title: Monitoring of clopidogrel-related platelet inhibition: correlation of nonresponse with clinical outcome in supra-aortic stenting.
abstract: OBJECTIVE
  Clopidogrel and aspirin are antiplatelet medications used in patients intended for endovascular stent placement. Although various studies have investigated individual responsiveness to clopidogrel in patients undergoing coronary interventions, there are no studies regarding patients undergoing stent placement of supra-aortic arteries supplying the brain. We analyzed platelet function in a near-patient setting to determine the effects of antiplatelet treatment in neurologic patients and correlated the results with clinical outcome after stent placement.
  
  
  METHODS
  The platelet function of 50 consecutive patients scheduled for neuro-interventional stent placement procedures was assessed by using point-of-care testing. All of the patients had symptomatic arteriosclerotic lesions. Clopidogrel effects were tested by impedance aggregometry. Fifty healthy blood donors without clopidogrel medication served as the control group.
  
  
  RESULTS
  Reference values for responders and nonresponders were established from the results of the healthy control group. Fourteen (28%) of 50 neurologic patients were stratified as clopidogrel nonresponders. Adverse events were registered in 5 (10%) of 50 patients, 1 of them with a permanent neurologic deficit (1 of 50 [2%]). All 5 of the patients with adverse events were nonresponders. There was a statistically significant correlation between adverse events and clopidogrel nonresponse (Fisher exact test, P = .001).
  
  
  CONCLUSIONS
  A significant rate of clopidogrel nonresponders could be identified in the treated patients. Our data strongly suggest a correlation of insufficient clopidogrel-related platelet inhibition with an increased risk of thromboembolic events in supra-aortic stent placement.
authors.affiliation: Department of Neuroradiology, Ludwig Maximilians University, Munich, Germany. smueller@med.uni-muenchen.de
authors.forename: S
authors.initials: S
authors.lastname: Müller-Schunk
authors.forename: J
authors.initials: J
authors.lastname: Linn
authors.forename: N
authors.initials: N
authors.lastname: Peters
authors.forename: M
authors.initials: M
authors.lastname: Spannagl
authors.forename: M
authors.initials: M
authors.lastname: Deisenberg
authors.forename: H
authors.initials: H
authors.lastname: Brückmann
authors.forename: T E
authors.initials: TE
authors.lastname: Mayer
mesh_terms: D000328:Adult; D000368:Aged; D001488:Basilar Artery / Q000473:pathology; D002343:Carotid Artery, Internal / Q000473:pathology; D000077144:Clopidogrel; D003251:Constriction, Pathologic; D016903:Drug Monitoring; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood / Q000473:pathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000494:pharmacology*; D015607:Stents / Q000009:adverse effects; D020521:Stroke / Q000097:blood / Q000473:pathology / Q000628:therapy*; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000494:pharmacology; D014711:Vertebral Artery / Q000473:pathology
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine