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Journal articles on the topic 'Rivaroxaban'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 July 2024

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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.

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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).

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Mardi, Parham, Bahareh Abbasi, Arman Shafiee, and Tara Afsharmoghaddam. "Pharmacogenetic Approach for the Prevention of Rivaroxaban’s ADRs: A Systematic Review and Meta-Analysis." Genetics Research 2023 (October 31, 2023): 1–11. http://dx.doi.org/10.1155/2023/6105320.

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Introduction. Pharmacogenetics is a potential approach that can be applied to decline the burden of rivaroxaban’s ADRs. The current systematic review and meta-analysis aim to identify genetic variants correlated with rivaroxaban exposure and evaluate their importance. Methods. We systematically searched PubMed, Web of Science, and Scopus databases for all observational and interventional studies. The fixed effect method was used to pool the data when the Q-test’s p value was higher than 0.1. We used random models when the p value was less than 0.1. Results. Data from ten studies (4721 participants) were analyzed in the current review. Qualitative synthesis from included studies found that two variants of ABCB1 (rs1045642 and rs2032582) and one variant of APOB (rs13306198) are potential contributors to rivaroxaban concentrations. Both wild homozygotes (AA) and heterozygotes (AC) of rs1045642 have significantly lower rivaroxaban concentrations compared to mutated homozygotes (CC) (SMD = 0.516, 95% CI: 0.115 to 0.917; SMD = 0.772, 95% CI: 0.088 to 1.455, respectively). Nevertheless, pooling unadjusted odds ratios did not yield a statistically significant correlation between rivaroxaban ADRs and genetic mutations. Conclusion. This study revealed that being an AC or CC for rs1045642 is attributed to a considerably higher rivaroxaban level in participants using rivaroxaban. That is to say, rs1045642 is a remarkable predictor of rivaroxaban metabolism. We concluded that identifying rs1045642 before drug administration might decrease ADRs although further studies adjusted for potential confounders are strongly suggested.

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4

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.

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5

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.

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Gencpinar, Tugra, Cagatay Bilen, Baris Kemahli, Kivanc Kacar, Pinar Akokay, Serdar Bayrak, and Cenk Erdal. "Effects of rivaroxaban on myocardial mitophagy in the rat heart." Turkish Journal of Thoracic and Cardiovascular Surgery 31, no. 3 (July 1, 2023): 301–8. http://dx.doi.org/10.5606/tgkdc.dergisi.2023.24385.

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Background: This study aims to demonstrate the efficacy of rivaroxaban’s pharmacokinetic effects on myocardial mitophagy in rats by inducing apoptosis. Methods: In this double-blind experiment, Wistar albino male rats were randomly divided into three groups for an experimental ischemia model: the sham group (Group 1; n=7), the control group (Group 2; n=7), and the drug group (Group 3; n=7). Rivaroxaban was perorally administered with gavage at 2 mg/ kg/day for 28 days in Group 3. The heart was surgically exposed, and ischemia was achieved by compressing the vessel around the proximal part of the left anterior descending coronary artery for 10 min. The heart tissue was then transected, removed, and morphologically and immunohistochemically examined under a light microscope. Results: Heart sections were immunohistochemically marked with caspase 3, caspase 9, APAF1, and Bcl-2 antibodies. Group 1 was compared to the rivaroxaban-treated group, and the pathways inducing apoptosis was increased (caspase 3, caspase 9, APAF1; p<0.015, p<0.004, and p<0.01, respectively) and Bcl-2, the molecule that inhibits apoptosis, was decreased (p<0.01) in Group 3. Conclusion: The present study provides an evidence that the mitophagy response is less in rivaroxaban-treated rats, showing the protective effect of rivaroxaban against acute ischemia. Rivaroxaban-treated rats may have reduced cell death in cardiomyocytes during myocardial infarction and thus have reduced damage to the heart tissue caused by myocardial infarction.

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7

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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8

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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9

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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10

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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11

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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12

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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13

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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14

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.

