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

P A Thürmann1

  • 1Institute of Clinical Pharmacology, University Witten/Herdecke, Wuppertal, Germany. thuermann@klinikum-wuppertal.de

Cardiology
|August 18, 1999
PubMed

Insights

Valsartan effectively reduced left ventricular mass in patients with essential hypertension and left ventricular hypertrophy (LVH). This angiotensin II receptor antagonist offers a significant therapeutic option for managing LVH and improving cardiovascular outcomes.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular disease.
  • Normalizing left ventricular mass is a key objective in antihypertensive therapy.

Purpose of the Study:

  • To compare the efficacy of valsartan (an angiotensin II receptor antagonist) with atenolol (a beta-blocker) in reducing left ventricular mass in patients with essential hypertension and LVH.

Main Methods:

  • A randomized, double-blind study involving 69 patients with essential hypertension and LVH.
  • Patients received either valsartan (80 mg/160 mg daily) or atenolol (50 mg/100 mg daily) for 8 months.
  • Echocardiography was used to assess left ventricular mass index (LVMI).

Main Results:

  • Both valsartan and atenolol significantly reduced blood pressure.
  • Valsartan treatment led to a greater reduction in LVMI (from 127 to 106 g/m²) compared to atenolol (from 127 to 117 g/m²).
  • Long-term valsartan treatment significantly reduced LVH in patients with essential hypertension.

Conclusions:

  • Valsartan is effective in reducing left ventricular hypertrophy in patients with essential hypertension.
  • Valsartan demonstrates a superior effect on LVH reduction compared to atenolol in this patient population.

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