The autonomic nervous system is implicated in the multifactorial pathogenesis of atrial fibrillation (AF) but few studies have attempted neural targeting for therapeutic intervention. We have demonstrated that short bursts of stimulation, at specific sites of left atrial ganglionated plexi (GPs), trigger fibrillation-inducing atrial ectopy and importantly continuous stimulation of these sites may not induce AV block, the 'conventional' marker used to locate GPs. We have shown that these ectopy-triggering GP (ET-GP) sites are anatomically stable and can be rendered inactive by either ablation at the site or by ablation between the site and the adjacent pulmonary vein (PV). This may have important implications for planning patient specific strategies for ablation of paroxysmal AF in the future.
Keywords: Atrial fibrillation; Autonomic nervous system; Catheter ablation; Humans.
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