Myocardial Ischemia and Infarction, Part I: ST Segment Elevation and Q Wave Syndromes

Myocardial Ischemia and Infarction: General Considerations

Myocardial cells require oxygen and other nutrients to function. Oxygenated blood is supplied by the coronary arteries. If severe narrowing or complete blockage of a coronary artery causes blood flow to become insufficient to meet oxygen and nutrient demands, ischemia of the heart muscle develops. This notion underlies the intuitive, “econometric” concept of ischemia as related to a mismatching (ratio) of supply “over” demand such that the denominator exceeds the numerator.

From a clinical perspective, myocardial infarctions (MIs) and myocardial ischemic events more broadly have been classified into two major groups or types. Type I MI is caused by abrupt total or near total blockage of blood flow (zero or near zero supply) through a major, epicardial coronary artery or one of its branches. Type I MIs, in turn, are subclassified into (1) those resulting from severe atherosclerotic disease, the most common substrate, and (2) those resulting from nonatherosclerotic occlusions (e.g., coronary artery dissection, coronary spasm, or embolism). Type II MIs, in contrast, occur when excessive oxygen demand causes severe ischemia despite the presence of normal or even increased myocardial blood supply. There are numerous causes of type II MIs (many of which are primarily noncardiac in etiology), as exemplified by those occurring with profound and sustained stresses due to hypoxemia, blood loss, tachyarrhythmia, or severe hypertension. Type II infarctions may occur in the context of chronic, nonocclusive coronary artery disease or cardiomyopathy. Thus, the two primary classification categories are not mutually exclusive. Clinicians should recognize that not uncommonly patients will have ischemia or MI due to a combination of atherosclerotic coronary disease and increased myocardial demand. We discuss the use of cardiac stress tests to unmask latent ischemia caused by partial coronary blockages in the next chapter.

Three key factors determine left ventricular myocardial oxygen demands: (1) the heart rate (chronotropic state), (2) the strength of its contractions (contractility or inotropic state), and (3) the systolic pressure developed in the main pumping chamber, which is usually the most important variable in determining the ventricular wall tension.

Myocardial ischemia, without MI, may occur transiently. For example, patients who experience typical angina pectoris (often but not always described as discomfort in the central chest area) often report this symptom with exertion, which increases all three determinants of myocardial oxygen demand. As noted, sustained ischemia of sufficient degree is the major cause of necrosis (MI) of a portion of the heart muscle.

The related term acute coronary syndrome (ACS) refers to conditions associated with an abrupt decrease in effective coronary artery perfusion. The designation of ACS includes unstable angina (especially that occurring at rest or with increasing severity or duration) and actual MI.

The layperson’s term heart attack refers to MI. However, keep in mind that what a patient or even another clinician has labeled a “heart attack” may or may not have been a bona fide MI. Furthermore, MI should not be confused with cardiac arrest (although cardiac arrest can be caused by acute MI; Chapter 21 ). Careful and critical review of available documentation, especially ECGs, serum cardiac biomarker levels, and relevant noninvasive (echocardiograms and computerized coronary tomography angiograms) and invasive (cardiac catheterization/angiography) studies, is essential to confirm this history.

Our discussion focuses primarily on ischemia and infarction of the left ventricle, the main pumping chamber of the heart. We also briefly discuss the important clinical topic of right ventricular infarction. We describe the typical serial changes involving pathologic ST elevations and Q waves in this chapter. Chapter 10 discusses the variability of ischemia-related ECG patterns, highlighting non-ST segment elevation ischemia/infarction and non-Q wave infarctions.

Transmural and Subendocardial Ischemia

A simplified cross-sectional diagram of the left ventricle is presented in Fig. 9.1 . The left ventricle can be divided into an outer layer ( epicardium or subepicardium ) and an inner layer ( endocardium or subendocardium ). This distinction is important because myocardial ischemia may primarily affect part of the inner layers, or it may be severe enough to affect virtually the entire thickness of the ventricular wall (i.e., subendocardial and subepicardial). This “through and through” combination is termed transmural ischemia.

Myocardial Blood Supply and Location of Infarction

The cardiac blood supply is delivered by the three main coronary arteries and their branches ( Fig. 9.2 ). Thus MIs associated with initial ST elevations tend to be localized to the general region (i.e., anterior vs. inferior) of the left ventricle supplied by one of these arteries or its major tributaries. The right coronary artery (RCA) most commonly supplies both the inferior (diaphragmatic) portion of the heart and the right ventricle. The left main coronary artery is short and divides into (1) the left anterior descending (LAD) branch, which generally supplies the ventricular septum and a large part of the left ventricular free wall, and (2) the left circumflex (LCx) coronary artery, which supplies the lateral wall of the left ventricle. This circulation pattern may be quite variable from one person to the next. In most individuals, the RCA also supplies the posterior and sometimes even a section of the lateral wall. Less commonly, the circumflex artery supplies the inferoposterior portion of the left ventricle.

