Intravenous iron therapy for patients with heart failure: expanding body of evidence

摘要

Anaemia (haemoglobin 12 g/dL in women and 13 g/dL inmen) represents a common co-morbidity in patients withheart failure (HF). The aetiology of anaemia in these patientsis oftenmultifactorial. Chronic gastrointestinal blood loss, vitamindeficiency, reduced iron availability from iron stores or impairedintestinal iron resorption caused by chronicinflammation as well as decreased erythropoietin availabilityor effect, malnutrition, and of course haemodilution amongstothers represent potential reasons.1,2 As anaemia is predictivefor mortality in HF, a direct association was initially suspected.However, solely increasing haemoglobin by erythropoiesisstimulating drugs failed in improving clinical outcome. In contrastto this, intravenous (i.v.) iron repletion in patients withHF and iron deficiency (ID) led to an increase in exercise capacityand reduced hospitalizations. Importantly, the effect of i.v.iron was independent from baseline haemoglobin levels. IDcan lead to impairment of the mitochondrial energy metabolismlong before it leads to impaired haematopoiesis detectablein peripheral blood/anaemia. Hepcidin, the centralregulator of iron homeostasis, is under normal circumstancesdown-regulated in ID, anaemia, and/or hypoxia. Lowerhepcidin leads to increased availability from iron stores andto a rise in intestinal iron absorption. However, chronic elevationof inflammatory mediators, as present in disease linked tochronic inflammation, as in HF, prompts to hepcidin up-regulation.This mechanism leads to ID in HF and also explains whyoral iron supplements are ineffective in patients with HFrEF.