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Brugada phenocopy following coronary artery bypass graft surgery
Journal of Electrocardiology 59 (2020) 134–139
Contents lists available at ScienceDirect
Journal of Electrocardiology journal homepage: www.jecgonline.com
Brugada phenocopy following coronary artery bypass graft surgery Yi Li a,⁎, Tong Liu b, Gary Tse b, Liang Tao a a
Department of Cardiothoracic Surgery, Wuhan Asia Heart Hospital Affiliated to Wuhan University of Science and Technology, Hubei, China Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China
b
a r t i c l e
i n f o
Available online xxxx
a b s t r a c t A 71-year old male with a history of inferior myocardial infarction and hypertension underwent coronary artery bypass graft (CABG) surgery. He had no family or personal history of syncope, sudden cardiac death or Brugada syndrome. A series of twelve-lead electrocardiograms showed type 1 and type 2 Brugada ECG patterns after procedure, but resolution of ST segment changes to five days later. The electrophysiological mechanisms underlying these changes will be discussed. © 2020 Elsevier Inc. All rights reserved.
Case presentation A 71-year-old male with a history of inferior wall myocardial infarction and hypertension was admitted for recurrent unstable angina episodes. He had no family or personal history of syncope, sudden cardiac death or Brugada syndrome. His initial 12-lead electrogram demonstrated abnormal Q waves in leads II, III, and aVF with no abnormalities in leads V1 to V3 (Fig. 1A). Coronary angiography revealed multi-vessel disease (MVD). Echocardiography showed widening of the ascending aorta (3.5 cm), mild tricuspid regurgitation and abnormal left ventricular diastolic function. The patient underwent coronary artery bypass graft (CABG) surgery. Three saphenous veins were anastomosed (endto-side) with obtuse marginal (OM) branch, the first diagonal (D1) branch and distal right coronary artery (RCA). The other end of saphenous veins anastomosed with the ascending aorta. His left internal mammary artery (LIMA) was used for revascularization between left anterior descending (LAD) branch and left subclavian artery (LSCA). The procedure time was 4 h and 35 min, with an aortic cross-clamp time (ACCT) of 76 min and cardiopulmonary bypass (CPB) time of 123 min. His ECG taken day 1 postoperatively showed J-point and ST segment elevation in lead V2, which became more pronounced on the next day (Fig. 1B) while echocardiography at bedside revealed a small amount (1.1 cm) of pericardial effusion at the roof of the right atrium and a 5.2 × 2.7 cm hematoma in the anterior mediastinum. On day 3, a type 2 Brugada ECG pattern was observed (Fig. 2A), progressing to a type 1 pattern on day 4 (Fig. 2B). A repeated ECG taken on day 4 with leads V1 and V2 placed on the 3rd intercostal space showed persistent Brugada patterns (Fig. 4A). However, the ECG abnormalities were ⁎ Corresponding author at: Wuhan Asia Heart Hospital Affiliated to Wuhan University of Science and Technology, Hubei, China. E-mail address: [email protected] (Y. Li).
https://doi.org/10.1016/j.jelectrocard.2020.02.006 0022-0736/© 2020 Elsevier Inc. All rights reserved.
