Brugada syndrome: report of the second consensus conference.

Brugada syndrome: report of the second consensus conference.
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布鲁格达综合征:第二次共识会议报告。

DOI:
10.1016/j.hrthm.2005.01.005
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发表时间:
2005
期刊:
影响因子:
5.5
通讯作者:
Wilde,Arthur
Wilde,Arthur
中科院分区:
医学2区
文献类型:
--
作者:
Antzelevitch,Charles;Brugada,Pedro;Borggrefe,Martin;Brugada,Josep;Brugada,Ramon;Corrado,Domenico;Gussak,Ihor;LeMarec,Herve;Nademanee,Koonlawee;PerezRiera,AndresRicardo;Shimizu,Wataru;Schulze-Bahr,Eric;Tan,Hanno;Wilde,Arthur

文献摘要

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自1992年作为临床实体引入以来,Brugada综合征已从一种罕见疾病发展为仅次于汽车事故的第二大死亡原因。心电图特征为右胸导联ST段明显抬高,该综合征与年轻人和其他健康成人的心源性猝死风险高相关,在婴儿和儿童中发生率较低。自发出现Brugada心电图的患者因室性心动过速/心室颤动而发生心律失常猝死的风险很高。Brugada综合征的ECG表现通常是动态的或隐蔽的,可能被钠通道阻滞剂、发热状态、迷走神经紧张剂、α-肾上腺素能激动剂、β-肾上腺素能阻滞剂、三环或四环抗抑郁药、葡萄糖和胰岛素联合用药、低钾血症和高钾血症、高钙血症以及酒精和可卡因毒性所掩盖或调节。近年来,报告的病例数量呈指数级上升,定义该疾病的临床、遗传、细胞、离子和分子方面的文章显著增加。2002年发表的第一次协商一致会议的报告侧重于诊断标准。本报告产生于2003年9月举行的第二次协商一致会议,根据现有的临床和基础科学数据,进一步阐述了诊断标准,并审查了风险分层计划以及治疗的装置和药理学方法。
Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.