Cocaine Cardiac Toxicity: Revisited

Abstract

Cocaine is a potent stimulant which affects cardiovascular system severely. The mechanism of cardiac toxicity depends on multiple factors. Cocaine increases sympathetic stimulation and causes excess catecholamine secretion. Besides, its indirect sympatho-mimetic effect also directly exerts cardiotoxic effect by different cellular, molecular, and ionic mechanisms, resulting in acute or chronic cardiovascular impairment. Cardiac arrhythmia and acute myocardial ischemia or infarction is the most common cause of cocaine-induced sudden cardiac death. Chronic cocaine abuse can develop sustained hypertension or myocarditis or cardiomyopathy leading to depressed left ventricular function. Therapy for cocaine induced cardiac toxicity generally includes use of benzo-diazepine agents, nitric oxide mediated vasodilators, alpha blockers and even calcium channel blockers. Beta blockers are relatively contraindicated in acute settings of cocaine cardiovascular toxicity. Hypersensitivity reaction to cocaine is often manifested by infiltration of eosinophilic or mononuclear cells without myocardial cell damage. Vascular dissection, endocarditis, and tricuspid valvular abnormalities are some less frequent manifestations in cocaine-induced cardiac toxicity.