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Iron status in patients with chronic heart failure

Open access
Jankowska, E. A., Malyszko, J., Ardehali, H., Koc-Zorawska, E., Banasiak, W., von Haehling, S., Macdougall, I. C., Weiss, G., McMurray, J. J. V., Anker, S. D., Gheorghiade, M., Ponikowski, P.·2013·European Heart Journal

Abstract

AIMS: The changes in iron status occurring during the course of heart failure (HF) and the underlying pathomechanisms are largely unknown. Hepcidin, the major regulatory protein for iron metabolism, may play a causative role. We investigated iron status in a broad spectrum of patients with systolic HF in order to determine the changes in iron status in parallel with disease progression, and to associate iron status with long-term prognosis. METHODS AND RESULTS: Serum concentrations of ferritin, transferrin saturation (Tsat), soluble transferrin receptor (sTfR), and hepcidin were assessed as the biomarkers of iron status in 321 patients with chronic systolic HF [age: 61 ± 11 years, men: 84%, left ventricular ejection fraction: 31 ± 9%, New York Heart Association (NYHA) class: 72/144/87/18] at a tertiary cardiology centre and 66 age- and gender-matched healthy subjects. Compared with healthy subjects, asymptomatic HF patients had similar haematological status, but increased iron stores (evidenced by higher serum ferritin without distinct inflammation, P < 0.01) with markedly elevated serum hepcidin (P < 0.001). With increasing HF severity, patients in advanced NYHA classes had iron deficiency (ID) (reduced serum ferritin, low Tsat, high sTfR), iron-restricted erythropoiesis (reduced haemoglobin, high red cell distribution width), and inflammation (high serum high-sensitivity-C-reactive protein and interleukin 6), which was accompanied by decreased circulating hepcidin (all P < 0.001). In multivariable Cox models, low hepcidin was independently associated with increased 3-year mortality among HF patients (P < 0.001). CONCLUSIONS: Increased level of circulating hepcidin characterizes an early stage of HF, and is not accompanied by either anaemia or inflammation. The progression of HF is associated with the decline in circulating hepcidin and the development of ID. Low hepcidin independently relates to unfavourable outcome.

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Metadata

Authors
Jankowska, E. A., Malyszko, J., Ardehali, H., Koc-Zorawska, E., Banasiak, W., von Haehling, S., Macdougall, I. C., Weiss, G., McMurray, J. J. V., Anker, S. D., Gheorghiade, M., & Ponikowski, P.
Venue
European Heart Journal
Published
2012-11-23
Volume
34
Issue
11
Pages
827-834
ISSN
  • 0195-668X (ISSN-L)
  • 1522-9645
OpenAlex
W2048830907
Cited by
273
References
44
FWCI
7.87
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Iron status in patients with chronic heart failure. https://app.cochat.ai/papers/10.1093/eurheartj/ehs377
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Jankowska, E. A., Malyszko, J., Ardehali, H., Koc-Zorawska, E., Banasiak, W., von Haehling, S., Macdougall, I. C., Weiss, G., McMurray, J. J. V., Anker, S. D., Gheorghiade, M., & Ponikowski, P. (2013). Iron status in patients with chronic heart failure. European Heart Journal. https://doi.org/10.1093/eurheartj/ehs377

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.