Key result
Everolimus-eluting stents resulted in lower endothelial cell activation and a lower risk of in-stent restenosis at 6 months compared to bare-metal stents (6 of 28 BMS patients developed restenosis).
Why the study?
Do everolimus-eluting stents reduce platelet and endothelial cell activation and restenosis compared to bare-metal stents in stable angina patients?
Observational (n=49)
Do everolimus-eluting stents reduce platelet and endothelial cell activation and restenosis compared to bare-metal stents in stable angina patients?
Everolimus-eluting stents induce less endothelial cell activation and are associated with a lower risk of in-stent restenosis compared to bare-metal stents in stable angina patients.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for everolimus-eluting stents in stable angina; prospective randomized trials needed before clinical adoption.
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.
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Szük et al. (2016) conducted an observational in Stable angina (n=49). Xience everolimus-eluting stents vs. Integrity bare-metal stents was evaluated on Platelet and endothelial cell activation biomarkers, and 6-month occurrence of restenosis or stent thrombosis. Everolimus-eluting stents resulted in lower endothelial cell activation and a lower risk of in-stent restenosis at 6 months compared to bare-metal stents (6 of 28 BMS patients developed restenosis).
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