2004
DOI: 10.1016/s0140-6736(04)17275-9
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Late thrombosis in drug-eluting coronary stents after discontinuation of antiplatelet therapy

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Cited by 1,266 publications
(318 citation statements)
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“…Owing to limitations of polymeric carriers in drug-eluting stents, [11][12][13][14][15][16][17][18][19][20][21] the development of polymer-free drug delivery platforms has potential applications in stents. 10 Surface modification using SAMs is one of the promising techniques for delivering drugs from metal implants without polymeric carriers.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Owing to limitations of polymeric carriers in drug-eluting stents, [11][12][13][14][15][16][17][18][19][20][21] the development of polymer-free drug delivery platforms has potential applications in stents. 10 Surface modification using SAMs is one of the promising techniques for delivering drugs from metal implants without polymeric carriers.…”
Section: Discussionmentioning
confidence: 99%
“…10 Most commercially available DESs use polymers to coat and release drugs. The limitations of using some polymeric carriers in DES are as follows: ͑a͒ polymer coatings undergo cracks, fissures, waviness, and other irregularities during stent expansion; 11 ͑b͒ inflammatory and hypersensitivity reactions to polymer coatings; [12][13][14][15][16][17][18] and ͑c͒ polymer coatings affect the normal vessel healing process 17,19,20 and this could cause late stent thrombosis. 18,19,21 Hence, there is a need for developing polymer-free drug delivery platform for coronary stents.…”
Section: Introductionmentioning
confidence: 99%
“…Both angioplasty and bare metal stents are associated with significant restenosis caused by neointimal hyperplasia that leads to a 14% incidence of reintervention (2). Recent reports have described late in-stent thrombosis in drug-eluting stents (3,4).…”
mentioning
confidence: 99%
“…Drug eluting stent technologies were composed of sustained drug release systems encapsulating anti-proliferative drugs to inhibit the proliferation of smooth muscle cells and they have been discovered to reduce the rate of in-stent restenosis [15,16]. Nevertheless, the anti-proliferative role of the drugs may impede endothelialization and blood is uncovered to the stent struts and/or to the surface coating, obviously increasing the proclivity of thrombosis [17,18]. Delayed or impaired endothelialization also limits the long-term success against restenosis [17,19].…”
Section: Introductionmentioning
confidence: 99%