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Journal articles on the topic 'Rivaroxaban'

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Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Petzold, Tobias, Manuela Thienel, Lisa Dannenberg, Philipp Mourikis, Carolin Helten, Aysel Ayhan, René M’Pembele, et al. "Rivaroxaban Reduces Arterial Thrombosis by Inhibition of FXa-Driven Platelet Activation via Protease Activated Receptor-1." Circulation Research 126, no. 4 (February 14, 2020): 486–500. http://dx.doi.org/10.1161/circresaha.119.315099.

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Rationale: A reduced rate of myocardial infarction has been reported in patients with atrial fibrillation treated with FXa (factor Xa) inhibitors including rivaroxaban compared with vitamin K antagonists. At the same time, low-dose rivaroxaban has been shown to reduce mortality and atherothrombotic events in patients with coronary artery disease. Yet, the mechanisms underlying this reduction remain unknown. Objective: In this study, we hypothesized that rivaroxaban’s antithrombotic potential is linked to a hitherto unknown rivaroxaban effect that impacts on platelet reactivity and arterial thrombosis. Methods and Results: In this study, we identified FXa as potent, direct agonist of the PAR-1 (protease-activated receptor 1), leading to platelet activation and thrombus formation, which can be inhibited by rivaroxaban. We found that rivaroxaban reduced arterial thrombus stability in a mouse model of arterial thrombosis using intravital microscopy. For in vitro studies, atrial fibrillation patients on permanent rivaroxaban treatment for stroke prevention, respective controls, and patients with new-onset atrial fibrillation before and after first intake of rivaroxaban (time series analysis) were recruited. Platelet aggregation responses, as well as thrombus formation under arterial flow conditions on collagen and atherosclerotic plaque material, were attenuated by rivaroxaban. We show that rivaroxaban’s antiplatelet effect is plasma dependent but independent of thrombin and rivaroxaban’s anticoagulatory capacity. Conclusions: Here, we identified FXa as potent platelet agonist that acts through PAR-1. Therefore, rivaroxaban exerts an antiplatelet effect that together with its well-known potent anticoagulatory capacity might lead to reduced frequency of atherothrombotic events and improved outcome in patients.

2

Hawes, Emily M., Allison M. Deal, Dorothy M. Adcock, Robert Gosselin, Cheryl Jeanneret, Kenneth D. Friedman, Stephan Moll, and Suzanne J. Francart. "Performance of coagulation tests in patients on therapeutic doses of rivaroxaban." Thrombosis and Haemostasis 111, no. 06 (2014): 1133–40. http://dx.doi.org/10.1160/th13-10-0871.

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SummaryKnowledge of anticoagulation status during rivaroxaban therapy is desirable in certain clinical situations. It was the study objective to determine coagulation tests most useful for assessing rivaroxaban’s anticoagulant effect. Peak and trough blood samples from 29 patients taking rivaroxaban 20 mg daily were collected. Mass spectrometry and various coagulation assays were performed. “On-therapy range” was defined as the rivaroxaban concentrations determined by LC-MS/ MS. A “misprediction percentage” was calculated based on how often results of each coagulation assay were in the normal reference range, while the rivaroxaban concentration was in the “on-therapy” range. The on-therapy range was 8.9 – 660 ng/ml. The misprediction percentages for prothrombin time (PT) and activated partial thromboplastin time (aPTT), using multiple reagents and coagulometers, ranged from 10% – 52% and 31% – 59%, respectively. PT, aPTT and activated clotting time (ACT) were insensitive to trough rivaroxaban: 59%, 62%, and 80% of samples had a normal result, respectively. Over 95% of PT and ACT values were elevated at peak. Four different rivaroxaban calibrated anti-Xa assays had R2 values >0.98, demonstrating strong correlations with rivaroxaban drug levels. In conclusion, PT, aPTT and ACT are often normal in patients on therapeutic doses of rivaroxaban. However, PT and ACT may have clinical utility at higher drug plasma levels. Rivaroxaban calibrated anti-factor Xa assays can accurately identify low and high on-therapy rivaroxaban drug levels and, therefore, have superior utility in all clinical situations where assessment of anticoagulation status may be beneficial.This trial is registered at www.clinicaltrials.gov (#NCT01743898).

