scholarly journals Evaluation of von Willebrand factor in COPD patients

2014 ◽  
Vol 40 (4) ◽  
pp. 373-379 ◽  
Author(s):  
Thiago Prudente Bártholo ◽  
Cláudia Henrique da Costa ◽  
Rogério Rufino
Keyword(s):  
Von Willebrand Factor ◽  
Medical Research Council ◽  
Control Group ◽  
X Rays ◽  
Copd Patients ◽  
Never Smokers ◽  
Von Willebrand ◽  
And Control ◽  
Willebrand Factor ◽  
Selection Phase

OBJECTIVE: To compare the absolute serum von Willebrand factor (vWF) levels and relative serum vWF activity in patients with clinically stable COPD, smokers without airway obstruction, and healthy never-smokers. METHODS: The study included 57 subjects, in three groups: COPD (n = 36); smoker (n = 12); and control (n = 9). During the selection phase, all participants underwent chest X-rays, spirometry, and blood testing. Absolute serum vWF levels and relative serum vWF activity were obtained by turbidimetry and ELISA, respectively. The modified Medical Research Council scale (cut-off score = 2) was used in order to classify COPD patients as symptomatic or mildly symptomatic/asymptomatic. RESULTS: Absolute vWF levels were significantly lower in the control group than in the smoker and COPD groups: 989 ± 436 pg/mL vs. 2,220 ± 746 pg/mL (p < 0.001) and 1,865 ± 592 pg/mL (p < 0.01). Relative serum vWF activity was significantly higher in the COPD group than in the smoker group (136.7 ± 46.0% vs. 92.8 ± 34.0%; p < 0.05), as well as being significantly higher in the symptomatic COPD subgroup than in the mildly symptomatic/asymptomatic COPD subgroup (154 ± 48% vs. 119 ± 8%; p < 0.05). In all three groups, there was a negative correlation between FEV1 (% of predicted) and relative serum vWF activity (r2 = −0.13; p = 0.009). CONCLUSIONS: Our results suggest that increases in vWF levels and activity contribute to the persistence of systemic inflammation, as well as increasing cardiovascular risk, in COPD patients.

scholarly journals Comparative analysis of prothrombotic activity in patients with myocardial infarction with non-obstructive and obstructive atherosclerotic lesions of the coronary arteries

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
VV Ryabov ◽  
D Vorobyeva ◽  
YUG Lugacheva ◽  
IV Kulagina
Keyword(s):  
Myocardial Infarction ◽  
Coronary Arteries ◽  
Von Willebrand Factor ◽  
Protein C ◽  
Control Group ◽  
Moderate Correlation ◽  
Blood Tests ◽  
Group A ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): The reported study was funded by RFBR, project number №19-315-90106 Aim To compare indicators of blood prothrombotic activity in patients with myocardial infarction with and without coronary arteries obstruction Material and methods. The study included 40 patients with AMI (19 patients in the main group and 21 patients in the control group). Three patients (15.7%) with acute myocarditis were excluded from the analysis. Hemostasiological and hematological blood tests were studied upon admission, on the 2nd, 4th, 7th days from hospitalization. Blood samples for protein C, antithrombin, von Willebrand factor (WF), plasminogen, homocysteine were performed on 4th ± 1 day from hospitalization. To determine the IgG / IgM antibodies to cardiolipin and β2-glycoprotein for the diagnosis of APS, the ORGENTEC Anti-β2-Glycoprotein I IgG / IgM ELISA enzyme immunoassay was used. Blood tests for lupus anticoagulant were performed using an ACL-Top 700 analyzer (Werfen) with HemosIL SynthASil dRVVT screen reagents / dRVVT confirm  and with a SCT screen / SCT confirm quartz activator. Results In patients with MINOCA a statistically higher level of homocysteine (p = 0.03) and a lower level of plasminogen (p = 0.007) are determined. Protein C, antithrombin, WF the presence of lupus anticoagulant, antibodies to cardiolipin and β2-glycoprotein no differences between the groups were detected, p &gt;0.05. MINOCA patients have a statistically higher platelet level on the 2nd and 4th day of AMI (p = 0.046 and p = 0.01 ) however the level of hemoglobin and hematocrit was statistically lower on the 4th day of AMI, (p = 0.008). In the main group, a moderate correlation was found between protein C and antithrombin (r = 0.65, p = 0.0001), antithrombin and von Willebrand factor (r = 0.54, p = 0.0001), between protein C and platelet level by 4th day (r = - 0.49, p = 0.04). In MINOCA patients a moderate negative correlation was found between homocysteine and plasminogen (r = -0.69, p = 0.002). In the control group, a high correlation was found between protein C and antithrombin (r = 0.96, p = 0.0001), a moderate correlation between protein C and plasminogen (r = 0.47, p = 0.03). In addition, a relationship was revealed between the presence of thrombosis according to ICAG data and the level of ejection fraction (r = 0.46, p = 0.04) in the control group, as well as between the presence of thrombosis and the level of fibrinogen upon admission (r = 0.55, p = 0.008). Conclusions Patients with MINOCA have a higher level of homocysteine and a lower level of plasminogen. For such indicators as protein C, antithrombin III, WF the presence of antibodies on the APS is not defined differences between groups. According to laboratory data patients with MINOCA showed higher levels of platelets but lower levels of hemoglobin and hematocrit in the early post-infarction period.

