Abstract

In‐stent restenosis (ISR) is a common and frequently resistant problem. The pathophysiology of in‐stent and nonstent restenosis is different, the former resulting primarily from intimal hyperplasia, while the latter is predominantly a consequence of negative late remodeling. Predictors of ISR are patient and lesion related. When approaching a patient with stent restenosis, false or pseudo‐restenosis must be considered. Angiography frequently fails to reveal pseudo‐restenosis, and, consequently, intravascular ultrasound can be essential in guiding the most effective strategy. Because of spontaneous neointimal regression, patients with asymptomatic stent restenosis often can be followed and treated medically. The mechanical approaches to ISR include balloon angioplasty alone, debulking plus PTCA, and restenting. For focal lesions (< 10 mm in length) balloon angioplasty at moderately high pressures is often effective. Following balloon dilatation, stent expansion and plaque extrusion equally account for the gain in lumen area. For more diffuse disease, debulking plus balloon angioplasty is preferred, although no randomized data are available. Only restenting is associated with a gain in MID that is comparable to the original stent implant and is not associated with reintrusion of neointima — INSTANT restenosis. Despite aggressive debulking with or without further stenting, diffuse stent restenosis often is resistant to purely mechanical treatment. Nonmechanical approaches, such as localized radiation therapy, will be required to effectively treat this difficult subset of patients.

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