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Outcomes assessment for chronic venous disease
Published in Peter Gloviczki, Michael C. Dalsing, Bo Eklöf, Fedor Lurie, Thomas W. Wakefield, Monika L. Gloviczki, Handbook of Venous and Lymphatic Disorders, 2017
Michael A. Vasquez, Linda Harris
There are no widely used tools to guide the assessment of risk status and the appropriate timing of the discontinuation of anticoagulation. Several studies have assessed risk of recurrence. In an evaluation of idiopathic DVT, prior pulmonary embolism (PE) increased the risk of recurrent PE and DVT (60% recurrent PE). However, risk of any recurrence after isolated calf or upper extremity DVT was rare.26 Recurrence was highest in patients who had multiple VTE, and 27.9% after a second DVT. Fewer data were available for multiple provoked VTE. Factors that increased risk included male gender, increased body weight, cancer, metastatic cancer, chemotherapy, continued oral contraceptives or hormone-replacement therapy, residual vein thrombosis, antithrombin deficiency, factor V Leiden, or G20210A. It is unknown whether these factors are additive. Several laboratory tests have been correlated with an increased risk of recurrence, including D-dimer level (>250 ng/mL after discontinuation of anticoagulation) and endogenous thrombin potential >100%. In the AUREC study, endogenous thrombin potential and D-dimer level were independent predictors of recurrence, and this was confirmed in other studies.27,28
Use of thrombomodulin-modified thrombin generation in uncomplicated pregnancy: the normal range and prothrombotic phenotype
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Feng Dong, Zhongxing Lv, Ping Di
The main TGT parameters were the following: (1) endogenous thrombin potential (ETP) (nM*min, the area under the curve) represented the amount of thrombin and was driven by the balance between procoagulants and anti-coagulants; (2) Lagtime (minutes, time to fibrin clot formed) represented the formation time of the first amounts of thrombin; (3) Peak Height (nM, maximal thrombin concentration); (4) Time to peak(ttPeak) (minutes, time to reach the maximal thrombin concentration). ETP ratio was a calculated value, which was the ETP in the presence of TM divided the ETP in the absence of TM. The ratio represented the anticoagulation role in PC system and could be taken as an index of procoagulant imbalance. All samples were tested in triplicate respectively and detected with an IQC (mixed plasma from normal people) to minimize the inter-assay variability.
Effects of platelets activated by different agonists on fibrin formation and thrombin generation
Published in Platelets, 2023
Ivan A. Muravlev, Anatoly B. Dobrovolsky, Olga A. Antonova, Svetlana G. Khaspekova, Alexey V. Mazurov
Platelets treated with the same agonists and prepared in the same way as in PRA (sedimentation in 96-well plates) were tested for their ability to accelerate thrombin generation. Tissue factor with minimum amount of phospholipids was used as a trigger reagent. As in PRA, in TGT platelets were exposed to endogenous thrombin formed after initiation of the coagulation cascade. Typical thrombin generation curves are given in Figure 3 and statistical data in Table II. Very low concentrations of thrombin were detected when the reaction was performed without platelets. Platelets which were not treated with exogenous agonists induced a 3- to 4-fold increase in endogenous thrombin potential (ETP), thrombin peak and maximum rate of thrombin generation. The effect on lag phase was much less pronounced: it shortened by about 15%. Incubation with exogenous agonists had no effect on lag phase and ETP (lag phase slightly shortened only in the presence of A23187) but markedly increased peak and maximum rate of thrombin generation. Thrombin generation was accelerated almost in the same order as fibrin formation in PRA: A23187 >> collagen > arachidonic acid > TRAP > ADP ≈ no agonist. Weak effect of TRAP in TGT could be explained by its competition with exogenous thrombin.
Platelets compensate for poor thrombin generation in type 3 von Willebrand disease
Published in Platelets, 2020
Timea Szanto, Vuokko Nummi, Annukka Jouppila, Herm Jan M. Brinkman, Riitta Lassila
TG was measured in platelet-poor (PPP) and -rich (PRP) plasma by Calibrated Automated Thrombography (CAT, Thrombinoscope, Maastricht, the Netherlands) [21–23]. Briefly, in 96-well microtiter plates, 80 μL of PPP/PRP were supplemented with 20 μL of either inner method Calibrator or tissue factor (TF) reagent comprised of 1 pM TF and 4 µM phospholipids in PPP (PPP Reagent Low), and compatibly 1 pM TF without exogenous phospholipids in PRP (PRP reagent). TG was initiated by FluCA reagent mixture (20 μL) (all reagents from Thrombinoscope, Stago). PPP was prepared by double (2000 g and 10 000 g, both 10 min), and PRP by a single (180 g, 10 min), centrifugation. Platelet count in PRP was adjusted to 150 × 109/L by adding autologous PPP. Adjusted final platelet count in PRP was confirmed with a Sysmex KX-21 cell calculator (Sysmex, Kobe, Japan). All measurements were carried out in triplicates for at least 60 min. We followed peak thrombin, endogenous thrombin potential (ETP), and lag time, and included 14 healthy controls.