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Coronary anomalies resulting in ischemia induced Brugada Phenocopy
International Journal of Cardiology 199 (2015) 75–76
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Coronary anomalies resulting in ischemia induced Brugada Phenocopy☆ Byron H. Gottschalk a, Daniel D. Anselm b, Adrian Baranchuk a,⁎ a b
Division of Cardiology, Electrophysiology and Pacing, Queen's University, Kingston General Hospital, Kingston, Ontario, Canada Libin Cardiovascular Institute of Alberta, Foothills Medical Centre, University of Calgary, Calgary, Alberta, Canada
a r t i c l e
i n f o
Article history: Received 2 July 2015 Accepted 2 July 2015 Available online 6 July 2015 Keywords: Brugada Phenocopy Brugada Syndrome Ischemia
We read the case report by Dendramis et al. with great interest and noted that their patient presented with typical ischemic type chest pain, rise in troponins, and a Type 1 Brugada ECG pattern [1]. The case is important as it expands our current understanding on ischemic causes of Brugada Phenocopy (BrP). BrPs are clinical entities that present with ECGs identical to those found in Brugada Syndrome (BrS) but are the result of various clinical circumstances [2,3]. They may be induced by a number of clinical conditions that are characterized into six etiological categories: (i) metabolic conditions; (ii) mechanical compression; (iii) myocardial ischemia & pulmonary embolism; (iv) myocardial & pericardial disease; (v) ECG modulations; and (vi) miscellaneous [4]. Diagnosis of BrP relies on a series of clinical and electrocardiographic features that differentiate BrP from BrS [5,6]. See www.brugadaphenocopy.com for more information. Dendramis et al. [1] present the case of a patient who developed typical chest pain, a marked increase in troponin I (TnI), and presented with a Type 1 Brugada ECG pattern. There was no sign of coronary atherosclerosis on percutaneous coronary angiography; however, two fistulous communications were identified. The first arose from the conus artery, likely connecting to a mediastinal vessel, while the second was found to arise from the atrial artery and likely connected to the right bronchial circulation. After resolution of the acute event, the ECG
☆ All authors had access to the data and a role in writing the manuscript. All authors approved the submission of the manuscript. ⁎ Corresponding author at: Cardiac Electrophysiology and Pacing, Kingston General Hospital, K7L 2V7, Queen's University, Canada. E-mail address: [email protected] (A. Baranchuk).
http://dx.doi.org/10.1016/j.ijcard.2015.07.009 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
normalized and the patient underwent a provocative challenge using flecainide, the results of which were negative. The authors [1] postulate that the fistulae resulted in temporary ischemia of the right ventricular outflow tract (RVOT) leading to the Brugada ECG pattern. This case is particularly interesting as it discusses an anatomic anomaly that presumably resulted in myocardial ischemia. Myocardial ischemia is a well-known etiology of BrP [7–9]; however, it may also unmask BrS through modulation of myocardial sodium channels [8]. In cases of Brugada patterns observed during ischemia, it is especially important to differentiate between the two conditions as longterm treatment may differ depending on the diagnosis. In this case, the negative provocative challenge, coupled with the patient's lack of personal or family history suggestive of BrS, confirms the diagnosis of BrP. It has been included in our database as a Type 1A BrP under the category of myocardial ischemia and pulmonary embolism. This is an important case in the category as it is the first description of confirmed BrP due to an anomaly in the coronary circulation. It provides evidence that atypical causes of myocardial ischemia may induce BrP and the diagnosis should be considered in such cases. We recommend use of the terminology Brugada Phenocopy in future manuscripts for consistency in the literature and to facilitate research on the phenomenon. Disclosures None. Funding None. References [1] G. Dendramis, C. Paleologo, D. Piraino, P. Assennato, Coronary artery fistulas and Brugada ECG pattern, a random association? Int. J. Cardiol. 197 (2015) 78–80. [2] D.D. Anselm, B.H. Gottschalk, A. Baranchuk, Brugada phenocopies: consideration of morphologic criteria and early findings from an international registry, Can. J. Cardiol. 30 (2014) 1511–1515. [3] A. Baranchuk, T. Nguyen, M.H. Ryu, F. Femenia, W. Zareba, A.A. Wilde, et al., Brugada phenocopy: new terminology and proposed classification, Ann. Noninvasive Electrocardiol. 17 (2012) 299–314. [4] D.D. Anselm, A. Baranchuk, Brugada phenocopy: redefinition and updated classification, Am. J. Cardiol. 111 (2013) 453. [5] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada Phenocopy International Registry and Online Educational Portal, 2015. Accessed July 1, 2015.
