Alcoholic Cardiomyopathy: Studies of Protein Metabolism

Abstract

It is now well known that cardiomyopathy may follow prolonged ingestion of ethanol in man. This myopathy appears to be unrelated to the associated liver dysfunction and damage. Studies with animal models have been difficult because of different diets, species of animal studied, and the duration of administration of ethanol. The results have also been inconsistent. However, what has emerged in the last decade is the general finding that although the heart may behave normally under “control” conditions, when an additional stress, either chemical or hemodynamic, is applied, the heart from the ethanol exposed animal reacts abnormally. As examples, little impairment of cardiac contractile action has been noted in alcohol exposed hearts unless there is the added stress of increased afterload (1,2). Similarly, both fast electrical pacing (3) and ischemia (4) produce a greater impairment of contractile action in the ethanol exposed heart than in the matched control. Further, in vitro studies with hearts from ethanol exposed animals show a decresed contractile response to increases in calcium when compared to the control (5).