DIFFERENTIAL EXPRESSION OF 92-KDA GELATINASE IN PRIMARY ATHEROSCLEROTIC VERSUS RESTENOTIC CORONARY LESIONS

Rupture of atherosclerotic plaque resulting in intravascular thrombosi s and myocardial infarction (MI), while a common sequelae of de novo a therosclerotic lesions, is an uncommon consequence of restenosis. We h ypothesize that the rarity of MI associated with restenotic lesions is a result of cellular and biochemical modifications induced by the loc al response to mechanical injury rendering the site resistant to ruptu re. Clinical and angiographic features of patients presenting with sym ptomatic primary (n = 24) or restenotic coronary lesions (n = 12) who underwent directional atherectomy were compared, Histologic analysis a nd immunostaining for 92-kDa gelatinase were performed on each atherec tomy specimen. There was no significant difference between the 2 group s regarding age, gender, incidence of diabetes, smoking, hypertension, hypercholesterolemia, or previous MI. Lesion length, extent, and dist ribution of disease and percent stenosis were not significantly differ ent between groups. However, 8% of primary lesions were hypercellular compared with 75% of restenotic specimens (p = 0.0001), Hypercellulari ty in restenotic specimens was shown by adjacent section staining to b e composed of smooth muscle cells. Ninety-two kDa gelatinase was expre ssed in 79% of primary lesions versus 0% of restenotic specimens (p = 0.0001). Thrombus was identified in 54% of primary lesions versus 22% of restenotic lesions (p <0.05). These findings suggest that, independ ent of clinical or angiographic influences, balloon injury induces inc reased lesion cellularity and reduced expression of 92-kDa gelatinase, possibly resulting in a reduced propensity for plaque rupture and thr ombosis. (C) 1997 by Excerpta Medica, Inc.