Baseline ferritin predicts myocardial iron uptake following intravenous iron therapy- a hypothesis generating study
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Aims
Iron deficiency (ID) is a common co-morbidity in heart failure (HF). Intravenous iron therapy improves outcomes. Several mechanisms have been proposed, including myocardial iron repletion. However, it is unknown if clinical iron markers predict the extent of this repletion. The aim of this study is to address this question by harnessing data from two clinical studies that evaluated changes in myocardial iron using cardiac magnetic resonance (CMR).
Methods and Results
We performed a post-hoc analysis of two previously published trials. The Myocardial-IRON trial measured change in myocardial iron, denoted by a decrease in CMR T1-mapping, at 7 and 30 days after FCM in patients with ID and HF. The STUDY trial measured myocardial and spleen iron at multiple timepoints after FCM in patients with ID without HF. In this post-hoc analysis, we examined the association between baseline iron markers (Tsat and ferritin) and change in myocardial iron in the weeks after FCM therapy. Changes in spleen iron were also examined, due its role as an intermediary in the redistribution of iron from iron-carbohydrate complexes such as FCM. In patients with or without HF, higher plasma ferritin at baseline predicted lower rise in myocardial iron in the weeks after therapy with FCM. In contrast, higher plasma ferritin at baseline predicted a greater rise in spleen iron.
Conclusions
These data point towards the hypothesis that functional ID, which is characterized by elevated ferritin, could limit myocardial iron repletion after IV iron therapy, by favoring iron trapping in the spleen.
