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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:261.)
© 2007 American Heart Association, Inc.

Editorials

Emerging Thrombotic Effects of Drug Eluting Stents

Ninian N. Lang; David E. Newby

From the Centre for Cardiovascular Science, University of Edinburgh, UK.

Correspondence to Dr Ninian N Lang, Centre for Cardiovascular Science, The University of Edinburgh, Chancellor’s Building, 49 Little France Crescent, Edinburgh, EH16 4SB, United Kingdom. E-mail ninian.lang@ed.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Drug eluting stents (DES) have been enthusiastically introduced into contemporary interventional cardiology practice. By delivering locally active doses of antiproliferative drugs, they have demonstrated an impressive capacity to inhibit restenosis caused by neointimal hyperplasia; a complication that has plagued uncoated "bare-metal" stents (BMS). DES coated with either paclitaxel or rapamycin (sirolimus) are now deployed in over 90% of coronary interventions in the United States.¹ However, clinical follow-up has revealed significant concerns relating to the incidence of late (> 30 days) stent thrombosis, especially in long stents and after discontinuation of dual antiplatelet therapy.² Stent thrombosis with DES has been attributed to various potential mechanisms (Figure), but delayed or incomplete stent endothelialization has been proposed as a major mechanism. In a recent autopsy study,³ DES showed reduced endothelialization (27±26% versus 66±25%), especially in those with evidence of stent thrombosis. However, patients with DES had stents that were almost twice as long and included those receiving DES for indications not approved by the Food and Drug Administration, including acute myocardial infarction. This selected autopsy group represents the extreme end of the spectrum and may not reflect the situation in the majority of patients who receive DES and survive.

View larger version (57K):   Proposed mechanisms of drug eluting stent thrombosis.

See page 400

The hypothesis that late stent thrombosis is attributable solely to delayed endothelialization contrasts with porcine models of coronary stent implantation. Although endothelialization may be more rapid than in humans, endothelial coverage of DES and BMS in a porcine model is almost complete . . . [Full Text of this Article]

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Antiproliferative Agents Alter Vascular Plasminogen Activator Inhibitor-1 Expression: A Potential Prothrombotic Mechanism of Drug-Eluting Stents

James A.S. Muldowney, III, John R. Stringham, Shawn E. Levy, Linda A. Gleaves, Mesut Eren, Robert N. Piana, and Douglas E. Vaughan
Arterioscler Thromb Vasc Biol 2007 27: 400-406. [Abstract] [Full Text] [PDF]