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The Many Faces of Early Repolarization Syndrome: a Single-Center Case

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1 69 2 70 3 71 4 The many faces of early repolarization syndrome: A 72 5 73 6 Q1 single-center case series 74 7 75 8 76 Q23 Aleksandr Voskoboinik, MBBS, PhD,* Henry Hsia, MD,* Joshua Moss, MD,* 9 † † 77 10 Vasanth Vedantham, MD, PhD,* Ronn E. Tanel, MD,* Akash Patel, MD,* 78 11 Q2 Julianne Wojciak, MS,* Natalie Downs, MS,* Melvin M. Scheinman, MD* 79 12 80 13 From the *Cardiology Division, University of California, San Francisco, San Francisco, California, and 81 14 † 82 Q3 15 Pediatric Cardiology Division, University of California, San Francisco, San Francisco, California. 83 16 84 17 85 fi 18 BACKGROUND Early repolarization syndrome (ERS) is a rare but of 10 patients had variants of uncertain signi cance on genetic 86 19 increasingly recognized cause of malignant ventricular arrhythmias. testing. Quinidine effectively suppressed arrhythmias in 5 of 5 pa- 87 20 tients but required dose escalation to .1 g/d in 3 of 5 patients. 88 21 OBJECTIVE The purpose of this study was to characterize the pre- Abnormal epicardial electrograms were recorded over the inferolat- 89 22 sentations and treatments of ERS at our institution. eral left ventricle in 2 patients who underwent mapping and were 90 23 91 METHODS We performed a retrospective chart review of all patients successfully ablated. Premature ventricular contraction triggers 24 were also targeted for ablation in 3 patients. 92 25 presenting to our institution between 2008 and 2019 with ERS. 93 26 Exclusion criteria included Brugada syndrome, positive provocative CONCLUSION ERS is a heterogeneous condition and may be asso- 94 27 testing with class I antiarrhythmic drugs, metabolic disturbances, ciated with both atrial and ventricular arrhythmias, atrioventricular 95 28 or structural heart disease. block, dynamic electrocardiographic changes, and variable triggers. 96 29 97 fi In addition to targeting premature ventricular contraction triggers, 30 Q5 RESULTS Of 10 patients identi ed with ERS, 8 were men with a 98 mapping and ablation of abnormal epicardial electrograms may be a 31 mean age of 30 6 17 years at diagnosis. Documented arrhythmias 99 32 included ventricular fibrillation in 7 of 10, polymorphic ventricular potential future treatment strategy. 100 33 tachycardia in 3 of 10, and monomorphic ventricular tachycardia in 101 34 3 of 10 patients. Atrial fibrillation was diagnosed in 3 of 10, and KEYWORDS Early repolarization syndrome; J wave; Ventricular 102 35 atrioventricular block was seen in 2 of 10. J waves and/or electro- fibrillation; Cardiac arrest; Catheter ablation 103 36 cardiographic early repolarization patterns were dynamic in 7 of 104 37 10. Arrhythmias occurred at rest in 8 of 10 and with exertion in 2 (Heart Rhythm 2019;-:1–9) 2019 Heart Rhythm Society. 105 38 © 106 of 10. Only 1 patient had a family history of sudden death, and 4 All rights reserved. 39 107 40 108 41 109 42 Introduction specifying the electrocardiographic (ECG) pattern 110 43 Our understanding of early repolarization syndrome (ERS) observed.3 111 44 has dramatically evolved over the past decade. The early 112 45 113 46 repolarization (ER) pattern, once thought to be a benign Methods 114 fi 47 nding, is now known to be associated with sudden death. We searched our institution’s Genetic Arrhythmia Registry to 115 1 48 The initial description of ERS by Haissaguerre et al of identify all patients between 2008 and 2019 with a diagnosis 116 49 Q6 QRS–ST-segment elevation in the inferior or lateral leads fi 117 50 of ERS. Patients also had to ful ll a diagnosis of at least 118 and a propensity for ventricular fibrillation (VF) has been 4 51 “possible” ERS with a Shanghai ERS score of 3. We 119 52 broadened. Moreover, debate exists as to whether ERS excluded Brugada syndrome (BrS), positive provocative 120 2 53 represents a repolarization or depolarization abnormality. testing with class I antiarrhythmic drugs, metabolic distur- 121 54 Putative genes, electrophysiological manifestations, and bances (eg, hypothermia), and ischemia (including coronary 122 55 fi 123 potential targets for ablation require further clari cation. spasm) as the primary causes of ECG changes. All patients 56 We sought to review all cases of ERS from our institution 124 57 underwent echocardiography to exclude structural heart dis- 125 58 with the aim of describing its range of presentations. We ease. Records were reviewed retrospectively to obtain demo- 126 59 follow the recent American Heart Association statement graphic data, clinical course, ECG changes, arrhythmias, 127 60 outcomes of electrophysiology studies, and events at 128 61 129 62 follow-up (Table 1). Supplemental Table 1 provides a sum- 130 63 Address reprint requests and correspondence: Dr. Aleksandr Voskoboi- mary of cardiac and genetic testing, and Supplemental 131 64 nik, Cardiology Division, University of California, San Francisco, San Fran- Figure 1 shows each patient’s ECG. The study was approved 132 65 Q4 cisco, CA. E-mail address: [email protected]. by our institutional review board. 