br Introduction Atrial fibrillation AF

Introduction Atrial fibrillation (AF) is the most clinically prevalent tachyarrhythmia [1,2]. AF is a potential risk factor for stroke, and AF-associated strokes are often severe, resulting in disability or death [3–6]. Anticoagulant therapy with the vitamin K antagonist warfarin reduces the risk of AF-related stroke [7]. However, warfarin has been underused for at-risk patients with AF in clinical practice [8,9]. Additionally, the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study showed that 26.3% of 4188 patients newly starting warfarin for AF discontinued therapy in the first year [10]. In a real-world setting, adherence to oral anticoagulation therapy is important for the prevention of stroke in at-risk patients with AF, because clinical outcomes such as mortality, stroke, and cardiovascular events are strongly dependent on the quality of anticoagulation and rate of warfarin discontinuation [11,12]. Recently, several non-vitamin K antagonist oral anticoagulants (NOACs) have been developed. Landmark phase 3 randomized clinical trials (RCTs) compared NOACs with warfarin and demonstrated that NOACs are at least as safe and effective as warfarin to prevent stroke/systemic embolisms in patients with non-valvular AF (NVAF) [13–17]. Current AF guidelines based on this evidence recommend the risk pd184352 and use of NOACs [18–21]. The average rates of adherence in RCTs can be remarkably high, owing to the attention study patients receive and to the selection of the patients [22]. In “real-world” practice, however, it is not clear whether the adherence and persistence of patients to NOACs are better than those to warfarin in patients with NVAF. Moreover, no reports have focused on this issue in Japanese patients with NVAF taking NOACs. The aim of this study was to evaluate NOAC persistence and to compare it with warfarin persistence in Japanese patients with NVAF who newly started these drugs.
Materials and methods
Results
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Disclosures
Conflict of interest
Acknowledgments
Introduction Catheter ablation of atrial fibrillation (AF) has rapidly evolved in this decade, and pulmonary vein isolation (PVI) is currently a well-standardized technique for treating paroxysmal AF. However, in patients with persistent AF, ablation therapy is still challenging because the arrhythmogenic substrate beyond the pulmonary veins (PVs) plays a role in the perpetuation of AF [1–3]. A tailored treatment approach for each AF patient seems reasonable owing to the multifactorial and progressive nature of AF. One factor that characterizes AF is the dominant frequency (DF). The DF is closely related to atrial refractoriness and degree of electrical remodeling [4]. A frequency gradient from the left atrium (LA) to the right atrium (RA) characterizes paroxysmal AF [5]. Patients with a rare type of AF with a right-to-left frequency gradient may suffer from a right atrial substrate and may be maintained on a right atrial driver. Therefore, measurement of regional DFs can be used as a guide to tailor an ablation strategy [6–8]. Magnetocardiography (MCG) is a body surface mapping method that noninvasively detects the magnetic field of the heart. Notably, the electrocardiography (ECG) signal is affected by interpatient differences in body characteristics and other physiological parameters, whereas the magnetic field is not distorted by its flow through the tissues such as lungs, muscles, and bones. This unique characteristic of magnetic fields results in better spatial resolution in MCG than in ECG [9]. Although it is well known that lead V1 on the ECG reflects RA DF [10,11], little is known about the ability of MCG to detect regional DFs in the atria. As the standard ECG leads are not specifically designed to record atrial activity, the multichannel and multiplane recording method of MCG (64 channels×3 planes) might offer an advantage over the standard ECG method in detecting atrial DFs. This study evaluated the relationship between DFs in the atria measured by MCG mapping and those measured by multisite intracardiac mapping.