Alcohol and heart muscle disease.

Ethanol consumption may induce acute and chronic effects on the myocardium. High-dose acute ethanol intake may induce a decrease in myocardial contraction and produce a variety of rhythm disturbances. These effects are more relevant in patients with underlying cardiomyopathy. Chronic ethanol intake may induce the development of a dilated cardiomyopathy, which is clinically and functionally similar to idiopathic dilated cardiomyopathy. Alcoholic cardiomyopathy is potentially reversible with abstinence. The prognosis depends on the persistence or abstinence of ethanol intake. There is a positive correlation between alcoholic cardiomyopathy and the presence of other ethanol-related diseases, such as skeletal myopathy and cirrhosis. In patients with a specific ethanol-related disease, the possible presence of other complications of alcoholism should be ruled out. Although there are several factors potentially implicated in the pathogenesis of alcohol-related myocardial damage, ethanol itself may induce direct myocardial lesions, which are dose-related and independent of nutrition, protein or ionic deficiencies. The most relevant pathogenic studies on alcoholic cardiomyopathy are based on the disruption of membrane permeability and ionic fluxes mediated by ethanol, inducing a decrease in the calcium transients through the sarcolemma and interfering with the excitation-contraction coupling of myocytes. Cell energy depletion or protein-turnover disruption may contribute to the deleterious effect of ethanol on the myocardium.