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Prevalence and prognostic significance of anemia in patients with congestive heart failure treated with standard vs high doses of enalapril.

Author(s): Terrovitis JV, Anastasiou-Nana MI, Alexopoulos GP, Tsolakis EJ, Margari ZJ, Drakos SG, Tsagalou EP, Papazoglou P, Efentakis S, Nanas JN

Affiliation(s): Heart Science Centre Harefield Hospital, Harefield, Middlesex, UK.

Publication date & source: 2006-03, J Heart Lung Transplant., 25(3):333-8. Epub 2006 Jan 6.

Publication type: Randomized Controlled Trial

BACKGROUND: Anemia is common in patients with congestive heart failure (CHF), although its etiology and pathophysiology remain largely unexplained. The purpose of this study was to examine the prognostic significance of a low hematocrit (Hct) in patients with CHF and the possible role of angiotensin-converting enzyme inhibition in anemia development. METHODS: Hct was measured at the time of enrollment of 160 patients with CHF, mean age 56 +/- 12 years, in New York Heart Association (NYHA) functional class 2.6 +/- 0.7 and with left ventricular ejection fraction of 20 +/- 9%. They were randomized to standard (mean: 17.9 +/- 4.3 mg/day) or high (mean: 42 +/- 19.3 mg/day) doses of enalapril. The follow-up duration was 2 years. Cox regression models were used to identify prognostic factors, and correlations among individual variables were tested. RESULTS: Mean baseline Hct was 42.7 +/- 5%. In multivariate analyses, low Hct (p = 0.036), older age (p = 0.022) and low systolic blood pressure (p = 0.032) were independent predictors of death within 2 years. A correlation was found between baseline Hct and NYHA class (Spearman's correlation coefficient: -0.183, p = 0.008). A significant decrease in Hct from 43.2 +/- 4.9% at baseline to 40.7 +/- 4.4% at 2 years was observed in the group treated with high doses of enalapril (p < 0.001). CONCLUSIONS: Low baseline Hct predicted poor 2-year prognosis in patients with CHF. Enalapril administered in high doses increased the incidence of anemia in this population. The underlying pathophysiologic mechanism and effects of maintaining a normal Hct on clinical outcomes remain to be determined.

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