Abstract 16024: High Frequency Driving Sites are Anchored by Fibrotic Regions in Chronic Atrial Fibrillation
Introduction: Stable high frequency sources and rotors have been described to drive episodes of atrial fibrillation (AF) but the mechanism for their stability is unknown. We used a chronic animal model of AF to test the hypothesis that fibrosis anchors sites of high frequency activation during AF, which may drive the arrhythmia..
Methods: Endocardial electrograms were measured with a Constellation catheter (Boston Scientific) placed in the left atrium (LA) of chronic AF dogs (n=6) (AF > 12 months). An EnSite (St. Jude) geometric shell was then fused with a LA wall created by segmenting a high resolution T1 Mapping MRI. Regions with the lowest 10% T1 in the LA wall, used as a surrogate measure of fibrosis, were included on the LA wall segmentation. Fibrosis densities were calculated from histology and correlated with T1 Mapping MRI. Electrograms recorded during AF were processed to determine the dominant frequency (DFs) at each recording site. A probability map with the highest 10% DF value for each minute of AF at each of the sites was created to determine the stability of the DF during the 30 min AF episode.
Results: Each AF animal had at least one site of high DF which was stable for at least 22.5 (75%) of a 30-minute AF episode and 82% of the high DF sites stabilized within 2 mm of a region of fibrosis (chi square test, p < 0.05). The mean DF was 8.5±1.2 Hz and the highest DF sites showed an average DF of 10.3±1.1 Hz. The region of T1 Mapping MRI detected fibrosis of the LA wall had an average value of 283±32 ms whereas the rest of the LA had an average value of 463±79 ms. Histology confirmed that that T1 Mapping MRI detected fibrosis had more fibrosis than other LA regions. (25±1% vs. 13±2%).
Conclusions: Fibrosis developed during chronic AF may provide a substrate that anchors sites of high DF. Cardiac T1 Mapping MRI provides a means to determine such fibrotic sites noninvasively. Ablating these sites may reduce the stability of these high frequency sources and eliminate the drivers of persistent AF.
Author Disclosures: N.A. Angel: None. E. Kholmovski: None. D.J. Dosdall: None. R.S. MacLeod: None. N. Marrouche: None. R. Ranjan: None.
- © 2015 by American Heart Association, Inc.