Prevalence and prognostic significance of J waves in patients experiencing ventricular fibrillation during acute coronary syndrome

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Archives of Cardiovascular Disease (2012) 105, 578 586 Available online at www.sciencedirect.com CLINICAL RESEARCH Prevalence and prognostic significance of J waves in patients experiencing ventricular fibrillation during acute coronary syndrome Prévalence et signification pronostique de la présence d une «onde J» chez les patients présentant une fibrillation ventriculaire au cours des syndromes coronaires aigus Linda Aïssou a, Jean-Sylvain Hermida a,b,, Sarah Traullé a,b, Astrid Delaverhne a, Momar Diouf c, Laurent Leborgne b,d, Maciej Kubala a, Geneviève Jarry d a Service de Rythmologie, Centre Hospitalier Universitaire Amiens-Picardie, France b Faculté de Médecine, Université de Picardie-Jules-Verne, France c Direction de la Recherche Clinique et Innovation, Centre Hospitalier Universitaire Amiens-Picardie, France d Unité de Soins Intensifs de Cardiologie, Centre Hospitalier Universitaire Amiens-Picardie, France Received 26 April 2012; accepted 5 July 2012 Available online 2nd October 2012 KEYWORDS Cardiac arrest; Acute coronary syndrome; Ventricular fibrillation; J wave Summary Background. J waves have been associated with idiopathic ventricular fibrillation (VF) and have also been described in patients with ischaemic VF. Aims. Our aim was to determine whether inferior and/or lateral J waves were associated with the occurrence of VF or in hospital mortality during acute coronary syndrome (ACS). Methods. Fifty-three patients (mean age 52 ± 10 years) experienced cardiac arrest due to VF during the first 48 hours of an ACS. These patients were entered in a retrospective casecontrol study. The control group was matched for age and sex and included 106 patients who experienced an ACS but without VF. Abbreviations: ACS, acute coronary syndrome; ECG, electrocardiogram; ER, early repolarization; ICD, implantable cardioverter defibrillator; LVEF, left ventricular ejection fraction; VF, ventricular fibrillation. Corresponding author. Service de Rythmologie, Centre Hospitalier Universitaire Amiens-Picardie, Hôpital Sud, 80054 Amiens cedex, France. E-mail address: hermida.jean-sylvain@chu-amiens.fr (J.-S. Hermida). 1875-2136/$ see front matter 2012 Elsevier Masson SAS. All rights reserved. http://dx.doi.org/10.1016/j.acvd.2012.07.005

J waves in ACS patients with ventricular fibrillation 579 Results. J waves were more frequent in the study group than in the control group (62% vs. 39%; P = 0.006). J waves (odds ratio [OR] 3.3, 95% confidence interval [CI] 1.5 7.1; P = 0.001) and left ventricular ejection fraction < 40% (53% vs. 14%; P < 0.001) (OR 7.9, 95% CI 3.5 18.0; P = 0.001) were associated with VF. Inhospital mortality was 15.1% in the study group versus 0.9% in the control group (OR 18.7, 95% CI 2.2 157.5; P = 0.008). VF (OR 18.3, 95% CI 2.3 835.9; P < 0.001) and the presence of J waves (OR 15.9. 95% CI 2.4 ; P < 0.001) were predictive of inhospital mortality. In patients who experienced VF, inhospital mortality was 24% when J waves were observed and 0% when J waves were absent (P = 0.02). Conclusions. Inferior and lateral J waves were observed more frequently in patients who experienced cardiac arrest due to VF associated with ACS than in the absence of cardiac arrest and were associated with higher inhospital mortality. 2012 Elsevier Masson SAS. All rights reserved. MOTS CLÉS Arrêt cardiaque ; Syndrome coronaire aigu ; Fibrillation ventriculaire ; «Onde J» Résumé Contexte. La présence des «ondes J» est associée aux fibrillations ventriculaires (FV) idiopathiques mais est également décrite chez les patients ayant eu une FV ischémique. Objectifs. Le but de cette étude a été de déterminer si l existence d «ondes J» dans les dérivations latérales et/ou inférieures de l ECG étaient associée au cours des syndromes coronariens aigus (SCA) à la survenue d une FV ou à la mortalité hospitalière. Méthodes. Cinquante-trois patients (âge moyen = 52 ± 10 ans) ayant présenté un arrêt cardiaque dû à une FV lors des 48 