Monary embolism, and prevention of recurrent DVT and pulmonary embolism in > 자유게시판

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Monary embolism, and prevention of recurrent DVT and pulmonary embolism in adults, and is now approved in the EU, in combination with antiplatelet agents, for the prevention of atherothrombotic events in adults who have acute coronary syndromes and elevated cardiac biomarkers [3,4,9]. The mechanisms of action of anticoagulant agents have an important role in the prolongation of clotting time in tests such as the prothrombin time (PT) test. VKAs interfere with the carboxylation of glutamate residues in Factors II, VII, IX and X, with the result that the coagulant activity of these factors is diminished. Direct Factor Xa inhibitors limit thrombogenesis via selective inhibition of Factor Xa without requiring cofactors such as antithrombin [10]. Direct thrombin inhibitors target thrombin and, likewise, do not require cofactors?2013 Samama et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Samama et al. Thrombosis Journal 2013, 11:11 http://www.thrombosisjournal.com/content/11/1/Page 2 ofsuch as antithrombin [11]. Both classes of anticoagulant agents have predictable, dose-dependent anticoagulant effects [12]. Rivaroxaban inhibits free Factor Xa and prothrombinase activity as well as clot-bound Factor Xa, thus effectively blocking thrombin generation [13]. Inhibition of Factor Xa activity by rivaroxaban is closely correlated to its plasma concentration. Anti-Factor Xa activity can be measured to indicate rivaroxaban exposure. As with apixaban and dabigatran, rivaroxaban does not require routine coagulation monitoring or dose titration (unlike VKAs and UFH). However, a reliable laboratory assay that could measure exposure to rivaroxaban may be necessary or helpful in certain clinical circumstances (e.g. prior PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/3081428 to urgent surgery, for perioperative management of those receiving rivaroxaban, for patients with thromboembolic or bleeding events, or for suspected overdose). Because rivaroxaban and other target-specific oral anticoagulants have different mechanisms of action from traditional anticoagulant agents, laboratory tests used for these traditional agents (such as PT/international normalised ratio [INR] or activated partial thromboplastin time) are not suitable for targetspecific oral anticoagulants [14]. This article will summarise the pharmacokinetics and pharmacodynamics of rivaroxaban and provide information and guidance on laboratory tests that can be PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/3081428 used for the measurement of rivaroxaban in clinical practice.At total daily oral doses of rivaroxaban of 5?0 mg, Cmax ranges (mean values) from 3-Chloro-5-cyclopropylpyridine 40 g/l to 400 g/l, and minimum plasma concentration (Ctrough) (mean values) from 8 g/l to 160 g/l (data derived from phase II studies of rivaroxaban in patients undergoing hip replacement surgery, patients with DVT or patients with acute coronary syndrome; Table 1) [17-19]. No relevant accumulation occurs beyond steady state in healthy individuals [20]. Elimination of rivaroxaban from plasma occurs with a 1-(5-(Aminomethyl)-2-nitrophenyl)ethanol terminal half-life of 5? hours in young individuals [3,20] and 11?3 hours in the elderly [3,21]. Rivaroxaban has a dual mode of elimination. Of the administered dose, approximately two-thirds undergoes metabolic degradation, half of which is eliminated renally and the other half by the hepatobil.