von Willebrand Factor Antigen, von Willebrand Factor Propeptide, and ADAMTS13 in Carotid Stenosis and Their Relationship with Cerebral Microemboli.

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.
Competing Interests: S.J.X.M. reports grants from Trinity College Dublin Innovation Bursary, Meath Foundation, Joint IICN/Merck Serono Fellowship in Neuroscience, The Vascular Neurology Research Foundation, unrestricted educational grant from Bayer HealthCare Ireland, and unrestricted educational grant from Verum Diagnostica, GmbH, outside the submitted work.S.T.L. reports grants from Meath Foundation, the Irish Institute of Clinical Neuroscience (IICN)/Novartis Ireland Fellowship Grant, the Irish Heart Foundation Stroke Prevention Bursary, the Vascular Neurology Research Foundation, Ireland, and unrestricted educational grant funding from Biogen Idec Ireland, outside the submitted work.D.J.H.M. reports grants from the Trinity College Dublin Innovation Bursary, Trinity College Dublin, Ireland, the Meath Foundation, Ireland, Joint IICN/Merck Serono Fellowship in Neuroscience, the Vascular Neurology Research Foundation, Bayer HealthCare Ireland, Verum Diagnostica, GmbH, the Irish Institute of Clinical Neuroscience (IICN)/Novartis Ireland Fellowship Grant, the Irish Heart Foundation Stroke Prevention Bursary, and Biogen Idec Ireland, during the conduct of the study.
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