Pulsed field ablation (PFA) has emerged as a promising non-thermal technique for pulmonary vein isolation (PVI) in atrial fibrillation (AF), providing myocardial tissue selectivity and a favorable safety profile by minimizing collateral damage to adjacent structures such as the esophagus and phrenic nerve (1). However, its effects on the sinoatrial (SA) node and the autonomic nervous system remain incompletely understood.

A 62-year-old woman with symptomatic paroxysmal AF (burden: 48%) underwent PVI using a circular PFA catheter under general anesthesia. During PFA delivery, key parameters include the pulse count, with each target site typically receiving at least three pulse applications to achieve PVI. The pulse voltage is generally set within a range of 1,500 V to 1,700 V, often starting at 1,500 V inside the pulmonary veins and potentially increasing to 1,600 V or 1,700 V for applications at the ostium or antrum. The catheter configuration features a specialized ablation catheter with two primary deployable shapes: a spindle-shaped configuration for ablation inside the pulmonary veins and a flower-shaped configuration (with six petals) to enhance contact and ablation at the pulmonary vein ostium and antrum regions. Anesthetic drugs include dexmedetomidine (loading dose of 0.5–1.0 μg/kg administered over 10 min before anesthesia induction and followed by a maintenance infusion of 0.2–0.7 μg/kg/h during the procedure) and propofol is administered at a reduced dose - typically 1.0–2.5 mg/kg for induction and 2–6 mg/kg/h for maintenance). During ablation of the right superior pulmonary vein (RSPV), frequent sinus tachycardia (cycle length ≈ 470 ms) was observed (Figures 1Panel a), which was not present during ablation of the other pulmonary veins. This phenomenon has been sporadically observed in other PFA procedures at our center, although it has not been systematically documented. At the end of the procedure, sinus rhythm remained stable, with a cycle length of 550–620 ms (Figures 1Panel b). One hour post-procedure, frequent sinoatrial (SA) block was noted on telemetry (Figures 1Panel c); the patient remained asymptomatic. Without pharmacological intervention, the bradyarrhythmia resolved spontaneously within five hours. No recurrence of AF or pauses exceeding 2 s were observed in Holters on the second day and at one month following the procedure.

Patient consent and ethnic approval (2014-014-01 Tianjin University Chest Hospital) was obtained by participants in this study. They cover all treatments, procedures, and publication of the manuscript with any accompanying images.

The transient SA block observed after RSPV ablation with PFA can be attributed to several interrelated factors, as supported by literature on the electrophysiological effects of PFA and relevant anatomical considerations.

Transient SA Nodal Injury Due to PFA: PFA creates large, symmetrical antral lesions through irreversible electroporation, which may transiently affect the SA node when applied in close proximity (2). In this case, the RSPV had a large, anteriorly oriented ostium, positioning it near the SA node region (3). The sinus tachycardia observed during RSPV ablation likely resulted from direct stimulation of the SA node by the electric field, a phenomenon commonly reported in PFA procedures due to its effects on cardiac tissue excitability (4). Subsequently, the delayed SA block may reflect reversible electroporation-induced stunning of the SA node or its microvasculature, similar to cases where PFA caused prolonged but self-resolving asystole without permanent damage (5). PFA lesions exhibit distinctive characteristics compared to radiofrequency ablation, generating larger tissue volumes that may extend unexpectedly beyond the tissue-electrode interface (2, 6). This physical property raises legitimate concerns about potential electrophysiological effects on the SA node, especially when the RSPV orifice of our patient was relatively large and extends forward, which makes it easier for the PFA catheter to approach the SA node (Figures 1Panel d). Extensive clinical experience generally supports the safety of PFA near the SAN, as evidenced by a multicenter study involving 616 cases of SVC isolation, which achieved 100% acute success with minimal transient SAN injury (0.3%) (7). Above are consistent with findings that PFA lesions often exhibit a transient peripheral zone of injury that recovers over hours, explaining the spontaneous resolution observed here (8). Additionally, transient edema resulting from reversible electroporation may contribute to delayed SA node dysfunction by compressing the nodal tissue or its microvasculature, consistent with the self-limiting nature of the observed block. The sinus tachycardia observed during RSPV ablation is likely a direct excitatory effect of the electric field on the SAN, rather than an indication of inadequate analgesia or anesthesia, as it was localized to the RSPV ablation and was not accompanied by other signs of light anesthesia.

Since no bradycardia occurred during the operation, we did not perform coronary angiography and therefore could not confirm whether the sinoatrial node artery was involved (15). Additionally, SA node mapping was not conducted to determine the relative distance between the sinoatrial node area and the right upper pulmonary vein.

Identification of Patients at Risk: Based on this case, we recommend using pre-procedural imaging (e.g., cardiac CT) to assess the anatomical relationship between the RSPV and the SAN region. Patients with a large, anteriorly oriented RSPV ostium may be at higher risk for transient SAN dysfunction during PFA. Intraoperative monitoring of sinus rhythm during RSPV ablation is crucial; the appearance of sinus tachycardia may serve as an early warning sign. Prolonged post-procedural monitoring (e.g., telemetry for 24 h) should be considered in such cases.

Recommendations for Monitoring: If sinus tachycardia occurs during RSPV ablation, we recommend continuous telemetry monitoring for at least 24 h post-procedure to detect delayed SA block. Asymptomatic bradyarrhythmias may not require active intervention but should be closely observed. Symptomatic or prolonged pauses may necessitate temporary pacing or pharmacological support.

In conclusion, the transient SA block observed in this patient likely resulted from PFA-induced reversible injury to the SA node, exacerbated by anatomical proximity and autonomic modulation. This case highlights the importance of vigilant post-procedural monitoring following PFA, especially when ablating veins near the SA node, and contributes to the growing body of evidence regarding PFA's unique electrophysiological effects.