© 1996 by European Society of Cardiology
Copyright © 1996, European Society of Cardiology
Alcohol and the heart: biochemical alterations
aMolecular and Metabolic Cardiology Group, Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, Bessemer Road, London, SE5 9PJ, UK
bMolecular and Metabolic Cardiology Group, Department of Cardiology, King's College School of Medicine and Dentistry, Bessemer Road, London, SE5 9PJ, UK
cDepartment of Cardiothoracic Surgery, National Heart and Lung Institute, Heart Science Centre, Harefield Hospital, Harefield, Middlesex, UB9 6JH, UK
* Corresponding author. Tel. (+44-171) 737 4000, ext. 4255; Fax (+44-171) 737 7434.
A considerable amount of attention has focused on the cardiovascular events associated with ethanol consumption. The available evidence suggests that moderate ethanol consumption is associated with reduced risk of coronary heart disease, i.e., vessel events. In contrast, this review is primarily concerned with ethanol and heart muscle damage. Clinical features of the consequences of prolonged and excessive ethanol consumption encompass defects in myocardial contractility and derangement of cellular architecture, including disarray of the contractile elements. Although the incidence of heart muscle abnormalities in alcohol misusers is generally higher than previously considered, the mechanisms are only just being elucidated. This process has been facilitated by laboratory based studies in which animals receive either a single dose of ethanol (acute studies) or a continuous supply of ethanol in their daily diets (chronic studies). Results from these models show that acute ethanol dosage causes a marked decrease in the synthesis of contractile proteins. This occurs in the absence of overt mitochondrial abnormalities: ATP concentrations are generally unaffected. Paradoxically, the synthesis of mitchondrial proteins is reduced. Use of metabolic inhibitors suggests that the deleterious effects of acetaldehyde contribute to these reductions in protein synthesis. In chronic studies, ethanol causes a reduction in the amount of contractile proteins, and two dimensional protein profiling implicates selective loss of individual myocardial proteins. The differential activities of lysosomal proteases may contribute to this patterned response. However, in chronic ethanol feeding, adaptive mechanisms also become important, as the synthesis of the myofibrillary proteins increases. Overall, the mechanisms inherent in these biochemical responses may contribute to the genesis of a distinct disease entity, alcoholic heart muscle disease.
KEYWORDS ks, fractional rate of protein synthesis; StRNA, specific radioactivity of amino-acyl-tRNA; Si, specific radioactivity of free amino acid in intracellular pools; Sp, specific radioactivity of free amino acid in extracellular pools
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