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      Resolution of a warfarin and dabigatran-resistant left atrial appendage thrombus with apixaban

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          Abstract

          The majority of embolisms associated with atrial fibrillation (AF) are from the left atrial appendage (LAA). To treat the existing thrombus, warfarin and novel anticoagulants have been used. However, there has been no clinical information regarding the difference of the effects of congealing the fibrinogenolysis system among these oral anticoagulants. Here, we report a case of persistent AF, in whom apixaban, factor Xa inhibitor resolved an LAA clot refractory to warfarin and direct thrombin inhibition. Factor Xa inhibitor, apixaban, could resolve the left appendage thrombosis refractory to warfarin and dabigatran.

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          Resolution of giant left atrial appendage thrombus with rivaroxaban.

          Georg Nickenig, Christoph Hammerstingl, B Pötzsch (2013)
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            Dabigatran and left atrial appendage thrombus.

            Gabriel Vanerio, A. Romero Vidal (2012)
            A 59-year-old white woman with previous history of arterial hypertension consulted because of palpitations. Atrial fibrillation of uncertain duration was diagnosed. She was not receiving anticoagulants. A trans-esophageal echocardiogram was performed, and a large left atrial appendage thrombus was detected. A strategy of rate control and anti-vitamin K treatment was started. On the subsequent days, we could not reach therapeutic INRs. Therefore, it was decided to stop warfarin and initiate dabigatran. We describe the evolution of the patient, the thrombus resolution, and a successful electrical cardioversion. In our comments, we summarize the natural history of left atrial thrombus, both with and without anticoagulant therapy. We also discuss the differences between warfarin and dabigatran.
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              Direct thrombin inhibitors, but not the direct factor Xa inhibitor rivaroxaban, increase tissue factor-induced hypercoagulability in vitro and in vivo

              E Perzborn, S Heitmeier, U Buetehorn … (2014)
              Background Increased hypercoagulability has been reported with low doses of direct thrombin inhibitors but not with direct factor Xa inhibitors. Objectives To compare the effects of rivaroxaban with those of melagatran and dabigatran on thrombin generation (TG) and tissue factor-induced hypercoagulability and to explore the possible involvement of the thrombin–thrombomodulin/activated protein C system. Methods In normal human plasma and in protein C-deficient plasma, TG was investigated in vitro in the presence and absence of recombinant human soluble thrombomodulin (rhs-TM). TG was determined by calibrated automated thrombography and an ELISA for prothrombin fragments 1+2 (F1+2). In an in vivo rat model, hypercoagulability was induced by tissue factor; levels of thrombin–antithrombin (TAT) and fibrinogen and the platelet count were determined. Results Rivaroxaban inhibited TG in a concentration-dependent manner. In the absence of rhs-TM, melagatran and dabigatran also inhibited TG concentration dependently. However, in the presence of rhs-TM, lower concentrations of melagatran (119–474 nmol L–1) and dabigatran (68–545 nmol L−1) enhanced endogenous thrombin potential, peak TG, and F1+2 formation in normal plasma but not in protein C-deficient plasma. In vivo, rivaroxaban dose-dependently inhibited TAT generation, whereas melagatran showed a paradoxical effect, with an increase in TAT and a small decrease in fibrinogen and platelet count at lower doses. Conclusion Low concentrations of the direct thrombin inhibitors melagatran and dabigatran enhanced TG and hypercoagulability, possibly via inhibition of the protein C system. In contrast, rivaroxaban reduced TG and hypercoagulability under all conditions studied, suggesting that it does not suppress this negative-feedback system.
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                Author and article information

                Contributors
                Yosuke Miwa
                Journal
                Journal ID (nlm-ta): J Arrhythm
                Journal ID (iso-abbrev): J Arrhythm
                Title: Journal of Arrhythmia
                Publisher: Elsevier
                ISSN (Print): 1880-4276
                ISSN (Electronic): 1883-2148
                Publication date PMC-release: 15 March 2016
                Publication date (Print): June 2016
                Publication date (Electronic): 15 March 2016
                Volume: 32
                Issue: 3
                Pages: 233-235
                Affiliations
                [0005]Department of Cardiology, Second Department of Internal Medicine, Kyorin University School of Medicine, Tokyo, Japan
                Author notes
                [* ]Correspondence to: Second Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan. Tel.: +81 422 47 5511; fax: +81 422 44 5137.Second Department of Internal Medicine, Kyorin University School of Medicine6-20-2 ShinkawaMitakaTokyo181-8611Japan y-miwa@ 123456ks.kyorin-u.ac.jp
                Article
                Publisher ID: S1880-4276(16)00031-4
                DOI: 10.1016/j.joa.2016.01.009
                PMC ID: 4913128
                PubMed ID: 27354873
                SO-VID: 7dc11a96-e312-463d-90bd-d949d071c53d
                Copyright © © 2016 Japanese Heart Rhythm Society
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 1 December 2015
                Date revision received : 11 January 2016
                Date accepted : 1 February 2016
                Categories
                Subject: Rapid Firing

                Keywords: factor xa inhibitor,left atrial appendage thrombus,direct thrombin inhibitor,atrial fibrillation
                Data availability:
                Keywords: factor xa inhibitor, left atrial appendage thrombus, direct thrombin inhibitor, atrial fibrillation

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