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Angiotensin II antagonism and the heart: valsartan in left ventricular hypertrophy.

Author(s): Thurmann PA

Affiliation(s): Institute of Clinical Pharmacology, University Witten/Herdecke, Wuppertal, Germany. thuermann@klinikum-wuppertal.de

Publication date & source: 1999, Cardiology., 91 Suppl 1:3-7.

Publication type: Clinical Trial; Randomized Controlled Trial

Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study the angiotensin II (AT(1) receptor) antagonist valsartan (Diovan((R)); 80 mg/160 mg q.d.) was compared with the beta-blocker atenolol (50 mg/100 mg q.d.) over 8 months in predominantly previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated with echocardiographic data. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001), and in the valsartan group (n = 9 with additional HCTZ) blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m(2) in the atenolol group and from 127 to 106 g/m(2) in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.

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