ABSTRACT
All forms of percutaneous coronary intervention (PCI) induce marked injury to the coronary or peripheral artery, and the injury response is critical to the longterm success or failure of the procedure. 1-3 The immediate response is platelet and thrombus activation, both of which induce cell activation with migration, proliferation and colonization and matrix synthesis.4-7 These cellular processes cause subsequent neointimal formation, with accumulation of fibroblasts/ myofibroblasts. Figure 28.1 is a high-power view of neointima from a human coronary artery. Neointimal thickening is the principal cause of in-stent restenosis, and may be of varying degrees through mechanisms not understood. Additionally, the adventitia thickens, and may contribute cells to the neointima in some circumstances.8-10 This latter process frequently causes vessel shrinkage, or negative remodeling, and is a principal cause of restenosis when a stent is not present to resist the constriction. 11-13 With stent placement, neointimal hyperplasia is the determining factor for in-stent restenosis, and is the major target of drug-eluting stents. 14, 15
The intracoronary stent improves long-term minimum luminal diameter and lowers restenosis rates. However, success of the stent is due to the geometric feature of a larger post-procedural lumen, allowing more late loss without causing severe stenoses. A bare (non-drug-eluting) stent possesses essentially no biological activity against neointima and hence does not limit neointimal thickening. Indeed, stenting is associated with increased neointima compared to balloon angioplasty. 6, 7 Itis only with the advent of brachytherapy and, more recently, drug-eluting stents that restenosis may finally be adequately controlled, through neointimal overgrowth limitation and preventing negative remodeling.
