LAUSR

Anaemia (haemoglobin <12 g/dL in women and <13 g/dL in men) represents a common co-morbidity in patients with heart failure (HF). The aetiology of anaemia in these patients is oftenmultifactorial. Chronic gastrointestinal blood loss, vitamin deficiency, reduced iron availability from iron stores or impaired intestinal iron resorption caused by chronic inflammation as well as decreased erythropoietin availability or effect, malnutrition, and of course haemodilution amongst others represent potential reasons. As anaemia is predictive for mortality in HF, a direct association was initially suspected. However, solely increasing haemoglobin by erythropoiesis stimulating drugs failed in improving clinical outcome. In contrast to this, intravenous (i.v.) iron repletion in patients with HF and iron deficiency (ID) led to an increase in exercise capacity and reduced hospitalizations. Importantly, the effect of i.v. iron was independent from baseline haemoglobin levels. ID can lead to impairment of the mitochondrial energy metabolism long before it leads to impaired haematopoiesis detectable in peripheral blood/anaemia. Hepcidin, the central regulator of iron homeostasis, is under normal circumstances down-regulated in ID, anaemia, and/or hypoxia. Lower hepcidin leads to increased availability from iron stores and to a rise in intestinal iron absorption. However, chronic elevation of inflammatory mediators, as present in disease linked to chronic inflammation, as in HF, prompts to hepcidin up-regulation. This mechanism leads to ID in HF and also explains why oral iron supplements are ineffective in patients with HFrEF.