title: Prolonged application of clopidogrel reduces inflammation after percutaneous coronary intervention in the porcine model.
abstract: OBJECTIVE
  We determined the effect of prolonged treatment with clopidogrel on C-reactive protein (CRP) concentrations and blood thrombogenicity after percutaneous transluminal coronary angioplasty followed by intracoronary brachytherapy in the porcine model. ANIMAL MODEL: All 48 pigs received antiplatelet therapy, including aspirin (325 mg, daily) and clopidogrel (300 mg, loading dose) 1 day before PCI, followed by a daily dose of clopidogrel (75 mg/day) in addition to aspirin. During PCI, one of two balloon-injured arteries was randomly assigned to receive immediate radiation treatment. Animals were sacrificed after 24 h, 1 month, and 3 months post-PCI. The pigs, which were sacrificed 3 months post-PCI, were divided into two groups. The first group received clopidogrel in addition to aspirin for 3 months, and the second group received clopidogrel in addition to aspirin for only 1 month after PCI and then aspirin alone.
  
  
  METHODS
  Blood was taken from all pigs before intervention, immediately after intervention, and before sacrifice. Serum CRP was measured by enzyme-linked immunosorbent assay. To analyze the procoagulant effects of PCI on blood thrombogenicity, a one-stage clotting assay was performed.
  
  
  RESULTS
  Clopidogrel treatment for 3 months reduced CRP levels more than did clopidogrel therapy for 1 month only at 3 months post-PCI (27.9+/-3.9 vs. 56.6+/-11.3 microg/ml; P=.019). Baseline CRP levels were found to be 50.4+/-4.8 microg/ml. Plasma clotting was not affected by prolonged clopidogrel therapy (322.8+/-59.3 s vs. 295.2+/-52.5 s; P=ns).
  
  
  CONCLUSIONS
  Prolonged treatment with clopidogrel reduced CRP levels post-PCI.
authors.affiliation: Department of Cardiology, Charité-Campus Benjamin Franklin, Berlin, Germany.
authors.forename: Yunus
authors.initials: Y
authors.lastname: Ayral
authors.forename: Ursula
authors.initials: U
authors.lastname: Rauch
authors.forename: Petra
authors.initials: P
authors.lastname: Goldin-Lang
authors.forename: Caroline
authors.initials: C
authors.lastname: Stellbaum
authors.forename: Carolin
authors.initials: C
authors.lastname: Deiner
authors.forename: Peter L
authors.initials: PL
authors.lastname: Schwimmbeck
authors.forename: Heinz-Peter
authors.initials: HP
authors.lastname: Schultheiss
authors.forename: Klaus
authors.initials: K
authors.lastname: Pels
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology; D001777:Blood Coagulation / Q000187:drug effects*; D001918:Brachytherapy / Q000009:adverse effects*; D002097:C-Reactive Protein / Q000378:metabolism*; D000077144:Clopidogrel; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D023421:Models, Animal; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D034421:Sus scrofa; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D010975:Platelet Aggregation Inhibitors; D002097:C-Reactive Protein; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin