title: Reduction of monocyte-platelet interaction and monocyte activation in patients receiving antiplatelet therapy after coronary stent implantation.
abstract: BACKGROUND
  Monocyte activation induces different procoagulant and proadhesive inflammatory responses and thus may play a role in thrombotic complications after coronary interventions. Monocyte-platelet interaction may trigger these effects inducing monocyte activation.
  
  
  OBJECTIVE
  To characterize the effect of antiplatelet vs anticoagulation therapy on monocyte-platelet interaction and monocyte function after intracoronary stenting.
  
  
  RESULTS
  Immediately before, and during the first 12 days after successful coronary stenting, monocyte-platelet conjugates and monocyte function were assessed by flow cytometric detection of GPIIb/IIIa (CD41) on monocytes and by monocyte surface exposure of Mac-1 (CD11b/CD18) and L-selectin (CD62L). Twenty patients receiving combined antiplatelet therapy (ticlopidine, aspirin) were compared to 20 patients with standard anticoagulation (phenprocoumon, overlapping heparin, aspirin). Before stenting, monocyte-platelet conjugates and Mac-1 surface expression in both groups were significantly increased, while L-selectin was significantly diminished. Anticoagulation did not change these variables significantly during the subsequent 12 days. In contrast, antiplatelet therapy reduced platelet-monocyte conjugates by 46 +/- 9.3% (mean +/- SEM, P = 0.0019) within 4 days, which was associated with a decrease in Mac-1 expression (28 +/- 6.7%, P = 0.0013) and an increase in L-selectin (56 +/- 15.0%, P = 0.0061).
  
  
  CONCLUSIONS
  After intracoronary stenting, combined antiplatelet therapy, but not anticoagulation, causes reduction of monocyte-platelet interaction, which is associated with monocyte deactivation. This may contribute to a decreased risk for thrombotic events.
authors.affiliation: Medizinische Klinik, Technische Universität München, Germany.
authors.forename: A E
authors.initials: AE
authors.lastname: May
authors.forename: F J
authors.initials: FJ
authors.lastname: Neumann
authors.forename: M
authors.initials: M
authors.lastname: Gawaz
authors.forename: I
authors.initials: I
authors.lastname: Ott
authors.forename: H
authors.initials: H
authors.lastname: Walter
authors.forename: A
authors.initials: A
authors.lastname: Schömig
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal; D000925:Anticoagulants / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D010644:Phenprocoumon / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D015607:Stents; D013927:Thrombosis / Q000503:physiopathology / Q000517:prevention & control*; D013988:Ticlopidine / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D013988:Ticlopidine; D010644:Phenprocoumon; D001241:Aspirin