Alteration Of Left Ventricular Early Diastolic Flow Propagation Velocity In Patients With Essential Hypertension And Its Clinical Significance

Objective To detect the alteration of left ventricular early diastolic flow propagation velocity (Vp) during left ventricular geometric remodeling in essential hypertension;to elucidate the relationship between left ventricular geometry and Vp as well as the changes of Vp after Valsartan therapy and to investigate its clinical significance. Methods We studied 105 patients with essential hypertension and 37 healthy volunteers. The left ventricular internal dimension at end diastole (LVIDd), interventricular septal thickness at end diastole (IVSd) and left ventricular posterior wall thickness at end diastole (LVPWd) was measured at the level of chordae tendineae of mitral valve from a cross sectional image in the parasternal long axis view by transthoracic M-mode echocardiography;and to calculate left ventricular ejection fraction (EF), left ventricular relative wall thickness (RWT) and left ventricular mass index (LVMI). From the apical four chamber view, diastolic mitral flow was recorded using pulsed Doppler and peak filling velocity in early diastole (E), peak filling velocity in atrial contraction (A), E/A ratio and early diastolic filling deceleration time (DT) were measured. Left ventricular early diastolic flow propagation velocity (Vp) was measured by color M-mode echocardiography from the apical four chamber view. Twenty hypertensive patients were treated with administration of Valsartan 80 ~ 160mg/d, and all parameters above were remeasured after 6 months. Results According to the control group's 95% range of normal value of left ventricular mass index and relative wall thickness, hypertensive patients were divided into four groups, i.e., normal geometry, concentric remodeling, concentric hypertrophy and eccentric hypertrophy. There were no significant differences in gender, age, heart rate and EF among all the groups (all P>0.05). Blood pressure was higher in each of hypertensive group than in the control group (all P<0.01), but there were no significant differences among hypertensive groups (all P>0.05). LVIDd was larger in the eccentric hypertrophy group than in any other groups (all P<0.01), however, it was smaller in concentric remodeling and concentric hypertrophy groups than in normal geometry and control groups (all P<0.05), and there was no significant difference between control group and normal geometry group (all P>0.05). IVSd and LVPWd were thicker in concentric hypertrophy group than in the rest groups (all P<0.01), but there were no significantdifferences among the rest groups (all P>0.05). RWT was higher in concentric hypertrophy group than in concentric remodeling group (PO.05), and it was higher in concentric remodeling and concentric hypertrophy groups than in any other groups (all PO.05 or 0.01) while there were no significant differences among them (all P>0.05). LVMI was higher in eccentric hypertrophy group than in concentric hypertrophy group (PO.05), and it was higher in eccentric hypertrophy group and concentric hypertrophy group than in the rest groups (all PO.01), but there were no significant differences among the rest groups (all P>0.05). Compared with control group and eccentric hypertrophy group, E and E/A ratio was lower, but A was higher in normal geometry group, concentric remodeling group and concentric hypertrophy group (all PO.05). There were no significant differences in E, A and E/A ratio between control group and eccentric hypertrophy group, and it was the same among control group, concentric remodeling group and concentric hypertrophy group (all P>0.05). DT was longer in concentric hypertrophy group than in the rest groups (all PO.01), and there were no significant differences among the rest groups (all P>0.05). Vp in each of hypertensive groups was significantly lower than in control group (all P<0.05 or 0.01). There were significant step-down changes among normal geometry, concentric remodeling, concentric hypertrophy and eccentric hypertrophy in VP (all PO.05 or 0.01). Spearman rank analysis showed there was a good correlation between VP and the progression of left ventricular geometric patterns (r=-0.62, P<0.0\). Multiple linear regression analysis showed that Vp was correlated with LVMI, systolic blood pressure and age in hypertensive patients (r=-0.40, P=0.02;r=-0.25, P=0.04;r=-0.20, P=0.0l, respectively), but other parameters have no correlation to Vp. After administration of Valsartan for 6 months, there was a significant reduction in systolic blood pressure, diastolic blood pressure, LVIDd, IVSd, LVPWd, RWT, LVMI and DT (all PO.05 or 0.01);and VP was improved significantly (PO.01) while there were no significant changes in heart rate, EF, E, A, and E/A ratio (all P>0.05). Conclusions Along with the progression of left ventricular geometric patterns of normal geometry, concentric remodeling, concentric hypertrophy and eccentric hypertrophy in order, there is a significant step-down change in Vp, and it reflects the degree of left ventricular diastolic dysfunction during left ventricular remodeling in hypertension accurately. LVMI, systolic blood pressure and age are important determinants of Vpin hypertensive patients. At the same time of decreasingblood pressure and LVMI efficiently in hypertensive patients, Valsartan can improve Vp significantly. Vp has important clinical value in assessment of left ventricular diastolic function, treatment effectiveness evaluation and the appraisal of the prognosis in hypertension.