Erythropoietin in Myocardial Infarction: Experimental Evidence and Clinical Studies

REVIEW, February 2011, VOL I ISSUE III, ISSN 2042-4884
10.5083/ejcm.20424884.26 , Cite or Link Using DOI
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Andreas Stein & Ilka Ott


Erythropoietin produced mainly in the kidney is the main regulator of erythropoiesis. Experimental studies identified additional, non-haematopoietic, protective effects during myocardial ischemia and reperfusion due to inhibition of apoptosis, stimulation of vasculogenesis and progenitor cell mobilisation. Based on these findings, five prospective, randomised, clinical trials have been performed. A short term regimen of erythropoietin was applied during PCI in patients with STEMI up to a cumulative dose of 100.000 IU. No changes in myocardial function or infarct size were observed after erythropoietin. Yet in two studies an increase in adverse events after erythropoietin was observed, whereas one study found an increase in major adverse clinical events in the control group. This review discusses experimental evidence of erythropoietin in acute myocardial infarction and its failure in clinical trials.

Evidence for beneficial effects of erythropoietin in
experimental myocardial infarction

Erythropoietin (EPO) is a member of the cytokine type I family and is mainly synthesised in the peritubular cells in the cortex-medullary border of the kidney. Under hypoxic conditions erythropoietin is released and increases the amount of circulating red blood cells by enhancing the development of precursor red cells and by protecting red blood cells from apoptosis. As a therapeutic agent eythropoietin became widely used in treating anaemia resulting from chronic kidney disease and myelodysplasia after chemotherapy or radiation.