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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Catheter ablation is a well-established, safe, and effective strategy to achieve rhythm control in patients with symptomatic atrial fibrillation (AF) who are either intolerant or refractory to pharmacologic rhythm control or who wish to avoid long-term use of anti-arrhythmic drugs. Historically, when vitamin-K antagonists (VKAs) were the only option for oral anticoagulation, catheter ablation was performed after interruption of the VKA for several days and a transition (bridge) to subcutaneous or parenteral anticoagulation, typically with low-molecular-weight heparin. This strategy, however, was cumbersome and fraught with bleeding complications. Furthermore, the COMPARE randomized trial and observational studies showed that the thromboembolic risk was 10 to 15-fold higher with VKAs and heparin bridging as compared to uninterrupted VKAs. After these results, uninterrupted VKAs with a therapeutic international normalized ratio (INR) became the standard of care for periprocedural anticoagulation, and patients would routinely undergo catheter ablation with INR ranging between 2 and 3.5.

This option, however, also has two important setbacks. First, ablation becomes contingent on a therapeutic INR on the day of the procedure. A supra-therapeutic INR may entail a decision to postpone the procedure or administer blood products for correction, whereas a sub-therapeutic INR would typically imply deferring ablation to another day or require IV heparin until an ideal INR is reached. Second, the use of uninterrupted VKAs conflicts with the ever growing use of direct oral anticoagulants (DOACs). Electrophysiologists planning catheter ablation for patients on DOACs are faced with the following decision: (1) transition to VKAs for uninterrupted periprocedural anticoagulation or (2) continue periprocedural DOAC.

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