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Schneckmann, R., M. Döring, S. Gerfer, S. Gorressen, S. Heitmeier, C. Helten, A. Polzin, et al. "Rivaroxaban attenuates neutrophil maturation in the bone marrow niche." Basic Research in Cardiology 118, no. 1 (August 14, 2023). http://dx.doi.org/10.1007/s00395-023-01001-5.

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AbstractPharmacological inhibition of factor Xa by rivaroxaban has been shown to mediate cardioprotection and is frequently used in patients with, e.g., atrial fibrillation. Rivaroxaban's anti-inflammatory actions are well known, but the underlying mechanisms are still incompletely understood. To date, no study has focused on the effects of rivaroxaban on the bone marrow (BM), despite growing evidence that the BM and its activation are of major importance in the development/progression of cardiovascular disease. Thus, we examined the impact of rivaroxaban on BM composition under homeostatic conditions and in response to a major cardiovascular event. Rivaroxaban treatment of mice for 7 days markedly diminished mature leukocytes in the BM. While apoptosis of BM-derived mature myeloid leukocytes was unaffected, lineage-negative BM cells exhibited a differentiation arrest at the level of granulocyte–monocyte progenitors, specifically affecting neutrophil maturation via downregulation of the transcription factors Spi1 and Csfr1. To assess whether this persists also in situations of increased leukocyte demand, mice were subjected to cardiac ischemia/reperfusion injury (I/R): 7 d pretreatment with rivaroxaban led to reduced cardiac inflammation 72 h after I/R and lowered circulating leukocyte numbers. However, BM myelopoiesis showed a rescue of the leukocyte differentiation arrest, indicating that rivaroxaban's inhibitory effects are restricted to homeostatic conditions and are mainly abolished during emergency hematopoiesis. In translation, ST-elevation MI patients treated with rivaroxaban also exhibited reduced circulating leukocyte numbers. In conclusion, we demonstrate that rivaroxaban attenuates neutrophil maturation in the BM, which may offer a therapeutic option to limit overshooting of the immune response after I/R.

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Weiss, Luisa, Wido Uhrig, Sarah Kelliher, Paulina B. Szklanna, Tadhg Prendiville, Shane P. Comer, Osasere Edebiri, et al. "Proteomic analysis of extracellular vesicle cargoes mirror the cardioprotective effects of rivaroxaban in patients with venous thromboembolism." PROTEOMICS – Clinical Applications, January 9, 2024. http://dx.doi.org/10.1002/prca.202300014.

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AbstractBackgroundVenous 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; yet, these remain poorly characterized. Extracellular vesicles (EVs) are considered proinflammatory messengers regulating a myriad of (patho)physiological processes and may be highly relevant to the pathophysiology of VTE. The effects of Rivaroxaban on circulating EVs in VTE patients remain unknown. We have established that differential EV biosignatures are found in patients with non‐valvular atrial fibrillation anticoagulated with Rivaroxaban versus warfarin. Here, we investigated whether differential proteomic profiles of circulating EVs could also be found in patients with VTE.Methods and ResultsWe performed comparative label‐free quantitative proteomic profiling of enriched plasma EVs from VTE patients anticoagulated with either Rivaroxaban or warfarin using a tandem mass spectrometry approach. Of the 182 quantified proteins, six were found to be either exclusive to, or enriched in, Rivaroxaban‐treated patients. Intriguingly, these proteins are involved in negative feedback regulation of inflammatory and coagulation pathways, suggesting that EV proteomic signatures may reflect both Rivaroxaban's anti‐coagulatory and anti‐inflammatory potential.ConclusionsThese differences suggest Rivaroxaban may have pleiotropic effects, supporting the reports of its emerging anti‐inflammatory and cardiovascular‐protective characteristics relative to warfarin.