resolved on day 5, with normalization of J point elevation and STsegment changes (Fig. 3). Pericardial effusion was spontaneously absorbed with anterior mediastinal hematoma organization according to echocardiography on day 5. Preoperative troponin was normal while postoperative peak of troponin was 1.14 ng/ml on day 1 and backed to normal within next 4 days. Electrolyte levels were normal throughout. Medications known to induce Brugada patterns were not prescribed. Discussion The main findings of this case are that patients undergoing CAGB can present with dynamic ECG changes that are suggestive of Brugada ECG patterns. There are two important issues that need to be addressed: (1) whether the ECGs were ischemia inducing true Brugada syndrome ECG pattern or Brugada phenocopy (BrP) associated to ischemia (or mechanical compression), and (2) the possible mechanisms underlying such ECG findings. BrPs are clinical entities that refer to ECG patterns which are identical to ECGs observed in Brugada syndrome [1]. However, they may have different etiologies, such as “metabolic conditions, mechanical compression, myocardial ischemia (including cases secondary to coronary anomalies and interventional procedure), pulmonary embolism, myocardial and pericardial disease, ECG modulations and miscellaneous conditions” [2–7]. These conditions must be distinguished from true Brugada syndrome as these are potential reversible causes and do not necessitate invasive treatments such as implantable cardioverter-defibrillator (ICD) insertion. Diagnosis of BrP is made on satisfying the following criteria: negative provocative testing using sodium channel blockers, negative genetic findings for SCN5A (not mandatory) and low pretest probability for Brugada syndrome [8]. In our case, the patient presented ECGs compatible with successively type 2 and type 1 Brugada ECG patterns had a low pretest probability of
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
135
Fig. 1. A. ECG) taken before CABG revealed Q waves in lead II, III and aVF with normal J-point in V1 and V2. Non-specific ST segment and T-wave changes were observed in V4 to V6. B. ECG taken 2 days operatively revealed J-point elevation in V2.
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Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
Fig. 2. A. On day 3, the ECG demonstrated a type 2 Brugada pattern in lead V2 with β-angle of 70.5°. Base of the triangle was 9.5 mm. B. ECG taken on day 4 revealed a type 1 Brugada pattern with high take-off less than 2 mm.
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
137
Fig. 3. ECG taken on day 5 revealed resolution of J-point and ST segment changes in the right precordial leads.
Brugada syndrome, and declined provocative testing and genetic testing. However, whether the ECG shown in Fig. 2B should be classified as type 1 BrP is controversial. This is because the high take-off observed in lead V2 did not meet the criteria of 2 mm rise, but there have been previously published BrP cases of coved pattern with a high take-off between 1 and 2 mm [9]. In any cases, because the J-point and ST segment changes are dynamics, it is possible that greater rises were not detected in-between the recorded ECGs. For detailed discussion on the morphological criteria of BrP, the reader is directed to this excellent reference here [10]. Some potential reasons for the origin of the Brugada ECG patterns following CABG include pericardial inflammation that results from cardiac surgery, mediastinal hematoma compression the RVOT and graft occlusion triggering acute ischemia [11]. It is worth mentioning that the higher electrode placement of leads V1–V3 should be ruled out first for which could form an rSr morphology similar to Brugada pattern in normal condition [12]. Although the P-wave in leads V1–V2 were different in Figs. 1 and 2, which may indicate the high electrode placement, the comparison of the ECG characteristics in leads V1–V2 placed on a different intercostal space (third) do not support this possibility in our case (Fig. 4B). The possible explanation for the different P waves is that the atrial depolarization is affected by mediastinal hematoma or pericardial effusion on the right atrium. Pericardiotomy-induced inflammation and stimulation of grafts can alter epicardial repolarization, thereby inducing ST-segment changes. Previously, cardiac compression
arising from mediastinal tumors or pectus excavatum have been reported causes of BrPs [13,14]. Although the compression of the mediastinal hematoma on the RV caused BrP has never been reported, it could still be a possible reason of the ECG pattern in lead V2. The J-point elevation in lead I and aVL can explicable by the pericardial effusion or anterior mediastinal hematoma, which can alter myocardial motion and the direction of repolarization. Furthermore, during cardiac surgery, the use of extracorporeal circulation and direct mechanical trauma can produce transient myocardial injury, leading to cellular edema and inflammation. Persistent incomplete right branch bundle block, ischemia-reperfusion injury, effects of general anesthetic agents could potentially lead to repolarization abnormalities [15]. Finally, perioperative myocardial ischemia or infarction should not be ignored although the patient had already received a treatment of CABG. It has been estimated that transient myocardial ischemia occurs in 33% of patients after CABG procedure. Early postoperative acute myocardial ischemia or infarction, which is major due to stenosis or occlusion of the saphenous vein graft (SVG) or the internal mammary artery (IMA) graft, IMA spasm and steal phenomenon of subclavian artery [16], may either induce a BrP [17] or unmask a true Brugada Syndrome (BrS) by modulating myocardial sodium channels [18]. Therefore, it is pivotal to distinct these causes to ensure that the patient is managed appropriately and prevent unnecessary and costly investigations [19]. The decreasing trend of plasma TnI levels and the absence of pathological Q waves in the ECG suggested a low possibility of perioperative myocardial
138
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
Fig. 4. A. ECG recorded on day 4 by moving VI and V2 electrodes to the 3rd ICS. A type 2 Brugada pattern was observed in lead V2. B. Comparison of the leads V1 and V2 recorded on day 4 and day 5. The P wave in lead V1 was bidirectional on day 4 and day 5 with electrodes placed correctly (black arrow), and the P wave was completely negative by moving lead V1 to the 3rd ICS on day 4 (red star) which consistent with high electrode placement performance. Similar changes appeared in lead V2. The atypical changes of QRS complex may be related to mediastinal hematoma, pericardial effusion and intraventricular conductive condition.
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
infarction. Nevertheless, imaging is needed to confirm or exclude acute myocardial ischemia such as conus branch of the RCA spasm or dissection [20,21], coronary steal effect [22] and transient mechanical compression on coronary artery or the graft. Conclusion We presented a case of transient and self-normalized BrP following CABG surgery with multiple contributory causes. Larger registry studied is needed to investigate the temporal trends of BrP ECG changes observed after CABG surgery. CRediT authorship contribution statement Yi Li: Conceptualization, Software, Formal analysis, Resources, Writing - original draft. Tong Liu: Methodology, Writing - review & editing, Supervision. Gary Tse: Investigation, Visualization, Project administration. Liang Tao: Validation, Data curation. References [1] Tse G, Liu T, Li KH, Laxton V, Chan YW, Keung W, et al. Electrophysiological mechanisms of Brugada syndrome: insights from pre-clinical and clinical studies. Front Physiol 2016;7:467. [2] Baranchuk A, Nguyen T, Ryu MH, Femenía F, Zareba W, Wilde A, et al. Brugada phenocopy: new terminology and proposed classification. Ann Noninvasive Electrocardiol 2012;17(4):299–314. [3] Zhang N, Liu T, Tse G, Yu S, Fu H, Xu G, et al. Brugada phenocopy in a patient with acute pulmonary embolism presenting with recurrent syncope. Oxf Med Case Reports 2017;2017(5):omx014. [4] Sreenivasan S, Monaghan M, Baranchuk A. Multifactorial Brugada phenocopy. JAMA Intern Med 2018;178(6):872–3. [5] Gottschalk BH, Anselm DD, Baranchuk A. Coronary anomalies resulting in ischemia induced Brugada phenocopy. Int J Cardiol 2015;199:75–6. [6] Gottschalk BH, Baranchuk A. Ischemia-induced Brugada phenocopy during balloon angioplasty. Int J Cardiol 2016;205:160.
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[7] Gottschalk BH, Anselm DD, Baranchuk A. Ischemic Brugada phenocopy during ablation of ventricular tachycardia. J Arrhythm 2016;32:156. [8] Gottschalk BH, Anselm DD, Brugada J, Brugada P, Wilde A, Chiale P, et al. Expert cardiologists cannot distinguish between Brugada phenocopy and Brugada syndrome electrocardiogram patterns. EP Europace 2016;18(7):1095–100. [9] Bayés de LA, Brugada J, Baranchuk A, Borggrefe M, Breithardt G, Goldwasser D, et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report. J Electrocardiol 2012;45(5):433–42. [10] Anselm DD, Gottschalk BH, Baranchuk A. Brugada phenocopies: consideration of morphologic criteria and early findings from an international registry. Can J Cardiol 2014;30(12):1511–5. [11] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy international registry and online educational portal. Available at http://www.brugadaphenocopy.com. [12] García-Niebla J, Baranchuk A, de Luna AB. True Brugada pattern or only high V1-V2 electrode placement? J Electrocardiol 2014;47(5):756–8. [13] Perez-Riera AR, Barbosa B, Daminello-Raimundo R, Resende Barbosa MPC, de Abreu LC. Brugada phenocopy caused by a compressive mediastinal tumor. Ann Noninvasive Electrocardiol 2018;23(3):e12509. [14] Siniorakis E, Arvanitakis S, Tzevelekos P, Panta S, Balanis A, Aivalioti F, et al. Pectus excavatum: right ventricular compromise with orthostatic syndrome and Brugada phenocopy. J Saudi Heart Assoc 2017;29(3):223–6. [15] Perez-Riera AR, Barbosa-Barros R, Daminello-Raimundo R, de Abreu LC, Baranchuk A. Unusual ST-segment elevation in the anterolateral precordial leads: ischemia, Brugada phenocopy, Brugada syndrome, all, or none? Circulation 2017;136(20): 1976–8. [16] Hirsch WS, Ledley GS, Kotler MN. Acute ischemic syndromes following coronary artery bypass graft surgery. Clin Cardiol 1998;21:625–32. [17] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia? Int J Cardiol 2014;177(2):619–20. [18] Di Diego JM, Antzelevitch