ALCOHOL AND HEART-MUSCLE DISEASE

Ethanol consumption may induce acute and chronic effects on the myocar dium. High-dose acute ethanol intake may induce a decrease in myocardi al contraction and produce a variety of rhythm disturbances. These eff ects are more relevant in patients with underlying cardiomyopathy. Chr onic ethanol intake may induce the development of a dilated cardiomyop athy, which is clinically and junctionally similar to idiopathic dilat ed cardiomyopathy. Alcoholic cardiomyopathy is potentially reversible with abstinence. The prognosis depends on the persistence or abstinenc e of ethanol intake. There is a positive correlation between alcoholic cardiomyopathy and the presence of other ethanol-related diseases, su ch as skeletal myopathy and cirrhosis. In patients with a specific eth anol-related disease, the possible presence of other complications of alcoholism should be ruled out. Although there are several factors pot entially 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 deficienc ies. 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 thr ough the sarcolemma and interfering with the excitation-contraction co upling of myocytes. Cell energy depletion or protein-turnover disrupti on may contribute to the deleterious effect of ethanol on the myocardi um.