Hypertension, Portal, Cardiomyopathies
Conditions
Keywords
Cardiac MRI, Hepatic MRI
Brief summary
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.
Detailed description
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.
Interventions
Multiparametric cardiac magnetic resonance, including functional and structural parameters
Sponsors
Study design
Eligibility
Inclusion criteria
1. noncirrhotic portal hypertension 2. age at least 18 years
Exclusion criteria
1. underlying cardiac disease, e.g., coronary heart disease/myocardial infarction, myocarditis, cardiomyopathies of other causes, congenital heart disease 2. patients who are using a intrauterinpessare for contraception 3. pregnant and breastfeeding women 4. patients with contraindications for MRI (not suitebale metallic implants) 5. patients with contraindications for MRI contrast agents (renal insufficiency, allergy)
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Myocardial T1 relaxation time | Measurement will be performed within 2 weeks after MRI scan. | T1 relaxation times will be obtained to asses acute myocardial injury and fibrosis. T1 maps will be analyzed using a segmental approach by region of interest analysis. T1 relaxation times are given in \[ms\]. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Myocardial T2 relaxation time | Measurement will be performed within 2 weeks after MRI scan. | T2 relaxation times will be obtained to asses myocardial edema. T2 maps will be analyzed using a segmental approach by region of interest analysis. T2 relaxation times are given in \[ms\]. |
| Myocardial ECV | Measurement will be performed within 2 weeks after MRI scan. | Myocardial extracellular volume will be obtained to asses extracellular space/myocardial fibrosis. ECV values will be calculated using a segmental approach by region of interest analysis of native and contrast-enhanced T1 relaxation maps. ECV values are given in \[%\]. |
| Myocardial strain | Measurement will be performed within 2 weeks after MRI scan. | Cardiac magnetic resonance feature-tracking will be used to asses left ventricular longitudinal, circumferential and radial strain. |
Countries
Germany