Cirrhotic Cardiomyopathy: Pathogenic Mechanisms and Management Strategies

Abstract

Cirrhotic cardiomyopathy is defined as attenuated systolic and diastolic contractile responses to stress stimuli, electrophysiological repolarization changes, including prolonged QT interval, and enlargement or hypertrophy of cardiac chambers. The abnormal ventricular function is manifested under conditions of physiological or pharmacological stress, such as liver transplantation and transjugular intrahepatic portosystemic shunt insertion. Attenuated myocardial beta-adrenergic receptor function, increased activity of cardiac contractility inhibitors such as tumor necrosis factor-alpha, nitric oxide and carbon monoxide, and apoptosis have been shown to play an important role in the pathogenesis of this condition. The diagnostic criteria include abnormal systolic contractile responses to stress, diastolic dysfunction at rest, and the absence of clinically significant primary cardiopulmonary disease. Current pharmacological treatment is nonspecific and directed towards alleviation of left ventricular failure. Liver transplantation is currently the only proven treatment with a specific effect on cirrhotic cardiomyopathy.