The term cirrhotic cardiomyopathy (CCM) was defined in 2005 according to expert consensus at the World Congress of Gastroenterology in Montreal as a clinical phenotype in patients with liver cirrhosis consisting of systolic and diastolic dysfunction and a complementary criterion, such as electrophysiological changes, without the presence of a known underlying cardiac disease. For a long time, CCM was considered to result from toxic effects of alcohol consumption. The current view is that CCM is a separate entity independent of the various etiologies of liver cirrhosis. Thus, generally impaired liver function and portal hypertension with splanchnic vasodilation leads to altered hemodynamic conditions with central hypovolemia, increased activation of volume and baroreceptors, especially of the sympathetic nervous system, resulting in a hyperdynamic syndrome with increased cardiac stress. However, the contribution of portal hypertension to CCM is unclear.~With new MRI techniques such as cardiac T1 and T2 mapping and extracellular volume fraction (ECV), quantitative parameters are available to detect pathologies of the myocardium before they become detectable with conventional techniques in cardiac MRI or echocardiography.~The aim of this study is to use multiparametric MRI to investigate any differences in myocardial structure and function in patients with noncirrhotic portal hypertension compared with a control group with liver cirrhosis and to investigate a quantifiable correlation between cardiac, hepatic, and splenic parameters.
The aim of this study is to use multiparametric MRI to investigate any differences in myocardial structure and function in patients with noncirrhotic portal hypertension compared with a control group with liver cirrhosis.