scholarly journals Immunohistological Evaluation of Von Willebrand Factor in the Left Atrial Endocardium and Atrial Thrombi from Cats with Cardiomyopathy

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1240
Author(s):  
Wan-Ching Cheng ◽  
Lois Wilkie ◽  
Tsumugi Anne Kurosawa ◽  
Melanie Dobromylskyj ◽  
Simon Lawrence Priestnall ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Left Atrial ◽  
Thrombus Formation ◽  
Clinical Signs ◽  
Naturally Occurring ◽  
Feline Model ◽  
Von Willebrand ◽  
And Control ◽  
Endocardial Endothelium ◽  
Willebrand Factor

Aortic thromboembolism (ATE) occurs in cats with cardiomyopathy and often results in euthanasia due to poor prognosis. However, the underlying predisposing mechanisms leading to left atrial (LA) thrombus formation are not fully characterised. von Willebrand Factor (vWF) is a marker of endothelium and shows increased expression following endothelial injury. In people with poor LA function and LA remodelling, vWF has been implicated in the development of LA thrombosis. In this study we have shown (1) the expression of endocardial vWF protein detected using immunohistofluorescence was elevated in cats with cardiomyopathy, LA enlargement (LAE) and clinical signs compared to cats with subclinical cardiomyopathy and control cats; (2) vWF was present at the periphery of microthrombi and macrothrombi within the LA where they come into contact with the LA endocardium and (3) vWF was integral to the structure of the macrothrombi retrieved from the atria. These results provide evidence for damage of the endocardial endothelium in the remodelled LA and support a role for endocardial vWF as a pro-thrombotic substrate potentially contributing to the development of ATE in cats with underlying cardiomyopathy and LAE. Results from this naturally occurring feline model may inform research into human thrombogenesis.

scholarly journals Intracardiac Hemostasis and Fibrinolysis Parameters in Patients with Atrial Fibrillation

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Noémi Klára Tóth ◽  
Zoltán Csanádi ◽  
Orsolya Hajas ◽  
Alexandra Kiss ◽  
Edina Nagy-Baló ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Femoral Vein ◽  
Endothelial Damage ◽  
Control Group ◽  
Thrombotic Risk ◽  
Von Willebrand ◽  
And Control ◽  
Willebrand Factor ◽  
Pai 1 ◽  
D Dimer

Aims. To identify intracardiac hemostasis or fibrinolysis abnormalities, which are associated with atrial fibrillation (AF) and increase the risk of thromboembolism.Patients and Methods. Patient group consisted of 24 patients with AF and control group included 14 individuals with other supraventricular tachycardia undergoing transcatheter radiofrequency ablation. Blood samples were drawn from the femoral vein (FV), left atrium (LA), and left atrial appendage (LAA) before the ablation procedure. Fibrinogen, factor VIII (FVIII) and factor XIII activity, von Willebrand factor (VWF) antigen, thrombin-antithrombin (TAT) complex, quantitative fibrin monomer (FM), plasminogen,α2-plasmin inhibitor, plasmin-α2-antiplasmin (PAP) complex, PAI-1 activity, and D-dimer were measured from all samples.Results. Levels of FVIII and VWF were significantly elevated in the FV and LA of AF patients as compared to controls. TAT complex, FM, PAP complex, and D-dimer levels were significantly elevated in the LA as compared to FV samples in case of both groups, indicating a temporary thrombotic risk associated with the catheterization procedure.Conclusions. None of the investigated hemostasis or fibrinolysis parameters showed significant intracardiac alterations in AF patients as compared to non-AF controls. AF patients have elevated FVIII and VWF levels, most likely due to endothelial damage, presenting at both intracardiac and systemic level.

