Tsiplenkova V G, Vikhert A M, Cherpachenko N M
J Am Coll Cardiol. 1986 Jul;8(1 Suppl A):22A-32A. doi: 10.1016/s0735-1097(86)80025-0.
The morphologic features of alcoholic cardiomyopathy in human sudden death compared with those of experimental alcoholic cardiomyopathy (6 weeks of alcohol administration and simultaneous inhibition of catalase activity) proved to be nearly identical. Regular and similar alterations in alcoholic cardiomyopathy in both human victims of sudden death and experimental rats are described as a complex of alterations characteristic of alcoholic cardiomyopathy. This complex of changes was used as the basis for morphologic diagnosis of endomyocardial biopsy in two groups of patients: I) chronic alcoholics (second to third stages), and II) patients with clinically diagnosed congestive cardiomyopathy. Typical signs of alcoholic cardiomyopathy were found in 9 of the 11 patients in the first group and in 6 of 18 in the second group. The fact that the features of alcoholic cardiomyopathy were not found in all cases of chronic alcoholism supports the hypothesis that the administration of alcohol itself is not sufficient for the development of this disease. The level of enzyme activity in the metabolism of alcohol appears to be of great importance. This hypothesis is confirmed by experiments with rats in which this disease developed only when there was simultaneous alcohol administration and inhibition of catalase activity. Histochemical study showed that the alterations of enzyme (both energetic and alcohol metabolism) in rats were similar to those found in the biopsy specimens from patients with alcoholic cardiomyopathy. Certain questions regarding the pathogenesis of alcoholic cardiomyopathy are discussed.
将人类猝死中的酒精性心肌病的形态学特征与实验性酒精性心肌病（给予酒精6周并同时抑制过氧化氢酶活性）的形态学特征相比较，结果证明两者几乎相同。在人类猝死受害者和实验大鼠的酒精性心肌病中，规律性且相似的改变被描述为酒精性心肌病的一系列特征性改变。这一系列变化被用作两组患者心内膜活检形态学诊断的基础：I）慢性酒精中毒者（第二至第三阶段），以及II）临床诊断为充血性心肌病的患者。在第一组的11名患者中有9名以及第二组的18名患者中有6名发现了酒精性心肌病的典型体征。并非在所有慢性酒精中毒病例中都发现酒精性心肌病的特征，这一事实支持了以下假说，即仅仅饮酒本身并不足以引发这种疾病。酒精代谢中的酶活性水平似乎至关重要。用大鼠进行的实验证实了这一假说，在这些实验中，只有当同时给予酒精并抑制过氧化氢酶活性时才会引发这种疾病。组织化学研究表明，大鼠体内酶（能量代谢酶和酒精代谢酶）的改变与酒精性心肌病患者活检标本中的改变相似。文中还讨论了有关酒精性心肌病发病机制的某些问题。
