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

Ann Intern Med. 2002 Sep 3;137(5 Part 1):321-6. doi: 10.7326/0003-4819-137-5_part_1-200209030-00007.

Abstract

Background: Chronic alcohol abuse has a dose-dependent toxic effect on the myocardium, leading to alcoholic cardiomyopathy. The fact that only a minority of persons with chronic alcoholism have this condition suggests the possibility of a genetic vulnerability. In this context, polymorphism of the angiotensin-converting enzyme (ACE) gene has been implicated in cardiac dysfunction.

Objective: To compare the ACE genotypes of alcoholic persons who have cardiomyopathy with those of comparable alcohol abusers who have normal cardiac function.

Design: Case-control study over a 2-year period.

Setting: An academic tertiary referral hospital in Barcelona, Spain.

Patients: 30 alcoholic men with symptomatic cardiomyopathy and 27 alcoholic men with normal cardiac function.

Measurements: Ethanol intake, cardiac status, left ventricular ejection fraction (LVEF), and ACE gene polymorphism.

Results: The DD ACE genotype was present in 57% of alcoholic persons with an LVEF less than 0.50 and in 7% of those with normal cardiac function. Compared with persons who had an I allele, the odds ratio for development of left ventricular dysfunction in alcoholic persons with the DD genotype was 16.4.

Conclusions: Vulnerability to cardiomyopathy among chronic alcohol abusers is partially genetic and is related to presence of the ACE DD genotype. This finding demonstrates genetic susceptibility to alcohol-induced myocardial damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Analysis of Variance
  • Cardiomyopathy, Alcoholic / genetics*
  • Cardiomyopathy, Alcoholic / physiopathology
  • Case-Control Studies
  • Electrocardiography
  • Genetic Predisposition to Disease*
  • Humans
  • Male
  • Middle Aged
  • Odds Ratio
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Stroke Volume / physiology
  • Ventricular Dysfunction, Left / physiopathology

Substances

  • Peptidyl-Dipeptidase A