CORONARY ANGIOPLASTY RESULTS IN LEUKOCYTE AND PLATELET ACTIVATION WITH ADHESION MOLECULE EXPRESSION - EVIDENCE OF INFLAMMATORY RESPONSES INCORONARY ANGIOPLASTY

Objectives. This study sought to characterize leukocyte and platelet a ctivation and adhesion molecule expression after coronary angioplasty. Background. Coronary angioplasty can be regarded as a clinical model of postischemic inflammation because this intervention leads to the re lease of inflammatory mediators as a result of plaque rupture and endo thelial injury. Methods. In 13 patients with stable angina (mean [+/-S EM] age 56.0 +/- 2.4 years, range 44 to 79), blood samples were drawn from the aorta and coronary sinus immediately before and immediately a nd 15 min after coronary angioplasty. Subsequently, leukocyte and plat elet functions were determined. Eleven control patients (57.5 +/- 2.3 years, range 52 to 78) underwent coronary arteriography.Results. Coron ary arteriography and angioplasty showed no difference in number of le ukocytes between the coronary sinus and the aorta. However, 15 min aft er coronary angioplasty, there was an increase in neutrophil CD18 and CD11b, monocyte CD14 and platelet glycoprotein Ilb/IIIa expression and a decrease in neutrophil L-selectin expression (189 +/- 25%, 163 +/- 27%, 158 +/- 35%, 141 +/- 22% and 31 +/- 10%, respectively, p < 0.01). In the control subjects, no change in adhesion molecule expression oc curred. Superoxide production and aggregation in ex vivo-stimulated ne utrophils collected from the coronary sinus 15 min after coronary angi oplasty was significantly decreased compared with that after coronary arteriography (54 +/- 12% vs. 106 +/- 30% and 58 +/- 11% vs. 102 +/- 2 9% respectively, p < 0.01). The reduced responses to phorbol ester sti mulation may be explained by previous in vivo activation of neutrophil s during coronary angioplasty. Conclusions. Coronary angioplasty incre ases neutrophil, monocyte and platelet adhesion molecule expression an d induces a significant decrease in ex vivo-stimulated neutrophil supe roxide generation and aggregation. These findings suggest that coronar y angioplasty triggers cellular activation with an inflammatory respon se that could contribute to restenosis. (C) 1997 by the American Colle ge of Cardiology.