Oral anticoagulation (OAC) has been the cornerstone for the treatment of atrial fibrillation (AF) patients. The vitamin K antagonist warfarin has been considered the drug of choice in stroke prevention with proven efficacy for more than 60 years. The great inter-patient and intra-patient dose variability and need for routine International Normalized Ratio (INR), are among the main disadvantages of warfarin. The direct-acting oral anticoagulants (DOACs), including direct thrombin inhibitors (dabigatran) and factors Xa inhibitors (apixaban, edoxaban, and rivaroxaban), are currently the therapy of choice for preventing thromboembolic events in patients with atrial fibrillation. Unlike warfarin and other vitamin K antagonists, the DOACs are administered in fixed doses and do not require routine laboratory monitoring.

Rivaroxaban is an oral inhibitor of free and clot-associated factor Xa through reversible, competitive interactions with its active site. Bioavailability following oral administration is dose-dependent, and it is highly bound to plasma proteins. Plasma levels peak 2 to 4 h following oral administration, partially excreted by the kidneys, and has a half-life depending on the dose and age. Factor Xa inhibitors variably affect prothrombin time (PT), with concentration-dependent PT prolongation. The sensitivity of the different assays varies widely, depending on the thromboplastin reagent, and it is recommended to check the sensitivity of PT in each institution. At therapeutic doses, rivaroxaban has a relatively weak effect on PT, but there is a more pronounced effect on supratherapeutic doses.

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