Abstract 16504: Heart Failure Enhanced Fibrillatory Activity in Small Pulmonary Vein and Left Atrium Tissue: Potential Mechanisms of Atrial Fibrillation
Introduction: HF predisposes to atrial fibrillation (AF) due to structural and electrical remodeling in the PV and LA. This study aimed to investigate whether heart failure (HF) can enhance pulmonary vein (PV) or left atrial (LA) arrhythmogenesis through modification of calcium homeostasis.
Methods and Results: Electrical activity and calcium regulation proteins were recorded in isolated LA and PVs from control rabbits and rabbits with rapid ventricular pacing-induced HF, using a multielectrode array system (64 microelectrodes, 8x8, 3,150x3,150 µm in area), conventional microelectrodes, and Western blot. Compared with control-PV (n=21), HF-PVs (n=8) had a higher incidence (88% vs. 38%, p<0.05) of rapid pacing-induced fibrillatory activity (FA, FIgure A) with a higher dominant frequency (DF, 23±1 vs. 19±1 Hz, p<0.05, Figure B-D), and higher incidences of early afterdepolarization (EAD, 50% vs. 6%, p<0.05), delayed afterdepolarization (DAD, 88% vs. 25%, p<0.05), and slower conduction velocity (Table). Similarly, HF-LA (n=8) had a higher incidence (88% vs. 36%, p<0.05) of rapid pacing-induced FA with higher DF (20±1 vs. 16±1 Hz, p<0.05), and higher incidences of EAD or DAD than control PV. HF-PV had a higher DF and larger area of FA than HF-LA. The protein expressions of Na+/Ca2+ exchanger and ryanodine receptors were increased, but the expression of sarcoplasmic reticulum Ca2+ ATPase was decreased in HF-PV and HF-LA, compared to control-PV and control-LA.
Conclusion: Automaticity and triggered activity contribute to the genesis of fibrillation in a small PV and LA substrate. HF-enhanced PV arrhythmogenesis may play an important role in the development of AF.
- © 2010 by American Heart Association, Inc.