133 66 134 67 135 68 1547-5271/$-see front matter © 2019 Heart Rhythm Society. All rights reserved. https://doi.org/10.1016/j.hrthm.2019.09.013 136 FLA 5.6.0 DTD HRTHM8145_proof 12 October 2019 8:47 pm ce 2 Heart Rhythm, Vol -,No-, - 2019 137 Q21 205 138 206 139 207 140 208 141 polymorphic 209 5 2y 18 mo 142 2y 210 143 211 144 212 ow 145 fl 213 146 214 147 215 148 216 149 217 150 218 151 219 abnormal substrate inferolateral epicardium abnormal substrate, mid-diastolic potentials during VT in the inferolateral epicardium 152 tract PVCs targeted 220 Targeted PVC trigger and Nil 8 y Nil 2 y Nil 6 mo Right ventricular out Nil 7 y 153 221 154 222 155 223 156 monomorphic ventricular tachycardia; PMVT 224 5 157 225 158 226 159 227 1 g/d), ICD 160 male; MMVT 228 , -blockers, sotalol, b 161 5 229 162 ecainide, ICD 230 fl PVCs, quinidine, cilostazol, ICD doses), ICD VT at doses), ICD quinidine successful 163 231 ICD Targeted PVC trigger, Isoproterenol suppressed Quinidine (required higher Quinidine (breakthrough 164 232 brillator; M 165 fi 233 166 234 167 235 168 236 169 utter, 237 fl 170 238 171 239 172 ventricular tachycardia. 240 173 5 241 PVCs multifocal PVCs, third- degree AV block arrhythmias, VF AV block, PVCs 174 implantable cardioverter-de 242 VF, PMVT, MMVT, unifocal PMVT, VF, unifocal PVCs Failed MMVT/organized fascicular MMVT, PMVT, third-degree VF, AFVF, AF, atrial Quinidine (required higher PMVTVFNilVF, PMVT, AF ICD, failed metoprolol, ICD Metoprolol, ICD ICD Nil Nil Nil 11 y 10 y 18 mo 175 5 243 176 244 177 245 brillation; VT 178 fi 246 179 female; ICD 247 5 180 248 181 249 182 ventricular 250 5 183 251 184 252 the inferior leads the inferior leads segment elevation inferiorly and anteriorly, transient inferior ST- segment elevation augmentation at longer coupling intervals elevation with J waves and augmentation at longer coupling intervals the inferior leads elevation segment elevation, terminal QRS notching in the inferior leads inferior leads 185 Terminal QRS notching in 253 186 254 187 electrocardiographic; F 255 188 5 256 189 257 190 258 191 259 192 260 193 261 194 atrioventricular; ECG 262 Previous syncope Presenting symptoms ECG changes Arrhythmias Treatment Ablation Follow-up premature ventricular contraction; VF 195 5 263 196 5 264 197 265 198 266 199 Age at diagnosis (y) 267 brillation; AV 200 fi 268 201 Summary of the clinical characteristics of patients in case series 269 202 atrial 270 203 5 271 AF 204 272 4 M 27 VF arrest 3 M 18 Syncope Terminal QRS notching in 56 M 55 M 46 Bradycardic arrest Presyncope Transient inferior ST- Intermittent J waves Table 1 Case Sex 1 F 20 VF arrest Global J waves with 2 F 17 VF arrest Global ST-segment ventricular tachycardia; PVC 910 M M 18 15 Syncope VF arrest Terminal QRS notching in Global ST-segment 7 M8 22 M 61 Polymorphic VT arrest Transient inferior ST- VF arrest Prominent J waves in the FLA 5.6.0 DTD HRTHM8145_proof 12 October 2019 8:47 pm ce Voskoboinik et al Early Repolarization Syndrome 3 273 Results and inferolateral J waves, more prominent at slower rates 341 274 (Figure 1B). She received amiodarone but continued to 342 275 Atrial fibrillation and ERS 343 276 have frequent multifocal premature ventricular contractions 344 277 Case 1 (PVCs) and developed further VF in the setting of brady- 345 278 cardia and pauses triggered by short-coupled PVCs. Isopro- 346 A 20-year-old woman was admitted following resuscitated 279 terenol infusion markedly decreased PVCs. A dual- 347 VF after collapsing in her kitchen. Her brother had died sud- 280 chamber ICD was implanted, and ibutilide was administered 348 281 denly at the age of 15. Postdefibrillation, the ECG showed 349 for persistent AF. During ibutilide infusion, the QRS width 282 atrial fibrillation (AF) with slow ventricular response and 350 and corrected QT interval prolonged, resulting in torsades 283 global J waves despite euthermia. These persisted beyond 351 284 de pointes. Its discontinuation combined with ventricular 352 her index presentation. Notably, J waves were apparent 285 pacing at higher rates facilitated hospital discharge. Three 353 only at slower rates and longer coupling intervals 286 months later, she presented following numerous shocks for 354 287 (Figure 1A) and were not accentuated with procainamide. 355 VF, with esmolol and theophylline failing to suppress com- 288 She received quinidine 325 mg thrice daily and an implant- 356 plex ventricular ectopy. Isoproterenol reduced PVCs but re- 289 able cardioverter-defibrillator (ICD).
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