Journal
JACC-CARDIOVASCULAR INTERVENTIONS
Volume 4, Issue 10, Pages 1057-1066Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jcin.2011.05.025
Keywords
inflammation; re-endothelialization; restenosis; stent thrombosis
Categories
Funding
- National Heart, Lung, and Blood Institute [HL85816, HL57506, HL73852, 1K08HL086672]
- Future Leaders in Cardiovascular Medicine Fellowship
- Michael Lerner Foundation
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Kimura Foundation
- Japan Foundation of Cardiovascular Research
- Grants-in-Aid for Scientific Research [22590794] Funding Source: KAKEN
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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. (J Am Coll Cardiol Intv 2011;4:1057-66) (C) 2011 by the American College of Cardiology Foundation
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