4.5 Article

Acute heart failure and iron deficiency: a prospective, multicentre, observational study

Journal

ESC HEART FAILURE
Volume 9, Issue 1, Pages 398-407

Publisher

WILEY PERIODICALS, INC
DOI: 10.1002/ehf2.13737

Keywords

Acute decompensated heart failure; Iron deficiency; Worsening heart failure; Comorbidity; Functional iron deficiency; Iron availability disorder

Funding

  1. Vifor Pharma, Ltd., Glattbrugg, Switzerland
  2. Dutch Network for Cardiovascular Research (WCN)

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The prevalence of iron deficiency in patients with acute heart failure is high, but some patients show improvement during treatment even without iron supplementation. Absolute iron deficiency is more likely to persist, while functional iron deficiency often resolves during treatment, possibly indicating reduced iron availability rather than a true deficiency.
Aims The prevalence and the natural course of iron deficiency (ID) in acute heart failure (AHF) are still unclear. We investigated the prevalence of ID in unselected patients admitted with AHF on admission, at discharge and up to 3 months thereafter. Methods and results In this prospective, multicentre, observational study, 742 patients admitted with AHF were enrolled. The main study outcome was the percentage of patients with ID (ferritin or ferritin 100-299 mu g/L and transferrin saturation <20% = functional ID) at admission (T0), after clinical stabilization prior to discharge (T1), and 10 +/- 6 weeks after discharge (T2). At T0, ID was present in 71.8% of the patients (44.1% absolute and 27.7% functional ID). At T1 and T2, ID was present in 56.4% (32.4% absolute and 24% functional ID) and 50.3% (36.8% absolute and 13.5% functional ID), respectively. Absolute ID persisted from T0 to T2 in 66% of the patients, while functional ID resolved in 56% of the patients. Ferritin (median [interquartile range] 124 mu g/L [56-247] to 150 mu g/L [73-277]), transferrin saturation (15% [10-20] to 18% [12-27]), and iron levels (9 mu mol/L [6-13] to 11 mu mol/L [8-16]) increased significantly (all P < 0.001) from T0 to T1. Transferrin saturation (to 21% [15-29]) and iron levels (to 13 mu mol/L [9-17]) also increased significantly (both P < 0.01) from T1 to T2 without iron supplementation. Conclusions Iron deficiency is highly prevalent in patients with AHF, but resolves during treatment in some patients, even without iron supplementation. Absolute ID is more likely to persist over time, whereas functional ID often resolves during treatment of AHF, representing probably a reduced iron availability rather than a true deficiency.

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