C. Acute myocardial ischemia: cellular mechanisms underlying ST segment elevation. J Electrocardiol 2014;47(4):486–90. [19] Xu G, Gottschalk BH, Pérez-Riera A, Barbosa-Barros R, Dendramis G, Carrizo AG, et al. Link between Brugada phenocopy and myocardial ischemia: results from the International Registry on Brugada Phenocopy. Pacing Clin Electrophysiol 2019;42: 658–62. [20] Agrawal S, Stevens S, Shirani J, Garg J, Nanda S. Ischemia-induced Brugada phenocopy. J Electrocardiol 2015;48(5):815–7. [21] Carrizo AG, Goransky A, Baranchuk A. Brugada phenocopy during right coronary artery dissection. J Electrocardiol 2017;50(6):969–71. [22] Guamán VC, Ferrando-Castagnetto F, Marichal P, Acquistapace F, Trujillo P, Baranchuk A. Brugada phenocopy secondary to extensive inferior wall ischemia induced by coronary steal effect. Ann Noninvasive Electrocardiol 2020;25(1):e12689.
Contents lists available at ScienceDirect
Journal of Electrocardiology journal homepage: www.jecgonline.com
Brugada phenocopy following coronary artery bypass graft surgery Yi Li a,⁎, Tong Liu b, Gary Tse b, Liang Tao a a
Department of Cardiothoracic Surgery, Wuhan Asia Heart Hospital Affiliated to Wuhan University of Science and Technology, Hubei, China Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China
b
a r t i c l e
i n f o
Available online xxxx
a b s t r a c t A 71-year old male with a history of inferior myocardial infarction and hypertension underwent coronary artery bypass graft (CABG) surgery. He had no family or personal history of syncope, sudden cardiac death or Brugada syndrome. A series of twelve-lead electrocardiograms showed type 1 and type 2 Brugada ECG patterns after procedure, but resolution of ST segment changes to five days later. The electrophysiological mechanisms underlying these changes will be discussed. © 2020 Elsevier Inc. All rights reserved.
Case presentation A 71-year-old male with a history of inferior wall myocardial infarction and hypertension was admitted for recurrent unstable angina episodes. He had no family or personal history of syncope, sudden cardiac death or Brugada syndrome. His initial 12-lead electrogram demonstrated abnormal Q waves in leads II, III, and aVF with no abnormalities in leads V1 to V3 (Fig. 1A). Coronary angiography revealed multi-vessel disease (MVD). Echocardiography showed widening of the ascending aorta (3.5 cm), mild tricuspid regurgitation and abnormal left ventricular diastolic function. The patient underwent coronary artery bypass graft (CABG) surgery. Three saphenous veins were anastomosed (endto-side) with obtuse marginal (OM) branch, the first diagonal (D1) branch and distal right coronary artery (RCA). The other end of saphenous veins anastomosed with the ascending aorta. His left internal mammary artery (LIMA) was used for revascularization between left anterior descending (LAD) branch and left subclavian artery (LSCA). The procedure time was 4 h and 35 min, with an aortic cross-clamp time (ACCT) of 76 min and cardiopulmonary bypass (CPB) time of 123 min. His ECG taken day 1 postoperatively showed J-point and ST segment elevation in lead V2, which became more pronounced on the next day (Fig. 1B) while echocardiography at bedside revealed a small amount (1.1 cm) of pericardial effusion at the roof of the right atrium and a 5.2 × 2.7 cm hematoma in the anterior mediastinum. On day 3, a type 2 Brugada ECG pattern was observed (Fig. 2A), progressing to a type 1 pattern on day 4 (Fig. 2B). A repeated ECG taken on day 4 with leads V1 and V2 placed on the 3rd intercostal space showed persistent Brugada patterns (Fig. 4A). However, the ECG abnormalities were ⁎ Corresponding author at: Wuhan Asia Heart Hospital Affiliated to Wuhan University of Science and Technology, Hubei, China. E-mail address: [email protected] (Y. Li).
