Stephen J X Murphy1,2, Soon Tjin Lim1,2,3, Fionnuala Hickey4, Justin A Kinsella5, Deirdre R Smith1,6, Sean Tierney7, Bridget Egan7, T Martin Feeley7,8, Sinéad M Murphy1,2,9, D Rónán Collins2,10, Tara Coughlan2,10, Desmond O'Neill2,10, Joseph A Harbison11, Prakash Madhavan12, Sean M O'Neill12, Mary-Paula Colgan12, James S O'Donnell13,14,15, Jamie M O'Sullivan14,15, George Hamilton16, Dominick J H McCabe1,2,3,6,9,15. 1. Department of Neurology, The Adelaide and Meath Hospital, Dublin incorporating the National Children's Hospital (AMNCH)/Tallaght University Hospital, Dublin, Ireland. 2. Stroke Service, AMNCH/Tallaght University Hospital, Dublin, Ireland. 3. Department of Clinical Neurosciences, Royal Free Campus, UCL Queen Square Institute of Neurology, London, United Kingdom. 4. Department of Clinical Medicine, Trinity Centre for Health Sciences, School of Medicine, Trinity College, Dublin, Ireland. 5. Department of Neurology, St Vincent's University Hospital and University College Dublin, Dublin, Ireland. 6. Vascular Neurology Research Foundation, C/O Dept of Neurology, AMNCH/Tallaght University Hospital, Dublin, Ireland. 7. Department of Vascular Surgery, AMNCH/Tallaght University Hospital, Dublin, Ireland. 8. Clinical Directorate, Dublin Midlands Hospital Group, Dublin Ireland. 9. Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Dublin, Ireland. 10. Age-Related Health Care Department, AMNCH/Tallaght University Hospital, Dublin, Ireland. 11. Department of Medicine for the Elderly/Stroke Service, St James's Hospital and School of Medicine, Trinity College Dublin, Dublin, Ireland. 12. Department of Vascular Surgery, St James's Hospital, Dublin, Ireland. 13. Department of Haematology, St James's Hospital, Dublin, Ireland. 14. Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland. 15. Irish Centre for Vascular Biology, Royal College of Surgeons in Ireland, Dublin, Ireland. 16. Department of Vascular Surgery, University Department of Surgery, Royal Free Hampstead NHS Trust, London, United Kingdom.
Abstract
BACKGROUND: The relationship between von Willebrand factor antigen (VWF:Ag), VWF propeptide (VWFpp), VWFpp/VWF:Ag ratio, ADAMTS13 activity, and microembolic signal (MES) status in carotid stenosis is unknown. METHODS: This prospective, multicenter study simultaneously assessed plasma VWF:Ag levels, VWFpp levels and ADAMTS13 activity, and their relationship with MES in asymptomatic versus symptomatic moderate-to-severe (≥50-99%) carotid stenosis patients. One-hour 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 transient ischemic attack (TIA)/ischemic stroke. VWF:Ag levels were higher (p = 0.049) and VWFpp/VWF:Ag ratios lower (p = 0.006) in early symptomatic than in asymptomatic patients overall, and in early symptomatic versus asymptomatic MES-ve subgroups (p ≤0.02). There were no intergroup differences in VWFpp expression or ADAMTS13 activity (p ≥0.05). VWF:Ag levels and ADAMTS13 activity decreased (p ≤ 0.048) and VWFpp/VWF:Ag ratios increased (p = 0.03) in symptomatic patients followed up from the early to late phases after TIA/stroke. Although there were no differences in the proportions of symptomatic and asymptomatic patients with blood group O, a combined analysis of early symptomatic and asymptomatic patients revealed lower median VWF:Ag levels in patients with blood group O versus those without blood group O (9.59 vs. 12.32 µg/mL, p = 0.035). DISCUSSION: VWF:Ag expression, a marker of endothelial ± platelet activation, is enhanced in recently symptomatic versus asymptomatic carotid stenosis patients, including in MES-ve patients, and decreases with ADAMTS13 activity over time following atherosclerotic TIA/ischemic stroke. Thieme. All rights reserved.
BACKGROUND: The relationship between von Willebrand factor antigen (VWF:Ag), VWF propeptide (VWFpp), VWFpp/VWF:Ag ratio, ADAMTS13 activity, and microembolic signal (MES) status in carotid stenosis is unknown. METHODS: This prospective, multicenter study simultaneously assessed plasma VWF:Ag levels, VWFpp levels and ADAMTS13 activity, and their relationship with MES in asymptomatic versus symptomatic moderate-to-severe (≥50-99%) carotid stenosis patients. One-hour 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 transient ischemic attack (TIA)/ischemic stroke. VWF:Ag levels were higher (p = 0.049) and VWFpp/VWF:Ag ratios lower (p = 0.006) in early symptomatic than in asymptomatic patients overall, and in early symptomatic versus asymptomatic MES-ve subgroups (p ≤0.02). There were no intergroup differences in VWFpp expression or ADAMTS13 activity (p ≥0.05). VWF:Ag levels and ADAMTS13 activity decreased (p ≤ 0.048) and VWFpp/VWF:Ag ratios increased (p = 0.03) in symptomatic patients followed up from the early to late phases after TIA/stroke. Although there were no differences in the proportions of symptomatic and asymptomatic patients with blood group O, a combined analysis of early symptomatic and asymptomatic patients revealed lower median VWF:Ag levels in patients with blood group O versus those without blood group O (9.59 vs. 12.32 µg/mL, p = 0.035). DISCUSSION: VWF:Ag expression, a marker of endothelial ± platelet activation, is enhanced in recently symptomatic versus asymptomatic carotid stenosis patients, including in MES-ve patients, and decreases with ADAMTS13 activity over time following atherosclerotic TIA/ischemic stroke. Thieme. All rights reserved.
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