240 Course of von Willebrand Factor in Patients Supported with HeartWare HVAD in Mid-Term Follow-Up

2011 ◽  
Vol 30 (4) ◽  
pp. S85-S86
Author(s):  
N. Dranishnikov ◽  
A. Stepanenko ◽  
A. Frumkin ◽  
J. Vierecke ◽  
M. Schweiger ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Von Willebrand ◽  
Willebrand Factor

Carotid enlargement and serum levels of von Willebrand factor in rheumatoid arthritis: a follow-up study

2012 ◽  
Vol 31 (12) ◽  
pp. 1727-1732 ◽  
Author(s):  
Mirjana Veselinovic ◽  
Vladimir Jakovljevic ◽  
Aleksandra Jurisic-Skevin ◽  
Slavco Toncev ◽  
Dragan M. Djuric
Keyword(s):  
Rheumatoid Arthritis ◽  
Von Willebrand Factor ◽  
Serum Levels ◽  
Follow Up Study ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals von Willebrand factor/ADAMTS13 ratio at presentation of acute ischemic brain injury is predictive of outcome

2020 ◽  
Vol 4 (2) ◽  
pp. 398-407 ◽  
Author(s):  
Alice Taylor ◽  
Chiara Vendramin ◽  
Deepak Singh ◽  
Martin M. Brown ◽  
Marie Scully
Keyword(s):  
Brain Injury ◽  
Von Willebrand Factor ◽  
Stroke Severity ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Mortality And Morbidity ◽  
Increased Risk ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Acute ischemic stroke (IS) and transient ischemic attack (TIA) are associated with raised von Willebrand factor (VWF) and decreased ADAMTS13 activity (ADAMTS13Ac). Their impact on mortality and morbidity is unclear. We conducted a prospective investigation of the VWF-ADAMTS13 axis in 292 adults (acute IS, n = 103; TIA, n = 80; controls, n = 109) serially from presentation until >6 weeks. The National Institutes of Health Stroke Score (NIHSS) and modified Rankin scale (mRS) were used to assess stroke severity. Presenting median VWF antigen (VWF:Ag)/ADAMTS13Ac ratios were: IS, 2.42 (range, 0.78-9.53); TIA, 1.89 (range, 0.41-8.14); and controls, 1.69 (range, 0.25-15.63). Longitudinally, the median VWF:Ag/ADAMTS13Ac ratio decreased (IS, 2.42 to 1.66; P = .0008; TIA, 1.89 to 0.65; P < .0001). The VWF:Ag/ADAMTS13Ac ratio was higher at presentation in IS patients who died (3.683 vs 2.014; P < .0001). A presenting VWF:Ag/ADAMTS13Ac ratio >2.6 predicted mortality (odds ratio, 6.33; range, 2.22-18.1). Those with a VWF:Ag/ADAMTS13Ac ratio in the highest quartile (>3.091) had 31% increased risk mortality. VWF:Ag/ADAMTS13Ac ratio at presentation of ischemic brain injury was associated with higher mRS (P = .021) and NIHSS scores (P = .029) at follow-up. Thrombolysis resulted in prompt reduction of the VWF:Ag/ADAMTS13Ac ratio and significant improvement in mRS on follow-up. A raised VWF:Ag/ADAMTS13Ac ratio at presentation of acute IS or TIA is associated with increased mortality and poorer functional outcome. A ratio of 2.6 seems to differentiate outcome. Prompt reduction in the ratio in thrombolysed patients was associated with decreased mortality and morbidity. The VWF:Ag/ADAMTS13Ac ratio is a biomarker for the acute impact of an ischemic event and longer-term outcome.

The anti-von Willebrand factor aptamer ARC1779 increases von Willebrand factor levels and platelet counts in patients with type 2B von Willebrand disease

2012 ◽  
Vol 108 (08) ◽  
pp. 284-290 ◽  
Author(s):  
Petra Jilma-Stohlawetz ◽  
Paul Knöbl ◽  
James C. Gilbert ◽  
Bernd Jilma
Keyword(s):  
Von Willebrand Factor ◽  
Plasma Concentrations ◽  
Fold Increase ◽  
Von Willebrand Disease ◽  
Platelet Counts ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Ristocetin Cofactor

