HEART-ECG in Acute Myocardial Infarction and Unstable Angina

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSIONST SEGMENT DEVIATION SCORE More than 15 mm indicates an area sufficiently large to attempt reperfusion THE TERMI

ACUTE MYOCARDIAL

INFARCTION AND UNSTABLE

ANGINA

A Bayés de Luna, F Furlanello, B.J Maron and D.P Zipes (eds.):

Arrhythmias and Sudden Death in Athletes 2000 ISBN: 0-7923-6337-X

J-C Tardif and M.G Bourassa (eds): Antioxidants and Cardiovascular Disease.

J Candell-Riera, J Castell-Conesa, S Aguadé Bruiz (eds): Myocardium at

Risk and Viable Myocardium Evaluation by SPET 2000.ISBN: 0-7923-6724-3

M.H Ellestad and E Amsterdam (eds): Exercise Testing: New Concepts for the

Douglas L Mann (ed.): The Role of Inflammatory Mediators in the Failing

Donald M Bers (ed.): Excitation-Contraction Coupling and Cardiac

Contractile Force, Second Edition 2001 ISBN: 0-7923-7157-7

Brian D Hoit, Richard A Walsh (eds.): Cardiovascular Physiology in the

Genetically Engineered Mouse, Second Edition 2001 ISBN 0-7923-7536-X

Pieter A Doevendans, A.A.M Wilde (eds.): Cardiovascular Genetics for Clinicians

Stephen M Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of

Pathology and Pathophysiology of Cardiovascular Disease 2001

ISBN 0-7923-7542-4

Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation 2001

ISBN 1-4020-0147-9

Pieter A Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New

Pathophysiological Concepts 2002 ISBN 1-4020-7022-5

Antonio Pacifico (ed.), Philip D Henry, Gust H Bardy, Martin Borggrefe,

Francis E Marchlinski, Andrea Natale, Bruce L Wilkoff (assoc eds):

Implantable Defibrillator Therapy: A Clinical Guide 2002

ISBN 1-4020-7143-4 Hein J.J Wellens, Anton P.M Gorgels, Pieter A Doevendans (eds.):

The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk

Previous volumes are still available

Developments in Cardiovascular Medicine

Academic Hospital, Maastricht

The Netherlands

and

Pieter A Doevendans, MD

Interuniversity Cardiology Institute of The Netherlands

Utrecht, The Netherlands

KLUWER ACADEMIC PUBLISHERS

NEW YORK, BOSTON, DORDRECHT, LONDON, MOSCOW

eBook ISBN: 0-306-48202-9

Print ISBN: 1-4020-7214-7

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Dordrecht

Determining the size of the area at risk, the severity

of ischemia, and identifying the site of occlusion inthe culprit coronary artery

A The ST segment deviation score

B The terminal QRS-ST segment pattern

C Specific ECG patterns indicating the site ofcoronary artery occlusion:

I Infero-posterior myocardial infarction with

or without right ventricular infarction

II Anterior wall myocardial infarction

Conduction disturbances in acute myocardialinfarction

A The sino-atrial region

B The AV nodal conduction system

C The sub-AV nodal conduction system

Myocardial infarction in the presence of abnormalventricular activation

A Left bundle branch block

B Paced ventricular rhythm

13

1324

43454953

65687679

Arrhythmias in acute myocardial infarction:

Incidence and prognostic significance

A Supraventricular arrhythmias

B Ventricular arrhythmiasThe electrocardiographic signs of reperfusion

The electrocardiogram in unstable anginaRecognition of multivessel and left main diseaseRecognition of critical narrowing of the left anteriordescending coronary artery

Risk Stratification

by: Hein J.J Wellens, Anton P.M Gorgels and Pieter A Doevendans

ISBN: 1-4020-7214-7

The publisher regrets that due to a publishing error, the incorrect series number

appears on the series page and the back cover The correct series number is

DICM245 The corrected series page appears below.

Kluwer Academic Publishers

A Bayés de Luna, F Furlanello, B.J Maron and D.P Zipes (eds.):

Arrhythmias and Sudden Death in Athletes 2000 ISBN: 0-7923-6337-X

J-C Tardif and M.G Bourassa (eds): Antioxidants and Cardiovascular Disease.

