INTRODUCTION

Restenosis is usually defined as a re-narrowing of the arterial lumen occurring after a vascular intervention intended to treat ischemic lesions. This loss of lumen area results from the injury caused by all forms of vascular intervention, including direct repair (patch angioplasty, endarterectomy) and intraluminal approaches (balloon angioplasty, atherectomy, stent angioplasty). While there are clear differences between arteries and veins (review in), this review will also include discussion of stenosis after vein bypass grafting or creation of arteriovenous fistula dialysis access because stenosis in these cases also results from injury.

Lumen enlargement after angioplasty or stenting is the result of a combination of plaque reduction (compression and embolization), plaque redistribution within or outside the lesion area, and vessel expansion (see review). Failure occurs at early times because of technical problems and thrombosis (e.g. small diameter vein graft, limited out-flow, or hypercoagulability) and later times (1-18 months) primarily because of injury-induced scarring. At much later times (> 18 months), failure primarily results from the ongoing atherosclerotic process. Although restenosis occurs within the con- text of atherosclerosis, the clinical features and genetic control of atherosclerosis and restenosis are different. Atherosclerosis develops slowly over decades, while restenosis occurs within months to years.

The costs of restenosis are considerable, since greater than 20% of all interventions fail because of restenosis. In the U.S. alone, it is estimated that as many as 200,000 cases of drug eluting stent (DES) restenosis occur every year (see review).