Editorial Delayed neointimal healing after drug-eluting stent implantation: seeing is believing

This editorial refers to ‘Angioscopic differences in neointimal coverage and in persistence of thrombus between sirolimus-eluting stents and bare metal stents after a 6-month implantation’ † by Takano et al., on page 2189 Ever since its introduction in 1977, the long-term benefit of percutaneous coronary intervention has been limited by the phenomenon of restenosis, i.e. recurrence of significant stenosis at the site of intervention. Whereas, after plain balloon angioplasty, restenosis is for roughly two-thirds due to negative vessel wall remodelling, the late lumen loss after stent implantation is virtually exclusively caused by neointimal hyperplasia, a proliferation of smooth muscle cells with deposition of abundant extracellular matrix. Over the last years, a multitude of anti-proliferative drugs have been tested, several of which have been found effective in inhibiting this neointimal hyperplasia when locally delivered from a polymer-encapsulated stent. The two compounds with the largest clinical experience are paclitaxel and sirolimus, a cytostatic macrocyclic lactone with both anti-inflammatory and anti-proliferative properties. Although the efficacy of these drug-eluting stents (DES) in preventing restenosis has been well established over the last years, recently, concerns have been raised about a possibly increased incidence of late stent thrombosis (more than 6 months after stent implantation) when compared with the very low incidence of late stent thrombosis after implan-tation of bare metal coronary stents (BMS). At the annua