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Morphologic and Functional Changes in Right‐Sided Cardiac Chambers in Patients With Chronic Liver Disease and Normal Pulmonary Artery Pressure
Author(s) -
Günay Nuran,
Erdem Şükran,
Güvenç Tolga Sinan,
Bulur Atilla,
Özdil Kamil,
Hasdemir Hakan,
Uyan Cihangir
Publication year - 2018
Publication title -
journal of ultrasound in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 91
eISSN - 1550-9613
pISSN - 0278-4297
DOI - 10.1002/jum.14516
Subject(s) - medicine , cardiology , pulmonary artery , pulmonary hypertension , diastole , blood pressure , coronary artery disease
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.