Brugada syndrome unmasked by lithium.
ABSTRACT A 38-year-old man was brought by emergency medical service after resuscitation following cardiac arrest. The patient was found pulseless with a wide complex tachycardia. The patient had bipolar disorder and was on lithium, lamotrigine, and ziprasidone. His electrolytes and lithium levels were normal. An electrocardiogram (EKG) was performed the next day and showed type 1 Brugada pattern. Lithium was held. Electrophysiologists made a diagnosis of drug-unmasked Brugada syndrome. Lithium can unmask Brugada syndrome through its ability to block sodium channels, even at subtherapeutic concentrations. Physicians need to be aware of this potentially fatal drug effect and should monitor EKGs of patients on lithium.
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ABSTRACT: Drug-induced Brugada syndrome (BrS) represents a great challenge for the prescribing clinicians as well as for those involved in the development of novel pharmaceuticals and in the regulatory bodies responsible with monitoring drug safety. Apart from well-known cardiac agents (mainly Class I antiarrhythmics), an increasing number of noncardiac agents, including psychotropic and anesthetic drugs, have been shown to induce the characteristic Brugada electrocardiogram pattern predisposing to fatal ventricular arrhythmias. Up to now, both repolarization and depolarization abnormalities are thought to be related to the development of ventricular fibrillation in BrS patients. This review highlights the mechanisms and the noncardiac medical agents that unmask a genetic predisposition to BrS.Pacing and Clinical Electrophysiology 08/2013; DOI:10.1111/pace.12234