Plasma levels of von Willebrand factor in the etiologic subtypes of ischemic stroke

Abstract

Summary. Background: Compared with coronary artery disease, there are few studies on von Willebrand factor (VWF) in ischemic stroke (IS). Moreover, there is little information on VWF in the etiologic subtypes of IS. Objectives: The aim of the present study was to investigate VWF in IS and in the etiologic subtypes of IS. Patients/methods: The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) is a case-control study comprising 600 patients and 600 matched controls. Etiologic IS subtype was defined according to the TOAST criteria. Blood sampling was performed in the acute phase and after 3 months. Results: The levels of VWF were increased in overall IS, at both time-points. The 3-month VWF levels were increased in the subtypes of large-vessel disease (LVD), cardioembolic (CE) stroke and cryptogenic stroke, but not in the subtype of smallvessel disease (SVD), as compared with the controls. The acute phase VWF levels were significantly increased in all four subtypes. In the multivariate regression analysis, with vascular risk factors as covariates, the 3-month VWF levels were associated with CE stroke and cryptogenic stroke, and the acute phase VWF levels with all subtypes. There were significant subtype-specific differences in VWF, with the highest levels in LVD and CE stroke. Conclusions: The present results show that VWF levels are increased in patients with IS. Furthermore, the VWF levels differ between etiologic IS subtypes and thus, it is important to consider etiologic subtypes in future studies of VWF in patients with IS.

Reperfusion of cerebral artery thrombosis by the GPIb–VWF blockade with the Nanobody ALX-0081 reduces brain infarct size in guinea pigs

“…18 In the prospective Rotterdam Study, the risk of ischemic stroke increased with rising levels of VWF in plasma, 19 and in the case-control SAHLSIS Study, VWF levels were found to be increased in ischemic stroke, both in the acute phase and 3 months after the event. 20 The inhibition of the GPIb-IX-V-vWF interaction may theoretically prevent pathologic thrombosis but may not have much influence on physiologic hemostasis, given the preeminent role of GPIb-VWF in platelet activation under high shear conditions 21 and may thus represent a particularly promising target for the treatment of ischemic stroke.…”

Fibrin D-Dimer, Tissue-Type Plasminogen Activator, von Willebrand Factor, and Risk of Incident Stroke in Older Men

“…4 The von Willebrand factor (vWF) is synthesized primarily by vascular endothelial cells and promotes platelet adhesion and aggregation, leading to thrombus formation. 1 Increased levels of vWF in stroke patients have been reported in several case-control studies, [5][6][7][8] but prospective studies have been inconsistent, with some showing a positive relationship 9,10 and others showing no relationship [11][12][13][14] between vWF and stroke risk. Fibrin D-dimer is the primary degradation product of cross-linked fibrin and is a marker of activated coagulation and fibrinolysis.…”

The role of von Willebrand factor in determining the risk of ischemic stroke in Hawler city: a case-control study

“…This result was in agreement with the other researchers. 2,12,13 The mechanism responsible for increase plasma vWF levels and the occurrence of ischemic stroke is due to inflammation resulting in endothelial cell activation, which leads to increase vWF secretion and subsequent reduce clearance of it. When vWF more release, it facilitates over platelet adhesion leading to secretion of excess active substances and excess generation of platelet plug which leading to thrombosis.…”

“…When vWF more release, it facilitates over platelet adhesion leading to secretion of excess active substances and excess generation of platelet plug which leading to thrombosis. [12][13][14] It has long been known that lipids abnormalities are a major risk factor for the onset of ischemic stroke. 15 Our data reveal that the mean fasting serum T.Ch level in patients with ischemic stroke was significantly higher (P <0.01) than the control group.…”