ABSTRACT
Introduction Medical therapy of coronary artery disease (CAD) has changed considerably in recent years. It is characterized by expanding the use of percutaneous coronary intervention (PCI) and continued conversion to minimally invasive percutaneous transluminal coronary angioplasty (PTCA) and stent therapy despite significant advances in pharmacological treatment and implementation of novel surgical techniques in treatment of the CAD (1). Introduction of stents showed a significant decrease in vessel remodeling and elastic recoil at the site of intervention and clearly demonstrated the superiority of stent implantation over PTCA alone with respect to restenosis in de novo coronary lesions. Extensive use of coronary stents to prevent restenosis has produced a new disease, in-stent restenosis. Unfortunately, this complication continues to be difficult to prevent; regardless of the treatment strategy, the rate of in-stent restenosis (20% to 60% after bare metal stent implantation) is still unacceptably high, depending on vessel and patient bias (2-5). This is particularly true in patients with diabetes and in some lesion sublets, such as bifurcated lesions, long diffuse lesions, and/or small vessels (5). However, it was also evident that neointimal proliferation is not affected by stenting technique (6). Thus, despite significant advances in the treatment of cardiovascular disease, intimal hyperplasia remains the most common cause of early failure after revascularization.