The Role Of High Von Willebrand Factor and Low ADAMTS13 Levels In The Risk Of Venous Thromboembolism

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1128-1128 ◽  
Author(s):  
Christiane Pereira Gouvea ◽  
Sandra Satiko Matsuda ◽  
Rodrigo Vaez ◽  
Patrícia Nunes Bezerra Pinheiro ◽  
Maria Aparecida Eiko Noguti ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Von Willebrand Factor ◽  
Control Group ◽  
Exclusion Criteria ◽  
Reference Category ◽  
Gender And Age ◽  
History Of ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Background Venous thromboembolism (VTE) is a common multicausal disease in the general population. von Willebrand factor (VWF) has been associated with VTE in epidemiological studies and recently VWF-mediated platelet adhesion has been shown to be critical for deep vein thrombosis (DVT) in mouse models. The large VWF multimers are cleaved by ADAMTS13 into smaller, less active multimers. Because of the key role of ADAMTS13, VWF and factor VIII (FVIII) in hemostasis and their close biological relationship, we aimed at investigating in the same population the effect of these proteins on VTE risk. Materials and Methods We included consecutive patients admitted to our anticoagulation clinic with a first objectively confirmed VTE event between January 2007 and July 2011. The study included only patients with DVT of the lower limbs and/or pulmonary embolism aged between 18-70 years, and without medical history of overt malignancy, arterial thrombosis, liver cirrhosis, renal failure on hemodialysis, connective tissue disease and other conditions characterized by chronic inflammation. Blood was collected at least 1 month after stopping anticoagulation and ≥ 6 months after VTE. Controls were recruited from friends or partners of patients, had no personal history of VTE and were matched to patients by gender and age. The other exclusion criteria for controls were the same as for patients, and in both groups pregnant or postpartum women at blood collection were excluded. ADAMTS13 and VWF antigens were determined by commercial ELISA and FVIII activity was measured using FVIII deficient plasma. High VWF (>150%) and FVIII (>150%) were defined by plasma levels of these proteins exceeding the 88th and 94th percentiles of the control group, respectively. To define low ADAMTS13 levels we used the 10th percentile of the controls (≤0.64 μg/ml). Odds ratios (OR) and 95% confidence intervals (CI) were presented adjusted for gender and age and medians with interquartile variation (25th-75th percentiles). Results 358 patients with a first objectively confirmed VTE event were admitted to our clinic, of whom 282 did not participate in the study due to the exclusion criteria (n= 249) and loss of follow-up or refusal (n= 33). Therefore, we included 76 patients (53 women, 70%) with a median age of 43 years (33-55 years) and 96 controls (66 women, 69%), with a median age of 42 years (31-52 years). In controls, there was a negative albeit weak correlation between ADAMTS13 levels and VWF (rs= -0.213 by Spearman coefficient, p= 0.037) and FVIII (rs= -0.251, p= 0.014). As expected, VTE was associated with high levels of VWF (OR 2.80, 95% CI 1.20-6.54) and FVIII (OR 3.02, 95% CI 1.08-8.43). Low ADAMTS13 levels were detected in 12 patients and 9 controls (OR 1.76, 95% CI 0.70-4.46). The population was dichotomized according to the 88th percentile of VWF of the controls. Median ADAMTS13 was lower in the group with VWF >p88 compared to the group with VWF ≤p88 in controls (0.80μg/ml, 0.63-0.94μg/ml vs. 0.98μg/ml, 0.81-1.23μg/ml, p= 0.051) and in patients (0.75μg/ml, 0.53-0.95μg/ml vs. 0.95μg/ml, 0.81-1.14μg/ml, p= 0.001). Next the population was categorized into subjects with VWF ≤p88 and ADAMTS13 >p10 (reference category: 52 patients, 79 controls), VWF ≤p88 and ADAMTS13 ≤p10 (4 patients, 6 controls), VWF >p88 and ADAMTS13 >p10 (12 patients, 8 controls) and VWF >p88 and ADAMTS13 ≤p10 (8 patients, 3 controls). The combination of high VWF and low ADAMTS13 increased VTE risk when compared to the reference category (OR 4.14; 95% CI 1.03-16.71). The risk did not substantially change with adjustment for acute phase proteins and ABO group, and it was attenuated when further adjusted for high FVIII (OR 3.41, 95% CI 0.80-14.70). No correlation was found between the time since the VTE event and levels of VWF, FVIII and ADAMTS13 (p>0.05). Conclusions our data suggest a potential effect of high VWF and low ADAMTS13 on VTE risk. An unbalance between these two interconnected proteins might have a role in the pathophysiology of VTE. Results should be interpreted with caution due to the wide 95% CI and to the attenuation of VTE risk with further adjustment for FVIII. In order to better explain our results studies with larger sample size are warranted. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Inhibition of von Willebrand factor–platelet glycoprotein Ib interaction prevents and reverses symptoms of acute acquired thrombotic thrombocytopenic purpura in baboons

