The SurfaceElectrocardiographyin Ischaemic HeartDiseaseCLINICAL AND IMAGINGCORRELATIONS ANDPROGNOSTIC IMPLICATIONS

A. Bayés de Luna, MD, FESC, FACCDirector of Cardiac Dep. Hospital Quiron, Barcelona

Professor of Medicine, Universidad Autonoma Barcelona

Director of Institut Catala de Cardiologia

Hospital Santa Creu I Sant Pau

St. Antoni M. Claret 167

ES-08025

Barcelona

Spain

M. Fiol-Sala, MDChief of the Intensive Coronary Care Unit

Intensive Coronary Care Unit

Hospital Son Dureta

Palma

Mallorca

Spain

With the collaboration of A. Carrillo†, D. Goldwasser*, J. Cino*,A. Kotzeva*, M. Riera†, J. Guindo* and R. Baranowski*∗From the Institut Catala de Cardiologica, Hospital Santa Creu I Sant Pau, Barcelona, Spain†From the Intensive Coronary Care Unit, Hospital Son Dureta, Palma, Mallorca, Spain

The SurfaceElectrocardiographyin Ischaemic HeartDisease

The SurfaceElectrocardiographyin Ischaemic HeartDiseaseCLINICAL AND IMAGINGCORRELATIONS ANDPROGNOSTIC IMPLICATIONS

A. Bayés de Luna, MD, FESC, FACCDirector of Cardiac Dep. Hospital Quiron, Barcelona

Professor of Medicine, Universidad Autonoma Barcelona

Director of Institut Catala de Cardiologia

Hospital Santa Creu I Sant Pau

St. Antoni M. Claret 167

ES-08025

Barcelona

Spain

M. Fiol-Sala, MDChief of the Intensive Coronary Care Unit

Intensive Coronary Care Unit

Hospital Son Dureta

Palma

Mallorca

Spain

With the collaboration of A. Carrillo†, D. Goldwasser*, J. Cino*,A. Kotzeva*, M. Riera†, J. Guindo* and R. Baranowski*∗From the Institut Catala de Cardiologica, Hospital Santa Creu I Sant Pau, Barcelona, Spain†From the Intensive Coronary Care Unit, Hospital Son Dureta, Palma, Mallorca, Spain

C© 2008 A. Bayes de Luna and M. Fiol-SalaPublished by Blackwell PublishingBlackwell Futura is an imprint of Blackwell Publishing

Blackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USABlackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UKBlackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia

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First published 2008

1 2008

ISBN: 978-1-4051-7362-9

Library of Congress Cataloging-in-Publication Data

Bayes de Luna, Antonio.The surface electrocardiography in ischemic heart disease : clinical and imaging

correlations and prognostic implications / A. Bayes de Luna, M. Fiol-Sala.p. ; cm.

Includes bibliographical references and index.ISBN 978-1-4051-7362-91. Coronary heart disease–Diagnosis. 2. Electrocardiography. I. Fiol-Sala, M. (Miguel)

II. Title.[DNLM: 1. Myocardial Ischemia–diagnosis. 2. Electrocardiography–methods. WG 300 B357s 2007]RC685.C6B36 2008616.1′2307543–dc22

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Contents

Foreword by Gunter Breihardt, vi

Foreword by Elliott M. Antman, vii

Introduction, ix

Part I The ECG in different clinicalsettings of ischaemic heart disease:correlations and prognosticimplications, 1

1 Anatomy of the heart: the importanceof imaging techniques correlations, 3

2 Electrocardiographic changes secondary tomyocardial ischaemia, 19

3 Electrocardiographic pattern of ischaemia:T-wave abnormalities, 30

4 Electrocardiographic pattern of injury:ST-segment abnormalities, 55

5 Electrocardiographic pattern of necrosis:abnormal Q wave, 128

Part II The ECG in different clinicalsettings of ischaemic heart disease:correlations and prognosticimplications, 195

6 Acute and chronic ischaemic heart disease:definition of concepts and classification, 197

7 Patients with acute chest pain: role of theECG and its correlations, 199

8 Acute coronary syndrome: unstable anginaand acute myocardial infarction, 209

9 Myocardial infarction with Q wave, 275

10 Myocardial infarction without Q wavesor equivalent: acute and chronic phase, 289

11 Clinical settings with anginal pain, outsidethe ACS, 297

12 Silent ischaemia, 302

13 Usefulness and limitations of the ECG in chronicischaemic heart disease, 304

14 The ECG as a predictor of ischaemicheart disease, 308

References, 310

Index, 325

Colour plate, facing page 12

v

Foreword by Gunter Breihardt

It is a great pleasure and honour for me to presentthis foreword to this new and exciting book.

Until recently, correlations between the ECG andthe structural changes of the heart have relied on ex-perimental studies and on studies done at autopsy,and only to a limited degree on modern imagingtechniques. When invasive coronary angiographycame into broad use, the general interest shiftedaway from the simple tool of the ECG that was con-sidered as low technology, leading to a gradual de-cline in interest in and knowledge of the ECG inischaemic heart disease. This is in contrast to whathas happened over many years in the field of ar-rhythmias where there has been a continuing learn-ing process with increasingly better interpretationof arrhythmias based on more and more sophisti-cated invasive electrophysiological studies.

Fortunately, some prominent and expert clinicalresearchers have kept their interest in the ECG alive.Among them is Antoni Bayes de Luna who, jointlywith Miquel Fiol Sala, now can be congratulatedfor the present book on clinical and imaging corre-lations and the prognostic implications of the sur-face ECG in ischaemic heart disease. Both authorsrightly state that they are authors and not editors ofa multi-author book. Look at the result: This bookhas a quite homogenous and unified presentationwhich can only be achieved if there is a commongenius behind it.

