Local Depolarization Abnormalities Are the Dominant Pathophysiologic Mechanism for Type 1 Electrocardiogram in Brugada Syndrome A Study of Electrocardiograms, Vectorcardiograms, and Body Surface Potential Maps During Ajmaline Provocation
Local Depolarization Abnormalities Are the Dominant Pathophysiologic Mechanism for Type 1 Electrocardiogram in Brugada Syndrome A Study of Electrocardiograms, Vectorcardiograms, and Body Surface Potential Maps During Ajmaline Provocation
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DOI：
10.1016/j.jacc.2009.11.033
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发表时间：
2010-02-23
影响因子：
24
通讯作者：
Tan, Hanno L.
中科院分区：
文献类型：
--
作者：
Postema, Pieter G.;van Dessel, Pascal F. H. M.;Tan, Hanno L.
目的：我们试图通过研究在急性激发试验中Brugada综合征（BrS）1型心电图（ECG）的发展过程中各种心电图去极化和/或复极化变量的变化，来获得对Brugada综合征（BrS）病理生理基础的新认识。方法对269例疑有BrS的患者进行了心房肌电激发，同时记录心电图、心向量图和62导联体表电位图，结果91例患者的心电图均为1型在BrS患者中，162例患者的检测结果为阴性（对照组），16例患者的检测结果异常。去极化异常在BrS患者中更为突出，并且通过较长的右心前区过滤QRS波群持续时间（142 +/- 23 ms vs. 125 +/- 14 ms，p < 0.01）和右终末传导延迟（60 +/- 11 ms vs. 53 +/- 9 ms，p < 0.01）映射到右心室（RV）。复极异常与去极异常保持一致，如稳定的低非偶极含量（12 +/- 8% vs. 8 +/-4%，p = NS），较低的空间QRS-T积分（33 +/- 12 mV）。ms vs. 40 +/- 16 mV。ms，p < 0.05），相似的空间QRS-T角（92 +/- 39度vs. 87 +/- 31度，p = NS），T峰-T末间期相似（143 +/- 36 ms vs. 138 +/- 25 ms，p = NS）和相似的T峰-Tend离散度（47 +/- 37 ms vs. 45 +/- 27 ms，p = NS）。结论1型BrS ECG主要以局部除极异常为特征，特别是RV（终末）传导延迟，通过补充无创心电图技术进行评估。我们无法确定复极异常的单独作用，但认为ECG上观察到的复极紊乱的典型体征继发于这些去极化异常。（J Am科尔心脏病学杂志2010; 55：789-97）（C）美国心脏病学会基金会2010年
ObjectivesWe 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.BackgroundBrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization.MethodsAjmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps.ResultsA 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 Tpeak-Tend dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS).ConclusionsThe 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. (J Am Coll Cardiol 2010; 55: 789-97) (C) 2010 by the American College of Cardiology Foundation