Background - Several disorders present reflex or persistent increase in vagal tone that may cause refractory symptoms even in a normal heart patient. Cardioneuroablation (CNA), the vagal denervation by RF ablation of the neuromyocardial interface, was developed to treat these conditions without pacemaker implantation. A theoretical limitation could be the reinnervation, that naturally grows in the first year, that could recover the vagal hyperactivity. This study aims to verify the vagal denervation degree in the chronic phase after CNA. Additionally, it intends to investigate the arrhythmias behavior after CNA. Methods - prospective longitudinal study with intra-patient comparison of 83 very symptomatic cases without significant cardiopathy, submitted to CNA, 49(59%) male, 47.3±17 years-old, having vagal paroxysmal atrial fibrillation 58(70%) or neurocardiogenic syncope 25(30%), NYHA Class < II and absence of significant comorbidities. CNA was performed in both atria by interatrial septum puncture, with irrigated conventional catheter and electroanatomic reconstruction. Ablation targeted the neuromiocardial interface by fragmentation mapping (AF-Nests) using the Velocity Fractionation software, conventional recording and anatomical localization of the ganglionated plexi. There were compared the time and frequency domain of the heart rate variability (HRV) and arrhythmias in 24h Holter pre-, 1-year-post- and 2-year-post-CNA. Clinical outpatient follow-up and serial Holter showed 80% asymptomatic cases at 40 months. Results - Time and frequency domain HRV demonstrated significant decrease in all autonomic parameters, showing an important parasympathetic and sympathetic activity reduction at 2 years-post-CNA (p<0.001). There was no difference in HRV between the 1-year- and 2-post-CNA (p>0.05) suggesting that the reinnervation has halted. There was also an important reduction in all brady- and tachyarrhythmias pre- vs. post-CNA, (p <0.01). Conclusions - There is an important and significant vagal and sympathetic denervation after 2 years of CNA with a significant reduction in brady and tachyarrhythmia in the whole group. There were no complications.

Background: Vagal hyperactivity is directly related to several clinical conditions as reflex/functional bradyarrhythmias and vagal atrial fibrillation (AF). Cardioneuroablation provides therapeutic vagal denervation through endocardial radiofrequency ablation for these cases. The main challenges are neuromyocardium interface identification and the denervation control and validation. The finding that the AF-Nest (AFN) ablation eliminates the atropine response and decreases RR variability suggests that they are related to the vagal innervation. Method: Prospective, controlled, longitudinal, nonrandomized study enrolling 62 patients in 2 groups: AFN group (AFN group 32 patients) with functional or reflex bradyarrhythmias or vagal AF treated with AFN ablation and a control group (30 patients) with anomalous bundles, ventricular premature beats, atrial flutter, atrioventricular nodal reentry, and atrial tachycardia, treated with conventional ablation (non-AFN ablation). In AFN group, ablation delivered at AFN detected by fragmentation/fractionation of the endocardial electrograms and by 3-dimensional anatomic location of the ganglionated plexus. Vagal response was evaluated before, during, and postablation by 5 s noncontact vagal stimulation at the jugular foramen, through the internal jugular veins (extracardiac vagal stimulation [ECVS]), analyzing 15 s mean heart rate, longest RR, pauses, and atrioventricular block. All patients had current guidelines arrhythmia ablation indication. Results: Preablation ECVS induced sinus pauses, asystole, and transient atrioventricular block in both groups showing a strong vagal response ( P =0.96). Postablation ECVS in the AFN group showed complete abolishment of the cardiac vagal response in all cases (pre/postablation ECVS= P <0.0001), demonstrating robust vagal denervation. However, in the control group, vagal response remained practically unchanged postablation ( P =0.35), showing that non-AFN ablation promotes no significant denervation. Conclusions: AFN ablation causes significant vagal denervation. Non-AFN ablation causes no significant vagal denervation. These results suggest that AFNs are intrinsically related to vagal innervation. ECVS was fundamental to stepwise vagal denervation validation during cardioneuroablation. Visual Overview A visual overview is available for this article.

The Selvester QRS score provides reliable quantification of myocardial fibrosis and was well correlated with MDCT in patients with HCM.

The vasovagal syncope is the most frequent cause of transient loss of consciousness, especially in young people without significant heart disease. The malignant cardioinhibitory form is caused by abrupt and intense vagal reflex with or without defined triggers. Refractory cases to preventive measures and pharmacological handling has been treated with definitive pacemaker implantation. Besides showing questionable results, pacemaker implantation is highly rejected by young patients. In the late 1990s, we proposed specific vagal denervation by catheter ablation and spectral mapping, for paroxysmal AF, functional bradyarrhythmias and severe cases of malignant cardioinhibitory syncope giving rise to cardioneuroablation. Recently, many authors worldwide have been reproducing the cardioneuroablation results where elimination or significant reduction of the vagal response were observed, which abolished symptoms in more than 75% of patients followed up to 14 years, without complications. Therefore, cardioneuroablation has shown to be a real therapeutic option in malignant syncope cardioinhibitory and in any exclusive vagal mediated bradyarrhythmia without the need for pacemaker implantation.

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