Structural and functional abnormalities are prominent in alcoholic cardiomyopathy (ACM). Histological features in affected subjects are almost identical to the characteristics of dilated cardiomyopathy. Quantitative morphometry, however, can distinguish between ACM and dilated cardiomyopathy. Biopsies from patients with ACM show increases in the activities of some myocardial enzymes (alpha-hydroxybutyric dehydrogenase, creatine kinase, lactate dehydrogenase, malic dehydrogenase) which are correlated with the bimodal distribution of alcohol intake and may represent an adaptive response. One-third of patients with ACM have serum antibodies against cardiac acetaldehyde-protein adducts. Animal models of ethanol toxicity have shown that acutely, alcohol and acetaldehyde reduce the synthesis of cardiac contractile proteins in vivo. Two-dimensional SDS-PAGE has also shown that in rats chronically fed alcohol, the relative amounts of over 10% of heart muscle proteins are altered. The heat shock proteins (HSP) Hsp60 and Hsp70 are decreased in alcohol-fed rats, as is desmin. Reduction in HSPs may indicate reduced myocardial protection whilst a fall in desmin may indicate structural defects. In conclusion, ACM is a complex process that is due to altered protein synthesis, the formation of acetaldehyde adducts and a reduction of cardiac HSPs and desmin. Both acetaldehyde and alcohol are myocardial perturbants.