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Morphologic and Functional Changes in Right-Sided Cardiac Chambers in Patients With Chronic Liver Disease and Normal Pulmonary Artery Pressure.
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.
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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