Iron is an essential component of two vital compounds: haemoglobin and myoglobin. The two share a basic Haeme architecture. Myoglobin is a single polypeptide chain containing iron and has a single oxygen-binding site. Haemoglobin carries 70% of the iron in the body and has a tetrameric structure and four oxygen-binding sites. Compared with haemoglobin, myoglobin has a higher affinity for oxygen, making it an efficient myocardial oxygen store.
The heart needs saturated iron supplies to maintain its oxygen stores and to remain an efficient pump of blood. The quality of blood as an oxygen carrier depends on its haemoglobin content, which is affected by iron saturation.
Over the past 20 years, research into the management of iron deficiency in patients with heart failure with reduced ejection fraction (HFrEF) showed improved exercise tolerance with intravenous iron repletion. Large randomised trials showed reduced heart failure hospitalisation, without affecting mortality.1 However, the HEART-FID trial did not show a difference between placebo and ferric carboxymaltose in terms of mortality, heart failure hospitalisations or the 6-minute walk distance.2
The IRONMAN study assessed the response of patients with HFrEF and iron deficiency to intravenous ferric derisomaltose (FDI). In a pre-specified COVID-19 sensitivity analysis, there was a borderline significant impact of intravenous FDI on the primary outcome of HFrEF hospitalisation and cardiovascular mortality, with improved quality of life at 4 months.1
Sze et al
3 undertook a post hoc analysis of the IRONMAN study in relation to the impact of age on the effects of intravenous FDI versus …
