Pathogenesis Of Clinical Events In Coronary Artery Disease. Clinical Observations

Studies on angina at rest showing that an increase of myocardial demand beyond a fixed supply is not the only or even the most frequent cause of acute myocardial ischemia open a new avenue in our understanding of ischemic heart disease. Functional factors that transiently interfere with regional coronary blood supply, such as coronary spasm, seem to play a major role in determining the clinical events associated with coronary atherosclerotic heart disease. These functional factors appear to be the major cause of angina at rest, nocturnal, post-prandial and cold-induced angina and for variable threshold of exertional angina.

Sudden death was also shown to be a possible consequence of coronary spasm which was shown to cause ventricular fibrillation and cardiac arrest during reversible ischemic episodes with or without anginal pain.

Myocardial infarction consistently occurs in the same vascular bed shown to undergo transient ischemic episodes before the onset of the final, irreversible one. The transient episodes were shown to be caused by coronary spasm. The irreversible episode could not be relieved by intracoronary nitrates. A platelet mural thrombus was found at post mortem at the site of demonstrated persistent spasm.

We suggest that coronary vasospasm and platelet aggregation may be responsible for the onset of acute myocardial infarction and, possibly, for the development of coronary thrombotic obstructions.

Thus, the clinical manifestations of ischemic heart disease may largely depend on the presence and severity of functional factors, transiently and acutely interfering with flow, along with a variable degree of coronary atherosclerosis. In turn, prognosis may be determined by the severity of acute functional factors and the extent to which the coronary circulation and the myocardium are already chronically jeopardized by organic lesions.