The heart: pathophysiology and clinical implications of cirrhotic cardiomyopathy

Abstract

Cirrhosis is associated with hyperdynamic circulation, which consists of peripheral vasodilatation and increased cardiac output. Peripheral vasodilatation is central to hyperdynamic circulation and portal hypertension in cirrhosis. However, those mechanisms underlying hyperdynamic circulation remain elusive, and are not fully understood. Most of the earlier research and attention have been focused on humoral factor abnormalities. Various gut-derived or locally produced humoral factors such as nitric oxide, endotoxin, endocannabinoids, and others have been implicated as possible mediators of hyperdynamic circulation development in cirrhosis. The associated cardiac dysfunction had been termed "cirrhotic cardiomyopathy (CCM)," which is an entity different from that seen in alcoholic heart muscle disease. Clinically, these patients present with sodium fluid retention, and strain often unmasks the presence of latent heart failure. No specific treatment can yet be recommended, but caution should be used with respect to procedures that may stress the heart such as shunt implantation and liver transplantation. Ultimately, additional research will be necessary to more accurately describe the prevalence, impact, and morbidity and survival rates for CCM, and to identify potential treatments.