The occurrence of systemic hemodynamic abnormalities in cirrhosis has been recognized for more than half a century. These hemodynamic changes consist of a reduced peripheral vascular resistance and a compensatory increase in cardiac output leading to the hyperdynamic circulatory syndrome. By contrast, evidence of cardiac abnormalities associated with cirrhosis is relatively new and still awaits full characterization. The cluster of cardiac abnormalities has been termed cirrhotic cardiomyopathy, defined as a chronic cardiac dysfunction in patients with cirrhosis, characterized by blunted contractile responsiveness to stress, and/or altered diastolic relaxation with electrophysiological abnormalities, in the absence of known cardiac disease1 (Table 1). Initially thought to be a consequence of a latent alcoholic cardiomyopathy in patients with alcoholic cirrhosis, it has become clear that cardiac abnormalities leave aside the etiology of the underlying liver disease.