J Candell-Riera, J Castell-Conesa, S Aguadé Bruiz (eds): Myocardium at

Risk and Viable Myocardium Evaluation by SPET 2000.ISBN: 0-7923-6724-3

M.H Ellestad and E Amsterdam (eds): Exercise Testing: New Concepts for the

New Century 2001 ISBN: 0-7923-7378-2

Douglas L Mann (ed.): The Role of Inflammatory Mediators in the Failing

Heart 2001 ISBN: 0-7923-7381-2

Donald M Bers (ed.): Excitation-Contraction Coupling and Cardiac

Contractile Force, Second Edition 2001 ISBN: 0-7923-7157-7

Brian D Hoit, Richard A Walsh (eds.): Cardiovascular Physiology in the

Genetically Engineered Mouse, Second Edition 2001 ISBN 0-7923-7536-X

Pieter A Doevendans, A.A.M Wilde (eds.): Cardiovascular Genetics for Clinicians

Stephen M Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of

Pathology and Pathophysiology of Cardiovascular Disease 2001

ISBN 0-7923-7542-4

Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation 2001

ISBN 1-4020-0147-9

Pieter A Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New

Pathophysiological Concepts 2002 ISBN 1-4020-7022-5

Daan Kromhout, Alessandro Menotti, Henry Blackburn (eds.): Prevention

of Coronary Heart Disease: Diet, Lifestyle and Risk Factors in the Seven

Countries Study 2002 ISBN 1-4020-7123-X

Antonio Pacifico (ed.), Philip D Henry, Gust H Bardy, Martin Borggrefe,

Francis E Marchlinski, Andrea Natale, Bruce L Wilkoff (assoc eds):

Implantable Defibrillator Therapy: A Clinical Guide 2002

ISBN 1-4020-7143-4 Hein J.J Wellens, Anton P.M Gorgels, Pieter A Doevendans (eds.):

The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk

Stratification 2002 ISBN 1-4020-7214-7

Previous volumes are still available

Developments in Cardiovascular Medicine

Pieter A Doevendans, M.D

Associate Professor of Cardiology,

Department of Cardiology

Academic Hospital Maastricht

University of Maastricht, the Netherlands

Anton P Gorgels, M.D

Associate Professor of Cardiology

Department of Cardiology

Academic Hospital Maastricht

University of Maastricht, the Netherlands

Over the years the cardiologists, residents, fellows and nursing staff, working atthe Department of Cardiology of the Academic Hospital of Maastricht, havecarefully collected the electrocardiograms published in this book We are verymuch indebted to them for their enthusiasm and willingness to donate thosepearls to us!

To have the electrocardiograms perfectly reproduced we had the good fortune

to have Adrie van den Dool working for us She and the medical photographygroup of the hospital did a perfect job, demonstrating again their ability tomake beautiful illustrations

Excellent secretarial assistance was provided by Birgit van den Burg, MiriamHabex, Vivianne Schellings and Willemijn Gagliardi We greatly appreciatedtheir pleasant, never complaining way of helping us again and again!

Manja Helmers played an important role in the final phase by expertlyproducing the layout of the manuscript

Hein J.J Wellens

Anton P.M Gorgels

Pieter A Doevendans

Chapter 1

Introduction

The electrocardiogram (ECG) remains the most accessible and inexpensive

diagnostic tool to evaluate the patient presenting with symptoms suggestive of

acute myocardial ischemia It plays a crucial role in decision making about the

aggressiveness of therapy especially in relation to reperfusion therapy, because

such therapy has resulted in a considerable reduction in mortality from acute

myocardial infarction

Several factors play a role in the amount of myocardial tissue that can be

salvaged by reperfusion therapy, such as the time interval between onset of

coronary occlusion and reperfusion, site and size of the jeopardized area, type

of reperfusion attempt (thrombolytic agent or an intracoronary catheter

intervention), presence or absence of risk factors for thrombolytic agents, etc

Most important in decision making on reperfusion therapy and the type of

intervention is to look for markers indicating a higher mortality rate from

myocardial infarction

The ECG is a reliable, inexpensive, non-invasive instrument to obtain that

information Recently it has become clear that both in anterior and inferior

myocardial infarction, the ECG frequently allows not only to identify the

infarct related coronary artery, but also the site of occlusion in that artery and

