Myocardial contractility in cirrhosis is impaired, particularly under stres
sful situations, in a phenomenon termed cirrhotic cardiomyopathy. impairmen
t of the cardiac P-adrenergic receptor and its signaling function appears t
o be involved in the pathogenesis of this disorder. Additional mechanisms t
hat may have a role include alterations in the physicochemical properties o
f the cardiomyocyte plasma membrane and abnormalities in circulating humora
l factors, such as nitric oxide, carbon monoxide, and catecholamines. The w
idespread use of orthotopic liver transplantation (OLT) and its associated
stresses on the cardiovascular system have highlighted this condition. Card
iac failure has emerged as an important cause of morbidity and mortality in
the liver transplant recipient. Unfortunately, pre-OLT recognition of cirr
hotic cardiomyopathy is suboptimal because of a lack of sensitive, noninvas
ive diagnostic tests. Similarly, the management of cirrhotic cardiomyopathy
is largely empirical because of a paucity of existing literature. Although
evidence suggests that cirrhotic cardiomyopathy may be reversible after OL
T, the natural history of this condition warrants further investigation.