Editorial
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World J Cardiol. Mar 26, 2014; 6(3): 81-86
Published online Mar 26, 2014. doi: 10.4330/wjc.v6.i3.81
Brugada phenocopy: A new electrocardiogram phenomenon
Daniel D Anselm, Jennifer M Evans, Adrian Baranchuk
Daniel D Anselm, Jennifer M Evans, Adrian Baranchuk, Division of Cardiology, Electrophysiology and Pacing, Queen’s University, Kingston General Hospital, Kingston, Ontario K7L 2V7, Canada
Author contributions: Anselm DD and Baranchuk A contributed equally to this work; Anselm DD wrote the manuscript including the initial draft and subsequent revisions; Evans JM revised the paper to meet grammatical and linguistic standards; Baranchuk A designed the manuscript, contributed to revisions and served as senior advisor; all authors read and approved the final manuscript.
Correspondence to: Adrian Baranchuk, MD, FACC, FRCPC, Associate Professor of Medicine, Division of Cardiology, Electrophysiology and Pacing, Queen’s University, Kingston General Hospital, 76 Stuart Street, Kingston, Ontario K7L 2V7, Canada. barancha@kgh.kari.net
Telephone: +1-613-5496666 Fax: +1-613-5481387
Received: November 11, 2013
Revised: December 24, 2013
Accepted: January 15, 2014
Published online: March 26, 2014
Processing time: 128 Days and 10.6 Hours
Core Tip

Core tip: Diagnostic distinctions between Brugada phenocopies (BrP) and Brugada syndrome (BrS) are: (1) BrP patients have a reversible underlying condition and upon resolution of this condition, the electrocardiogram normalizes; (2) BrP patients have a low pretest probability of BrS as opposed to a high pretest probability in patients with true congenital BrS; and (3) BrP patients have a negative sodium channel blocker test, while patients with BrS have a positive test. The different electrocardiographic response to the provocative challenge highlights a pathophysiological divergence when comparing BrP and BrS. This suggests alternative underlying mechanisms with various genetic, structural and environmental interactions yet to be elucidated.