Pannone Luigi, Monaco Cinzia, Sorgente Antonio, Vergara Pasquale, Calburean Paul-Adrian, Gauthey Anaïs, Bisignani Antonio, Kazawa Shuichiro, Strazdas Antanas, Mojica Joerelle, Lipartiti Felicia, Al Housari Maysam, Miraglia Vincenzo, Rizzi Sergio, Sofianos Dimitrios, Cecchini Federico, Osório Thiago Guimarães, Paparella Gaetano, Ramak Robbert, Overeinder Ingrid, Bala Gezim, Almorad Alexandre, Ströker Erwin, Pappaert Gudrun, Sieira Juan, Brugada Pedro, La Meir Mark, Chierchia Gian Battista, de Asmundis Carlo
Heart Rhythm Management Centre, Postgraduate Program in Cardiac Electrophysiology and Pacing, Universitair Ziekenhuis Brussel-Vrije Universiteit Brussel, European Reference Networks Guard-Heart, Brussels, Belgium.
Cardiac Surgery Department, Universitair Ziekenhuis Brussel-Vrije Universiteit Brussel, Brussels, Belgium.
Heart Rhythm. 2022 Mar;19(3):397-404. doi: 10.1016/j.hrthm.2021.09.032. Epub 2021 Oct 1.
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.
The purpose of this study was to analyze aEGM from high-density RVOT-EPI electroanatomic mapping (EAM).
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.
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.
Two different types of aEGMs are described from BrS high-density epicardial mapping. This might correlate with depolarization and repolarization abnormalities.
Brugada综合征(BrS)的发病机制以及右心室流出道心外膜(RVOT-EPI)中发现的异常心内膜电图(aEGMs)存在争议。
本研究旨在分析高密度RVOT-EPI电解剖标测(EAM)中的aEGM。
回顾性纳入所有使用HD-Grid导管进行RVOT-EPI EAM以诊断BrS的患者。在阿义马林给药前后获取标测图,所有患者均同时进行无创心电图成像,并标注RVOT-EPI最晚激动时间(RVOTat)。高频电位(HFPs)定义为在远场心室心内膜电图期间或之后出现的心室电位,显示局部激动时间(HFPat)。低频电位(LFPs)定义为在近场心室激动后出现的aEGMs,显示碎裂或延迟成分。它们从体表心电图的激动时间定义为LFPat。
连续15例患者纳入研究。在阿义马林给药前的EAM中,7例患者(46.7%)显示LFPs。所有患者在阿义马林给药前后均显示HFPs,给药后显示LFPs。阿义马林给药后,平均HFPat(134.4对65.3毫秒,P<.001)、平均LFPat(224.6对113.6毫秒,P<.001)和平均RVOTat(124.8对55.9毫秒,P<.001)增加。阿义马林给药前(ρ = 0.76)和给药后(ρ = 0.82),RVOTat与HFPat相关,而阿义马林给药前(P<.001)和给药后(P<.001),RVOTat均短于LFPat。有心脏性猝死未遂病史的BrS患者在阿义马林给药后aEGMs更长。
从BrS高密度心外膜标测中描述了两种不同类型的aEGMs。这可能与去极化和复极化异常相关。