The aim of this book is to present better cor-relations between the structure of the heart, itsvarious walls, especially those of the left ventricle,and their relationship with the torso. This will helpto eliminate much of the confusion in the inter-pretation of the ECG and the terms used, whichhas arisen over several decades and still continuestoday. The authors not only point to the limitations

of still used classifications and correlations but theyalso present solutions to these problems based onrecent anatomic–electrocardiographic correlations.Their presentation is based on the recent pioneeringwork, initiated by Antoni Bayes de Luna, on the useof magnetic resonance imaging and its correlationswith the ECG.

This book deserves the attention of all those whotake care of the ever-increasing number of patientswith ischaemic heart disease. It is a treasure anda must for everyone who is involved in manag-ing patients with ischaemic heart disease, be it aspractitioner, internist, cardiologist or as intensivecare physician or interventionalist, as teacher oras student – all will benefit from the vast experi-ence of the authors and from the information fromtheir own studies and the literature that they haveassembled.

The reader and eager student of this book willappreciate that the most important messages of eachchapter are summarised in a box that emphasises thedidactic claim of this work.

This book has the potential to become the ‘bible’in this field for generations to come, hopefullyworldwide.

Gunter Breithardt, MD, FESC, FACC, FHRSProfessor of Medicine (Cardiology)

Head of the Department of Cardiologyand Angiology; and

Head of the Department ofMolecular Cardiology of the

Leibniz-Institute for Arteriosclerosis Research,Westphalian Wilhelms – University of Munster,

Munster, Germany

May 2007Munster, Germany

vi

Foreword by Elliott M. Antman

Medical decision-making consists of a five-step pro-cess including obtaining a medical history fromthe patient, selecting the appropriate diagnostictests, interpreting the results of the diagnostic tests,weighing the risks and benefits of additional testingor potential therapeutic interventions, and agree-ing on a plan of a therapeutic approach in con-junction with the patients wishes. A diagnostic testthat optimizes sensitivity and specificity is partic-ularly attractive clinically, since it is used to am-plify the prior probability that a particular diag-nostic condition is present. Given the escalatingcost of health care, a diagnostic test is especiallyattractive if it is inexpensive. Diagnostic tests thatcontain these features and utilize equipment thatis universally available are more likely to stand thetest of time in clinical medicine. One such diag-nostic test – the electrocardiogram – stands out asa shining example of a successful diagnostic test.It is a well accepted component of the diagnos-tic toolbox of health care professionals around theworld.

Einthoven is often credited as the individualwho introduced the electrocardiogram to clinicalmedicine. After applying a string galvanometer torecord the hearts electrical signals on the surface ofthe body, it was in 1895 that he introduced the fivedeflections P, Q, R, S, and T. Willem Einthoven washonored in 1924 for his invention of the electro-cardiograph by receiving the Nobel Prize in Phys-iology or Medicine. In 1934, Frank Wilson intro-duced the concept of unipolar leads, and in 1938the American Heart Association and Cardiac Soci-ety of Great Britain defined the standard positionsand wiring of the chest leads V1–V6. In 1942, Gold-berger introduced the technique for increasing thevoltage of Wilsons unipolar leads, thus creating theaugmented limb leads aVR, aVL, and aVF. In com-

bination with Einthovens three limb leads, the sixprecordial leads, and the augmented unipolar leadsform the 12-lead electrocardiogram recording pat-tern as we know it today.

With the passage of time, many new and highlysophisticated imaging and biochemical test havebeen introduced into clinical medicine. Some mightargue that the 12-lead electrocardiogram has lostsome its luster but a more penetrating analysis ofthe situation shows that this is not the case. The newimaging and biochemical tests amplify and extendour ability to interpret the 12-lead electrocardio-gram in ways that we did not realize were possiblein the past.

One of the most important applications of thesurface electrocardiogram is in evaluation of pa-tients with ischemic heart disease. This elegant text-book by Drs. A. Bayes de Luna and M. Fiol-Sala isa refreshing modernistic look at the surface elec-trocardiogram by two internationally recognizedexperts in the field. They provide the reader, ina single volume, a richly illustrated resource thatintegrates clinical findings, contemporary imagingmodalities, cutting edge biomarker findings witha 100-year old diagnostic test – the 12-lead sur-face electrocardiogram. The book is divided intotwo parts. First, electrocardiographic patterns of is-chemia, injury, and infarction are discussed. Polarmaps, vectorial illustrations, and simple diagramsillustrating the relationship between myocyte ac-tion potentials and the surface electrocardiogramare appealing for both the novice and experiencedreader. The second part of the book explores theuse of the surface electrocardiogram in a variety ofclinical settings of ischemic heart disease, touchingon the correlations with coronary anatomy and theprognostic implications that can be gleaned fromthe ECG.

vii

viii Foreword

This textbook by Bayes de Luna and Fiol Sala isa marvelous example of what can be accomplishedwhen clinicians who are comfortable at the patient’sbedside also have the visionary insight to incor-porate new knowledge from contemporary cardiacimaging procedures into a fresh view of an older,but still extremely useful, diagnostic test. As withthe classical 12-lead electrocardiogram itself, read-ers of this textbook will find themselves returningto it over and over again because of the depth andbreadth of its clinical usefulness.

