Multimodal Cardiovascular Imaging: Principles and Clinical Applications

Chapter 7. Electrocardiography of Ischemic Heart Disease

Henrik Engblom; David G. Strauss

Introduction

The 12-lead electrocardiogram (ECG) is still the most frequently used diagnostic method in patients with suspected ischemic heart disease (IHD). Practically all patients presenting at the emergency room with chest pain have an ECG recorded to exclude or confirm unstable IHD and ongoing myocardial ischemia. In many regions, ECG is recorded in ambulances on patients with typical or atypical chest pain, dizziness, fainting, irregular heartbeat, and other clinical symptoms or signs. Furthermore, inducible ECG changes found during an exercise or pharmacologic stress test are frequently used to diagnose significant coronary artery stenosis in the situation of stable IHD. The frequent use of ECG as a diagnostic method in suspected IHD worldwide is due to several factors. First, the ECG provides a unique perspective of the condition of the myocardium by exploring its electrical activity, which is not depicted by other imaging modalities of the heart. Second, it is an inexpensive examination that is not associated with any risk for the patient, and it can be performed within a few minutes. Third, the technique is widely available, even in the developing parts of the world. Finally, the medical community has a long experience with the method because it has been around for more than 100 years.

Currently, the standard clinical ECG is displayed in 12 leads, 6 limb leads, and 6 precordial leads. This results in 12 views of the electrical activity of the myocardium. Body surface potential mapping (BSPM) is a method that provides additional views of the body surface potential distribution by performing recordings at multiple sites (24-240 sites) on the body surface. BSPM has evolved from the so-called classical forward and inverse problems of ECG. The former focuses on how the electrical activity from electrical sources present in the heart is propagated to the epicardium (near-field problem) or to the body surface (far-field problem).1 The latter focuses on how the electrical activity recorded at the body surface can be used to derive details about the electrical activity in the heart (ie, epicardial potentials).2 Both problems require high spatial resolution information from the body surface, which can be obtained through BSPM. Thus, BSPM has previously been shown to be useful for detecting myocardial infarction.3-6 BSPM will not be discussed further in this chapter.

Although there are clear advantages to using additional leads in certain circumstances, problems may occur even when using only the 10 electrodes of the standard 12-lead ECG. Multiple electrodes and wires interfere with auscultation, echocardiograms, resuscitation efforts, and chest x-rays. Noise levels due to limb movement detected by multiple leads make interpretation difficult, and the discomfort to patients caused by so many electrodes tends to be high. Additionally, rapid and accurate electrode placement can be difficult in emergency situations. Fewer electrodes placed at more easily accessed locations could facilitate ECG acquisition for both patients and staff. An example of a reduced lead set is the EASI lead system, which uses five torso electrodes, four recording and one ground. The EASI lead system has been shown to emulate the 12-lead ECG reasonably well,7-13 which can be advantageous in the emergency situation.14 Reduced-lead systems will not be discussed further in this chapter.

In vectorcardiography, the sum of the heart's electrical activity in three-dimensional space throughout the cardiac cycle is traced by using only three orthogonal leads, Vx, Vy, and Vz. Vectorcardiography has been shown to have substantial potential for monitoring patients with acute myocardial infarction15,16 and may help in identifying candidates for emergency coronary angiography.16 It has also been shown to correlate with enzymatically estimated infarct size.17 The use of vectorcardiography in IHD will be discussed further in subsequent parts of this chapter.

The rest of this chapter will focus on the pathophysiologic basis of ECG changes in IHD and the use of the standard 12-lead ECG for characterizing different aspects of this disease.

ECG Aspects of Myocardial Ischemia

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Pathophysiology of Myocardial Ischemia Due to Decreased Blood Supply

Myocardial ischemia is defined as an insufficient oxygen supply of the myocardium in relation to its oxygen demand. To put acute ischemia-related ECG changes into perspective of the serial events occurring in the myocardium in the situation of acute coronary occlusion, the following section will discuss the so-called ischemic cascade.18

Before discussing the consequences of myocardial ischemia, it is important to understand the cause of it. Blood flow to the myocardium can be partially reduced due to a coronary stenosis or completely absent due to coronary occlusion. The major pathophysiologic basis of coronary stenosis and occlusion is the formation of an atherosclerotic plaque in the coronary vessel wall. The severity of a coronary stenosis depends on the degree at which the stenosis obstructs the arterial lumen. If the atherosclerotic plaque becomes unstable and ruptures, the formation of a thrombus in situ starts, which results in occlusion of the coronary artery. Coronary occlusion can also result from embolization19 or spasm20,21 of the coronary artery.

The Ischemic Cascade in Coronary Occlusion

A sudden coronary occlusion, in the absence of a significant coronary collateral flow, results in transmural myocardial ischemia, which is the initial step of the ischemic cascade (Fig. 7–1). The steps of the ischemic cascade caused by sudden loss of coronary blood flow can be described as follows:

Figure 7–1.

