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The Potential of Plants as Treatments for Venous Thromboembolism
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Lilitha L. Denga, Namrita Lall
Coagulation is a physiological mechanism that prevents excessive bleeding by converting blood from a liquid to a gel state. Coagulation is regulated in a physiological pathway known as the coagulation cascade (Schenone, Furie, and Furie 2004). VTE is a condition where coagulation is upregulated, resulting in thrombosis and subsequently PE (Koupenova et al. 2017).
Postoperative Bleeding
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
The coagulation system is comprised of primary and secondary hemostasis. Platelet plug formation is the endpoint for primary hemostasis, while secondary hemostasis centers around thrombin. Thrombin is an enzyme that converts fibrinogen to fibrin and simultaneously activates platelet aggregation and the intrinsic and extrinsic pathways. Massive blood loss presents a challenge to the coagulation system. With loss of coagulation factors and thrombocytopenia comes coagulopathy (Curnow et al., 2016).
Congenital and acquired disorders of coagulation
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Jeanne M Lusher, Roshni Kulkarni
Acquired coagulation disorders are abnormalities in blood coagulation secondary to a large number of disorders. In contrast to the inherited coagulation disorders, which are often characterized by a single-factor deficiency, acquired disorders are complex and associated with multiple haemostatic abnormalities, including thrombocytopenia, platelet function defects, and vascular abnormalities. Furthermore, there is poor correlation between severity of bleeding and laboratory tests. While no specific replacement therapy exists, treatment of the underlying disorder is sometimes helpful in ameliorating the bleeding. The following are the most common acquired bleeding disorders.
Application of anti-Xa assay in monitoring unfractionated heparin therapy in contemporary antithrombotic management
Published in Expert Review of Hematology, 2023
Michael Safani, Steve Appleby, Ryan Chiu, Emmanuel J Favaloro, Emanuel T. Ferro, Jimmy Johannes, Milan Sheth
The coagulation pathways represent a cascade of events intended to provide a balance between procoagulant and anticoagulant processes and maintain hemostasis. Primary hemostasis consists of platelet activation, aggregation, and thrombus formation and aims to form a plug at the site of exposed endothelial cells due to tissue damage. Secondary hemostasis, as measured by the pathology laboratory, conventionally comprises three coagulation pathways. The intrinsic pathway is activated by endothelial damage and collagen exposure and includes factors I, II, IX, X, XI, and XII. The extrinsic pathway is activated by release of tissue factor by damaged endothelium and includes factors I, II, VII, and X. The common pathway consists of factors I, II, V, VIII, X. The intrinsic and extrinsic pathways converge to form a common pathway and at a specific point to activate fibrinogen to form fibrin polymer. In vivo, the final stages of primary and secondary hemostasis are marked by binding of fibrin polymers to platelets to secure and stabilize the platelet plug [37–41].
The antithrombosis effect of dehydroandrographolide succinate: in vitro and in vivo studies
Published in Pharmaceutical Biology, 2022
Bowen Yin, Shuhua Zhang, Yuxi Huang, Yuanzhu Long, Yiguo Chen, Shiyun Zhao, Aiqun Zhou, Minghua Cao, Xiaoming Yin, Daya Luo
We tested the activity of multiple coagulation factors in intrinsic and extrinsic pathways to explore the detailed mechanism by which DAS promoted secondary hemostasis. Through in vivo medication experiments in SD rats, we found that the MIC of FX was 100 mg/kg, the MIC of FV and FVII was 200 mg/kg, the MIC of FVIII was 300 mg/kg, and the MIC of FIX and FXI was 400 mg/kg. Compared with control conditions (FIIa = 89.21 ± 21.72%, FVa = 304.12 ± 79.65%, FVIIa = 324.19 ± 48.03%, FVIIIa = 524.79 ± 115.47%, FIX = 85.49 ± 27.87%, FXa = 34.90 ± 7.40%, FXIa = 38.12 ± 10.33%, FXIIa = 180.00 ± 25.33%), low-dose DAS activated the coagulation factors FV (470.84 ± 45.28%), FVII (600.46 ± 50.81%) and FX (89.93 ± 11.97%) (p < 0.05); medium-dose DAS activated the coagulation factors FV (443.44 ± 75.04%), FVII (632.12 ± 84.58%), FVIII (679.92 ± 143.34%), FIX (119.17 ± 31.12%), FX (89.88 ± 19.70%), and FXI (65.08 ± 15.39%) (p < 0.05); and high-dose DAS activated the coagulation factors FII (114.76 ± 23.92%), FV (414.84 ± 100.65%), FVII (790.66 ± 225.56%), FVIII (672.59 ± 179.16%), FX (102.76 ± 29.41%), FXI (65.47 ± 34.08%), and FXII (311.86 ± 146.20%) (p < 0.05). Aspirin had no effect on the activity of most coagulation factors, but it reduced the activity of FII (61.83 ± 8.95%) and FVIII (306.60 ± 29.96%) (p < 0.05) (Figure 5). Therefore, DAS might exert a potential procoagulant effect by enhancing the activity of various coagulation factors, and aspirin inhibited coagulation factors.
The role of viscoelastic testing in assessing peri-interventional platelet function and coagulation
Published in Platelets, 2022
Udaya S. Tantry, Jan Hartmann, Matthew D. Neal, Herbert Schöechl, Kevin P. Bliden, Seema Agarwal, Dan Mason, Joao D. Dias, Elisabeth Mahla, Paul A. Gurbel
A close interplay between platelets and coagulation is essential for the generation of a platelet-fibrin clot during hemostasis. In patients presenting with acute coronary syndromes, stroke, venous thromboembolism in the presence of existing endothelial dysfunction, systemic prothrombotic phenotype (hypercoagulability) results in a strong and occlusive platelet-fibrin clot[1]. Conversely, impaired hemostasis due to low platelet count or low coagulation proteins, and drug-induced inhibition of platelets or coagulation carries an increased risk for spontaneous and peri-interventional bleeding [2–6]. Laboratory tests such as blood count, international normalized ratio/prothrombin time (INR/PTI) and partial thromboplastin time, and Clauss fibrinogen are the current standard methods to assess platelet count and coagulation proteins. However, these tests have a long turnaround time, reflect a single aspect of coagulation, and therefore are suboptimal whenever urgent therapeutic decisions are requested peri-operatively, peri-interventional, or during trauma management [7].