Abstract

Drug-eluting stents (DES) are widely used in percutaneous coronary intervention and have resulted in significant reductions in target-vessel revascularization as compared with bare-metal stents (BMS) in randomized, controlled trials and in unrestricted patient and lesion subsets.1,2 Comprehensive analyses have proven the safety of sirolimus-eluting stents (SES) and paclitaxel-eluting stents (PES) compared with BMS, with similar rates of death and myocardial infarction after as much as 4 years of follow-up2,3; however, a valid safety concern remains, given that DES increase the risk of late (>30 days) and very late (>1 year) stent thrombosis compared with BMS. Our understanding of the risk factors for stent thrombosis has been derived from experimental models, pathological findings, and clinical trials. The mechanisms underlying the increased thrombogenicity of DES are multifactorial and include patient, lesion, and procedural factors, as well as compliance with and response to antiplatelet therapy.4–6 However, all currently available DES may be susceptible to late and very late stent thrombosis because of the delayed arterial healing and impaired endothelialization that accompany the drugs used to inhibit neointimal hyperplasia. We can postulate that the rate of healing varies from patient to patient, and even from lesion to lesion within the same patient, but we do not have a method to assess or measure healing after stenting. Therefore, we have empirically recommended that dual-antiplatelet therapy be extended for at least 12 months after DES implantation in an effort to reduce events during the period when the stent is prone to thrombus formation.7 Articles see pp 20 and 28 In terms of assessing the mechanisms of stent failure, including restenosis and stent thrombosis, intravascular ultrasound (IVUS) has been helpful. Subacute stent thrombosis (<30 days) in BMS and DES alike often has a cause that is identifiable by IVUS, such as severe …

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