Abstrait

Possible Benefits of Direct Oral Anticoagulants for the Electrophysiological Substrate Properties of Atrial Fibrillation: Can these New Agents have Antiatrial Fibrillation Actions?

Higa S*, Chen YJ and Chen SA

Atrial Fibrillation (AF) is the most common sustained cardiac arrhythmia, and is associated with thromboembolic events. Previous studies also have shown a close relationship between AF and heart failure, and heart failure can be one of the most important risk factors for AF. Therefore, heart failure animal models have been established to investigate the structural and electrical remodeling for AF substrates and suggested that the structural and/or electrical remodeling caused by heart failure may play an important role in AF genesis. Several recent studies have demonstrated that Direct Oral Anticoagulants (DOACs) can directly modulate the mechanical and electrophysiological properties of the Left Atrium (LA) and Pulmonary Veins (PVs) and suggest that DOACs may have a beneficial effect of anti-AF actions via preventing AF progression in addition to their anti-thrombotic action. Therefore, DOACs may affect the natural course of AF progression causing a transition from a paroxysmal to persistent form. Although, many clinical studies need to be conducted to evaluate the additional effects of DOACs, it would have a great impact on clinical practice. In this manuscript, I will focus on recent studies regarding: The effects of thrombin, factor Xa, and its inhibitors on tissue inflammation and fibrosis. The beneficial effects of thrombin inhibitors on the AF substrate in a heart failure animal model. The role of the PV myocardium on AF arrhthmogenesis in a heart failure animal model. The beneficial effects of DOACs on the electrophysiological properties of the atrium and PVs. Finally, I will discuss about the significant impact of AF progression and the possible benefits of DOACs on the clinical outcomes of catheter ablation of AF and the future direction of clinical research to evaluate the beneficial effects of DOACs on AF substrates.