Elliott M. AntmanSenior Investigator, TIMI Study Group

Professor of Medicine, Harvard Medical School; andDirector of the Samuel A. Levine Cardiac Unit

at the Brigham & Women’s HospitalCardiovascular Division

Brigham & Women’s HospitalBoston

USA

May 2007Boston, USA

Introduction

The electrocardiogram (ECG), which was discov-ered more than 100 years ago and has just celebratedits first century, appears to be more alive than ever.Until recently its utility was especially importantfor identifying different ECG morphological abnor-malities, including arrhythmias, blocks at all levels,pre-excitation, acute coronary syndromes, as wellas Q-wave acute myocardial infarction, for whichECG was the ‘gold-standard’ diagnostic technique.

An authentic re-evaluation of ECG has been evi-denced in the last years as a result of the great impor-tance it acquired in the risk stratification and prog-nosis of different heart diseases. Every year there ismore and more information that demonstrates thatECG provides new and important data, and its ap-plications are growing and will be expanded in thefuture. It has been recently confirmed that ECG al-lows us to approach with high reliability the molec-ular mechanisms that explain some heart diseases,such as chanellopathies. For example, the correla-tion between ECG changes and the genes involvedin long QT syndrome is well known.

Although the usefulness of the surface ECG is im-portant in all types of heart diseases, it stands outparticularly in the case of ischaemic heart disease(IHD), for various reasons. The ECG is the key di-agnostic tool both in the acute phase of IHD (acutecoronary syndromes, ACSs) and in the chronic one(Q-wave infarction). Furthermore, it is crucial forrisk stratification in patients with acute ischaemicpain. The ACSs are nowadays divided into two types:with or without ST-segment elevation. This is ex-tremely important in the decision making to usefibrinolytic therapy. In the case of an ACS, espe-cially with ST-segment elevation (STE-ACS), a care-ful evaluation of ST-segment deviations in differentleads allows us to ascertain not only the occludedartery but also the site of occlusion. Therefore, it

helps to stratify the risk and, consequently, to takethe most appropriate therapeutic decision.

In the chronic phase of Q-wave infarction, theECG is also very useful, since the identification ofdifferent ECG patterns of infarction permits us tohave a reliable approximation of the infarcted area.

Lastly, the ECG is of great importance, as thenumber of patients with IHD is very large, andtherefore the repercussion to properly understandthe ECG changes may have an extraordinary socialand economic impact.

Nevertheless, in spite of all above-mentioned ar-guments, there are few books that have dealt in aglobal manner with the value of ECG in IHD. Over30 years ago Schamroth and Goldberger wrote twoimportant works, dedicated more to the chronicphase of IHD, which have inevitably become out-dated in many aspects. More recently, two groups,those of Wellens and Sclarovsky, which have pub-lished pioneer studies on the importance of the ECGin the acute phase of IHD, have published two excel-lent books that brilliantly deal with the ECG’s rolein the acute phase of this disease. We neverthelessconsidered that in the overall context of the ECG’simportance in IHD there remained a space to fillin this field. That is what we intend to do with thispublication.

One of the most important and new aspects ofthe book is the great number of correlations notonly with coronariography but also with echocar-diography, isotopic studies and new imaging tech-niques, especially cardiovascular magnetic reso-nance (CMR), and also in some cases with coronarymultidetector computer tomography (CMDCT).All these correlations have given us a huge amountof important and new information.

We explain the ECG pattern of chronic Q-wavemyocardial infarction (MI) based on the correlation

ix

x Introduction

with the VCG loops. We consider that the ECG-VCGcorrelation is the most didactic way to explain ECG(Bayes de Luna 1977, 1999). However, we only com-ment in this book the ECG criteria for diagnosis ofchronic-Q wave MI because there is not agreementsupporting that the VCG criteria present better ac-curacy than ECG criteria (Hurd 1981, Warner 1982)T and the use of VCG is more time-consuming andhas not become popular in clinical practice. In orderto set up its real importance could be mandatory inthe era of imaging techniques to perform a com-parative study of ECG and VCG criteria with thestandars of cardiovascular magnetic resonance.

When necessary, we also comment on therole of other non-invasive electrocardiographictechniques, especially exercise ECG and Holtermonitoring. Just a few remarks are given on othernon-invasive electrocardiological techniques. Theinvasive electrophysiological techniques are usu-ally not useful for risk stratification but are nec-essary in case of resynchronisation and implantablecardioverter-defibrillator implantation or ablationprocedures.

We have two parts in this book. In the first one,following comments on the most important as-pects of the heart’s anatomy related to IHD onthe basis of coronariographic and imaging correla-tions, we discuss the concept of the ECG patterns ofischaemia, injury and infarction, the electrophysio-logical mechanisms that explain them and the cor-relation that exists between the presence of thesepatterns in different leads and the myocardial areainvolved. Correlations between ECG curves andvectorcardiographic loops constitute the key to un-derstand the ECG morphologies. For this reason,the two above-mentioned techniques of electricalactivity recording are often represented together inthis book. Nevertheless, in clinical practice the sur-face ECG alone allows for making a correct diag-nosis in most cases. Of particular interest is thepossibility to locate the place of coronary occlu-sion in patients with STE-ACS, thanks to the ap-plication of sequential algorithms, and to identifythe typical and atypical ECG patterns of STE-ACS,and to define properly the classification of non (N)STE-ACS. Also important is the new classification ofinfarction in case of Q-wave MI based on our ex-perience with contrast-enhanced (CE)-CMR cor-relations. All this represents a new approach to

understand the ECG curves generated during acuteand chronic ischaemia.

