive to attain and keep current. It does not try to contain everything
a subspecialist should know about the field. The textbook is consistent with the ESC
Guidelines and with best practice. The book has 120 contributors from 12 European
countries who were chosen as much for their ability as writers as for their knowledge.
The result is a balanced, expert and comprehensive review of each topic. It covers the
entire field of cardiovascular medicine and, unlike other texts, the first six chapters are
dedicated to diagnostic imaging. Imaging modalities are also discussed within the
subsequent chapters on different disorders and diseases and referenced back to the first
chapters.
Easy to navigate and lavishly illustrated
All chapters follow the same format so that there are no inconsistencies in style or
content. Each chapter opens with a brief ‘Summary’ box detailing the scope of the
chapter and ends with a ‘Personal perspectives’ box in which the author outlines state-ofthe-art and future directions for the area. The ESC Textbook of Cardiovascular Medicine
is succinct, focused and practical to use. Only key references are included so that
readability is not inhibited by overly dense text. It is also visually appealing, with an
image on every two-page spread. There are over 700 full colour images and over 230
informative tables. All of the illustrations (and many of the ECG traces too) have been

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redrawn to ensure consistency of style and quality. This truly outstanding art programme
means that techniques and concepts are easy to grasp.

Accompanying online version and CME accreditation
An online version of The ESC Textbook of Cardiovascular Medicine is provided with
each printed copy. A card with the website address and a unique access number is bound
into every book. The unique access number is used when registering, at which point a
user name and password can be chosen. Using the website is straightforward and
technical help is available if needed. The online version contains all the text and images
from The ESC Textbook of Cardiovascular Medicine as well as: l an excellent full text
search facility; l downloadable PDF chapter files; l links from reference lists to PubMed;
l a database of video clips supplied by the authors; l chapter-based CME multiple choice
questions. The provision of high-quality CME for cardiologists and trainees in Europe is
a key priority of the ESC. In line with this aim, accreditation of chapters in The ESC
Textbook of Cardiovascular Medicine is awarded by EBAC (The European Board for
Accreditation in Cardiology). Having read a chapter, you are required to submit your
answers to a set of multiple choice questions relating to the chapter’s content. Your score
is then displayed and feedback is given on the correctly answered questions. Feedback is
not given on incorrect answers so that the test may be attempted again. Having
successfully completed a chapter (achieving a pass mark of 60% or above), you can
download an EBAC certificate from the website. The editors wish to acknowledge the
great help provided to them by the editorial staff at Blackwell Publishing. Gina Almond
and Julie Elliott, in particular, have been engaged and involved in the production of this
book from start to finish.
A. John Camm
Thomas F. Lüscher
Patrick W. Serruys

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Contents

1
The Morphology of the Electrocardiogram ………………………………....………………… 1
Antoni Bayés Luna, Velislav N. Batchvarov & Marek Malik

2
Cardiac Ultrasound ………………………………………………………………………………………. 37
Jos Roelandt & Raimund Erbel

3
Cardiovascular Magnetic Resonance ………………………………………………………….... 95
Dudley J. Pennell, Frank E. Rademakers & Udo P. Sechtem

4
Cardiovascular Computerized Tomography ………………………………………………… 115
Pim J. Feyter & Stephan Achenbach

5
Nuclear Cardiology ……………………………………………………………………………………. 141
Philipp A. Kaufmann, Paolo G. Camici & S. Richard Underwood

6
Invasive Imaging and Haemodynamics ………………………………………………………. 159
Christian Seiler & Carlo Di Mario

7
Genetics of Cardiovascular Diseases ………………………………………………............ 189
Silvia G. Priori, Carlo Napolitano, Stephen Humphries, Maria Cristina Digilio,
Paul Kotwinski & Bruno Marino

8

Clinical Pharmacology of Cardiovascular Drugs ……………………………………….…. 219
Aroon Hingorani, Patrick Vallance & Raymond MacAllister

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9
Prevention of CVD: Risk Factor Detection and Modification …………………….…. 243
Joep Perk, Annika Rosengren & Jean Dallongeville

10
Hypertension …………………………………………………………………………………………….. 271
Sverre E. Kjeldsen, Henrik M. Reims, Robert Fagard & Giuseppe Mancia

11
Diabetes Mellitus and Metabolic Syndrome ………………………………………………. 301
Francesco Cosentino, Lars Ryden & Pietro Francia

12
Acute Coronary Syndromes: Pathophysiology, Diagnosis and Risk
Stratification ………………………………………………………………………………………….….. 333
Christian W. Hamm, Christopher Heeschen, Erling Falk & Keith A.A. Fox

