Drug-Eluting Stent Update 2007

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. 1Long-term follow-up (Ͼ6 years) in patients with bare metal stents (BMS) shows that tissue proliferation reaches its peak at around 6 to 12 months and then regresses. 2This 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 al 3 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. 3A similar catch-up phenomenon was observed after implantation of paclitaxel-eluting stents (PES) and tacrolimus-eluting stents in porcine models. 4,5Conversely, 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 -10However, 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. 11The 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.