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Brugada phenocopy in the context of intracranial hemorrhage
IJCA-18772; No of Pages 2 International Journal of Cardiology xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Brugada phenocopy in the context of intracranial hemorrhage Carlos Labadet a,⁎, Byron H. Gottschalk b, Mirza Rivero a, Claudio Hadid a, Juan Fuselli a, Daniel D. Anselm b, Adrian Baranchuk b a b
Servicio de Cardiología, Hospital Universitario C.E.M.I.C., Buenos Aires, Argentina Department of Cardiology, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada
a r t i c l e
i n f o
Article history: Received 21 August 2014 Accepted 26 August 2014 Available online xxxx Keywords: Brugada ECG pattern Intracranial hemorrhage Brugada phenocopy
An 85-year-old man was admitted to the ICU with syncope preceded by prodromal symptoms and complicated by head trauma. He had a history of hypertension, dyslipidemia, paroxysmal atrial fibrillation, mild chronic renal failure, and an aortic valve replacement seven years prior. His medications included enalapril 10 mg, amlodipine 5 mg, atorvastatin 10 mg, aspirin 100 mg, and amiodarone 200 mg. Physical examination revealed a blood pressure of 150/60 mm Hg, and a right lid hematoma. A 12-lead ECG at admission demonstrated sinus rhythm, first degree AV block (PR interval 220 ms) (Fig. 1A). A head CT scan demonstrated an orbital floor fracture, temporo-parietal subarachnoid hemorrhage (SAH) as well as sylvian cistern, falx, and right parasellar hematomas. Intracranial angiography ruled out an aneurysmal cause of the SAH. The patient was subsequently treated with nimodipine 60 mg q4h PO, metoclopramide 10 mg IV, and levetiracetam 500 mg BID PO. Twelve hours following admission, an ST-elevation was noted on the ICU monitor, which prompted an evaluation on surface ECG that demonstrated an isolated ST-elevation in V2 (Fig. 1B). A subsequent ECG, taken 1 h later, demonstrated ST-elevation in lead V2 consistent with a Type 2 Brugada ECG pattern (Fig. 1C). The ECG normalized within 9 h, resembling the admission ECG (Fig. 1D). Cardiac Troponin-T values were within normal limits and an echocardiogram revealed mild left ventricular hypertrophy with preserved ejection fraction and moderate aortic stenosis. A head CT scan performed 48 h after admission demonstrated an insular hematoma with intraventricular hemorrhage.
⁎ Corresponding author. Tel.: +54 114 447 7247; fax: +54 114 866 2985. E-mail address: [email protected] (C. Labadet).
The patient underwent an electrophysiological study that revealed slight AV node conduction delay (Wenckeback point 510 ms) and no arrhythmia inducibility. A sodium channel blocker test with flecainide 400 mg PO failed to induce a Type-1 Brugada ECG pattern. Based on this result and the clinical circumstances under which the Brugada ECG pattern was observed, a diagnosis of Type-2 Brugada phenocopy was made. After recovery, the patient was discharged without other complications. Brugada phenocopies (BrP) are clinical entities characterized by ECG patterns identical to congenital Brugada syndrome (BrS) but are elicited by various clinical circumstances [1,2]. They are classified according to the ECG pattern they present with: Type-1 BrP present with Type-1 Brugada ECG pattern, while Type-2 BrP present with Type-2 Brugada ECG pattern. Furthermore, they are sub-classified according to whether all the diagnostic criteria have been met: Class A BrP have met all the mandatory diagnostic criteria, including a negative sodium channel blocker provocative test; Class B includes highly suspected BrP, however not all criteria have been met and Class C includes cases of suspected BrP where provocative testing is not justified such as recent surgical RVOT manipulation or inappropriate ECG filters [3]. To our knowledge, this is the first case to document a confirmed, Type 2A BrP caused by a neurological condition. Cardiac complications of neurologic disease have been well documented in the literature [4]. ECG alterations including, but not limited to, ST-segment elevation have been associated with neurological disorders such as SAH and intracerebral hemorrhage [4–6]. Goldberger et al. [6] described a case of dramatic ECG changes, including a Brugada ECG pattern, associated with catastrophic neurologic syndrome. The authors postulated that the Brugada ECG pattern could have been unmasked, either by propofol infusion or by the patient's febrile state (in which case, a “true” Brugada syndrome needs to be ruled out). Our patient was afebrile and did not receive propofol. He did receive metoclopramide, a drug that is preferably avoided in BrS as it may unmask the ECG pattern [7]. However, historical features along with the negative flecainide test allow us to suspect that the ECG pattern was not BrS unmasked by metoclopramide. Rather, we believe the Brugada ECG manifestations were due to neurological dysfunction as a consequence of hematoma formation. The insula is a region that, when damaged, has been implicated in ECG abnormalities including ST-segment elevation, QT prolongation and arrhythmias [4, 8–10]. When damaged, the insula modulates central and peripheral cardiac autonomic changes thought to increase the risk of arrhythmias [8].
