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CASE International Journal of Arrhythmia 2016;17(1):60-63 REPORTS doi: http://dx.doi.org/10.18501/arrhythmia.2016.010 Management of Aborted Sudden Cardiac Arrest with J Wave Syndrome Ki Hong Lee, MD; Hyung Wook Park, MD, PhD The Heart Research center of Chonnam National University Hospital, Cardiovascular Research Institute of Chonnam National University, Gwangju, Korea Received: November 16, 2015 Accepted: March 28, 2016 Correspondence: Hyung Wook Park, MD, PhD Associate Professor, Cardiovascular Medicine, Chief of Cardiovascular Medicine, The Heart Center of Chonnam National University Hospital, 42 Jaebongro, Dong-gu, Gwangju, Republic of Korea, 501-757 Tel: 82-62-220-6572 Fax: 82-62-223-3105 E-mail: [email protected] Copyright © 2016 The Official Journal of Korean Heart Rhythm Society Editorial Board & MMK Co., Ltd. ABSTRACT We report the case of a 19-year-old male who successfully recovered from sudden cardiac arrest. Careful evaluation did not reveal any electrical or structural abnormalities. He underwent implantable cardioverter defibrillator (ICD) implantation, with a diagnosis of idiopathic ventricular fibrillation (VF). Three months later, VF recurred and was successfully terminated by ICD shock. Electrocardiogram (ECG) revealed a slurred type J point elevation at the inferolateral leads with a horizontal/descending ST segment change, which was not present during the initial hospitalization. Cilostazol was prescribed to prevent further lethal ventricular arrhythmias. Subsequently, no arrhythmic events were reported, and the J wave disappeared at the follow-up ECG. However, recurrent VF episodes with an interval of 1–2 weeks occurred 1 year later, and were terminated by ICD shock. Simultaneous ECG revealed a J point elevation at the inferolateral leads. Cilostazol was replaced by quinidine. Subsequently, no arrhythmic event recurred for over 12 months. Serial follow-up ECG is needed to identify masked inherited primary arrhythmic syndromes in sudden cardiac arrest survivors diagnosed with idiopathic VF. Cilostazol and quinidine might be good therapeutic options to prevent further lethal events in cases where the J wave syndrome is present with recurrent ventricular arrhythmias. Key Words: ■Heart Arrest ■Arrhythmias, Cardiac ■Anti-Arrhythmia Agents Introduction majority of survivors. IPAS is often revealed during serial followup examinations because electrocardiographic abnormalities of Lethal ventricular arrhythmias can occur even in the absence of IPAS tend to change spontaneously. The J wave syndrome is a structural heart disease. Inherited primary arrhythmia syndrome recently discovered form of IPAS and is an important cause of (IPAS) is a rare condition, but is often associated with high SCA in relatively young patients. We report the case of a 19-year- mortality rates. Despite meticulous evaluation, the underlying old male who survived SCA and a diagnosis of J wave syndrome cause of sudden cardiac arrest (SCA) remains idiopathic in a was made subsequently. 60 Management of J Wave Syndrome Case horizontal/descending ST segment change (Figure 2). Cilostazol was prescribed to prevent further lethal ventricular arrhythmias. A 19-year-old male was transferred to the emergency Nevertheless, recurrent VF episodes with an interval of 1 to 2 department with aborted sudden cardiac arrest. He had no weeks occurred 1 year later, and were terminated by ICD shock previous history of hypertension, diabetes mellitus, dyslipidemia, (Figure 3). At that time, ECG also demonstrated a J point or other cardiac problems. He was a student with ordinary activity elevation at the inferolateral lead, which was not apparent during levels. Cardiac arrest developed during sleep. When the the ‘no-event’ period. To minimize shock therapy, cilostazol was emergency team arrived, an automated external defibrillator switched with quinidine, as class Ic anti-arrhythmic agents directly demonstrated ventricular fibrillation (VF), which was terminated inhibit Ito, thereby decreasing the J point elevation resulting in by three rounds of defibrillation. After the successful recovery of decreased the transmural dispersion of repolarization and spontaneous circulation, the patient underwent hypothermia refractoriness. No arrhythmic events were reported subsequently treatment. Subsequently, careful evaluation was performed to and ECG revealed no J wave. identify the cause of sudden cardiac arrest. None of the examinations performed, including electrocardiogram (ECG), Discussion holter monitoring, coronary angiogram, brain computer tomography, and flecainide or epinephrine drug challenge test, The early repolarization pattern in ECG, known as the J wave, revealed any abnormalities. Electrophysiological studies did not is considered to be benign. Recent studies, however, have reported induce any ventricular tachycardia. Finally, a diagnosis of that the J wave may be associated with an increased risk of death.1,2 idiopathic VF was made and the patient underwent implantable Additionally, early repolarization has been reported to be cardioverter-defibrillator (ICD) implantation to protect him associated with recurrent VF in cardiac arrest survivors.3 Rosso et from further lethal ventricular arrhythmias. al. have termed early repolarization with a horizontal/descending The patient had an uneventful recovery after being discharged ST segment as “malignant”, because it was more strongly from the hospital. However, 3 months later, an ICD shock correlated with idiopathic