Letter to the Editor Decreased circulatory erythropoietin in hyperacute phase of myocardial ischemia Emin Alioglu a,1 , Ertugrul Ercan b, ⁎ , Gulden Sonmez Tamer c,2 , Can Duman c,2 , Ugur Turk a,1 , Istemihan Tengiz a,1 , Nurullah Tuzun a,1 , Serkan Saygi d,3 a Central Hospital, Department of Cardiology, Izmir, Turkey b Faculty of Medicine, Department of Cardiology, Canakkale Onsekiz Mart University, Turkey c Department of Biochemistry, Kocaeli University, Kocaeli, Turkey d Karsiyaka State Hospital, Department of Cardiology, Izmir, Turkey Received 8 December 2008; accepted 14 December 2008 Available online 25 January 2009 Abstract Purpose: Erythropoietin provides cellular protection by inhibiting apoptosis. Myocardial damage related to the cardiac ischemia is more prominent especially in the first 6 h. In the present study, circulatory erythropoietin levels in response to cardiac ischemia were evaluated. Materials and methods: Patients with stable angina who underwent balloon angioplasty (study group, n = 55) and hospitalized for coronary angiography (as control group, n =23) were enrolled into the study. Serum erythropoietin levels were measured in both groups in baseline, 6 and 18 h after the procedure. Results: Coronary balloon inflation time was accepted as duration of myocardial ischemia. Study group showed significant erythropoietin reduction at sixth hour compared to control group. Erythropoietin reduction at sixth hour was significantly correlated with duration of myocardial ischemia. Conclusion: Decreased circulatory erythropoietin levels in the early phase of acute cardiac ischemia may accelerate the apoptotic activity. Recombinant erythropoietin replacement to prevent erythropoietin decrease following cardiac ischemia may have negative effect on myocyte loss. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Erythropoietin; Ischemia; Apoptosis 1. Introduction Erythropoietin (EPO) is a glycoprotein hormone impli- cated in the regulation of red blood cell production [1,2]. It is produced in response to hypoxia by the kidney [3,4]. EPO is needed for the heamotopoiesis [4]. Recently, non-heamoto- poetic effects of EPO have been established on the myocardium [5–7]. Recombinant EPO has been shown to have cardio protective effects in animal researches [8,9]. EPO provides cellular protection by inhibiting apoptosis [10,11]. Myocardial damage related to the cardiac ischemia is more prominent especially in the first 6 h. In the present International Journal of Cardiology 146 (2011) e49 – e52 www.elsevier.com/locate/ijcard ⁎ Corresponding author. +90 286 218 9303, +90 533 521 6481 (Mobile); fax: +90 286 218 0018. E-mail addresses: dreminalioglu@yahoo.com (E. Alioglu), ertugrulercan@yahoo.com (E. Ercan), guldensonmez@yahoo.com (G. Sonmez Tamer), canduman@yahoo.com (C. Duman), droturk@yahoo.com (U. Turk), dritengiz@yahoo.com (I. Tengiz), drnurullahtuzun@yahoo.com (N. Tuzun), serkankard@yahoo.com (S. Saygi). 1 Tel.: +90 232 341 6767; fax: +90 232 341 6868. 2 Tel.: +90 222 243 4 436; fax: +90 222 333 0 321. 3 Tel.: +90 232 366 8888; fax: +90 232 3668530. 0167-5273/$ - see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2008.12.184