Iron and Exercise in Heart Failure: How to Assess Relevant Changes?

Abstract

Both the clinical picture and the prognosis of patients with chronic heart failure (HF) are characterized by impaired exercise tolerance and dyspnea; the impact of respiratory muscle dysfunction on these symptoms has been evaluated since the early 1990s. Recent studies have shown that iron deficiency (ID) is very common in patients with HF and its prevalence increases with increasing New York Heart Association class or accompanying anemia. Overall, it appears that at least one third of all patients with HF is affected; other authors estimate that up to half of all patients have ID. Patients with chronic HF develop iron deficiency through deranged iron absorption or by diminished availability of iron in the reticuloendothelial system. Iron deficiency seems more prevalent in patients with HF than anemia and both cause reduced exercise capacity. The presence of ID may have multifaceted clinical consequences, not only directly related to impaired erythropoiesis, but also to marked impairment of oxidative metabolism, cellular energetics, and cellular immune mechanisms. Iron deficiency with and without anemia is accompanied by reduced aerobic performance and subjective complaints of poor physical condition. Its correction improves cognitive, symptomatic, and exercise performance. Interestingly, intravenous iron supplementation with ferric carboxymaltose has been shown to improve exercise capacity in patients with and without additional anemia as well as patients’ overall wellbeing. In general, the aim of treatment is to supply enough iron to normalize hemoglobin concentrations and to replenish iron stores, and thus improve quality of life. Two distinct approaches exist: first, prevention strategies targeted at populations at risk and, second, active iron supplementation approaches in patients with either confirmed ID or those who have already developed ID anemia. Clinically, it would be helpful to detect the earliest changes in red cell indices that reflect iron-restricted erythropoiesis. One approach would be to identify newly formed iron-deficient cells as they are released from the bone marrow as reticulocytes. It would be also helpful to analyze the complex interplay between ID and exercise response in patients with chronic HF. The study by Enjuanes et al published in Revista Espanola de Cardiologia therefore comes as a welcome addition to the ID in HF portfolio. The authors present data from patients with chronic HF