In the second part we explain a detailed globalapproach that has to be done in patients with acuteprecordial pain, emphasising on the importance ofECG changes, first to diagnose the ischaemic originand later to stratify the risk in different types of ACS.Other electrocardiographic features of ACS, such ascoexisting arrhythmias, conduction disturbances,ECG changes following fibrinolytic treatment andmechanical complications and the ECG character-istics of atypical ACSs, are also presented. Further-more, we comment on the new, current conceptsof MI with and without Q wave, the ECG mark-ers of poor prognosis in chronic IHD and the ECGcharacteristics of other clinical settings with angi-nal pain outside the acute phase of ACS as chronicstable angina, X syndrome, silent ischaemia, etc.Finally, the capacity of ECG as marker of IHD isalso discussed.

The information given in this book may help toperform the best diagnosis in patients with acutethoracic pain and to take decisions, sometimes inan urgent manner, for the best approach of manage-ment in patients with acute and chronic IHDs. Wewould like to emphasise that we are not the editors,but the authors of the book. This is important, be-cause all the information is given in a homogeneousmanner, without the presence of contradictoryopinions that often appear in ‘edited’ books. Also,the presence of frequent cross-references within thetext makes the content of the book easier to fol-low. We are aware that we are often repetitive, es-pecially when we comment on the new concepts ofACS with or without STE and the new classificationof Q-wave MI based on CMR correlations. How-ever, we consider that this may be helpful especiallyfor the readers who are not too much involved inthe topic and also for consultants of some specifictopic.

We express our gratitude to E. Antman, pioneerin many aspects of IHD, who has written a gen-erous Foreword to this book, for his support andcollaboration. We have written together a mono-graph related to the role of surface ECG in patientswith acute thoracic pain and ST-segment elevationMI, which has been mostly included in this book,and for that he may also be considered co-author ofthe book. Also my thanks to Gunter Breithardt, an

Introduction xi

expert and pioneer in electrocardiology, because hehas also written an outstanding Foreword empha-sising the electrocardiographic aspects of the book.We also appreciate very much the advice and friend-ship of Y. Birnbaum, J. Cinca, P. Clemensen, A.Gorgels, K. Nikus, O. Pahlm, G. Pohost, W. Roberts,S. Sclarovsky, S. Stern, G. Wagner, H. Wellens andW. Zareba, with whom we shared many aspects ofthe new ideas expressed in this book.

Finally, we would like to thank the help espe-cially of J. Cino, A. Carrillo, A. Kotzeva, M. Riera, J.Guindo, D. Goldwasser and R. Baranowski for theircollaboration, and also of T. Bayes-Genıs, A. Boix,R. Elosua, P. Farres, J. Guerra, A. Martinez Rubio,J. Gurri, M. Santalo, J. Puig, I. Ramirez, J. Riba,

E. Rodriguez, P. Torner, T. Anivarro, M.T. Subiranaand X. Vinolas, who collaborated in the selection oficonography and in many other aspects. A specialmention of gratitude to the Cardiovascular Imag-ing Unit of Saint Paul Hospital (G. Pons, F. Car-reras, R. Leta and S. Pujadas) for its outstandingcontribution with the CMR and CMDCT figures.Many thanks also to Montserrat Saurı, who gaveus her valuable secretarial support; to Josep Sarriofor some of the drawings; and to Prous Science andBlackwell Publishing for their invaluable work in allthe printing process of the book in its Spanish andEnglish versions.

Antoni Bayes de LunaMiquel Fiol-Sala

I PART I

Electrocardiographicpatterns of ischaemia,injury and infarction

1 CHAPTER 1

Anatomy of the heart: theimportance of imaging techniquescorrelations

The surface electrocardiography (ECG) in bothacute and chronic phase of ischaemic heart dis-ease (IHD) may give crucial information about thecoronary artery involved and which is the area ofmyocardium that is at risk or already infarcted.This information jointly with the ECG–clinical cor-relation is very important for prognosis and riskstratification, as will be demonstrated in this book.Therefore, we will give in the following pages anoverview of the anatomy of the heart, especially theheart walls and coronary tree, and emphasise thebest techniques currently used for its study.

For centuries, since the pioneering works ofVesalio, Leonardo da Vinci, Lower and Bourgery-Jacob, pathology has been a unique method to studythe anatomy of the heart. Since the end of the nine-teenth century, the visualisation of the heart in vivohas been possible by X-ray examination. The last40–50 years started the era of invasive imaging tech-niques with cardiac catheterisation (angiographyand coronary angiography) and modern non-invasive imaging techniques, first with echocardio-graphy and later with isotopic studies, scannerand cardiovascular magnetic resonance (CMR).These techniques open a new avenue to study notonly the anatomy of the heart, coronary arteries andgreat vessels but also the myocardial function andperfusion, and the characterisation of the valves,pericardium, etc.

The coronary angiography (Figure 1.1) is espe-cially important in the acute phase for diagnosingthe disease and correlating the place of occlusionwith the ST-segment deviations. It is also usefulin the chronic phase of the disease. However, inthe chronic phase of Q-wave myocardial infarc-tion (MI) the ECG does not usually predict the

state of the coronary tree, because the revascu-larisation treatment has modified, sometimes verymuch, the characteristics of the occlusion respon-sible for the MI. Furthermore, the catheterisa-tion technique may give important information foridentifying hypokinetic or akinetic areas. The lattermay be considered comparable to infarcted areas(Shen, Tribouilloy and Lesbre, 1991; Takatsu et al.,1988; Takatsu, Osugui and Nagaya, 1986; Warneret al., 1986). Currently, in some cases, the non-invasive coronary multidetector computer tomog-raphy (CMDCT) may be used (Figure 1.1).

