title: Anemia and change in hemoglobin over time related to mortality and morbidity in patients with chronic heart failure: results from Val-HeFT.
abstract: BACKGROUND
  Anemia is known to be a prognostic marker for patients with heart failure. However, little is known about the prognostic value of changes in hemoglobin (Hgb) over time or about the causes of anemia.
  
  
  RESULTS
  Retrospective analysis of Valsartan Heart Failure Trial data indicated that the quartile of patients with the biggest average decrease in Hgb over 12 months (from 14.2 to 12.6 g/dL) had significantly (P< or =0.01) increased risk of subsequent hospitalization (hazard ratio [HR], 1.47), morbid events (HR, 1.41), and death (HR, 1.6) compared with the quartile that exhibited little change in Hgb over 12 months (from 13.7 to 13.8 g/dL). Increasing Hgb was significantly associated with lower mortality in patients with (HR, 0.78) and without (HR, 0.79) anemia at baseline. Anemia at baseline and the changes in Hgb were independently associated with serum albumin, blood pressure, glomerular filtration rate, B-type natriuretic peptide, and C-reactive protein. Lack of anemia at baseline and increases in Hgb over 12 months were not associated with smaller left ventricular diameters or higher ejection fractions.
  
  
  CONCLUSIONS
  Changes in Hgb over 12 months were inversely associated with subsequent risk of mortality and morbidity, independently of the effects of baseline anemia and other important predictors. Several factors were independently related to anemia at baseline and changes in Hgb, suggesting multiple causes of anemia in patients with heart failure. These findings raise important questions about the optimal level of Hgb in patients with moderate to severe heart failure and how to achieve them.
authors.affiliation: VA Medical Center, Minneapolis, MN 55417, USA. anand001@umn.edu
authors.forename: Inder S
authors.initials: IS
authors.lastname: Anand
authors.forename: Michael A
authors.initials: MA
authors.lastname: Kuskowski
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Rector
authors.forename: Viorel G
authors.initials: VG
authors.lastname: Florea
authors.forename: Robert D
authors.initials: RD
authors.lastname: Glazer
authors.forename: Allen
authors.initials: A
authors.lastname: Hester
authors.forename: Yann Tong
authors.initials: YT
authors.lastname: Chiang
authors.forename: Nora
authors.initials: N
authors.lastname: Aknay
authors.forename: Aldo P
authors.initials: AP
authors.lastname: Maggioni
authors.forename: Cristina
authors.initials: C
authors.lastname: Opasich
authors.forename: Roberto
authors.initials: R
authors.lastname: Latini
authors.forename: Jay N
authors.initials: JN
authors.lastname: Cohn
mesh_terms: D000368:Aged; D000740:Anemia / Q000097:blood* / Q000401:mortality*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy / Q000401:mortality*; D006454:Hemoglobins; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009017:Morbidity; D015999:Multivariate Analysis; D015995:Prevalence; D011379:Prognosis; D016019:Survival Analysis; D013777:Tetrazoles / Q000627:therapeutic use; D014633:Valine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D006454:Hemoglobins; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine