Cardiotoxicity of cocaine use by humans and rodents: Synergisms of concomitant cocaine plus alcohol exposure

As cocaine abuse has become widespread, the number of cocaine related cardiovascular events, such as angina pectoris, myocardial ischemia and infarction, cardiac myopathy, left ventricular hypertrophy, and sudden death has increased substantially [1-15]. These occur in young subjects, a significant percentage of whom had no evidence of atherosclerotic coronary artery disease on subsequent angiography [10,11,18-21]. Twice as many men as women experience cocaine related cardiac ischemic events, at least partly caused by a greater frequency of cocaine use in men. The concomitant use of cigarettes and/or ethanol is pervasive, with up to 75% of cocaine users admitting to each. Although myocardial ischemia, infarction, and sudden death are most likely to occur in chronic cocaine users, they have been reported in first time users as well. These events can occur from any route of administration and with a large or small amount of the drug [3,4,8,9,20-29]. It is thought that the pathophysiology of cocaine-related myocardial ischemia and infarction is most likely multidimensional, and that it is caused by individual and/or combined conditions including increased myocardial oxygen demand in the setting of limited or fixed supply, marked coronary artery vasoconstriction, and enhanced platelet aggregation and thrombus formation [1].