title: Iron deficiency: an ominous sign in patients with systolic chronic heart failure.
abstract: OBJECTIVE
  Beyond erythropoiesis, iron is involved in numerous biological processes crucial for maintenance of homeostasis. Patients with chronic heart failure (CHF) are prone to develop iron deficiency (ID), and iron supplementation improves their functional status and quality of life. We sought to examine the relationship between ID and survival in patients with systolic CHF.
  
  
  RESULTS
  In a prospective observational study, we evaluated 546 patients with stable systolic CHF [age: 55 +/- 11 (mean +/- standard deviation) years, males: 88%, left ventricular ejection fraction: 26 +/- 7%, New York Heart Association (NYHA) class (I/II/III/IV): 57/221/226/42]. Iron deficiency was defined as: ferritin <100 microg/L, or 100-300 microg/L with transferrin saturation <20%. The prevalence of ID was 37 +/- 4% [+/-95% confidence intervals (CI)] in the entire CHF population (32 +/- 4 vs. 57 +/- 10%-in subjects without vs. with anaemia defined as haemoglobin level <12 g/dL in women and <13 g/dL in men, P < 0.001). In a multiple logistic model, ID was more prevalent in women, those in the advanced NYHA class, with higher plasma N-terminal pro-type B natriuretic peptide and higher serum high-sensitivity C-reactive protein (all P < 0.05). At the end of follow-up (mean duration: 731 +/- 350 days), there were 153 (28%) deaths and 30 (6%) heart transplantations (HTX). In multivariable models, ID (but not anaemia) was related to an increased risk of death or HTX (adjusted hazard ratio 1.58, 95% CI 1.14-2.17, P < 0.01).
  
  
  CONCLUSIONS
  In patients with systolic CHF, ID is common and constitutes a strong, independent predictor of unfavourable outcome. Iron supplementation may be considered as a therapeutic approach in these patients to improve prognosis.
authors.affiliation: Department of Heart Diseases, Wroclaw Medical University, Centre for Heart Diseases, Military Hospital, ul. Weigla 5, Wroclaw, Poland. ewa.jankowska@antro.pan.wroc.pl
authors.forename: Ewa A
authors.initials: EA
authors.lastname: Jankowska
authors.forename: Piotr
authors.initials: P
authors.lastname: Rozentryt
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Witkowska
authors.forename: Jolanta
authors.initials: J
authors.lastname: Nowak
authors.forename: Oliver
authors.initials: O
authors.lastname: Hartmann
authors.forename: Beata
authors.initials: B
authors.lastname: Ponikowska
authors.forename: Ludmila
authors.initials: L
authors.lastname: Borodulin-Nadzieja
authors.forename: Waldemar
authors.initials: W
authors.lastname: Banasiak
authors.forename: Lech
authors.initials: L
authors.lastname: Polonski
authors.forename: Gerasimos
authors.initials: G
authors.lastname: Filippatos
authors.forename: John J V
authors.initials: JJ
authors.lastname: McMurray
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
authors.forename: Piotr
authors.initials: P
authors.lastname: Ponikowski
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D002908:Chronic Disease; D018572:Disease-Free Survival; D005260:Female; D005293:Ferritins / Q000097:blood; D054143:Heart Failure, Systolic / Q000150:complications* / Q000378:metabolism; D006801:Humans; D000090463:Iron Deficiencies; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D011379:Prognosis; D011446:Prospective Studies; D014168:Transferrin / Q000378:metabolism
chemical_list: D010446:Peptide Fragments; D014168:Transferrin; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein; D005293:Ferritins