Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis.
Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis.
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DOI:
10.1016/j.jcin.2011.05.025
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发表时间:
2011-10
影响因子:
11.3
通讯作者:
Simon, Daniel I.
中科院分区:
文献类型:
--
作者:
Inoue, Teruo;Croce, Kevin;Morooka, Toshifumi;Sakuma, Masashi;Node, Koichi;Simon, Daniel I.
The cellular and molecular processes that control vascular injury responses following PCI involve a complex interplay among vascular cells and progenitor cells that control arterial remodeling, neoinitimal proliferation and reendothelialization. Drug eluting stents (DES) improve the efficacy of peructaneous coronary intervention (PCI) by modulating vascular inflammation and preventing neointimal proliferation and restenosis. Although positive effects of DES reduce inflammation and restenosis, negative effects delay reendothelialization and impair endothelial function. Delayed reendothelialization and impaired endothelial function may be linked to stent thrombosis and adverse clinical outcomes following DES use. Compared with BMS, DES may also differentially modulate mobilization, homing and differentiation of vascular progenitor cells involved reendothelialization 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.
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