title: Leukocyte activation after coronary stenting in patients during the subacute phase of a previous ST-elevation myocardial infarction.
abstract: OBJECTIVE
  To study leukocyte activation after percutaneous coronary intervention in patients with previous ST elevation myocardial infarction.
  
  
  METHODS
  Neutrophil and monocyte activation (by flow cytometric assessment of the surface expression of CD11b and CD62L adhesion molecules) was assessed in 39 patients during the subacute period of a previous ST elevation myocardial infarction initially treated with fibrinolytic agents, before and after diagnostic coronary angiography (coronary angiography control phase) as well as before and after stent implantation (percutaneous coronary intervention phase). Simultaneous evaluation of C-reactive protein (C-reactive protein immonoturbidimetry) and plasma cytokine levels (interleukins-1, -6, -10 and tumor necrosis alpha by immunoassay) was also performed. To track the earliest detectable change in the first few minutes after stent deployment, all measurements were performed before and 60 min after the procedures.
  
  
  RESULTS
  CD11b expression increased 1 h after stent deployment in neutrophils (P<0.0001) and monocytes (P<0.0001). A comparable increase, however, was also observed after coronary angiography (neutrophils, P=0.03; monocytes, P=0.01), although the increase of CD11b expression was greater after percutaneous coronary intervention on both neutrophils (90 vs. 40%, P=0.014) and monocytes (65 vs. 33%, P=0.04). CD62L expression decreased significantly after percutaneous coronary intervention (neutrophils, P=0.01; monocytes, P=0.006), but remained unchanged after coronary angiography. Plasma cytokine and C-reactive protein concentrations did not change after the procedures.
  
  
  CONCLUSIONS
  CD62L appears to be a specific and reliable early cellular biomarker of leukocyte activation after percutaneous coronary intervention, when this procedure is performed in patients with previous ST elevation myocardial infarction. Whether this marker represents also a potential predictor of future events and/or restenosis in this group of patients remains to be defined.
authors.affiliation: Cardiology Department, Democritus University of Thrace, Alexandroupolis, and 2nd Cardiology Department, Papanikolaou General Hospital, Thessaloniki, Greece. dstakos@med.duth.gr
authors.forename: Dimitrios A
authors.initials: DA
authors.lastname: Stakos
authors.forename: Ioannis
authors.initials: I
authors.lastname: Kotsianidis
authors.forename: Dimitrios N
authors.initials: DN
authors.lastname: Tziakas
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Spanoudakis
authors.forename: Georgios
authors.initials: G
authors.lastname: Chalikias
authors.forename: Georgios
authors.initials: G
authors.lastname: Bourikas
authors.forename: Georgios
authors.initials: G
authors.lastname: Katsaris
authors.forename: Harisios
authors.initials: H
authors.lastname: Boudoulas
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D039481:CD11b Antigen / Q000097:blood; D006801:Humans; D019041:L-Selectin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000628:therapy*; D018375:Neutrophil Activation / Q000276:immunology*; D015607:Stents; D013997:Time Factors
chemical_list: D039481:CD11b Antigen; D019041:L-Selectin