It is widely known that liver cirrhosis, regardless of the etiologies is accompanied by severe
hemodynamic changes. The principal pathophysiological mechanisms are the hyperdynamic
circulation with increased cardiac output, heart rate along with reduced systemic vascular resistance.
Thus, counteractive mechanisms may develop that eventually lead to systolic as well as diastolic dysfunction
and rhythm disturbances, in order to keep a steady homeostasis in the human body.
Literally, blunted contractile responsiveness to physical or pharmacological stress, impaired diastolic
relaxation and electrophysiological changes, primarily QT interval prolongation, do occur
progressively in a cirrhotic patient with no known preexisting cardiac disease. This condition is
identified as cirrhotic cardiomyopathy (CCM), an entity different from that seen in alcoholic cardiac
For the past decades, clinicians did study and attempt to understand the pathophysiology and clinical
significance of this process. Indeed, various factors have been identified acting at the molecular
and cellular level.
Electrocardiography, echocardiography and various serum biomarkers are the main tools that help
healthcare practitioners to point to the correct diagnosis.
Noteworthy, the subjects that suffer from cirrhotic cardiomyopathy may progress to heart failure
during invasive procedures such as surgery, insertion of a transjugular intrahepatic portosystemic
shunting (TIPS) and liver transplantation. Besides, several studies have illustrated that CCM is a
contributing factor, or even a precipitant, of hepatorenal syndrome (HRS), a conceivable reversible
kidney failure in patients with liver cirrhosis and ascites.
The treatment is the same as it is in the patients with liver cirrhosis and heart failure and there is no
particular treatment for cirrhotic cardiomyopathy. Hence, it is of utmost importance to clearly comprehend
the pathophysiology of this disease in order to design more accurate diagnostic tools and
definitive treatments in a way to prevent the complications of cirrhosis and overt heart failure.
The objective of this review is to describe in a comprehensive way the pathological alterations that
occur in the cardiovascular system of cirrhotic patients. It will also point the limitations that remain in
the diagnosis and treatment strategies and more importantly, this review will alert the clinicians in the
modern era to further observe and record additional pathological changes in this subset of patients.