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The ischemic cascade. The sequential events occurring after onset of myocardial ischemia are shown. ECG, electrocardiogram.

Myocardial ischemia: As the coronary artery is occluded, the perfusion to the part of the myocardium supplied by the occluded vessel is terminated, and this part of the myocardium becomes ischemic.
Diastolic dysfunction: Soon after the coronary vessel has been occluded, diastolic dysfunction can be observed in the myocardium supplied by the occluded vessel. The diastolic dysfunction is due to impaired myocardial relaxation. The relaxation is the first to be affected by the ischemia because it is the most energy-demanding process of the cardiac cycle. Normally, the myocytes relax by pumping cytosolic Ca2+ into the sarcoplasmatic reticulum or out of the cell. This process requires adenosine triphosphate (ATP). As the coronary artery becomes occluded, the oxygen supply to the myocardium distal to the occlusion is interrupted. The lack of oxygen results in a shift of the aerobic metabolism to anaerobic glycolysis within seconds.22 The high-energy phosphate reserve, available predominantly as creatine phosphate, is almost completely exhausted after 30 seconds of ischemia. Thus, there is an imbalance between ATP production and consumption.23 The latter exceeds the former, and the earliest result is dysfunctional myocyte relaxation.
Systolic dysfunction: As the ischemia persists, Ca2+ accumulates in the cytosol, which becomes acidotic and exhibits an increase in phosphate concentration.24,25 This eventually causes impairment of myocyte contractility and systolic dysfunction, which is the next step in the ischemic cascade.
ECG changes: The earliest and most consistent ECG alterations due to acute transmural ischemia are increased T wave amplitude and ST-segment elevation in ECG leads above the ischemic zone. These ECG changes occur due to injury currents induced in the border zone between ischemic and nonischemic myocardium.26-28 These ST-segment changes are discussed in detail later.
Angina pectoris: Eventually the accumulation of metabolites in the ischemic myocardium causes development of chest pain, so-called angina pectoris.29 The chest pain is often experienced in conjunction with pain radiating to the arms, neck, jaw, shoulders, or back. The accumulated metabolites (including adenosine) stimulate afferent cardiac nerves that fuse with afferent nerves from the organs mentioned earlier, explaining why myocardial ischemia can be experienced as extrathoracic pain.
Myocardial infarction: If the ischemia is severe enough and persists long enough without restoration of blood flow, the ultimate fate of the myocytes supplied by the occluded vessel is irreversible injury (cell death). If ischemia persists, the myocardial infarction will evolve from the endocardial border and progress toward the epicardium in a wave-front manner.30 If there is no restoration of blood flow, the infarction will ultimately involve the full thickness of the myocardial muscle wall, transmural myocardial infarction. Thus, the duration of ischemia is a major determinant of the transmural extent of infarction.31

Transmural Ischemia Due to Coronary Occlusion: ST-Segment Deviation

The ST-segment coincides with and is the result of the plateau phase of the ventricular transmembrane action potential. Under normal conditions, the ST segment is isoelectric because the transmembrane voltage remains at approximately the same levels in all ventricular myocytes during that time. Ischemia can reduce the resting membrane potential, shorten the duration of the action potential, and reduce the amplitude of the action potential plateau phase. These alterations of the electrical properties in ischemic myocardium result in abnormal voltage gradients between normal and ischemic myocardium. This voltage gradient induces an injury current, seen as deviation of the ST segment on the body surface ECG. As mentioned earlier, these injury currents arise in the border zones between normal and ischemic myocardium.26-28

There are two types of injury currents, a diastolic injury current and a systolic injury current. In the situation of transmural ischemia, the diastolic injury current causes a negative displacement (depression) of the diastolic TQ baseline due to a reduced resting membrane potential. This can partly be explained by increased extracellular K+ in the ischemic zone.32 As a result, a lead overlying the ischemic myocardium will detect a negative deflection during electrical diastole.

There is evidence suggesting that ST-segment elevation partly originates from a true elevation of ST segment caused by systolic injury currents. The shortening of the action potential and the decrease in its amplitude cause injury current to flow during electrical systole and cause ST-segment elevation and hyperacute tall T waves.33 Thus, ST-segment elevation can be explained by baseline depression or true ST-segment elevation or both,34-37 which is illustrated in Fig. 7–2. ST-segment elevation is measured at the J point, the time where the QRS complex ends and the ST segment starts.

Figure 7–2.

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Typical myocardial cell action potentials (upper curves) and body surface electrocardiograms (lower curves) that represent various degrees of ischemia (b), injury (c), and cell death (necrosis). Curves labeled "a" represent the normal pattern. Reproduced with permission from Selvester et al.46

If the ischemic injury is transmural, the overall ST vector is directed toward an overlying lead that then exhibits ST-segment elevation. Hence, transmural ischemia can be seen as ST-segment depression in leads in which the lead axis is opposite to the leads with ST-segment elevation. This can be seen, for example, when the posterolateral left ventricular (LV) wall is subject to transmural ischemic injury, when the typical change in the standard 12-lead ECG is ST-segment depression in leads V1 and V2.38 This is because the ST vector is directed away from the exploring V1 and V2 electrodes. Thus, in this situation, ST-segment depression should be considered indicative of transmural ischemic injury.