3

Jennings, Sin-Ling T., Khanh N. P. Manh, and Jusilda Bita. "Morbidly Obese Patient on Rivaroxaban Presents With Recurrent Upper Extremity Deep Vein Thrombosis: A Case Report." Journal of Pharmacy Practice 33, no. 5 (June 23, 2019): 712–19. http://dx.doi.org/10.1177/0897190019851358.

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A morbidly obese patient with history of deep vein thrombosis and pulmonary embolism was diagnosed with an acute left upper extremity deep vein thrombosis and started on rivaroxaban. Three months later, the patient returned with swelling in the right arm and was found to have a right brachial thrombosis. Anticoagulant therapy was switched to a low-molecular-weight heparin, and patient was discharged on enoxaparin along with an order to follow-up with a hematologist. Subanalyses from randomized controlled trials, pharmacokinetic/pharmacodynamic, and real-world studies suggest that rivaroxaban may be effective and safe in morbidly obese patients for primary and secondary prevention of venous thromboembolism. However, the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis does not recommend the use of direct-acting oral anticoagulants in this population. If used, drug levels should be monitored to guide the therapy. Due to the disparity in data to show efficacy and safety of rivaroxaban in morbidly obese subjects, the interpatient variability of rivaroxaban’s effects in subjects, and the lack of defined therapeutic range for rivaroxaban drug concentration, rivaroxaban should be used cautiously in this population.

4

Weiss, Luisa, Paulina Szklanna, Tadhg Prendiville, Karl Egan, Sarah Kelliher, Aine Lennon, Eugene Dillon, et al. "Comprehensive Multi-Parameter Characterisation of Circulating Extracellular Vesicles from Rivaroxaban-Treated VTE Patients Reveals Reduced Inflammation and Ameliorated Endothelial Dysfunction." Blood 138, Supplement 1 (November 5, 2021): 3210. http://dx.doi.org/10.1182/blood-2021-146131.

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Abstract Venous Thromboembolism (VTE) remains a significant cause of morbidity and mortality worldwide. Rivaroxaban, a direct oral factor Xa inhibitor, mediates anti-inflammatory and cardiovascular-protective effects besides its well-established anticoagulant properties, however, these remain poorly characterized. Extracellular vesicles (EVs) are important circulating messengers regulating a myriad of biological and pathological processes and may be highly relevant to the pathophysiology of VTE as they reflect alterations in platelet and endothelial biology. However, the effects of Rivaroxaban on circulating pro-inflammatory EVs in VTE patients remain unknown. We hypothesized that rivaroxaban's anti-inflammatory properties are reflected upon differential molecular profiles of circulating EVs. Single-episode VTE patients anticoagulated with 20 mg Rivaroxaban or warfarin at a target INR of 2.0-3.0, respectively, who had commenced therapy no sooner than 3 months previously were recruited following informed written consent at the Mater Misericordiae University Hospital, Dublin, Ireland. Patient data including age, sex, BMI, prevalent risk factors and comorbidities were collected. Patients on warfarin therapy had a time in therapeutic range of at least 55% and an INR in target range at time of blood sampling. Exclusion criteria included known pro-inflammatory conditions, active malignancy, recurrent VTE, antiphospholipid syndrome, bleeding or platelet function disorders, use of anti-platelet drugs, and thrombocytopenia. To address the hypothesis, we firstly used a combination of Nanoparticle Tracking Analysis (NTA) and flow cytometry to comprehensively characterise differences in the concentration and size of small (0-200 nm) and large (200-1000 nm) circulating EVs, respectively. Statistical analysis revealed a trend towards reduced levels of circulating small and large EVs in Rivaroxaban-treated VTE patients compared with matched warfarin controls. Moreover, small and large EVs measured in the patients plasma correlated strongly and highly significantly (r=0.804, p<0.0001), indicating a concomitant decrease in both populations. As circulating EVs are considered pro-coagulant and pro-inflammatory, these results may point towards an ameliorated baseline pro-inflammatory state of VTE patients anticoagulated with Rivaroxaban. To further uncover Rivaroxaban-mediated alterations, we next compared proteomic profiles of circulating EVs. We robustly quantified over 300 vesicular proteins. Statistical analysis of the protein expression level using a student's t-test with a false discovery rate of 5% and a minimal fold change of 0.1 identified differential protein expression of a tightly regulated cluster of proteins involved in negative feedback regulation of inflammatory and coagulation pathways in Rivaroxaban-treated patients, which may in part contribute to the superior outcomes of Rivaroxaban-treated patients seen in recent clinical trials. Furthermore, we recently established that Rivaroxaban potentially ameliorates endothelial dysfunction in a cohort of non-valvular atrial fibrillation patients. Therefore, we aimed to also assess circulating markers of endothelial activation (Intercellular Adhesion Molecule 1 [ICAM-1] and Tissue Factor Pathway Inhibitor [TFPI]). Intriguingly, Rivaroxaban-treated patients exhibited an increase in plasma TFPI levels with a simultaneous decrease in soluble ICAM-1, potentially pointing towards ameliorated endothelial dysfunction in Rivaroxaban-treated VTE patients relative to warfarin. Collectively, we established that EV proteomic signatures are powerful biological sensors of Rivaroxaban's anti-inflammatory potential. Moreover, Rivaroxaban therapy may ameliorate endothelial dysfunction relative to warfarin. These findings are of translational relevance towards characterizing the anti-inflammatory and cardiovascular-protective mechanisms associated with Rivaroxaban therapy. Disclosures Kevane: Leo Pharma: Research Funding. Murphy: Bayer Pharma: Research Funding. Ni Ainle: Daiichi-Sankyo: Research Funding; Actelion: Research Funding; Leo Pharma: Research Funding; Bayer Pharma: Research Funding. Maguire: Bayer Pharma: Research Funding; Actelion: Research Funding.