therefore the size of the jeopardized area Obviously, the more proximal the

occlusion, the larger the area at risk and the more aggressive the reperfusion

attempt The ECG will also give an indication of the size of the jeopardized

area by making an ST segment deviation score and tell us about the severity

and reversibility of cardiac ischemia by analyzing the pattern of the QRS and

the beginning of ST segment elevation

It will inform us about other factors of importance for the management and

prognosis of the patient such as heart rate, width of the QRS complex, presence

of abnormalities in impulse formation and conduction, and presence or absence

of a prior infarction

Following reperfusion therapy the ECG can inform us about the result and

help us to select which patient should receive a rescue angioplasty in case of

failure of thrombolytic therapy

At present, decision making on management of acute myocardial

infarction should be individualized and the purpose of this book is to show that

the ECG is an indispensable tool to reach that goal

Often the patient with an acute coronary syndrome presents with different

ST-T segment patterns such as ST elevation, ST depression and T wave

inversion In recent years it has become clear that the ECG at presentation

allows immediate risk stratification across the whole spectrum of acute

coronary syndromes For example, we learned that the patient with extensive

ST segment depression may have a worse long term prognosis that the patient

with an acute myocardial infarction

Risk of the patient with acute myocardial ischemia will depend on site and

severity of coronary artery disease Therefore the identification of the patient

with left main stenosis, severe three vessel disease or proximal narrowing of

the left anterior descending branch is of obvious importance Again, also under

THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA

these circumstances the ECG allows us to select those patients who needinvasive diagnostic studies

4

Determining the size of the area at risk, the severity of

ischemia, and identifying the site of occlusion in the culprit coronary artery

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

ST SEGMENT DEVIATION SCORE

More than 15 mm indicates an area sufficiently large to attempt

reperfusion

THE TERMINAL QRS-ST SEGMENT PATTERN

Grade III ischemia indicates poorer short and long term prognosis

SPECIFIC ECG PATTERNS: IDENTIFYING THE SITE OF

OCCLUSION IN THE CULPRIT CORONARY ARTERY

I Infero posterior infarction

ST elevation in lead II higher than in lead III

ST iso-electric or elevated in lead I

ST iso-electric or depressed with negative T wave in lead

Proximal (with right ventricular infarction) or distal RCA?

Proximal RCA

ST elevation with positive T wave in lead

Distal RCA

Iso electric ST with positive T wave in lead

Posterior wall involvement?

ST depression in precordial leads

Lateral wall involvement?

ST elevation in leads I, AVL, and

Atrial infarction?

Pta segment elevation in lead II

Anterior wall infarction

LAD occlusion proximal to first septal and first diagonal branch

Acquired right bundle branch block

ST elevation lead AVR

ST elevation > 2mm in lead

ST depression in leads II, III and AVF

LAD occlusion distal to first septal and proximal to first diagonal branch

ST depression lead III> Lead II

Q in lead AVL

LAD occlusion distal to first diagonal and proximal to first septal branch

Signs of occlusion proximal to first septal branch

ST depression in lead AVL

Distal LAD occlusion

Q waves in leadsAbsence of ST depression in leads II, III and AVF

II

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

In acute myocardial infarction (MI) the surface electrocardiogram (ECG)

allows risk assessment in the individual patient by estimating the size of the

area involved This will be of help in selecting those patients most likely to

profit from reperfusion of that area Risk on admission can be assessed from

several variables 1) The total score of ST segment deviation reflecting the

severity of ischemia and global size of the ischemic area (1-3), 2) the heart rate

(3-5), 3) QRS width (3), 4) the terminal QRS-ST segment pattern (6,7), and 5),

by identifying the leads showing ST segment deviation, because they reflect the

site and size of the ischemic process As will be shown in this chapter the latter

usually allows to identify not only the culprit coronary artery, but also the site

of occlusion in that artery and thereby the area at risk This is important

because coronary arteries differ as far as the size of the ventricular area that

they perfuse In general the left anterior descending coronary artery (LAD)

supplies 50% of left ventricular mass and the right coronary artery (RCA) and

circumflex coronary artery (CX) each 25%

The size of a MI may differ between patients because of individual

variations of the coronary artery system and the site of occlusion in the culprit

vessel (proximal or distal) Also collateral circulation or multivessel ischemia

will influence the extent of the ischemic area This may sometimes lead to

paradoxical situations: ST segment elevation in the precordial leads can be

caused by RCA occlusion and ST segment elevation in the inferior leads by

LAD occlusion

To understand the findings on the ECG, it is helpful to look at the pattern

of ST segment elevation and depression in the different leads by applying the

vectorial concept of electrical forces (8)

