Pulsed field ablation in patients with complex consecutive atrial tachycardia in conjunction with ultra-high density mapping: Proof of concept.

INTRODUCTION: Catheter-ablation (CA) of consecutive left atrial tachycardias (LAT) can be challenging. Pulsed field ablation (PFA) yields a novel nonthermal CA technology for treatment of atrial fibrillation (AF). There is no data regarding PFA of LAT. This study sought to investigate PFA of consecutive LAT following prior CA of AF. METHODS: Consecutive patients with LAT underwent ultrahigh-density (UHDx) mapping. Subsequent to identification of the AT mechanism, PFA was performed at the assumed critical sites for LAT maintenance. Continuous ablation lines were performed if required and evaluated with pre- and post-PFA HDx-mapping. RESULTS: Fifteen patients (age 70 ± 10, male 73%) who underwent 3.6 ± 2 prior AF-CA procedures were included. The total mean procedure and fluoroscopy times were 141 ± 43 and 18 ± 10 min, respectively. All 19 of 19 (100%) LAT were successfully ablated with PFA. Two AT located at the right atria required RF-ablation. LAT were identified as localized reentry (n = 1) and macro-reentry LAT (n = 18) and targeted with PFA. All LAT terminated with PFA either to sinus rhythm (9/15) or a secondary AT (6/15 and subsequently to SR); 63% (12/19) terminated with the first PFA-application. All lines (13 roof, 11 anterior, 1 mitral) were blocked. LA-posterior-wall isolation (LAPWI) was successfully achieved when performed (10/10). AF/AT free survival was 80% (12/15) after 153 [88-207] days of follow-up. No procedure-related complications occurred. CONCLUSION: PFA of consecutive LAT is feasible and safe. Successful creation of ablation lines and LAPWI can be achieved in a short time. PFA may offer the opportunity for effective ablation of atrial arrhythmias beyond AF.

Impact of the ablation technique on release of the neuronal injury marker S100B during pulmonary vein isolation.

AIMS: S100B, a well-known damage-associated molecular pattern protein is released acutely by central and peripheral nerves and upon concomitant denervation in pulmonary vein isolation (PVI). We aimed to investigate whether the ablation technique used for PVI impacts S100B release in patients with paroxysmal atrial fibrillation (AF). METHODS AND RESULTS: The study population consisted of 73 consecutive patients (age: 62.7 ± 10.9 years, 54.8% males) undergoing first-time PVI with either radiofrequency (RF; n = 30) or cryoballoon (CB; n = 43) for paroxysmal AF. S100B determined from venous plasma samples taken immediately before and after PVI increased from 33.5 ± 1.8 to 91.1 ± 5.3 pg/mL (P < 0.0001). S100B release in patients undergoing CB-PVI was 3.9 times higher compared to patients with RF-PVI (ΔS100B: 21.1 ± 2.7 vs. 83.1 ± 5.2 pg/mL, P < 0.0001). During a mean follow-up of 314 ± 186 days, AF recurrences were observed in 18/71 (25.4%) patients (RF-PVI: n = 9/28, CB-PVI: n = 9/43). Univariate Cox regression analysis indicated that an increase in S100B was associated with higher freedom from AF in follow-up (hazard ratio per 10 pg/mL release of S100B: 0.83; 95% confidence interval: 0.72-0.95; P = 0.007). CONCLUSION: The ablation technique used for PVI has an impact on the release of S100B, a well-established biomarker for neural damage.

Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation.

Atrial fibrillation (AF), the most common sustained heart rhythm disorder worldwide, is linked to dysfunction of the intrinsic cardiac autonomic nervous system (ICNS). The role of ICNS damage occurring during catheter-based treatment of AF, which is the therapy of choice for many patients, remains controversial. We show here that the neuronal injury marker S100B is expressed in cardiac glia throughout the ICNS and is released specifically upon catheter ablation of AF. Patients with higher S100B release were more likely to be AF free during follow-up. Subsequent in vitro studies revealed that murine intracardiac neurons react to S100B with diminished action potential firing and increased neurite growth. This suggests that release of S100B from cardiac glia upon catheter-based treatment of AF is a hallmark of acute neural damage that contributes to nerve sprouting and can be used to assess ICNS damage.