EPC mobilization after erythropoietin treatment in acute ST-elevation myocardial infarction: the REVEAL EPC substudy.

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.

Aldehyde dehydrogenase activity allows reliable EPC enumeration in stored peripheral blood samples.

Background: Interest in the biology of endogenous progenitor cells (EPCs) continues to grow as evidence of their role in vascular repair mounts. EPC enumeration requires specialized laboratory techniques and is performed immediately after sample acquisition, limiting the clinical contexts in which EPC enumeration can be performed and the ability to increase sample sizes through multi-center participation.

Methods: We compared the numbers of EPCs enumerated in samples processed immediately after acquisition (n = 36) with EPCs enumerated in specimens stored for 24 hours or after cryopreservation of mononuclear cells (MNC) using two EPC identification strategies: cell surface marker expression (CD133/CD34) and aldehyde dehydrogenase activity (ALDH(br) cells).

Unfractionated heparin reduces the anti-platelet effects of abciximab but not eptifibatide during PCI.

In 29 patients undergoing percutaneous coronary intervention (PCI), we obtained blood samples at baseline, 10 minutes after standard weight-based abciximab (n=15) or double-bolus eptifibatide (n=14) and 5 minutes after unfractionated heparin (UFH; 70 U/kg bolus). The median percent inhibition was significantly higher in the eptifibatide group compared with the abciximab group both before (96.5% [94-100] vs.

Simultaneous testing of the heparin effect on the soluble phase and platelet component of hemostasis.

Background: This study assessed the anticoagulant effect of heparin on both platelet activity and soluble phase coagulation.

Methods And Results: Blood samples were collected from 32 patients undergoing cardiac catheterization before and 5 minutes after a heparin injection (2000 U). Activated clotting time (ACT), activated partial thromboplastin time (aPTT), and whole blood platelet aggregation [adenosine diphosphate (ADP) and collagen] were compared with the flow device variables platelet hemostasis time (PHT) and collagen-induced thrombus formation (CITF).