IN-STENT RESTENOSIS - CONTRIBUTIONS OF INFLAMMATORY RESPONSES AND ARTERIAL INJURY TO NEOINTIMAL HYPERPLASIA

Objectives. We examined the relative contributions of inflammation and arterial injury to neointimal formation in a porcine coronary overstr etch restenosis model. Background. Previous studies established that s tents cause neointimal proliferation proportional to injury, Although inflammation has been postulated to be a major contributor to restenos is after angioplasty, there is a paucity of data on the relation betwe en inflammation and subsequent neointimal formation. Methods. Twenty-o ne pigs underwent balloon injury followed by implantation of oversized , tubular, slotted stents (stent/artery ratio 1.2:1) in the left anter ior descending coronary artery, Morphometric analysis of the extent of injury (graded as injury score 0 to 3) and inflammation (graded as in flammation score 0 to 3) 1 month later was assessed and correlated wit h neointimal formation.Results. An inflammatory reaction was observed in 20 of 21 pigs, and significant positive correlations were found bet ween the degree of arterial injury and the extent of the inflammatory reaction (r = 0.80, p < 0.01) and between the extent of inflammatory r eaction and the neointimal thickness (r = 0.75, p < 0.01), neointimal area (r = 0.53, p = 0.01) and percent area stenosis (r = 0.66, p < 0.0 1) within the stents, Importantly, there were areas with inflammation only in the absence of injury, and vice versa, that were also associat ed with neointimal hyperplasia. Conclusions. These data suggest that t he inflammatory reaction plays an equally important role as arterial i njury in neointimal formation after coronary stenting, and that, anti- inflammatory approaches may be of value to reduce in-stent restenosis. (C) 1998 by the American College of Cardiology.