ABSTRACT
Coronary stenting is increasingly used during coronary interventions, and currently stents are implanted in most patients undergoing percutaneous catheter-based procedures.1-3 New stent designs may be readily delivered to the target lesion, are easily deployed, and can match almost every potential anatomic demand.3 The widespread adoption of coronary stenting relies on its ability to guarantee an optimal immediate angiographic result. Seminal studies both from Europe and from America demonstrated that stents are able to reduce the risk of restenosis when compared with balloon angioplasty.1,2 Some patients, however, still develop restenosis after stent implantation. In fact, coronary stenting elicits a more profound neointimal response than conventional balloon angioplasty.1 Restenosis after balloon angioplasty is the result of acute vessel recoil, vascular remodeling, and neointimal proliferation.4 Conversely, in-stent restenosis is largely dependent on severe neointimal tissue growth, which eventually obstructs the stent lumen.5 Therefore, treatment of in-stent restenosis is not an easy task, representing a technical and clinical challenge affecting a significant number of patients.6 Currently, instent restenosis constitutes a major health problem affecting up to 150 000 patients annually in the USA alone.6 In other words, restenosis, the main drawback of balloon angioplasty since its inception 25 years ago, still persist as the Achilles’ heel of the technique in the stent era.