premières heures d un SCA, ont été inclus dans une étude cas-témoin rétrospective. Le groupe témoin a été apparié pour l âge et le sexe. Il comprend 106 patients qui ont eu un SCA mais sans arrêt cardiaque par FV. Résultats. Les «ondes J» ont été plus fréquentes dans le groupe FV que dans le groupe témoin sans FV (62 % vs 39 % ; p = 0,006). La présence d «ondes J» (OR 3,3, CI 1,5 7,1 ; p = 0,001) et d une FEVG < 40 % (53 % vs 14 % ; p < 0,001) (OR 7,9, CI 3,5 18,0 ; p = 0,001) sont apparues associées à la survenue d une FV. La mortalité hospitalière a été de 15,1 % dans le groupe FV contre 0,9 % dans le groupe témoin (OR 18,7, CI 2,2 157,5 ; p = 0,008). La survenue d une FV (OR 18,3, CI 2,3 835,9 ; p < 0,001) et la présence d «ondes J» (OR 15,9 CI 2,4 ; p < 0,001) ont été prédictives de la mortalité hospitalière. Chez les patients ayant eu une FV, la mortalité hospitalière a été de 24 % en présence d une «onde J» et nulle en l absence d «onde J» (p = 0,02). Conclusions. Au cours des 48 premières heures d un SCA, des «ondes J» en position latérales et ou inférieures ont été observées plus fréquemment chez les patients ayant eu une FV et sont apparues associées à une mortalité hospitalière plus élevée. 2012 Elsevier Masson SAS. Tous droits réservés. Background J point elevation with QRS notching or slurring may be associated with ST-segment elevation and characterizes the early repolarization (ER) pattern when localized in inferolateral electrocardiogram (ECG) leads. The ER pattern has been identified for many decades and was considered to be a normal variant [1 3]. Recently, ER has been described in patients with idiopathic ventricular fibrillation (VF), in several case reports [4 12] then in case-control studies [13 16]. The prevalence of ER in patients with idiopathic VF has been reported to be 23 to 58% [13 17] versus 5 to 9% in the general population [14,16,18]. In athletes, ER was present in 28.6% of cases and 7.6% of controls [13]. The presence of ER in patients with idiopathic VF currently defines the ER syndrome [19]. Although Brugada syndrome and ER syndrome differ according to the magnitude and localization of J point elevation, they are believed to represent a broad continuum. The generic term of J wave syndrome has been proposed [19]. The significance of J waves, reflecting either ER or ventricular depolarization abnormality, is still being debated [20,21]. Inferior and/or lateral J waves have also been reported in patients with chronic coronary artery disease [22], previous myocardial infarction [22,23], acute myocardial ischaemia [24] or ischaemic VF [25,26], patients resuscitated from cardiac arrest [27], patients with arrhythmogenic right ventricular dysplasia-cardiomyopathy [28], children with hyperactivity disorder [29] and patients with short QT syndrome [30] or Wolff Parkinson White syndrome [31]. J waves may be a sign of a primary electrical abnormality, structural cardiac disease or both. The aim of this study was to determine whether inferior and/or lateral J waves were associated with the occurrence of VF or inhospital mortality during acute coronary syndrome (ACS). Methods Patients We conducted a retrospective case-control study and reviewed the medical records of 98 consecutive patients hospitalized in the coronary care unit of our institution

580 L. Aïssou et al. Figure 1. Flow-chart of patients included in or excluded from the study. ACS: acute coronary syndrome; AV: atrioventricular; CCU: cardiac care unit; LBBB: left bundle branch block; PTCA: percutaneous transluminal coronary angioplasty; VF: ventricular fibrillation. between 2008 and 2010 with the diagnosis of resuscitated cardiac arrest. The study was approved by the Amiens ethics committee. The Amiens-Picardie University Hospital is a tertiary referral centre for the Picardie administrative region (1.9 million inhabitants); it also directly receives cases of cardiac arrest occurring in its own health territory and in the city of Amiens (total population 520,000 inhabitants) via emergency services. Patients were included in the study group when cardiac arrest was due to spontaneous primary VF occurring < 48 