Richardson P J, Patel V B, Preedy V R
Department of Cardiology, King's College School of Medicine and Dentistry, London, UK.
Novartis Found Symp. 1998;216:35-45; discussion 45-50. doi: 10.1002/9780470515549.ch4.
Structural and functional abnormalities are prominent in alcoholic cardiomyopathy (ACM). Histological features in affected subjects are almost identical to the characteristics of dilated cardiomyopathy. Quantitative morphometry, however, can distinguish between ACM and dilated cardiomyopathy. Biopsies from patients with ACM show increases in the activities of some myocardial enzymes (alpha-hydroxybutyric dehydrogenase, creatine kinase, lactate dehydrogenase, malic dehydrogenase) which are correlated with the bimodal distribution of alcohol intake and may represent an adaptive response. One-third of patients with ACM have serum antibodies against cardiac acetaldehyde-protein adducts. Animal models of ethanol toxicity have shown that acutely, alcohol and acetaldehyde reduce the synthesis of cardiac contractile proteins in vivo. Two-dimensional SDS-PAGE has also shown that in rats chronically fed alcohol, the relative amounts of over 10% of heart muscle proteins are altered. The heat shock proteins (HSP) Hsp60 and Hsp70 are decreased in alcohol-fed rats, as is desmin. Reduction in HSPs may indicate reduced myocardial protection whilst a fall in desmin may indicate structural defects. In conclusion, ACM is a complex process that is due to altered protein synthesis, the formation of acetaldehyde adducts and a reduction of cardiac HSPs and desmin. Both acetaldehyde and alcohol are myocardial perturbants.
结构和功能异常在酒精性心肌病（ACM）中很突出。受影响个体的组织学特征与扩张型心肌病的特征几乎相同。然而，定量形态学可以区分ACM和扩张型心肌病。ACM患者的活检显示某些心肌酶（α-羟丁酸脱氢酶、肌酸激酶、乳酸脱氢酶、苹果酸脱氢酶）的活性增加，这些酶与酒精摄入的双峰分布相关，可能代表一种适应性反应。三分之一的ACM患者有针对心脏乙醛蛋白加合物的血清抗体。乙醇毒性的动物模型表明，急性情况下，酒精和乙醛会在体内减少心脏收缩蛋白的合成。二维SDS-PAGE也显示，长期喂食酒精的大鼠中，超过10%的心肌蛋白相对含量发生改变。热休克蛋白（HSP）Hsp60和Hsp70在喂食酒精的大鼠中减少，结蛋白也减少。热休克蛋白的减少可能表明心肌保护作用降低，而结蛋白的减少可能表明结构缺陷。总之，ACM是一个复杂的过程，是由于蛋白质合成改变、乙醛加合物的形成以及心脏热休克蛋白和结蛋白的减少。乙醛和酒精都是心肌干扰物。
