title: [To the potential use of alcoholic cardiomyopathy echocardiography assessment of forming].
abstract: Chronic alcohol abuse leads not only to a significant human psychic and social degradation, but also promotes the alcoholic cardiomyopathy formation, that is one of the leading causes of high mortality of alcoholics. However, to date in clinic there are no unified approaches in the prevention and treatment of alcoholic cardiomyopathy, first of all, due to the lack of the adequate model in the experimental pharmacology, which can assess the stages of formation of alcoholic cardiomyopathy objective and in real time, and thus create the basis for the search and study the mechanisms of action of drugs for the treatment of this serious disease. Studing the possibility of echocardiography using in experiments with rats exposed to prolonged forced alcoholism is one of the approaches to solve this problem. It was shown that the significant changes of intracardiac echocardiography hemodynamics corresponding to the known from the clinic, begining to form from the 20th week of systematic consumption of alcohol by rats. At this time interval the reduction in inotropic function of the heart in alcoholized rats compared to control is observed: fraction shortening (FS) is 41.9% (40.3-42.2) and 51.3% (48.8-59.1) respectively, and ejection fraction (EF) 78.8 (77.4-79.2) and 87.5% (84.6-92.4) respectively, p = 0.0215. The dilated heart failure develops in the rats from the 24 week of regular alcohol consumption, as evidenced not only by dynamic reducing of FS and FV, but also by the dilatation ofthe heart. For example, the end-systolic size of the left ventricle in animals consuming alcohol compared with control increased more than 2 times (4.31 mm (3.80-4.41) and 2.0 mm (1.85-2.36); p = 0.0008, and the end-diastolic dimension was 5.95 mm (5.13-6.37) and 4.52 mm (3.85-4.90) respectively; p = 0.0171. Thus, the echocardiographic picture characteristic for alcoholic dilated cardiomyopathy is formed by the end of the 24th week of chronic alcoholiation.
authors.forename: S A
authors.initials: SA
authors.lastname: Kryzhanovskiĭ
authors.forename: L G
authors.initials: LG
authors.lastname: Kolik
authors.forename: I B
authors.initials: IB
authors.lastname: Tsorin
authors.forename: E O
authors.initials: EO
authors.lastname: Ionova
authors.forename: V N
authors.initials: VN
authors.lastname: Stoliaruk
authors.forename: M B
authors.initials: MB
authors.lastname: Vititnova
authors.forename: A V
authors.initials: AV
authors.lastname: Nadorova
authors.forename: S B
authors.initials: SB
authors.lastname: Seredenin
mesh_terms: D000818:Animals; D002310:Cardiomyopathy, Alcoholic / Q000175:diagnosis* / Q000503:physiopathology; D004452:Echocardiography; D000431:Ethanol / Q000633:toxicity*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D051381:Rats
chemical_list: D000431:Ethanol