Alcoholic and cocaine-associated cardiomyopathies

Abstract

Alcohol and cocaine use are associated with significant cardiovascular complications, including cardiomyopathy. The pathophysiologic mechanisms underlying the development of these toxic cardiomyopathies vary depending on the inciting agent but include direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. The typical patient with alcoholic cardiomyopathy is a long-term excessive alcohol consumer who is otherwise indistinguishable from other patients with nonischemic cardiomyopathy. The typical patient with cocaine cardiomyopathy is a young male smoker who presents with signs of adrenergic excess. Management of these patients is similar to that of patients with other forms of dilated cardiomyopathy, although beta-blockers should be avoided in patients with cocaine-associated heart failure and benzodiazepines should be given in this setting to blunt adrenergic excess. Left ventricular function may improve dramatically with abstinence from alcohol or cocaine. Unfortunately, the rate of recidivism is high and left ventricular dysfunction and symptomatic heart failure often recurs.