Rivaroxaban: A New Treatment Paradigm in the Setting of Vascular Protection?

The pathophysiology of atherosclerosis involves a diseased endothelium, lipid accumulation and low-grade inflammation. In later stages of coronary artery disease (CAD) and peripheral arterial disease (PAD), plaque rupture may induce atherothrombosis caused by fibrin formation and platelet activation, leading to vessel occlusion with subsequent organ damage such as myocardial infarction, stroke or limb ischaemia. Because of the high disease burden associated with CAD and PAD, there is a need for continuous vascular protection beyond currently available treatments including antiplatelet agents. Due to its central role in the coagulation cascade, inhibition of factor Xa, with the subsequent reduced thrombin formation that impacts not only fibrin but also platelets, may provide additional benefit over using antiplatelets alone. Evidence from Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction-51 (ATLAS-ACS 2-TIMI 51) supports the use of the direct, oral, factor Xa inhibitor rivaroxaban (2.5 mg twice-daily [bid] and 5 mg bid) in reducing mortality and morbidity in patients with acute coronary syndrome, when combined with antiplatelets. Here, we review the role of rivaroxaban in three clinical trials of CAD and/or PAD: Cardiovascular OutcoMes for People using Anticoagulation StrategieS (COMPASS), Vascular Outcomes studY of ASA alonG with rivaroxaban in Endovascular or surgical limb Revascularization for PAD (VOYAGER PAD) and Cardiovascular Outcome Modification, Measurement AND Evaluation of Rivaroxaban in patients with Heart Failure (COMMANDER HF).