Abstract

Heart failure syndromes represent a principal cause of morbidity and mortality in the Western world.1 The importance of measures for diagnosis, surveillance, and treatment of patients with chronic heart failure (CHF) are likely to attract increasing attention as the prevalence of the syndrome will rise with the ageing of the population. One of the most studied clinical determinants of outcome in patients with CHF is haemoglobin level.2 There are many reports showing that anaemia is associated with a reduced quality of life and increased mortality in these patients.2 However, many questions remain that pertain to the precise mechanisms of anaemia, the need to treat it, and the desired haemoglobin goals. Erythropoietin (Epo) is a 34 kDa glycoprotein synthesized by renal peritubular cells, but also by neuronal and hepatic macrophages and other cells.3 The output signals that control Epo homeostasis are principally provided by a set of transcription factors that ‘sense’ changes in oxygen levels and are termed accordingly as hypoxia-inducible factors. The Epo receptor is found most abundantly in bone marrow erythroid progenitor cells, although other tissues also express it. Aside from the well described action of Epo as a proliferative enhancer of erythropoiesis, in recent … *Corresponding author. Tel: +972 3 6974762, Fax: +972 3 546 9832, Email: jacobg{at}post.tau.ac.il

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