According to current guidelines,39 the predetermined threshold for ST-segment elevation (age, sex, and ECG lead dependent)40-42 should be exceeded in two or more anatomically contiguous ECG leads in order to be indicative of acute transmural myocardial ischemia. The currently recommended threshold values of ST-segment changes are listed in Table 7–1.

Table 7–1. Threshold Values for ST-Segment Changes

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Table 7–1. Threshold Values for ST-Segment Changes

ST-Segment Elevation

ST-Segment Depression

For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.

For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.

For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).

For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.

For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.

For men and women, the threshold value for abnormal J-point elevation in V7 through V9 should be 0.05 mV (0.5 mm).

ST-segment elevation can also occur in the absence of myocardial ischemia. In the situation of early repolarization, ST-segment elevation is characterized by J-point elevation and rapid upslope or normal ST segment, which is considered a normal variant. ST-segment elevation can also be associated with pericarditis, elevated serum potassium, acute myocarditis, Osborne waves (caused by hypothermia), and certain cardiac tumors. Thus, it can be a clinical challenge to differentiate acute transmural ischemia from other causes of ST-segment elevation. However, criteria have been suggested that can be applied to differentiate ST-segment elevation caused by acute myocardial ischemia from that resulting from other causes.43

Clinical Implications

The ECG is still the most important diagnostic method in the situation of suspected acute coronary occlusion. All patients who present at the emergency department with symptoms associated with myocardial ischemia should undergo an ECG examination. If ST-segment elevation above the predetermined thresholds (see Table 7–1) is seen in two or more anatomically contiguous body surface ECG leads in the situation of suspected acute coronary syndrome, the patient is likely to suffer from transmural ischemia due to a coronary occlusion and is in need of acute reperfusion therapy. Development of infarction after such an event is clinically referred to as ST-segment elevation myocardial infarction (STEMI). Patients who develop infarction with ST-segment elevation below the predetermined thresholds or without ST-segment elevation are clinically diagnosed as having non–ST-segment elevation myocardial infarction (NSTEMI).

ECG Aspects of Myocardial Infarction

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Pathophysiology of Myocardial Infarction

The definition of myocardial infarction is, as discussed earlier, cell death due to prolonged myocardial ischemia. Cell death can be identified pathologically by identification of specific histologic patterns such as coagulation or contraction-band necrosis. By pathology, the infarction can be localized and quantified, as well as classified, according to the timing of the infarction (acute, healing, or healed) by description of the ultrastructure of the infarction and the presence of polymorphonuclear leukocytes.

The clinical diagnosis of acute myocardial infarction is defined by a rise of cardiac biomarkers such as creatine kinase isoenzyme MB (CK-MB) and cardiac troponin T or I (cTnT or cTnI) together with evidence of myocardial ischemia with at least one of the following: (1) symptoms of ischemia; (2) ECG changes indicative of acute ischemia/infarction; (3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.44

Infarct-Related ECG Changes

The final stage of the ischemic cascade is, as previously discussed, myocardial infarction. Because the acute injury currents have subsided, the remaining ECG abnormalities are due to the resulting infarction. The infarction will affect the local activation sources of the myocardium seen as changes primarily in the QRS complex. The infarction might also cause persistent alteration of the repolarization, resulting in remaining T wave alterations.45 The magnitude and extent of infarct-related QRS complex changes in different leads depend on the location and extent of infarction.

The myocardial activation (depolarization) vector is the result of all parts of the myocardium that are being depolarized at a given time point. The result of the time-resolved propagation of the depolarization vector during the cardiac cycle is what causes the deflections of the QRS complex seen in different leads. The degree to which the normal depolarization vector changes after an acute myocardial infarction depends on the characteristics of the infarction such as the location, size, endocardial extent, and transmural extent.

The Pathologic Q Wave

If the initial depolarization forces are directed away from an exploring lead, the initial QRS deflection in that lead is negative and results in a Q wave. Presence of Q waves in leads that normally do not exhibit initial negative depolarization forces can be a sign of myocardial infarction in the underlying myocardium. Myocardial infarction can, however, result in other changes in the QRS complex depending on its location. If the infarction is isolated to the posterolateral LV wall, the alteration in the QRS complex is not the appearance of Q waves, but rather prominent R waves in leads V1 and V2. In fact, 10% of all infarcts are limited to the basal parts of the LV and do not produce Q waves.46 Still, the terms Q wave myocardial infarction (QWMI) and non–Q wave myocardial infarction (non-QWMI) are well-established clinical entities, although the differences in infarct characteristics between QWMI and non-QWMI are not completely understood. Furthermore, the prognostic impact of Q wave development is still controversial.47 Historically, the development of pathologic Q waves after acute coronary occlusion has been associated with transmural myocardial infarction. Based on animal studies, Prinzmetal et al48 stated that transmural myocardial infarction was required for pathologic Q waves to appear. More recently, however, histopathology49-51 studies have shown that Q waves in the ECG are not as closely related to transmural myocardial infarction as previously reported. In the past, however, it has been difficult to establish the pathologic basis for Q waves in humans due to lack of accurate in vivo methodology. Recent advances of different imaging modalities have enabled studies of the pathophysiologic basis of infarct-related ECG changes. Such studies are discussed in the last section of this chapter.

