Haïssaguerre Michel, Nademanee Koonlawee, Sacher Frédéric, Cheniti Ghassen, Hocini Mélèze, Surget Elodie, Dubois Rémi, Vigmond Edward, Bernus Olivier
Univ. Bordeaux, CRCTB U1045, Inserm, Bordeaux, France; IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France; Bordeaux University Hospital, Bordeaux, France.
Bumrungrad Hospital, Bangkok, Thailand.
Heart Rhythm. 2022 Mar;19(3):417-426. doi: 10.1016/j.hrthm.2021.10.030. Epub 2021 Nov 1.
The Brugada pattern manifests as a spontaneous variability of the electrocardiographic marker, suggesting a variability of the underlying electrical substrate.
The purpose of this study was to investigate the response of the epicardial substrate of Brugada syndrome (BrS) to programmed ventricular stimulation and to Na blocker infusion.
We investigated 6 patients (all male; mean age 54 ± 14 years) with BrS and recurrent ventricular fibrillation. Five had no type 1 BrS electrocardiogram pattern at admission. They underwent combined epicardial-endocardial mapping using multielectrode catheters. Changes in epicardial electrograms were evaluated during single endocardial extrastimulation and after low-dose ajmaline infusion (0.5 mg/kg in 5 minutes).
All patients had a region in the anterior epicardial right ventricle with prolonged multicomponent electrograms. Single extrastimulation prolonged late epicardial components by 59 ± 31 ms and in 4 patients abolished epicardial components at some sites, without reactivation by surrounding activated sites. These localized blocks occurred at an initial coupling interval of 335 ± 58 ms and then expanded to other sites, being observed in up to 40% of epicardial sites. Ajmaline infusion prolonged electrogram duration in all and produced localized blocks in 62% of sites in the same patients as during extrastimulation. Epicardial conduction recovery after ajmaline occurred intermittently and at discontinuous sites and produced beat-to-beat changes in local repolarization, resulting in an area of marked electrical disparity. These changes were consistent with models based on microstructural alterations under critical propagation conditions.
In BrS, localized functional conduction blocks occur at multiple epicardial sites and with variable patterns, without being reactivated from the surrounding sites.
Brugada波表现为心电图标志物的自发变异性，提示潜在电基质的变异性。
本研究旨在探讨Brugada综合征（BrS）的心外膜基质对程序性心室刺激和钠通道阻滞剂输注的反应。
我们研究了6例（均为男性；平均年龄54±14岁）患有BrS和复发性室颤的患者。5例入院时无1型BrS心电图模式。他们使用多电极导管进行了心外膜-心内膜联合标测。在单次心内膜额外刺激期间和低剂量阿义马林输注（5分钟内0.5mg/kg）后，评估心外膜电图的变化。
所有患者的心外膜右心室前壁均有一个多成分电图延长的区域。单次额外刺激使心外膜晚期成分延长59±31毫秒，4例患者的某些部位心外膜成分消失，周围激活部位未重新激活。这些局部阻滞发生在初始耦合间期为335±58毫秒时，然后扩展到其他部位，在心外膜部位中高达40%可观察到。阿义马林输注使所有患者的电图持续时间延长，并在与额外刺激相同的患者中62%的部位产生局部阻滞。阿义马林后心外膜传导恢复间歇性且在不连续部位发生，并导致局部复极逐搏变化，形成明显的电差异区域。这些变化与基于临界传播条件下微观结构改变的模型一致。
在BrS中，局部功能性传导阻滞发生在多个心外膜部位，且模式可变，周围部位不会重新激活。
