The cirrhotic heart: cirrhotic cardiomyopathy and circulatory derangement

Cirrhotic cardiomyopathy has recently gained the dignity of a new clinical entity. The knowledge of subtle cardiostructural changes that can be detected even in the early stages of preascitic cirrhosis have contributed to a better understanding of the cardiovascular derangement observed as disease severity progresses. Diastolic dysfunction is frequently detected in this setting and structural changes in the heart are being characterized. Decompensated cirrhosis is characterized by decreased arterial blood pressure and peripheral vascular resistances, increased cardiac output and heart rate in the setting of hyperdynamic circulation favoured by total blood volume expansion, circulatory overload and overactivity of the endogenous vasoactive systems. Peripheral vasodilation prevents heart failure. Reduced heart responses to stressful conditions such as changes in cardiac loading conditions in presence of further deterioration of liver function, e.g. refractory ascites, hepatorenal syndrome, spontaneous bacterial peritonitis and bleeding esophageal varices, have recently been identified. Considering the availability of therapeutic interventions (paracentesis, transjugular intrahepatic porto-systemic shunt-TIPS, peritoneovenous shunt, liver transplantation) currently employed to manage the life-threatening complications of the most advanced phases of cirrhosis, knowledge of their impact on cardiovascular function is of paramount importance. Therapeutic interventions targeted to prevent and manage cardiovascular deterioration are being performed.