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ORIGINAL ARTICLE
Year : 2016  |  Volume : 13  |  Issue : 1  |  Page : 11-17

Right ventricle morphology and function in systemic hypertension


Department of Cardiology, Cairo University, Giza, Egypt

Correspondence Address:
Noha H Hanboly
Department of Cardiovascular, Cairo University, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0189-7969.173854

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Background: Functional and structural consequences of hypertension on the right ventricle (RV) have received scarce attention due to the complex shape and orientation. The aim of the current study is to study the RV systolic and diastolic function in untreated hypertensive patients using two-dimensional speckle tracking analysis and correlating the findings with the morphological and functional changes of the left ventricle. Methods: This cross-sectional study involved 80 patients with mild to moderate untreated systemic hypertension and 40 healthy controls. M-mode echocardiography measurements of the right ventricular wall (RVW) diastolic thickness, tricuspid annular plane systolic excursion, left ventricular (LV) dimensions, and systolic function were performed. Pulsed Doppler echocardiography was used to measure peak early (TE) and peak atrium (TA) right ventricular diastolic filling velocities. Similar parameters of the LV diastolic filling were recorded. Tissue Doppler imaging (TDI) was done to determine the left and right myocardial annular velocities. Mean pulmonary artery pressure (MPAP) was measured noninvasively by the estimation of pulmonary artery acceleration time (AT). Apical 4-chamber images were acquired at high frame rate to extract RV peak systolic strains. Results: The current study revealed significantly thicker RVW in hypertensive group (5.3 vs. 2.8 mm in controls, P < 0.001). The RV diastolic dysfunction (RVDD) defined as tricuspid E/A ratio <0.8 was recorded in 60% of the hypertensive group. Significant positive correlation was found between tricuspid and mitral E/A ratio. Pulmonary AT was significantly reduced in hypertensive group (128.1 ± 5.4 vs. 143.6 ± 1.8 ms in healthy group, P < 0.001). Pulmonary artery systolic pressure (PASP) was significantly elevated in untreated hypertensive group 39.3 ± 7.8 mm Hg. The RV diameter was 2.2 and 2.1 cm in controls and hypertensive group (P = 0.011). Global RV systolic strain values were remarkably reduced in hypertensive group (−19.6 ± 1.4 vs. −24.1 ± 2.2% in controls, P < 0.001). Conclusions: The RV diastolic and systolic dysfunction was found in 60% and 30%, respectively, in the hypertensive group. Body mass index is a predictor of RVDD while several variables were found to be significantly (P < 0.001) associated with RV systolic dysfunction. These variables were left atrium dimensions, systolic blood pressure, and PASP. Possible causes of these structural and functional changes in the RV are translation of the increased LV filling pressure in the pulmonary circulation and interaction of the right and left ventricle.


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