Background

The pathogenesis of Brugada syndrome (BrS) and consequently of abnormal electrograms (aEGMs) found in the epicardium of the right ventricular outflow tract (RVOT-EPI) is controversial.

Objective

The purpose of this study was to analyze aEGM from high-density RVOT-EPI electroanatomic mapping (EAM).

Methods

All patients undergoing RVOT-EPI EAM with the HD-Grid catheter for BrS were retrospectively included. Maps were acquired before and after ajmaline, and all patients had concomitant noninvasive electrocardiographic imaging with annotation of RVOT-EPI latest activation time (RVOTat). High-frequency potentials (HFPs) were defined as ventricular potentials occurring during or after the far-field ventricular EGM showing a local activation time (HFPat). Low-frequency potentials (LFPs) were defined as aEGMs occurring after near-field ventricular activation showing fractionation or delayed components. Their activation time from surface ECG was defined as LFPat.

Results

Fifteen consecutive patients were included in the study. At EAM before ajmaline, 7 patients (46.7%) showed LFPs. All patients showed HFPs before and after ajmaline and LFPs after ajmaline. Mean HFPat (134.4 vs 65.3 ms, P <.001), mean LFPat (224.6 vs 113.6 ms, P <.001), and mean RVOTat (124.8 vs 55.9 ms, P <.001) increased after ajmaline. RVOTat correlated with HFPat before (ρ = 0.76) and after ajmaline (ρ = 0.82), while RVOTat was shorter than LFPat before (P <.001) and after ajmaline (P <.001). BrS patients with history of aborted sudden cardiac death had longer aEGMs after ajmaline.

Conclusion

Two different types of aEGMs are described from BrS high-density epicardial mapping. This might correlate with depolarization and repolarization abnormalities.

中文翻译：

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Brugada 综合征的高密度心外膜标测：去极化和复极化异常

背景

Brugada 综合征 (BrS) 的发病机制以及因此在右心室流出道心外膜 (RVOT-EPI) 中发现的异常电图 (aEGM) 的发病机制是有争议的。

客观的

本研究的目的是分析来自高密度 RVOT-EPI 电解剖标测 (EAM) 的 aEGM。

方法

回顾性纳入了所有接受 RVOT-EPI EAM 并使用 HD-Grid 导管治疗 BrS 的患者。在ajmaline之前和之后获取地图，所有患者都进行了伴随无创心电图成像，并标注了RVOT-EPI最近激活时间（RVOTat）。高频电位 (HFPs) 定义为显示局部激活时间 (HFPat) 的远场心室 EGM 期间或之后发生的心室电位。低频电位 (LFP) 被定义为在近场心室激活后发生的 aEGM，显示出分级或延迟成分。他们从表面心电图的激活时间被定义为 LFPat。

结果

研究中包括 15 名连续患者。在阿吉马林之前的 EAM 中，7 名患者 (46.7%) 出现 LFP。所有患者在阿吉马林前后均出现 HFP，在阿吉马林后出现 LFP。平均 HFPat（134.4 vs 65.3 ms，P <.001）、平均 LFPat（224.6 vs 113.6 ms，P <.001）和平均 RVOTat（124.8 vs 55.9 ms，P <.001）在阿吉马林后增加。RVOTat 与 Ajmaline 之前 (ρ = 0.76) 和之后 (ρ = 0.82) 的 HFPat 相关，而 RVOTat 比 Ajmaline 之前 ( P  <.001) 和之后 ( P <.001) 的 LFPat 短。有流产心源性猝死病史的 BrS 患者在阿吉马林后的 aEGM 时间更长。

结论

BrS 高密度心外膜标测描述了两种不同类型的 aEGM。这可能与去极化和复极化异常有关。