S J X Murphy1,2, S T Lim1,2, J A Kinsella3, S Tierney4, B Egan4, T M Feeley4,5, S M Murphy1,2,6, R A Walsh1,6, D R Collins7,2, T Coughlan7,2, D O'Neill7,2, J A Harbison8, P Madhavan9, S M O'Neill9, M P Colgan9, D Cox10,11, N Moran10,11, G Hamilton12, J F Meaney13, D J H McCabe14,15,16,17,18,19,20. 1. Department of Neurology, AMNCH/Tallaght University Hospital, Dublin, Ireland. 2. Stroke Service, AMNCH/Tallaght University Hospital, Dublin, Ireland. 3. Department of Neurology, St Vincent's University Hospital, University College Dublin, Dublin, Ireland. 4. Department of Vascular Surgery, AMNCH/Tallaght University Hospital, Dublin, Ireland. 5. Dublin Midlands Hospital Group, Dublin, Ireland. 6. Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Dublin, Ireland. 7. Age-Related Health Care Department, AMNCH/Tallaght University Hospital, Dublin, Ireland. 8. Department of Medicine for the Elderly/Stroke Service, St. James's Hospital/Trinity College Dublin, Dublin, Ireland. 9. Department of Vascular Surgery, St. James's Hospital/Trinity College Dublin, Dublin, Ireland. 10. Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland. 11. Irish Centre for Vascular Biology, Dublin, Ireland. 12. Department of Vascular Surgery, University Department of Surgery, Royal Free Hampstead NHS Trust, London, UK. 13. Department of Radiology, Centre for Advanced Medical Imaging, St. James's Hospital/Trinity College Dublin, Dublin, Ireland. 14. Vascular Neurology Research Foundation, C/O Department of Neurology, The Adelaide and Meath Hospital, Dublin, Incorporating the National Children's Hospital (AMNCH)/Tallaght University Hospital, Tallaght, Dublin 24, Ireland. dominick.mccabe@tuh.ie. 15. Department of Neurology, AMNCH/Tallaght University Hospital, Dublin, Ireland. dominick.mccabe@tuh.ie. 16. Stroke Service, AMNCH/Tallaght University Hospital, Dublin, Ireland. dominick.mccabe@tuh.ie. 17. Department of Clinical Neurosciences, Royal Free Campus, UCL Queen Square Institute of Neurology, London, UK. dominick.mccabe@tuh.ie. 18. Irish Centre for Vascular Biology, Dublin, Ireland. dominick.mccabe@tuh.ie. 19. Stroke Clinical Trials Network Ireland, Dublin, Ireland. dominick.mccabe@tuh.ie. 20. Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Dublin, Ireland. dominick.mccabe@tuh.ie.
Abstract
BACKGROUND: Assessment of 'high on-treatment platelet reactivity (HTPR)' could enhance understanding of the pathophysiology of first or recurrent vascular events in carotid stenosis patients on antiplatelet therapy. METHODS: This prospective, multi-centre study assessed antiplatelet-HTPR status and its relationship with micro-emboli signals (MES) in asymptomatic vs. symptomatic ≥ 50-99% carotid stenosis. Platelet function/reactivity was assessed under 'moderately high shear stress' with the PFA-100® and 'low shear stress' with VerifyNow® and Multiplate® analysers. Bilateral 1-h transcranial Doppler ultrasound of the middle cerebral arteries classified patients as MES + ve or MES - ve. RESULTS: Data from 34 asymptomatic patients were compared with 43 symptomatic patients in the 'early phase' (≤ 4 weeks) and 37 patients in the 'late phase' (≥ 3 months) after TIA/ischaemic stroke. Median daily aspirin doses were higher in early symptomatic (225 mg; P < 0.001), but not late symptomatic (75 mg; P = 0.62) vs. asymptomatic patients (75 mg). There was a lower prevalence of aspirin-HTPR in early (28.6%; P = 0.028), but not late symptomatic (38.9%; P = 0.22) compared with asymptomatic patients (56.7%) on the PFA-100®, but not on the VerifyNow® or Multiplate® (P ≤ 0.53). Early symptomatic patients had a higher prevalence of aspirin-HTPR on the PFA-100® (28.6%) vs. VerifyNow® (9.5%; P = 0.049), but not Multiplate® assays (11.9%, P = 0.10). There was no difference in aspirin-HTPR prevalence between any symptomatic vs. asymptomatic MES + ve or MES - ve subgroup. DISCUSSION: Recently symptomatic moderate-severe carotid stenosis patients had a lower prevalence of aspirin-HTPR than their asymptomatic counterparts on the PFA-100®, likely related to higher aspirin doses. The prevalence of antiplatelet-HTPR was positively influenced by higher shear stress levels, but not MES status.