A THE ST SEGMENT DEVIATION SCORE

The number of ECG leads showing ST segment deviation (elevation or

depression) and the ST segment deviation score (using the sum of ST segment

deviation in all 12 leads) are markers for the extent of the ischemic area in

acute coronary syndromes (9)

Soon after the introduction of thrombolytic therapy for treatment of acute

MI, it was shown that the greatest reduction in infarct size could be obtained in

patients showing a large ST segment deviation score (1,10,11) The absolute

ST segment deviation score was especially of great value in estimating the

extent of posterior ischemia in patients with infero-posterior infarction (12,13)

Hathaway et al (3) using the information from the GUSTO-I study showed

that the sum of absolute ST segment deviation added major information about

the area at risk and 30 days mortality of acute MI when included in a

nomogram for risk stratification on admission As shown in table 2-1 also

included in their nomogram were data on systolic blood pressure, heart rate,

QRS duration, age, height, diabetes, Killip class, prior MI and prior coronary

artery bypass grafting

9

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

It is important to know that in the very acute phase of ischemia locally

marked ST segment elevation may occur With ongoing ischemia the amount

of ST segment deviation stabilizes after 1 to 4 hours which is the time when

usually the first ECG is made (9)

For practical purposes it is useful to accept a 15mm value of ST segment

deviation as a figure indicating a large area at risk As will be discussed later,

especially in the precordial leads in anterior wall MI there may be a

discrepancy between the area at risk as determined from the ST segment

deviation score and ECG findings indicating the site of occlusion in the culprit

coronary artery

SEVERITY OF CARDIAC ISCHEMIA

As pointed out by Sclarovsky and Birnbaum (6,7) typical patterns of the end of

the QRS complex and ST segment morphology may be of prognostic

signifi-cance in acute myocardial infarction They divided the ischemic changes after

occlusion of the coronary artery into three grades (figs 2.1 and 2.2) Grade I is

characterized by tall, peaked, symmetrical T waves without ST segment

elevation Grade II shows ST segment elevation without changes in the

terminal portion of the preceding QRS complex; while in grade III ischemia,

apart from ST segment elevation, changes are present in the last part of the

QRS complex such as an increase in the amplitude of the R wave and

disappearance of the S wave

These serial ECG changes following acute coronary occlusion are related

to severity and size of the ischemic area However, decision making on

necessity and type of reperfusion therapy is usually based on the admission

ECG Sclarovsky and Birnbaum therefore called attention to two important

signs indicating distortion of the terminal portion of the QRS in grade III

ischemia: presence of the junction point more than 50% of the height of the R

wave in leads with a qR configuration, and disappearance of the S wave in

leads expected to have an RS configuration (6,7)

Several studies looked at the prognostic significance of the three grades of

ischemia on presentation (14-17) They indicated that ischemia grading on the

admission ECG correlated with in-hospital mortality, final infarct size, severity

of left ventricular dysfunction and late mortality Grade III ischemia had the

most ominous prognosis doubling early and late mortality as compared to grade

II ischemia It was also shown that early reperfusion therapy (within 2 hours

after onset of symptoms) resulted in similar beneficial results in grade II and

grade III ischemia This was no longer the case when such therapy was applied

later, grade III ischemia patients having a significantly higher in-hospital

mortality (18) This suggests that ischemia grading in relation to time interval

after onset of complaints can also give an indication of the reversibility of

cardiac ischemia The same authors also showed a higher incidence of

complications in grade III patients during hospital admission such as high

11

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

degree AV block and reinfarction (19) These date suggest that an early

primary percutaneous coronary intervention should be considered in patients

presenting with grade III ischemia

Birnbaum and Sclarovsky discussed why patients with grade III ischemia

on the admission ECG have worse short and long term prognosis and less

benefit from reperfusion therapy (7) They came to the conclusion that the

difference in infarct size between grade II and Grade III ischemia patients is

probably due to faster progression of necrosis in grade III ischemia possibly

related to thickness of the ventricular wall, lack of collaterals and lack of

protection by ischemic preconditioning (7)

