Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia?

Abstract

We read the casereport by Jiang et al. with great interest and notedthat their patient presented with a Type-1 Brugada ECG pattern after aradiofrequency catheter ablation procedure for atrial fibrillation [1].The caseis important asit contributesto thegrowingbodyof literatureon Brugada phenocopy (BrP) [2,3].BrP are clinical entities that present with ECGs identical to those oftrueBrugadasyndrome(BrS)butareelicitedbyvariousclinicalcircum-stances [2,3]. They may be induced by a number of clinical conditionsthat are characterized into six etiological categories: (i) metabolicconditions; (ii) mechanical compression; (iii) myocardial ischemia p (iv) myocardial & pericardial disease; (v) ECGmodulations; and (vi) miscellaneous [4]. The hallmark to diagnosislies in a series of electrocardiographic and clinical features (Table 1)that aim to differentiate BrP from BrS [5,6]. More information onthe condition and a stepwise diagnostic approach can be found at theinternational registry and online educational portal for BrP (www.brugadaphenocopy.com).In the case presented by Jiang et al. [1], the patient developed aBrugada ECG pattern and a marked increase in troponin I (TnI) follow-ing an ablation procedure for atrial fibrillation. We agree with theauthors that the mechanism behind this phenomenon was unlikelydue to coronary vasospasm as the ST-elevations were sustained over anumber of days. Michael et al. described a similar case of ST-segmentelevations that occurred during an ablation procedure for atrialfibrillation [7]. An urgent coronary angiogram revealed a sub-totalocclusion within the inferior branch of the 1st diagonal. We suspectthat ischemia was alsothelikely mechanismbehindST-segment eleva-tions and increased TnI in the present case [1]. Blood clots may beextremely small, and lysis of these clots can occur in a matter of mi-nutes.Itisconceivabletherefore,thatthiswasanembolicphenomenonthat was not captured by coronary angiography.As previously discussed by our group [3], ischemia may eitherinduce a BrP [5] or modulate myocardial sodium channels resulting intheunmaskingoftrueBrS[8].Aprovocativetestusingasodiumchannelblocker was therefore mandatory in this case. The negative result,coupled with the patient's lack of personal or family history suggestiveof BrS, allows us to confirm the diagnosis of BrP in this case. It will beincluded in our database as a Type 1A BrP under the category of ische-mia and pulmonary embolism. We recommend the authors use theterminologyBrugadaphenocopyinthefutureforconsistencyintheliter-ature and to facilitate future research on this clinical phenomenon.Conflict of interestNoneReferences