Department of Cardiovascular Medicine, Dokkyo Medical University, Tochigi, Japan.
JACC Cardiovasc Interv. 2011 Oct;4(10):1057-66. doi: 10.1016/j.jcin.2011.05.025.
The cellular and molecular processes that control vascular injury responses after percutaneous coronary intervention involve a complex interplay among vascular cells and progenitor cells that control arterial remodeling, neointimal proliferation, and re-endothelialization. Drug-eluting stents (DES) improve the efficacy of percutaneous coronary intervention by modulating vascular inflammation and preventing neointimal proliferation and restenosis. Although positive effects of DES reduce inflammation and restenosis, negative effects delay re-endothelialization and impair endothelial function. Delayed re-endothelialization and impaired endothelial function are linked to stent thrombosis and adverse clinical outcomes after DES use. Compared with bare-metal stents, DES also differentially modulate mobilization, homing, and differentiation of vascular progenitor cells involved in re-endothelialization and neointimal proliferation. The effects of DES on vascular inflammation and repair directly impact clinical outcomes with these devices and dictate requirements for extended-duration dual antiplatelet therapy.
经皮冠状动脉介入治疗后血管损伤反应的细胞和分子过程涉及血管细胞和祖细胞之间的复杂相互作用，这些细胞和祖细胞控制着动脉重塑、新生内膜增殖和再内皮化。药物洗脱支架 (DES) 通过调节血管炎症和预防新生内膜增殖和再狭窄，提高了经皮冠状动脉介入治疗的疗效。虽然 DES 的积极作用降低了炎症和再狭窄，但负面影响延迟了再内皮化并损害了内皮功能。再内皮化延迟和内皮功能受损与支架血栓形成和 DES 使用后的不良临床结局有关。与裸金属支架相比，DES 还可调节参与再内皮化和新生内膜增殖的血管祖细胞的动员、归巢和分化。DES 对血管炎症和修复的影响直接影响这些器械的临床结局，并决定了对延长时间双重抗血小板治疗的要求。
