The greatest insights in science are obtained through integrative approaches that combine the best aspects emerging and traditional technologies. The study by Veerman et al1 that appears in this issue of Circulation Research thoughtfully integrates big data high throughput technology, small data molecular approaches, and electrophysiological methods to draw conclusions important both to the understanding of Brugada syndrome and normal ventricular function. Article, see p 537 More than 2 decades ago, Josep and Pedro Brugada first described a syndrome of ST-segment elevation, right bundle branch block, a high incidence of polymorphic ventricular tachycardia and ventricular fibrillation, and increased risk of sudden cardiac death.2 Research dating back to 1991 has described that the induction of phase 2 reentry by sodium channel block which was thought to be the cause of life-threatening arrhythmias in this syndrome,3 and which later became known as Brugada syndrome.4,5 In 1998, Chen et al6 showed linkage of the Brugada syndrome with a mutation in the SCN5A gene encoding the α subunit of the cardiac sodium channel protein. Because of the dynamic and temporary nature of the Brugada ECG pattern, sodium channel blockers (eg, ajmaline, flecainide, or procainamide) have been administered to unmask type 1 ECG patterns.7 Since the discovery of the SCN5A mutation, a total of 12 Brugada syndrome susceptibility genes have been identified (Brugada susceptibility [BrS] 1–12). Type 1 BrS or BrS1, caused by the loss-of-function mutation in the SCN5A-encoded subunit of the sodium channel, represents the most common genetic substrate for BrS accounting for ≤30% of the disorder.8,9 Furthermore, mutations of the L-type calcium channel α1, β2, and α2δ subunits encoded by CACNA1, CACNB2B, and CACNA2B are estimated to cause 10% to 15% of Brugada syndrome.10,11 Functional analyses have shown that …

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当高通量遇到力学研究时

通过将新兴技术和传统技术的最佳方面相结合的综合方法，可以获得对科学的最深刻见解。Veerman等[1]的研究周到地考虑了大数据高通量技术，小数据分子方法和电生理方法，以得出对理解Brugada综合征和正常心室功能均重要的结论。文章，见p537。二十多年前，Josep和Pedro Brugada首先描述了一种ST段抬高综合征，右束支传导阻滞，多形性室性心动过速和室颤的发生率高，以及心脏猝死的风险增加。2 1991年的研究表明，钠通道阻滞诱导2期再进入，这被认为是该综合征危及生命的心律不齐的原因3，后来被称为Brugada综合征。4,51998年Chen等[6]显示Brugada综合征与编码心脏钠通道蛋白α亚基的SCN5A基因突变有关。由于Brugada ECG模式的动态和暂时性，已施用钠通道阻滞剂（例如，阿马琳，氟卡尼或普鲁卡因酰胺）来掩盖1型ECG模式。7自从发现SCN5A突变以来，总共有12种Brugada综合征易感基因已被鉴定（Brugada易感性[BrS] 1-12）。类型1 BrS或BrS1，