BACKGROUND: Assessment of 'high on-treatment platelet reactivity (HTPR)' could enhance understanding of the pathophysiology of first or recurrent vascular events in carotid stenosispatients on antiplatelet therapy. METHODS: This prospective, multi-centre study assessed antiplatelet-HTPR status and its relationship with micro-emboli signals (MES) in asymptomatic vs. symptomatic ≥ 50-99% carotid stenosis. Platelet function/reactivity was assessed under 'moderately high shear stress' with the PFA-100® and 'low shear stress' with VerifyNow® and Multiplate® analysers. Bilateral 1-h transcranial Doppler ultrasound of the middle cerebral arteries classified patients as MES + ve or MES - ve. RESULTS: Data from 34 asymptomatic patients were compared with 43 symptomatic patients in the 'early phase' (≤ 4 weeks) and 37 patients in the 'late phase' (≥ 3 months) after TIA/ischaemic stroke. Median daily aspirin doses were higher in early symptomatic (225 mg; P < 0.001), but not late symptomatic (75 mg; P = 0.62) vs. asymptomatic patients (75 mg). There was a lower prevalence of aspirin-HTPR in early (28.6%; P = 0.028), but not late symptomatic (38.9%; P = 0.22) compared with asymptomatic patients (56.7%) on the PFA-100®, but not on the VerifyNow® or Multiplate® (P ≤ 0.53). Early symptomatic patients had a higher prevalence of aspirin-HTPR on the PFA-100® (28.6%) vs. VerifyNow® (9.5%; P = 0.049), but not Multiplate® assays (11.9%, P = 0.10). There was no difference in aspirin-HTPR prevalence between any symptomatic vs. asymptomatic MES + ve or MES - ve subgroup. DISCUSSION: Recently symptomatic moderate-severe carotid stenosispatients had a lower prevalence of aspirin-HTPR than their asymptomatic counterparts on the PFA-100®, likely related to higher aspirin doses. The prevalence of antiplatelet-HTPR was positively influenced by higher shear stress levels, but not MES status.
Authors: Dominick J H McCabe; Paul Harrison; Ian J Mackie; Paul S Sidhu; Andrew S Lawrie; Gordon Purdy; Samuel J Machin; Martin M Brown Journal: Platelets Date: 2005-08 Impact factor: 3.862
Authors: Justin A Kinsella; W Oliver Tobin; Sean Tierney; Timothy M Feeley; Bridget Egan; Tara Coughlan; D Ronan Collins; Desmond O'Neill; Joseph A Harbison; Colin P Doherty; Prakash Madhavan; Dermot J Moore; Sean M O'Neill; Mary-Paula Colgan; Maher Saqqur; Raymond P Murphy; Niamh Moran; George Hamilton; Dominick J H McCabe Journal: J Neurol Sci Date: 2017-03-14 Impact factor: 3.181
Authors: S Claiborne Johnston; J Donald Easton; Mary Farrant; William Barsan; Robin A Conwit; Jordan J Elm; Anthony S Kim; Anne S Lindblad; Yuko Y Palesch Journal: N Engl J Med Date: 2018-05-16 Impact factor: 91.245