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Eur Heart J. 2014 Sep 21;35(36):2468-76. doi: 10.1093/eurheartj/ehu235. Epub 2014 Jun 13.

Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure.

Author information

1
Laboratory for Applied Research on Cardiovascular System, Department of Heart Diseases, Wrocław Medical University, Wrocław, Poland Cardiology Department, Centre for Heart Diseases, Military Hospital, ul. Weigla 5, Wrocław 50-981, Poland ewa.jankowska@umed.wroc.pl.
2
Laboratory of Molecular and Cellular Immunology, Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.
3
Cardiology Department, Centre for Heart Diseases, Military Hospital, ul. Weigla 5, Wrocław 50-981, Poland Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland.
4
Cardiology Department, Municipal Hospital, Inowrocław, Poland.
5
Cardiology Department, Centre for Heart Diseases, Military Hospital, ul. Weigla 5, Wrocław 50-981, Poland.
6
Division of Applied Cachexia Research, Department of Cardiology, Charité Medical School, Berlin, Germany Department of Innovative Clinical Trials, University Medical Centre Göttingen, Göttingen, Germany.
7
Department of Cardiology, Attikon University Hospital, University of Athens Medical School, Greece.
8
National Heart and Lung Institute, Imperial College, London, UK.

Abstract

AIM:

Acute heart failure (AHF) critically deranges haemodynamic and metabolic homoeostasis. Iron is a key micronutrient for homoeostasis maintenance. We hypothesized that iron deficiency (ID) defined as depleted iron stores accompanied by unmet cellular iron requirements would in this setting predict the poor outcome.

METHODS AND RESULTS:

Among 165 AHF patients (age 65 ± 12 years, 81% men, 31% de novo HF), for ID diagnosis we prospectively applied: low serum hepcidin reflecting depleted iron stores (<14.5 ng/mL, the 5th percentile in healthy peers), and high-serum soluble transferrin receptor (sTfR) reflecting unmet cellular iron requirements (≥1.59 mg/L, the 95th percentile in healthy peers). Concomitance of low hepcidin and high sTfR (the most profound ID) was found in 37%, isolated either high sTfR or low hepcidin was found in 29 and 9% of patients, and 25% of subjects demonstrated preserved iron status. Patients with low hepcidin and high sTfR had peripheral oedema, high NT-proBNP, high uric acid, low haemoglobin (P < 0.05), and 5% in-hospital mortality (0% in remaining patients). During the 12-month follow-up, 33 (20%) patients died. Those with low hepcidin and high sTfR had the highest 12-month mortality [(41% (95% CI: 29-53%)] when compared with those with isolated high sTfR [15% (5-25%)], isolated low hepcidin [7% (0-19%)] and preserved iron status (0%) (P < 0.001). Analogous mortality patterns were seen separately in anaemics and non-anaemics.

CONCLUSION:

Iron deficiency defined as depleted body iron stores and unmet cellular iron requirements is common in AHF, and identifies those with the poor outcome. Its correction may be an attractive therapeutic approach.

KEYWORDS:

Acute heart failure; Hepcidin; Iron status; Mortality; Soluble transferrin receptor

PMID:
24927731
DOI:
10.1093/eurheartj/ehu235
[Indexed for MEDLINE]

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