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Increased platelet count and leucocyte–platelet complex formation in acute symptomatic compared with asymptomatic severe carotid stenosis
  1. D J H McCabe1,2,
  2. P Harrison2,4,
  3. I J Mackie2,
  4. P S Sidhu1,
  5. G Purdy2,
  6. A S Lawrie2,
  7. H Watt3,
  8. S J Machin2,
  9. M M Brown1
  1. 1Stroke Research Group, Institute of Neurology, National Hospital for Neurology and Neurosurgery, University College London, London, UK
  2. 2The Haemostasis Research Unit, Department of Haematology, University College London, London, UK
  3. 3The Dementia Research Group, Institute of Neurology, National Hospital for Neurology and Neurosurgery, and Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. 4Oxford Haemophilia Centre and Thrombosis Unit, Churchill Hospital, Oxford, UK
  1. Correspondence to:
 Dr D J H McCabe
 University Department of Clinical Neurosciences, Royal Free and University College Medical School, The Royal Free Hospital Hampstead, Pond St, London NW3 2PF, England; d.mccabemedsch.ucl.ac.uk

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 (⩾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.

Conclusion: Increased platelet count and leucocyte–platelet complex formation may contribute to the early excess risk of stroke in patients with recently symptomatic carotid stenosis.

  • CDUS, colour Doppler ultrasound
  • FBC, full blood count
  • MPV, mean platelet volume
  • TIA, transient ischaemic attack
  • ischaemic stroke or TIA
  • carotid stenosis
  • flow cytometry
  • platelet activation
  • leucocyte–platelet complexes

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Footnotes

  • Dr McCabe was funded by a grant from the Brain Research Trust, England. Professor Brown’s Chair in Stroke Medicine is supported by The Reta Lila Weston Trust for Medical Research, U.K. The ultrasound laboratory at Atkinson Morley’s Hospital was funded by the Wellcome Trust and the Neurosciences Research Foundation.

  • Competing interests: none declared

  • The 21 gauge Butterfly needles were purchased from Venisystems, Abbott, Ireland, and the Vacutainer system and Luer adaptors from Becton Dickinson Vacutainer Systems, UK. The anti-IgM-fluorescein isothiocyanate (FITC)-conjugated isotype control mouse monoclonal antibody used in the PAC1 assays was purchased from Sigma-Aldrich Inc., St Louis, USA, and the anti-PAC1-FITC-conjugated IgMκ mouse monoclonal test antibody was purchased from Becton Dickinson, San Jose, USA. The anti-CD45-R-phycoerythrin-cyanine 5 (RPE-Cy5) antibody used in the leucocyte–platelet complex assays was purchased from Dako, Glostrup, Denmark. All other mouse monoclonal antibodies used in the flow cytometry studies were purchased from Immunotech, Beckman Coulter, Marseille, France.