The era of modern non-invasive imaging tech-niques started with echocardiography, which isvery easy to perform and has a good cost-effectiverelation. This technique plays an important role, es-pecially in the acute phase, in the detection of left-ventricular function and mechanical complicationsof acute MI (Figures 1.2, 8.28 and 8.29). Also, it isvery much used in chronic ischaemic-heart-diseasepatients for the study of left-ventricular functionand also detection of hypokinetic and akinetic areas(Bogaty et al., 2002; Matetzky et al., 1999; Mitamuraet al., 1981). However, echocardiography tends tooverestimate the area that is at risk or necrosed,and thus its reliability is good but not excellent.The techniques of echo stress and especially iso-topic studies (single-photon emission computedtomography, SPECT) have proved to be very re-liable for detecting perfusion defects and necroticareas (Gallik et al., 1995; Huey et al., 1988; Zafriret al., 2004) (Figure 1.3). They are very usefulin cases where there is dubious precordial painwith positive exercise testing without symptoms(Figure 4.58). It has been demonstrated, however,that in some cases (non-Q-wave infarction) the

3

4 PART I Electrocardiographic patterns of ischaemia, injury and infarction

(A)

(B)

Figure 1.1 (A) Normal case: coronary angiography (left)and three-dimensional volume rendering of CMDCT (right)showing normal LAD and LCX artery. The latter is partiallycovered by left appendix in CMDCT. The arrow points outLAD. (B) Normal case: coronary arteriography (left) andthree-dimensional volume rendering of CMDCT (right)showing normal dominant RCA. (C) 85-year-old man withatypical anginal pain: (a) Maximal intensity projection(MIP) of CMDCT with clear tight mid-LAD stenosis thatcorrelates perfectly with the result of coronaryangiography performed before PCI (b). (D) Similar case as(C) but with the stenosis in the first third of RCA ((a–d)CMDCT and (e) coronary arteriography). (E) Similar case as(C) and (D) but with the tight stenosis in the LCX beforethe bifurcation ((a) and (b) CMDCT and (c) coronaryangiography). (F) These images show that CMDCT may alsodemonstrate the presence of stenosis in distal vessels, inthis case posterior descending RCA ((a–b) CMDCT and (c))

coronary angiography). (G) These images show thatCMDCT (a, b) may delimitate the length of total occlusionand visualise the distal vessels (see arrows in (b), the yellowones correspond to distal RCA retrograde flow from LAD)that is not possible to visualise with coronary angiography(c). (H) A 42-year-old man sports coach with a stentimplanted in LAD by anginal pain 6 months before. Thepatient complains of atypical pain and present state ofanxiety that advises to perform a CMDCT to assure thegood result and permeability of the stent. In the MIP ofCMDCT (a–c) was well seen the permeability of the stentbut also a narrow, long and soft plaque in left main trunkwith a limited lumen of the vessel (see (d) rounded circle)that was not well seen in the coronary angiography (e) butwas confirmed by IVUS (f). The ECG presents not very deepnegative T wave in V1–V3 along all the follow-up. Thisfigure can be seen in colour, Plate 1.

extension of the infarction may be underestimatedand that in presence of the left bundle branch block(LBBB) the estimation of some perfusion defects isdoubtful.

The most recent imaging techniques are CMR(Figure 1.4) and CMDCT (Figure 1.1). The latter isused for non-invasive study of coronary tree. CMR,which may also be used for perfusion and func-

tion studies of the myocardium, gives us the best ‘invivo’ anatomic information about the heart. Thus,this technique, in conjunction with gadolinium in-jection and contrast-enhanced CMR (CE-CMR),is very useful for identifying and locating MI, aswell as for determining its transmurality with ex-traordinary reliability, comparable to pathologicalstudies (Bayes de Luna et al., 2006a–c; Cino et al.,

CHAPTER 1 Anatomy of the heart: the importance of imaging techniques correlations 5

(D)

(C)

Figure 1.1 (Continued )

2006; Moon et al., 2004; Salvanayegam, 2004; Wuet al., 2001). This is why CE-CMR has become thegold-standard technique for studying correlationsbetween ECG findings and infarcted myocardial ar-eas in the chronic phase of IHD (Bayes de Lunaet al., 2006a–c; Cino et al., 2006; Engblom et al.,2002, 2003). Also, CE-CMR may distinguish ac-cording to location the hyperenhancement areas be-tween ischaemic and non-ischaemic patients (Fig-ure 1.5) and may show in vivo the sequence of theevolving transmural MI (Mahrholdt et al., 2005a,b) (Figure 8.5). The reproducibility of CE-CMRalong time, especially after the acute phase, is verygood. It also has the advantage of not producingradiation. The current limitation of CMR, whichwill probably be solved in the next few years, isthe study of coronary tree. Currently, this may beperformed non-invasively by CMDCT (see aboveFig 1.1).

The heart walls and theirsegmentation: cardiac magneticresonance (Figures 1.4–1.14)The heart is located in the central-left part of thethorax (lying on the diaphragm) and is oriented an-teriorly, with the apex directed forwards, and fromright to left (Figure 1.4).

The left ventricle (LV) is cone shaped. Althoughits borders are imprecise, classically (Myers et al.,1948a, b; Myers, Howard and Stofer, 1948), it hasbeen divided, except in its inferomost part the apex,into four walls, till very recently named septal, ante-rior, lateral and inferoposterior. In the 1940s–1950sthe inferoposterior wall was named just posterior(Goldberger, 1953) (Figure 1.6A), probably becauseit was considered opposed to the anterior wall. Lateron (Perloff, 1964), only the basal part of this wall,which was thought to bend upwards, was consid-ered really a posterior wall (Figure 1.6B). Therefore,

6 PART I Electrocardiographic patterns of ischaemia, injury and infarction

(E)

(F)

Figure 1.1 (Continued )

it was named ‘true posterior’ and the rest of the walljust ‘inferior wall’ (Figure 1.6). According to that,for more than 40 years the terms ‘true’ or ‘strictposterior infarction’, ‘injury’ and ‘ischaemia’ havebeen applied, when it was considered that the basalpart of the inferoposterior wall was affected. Thecommittee of the experts of the International So-ciety of Computerised ECG (McFarlane and VeitchLawrie, 1989), in accordance with the publicationsof Selvester and Wagner, has named these walls an-terosuperior, anterolateral, posterolateral and in-ferior, respectively. However, this nomenclaturehas not been popularised, and the classical names(Figure 1.7A) are still mostly used in the major-

ity of papers (Roberts and Gardin, 1978), ECGbooks (Figure 1.7B to D), task force (Surawicz etal., 1978) and statements (Hazinsky, Cummis andField, 2000).

Later on, in the era of imaging techniques, theheart was transected into different planes (Figure1.7) and different names were given to the heartwalls by echocardiographists and experts in nuclearmedicine. However, recently, the consensus of theNorth American Societies for Imaging (Cerqueira,Weissman and Disizian, 2002) divided the LV in17 segments and 4 walls: septal, anterior, lateraland inferior (Figures 1.8 and 1.9). This consensusstates that the classical inferoposterior wall should

CHAPTER 1 Anatomy of the heart: the importance of imaging techniques correlations 7

(G)

(H)

Figure 1.1 (Continued )

be called inferior ‘for consistency’, and segment 4should be called inferobasal instead of posteriorwall. Therefore the word ‘posterior’ has to be sup-pressed. Figures 1.8 and 1.9 show the 17 segmentsinto which the four left-ventricular walls are divided(6 basal, 6 medial, 4 inferior and the apex), and theright side of Figure 1.9 shows the heart walls withtheir corresponding segments on a polar ‘bull’s-eye’map, as used by specialists in nuclear medicine. Now

we will explain, thanks to correlations with CMR,why we consider that this terminology (Cerqueira,Weissman and Disizian, 2002) is the best and it willbe used further in this book. Page 16 shows the evo-lution of the terminology given to the wall that lieson the diaphragm.

If we consider that the heart is located in thethorax in a strictly posteroanterior position, as ispresented by anatomists and by experts in nuclear

8 PART I Electrocardiographic patterns of ischaemia, injury and infarction

Figure 1.2 Echocardiography: see example of volumes,wall thickening and myocardium mass in a normal caseand in a patient with post-MI. Above: (A) End-diastolic and(B) end-systolic apical long-axis views of a normal leftventricle. The endocardial and epicardial contours aretraced and the built-in computer software of theultrasound system allows calculation of volumes, wallthickening and myocardial mass. Below: Segmental wall

function analysis: post-infarct lateral wall hypokinesisshown in the four view. The left ventricle is dilated.Superposition of the traced endocardial contours at enddiastole (A) and end systole (B) shows the hypokinesis andcompensatory hyperkinesis of the interventricular septum.(C) It shows the superimposed end-diastolic andend-systolic contours. (Adapted from Camm AJ, Luscher TFand Serruys PW, 2006.)

medicine, and in the transverse section of CMRimages (Figure 1.10A–C), we may understand thatin case of involvement (injury or infarction) ofbasal part of inferior wall (classically called pos-terior wall) especially when in lean individuals themajority of inferior wall is placed in a posterior po-sition (Figure 1.13C), an RS (R) and/or ST-segmentdepression in V1 will be recorded (Figure 1.10D).However, now, thanks to magnetic resonance cor-relations (Figure 1.11), we have evidence that the

The usefulness of invasive and non-invasiveimaging techniques and their correlations withECG in IHD:� Non-invasive imaging techniques, especiallySPECT, are very useful in detecting perfusion de-fects during exercise test.� We will present in this book the importance ofECG–coronary angiography correlations to iden-tify the artery occlusion site and the myocardialarea at risk.� The role of coronary angiography, and inspecial circumstances, of non-invasive detection

of coronary tree by CMDCT in chronic-heart-disease patients, will be commented.� In chronic Q-wave MI we will emphasise theimportance of the ECG–CMR correlations toidentify and locate the area of infarction.� ECG is very useful in coronary care unit and isalso used routinely in the chronic phase.� X-ray examination still plays some role es-pecially in the acute phase (heart enlargementand pulmonary oedema) and in the detectionof aneurysms and calcifications, visualisation ofheart valves, pacemakers, etc.

sagittal view of the heart is, in respect to the tho-rax, located with an oblique right-to-left inclinationand not in a strictly posteroanterior position, as wasusually presented by anatomists, nuclear medicineand the transverse section of CMR (Figure 1.10).This helps us to understand how the RS (R) or pre-dominant ST-segment depression patterns in V1 isthe consequence of the infarction of or injury to thelateral, not the inferobasal, segment (classical poste-rior wall) (Figure 1.12). However, we have to remind

CHAPTER 1 Anatomy of the heart: the importance of imaging techniques correlations 9

(A)

(B)

Figure 1.3 Examples of correlation exercise test – isotopicimages (SPECT). (A) Above: Observe the three heart planes(see Figure 1.4B) used by nuclear medicine experts (andother imaging techniques) to transect the heart:(1) short-axis (transverse) view (SA), (2) vertical long-axisview (VLA) (oblique sagittal-like) and (3) horizontallong-axis (HLA) view. Below: Normal case of perfusion ofleft ventricle. On the middle is (B) the bull’s-eye image ofthis case. The segmentation of the heart used in this bookis shown (Cerqueira, Weissman and Disizian, 2002). On (A)transections of the three axes are shown. The short-axistransections is at the mid-apical level (see Figure 1.8 forsegmentation). (B) Above: In the three planes (SA, VLA and

