Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy.

Background & Aims: Cirrhotic cardiomyopathy is a recently recognized entity, but detailed cellular and molecular mechanisms remain unclarified. We aimed to elucidate the role of myosin heavy chain isoform shifts and their relation to calcium transients in the contractile kinetics of cirrhotic rats.

Methods: Cirrhosis was induced in male Lewis Brown-Norway rats by bile duct ligation (BDL).

Role of cardiac myofilament proteins titin and collagen in the pathogenesis of diastolic dysfunction in cirrhotic rats.

Background & Aims: Significance of diastolic dysfunction in cirrhotic cardiomyopathy has been brought to the forefront with several reports of unexpected heart failure following liver transplantation and transjugular intrahepatic portosystemic stent-shunt, but the etiology remains unclear. The present study investigated the role of passive tension regulators - titin and collagen - in the pathogenesis of this condition.

Methods: Cirrhosis was induced by bile duct ligation (BDL) in rats, while controls underwent bile duct inspection with no ligation.

Cardiac dysfunction in cirrhosis.

Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation.