Differences between activities of coagulation factors after one month of therapy with different direct oral anticoagulant in pulmonary embolism patients

Abstract

Summary What is known and Objective Direct oral anticoagulants (DOACs) are frequently used for the treatment of pulmonary embolism (PE), but both clinical and laboratory data comparing their efficacy and safety are conflicting. This study investigated and compared the impact of three DOACs (apixaban, rivaroxaban and dabigatran) on coagulation cascade in acute PE patients. Methods After the initial treatment, acute PE patients were randomly allocated to one of three groups, and treatment continued using one of the three DOACs. Following 1 month of treatment, the activity of factors II, VII and VIII, as well as protein C, antithrombin, D‐dimer and fibrinogen, were measured, and the values were compared between the groups. Results and Discussion One hundred consecutive PE patients were included. The mean values for the activity of factors II and VII and protein C were higher in patients on apixaban than in patients on rivaroxaban (1.45 ± 1.12 (IU/mL) vs 1.13 ± 0.92 (IU/mL), P < 0.001; 1.24 ± 1.10 (IU/mL) vs 1.05 ± 0.98 (IU/mL), P = 0.024 and 1.15 ± 0.62 vs 1.02 ± 0.68 (IU/mL), P = 0.019, respectively). The mean of factor II activity and the median of factor VIII activity were also significantly higher in patients on apixaban than in patients on dabigatran (1.45 ± 1.12 vs 1.20 ± 0.96 (IU/mL), P = 0.003 and 2.9 (2.0‐4.0) vs 2.1 (1.5‐2.7) (IU/mL), P = 0.001, respectively). No difference was noticed in D‐dimer concentrations, or in the activity of the other factors measured. Additionally, no difference was noticed between the rivaroxaban and dabigatran groups. What is new and Conclusion Apixaban had a significantly higher thrombin activity, above the laboratory determined normal range, compared to patients on rivaroxaban and dabigatran. This higher thrombin activity in patients on apixaban may contribute to a better haemostatic response during the therapy or increased prothrombotic state after therapy interruption.

Research progress on biomarkers of pulmonary embolism

“…21 Distortion of coagulation factors in blood also induces the occurrence of PE. Until now, the highly acknowledged predisposing coagulation-related factors in blood for PE have been already identified to mainly include coagulation factor II, factor IV, factor VII, factor VIII, factor V Leiden, factor X, factor XIII, prothrombin fragment 1 + 2, antithrombin III, tissue factor, protein C, and protein S. [22][23][24] Nils Kucher et al proposed that PE patients had lower levels of FXIII A subunit antigen, compared with those who have suspected but excluded PE. 25 Recent report shows that factor II and X activity can be used as the therapeutic markers of warfarin in Chinese PE patients.…”

D-Dimer and Fibrinogen Values according to the Localization of Deep Venous Thrombosis

“…3 D-dimer and fibrinogen are sensitive, but nonspecific, biomarkers used for the diagnosis of venous thromboembolism (VTE). 4 5 6 7 8 9 10 D-dimer to fibrinogen ratio may be a better predictor for the diagnosis and the outcomes of VTE, with a higher specificity than D-dimer alone. 11 When used in the diagnosis of VTE as an isolated marker, specificity of D-dimer is below 50%.…”