Pathophysiology of restenosis: interaction of thrombosis, hyperplasia, and/or remodeling.
In response to arterial injury, a series of intravascular changes take place that lead to restenosis: thrombosis, neointimal hyperplasia, and remodeling of the vessel. Neointima formation involves thrombosis, recruitment (migration), and recruitment/cell proliferation. To determine the source of neointimal cells that accumulate at the site of injury, pig models of stented and catheterized arteries were examined. The phases of neointima formation can each be seen in the pig in which neointimal cells come from nearby arterial tissue. The pig model was also employed to assess the effect of different degrees of force exerted by self-expanding stents on the arterial wall. In this model, the luminal area increased in response to chronic stent force. Slow expansion may help prevent neointimal hyperplasia and maintain luminal patency without causing damage to the artery.
Schwartz
R S
RS
Department of Cardiovascular Diseases and Internal Medicine, Mayo Medical School, Rochester, Minnesota 55905, USA.
D015906:Angioplasty, Balloon, Coronary / Q000295:instrumentation*; D000818:Animals; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D003328:Coronary Thrombosis / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D004868:Equipment Failure; D005352:Fibromuscular Dysplasia / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D006965:Hyperplasia / Q000473:pathology / Q000503:physiopathology; D012008:Recurrence; D019233:Retreatment; D015607:Stents; D017539:Tunica Intima / Q000473:pathology / Q000503:physiopathology