Preedy V R, Richardson P J
Department of Clinical Biochemistry, King's College School of Medicine, London, UK.
Br Med Bull. 1994 Jan;50(1):152-63. doi: 10.1093/oxfordjournals.bmb.a072873.
Although the beneficial effects of mild or moderate ethanol consumption have been implied with respect to coronary artery disease, excessive ethanol consumption can result in alcoholic heart muscle disease (AHMD). The latter is characterized by features consistent with dilated cardiomyopathy with concomitant ventricular dysfunction and histopathological abnormalities. By definition, no other cause for the abnormalities in AHMD is demonstrated, other than excessive alcohol consumption. The metabolic basis of AHMD is probably multi-factorial, and the alterations of myocardial biochemistry are contributing factors for the precipitation and progression of the disease. The latter may reverse with abstention. Evidence is provided to support the contention that the abnormalities include central defects in protein metabolism, which perhaps are engendered by free radicals and/or the formation of acetaldehyde adducts. The latter may initiate the formation of auto-antibodies, therefore providing an auto-immune basis for AHMD in chronic alcohol misuse. Evidence is also provided to show that acetaldehyde is a potent perturbant of protein synthesis, and reduces the formation of new contractile proteins.
尽管适度饮酒对冠状动脉疾病有潜在益处，但过度饮酒会导致酒精性心肌病（AHMD）。后者的特征与扩张型心肌病一致，伴有心室功能障碍和组织病理学异常。根据定义，除过度饮酒外，未发现其他导致AHMD异常的原因。AHMD的代谢基础可能是多因素的，心肌生物化学改变是该疾病发生和进展的促成因素。后者可能会随着戒酒而逆转。有证据支持这样的观点，即异常包括蛋白质代谢的核心缺陷，这可能是由自由基和/或乙醛加合物的形成引起的。后者可能引发自身抗体的形成，从而为长期酗酒导致的AHMD提供自身免疫基础。也有证据表明乙醛是蛋白质合成的强力干扰物，并减少新收缩蛋白的形成。
