European Journal of Biomedical and Pharmaceutical Sciences

RIVAROXABAN BEYOND INHIBITING THROMBOSIS: TARGETING INFLAMMATION AND ATHEROSCLEROSIS

*Carlos V. Serrano, Pedro H. M. Cellia, Bruna R. Scarpa, Priscilla Teixeira Céo Frisso, Otavio R. Coelho, Alvaro Avezum Junior

ABSTRACT

Recent evidence has described beneficial clinical effects among patients with stable coronary artery disease (CAD), peripheral artery disease (PAD), and/or stroke when low-dose rivaroxaban (anti-factor Xa) was added to aspirin. A decrease on atherothrombotic events was observed, in part, by optimization of vascular protection. While the function of platelets is well recognized, substantiation is being composed on the role of coagulation factors to the developments of both atherosclerosis and atherothrombosis. Coagulation factors participate importantly on thrombus formation, meaning fibrin materialization and platelet activation and aggregation. In addition, these factors facilitate numerous pathophysiologic mechanisms through activation of protease‐activated‐receptors (PARs). Consequently, the association of anticoagulant to antiplatelet has obtained interest in secondary prevention for CAD/PAD as residual atherothrombotic risks are reduced. In this review, based on these recent findings, we emphasize the importance of factor Xa inhibition on protease-activated receptor (PAR) inactivation. PARs participate markedly on the pathophysiology of atherothrombosis. Key points:  Combining low-dose rivaroxaban to aspirin improves cardiovascular outcomes in patients with stable atherosclerotic vascular disease.  Coagulation and inflammatory pathways via factor Xa-mediated PAR activation on the arterial wall, and the resulting contribution to atherosclerosis, have been well documented.  Rivaroxaban can experimentally attenuate miointimal formation after mechanical vascular injury.  Inhibition of the factor Xa-PAR-2 pathway may minimize cardiac injury and dysfunction after myocardial infarction.

Keywords: Rivaroxaban; atherosclerosis; inflammation; factor Xa; protease-activated receptor; coronary artery disease.