Pathophysiology of coronary artery restenosis.
All forms of percutaneous coronary intervention confer injury on the vessel. The arterial response to that injury is the basis for long-term outcome. The stent prevents remodeling but enhances neointimal formation, and it is this neointima that is principally responsible for in-stent restenosis. Neointima forms in response to thrombus, inflammation, intimal and medial dissections, and elastic recoil of the arterial wall when a stent is not placed. Current efforts to solve restenosis center on limiting neointimal hyperplasia through drug-eluting stents and vascular brachytherapy. This article reviews arterial injury during revascularization in both patients and animal models and discusses the nature and formation of neointimal hyperplasia.
Schwartz
Robert S
RS
Minnesota Cardiovascular Research Institute, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA.
Henry
Timothy D
TD
D000800:Angioplasty, Balloon / Q000009:adverse effects; D000818:Animals; D023903:Coronary Restenosis / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000293:injuries* / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D015607:Stents / Q000009:adverse effects; D017539:Tunica Intima / Q000473:pathology*