Determination of ADAMTS13 Antigen and Activity Levels in Patients with Acute Myocardial Infarction and Acute Ischemic Stroke.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3987-3987
Author(s):  
Ningzheng Dong ◽  
Fang Liu ◽  
Shundong Ji ◽  
Changgeng Ruan
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ischemic Stroke ◽  
General Population ◽  
Von Willebrand Factor ◽  
Arterial Thrombosis ◽  
Activity Levels ◽  
Adamts13 Activity ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract von Willebrand factor-cleaving protease (ADMTS13) is a metalloproteases regulating von Willebrand factor multimers size in plasma, its activity decrease has been reported in many physiological and pathological conditions. But information on ADAMTS13 in arterial thrombosis disease and in the general population is limited. In this study, we investigated the ADAMTS13 antigen and activity levels in 87 healthy control subjects of different ages, in 93 patients with acute myocardial infarction (AMI) and in 30 patients with acute ischemic stroke (AIS). ADAMTS13 Antigen levels were measured using a sandwich ELISA, and ADAMTS13 activity levels were analyzed by the FRETS-VWF73 method. A pool of plasma obtained from 40 blood donors was used as reference and was defined to contain 100% of the protease. The individual subject of the pool was not included in the study. Compared with 50 sex- and age-matched control subjects, ADAMTS13 antigen and activity levels were significantly lower in patients with arterial thrombosis diseases. Antigen levels were 87.8±19.8%, 61.8±18.8%, and 70.2±15.5% respectively in control, AMI and ASI patients. ADAMTS13 activity were 81.7±13.9%, 59.2±22.1% and 65.4±15.8% respectively. In the 87 healthy subjects, the range of ADAMTS13 activity is from 46.3% to 119.0%, and antigen is from 60.8% to 141.9%. In different age groups (17 to 20 years old, 21 to 40 years old, 41 to 60 years old, and older than 60 years old), ADAMTS13 antigen levels were 76.0%, 109.7%, 99.3%, and 74.5% respectively, and activity levels were 80.8%, 81.1%, 77.9%, and 87.3% respectively. It seems the antigen reached the highest level in people from 21 to 40 years old, then gradually decreased with age. The antigen and activity mean in males (87.1% and 80.8%) was lower than that in females (94.7% and 86.1%), but the difference is not significant (p=0.145 and p=0.124). In conclusion, the decrease of ADAMTS13 antigen and activity in AMI and AIS patients indicated ADMATS13 might contribute to arterial thrombosis, and the plasma ADAMTS13 antigen level in the general population was significantly affected by age.

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

2020 ◽  
Author(s):  
Stephen J. X. Murphy ◽  
Soon Tjin Lim ◽  
Fionnuala Hickey ◽  
Justin A. Kinsella ◽  
Deirdre R. Smith ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Carotid Stenosis ◽  
Blood Group ◽  
Von Willebrand Factor ◽  
Adamts13 Activity ◽  
Von Willebrand Factor Antigen ◽  
Asymptomatic Patients ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Antigen

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.

scholarly journals Low ADAMTS13 Activity Correlates with Increased Mortality in COVID-19 Patients

2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S6-S7
Author(s):  
Joseph Sweeney ◽  
Mohammad Barouqa ◽  
Gregory Krause ◽  
Jesus Gonzalez Lugo ◽  
Shafia Rahman ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Hospitalized Patients ◽  
Activity Level ◽  
Activity Levels ◽  
Adamts13 Activity ◽  
Cut Point ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor ◽  
D Dimer

