Document Detail


Mechanisms of alcoholic heart disease.
MedLine Citation:
PMID:  19124444     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Compromised heart function is regularly seen in patients with chronic alcohol ingestion and is often manifested as cardiomegaly, reduced myocardial contractility (with concomitant reductions in ejection fraction and stroke volume), myocardial fibrosis, enhanced risk of stroke and hypertension, and disruptions in the myofibrillary structure. A number of mechanisms including oxidative damage, deposition of triglycerides, altered fatty acid extraction, decreased myofilament Ca(2+) sensitivity, and impaired protein synthesis have been proposed for the development of alcoholic cardiomyopathy. Nonetheless, the underlying mechanism(s) has not been delineated. Several alcohol metabolites have been identified as specific toxins of myocardial tissue, including ethanol, its first and major metabolic product--acetaldehyde--and fatty acid ethyl esters. Acetaldehyde directly impairs cardiac contractile function, disrupts cardiac excitation-contraction coupling and promotes oxidative damage and lipid peroxidation. Unfortunately, the most direct approach to studying this (direct administration of acetaldehyde) is impossible, since direct intake of acetaldehyde is highly toxic and unsuitable for chronic studies. In order to overcome this obstacle, transgenic mice have recently been produced to artificially alter ethanol/acetaldehyde metabolism, resulting in elevated acetaldehyde levels after ethanol ingestion. This review will summarize some of the postulated mechanisms for alcoholic cardiomyopathy, with special emphasis on animal models.
Authors:
Jun Ren; Loren E Wold
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2008-08-21
Journal Detail:
Title:  Therapeutic advances in cardiovascular disease     Volume:  2     ISSN:  1753-9447     ISO Abbreviation:  -     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2009-01-06     Completed Date:  2009-02-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101316343     Medline TA:  Ther Adv Cardiovasc Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  497-506     Citation Subset:  IM    
Affiliation:
University of Wyoming College of Health Sciences, Laramie, WY 82071, USA. jren@uwyo.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathy, Alcoholic / metabolism*,  physiopathology*
Central Nervous System Depressants / adverse effects*
Ethanol / adverse effects*
Humans
Oxidative Stress / physiology*
Grant Support
ID/Acronym/Agency:
1R01 AA013412/AA/NIAAA NIH HHS; 5P20RR016474/RR/NCRR NIH HHS; R15 AA13575/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Central Nervous System Depressants; 64-17-5/Ethanol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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