Mechanisms of ethanol-induced cardiac damage.

Although the extent of excessive ethanol consumption merits serious concern, and the association between such consumption and dilated cardiomyopathy is increasingly recognised, the pathogenesis and factors that determine patient susceptibility are still poorly known. Until the 1950s the cause of ethanolinduced cardiomyopathy was supposed to be nutritional deficiencies (that is, disturbances of nutrient handling or limitations in supply). Though dietary deficiencies (for example, thiamine) can cause cardiomyopathy, the distinction between alcoholic heart muscle disease (AHMD) and beriberi heart disease was demonstrated only when cardiac dysfunction was shown to occur in the absence of nutritional deficiencies and when AHMD failed to respond to thiamine.' Furthermore, the use of appropriate pair-feeding regimens using nutritionally complete liquid diets has also shown that experimental alcohol-induced cardiac abnormalities can occur without overt nutritional deficiencies.2