SLOW PATHWAY ABLATION FOR ATRIOVENTRICULAR REENTRANT TACHYCARDIA SIGNIFICANTLY ALTERS THE AUTONOMIC MODULATION OF FAST ATRIOVENTRICULAR NODAL PATHWAY
Tématický okruh: Poruchy rytmu, kardiostimulace1 II. interní klinika, VFN Praha, Praha, 2 Klinika kardiologie, Institut klinické a experimentální medicíny, Praha
Background: It is believed that slow pathway ablation for atrioventricular reentrant tachycardia (AVNRT) has limited impact on fast pathway conduction properties. Atrioventricular (AV) nodal turbulence (AVNT), 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 AVNT.
Methods: The electrophysiological study was performed in 6 patients (3 men, mean age 53±15 years) undergoing catheter ablation for AVNRT. The stimulation protocol consisting of series of isolated extrastimuli delivered from right ventricle apex during constant atrial pacing at 100bpm was performed immediately prior to and 6±3min after successful slow pathway ablation. Averaged post-VPCs profiles of AV conduction intervals derived from surface ECG and intracardiac electrogram were analyzed. The descriptors of AVNT, Turbulence Onset (TOAV) and Slope (TSAV), were assessed.
Results: Slow pathway ablation resulted in suppression of AV nodal responsiveness to VPC. The Figure shows representative post-VPC dynamics of AV intervals before and after ablation. However ablation had only borderline effect on TOAV, progress of TSAV was significant (TOAV: -2.5±2.1% vs. -1.1±1.4%, p=0.07; TSAV: 1.1±0.8vs. 0.6±0.6; p=0.02).
Conclusion: It is feasible to detect the AVNT by the use of 2-channel atrial and ventricular pacing in order to eliminate the direct effect of heart rate variability on AV conduction. Slow pathway ablation had impact on modulation of AV nodal fast pathway conduction. It is not clear whether a direct thermal injury to AV node or a local vagal denervation is responsible for this effect.
Methods: The electrophysiological study was performed in 6 patients (3 men, mean age 53±15 years) undergoing catheter ablation for AVNRT. The stimulation protocol consisting of series of isolated extrastimuli delivered from right ventricle apex during constant atrial pacing at 100bpm was performed immediately prior to and 6±3min after successful slow pathway ablation. Averaged post-VPCs profiles of AV conduction intervals derived from surface ECG and intracardiac electrogram were analyzed. The descriptors of AVNT, Turbulence Onset (TOAV) and Slope (TSAV), were assessed.
Results: Slow pathway ablation resulted in suppression of AV nodal responsiveness to VPC. The Figure shows representative post-VPC dynamics of AV intervals before and after ablation. However ablation had only borderline effect on TOAV, progress of TSAV was significant (TOAV: -2.5±2.1% vs. -1.1±1.4%, p=0.07; TSAV: 1.1±0.8vs. 0.6±0.6; p=0.02).
Conclusion: It is feasible to detect the AVNT by the use of 2-channel atrial and ventricular pacing in order to eliminate the direct effect of heart rate variability on AV conduction. Slow pathway ablation had impact on modulation of AV nodal fast pathway conduction. It is not clear whether a direct thermal injury to AV node or a local vagal denervation is responsible for this effect.
