Variable aetiologies contributing to the anaemia of systolic heart failure are important to individual patient management.

The anaemia of chronic left ventricular systolic dysfunction (LVSD) or systolic heart failure is common, increases over time,1 and is linked with a bad clinical outcome. It is often considered an expression of the chronic vascular inflammation of endstage disease similar to that seen in conjunction with many other chronic disease states. Failure of haematinic function, particularly renal erythropoietin (Epo) synthesis and release, is also seen as a key mechanism and is cited as a major justification for considering exogenous Epo therapy in this disease. Westenbrink et al .2 from Groningen contribute a simple but critical clinical paper highlighting that variable mechanisms contribute to this clinical setting. By defining these carefully, Westenbrink shows that notwithstanding the impact of altered Epo kinetics and dynamics, many of these patients might also have ‘simple’ dilutional anaemia related to poorly perceived and asymptomatic fluid imbalance. This simple finding has important implications for management. The anaemia of LVSD is readily identified by simple measurement; its haematological severity begets a poor outcome. Its prevalence is poorly defined due to the application of variable diagnostic cut-offs. Haematinic deficiencies secondary to poor nutrition, poor micronutrient absorption, and/or chronic gastrointestinal bleeding are common in LVSD and might contribute to a third of cases.3 In the absence of haematinic deficiency, reduced Epo production, (controlling proliferation and differentiation of erythroid cells) may also be involved. As the primary stimulus for Epo release is renal hypoxia, it is understandable that this might be implicated given that reduced renal perfusion is common in LVSD. Anaemia would result if Epo release was insufficient to meet the demands of normal erythropoiesis. Opasich et al .4 have already reported that 76% of their sample of anaemic chronic heart failure patients showed impaired … *Corresponding author. Tel: +44 121 507 4476 5080; fax: +44 121 554 4854. E-mail address : robert.macfadyen{at}swbh.nhs.uk