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Drug‐Induced Brugada Syndrome by Noncardiac Agents
Author(s) -
LETSAS KONSTANTINOS P.,
KAVVOURAS CHARALAMPOS,
KOLLIAS GEORGE,
TSIKRIKAS SPYRIDON,
KORANTZOPOULOS PANAGIOTIS,
EFREMIDIS MICHALIS,
SIDERIS ANTONIOS
Publication year - 2013
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/pace.12234
Subject(s) - medicine , brugada syndrome , drug , ventricular fibrillation , anti arrhythmia agents , sudden cardiac death , cardiology , drug development , intensive care medicine , pharmacology , atrial fibrillation
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.

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