BACKGROUND: There is evidence that endothelial coverage of drug-eluting stents might be delayed or absent, a risk factor for late thrombotic events. We studied the effects of different drug-polymer-device iterations on endothelium-dependent coronary vasomotion. Systemic markers of endothelial inflammation were correlated with coronary vasomotor changes. METHODS AND RESULTS: Patients with paclitaxel-eluting stents (n=11), sirolimus-eluting stents (n=21), biolimus A9-eluting stents (n=28), zotarolimus-eluting stents (n=10), and bare-metal stents (n=13) were studied 10, 9, 9, 9, and 12 months after implantation, respectively. Endothelium-dependent coronary vasomotion was tested proximally and distally to the stent and at a reference vessel segment during atrial pacing at increasing heart rates by quantitative coronary angiography. Indexes of platelet-monocyte binding and other biomarkers were studied in a subgroup of 19 patients. The baseline characteristics and hemodynamics of the patients in the different stent groups were comparable. Significant differences were observed across the 5 stent groups, concerning the vasomotion of segments proximal (P=0.006) and distal (P=0.003) to the stent. Normal vasomotion (vasodilatation) was maintained in the biolimus A9-eluting stent, zotarolimus-eluting stent, and bare-metal stent groups, whereas vasoconstriction was observed in the sirolimus-eluting stent and paclitaxel-eluting stent groups. Platelet-monocyte binding in whole blood showed a significant inverse correlation with vasomotion in reference but not in segments adjacent to the stent (r=-0.57; P=0.01). CONCLUSIONS: Paclitaxel-eluting stents and sirolimus-eluting stents seem to cause endothelial dysfunction of the implanted vessel, whereas biolimus A9-eluting stents and zotarolimus-eluting stents behave more closely to bare-metal stents, with preserved endothelial vasomotor response. Coronary vasoconstriction was not associated with detectable systemic endothelial activation.
BACKGROUND: There is evidence that endothelial coverage of drug-eluting stents might be delayed or absent, a risk factor for late thrombotic events. We studied the effects of different drug-polymer-device iterations on endothelium-dependent coronary vasomotion. Systemic markers of endothelial inflammation were correlated with coronary vasomotor changes. METHODS AND RESULTS:Patients with paclitaxel-eluting stents (n=11), sirolimus-eluting stents (n=21), biolimus A9-eluting stents (n=28), zotarolimus-eluting stents (n=10), and bare-metal stents (n=13) were studied 10, 9, 9, 9, and 12 months after implantation, respectively. Endothelium-dependent coronary vasomotion was tested proximally and distally to the stent and at a reference vessel segment during atrial pacing at increasing heart rates by quantitative coronary angiography. Indexes of platelet-monocyte binding and other biomarkers were studied in a subgroup of 19 patients. The baseline characteristics and hemodynamics of the patients in the different stent groups were comparable. Significant differences were observed across the 5 stent groups, concerning the vasomotion of segments proximal (P=0.006) and distal (P=0.003) to the stent. Normal vasomotion (vasodilatation) was maintained in the biolimus A9-eluting stent, zotarolimus-eluting stent, and bare-metal stent groups, whereas vasoconstriction was observed in the sirolimus-eluting stent and paclitaxel-eluting stent groups. Platelet-monocyte binding in whole blood showed a significant inverse correlation with vasomotion in reference but not in segments adjacent to the stent (r=-0.57; P=0.01). CONCLUSIONS:Paclitaxel-eluting stents and sirolimus-eluting stents seem to cause endothelial dysfunction of the implanted vessel, whereas biolimus A9-eluting stents and zotarolimus-eluting stents behave more closely to bare-metal stents, with preserved endothelial vasomotor response. Coronary vasoconstriction was not associated with detectable systemic endothelial activation.
Authors: Pietro Giudice; Tiziana Attisano; Marco Di Maio; Elisabetta M Bellino; Maria V Polito; Cesare Baldi; Francesco Vigorito; Michele R Di Muro; Salvatore D Tomasello; Alfredo R Galassi; Federico Piscione Journal: Interv Med Appl Sci Date: 2014-12-22
Authors: Olivier Muller; Jozef Bartunek; Michalis Hamilos; Catalina Trana Berza; Fabio Mangiacapra; Argyrios Ntalianis; Kristof Vercruysse; Christian Duby; William Wijns; Bernard De Bruyne; Guy R Heyndrickx; Marc Vanderheyden; Josefin-Beate Holz; Emanuele Barbato Journal: J Cardiovasc Transl Res Date: 2012-12-12 Impact factor: 4.132
Authors: Rod R Jose; Waseem K Raja; Ahmed M S Ibrahim; Pieter G L Koolen; Kuylhee Kim; Abdurrahman Abdurrob; Jonathan A Kluge; Samuel J Lin; Gillian Beamer; David L Kaplan Journal: J Biomed Mater Res B Appl Biomater Date: 2014-11-11 Impact factor: 3.368
Authors: Emanuele Barbato; Arnold Herman; Edouard Benit; Luc Janssens; Jacques Lalmand; Etienne Hoffer; Patrick Chenu; Antoine Guédès; Luc Missault; Bruno Pirenne; François Cardinal; Steven Vercauteren; William Wijns Journal: J Cardiovasc Transl Res Date: 2013-10-19 Impact factor: 4.132
Authors: Luigi Di Serafino; Jaydeep Sarma; Karen Dierickx; Ioannis Ntarladimas; Stylianos A Pyxaras; Leen Delrue; Bernard De Bruyne; William Wijns; Emanuele Barbato; Jozef Bartunek Journal: J Cardiovasc Transl Res Date: 2013-12-06 Impact factor: 4.132