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Erythropoietin (EPO) is an important regulator of the production red blood cells, and cloning of the gene led to the development of recombinant human EPO preparation, rhEPO.1 EPO caught the public eye when some leading athletes started to take it to increase the oxygen-carrying capacity of the blood and, thereby, to achieve enhanced athletic performance. Thus, they were conveniently able to achieve the polycythaemia that others acquired by living at high altitude. Better athletic performance did, however, come at a serious price for some, as reports of increased heart attacks and strokes filtered in, so that this use of EPO for enhanced sports performance is now banned. In contrast, the legitimate use of rhEPO as a cytokine in the treatment of anaemias of chronic renal disease or cancer has improved the quality of life of those seriously ill persons. The questions evaluated in this Editorial are whether the benefits of rhEPO extend beyond its haematological use for treatment of these chronic anaemias and whether it has cardiovascular protective qualities.
Indeed, EPO is also clinically used for the treatment of the anaemia of chronic heart failure. However, strong experimental data2 do not translate into simple clinical benefit. Rather, despite increasing the haemoglobin, there are potential side effects that include worsening hypertension, thrombotic events and endothelin activation.3
The ever-present problem is whether the benefits of therapeutic rhEPO more than balance the side effects that have surfaced. In this regard, the present study by Ludman et al4 published in Heart is highly relevant (see page 1560). The experimental background is that EPO is a promoter of cardiac protective paths such as the reperfusion injury salvage kinase (RISK) and Janus Kinase/ Signal Transducer and Activator of Transcription factor (JAK-STAT) paths.2 5 Thus, EPO should be able to promote protection …