The Pathogenesis of Venous Thromboembolism: Evidence for Multiple Interrelated Causes

Abstract

Additional thrombophilic defects and exogenous risk factors increase the risk for VTE in persons with hereditary deficiencies of protein S, protein C, or antithrombin and provide evidence that multiple genetic and environmental risk factors contribute to VTE.

Different risk of deep vein thrombosis and pulmonary embolism in carriers with factor V Leiden compared with non-carriers, but not in other thrombophilic defects. Results from a large retrospective family cohort study

“…[13][14][15][16][17] Between May 1998 and July 2004, first-degree relatives aged 15 ABSTRACT years or older of consecutive patients (probands) with documented venous thrombosis (i.e. deep vein thrombosis or pulmonary embolism) or any documented arterial thrombosis before the age of 50 years, were enrolled after obtaining informed consent.…”

Profilaxia da trombose venosa profunda: aplicação prática e conhecimento teórico em um hospital geral

“…Stasis, endothelial lesion and hypercoagulability, combined or alone, are factors associated with its etiopathogenic genesis. 1 DVT, which has multidisciplinary occurrence, is a frequent and severe entity, mainly resulting from other surgical or clinical affections. Its most severe complications are acute pulmonary embolism (PE) and late postthrombotic syndrome.…”

Progressive chromogenic anti-factor Xa assay and its use in the classification of antithrombin deficiencies

“…The relative risk of VTE in patients with AT deficiency was estimated to be approximately 25-50-fold [29][30][31][32]. AT deficiency also represents an increased risk of pulmonary embolism and recurrence of VTE [16,33,34].…”

“…The diluted plasma was incubated with 50 μL 12 nkat/mL FXa for 300 s at 37 °C. Then, 50 μL 1.25 mg/mL BIO-PHEN CS-11 (32) [Suc-IIe-Gly-(γPip)Gly-Arg-pNA, HCl] chromogenic substrate (Hyphen BioMed, Neuville sur Oise, France) was added and the release of pNA by uninhibited FXa was recorded at 405 nm for 60 s. The same assay components were used for the determination of hc activity, with the following exceptions: in this case polybrene was replaced by 1 U/mL heparin in the dilution buffer, the dilution of plasma samples was 50-fold and the incubation with FXa was shortened to 60 s. The ΔA/min values were converted to percentage of mean normal anti-FXa activity. Calibration curve was set-up by measurement on dilutions of HemosIL™ Calibration plasma (Instrumentation Laboratory, Milano, Italy) recalibrated on the mean p-anti-FXa activity and hc-anti-FXa activity in the reference population as 100%.…”

“…Anti-FXa determinations were also performed on the plasma samples from 24 first-degree relatives of the patients, in which causative AT mutation was excluded by DNA sequencing. The reference sample group consisted of 188 apparently healthy individuals, 104 females and 84 males, median age: 34 [interquartile range (IQR): [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. Exclusion criteria for the healthy group were the history of arterial and venous thrombosis and, in the case of women, being on oral contraceptive or pregnancy.…”