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Updated: Jun 29, 2025

Comprehensive Echocardiographic Assessment of Right Ventricle Function in a Rat Model of Pulmonary Arterial Hypertension
Published on: January 20, 2023
Pattern of Right Ventricular Changes in Patients with Uncomplicated Systemic Hypertension at a Tertiary Centre in
R K Moronkola1, A C Mbakwem2, A O Ajibare1
1Department of Medicine, Lagos State University Teaching Hospital, Ikeja, Lagos, Nigeria
Background And Aims:
Hypertension is an independent risk factor for cardiovascular complications. The effect of systemic hypertension on the right ventricle (RV) has received less attention probably due to its complex structure and location. The aim of the study was to assess the effect of systemic hypertension on the structure and function of the right ventricle using transthoracic echocardiography.
Method:
One hundred hypertensives and 100 healthy controls were recruited into the study. Transthoracic echocardiography was used to measure RV wall thickness (RVWT) in diastole, RV internal dimensions in diastole, tricuspid annular plane systolic excursion (TAPSE), right ventricular filling velocities (TE and TA), and RV systolic excursion velocity (RVSm). These measurements were repeated on the left ventricle.
Results:
There was significantly thicker RV wall (0.51 + 0.08cm vs 0.44+0.08cm; p=0.001) in the hypertensive group and higher frequency of RV hypertrophy (48.45% vs 18.75%; p<0.001). Tricuspid annular plane systolic excursion (TAPSE) and the tricuspid annular peak systolic excursion velocity (TSm) were significantly lower in the hypertensive group (2.34+0.45cm vs 2.50+0.36cm; p=0.008, and 11.70+3.03cm/s vs 12.60+2.93cm/s p=0.039, respectively), though no participant had abnormal TAPSE. Tricuspid E/A ratio was lower in the hypertensive group (1.13+ 0.33 vs 1.24+0.27; p=0.011). The tricuspid E/A ratio had positive correlation with mitral E/A ratio.
Conclusion:
Right ventricular structural and functional changes are found in systemic hypertension, even in the absence of other systemic complications. These changes could have been mediated by ventricular interdependence and altered humoral factors.
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