13
Management of Acute Coronary Syndromes ……………………………………….…….. 367
Eric Boersma, Frans de Werf & Felix Zijlstra

14
Chronic Ischaemic Heart Disease ………………………………………………………….……. 391
Filippo Crea, Paolo G. Camici, Raffaele De Caterina & Gaetano A. Lanza

15
Management of Angina Pectoris ………………………………………………………………... 391
Kim Fox, Henry Purcell, John Pepper & William Wijns

16
Myocardial Disease ……………………………………………………………….………………...… 453
Otto M. Hess, William McKenna, Heinz-Peter Schultheiss, Roger Hullin, Uwe Kühl,
Mathias Pauschinger, Michel Noutsias & Srijita Sen-Chowdhry

17
Pericardial Diseases …………………………………………………………………………………... 517
Bernhard Maisch, Jordi Soler-Soler, Liv Hatle & Arsen D. Ristic

18
Tumours of the Heart …………………………………………………………………………......... 535
Mary N. Sheppard, Annalisa Angelini, Mohammed Raad & Irina Savelieva

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19
Congenital Heart Disease in Children and Adults ……………………………………….. 553
John E. Deanfield, Robert Yates & Vibeke E. Hjortdal

20
Pregnancy and Heart Disease ………………………………………………………………….…. 607
Patrizia Presbitero, Giacomo G. Boccuzzi, Christianne J.M. Groot & Jolien W. RoosHesselink

21

Valvular Heart Disease ………………………………………………………………………………. 625
Alec Vahanian, Bernard Iung, Luc Pierard, Robert Dion & John Pepper

22
Infective Endocarditis ……………………………………………………………………...…..……. 671
Werner G. Daniel & Frank A. Flachskampf

23
Heart Failure: Epidemiology, Pathophysiology and Diagnosis …………………….. 685
John McMurray, Michel Komajda, Stefan Anker & Roy Gardner

24
Management of Chronic Heart Failure ……………………………………………………..... 721
Karl Swedberg, Bert Andersson, Christophe Leclercq & Marko Turina

25
Pulmonary Hypertension ………………………………………………….………………………… 759
Nazzareno Galiè & Gerald Simonneau

26
Cardiac Rehabilitation ………………………………………………………………………………… 783
Stephan Gielen, Dirk Brutsaert, Hugo Saner & Rainer Hambrecht

27
Bradycardia ……………………………………………………………………………………………..… 807
Lukas Kappenberger, Cecilia Linde & William D. Toff

28
Supraventricular Tachycardia …………………………………………………………………… 831
Jerónimo Farré, Hein J.J. Wellens, José A. Cabrera & Carina Blomström-Lundqvist

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29
Atrial Fibrillation: Epidemiology, Pathogenesis and Diagnosis ……………………. 871
Harry J.G.M. Crijns, Maurits A. Allessie & Gregory Y.H. Lip

30
Atrial Fibrillation: Treatment ………………………………………………………….………….. 891
Etienne Aliot, Christian de Chillou, Pierre Jaïs & S. Bertil Olsson

31
Syncope …………………………………………………………………………………………………….. 931
Michele Brignole, Jean-Jacques Blanc & Richard Sutton

32
Ventricular Tachycardia ……………………………………………………………………………… 949
Lars Eckardt, Pedro Brugada, John Morgan & Günter Breithardt

33
Sudden Cardiac Death and Resuscitation ……………………………………………………. 973
Stefan H. Hohnloser, Alessandro Capucci & Peter J. Schwartz

34
Diseases of the Aorta and Trauma to the Aorta and the Heart …………….……… 993
Christoph A. Nienaber, Axel Haverich & Raimund Erbel

35
Peripheral Arterial Occlusive Disease ……………………………………………………….. 1033

Giancarlo Biamino, Andrej Schmidt, Iris Baumgartner, Dierk Scheinert, Marco Roffi &
Felix Mahler

36
Venous Thromboembolism ………………………………………………………………………. 1076
Sebastian M. Schellong, Henri Bounameaux & Harry R. Büller

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TETC01 12/2/05 18:09 Page 1

1

The Morphology of
the Electrocardiogram
Antoni Bayés de Luna, Velislav N. Batchvarov and
Marek Malik