5

Duggan, Sean T., Lesley J. Scott, and Greg L. Plosker. "Rivaroxaban." Drugs 69, no. 13 (September 2009): 1829–51. http://dx.doi.org/10.2165/11200890-000000000-00000.

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6

Duggan, Sean T. "Rivaroxaban." American Journal Cardiovascular Drugs 12, no. 1 (February 2012): 57–72. http://dx.doi.org/10.2165/11208470-000000000-00000.

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7

Mueck, Wolfgang, Anthonie W. A. Lensing, Giancarlo Agnelli, Hervé Decousus, Paolo Prandoni, and Frank Misselwitz. "Rivaroxaban." Clinical Pharmacokinetics 50, no. 10 (October 2011): 675–86. http://dx.doi.org/10.2165/11595320-000000000-00000.

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8

Kakar, P., T. Watson, and G. Y. H. Lip. "Rivaroxaban." Drugs of Today 43, no. 3 (2007): 129. http://dx.doi.org/10.1358/dot.2007.43.3.1067345.

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9

Rees, Sharon. "RIVAROXABAN." Journal of Prescribing Practice 3, no. 6 (June 2, 2021): 210–12. http://dx.doi.org/10.12968/jprp.2021.3.6.210.

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10

Chen, Terry, and Sum Lam. "Rivaroxaban." Cardiology in Review 17, no. 4 (July 2009): 192–97. http://dx.doi.org/10.1097/crd.0b013e3181aa2154.

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11

Dennis, J. Cada, L. Levien Terri, R. Woodruff Christopher, and E. Baker Danial. "Rivaroxaban." Hospital Pharmacy 46, no. 12 (December 2011): 960–70. http://dx.doi.org/10.1310/hpj4612-960.

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12

Kubitza, D., F. Misselwitz, and E. Perzborn. "Rivaroxaban." Hämostaseologie 27, no. 04 (2007): 282–89. http://dx.doi.org/10.1055/s-0037-1617095.

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ZusammenfassungRivaroxaban (Xarelto®), ein neuartiger oraler, direkter Faktor-Xa-Hemmer, ist in klinischer Entwicklung zur Prävention und Behandlung thromboembolischer Erkrankungen. Rivaroxaban hemmt die Clot-assoziierte und die freie Faktor-Xa-Aktivität, die Prothrombinase, und die Thrombinbildung. In Tiermodellen verhinderte Rivaroxaban die Bildung und das Wachstum venöser und arterieller Thromben. Rivaroxaban hat eine hohe orale Bioverfügbarkeit, schnellen Wirkeintritt und vorhersagbare Pharmakokinetik. In Phase-II-Studien zur Prävention venöser Thromboembolien (VTE) nach großen orthopädischen Operationen und zur Behandlung tiefer Venenthrombosen war Rivaroxaban wirksam und gut verträglich. In einer Phase-III-Studie zeigte Rivaroxaban höhere Wirksamkeit als Enoxaparin zur Vorbeugung von VTEs bei Kniegelenkersatzoperationen bei vergleichbar niedrigen Blutungsraten. Rivaroxaban wird zudem zur Therapie und Sekundärprävention von VTEs, zur Schlaganfallprophylaxe bei Vorhofflimmern und zur Sekundärprävention bei Patienten mit akutem Koronarsyndrom geprüft. Rivaroxaban ist eine vielversprechende Alternative zur aktuellen Therapie mit Antikoagulanzien bei thromboembolischen Erkrankungen.

