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肝硬化中的心脏功能障碍。

Cardiac dysfunction in cirrhosis.

作者信息

Lee Ralph F, Glenn Tamara K, Lee Samuel S

机构信息

Liver Unit, University of Calgary, Calgary, AB, Canada.

出版信息

Best Pract Res Clin Gastroenterol. 2007;21(1):125-40. doi: 10.1016/j.bpg.2006.06.003.

DOI:10.1016/j.bpg.2006.06.003
PMID:17223501
Abstract

Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation. These abnormalities have been termed cirrhotic cardiomyopathy. The pathogenic mechanisms that underlie this syndrome include impairment of the beta-adrenergic receptor signalling, cardiomyocyte plasma membrane function, intracellular calcium kinetics, and humoral factors such as endogenous cannabinoids, nitric oxide and carbon monoxide. Cirrhotic cardiomyopathy is believed to contribute to the cardiac dysfunction that can be observed in patients with transjugular intrahepatic portosystemic stent-shunt insertion and liver transplantation. Insufficient cardiac contractile function may also play a role in the pathogenesis of hepatorenal syndrome precipitated by spontaneous bacterial peritonitis. In this review, the clinical features, pathogenic mechanisms, clinical consequences and management options for cirrhotic cardiomyopathy are discussed.

摘要

已知肝硬化与多种心血管异常有关。这些异常包括心输出量增加、动脉压降低和总外周阻力降低。尽管肝硬化患者的基线心输出量增加,但在面对药物、生理和手术应激时,其收缩和舒张功能减弱,同时还存在QT间期延长等心脏电活动异常。这些异常被称为肝硬化性心肌病。该综合征的发病机制包括β-肾上腺素能受体信号传导受损、心肌细胞质膜功能障碍、细胞内钙动力学异常以及内源性大麻素、一氧化氮和一氧化碳等体液因子异常。肝硬化性心肌病被认为与经颈静脉肝内门体分流术和肝移植患者中观察到的心脏功能障碍有关。心脏收缩功能不足也可能在自发性细菌性腹膜炎诱发的肝肾综合征发病机制中起作用。在这篇综述中,将讨论肝硬化性心肌病的临床特征、发病机制、临床后果及治疗选择。

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