Myocardial contractility in cirrhosis is impaired, particularly under stressful situations, in a phenomenon termed cirrhotic cardiomyopathy. Impairment of the cardiac beta-adrenergic receptor and its signaling function appears to be involved in the pathogenesis of this disorder. Additional mechanisms that may have a role include alterations in the physicochemical properties of the cardiomyocyte plasma membrane and abnormalities in circulating humoral factors, such as nitric oxide, carbon monoxide, and catecholamines. The widespread use of orthotopic liver transplantation (OLT) and its associated stresses on the cardiovascular system have highlighted this condition. Cardiac failure has emerged as an important cause of morbidity and mortality in the liver transplant recipient. Unfortunately, pre-OLT recognition of cirrhotic cardiomyopathy is suboptimal because of a lack of sensitive, noninvasive diagnostic tests. Similarly, the management of cirrhotic cardiomyopathy is largely empirical because of a paucity of existing literature. Although evidence suggests that cirrhotic cardiomyopathy may be reversible after OLT, the natural history of this condition warrants further investigation.