Summary
The 12-lead electrocardiogram (ECG) is the single most
commonly performed investigation. Almost every
hospitalized patient will undergo electrocardiography,
and patients with known cardiovascular disease will do
so many times. In addition, innumerable ECGs recorded
are made for life insurance, occupational fitness and
routine purposes. Most ECG machines are now able to
read the tracing; many of the reports are accurate but
some are not. However, an accurate interpretation of
the ECG requires not only the trace but also clinical

details relating to the patient. Thus, every cardiologist
and physician/cardiologist should be able to understand
and interpret the 12-lead ECG. Nowadays, many
other groups, for example accident and emergency
physicians, anaesthetists, junior medical staff, coronary
care, cardiac service and chest pain nurses, also need a

good grounding in this skill. In the last several decades
a variety of new electrocardiographic techniques, such
as short- and long-term ambulatory ECG monitoring
using wearable or implantable devices, event ECG
monitoring, single averaged ECGs in the time,
frequency and spatial domains and a variety of stress
recoding methods, have been devised. The cardiologist,
at least, must understand the application and value of
these important clinical investigations. This chapter
deals comprehensively with 12-lead electrocardiography
and the major pathophysiological conditions that can
be revealed using this technique. Cardiac arrhythmias
and other information from ambulatory and averaging
techniques are explained only briefly but are more fully
covered in other chapters, for example those devoted to
specific cardiac arrhythmias.

since rhythm abnormalities are dealt with elsewhere in
this book.

Introduction

Broadly speaking, electrocardiography, i.e. the science and

practice of making and interpreting recordings of cardiac
electrical activity, can be divided into morphology and
arrhythmology. While electrocardiographic morphology
deals with interpretation of the shape (amplitude, width
and contour) of the electrocardiographic signals, arrhythmology is devoted to the study of the rhythm (sequence
and frequency) of the heart. Although these two parts of
electrocardiography are closely interlinked, their methodological distinction is appropriate. Intentionally, this
chapter covers only electrocardiographic morphology

Morphology of the ECG

The electrocardiogram (ECG), introduced into clinical
practice more than 100 years ago by Einthoven, comprises
a linear recording of cardiac electrical activity as it occurs
over time. An atrial depolarization wave (P wave), a
ventricular depolarization wave (QRS complex) and a
ventricular repolarization wave (T wave) are successively

1

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TETC01 12/2/05 18:09 Page 2

Chapter 1

QRS
ST interval

PR interval

PR
segment

ST
segment
T wave

P wave

Figure 1.1 ECG morphology recorded
in a lead facing the left ventricular free
wall showing the different waves and
intervals. Shading, atrial repolarization
wave.

QT interval

recorded for each cardiac cycle (Fig. 1.1). During normal
sinus rhythm the sequence is always P–QRS–T. Depending on heart rate and rhythm, the interval between
waves of one cycle and another is variable.

An electrode that faces the head of the vector records a
positive deflection.
To ascertain the direction of a wavefront, the ECG is
recorded from different sites, termed ‘leads’. When recording the 12-lead ECG six frontal leads (I, II, III, aVR, aVL,
aVF) and six horizontal leads (V1–V6) are used. There
are three bipolar leads in the frontal plane that connect
the left to right arm (I), the left leg to right arm (II) and the

left leg to left arm (III). According to Einthoven’s law, the
voltage in each lead should fit the equation II = I + III.
These three leads form Einthoven’s triangle (Fig. 1.3A).
Bailey obtained a reference figure (Bailey’s triaxial system) by shifting the three leads towards the centre.
There are also three augmented bipolar leads (aVR, aVL
and aVF) in the frontal plane (Fig. 1.3B). These are de-

Electrophysiological principles [1–6]
The origin of ECG morphology may be explained by the
dipole-vector theory, which states that the ECG is an
expression of the electro-ionic changes generated during
myocardial depolarization and repolarization. A pair of
electrical charges, termed a dipole, is formed during both
depolarization and repolarization processes (Fig. 1.2).
These dipoles have a vectorial expression, with the head
of the vector located at the positive pole of a dipole.

+++–––
–––+++

––––––
++++++
Na

Depolarization
dipole

–––––+
+++++–

–+

Na

K

Ca Na

1

Ca

+++++–
–––––+

2

––++++
++––––

Na

Ca

Ca

0

Na

3

+–

Ca

K

++++++
––––––

++++++
––––––
K

K

T

ST

Na

Ca

B
Na+ Ca2+

Outside + + + + + +

Na+

K+

– – – –

Cell membrane
Sarc.
Ret.

Ca2+

Na+ Ca2+

K+

– –

+ + + + + + + + + + + +

K+

Int. cel.

K

++++++
––––––

Na

Ca Na
A

Repolarization
dipole

Ionic pump

2

Na+ Na+ Ca2+

Direction of
phenomenon
Vector
Dipole

–+

Figure 1.2 Scheme of electro-ionic
changes that occur in the cellular
depolarization and repolarization in the
contractile myocardium. (A) Curve of
action potential. (B) Curve of the
electrogram of a single cell (repolarization
with a dotted line) or left ventricle
(normal curve of ECG with a positive
continuous line). In phase 0 of action
potential coinciding with the Na+

entrance, the depolarization dipole (−+)
and, in phase 2 with the K + exit, the
repolarization dipole (+−), are originated.
At the end of phase 3 of the action
potential an electrical but not ionic
balance is obtained. For ionic balance
an active mechanism (ionic pump)
is necessary.

