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European Journal of Heart Failure 2004 6(7):937-945; doi:10.1016/j.ejheart.2004.09.005
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© 2004 European Society of Cardiology

Effect of valsartan added to background ACE inhibitor therapy in patients with heart failure: results from Val-HeFT

Henry Kruma,*, Peter Carsonb, Csaba Farsangc, Aldo P. Maggionid, Robert D. Glazere, Nora Aknaye, Yann-Tong Chiange and Jay N. Cohnf

a Monash University Medical School, Alfred Hospital Melbourne, Australia
b Department of Veterans' Affairs, Medical Center Washington, DC, United States
c Semmelweis University, 1st Department of Internal Medicine Budapest, Hungary
d ANMCO Research Center Florence, Italy
e Novartis Pharmaceuticals Corporation, East Hanover New Jersey, United States
f Cardiovascular Division, Department of Medicine, University of Minnesota Medical School Minneapolis, Minnesota, United States

* Corresponding author. NHMRC Center of Clinical Research Excellence in Therapeutics, Department of Epidemiology and Preventive Medicine and Department of Medicine, Monash Medical School, Alfred Hospital, Prahran, Victoria 3181, Australia. Tel.: +61 3 9903 0042; Fax: +61 3 9903 0556. E-mail address: henry.krum{at}med.monash.edu.au


   Abstract

Aims: To investigate the effect of valsartan in the Valsartan-Heart Failure Trial (Val-HeFT) when added to angiotensin-converting enzyme inhibitor (ACEi) alone in patients with heart failure (HF).

Methods: Subjects in Val-HeFT receiving ACEi but not beta-blocker at baseline were analysed; 1532 were assigned to valsartan and 1502 assigned to placebo. Primary outcome events (all-cause mortality, hospitalisation for adjudicated heart failure, sudden death with resuscitation and need for >4 h of parenteral therapy for worsening heart failure) were monitored.

Results: Mortality was not affected by valsartan but morbidity endpoints were significantly reduced (36.3% in placebo, 31.0% in valsartan, p=0.002) in patients receiving an ACEi but no beta-blocker. Quality of life (QOL) was significantly improved, ejection fraction (EF) significantly increased, left ventricular (LV) diameter significantly reduced and plasma B-type natriuretic peptide, norepinephrine and aldosterone levels significantly reduced with valsartan compared to placebo. The morbidity benefit was significant in patients on ACEi doses below the median (22% reduction, p=0.003) and not statistically significant in those receiving ACEi doses above the median (14% reduction, p=0.143).

Conclusion: Valsartan reduces heart failure hospitalisations and slows LV remodelling in patients treated with an ACEi in the absence of beta-blockade, particularly in those on lower doses of ACEi.

Key Words: Chronic heart failure • Valsartan • Angiotensin receptor blockade • ACE-inhibition • Mortality

Received May 6, 2004; Revised August 12, 2004; Accepted September 20, 2004


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