title: Shear-induced platelet aggregation in cerebral ischemia.
abstract: OBJECTIVE
  Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents.
  
  
  METHODS
  The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in citrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents.
  
  
  RESULTS
  Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shear-induced platelet aggregation with platelet count, agonist-induced platelet aggregation, fibrinogen level, or beta-thromboglobulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it.
  
  
  CONCLUSIONS
  These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the increase of larger von Willebrand factor multimers, and is corrected by ticlopidine but not by low-dose aspirin.
authors.affiliation: Department of Neurology, Tokyo Women's Medical College, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Uchiyama
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: S
authors.initials: S
authors.lastname: Maruyama
authors.forename: M
authors.initials: M
authors.lastname: Handa
authors.forename: Y
authors.initials: Y
authors.lastname: Ikeda
authors.forename: M
authors.initials: M
authors.lastname: Fukuyama
authors.forename: I
authors.initials: I
authors.lastname: Itagaki
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology; D002545:Brain Ischemia / Q000097:blood*; D002544:Cerebral Infarction / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006403:Hematologic Tests / Q000379:methods; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count; D013988:Ticlopidine / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors; D001620:beta-Thromboglobulin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D001620:beta-Thromboglobulin; D014841:von Willebrand Factor; D005340:Fibrinogen; D013988:Ticlopidine; D001241:Aspirin