Cirrhosis-Associated Cardiomyopathy

Liver cirrhosis is the 12 th leading cause of death in the US. The heart is one of the most adversely affected organs in liver cirrhosis. Cirrhosis-induced cardiomyopathy describes the cardiac dysfunction in patients with cirrhosis characterized by impaired contractile response to stress and/or altered diastolic relaxation with electrophysiologic abnormalities in the absence of other known cardiac disease. The current definition of cirrhosis-induced cardiomyopathy does not take into account recent evidence of resting contractile and relaxation dysfunction that can be appreciated by advanced imaging tools such as Doppler tissue imaging and cardiac magnetic resonance imaging. Cirrhosis-induced cardiomyopathy is caused by cellular as well as physiological mechanisms including but not limited to: beta adrenergic receptor dysfunction, calcium channelopathy, elevated levels of catecholamines, elevated levels of nitric oxide, carbon monoxide and hydrogen sulphide and stimulation of endogenous cannabinoid pathways capable of producing negative inotropic, relaxation, and electrophysiological defects. Currently there is no specific therapy for cirrhosis-induced cardiomyopathy. There is some evidence that short courses of beta blockers may restore prolonged QT interval to normal values. Also, there is an emerging evidence for a role of aldosterone antagonists in reducing myocardial hypertrophy. Liver transplantation may revert cardiac dysfunction, but surgery and shunt insertion may also aggravate the condition. More standardized tools are needed to screen for and treat cirrhosis-induced cardiomyopathy.