http://dx.doi.org/10.1016/j.ijcard.2014.08.151 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Labadet C, et al, Brugada phenocopy in the context of intracranial hemorrhage, Int J Cardiol (2014), http://dx.doi.org/ 10.1016/j.ijcard.2014.08.151
e2
C. Labadet et al. / International Journal of Cardiology xxx (2014) xxx–xxx
Fig. 1. A: Admission ECG demonstrating sinus rhythm and first degree AV block. B: An ECG 12 h after admission demonstrating ST-segment elevation in lead V2 (arrow). C: An ECG 13 h after admission demonstrating ST-segment elevation in lead V2 (Type- 2 or saddleback) Brugada ECG pattern (arrowhead). D: An ECG 22 h after admission depicting resolution of the STsegment elevation in lead V2.
Švigelj et al. [9] described the case of a patient with SAH who developed ST-segment elevation and cardiac arrhythmia due to a hematoma in the left insular region. Upon removal of the hematoma, the arrhythmias resolved demonstrating reversibility of the region's autonomic dysfunction. Furthermore, insular lesions in stroke patients have also been implicated in ECG abnormalities and adverse outcomes [10]. Our patient presented with SAH and intracerebral hematomas in various regions. Twelve hours following admission, he developed ST-segment elevation that progressed to a Type-2 Brugada ECG pattern. A subsequent CT scan at 48 h post admission demonstrated an insular hematoma. We postulate that the insular hemorrhage, or subsequent hematoma formation, produced a mass effect on the insula resulting in autonomic nervous system imbalances that caused the ventricular repolarization abnormality and the Brugada ECG pattern [8]. Furthermore, we speculate sufficient reduction of this mass effect, 9 h after the ECG pattern presented, resulted in restoration of proper insular function, and therefore resolution of the ECG pattern. We present the case of a man who presented with head trauma and intracranial hemorrhage including SAH that subsequently developed a Type-2 BrP. This case is important as it contributes to the growing body of literature on BrP. It has been included as a Type 2A BrP in the International Registry of Brugada Phenocopies at www.brugadaphenocopy.com [2].
Conflict of interest None. References [1] Baranchuk A, Nguyen T, Ryu MH, et al. Brugada phenocopy: new terminology and proposed classification. Ann Noninvasive Electrocardiol 2012;17:299–314. [2] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy international registry and online educational portal. http://www.brugadaphenocopy.com. [Accessed August 2014]. [3] Gottschalk B, Anselm DD, Baranchuk A. Brugada phenocopy: morphological classification and importance of provocative testing. Ann Noninvas Electrocardiol 2014 [In press]. [4] Baranchuk A, Nault MA, Morillo CA. The central nervous system and sudden cardiac death: what should we know? Cardiol J 2009;16:105–12. [5] Saritemur M, Akoz A, Kalkan K, Emet M. Intracranial hemorrhage with electrocardiographic abnormalities and troponin elevation. Am J Emerg Med 2013;31: 271.e5–7. [6] Goldberger ZD, Creutzfeldt CJ, Goldberger AL. Catastrophic neurologic syndrome with dramatic ECG changes. J Electrocardiol 2014;47:80–3. [7] Postema PG, Wolpert C, Amin AS, et al. Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (http:// www.brugadadrugs.org). Heart Rhythm 2009;6:1335–41. [8] Koppikar S, Baranchuk A, Guzman JC, Morillo CA. Stroke and ventricular arrhythmias. Int J Cardiol 2013;168:653–9. [9] Svigelj V, Grad A, Tekavcic I, Kiauta T. Cardiac arrhythmia associated with reversible damage to insula in a patients with subarachnoid hemorrhage. Stroke 1994;25:1053–5. [10] Christensen H, Boysen G, Christensen AF, Johannesen HH. Insular lesions, ECG abnormalities, and outcome in acute stroke. J Neurol Neurosurg Psychiatry 2005;76:269–71.
