Heart failure & cardiomyopathiesCohort study
Intravenous iron therapy results in rapid and sustained rise in myocardial iron content through a novel pathway
- Prospective observational study
- mechanistic study in mice and cells
Authors' conclusion
Intravenous 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.
Study context
- Population
- Patients receiving ferric carboxymaltose for iron deficiency
- Participants
- 12 patients
Main finding
As reported in the abstract
Myocardial iron uptake (myocardial MR T1 relaxation time in patients; plasma iron markers)
- Myocardial T1 dropped maximally 3 h post-FCM, remaining low 42 days later
- Splenic T1 dropped maximally at 14 days, recovering by 42 days
- Plasma non-transferrin-bound iron (NTBI) peaked at 3 h; ferritin peaked at 14 days
- Changes in liver T1 diverged among patients
Observational data: associations, not effects.
Further findings
Myocardial labile iron pool in mice
- Myocardial labile iron pool (LIP) rose 1 h and remained elevated 42 days after ferric carboxymaltose (FCM)
Labile iron pool in cardiomyocytes
- FCM raised LIP rapidly; prevented by inhibitors of T-type and L-type calcium channels and divalent metal transporter 1
Original publication
Intravenous iron therapy results in rapid and sustained rise in myocardial iron content through a novel pathway. Eur Heart J. Published 25 June 2024. doi:10.1093/eurheartj/ehae359
Summarised from the published abstract; every number is checked against it