Abstract

Brugada phenocopies(BrP) are clinical entities that are etiologically distinct from true congenital Brugada syndrome. BrP are characterized by type 1 or type 2 Brugada electrocardiogram(ECG) patterns in precordial leads V1-V3. However, BrP are elicited by various un-derlying clinical conditions such as myocardial ischemia, pulmonary embolism, electrolyte abnormalities, or poor ECG filters. Upon resolution of the inciting underlying pathological condition, the BrP ECG subsequently nor-malizes. To date, reports have documented BrP in the context of singular clinical events. More recently, recur-rent BrP has been demonstrated in the context of re-current hypokalemia. This demonstrates clinical repro-ducibility, thereby advancing the concept of this new ECG phenomenon. The key to further understanding the pathophysiological mechanisms behind BrP requires experimental model validation in which these phenom-ena are reproduced under strictly controlled environ-mental conditions. The development of these validation models will help us determine whether BrP are tran-sient alterations of sodium channels that are not repro-ducible with a sodium channel provocative test or al-ternatively, a malfunction of other ion channels. In this editorial, we discuss the conceptual emergence of BrP as a new ECG phenomenon, review the progress made to date and identify opportunities for further investiga-tion. In addition, we also encourage investigators that are currently reporting on these cases to use the term BrP in order to facilitate literature searches and to help establish this emerging concept.

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