hours after onset of ACS. ACS was defined as a rise in cardiac troponin concentration with one value above the 99th percentile of the upper reference limit and at least: symptoms of ischaemia; ECG changes indicative of new ischaemia; development of pathological Q waves; or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality [32]. To obtain a homogeneous group of cases with VF at the early phase of ACS, we excluded patients found in asystole without documented previous spontaneous VF (n = 13) and patients with VF without ACS (n = 10), VF occurring during or after the revascularization procedure (n = 8), left bundle branch block on the postcardiac arrest ECG (n = 8), VF occurring > 48 hours after the onset of ACS (n = 3) and third-degree atrioventricular block (n = 3). The study group finally comprised 53 patients (41 men and 12 women) with a mean age of 52 ± 10 years (range 34 76 years; Fig. 1). The control group comprised two age- and sex-matched controls for each patient. Controls were selected from a cohort of patients with ACS but without cardiac arrest due to VF or left bundle branch block, admitted to the coronary care unit during the same period (n = 106). The list of patients in the study and control groups was obtained from our institution s electronic medical records system (Département d Informatique Médicale). The following data were collected: cardiovascular risk factors; treatment on arrival; previously known coronary artery disease; localization of the ACS; revascularization procedure; thrombolytic therapy; and left ventricular ejection fraction (LVEF) on echocardiography performed during the first 48 hours. The presence of diabetes, hypertension or dyslipidaemia was assessed by patient self-reporting and according to the presence of specific treatment on arrival. The diagnosis of previous coronary artery disease was accepted only when the patient had had a previous anatomical and/or functional evaluation showing coronary artery disease. Localization of the ACS was assessed by the results of coronary angiography and by a 12-lead ECG. Electrocardiogram analysis Blinded evaluation of the ECG was performed by two cardiologists (L.A,. S.T.); in the case of disagreement, a consensus was reached after a third blinded analysis (J.-S.H.). PR intervals, QRS durations and QTc intervals (Bazett s formula) [33] were measured on the ECG recorded on the day of onset of the ACS and VF. J waves were defined as in the study by Haïssaguerre et al.: The amplitude of J-point elevation had

J waves in ACS patients with ventricular fibrillation 581 Figure 2. Ventricular fibrillation (VF) in a patient with J waves. Presence of QRS notching in leads II, III and avf during an inferior acute coronary syndrome (ACS) in a 58-year-old man. Small notching is visible before VF but is not enhanced. The 12-lead electrocardiogram was recorded on the first day of the ACS. to be at least 1 mm (0.1 mv) above the baseline level, either as QRS slurring (a smooth transition from the QRS segment to the ST segment) or notching (a positive J deflection inscribed on the S wave) in the inferior lead (II, III, and avf), lateral lead (I, avl and V4 to V6) or both. The anterior precordial leads (V1 to V3) were excluded from the analysis to avoid the inclusion of patients with right ventricular dysplasia or the Brugada syndrome. (Fig. 2) [14]. As QRS slurring was sometimes difficult to distinguish from ST-segment elevation related to myocardial infarction, we therefore also analysed the ECG after return of the ST segment to the isoelectric line (Fig. 3). Due to the description of J wave spontaneous variations in the literature, we considered for analysis all ECGs recorded during hospitalization. Therapeutic hypothermia was performed in all 52 patients in the study group with out-of-hospital cardiac arrest (Fig. 1). ECGs recorded during therapeutic hypothermia were excluded to avoid confusion with Osborne wave. differences and 95% CIs were computed for continuous variables. Differences between patients with or without J waves were assessed by a t test for continuous variables and by the Chi 2 test for categorical