903-15 Expression of 92 kDa Gelatinase in Primary Atherosclerotic vs Restenotic Coronary Lesions: Evidence for Mechanical Plaque Stabilization

Abstract

Rupture of atherosclerotic plaque resulting in intravascular thrombosis and myocardial infarction (MI), while a common sequelae of primary atherosclerotic lesions, is an uncommon consequence of restenosis. We hypothesize that the rarity of MI associated with restenotic lesions is a result of cellular and biochemical modifications induced by the local response to balloon injury rendering the site resistant to rupture (plaque stabilization). Clinical and angiographic features of pts presenting with symptomatic primary (n = 24) or restenotic coronary lesions (n = 12) who underwent directional atherectomy were compared. Histologic analysis and immunostaining forthe matrix degrading enzyme, 92 kDa gelatinase, were performed on each atherectomy specimen. There was no significant difference between the 2 groups regarding age, gender, incidence of diabetes, smoking, hypertension, hypercholesterolemia or previous MI. Extent and distribution of disease, vessel caliber and % stenosis were not significantly different between groups. However, 8% of primary lesions were hypercellular compared to 75% (p = 0.0001) of restenotic specimens. 92 kDa gelatinase was expressed in 79% of primary lesions vs 0% of restenotic specimens (p = 0.0001). Thrombus was identified in 54% of primary lesions vs 22% of restenotic lesions (p < 0.05). These findings suggest that, independent of clinical or angiographic influences, balloon injury induced increased lesion cellularity and reduced expression of 92 kDa gelatinase, possibly conferring less propensity for plaque rupture and thrombosis.