title: Increased platelet count and leucocyte-platelet complex formation in acute symptomatic compared with asymptomatic severe carotid stenosis.
abstract: OBJECTIVE
  The risk of stroke in patients with recently symptomatic carotid stenosis is considerably higher than in patients with asymptomatic stenosis. In the present study it was hypothesised that excessive platelet activation might partly contribute to this difference.
  
  
  METHODS
  A full blood count was done and whole blood flow cytometry used to measure platelet surface expression of CD62P, CD63, and PAC1 binding and the percentage of leucocyte-platelet complexes in patients with acute (0-21 days, n = 19) and convalescent (79-365 days) symptomatic (n = 16) and asymptomatic (n = 16) severe (> or =70%) carotid stenosis. Most patients were treated with aspirin (37.5-300 mg daily) although alternative antithrombotic regimens were more commonly used in the symptomatic group.
  
  
  RESULTS
  The mean platelet count was higher in patients with acute and convalescent symptomatic compared with asymptomatic carotid stenosis. There were no significant differences in the median percentage expression of CD62P and CD63, or PAC1 binding between the acute or convalescent symptomatic and asymptomatic patients. The median percentages of neutrophil-platelet (p = 0.004), monocyte-platelet (p = 0.046), and lymphocyte-platelet complexes (p = 0.02) were higher in acute symptomatic than in asymptomatic patients. In patients on aspirin monotherapy, the percentages of neutrophil-platelet and monocyte-platelet complexes (p = 0.03) were higher in acute symptomatic (n = 11) than asymptomatic patients (n = 14). In the convalescent phase, the median percentages of all leucocyte-platelet complexes in the symptomatic group dropped to levels similar to those found in the asymptomatic group.
  
  
  CONCLUSIONS
  Increased platelet count and leucocyte-platelet complex formation may contribute to the early excess risk of stroke in patients with recently symptomatic carotid stenosis.
authors.affiliation: University Department of Clinical Neurosciences, Royal Free and University College Medical School, The Royal Free Hospital Hampstead, Pond St, London NW3 2PF, England. d.mccabe@medsch.ucl.ac.uk
authors.forename: D J H
authors.initials: DJ
authors.lastname: McCabe
authors.forename: P
authors.initials: P
authors.lastname: Harrison
authors.forename: I J
authors.initials: IJ
authors.lastname: Mackie
authors.forename: P S
authors.initials: PS
authors.lastname: Sidhu
authors.forename: G
authors.initials: G
authors.lastname: Purdy
authors.forename: A S
authors.initials: AS
authors.lastname: Lawrie
authors.forename: H
authors.initials: H
authors.lastname: Watt
authors.forename: S J
authors.initials: SJ
authors.lastname: Machin
authors.forename: M M
authors.initials: MM
authors.lastname: Brown
mesh_terms: D000208:Acute Disease; D000368:Aged; D001241:Aspirin / Q000627:therapeutic use; D016893:Carotid Stenosis / Q000150:complications* / Q000503:physiopathology*; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D005434:Flow Cytometry; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008297:Male; D015539:Platelet Activation; D010976:Platelet Count; D012720:Severity of Illness Index; D020521:Stroke / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D005343:Fibrinolytic Agents; D001241:Aspirin