QTc shortening effect of ganglionated plexi ablation: A miraculous phenomenon?

We have read with interest the paper by Aksu and colleagues in a recent issue of the Journal. They investigated the dynamics of the heart rate‐corrected QT interval (QTc) after the cardioneuroablation for functional bradyarrhythmias and compared “regular” patients and those with cardioneuroablation accompanied by pulmonary vein isolation for concomitant atrial fibrillation. Let us put aside an unexpected finding of a greater effect in the less extensive, “cardioneuroablation alone” group. Because pulmonary vein antra are rich in neural tissue, their ablation offers additive denervation effects on top of selective ganglionic plexi ablation. Consequently, enhancement instead of paradoxical attenuation of the QTc dynamics would be a plausible expectation. This remains to be elucidated because the between‐group difference in outcome cannot be explained (as authors attempted) by relatively small differences in baseline characteristics. The gradual QTc shortening early after the procedure reaching the considerable difference of ~35ms after 9–12 months is a rather peculiar and unprecedented observation. Other authors suggested that, conversely, QTc prolongation may occur in patients after atrial fibrillation ablation, perhaps due to collateral ganglionic plexi ablation. Rare reports on malignant ventricular arrhythmias after atrial fibrillation ablation sometimes accompanied by a new manifestation of long QT triggered the investigations of whether these adverse events can be caused by the denervation of the ventricular myocardium. One study confirmed significant QTc prolongation by ~25ms immediately after the atrial fibrillation ablation, by ~10–15ms after 1 day, and by ~5–10ms after 1 and 3 months (already nonsignificant). The other study did not find any meaningful change in QTc both after 1 day and 3 months following the atrial fibrillation ablation. One may argue that such patients were much older and likely had more comorbidities compared to typical candidates of cardioneuroablation. Also, their ganglionic plexi were targeted incompletely, especially when distant from pulmonary vein antra, with relatively modest heart rate acceleration by 16 and 11 bpm, respectively. Therefore, we would like to present the results (not published so far) from our cohort of 108 patients (mean age: 39 years) who underwent anatomically navigated biatrial cardioneuroablation. After a mean radiofrequency time of 16min, heart rate accelerated by 21 bpm, and complete denervation of sinoatrial and atrioventricular nodes was achieved as assessed by extracardiac vagal nerve stimulation. The QTc was significantly prolonged by ~25–30ms immediately after the procedure (highly significant), by ~5–10ms after 1 day (borderline significant), returned to baseline level after 3 months, and became shorter by ~5ms after 1 year (borderline significant). The QTc dynamics was comparable to that observed in Chikata's study. In conclusion, we observed only short‐living QTc prolongation after cardioneuroablation that should not convey a long‐term risk. On the other hand, we cannot confirm clinically relevant QTc shortening with potential treatment implications. The study by Aksu and colleagues represent a clear outlier in the data concerning repolarization characteristics after ganglionic plexi ablation. Their electrogram‐guided variant of cardioneuroablation can hardly explain this striking difference. Perhaps QT measurements by suboptimum method deserve to be reviewed to escape from Wonderland.