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Over 1.5 million percutaneous coronary revascularisation procedures are performed annually world wide, most being intracoronary stenting. Despite enormous advances in devices, the major limitation is in-stent stenosis (ISS) (reviewed by Bennett and O'Sullivan1). Although ISS rates are 10–20% in selected patients, we now stent total occlusions, saphenous vein bypass grafts, both angioplasty and ISS sites, diabetic patients, and small vessels. Thus, real ISS rates are much higher, up to 59% in some high risk lesions.
Until recently, the only effective treatment for ISS was brachytherapy. Brachytherapy reduces target vessel revascularisation rates and binary restenosis rates, and increases minimum luminal diameters (MLDs) compared with control vessels, maintained to three years.1 Although effective, brachytherapy is not universally accepted, due predominantly to late thrombosis and the logistics of administering radioactivity. In contrast, drug eluting stents containing the immunosuppressive agent rapamycin and the antimitotic agent paclitaxel have shown encouraging reductions in ISS in de novo lesions,2,3 and possibly in ISS lesions. This review examines the pathology of ISS and how drugs bound to stents interrupt the normal response to vessel injury.
MECHANISMS OF RESTENOSIS
Overdistension of the diseased vessel causes endothelial disruption, internal elastic lamina fracture, and medial dissection. Lumen enlargement is caused by a combination of plaque reduction (compression/embolisation), axial plaque redistribution towards the proximal and distal segments outside the stent, plaque extrusion, and vessel expansion. Many processes then contribute to restenosis (fig 1 and table 1).