13

Abdullaev, Sherzod, and Ranokhon Igamberdieva. "MO162: Renal Function During Long-Term Use of Oral Anticoagulants in Patients with Atrial Fibrillation." Nephrology Dialysis Transplantation 37, Supplement_3 (May 2022). http://dx.doi.org/10.1093/ndt/gfac066.064.

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Abstract BACKGROUND AND AIMS Long-term oral anticoagulant should be recommended in patients with atrial fibrillation (AF) and CHA2DS2VASc score ≥ 1 for stroke prevention. Warfarin and different direct oral anticoagulants are metabolized differently by the kidney. The impact on renal function during long-term use of oral anticoagulants in the patients with AF remains unclear. The aim of our study was to compare rivaroxaban's and warfarin's impact on the decline in renal function in patients with AF. METHOD This study included patients with non-valvular AF from 2016 to 2020, mainly through the medical history of the Republican nephrology inpatient departments. Baseline estimated glomerular filtration rate (eGFR), follow-up eGFR and the change in eGFR between 2-year eGFR and baseline eGFR were compared between different anticoagulants after propensity score matching. The primary study endpoint was acute kidney injury (AKI). A total of 289 patients were enrolled (n = 131 rivaroxaban, n = 158 warfarin) in this study, and the mean observation time was 2.9 ± 0.8 years. RESULTS During the observation period, there was a significantly higher incidence of AKI during follow-up in the warfarin group than in the rivaroxaban group before and after propensity score matching (before: warfarin versus rivaroxaban: 8.9% versus 4.6%, P < .001; after: warfarin versus rivaroxaban: 8.2% versus 3.8%, P < .001). The change in eGFR between 2-year eGFR and baseline eGFR did not differ between the warfarin and rivaroxaban groups after propensity score matching (warfarin versus rivaroxaban: − 1.31 ± 20.31 versus –1.82 ± 16.23 mL/min/1.73 m2, P = .452). CONCLUSION During the mean observation time of 2.9 ± 0.8 years, warfarin was associated with a higher incidence of AKI compared with rivaroxaban. The decline in renal function did not differ among warfarin and rivaroxaban groups.

14

"Rivaroxaban." Reactions Weekly 1853, no. 1 (May 2021): 425. http://dx.doi.org/10.1007/s40278-021-95291-x.

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15

"Rivaroxaban." Reactions Weekly 1854, no. 1 (May 2021): 318. http://dx.doi.org/10.1007/s40278-021-95649-7.

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16

"Rivaroxaban." Reactions Weekly 1854, no. 1 (May 2021): 319. http://dx.doi.org/10.1007/s40278-021-95650-6.

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17

"Rivaroxaban." Reactions Weekly 1838, no. 1 (January 2021): 480. http://dx.doi.org/10.1007/s40278-021-89797-5.

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18

"Rivaroxaban." Reactions Weekly 1839, no. 1 (January 2021): 278. http://dx.doi.org/10.1007/s40278-021-90116-9.

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19

"Rivaroxaban." Reactions Weekly 1840, no. 1 (January 2021): 330. http://dx.doi.org/10.1007/s40278-021-90473-x.

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"Rivaroxaban." Reactions Weekly 1837, no. 1 (January 2021): 628. http://dx.doi.org/10.1007/s40278-021-89227-9.

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21

"Rivaroxaban." Reactions Weekly 1837, no. 1 (January 2021): 627. http://dx.doi.org/10.1007/s40278-021-89226-9.

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"Rivaroxaban." Reactions Weekly 1837, no. 1 (January 2021): 626. http://dx.doi.org/10.1007/s40278-021-89225-9.

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"Rivaroxaban." Reactions Weekly 1837, no. 1 (January 2021): 625. http://dx.doi.org/10.1007/s40278-021-89224-9.