variables. Interobserver agreement was determined by overall proportion of agreement and kappa score for the diagnosis of J waves. A multivariate logistic regression model (forward conditional model) was used to identify the factors associated with the occurrence of VF and with inhospital mortality. Data that were significantly different (P < 0.05) between study and control patients in univariate analysis were included in the logistic regression ( J waves, RR interval, QTc interval, anterior localization of the ACS, LVEF). An exact logistic model was used for inhospital mortality due to the sparse distribution of the variables. ORs were calculated with 95% CIs. P values were two-sided and values < 0.05 were considered significant. SPSS software (version 11) was used for all analysis. Statistical analysis Differences between cases and controls were assessed using a generalized linear mixed model with the SAS Glimmix procedure. Odds ratios (ORs) and their 95% confidence intervals (95% CIs) were computed for categorical variables and mean Results The characteristics of patients included in the study and control groups are summarized in Table 1. The two groups were similar in terms of age, sex ratio, cardiovascular risk factors, treatment with beta-blockers, history of coronary artery

582 L. Aïssou et al. Figure 3. Diagnosis of J waves during acute coronary syndrome (ACS). (A) Patient who experienced cardiac arrest at the initial phase of an anterior ACS; J waves are already visible during the phase of ST-segment elevation. (B) Inferolateral ACS with ST-segment elevation in leads II, III, avf, V4 and V6 but with no visible notching; detection of J waves in leads V5 to V6 after return of the ST segment to the isoelectric line. disease, extent of coronary artery disease and ACS treatment modalities. The localization of the ACS was more often anterior than non-anterior in patients who experienced cardiac arrest due to VF. A significantly lower LVEF and a significantly longer QTc interval were observed in the study group. Prevalence of J waves The total prevalence of J waves in patients with ACS was 47%. The prevalence of J waves was higher in the study group than in the control group (62% vs. 39%; P = 0.006). In the 74 patients in whom J waves were observed, 33 (45%) patients had been resuscitated from a cardiac arrest. J waves were mainly localized in the inferolateral leads (53%) compared with inferior leads only or lateral leads only. The distribution of J waves in these leads was similar in the study and control groups (Table 2). The amplitude of J waves was not significantly higher in the study group (Table 2). On logistic regression, the presence of J waves was associated with VF, with an OR of 3.3 (95% CI 1.5 7.1; P = 0.001). LVEF < 40% was also associated with the presence of VF (OR 7.9, 95% CI 3.5 18.0; P = 0.001) compared with the control group (53% vs 14%; P < 0.001; Table 1). RR interval, QTc interval and anterior localization of the ACS were not associated with VF in the regression model. The interobserver agreement for the diagnosis of J waves on ECG was 91% with a kappa score of 0.82. Inhospital mortality and J waves Inhospital mortality was 15.1% in the study group versus 0.9% in the control group (OR 18.7, 95% CI 2.2 157.5; P = 0.008). On multivariate logistic regression, VF (OR 18.3 95% CI 2.3 835.9; P < 0.001) and the presence of J waves (OR 15.9, 95% CI 2.4 ; P < 0.001) were predictive of inhospital mortality. RR interval, QTc interval, LVEF and anterior localization of the ACS were not associated with inhospital mortality in the regression model. Comparison between the four subgroups of patients with or without J waves and according to the presence or absence of VF is shown in Table 3. Mortality was higher in patients in whom J waves were present after the episode of VF than in patients without J waves (24% vs. 0%; P = 0.02) (Fig. 4), whereas LVEF (42 ± 13% vs. 43 ± 13%; P = 0.6) and age (51 ± 8 years vs. 56 ± 13 years; P = 0.1) were not different between the two groups (Table 3). Death occurred in the context of post cardiac arrest syndrome for all the patients in the study group.

