RESUMO
Introduction: Unsuccessful endocardial ablation for perimitral atrial flutter (AFL) could be attributed by the epicardial bridging. Objective: This study aimed to investigate the electrophysiological characteristics of epicardial breakthrough during catheter ablation of perimitral AFL. Materials and methods: This retrospective study recruited 40 patients who received successful catheter ablation of perimitral AFL from January 2016 to June 2021. The patients were divided into two groups: group 1 (n = 18) successful endocardial ablation, and group 2 (n = 22) successful epicardial ablation following unsuccessful endocardial ablation owing to incomplete mitral block or unachievable termination AFL. The local electrogram (EGM) interval of coronary sinus (CS) duration perimitral AFL was measured before catheter ablation. Results: There was no significant difference in the baseline characteristics between the two groups. In group 2, 60% of successful epicardial ablation was performed in intra-CS ablation and 40% in VOM ethanol infusion. Group 2 patients had a longer EGM interval of distal CS than that in group 1 (CS1-2: 64.2 17.5 vs. 42.4 0.09 ms, P = 0.008, CS3-4: 57.13 19.4 vs. 43.8 7.5 ms; P = 0.001). The conduction velocity at successful site was slower in group 2 compared to group 1 (0.18 0.05 vs. 0.75 0.19 m/s, P = 0.040). In the multivariate analysis, distal EGM interval (CS1-2) was identified as independent predictor of the need of epicardial ablation with the optimal cutoff of 49 ms. Conclusion: Longer EGM interval in distal CS during perimitral AFL was observed in perimitral AFL patients with epicardial breakthrough following endocardial-failed ablation, which may be associated with the need of epicardial ablation.
RESUMO
Long QT syndrome (LQTS) is commonly presented with life-threatening ventricular arrhythmias (VA). Renal artery denervation (RDN) is an alternative antiadrenergic treatment that attenuates sympathetic activity. We aimed to evaluate the efficacy of RDN on preventing VAs in LQTS rabbits induced by drugs. The subtypes of LQTS were induced by infusion of HMR-1556 for LQTS type 1 (LQT1), erythromycin for LQTS type 2 (LQT2), and veratridine for LQTS type 3 (LQT3). Forty-four rabbits were randomized into the LQT1, LQT2, LQT3, LQT1-RDN, LQT2-RDN, and LQT3-RDN groups. All rabbits underwent cardiac electrophysiology studies. The QTc interval of the LQT2-RDN group was significantly shorter than those in the LQT2 group (650.08 ± 472.67 vs. 401.78 ± 42.91 ms, p = 0.011). The QTc interval of the LQT3-RDN group was significantly shorter than those in the LQT3 group (372.00 ± 22.41 vs. 335.70 ± 28.21 ms, p = 0.035). The VA inducibility in all subtypes of the LQT-RDN groups was significantly lower than those in the LQT-RDN groups, respectively (LQT1: 9.00 ± 3.30 vs. 47.44 ± 4.21%, p < 0.001; LQT2: 11.43 ± 6.37 vs. 45.38 ± 5.29%, p = 0.026; LQT3: 10.00 ± 6.32 vs. 32.40 ± 7.19%, p = 0.006). This study demonstrated the neuromodulation of RDN leading to electrical remodeling and reduced VA inducibility of the ventricular substrate in LQT models.
