title: Coronary angioplasty results in leukocyte and platelet activation with adhesion molecule expression. Evidence of inflammatory responses in coronary angioplasty.
abstract: OBJECTIVE
  This study sought to characterize leukocyte and platelet activation 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 release of inflammatory mediators as a result of plaque rupture and endothelial injury.
  
  
  METHODS
  In 13 patients with stable angina (mean [ +/- SEM] age 56.0 +/- 2.4 years, range 44 to 79), blood samples were drawn from the aorta and coronary sinus immediately before and immediately and 15 min after coronary angioplasty. Subsequently, leukocyte and platelet functions were determined. Eleven control patients (57.5 +/- 2.3 years, range 52 to 78) underwent coronary arteriography.
  
  
  RESULTS
  Coronary arteriography and angioplasty showed no difference in number of leukocytes between the coronary sinus and the aorta. However, 15 min after coronary angioplasty, there was an increase in neutrophil CD18 and CD11b, monocyte CD14 and platelet glycoprotein IIb/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 occurred. Superoxide production and aggregation in ex vivo-stimulated neutrophils collected from the coronary sinus 15 min after coronary angioplasty was significantly decreased compared with that after coronary arteriography (54 +/- 12% vs. 106 +/- 30% and 58 +/- 11% vs. 102 +/- 29%, respectively, p < 0.01). The reduced responses to phorbol ester stimulation may be explained by previous in vivo activation of neutrophils during coronary angioplasty.
  
  
  CONCLUSIONS
  Coronary angioplasty increases neutrophil, monocyte and platelet adhesion molecule expression and induces a significant decrease in ex vivo-stimulated neutrophil superoxide generation and aggregation. These findings suggest that coronary angioplasty triggers cellular activation with an inflammatory response that could contribute to restenosis.
authors.affiliation: Heart Institute, School of Medicine, University of São Paulo, Brazil.
authors.forename: C V
authors.initials: CV
authors.lastname: Serrano
authors.forename: J A
authors.initials: JA
authors.lastname: Ramires
authors.forename: M
authors.initials: M
authors.lastname: Venturinelli
authors.forename: S
authors.initials: S
authors.lastname: Arie
authors.forename: E
authors.initials: E
authors.lastname: D'Amico
authors.forename: J L
authors.initials: JL
authors.lastname: Zweier
authors.forename: F
authors.initials: F
authors.lastname: Pileggi
authors.forename: P L
authors.initials: PL
authors.lastname: da Luz
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000378:metabolism / Q000628:therapy*; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D015539:Platelet Activation; D012008:Recurrence; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
chemical_list: D015815:Cell Adhesion Molecules; D013481:Superoxides