The effect of valsartan on left ventricular myocardial functions in hypertensive patients with left ventricular hypertrophy.

It has been shown by various diagnostic methodologies that angiotensin receptor blockage reduces left ventricular mass, improves diastolic function and increases contractility in hypertensive left ventricular hypertrophy (LVH). We planned to detect the effect of angiotensin receptor blockage on midwall mechanics and myocardial dynamics in hypertensive patients with LVH. Angiotensin 2 type 1 receptor blocker (valsartan 80-160 mg) was administered to 38 previously untreated hypertensive patients with LVH for 6 months. Left ventricular midwall mechanics and tissue Doppler velocities were measured at baseline and at the end of the study. Mean blood pressure was reduced from 152 ± 14/92 ± 8 to 131 ± 14/83 ± 9 mmHg (P <0.05). Left ventricular mass index was decreased from 135 ± 15 to 114 ± 14 g/m(2) (P <0.001). Midwall fractional shortening was increased from 19.0 ± 4 to 22.4 ± 3% (P <0.05). Circumferential end-systolic wall stress was decreased from 131 ± 44 to 119 ± 37 × 10(3) dyn/cm(2) (P <0.05). Left ventricular interventricular septal myocardial tissue peak systolic velocity was increased from 6.7 ± 1 to 8.1 ± 0.9 cm/s (P <0.001) and lateral wall myocardial tissue peak systolic velocity was increased from 7.5 ± 1 to 9.0 ± 1 cm/s (P <0.001), and E/E(m) ratio was significantly decreased (11.0 ± 0.3 to 8.90 ± 0.1, P <0.05) with 6-month valsartan therapy. This study suggests that valsartan exhibits not only blood pressure-lowering qualities but also cardioprotective actions in patients with hypertension because it enhances regression of LVH and improves left ventricular myocardial contractility and relaxation.