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- W2150391242 endingPage "506" @default.
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- W2150391242 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 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." @default.
- W2150391242 created "2016-06-24" @default.
- W2150391242 creator A5032451475 @default.
- W2150391242 creator A5054154054 @default.
- W2150391242 date "2008-09-30" @default.
- W2150391242 modified "2023-10-17" @default.
- W2150391242 title "Mechanisms of alcoholic heart disease" @default.
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- W2150391242 doi "https://doi.org/10.1177/1753944708095137" @default.
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- W2150391242 hasPublicationYear "2008" @default.
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