J waves in ACS patients with ventricular fibrillation 583 Table 1 Comparison of patients in the study and control groups. Characteristics Study group (n = 53) Control group (n = 106) P Demographic and clinical Age (years) 52 ± 10 52 ± 10 0.8 Men 41 (77) 82 (77) 1 Ethnicity White 53 105 Black 0 1 Diabetes mellitus 10 (18) 1 (0.9) 0.1 Hypertension 13 (24) 27 (25) 1 Dyslipidaemia 19 (35) 29 (27) 0.3 Smoker 35 (66) 75 (70) 0.6 Beta-blocker 5 (9) 11 (10) 0.8 Electrocardiographic RR interval (ms) 759 ± 157 880 ± 172 0.002 PR interval (ms) 166 ± 37 156 ± 26 0.1 QRS (ms) 92 ± 10 90 ± 11 0.2 QTc interval (ms) 444 ± 33 422 ± 29 < 0.001 CAD Previous CAD 4 (7) 4 (3) 0.4 STEMI 47 (89) 102 (96) 0.07 Extent of the CAD 1 vessel 31 (59) 61 (58) 0.9 2 vessels 14 (26) 27 (25) 0.8 3 vessels 8 (15) 18 (17) 0.8 ACS localization Anterior 31 (59) 37 (35) 0.006 Inferior 17 (32) 61 (57) 0.002 Lateral 5 (9) 8 (8) 0.7 Treatment of ACS Thrombolysis 19 (36) 41 (39) 0.4 Rescue PCI 5 (9) 9 (8) 0.9 Revascularization procedures 49 (92) 87 (82) 0.09 No revascularization therapy 3 (6) 10 (9) 0.4 LVEF (%) 42 ± 13 52 ± 10 < 0.001 LVEF < 40% 28 (53) 15 (14) < 0.001 Data are mean ± standard deviation or number (%). ACS: acute coronary syndrome; CAD: coronary artery disease; LVEF: left ventricular ejection fraction; PCI: percutaneous coronary intervention; STEMI: ST-segment elevation myocardial infarction; VF: ventricular fibrillation. Table 2 Prevalence amplitude and localization of J waves in the study group versus the control group. Study group (n = 53) Control group (n = 106) P J waves 33 (62) 41 (39) 0.006 Localization of J waves Inferior 8 (24) 13 (32) 0.6 Lateral 5 (15) 9 (22) 0.6 Inferolateral 20 (61) 19 (46) 0.2 Amplitude of J waves (mm) 1.8 ± 0.5 1.4 ± 0.5 0.7 Number of electrocardiograms screened per patient 13 ± 9 11 ± 5 0.3 Data are mean ± standard deviation or number (%).

584 L. Aïssou et al. Table 3 Comparison of patients with or without J waves according to the presence or absence of ventricular fibrillation. J waves (n = 74) Absence of J waves (n = 85) VF (1) (n = 33) No VF (2) (n = 41) P (1) vs. (2) VF (3) (n = 20) No VF (4) (n = 65) P (3) vs. (4) Age (years) 51 ± 8 51 ± 9 0.9 54 ± 13 53 ± 11 0.5 P = 0.2 vs. (1) P = 0.5 vs. (2) Men 28 (85) 35 (85) 0.1 13 (65) 47 (72) 0.6 P = 0.2 vs. (1) P = 0.2 vs. (2) RR interval (ms) 770 ± 147 852 ± 180 0.1 741 ± 177 903 ± 165 0.01 P = 0.6 vs. (1) P = 0.2 vs. (2) PR interval (ms) 170 ± 29 158 ± 29 0.1 160 ± 24 155 ± 24 0.4 P = 0.6 vs. (1) P = 0.6 vs. (2) QRS (ms) 95 ± 9 90 ± 10 0.06 88 ± 11 89 ± 12 0.7 P = 0.02 vs. (1) P = 0.5 vs. (2) QTc interval (ms) 445 ± 30 424 ± 28 0.003 442 ± 37 421 ± 30 0.02 P = 0.8 vs. (1) P = 0.5 vs. (2) ACS localization Anterior 17 (51) 15 (37) 0.2 14 (70) 22 (34) 0.005 P = 0.2 vs. (1) P = 0.8 vs. (2) Inferior 13 (40) 25 (61) 0.1 4 (20) 36 (55) 0.005 P = 0.2 vs. (1) P = 0.7 vs. (2) Lateral 3 (9) 1 (2) 0.3 2 (10) 7 (11) 0 P = 0.9 vs. (1) P = 0.1 vs. (2) Revascularization procedure 31 (94) 35 (85) 0.3 18 (90) 52 (80) 0.5 P = 0.6 vs. (1) P = 0.6 vs. (2) Thrombolysis 13 (40) 15 (37) 0.8 6 (30) 26 (40) 0.6 P = 0.6 vs. (1) P = 0.8 vs. (2) LVEF 42 ± 13 53 ± 9 < 0.001 43 ± 13 52 ± 11 0.008 P = 0.6 vs. (1) P = 0.7 vs. (2) Inhospital mortality 8 (24) 1 (2.4) 0.009 0 0 P = 0.02 vs. (1) P = 0.4 vs. (1) Data are mean ± standard deviation or number (%). ACS: acute coronary syndrome; LVEF: left ventricular ejection fraction; VF: ventricular fibrillation Discussion This study has shown that in patients with ACS, inferior and lateral J waves were more frequently observed in the presence of VF than in the absence of VF. The presence of J waves was also associated with higher inhospital mortality compared with in ACS patients without VF. Prevalence of J waves and ventricular fibrillation during acute coronary syndrome The abnormal distribution of a transient outward current through the ventricular wall leads to the presence of a prominent action potential notch in epicardium but not endocardium and to a voltage gradient that manifests as a J wave [34]. Experimental studies have shown that J waves are secondary to a form of transmural electrical heterogeneity, which is accentuated during acute ischaemia, increasing the risk of malignant arrhythmias [35]. The mechanism of J waves is shared by other causes of VF, such as Brugada syndrome or idiopathic VF, regardless of their inferolateral or anterior localization. Prominent J waves have been reported