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Abstract Background Pulmonary vein isolation (PVI) is a cornerstone therapy for paroxysmal atrial fibrillation (PAF). The variations in nonlinear heart rate variability (HRV) between patients with and without recurrences remain unclear. We aimed to characterize the nonlinear HRV before and after PVI in patients with and without recurrence. Methods Twenty‐five drug‐refractory PAF patients (56.0 ± 9.1 years old, 20 males) who received PVI were enrolled. Holter electrocardiography were performed before, 1–3, and 6–12 months after PVI. After 8.2 ± 2.5 months of follow‐ups after PVI, patients were divided into two groups: the recurrence (n = 8) and non‐recurrence (n = 17) groups. Linear and nonlinear HRV variables were analyzed, including the Poincaré Plot analysis and the Detrended Fluctuation Analysis (DFA). Results The non‐recurrence group, but not the recurrence group, had decreased high‐frequency component (HF), the root mean square of successive RR interval differences (RMSSD), and the Poincaré Plot index SD1 1–3 months after PVI and increased DFAslope2 6–12 months after PVI. The non‐recurrence group's LF/HF ratio and DFAslope1 decreased significantly 1–3 and 6–12 months after PVI, respectively, whereas there was no significant change in the recurrence group after PVI. Conclusions Significantly reduced vagal tone 1–3 months after PVI, increased long‐term fractal complexity 6–12 months after PVI, and decreased sympathetic tone as well as short‐term fractal complexity 1–3 and 6–12 months after PVI led to a better AF‐free survival after PVI. These findings suggest that neuromodulation and heart rate dynamics play crucial roles in AF recurrence following PVI.

Abstract Background The autonomic activity plays a critical role in generating paroxysmal atrial fibrillation (PAF). This study aimed to evaluate the changes in the autonomic nerve activity before and after PAF events in patients with and without ischemic heart disease (IHD). Methods The study included 49 patients (71.43 ± 12.24 years old, 26 males) with PAF events lasting more than 30 s during 24‐hr ambulatory Holter monitoring. The 20‐min intervals before and after PAF events were divided into eight segments of 5 min each. Heart rate variability (HRV) analyses of the time and frequency domains were applied to each time segment. Results Patients with IHD had significant increases in the root mean square successive differences (r‐MSSD, p = .008) and HF component (p = .04), followed by a significant increase in the LF/HF ratio (p = .02) preceding the onset of PAF. Patients without IHD had only a significant increase in the r‐MSSD (p = .045) preceding the onset of PAF. During the termination of PAF events, patients in both the IHD and control groups had a significantly decreased r‐MSSD and HF, respectively. Conclusion Ischemic heart disease causes a sympathovagal imbalance in the initiation of PAF. Decreased parasympathetic activity regulated the termination of PAF in both the IHD and control groups. The modification of the autonomic nervous system (ANS) activity should be individualized due to the autonomic complexity in AF arrhythmogenesis and termination.