The main findings in the current study are as follows: (1) in patients with paroxysmal AF, mean SCL, BCL, and ERP of the AVN were all shortened immediately after circumferential PVI regardless of the level of RF power used for ablation, and (2) the recurrences of AFL and AF/AFL during 1-year follow-up were higher in those who underwent HPSD ablation compared with those who underwent conventional ablation.
Several studies reported that PVI in patients with AF increases the resting heart rate and attenuates the heart rate variability [2, 13, 14]. These phenomena were largely explained by the modulative effect on the sympathovagal balance of the intrinsic cardiac autonomic nervous system. It is well-known that intracardiac GPs are located at the roots of PVs and that the GPs are neurally connected to the sinoatrial node [15, 16]. Due to the anatomical proximity of the GPs and PV antrum, changes in the sympathovagal balance after PVI also affect the neurally connected sinoatrial node, which can lead to a faster resting heart rate. Consistent with these findings, the shortening of SCL was commonly observed in both groups in our study. In our HPSD strategy delivering (500 J in the anterior walls) led to similar changes in SCL, BCL, and ERP of the AVN, which could indicate that such amount of energy is sufficient to impact the superior left and right atrial GPs. Because the inferior left and right GPs are not anatomically covered by the current PVI scheme, neither of the ablation strategies can cause any effect on those GPs [17]. Considering that acetylcholinesterase-positive cells are located in the subendocardial atrial myocardium, shallow lesion formation by HPSD might induce a vagal denervation effect [18].
Changes in the electrophysiologic property of AVN during AF ablation have not been reported in humans. An animal study by Zhang et al. [19] showed that ablations of the cardiac anterior right GP and inferior right GP had a negative dromotropic effect on AVN, lasting for only a short period. Another canine study on the acute effect of GP ablation showed no significant changes in the AVN function [20]. This discrepancy in the response of AVN by GP ablations could be explained by the variable destructed contents of parasympathetic and sympathetic elements of the GPs. Adrenergic and cholinergic nerves are highly collocated in GPs, indicating that it is difficult to selectively target either parasympathetic or sympathetic neurons during the ablation procedures [21]. The shortening of the BCL and ERP of the AVN, which was observed immediately after AF ablation in our study, could be explained by the vagal modulation effect.
In previous studies, increased heart rate after PVI persisted for 3 to 6 months or up to 12 months [2, 4, 13]. In contrast, our results did not show significant changes in the mean heart rate between pre- and post-ablation 24-h Holter monitoring. A possible reason for this discrepancy is that the pre-ablation mean heart rate might have been overestimated because almost all patients showed an episode of paroxysmal AF in the pre-ablation Holter test.
Several studies reported that vagal denervation effect by PVI was associated with a lower recurrence of atrial tachyarrhythmia after ablation [2, 13, 22], while others did not report such beneficial effect of PVI on clinical recurrence [4, 14]. In our study population, there was no significant difference in the post-PVI shortening of SCL, BCL, and ERP of the AVN between patients with AF/AFL recurrence after ablation and those without (Additional file 1: Table S1). Albeit the relatively small number of patients and short follow-up duration of our study, the incidence of AFL recurrence was higher in the HPSD group than in the conventional ablation group (Fig. 3). Another large-scale study showed similar results recently [10], and the higher recurrence of AFL in patients treated with the HPSD method is a major concern. Although the very low risk of esophageal injury is one of the main advantages of HPSD ablation over conventional ablation, shallow lesion formation might contribute to the recurrence of AFL. Bortone et al. [9] showed that the delivery of higher power compared with conventional energy guided by unipolar modification leads to higher single pass PVI, shorter procedural time, and equivalent clinical outcome. The energy delivery per point was higher in Bortone et al. (412.3 ± 39.4 J) than in our study (300–500 J), which is the most likely explanation for the higher recurrence in the HPSD group in our study. Furthermore, the minimal time for chronic lesion formation at 50 W was suggested as 11.0 s [23], which is beyond the value used in our study. Mohanty et al. [24] reported that the lesion duration of < 10 s per point was associated with conduction recovery and a high rate of conduction recovery in the LA posterior wall facing the esophagus in patients who underwent HPSD AF ablation. The optimal duration of energy delivery in HPSD ablation to create a durable lesion in AF is still unclear yet. Furthermore, we consider the risk of the conduction recovery due to the lower total energy delivery in the HPSD method based on our result. When we compared the perimeters of circumferential PVI except for carina sites according to the ablation methods, there were no significant differences in the lesion perimeters (Additional file 1: Table S5). Finally, one animal experiment showed that a power greater than 40 W in fixed ablation index did not lead to higher lesion volume [25], which might have contributed to the higher AF/AFL recurrence in patients in the HPSD group.
We aimed to evaluate the change of the electrophysiologic parameters as an indirect measure of the cardiac autonomic function and compare the arrhythmic recurrence after PVI according to the different RF power. However, there are several limitations to the current study. First, this was a single-center observational study from a prospective cohort registry, and the conventional ablation group included patients who underwent PVI with a range of RF power (20 to 40 watts). Second, among the total of 239 patients, only 127 patients who had undergone Holter tests at all time points during the 1-year follow-up (i.e., baseline, 3, 6, and 12 months after ablation) were included in the analysis of mean heart rate. Third, we did not measure the heart rate variability through Holter monitoring, which could be useful for tracking the long-term changes in sympathovagal neurocardiac function. It may be postulated that elevated sympathetic tone resulting from pain or physical discomfort during the invasive ablation procedure could have contributed to the heightened sympathetic tone; however, it is highly unlikely because we titrated the sedatives and analgesics according to the level of pain and consciousness and all patients well-tolerated the procedure. Fourth, we could not compare and present the rates of the first pass isolation, vagal response during PVI, such as sinus pause, and the steam pop according to the different ablation methods due to the lack of data.