Blood ◽  
2012 ◽  
Vol 120 (17) ◽  
pp. 3611-3614 ◽  
Author(s):  
Hendrik B. Feys ◽  
Jan Roodt ◽  
Nele Vandeputte ◽  
Inge Pareyn ◽  
Harald Mottl ◽  
...  
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
Von Willebrand Factor ◽  
Platelet Glycoprotein ◽  
Control Group ◽  
Severe Thrombocytopenia ◽  
Thrombocytopenic Purpura ◽  
Platelet Aggregates ◽  
New Treatment ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract The pathophysiology of thrombotic thrombocytopenic purpura (TTP) can be explained by the absence of active ADAMTS13, leading to ultra-large von Willebrand factor (UL-VWF) multimers spontaneously interacting with platelets. Preventing the formation of UL-VWF–platelet aggregates therefore is an attractive new treatment strategy. Here, we demonstrate that simultaneous administration of the inhibitory anti-VWF monoclonal antibody GBR600 and the inhibitory anti-ADAMTS13 antibody 3H9 to baboons (prevention group) precluded TTP onset as severe thrombocytopenia and hemolytic anemia were absent in these animals. In addition, partial VWF inhibition was not enough to prevent thrombocytopenia, demonstrating the specificity of this therapeutic strategy. GBR600 treatment of baboons during acute TTP (treatment group) resulted in a rapid recovery of severe thrombocytopenia similar to the platelet count increases observed in TTP patients treated by plasma exchange. Baboons in the control group only injected with 3H9 developed early stages of TTP as previously described. Hence, inhibiting VWF-GPIb interactions is an effective way to prevent and treat the early symptoms of acquired TTP in baboons.

scholarly journals Elevated Plasma von Willebrand Factor Antigen and Activity Levels Are Associated With the Severity of Coronary Stenosis

2020 ◽  
Vol 26 ◽  
pp. 107602961990055
Author(s):  
Bin Yan ◽  
Qi Wang ◽  
Weipeng Du ◽  
Suping Zhai ◽  
Chaoyang Gou ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Coronary Stenosis ◽  
Vital Role ◽  
Control Group ◽  
Activity Levels ◽  
Gensini Score ◽  
Subendothelial Matrix ◽  
Artery Disease ◽  
Von Willebrand ◽  
Willebrand Factor

von Willebrand factor (VWF) acts as a bridge between platelets and the subendothelial matrix following vessel damage and plays a vital role in coronary artery disease (CAD). The aim of this study was to investigate the association between VWF and the severity of coronary stenosis quantified by the Gensini score in acute myocardial infarction (AMI), the most dangerous complication of CAD. Plasma VWF antigen (VWF: Ag) and VWF-collagen binding (VWF: CB) in normal controls (n = 123) and in patients with AMI (n = 205) were tested, and then the patients were divided based on Gensini scores. The levels of VWF: Ag and VWF: CB in patients with AMI were significantly higher than those in the control group ( P < .001). Plasma levels of VWF: Ag and VWF: CB were positively correlated with both Gensini score and the number of affected vessels. Both VWF: Ag and VWF: CB were independent factors for coronary stenosis, adjusting confounding factors. Thus, the levels of VWF: Ag and VWF: CB were positively correlated with the severity of coronary stenosis. Screening of VWF at time of AMI may have prognostic value in terms of the severity of coronary stenosis.

