Abstract 20012: The Impact of an Anti-CD34 Stent Surface Modification on the Acute Attachment of Circulating Blood Cells in a Human Shunt Model
Background: The risk of stent thrombosis can potentially be reduced by accelerated re-growth of a functional endothelium. Circulating endothelial progenitor cells (EPCs), which differentiate into arterial endothelial cells, can be ‘captured’ by CD34 antibodies immobilized on stent struts, leading to healing of the stented-artery. Therefore the goal of this project was to evaluate the acute interaction of EPC-capturing stents with human blood in an ex vivo arterio-venous shunt.
Methods and Results: Seven patients undergoing elective percutaneous coronary intervention (PCI) were selected. Silastic tubing was then cannulated between the arterial and venous sheaths forming an arterio-venous shunt. Each silastic tubing had both (1) 316L stainless steel stent with antihuman-CD34 monoclonal antibody and (2) bare metal (316L) stent. The flow condition within the shunt was adjusted and continuously monitored throughout the procedure to ensure coronary flow rates. After 60–90 minutes, the silastic tubing was removed and stents were fixed in 10% formalin. Scanning electron microscopy (SEM) and confocal microscopy were utilized to determine morphology and cell coverage of the luminal surface of stents. All procedures were approved by the institute's IRB committee. SEM analysis of the stent struts demonstrated a decrease in inflammatory (leukocytes) cells and fibrin/platelet deposition within the anti-CD34 stents as compared to the bare metal stents. Moreover, EPC-like round cells were observed attached to the anti-CD34 stent struts. Confocal microscopy confirmed SEM results of decrease inflammatory cells and thrombotic material in the anti-CD34 stents as compared to bare metal stents.
Conclusions: Anti-CD34 stents acutely inhibited leukocyte attachment and pro-thrombotic material as compared to a bare metal stent in a human ex vivo shunt model.
- © 2010 by American Heart Association, Inc.