Nagase Satoshi, Kusano Kengo Fukushima, Morita Hiroshi, Nishii Nobuhiro, Banba Kimikazu, Watanabe Atsuyuki, Hiramatsu Shigeki, Nakamura Kazufumi, Sakuragi Satoru, Ohe Tohru
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
J Am Coll Cardiol. 2008 Mar 25;51(12):1154-61. doi: 10.1016/j.jacc.2007.10.059.
We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS).
Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave.
In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of pilsicainide.
Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of pilsicainide and in all of the 19 patients after the administration of pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of pilsicainide administration.
Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
我们研究了Brugada综合征（BrS）患者复极异常与伴有终末T波倒置的穹窿型ST段抬高（1型心电图[ECG]）之间的关系。
最近的实验研究表明，右心室动作电位（AP）切迹的加重优先延长心外膜AP，导致T波倒置。
对19例BrS患者和3例对照者，使用右心室流出道的局部单极电图直接检测心外膜和心内膜的激活-恢复间期（ARIs）和复极时间（RTs）。在服用吡西卡尼前后检查体表心电图、ARI和RT。
19例BrS患者中，10例在服用吡西卡尼前观察到1型ECG，19例患者在服用吡西卡尼后均观察到1型ECG。我们发现，在基线条件下，所有9例无1型ECG的BrS患者以及所有对照者中，无论是否服用吡西卡尼，心外膜的ARI和RT均短于心内膜。然而，在基线条件下表现为1型ECG的10例BrS患者中的8例以及服用吡西卡尼后的所有BrS患者中，观察到心外膜ARI长于心内膜ARI。此外，无论是否服用吡西卡尼，所有表现为1型ECG的患者中心外膜RT均长于心内膜RT。
我们的数据支持以下假设，即与1型BrS ECG相关的负向T波是由于右心室流出道区域AP切迹加重继发的心外膜AP优先延长所致。