Clinical Implications

The resting standard 12-lead ECG is often used clinically to report on the presence of myocardial infarction based on infarct-related QRS and T wave changes. A newly detected pathologic Q wave is a common cause for outpatients to be referred to a cardiologist in order to rule out or confirm coronary artery disease. Thus, it is important to understand the ability and limitations of the standard 12-lead to detect and quantify myocardial infarction.

Quantitative Assessment of Myocardial Ischemia and Infarction Using the 12-Lead ECG

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ECG Analysis of Ischemia Location, Size, and Severity

Figure 7–3 is an illustration and mathematical characterization of solid angle theory by Holland and Arnsdorf52 in the 1970s, produced at a time when many investigators were using epicardial and precordial ST-segment mapping to determine the size and severity of ischemia.53,54 Holland et al55 performed a series of experiments in pigs and showed that the amount of ST-segment elevation is affected by the size and shape of the ischemic zone in relation to the anatomic location of the ECG lead.

Figure 7–3.

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Mathematical and pictorial characterization of solid angle theory. The amount of observed ST-segment elevation is proportional to the solid angle (Ω), defined as the area of spherical surface cut off a unit sphere (inscribed about the recording electrode) by a cone formed by drawing lines from the recording electrode to every point along the ischemic boundary. The ischemic boundary is a source of electrical current flow established by differences in the transmembrane potentials of the normal (VN) and ischemic (VI) cells during electrical systole and diastole. Thus, the amount of observed ST-segment elevation is determined by the size and shape of the ischemic zone, along with the difference in potential between ischemic and normal cells, and a term (K) to correct for differences in conductivity between the intra- and extracellular spaces. Reprinted from Holland RP, Arnsdorf MF. Solid angle theory and the electrocardiogram: physiologic and quantitative interpretations. Prog Cardiovasc Dis. 1977;19:431-457, Copyright 1977, with permission from Elsevier.

In the 1980s, as thrombolytic therapy moved into widespread use, investigators sought to use the 12-lead ECG to quantify the size of ischemia. In 1988, Aldrich et al56 developed an ST-segment deviation score for use in acute anterior and inferior myocardial infarction, and later, a score was developed for posterolateral myocardial infarction.57 The scores were developed by assessing the relationship between the predischarge ECG QRS score estimation of final infarct size and the number of leads with and the amount of ST-segment deviation on the presenting ECG. Because the patients did not receive reperfusion therapy, it was assumed that the entire region of ischemic myocardium at risk would infarct. The Aldrich score has been used in multiple studies to estimate myocardium at risk.58,59 However, it did not have a strong correlation with myocardial perfusion single photon emission computed tomography (SPECT) measurements of ischemia size.60 Simplified ECG approaches to estimate myocardium at risk are confounded by differences in distance between each LV wall and individual electrodes and by the fact that the magnitude of the ischemic vector is proportional to 1/distance2.

In contrast to the 12-lead ECG, where the amount of ST-segment elevation in each lead is affected by the distance and location of the individual lead according to the solid angle theorem,52 a single vector from a vectorcardiography might better correlate with the size of ischemic myocardium. Prior studies have used continuous monitoring of vectorcardiography changes to quantify myocardial ischemia and infarction.61-65 In addition, the Frank vectorcardiography lead system66 has been used to compare ST-vector magnitude changes to myocardial perfusion SPECT estimates of the size and severity of ischemia.67-69 A recent study used the inverse Dower transformation to convert the 12-lead ECG to a vectorcardiogram and projected the vector to a model of the LV to localize ischemia. In addition, the ST-vector magnitude was shown to correlate with ischemia size by myocardial perfusion SPECT.70

The Sclarovsky-Birnbaum ischemia grading system was introduced in 1990 and is now considered to be a method for estimating the severity of ischemia.71,72 It is based on assessment of changes in the terminal part of the QRS complex and in the ST segment. The ischemia grading system consists of three grades representing increasing severity: grade I is characterized by tall upright T waves without ST-segment elevation, grade II is characterized by ST-segment elevation in at least two adjacent leads without terminal QRS distortion, and grade III is characterized by ST-segment elevation with terminal QRS distortion in two or more adjacent leads. Observational studies have shown that patients with grade III ischemia have worse prognosis, larger myocardial infarction size, and less benefit from reperfusion therapy.73-75

ECG Acuteness (Time-Course) of Ischemia

The Anderson-Wilkins score for estimating the acuteness of ischemia was introduced in 1995.76,77 It describes a continuous scale from 4.0 (hyperacute) to 1.0 (subacute) based on the comparative hyperacute T waves versus abnormal Q waves in each of the leads with ST-segment elevation or tall T waves. The Anderson-Wilkins score considers each standard lead (except aVR) with at least 0.1-mV ST-segment elevation or tall T waves based on the criteria of Gambill et al.78 Acuteness phase is designated for each of these leads based on the presence or absence of a tall T wave or an abnormal Q wave (Table 7–2), with phase 1A being the most acute (early ischemia) and phase 2B being the least acute (late ischemia/completed infarct).

