The impact of hypertension and hypertension-related left ventricle hypertrophy on right ventricle function.Echocardiography. 2007 Apr; 24(4):374-84.E
The aim of our study is to determine the effect of hypertension and hypertension-related left ventricle hypertrophy on right ventricle (RV) morphology and function by using RV standard Doppler echocardiographic indices, myocardial Doppler imaging, and strain/strain rate imaging indices.
We studied 35 patients with arterial hypertension and 30 age- and sex-adjusted control subjects who had no other pathological conditions. Standard transthoracic Doppler echocardiographical measurements, pulsed-wave tissue Doppler from tricuspid anulus (Peak systolic-st, peak early diastolic-et, peak late diastolic velocity-at), reconstructed spectral pulsed-wave tissue Doppler velocities (peak systolic-S, peak early-E, peak late diastolic velocity-A), and strain/strain rate imaging of RV free wall mid region (peak systolic strain-in, peak systolic strain rate-SR) were obtained.
Age, body surface area, blood pressure, and heart rate were comparable between two groups. Hypertensive subjects had significantly increased LV end-diastolic septal and posterior wall thickness, left atrial diameter, LV mass, LV mass index, and relative wall thickness during diastole. At the level of right ventricular lateral tricuspid annulus without systolic changes, the majority of diastolic measurements were altered in hypertensives (early diastolic velocity et; 13 +/- 2 vs. 18 +/- 4 m/sec, P < 0.0001, late diastolic velocity at; 20 +/- 4 vs. 14 +/- 3 m/sec, P < 0.0001, early to late diastolic velocity ratio; 0.69 +/- 0.14 vs. 1.32 +/- 0.38, P < 0.0001). The velocity data from two-dimensional color myocardial imaging at the level of RV free wall mid region again showed altered diastolic measurements in hypertensives (E; 8.01 +/- 2.6 vs. 10.4 +/- 3.14 m/sec, P < 0.001, A; 11.5 +/- 2.6 vs. 9.12 +/- 3.7 m/sec, P < 0.0001, E/A ratio; 0.75 +/- 0.41 vs. 1.87 +/- 0.48, P < 0.00). The peak systolic strain of RV free wall mid region was significantly lower in hypertensive individuals than controls (25.666 +/- 5.64 vs. 30.03 +/- 6.78%, P < 0.05). No significant differences were found in other parameters of RV function between hypertensive and control subjects.
The present study demonstrates that besides the manifest morphologic LV adaptations, significant RV functional alterations can be determined by TDI and strain/strain rate imaging in patients arterial hypertension. Both tissue velocities by TDI and strain imaging may be new tools to define and quantitate subtle change in systolic and diastolic function of right ventricular function in arterial hypertension that cannot be determined in standard echocardiographic parameters.