The mechanism for the cardiac damage produced by alcohol remains unclear. Several theories have arisen over many years. Original theories regarding the mechanism focused on nutritional deficiencies (eg thiamine deficiency), secondary exposures (eg tobacco, cobalt, arsenic) and other comorbidities (eg hypertension). Although these mechanisms continue to play a role in selected patients, most evidence in the literature indicates that the effects of alcohol on the myocardium are independent of these factors and that the effect is a direct toxic result of ethanol or its metabolites.