If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Oxidative Stress (OS) is thought to be a mediator of atrial fibrillation (AF), but the precise role of OS in AF is unknown. We assessed reactive oxygen species (ROS) scavenging on slow conduction and maintenance of rotational drivers.
We hypothesized that ROS are dynamically involved in a vulnerable substrate and that ROS scavenging reduces AF drivers and arrhythmogenic slow conduction zones.
AF was induced in 48 dogs by rapid atrial pacing (RAP) for 3-14 weeks. Epicardial high-density mapping was performed (130 electrodes, dist. 2.5mm) in the atrial regions: posterior left atrium (PLA), left atrial free wall (LAFW), left atrial appendage (LAA), posterior right atrium (PRA), right atrial free wall (RAFW), right atrial appendage (RAA). N-acetylcysteine (NAC) was given intravenously (100mg/kg) in 15 AF dogs. We mapped all atrial regions pre and post NAC. We detected rotational activity in activation time maps and quantified slow conduction as activation delay in neighboring electrodes.
We detected rotational activity in all regions (Figure A) with the stability of 376±255ms in the LAA, 422±174ms in the PLA, and 317±174ms in the LAFW (Figure B). The cycle length of rotational activity was shorter in the PLA (CL 94±7 ms) compared to other regions (P<0.05) (Figure C) and increased in remote regions with increasing distance to the PLA (Figure D). After providing NAC, rotational activities reduced in the left atrium by 40% in the LAFW, by 39% in the PLA, and by 12% in the LAFW (Figure E).
Acute scavenging of ROS reduces arrhythmogenic slow conduction and AF triggers. These results show that ROS is dynamically involved in the maintenance of AF.