ObjectivesThis study investigated the effect of electrical stimulation of aortic root ventricular ganglionated plexi (GP) on atrial fibrillation (AF) inducibility. BackgroundThe ventricular GP are interconnected with atrial GP to govern heart function, although the effect of ventricular GP modification on control of AF remains unknown. MethodsEffective refractory periods (ERPs) of test pulmonary veins (PVs) were measured at baseline and during high-level (HL-ES) and low-level (LL-ES) electrical stimulation of the aortic root GP. The arrhythmogenic threshold of acetylcholine and isoproterenol was determined at baseline and during HL-ES and LL-ES. Moreover, AF was induced at PVs by programmed electrical stimulation after HL-ES or LL-ES. Immunohistochemistry staining was performed to examine the autonomic activity from aortic root GP to the PVs. ResultsCompared with the baseline group, HL-ES of aortic root GP significantly shortened atrial ERP (95 ± 13 ms vs. 122 ± 9 ms) and PV ERP (104 ± 11 ms vs. 131 ± 12 ms); decreased the threshold concentration of AF by both acetylcholine (1.3 ± 0.2 μmol/l vs. 3.2 ± 0.3 μmol/l) and isoproterenol (0.3 ± 0.1 μmol/l vs. 1.3 ± 0.2 μmol/l); and increased the AF-inducing rate from PVs (90% vs. 30%). In contrast, LL-ES of the GP prevented the shortening of ERP and PV ERP to 125 ± 10 ms and 133 ± 11 ms, respectively; increased threshold levels of acetylcholine and isoproterenol to 5.7 ± 0.4 μmol/l and 3.2 ± 0.3 μmol/l; and decreased the AF-inducing rate to 5%. We also found that the biotinylated dextran amine–containing varicose fibers projected directly from the aortic root GP to the left PVs. ConclusionsThese findings suggest that autonomic innervations of left PVs partly originated from aortic root ventricular GP. Moreover, LL-ES of aortic root ventricular GP suppressed AF inducibility and arose from PVs mediated by the autonomic nervous system.