ArticleThrombosis research2016
Rivaroxaban improves patency and decreases inflammation in a mouse model of catheter thrombosis.
Article in Thrombosis research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The Impairment in Kidney Function in the Oral Anticoagulation Era. A Pathophysiological Insight.Cardiovascular drugs and therapy · 2021Pooled it
- Rivaroxaban versus warfarin: differential effects on oxidative stress and fibrinolytic markers in atrial fibrillation.Frontiers in pharmacology · 2026Article
- Beyond Anticoagulation: A Comprehensive Review of Non-Vitamin K Oral Anticoagulants (NOACs) in Inflammation and Protease-Activated Receptor Signaling.International journal of molecular sciences · 2024Review
- The effect of rivaroxaban on biomarkers in blood and plasma: a review of preclinical and clinical evidence.Journal of thrombosis and thrombolysis · 2023Review
- Crosstalk between septic shock and venous thromboembolism: a bioinformatics and immunoassay analysis.Frontiers in cellular and infection microbiology · 2023Article
- Prophylactic rivaroxaban in the early post-discharge period reduces the rates of hospitalization for atrial fibrillation and incidence of sudden cardiac death during long-term follow-up in hospitalized COVID-19 survivors.Frontiers in pharmacology · 2023Article
- Overall Hemostatic Potential Assay Detects Risk of Progression to Post-Thrombotic Syndrome in Anticoagulated Patients following Deep Vein Thrombosis.Diagnostics (Basel, Switzerland) · 2022Article
- Promising drug repurposing approach targeted for cytokine storm implicated in SARS-CoV-2 complications.Immunopharmacology and immunotoxicology · 2021Review
- Role of miR-92a-3p, oxidative stress, and p38MAPK/NF-κB pathway in rats with central venous catheter related thrombosis.BMC cardiovascular disorders · 2020Article
- Comparison of Inflammatory Mediators in Patients With Atrial Fibrillation Using Warfarin or Rivaroxaban.Frontiers in cardiovascular medicine · 2020Article
- Rivaroxaban improves vascular response in LPS-induced acute inflammation in experimental models.PloS one · 2020Article
- A prospective evaluation of rivaroxaban on haemostatic parameters in apparently healthy dogs.Veterinary medicine and science · 2019Article
- Rivaroxaban attenuates thrombosis by targeting the NF-κB signaling pathway in a rat model of deep venous thrombus.International journal of molecular medicine · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
introductionDysfunction of indwelling central venous catheters (CVC) due to tissue ingrowth or clotting is common. The study objective was to determine if the oral anticoagulant rivaroxaban (RIVA) improved CVC patency and inflammation in mice. MATERIALS AND
methodsPolyurethane catheters (0.5cm length) were placed unilaterally into the external jugular vein (EJV) of mice, which subsequently underwent daily gavage with either vehicle or RIVA (5mg/kg). CVC patency, as assessed by B-mode and Doppler ultrasound, and hematocrit were measured at 3, 7, 14 or 21days (n=8-11 mice/group/time-point). Plasma monocyte chemotactic protein-1 (MCP-1) levels were assessed by ELISA, EJV matrix metalloproteinase-9 (MMP-9) levels by western immunoblotting, and cell proliferation (anti-Ki67), macrophage infiltration (anti-MAC387) by immunostaining of EJV tissues. RESULTS AND
conclusionsCVC patency was significantly improved in RIVA-treated mice compared to vehicle-treated (93.8% vs. 62.9%) with the probability of patency in RIVA-treated mice being 1.5 times that in vehicle-treated (relative risk [RR], 1.50, 95% confidence interval [CI], 1.14-1.95, p=0.002). Plasma MCP-1 levels were lower in RIVA-treated mice vs. vehicle-treated at 21days (389±260 vs. 804±292ng/mL, p=0.005). Cell proliferation was less at day 7 in EJV from the RIVA-treated mice than vehicle-treated (5.0%±3.0 vs. 11.5%±3.6, p=0.0006), as were MMP-9 protein levels. There were no differences in hematocrit between vehicle and RIVA-treated groups at any time point. In conclusion, these data indicate RIVA lowers inflammation and improves CVC patency in a mouse model, supporting future studies to assess RIVA for improving CVC patency in patients.
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