Liver cirrhosis is associated with several cardiovascular abnormalities. Despite an increased baseline cardiac output, cirrhotic patients have a suboptimal ventricular response to stress. This phenomenon is called cirrhotic cardiomyopathy. The pathogenesis of this syndrome is multifactorial and includes diminished beta-adrenergic receptor signal transduction, cardiomyocyte cellular plasma membrane dysfunction, and increased activity or levels of cardiodepressant substances such as cytokines, endogenous cannabinoids, and nitric oxide. Although cirrhotic cardiomyopathy is usually clinically mild or silent, overt heart failure can be precipitated by stresses such as liver transplantation or transjugular intrahepatic portosystemic shunt insertion. Moreover, cirrhotic cardiomyopathy may play a role in the pathogenesis of hepatorenal syndrome. Treatment of this condition is mainly supportive. Orthotopic liver transplantation appears to improve or normalize the condition, generally after a period of several months.