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      Improving Outcomes in Congestive Heart Failure: Val-HeFT


      S. Karger AG

      Quality of life, Mortality, Val-HeFT, AT1 receptor blocker

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          The aims of the treatment of heart failure are to improve the quality of life and slow the progression of cardiac disease. Improvement of quality of life is best assessed by questionnaire; progression of the disease is assessed by measuring mortality and morbidity. The agenda for the future is to establish intermediate markers for progression of cardiac disease that can be substituted for morbidity and mortality, and thus improve the efficiency and shorten the follow-up of clinical trials. At present, polypharmacy is required to achieve optimal improvements in quality and duration of life. Furthermore, some drugs may favorably affect one end point and adversely affect the other; for example, beta-blockers may exert adverse short-term effects on quality of life but may slow progression of the disease. Certain inotropic drugs may reduce symptoms but shorten life expectancy. Angiotensin-converting enzyme (ACE) inhibitors have exerted favorable effects on both quality of life and mortality, but the magnitude of these benefits has been disappointingly small. Persistent angiotensin-induced vasoconstriction and endocrine effects, despite ACE inhibition, is one possible explanation. The Valsartan in Heart Failure Trial (Val-HeFT) has been designed to test the efficacy and safety of the AT<sub>1</sub> receptor blocker (ARB) valsartan in combination with ACE inhibitors and all other prescribed therapies in patients with heart failure. The study is powered to detect a mortality benefit and should therefore establish the role of ARBs in this patient group. When this trial and other ongoing studies are completed, we will be more able to define the role of ARBs in the treatment of heart failure.

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          Author and article information

          S. Karger AG
          August 1999
          06 August 1999
          : 91
          : Suppl 1
          : 19-22
          Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minn., USA
          47284 Cardiology 1999;91(suppl 1):19–22
          © 1999 S. Karger AG, Basel

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          Page count
          References: 25, Pages: 4


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