Circulation, Vol 58, 965-970, Copyright © 1978 by American Heart Association
RJ Bing
Changes in cardiac metabolism in myocardial failure and after alcohol
ingestion are discussed. The main effect of alcohol ingestion is loss of
cardiac contractility. Since heart muscle does not contain alcohol
dehydrogenase, its toxicity is probably the result of a direct toxic effect
of ethanol and acetaldehyde on the myocardial cell, possibly involving
various membrane systems. Alcohol inhibits mitochondrial respiration and
the activity of enzymes in the tricarboxylic acid cycle, and its interferes
with both mitochondrial calcium uptake and binding. Ethanol profoundly
affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial
protein synthesis and inhibits Ca++- activated myofibrillar ATPase. In
myocardial failure, a series of possibilities may be responsible for the
loss of contractility. Excitation-contraction coupling could be disturbed
at the level of the sarcolemma, at the sarcoplasmic reticulum, at the
mitochondria, and between calcium and the regulatory proteins. Deficiencies
in Ca++ delivery systems of excitation-contraction coupling on the myosin
ATPase activity could be responsible for the dimunition in cardiac
contractility. Mitochondrial function may also be involved, since
mitochondria from failing human hearts are defective with respect to
respiratory control and calcium accumulation. Under certain conditions, the
relationship of mitochondria to calcium sequestration is very important in
influencing contractility. The involvement of contractile and regulatory
proteins in myocardial failure cannot be excluded.
ARTICLES
Cardiac metabolsim: its contributions to alcoholic heart disease and myocardial failure
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