EPC mobilization after erythropoietin treatment in acute ST-elevation myocardial infarction: the REVEAL EPC substudy
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EPC mobilization after erythropoietin treatment in acute ST-elevation myocardial infarction: the REVEAL EPC substudy Thomas J. Povsic • Samer S. Najjar • Kristi Prather • Jiying Zhou • Stacie D. Adams • Katherine L. Zavodni • Francine Kelly • Laura G. Melton • Vic Hasselblad • John F. Heitner Subha V. Raman • Gregory W. Barsness • Manesh R. Patel • Raymond J. Kim • Edward G. Lakatta • Robert A. Harrington • Sunil V. Rao
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Ó Springer Science+Business Media New York 2013
Abstract Erythropoietin (EPO) was hypothesized to mitigate reperfusion injury, in part via mobilization of endothelial progenitor cells (EPCs). The REVEAL trial found no reduction in infarct size with a single dose of EPO (60,000 U) in patients with ST-segment elevation myocardial infarction. In a substudy, we aimed to determine the feasibility of cryopreserving and centrally analyzing EPC levels to assess the relationship between EPC numbers, EPO administration, and infarct size. As a prespecified substudy, mononuclear cells were locally cryopreserved before as well as 24 and 48–72 h after primary percutaneous coronary intervention. EPC samples were collected in 163 of 222 enrolled patients. At least one sample was obtained from 125 patients, and all three time points were available in 83 patients. There were no significant differences in the absolute EPC numbers over time or between EPO- and placebotreated patients; however, there was a trend toward a greater increase in EPC levels from 24 to 48–72 h postintervention in patients receiving C30,000 U of EPO (P = 0.099 for CD133? cells, 0.049 for CD34? cells, 0.099 for ALDHbr
cells). EPC numbers at baseline were inversely related to infarct size (P = 0.03 for CD133? cells, 0.006 for CD34? cells). Local whole cell cryopreservation and central EPC analysis in the context of a multicenter randomized trial is feasible but challenging. High-dose (C30,000 U) EPO may mobilize EPCs at 48–72 h, and baseline EPC levels may be inversely associated with infarct size.
T. J. Povsic (&) K. Prather L. G. Melton V. Hasselblad M. R. Patel R. A. Harrington S. V. Rao Duke Clinical Research Institute, Duke University Medical Center, Box 103208, Durham, NC 27710, USA e-mail: [email protected]
S. S. Najjar E. G. Lakatta Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA
Keywords Erythropoietin Endothelial progenitor cells Myocardial infarction Cryopreservation
Extensive preclinical literature suggests a benefit of erythropoietin (EPO) on ischemia reperfusion injury [1, 2]. Although EPO may theoretically limit myocardial injury based on anti-apoptotic and direct angiogenic signaling, EPO is also a direct mobilizer of endothelial progenitor cells (EPCs) [3, 4], which in preclinical models contribute directly to EPO-induced angiogenesis [5] and may be related to degree of myocardial salvage [6].
J. F. Heitner New York Methodist Hospital, Brooklyn, NY, USA
T. J. Povsic J. Zhou S. D. Adams K. L. Zavodni F. Kelly M. R. Patel R.
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