Abstract Systemic inflammation and coagulopathy are characteristic hallmarks of COVID19. “COVID coagulopathy” manifests mainly as a prothrombotic state affecting both large and small blood vessels, and presenting as arterial, venous, and microangiopathic thrombotic events with von Willebrand factor (VWF) and soluble thrombomodulin increased in hospitalized patients. The causes of coagulopathy are poorly understood. Aim: To investigate the relationship between von Willebrand factor (VWF) biomarkers, intravascular hemolysis, coagulation, and organ damage in COVID19 patients and to study their association with disease severity and mortality. Methods: 181 hospitalized adult COVID19 patients were randomly selected with a balanced distribution of survivors and non-survivors during the period of March 26th 2020 to May 5th 2020. The medical records and laboratory values were reviewed. Statistical analysis was performed using R studio V.3.6.2. Results: Patients who died (n=90) had significantly lower ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) activity, elevated lactate dehydrogenase levels, increased schistocyte/RBC fragment counts, and elevated VWF antigen and activity levels compared to patients discharged alive (n=91). In 31 patients, we measured several of these biomarkers on two or more occasions. The trending of ADAMTS13 activity illustrated that it is not steady throughout the hospitalization course. ADAMTS13 activity levels tended to improve and/or reach normal levels in patients that survived, yet ADAMTS13 activity levels worsened in most patients that died. Likewise, the VWF antigen and activity levels tended to decrease in patients that survived whereas tended to increase well above the normal range (2-3 folds) in patients that died. D-Dimer levels trended downwards in survivors, sometimes to levels less than 1 µg/ml, yet tended to increase in patients who died. Given the relationship between ADAMTS13 activity and mortality, we wanted to determine a cut-point of initial ADAMTS13 activity (within 72 hours from admission) to predict mortality. 102 patients in our cohort had an ADAMTS13 activity measurement within this timeframe. We determined that this optimal cut-point of initial ADAMTS13 activity was 43% using Youden’s J statistic. Only 30% of patients who had an ADAMTS13 activity level of less than 43% on admission survived, yet 60% of patients survived who had an ADAMTS13 activity level of greater than 43% on admission. Conclusions: COVID-19 may present with low ADAMTS13 activity in a subset of hospitalized patients. Presence of schistocytes/RBC fragment and elevated D-dimer levels on admission may warrant a work-up for ADAMTS13 activity and VWF antigen and activity levels. These findings indicate the need for future investigation to study the relationship between endothelial and coagulation activation and the efficacy of treatments aimed at prevention and/or amelioration of microangiopathy in COVID-19.

Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

1992 ◽  
Vol 68 (06) ◽  
pp. 678-682 ◽  
Author(s):  
F Andreotti ◽  
D R Hackett ◽  
A W Haider ◽  
M C Roncaglioni ◽  
G J Davies ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasminogen Activator Inhibitor ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor

SummaryPlasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and ≥ 50% resolution of maximal ST-deviation on the electrocardiogram.Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.

Decreased beta2-Glycoprotein I Plasma Levels as a Risk Factor for Myocardial Infarction in Men.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1813-1813
Author(s):  
Bas De Laat ◽  
Philip G. de Groot ◽  
Ronald H.W.M. Derksen ◽  
Rolf T. Urbanus ◽  
Koen Mertens ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Confidence Interval ◽  
Von Willebrand Factor ◽  
Plasma Levels ◽  
Odds Ratio ◽  
Arterial Thrombosis ◽  
Glycoprotein I ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Background: Several factors influence the occurrence of acute myocardial infarction. One of these factors is thought to be Von Willebrand Factor which serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2- glycoprotein I is able to inhibit platelet binding to von Willebrand Factor by binding to the A1 domain of Von Willebrand Factor 1. This could indicate that beta2-glycoprotein I possesses antithrombotic properties with respect to arterial thrombosis. In the present study we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. Methods and Results: We have measured beta2-glycoprotein I and Von Willebrand Factor antigen levels in 539 men with a first myocardial infarction and in 611 control subjects who participated in the case-control Study of Myocardial Infarction Leiden (SMILE). Although we did not find a profound effect of beta2-glycoprotein I plasma levels on myocardial infarction in the overall population (odds ratio 0.93, 95% confidence interval 0.65–1.33), there appeared to be a dose-dependent protective effect of increasing beta2-glycoprotein I plasma levels on myocardial infarction in men of 60 years and older. In this age group we found an odds Ratio of 0.44 (95% confidence interval 0.25–0.77) for high beta2-glycoprotein I levels compared to low levels. Furthermore, high plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of Von Willebrand Factor. In addition, we studied a possible association between age and Von Willebrand Factor and beta2-glycoprotein I plasma levels. It appeared that both Von Willebrand Factor and beta2-glycoprotein I plasma levels increased with age, but a larger increase in Von Willebrand Factor plasma levels was observed than in beta2-glycoprotein I plasma levels (13.7 % every 10 years versus 5.7% every 10 years). Conclusions: In this study high circulating levels of beta2-glycoprotein I appeared to be associated with a lower risk of myocardial infarction in men over 60 years. In addition we observed a larger increase in Von Willebrand Factor levels with age than beta2- glycoprotein I levels. As beta2-glycoprotein I possesses antithrombotic properties by inhibiting the activity of Von Willebrand Factor in-vitro, this might indicate that during aging the haemostatic balance slowly shifts to a more prothrombotic state 1. Future in-vivo experiments are needed to investigate the exact contribution of beta2-glycoprotein I on the pathophysiology of myocardial infarction and arterial thrombosis in general.

Sign in / Sign up

Export Citation Format

Share Document