title: Antiplatelet effect of ticlopidine after coronary stenting.
abstract: OBJECTIVE
  This study sought to investigate the contribution of ticlopidine to the inhibition of platelet activation after coronary stent placement.
  
  
  BACKGROUND
  After coronary stenting, antiplatelet therapy with aspirin and ticlopidine improves stent patency compared with anticoagulation. However, the specific role of ticlopidine has not been elucidated.
  
  
  METHODS
  After successful coronary stent placement, we randomized 22 patients to receive ticlopidine and aspirin (ticlopidine group) and 25 to receive aspirin alone (aspirin group). Surface expression on platelets of the activated fibrinogen receptor and of P-selectin was assessed by flow cytometry.
  
  
  RESULTS
  In the aspirin group the percent of platelets with activated fibrinogen receptors increased between days 1 and 5 (p = 0.001), whereas there were no substantial changes in the ticlopidine group. The percent of P-selectin-positive platelets did not change significantly in the aspirin group but decreased in the ticlopidine group (p = 0.019). At day 5 after the intervention, the percent of platelets with activated fibrinogen receptors in the ticlopidine group was significantly lower (median [interquartile range]: 8.5 [3.1 to 17.8] vs. 18.1 [8.5 to 35.5], p = 0.025), and there was a trend to fewer P-selectin-positive platelets than in the aspirin group (5.8 [3.4 to 9.5] vs. 8.8 [4.0 to 15.8], p = 0.073).
  
  
  CONCLUSIONS
  Combined antiplatelet therapy with ticlopidine plus aspirin is superior to treatment with aspirin alone in suppressing platelet activation after coronary stenting.
authors.affiliation: Deutsches Herzzentrum und 1. Medizinische Klinik der Technischen Universität München, Munich, Germany. neumann@med1.med.tu-muenchen.de
authors.forename: F J
authors.initials: FJ
authors.lastname: Neumann
authors.forename: M
authors.initials: M
authors.lastname: Gawaz
authors.forename: T
authors.initials: T
authors.lastname: Dickfeld
authors.forename: A
authors.initials: A
authors.lastname: Wehinger
authors.forename: H
authors.initials: H
authors.lastname: Walter
authors.forename: R
authors.initials: R
authors.lastname: Blasini
authors.forename: A
authors.initials: A
authors.lastname: Schomig
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal; D001241:Aspirin / Q000627:therapeutic use; D003251:Constriction, Pathologic; D003327:Coronary Disease / Q000473:pathology / Q000628:therapy*; D004359:Drug Therapy, Combination; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010976:Platelet Count; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D015607:Stents; D013988:Ticlopidine / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D013988:Ticlopidine; D001241:Aspirin