Please cite this article as: Labadet C, et al, Brugada phenocopy in the context of intracranial hemorrhage, Int J Cardiol (2014), http://dx.doi.org/ 10.1016/j.ijcard.2014.08.151
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Brugada phenocopy in the context of intracranial hemorrhage Carlos Labadet a,⁎, Byron H. Gottschalk b, Mirza Rivero a, Claudio Hadid a, Juan Fuselli a, Daniel D. Anselm b, Adrian Baranchuk b a b
Servicio de Cardiología, Hospital Universitario C.E.M.I.C., Buenos Aires, Argentina Department of Cardiology, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada
a r t i c l e
i n f o
Article history: Received 21 August 2014 Accepted 26 August 2014 Available online xxxx Keywords: Brugada ECG pattern Intracranial hemorrhage Brugada phenocopy
An 85-year-old man was admitted to the ICU with syncope preceded by prodromal symptoms and complicated by head trauma. He had a history of hypertension, dyslipidemia, paroxysmal atrial fibrillation, mild chronic renal failure, and an aortic valve replacement seven years prior. His medications included enalapril 10 mg, amlodipine 5 mg, atorvastatin 10 mg, aspirin 100 mg, and amiodarone 200 mg. Physical examination revealed a blood pressure of 150/60 mm Hg, and a right lid hematoma. A 12-lead ECG at admission demonstrated sinus rhythm, first degree AV block (PR interval 220 ms) (Fig. 1A). A head CT scan demonstrated an orbital floor fracture, temporo-parietal subarachnoid hemorrhage (SAH) as well as sylvian cistern, falx, and right parasellar hematomas. Intracranial angiography ruled out an aneurysmal cause of the SAH. The patient was subsequently treated with nimodipine 60 mg q4h PO, metoclopramide 10 mg IV, and levetiracetam 500 mg BID PO. Twelve hours following admission, an ST-elevation was noted on the ICU monitor, which prompted an evaluation on surface ECG that demonstrated an isolated ST-elevation in V2 (Fig. 1B). A subsequent ECG, taken 1 h later, demonstrated ST-elevation in lead V2 consistent with a Type 2 Brugada ECG pattern (Fig. 1C). The ECG normalized within 9 h, resembling the admission ECG (Fig. 1D). Cardiac Troponin-T values were within normal limits and an echocardiogram revealed mild left ventricular hypertrophy with preserved ejection fraction and moderate aortic stenosis. A head CT scan performed 48 h after admission demonstrated an insular hematoma with intraventricular hemorrhage.
⁎ Corresponding author. Tel.: +54 114 447 7247; fax: +54 114 866 2985. E-mail address: [email protected] (C. Labadet).
The patient underwent an electrophysiological study that revealed slight AV node conduction delay (Wenckeback point 510 ms) and no arrhythmia inducibility. A sodium channel blocker test with flecainide 400 mg PO failed to induce a Type-1 Brugada ECG pattern. Based on this result and the clinical circumstances under which the Brugada ECG pattern was observed, a diagnosis of Type-2 Brugada phenocopy was made. After recovery, the patient was discharged without other complications. Brugada phenocopies (BrP) are clinical entities characterized by ECG patterns identical to congenital Brugada syndrome (BrS) but are elicited by various clinical circumstances [1,2]. They are classified according to the ECG pattern they present with: Type-1 BrP present with Type-1 Brugada ECG pattern, while Type-2 BrP present with Type-2 Brugada ECG pattern. Furthermore, they are sub-classified according to whether all the diagnostic criteria have been met: Class A BrP have met all the mandatory diagnostic criteria, including a negative sodium channel blocker provocative test; Class B includes highly suspected BrP, however not all criteria have been met and Class C includes cases of suspected BrP where provocative testing is not justified such as recent surgical RVOT manipulation or inappropriate ECG filters [3]. To our knowledge, this is the first case to document a confirmed, Type 2A BrP caused by a neurological condition. Cardiac complications of neurologic disease have been well documented in the literature [4]. ECG alterations including, but not limited to, ST-segment elevation have been associated with neurological disorders such as SAH and intracerebral hemorrhage [4–6]. Goldberger et al. [6] described a case of dramatic ECG changes, including a Brugada ECG pattern, associated with catastrophic neurologic syndrome. The authors postulated that the Brugada ECG pattern could have been unmasked, either by propofol infusion or by the patient's febrile state (in which case, a “true” Brugada syndrome needs to be ruled out). Our patient was afebrile and did not receive propofol. He did receive metoclopramide, a drug that is preferably avoided in BrS as it may unmask the ECG pattern [7]. However, historical features along with the negative flecainide test allow us to suspect that the ECG pattern was not BrS unmasked by metoclopramide. Rather, we believe the Brugada ECG manifestations were due to neurological dysfunction as a consequence of hematoma formation. The insula is a region that, when damaged, has been implicated in ECG abnormalities including ST-segment elevation, QT prolongation and arrhythmias [4, 8–10]. When damaged, the insula modulates central and peripheral cardiac autonomic changes thought to increase the risk of arrhythmias [8].
