title: Naproxen treatment prevents periprocedural inflammatory response but not myocardial injury after percutaneous coronary intervention.
abstract: OBJECTIVE
  Recent studies have documented that elevation of C-reactive protein (CRP) levels after percutaneous coronary intervention (PCI) have been predictive of adverse outcome. This study was performed to test the hypothesis that preprocedural use of naproxen sodium is associated with a reduction in the extent of inflammatory response and myocardial injury after PCI.
  
  
  METHODS
  Ninety-seven patients who were scheduled for elective PCI were randomized either for naproxen sodium (500 mg bid) (n:39, 75% male, 59+/-10 years) or control (n:58, 76% male, 60+/-10 years). All patients were troponin negative before the procedure. Blood samples for CRP, Troponin I and CK-MB were collected at baseline and after the procedure.
  
  
  RESULTS
  The characteristics were similar between the two groups. After coronary stenting, the rise in CRP levels was significantly higher in controls than those treated with naproxen (DeltaCRP=6.4 mg/L in the controls and 0.43 mg/L in the naproxen group, p<0.0001). The incidence of any troponin I elevation or CK-MB elevation above upper limit of normal was not statistically different between groups. During follow up (12+/-2 months), major cardiac adverse events (death, myocardial infarction, and revascularization of target lesion) was similar between groups.
  
  
  CONCLUSIONS
  Our data show that naproxen pretreatment leads to significant suppression in PCI related CRP elevation. However this improvement in CRP levels was not associated with any significant reduction in post-PCI myonecrosis.
authors.affiliation: Ankara University School of Medicine, Cardiology Department, Ankara, Turkey. cagdas_2005@yahoo.com
authors.forename: Cagdas
authors.initials: C
authors.lastname: Ozdol
authors.forename: Sadi
authors.initials: S
authors.lastname: Gulec
authors.forename: Uzeyir
authors.initials: U
authors.lastname: Rahimov
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Atmaca
authors.forename: Sibel
authors.initials: S
authors.lastname: Turhan
authors.forename: Cetin
authors.initials: C
authors.lastname: Erol
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000032:analysis; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form / Q000097:blood; D004338:Drug Combinations; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000517:prevention & control*; D007432:Intraoperative Period; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D009288:Naproxen / Q000627:therapeutic use*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D004338:Drug Combinations; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D009288:Naproxen; D002097:C-Reactive Protein; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form; D013988:Ticlopidine; D001241:Aspirin