HLA) see (A) normal uptake at rest (Re) and during exercise(Ex) can be observed. Middle: Abnormal uptake onlyduring exercise of segments 7, 13 and 17 (see Figure 1.8) ina patient with angina produced by distal involvement ofnot long LAD. The basal part of the anterior wall of leftventricle is not involved. Below: Abnormal uptake duringrest and exercise in a patient in chronic phase of MIproduced by distal occlusion of very long LAD that wrapsthe apex involving part of inferior wall (segments 7, 13 and17 and also 15) (see Figure 1.8), without residual ischaemiaon exercise. In this case the image of abnormal uptake ispersistent during rest. See in all cases the ECG patterns thatmay be found. This figure can be seen in colour, Plate 2.

10 PART I Electrocardiographic patterns of ischaemia, injury and infarction

(A)

(B)

Figure 1.4 Cardiac magnetic resonance imaging (CMR).(A) Transections of the heart following the classical humanbody planes: (1) frontal plane, (2) horizontal plane and(3) sagittal plane. (B) Transections of the heart followingthe heart planes that cut the body obliquely. These are theplanes used by the cardiac imaging experts: (1) short-axis(transverse) view, in this case at mid-level (see B(1));(2) horizontal long-axis view;

(3) vertical long-axis view (oblique sagittal-like). Check thegreat difference between the sagittal plane according tohuman body planes (A(3)) and the heart planes (B(3). (B) Itshows the four walls of the heart with the classical names:septal (S), anterior (A), lateral (L) and inferoposterior.Currently, the inferoposterior wall is named for consistencyjust inferior (I) (see p. 16 and Figure 1.8).

Hyperenhancement patterns

Ischaemic

A. Subendocardial infarct A. Mid-wall HE

. Idioparthi dilared cardiomyopathy

. Myocarditis

B. Transmular infarct

B. Epicardial HE

C. Global endocardial HE

. Sarcoidosis, myocarditis, Anderson-Fabry, Chags disease

. Amyloidosis, systemic selerosis. post-cardiac transplantation

. Hypertrophic cardiomyopathy

. Sarcoidosis

. Myocarditis

. Anderson-fabry

. Chas disease

. Right ventricular pressure overload (e.g. congenital heart disease,

pulmonary HTN)

Non-ischaemic

Figure 1.5 Hyperenhancement patterns found in clinicalpractice. If hyperenhancement is present, thesubendocardium should be involved in patients with

ischaemic disease. Isolated mid-wall or subepicardialhyperenhancement strongly suggests a ‘non-ischaemic’etiology. (Taken from Marhrholdt, 2005.)

CHAPTER 1 Anatomy of the heart: the importance of imaging techniques correlations 11

Anterior infarct

Anterior infarct

LV LV

Goldberger, 1953

Perloff, 1964

V4 V4

Posterior infarct

True posterior infarct

Figure 1.6 Above: The concept of anterior and posteriorinfarction according to Goldberger (1953). Below: Theconcept of anterior and true or strict posterior infarction isshown according to Perloff (1964). The other part of thewall that lies on the diaphragm became to be namedinferior (see p. 16).

that in the majority of cases except for very lean in-dividuals (see Figure 1.13C), the part of the inferiorwall that is really posterior just involves the areaof late depolarisation (segment 4, or inferobasal).Therefore, in case of MI of this area, there wouldnot be changes in the first part of QRS, because thisMI does not originate a Q wave or an equivalentwave (Durrer et al., 1970).

The CMR technique gives us real informa-tion about the in vivo heart’s anatomy (Blackwell,Cranney and Pohost, 1993; Pons-Llado and Car-reras, 2005) (Figure 1.4). In this regard, the follow-ing are important:(a) CMR patterns of the frontal, horizontal andsagittal planes of the heart following the humanbody planes are shown in Figure 1.4A. This allowsus to know with precision the heart’s location withinthe thorax. In this figure we can observe these tran-sections, performed at the mid-level of the heart.(b) Nevertheless, bearing in mind the three-dimensional location of the heart within the tho-rax, in order to correlate the left ventricular wallsamongst themselves and, above all, to locate thedifferent segments into which they can be divided,it is best to perform transections following the

