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酒精性心肌病。

Alcoholic cardiomyopathy.

机构信息

Dipartimento Cardiovascolare, Ospedali Riuniti, Bergamo, Italy.

出版信息

J Cardiovasc Med (Hagerstown). 2010 Dec;11(12):884-92. doi: 10.2459/JCM.0b013e32833833a3.

Abstract

The myocardial depressant effects of excessive ethanol consumption have long been known. Excessive alcohol intake is reported in a wide range (3-40%) of patients with idiopathic dilated cardiomyopathy; furthermore, chronic excessive alcohol consumption may lead to progressive and chronic cardiac dysfunction and can be a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy (ACM). The pathophysiological mechanisms underlying ACM are poorly understood. Excessive alcohol consumption has been associated with left-ventricular myocyte loss in some animal models but not in all studies. In addition, heavy drinking may cause myocyte dysfunction, due to abnormalities in calcium homeostasis, and cause elevated levels of norepinephrine. Increasing doses of ethanol have been associated with a negative inotropic effect on myocytes in animal experiments. In this review, we evaluate the epidemiology, current pathophysiological mechanisms and possible role of factors that influence ACM and discuss its clinical presentation, prognosis and treatment.

摘要

长期以来,人们一直知道过量饮酒会导致心肌抑制作用。据报道,在广泛范围内(3%-40%)的特发性扩张型心肌病患者中存在过量饮酒的情况;此外,长期过量饮酒可能导致进行性和慢性心功能障碍,并且可能是扩张型心肌病的一个潜在原因,称为酒精性心肌病(ACM)。ACM 的病理生理机制尚未完全清楚。在一些动物模型中,过量饮酒与左心室心肌细胞丢失有关,但并非所有研究都如此。此外,大量饮酒可能会导致心肌细胞功能障碍,这是由于钙稳态异常引起的,并导致去甲肾上腺素水平升高。动物实验中,随着乙醇剂量的增加,心肌细胞出现负性肌力作用。在这篇综述中,我们评估了 ACM 的流行病学、当前的病理生理机制以及可能影响 ACM 的因素的作用,并讨论了其临床表现、预后和治疗。

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