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World J Gastroenterol. Nov 14, 2014; 20(42): 15492-15498
Published online Nov 14, 2014. doi: 10.3748/wjg.v20.i42.15492
Cirrhotic cardiomyopathy: A cardiologist’s perspective
Natig Gassanov, Evren Caglayan, Nasser Semmo, Gero Massenkeil, Fikret Er
Natig Gassanov, Fikret Er, Department of Internal Medicine I, Klinikum Gütersloh, 33332 Gütersloh, Germany
Evren Caglayan, Department of Internal Medicine III, University of Cologne, 50937 Cologne, Germany
Nasser Semmo, Hepatology, Department of Clinical Research, University of Bern, 3010 Bern, Switzerland
Gero Massenkeil, Department of Internal Medicine II, Klinikum Gütersloh, 33332 Gütersloh, Germany
Author contributions: Gassanov N, Caglayan E and Er F drafted and wrote the entire manuscript; Semmo N and Massenkeil G made substantial contributions to conception and design of the pathophysiology and treatment part of the manuscript.
Correspondence to: Natig Gassanov, MD, Department of Internal Medicine I, Klinikum Gütersloh, 33332 Gütersloh, Germany. natig.gassanov@klinikum-guetersloh.de
Telephone: +49-5241-8324402 Fax: +49-221-47832712
Received: October 30, 2013
Revised: April 1, 2014
Accepted: June 12, 2014
Published online: November 14, 2014
Processing time: 383 Days and 14.7 Hours
Abstract

Cardiac dysfunction is frequently observed in patients with cirrhosis, and has long been linked to the direct toxic effect of alcohol. Cirrhotic cardiomyopathy (CCM) has recently been identified as an entity regardless of the cirrhosis etiology. Increased cardiac output due to hyperdynamic circulation is a pathophysiological hallmark of the disease. The underlying mechanisms involved in pathogenesis of CCM are complex and involve various neurohumoral and cellular pathways, including the impaired β-receptor and calcium signaling, altered cardiomyocyte membrane physiology, elevated sympathetic nervous tone and increased activity of vasodilatory pathways predominantly through the actions of nitric oxide, carbon monoxide and endocannabinoids. The main clinical features of CCM include attenuated systolic contractility in response to physiologic or pharmacologic strain, diastolic dysfunction, electrical conductance abnormalities and chronotropic incompetence. Particularly the diastolic dysfunction with impaired ventricular relaxation and ventricular filling is a prominent feature of CCM. The underlying mechanism of diastolic dysfunction in cirrhosis is likely due to the increased myocardial wall stiffness caused by myocardial hypertrophy, fibrosis and subendothelial edema, subsequently resulting in high filling pressures of the left ventricle and atrium. Currently, no specific treatment exists for CCM. The liver transplantation is the only established effective therapy for patients with end-stage liver disease and associated cardiac failure. Liver transplantation has been shown to reverse systolic and diastolic dysfunction and the prolonged QT interval after transplantation. Here, we review the pathophysiological basis and clinical features of cirrhotic cardiomyopathy, and discuss currently available limited therapeutic options.

Keywords: Cirrhosis; Cardiomyopathy; Pathogenesis; Hyperdynamic circulation; Diastolic dysfunction

Core tip: Currently, little is known about the pathogenesis, diagnostic parameters and therapeutic principles of the cirrhotic cardiomyopathy. Increased cardiac output due to hyperdynamic circulation seems to be a pathophysiological hallmark of the disease. The main clinical features of cirrhotic cardiomyopathy include attenuated systolic contractility in response to physiologic or pharmacologic strain, diastolic dysfunction, electrical conductance abnormalities and chronotropic incompetence. Here, we review the pathophysiological basis and clinical features of cirrhotic cardiomyopathy, and discuss currently available therapeutic options.