to occur in ACS [24,25] but their prevalence has not been specifically assessed. Data are available for patients with cardiac arrest and patients with chronic coronary disease. The presence of J waves in patients following cardiac arrest, including VF, asystole and pulseless electrical pattern, was studied by Lelloucheet al.; J waves were present in 36% of all cases and in 9% of cases in which an acute coronary lesion was diagnosed. This value is lower than the 47% prevalence we observed in the context of ACS. The difference could be explained by the fact that cardiac arrest not only includes patients with VF but also patients with asystole or pulseless ventricular activity in 23% of cases with an acute coronary lesion [36]. In patients with chronic coronary artery disease, prior myocardial infarction and implantation of an implantable

J waves in ACS patients with ventricular fibrillation 585 Figure 4. Prevalence of J waves in those with ventricular fibrillation (VF) during acute coronary syndrome and inhospital mortality. The prevalences of J waves in the study and control groups are shown in the centre of the figure. Inhospital mortality is shown on each side for the four subgroups, which are: (1) J wave and VF; (2) J wave and no VF; (3) absence of J wave and VF; (4) absence of J wave and no VF. Same subgroups as in Table 3. cardioverter defibrillator (ICD) as primary prevention, the prevalence of ER was 32% following appropriate therapy with an ICD and 8% in the absence of ICD therapy [22]. The prevalence of ER in this study was also lower than that reported in our series, but this study was performed after healing of the myocardial infarction and not at the acute phase, which may explain the difference. Inferior or inferolateral localization and an amplitude of J waves > 0.2 mv, alone or in combination, have been associated with a higher risk of unexpected death in large cohorts of the general population [23,37,38]. Recently, it was found that the presence of early repolarization was associated with a favourable long-term prognosis when the ST segment had an ascending aspect as opposed to an horizontal or descending pattern [39]. This particularity has also been found in patients with idiopathic VF [40] and may explain the low predictive value of the presence of an isolated J wave. We found a non-significant trend towards a higher amplitude of J waves and more frequent inferolateral localization in the study group compared with in controls (Table 2). According to the ACS, the analysis of the morphology of the ST-segment elevation was not undertaken in our study. Prognostic significance of J waves The prevalence of J waves was two-fold higher in patients experiencing VF during ACS (62%) than in patients with idiopathic VF in the study by Haïssaguerre et al. (31%) [14]. In contrast, the prevalence of J waves was only 5 to 9% in control populations [14,16,18]. A high inhospital mortality was observed in the study group in the presence of J waves (24%) versus no mortality in the absence of J waves (Fig. 4). These results indicate that J waves could be related not only to a predisposing state but also to an acquired condition. J waves may reflect the severity of myocardial ischaemia due to both ACS and cardiac arrest. The duration of the cardiac arrest also could explain the association of post-arrest J waves to inhospital mortality in the context of postcardiac arrest syndrome. Study imitations ECGs were not available to check for the presence of J waves before VF, as, in > 90% of cases, ACS was the first manifestation of coronary artery disease (Table 1). This limitation was also reported by Haïssaguerre et al. [14]. In this work, a prior ECG was available in one third of patients to document the existence of J waves before the episode of idiopathic VF. A detailed prospective study of the chronology of onset of J waves and variations in patients with cardiac arrest and ACS may be of interest in future investigations. Only one black patient and no Asian patients were included in this study; the results may therefore only apply to the Caucasian population. Conclusions In patients with ACS, inferior and lateral J waves seemed to be observed more frequently in the presence of VF than in the absence of VF. The presence of J waves is associated with higher inhospital mortality compared with in ACS patients without VF. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.

