Angiotensin II antagonism and the heart: Valsartan in left ventricular hypertrophy

Authors
Citation
Pa. Thurmann, Angiotensin II antagonism and the heart: Valsartan in left ventricular hypertrophy, J CARDIO PH, 33, 1999, pp. S33-S36
Citations number
27
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
01602446 → ACNP
Volume
33
Year of publication
1999
Supplement
1
Pages
S33 - S36
Database
ISI
SICI code
0160-2446(1999)33:<S33:AIAATH>2.0.ZU;2-M
Abstract
Left ventricular hypertrophy (LVH) represents an independent risk factor fo r cardiovascular morbidity and mortality, and normalization of left ventric ular mass has become a desirable goal of antihypertensive treatment. In a r andomized, double-blind study, the angiotensin II (AT(1)-receptor) antagoni st valsartan (Diovan(R); 80-160 mg q.d.) was compared with the beta-blocker atenolol (50-100 mg q.d.) over 8 months in previously untreated patients w ith essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated by echocardiography. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], ini tial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001). In the valsartan group (n = 9 with HCTZ), blood pressure decreased from 163 /101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased fr om 127 to 117 g/m(2) in the atenolol group and from 127 to 106 g/m(2) in th e valsartan group. Long-term treatment with valsartan resulted in a signifi cant reduction of LVH in patients with essential hypertension.