OCCLUSION IN THE CULPRIT CORONARY ARTERY

In cardiac ischemia the direction and displacement of the ST segment is

determined by the sum of direction and magnitude of all ST vectors at that

point in time The resulting main vector will point in the direction of the most

pronounced ischemia This results in ST elevation in that area The opposite

area will record (reciprocal) ST segment depression Although no ischemia

may be present in that area, this is not excluded by the reciprocal changes The

lead perpendicular to the dominant vector will record an iso-electrical ST

segment (6) This vectorial concept is particularly useful when analyzing the

frontal plane leads In the horizontal plane the electrodes may be so close to the

myocardium that the local vector overrules the far field electrical forces

Infarction patterns are usually classified as inferoposterior and anterior It

will be shown that additional information from the ECG allows the recognition

of the culprit coronary artery and frequently the location of the occlusion in

that artery

I Infero-posterior wall infarction

Infero-posterior wall infarction is either caused by the occlusion of the RCA or

the CX and is characterized by ST segment elevation in leads II, III and AVF

Discriminating ECG features between these two coronary arteries are based

upon the specific anatomic location of these vessels

Coronary patho-anatomy

The perfusion areas of the RCA (1) and the CX are depicted in figure 2.3 The

RCA originates from the right aortic sinus It passes down the right

atrioventricular groove towards the crux, where it crosses the interventricular

septum and continues to the postero(lateral) area of the left ventricle The

following side branches are of importance: 2) The conus branch This branch

may provide blood flow to the basal part of the interventricular septum in case

of a proximal LAD occlusion(20) 3) The sinoatrial branch This vessel

originates in 60% from the RCA, and in about 40% from the CX (11 in fig 2.3)

13

and rarely from both arteries Involvement of this vessel may lead to sinus nodeischemia with sinus bradycardia, sino-atrial block and atrial infarction and mayfavor the occurrence of atrial fibrillation 4) The right ventricular branch, whichperfuses the anterolateral part of the right ventricle The RCA before the right

ventricular branch is called the proximal, thereafter the distal RCA Occlusion

of the proximal RCA leads to right ventricular (RV) infarction, with diminishedfunction of the RV, possibly leading to underfilling of the LV with hypotensionand cardiogenic shock In proximal RCA occlusion there is also a highincidence of high degree AV nodal conduction disturbances (see chapter 3) 5)The distal RCA has the acute marginal branch perfusing the posterior area ofthe RV 6) The posterior descending branch which brings blood to theinferobasal septum and the posteromedial papillary muscle Obstruction of flowleads to septal involvement, and possibly papillary muscle dysfunction andmitral regurgitation It may also result in block or conduction delay in theposterior fascicle of the left bundle branch, especially when also the proximalLAD is narrowed or occluded 7) The branch to the AV node 8) Theposterolateral branch(es) In case of a dominant RCA, occlusion may result in

posterior wall infarction, and even left lateral involvement The CX originates

from the main stem of the left coronary artery (9) and runs through the leftatrioventricular groove The CX usually gives one to three large obtusemarginal branches (12) supplying the free wall of the LV from superior to

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 15

inferior along the lateral border In case of a dominant CX one or more medial

posterobasal branches may arise from this vessel (13 in fig 2.3)

Dominance

The RCA is dominant in about 70% of cases, passing the interventricular

septum, giving rise to posterolateral branches In 30% of patients no RCA

dominance is present, the CX being dominant in about half of them In those

cases the CX is large and continues down to the diafragmatic surface of the

LV, where it gives rise to the posterolateral branches, reaching the crux, ending

in the posterior descending branch with a branch to the AV node It is very

important to recognize which vessel is dominant because this identifies patients

at risk for extensive myocardial damage with complications of heart failure,

ventricular arrhythmias and death

RCA or CX occlusion in acute inferior wall myocardial infarction?

Because of the different anatomic structures perfused and the resulting clinical

consequences in case of ischemia and necrosis, it is important to identify the

culprit coronary artery in infero posterior wall infarction As pointed out

before, both vessels perfuse the inferior part of the left ventricle, but the RCA

more specifically the medial part including the inferior septum, whereas the CX

perfuses the left postero basal and lateral area This results in a ST segment

vector directed inferior and rightward in case of a RCA occlusion versus an

inferior and leftward vector in CX occlusion (figure 2.4) In RCA occlusion the

ST vector will therefore result in more ST elevation in III than in II leading to

ST depression in lead I In case of CX occlusion the vector will point towards

lead II, leading to ST elevation or an isoelectric ST segment in lead I When the

vector points towards AW, the ST vector is perpendicular to lead I, resulting

in an iso-electric ST segment in lead I In our experience ST segmentdepression in lead I is predictive for RCA occlusion in 86%, and an iso-electric

or positive ST segment for CX occlusion in 77% Differences in dominancelead to absence of a 100% positive predictive accuracy

