Thrombosis After Stent Implantation: How Much of a Problem Is There?

Ioannis Iakovou


Future Cardiol. 2008;4(3):261-267. 

In This Article

Abstract and Introduction

Drug-eluting stents reduce the occurrence of in-stent restenosis and the need for subsequent target vessel revascularization when compared with bare-metal stents. However, drug-eluting stents may be associated with delayed (or absent) endothelialization, localized hypersensitivity reactions and late stent thrombosis. Stent thrombosis is a catastrophic event, resulting in life-threatening complications. Although larger, adequately powered, randomized trials are needed to fully assess the net clinical effects of drug-eluting stents compared with bare-metal stents, the evidence, thus far, appears to suggest that the net clinical benefit of drug-eluting stents may outweigh their risks. Premature discontinuation of antiplatelet therapy is the most important predictor of stent thrombosis; therefore, patients who are candidates for implantation of drug-eluting stents should be screened for their ability to receive and tolerate uninterrupted antiplatelet therapy longer than is necessary with bare-metal stents.

Stent thrombosis (ST) is the sudden occlusion of a stented coronary artery due to thrombus formation. The clinical consequences of ST are frequently catastrophic and include death in 20-48% or major myocardial infarction (MI) in 60-70% of the cases.[1,2,3,4,5] When bare-metal stents (BMS) were first introduced, ST was a common complication. Most episodes occurred within 2 weeks of stent implantation and often resulted in MI and, not infrequently, death.[3] Technical improvements, such as the use of adequately sized balloons and high-pressure deployment, helped to substantially decrease thrombosis rates.[3,6] In addition, a regimen of dual-antiplatelet therapy (aspirin plus a thienopyridine) was found to further reduce the incidence of ST.[3] Dual-antiplatelet therapy is prescribed for 4 weeks after BMS implantation, the time required for stent endothelialization to occur. Late ST (>30 days) after the implantation of a BMS is rare. This complication first appeared when intracoronary radiation (brachytherapy) was introduced as a treatment for in-stent restenosis.[7,8] Intracoronary radiation was found to delay re-endothelialization in animals, thus predisposing to late ST. Prolonging the duration of dual-antiplatelet therapy to 6-12 months largely resolved this problem.[7,8] Similar to brachytherapy, drug-eluting stents (DES) have an antiproliferative effect that delays stent re-endothelialization. For this reason, DES trials have initially mandated dual-antiplatelet therapy for 3-6 months, as well as the indefinite use of aspirin.[9]

Stent platforms, polymer coating, eluted drug and other factors might contribute to DES thrombogenicity.[5] First, stent design might influence the degree of platelet activation after coronary stent deployment. Second, both the polymer coating and the medication with which it is impregnated might influence the propensity for thrombosis.[5]

What is the pathologic basis of DES thrombosis? Virmani et al. initially proposed that a hypersensitivity reaction could contribute to the development of this event by describing a case of fatal acute MI and cardiac rupture as a result of late thrombosis of a Cypher® stent (Cordis Corporation, FL, USA) deployed 18 months previously.[10] The hypersensitivity reaction could be caused by the metallic stent, polymer or the drug. There is a likely spectrum of allergic responses to DES in sensitive patients, varying from benign reactions to excessive inflammation with medial destruction and aneurysm formation with late in-stent thrombosis. In addition, despite animal data demonstrating complete coverage at 30 days, DES strut endothelialization is reduced in humans with oronary artery disease.[11,12]


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