Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia? Byron H. Gottschalk, Daniel D. Anselm, Adrian Baranchuk PII: DOI: Reference:

S0167-5273(14)01832-4 doi: 10.1016/j.ijcard.2014.09.112 IJCA 18888

To appear in:

International Journal of Cardiology

Received date: Accepted date:

7 September 2014 20 September 2014

Please cite this article as: Gottschalk Byron H., Anselm Daniel D., Baranchuk Adrian, Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia?, International Journal of Cardiology (2014), doi: 10.1016/j.ijcard.2014.09.112

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

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Byron H Gottschalk, BMSc, Daniel D. Anselm, MD, Adrian Baranchuk, MD FACC FRCPC

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Division of Cardiology, Electrophysiology and Pacing, Queen’s University, Kingston General Hospital, Kingston, Ontario, Canada

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Letter to the Editor

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Word Count: 418

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Key Words: Brugada Phenocopy; Brugada Syndrome; ischemia;

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Disclosures: None

Corresponding Author:

Adrian Baranchuk, MD FACC FRCPC Associate Professor of Medicine Cardiac Electrophysiology and Pacing Kingston General Hospital K7L 2V7 Queen's University Ph: 613 549 6666 ext 3801 Fax: 613 548 1387 Email: [email protected]

ACCEPTED MANUSCRIPT We read the case report by Jiang et al. with great interest and noted that their patient presented with a Type-1 Brugada ECG pattern after a radiofrequency catheter

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ablation procedure for atrial fibrillation [1]. The case is important as it contributes to the

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growing body of literature on Brugada Phenocopy (BrP) [2, 3].

BrP are clinical entities that present with ECGs identical to those of true Brugada

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Syndrome (BrS) but are elicited by various clinical circumstances [2, 3]. They may be

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induced by a number of clinical conditions that are characterized into six etiological categories: (i) metabolic conditions; (ii) mechanical compression; (iii) myocardial

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ischemia & pulmonary embolism; (iv) myocardial & pericardial disease; (v) ECG modulations; and (vi) miscellaneous [4]. The hallmark to diagnosis lies in a series of

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electrocardiographic and clinical features (Table 1) that aim to differentiate BrP from BrS [5, 6]. More information on the condition and a stepwise diagnostic approach can be

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found at the international registry and online educational portal for BrP (www.brugadaphenocopy.com). In the case presented by Jiang et al. [1], the patient developed a Brugada ECG pattern and a marked increase in troponin I (TnI) following an ablation procedure for atrial fibrillation. We agree with the authors that the mechanism behind this phenomenon was unlikely due to coronary vasospasm as the ST-elevations were sustained over a number of days. Michael et al. described a similar case of ST-segment elevations that occurred during an ablation procedure for atrial fibrillation [7]. An urgent coronary angiogram revealed a sub-total occlusion within the inferior branch of the 1st diagonal. We suspect that ischemia was also the likely mechanism behind ST-segment elevations and increased TnI in the present case [1]. Blood clots may be extremely small, and lysis

ACCEPTED MANUSCRIPT of these clots can occur in a matter of minutes. It is conceivable therefore, that this was an embolic phenomenon that was not captured by coronary angiography.

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As previously discussed by our group [3], ischemia may either induce a BrP [5] or

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modulate myocardial sodium channels resulting in the unmasking of true BrS [8]. A provocative test using a sodium channel blocker was therefore mandatory in this case.

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The negative result, coupled with the patient’s lack of personal or family history

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suggestive of BrS, allows us to confirm the diagnosis of BrP in this case. It will be included in our database as a Type 1A BrP under the category of ischemia and pulmonary

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embolism. We recommend the authors use the terminology Brugada Phenocopy in the future for consistency in the literature and to facilitate future research on this clinical

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phenomenon.

ACCEPTED MANUSCRIPT References

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Tables

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[1] Jiang C, Wang R, Lu W, Han B. A Brugada-like electrocardiogram pattern induced after radiofrequency catheter ablation of atrial fibrillation. Int J cardiol. 2014 (In press). [2] Anselm DD, Evans JM, Baranchuk A. Brugada phenocopy: A new electrocardiogram phenomenon. World J Cardiol. 2014;6:81-86. [3] Baranchuk A, Nguyen T, Ryu MH, Femenia F, Zareba W, Wilde AA, et al. Brugada phenocopy: new terminology and proposed classification. Ann Noninvasive Electrocardiol. 2012;17:299-314. [4] Anselm DD, Baranchuk A. Brugada phenocopy: redefinition and updated classification. Am J Cardiol. 2013;111:453. [5] Gottschalk BH, Anselm DD, Baranchuk A. Brugada Phenocopy international registry and online educational portal. 2014. Accessed September 4, 2014. www.brugadaphenocopy.com. [6] Anselm DD, Baranchuk A. Terminological clarification of Brugada Phenocopy, Brugada Syndrome, and the Brugada ECG pattern: re. early repolarization pattern in patients with provocable Brugada Phenocopy: a marker of additional arrhythmogenic cardiomyopathy. Int J Cardiol. 2014;171:288. [7] Michael KA, Redfearn DP, Simpson CS, Baranchuk A. An unusual complication of a pulmonary vein isolation. J Interv Card Electrophysiol. 2009;25:203-205. [8] Di Diego JM, Antzelevitch C. Acute myocardial ischemia: Cellular mechanisms underlying ST segment elevation. J Electrocardiol. 2014;47:486-490.

Table 1. Diagnostic criteria for Brugada Phenocopy and Differentiation from Brugada Syndrome Diagnostic criteria for Brugada Phenocopy I. An ECG pattern of either Type-1 or Type-2 Brugada morphology II. The patient has an underlying condition that is identifiable III. Resolution of the ECG pattern upon resolution of the underlying condition IV. Low clinical pretest probability for BrS determined by a lack of symptoms, medical history, and family history V. A negative provocative test with sodium channel blocker such as ajmaline, flecainide, or procainamide (not mandatory if surgical RVOT manipulation has occurred within the last 96 hours) VI. The results of genetic testing are negative (not mandatory as the SCN5A mutation is identifiable by only 20% to 30% of probands for BrS)

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

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