SummaryBlockade of hyperactive von Willebrand factor (VWF) by ARC1779 blunted the platelet drop induced by desmopressin in patients with type 2B von Willebrand disease (VWD). Thus, we hypothesised that ARC1779 may increase VWF levels and correct thrombocytopenia. Three thrombocytopenic patients suffering from type 2B VWD received a loading dose of 0.23 mg/kg ARC1779 followed by 4 μg/kg/min intravenously for 72 hours in a prospective clinical trial. ARC1779 was well tolerated and safe. Plasma concentrations of ARC1779 increased to 76 μg/ml (59–130) leading to an immediate decrease of free VWF A1 domains. VWF/FVIII levels increased as early as 12 h after start of infusion, peaked near the end of infusion, and returned to baseline at follow-up. VWF ristocetin cofactor activity (VWF:RCo) showed a median 10-fold increase 8 hours after end of infusion, while the median VWF-antigen and FVIII increase was less (5-fold and 4-fold, respectively). Most importantly inhibition of hyperactive VWF rapidly increased platelet counts from 40x109/l (38–58 x109/l) to a maximum of 146 x109/l (107–248 x109/l). In conclusion, ARC1779 markedly increases VWF/FVIII levels and most importantly improves or even corrects thrombocytopenia in VWD type 2B patients. This underscores the in vivo potency of ARC1779.

scholarly journals Increased SERUM VON Willebrand Levels in Chronic Lymphocytic Leukemia (CLL) Patients Are Related to a Shorter Time to Treatment

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5547-5547
Author(s):  
Thommais Tryfou ◽  
Paraskevi Papaioannou ◽  
Panagiotis Repousis ◽  
Annita Ioanna Gkioka ◽  
Sotirios Sachanas ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Chronic Lymphocytic Leukemia ◽  
Von Willebrand Factor ◽  
Conflicts Of Interest ◽  
Umbilical Vein ◽  
Lymphocytic Leukemia ◽  
Endothelial Cell Proliferation ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract CLL is a frequent and usually indolent disease that require only follow-up in about 2/3 of patients while the rest 1/3 of patients are symptomatic, have a worse outcome and need to be treated. The role of angiogenesis in CLL prognosis remains unclear. It has been shown that CLL plasma promotes von Willebrand factor (vWF) secretion, and expression in human umbilical vein endothelial cell cultures (HUVECs) [1]. Therefore, we investigated whether serum vWF levels in CLL patients at diagnosis could provide prognostic information. Patients and methods: 33 CLL patients were studied of whom 55%, 32% and 13% were Binet staged A, B and C respectively. 45% never required treatment while 55% required treatment either at the time of diagnosis or during their follow-up. The time to first treatment (TFT) was 34 months. Serum vWF was measured by ELISA (R&D Quantiquine, duo Set) in frozen sera drawn at patients' diagnosis and in 10 healthy individuals (HI). Measurements were performed in duplicate according to the manufacturer's instructions. Statistical analysis was performed by conventional methods, using the SPSS v.22 software. P values below 0,05 were considered statistically significant. Results: Serum vWF levels ranged from 178,5 to 14353,5 pg/ml (median 1028,5) in patients and from 374,6 to 1141,3 pg/ml (median 528,5) in HI, the difference being statistically significant (p< 0,05). Patients with Serum vWF levels above 528,5 pg/ml (median normal value) had a significantly shorter TFT than the others (p=0,01) as shown in figure. Otherwise, serum vWF levels correlated only with hypogammaglobulinemia (p=0,04). Conclusion: Serum vWF levels were increased in CLL patients. Importantly, we showed for the first time, to our knowledge, that higher vWF levels correlated with a shorter TFT, suggesting that increased vWF levels reflect active neoangiogenesis that in turn, contributes to a more aggressive disease behavior. [1] Shahidi M et al, Induction of endothelial cell proliferation and von Willebrand factor expression and secretion by leukemic plasma of patients with chronic lymphocytic leukemia before and after inhibition of NF-κB. Blood Coagul Fibrinolysis. 2016 Sep;27(6):711-6. Figure. Figure. Disclosures No relevant conflicts of interest to declare.