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The Morphology of the Electrocardiogram

A

B

C

D

+

–
I

–120º

–

–

–60º

–

+

I

+VR

+VL

–150º

–30º

–

–

––180º
+
II

III

0º

+I

III

II

V1
V3R

+150º

+

+30º

+
+120º

+III

+90º

+60º

V2
V3 V4 V4 V6 V7

V4R

+II

+VF
+

+

Figure 1.3 (A) Einthoven’s triangle. (B) Einthoven’s triangle superimposed on a human thorax. Note the positive (continuous line) and
negative (dotted line) part of each lead. (C) Bailey’s hexaxial system. (D) Sites where positive poles of the six precordial leads are located.

A

this occurs is shown in Fig. 1.4. This concept is useful for
understanding how the ECG patterns of ischaemia and
injury are generated (see Fig. 1.17).

Normal characteristics
A
LV

Heart rate

B

B
Figure 1.4 Correlation between global action potential, i.e.
the sum of all relevant action potentials, of the subendocardial
(A) and subepicardial (B) parts of the left ventricle and the ECG

waveform. Depolarization starts first in the furthest zone
(subendocardium) and repolarization ends last in the furthest
zone (subendocardium). When the global action potential of
the nearest zone is ‘subtracted’ from that of the furthest zone,
the ECG pattern results. (LV = left ventricle.)

scribed as ‘augmented’ because, according to Einthoven’s
law, their voltage is higher than that of the simple bipolar
leads. By adding these three leads to Bailey’s triaxial system, Bailey’s hexaxial system is obtained (Fig. 1.3C). In
the horizontal plane, there are six unipolar leads (V1–V6)
(Fig. 1.3D).
One approach to understanding ECG morphology is
based on the concept that the action potential of a cell
or the left ventricle (considered as a huge cell that
contributes to the human ECG) is equal to the sum of
subendocardial and subepicardial action potentials. How

Normal sinus rhythm at rest is usually said to range
from 60 to 100 b.p.m. but the nocturnal sleeping heart
rate may fall to about 50 b.p.m. and the normal daytime resting heart rate rarely exceeds 90 b.p.m. Several
methods exist to assess heart rate from the ECG. With the
standard recording speed of 25 mm/s, the most common
method is to divide 300 by the number of 5-mm spaces
(the graph paper is divided into 1- and 5-mm squares)
between two consecutive R waves (two spaces represents
150 b.p.m., three spaces 100 b.p.m., four spaces 75 b.p.m.,
five spaces 60 b.p.m., etc.).

Rhythm
The cardiac rhythm can be normal sinus rhythm (emanating from the sinus node) or an ectopic rhythm (from a

site other than the sinus node). Sinus rhythm is considered to be present when the P wave is positive in I, II,
aVF and V2–V6, positive or biphasic (+/–) in III and V1,
positive or –/+ in aVL, and negative in aVR.

PR interval and segment
The PR interval is the distance from the beginning of the
P wave to the beginning of the QRS complex (Fig. 1.1).
The normal PR interval in adult individuals ranges from

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4

Chapter 1

0.12 to 0.2 s (up to 0.22 s in the elderly and as short as
0.1 s in the newborn). Longer PR intervals are seen in cases
of atrioventricular (AV) block and shorter PR intervals in
pre-excitation syndromes and various arrhythmias. The
PR segment is the distance from the end of the P wave to
QRS onset and is usually isoelectric. Sympathetic overdrive may explain the down-sloping PR segment that
forms part of an arc with the ascending nature of the ST
segment. In pericarditis and other diseases affecting the
atrial myocardium, as in atrial infarction, a displaced and
sloping PR segment may be seen.