ventricular fibrillation among all types occurred, which was revealed to be a VF event at ICD of early repolarization.4 In the present case report, a horizontal/ interrogation (Figure 1). At that time, a simultaneous ECG descending type of early repolarization pattern was documented demonstrated the presence of a newly developed J point elevation in the ECG. This abnormal pattern, which exhibited dynamic at the inferolateral lead, which was of the slurred type with a changes with time, might cause recurrent VF episodes. Figure 1. Interrogated intracardiac electrogram from an implantable cardioverter defibrillator (ICD). Ventricular fibrillation was present and was terminated by ICD shock 36 J. 61 International Journal of Arrhythmia 2016;17(1):60-63 Figure 2. Electrocardiogram (ECG) after successful defibrillation from ventricular fibrillation. A newly developed J point elevation at the inferolateral lead of the slurred type with a horizontal/descending ST segment change was detected by ECG. Figure 3. Interrogated intracardiac electrogram from an implantable cardioverter defibrillator (ICD). Ventricular fibrillation (VF) was detected and was terminated by ICD shock 36 J. Recurrent VF episodes occurred at 1-2 week intervals. The J wave is formed due to an outward shift in the balance of sodium current (INa). The loss of the action potential dome in the the membrane ionic currents at the end of the phase 1 and phase 2 epicardium, but not in the endocardium, results in the action potentials. In these phases, an outward current occurs development of a marked transmural dispersion of repolarization mainly due to the activation of the transient outward current (Ito), and refractoriness. This event is responsible for the development while the inward current is a result of the activation of an inward of a vulnerable window during which a premature impulse or calcium current (ICa) and an inactivating component of an inward extrasystole can induce a reentrant arrhythmia.5-7 62 Management of J Wave Syndrome Although the primary therapy for VF is ICD implantation, Cardiovasc Electrophysiol. 2011;22:131-136. shock reduction and the prevention of recurrent ventricular 4) Rosso R, Glikson E, Belhassen B, Katz A, Halkin A, Steinvil A, arrhythmia should be considered. A pharmacologic intervention, Viskin S. Distinguishing "benign" from "malignant early which either decreases the membrane outward currents, or repolarization": The value of the ST-segment morphology. Heart increases the inward currents, prevents the loss of the action Rhythm. 2012;9:225-229. potential dome in the right ventricular epicardium. Quinidine has 5) Antzelevitch C, Brugada P, Brugada J, Brugada R, Towbin JA, been shown to directly inhibit the Ito in addition to a secondary Nademanee K. Brugada syndrome: 1992-2002: A historical inhibition due to an increase in the heart rate by a vagolytic perspective. J Am Coll Cardiol. 2003;41:1665-1671. action.5,7 Experimental studies have shown quinidine to be 6) Priori SG, Napolitano C, Gasparini M, Pappone C, Della Bella P, effective in restoring the epicardial action potential dome, thus Brignole M, Giordano U, Giovannini T, Menozzi C, Bloise R, normalizing the ST-segment and preventing phase 2 reentry and Crotti L, Terreni L, Schwartz PJ. Clinical and genetic heterogeneity polymorphic VT.8 Cilostazol, an oral phosphodiesterase type-III of right bundle branch block and ST-segment elevation syndrome: inhibitor has been shown to increase the ICa due to the inhibition A prospective evaluation of 52 families. Circulation . of the phosphodiesterase activity in the ventricular myocytes and decreases the Ito due to an increased heart rate which again is secondary to an increased ICa in the sinus node.9 In the present case report, the patient underwent ICD implantation with the initial diagnosis of idiopathic VF. However, J point elevation occurred during late follow-up, which was related 2000;102:2509-2515. 7) Yan GX, Antzelevitch C. Cellular basis for the brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation. 1999;100:1660-1666. 8) Antzelevitch C. The brugada syndrome: Ionic basis and arrhythmia mechanisms. J Cardiovasc Electrophysiol. 2001;12:268-272. with recurrent ventricular arrhythmia, and potential preventive 9) Matsui K, Kiyosue T, Wang JC, Dohi K, Arita M. Effects of strategies were indicated. Pharmacological therapy with cilostazol pimobendan on the l-type Ca2+ current and developed tension in and quinidine successfully suppressed lethal ventricular guinea-pig ventricular myocytes and papillary muscle: Comparison arrhythmias. Therefore, careful and serial follow-up evaluation is essential in patients with idiopathic VF because unrevealed IPAS with ibmx, milrinone, and cilostazol. Cardiovasc Drugs Ther. 1999;13:105-113. might be present. Additional therapeutic strategies may be considered to prevent and minimize the occurrence of further lethal arrhythmias. References 1) Tikkanen JT, Junttila MJ, Anttonen O, Aro AL, Luttinen S, Kerola T, Sager SJ, Rissanen HA, Myerburg RJ, Reunanen A, Huikuri HV. Early repolarization: Electrocardiographic phenotypes associated with favorable long-term outcome. Circulation. 2011;123:26662673. 2) Gussak I, Antzelevitch C. Early repolarization syndrome: Clinical characteristics and possible cellular and ionic mechanisms. J Electrocardiol. 2000;33:299-309 3) Lellouche N, Sacher F, Jorrot P, Cariou A, Spaulding C, Aurore A, Combes X, Fichet J, Teiger E, Jais P, Dubois-Rande JL, Haissaguerre M. Sudden cardiac arrest: ECG repolarization after resuscitation. J 63