ABSTRACT
The use of intracoronary stents has become the first choice of therapy in interventional cardiology, representing 70-80% of all percutaneous coronary interventions in the United States and Europe.1,2 Metallic coronary stents reduce the incidence of restenosis compared to balloon angioplasty by opposing elastic recoil and late remodeling of the vessel.3,4 However, an excessive neointimal hyperplasia inside the stent still induces a restenosis frequency in up to 10-30% of the treated patients.1 This ‘in-stent’ restenosis is a local, chronic response of the vessel wall to a foreign body, which involves a cascade of thrombotic, proliferative, and inflammatory phases.5 Many different cell types: platelets, smooth muscle cells (SMCs), myofibroblasts, endothelial cells, and inflammatory cells, are recruited to play a pivotal role in this wound healing phenomenon, with the subsequent release of several growth factors which, on their turn, again stimulate the fibromuscular proliferative response of the vessel wall.
