title: Effects of persistent platelet reactivity despite aspirin therapy on cardiac troponin I and creatine kinase-MB levels after elective percutaneous coronary interventions.
abstract: BACKGROUND
  Creatinine kinase-MB (CK-MB) and cardiac troponin I (cTnI) elevations are highly specific for myonecrosis after percutaneous coronary intervention (PCI). Aspirin is used to prevent thrombotic complications. Several studies have shown that some individuals exhibit a reduced or completely missing antiplatelet response to aspirin. The aim of this study is to investigate the effects of platelet reactivity despite aspirin therapy on CK-MB and cTnI levels after elective percutaneous coronary interventions despite 600 mg loading dose of clopidogrel.
  
  
  METHODS
  One hundred fourteen (mean age 61.2+/-9.3 years, 78.1% male) patients receiving 300 mg daily enteric coated aspirin for at least 7 days with documented coronary artery disease were included in the study. Platelet reactivity despite aspirin was measured by platelet function analyzer (PFA)-100 collagen/epinephrine cartridge. Blood samples for CK-MB and cTnI were obtained before and at 6, 24, and 36 h after the PCI. Persistent platelet reactivity was defined when collagen/epinephrine closure time<165 s.
  
  
  RESULTS
  A total of 87 (76.4%) patients were noted to have normal platelet reactivity (Group A), and 27 (23.6%) had persistent platelet reactivity (Group B). The elevations of CK-MB and cTnI levels were statistically significant within the groups (both P<0.001). However, there were no significant differences in the CK-MB and cTnI levels of the groups at baseline and after PCI for all studied hours.
  
  
  CONCLUSIONS
  Persistent platelet reactivity was not associated with increased risk of CK-MB, cTnI elevations in low-to-intermediate risk PCI patients.
authors.affiliation: Department of Cardiology, Baskent University Faculty of Medicine, Ankara, Turkey. gulmezoyku@yahoo.com
authors.forename: Oyku
authors.initials: O
authors.lastname: Gulmez
authors.forename: Aylin
authors.initials: A
authors.lastname: Yildirir
authors.forename: Gamze
authors.initials: G
authors.lastname: Kaynar
authors.forename: Didem
authors.initials: D
authors.lastname: Konas
authors.forename: Alp
authors.initials: A
authors.lastname: Aydinalp
authors.forename: Cagatay
authors.initials: C
authors.lastname: Ertan
authors.forename: Bulent
authors.initials: B
authors.lastname: Ozin
authors.forename: Haldun
authors.initials: H
authors.lastname: Muderrisoglu
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood / Q000628:therapy*; D052279:Creatine Kinase, MB Form / Q000097:blood*; D004351:Drug Resistance; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D009336:Necrosis; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests; D013608:Tablets, Enteric-Coated; D013927:Thrombosis / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors; D019210:Troponin I / Q000097:blood*; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D013608:Tablets, Enteric-Coated; D019210:Troponin I; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form; D013988:Ticlopidine; D001241:Aspirin