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本文引用的文献

1
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.局部去极化异常是 1 型 Brugada 综合征心电图的主要病理生理机制：一项关于心电图、向量心电图和哇巴因激发时体表电位图的研究。
J Am Coll Cardiol. 2010 Feb 23;55(8):789-97. doi: 10.1016/j.jacc.2009.11.033.
2
SCN5A mutations and the role of genetic background in the pathophysiology of Brugada syndrome.SCN5A突变及遗传背景在Brugada综合征病理生理学中的作用。
Circ Cardiovasc Genet. 2009 Dec;2(6):552-7. doi: 10.1161/CIRCGENETICS.109.853374. Epub 2009 Sep 29.
3
Mechanism of right precordial ST-segment elevation in structural heart disease: excitation failure by current-to-load mismatch.结构性心脏病患者心前区右侧 ST 段抬高的机制：电流与负荷不匹配导致的激动失败。
Heart Rhythm. 2010;7(2):238-48. doi: 10.1016/j.hrthm.2009.10.007. Epub 2009 Oct 12.
4
Ventricular late potential in patients with apparently normal electrocardiogram; predictor of Brugada syndrome.心电图看似正常的患者的心室晚电位；Brugada综合征的预测指标。
Pacing Clin Electrophysiol. 2010 Mar;33(3):266-73. doi: 10.1111/j.1540-8159.2009.02621.x. Epub 2009 Dec 1.
5
Exercise-induced ECG changes in Brugada syndrome.布加综合征运动诱发的心电图改变。
Circ Arrhythm Electrophysiol. 2009 Oct;2(5):531-9. doi: 10.1161/CIRCEP.109.862441. Epub 2009 Aug 24.
6
Absence of pathognomonic or inflammatory patterns in cardiac biopsies from patients with Brugada syndrome.Brugada综合征患者心脏活检中缺乏特征性或炎症性模式。
Circ Arrhythm Electrophysiol. 2009 Feb;2(1):16-23. doi: 10.1161/CIRCEP.107.737882. Epub 2008 Dec 7.
7
Slow and discontinuous conduction conspire in Brugada syndrome: a right ventricular mapping and stimulation study.缓慢且不连续传导在Brugada综合征中共同起作用：一项右心室标测与刺激研究。
Circ Arrhythm Electrophysiol. 2008 Dec;1(5):379-86. doi: 10.1161/CIRCEP.108.790543. Epub 2008 Dec 2.
8
Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org).药物与 Brugada 综合征患者：文献回顾、建议和最新网站（www.brugadadrugs.org）。
Heart Rhythm. 2009 Sep;6(9):1335-41. doi: 10.1016/j.hrthm.2009.07.002. Epub 2009 Jul 8.
9
Differential effects of cardiac sodium channel mutations on initiation of ventricular arrhythmias in patients with Brugada syndrome.心脏钠通道突变对Brugada综合征患者室性心律失常起始的不同影响。
Heart Rhythm. 2009 Apr;6(4):487-92. doi: 10.1016/j.hrthm.2009.01.031. Epub 2009 Jan 31.
10
Functional effects of KCNE3 mutation and its role in the development of Brugada syndrome.KCNE3 突变的功能效应及其在 Brugada 综合征发生发展中的作用。
Circ Arrhythm Electrophysiol. 2008 Aug;1(3):209-18. doi: 10.1161/CIRCEP.107.748103.

Brugada 综合征的病理生理学机制：去极化与复极化。

The pathophysiological mechanism underlying Brugada syndrome: depolarization versus repolarization.

机构信息

Department of Cardiology, Academic Medical Center Amsterdam, Amsterdam, The Netherlands.

出版信息

J Mol Cell Cardiol. 2010 Oct;49(4):543-53. doi: 10.1016/j.yjmcc.2010.07.012. Epub 2010 Jul 24.

DOI:10.1016/j.yjmcc.2010.07.012
PMID:20659475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2932806/
Abstract

This Point/Counterpoint presents a scholarly debate of the mechanisms underlying the electrocardiographic and arrhythmic manifestations of Brugada syndrome (BrS), exploring in detail the available evidence in support of the repolarization vs. depolarization hypothesis.

摘要

本观点对论呈现了一场关于 Brugada 综合征（BrS）心电图和心律失常表现背后机制的学术辩论，详细探讨了支持复极与去极化假说的现有证据。