Integrity^® bare-metal coronary stent-induced platelet and endothelial cell activation results in a higher risk of restenosis compared to Xience^® everolimus-eluting stents in stable angina patients

Abstract

Drug-eluting stenting (DES) has become a reliable tool for coronary stenting; however, its direct effects on platelet and endothelium function differ from those of bare-metal stenting (BMS). This study involved a periprocedural analysis of various biomarkers of cellular activation after elective DES (Xience^®, Abbott Vascular, Santa Clara, CA, USA) or BMS (Integrity^®, Medtronic, Minneapolis, MI, USA). Forty-nine stable angina patients were recruited: 28 underwent BMS, and 21 received everolimus-eluting stents. Samples were collected (i) prior to stenting, (ii) at 24 hours after procedure, and (iii) after 1 month of dual antiplatelet therapy. Platelet activation was analyzed by surface P-selectin positivity in parallel with plasma levels of soluble P-selectin, CD40L and platelet-derived growth factor (PDGF). Endothelial cell (EC) activation was detected by measuring markers of early (von Willebrand factor) and delayed response (VCAM-1, ICAM-1, E-selectin). Patients were followed for 6 months for the occurrence of restenosis or stent thrombosis. Increased platelet activation was sustained regardless of stent type or antiplatelet medication. Concentrations of most EC markers were more elevated after BMS than after DES. No stent thrombosis was seen, but six BMS subjects displayed restenosis with significantly higher sCD40L (779 [397–899] vs. 381 [229–498] pg/mL; p = 0.032) and sICAM-1 (222 [181–272] vs. 162 [153–223] ng/mL; p = 0.046) levels than in those without complication, while DES patients exhibited significantly decreased PDGF (572 [428–626] vs. 244 [228–311] pg/mL; p = 0.004) after 1 month. Nonresponsiveness to antiplatelet drugs did not influence these changes. In conclusion, the degree of platelet and EC activation suggests that Xience^® DES may be regarded a safer coronary intervention than Integrity^® BMS, with a lower risk of in-stent restenosis.

Keywords:

• Coronary stenting
• endothelial injury
• inflammation
• platelet activation
• soluble marker
• therapeutic responsiveness

Acknowledgments

Béla Nagy Jr was supported by a Lajos Szodoray Grant of the University of Debrecen. The authors thank Annamária Bereczky, Erzsébet Halász, and Mária Szabó for their excellent technical assistance. They also thank David Durham (University of Szeged) for the linguistic corrections of the manuscript.

Declaration of interest

The authors declare that there is no conflict of interest.

Supplemental material

Supplemental data for this article can be accessed at www.tandfonline.com/iplt.