Abstract 20685: Differences in Atrial Fibrillation Characteristics Between Normal and Heart Failure Atria — A Tale of Two Substrates
Introduction: AF substrate is different in normal vs diseased hearts. Both fibrosis and autonomic remodeling contribute to AF substrate in heart failure (HF). We examined differences in AF electrogram (EGM) characteristics between the normal and HF left atrium.
Methods: Epicardial mapping was performed in the posterior left atrium (PLA), pulmonary veins (PVs) and left atrial appendage (LAA) in 7 normal dogs (Gp I) and 8 HF dogs (ventricular pacing at 240/min for 3 weeks) (Gp II). In Gp I, AF was induced by vagal stimulation. In Gp II, AF was induced in the presence and absence of double autonomic blockade. Frequency content of AF EGMs was assessed by the following: fractional interval (FI), dominant frequency (DF), organization index (OI) and Shannon's entropy (ShEn). HF atria were immunostained for autonomic nerves (acetylcholinesterase, dopamine beta-hydroxylase).
Results: In addition to increased atrial fibrosis, HF resulted in a significant increase in the number of autonomic ganglia in the PLA (Gp I vs Gp II=1.0±1.4 vs 3.6±3.3, p<0.05). HF resulted in decreased fractionation (i.e. increased FI) in the PLA and LAA (example in fig 1; fig 2A) and an increase in heterogeneity of FI in the PLA (figs 2B). HF decreased DF and increased OI in all regions (figs 2C, D). ShEn did not change with HF. In HF, double autonomic blockade significantly decreased DF in the PVs (7.0±0.9 Hz vs 5.96±0.4 Hz, p<0.05).
Conclusions: HF results in slowing and organization of AF in the left atrium and PVs, with AF becoming less fractionated but with fractionation becoming more heterogeneous in the PLA. EGM changes in the HF PVs are at least partially mediated by autonomic remodeling, with the remaining EGM changes likely due to fibrosis. These findings suggest that ablation approaches in HF should not only include the creation of ablation lines in the left atrium, but should also target the autonomic innervation of the PVs.
- © 2010 by American Heart Association, Inc.