title: Alcoholic cardiomyopathy: clinical and experimental pathological changes.
abstract: In this review we survey the features of alcohol-induced lesions in the heart, in both the clinical and laboratory-animal setting. The data indicates a diverse range of lesions that contribute to the genesis of the entity alcoholic cardiomyopathy (also referred to as alcoholic heart muscle disease). Biopsies of affected patients reveal lesions similar to dilated cardiomyopathy though quantitative morphometry can distinguish between the two disorders. Biochemical analysis reveals an increase in the activities of some enzymes, though the pathogenetic nature of these alterations are unknown, but may well be adaptive. The induction of ischaemia in acute ethanol exposure may contribute to the heart muscle damage, though long term experimental studies indicate that heat shock proteins are reduced, making the heart more vulnerable to cardiac dysfunction. Changes in the rate of protein turnover induced by alcohol appear to be a central feature in animal studies and it is very likely that similar changes occur in man.
authors.affiliation: Rayne Institute, Department of Clinical Biochemistry, London.
authors.forename: V R
authors.initials: VR
authors.lastname: Preedy
authors.forename: P J
authors.initials: PJ
authors.lastname: Richardson
mesh_terms: D000079:Acetaldehyde / Q000493:pharmacokinetics; D000818:Animals; D001706:Biopsy; D002310:Cardiomyopathy, Alcoholic / Q000473:pathology*; D002311:Cardiomyopathy, Dilated / Q000473:pathology; D000431:Ethanol / Q000493:pharmacokinetics; D006360:Heat-Shock Proteins / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D017202:Myocardial Ischemia / Q000473:pathology; D009206:Myocardium / Q000473:pathology
chemical_list: D006360:Heat-Shock Proteins; D000431:Ethanol; D000079:Acetaldehyde