The acute and chronic toxic effects of alcohol on skeletal and cardiac muscle are clinically important. Muscle weakness and atrophy are the main manifestations of skeletal myopathy, and arrhythmias and progressive left-ventricular dysfunction are those of cardiomyopathy. Most patients remain asymptomatic from these effects for a long time. Myocyte atrophy and death are the main pathological findings. A clear dose-related effect has been established with ethanol consumption, with gender and some specific gene polymorphisms being factors of increased susceptibility to alcohol-induced muscle damage. Pathogenic mechanisms are pleiotropic, the most relevant being disturbances in carbohydrate, protein, and energy cell turnover, signal transduction, and induction of apoptosis and gene dysregulation. Ethanol abstinence is the only effective treatment, although controlled drinking is useful in patients who do not achieve abstinence. Persistent high-dose consumption results in deterioration of muscle and heart function, with a high mortality due to arrhythmias and progression of heart failure.
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