https://doi.org/10.1016/j.jelectrocard.2020.02.006 0022-0736/© 2020 Elsevier Inc. All rights reserved.
resolved on day 5, with normalization of J point elevation and STsegment changes (Fig. 3). Pericardial effusion was spontaneously absorbed with anterior mediastinal hematoma organization according to echocardiography on day 5. Preoperative troponin was normal while postoperative peak of troponin was 1.14 ng/ml on day 1 and backed to normal within next 4 days. Electrolyte levels were normal throughout. Medications known to induce Brugada patterns were not prescribed. Discussion The main findings of this case are that patients undergoing CAGB can present with dynamic ECG changes that are suggestive of Brugada ECG patterns. There are two important issues that need to be addressed: (1) whether the ECGs were ischemia inducing true Brugada syndrome ECG pattern or Brugada phenocopy (BrP) associated to ischemia (or mechanical compression), and (2) the possible mechanisms underlying such ECG findings. BrPs are clinical entities that refer to ECG patterns which are identical to ECGs observed in Brugada syndrome [1]. However, they may have different etiologies, such as “metabolic conditions, mechanical compression, myocardial ischemia (including cases secondary to coronary anomalies and interventional procedure), pulmonary embolism, myocardial and pericardial disease, ECG modulations and miscellaneous conditions” [2–7]. These conditions must be distinguished from true Brugada syndrome as these are potential reversible causes and do not necessitate invasive treatments such as implantable cardioverter-defibrillator (ICD) insertion. Diagnosis of BrP is made on satisfying the following criteria: negative provocative testing using sodium channel blockers, negative genetic findings for SCN5A (not mandatory) and low pretest probability for Brugada syndrome [8]. In our case, the patient presented ECGs compatible with successively type 2 and type 1 Brugada ECG patterns had a low pretest probability of
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
135
Fig. 1. A. ECG) taken before CABG revealed Q waves in lead II, III and aVF with normal J-point in V1 and V2. Non-specific ST segment and T-wave changes were observed in V4 to V6. B. ECG taken 2 days operatively revealed J-point elevation in V2.
136
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
Fig. 2. A. On day 3, the ECG demonstrated a type 2 Brugada pattern in lead V2 with β-angle of 70.5°. Base of the triangle was 9.5 mm. B. ECG taken on day 4 revealed a type 1 Brugada pattern with high take-off less than 2 mm.
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
137
Fig. 3. ECG taken on day 5 revealed resolution of J-point and ST segment changes in the right precordial leads.