A Comprehensive Study on Hemostasis in CAPD Patients Treated with Erythropoietin

2002 ◽  
Vol 22 (5) ◽  
pp. 582-592 ◽  
Author(s):  
Jolanta Malyszko ◽  
Ewa Suchowierska ◽  
Jacek S. Malyszko ◽  
Michal Mysliwiec
Keyword(s):  
Platelet Aggregation ◽  
Tissue Factor ◽  
Von Willebrand Factor ◽  
Factor Vii ◽  
Clot Lysis ◽  
Control Group ◽  
Primary Role ◽  
Baseline Values ◽  
Von Willebrand ◽  
Willebrand Factor

Objective Bleeding diathesis and simultaneous thrombotic complications may be seen in dialyzed patients. Erythropoietin (EPO) may shift the precarious balance of the hemostatic system toward thrombosis. Platelets and tissue factor (TF) play a major role in plug formation. Tissue factor pathway inhibitor (TFPI) appears to play a primary role in regulating TF-induced coagulation. Thrombin activatable fibrinolysis inhibitor (TAFI) is a key protein linking coagulation and fibrinolysis. The aim of the study was to assess whether 6 months of EPO therapy affects platelet function, that is, platelet aggregation and P-selectin level; moieties of the extrinsic coagulation pathway: TF, TFPI, and TFPI/Xa complexes, and factors VII and X; markers of ongoing coagulation: thrombin–antithrombin complexes (TAT) and prothrombin fragments 1+2; a marker of ongoing fibrinolysis: plasmin–antiplasmin complexes (PAP); fibrinolytic activity: euglobulin clot lysis time (ECLT); and markers of endothelial cell injury: von Willebrand factor, thrombomodulin, E-selectin, and TAFI, in continuous ambulatory peritoneal dialysis (CAPD) patients. Patients and Methods 22 patients on CAPD were given EPO 6000 U/week. 12 patients with chronic renal failure and 12 healthy volunteers served as control groups. All parameters were studied before, and after 1, 3, and 6 months of EPO therapy. Setting Department of Nephrology and Internal Medicine, Medical Academy of Bialystok, Poland. Results Platelet aggregation in whole blood did not change significantly during EPO treatment. A significant rise in arachidonic acid-induced platelet aggregation in platelet-rich plasma was observed after 3 and 6 months, and in collagen-induced platelet aggregation after 6 months of EPO therapy, compared to the baseline values. The TFPI concentration decreased significantly after 6 months of EPO therapy. The activity of factor VII increased transiently after 1 month of EPO therapy, compared to the baseline values. The TAFI concentration and activity in the CAPD group were significantly higher than in the control group. Erythropoietin therapy resulted in a significant decrease in TAFI concentration and activity after 6 months of EPO treatment. The ECLT was shortened significantly as early as after 1 month of EPO therapy. Thrombomodulin, von Willebrand factor concentration and activity, PAP, TAT, TFPI/Xa complexes, prothrombin fragments 1+2, factor X activity, P-selectin, E-selectin, and lipoprotein(a) did not change significantly during EPO treatment. Conclusion Erythropoietin treatment has a minimal effect on hemostasis in CAPD patients. A tendency toward a decline in TAFI is of unknown clinical relevance so far, and awaits further research.

Indicators of hemostasis in non-alcoholic liver steatosis (experimental and clinical study)

2021 ◽  
Vol 22 (3) ◽  
pp. 17-21
Author(s):  
A. M. Miftakhova ◽  
Keyword(s):  
Platelet Aggregation ◽  
Von Willebrand Factor ◽  
Liver Steatosis ◽  
Control Group ◽  
Thrombin Time ◽  
Alcoholic Fatty Liver ◽  
Mass Coefficient ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Alcoholic Fatty Liver Disease