St Segment Elevation Ischemia and Acute Myocardial Infarction

STEMI is characterized by severe ischemia and ultimately necrosis of a portion of the entire (or nearly the full) thickness of a portion of the left (and sometimes right) ventricular wall. As noted, most, but not all, patients who present with acute STEMI have underlying atherosclerotic coronary artery disease. The usual pathophysiology of STEMI, sometimes evolving into a Q wave MI, relates to complete or near complete blockage of one of the major epicardial coronary arteries by a ruptured or eroded (ulcerated) atherosclerotic plaque, an event followed by the formation of a clot (thrombus) at this intracoronary site. The “culprit artery” thrombus, the proximate cause of the STEMI, is composed of platelets and fibrin, thereby blocking blood flow to downstream myocardial tissue.

As noted, multiple factors other than atherosclerotic plaque disruption may initiate or contribute to acute STEMI, including spontaneous coronary artery dissection, coronary emboli, spontaneous or drug-induced (e.g., cocaine) coronary vasospasm, and the syndrome known as stress ( takotsubo ) cardiomyopathy (see the next section and Chapter 10 ). The acronym MINOCA to indicate the syndrome of m yocardial i nfarction without o bstructive c oronary a rteries (or atherosclerosis) is increasingly used, with multiple specific causes as described at the end of this chapter.

Not surprisingly, the more extensive and severe MIs are the most likely to produce changes in both myocardial repolarization (ST-T) and depolarization (QRS complex). The earliest ECG changes seen with acute transmural ischemia/infarction due to major coronary occlusion typically occur in the ST-T complex in two major, sequential phases:

• 1.

  The acute phase is marked by the appearance of ST segment elevations, sometimes accompanied by tall positive (so-called hyperacute) T waves in multiple (usually two or more) leads. The term STEMI refers specifically to MIs with new or increased elevation of the ST segment, sometimes with prominent T waves, which are usually associated with complete or near complete occlusion of an epicardial coronary artery. Reciprocal ST depressions may occur in leads whose positive poles are directed about 180 degrees from those showing ST elevations. Thus an inferior MI may be marked by ST elevations in leads II, III, and aVF, along with reciprocal ST depressions in I and aVL. ST depressions may also be present in V ₁ to V ₃ if there is associated lateral or posterior wall involvement.

• 2.

  The subacute / evolving phase occurs hours or days later and is characterized by decreasing ST elevations and the appearance of T wave inversions in leads that previously showed ST elevations.

Clinicians also describe ST elevation MIs from the ECG in terms of the presumed location of the infarct. Anterior means that the infarct involves the front or lateral wall of the left ventricle, whereas inferior indicates involvement of the lower (diaphragmatic) wall of the left ventricle ( Fig. 9.3 ). For example, with an acute anterior wall MI, the ST segment elevations and tall hyperacute T waves typically appear in two or more of the anterior leads (chest leads V ₁ to V ₆ and extremity leads I and aVL) ( Fig. 9.4 ). With an inferior wall MI the ST segment elevations and tall hyperacute T waves are seen in two or more of the inferior leads II, III, and aVF ( Fig. 9.5 ).

The ST segment elevation pattern seen with acute MI is technically called a current of injury and indicates that damage involves the epicardial (outer) layer of the heart as a result of severe ischemia. The exact reasons that acute MI produces ST segment elevation are complicated and not fully known. What follows is a very brief overview of the mechanism of the injury current as reflected in ST deviations.

Under normal conditions, no net current flows at the time ST segment is inscribed because the myocardial fibers all attain about the same voltage level during the corresponding (plateau) phase of the ventricular action potential. Severe ischemia, with or without actual infarction, alters the balance of electrical charges across the myocardial cell membranes. As a result, a voltage gradient forms between normal and ischemic cells during the plateau phase (and other phases) of their action potentials. This voltage gradient leads to current flow—the current of injury. The emergence of the ST segment deviations on the body surface ECG is related to these cellular injury currents through a complex mechanistic set of interactions.

The ST segment elevations seen with acute MI may have different morphologies ( Fig. 9.6 ). Notice that the ST segment may be plateau-shaped or dome-shaped. Sometimes it is obliquely elevated, or it may retain its concave (unsloping) appearance. ^b

b Marked ST elevations and tall, positive T waves in the context of STEMI are sometimes informally referred to as the “tombstone” pattern because of their appearance and ominous prognosis. The more technical term is a monophasic current of injury pattern.