Table 7–2. Algorithm for Designating the ECG-Time Phase

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Table 7–2. Algorithm for Designating the ECG-Time Phase

Tall T Wave Present (A)

Tall T Wave Absent (B)

Q wave absent (1)

1A = 4 points

1B = 3 points

Q wave present (2)

2A = 2 points

2B = 1 point

ECG, electrocardiogram.

The acuteness score is calculated by the following formula:

The Anderson-Wilkins acuteness score has demonstrated clinical prognostic value. The score was predictive of 1-year mortality after myocardial infarction (P = .04), whereas time from symptom onset to reperfusion was not predictive of mortality (P = .60).79 In addition, ECG estimates of the relationship between ischemia size and final myocardial infarct size have suggested that the Anderson-Wilkins acuteness score predicts myocardial salvage.79

ECG Characterization of Infarction

After the description by Pardee80 in 1920 of the ECG changes of myocardial infarction, multiple studies looked at the ability of the ECG to detect and localize myocardial infarction with varying results.81

Pathology studies in the 1950s and 1960s reported a low sensitivity of conventional ECG criteria for myocardial infarction.82-84 However, pathology studies often involved the sickest patients with multiple infarcts. In the 1970s, Savage et al85 used detailed postmortem histologic analyses of hearts with computer digitization of infarct location in patients with single, well-circumscribed infarcts to document the relationship between ECG changes and infarct location. They showed that anteroseptal myocardial infarctions were associated with Q waves or markedly diminished R waves in V1 to V3; that inferior myocardial infarctions were associated with Q waves or markedly diminished R waves in II, III, and aVF; and that significant apical myocardial infarction was associated with Q waves or markedly diminished R waves in V4 to V6.85 This led to the detailed testing of the so-called Selvester QRS scoring system to identify, localize, and quantify myocardial infarction.

Traditionally, the Minnesota coding system has been used to diagnose myocardial infarction.86 The Minnesota coding system was developed to detect rather than quantify the amount of infarction from ECG changes. Pahlm et al87 have shown that the Minnesota coding system correlates poorly with anatomically determined infarct size.

QRS Infarct Scoring in the Absence of ECG Confounding Factors

Based on mapping data of the electrical depolarization in isolated human hearts by Durrer et al,88 Selvester and colleagues developed a computer simulation of the human ventricular depolarization. This computerized model was used to derive a QRS scoring system by simulating infarction in different parts of the LV.89,90

In the 1980s, different versions of the Selvester QRS score were evaluated.91-96 In the 1985 version of the QRS score, it was noted that the score performed best in patients 40 to 50 years old.95 False-positive points were most common in younger males who have increased voltages and older females who have lower voltages.95 Later work reevaluated the specificity of the QRS score in approximately 3000 normal patients and made age and sex adjustments to the score.97 Absolute amplitude criteria (not ratios) were normalized to age 55 by increasing them 1% per year for age 20 to 54 and decreasing them 1% per year for ages greater than 55 years. For females, duration and amplitude criteria were further decreased by 10%. In addition, some R and S amplitude criteria in the precordial leads were tightened by 0.1 to 0.2 mV.

Numerous studies have tested the potential clinical utility of QRS scoring, including the ability to predict LV ejection fraction,98 prognosis,99,100 and response following coronary artery bypass surgery.101

QRS Infarct Scoring in the Presence of Hypertrophy and Conduction Defects

Bundle branch and fascicular blocks can have multiple etiologies, including myocardial infarction, degenerative changes that occur at the base of the septum around the aortic-mitral annulus, idiopathic sclerosis of the conduction system, and increased mechanical stress and strain on the fibrous skeleton of the conduction system.102 Fascicular blocks, bundle branch blocks, and hypertrophy have traditionally been thought to simulate or conceal the typical ECG signs of myocardial infarction.103,104 However, computer simulations suggested that once the correct underlying activation sequence is taken into account, modified ECG criteria can be developed to detect and quantify myocardial infarction in each of these conduction/hypertrophy (ECG confounding factor) subtypes.46,105 Until recently, the QRS scores for use in the presence of confounders had not been systematically evaluated due to the inability to collect a sufficient number of patients with infarcts and each of the conduction/hypertrophy subtypes. Using late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR) as a reference standard for myocardial infarction or scar, the QRS scores for use in the presence of hypertrophy and conduction defects correlated with CMR infarct/scar size (r = 0.60-0.80; P < .001).106 Subsequent studies have shown that these QRS scores may have clinical value in predicting the risk of implantable defibrillator shocks107 and response to cardiac resynchronization therapy.108,109

The following will discuss how the different conduction and hypertrophy types affect electrical activation and the ability to detect myocardial infarction or scar.

