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(Circulation. 2007;116:961-968.)
© 2007 American Heart Association, Inc.

Advances in Interventional Cardiology

Drug-Eluting Stent Update 2007

Part II: Unsettled Issues

Joost Daemen, MD; Patrick W. Serruys, MD, PhD

From Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands.

Correspondence to Professor P.W. Serruys, MD, PhD, Thoraxcenter, Ba-583, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. E-mail p.w.j.c.serruys@erasmusmc.nl

Key Words: stents • restenosis • thrombosis • myocardial infarction • diabetes mellitus

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

	Introduction

 
Restenosis has been called the Achilles heel of coronary stenting and is caused by a combination of factors, including neointimal proliferation, elastic recoil, reorganization of thrombus, remodeling, and inflammation.¹ Long-term follow-up (>6 years) in patients with bare metal stents (BMS) shows that tissue proliferation reaches its peak at around 6 to 12 months and then regresses.² This pattern fits with the observed increase in revascularization rates up to 1 year, after which a plateau occurs. After drug-eluting stent (DES) implantation, Carter et al³ showed a late catch-up of restenosis in sirolimus-eluting stents (SES) in porcine models. Although a 50% reduction of restenosis was observed at 30 days, restenosis rates for SES and BMS were equivalent at 6 months.³ A similar catch-up phenomenon was observed after implantation of paclitaxel-eluting stents (PES) and tacrolimus-eluting stents in porcine models.^4,5 Conversely, in humans, there does not seem to be reason for concern about late catch-up for up to 4 years on both clinical and angiographic end points.^6–10 However, several long-term DES studies showed that, in contrast to BMS, the neointima continued to grow up to 2 years as assessed by intravascular ultrasound.¹¹ The discrepancy between porcine and clinical data is influenced by the temporal differences in arterial response in humans compared with animal models but also may be due to differences in species response to sirolimus and paclitaxel and physiological stimuli for neointimal formation.

	Trading Restenosis for Thrombosis and Late Mortality?

 
The Problem of Restenosis
Restenosis has always been considered a benign and harmless entity. However, recent studies assessing the clinical presentation and long-term outcome . . . [Full Text of this Article]

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