QT interval
The QT interval represents the sum of depolarization (QRS
complex) and repolarization (ST segment and T wave)
(Fig. 1.1). Very often, particularly in cases of a flat T wave
or in the presence of a U wave, it is difficult to measure the
QT interval accurately. It is usual to perform this measurement using a consistent method in order to ensure
accuracy if the QT interval is studied sequentially. The
recommended method is to consider the end of repolarization as the point where a tangent drawn along the
descending slope of the T wave crosses the isoelectric line.
The best result may be obtained by measuring the median
duration of QT simultaneously in 12 leads. Automatic
measurement may not be accurate but is often used clinically [7].
It is necessary to correct the QT interval for heart rate
(QTc). Different heart rate correction formulae exist. The
most frequently used are those of Bazett and Fridericia:
Bazett (square root) correction: QT corrected
= QT measured/RR interval (s)0.5
Fridericia (cube root) correction: QT corrected
= QT measured/RR interval (s)0.33
Although these correction methods are not accurate
and are highly problematic in cases when a very precise
QTc value is needed, their results are satisfactory in standard clinical practice. Because of its better accuracy the
Fridericia formula is preferred to that of Bazett.
A long QT interval may occur in the congenital long
QT syndromes or can be associated with sudden death
[8], heart failure, ischaemic heart disease, bradycardia,
some electrolyte disorders (e.g. hypokalaemia and hypocalcaemia) and following the intake of different drugs.
Generally, it is believed that if a drug increases the QTc
by more than 60 ms, torsade de pointes and sudden

cardiac death might result. However, torsade de pointes
rarely occurs unless the QTc exceeds 500 ms [9]. A short
QT interval can be found in cases of early repolarization,
in association with digitalis and, rarely, in a genetic disorder associated with sudden death [10].

P wave
This is the atrial depolarization wave (Fig. 1.1). In general, its height should not exceed 2.5 mm and its width
should not be greater than 0.1 s. It is rounded and positive but may be biphasic in V1 and III and –/+ in aVL. The
atrial repolarization wave is of low amplitude and usually
masked by coincident ventricular depolarization (QRS
complex) (see shading in Fig. 1.1).

QRS complex
This results from ventricular depolarization (Figs 1.1 and
1.5). According to Durrer et al. [11], ventricular depolarization begins in three different sites in the left ventricle
and occurs in three consecutive phases that give rise to
the generation of three vectors [6].
The ventricular depolarization signal is often described
generically as a QRS complex. Usually the deflection is
triphasic and, provided that the initial wave is negative
(down-going), the three waves are sequentially known
as Q, R and S. If the first part of the complex is up-going
the deflection is codified as an R wave, etc. If the R or S
wave is large in amplitude, upper case letters (R, S) are
used, but if small in amplitude, lower case letters (r, s)
are used. A normal or physiological initial negative wave
of the ventricular depolarization waveform is called a q
wave. It must be narrow (< 0.04 s) and should not usually
exceed 25% of the amplitude of the following R wave,
though some exceptions exist mainly in leads III, aVL

and aVF. If the initial deflection is wider or deeper, it is
known as a Q wave. Different morphologies are presented in Fig. 1.5.
The QRS width should not exceed 0.095 s and the R
wave height should not exceed 25 mm in leads V5 and V6
or 20 mm in leads I and aVL, although a height greater
than 15 mm in aVL is usually abnormal.

ST segment and T wave
The T wave, together with the preceding ST segment, is
formed during ventricular repolarization (Fig. 1.1). The
T wave is generally positive in all leads except aVR, but
may be negative, flattened or only slightly positive in V1,
and flattened or slightly negative in V2, III and aVF. The
T wave presents an ascending slope with slower inscription than the descending slope. In children, a negative
T wave is normal when seen in the right precordial leads
(paediatric repolarization pattern) (Fig. 1.6F). Under
normal conditions, the ST segment is isoelectric or shows
only a slight down-slope (< 0.5 mm). Examples of normal
ST–T wave variants are displayed in Fig. 1.6 (the figure
caption provides comment on these patterns). Occasion-

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The Morphology of the Electrocardiogram

A

40

40
30
20
>60

0
>6
40

0

0

60
*1

40
30

40–60
–6

ally, after a T wave, a small U wave can be observed, usually showing the same polarity as the T wave (Fig. 1.1).

–6

30

20

2
*

–2

0

40

*

3

10

Electrocardiographic morphological
abnormalities

30
* = 0 ms

20

Electrocardiography can be considered the test of choice
or the gold standard for the diagnosis of AV blocks,
abnormal intra-atrial and intraventricular conduction,
ventricular pre-excitation, most cardiac arrhythmias and,
to some extent, acute myocardial infarction. However, in

other cases, such as atrial and ventricular enlargement,
abnormalities secondary to chronic coronary artery disease (ECG pattern of ischaemia, injury or necrosis), other
repolarization abnormalities and certain arrhythmias,
electrocardiography provides useful information and may
suggest the diagnosis based on predetermined electrocardiographic criteria. However, these criteria have lesser
diagnostic potential compared with other electrocardiology or imaging techniques (e.g. echocardiography in atrial
or ventricular enlargement). In some circumstances, electrocardiography is the technique of choice and the electrocardiographic criteria in use are diagnostic for those
conditions (e.g. bundle branch block), while for other conditions (e.g. cavity enlargement) the criteria are only indicative. In order to know the real value of the ECG criteria
in these cases, it is important to understand the concepts
of sensitivity, specificity and predictive accuracy [1].

