Cardiovascular Centre Aalst, OLV Hospital, Moorselbaan 164, Aalst, Belgium
Circ Cardiovasc Interv. 2008 Dec;1(3):193-200. doi: 10.1161/CIRCINTERVENTIONS.108.797928.
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.
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).
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.
有证据表明，药物洗脱支架的内皮覆盖可能会延迟或缺失，这是导致晚期血栓形成事件的一个风险因素。我们研究了不同药物-聚合物-器械迭代对内皮依赖性冠状动脉血管舒缩的影响。系统内皮炎症标志物与冠状动脉血管舒缩变化相关。
分别在紫杉醇洗脱支架（n=11）、西罗莫司洗脱支架（n=21）、依维莫司洗脱支架（n=28）、佐他莫司洗脱支架（n=10）和裸金属支架（n=13）植入后 10、9、9、9 和 12 个月，对患者进行研究。通过定量冠状动脉造影，在心房起搏时，以递增的心率，在支架近端和远端以及参考血管节段测试内皮依赖性冠状动脉血管舒缩。在 19 例患者的亚组中研究了血小板-单核细胞结合和其他生物标志物的指标。不同支架组患者的基线特征和血液动力学参数具有可比性。在支架近端（P=0.006）和支架远端（P=0.003）的 5 个支架组之间观察到显著差异。在依维莫司洗脱支架、佐他莫司洗脱支架和裸金属支架组中，血管舒缩保持正常（血管扩张），而在西罗莫司洗脱支架和紫杉醇洗脱支架组中，血管收缩。全血中血小板-单核细胞结合与参考节段而非支架相邻节段的血管舒缩呈显著负相关（r=-0.57；P=0.01）。
紫杉醇洗脱支架和西罗莫司洗脱支架似乎会导致植入血管的内皮功能障碍，而依维莫司洗脱支架和佐他莫司洗脱支架的表现更接近裸金属支架，保留了内皮血管舒缩反应。冠状动脉收缩与可检测的系统性内皮激活无关。
