Lecture: Cirrhotic cardiomyopathy

Today’s lecture focused on the liver-heart axis, with portal hypertension and the hyperdynamic circulatory state and the effect it has on the otherwise normal heart.  In fact over half of cirrhotics will display cardiac abnormalities, mostly in the form of electrophysiologic changes.

Cardiac abnormalities come in three forms: 1. electrophysiologic changes (usually a prolonged QT interval or electromechanical dyssynchrony); 2. diastolic dysfunction (cardiomyocyte hypertrophy and fibrosis means inadequate relaxation and poor compliance to passive filling); and 3. systolic dysfunction (changes in beta adrenergic signaling, calcium availability and and increase in contractile suppressants like endotoxin, nitric oxide and carbon monoxide impair inotropy and chronotropy).

The prevalence, natural history and treatment of cirrhotic cardiomyopathy is still unknown.  Although overt heart failure is rare in the cirrhotic patient, cirrhotic cardiomyopathy may play a pivotal role in other relevant conditions like spontaneous bacterial peritonitis and hepatorenal syndrome.

The working definition of cirrhotic cardiomyopathy is:  

“A cardiac dysfunction in patients with cirrhosis characterized by impaired contractile responsiveness to stress and/or altered diastolic relaxation with electrophysiological abnormalities (in the absence of other known cardiac disease).”
 
 
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