A. Cuocolo et al., Effects of valsartan on left ventricular diastolic function in patients with mild or moderate essential hypertension: comparison with enalapril, J HYPERTENS, 17(12), 1999, pp. 1759-1766
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective This study compares the effects of an AT(1) angiotensin II recept
or antagonist (valsartan) with those of an ACE inhibitor (enalapril) on lef
t ventricular (LV) diastolic function in patients with mild or moderate ess
ential hypertension and no evidence of LV hypertrophy at echocardiography.
Methods A total of 24 patients (10 men, mean age 47 +/- 8 years) underwent
radionuclide ambulatory monitoring (Vest) of LV function at rest and during
upright bicycle exercise testing before and after two 4-week treatment per
iods with valsartan (80-160 mg/day orally) and enalapril (20-40 mg/day oral
ly) according to a double-blind, crossover randomization scheme.
Results In the overall population no differences between the two treatments
were found in LV peak filling rate (PFR) either at rest or at peak exercis
e. In a subgroup analysis it was found that baseline PFR was normal (= 2.5
EDV/sec) in 12 patients (subgroup A) and impaired (< 2.5 EDV/sec) in the re
maining 12 (subgroup B). In both subgroups. valsartan and enalapril induced
a significant and comparable reduction of systolic and diastolic blood pre
ssure. In subgroup A, valsartan and enalapril did not induce significant ch
anges in PFR. In subgroup B, valsartan increased PFR both at rest (from 2.0
+/- 0.3 to 2.4 +/- 0.3 EDV/sec, P < 0.01) and at peak exercise (from 4.1 /- 1.1 to 4.4 +/- 1.0 EDV/s, P < 0.05), whereas enalapril did not change PF
R either at rest (2.0 +/- 0.4 EDV/s, P < 0.01 versus valsartan) or at peak
exercise (3.7 +/- 1.1 EDV/sec, P< 0.05 versus valsartan).
Conclusions Valsartan-induced renin-angiotensin system blockade is able to
improve LV filling in patients with mild or moderate essential hypertension
and impaired diastolic function. These findings support the hypothesis of
a contribution of the renin-angiotensin system in the control of LV diastol
ic function in these patients. J Hypertens 1999, 17:1759-1766 (C) Lippincot
t Williams & Wilkins.