Ethanol induced cardiovascular disease.

Although the beneficial effects of mild or moderate ethanol consumption have been implied with respect to coronary artery disease, excessive ethanol consumption can result in alcoholic heart muscle disease (AHMD). The latter is characterized by features consistent with dilated cardiomyopathy with concomitant ventricular dysfunction and histopathological abnormalities. By definition, no other cause for the abnormalities in AHMD is demonstrated, other than excessive alcohol consumption. The metabolic basis of AHMD is probably multi-factorial, and the alterations of myocardial biochemistry are contributing factors for the precipitation and progression of the disease. The latter may reverse with abstention. Evidence is provided to support the contention that the abnormalities include central defects in protein metabolism, which perhaps are engendered by free radicals and/or the formation of acetaldehyde adducts. The latter may initiate the formation of auto-antibodies, therefore providing an auto-immune basis for AHMD in chronic alcohol misuse. Evidence is also provided to show that acetaldehyde is a potent perturbant of protein synthesis, and reduces the formation of new contractile proteins.