Brugada syndrome, and declined provocative testing and genetic testing. However, whether the ECG shown in Fig. 2B should be classified as type 1 BrP is controversial. This is because the high take-off observed in lead V2 did not meet the criteria of 2 mm rise, but there have been previously published BrP cases of coved pattern with a high take-off between 1 and 2 mm [9]. In any cases, because the J-point and ST segment changes are dynamics, it is possible that greater rises were not detected in-between the recorded ECGs. For detailed discussion on the morphological criteria of BrP, the reader is directed to this excellent reference here [10]. Some potential reasons for the origin of the Brugada ECG patterns following CABG include pericardial inflammation that results from cardiac surgery, mediastinal hematoma compression the RVOT and graft occlusion triggering acute ischemia [11]. It is worth mentioning that the higher electrode placement of leads V1–V3 should be ruled out first for which could form an rSr morphology similar to Brugada pattern in normal condition [12]. Although the P-wave in leads V1–V2 were different in Figs. 1 and 2, which may indicate the high electrode placement, the comparison of the ECG characteristics in leads V1–V2 placed on a different intercostal space (third) do not support this possibility in our case (Fig. 4B). The possible explanation for the different P waves is that the atrial depolarization is affected by mediastinal hematoma or pericardial effusion on the right atrium. Pericardiotomy-induced inflammation and stimulation of grafts can alter epicardial repolarization, thereby inducing ST-segment changes. Previously, cardiac compression
arising from mediastinal tumors or pectus excavatum have been reported causes of BrPs [13,14]. Although the compression of the mediastinal hematoma on the RV caused BrP has never been reported, it could still be a possible reason of the ECG pattern in lead V2. The J-point elevation in lead I and aVL can explicable by the pericardial effusion or anterior mediastinal hematoma, which can alter myocardial motion and the direction of repolarization. Furthermore, during cardiac surgery, the use of extracorporeal circulation and direct mechanical trauma can produce transient myocardial injury, leading to cellular edema and inflammation. Persistent incomplete right branch bundle block, ischemia-reperfusion injury, effects of general anesthetic agents could potentially lead to repolarization abnormalities [15]. Finally, perioperative myocardial ischemia or infarction should not be ignored although the patient had already received a treatment of CABG. It has been estimated that transient myocardial ischemia occurs in 33% of patients after CABG procedure. Early postoperative acute myocardial ischemia or infarction, which is major due to stenosis or occlusion of the saphenous vein graft (SVG) or the internal mammary artery (IMA) graft, IMA spasm and steal phenomenon of subclavian artery [16], may either induce a BrP [17] or unmask a true Brugada Syndrome (BrS) by modulating myocardial sodium channels [18]. Therefore, it is pivotal to distinct these causes to ensure that the patient is managed appropriately and prevent unnecessary and costly investigations [19]. The decreasing trend of plasma TnI levels and the absence of pathological Q waves in the ECG suggested a low possibility of perioperative myocardial
138
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
Fig. 4. A. ECG recorded on day 4 by moving VI and V2 electrodes to the 3rd ICS. A type 2 Brugada pattern was observed in lead V2. B. Comparison of the leads V1 and V2 recorded on day 4 and day 5. The P wave in lead V1 was bidirectional on day 4 and day 5 with electrodes placed correctly (black arrow), and the P wave was completely negative by moving lead V1 to the 3rd ICS on day 4 (red star) which consistent with high electrode placement performance. Similar changes appeared in lead V2. The atypical changes of QRS complex may be related to mediastinal hematoma, pericardial effusion and intraventricular conductive condition.
Y. Li et al. / Journal of Electrocardiology 59 (2020) 134–139
infarction. Nevertheless, imaging is needed to confirm or exclude acute myocardial ischemia such as conus branch of the RCA spasm or dissection [20,21], coronary steal effect [22] and transient mechanical compression on coronary artery or the graft. Conclusion We presented a case of transient and self-normalized BrP following CABG surgery with multiple contributory causes. Larger registry studied is needed to investigate the temporal trends of BrP ECG changes observed after CABG surgery. CRediT authorship contribution statement Yi Li: Conceptualization, Software, Formal analysis, Resources, Writing - original draft. Tong Liu: Methodology, Writing - review & editing, Supervision. Gary Tse: Investigation, Visualization, Project administration. Liang Tao: Validation, Data curation. References [1] Tse G, Liu T, Li KH, Laxton V, Chan YW, Keung W, et al. Electrophysiological mechanisms of Brugada syndrome: insights from pre-clinical and clinical studies. Front Physiol 2016;7:467. [2] Baranchuk A, Nguyen T, Ryu MH, Femenía F, Zareba W, Wilde A, et al. Brugada phenocopy: new terminology and proposed classification. Ann Noninvasive Electrocardiol 2012;17(4):299–314. [3] Zhang N, Liu T, Tse G, Yu S, Fu H, Xu G, et al. Brugada phenocopy in a patient with acute pulmonary embolism presenting with recurrent syncope. Oxf Med Case Reports 2017;2017(5):omx014. [4] Sreenivasan S, Monaghan M, Baranchuk A. Multifactorial Brugada phenocopy. JAMA Intern Med 2018;178(6):872–3. [5] Gottschalk BH, Anselm DD, Baranchuk A. Coronary anomalies resulting in ischemia induced Brugada phenocopy. Int J Cardiol 2015;199:75–6. [6] Gottschalk BH, Baranchuk A. Ischemia-induced Brugada phenocopy during balloon angioplasty. Int J Cardiol 2016;205:160.
