title: Platelet degranulation and monocyte-platelet complex formation are increased in the acute and convalescent phases after ischaemic stroke or transient ischaemic attack.
abstract: Flow cytometric studies suggest that platelets are activated in ischaemic stroke or transient ischaemic attack (TIA). However, few studies have measured circulating leucocyte-platelet complexes in this patient population. Whole blood flow cytometry was used to quantify the expression of CD62P-, CD63-, and PAC1-binding, and the percentages of leucocyte-platelet complexes in acute (1-27 d, n = 79) and convalescent (79-725 d, n = 70) ischaemic cerebrovascular disease (CVD) patients compared with controls without CVD (n = 27). We performed a full blood count, and measured plasma levels of soluble P-selectin, soluble E-selectin, and von Willebrand factor antigen (VWF:Ag) as additional markers of platelet and/or endothelial cell activation. The median percentage CD62P expression and the median percentage monocyte-platelet complexes were higher in both acute and convalescent CVD patients than controls (P </= 0.02). The mean white cell count and mean VWF:Ag levels were significantly elevated in the acute and convalescent phases after ischaemic stroke or TIA (P </= 0.02). Otherwise, there was no significant increase in any other marker of platelet or endothelial activation in CVD patients. There was a positive correlation between the percentage expression of CD62P and the percentages of both neutrophil-platelet and monocyte-platelet complexes in the acute phase, and the percentages of all leucocyte-platelet complexes in the convalescent phase after ischaemic CVD. This study provides evidence for ongoing excessive platelet and/or endothelial activation in ischaemic CVD patients despite treatment with antithrombotic therapy.
authors.affiliation: Stroke Research Unit, Department of Headache, Brain Injury and Rehabilitation, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, University College London, London, UK. d.mccabe@ion.ucl.ac.uk
authors.forename: Dominick J H
authors.initials: DJ
authors.lastname: McCabe
authors.forename: Paul
authors.initials: P
authors.lastname: Harrison
authors.forename: Ian J
authors.initials: IJ
authors.lastname: Mackie
authors.forename: Paul S
authors.initials: PS
authors.lastname: Sidhu
authors.forename: Gordon
authors.initials: G
authors.lastname: Purdy
authors.forename: Andrew S
authors.initials: AS
authors.lastname: Lawrie
authors.forename: Hilary
authors.initials: H
authors.lastname: Watt
authors.forename: Martin M
authors.initials: MM
authors.lastname: Brown
authors.forename: Samuel J
authors.initials: SJ
authors.lastname: Machin
mesh_terms: D000208:Acute Disease; D000368:Aged; D015415:Biomarkers / Q000032:analysis; D001792:Blood Platelets / Q000473:pathology*; D016022:Case-Control Studies; D002448:Cell Adhesion; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood; D017493:Leukocyte Common Antigens / Q000032:analysis; D007962:Leukocytes / Q000473:pathology*; D008297:Male; D010799:Phycoerythrin / Q000032:analysis; D015539:Platelet Activation; D010973:Platelet Adhesiveness; D018709:Statistics, Nonparametric; D020521:Stroke / Q000097:blood* / Q000473:pathology
chemical_list: D015415:Biomarkers; D010799:Phycoerythrin; D017493:Leukocyte Common Antigens