Figure 2.5, left, shows an example of an acute inferior wall infarction due

to RCA occlusion Marked ST elevation is present in the inferior leads LeadIII shows the most pronounced elevation, being higher than in II, resulting in adepressed ST segment in lead I Note that also the ST segment in lead AVL isnegative A greater ST segment depression in lead AVL than in lead I has alsobeen found to be highly predictive for RCA occlusion (21) The least negative

ST segment is found in lead AVR, indicating an almost perpendicularorientation of the ST vector in that lead ST segment elevation in lead AVR inthe setting of inferior wall infarction is rare and suggests in our experienceadditional proximal left coronary artery disease, or a dominant posterior

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION

Posterior wall involvement

Posterior wall involvement is diagnosed by finding reciprocal ST segment

depression in the precordial leads When present in RCA occlusion, it indicates

dominance of this vessel

In case of CX occlusion posterior wall involvement is almost obligatory

Absence of precordial ST depression in inferior wall infarction is therefore

strongly suggestive of RCA involvement (22) In figure 2.5, left, an example is

given of posterior wall involvement in RCA occlusion ST depression is

present in leads to with deepest negativity in lead In figure 2.5, right,

a CX occlusion is shown with ST depression in leads to

Recent data indicate that larger infarctions, more postinfarction

complications and a higher mortality rate occur in patients with precordial

ST-depression (20-22) As pointed out by Birnbaum et al (23) when the greatest

amount of ST depression is seen in leads 3-vessel disease and a low left

ventricular ejection fraction should be suspected

Isolated ST depression in the precordial leads may present the difficulty to

differentiate acute CX occlusion, resulting in true posterior wall infarction,

from nonocclusive anterior myocardial ischemia It has been suggested that in

that situation maximal ST depression in or is predictive for acute CX

occlusion (24-26) Also the recording of qR complexes with ST segment

elevation in leads has been recommended to diagnose a CX occlusion

(27,28)

Lateral wall involvement

Lateral wall involvement is reflected by ST segment elevation in leads and

It can be seen in both RCA or CX occlusion, but occurs more frequently in

the latter Independent of the vessel involved, ST segment elevation in these

leads implies a larger ischemic area and the need for aggressive reperfusion

therapy (29)

Figure 2.6 shows an inferior wall infarction due to RCA occlusion as

assessed by the typical changes in the extremity leads and the absence of ST

depression in the precordials ST elevation in and indicates lateral

involvement and therefore the presence of a dominant RCA

Figure 2.7 shows an example of a CX occlusion: there is only minor ST

elevation in the inferior leads, with most ST elevation in lead I, suggesting a

non dominant CX The vector in the frontal plane suggests a more high lateral

localization of the ischemia, consistent with a not very large obtuse marginal

branch Most ischemia is found in the left posterior wall, due to a prominent

posterolateral branch

17

descending branch perfusing large parts of the septum Figure 2.5, right, shows

inferior wall infarction due to a CX occlusion Most ST elevation is seen in

lead II, resulting in a positive ST segment in lead I The ST segment in AVR is

iso-electric indicating that the ST vector is perpendicular to that lead This

results in a markedly negative ST segment in lead AVL

RV infarction

In RCA occlusion the presence of RV involvement is important because it identifies a subgroup of patients at high risk (30-42) Clinically the patient may present with hypotension, frequently combined with bradycardia, due to sinus bradycardia or high degree AV nodal block AV-nodal conduction disturbances and late VT are more frequently encountered in inferior wall MI with RV involvement As also discussed in chapter 3, patients with AV nodal conduction disturbances have a higher mortality than patients without AV nodal conduction disturbances, also in the thrombolytic era (30-33) Diagnosing RV-involvement in inferior wall infarction is difficult from the standard 12 lead ECG The reason being that precordial leads overlying the RV

frequently record ST depression due to reciprocal ST segment changes

of ischemia of the posterior wall.

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 19

Therefore it is necessary to record the right precordial leads Figure 2.6

(right panel) shows ST elevation in the right precordial leads to

has been found to be especially useful for diagnosing right ventricular

involvement ST-elevation of predicts an occlusion proximal to the

RV-branch with an accuracy of 90% and ST-segment depression an

occlusion of the CX (fig 2.8) with an accuracy of 100% (43) An isoelectric

ST-segment predicts distal RCA occlusion (fig 2.9) It is important to stress

that sufficient ST-segment elevation in the inferior leads of the standard ECG

(at least 2mm) is needed to use the right precordial leads for determining the

site of coronary artery occlusion.