139
[7] Gottschalk BH, Anselm DD, Baranchuk A. Ischemic Brugada phenocopy during ablation of ventricular tachycardia. J Arrhythm 2016;32:156. [8] Gottschalk BH, Anselm DD, Brugada J, Brugada P, Wilde A, Chiale P, et al. Expert cardiologists cannot distinguish between Brugada phenocopy and Brugada syndrome electrocardiogram patterns. EP Europace 2016;18(7):1095–100. [9] Bayés de LA, Brugada J, Baranchuk A, Borggrefe M, Breithardt G, Goldwasser D, et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report. J Electrocardiol 2012;45(5):433–42. [10] Anselm DD, Gottschalk BH, Baranchuk A. Brugada phenocopies: consideration of morphologic criteria and early findings from an international registry. Can J Cardiol 2014;30(12):1511–5. [11] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy international registry and online educational portal. Available at http://www.brugadaphenocopy.com. [12] García-Niebla J, Baranchuk A, de Luna AB. True Brugada pattern or only high V1-V2 electrode placement? J Electrocardiol 2014;47(5):756–8. [13] Perez-Riera AR, Barbosa B, Daminello-Raimundo R, Resende Barbosa MPC, de Abreu LC. Brugada phenocopy caused by a compressive mediastinal tumor. Ann Noninvasive Electrocardiol 2018;23(3):e12509. [14] Siniorakis E, Arvanitakis S, Tzevelekos P, Panta S, Balanis A, Aivalioti F, et al. Pectus excavatum: right ventricular compromise with orthostatic syndrome and Brugada phenocopy. J Saudi Heart Assoc 2017;29(3):223–6. [15] Perez-Riera AR, Barbosa-Barros R, Daminello-Raimundo R, de Abreu LC, Baranchuk A. Unusual ST-segment elevation in the anterolateral precordial leads: ischemia, Brugada phenocopy, Brugada syndrome, all, or none? Circulation 2017;136(20): 1976–8. [16] Hirsch WS, Ledley GS, Kotler MN. Acute ischemic syndromes following coronary artery bypass graft surgery. Clin Cardiol 1998;21:625–32. [17] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy induced by ischemia or Brugada syndrome unmasked by ischemia? Int J Cardiol 2014;177(2):619–20. [18] Di Diego JM, Antzelevitch C. Acute myocardial ischemia: cellular mechanisms underlying ST segment elevation. J Electrocardiol 2014;47(4):486–90. [19] Xu G, Gottschalk BH, Pérez-Riera A, Barbosa-Barros R, Dendramis G, Carrizo AG, et al. Link between Brugada phenocopy and myocardial ischemia: results from the International Registry on Brugada Phenocopy. Pacing Clin Electrophysiol 2019;42: 658–62. [20] Agrawal S, Stevens S, Shirani J, Garg J, Nanda S. Ischemia-induced Brugada phenocopy. J Electrocardiol 2015;48(5):815–7. [21] Carrizo AG, Goransky A, Baranchuk A. Brugada phenocopy during right coronary artery dissection. J Electrocardiol 2017;50(6):969–71. [22] Guamán VC, Ferrando-Castagnetto F, Marichal P, Acquistapace F, Trujillo P, Baranchuk A. Brugada phenocopy secondary to extensive inferior wall ischemia induced by coronary steal effect. Ann Noninvasive Electrocardiol 2020;25(1):e12689.