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Alalawneh, Majdoleen, Ahmed Awaisu, Ibtihal Abdallah, Hazem Elewa, Mohammed Danjuma, Kamal M. Matar, Akram M. ElKashlan, Yasser Elshayep, Fathy Ibrahim, and Ousama Rachid. "Pharmacokinetics of single‐dose rivaroxaban under fed state in obese vs. non‐obese subjects: An open‐label controlled clinical trial (RIVOBESE‐PK)." Clinical and Translational Science 17, no. 6 (June 2024). http://dx.doi.org/10.1111/cts.13853.

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AbstractThe evidence of rivaroxaban's pharmacokinetics in obese compared with non‐obese populations remains inconclusive. We aimed to compare the pharmacokinetic profile of rivaroxaban between obese and non‐obese populations under fed state. Participants who met the study's eligibility criteria were assigned into one of two groups: obese (body mass index ≥35 kg/m2) or non‐obese (body mass index 18.5–24.9 kg/m2). A single dose of rivaroxaban 20 mg was orally administered to each participant. Nine blood samples over 48 h, and multiple urine samples over 18 h were collected and analyzed for rivaroxaban concentration using ultra‐performance liquid chromatography coupled with tandem mass detector. Pharmacokinetic parameters were determined using WinNonlin software. Thirty‐six participants were recruited into the study. No significant changes were observed between obese and non‐obese participants in peak plasma concentration, time to reach peak plasma concentration, area under the plasma concentration–time curve over 48 h or to infinity, elimination rate constant, half‐life, apparent volume of distribution, apparent clearance, and fraction of drug excreted unchanged in urine over 18 h. Rivaroxaban's exposure was similar between the obese and non‐obese subjects, and there were no significant differences in other pharmacokinetic parameters between the two groups. These results suggest that dose adjustment for rivaroxaban is probably unwarranted in the obese population.

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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.

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Khidhir, Angela. "Abstract 12256: Symptomatic Supratherapeutic International Normalized Ratio on Rivaroxaban: A Case Report and a Systematic Review." Circulation 146, Suppl_1 (November 8, 2022). http://dx.doi.org/10.1161/circ.146.suppl_1.12256.

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Rivaroxaban is a direct oral anticoagulant that works by inhibiting factor Xa. Direct anticoagulants have largely replaced direct vitamin K inhibitors (VKAs) due to the increased risk of major hemorrhages and the need for regular monitoring and dose adjustments. However, there have been multiple reports of elevated international normalized ratio (INR) and incidents of bleeding in patients on rivaroxaban, which brings into question the potential need for monitoring. The purpose of this review is to differentiate the patients that may benefit from regular monitoring and to propose future directions for implementation of monitoring. Here we report a case of an INR of 4.8 in a patient who presented with a gastrointestinal bleed and a drop of five gm/dL in hemoglobin four days after starting rivaroxaban following right femoral popliteal bypass graft stenting. The patient had no liver or kidney abnormalities and was not taking any medication or consuming any foods that could introduce any significant drug interaction. Additionally, we conducted a systematic review of similar reports in the literature with the goal of identifying the factors that could influence rivaroxaban’s levels in the blood or its influence on the INR. We reviewed PubMed using keywords including; “rivaroxaban”, “anti-Xa”, “DOAC”, “elevated”, “INR”, “bleeding”, “hemorrhage”, “pharmacology”, and “pharmacokinetics”. The literature revealed reports of INRs up to 5.2. Reviewing the pharmacokinetics of rivaroxaban indicated possibly higher drug levels in Caucasians, patients with a low body mass index (BMI), and patients with polymorphisms in the genes coding for CYP3A4, CYP2J2, or p-glycoprotein, assuming no renal or liver disease and no significant drug-drug or drug-food interactions. INR can be falsely normal if the thromboplastin reagent used to monitor the INR on warfarin is not sensitive to the changes in INR due to rivaroxaban. We suggest finding a thromboplastin reagent that is sensitive to INR changes with rivaroxaban, which could yield clinically relevant INRs on rivaroxaban allowing for accurate monitoring. We then suggest conducting studies to evaluate the cost effectiveness of regular monitoring in at-risk patients.

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

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

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

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

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

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"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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"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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"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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"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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