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Trials  2001 

ELITE II and Val-HeFT are different trials: together what do they tell us?

DOI: 10.1186/cvm-2-5-240

Keywords: ACE inhibition, angiotensin receptor antagonism, heart failure, prognosis

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Despite progress over recent decades in the prevention and treatment of cardiovascular disease, heart failure continues to place a significant and increasing burden on patients and healthcare systems worldwide. In the USA alone, an estimated four million to five million people suffer from chronic heart failure, where it has an estimated five-year mortality rate of 50% and is the leading cause of hospitalisation in age groups 65 years and older [1,2].Typically, a patient with heart failure has reduced cardiac output, elevated filling pressures, and increased peripheral vascular resistance. Heart failure is not a homogenous disease process, however, and this makes the study of heart failure potentially complex, and makes the comparison between different patient cohorts in different clinical trials difficult.Angiotensin-converting enzyme (ACE) inhibitors are the treatment of choice in heart failure, with proven ability to reduce morbidity and mortality [3]. More recently, however, reporting of data from large-scale clinical trials has focused attention on the potential role of angiotensin II antagonists. Two such trials – the Losartan Heart Failure Survival Study (ELITE II) and the Valsartan Heart Failure Trial (Val-HeFT) – are reviewed below.Both ELITE II [4] and Val-HeFT [5] evaluated the efficacy of a selective angiotensin II receptor antagonist on morbidity and mortality in patients with symptomatic heart failure. There are essential differences however, in the design of these trials that must be taken into consideration when comparing these two studies and interpreting the clinical impact of the results. The bottom line, as detailed in this communication, is that the trials address very different hypotheses and provide complementary but different types of information; too much comparison is simply inappropriate.The questions addressed reflect the most essential differences between the two trials. The primary hypothesis in the ELITE II study was that losartan would


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