ALCOHOL AND THE HEART - BIOCHEMICAL-ALTERATIONS

A considerable amount of attention has focused on the cardiovascular e vents associated with ethanol consumption. The available evidence sugg ests that moderate ethanol consumption is associated with reduced risk of coronary heart disease, i.e., vessel events. In contrast, this rev iew is primarily concerned with ethanol and heart muscle damage. Clini cal features of the consequences of prolonged and excessive ethanol co nsumption encompass defects in myocardial contractility and derangemen t of cellular architecture, including disarray of the contractile elem ents. Although the incidence of heart muscle abnormalities in alcohol misusers is generally higher than previously considered, the mechanism s are only just being elucidated. This process has been facilitated by laboratory based studies in which animals receive either a single dos e of ethanol (acute studies) or a continuous supply of ethanol in thei r daily diets (chronic studies). Results from these models show that a cute ethanol dosage causes a marked decrease in the synthesis of contr actile proteins. This occurs in the absence of overt mitochondrial abn ormalities: ATP concentrations are generally unaffected. Paradoxically , the synthesis of mitchondrial proteins is reduced. Use of metabolic inhibitors suggests that the deleterious effects of acetaldehyde contr ibute to these reductions in protein synthesis. In chronic studies, et hanol causes a reduction in the amount of contractile proteins, and tw o dimensional protein profiling implicates selective loss of individua l myocardial proteins. The differential activities of lysosomal protea ses may contribute to this patterned response. However, in chronic eth anol feeding, adaptive mechanisms also become important, as the synthe sis of the myofibrillary proteins increases. Overall, the mechanisms i nherent in these biochemical responses may contribute to the genesis o f a distinct disease entity, alcoholic heart muscle disease.