title: Platelet reactivity in patients with subacute stent thrombosis compared with non-stent-related acute myocardial infarction.
abstract: BACKGROUND
  Recent case control studies suggest that patients with subacute stent thrombosis (SAT) have increased platelet reactivity. However, SAT often presents as acute myocardial infarction (AMI), which is also associated with augmented platelet activation. We therefore compared platelet reactivity in patients with SAT and patients with AMI unrelated to stenting.
  
  
  METHODS
  We identified 20 patients with SAT, 20 patients with ST-elevation AMI who underwent primary percutaneous coronary intervention (PCI), and 20 patients who underwent stenting without SAT occurrence (stable control group). Platelet function was measured > or = 3 days after PCI in the SAT (repeat procedure) and AMI groups and > or = 3 months after stenting in the stable group. All patients received aspirin and clopidogrel. Platelet reactivity was evaluated by aggregation in response to 5 and 20 micromol/L of adenosine diphosphate and 1.5 mmol/L arachidonic acid, and by flow cytometric determination of P-selectin and glycoprotein IIb/IIIa activation.
  
  
  RESULTS
  Clinical characteristics were similar among the groups. Platelet testing was performed 4.9 +/- 1.7, 3.1 +/- 0.3, and 108 +/- 22 days after PCI in the SAT, AMI, and stable groups, respectively. The SAT group had higher platelet aggregation and activation markers than the stable group. However, platelet aggregation and activation was very similar in the SAT and AMI groups.
  
  
  CONCLUSIONS
  Patients with SAT have increased platelet reactivity, compared with patients who do not develop SAT following stenting. However, the augmented platelet reactivity does not appear to differ from patients with AMI unrelated to stenting. This study highlights the need for large prospective studies to determine whether platelet hyperreactivity increases the risk of SAT.
authors.affiliation: The Methodist Hospital Research Institute and the Methodist DeBakey Heart Center, The Methodist Hospital, Houston, TX 77030, USA.
authors.forename: Eli I
authors.initials: EI
authors.lastname: Lev
authors.forename: Carlos L
authors.initials: CL
authors.lastname: Alviar
authors.forename: Mehmet E
authors.initials: ME
authors.lastname: Arikan
authors.forename: Bijal P
authors.initials: BP
authors.lastname: Dave
authors.forename: Juan F
authors.initials: JF
authors.lastname: Granada
authors.forename: Timothy
authors.initials: T
authors.lastname: DeLao
authors.forename: Armando
authors.initials: A
authors.lastname: Tellez
authors.forename: Kelly
authors.initials: K
authors.lastname: Maresh
authors.forename: Neal S
authors.initials: NS
authors.lastname: Kleiman
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000077144:Clopidogrel; D003327:Coronary Disease / Q000503:physiopathology / Q000628:therapy*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D015539:Platelet Activation; D010974:Platelet Aggregation; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015607:Stents / Q000009:adverse effects*; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology*; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine