This study adopts a strategy combining basic research with clinical investigation to systematically explore the therapeutic value of cardioneuroablation in the treatment of vagally-mediated bradycardia. The study design fully considers the complexity of the scientific question and the feasibility of clinical translation. Through rigorous experimental design and standardized operational procedures, the reliability and reproducibility of the study results are ensured.

In recent years, cardiac ganglionated plexus (GP) ablation has emerged as a novel minimally invasive electrophysiological intervention. By targeting and ablating overactive GPs, this technique aims to suppress aberrant vagal signaling and alleviate symptoms of bradycardia. It offers distinct advantages, including a mechanism-targeted approach and the avoidance of permanent device implantation. Previous studies have demonstrated the feasibility and clinical potential of this technique in patients with vasovagal syncope, particularly the cardioinhibitory type. Therefore, developing such a "device-free" interventional therapy addresses a pressing clinical need and holds significant medical importance. Results from preliminary small-scale clinical studies suggest that GP ablation can significantly reduce syncope recurrence, improve quality of life, and increase resting heart rate. However, higher-level evidence regarding the efficacy and safety of cardiac GP ablation for the treatment of symptomatic bradycardia is still lacking. Consequently, this study combines basic and clinical research to address the unresolved questions regarding cardioneuroablation, aiming to fill this evidence gap and establish an evidence-based therapeutic strategy for patients with significant, vagally-mediated bradycardia.

Inclusion Criteria:

1. Age range: 18 - 65 years old
2. Have symptoms related to bradycardia (syncope, dizziness, blackout, palpitations, fatigue, listlessness, inability to concentrate and decreased activity endurance, etc.)
3. Meet one of the following conditions: ①Dynamic electrocardiogram shows an average heart rate of less than 50 beats per minute or there is a heart arrest lasting more than 3 seconds during the day; ②Transient second or third degree atrioventricular conduction block without hemodynamic disorders during the day
4. The atropine test showed that the sinus heart rate increased by ≥ 25%, or the heart rate was ≥ 90 beats per minute, or the atrioventricular conduction block was significantly improved to be no more than first-degree atrioventricular conduction block.

Exclusion Criteria:

1. A history of severe trauma caused by bradycardia
2. Regular use of antiarrhythmic drugs within the past 3 months
3. Prior implantation of a cardiac pacemaker
4. Existing implantation of, or indication for implantation of, electronic devices with pacing function, such as cardiac contractility modulators (CCMs), implantable cardioverter-defibrillators (ICDs), or cardiac resynchronization therapy (CRT) devices
5. Bradycardia or atrioventricular block caused by medications or other reversible factors (e.g., hyperkalemia, hypothyroidism)
6. Bradycardia or atrioventricular block associated with obstructive sleep apnea syndrome (OSAS)
7. Coronary revascularization within the past 3 months, or unstable coronary heart disease despite standardized medical treatment or revascularization
8. Stroke or transient ischemic attack (TIA) within the past 3 months
9. A history of open-heart surgery
10. Severe congenital heart disease
11. Complicated with severe ventricular arrhythmia
12. Severe cardiac insufficiency with left ventricular ejection fraction (LVEF) ≤ 35%
13. Severe cardiomyopathy, such as hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM), or cardiac amyloidosis
14. Severe aortic or mitral valve stenosis
15. Pregnancy or lactation period
16. Expected survival time of less than 1 year
17. Refusal to sign the informed consent form
18. Other conditions deemed ineligible by the researchers