Cirrhotic cardiomyopathy as a problem in liver transplantation

Liver cirrhosis is an important cause of mortality, and access to liver transplantation has significantly improved its prognosis. However, most patients in the liver transplant waiting list have end-stage liver disease. Due to the marked peripheral vasodilatation in end-stage cirrhosis that masks a latent myocardial dysfunction, cardiac abnormalities at rest are usually subclinical and escape the attention of physicians. However, when challenged, the systolic and diastolic functions are attenuated. In addition to these contractile abnormalities, morphological changes can be observed such as cardiac chamber enlargement or hypertrophy, and changes in electrophysiological repolarization, including a prolonged QT interval. A combination of these cardiac abnormalities is termed cirrhotic cardiomyopathy. Liver transplantation induces significant cardiovascular stress. Clamping of the inferior vena cava and portal vein, hemorrhage and infusion therapy, and ischemia/reperfusion all cause hemodynamic fluctuation. This increases the cardiac workload, and thus, subclinical ventricular dysfunction may manifest earlier as overt heart failure during surgery and in the postoperative period. However, because liver transplantation is the only definitive treatment for end-stage liver failure and also appears to reverse cardiomyopathy, it is important to understand the changes in the cardiovascular system during this intervention. Although evidence suggests that cirrhotic cardiomyopathy may be reversible after orthotopic liver transplantation, further investigation is needed. This review focuses on cirrhotic cardiomyopathy before, during, and after liver transplantation. MedLine, Scopus databases were searched for publications up to 2024.