title: Differential prognostic impact of high on-treatment platelet reactivity among patients with acute coronary syndromes versus stable coronary artery disease undergoing percutaneous coronary intervention.
abstract: BACKGROUND
  High on-treatment platelet reactivity (HTPR) after clopidogrel is associated with a higher risk of cardiovascular events after percutaneous coronary intervention (PCI). However, it remains unclear whether HTPR is of similar prognostic value for different clinical presentations.
  
  
  METHODS
  We compared the prognostic impact of HTPR, measured by the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA), on outcomes between 1,095 patients with acute coronary syndromes (ACS) and 1,329 patients with stable coronary artery disease (CAD) who were treated with PCI. Before PCI, patients received optimal clopidogrel treatment (75 mg daily for at least 5 days or if <5 days, 300-600 mg loading), and platelet reactivity was measured at 24 to 48 hours after PCI. The primary end point was a composite of death, myocardial infarction, stent thrombosis, or stroke.
  
  
  RESULTS
  During follow-up (median, 22.0 months), HTPR was independently associated with higher risks of the primary end point (hazard ratio [HR] 2.03, 95% CI 1.30-3.18, P = .002) and mortality (HR 3.46, 95% CI 1.18-10.18, P = .02) in patients with ACS. By contrast, for patients with stable CAD, HTPR was not associated with adjusted risks of the primary end point (HR 1.00, 95% CI 0.71-1.39, P = .98) or mortality (HR 0.74, 95% CI 0.36-1.51, P = .41). Significant interactions were present between HTPR status and clinical presentations for the primary end point (P = .02) and mortality (P = .04).
  
  
  CONCLUSIONS
  There was a substantial interaction between platelet reactivity on clopidogrel and clinical presentations on cardiovascular events after PCI. High on-treatment platelet reactivity was significantly associated with higher risks of cardiovascular events in ACS patients, whereas this association was absent in stable CAD patients.
authors.affiliation: Department of Cardiology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
authors.forename: Duk-Woo
authors.initials: DW
authors.lastname: Park
authors.forename: Jung-Min
authors.initials: JM
authors.lastname: Ahn
authors.forename: Hae-Geun
authors.initials: HG
authors.lastname: Song
authors.forename: Jong-Young
authors.initials: JY
authors.lastname: Lee
authors.forename: Won-Jang
authors.initials: WJ
authors.lastname: Kim
authors.forename: Soo-Jin
authors.initials: SJ
authors.lastname: Kang
authors.forename: Sung-Cheol
authors.initials: SC
authors.lastname: Yun
authors.forename: Seung-Whan
authors.initials: SW
authors.lastname: Lee
authors.forename: Young-Hak
authors.initials: YH
authors.lastname: Kim
authors.forename: Cheol Whan
authors.initials: CW
authors.lastname: Lee
authors.forename: Seong-Wook
authors.initials: SW
authors.lastname: Park
authors.forename: Seung-Jung
authors.initials: SJ
authors.lastname: Park
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000401:mortality / Q000601:surgery; D000368:Aged; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000401:mortality / Q000601:surgery; D005260:Female; D005500:Follow-Up Studies; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention / Q000379:methods* / Q000401:mortality; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D010979:Platelet Function Tests; D011379:Prognosis; D020521:Stroke / Q000139:chemically induced; D013927:Thrombosis / Q000139:chemically induced; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine