Exploration of new diagnostic and therapeutic methods for atrial fibrillation

• Published in: SHIKOKU ACTA MEDICA Vol. 79; no. 1.2; pp. 43 - 52
• Main Author: Soeki, Takeshi
• Format: Journal Article
• Language: Japanese
• Published: Tokushima Medical Association 2023
• Subjects: anticoagulant therapy; atrial fibrillation; biomarker; catheter ablation; inflammation
• ISSN: 0037-3699; 2758-3279
• DOI: 10.57444/shikokuactamedica.79.1.2_43

Atrial fibrillation （AF） is one of the most common arrhythmia.　Various tools such as portable electrocardiogram （ECG） and implantable cardiac monitor have been available for diagnosis of AF.　In addition, the treatment for AF has progressed remarkably in accompany with the development of anticoagulant therapy and catheter ablation.　However, it remains unknown about the pathophysiology of AF such as inflammation.　In this regard, there is still room for the further progress in diagnostic and therapeutic methods for AF.　We reported previously that local production of pentraxin （PTX） 3 in the left atrium might reflect the local inflammation of AF.　In addition, we also reported that local production of microRNA （miR）-328 in the left atrium might be involved in the process of atrial remodeling in patients with AF.　Based on these results, it is suggested that plasma concentrations of PTX3 or miR-328 might be used as a new biomarker for AF.　For the development of preventive strategies, the ability to identify risk markers for new-onset AF is critical.　We have shown that a new combined score including age, premature atrial contraction count, maximum RR interval, and left atrial diameter could help characterize the risk of new-onset AF.　Activated factor X （FXa）, which contributes to chronic inflammation via protease-activated receptor 2 （PAR-2）, might play an important role in AF arrhythmogenesis.　We have recently shown that angiotensin II-treated PAR-2 deficient mice had a lower incidence of AF and less atrial fibrosis compared to wild-type mice treated with angiotensin II.　We also have shown that rivaroxaban, but not warfarin, reduced AF inducibility and collagen volume fraction in the atrium.　These findings suggested the possibility of Xa inhibitors as therapeutic agents for the onset and progression of AF through the new mechanism.　I would like to continue working on the development of new diagnostic and therapeutic methods for arrhythmia including AF.