Department of Internal Medicine, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232, USA.
Am J Emerg Med. 2010 Feb;28(2):256.e7-8. doi: 10.1016/j.ajem.2009.05.020.
Brugada syndrome is characterized by the electrocardiographic (ECG) pattern of right bundle-branch block (RBBB) with a high take-off, coved ST-segment elevation in the precordial leads V1 to V3, and the risk of sudden cardiac death. Typically, there is no evidence of structural heart disease. In many cases, Brugada syndrome has been linked to a mutation of the gene SCN5A, which encodes for the fast cardiac sodium channel. In patients with the Brugada syndrome, pharmacologic sodium channel blockade can increase the degree of ST-segment elevation. Interestingly, even in patients with a normal baseline ECG and no clinical suggestion of the Brugada syndrome, toxic doses of class I antiarrhythmic agents as well as toxicities with several nonantiarrhythmic drugs that possess sodium channel blocking properties can induce the Brugada ECG abnormality. Specifically, the beta-receptor blocker propranolol, at high doses, binds to the cardiac sodium channels and inhibits sodium uptake. In this report, we describe a case of severe propranolol toxicity, which resulted in the Brugada ECG pattern in an otherwise healthy individual who had no clinical or ECG suggestion of the genetically determined Brugada syndrome.
Brugada 综合征的特征为心电图(ECG)呈右束支传导阻滞(RBBB)伴 RBBB 起始陡峭、前间壁导联 V1 至 V3 的 ST 段抬高呈穹隆状,且有发生心源性猝死的风险。通常,无结构性心脏病的证据。在许多情况下,Brugada 综合征与 SCN5A 基因突变相关,该基因编码快速型心肌钠离子通道。在 Brugada 综合征患者中,药物性钠离子通道阻断可增加 ST 段抬高的程度。有趣的是,即使在基线 ECG 正常且无 Brugada 综合征临床提示的患者中,I 类抗心律失常药物的中毒剂量以及具有钠离子通道阻断特性的几种非抗心律失常药物的毒性也可诱发 Brugada 心电图异常。具体而言,高剂量的β受体阻滞剂普萘洛尔与心肌钠离子通道结合并抑制钠离子摄取。在本报告中,我们描述了一例严重的普萘洛尔中毒病例,该患者在无基因决定的 Brugada 综合征的临床或 ECG 提示的情况下出现了 Brugada 心电图模式,该患者身体健康。