• Stephen L Rennyson and Laszlo Littmann.
• Department of Internal Medicine, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232, USA.
• Am J Emerg Med. 2010 Feb 1; 28 (2): 256.e7-8.

AbstractBrugada 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.

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