Stepan Havranek1, Lucie Souckova, Jan Simek, Dan Wichterle. 1. 2nd Department of Medicine - Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, U Nemocnice 2, Prague, 128 08, Czech Republic, stepan.havranek@lf1.cuni.cz.
Abstract
PURPOSE: Atrioventricular (AV) conduction turbulence, biphasic dromotropic response of AV node to single ventricular premature contraction (VPC), consists of early shortening and later prolongation of AV conduction intervals due to the direct electrophysiological mechanisms and perturbation in autonomic modulation. We investigated the acute effect of radiofrequency catheter ablation of slow pathway on AV turbulence. METHODS: The electrophysiological study was performed in 18 patients (7 men, mean age 49 ± 15 years) undergoing catheter ablation for AV nodal reentrant tachycardia. The stimulation protocol consisting of series of isolated VPC (coupling interval of 273 ± 23 ms) delivered from right ventricle apex during constant atrial pacing at 100 bpm was performed immediately prior to and 8 ± 4 min after successful slow-pathway ablation. Averaged post-VPCs profiles of AV conduction intervals were analyzed by purpose-written software. The descriptors of AV turbulence, turbulence onset (TOAV), turbulence slope (TSAV), and AV recovery (R AV) were assessed. RESULTS: Slow-pathway ablation suppressed the AV nodal responsiveness to VPC as evidenced by significant reduction of AV turbulence indices: TOAV: -6.4 ± 7.5 % vs. -4.3 ± 6.1 % (p < 0.05); TSAV: 2.0 ± 2.6 ms/RRi vs. 1.0 ± 0.7 ms/RRi (p < 0.05); and R AV: -13.8 ± 7.3 % vs. -6.5 ± 12.7 % (p < 0.05). CONCLUSIONS: Slow-pathway ablation significantly attenuated both vagal and non-autonomic modulation of AV nodal conduction. This effect is likely due to direct thermal injury of AV node associated with the change of properties of AV nodal fast-pathway although specific alteration of peri-AV nodal ganglionated plexi or their neural inputs into the AV node cannot be excluded.
PURPOSE:Atrioventricular (AV) conduction turbulence, biphasic dromotropic response of AV node to single ventricular premature contraction (VPC), consists of early shortening and later prolongation of AV conduction intervals due to the direct electrophysiological mechanisms and perturbation in autonomic modulation. We investigated the acute effect of radiofrequency catheter ablation of slow pathway on AV turbulence. METHODS: The electrophysiological study was performed in 18 patients (7 men, mean age 49 ± 15 years) undergoing catheter ablation for AV nodal reentrant tachycardia. The stimulation protocol consisting of series of isolated VPC (coupling interval of 273 ± 23 ms) delivered from right ventricle apex during constant atrial pacing at 100 bpm was performed immediately prior to and 8 ± 4 min after successful slow-pathway ablation. Averaged post-VPCs profiles of AV conduction intervals were analyzed by purpose-written software. The descriptors of AV turbulence, turbulence onset (TOAV), turbulence slope (TSAV), and AV recovery (R AV) were assessed. RESULTS: Slow-pathway ablation suppressed the AV nodal responsiveness to VPC as evidenced by significant reduction of AV turbulence indices: TOAV: -6.4 ± 7.5 % vs. -4.3 ± 6.1 % (p < 0.05); TSAV: 2.0 ± 2.6 ms/RRi vs. 1.0 ± 0.7 ms/RRi (p < 0.05); and R AV: -13.8 ± 7.3 % vs. -6.5 ± 12.7 % (p < 0.05). CONCLUSIONS: Slow-pathway ablation significantly attenuated both vagal and non-autonomic modulation of AV nodal conduction. This effect is likely due to direct thermal injury of AV node associated with the change of properties of AV nodal fast-pathway although specific alteration of peri-AV nodal ganglionated plexi or their neural inputs into the AV node cannot be excluded.