heart planes that are perpendicular to each other(see Figure 1.4B), as has been already done innuclear medicine (Figure 1.3; see Plate 2). Theseplanes transect the heart following the heart planes(Figure 1.4B) and are the following: horizontal long-axis view, short-axis view (transverse) and verticallong-axis view (oblique sagittal-like). In reality theoblique sagittal-like view (Figure 1.11B) presents,as we have said, an oblique right to left and nota strict posteroanterior direction (compare Figure1.4A(3) with Figures 1.4B(3) and 1.11B). There-fore in the presence of infarction of the inferobasalpart of inferior wall (classically called posterior wall)and especially when the infarction involves the mid-inferior wall if it is located posteriorly, as happens invery lean individuals (Figure 1.13C), the vector ofinfarction generated in this area is directed forwardsand from right to left and is recorded as RS mor-phology in V2–V3, but not in V1 where it presentsa normal rS morphology (Figure 1.12B). On thecontrary, the vector of infarction, in the case of in-farction involving the lateral wall, may generate anRS pattern in V1 (Bayes de Luna, Batchvarov andMalik, 2006; Bayes de Luna, Fiol and Antman, 2006;Cino et al., 2006) (Figure 1.12C) (see legend Figure1.12).(c) The longitudinal vertical plane (Figures 1.3(2),1.8C and 1.11B; see Plate 2) is not fully sagittal withrespect to the anteroposterior position of the tho-rax, but rather oblique sagittal, as it is directed fromright to left. (The sagittal-like axis follows the CDline in Figure 1.11A.) Compare Figures 1.4B(3) and1.11B with the true sagittal view – Figure 1.4A(3).The view of this plane, as seen from the left side(oblique sagittal), allows us to correctly visualise theanterior and the inferior heart walls (Figure 1.11B).We can clearly see that the inferior wall has a por-tion that lies on the diaphragm until, at a certainpoint, sometimes it changes its direction and be-comes posterior (classic posterior wall), now calledinferobasal segment. This posterior part is more orless important, depending on, among other factors,the body-build. We have found (Figure 1.13) that inmost cases the inferior wall remains flat (C shape)(Figure 1.13B). However, sometimes a clear basalpart bending upwards (G shape) (Figure 1.13A) isseen. Only rarely, usually in very lean individuals,does the great part of the inferior wall present a clearposterior position (U shape) (Figure 1.13C).

12 PART I Electrocardiographic patterns of ischaemia, injury and infarction

(A)

(D)

(B) (C)

Frontal view

Inferior Inferoposterior Direct posterior Posterolateral

Figure 1.7 (A) The left ventricle may be divided into fourwalls that till very recently were usually named anterior(A), inferoposterior (IP) or diaphragmatic, septal (S) andlateral (L). However, according to the arguments given inthis book, we consider that the ‘inferoposterior’ wall hasto be named just ‘inferior’ (see p. 16). (B–D) Differentdrawings of the inferoposterior wall (inferior + posteriorwalls) according to different ECG textbooks (see inside thefigure). In all of them the posterior wall corresponds to the

basal part of the wall lying on the diaphragm that wasthought to bend upwards. It was considered that the heartwas located strictly in a posteroanterior position in thethorax (Figures 1.10D and 1.12A). The cardiovascularmagnetic resonance (CMR) gives us the information thatthe inferoposterior wall lies flat, even in its basal part, inaround two-third of cases (Figure 1.13) and make evidentthat the heart is always placed in an oblique position(Figure 1.12B,C).

Therefore, often, the posterior wall does not ex-ist and for this reason, the name ‘inferior wall’seems clearly better than the name ‘inferoposte-rior’. On the other hand, the anterior wall is, infact, superoanterior, as is clearly appreciated inFigure 1.11B. However, in order to harmonise theterminology with imaging experts and to avoidmore confusion, we consider that the names ‘ante-rior wall’ and ‘inferior wall’ are the most adequatefor its simplification and also, because when an in-farct exists in the anterior wall, the ECG repercus-sion is in the horizontal plane (HP; V1–V6) andwhen it is in the inferior wall – even in the infer-obasal segment – it is in the frontal plane (FP).

(d) The longitudinal HP (Figures 1.3(3) and 1.8B;see Plate 2) is directed from backwards to forwardsfrom rightwards to leftwards, and slightly cephalo-caudally. In Figure 1.8A (arrows), one can appre-ciate how, following the line AB, the heart can beopened like a book (Figure 1.8B).(e) The transverse plane (Figures 1.4B(1), 1.3A(1)and 1.8A), with respect to the thorax, is directed pre-dominantly cephalocaudally and from right to left,and it crosses the heart, depending on the transec-tion performed, at the basal level, mid-level or apicallevel (Figure 1.8A). Thanks to these transverse tran-sections performed at different levels, we are able toview the right ventricle (RV) and the left-ventricular

Plate 1 (A) Normal case: coronary angiography (left) and three-dimensional volume rendering of CMDCT (right) showingnormal LAD and LCX artery. The latter is partially covered by left appendix in CMDCT. The arrow points out LAD.(B) Normal case: coronary arteriography (left) and three-dimensional volume rendering of CMDCT (right) showing normaldominant RCA. (C) 85-year-old man with atypical anginal pain: (a) Maximal intensity projection (MIP) of CMDCT with cleartight mid-LAD stenosis that correlates perfectly with the result of coronary angiography performed before PCI (b). (D)Similar case as (C) but with the stenosis in the first third of RCA ((a–d) CMDCT and (e) coronary arteriography). (E) Similarcase as (C) and (D) but with the tight stenosis in the LCX before the bifurcation ((a) and (b) CMDCT and (c) coronaryangiography). (F) These images show that CMDCT may also demonstrate the presence of stenosis in distal vessels, in thiscase posterior descending RCA ((a–b) CMDCT and (c)) coronary angiography). (G) These images show that CMDCT (a, b)may delimitate the length of total occlusion and visualise the distal vessels (see arrows in (b), the yellow ones correspondto distal RCA retrograde flow from LAD) that is not possible to visualise with coronary angiography (c). (H) A 42-year-oldman sports coach with a stent implanted in LAD by anginal pain 6 months before. The patient complains of atypical painand present state of anxiety that advises to perform a CMDCT to assure the good result and permeability of the stent. Inthe MIP of CMDCT (a–c) was well seen the permeability of the stent but also a narrow, long and soft plaque in left maintrunk with a limited lumen of the vessel (see (d) rounded circle) that was not well seen in the coronary angiography (e)but was confirmed by IVUS (f). The ECG presents not very deep negative T wave in V1–V3 along all the follow-up.

Plate 1 (Continued )

Plate 1 (Continued )

Plate 1 (Continued )