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 underlying 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 normalizes. To date, reports have documented BrP in the context of singular clinical events. More recently, recurrent BrP has been demonstrated in the context of recurrent hypokalemia. This demonstrates clinical reproducibility, 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 phenomena are reproduced under strictly controlled environmental conditions. The development of these validation models will help us determine whether BrP are transient alterations of sodium channels that are not reproducible with a sodium channel provocative test or alternatively, 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 investigation. 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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