Aim. Assessment of the morphological changes of the liver on the model of non-alcoholic steatosis in laboratory animals and hemostasis parameters in animals and patients with steatosis. Materials and methods. The experimental part of the study was conducted on 18 white rats divided into 2 groups: control (intact animals) and “Steatosis” (animals with liver steatosis modeled in laboratory conditions). The clinical part was performed on 52 patients with non-alcoholic fatty liver disease (the clinical form is non-alcoholic liver steatosis), with an average age of 43.0 ± 11.1 years and a body mass index of 37.2 ± 2.6. The control group consisted of 20 practically healthy individuals. At the end of the experiment, on the 30th day, the animals were removed from the experiment, direct blood sampling was performed from the right atrium, the liver mass and mass coefficient were determined, and a histological examination of the liver was performed. Laboratory tests included the determination of the following indicators of hemostasis in blood plasma: activity of the von Willebrand factor, platelet aggregation with ADP, collagen and ristocetin; prothrombin time, Quick prothrombin, international normalized ratio, thrombin time, activated partial thromboplastin time (APTT), fibrinogen and Hageman-dependent fibrinolysis. Results. In the experiment, the mass coefficient of the liver was significantly higher in the “Steatosis” group compared to the control group (3.75 (3.38-3.99) and 3.5 (3.3-3.6), respectively) (p = 0.009). Structural reorganization of the liver confirms the development of steatosis in animals. In animals with steatosis, a change in indicators reflecting the activity of the plasma link according to the external mechanism of coagulation was found: an elongation of the prothrombin time (p = 0.034), a decrease in the prothrombin index according to Quick (p = 0.018), an increase in INR (p = 0.027). APTT and thrombin time in animals with steatosis are higher than in the control, but these changes are not statistically significant (p = 0.181 and p = 0.364, respectively). The concentration of fibrinogen, Hageman-dependent fibrinolysis, platelet aggregation with ADP and the activity of the von Willebrand factor did not have statistically significant differences when comparing the two groups. In patients with steatosis, the number of platelets did not significantly differ from the control (p = 0.082). However, there was a decrease in aggregation with collagen (p = 0.002) and with ADP (p = 0.02). Platelet aggregation with ristocetin and the activity of the von Willebrand factor was higher than in the control (p = 0.001 and p = 0.01, respectively). In patients with steatosis, there was an extension of the APTT and an increase in the concentration of fibrinogen in comparison with the control, but these indicators did not go beyond the reference values of the set. The thrombin time was significantly prolonged in patients with steatosis in comparison with practically healthy individuals (p < 0.001). Conclusion. Non-alcoholic fatty liver disease is accompanied by a violation of the functioning of both vascular-platelet and coagulation hemostasis. There is a violation of the aggregation properties of platelets, signs of endothelial damage, hepatic coagulopathy.

Evaluation of ADAMTS-13 Activity and VWF:Ag Levels in Patients with Ischemic Stroke.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3507-3507
Author(s):  
Manuela Krause ◽  
Martina Boehm ◽  
Ingrid Stier-Brueck ◽  
Inge Scharrer
Keyword(s):  
Ischemic Stroke ◽  
Von Willebrand Factor ◽  
Thrombus Formation ◽  
The Elderly ◽  
Control Group ◽  
Healthy Controls ◽  
First Onset ◽  
The Mean ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Background: The role of von Willebrand factor cleaving protease (ADAMTS-13) in the pathogenesis of ischemic stroke is still undefined. ADAMTS-13 cleaves ultra-large multimers of von Willebrand factor (ULVWF), and is believed to regulate the size thus the activity of VWF, especially on sites of high shear stress. By assuming the hypothesis, that a deficiency of ADAMTS-13 influences the thrombotic tendency such as intravascular aggregation and platelet thrombus formation, we analysed adult patients with onset of cerebral ischemia. Methods and Patients: 158 unrelated patients (female:89 /male:69) with an objectively confirmed ischemic stroke (n=126) or TIA (n=32), median age at first onset:42 years (range:17–71 years), and 82 healthy subjects, median age:28 years (range:16–52 years), were studied. In our study group we analysed on the one hand 95 patients (pts) with early onset of stroke/TIA <45 years (median age:32 years), and on the other hand 63 elderly pts >45 years (median age:54 years). None of the pts enrolled had overt evidence of autoimmune or malignancy disease. ADAMTS13 was measured with an assay based on the positive correlation between multimeric size and Ristocetin Cofactor activity of the VWF. Results: In our population the ADAMTS-13 activity was in median 95% (range= 40–185%) significantly higher than 91% (range=52–150%) among controls (p=0.002; OR 0.54). In the subgroup analysis we found no statistical differences in the mean ADAMTS-13 activities among pts with early onser (99% vs 91%; p=0.76, OR 0.93), and among pts with onset at age 45 years as compared to healthy controls (88% vs 91%; p=0.30, OR 1.25). Furthermore, we found statistical differences in the mean VWF:Ag levels among all pts as compared to healthy controls (135% vs 110%; p=0.01, OR 0.63), and in the elderly pts (140% vs 110%; p=0.01, OR 1.63). The young pts showed no statistical differences in the mean VWF:Ag levels compared with the control group (127% vs 110%; p=0.98, OR 0.99). Conclusion: The results from this study show that higher levels of ADAMTS-13 activity and VWF:Ag as compared to healthy controls are associated with ischemic stroke/TIA. Only in the elderly pts we observed a tendency to a negative association between ADAMTS-13 and VWF (lower ADAMTS-13 levels and higher levels of VWF:Ag). It may be, that higher ADAMTS-13 levels have a relevance to prevent thrombotic events. Further studies are needed to confirm whether the relationship between VWF and ADAMTS-13 plays an additional role in the pathogenesis on the onset of ischemic stroke.

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