title: Rapid assessment of glycoprotein IIb/IIIa blockade with the platelet function analyzer (PFA-100) during percutaneous coronary intervention.
abstract: BACKGROUND
  The platelet function analyzer PFA-100 (Dade Behring, Miami, Fla) evaluates platelet function by determining the time to occlusion of an aperture in a membrane coated with collagen and adenosine diphosphate or epinephrine as whole blood flows under shear stress conditions. Platelet aggregation causes aperture occlusion, and results are reported as closure time (CT). Interindividual variability is observed in the level of platelet inhibition achieved with use of the current abciximab dosing regimen (0.25-mg/kg bolus + 10-microg/min infusion for 12 hours). The relationships between specific levels of platelet inhibition and clinical efficacy and safety have not been fully established.
  
  
  RESULTS
  We prospectively studied platelet function in 27 patients receiving abciximab during percutaneous coronary intervention. This evaluation included determinations of platelet-rich plasma aggregometry, receptor occupancy studies (D3 assay), and CT measurements at baseline and 10 minutes, 4 hours, 12 hours, and 24 hours after the bolus. All patients received abciximab, aspirin, and heparin; patients undergoing coronary stent implantation received aspirin and ticlopidine after the procedure. CT results were reported within 10 minutes after initiation of testing. For 96% of patients, CT was 300 seconds (maximum CT) immediately after abciximab bolus and remained so throughout the infusion. At 24 hours we observed variable recovery from platelet inhibition and in 72% of patients CT returned to normal (< or =130 seconds).
  
  
  CONCLUSIONS
  Findings with the PFA-100 were similar to results observed with platelet aggregometry and receptor occupancy measurements. Most patients treated with abciximab exhibit normalized platelet function at 24 hours despite moderate levels of receptor occupancy, suggesting dissociation between occupancy and function.
authors.affiliation: Duke Clinical Research Institute, Durham, NC 27710, USA.
authors.forename: M
authors.initials: M
authors.lastname: Madan
authors.forename: S D
authors.initials: SD
authors.lastname: Berkowitz
authors.forename: D J
authors.initials: DJ
authors.lastname: Christie
authors.forename: L K
authors.initials: LK
authors.lastname: Jennings
authors.forename: A C
authors.initials: AC
authors.lastname: Smit
authors.forename: K N
authors.initials: KN
authors.lastname: Sigmon
authors.forename: S
authors.initials: S
authors.lastname: Glazer
authors.forename: J E
authors.initials: JE
authors.lastname: Tcheng
mesh_terms: D000077284:Abciximab; D000293:Adolescent; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000493:pharmacokinetics / Q000627:therapeutic use*; D000925:Anticoagulants / Q000493:pharmacokinetics / Q000627:therapeutic use; D001241:Aspirin / Q000493:pharmacokinetics / Q000627:therapeutic use; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy*; D004359:Drug Therapy, Combination; D004867:Equipment Design; D006493:Heparin / Q000493:pharmacokinetics / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000295:instrumentation*; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000493:pharmacokinetics / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors* / Q000378:metabolism; D011446:Prospective Studies
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin; D001241:Aspirin; D000077284:Abciximab