Key result
Intravenous iron therapy with ferric carboxymaltose leads to rapid increases in plasma non-transferrin-bound iron, which is transported directly to cardiomyocytes and remains labile for weeks.
Why the study?
Does intravenous iron therapy with ferric carboxymaltose lead to clinically relevant myocardial accumulation of non-transferrin-bound iron?
Does intravenous iron therapy with ferric carboxymaltose lead to clinically relevant myocardial accumulation of non-transferrin-bound iron?
Intravenous iron therapy with ferric carboxymaltose leads to rapid myocardial accumulation of non-transferrin-bound iron via non-canonical pathways, which remains labile for weeks.
Graphical AbstractIron deposition in the myocardium following intravenous iron therapy—by the non-canonical pathway but not the canonical pathway (created with BioRender. com). Plasma NTBI levels increase rapidly after intravenous iron therapy with FCM and are transported directly to the cardiomyocyte through NTBI transporters such as L-type and T-type calcium channels and divalent metal transporter 1 within hours (non-canonical pathway). Iron taken up by the myocardium remains in a labile form for weeks after FCM. FCM, ferric carboxymaltose; NTBI, non-transferrin bound iron; TfR, transferrin receptorOpen in new tabDownload slide
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Haehling et al. (2024) conducted an editorial in Myocardial iron deposition. Intravenous iron therapy (ferric carboxymaltose) was evaluated. Intravenous iron therapy with ferric carboxymaltose leads to rapid increases in plasma non-transferrin-bound iron, which is transported directly to cardiomyocytes and remains labile for weeks.
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