In left bundle branch block (LBBB), ventricular electrical activation begins in the endocardium of the right ventricle (RV) and proceeds through the septum to the endocardium of the LV (Fig. 7–4C).46,110,111 With a septum of normal thickness, this takes approximately 40 ms, and it then takes an additional 50 ms for electrical activation to reenter the Purkinje network and propagate through the anterosuperior and inferior walls. The posterolateral wall is activated last in another 50 ms, producing a total QRS duration of at least 140 ms.112 This is consistent with the Grant and Dodge113 observation that the QRS duration in new-onset LBBB is consistently greater than 140 ms, and thus, patients with a QRS duration of 120 to 140 ms likely do not have LBBB, but rather a combination of LV hypertrophy (LVH) and/or left anterior fascicular block (LAFB). The criteria for LBBB QRS scoring in the limb leads (I, II, aVL, and aVF) are similar to criteria in other conduction types in that Q waves and small R waves are signs of myocardial infarction. However, the criteria are drastically different in the precordial leads, where an anteroseptal myocardial infarction causes large R waves in leads V1 and V2, rather than Q waves as in normal conduction (Fig. 7–5).

Figure 7–4.

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Ventricular activation sequences, electrocardiogram waveforms, and vector loops (vectorcardiograms) in the frontal and transverse planes. The frontal and transverse planes are shown in normal conduction (A), left anterior fascicular block (LAFB) + right bundle branch block (RBBB) (B), and left bundle branch block (LBBB) (C). Colored lines represent areas of myocardium activated within the same 10-ms period (isochrones). Numbers represent milliseconds since beginning of activation. Modified from Strauss DG, Selvester RH. The QRS complex—a biomarker that "images" the heart: QRS scores to quantify myocardial scar in the presence of normal and abnormal ventricular conduction. J Electrocardiol. 2009;42:85-96, Copyright 2009, with permission from Elsevier.

Figure 7–5.

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Electrical activation sequence in left bundle branch block (LBBB) and the effect of septal scar. A. LBBB conduction begins in the endocardium of the right ventricle (RV), and electrical forces from the septum and RV free wall go in opposite directions and cancel each other out, producing an isoelectric segment or small R wave in leads V1 to V3. However, in the presence of septal scar (B), the RV free wall forces are unopposed, producing large R waves in leads V1 to V3. LV, left ventricle. Modified from Strauss et al.106

In right bundle branch block (RBBB), ventricular activation of the LV is unaffected, but RV activation does not occur until the activation wave front proceeds through the septum. Thus, the RV free wall is activated late, producing a late positive deflection (R or R′) in leads V1 and V2.46,111,114 This confounds the diagnosis of posterolateral infarcts; thus, the scoring system's R wave criteria in V1 and V2 are modified. In addition, there is a change in V1 and V2 for large anterior infarcts.

Ventricular hypertrophy and chamber enlargement frequently occur in combination with conduction defects. Although most ECG criteria for ventricular hypertrophy consider only QRS voltage changes,115 the combined Cornell time-voltage index or QRS area measurement improves the diagnosis of LVH.116 Consideration of the time effects of hypertrophy can be especially important when patients have combinations of hypertrophy and conduction defects.112 The LVH QRS score should be applied to patients who have LVH (by ECG voltage criteria) without other conduction defects. The QRS score criteria for the other conduction types can be applied even if LVH is present. The principal differences between the LVH and no-confounder QRS score is that QS complexes (Q waves without an R wave) in V1 to V3 do not always receive points, but notches in the first 40 ms of these leads do receive points.

RV hypertrophy (RVH) causes large R waves in V1 and V2 that can mimic posterolateral infarcts in all conduction types except LBBB, where RVH mimics anteroseptal infarcts. If large R waves are present, then the P waves should be analyzed for signs of right atrial overload (RAO), which generally accompanies RVH.46 If the P waves suggest RAO, then large R waves in V1 and V2 should be assumed to be due to RVH and should not receive QRS points.

LAFB only causes 20-ms prolongation104,117; however, additional LVH can cause a total QRS duration of up to 140 ms or more.46,118 Thus, patients with intermediate QRS duration between 120 and 140 ms likely have LAFB and LVH or LVH alone, and not LBBB.113 Figure 7–4B shows combined activation of LAFB and RBBB. Left posterior fascicular block (LPFB) does not affect the scoring system because it was included in the computer simulations for inferior infarcts.105

Multimodal Imaging to Uncover the Pathophysiologic Basis for ECG Changes Related to Myocardial Ischemia and Infarction

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In order to understand the pathophysiologic basis for ECG changes related to myocardial ischemia and infarction, it is of great importance to have access to other diagnostic imaging modalities. The following section discusses examples of situations where multimodal imaging strategies have been applied in order to better understand the ECG mechanisms and findings in IHD.

