| Literature DB >> 31961030 |
Konstantinos Vlachos1, Giuseppe Mascia2, Claire A Martin1,3, George Bazoukis4, Antonio Frontera1, Ghassen Cheniti1, Konstantinos P Letsas4, Micheal Efremidis4, Stamatis Georgopoulos4, Charis Gkalapis5,6, Josselin Duchateau1, Thomas Parmbrun1, Nicholas Derval1, Mélèze Hocini1, Michel Haissaguerre1, Pierre Jais1, Frédéric Sacher1.
Abstract
The incidence of atrial fibrillation (AF) in Brugada syndrome (BrS) has been reported at between 9% and 53% by different series, but the true prevalence is unknown. However, AF may be the presenting feature in some patients. The underlying mechanisms for AF may be a combination of multiple factors, genetic or acquired, that may impact upon autonomic function, atrial structure, and conduction velocities or other unknown factors. The presence of AF has been associated with a more malignant course, with a greater incidence of syncope and ventricular arrhythmias, thus acting as marker of more advanced disease. Regarding the management of patients with AF, antiarrhythmic drugs effective in preventing malignant arrhythmias in BrS such as quinidine or invasive treatment with pulmonary vein isolation (PVI) may be useful in AF treatment. In this review, we aim to present the current perspectives regarding the genetics, pathophysiology, management, and prognosis of AF in patients with BrS.Entities:
Keywords: Brugada syndrome; arrhythmia mechanism; atrial fibrillation; genetics
Mesh:
Substances:
Year: 2020 PMID: 31961030 DOI: 10.1111/jce.14361
Source DB: PubMed Journal: J Cardiovasc Electrophysiol ISSN: 1045-3873