586 L. Aïssou et al. Acknowledgements The authors thank Dr. F. Sacher (CHU Bordeaux) for his contribution to the ECG interpretation. References [1] Klatsky AL, Oehm R, Cooper RA, et al. The early repolarization normal variant electrocardiogram: correlates and consequences. Am J Med 2003;115:171 7. [2] Mehta M, Jain AC, Mehta A. Early repolarization. Clin Cardiol 1999;22:59 65. [3] Wasserburger RH, Alt WJ. The normal RS-T segment elevation variant. Am J Cardiol 1961;8:184 92. [4] Aizawa Y, Tamura M, Chinushi M, et al. Idiopathic ventricular fibrillation and bradycardia-dependent intraventricular block. Am Heart J 1993;126:1473 4. [5] Daimon M, Inagaki M, Morooka S, et al. Brugada syndrome characterized by the appearance of J waves. Pacing Clin Electrophysiol 2000;23:405 6. [6] Garg A, Finneran W, Feld GK. Familial sudden cardiac death associated with a terminal QRS abnormality on surface 12-lead electrocardiogram in the index case. J Cardiovasc Electrophysiol 1998;9:642 7. [7] Kalla H, Yan GX, Marinchak R. Ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a Brugada syndrome variant. J Cardiovasc Electrophysiol 2000;11:95 8. [8] Otto CM, Tauxe RV, Cobb LA, et al. Ventricular fibrillation causes sudden death in Southeast Asian immigrants. Ann Intern Med 1984;101:45 7. [9] Shinohara T, Takahashi N, Saikawa T, et al. Characterization of J wave in a patient with idiopathic ventricular fibrillation. Heart Rhythm 2006;3:1082 4. [10] Takagi M, Aihara N, Takaki H, et al. Clinical characteristics of patients with spontaneous or inducible ventricular fibrillation without apparent heart disease presenting with J wave and ST segment elevation in inferior leads. J Cardiovasc Electrophysiol 2000;11:844 8. [11] Takeuchi T, Sato N, Kawamura Y, et al. A case of a short-coupled variant of torsades de Pointes with electrical storm. Pacing Clin Electrophysiol 2003;26:632 6. [12] Ueyama T, Shimizu A, Esato M, et al. A case of a concealed type of Brugada syndrome with a J wave and mild ST-segment elevation in the inferolateral leads. J Electrocardiol 2007;40:39 42. [13] Cappato R, Furlanello F, Giovinazzo V, et al. J wave, QRS slurring, and ST elevation in athletes with cardiac arrest in the absence of heart disease: marker of risk or innocent bystander. Circ Arrhythm Electrophysiol 2010;3:305 11. [14] Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358:2016 23. [15] Nam GB, Kim YH, Antzelevitch C. Augmentation of J waves and electrical storms in patients with early repolarization. N Engl J Med 2008;358:2078 9. [16] Rosso R, Kogan E, Belhassen B, et al. J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. J Am Coll Cardiol 2008;52:1231 8. [17] Merchant FM, Noseworthy PA, Weiner RB, et al. Ability of terminal QRS notching to distinguish benign from malignant electrocardiographic forms of early repolarization. Am J Cardiol 2009;104:1402 6. [18] Nam GB, Ko KH, Kim J, et al. Mode of onset of ventricular fibrillation in patients with early repolarization pattern vs Brugada syndrome. Eur Heart J 2010;31:330 9. [19] Antzelevitch C, Yan GX. J wave syndromes. Heart Rhythm 2010;7:549 58. [20] Antzelevitch C, Yan GX, Viskin