In a minority of cases of RV involvement the precordial lead shows elevation The sensitivity of ST elevation in lead is 24% but the specificity100% Figure 2.10 shows an acute inferior wall infarction due to RCAocclusion In lead the ST segment is elevated, indicating RV involvement.Even less frequent than ST elevation in only, as the result of RVinvolvement, is the finding of more leftward precordial leads with STelevation An example is shown in figure 2.11 The extremity leads indicateinferior wall infarction due to RCA occlusion The precordial leads todisplay ST elevation, most prominent in consistent with RV involvement.Lack of posterior wall ischemia leads to these findings because of ischemia ofthe relatively thin RV anterior wall This is confirmed by the positive rightprecordial leads (right panel).

ST-SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 21

Isolated RV infarction

Rarely the ECG shows only minor or no changes in the inferior leads and STelevation is only seen in leads and in the right precordial area Anexample is given in figure 2.12 This picture reflects a predominant RVinfarction and is related to a non dominant RCA, a collaterally filled RCA or anisolated occlusion of a RV branch (44) It may also be seen after occlusion ofthe RV branch following PTCA or stenting of the right coronary artery (45)

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 23

Atrial infarction

Atrial infarction may occur when a RCA or CX occlusion is proximal to thesinoatrial branch An example is given in figure 2.6 It shows slight elevation ofthe baseline following the P wave, best seen in lead II This Pta segmentelevation reflects the repolarization phase of the P wave The presence of atrialinfarction not only identifies a proximal RCA or CX occlusion, but isfrequently accompanied by sinus node dysfunction, sino-atrial conductiondisturbances and episodes of atrial fibrillation

AV nodal block

AV nodal block is common in inferior wall infarction, especially in case of aproximal RCA occlusion ECG features, prognostic significance andmanagement are discussed in chapter 3

Difficulties in diagnosing CX occlusion

One of the pitfalls in diagnosing acute MI is the underestimation of the areainvolved in CX infarction This is due to several causes: 1) The left ventriculararea supplied by the CX is activated in the second half of the QRS complex andtherefore both abnormalities in activation and repolarization may be obscured

by preceding and ongoing activation and repolarization of other areas of theheart 2) Posterior wall ischemia may only become manifest by ST segmentdepression and therefore unstable angina rather than MI is diagnosed In thatsetting it has been suggested that presence of maximal ST depression in leads

or is predictive for acute CX occlusion (24-26) Also the use ofadditional leads has been recommended (27,28) A finding in CXocclusion can be delayed activation of the posterolateral wall This can berecognized as a late positive deflection in lead I, and a late negative deflection

in leads III and AVF indicating that the terminal activation vector points to theleft baso lateral area (fig 2.5, right)

A clue pointing to an extensive CX infarction is shown in figure 2.13 Itshows an inferior wall infarction with an iso-electric ST segment in lead I,consistent with a CX occlusion The left and right precordial leads are inaccordance with that diagnosis

Suggestive of CX dominance is the clearly prolonged PR interval,indicating AV nodal involvement

II Anterior wall infarction

The left anterior descending branch (LAD) is usually the largest coronaryartery and supplies the anterior, lateral, septal and in 70% of humans the infero-apical segment of the left ventricle (figure 2.14) It also perfuses the bundle ofHis and the proximal part of the bundle branches The size of the ischemic areaand the prognosis is dependent on the site of occlusion in the LAD Dependingupon the site of LAD occlusion, apart from ST segment elevation in theprecordial leads, specific changes will occur in the extremity and lateral leads

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 25

Involvement of the distal AV conduction system leads to impaired conduction,

varying from intra hissal block to right bundle branch block (RBBB) with or

without left fascicular block, to complete sub AV nodal block (46) The clinical

picture may include heart failure and in the subacute phase ventricular

tachycardia and fibrillation may occur, leading to increased in-hospital and one

year mortality (47,48)

Anterior wall infarction is diagnosed by the presence of ST elevation in the

precordial leads to The challenge in anterior wall infarction is to

recognize the size of the area at risk and the site of the occlusion in the LAD

This information can be obtained by observing additional changes in the other

precordial and extremity leads

The ST segment vector to localize the site of ischemia

The anteroseptal area of the left ventricle which is perfused by the LAD can be

divided into 3 main parts: 1) The basoseptal part, supplied by the first septal

branch(es), 2) The lateral basal part, perfused by the first diagonal branch(es),

or intermediate branch, 3) The inferoapical part, receiving blood from the distal

