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Pathogenetic mechanisms underlying the clinical events associated with atherosclerotic heart disease.

The demonstration that an increase of myocardial demand beyond a fixed supply is not the only or even the most frequent cause of acute myocardial ischemia opens 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, postprandial, and cold-induced angina and for variable threshold of exertional angina. Coronary spasm was shown to cause ventricular fibrillation and cardiac arrest during transient reversible ischemic episodes with or without anginal pain and thus can be one of the causes of sudden death. 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 that transiently and acutely interfere with coronary flow, along with an extremely variable degree of coronary atherosclerosis. In turn, prognosis may be determined by the presence and severity of acute functional factors and the extent to which the coronary circulation and the myocardium are already chronically jeopardized. Therefore, diagnosis, treatment and prevention of ischemic heart disease should be focused not only on the detection, treatment and prevention of coronary atherosclerosis, but also on the identification of the factors that transiently interfere with coronary blood supply and of their mechanisms, treatment and prevention.