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[6] D.D. Anselm, A. Baranchuk, 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. 171 (2014) 288. [7] D.D. Anselm, R. Barbosa-Barros, L. de Sousa Belém, R. Nogueira de Macedo, A.R. PérezRiera, A. Baranchuk, Brugada phenocopy induced by acute inferior ST-segment
elevation myocardial infarction with right ventricular involvement, Inn. Card. Rhythm Manag. 4 (2013) 1092–1094. [8] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia? Int. J. Cardiol. 177 (2014) 619–620. [9] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada syndrome unmasked by ischemia needs full risk evaluation, Intern. Emerg. Med. 10 (2015) 111–112.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Coronary anomalies resulting in ischemia induced Brugada Phenocopy☆ Byron H. Gottschalk a, Daniel D. Anselm b, Adrian Baranchuk a,⁎ a b
Division of Cardiology, Electrophysiology and Pacing, Queen's University, Kingston General Hospital, Kingston, Ontario, Canada Libin Cardiovascular Institute of Alberta, Foothills Medical Centre, University of Calgary, Calgary, Alberta, Canada
a r t i c l e
i n f o
Article history: Received 2 July 2015 Accepted 2 July 2015 Available online 6 July 2015 Keywords: Brugada Phenocopy Brugada Syndrome Ischemia
We read the case report by Dendramis et al. with great interest and noted that their patient presented with typical ischemic type chest pain, rise in troponins, and a Type 1 Brugada ECG pattern [1]. The case is important as it expands our current understanding on ischemic causes of Brugada Phenocopy (BrP). BrPs are clinical entities that present with ECGs identical to those found in Brugada Syndrome (BrS) but are the result of various clinical circumstances [2,3]. They may be induced by a number of clinical conditions that are characterized into six etiological categories: (i) metabolic conditions; (ii) mechanical compression; (iii) myocardial ischemia & pulmonary embolism; (iv) myocardial & pericardial disease; (v) ECG modulations; and (vi) miscellaneous [4]. Diagnosis of BrP relies on a series of clinical and electrocardiographic features that differentiate BrP from BrS [5,6]. See www.brugadaphenocopy.com for more information. Dendramis et al. [1] present the case of a patient who developed typical chest pain, a marked increase in troponin I (TnI), and presented with a Type 1 Brugada ECG pattern. There was no sign of coronary atherosclerosis on percutaneous coronary angiography; however, two fistulous communications were identified. The first arose from the conus artery, likely connecting to a mediastinal vessel, while the second was found to arise from the atrial artery and likely connected to the right bronchial circulation. After resolution of the acute event, the ECG
☆ All authors had access to the data and a role in writing the manuscript. All authors approved the submission of the manuscript. ⁎ Corresponding author at: Cardiac Electrophysiology and Pacing, Kingston General Hospital, K7L 2V7, Queen's University, Canada. E-mail address: [email protected] (A. Baranchuk).
http://dx.doi.org/10.1016/j.ijcard.2015.07.009 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
normalized and the patient underwent a provocative challenge using flecainide, the results of which were negative. The authors [1] postulate that the fistulae resulted in temporary ischemia of the right ventricular outflow tract (RVOT) leading to the Brugada ECG pattern. This case is particularly interesting as it discusses an anatomic anomaly that presumably resulted in myocardial ischemia. Myocardial ischemia is a well-known etiology of BrP [7–9]; however, it may also unmask BrS through modulation of myocardial sodium channels [8]. In cases of Brugada patterns observed during ischemia, it is especially important to differentiate between the two conditions as longterm treatment may differ depending on the diagnosis. In this case, the negative provocative challenge, coupled with the patient's lack of personal or family history suggestive of BrS, confirms the diagnosis of BrP. It has been included in our database as a Type 1A BrP under the category of myocardial ischemia and pulmonary embolism. This is an important case in the category as it is the first description of confirmed BrP due to an anomaly in the coronary circulation. It provides evidence that atypical causes of myocardial ischemia may induce BrP and the diagnosis should be considered in such cases. We recommend use of the terminology Brugada Phenocopy in future manuscripts for consistency in the literature and to facilitate research on the phenomenon. Disclosures None. Funding None. References [1] G. Dendramis, C. Paleologo, D. Piraino, P. Assennato, Coronary artery fistulas and Brugada ECG pattern, a random association? Int. J. Cardiol. 197 (2015) 78–80. [2] D.D. Anselm, B.H. Gottschalk, A. Baranchuk, Brugada phenocopies: consideration of morphologic criteria and early findings from an international registry, Can. J. Cardiol. 30 (2014) 1511–1515. [3] A. Baranchuk, T. Nguyen, M.H. Ryu, F. Femenia, W. Zareba, A.A. Wilde, et al., Brugada phenocopy: new terminology and proposed classification, Ann. Noninvasive Electrocardiol. 17 (2012) 299–314. [4] D.D. Anselm, A. Baranchuk, Brugada phenocopy: redefinition and updated classification, Am. J. Cardiol. 111 (2013) 453. [5] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada Phenocopy International Registry and Online Educational Portal, 2015. Accessed July 1, 2015.
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B.H. Gottschalk et al. / International Journal of Cardiology 199 (2015) 75–76
[6] D.D. Anselm, A. Baranchuk, 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. 171 (2014) 288. [7] D.D. Anselm, R. Barbosa-Barros, L. de Sousa Belém, R. Nogueira de Macedo, A.R. PérezRiera, A. Baranchuk, Brugada phenocopy induced by acute inferior ST-segment
elevation myocardial infarction with right ventricular involvement, Inn. Card. Rhythm Manag. 4 (2013) 1092–1094. [8] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia? Int. J. Cardiol. 177 (2014) 619–620. [9] B.H. Gottschalk, D.D. Anselm, A. Baranchuk, Brugada syndrome unmasked by ischemia needs full risk evaluation, Intern. Emerg. Med. 10 (2015) 111–112.