Since a significant fraction of the population are heavy consumers of ethanol, and recent postmortem studies suggest that most alcoholics have some degree of cardiac abnormality, elucidation of the basis for alcoholic cardiomyopathy is of some importance. Intoxicating amounts of ethanol depress ventricular function acutely and effect leakage of myocardial cell components.
On the basis of studies in three animal species and in man, it would appear that the cumulative effects of chronic ethanol intake can, without evident malnutrition, depress ventricular function and produce metabolic and morphologic abnormalities of the myocardium before clinical manifestations. Progression of the disease to produce heart failure, arrhythmias, or thromboembolism, separately or in combination, occurs under multiple circumstances that are not clearly defined. These would appear to include the cumulative effects without superimposed factors, an intensified drinking episode, simultaneous exposure to trace metals in excess, and occasional specific nutritional deficiency or superimposed infection. The low incidence of nutritional complications such as cirrhosis, peripheral neuritis, and delirium tremens associated with cardiomyopathy supports the view that the cardiac abnormality is commonly not dependent on malnutrition. Finally, clinical data indicate that cessation of alcohol intake will reverse the disease or interrupt its progression in many patients. Anticoagulant therapy is recommended at least during the early recovery stage.
- © 1971 American Heart Association, Inc.