Inhibition of Von Willebrand Factor (VWF) by ARC1779 Normalizes Von Willebrand Factor/FVIII Levels and Corrects Thrombocytopenia in VWD Type 2b Patients,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3377-3377
Author(s):  
Petra Jilma-Stohlawetz ◽  
Paul Knoebl ◽  
Ingrid Pabinger ◽  
James Gilbert ◽  
Robert G. Schaub ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Von Willebrand Factor ◽  
Repeated Measures ◽  
Plasma Concentrations ◽  
Von Willebrand Disease ◽  
Hepatitis C Infection ◽  
Platelet Counts ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Abstract 3377 Introduction: Infusion of the anti-VWF aptamer ARC1779 effectively elevated platelet counts in some patients with congenital thrombocytopenic purpura, and blunted the platelet drop induced by desmopressin in patients with type 2b von Willebrand disease (VWD). Thus, we hypothesized that ARC1779 may increase VWF levels and correct thrombocytopenia by blocking the hyperactive VWF A1 domain in type 2b VWD. Methods: Thrombocytopenic patients suffering from type 2b VWD received intravenous infusions of ARC1779 (4 mcg/kg/min) for 72 hours in a prospective clinical trial. Patients were monitored using previsouly published assays (Thromb Haemost. 2010;104:563–70). Data are provided as median and the range and were tested for significance by repeated measures analysis of variance. Results: All patients had moderate thrombocytopenia, low levels of VWF:RCo, VWF:CBA, FVIII:C, and collagen/ADP closure times >300s (platelet function analyzer PFA-100). ARC1779 was well tolerated and safe even in a patient who suffered from active chronic gastrointestinal bleeding due to angiodysplasias before start of infusion. Plasma concentrations of ARC1779 increased to 76 mcg/mL (59–130) which suppressed free VWF A1 domains in the REAADS assay to a minimum of <3 to 5%. Consistent with the estimated in vivo half-life of VWF, VWF/FVIII levels increased as early as 12h after start of infusion, peaked near the end of infusion, and returned to baseline at follow-up. That was best exemplified by VWF:RCo levels which increased from 32% (26–45%) 10-fold to 367% (215–418%) 8h after end of infusion, and decreased again to 33% (20–40%) during follow up. Similarly VWF:CBA levels increased 16-fold (8 to 69-fold), VWF: Ag levels 5.2 fold (3 to 27-fold), and FVIII levels 4.3 fold (3 to 6-fold). Most importantly inhibition of hyperactive VWF rapidly increased platelet counts from 40/nL (38–58/nL) to a maximum of 146/nL (107–248/nL). This was observed although patients were suffering from chronic liver disease due to hepatitis C infection or associated immune thrombocytopenia, which could have blunted the platelet response. All changes were statistically significant (p<0.007). Conclusion: This clinical trial underscores the therapeutic efficacy of the VWF A1 antagonist aptamer ARC1779. ARC1779 significantly increases VWF/FVIII levels and most importantly improves or even corrects thrombocytopenia in VWD type 2b patients. This could facilitate (i) the collection of autologous platelets for platelet transfusions pre-operatively or (ii) interferon therapy in patients whose HCV therapy could not be initiated or had to be stopped due to thrombocytopenia. As angiodysplasias may be caused by defective or deficient VWF (Blood 2011;117:1071–80), it may also be tempting to further investigate the potential of chronic anti-VWF aptamer therapy to treat angiodysplasia. Disclosures: Knoebl: Archemix Corp.: Consultancy. Pabinger:Archemix Corp.: Consultancy. Gilbert:Archemix Corp.: previous employment. Schaub:Archemix Corp.: Consultancy, previous employment. Jilma:Archemix Corp.: Consultancy, Research Funding.

Course of von Willebrand factor in recipients of axial-flow and centrifugal blood pumps in up to 12 months of follow-up

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
N Dranishnikov ◽  
A Stepanenko ◽  
A Frumkin ◽  
J Vierecke ◽  
EV Potapov ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Axial Flow ◽  
Blood Pumps ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Effect of Acute Myocardial Infarction on a Disintegrin and Metalloprotease with Thrombospondin Motif 13 and Von Willebrand Factor and Their Relationship with Markers of Inflammation

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Abeer A. Al-Masri ◽  
Syed Shahid Habib ◽  
Ahmad Hersi ◽  
Hana Al Zamil
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Von Willebrand Factor ◽  
Study Objective ◽  
Control Subjects ◽  
Markers Of Inflammation ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Thrombospondin Motif

Objectives. Coagulation mechanisms and fibrinolytic assembly are important components role players of acute myocardial infarction (AMI) progression. Our study objective was to see the serial variations in the levels of Von Willebrand factor (VWF) and A Disintegrin and Metalloprotease with ThromboSpondin motif (ADAMTS13) over the course of AMI and to determine their relationship with the cardiovascular risk markers and the patient’s clinical characteristics. Methods. This project was done at the departments of Emergency Medicine, Physiology and Cardiac sciences of King Saud University Medical City. We studied ADAMTS13, VWF, fibrinogen, and CRP levels in 80 patients with AMI when patients were admitted; post AMI by 3-4 days and at follow-up of 3 months. We compared them with a control group consisting of 36 subjects. Results. AMI had significantly lower levels of ADAMTS13 at AMI and after 3-4 days; at follow-up the difference in levels was nonsignificant, when compared with controls. Similarly, VWF levels were significantly higher in AMI and remained high even at follow-up compared to control subjects. VWF/ADAMTS13 ratio was also significantly higher at AMI and 3-4 days while at follow-up difference was nonsignificant compared to control subjects. Regression analysis between hsCRP and ADAMTS13 showed an inverse relationship (r=0.376,p<0.01), while correlation with VWF was significantly positive (r=0.337,p<0.01). Conclusions. Increased levels of VWF and reduced levels of ADAMTS13 activity may contribute to the pathogenesis of acute myocardial infarction and might prove to be important mediators of AMI progression.

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