Pacific Rim Electrophysiology Research Institute, 1700 Cesar E. Chavez Avenue, Los Angeles, CA 90033, USA.
Circulation. 2011 Mar 29;123(12):1270-9. doi: 10.1161/CIRCULATIONAHA.110.972612. Epub 2011 Mar 14.
The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (Vt/VF) in patients with the Brugada syndrome (BrS) remains unelucidated. However, several studies have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electrophysiological substrate. We hypothesized that in patients with BrS who have frequent recurrent VF episodes, the substrate site is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified at this location, which would serve as the target site for catheter ablation.
We studied 9 symptomatic patients with the BrS (all men; median age 38 years) who had recurrent VF episodes (median 4 episodes) per month, necessitating implantable cardioverter defibrillator discharge. Electroanatomic mapping of the right ventricle, both endocardially and epicardially, and epicardial mapping of the left ventricle were performed in all patients during sinus rhythm. All patients had typical type 1 Brugada ECG pattern and inducible Vt/VF; they were found to have unique abnormal low voltage (0.94±0.79 mV), prolonged duration (132±48 ms), and fractionated late potentials (96±47 ms beyond QRS complex) clustering exclusively in the anterior aspect of the RVOT epicardium. Ablation at these sites rendered Vt/VF noninducible (7 of 9 patients [78%]; 95% confidence interval, 0.40 to 0.97, P=0.015) and normalization of the Brugada ECG pattern in 89% (95% confidence interval, 0.52 to 0.99; P=0.008). Long-term outcomes (20±6 months) were excellent, with no recurrent Vt/VF in all patients off medication (except 1 patient on amiodarone).
The underlying electrophysiological mechanism in patients with BrS is delayed depolarization over the anterior aspect of the RVOT epicardium. Catheter ablation over this abnormal area results in normalization of the Brugada ECG pattern and prevents Vt/VF, both during electrophysiological studies as well as spontaneous recurrent Vt/VF episodes in patients with BrS.
导致 Brugada 综合征（BrS）患者心电图异常模式和室性心动过速/心室颤动（Vt/VF）的潜在电生理机制仍未阐明。然而，多项研究表明，右心室流出道（RVOT）可能是电生理基质所在部位。我们假设在 BrS 患者中，反复发生 VF 发作的患者，其基质部位是 RVOT 心外膜或心内膜上；在此部位可识别到异常电活动，该部位将作为导管消融的靶点。
我们研究了 9 例有症状的 BrS 患者（均为男性；中位年龄 38 岁），他们每月反复发作 VF（中位 4 次），需要植入式心脏复律除颤器放电。所有患者在窦性心律时均行右心室心内膜和心外膜电标测以及左心室心外膜标测。所有患者均有典型的 1 型 Brugada 心电图模式和可诱发的 Vt/VF；发现其具有独特的异常低电压（0.94±0.79 mV）、长持续时间（132±48 ms）和晚期碎裂电位（QRS 波群后 96±47 ms），这些均局限于 RVOT 心外膜的前侧。在此部位消融可使 Vt/VF 不再可诱发（9 例中有 7 例[78%]；95%置信区间，0.40 至 0.97，P=0.015），89%（95%置信区间，0.52 至 0.99；P=0.008）的 Brugada 心电图模式恢复正常。长期结果（20±6 个月）良好，所有患者停药后均未再发生 Vt/VF（除 1 例服用胺碘酮外）。
BrS 患者的潜在电生理机制是 RVOT 心外膜前侧延迟去极化。在此异常区域行导管消融可使 Brugada 心电图模式正常化，并预防 Vt/VF，无论是在电生理研究中还是在 BrS 患者的自发性反复 Vt/VF 发作中。
