title: The effect of antiplatelet drugs clopidogrel and aspirin is less immediately after stent implantation.
abstract: BACKGROUND
  A decreased effect of clopidogrel or aspirin on platelets corresponds to an increased risk of major adverse coronary events. The aim was to investigate if the inhibition of platelet function by clopidogrel and aspirin is equal at two different time points: immediately after percutaneous coronary intervention (PCI) and one day thereafter.
  
  
  METHODS
  Platelet function was assessed by the Vasodilator Stimulated Phosphoprotein (VASP) phosphorylation assay, Impedance Aggregometry, Platelet Function Analyzer and the Cone and Platelet Analyzer in 30 patients on chronic treatment with clopidogrel and aspirin.
  
  
  RESULTS
  Inhibition of platelets by clopidogrel and aspirin was less post PCI than one day after PCI as measured with the VASP assay and aggregometry: the platelet reactivity index, the adenosine diphosphate/prostaglandin and the arachidonic acid -induced platelet aggregation were 23% (p=0.009), 75% (p=0.001) and 127% (p<0.001) higher post PCI than one day after PCI, respectively. The collagen/adenosine diphosphate closure time was 30% higher after PCI compared to one day thereafter (p=0.047), which could in part be due to a two-fold increase in von Willebrand factor-ristocetin cofactor activity one day after PCI (p=0.001).
  
  
  CONCLUSIONS
  Inhibition of platelets by clopidogrel and aspirin was less immediately post PCI as compared to one day thereafter. This indicates that the time point of platelet function testing is important for the determination of cut-off points and the definition of nonresponsiveness to antiplatelet drugs.
authors.affiliation: Department of Clinical Pharmacology, Medical University of Vienna, Austria.
authors.forename: Jolanta M
authors.initials: JM
authors.lastname: Siller-Matula
authors.forename: Katrin
authors.initials: K
authors.lastname: Haberl
authors.forename: Knut
authors.initials: K
authors.lastname: Prillinger
authors.forename: Simon
authors.initials: S
authors.lastname: Panzer
authors.forename: Irene
authors.initials: I
authors.lastname: Lang
authors.forename: Bernd
authors.initials: B
authors.lastname: Jilma
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000980:Antiplatyhelmintic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D001241:Aspirin / Q000008:administration & dosage* / Q000009:adverse effects; D015815:Cell Adhesion Molecules / Q000097:blood; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy / Q000628:therapy; D005260:Female; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008840:Microfilament Proteins / Q000097:blood; D008875:Middle Aged; D010750:Phosphoproteins / Q000097:blood; D010974:Platelet Aggregation / Q000187:drug effects; D010979:Platelet Function Tests / Q000379:methods; D015607:Stents; D013988:Ticlopidine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives*; D013997:Time Factors; D014841:von Willebrand Factor / Q000378:metabolism; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D000980:Antiplatyhelmintic Agents; D015815:Cell Adhesion Molecules; D008840:Microfilament Proteins; D010750:Phosphoproteins; D000098662:Vasodilator-Stimulated Phosphoprotein; D014841:von Willebrand Factor; D006493:Heparin; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin