ABSTRACT
There is ample evidence that acute or chronic alcohol ingestion may be a myocardial depressant. There is also evidence that acute or chronic alcohol ingestion may be a skeletal muscle depressant. In one study in asymptomatic alcoholics, almost one third of the men and half of the women showed histologic evidence of deltoid muscle myopathy with accompanying muscle weakness and depression of ejection fraction [1]. Low doses of ethanol, even as little as two cocktails, have been shown to be able to decrease myocardial contractility in normal subjects [2-5]. If the subject is alcoholic or already has some cardiac muscle disease on which alcohol is superimposed, the depressant effect of acute alcohol ingestion is exaggerated [6,7]. Partly responsible for the deleterious effects of alcohol in patients who have cardiac disease is the finding that in such patients alcohol acts as a vasoconstrictor [8]. However, when a decreased afterload is necessary for improving the function of a heart in Class 3 or 4 heart failure, the peripheral vasodilatory effects of a few drinks of a moderate amount of alcohol may not produce any hemodynamic deterioration [9].