30

VL
B

3

V6
1

2

30°

V1

VF

Figure 1.5 (A) The three initial points (1, 2, 3) of ventricular

depolarization are marked by asterisks. The isochrone lines
of the depolarization sequence can also be seen (time shown
in ms). (B) The first vector corresponds to the sum of
depolarization of the three points indicated in (A) and because
it is more potent than the forces of the right vector, the global
direction of vector 1 will be from left to right. The second
vector corresponds to depolarization of the majority of the
left ventricle and usually is directed to the left, downward
and backward. The third vector represents the depolarization
of basal parts of the septum and right ventricle.

A

B
V4

C

Atrial abnormalities
Electrocardiographic patterns observed in patients with
atrial hypertrophy and atrial dilation (atrial enlargement) and with atrial conduction block are encompassed
by this term (Fig. 1.7).

D
V5

E
V2

F

Figure 1.6 Different morphologies of normal variants of the ST segment and T wave in the absence of heart disease. (A) Normal ST/T
wave. (B) Vagotonia and early repolarization. (C) Sympathetic overdrive. ECG of a 22-year-old male obtained with continuous Holter
monitoring during a parachute jump. (D) Straightening of ST with symmetric T wave in a healthy 75-year-old man without heart
disease. (E) Normal variant of ST ascent (saddle morphology) in a 20-year-old man with pectus excavatum. (F) Normal repolarization
in a 3-year-old child.

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Chapter 1
A

C

B
3

2

1

2
mm

mm

2
mm

6

1

Right atrium

1

Right atrium

Left atrium

Left atrium

Right atrium
Left atrium

0.10 s

0.10 s

0.12 s

Normal P wave

RAE

LAE
Figure 1.7 Schematic diagrams of atrial
depolarization in (A) normal P wave,
(B) right atrial enlargement (RAE) and
(C) left atrial enlargement (LAE) with
interatrial conduction block. An example
of each of these P waves is shown beneath
each diagram.

Right atrial enlargement (Fig. 1.7B)
Right atrial enlargement is usually present in patients
with congenital and valvular heart diseases affecting the
right side of the heart and in cor pulmonale.
Diagnostic criteria
The diagnostic criteria of right atrial abnormality are based
on P-wave amplitude abnormalities (≥ 2.5 mm in II
and/or 1.5 mm in V1) and ECG features of associated
right ventricular abnormalities.

Left atrial enlargement (Fig. 1.7C)
Left atrial enlargement is seen in patients with mitral and
aortic valve disease, ischaemic heart disease, hypertension
and some cardiomyopathies.
Diagnostic criteria
1 P wave with duration ≥ 0.12 s especially seen in leads I
or II, generally bimodal, but with a normal amplitude.
2 Biphasic P wave in V1 with a terminal negative
component of at least 0.04 s. Criteria 1 and 2 have good
specificity (close to 90%) but less sensitivity (< 60%).

3 P wave with biphasic (±) morphology in II, III and aVF
with duration ≥ 0.12 s, which is very specific (100%
in valvular heart disease and cardiomyopathies) but
has low sensitivity for left atrial abnormality [12,13].

left atrial abnormality. Usually the negative part in V1
may be less prominent than in atrial hypertrophy or
dilation, although it is not surprising that the morphology of left atrial abnormality and atrial block are similar
because the features of left atrial abnormality are more
dependent on delayed interatrial conduction than on
atrial dilation.
advanced interatrial block with left atrial
retrograde activation
This is characterized by a P wave with duration ≥ 0.12 s
and with biphasic (±) morphology in II, III and aVF. A
biphasic P-wave morphology in V1 to V3/V4 is also frequent (see below). This morphology is a marker for
paroxysmal supra-ventricular tachyarrhythmias [12,13]
and is very specific (100%) for left atrial enlargement.

Ventricular enlargement
The electrocardiographic concept of enlargement of the
right and left ventricle encompasses both hypertrophy and
dilation and, of course, the combination. The diagnostic
criteria for ventricular enlargement when QRS duration
is less than 120 ms are set out below. The criteria for the
diagnosis of right and/or left ventricular enlargement
combined with intraventricular block (QRS duration
≥ 120 ms) are defined elsewhere [1,5,14,15].

