Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands.
J Am Coll Cardiol. 2010 Feb 23;55(8):789-97. doi: 10.1016/j.jacc.2009.11.033.
We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing.
BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization.
Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps.
A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p < 0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV.ms vs. 40 +/- 16 mV.ms, p < 0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees , p = NS), similar T(peak)-T(end) interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar T(peak)-T(end) dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS).
The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities.
通过研究在阿义马林激发试验中出现特征性 1 型 Brugada 综合征（BrS）心电图时各种心电图去极化和/或复极化变量的变化，我们试图深入了解 BrS 的病理生理基础。
BrS 与心源性猝死有关。尽管其病理生理基础尚未解决，但据信存在异常心脏去极化或异常复极化。
对 269 例疑似 BrS 患者进行阿义马林激发试验，同时记录心电图、向量心电图和 62 导体表电位图。
91 例患者（BrS 患者）诱发 1 型心电图，162 例患者试验结果阴性（对照组），16 例患者试验结果异常。与对照组相比，去极化异常在 BrS 患者中更为明显，且通过更长的右胸前滤波 QRS 复合波时限（142 ± 23 ms 比 125 ± 14 ms，p < 0.01）和右心尖终端传导延迟（60 ± 11 ms 比 53 ± 9 ms，p < 0.01）定位于右心室（RV）。复极异常与去极化异常一致，表现为稳定的低非极性含量（12 ± 8%比 8 ± 4%，p = NS）、较低的空间 QRS-T 积分（33 ± 12 mV.ms 比 40 ± 16 mV.ms，p < 0.05）、相似的空间 QRS-T 角度（92 ± 39 度比 87 ± 31 度，p = NS）、相似的 T(peak)-T(end) 间期（143 ± 36 ms 比 138 ± 25 ms，p = NS）和相似的 T(peak)-T(end) 离散度（47 ± 37 ms 比 45 ± 27 ms，p = NS）。
1 型 BrS 心电图的特征主要为局限性去极化异常，特别是 RV 的（终末）传导延迟，这可通过补充的非侵入性心电图技术进行评估。我们不能确定复极异常的单独作用，但建议心电图上看到的典型复极异常征象是继发于这些去极化异常。