Furthermore, the morphology of the ST elevations may vary from one time to the next in the same individual during STEMI.

Pathologic ST segment elevations (and reciprocal ST depressions) are the earliest ECG signs of infarction and are generally seen within minutes of blood flow occlusion. As noted, relatively tall, positive (hyperacute) T waves may also be seen at this time ( Figs. 9.7 and 9.8 ). These T waves have the same significance as the ST elevations. In some cases, hyperacute T waves actually precede the ST elevations.

Guidelines for assessing whether ST segment (and associated J point) elevations are likely caused by acute ischemia have been proposed. However, invoking overly rigid criteria is of limited use because of false positives (from normal variants, left ventricular hypertrophy, left bundle branch block, etc., as described in Chapter 10 ) and also false negatives. For example, T wave positivity may precede ST elevations; the ST elevations may be less than 1 to 2 mm in amplitude, and ST elevations may not be present in multiple adjacent leads. ^c

c Consider an inferolateral MI with ST elevations in II, III, aVF, and V ₆ or one involving occlusion of the left main coronary artery with primary ST elevations in leads aVR and V ₁ (see Chapter 10 ). The leads here are not “contiguous.”

Clinicians should also be aware that ST changes in acute ischemia may evolve rapidly with a patient under observation. If the initial ECG is not diagnostic of STEMI but the patient continues to have symptoms consistent with myocardial ischemia, obtaining serial ECGs at 5- to 10-minute intervals (or continuous 12-lead ST segment monitoring) is strongly recommended.

Keep in mind that ECG evidence of infarction may relate not only to ST deviations (current of injury patterns) but also to T wave inversions and sometimes to the appearance of pathologic Q waves.

After a variable time lag (usually hours to a few days) the elevated ST segments start to return to the baseline. At the same time, the T waves become inverted (negative) in leads that previously showed ST segment elevations. This phase of T wave inversions is called the evolving or subacute phase of the infarction. Thus with an anterior/anterolateral wall infarction the T waves become inverted in one or more of the anterior leads (V ₁ to V ₆ , I, aVL). With an inferior wall infarction, the T waves become inverted in one or more of the inferior leads (II, III, aVF). These T wave inversions are illustrated in Figs. 9.4 and 9.5 . The spontaneous sequence of evolving ST-T changes may be substantially altered by percutaneous interventions designed to produce reperfusion of an occluded coronary artery.

As described further in this chapter, the evolution of ST-T changes with what begins as a STEMI event may cause confusion. Within hours to days, the ST segments begin to return to baseline and the T waves become inverted. These evolving findings should be termed as “consistent with an evolving STEMI” and not diagnosed as non-ST elevation MI.

QRS Changes: Pathologic Q Waves of Infarction

MI, particularly when large and transmural, often produces distinctive changes in the QRS (depolarization) complex. The characteristic depolarization sign is the appearance of new Q waves. Why do certain MIs lead to pathologic Q waves? Recall that a Q wave is simply an initial negative deflection of the QRS complex. If the entire QRS complex is negative, it is called a QS complex :

A Q wave (negative initial QRS deflection) in any lead indicates that the electrical voltages are directed away from that particular lead. With a transmural infarction, necrosis of heart muscle occurs in a localized area of the ventricle. As a result the electrical voltages produced by this portion of the myocardium disappear. Instead of positive (R) waves over the infarcted area, Q waves are often recorded (either a QR or QS complex).

As discussed in the next chapter, the common clinical tendency to equate pathologic Q waves with transmural necrosis is an oversimplification. Not all transmural infarcts lead to Q waves, and not all Q wave infarcts correlate with transmural necrosis.

The new Q waves of an MI generally appear within the first day or so of the infarct. With an anterior/anterolateral wall infarction, these Q waves are seen in one or more of leads V ₁ to V ₆ , I, and aVL (see Fig. 9.4 ). With an inferior wall MI the new Q waves appear in leads II, III, and aVF (see Fig. 9.5 ).

In summary, abnormal Q waves, in the appropriate context, are characteristic markers of infarction. They signify the loss of positive electrical voltages (potential), which is caused by the death of heart muscle.

More Specific ECG Localization of Infarctions

As mentioned earlier, MIs are generally localized to a specific portion of the left ventricle, affecting either the anterior or the inferior wall. Anterior infarctions are often further designated by ECG readers as anteroseptal, anterior free wall, or high lateral depending on the leads that show signs of the infarction ( Figs. 9.9–9.11 ). However, these traditional ECG-MI correlations, also including terms such as anterolateral or anteroapical, are at best approximate and often misleading or ambiguous compared with more direct anatomic determinations of infarct location obtained with imaging (echocardiographic or magnetic resonance), angiogram, radionuclide, or postmortem studies.