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24

"Rivaroxaban." Reactions Weekly 1851, no. 1 (April 2021): 331. http://dx.doi.org/10.1007/s40278-021-94421-3.

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"Rivaroxaban." Reactions Weekly 1856, no. 1 (May 2021): 358. http://dx.doi.org/10.1007/s40278-021-96351-9.

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"Rivaroxaban." Reactions Weekly 1842, no. 1 (February 2021): 327. http://dx.doi.org/10.1007/s40278-021-91063-3.

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"Rivaroxaban." Reactions Weekly 1842, no. 1 (February 2021): 328. http://dx.doi.org/10.1007/s40278-021-91064-3.

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"Rivaroxaban." Reactions Weekly 1843, no. 1 (February 2021): 320. http://dx.doi.org/10.1007/s40278-021-91422-z.

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"Rivaroxaban." Reactions Weekly 1841, no. 1 (February 2021): 214. http://dx.doi.org/10.1007/s40278-021-90716-x.

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"Rivaroxaban." Reactions Weekly 1844, no. 1 (February 2021): 397. http://dx.doi.org/10.1007/s40278-021-91844-2.

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"Rivaroxaban." Reactions Weekly 1844, no. 1 (February 2021): 396. http://dx.doi.org/10.1007/s40278-021-91843-2.

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"Rivaroxaban." Reactions Weekly 1844, no. 1 (February 2021): 398. http://dx.doi.org/10.1007/s40278-021-91845-2.

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"Rivaroxaban." Reactions Weekly 1846, no. 1 (March 2021): 286. http://dx.doi.org/10.1007/s40278-021-92534-6.

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"Rivaroxaban." Reactions Weekly 1849, no. 1 (April 2021): 385. http://dx.doi.org/10.1007/s40278-021-93769-9.

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"Rivaroxaban." Reactions Weekly 1852, no. 1 (April 2021): 384. http://dx.doi.org/10.1007/s40278-021-94837-7.

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36

"Rivaroxaban." Reactions Weekly 1913, no. 1 (July 2022): 389. http://dx.doi.org/10.1007/s40278-022-18539-2.

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"Rivaroxaban." Reactions Weekly 1920, no. 1 (August 20, 2022): 420. http://dx.doi.org/10.1007/s40278-022-21957-9.

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"Rivaroxaban." Reactions Weekly 1907, no. 1 (May 2022): 428. http://dx.doi.org/10.1007/s40278-022-15687-4.

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"Rivaroxaban." Reactions Weekly 1927, no. 1 (October 8, 2022): 470. http://dx.doi.org/10.1007/s40278-022-25206-3.

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"Rivaroxaban." Reactions Weekly 1923, no. 1 (September 10, 2022): 439. http://dx.doi.org/10.1007/s40278-022-23302-7.

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"Rivaroxaban." Reactions Weekly 1923, no. 1 (September 10, 2022): 438. http://dx.doi.org/10.1007/s40278-022-23301-7.

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"Rivaroxaban." Reactions Weekly 1922, no. 1 (September 3, 2022): 519. http://dx.doi.org/10.1007/s40278-022-22804-0.

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"Rivaroxaban." Reactions Weekly 1922, no. 1 (September 3, 2022): 522. http://dx.doi.org/10.1007/s40278-022-22807-0.

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"Rivaroxaban." Reactions Weekly 1922, no. 1 (September 3, 2022): 520. http://dx.doi.org/10.1007/s40278-022-22805-0.

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"Rivaroxaban." Reactions Weekly 1922, no. 1 (September 3, 2022): 521. http://dx.doi.org/10.1007/s40278-022-22806-0.

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"Rivaroxaban." Reactions Weekly 1922, no. 1 (September 3, 2022): 523. http://dx.doi.org/10.1007/s40278-022-22808-0.

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"Rivaroxaban." Reactions Weekly 1903, no. 1 (April 2022): 337. http://dx.doi.org/10.1007/s40278-022-13899-5.

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"Rivaroxaban." Reactions Weekly 1918, no. 1 (August 6, 2022): 439. http://dx.doi.org/10.1007/s40278-022-20896-x.

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"Rivaroxaban." Reactions Weekly 1909, no. 1 (June 2022): 490. http://dx.doi.org/10.1007/s40278-022-16777-0.

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"Rivaroxaban." Reactions Weekly 1909, no. 1 (June 2022): 491. http://dx.doi.org/10.1007/s40278-022-16778-0.

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