Key result
Rivaroxaban reduced levels of key inflammation and coagulation biomarkers to a similar extent as VKAs in patients with atrial fibrillation, with the exception of F1.2 which was reduced by VKA but not rivaroxaban.
Why the study?
This substudy evaluated the effects of rivaroxaban versus a vitamin-K antagonist on coagulation and inflammation biomarkers in patients with nonvalvular AF scheduled for cardioversion without adequate baseline anticoagulation.
Does rivaroxaban reduce biomarkers of coagulation and inflammation compared to VKA in patients with nonvalvular AF scheduled for cardioversion?
RCT (n=958)
Open-label
2:1
Yes
Does rivaroxaban reduce biomarkers of coagulation and inflammation compared to VKA in patients with nonvalvular AF scheduled for cardioversion?
Absolute Event Rate: 2.7% vs -53%
p-value: p=<0.001
Rivaroxaban reduces key biomarkers of coagulation and inflammation to a similar extent as VKAs in patients with AF undergoing cardioversion, supporting its anti-inflammatory and anticoagulant effects.
Rivaroxaban matches VKA effects on key biomarkers in AF cardioversion; extends RCT evidence supporting its use as an alternative.
Introduction This X-VeRT (eXplore the efficacy and safety of once-daily oral riVaroxaban for the prevention of caRdiovascular events in patients with nonvalvular aTrial fibrillation scheduled for cardioversion) substudy evaluated the effects of treatment with rivaroxaban or a vitamin-K antagonist (VKA) on levels of biomarkers of coagulation (D-dimer, thrombin–antithrombin III complex [TAT] and prothrombin fragment [F1.2]) and inflammation (high sensitivity C-reactive protein [hs-CRP] and high-sensitivity interleukin-6 [hs-IL-6]) in patients with atrial fibrillation (AF) who were scheduled for cardioversion and had not received adequate anticoagulation at baseline (defined as, in the 21 days before randomization: no oral anticoagulant; international normalized ratio <2.0 with VKA treatment; or <80% compliance with non-VKA oral anticoagulant treatment). Methods Samples for biomarker analysis were taken at baseline (n = 958) and treatment completion (42 days after cardioversion; n = 918). The influence of clinical characteristics on baseline biomarker levels and the effect of treatment on changes in biomarker levels were evaluated using linear and logistic models. Results Baseline levels of some biomarkers were significantly associated with type of AF (D-dimer and hs-IL-6) and with history of congestive heart failure (hs-CRP, D-dimer, and hs-IL-6). Rivaroxaban and VKA treatments were associated with reductions from baseline in levels of D-dimer (−32.3 and −37.6%, respectively), TAT (−28.0 and −23.1%, respectively), hs-CRP (−12.5 and −17.9%, respectively), and hs-IL-6 (−9.2 and −9.8%, respectively). F1.2 levels were reduced from baseline in patients receiving a VKA (−53.0%) but not in those receiving rivaroxaban (2.7%). Conclusion Anticoagulation with rivaroxaban reduced levels of key inflammation and coagulation biomarkers to a similar extent as VKAs, with the exception of F1.2. Further investigation to confirm the value of these biomarkers in patients with AF is merited.
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Kirchhof et al. (2020) conducted an RCT in Nonvalvular atrial fibrillation scheduled for cardioversion (n=958). Rivaroxaban vs. Vitamin-K antagonist (VKA) was evaluated on Change in prothrombin fragment 1+2 (F1.2) levels from baseline to end of treatment (p=<0.001). Rivaroxaban reduced levels of key inflammation and coagulation biomarkers to a similar extent as VKAs in patients with atrial fibrillation, with the exception of F1.2 which was reduced by VKA but not rivaroxaban.
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