Evidence map›Paper›PMID 38917062›Full record

Observational studyEuropean heart journal2024

Intravenous iron therapy results in rapid and sustained rise in myocardial iron content through a novel pathway.

Mayra Vera-Aviles, Syeeda Nashitha Kabir, Akshay Shah, Paolo Polzella, Dillon Yee Lim, Poppy Buckley, Charlotte Ball, Dorine Swinkels, Hanke Matlung, Colin Blans and 7 more

Abstract readObservational Study
In one paragraph

Observational study in European heart journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Rationale and design of the RISE-HF trial: sucrosomial iron in heart failure.International journal of cardiology. Heart & vasculature · 2026
    Article
  7. Iron overload induced by ferric derisomaltose and ferric carboxymaltose both increase FGF-23 levels and lead to osteomalacia and bone loss in normal mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  8. Iron Deficiency as a Modifiable Risk Factor in Heart Failure: Evidence and Recommendations.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026
    Review
  9. Article
  10. Article
  11. Iron Deficiency in Heart Failure: Cellular Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Mayra Vera-AvilesDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.
Syeeda Nashitha KabirDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.ORCID 0000-0003-1811-8683
Akshay ShahNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-1869-2231
Paolo PolzellaDepartment of Clinical Haematology, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
Dillon Yee LimDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.ORCID 0000-0002-3619-2548
Poppy BuckleyDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.
Charlotte BallDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.
Dorine SwinkelsDepartment of Laboratory Medicine, Iron Expertise Centre, Radboud University Medical Centre, Nijmegen, The Netherlands.ORCID 0000-0002-1040-9446
Hanke MatlungSanquin Diagnostic Services, Amsterdam, The Netherlands.
Colin BlansSanquin Diagnostic Services, Amsterdam, The Netherlands.
Philip HoldshipDepartment of Earth Sciences, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-6246-3620
Jeremy NugentDepartment of Chemistry, Chemistry Research Laboratory, University of Oxford, Oxford, United Kingdom.
Edward AndersonDepartment of Chemistry, Chemistry Research Laboratory, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-4149-0494
Michael DesboroughDepartment of Clinical Haematology, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.ORCID 0000-0002-1951-5616
Stefan PiechnikOxford Centre for Clinical Magnetic Resonance Research (OCMR), University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-0268-5221
Vanessa FerreiraOxford Centre for Clinical Magnetic Resonance Research (OCMR), University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-0046-7634
Samira Lakhal-LittletonDepartment of Physiology, Anatomy & Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.ORCID 0000-0001-7797-1567

Funding

British Heart FoundationBritish Heart Foundation Centre for ResearchCentre for Research Excellence HSR00031EPSRCMedical Research Council MR/V009567/1Medical Research Council MR/V009567/1/National Institute for Health and Care Research Academic Clinical Lectureship awardWellcome Trust
6 · The paper itself

Abstract

BACKGROUND AND

aimsIntravenous iron therapies contain iron-carbohydrate complexes, designed to ensure iron becomes bioavailable via the intermediary of spleen and liver reticuloendothelial macrophages. How other tissues obtain and handle this iron remains unknown. This study addresses this question in the context of the heart.

methodsA prospective observational study was conducted in 12 patients receiving ferric carboxymaltose (FCM) for iron deficiency. Myocardial, spleen, and liver magnetic resonance relaxation times and plasma iron markers were collected longitudinally. To examine the handling of iron taken up by the myocardium, intracellular labile iron pool (LIP) was imaged in FCM-treated mice and cells.

resultsIn patients, myocardial relaxation time T1 dropped maximally 3 h post-FCM, remaining low 42 days later, while splenic T1 dropped maximally at 14 days, recovering by 42 days. In plasma, non-transferrin-bound iron (NTBI) peaked at 3 h, while ferritin peaked at 14 days. Changes in liver T1 diverged among patients. In mice, myocardial LIP rose 1 h and remained elevated 42 days after FCM. In cardiomyocytes, FCM exposure raised LIP rapidly. This was prevented by inhibitors of NTBI transporters T-type and L-type calcium channels and divalent metal transporter 1.

conclusionsIntravenous iron therapy with FCM delivers iron to the myocardium rapidly through NTBI transporters, independently of reticuloendothelial macrophages. This iron remains labile for weeks, reflecting the myocardium's limited iron storage capacity. These findings challenge current notions of how the heart obtains iron from these therapies and highlight the potential for long-term dosing to cause cumulative iron build-up in the heart.

Indexed as

Ferric CompoundsIronLiverMaltoseMyocardiumAdultAnemia, Iron-DeficiencyAnimalsFemaleHumansInfusions, IntravenousMagnetic Resonance ImagingMaleMiceMiddle AgedMyocytes, Cardiacferric carboxymaltoseFerric CompoundsIronMaltoseFerric carboxymaltoseIntravenous iron therapyLabile ironMagnetic resonanceMyocardiumNon-transferrin-bound iron

Identifiers

PMID38917062
PMCPMC11544312

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.