Myocardial Ischemia by ECG Compared with Myocardial Perfusion SPECT

Myocardial perfusion SPECT is considered the gold standard for quantification of myocardial perfusion defects. As mentioned earlier, the Aldrich score was shown not to have a strong correlation with myocardial perfusion SPECT.60 Myocardial perfusion SPECT has enabled further studies of ECG measures of ischemia. Recently, Ubachs et al119 showed that the distribution of ST-segment elevation during acute coronary occlusion can be used to locate the ischemic area depicted by myocardial perfusion SPECT (Fig. 7–6). Other approaches for localizing and quantifying the extent of myocardial ischemia during acute coronary occlusion have been proposed and compared with myocardial perfusion SPECT (Figs. 7–7 and 7–8).120-122

Figure 7–6.

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Polar plot representation of myocardium at risk (MaR). Polar plots generated from rest technetium 99m–tetrofosmin single photon emission computed tomography (SPECT) perfusion, cardiovascular magnetic resonance imaging (MRI) wall thickening, and electrocardiography (ECG) for all patients (patient numbers are shown) with left anterior descending artery (LAD), right coronary artery (RCA), and left circumflex artery (LCx) occlusion. Underneath each polar plot, the designated culprit arteries by the two observers are stated as observer 1/observer 2. Note the similarity in the location of MaR by the three modalities. Reproduced with permission from Ubachs et al.119

Figure 7–7.

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The display of ischemic myocardium from simulated (DIMS) electrocardiography (ECG) method. A. Twelve-lead ECGs for three patients who underwent prolonged coronary angioplasty. The ECGs were recorded before balloon deflation. Patient 1 had a left circumflex artery occlusion, patient 2 had a right coronary artery occlusion, and patient 3 had a left anterior descending artery occlusion. B. The single photon emission computed tomography (SPECT; left column) and DIMS-ECG (right column) polar plots for the same three patients. Color scales show the distribution of ischemic to nonischemic myocardium for SPECT and the predicted ischemic to nonischemic scale for DIMS-ECG. Reproduced with permission from Galeotti et al.121

Figure 7–8.

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ST compass method. A. To create ST compass plots, the level of ST-segment deviation in each lead is measured automatically in the J point, and each ST measurement is plotted in the ST compass. ST-segment elevation is marked as an arrow from the center of the compass in the positive direction of the relevant lead. ST-segment depression is marked as an arrow from the center of the compass pointing in the opposite direction of the lead in question. The size of the arrow is determined by the magnitude of the ST-segment deviation. Finally, the ST injury vector that best fits all measured ST-segment deviations can be estimated. ST compass method. B. Examples of MPIs and ST injury vectors for three acute myocardial infarction patients with occlusion of the left anterior descending artery (LAD), right coronary artery (RCA), and left circumflex artery (LCx). There is strong agreement between the anatomic location of ischemia and the corresponding ST injury vector. The LAD patient shows apical anterior ischemia resulting in a large-magnitude anterolateral ST injury vector. The RCA patient shows inferior (slightly septal) ischemia resulting in a medium-magnitude posteroinferior (slightly septal) ST injury vector direction. The LCx patient has inferior (slightly lateral) ischemia, which results in a posteroinferior (slightly lateral) ST injury vector of medium magnitude. ECG, electrocardiogram; MPI, myocardial perfusion imaging; SPECT, single photon emission computed tomography. Reproduced with permission from Andersen MP, Terkelsen CJ, Sorensen JT, et al. The ST injury vector: electrocardiogram-based estimation of location and extent of myocardial ischemia. J Electrocardiol. 2010;43:121-131.

Infarct Characteristics by ECG Compared with CMR

Currently, LGE CMR is considered the gold standard for infarct visualization in vivo. In order to determine the location of infarction based on infarct-related ECG changes, Bayes de Luna et al123 suggested a novel terminology based on LGE CMR findings of infarct location in relation to the 17-segment model124 used to standardize description of different parts of the LV (Fig. 7–9). Thus, the 17-segment model facilitates multimodal imaging approaches.

Figure 7–9.

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The electrocardiogram (ECG) patterns of Q wave myocardial infarction or Q wave equivalents with the names given to myocardial infarction and related infarction area documented by cardiovascular magnetic resonance (CMR). Purple color indicates area of infarction. Reproduced with permission from Bayes de Luna et al.123

Recent imaging studies125-128 have confirmed previous histopathology findings49-51 that the association between pathologic Q waves and transmural myocardial infarction is weaker than previously presumed. Using CMR, it has been shown that endocardial extent of infarction seems to be more important for presence of pathologic Q waves than transmural extent of infarction (Fig. 7–10).129 Furthermore, it was shown that the Selvester QRS scoring system can be used to estimate transmural extent of infarction in patients with early reperfused acute myocardial infarction.127

Figure 7–10.

