This editorial refers to ‘A single dose of erythropoietin in ST-elevation myocardial infarction’ by A.A. Voors et al., doi:10.1093/eurheartj/ehq304
Contemporary management of patients with acute myocardial infarction (AMI) is based on the widely established concept of opening the infarct-related artery in order to achieve early reperfusion and salvage the myocardium. Although the introduction of thrombolytic therapy and subsequently percutanoeus coronary intervention (PCI) dramatically improved the outcome in AMI, many patients who survive an acute phase of AMI still demonstrate extensive, irreversible damage of the myocardium and ultimately develop cardiac remodelling and heart failure (HF) which unfavourably affect mortality and morbidity.1,2 Thus, prevention or attenuation of remodelling is considered an important therapeutic goal during both the early and later stages after AMI. The size of the infarcted area correlates with resultant haemodynamic derangements and neurohormonal activation, and is a key predictor of left ventricle (LV) remodelling and development of HF.1 There is a constant interest in and search for therapies limiting infarct size, which can be an adjuvant to early reperfusion strategies.
AMI triggers an increase in the blood levels of inflammatory and haematopoietic cytokines capable of mobilizing numerous types of stem/progenitor cells.3 It can be a self-repair mechanism in which progenitor/stem cells can contribute to myocardial and vascular regeneration after acute injury. Among these cytokines, erythropoietin (EPO), a hormone involved in the regulation of erythropoiesis, may play an important role. Apart from being a stimulus for progenitor cell mobilization,4 EPO itself exerts potent protective effects within the cardiovascular system,5 thus carrying the potential to be a promising agent for the treatment of AMI.
EPO protects the heart and the vessels: experimental evidence for practising cardiologists
EPO has been traditionally viewed as a haematopoietic cytokine produced by the kidney in response to hypoxia.6,7 EPO promotes proliferation, differentiation, and survival of bone marrow erythroid …