Right ventricular enlargement

Interatrial block
partial block
P-wave morphology is very similar to that seen with

Right ventricular enlargement (RVE) is found particularly in cases of congenital heart disease, valvular
heart disease and cor pulmonale. Figure 1.8 shows that

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The Morphology of the Electrocardiogram
Table 1.1 Electrocardiographic criteria of
right ventricular enlargement

Criterion

Sensitivity (%)

Specificity (%)

V1

R/S V1 ≥ 1
R V1 ≥ 7 mm
qR in V1
S in V1 < 2 mm
IDT in V1 ≥ 0.35 s

6
2
5
6
8

98
99
99
98
98

V5-V6

R/S V5–V6 ≤ 1
R V5–V6 < 5 mm
S V5–V6 ≥ 7 mm

16
13
26

93
87
90

V1 + V6

RV1 + SV5-V6 > 10.5 mm

18

94

ÂQRS

ÂQRS ≥ 110°
SI, SII, SIII

15
24

96
87

IDT, intrinsicoid deflection (time from QRS onset to R wave peak).

Table 1.2 Morphologies with dominant R or R′ (r′ ) in V1
Clinical setting

QRS width

P-wave morphology in V1

< 0.12 s

Various changes

< 0.12 s
< 0.12 s

Normal
Normal

Typical right bundle branch block

From < 0.12 to ≥ 0.12 s

Normal

Atypical right bundle branch block
Ebstein’s disease
Arrhythmogenic right ventricular dysplasia
Brugada’s syndrome

Often ≥ 0.12 s
Often ≥ 0.12 s
Sometimes ≥ 0.12 s

Often tall, peaked and + or ±
Often abnormal
Normal

Right ventricular or biventricular enlargement
(hypertrophy)

< 0.12 s

Often tall and peaked

Wolff–Parkinson–White syndrome

From < 0.12 to ≥ 0.12 s

Normal P, short PR

Lateral myocardial infarction

< 0.12 s

Normal P

No heart disease
Incorrect electrode placement
Normal variant (post-term infants, scant
Purkinje fibres in anteroseptal zone)
Chest anomalies

the ECG pattern in V1 (prominent R wave) is related
more to the degree of RVE than to its aetiology.
Diagnostic criteria
The electrocardiographic criteria most frequently used
for the diagnosis of RVE are shown in Table 1.1, along
with their sensitivities (low) and specificities (high). The
differential diagnosis of an exclusive or dominant R wave
in V1 (R, Rs or rSR′ pattern) is given in Table 1.2.
1 Morphology in V1: morphologies with a dominant
or exclusive R wave in V1 are very specific, but not
so sensitive (< 10%) for the diagnosis of RVE.
Nevertheless, other causes that may cause a dominant

R pattern in V1 must be excluded (see Table 1.2). An
rS or even QS morphology in V1, together with RS in
V6, may often be observed in chronic cor pulmonale,
even in advanced stages or in the early stages of RVE
of other aetiologies (Fig. 1.8).

Valve heart
disease
1

2

Cor
pulmonale
3

4

Congenital heart
disease
5

6

Figure 1.8 ECG pattern of right ventricular enlargement:
note that QRS in V1 depends more on the severity of
right ventricular enlargement than on aetiology of the
disease. 1, 3 and 5 represent examples of mild mitral
stenosis, cor pulmonale and congenital pulmonary
stenosis respectively, while 2, 4 and 6 are cases of severe

and long-standing mitral stenosis, cor pulmonale with
severe pulmonary hypertension, and congenital pulmonary
stenosis respectively.

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Chapter 1

2 Morphology in V6: the presence of forces directed
to the right expressed as an S wave in V5–V6 is one
of the most important ECG criteria.
3 Frontal plane QRS electrical axis (ÂQRS): ÂQRS ≥ 110°
is a criterion with low sensitivity but high specificity
(95%) provided that left posterior hemiblock, an
extremely vertical heart position and lateral left
ventricular wall infarction have been excluded.
4 SI, SII, SIII: an S wave in the three bipolar limb leads
is frequently seen in chronic cor pulmonale with
a QS or rS pattern in V1 and an RS pattern in V6.
The possibility of this pattern being secondary to
a positional change or simply to peripheral right
ventricular block must be excluded [16].
The combination of more than one of these criteria

increases the diagnostic likelihood. Horan and Flowers
[15] have published a scoring system based on the
most frequently used ECG criteria for right ventricular
enlargement.

V6

V1

A

V1

V6

B

Figure 1.9 The most characteristic ECG feature of left
ventricular enlargement is tall R waves in V5–6 and deep
S waves in V1–2. The presence of a normal septal q wave
depends on whether septal fibrosis is present. This figure
shows two examples of aortic valvular disease both with left
ventricular enlargement: (A) no fibrosis and a normal septal
q wave; (B) abnormal ECG (ST/T with strain pattern) and no
septal q wave due to extensive fibrosis.

