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Mechanisms of alcoholic heart disease

¹ University of Wyoming College of Health Sciences, Laramie, WY 82071, USA
² Center for Cardiovascular and Pulmonary Research The Research Institute at Nationwide Children's Hospital and the Department of Pediatrics The Ohio State University Columbus, OH 43205, USA

^* To whom correspondence should be addressed.

	Abstract

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 Ca²⁺ 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.

Key Words: ethanol, acetaldehyde, alcoholic cardiomyopathy, oxidative stress

First published on August 21, 2008, doi:10.1177/1753944708095137

Therapeutic Advances in Cardiovascular Disease 2008;2:497.

A more recent version of this article appeared on December 1, 2008


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