Myocardial Ischemia, Injury and Infarction

Insufficient blood supply to the myocardium can result in myocardial ischemia, injury or infarction, or all three. Atherosclerosis of the larger coronary arteries is the most common anatomic condition to diminish coronary blood flow. The branches of coronary arteries arising from the aortic root are distributed on the epicardial surface of the heart. These in turn provide intramural branches that supply the cardiac muscle. Myocardial ischemia generally appears first and is more extensive in the sub-endocardial region since these deeper myocardial layers are farthest from the blood supply, with greater intramural tension and need for oxygen.
Subendocardial ischemia

Ischemia in this area prolongs local recovery time. Since repolarization normally proceeds in an epicardial-to-endocardial direction, delayed recovery in the subendocardial region due to ischemia does not reverse the direction of repolarization but merely lengthens it. This generally results in a prolonged QT interval or increased amplitude of the T wave or both as recorded by the electrodes overlying the subendocardial ischemic region.
Subepicardial or transmural ischemia

Transmural ischemia is said to exist when ischemia extends subepicardially. This process has a more visible effect on recovery of subepicardial cells compared with subendocardial cells. Recovery is more delayed in the subepicardial layers, and the subendocardial muscle fibers seem to recover first. Repolarization is endocardial-to-epicardial, resulting in inversion of the T waves in leads overlying the ischemic regions.
Injury

Injury to the myocardial cells results when the ischemic process is more severe. Subendocardial injury on a surface ECG is manifested by ST segment depression, and subepicardial or transmural injury is manifested as ST segment elevation. In patients with coronary artery disease, ischemia, injury and myocardial infarction of different areas frequently coexist, producing mixed and complex ECG patterns.
Myocardial infarction

The term infarction describes necrosis or death of myocardial cells. Atherosclerotic heart disease is the most common underlying cause of myocardial infarction. The left ventricle is the predominant site for infarction; however, right ventricular infarction occasionally coexists with infarction of the inferior wall of the left ventricle. The appearance of pathological Q waves is the most characteristic ECG finding of transmural myocardial infarction of the left ventricle. A pathological Q wave is defined as an initial downward deflection of a duration of 40 msec or more in any lead except III and aVR.

The Q wave appears when the infarcted muscle is electrically inert and the loss of forces normally generated by the infarcted area leaves unbalanced forces of variable magnitude in the opposite direction from the remote region, for example, an opposite wall. These forces can be represented by a vector directed away from the site of infarction and seen as a negative wave (Q wave) by electrodes overlying the infarcted region.

During acute myocardial infarction, the central area of necrosis is generally surrounded by an area of injury, which in turn is surrounded by an area of ischemia. Thus, various stages of myocardial damage can coexist. The distinction between ischemia and necrosis is whether the phenomenon is reversible. Transient myocardial ischemia that produces T wave, and sometimes ST segment abnormalities, can be reversible without producing permanent damage and is not accompanied by serum enzyme elevation.


Two types of myocardial infarction can be observed electrocardiographically:

  • Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is not always present; hence, the term Q-wave infarction may be preferable for ECG description
  • Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities.
  • Elevation of serum enzymes is expected in both types of infarction. In the absence of enzyme elevation, ST and T wave abnormalities are interpreted as due to injury or ischemia rather than infarction.
Site of infarction

The ECG has been used to localize the site of ischemia and infarction. Some leads depict certain areas; the location of the infarct can be detected fairly accurately from analysis of the 12-lead ECG. Leads that best detect changes in commonly described locations are classified as follows:

Inferior (or diaphragmatic) wall: II, II and aVF
Septal: V1 and V2
Anteroseptal: V1, V2, Vf3 and sometimes V4
Anterior: V3, V4 and sometimes V2

Apical: V3, V4 or both
Lateral: I, aVL, V5 and V6
Extensive anterior: I, aVL and V1 through V6
Posterior wall infarction does not produce Q wave abnormalities in conventional leads and is diagnosed in the presence of tall R waves in V1 and V2. The classic changes of necrosis (Q waves), injury (ST elevation), and ischemia (T wave inversion) may all be seen during acute infarction. In recovery, the ST segment is the earliest change that normalizes, then the T wave; the Q wave usually persists. Therefore, the age of the infarction can be roughly estimated from the appearance of the ST segment and T wave. The presence of the Q wave in the absence of ST and T wave abnormality generally indicates prior or healed infarction. Although the presence of a Q wave with a 40 msec duration is sufficient for diagnosis, criteria defining the abnormal depth of Q waves in various leads have been established. For example, in lead I, the abnormal Q wave must be more than 10 percent of QRS amplitude. In leads II and aVF, it should exceed 25 percent, and in aVL it should equal 50 percent of R wave amplitude. Q waves in V2 through V6 are considered abnormal if greater than 25 percent of R wave amplitude.
The Q wave generally indicates myocardial necrosis, although similar patterns may be produced by other conditions, such as WPW syndrome, connected transportation of the great vessels, etc. ST-segment elevation can be observed in conditions other than acute myocardial infarction.

ST segment elevation and T wave abnormalities

Other causes of ST segment elevation include the following:

  • Acute pericarditis: ST elevation in acute pericarditis is generally diffuse and does not follow the pattern of blood supply. As a rule these changes are not accompanied by reciprocal depression of the ST segment in other leads.
  • Early repolarization: In some patients without known heart disease, particularly young patients, early takeoff of the ST segment may be seen.
  • Ventricular aneurysm: After acute myocardial infarction, the ST segment usually normalizes. However, in the presence of a persistent aneurysm in the region of infarction, ST segment elevation may persist indefinitely.
Abnormal T waves can be seen in a variety of conditions other than myocardial ischemia, including:

  • Hyperventilation
  • Cerebrovascular disease
  • Mitral valve prolapse
  • Right or left ventricular hypertrophy
  • Conduction abnormalities (right or left bundle branch block)
  • Ventricular preexcitation
  • Myocarditis
  • Electrolyte imbalance
  • Cardioactive drugs such as digitalis and antiarrhythmic agents
  • No obvious cause, particularly in women
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