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Withdrawal may reverse chronic alcohol-induced cardiac depression in models; leaves open reversibility in human cardiomyopathy.
In order to investigate the reversibility of chronic alcohol cardiac depression, hamsters were fed with 50% ethanol for 3 1/2 months, reaching serum alcohol levels of 0.13 +/- 0.11 g/dl (mean +/- SD). Alcohol was then withdrawn for 2 days. Isolated hearts were perfused according to a modified Langendorff method. Energy metabolites were studied using 31P magnetic resonance spectroscopy of isolated perfused hearts standardized by HPLC analysis of freeze-clamped tissue. Total intracellular calcium [Ca2+]i was measured with atomic absorption spectrophotometry, marking the extracellular space in vivo with K(CoEDTA). In alcohol-treated hamster hearts developed pressure was significantly depressed compared to controls. End-diastolic pressure was significantly increased. Coronary flow was not changed, whereas oxygen consumption and high-energy phosphate levels were significantly depressed. Intracellular pH was significantly decreased. [Ca2+]i was significantly increased. Heart weights were significantly lower. After alcohol withdrawal ventricular function, high-energy phosphate levels, and [Ca2+]i were not significantly different from control. The results indicate that chronic alcohol consumption depresses ventricular function and energy levels and also leads to myocardial acidosis. The increase in intracellular calcium likely causes mitochondrial dysfunction. Withdrawal of alcohol is associated with reversibility of functional and energetic cardiac depression.
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Auffermann et al. (1989) studied this question.
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