Introduction: The mechanism(s) underlying complex fractionated atrial electrograms (CFAE) is not well understood. We hypothesized that CFAE may be caused by enhanced activity of the intrinsic cardiac autonomic nervous system.
Methods and results: In 35 anesthetized dogs, via a right or left thoracotomy, sustained atrial fibrillation was induced by local application of acetylcholine (ACh; 10, 100 mM) to the surface of the atrial appendage (AA) or by injection of ACh (10 mM) into the ganglionated plexi (GP). Fast Fourier transform analysis was performed from recordings at AA, atrial sites near the AA, mid portion of the atrium, atrial sites near the GP, and the pulmonary veins. After AF was induced with ACh either by topical application to the AA or by direct injection into the GP, CFAE exhibited a significant gradient of progressively decreasing dominant frequency and incidence of CFAE (CFAE%) from the GP toward distant sites, while regularity index progressively decreased in the opposite direction. Ablation of GP markedly attenuated CFAE and eliminated these gradients.
Conclusions: These results suggest CFAE may result from activation of the intrinsic cardiac autonomic nervous system in these animal models of sustained AF. Ablation of GP attenuates CFAE and eliminates the DF gradient.