Structural cardiac morphological changes develop in a considerable number of chronic alcoholics, and preclinical cardiomyopathy is frequent especially among those with alcoholic liver disease. Alcohol exerts an acute albeit transient toxic effect on cardiac performance resulting in an impaired contraction of the myocardium. The effect is dose-dependent at rest, whereas compensatory mechanisms counterbalance the alcohol-induced changes during exercise. Similar cardiovascular reactions are recorded in patients with coronary artery disease, in whom the vasodilatory effect is measurable. In predisposed individuals heavy alcohol intake may induce atrial fibrillation or even malignant arrhythmias. Arterial hypertension is often found during the period following an alcohol excess, but this effect seems to be reversible. Alcohol intake inhibits aggregation of blood platelets and induces an increase in the level of high density lipoprotein cholesterol inhibiting atherogenesis. These mechanisms may well be dominant factors in the interpretation of the obvious protective effect of alcohol as seen in the U- or J-shaped relation between daily alcohol consumption and rate of survival. This relation clearly demonstrates a lower mortality among people consuming one to two drinks per day compared with both those who drink more and with alcohol abstainers, justifying that these people should continue their drinking habits unless they have diseases contraindicating alcohol consumption or have an increased risk of developing chronic alcoholism.