http://dx.doi.org/10.1016/j.ijcard.2014.08.151 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Labadet C, et al, Brugada phenocopy in the context of intracranial hemorrhage, Int J Cardiol (2014), http://dx.doi.org/ 10.1016/j.ijcard.2014.08.151
e2
C. Labadet et al. / International Journal of Cardiology xxx (2014) xxx–xxx
Fig. 1. A: Admission ECG demonstrating sinus rhythm and first degree AV block. B: An ECG 12 h after admission demonstrating ST-segment elevation in lead V2 (arrow). C: An ECG 13 h after admission demonstrating ST-segment elevation in lead V2 (Type- 2 or saddleback) Brugada ECG pattern (arrowhead). D: An ECG 22 h after admission depicting resolution of the STsegment elevation in lead V2.
Švigelj et al. [9] described the case of a patient with SAH who developed ST-segment elevation and cardiac arrhythmia due to a hematoma in the left insular region. Upon removal of the hematoma, the arrhythmias resolved demonstrating reversibility of the region's autonomic dysfunction. Furthermore, insular lesions in stroke patients have also been implicated in ECG abnormalities and adverse outcomes [10]. Our patient presented with SAH and intracerebral hematomas in various regions. Twelve hours following admission, he developed ST-segment elevation that progressed to a Type-2 Brugada ECG pattern. A subsequent CT scan at 48 h post admission demonstrated an insular hematoma. We postulate that the insular hemorrhage, or subsequent hematoma formation, produced a mass effect on the insula resulting in autonomic nervous system imbalances that caused the ventricular repolarization abnormality and the Brugada ECG pattern [8]. Furthermore, we speculate sufficient reduction of this mass effect, 9 h after the ECG pattern presented, resulted in restoration of proper insular function, and therefore resolution of the ECG pattern. We present the case of a man who presented with head trauma and intracranial hemorrhage including SAH that subsequently developed a Type-2 BrP. This case is important as it contributes to the growing body of literature on BrP. It has been included as a Type 2A BrP in the International Registry of Brugada Phenocopies at www.brugadaphenocopy.com [2].
Conflict of interest None. References [1] Baranchuk A, Nguyen T, Ryu MH, et al. Brugada phenocopy: new terminology and proposed classification. Ann Noninvasive Electrocardiol 2012;17:299–314. [2] Gottschalk BH, Anselm DD, Baranchuk A. Brugada phenocopy international registry and online educational portal. http://www.brugadaphenocopy.com. [Accessed August 2014]. [3] Gottschalk B, Anselm DD, Baranchuk A. Brugada phenocopy: morphological classification and importance of provocative testing. Ann Noninvas Electrocardiol 2014 [In press]. [4] Baranchuk A, Nault MA, Morillo CA. The central nervous system and sudden cardiac death: what should we know? Cardiol J 2009;16:105–12. [5] Saritemur M, Akoz A, Kalkan K, Emet M. Intracranial hemorrhage with electrocardiographic abnormalities and troponin elevation. Am J Emerg Med 2013;31: 271.e5–7. [6] Goldberger ZD, Creutzfeldt CJ, Goldberger AL. Catastrophic neurologic syndrome with dramatic ECG changes. J Electrocardiol 2014;47:80–3. [7] Postema PG, Wolpert C, Amin AS, et al. Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (http:// www.brugadadrugs.org). Heart Rhythm 2009;6:1335–41. [8] Koppikar S, Baranchuk A, Guzman JC, Morillo CA. Stroke and ventricular arrhythmias. Int J Cardiol 2013;168:653–9. [9] Svigelj V, Grad A, Tekavcic I, Kiauta T. Cardiac arrhythmia associated with reversible damage to insula in a patients with subarachnoid hemorrhage. Stroke 1994;25:1053–5. [10] Christensen H, Boysen G, Christensen AF, Johannesen HH. Insular lesions, ECG abnormalities, and outcome in acute stroke. J Neurol Neurosurg Psychiatry 2005;76:269–71.
Please cite this article as: Labadet C, et al, Brugada phenocopy in the context of intracranial hemorrhage, Int J Cardiol (2014), http://dx.doi.org/ 10.1016/j.ijcard.2014.08.151