title: Intravenous iron alone for the treatment of anemia in patients with chronic heart failure.
abstract: OBJECTIVE
  This study was undertaken to assess the hematologic, clinical, and biochemical response to intravenous iron in patients with chronic heart failure (CHF) and anemia.
  
  
  BACKGROUND
  Anemia is common in patients with CHF and is associated with higher morbidity and mortality. The combination of erythropoietin (EPO) and iron increases hemoglobin (Hb) and improves symptoms and exercise capacity in anemic CHF patients. It is not known whether intravenous iron alone is an effective treatment for anemia associated with CHF.
  
  
  METHODS
  Sixteen anemic patients (Hb < or =12 g/dl) with stable CHF (age 68.3 +/- 11.5 years, 12 men, 9 participants New York Heart Association [NYHA] functional class II and the remainder class III, left ventricular ejection fraction 26 +/- 13%) received a maximum of 1 g of iron sucrose by bolus intravenous injections over a 12-day treatment phase in an outpatient setting. Mean follow-up was 92 +/- 6 days.
  
  
  RESULTS
  Hemoglobin rose from 11.2 +/- 0.7 to 12.6 +/- 1.2 g/dl (p = 0.0007), Minnesota Living with Heart Failure (MLHF) score fell (denoting improvement) from 33 +/- 19 to 19 +/- 14 (p = 0.02), 6-min walk distance increased from 242 +/- 78 m to 286 +/- 72 m (p = 0.01), and all patients recorded NYHA class II at study end (p < 0.02). Changes in MLHF score and 6-min walk distance related closely to changes in Hb (r = 0.76, p = 0.002; r = 0.56, p = 0.03, respectively). Of all baseline measurements, only iron and transferrin saturation correlated with increases in Hb (r = 0.60, p = 0.02; r = 0.60, p = 0.01, respectively). There were no adverse events relating to drug administration or during follow-up.
  
  
  CONCLUSIONS
  Intravenous iron sucrose, when used without concomitant EPO, is a simple and safe therapy that increases Hb, reduces symptoms, and improves exercise capacity in anemic patients with CHF. Further assessment of its efficacy should be made in a multicenter, randomized, placebo-controlled trial.
authors.affiliation: Department of Clinical Cardiology, The Heart Hospital, London, United Kingdom. aidan@bolgers.org
authors.forename: Aidan P
authors.initials: AP
authors.lastname: Bolger
authors.forename: Frederick R
authors.initials: FR
authors.lastname: Bartlett
authors.forename: Helen S
authors.initials: HS
authors.lastname: Penston
authors.forename: Justin
authors.initials: J
authors.lastname: O'Leary
authors.forename: Noel
authors.initials: N
authors.lastname: Pollock
authors.forename: Raffi
authors.initials: R
authors.lastname: Kaprielian
authors.forename: Callum M
authors.initials: CM
authors.lastname: Chapman
mesh_terms: D000368:Aged; D000740:Anemia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D002303:Cardiac Output, Low / Q000150:complications*; D002908:Chronic Disease; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage* / Q000627:therapeutic use; D000077605:Ferric Oxide, Saccharated; D005767:Gastrointestinal Diseases / Q000150:complications; D005937:Glucaric Acid; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007275:Injections, Intravenous; D007501:Iron / Q000097:blood; D008297:Male; D008875:Middle Aged; D010807:Physical Endurance; D011446:Prospective Studies; D014168:Transferrin / Q000378:metabolism; D016138:Walking
chemical_list: D005290:Ferric Compounds; D006454:Hemoglobins; D014168:Transferrin; D007501:Iron; D000077605:Ferric Oxide, Saccharated; D005937:Glucaric Acid