LAD, frequently wrapped around the apex (figure 2.14, left panel)

As shown in a recent study by Engelen et al (49) occlusions at different sites(figure 2.14, right panel) lead to 4 electrocardiographically different pictures:

1 Proximal of the septal and diagonal branches This results in ischemia of all

3 named areas 2 Distal of the first septal and diagonal branches This leads toischemia of the inferoapical area only 3 Occlusion before the first diagonalbut distal of the first septal branch This leads to ischemia of the baso lateralwall and the infero apical wall but not the basal septum 4 Proximal before thefirst septal but distal of the first diagonal branch This leads to ischemia of theseptum and the inferoapical area, whereas the basolateral area remains free Inthe study by Engelen et al (49) the incidence of these sites of occlusion in theLAD territory were as follows: 40%, 40%, 10% and 10% respectively.Obviously, risk varies with these different sites of occlusion

LAD occlusion proximal to the first septal and the first diagonal branch High risk!

Typically the ECG shows one or more of the following findings Acquiredright bundle branch block, ST elevation in AVR, ST elevation of more than2mm in lead and ST depression in the inferior leads and in lead (42-44)

An example is given in fig 2.15 Figure 2.16 depicts the likely mechanism of

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 27

these findings: Global involvement of the left ventricle with contribution to the

ECG from all ischemic areas Because of the larger mass of the basal part the

vector of the ST segment will point in the superior direction (figure 2.16, left

panel) In the frontal plane this results in ST elevation in leads AVR and AVL

as the consequence of basal septal and lateral ischemia (figure 2.16, right

panel) The more cranially positioned lead will also record ST elevation

This upward orientation of the ST vector causes reciprocal ST depression in the

inferior leads (50) and also sometimes in the lateral leads Frequently

the ST vector points not only upward but somewhat more to the left than to the

right This results in more ST elevation in AVL than in AVR, and more ST

depression in lead III than in lead II Local conduction delay in the lateral leads

may lead to widening of the Q wave in lead AVL

Statistical values of criteria to identify a proximal occlusion are listed in table

2.2

Distal LAD occlusion Low risk.

Figure 2.17 shows an example of an acute anterior wall infarction due to adistal LAD occlusion (behind the major proximal septal and diagonalbranches) Typical findings are the presence of Q waves in leads andand the absence of ST depression in the inferior leads (53,54)

In this situation there is ischemia in the infero-apical part therefore the STvector will point inferiorly (figure 2.18 left panel)

The ST segment in the inferior leads will become isoelectric or evenpositive (figure 2.18, right panel) The Q waves in the left precordial leads arelikely due to the combination of local conduction delay in that area combinedwith persistence of the regular septal q wave in these leads

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 29

LAD occlusion distal to the first septal branch, but proximal to the first diagonal branch Intermediate risk.

Figure 2.19 shows the ECG of an acute anterior wall infarction with anocclusion site distal to the first septal, but proximal to the first diagonal branch.Typical features are: ST elevation in lead AVL and the left lateral leads and STdepression in lead III which is more pronounced than in lead II Figure 2.20shows a diagram with the distribution of ischemia in that situation, leading tothe ST segment vector pointing in a left lateral direction (left panel) Because

of that direction of the ST segment vector the difference in ST depressionbetween leads III and II is now much more pronounced than in the LADocclusion proximal to both the first septal and the first diagonal (fig 2.15)

SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 31

LAD occlusion distal to the first diagonal branch but proximal to the first

septal branch Intermediate risk

In this situation, the baso-lateral area is not involved, because the occlusion site

is distal to the first diagonal or intermediate branch (fig 2.21) Signs of an

occlusion proximal to the first septal branch are present such as ST elevation in

AVR and >2mm in with ST depression in In this situation the right

precordial lead has also been described to show ST elevation (55).

However, lead AVL now shows ST depression and the inferior leads positive

ST segments.

Figure 2.22 shows a diagrammatic presentation to explain the findings.

The left panel shows the rightward orientation of the ST segment vector,

leading (right panel) to most negativity of the ST segment in AVL and most

positivity in lead III, whereas leads AVR and II are less positive, or isoelectric.

Negativity in lead AVL is highly specific for an occlusion site below the first

diagonal branch (table 2.2).