Chapter 8 Myocardial Infarction and Ischemia, I ST Segment Elevation and Q Wave Syndromes
This chapter and the next (forming one unit) examine one of the most important topics in clinical electrocardiography and clinical medicine—the diagnosis of myocardial ischemia and infarction∗ (ischemic heart disease), including ST segment elevation myocardial infarction (STEMI). Basic terms and concepts are briefly discussed first.
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 the blood flow to become inadequate, ischemia of the heart muscle develops. Ischemia means literally “to hold back blood.”
Myocardial ischemia may occur transiently. For example, patients who experience angina pectoris with exercise are having transient myocardial ischemia. If the ischemia is more severe, necrosis of a portion of heart muscle may occur. Myocardial infarction (MI) refers to myocardial necrosis (or, in nontechnical parlance—a “heart attack”).
This discussion focuses primarily on ischemia and infarction of the left ventricle, the predominant pumping chamber of the heart. The important clinical topic of right ventricular infarction is also discussed briefly.
A simplified cross-sectional diagram of the left ventricle is presented in Figure 8-1. Notice that the left ventricle consists of an outer layer (epicardium or subepicardium) and an inner layer (subendocardium). This distinction is important because myocardial ischemia may be limited to just the inner layer, or it may affect virtually the entire thickness of the ventricular wall (transmural ischemia).
Figure 8-1 Cross section of the left ventricle showing the difference between a subendocardial infarct, which involves the inner half of the ventricular wall, and a transmural infarct, which involves the full thickness (or almost the full thickness) of the wall. As discussed in the text, pathologic Q waves may be a marker of transmural infarction. However, not all transmural myocardial infarctions produce abnormal Q waves; in some cases, subendocardial (nontransmural) infarctions are associated with Q waves.
The cardiac blood supply is delivered by the three main coronary arteries and their branches (Fig. 8-2). The right coronary artery supplies both the inferior (diaphragmatic) portion of the heart and the right ventricle. The left main coronary artery is short and divides into the left anterior descending coronary artery, which generally supplies the ventricular septum and a large part of the left ventricular free wall, and the left circumflex coronary artery, which supplies the lateral wall of the left ventricle. This circulation pattern may be variable. Sometimes, for example, the circumflex artery also supplies the inferoposterior portion of the left ventricle. MIs tend to be localized to the region (e.g., anterior or inferior) of the left ventricle supplied by one of these arteries or their branches.
The serial, typical effects involving STEMI and Q wave MI on the ECG are examined in this chapter. Chapter 9 discusses the diversity of ECG patterns associated with non–ST segment elevation ischemia and non–Q wave infarctions.
“Transmural” MI is characterized by ischemia and ultimately necrosis of a portion of the entire (or nearly the entire) thickness of the left ventricular wall. Most patients who present with acute MI have underlying atherosclerotic coronary artery disease. The pathophysiology of acute STEMI and subsequent evolving Q wave MI most often relates to occlusion of one of the coronary arteries by a ruptured atherosclerotic plaque, followed by the formation of a clot at this site. The clot in the “culprit artery” is composed of platelets and fibrin, blocking the blood flow downstream.
1. The acute phase is marked by the appearance of ST segment elevations and sometimes tall positive (hyperacute) T waves in multiple (usually two or more) leads. The term “STEMI” refers to this phase.
Transmural MIs can also be described in terms of the location of the infarct. Anterior means that the infarct involves the anterior or lateral wall of the left ventricle, whereas inferior indicates involvement of the inferior (diaphragmatic) wall of the left ventricle (Fig. 8-3). The anatomic location of the infarct determines the leads in which the typical ECG patterns appear. For example, with an acute anterior wall MI, the ST segment elevations and tall hyperacute T waves appear in one or more of the anterior leads (chest leads V1 to V6 and extremity leads I and aVL) (Fig. 8-4). With an inferior wall MI the ST segment elevations and tall hyperacute T waves are seen in inferior leads II, III, and aVF (Fig. 8-5).
Figure 8-4 A, Acute phase of an anterior wall infarction: ST segment elevations and new Q waves. B, Evolving phase: deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A and B, notice the reciprocal ST-T changes in the inferior leads (II, III, and aVF).
Figure 8-5 A, Acute phase of an inferior wall myocardial infarction: ST segment elevations and new Q waves. B, Evolving phase: deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, V2, V4).
An important (but not always present) feature of the ST-T changes seen with STEMI is their reciprocity. The anterior and inferior leads tend to show inverse patterns. Thus in an anterior infarction with ST segment elevations in two or more of leads V1 to V6, I, and aVL, ST segment depression is often seen in leads II, III, and aVF. Conversely, with an acute inferior wall infarction, leads II, III, and aVF show ST segment elevation, with reciprocal ST depressions often seen in one or more of leads V1 to V3, I, and aVL. Reciprocal changes are illustrated in Figures 8-4 and 8-5.
The ST segment elevation seen with acute MI is called a current of injury and indicates that damage has occurred to the epicardial (outer) layer of the heart as a result of severe ischemia. The exact reasons that acute MI produces ST segment elevation are complex and not fully understood. Normally the ST segment is isoelectric (neither positive nor negative) because no net current flow is occurring at this time. MI alters the electrical charge on the myocardial cell membranes in a number of ways. As a result, current flow becomes abnormal (current of injury) and produces ST segment deviations.
The ST segment elevations (and reciprocal ST depressions) are the earliest ECG signs of infarction, and are generally seen within minutes of blood flow occlusion. Tall, positive (hyperacute) T waves may also be seen at this time (Figs. 8-7 and 8-8). These T waves have the same significance as the ST elevations. In some cases, hyperacute T waves actually precede the ST elevations.
Figure 8-7 Chest leads from a patient with acute anterior ST segment elevation myocardial infarction (STEMI). A, In the earliest phase of the infarction, tall, positive (hyperacute) T waves are seen in leads V2 to V5B, Several hours later, marked ST segment elevation is present in the same leads (current of injury pattern), and abnormal Q waves are seen in leads in V1 and V2.
Figure 8-8 Hyperacute T waves with anterior ST segment elevation myocardial infarction (STEMI). This patient was complaining of severe chest pain. Notice the very tall (hyperacute) T waves in the chest leads. In addition, slight ST segment elevations are present in lead aVL and reciprocal ST depressions are seen in leads II, III, and aVF. Notice the atrial premature beat (APB) in lead V4.
Guidelines for assessing whether ST segment (and usually J point) elevations are due to acute ischemia have been suggested. However, strict criteria are limited because of false-positives (due to normal variants, left ventricular hypertrophy, etc., as described in Chapter 9) and false-negatives (e.g., T wave positivity may precede ST elevations or the ST elevations may be less than 1-2 mm).
Clinicians should be aware that ST changes in acute ischemia may evolve with the patient under observation. If the initial ECG is not diagnostic of STEMI but the patient continues to have symptoms consistent with myocardial ischemia, serial ECGs at 5- to 10-minute intervals (or continuous 12-lead ST segment monitoring) should be performed.
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 in leads that previously showed ST segment elevations. This phase of T wave inversions is called the evolving phase of the infarction. Thus with an anterior wall infarction the T waves become inverted in one or more of the anterior leads (V1 to V6, 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. 8-4 and 8-5.)
Key Clinical Correlates
Of major importance is the finding that acute reperfusion therapies with percutaneous coronary interventions (angioplasty procedures) or intravenous thrombolytic medications have been shown consistently to improve mortality rate only for acute STEMI.
Furthermore, the earlier such therapy is given after the onset of the acute STEMI the more likely it is to reduce the size of the infarct and the risk of major complications, including heart failure and death.