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Morphologic and Functional Changes in Right-Sided Cardiac Chambers in Patients With Chronic Liver Disease and Normal
Nuran Günay1, Şükran Erdem1, Tolga Sinan Güvenç2
1Departments of Cardiology, Ümraniye Research and Tranining Hospital, Istanbul, Turkey.
Insights
Chronic liver disease (CLD) increases right ventricular free wall thickness, even with normal pulmonary pressure, indicating cirrhotic cardiomyopathy. However, RV function remains unaffected in the absence of pulmonary hypertension.
Area of Science:
- Cardiology
- Hepatology
- Echocardiography
Background:
- Chronic liver disease (CLD) can lead to cardiovascular complications.
- Cirrhotic cardiomyopathy is a known complication, but its effects on right-sided heart chambers in the absence of pulmonary hypertension require further investigation.
Purpose of the Study:
- To evaluate the structural and functional impact of CLD on right-sided heart chambers (right ventricle and right atrium) in patients without pulmonary hypertension.
- To correlate echocardiographic findings with disease severity.
Main Methods:
- Echocardiographic assessment of right ventricular (RV) and right atrial (RA) dimensions, systolic/diastolic function, and myocardial strain in 51 CLD patients and 25 controls.
- Classification of CLD patients using Model of End-Stage Liver Disease and Child-Pugh scores.
Main Results:
- CLD patients exhibited significantly increased RV free wall thickness compared to controls (P < .001).
- No significant differences were observed in RV/RA dimensions, conventional RV systolic/diastolic function indices, or strain imaging between groups.
- RV end-diastolic diameter and RA area correlated with RV free wall thickness in CLD patients.
Conclusions:
- CLD is associated with increased RV free wall thickness, suggesting cirrhotic cardiomyopathy, even with normal pulmonary artery pressure.
- Cirrhotic cardiomyopathy does not impair RV systolic or diastolic function in the absence of pulmonary hypertension.
Objectives:
To investigate the effects of chronic liver disease (CLD) on the structural and functional characteristics of right-sided heart chambers in patients with normal pulmonary artery pressure.
Methods:
Fifty-one patients with known CLD but without pulmonary hypertension or other cardiovascular conditions were consecutively enrolled, along with 25 age- and sex-matched participants. Patients with CLD were classified according to the Model of End-Stage Liver Disease score and Child-Pugh classification. Right ventricular (RV) and right atrial (RA) dimensions, indices of RV systolic/diastolic function, and myocardial strain were measured by standard echocardiographic methods.
Results:
Patients in the study group had similar RV end-diastolic, end-systolic, and RA dimensions compared to controls. Similarly, neither the conventional indices of RV systolic/diastolic function nor the strain imaging findings were different between groups (P > .05). Only RV free wall thickness was significantly higher in the study group (mean ± SD, 4.15 ± 0.64 versus 3.75 ± 0.37 mm; P < .001). Right ventricular end-diastolic diameter (P = .018; r = 0.334) and RA area (P = .017; r = 0.335) had a significant correlation with RV free wall thickness in patients with CLD. Patients treated with beta blockers were found to have a significant reduction in mean RV free wall strain compared to patients who did not receive beta blocker treatment (-20.37 ± 6.6 versus -24.07 ± 6.52; P = .04).
Conclusions:
Patients with CLD had increased RV free wall thickness despite normal systolic pulmonary pressure, presumably secondary to cirrhotic cardiomyopathy. In the absence of pulmonary hypertension, however, cirrhotic cardiomyopathy did not cause impaired RV systolic or diastolic function.
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