S. Rationale for the use of the terms J-wave syndromes and early repolarization. J Am Coll Cardiol 2011;57:1587 90. [21] Surawicz B, Macfarlane PW. Inappropriate and confusing electrocardiographic terms: J-wave syndromes and early repolarization. J Am Coll Cardiol 2011;57:1584 6. [22] Patel RB, Ng J, Reddy V, et al. Early repolarization associated with ventricular arrhythmias in patients with chronic coronary artery disease. Circ Arrhythm Electrophysiol 2010;3: 489 95. [23] Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361:2529 37. [24] Shinde R, Shinde S, Makhale C, et al. Occurrence of J waves in 12-lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol 2007;30:817 9. [25] Jastrzebski M, Kukla P. Ischemic J wave: novel risk marker for ventricular fibrillation. Heart Rhythm 2009;6:829 35. [26] Maruyama M, Atarashi H, Ino T, et al. Osborn waves associated with ventricular fibrillation in a patient with vasospastic angina. J Cardiovasc Electrophysiol 2002;13:486 9. [27] Jain U, Wallis DE, Shah K, et al. Electrocardiographic J waves after resuscitation from cardiac arrest. Chest 1990;98: 1294 6. [28] Peters S, Selbig D. Early repolarization phenomenon in arrhythmogenic right ventricular dysplasia-cardiomyopathy and sudden cardiac arrest due to ventricular fibrillation. Europace 2008;10:1447 9. [29] Nahshoni E, Sclarovsky S, Spitzer S, et al. Early repolarization in young children with attention-deficit/hyperactivity disorder versus normal controls: a retrospective preliminary chart review study. J Child Adolesc Psychopharmacol 2009;19: 731 5. [30] Watanabe H, Makiyama T, Koyama T, et al. High prevalence of early repolarization in short QT syndrome. Heart Rhythm 2010;7:647 52. [31] Mizumaki K, Nishida K, Iwamoto J, et al. Early repolarization in Wolff-Parkinson-White syndrome: prevalence and clinical significance. Europace 2011;13:1195 200. [32] Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50: 2173 95. [33] Bazett HG. An analysis of the time-relations of electrocardiograms. Heart 1920;7:353 70. [34] Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372 9. [35] Gussak I, Antzelevitch C. Early repolarization syndrome: clinical characteristics and possible cellular and ionic mechanisms. J Electrocardiol 2000;33:299 309. [36] Lellouche N, Sacher F, Jorrot P, et al. Sudden cardiac arrest: ECG repolarization after resuscitation. J Cardiovasc Electrophysiol 2011;22:131 6. [37] Haruta D, Matsuo K, Tsuneto A, et al. Incidence and prognostic value of early repolarization pattern in the 12-lead electrocardiogram. Circulation 2011;123:2931 7. [38] Sinner MF, Reinhard W, Muller M, et al. Association of early repolarization pattern on ECG with risk of cardiac and allcause mortality: a population-based prospective cohort study (MONICA/KORA). PLoS Med 2010;7:e1000314. [39] Tikkanen JT, Junttila MJ, Anttonen O, et al. Early repolarization: electrocardiographic phenotypes associated with favorable long-term outcome. Circulation 2011;123: 2666 73. [40] Rosso R, Glikson E, Belhassen B, et al. Distinguishing benign from malignant early repolarization: the value of the STsegment morphology. Heart Rhythm 2012;9:225 9.