ABSTRACT

The use of coronary stents has increased exponentially since their introduction into clinical practice in the early 1990s. It is currently estimated that stents are used in 60-70% of all percutaneous coronary revascularization procedures. Enthusiasm for the widespread use of stents is based not only on the ability to achieve a large, smooth lumen and effectively treat acute or threatened vessel closure but also upon their ability to reduce restenosis.1-4 However, with the increased use of coronary stents, in-stent restenosis has developed as an important clinical problem. The reaction to the placement of a coronary stent has been shown to involve both the stented and adjacent vessel and consists of a combination of intimal hyperplasia and tissue remodeling, which tapers off as the distance from the stented segment increases.5 In-stent restenosis is generally defined as a 50% or greater narrowing within, or at the proximal or distal sites of (or 5 mm from) a previously placed stent.6 Recurrent in-stent restenosis is defined as a 50% or greater stenosis, which occurs more than 1 month after treatment of in-stent restenosis. Rates of primary and recurrent in-stent restenosis vary considerably depending on many factors including whether the initial lesion was ‘focal’ ( 10 mm in length) or diffuse ( 10 mm in length).