Angiotensin-converting enzyme gene polymorphism is associated with vulnerability to alcoholic cardiomyopathy

Abstract

Approximately 15% to 40% of all cases of dilated cardiomyopathy in western countries are related to alcohol abuse (1). Ethanol has a progressive and dose-dependent toxic effect on cardiac function, independent of malnutrition, thiamin deficiency, or electrolyte disturbances (2). We previously established a relationship between the total lifetime dose of alcohol consumed and the depression of left ventricular ejection fraction (LVEF); however, the quantity of alcohol consumed accounted for only about one third of the effect of alcohol (r 0.34) (2). Of note, we have encountered alcoholic persons with high levels of alcohol consumption who have no evidence of myocardial impairment, whereas other alcoholic persons with less consumption display considerable loss of contractile capacity. In this context, we have previously suggested the possibility of a genetic vulnerability to the effects of alcohol on the myocardium (3, 4). Researchers have recently focused on the possible importance of angiotensin-converting enzyme (ACE) as an influence on skeletal muscle performance (5, 6), cardiac hypertrophy (7–9), myocardial function (10, 11), and overall cardiac mortality (12). Therefore, we sought to evaluate the possibility that ACE gene polymorphism may play a role in the development of alcoholic cardiomyopathy. In this study, we compared alcoholic persons who have depressed LVEF with alcoholic persons who showed no evidence of cardiac dysfunction.