News on angiotensin II and atrial fibrillation: from the molecular to the pathophysiological
Artículo de revista
Universidad de Cartagena
Introduction: atrial fibrillation is the most prevalent arrhythmia in the world, having high morbidity and mortality rates. Numerous studies have shown the involvement of the angiotensin renin system in the pathogenesis of atrial fibrillation, and in several of these, the underlying mechanism involving a process of atrial tissue remodeling is speculated. Objective: present literature related to the pathophysiological mechanisms of Atrial Fibrillation, its impact on cardiovascular risk, and related aspects between angiotensin II and atrial fibrillation. Methods: a non-systematic review of the available literature was conducted using key terms such as "Atrial Fibrillation" and "Angiotensin II", in addition to synonyms, which were combined with the "AND" and "OR" connectors, both in English and Spanish, in the PubMed, ScienceDirect, Embase, EBSCO, and MEDLINE databases. Results: atrial fibrosis is a structural alteration that facilitates the maintenance of atrial fibrillation, Angiotensin II contributes to this process extensively by stimulating inflammatory processes, decreasing the activity of collagenase, increased expression of MAPK, and changes in cardiac electrophysiological properties through binding to the AT1 receptor. Conclusions: getting to know the pathophysiology of atrial fibrillation at the molecular level, allows to further elucidate the context and possible complications of affected patients, facilitating the generation of hypotheses that contribute to the timely, accurate and effective diagnosis, the development of new therapeutic targets, as well as a better approach in the clinical area.