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Three cases illustrating the importance of the endocardial extent of infarction and its location for the QRS score. A. A small transmural, non–Q wave myocardial infarction in the inferior left ventricular (LV) wall with a QRS score of 0 and myocardial infarction size of 2% of the LV by late gadolinium-enhanced (LGE) cardiovascular magnetic resonance (CMR). B. A nontransmural, Q wave myocardial infarction in the inferior LV wall with a QRS score of 8 with the following criteria met: Q duration >30 ms in lead II; Q duration >40 ms and R/Q ratio <1 in lead aVF; R duration >40 ms in lead V1; R duration >50 ms in lead V2; and Q duration >30 ms in lead V6. Infarct size by LGE CMR was only 7% of the LV. The endocardial extent, however, measured 24% of the LV endocardial extent, closely resembling the QRS score of 8 (24% of the LV). C. A transmural, non–Q wave myocardial infarction in the posterolateral LV wall. This patient had prominent R waves and small S waves in V1 and V2 suggestive of posterolateral myocardial infarction. Arrows indicate either myocardial infarction by LGE CMR or QRS changes generating QRS points. 2ch, two-chamber long axis view. Reproduced with permission from Engblom et al.127

Recovery of infarct-related ECG changes after acute myocardial infarction has previously been described.130-132 Until recently, however, it has been difficult to establish the anatomic correlate of these changes due to lack of an accurate in vivo method for infarct visualization. Recently, the recovery of infarct-related QRS changes in relation to infarct involution during the first year after reperfused myocardial infarction as assessed by CMR has been demonstrated.133 This study showed that the timing and magnitude of the recovery of QRS changes was similar to that observed for infarct involution (Fig. 7–11).

Figure 7–11.

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Changes in hyperenhanced myocardium in relation to changes in two representative electrocardiogram leads over time affecting the QRS score in a patient with a right coronary artery occlusion. Note the QRS notch (arrows) in the QS complex in aVF seen on days 7 to 365, indicating viable myocardium in the peri-infarction zone, which decreases the QRS score. Also note the increasing R wave amplitude and decreasing Q wave amplitude and duration over time in lead II, also affecting the QRS score. Reproduced with permission from Engblom et al.133

Figure 7–12 shows the ECG and CMR images from a patient with LBBB and inferior and posterolateral infarcts, demonstrating how infarcts can be detected even in the presence of LBBB.

Figure 7–12.

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Electrocardiogram (ECG) and short axis cardiovascular magnetic resonance (CMR) images from a patient with left bundle branch block and ischemic cardiomyopathy due to inferior and posterolateral infarcts comprising 23% of the left ventricle (LV) by CMR and that received 8 QRS points (ECG-estimated scar = 24%). Note the large S/S′ ratio in V1 and V2, which reflects posterolateral scar. For the CMR images, the regions with solid scar ("core") are shown in red, and the regions with heterogeneous scar and live myocardium ("gray zone") are shown in yellow. For comparison with the QRS score, total CMR scar was defined as core + 1/2 gray. Reproduced with permission from Strauss et al.106

It is desirable to further develop multimodal approaches for two- and three-dimensional coregistrations of advanced ECG imaging and non-ECG imaging techniques to enable better understanding of the pathophysiologic basis of IHD and perhaps to improve management of patients suffering from IHD.

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Chapter 7. Electrocardiography of Ischemic Heart Disease

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Introduction

ECG Aspects of Myocardial Ischemia

Pathophysiology of Myocardial Ischemia Due to Decreased Blood Supply

The Ischemic Cascade in Coronary Occlusion

Figure 7–1.

Transmural Ischemia Due to Coronary Occlusion: ST-Segment Deviation

Figure 7–2.

Clinical Implications

ECG Aspects of Myocardial Infarction

Pathophysiology of Myocardial Infarction

Infarct-Related ECG Changes

The Pathologic Q Wave

Clinical Implications

Quantitative Assessment of Myocardial Ischemia and Infarction Using the 12-Lead ECG

ECG Analysis of Ischemia Location, Size, and Severity

Figure 7–3.

ECG Acuteness (Time-Course) of Ischemia

ECG Characterization of Infarction

QRS Infarct Scoring in the Absence of ECG Confounding Factors

QRS Infarct Scoring in the Presence of Hypertrophy and Conduction Defects

Figure 7–4.

Figure 7–5.

Multimodal Imaging to Uncover the Pathophysiologic Basis for ECG Changes Related to Myocardial Ischemia and Infarction

Myocardial Ischemia by ECG Compared with Myocardial Perfusion SPECT

Figure 7–6.

Figure 7–7.

Figure 7–8.

Infarct Characteristics by ECG Compared with CMR

Figure 7–9.

Figure 7–10.

Figure 7–11.

Figure 7–12.

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References

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