Increased platelet count and excessive platelet activation in :增加血小板计数和血小板过度激活在
Increased platelet count and excessive platelet activation in
symptomatic compared with asymptomatic severe carotid stenosis
††,†Dominick J. H. McCabe*, Paul Harrison, Paul S. Sidhu*, Ian J. Mackie,
††‡†Andrew S. Lawrie, Gordon Purdy, Hilary Watt, Samuel J. Machin,
Martin M. Brown FRCP*.
†Stroke Research Group *, Institute of Neurology, and The Haemostasis Research Unit ,
Department of Haematology, University College London, London, United Kingdom.
‡The Dementia Research Group , Institute of Neurology, The National Hospital for Neurology & Neurosurgery, and The Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom.
#Oxford Haemophilia Centre and Thrombosis Unit , Churchill Hospital, Oxford, United
Kingdom.
Address for Correspondence: Dr. Dominick 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.
Telephone: –44-20-77940500, Ext 4363. Fax: -44-20-78302754.
e-mail: d.mccabe@ion.ucl.ac.uk
Background: The risk of stroke in patients with recently symptomatic severe carotid stenosis is considerably higher than in patients with asymptomatic stenosis. We hypothesised that excessive platelet activation might partly contribute to this difference.
Methods: We performed a full blood count, and used whole blood flow cytometry to measure platelet surface expression of CD62P, CD63 and PAC1 binding, and the absolute number of neutrophil-platelet, monocyte-platelet and lymphocyte-platelet complexes in acute (0-21 days, n = 19) and convalescent (79-365 days, n = 16) symptomatic compared with asymptomatic severe (? 70%) carotid stenosis patients (n =
16). The majority of patients were treated with aspirin (37.5 to 300 mg daily), although alternative antithrombotic regimens were more commonly used in the symptomatic group.
Results: The mean platelet count was higher in acute and convalescent symptomatic than asymptomatic patients. The median absolute number of neutrophil-platelet complexes
was higher in acute symptomatic patients (p = 0.03), and the median absolute numbers of CD62P- and PAC1-positive platelets were higher in convalescent symptomatic than asymptomatic patients (p ? 0.037). Otherwise, there were no significant differences in platelet activation status between symptomatic and asymptomatic patients.
Conclusions: Increased platelet production and excessive platelet activation / leucocyte-platelet complex formation may contribute to the excess risk of stroke in patients with recently symptomatic severe carotid stenosis.