Abstract
As cocaine abuse has become widespread, it has been associated with various cardiovascular complications, including angina pectoris, myocardial infarction, and sudden cardiac death. Cocaine's principal effects on the cardiovascular system are mediated via alpha-adrenergic stimulation and include (a) an increase in the determinants of myocardial oxygen demand (heart rate and systemic arterial pressure) and (b) a concomitant decrease in myocardial oxygen supply (caused by vasoconstriction of the epicardial coronary arteries). Cocaine-induced coronary arterial vasoconstriction is enhanced at sites of atherosclerotic narrowing. Delayed or recurrent vasoconstriction of the coronary arteries may occur hours after the serum cocaine concentration has declined and appears to be caused by cocaine's major metabolites. Beta-adrenergic blocking agents may exacerbate cocaine-induced coronary arterial vasoconstriction, thereby increasing the magnitude of myocardial ischemia. Concomitant cigarette smoking exacerbates the deleterious effects of cocaine on myocardial oxygen supply and demand substantially.
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