A

1972

1980

1988

B

1973

1982

1989

Left ventricular enlargement
Left ventricular enlargement, or ischaemic heart disease,
is found particularly in hypertension, valvular heart disease, cardiomyopathies and in some congenital heart
diseases.
In general, in patients with left ventricular enlargement, the QRS voltage is increased and is directed more
posteriorly than normal. This explains why negative QRS
complexes predominate in the right precordial leads. Occasionally, probably related to significant cardiac laevorotation or with more significant hypertrophy of the left
ventricular septal area than of the left ventricular free wall,
as occurs in some cases of apical hypertrophic cardiomyopathy, the maximum QRS is not directed posteriorly.
In this situation a tall R wave may be seen even in V2.
The normal q wave in V6 may not persist if hypertrophy is associated with fibrosis and/or partial left
bundle branch block. In Fig. 1.9, the ECG from a case of
aortic valvular disease without septal fibrosis shows a
q wave in V6 and a positive T wave, whereas the ECG
from another case with fibrosis does not have a q wave in
V6 [17,18]. The ECG pattern is more related to disease
evolution than to the haemodynamic overload (Fig. 1.10),
although a q wave in V5–V6 remains more frequently in

long-standing aortic regurgitation than in aortic stenosis.
The pattern of left ventricular enlargement is usually fixed
but may be partially resolved with medical treatment of
hypertension or surgery for aortic valvular disease.
Diagnostic criteria
Various diagnostic criteria exist (Table 1.3). Those with
good specificity (≥ 95%) and acceptable sensitivity

Figure 1.10 Examples of different ECG morphologies seen
during the evolution of aortic stenosis (A) and aortic
regurgitation (B).

(40–50%) include the Cornell voltage criteria and the
Romhilt and Estes scoring system.

Intraventricular conduction blocks
Ventricular conduction disturbances or blocks can occur
on the right side or on the left. They can affect an entire
ventricle or only part of it (divisional block). The block
of conduction may be first degree (partial block or conduction delay) when the stimulus conducts but with

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TETC01 12/2/05 18:09 Page 9

The Morphology of the Electrocardiogram

Table 1.3 Electrocardiographic criteria of left ventricular enlargement
Voltage criteria

Sensitivity (%)

Specificity (%)

RI + SIII > 25 mm
R aVL > 11 mm
R aVL > 7.5 mm
SV1 + RV5–6 ≥ 35 mm (Sokolow–Lyon)
RV5–6 > 26 mm
Cornell voltage criterion: R aVL + SV3 > 28 mm (men) or 20 mm (women)
Cornell voltage duration: QRS duration × Cornell voltage > 2436 mm/seg
In V1–V6, deepest S + tallest R > 45 mm
Rohmilt–Estes score > 4 points
Rohmilt–Estes score > 5 points

10.6
11
22
22
25
42
51
45
55
35

100
100
96

100
98
96
95
93
85
95

delay, third degree (advanced block) when passage of
the wavefront is completely blocked, and second degree
when the stimulus sometimes passes and sometimes
does not.

Partial or first-degree RBBB
In this case, activation delay of the ventricle is less
delayed. The QRS complex is 0.1–0.12 s in duration, but
V1 morphology is rsR′ or rsr′.

Advanced or third-degree right bundle branch block
Advanced (third degree) left bundle branch block

(Fig. 1.11)
Advanced right bundle branch block (RBBB) represents
complete block of stimulus in the right bundle or within
the right ventricular Purkinje network. In this situation,
activation of the right ventricle is initiated by condution
through the septum from the left-sided Purkinje system.
Diagnostic criteria
1 QRS ≥ 0.12 s with slurring in the mid-final portion of
the QRS.

2 V1: rsR′ pattern with a slurred R wave and a negative
T wave.
3 V6: qRs pattern with S-wave slurring and a positive
T wave.
4 aVR: QR with evident R-wave slurring and a negative
T wave.
5 T wave with polarity opposite to that of the slurred
component of the QRS.

(Fig. 1.12)
Advanced left bundle branch block (LBBB) represents
complete block of stimulus in the left bundle or within
the left ventricular Purkinje network. In this situation,
activation of the left ventricle is initiated by conduction
through the septum from the right-sided Purkinje system.
Diagnostic criteria
1 QRS ≥ 0.12 s, sometimes over 0.16 s, especially with
slurring in the mid-portion of the QRS.
2 V1: QS or rS pattern with a small r wave and a positive
T wave.
3 I and V6: a single R wave with its peak after the initial
0.06 s (delayed intrinsicoid deflection).
4 aVR: a QS pattern with a positive T wave.
5 T waves with their polarity usually opposite to
the slurred component of the QRS complex.

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Figure 1.11 ECG in a case of advanced
right bundle branch block.

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