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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
In addition to cascade amplification and fibrinogen conversion, thrombin is a potent activator of platelets (Brass 2003). Studies have shown that the protein components of platelets provide virtually all the specificity required for procoagulant activity and subsequent thrombin generation (Monroe, Hoffman, and Roberts 2002). Thrombin activates platelets and localizes them near a site of exposed TF, resulting in the release of partially active FV, FVIII and FIX (Manly, Boles, and Mackman 2011). Thrombin then cleaves the partially activated coagulation factors to fully active forms, which rapidly bind to the activated platelet (Figure 17.3).
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).
Haemostasis
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The propagation phase begins formation with the tenase (IXa–VIIIa) complex on platelet surfaces. The tenase complex generates large amounts of factor Xa that interacts with factor Va, forming the prothrombinase (factors Va–Xa) complex, which catalyses the conversion of prothrombin (factor II) to thrombin (factor IIa). Thrombin converts fibrinogen into fibrin monomers, which polymerize to form a stable fibrin clot. This burst of thrombin generation also produces a positive feedback by activating factors V, VIII and XI (Figure 53.4).
Clinical safety of low-dose anticoagulation with fondaparinux in patients undergoing peripheral endovascular treatment due to critical limb-threatening ischaemia – a pilot study
Published in Acta Cardiologica, 2021
Sorin Giusca, Michael Lichtenberg, Christoph Eisenbach, Grigorios Korosoglou
From a pathophysiological point of view, it has become increasingly recognised that arterial thrombosis results from a complex interplay of both platelet aggregation and thrombin formation. Thrombin plays a central role in clot formation by both stimulating platelet activation and catalysing procoagulant pathways, which results in fibrin deposition [15]. In the same line, earlier experimental studies demonstrated that the initiation of blood coagulation in the arterial system combines the activation of both plasmatic and cellular components of the coagulation system [16]. From a clinical point of view, acute coronary syndromes and CLTI share significant similarities, both events being the endpoint in a cascade of atherothrombotic processes, occurring in the coronary and peripheral vascular territory, respectively [17]. Recent data from amputation specimens of patients with CLTI on the other hand, showed that atherothrombotic occlusions are frequently observed in such patients, especially in BTK occlusive disease in the presence of insignificant atherosclerotic disease [7]. These data together with previous experimental observations further support the notion of a dual pathway inhibition, i.e. the therapeutic administration of anticoagulation and antiplatelet agents in patients with PAD, especially after percutaneous interventions, which itself leads to platelet hyperreactivity due to endothelial activation after balloon dilatation [18].
Biochemical and immunological aspects of COVID-19 infection and therapeutical intervention of oral low dose cytokine therapy: a systematic review
Published in Immunopharmacology and Immunotoxicology, 2021
Ratheesh M, Sheethal S, Svenia P. Jose, Sony Rajan, Sulumol Thomas, Tariq Jagmag, Jayesh Tilwani
Coagulation pathway is responsible for clot formation with the help of thrombin by the activation of platelets and conversion of fibrinogen to fibrin. Thrombin can intensify inflammatory condition through proteinase activated receptors (PARs). PAR-1 is the major thrombin receptor which facilitates platelet aggregation along with the relationships between coagulation, fibrosis and inflammation. So, thrombin is strictly controlled by a negative feedback mechanism and is assisted by physiological anticoagulants [46]. During an inflammatory condition, all these mechanisms will be compromised by an imbalanced production and consumption of anticoagulants. This will induce microthrombosis and cause intravascular coagulation which will finally lead to multiple organ failure. Evidence show that intravascular thrombosis and fibroproliferative lung disease are the common medical conditions seen in patients with severe SAR-CoV-2 infection and non survivors [13,46,47].
Aspirin and low-dose rivaroxaban – the dual pathway concept in patients with stable atherosclerotic disease: a comprehensive review
Published in Expert Review of Cardiovascular Therapy, 2020
Eliot Parascandolo, Alon Eisen
Rivaroxaban is another anti-thrombotic drug which primarily works on the coagulation cascade. Rivaroxaban works via direct, selective, and reversible inhibition of free and bound Factor Xa. The drug works on both the intrinsic and extrinsic pathways leading to an inhibition of prothrombin activator which would subsequently activate prothrombin to thrombin. Thrombin activates platelets and catalyzes the conversion of fibrinogen to fibrin which stabilizes platelet aggregates. Blocking this action diminishes clot formations via inhibition of the secondary hemostatic system. Rivaroxaban is efficacious at lowering the risk of MI and mortality in patients with a recent acute coronary syndrome [10]. Its current indications include: stroke prevention in non-valvular atrial fibrillation, treatment of pulmonary embolism/deep vein thrombosis, and prevention of venous thromboembolism (VTE), prevention of atherothrombotic events in adults with CAD, prevention of atherothrombotic events in adults with PAD, secondary prevention in ACS, and prevention of VTE after elective hip/knee replacement surgery [11].