Key result
Cellular cholesterol defects, coronary spasm, and vasodilators during CPB drive MI pathophysiology.
This review discusses the pathogenesis of ischemic heart disease, emphasizing cholesterol metabolism, coronary spasm, and mechanisms of ischemic injury.
Supports targeting cholesterol defects and spasm in MI risk; leaves open prospective trials for clinical translation.
Primary prevention of death from ischemic heart disease requires further understanding of the pathogenesis of this disorder. Cellular defects of cholesterol metabolism may be more significant markers that serum lipid levels for the identification and treatment of atherosclerotic risk. Coronary spasm has been shown to be an important cause of ischemia in the presence and absence of atherosclerotic lesions. Careful manipulation of physiologic variables with vasodilator agents during cardiopulmonary bypass can substantially alter the myocardial oxygen supply-demand relation, thereby minimizing ischemic injury. The cellular basis for loss of mechanical function during ischemia and the factors that determine irreversible injury are yet unknown.
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Shine et al. (1977) conducted a review in Myocardial Infarction. Cellular defects of cholesterol metabolism, coronary spasm, and physiologic manipulation with vasodilators during cardiopulmonary bypass are key factors in the pathophysiology of myocardial infarction.
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