Rivaroxaban is a direct oral anticoagulant that has similar efficacy to warfarin in the management of non-valvular atrial fibrillation (NVAF) and venous thromboembolism (VTE) and is currently prescribed in preference to warfarin. Rivaroxaban inhibits activated factor X (FXa), which converts prothrombin to thrombin. However, thrombin and FXa also mediate pro-inflammatory signaling, leading to further activation of coagulation. Recent studies revealed that Rivaroxaban downregulated pro-inflammatory protein expression and reduced complement activation, while warfarin failed to do so. Therefore, long-term inhibition of FXa may confer additional benefits that are unrelated to Rivaroxaban’s anticoagulant function but rather, are mediated by inhibition of pro-inflammatory signalling. Extracellular vesicles (EVs) are pro-inflammatory mediators that regulate many physiological and pathological processes. It is likely that the well-characterized anti-inflammatory effects of Rivaroxaban will be mirrored by similar effects upon plasma EVs. The RIVEVE study aims to characterize the influence of Rivaroxaban upon circulating pro-inflammatory EVs using a combination of single vesicle analysis and proteomics.