Author + information
- Received April 18, 2013
- Accepted May 7, 2013
- Published online October 22, 2013.
- Tsukasa Kamakura, MD∗,†,
- Hiro Kawata, MD∗,
- Ikutaro Nakajima, MD∗,
- Yuko Yamada, MD∗,
- Koji Miyamoto, MD∗,
- Hideo Okamura, MD∗,
- Takashi Noda, MD, PhD∗,
- Kazuhiro Satomi, MD, PhD∗,
- Takeshi Aiba, MD, PhD∗,
- Hiroshi Takaki, MD, PhD∗,
- Naohiko Aihara, MD∗,
- Shiro Kamakura, MD, PhD∗∗ (, )
- Takeshi Kimura, MD, PhD† and
- Wataru Shimizu, MD, PhD‡
- ∗Division of Arrhythmia and Electrophysiology, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan
- †Division of Cardiology, Department of Cardiovascular Medicine, Kyoto University, Kyoto, Japan
- ‡Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan
- ↵∗Reprint requests and correspondence:
Dr. Shiro Kamakura, Division of Arrhythmia and Electrophysiology, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, 565-8565 Suita, Japan.
Objectives The aim of this study was to investigate the significance of non-type 1 anterior early repolarization (NT1-AER) combined with inferolateral early repolarization syndrome (ERS).
Background Inferolateral ERS might be a heterogeneous entity, although it excludes type 1 Brugada syndrome (BS).
Methods Of 84 patients with spontaneous ventricular fibrillation, 31 ERS patients were divided into 2 groups. The ERS(A)-group consisted of inferolateral ER and NT1-AER—that is, notching or slurring with J-wave ≥1 mm at the end of QRS to early ST segment in any of V1 to V3 leads, in which the ST-T segment did not change to a coved pattern in the standard and high costal (second and third) electrocardiographic recordings even after drug provocation tests (n = 12). The other, ERS(B)-group, showed only inferolateral ER (n = 19). Clinical characteristics and outcomes were compared between the ERS groups, 40 patients with type-1 BS (BS-group), and 13 patients with idiopathic ventricular fibrillation lacking J-wave (IVF-group).
Results Ventricular fibrillation occurred during sleep or near sleep in 10 of 12 patients in ERS(A)-group and in 22 of 40 patients in BS-group but in 2 of 19 patients in ERS(B)-group and in 1 of 13 patients in IVF-group (ERS[A] vs. ERS[B], p < 0.0001). Ventricular fibrillation recurrence was significantly higher in ERS(A)-group (58%), particularly in patients with J waves in the high lateral lead, and BS-group (55%), compared with ERS(B)-group (11%) and IVF-group (15%) (ERS[A] vs. ERS[B], p = 0.012).
Conclusions Inferolateral ERS comprises heterogeneous ER subtypes with and without NT1-AER. Coexistence of NT1-AER was a key predictor of poor outcome in patients with ERS.
J-wave or early repolarization (ER) is a common electrocardiographic finding that affects 1% to 13% of individuals and is characterized by the elevation of the J point with notching or slurring on electrocardiogram (ECG) followed by ST-segment elevation (1–3). Although this condition had been considered benign, Haïssaguerre et al. (1) demonstrated patients with J waves in the inferolateral lead (I, II, III, aVL, aVF, and V4 to V6) were likely to be associated with idiopathic ventricular fibrillation (IVF) and reported this entity as inferolateral early repolarization syndrome (ERS) in 2008. Since then, the J-wave has come to be known as a possible indicator of an increased risk for death due to cardiac arrhythmia.
Brugada syndrome (BS) is another clinical entity that causes sudden death because of ventricular fibrillation (VF) in patients with apparently structurally normal hearts and is characterized by coved ST-segment elevation in the right precordial leads (V1 to V3) (4,5). Yan and Antzelevitch, with a canine Brugada model (6), demonstrated that this peculiar ST-segment elevation in the anterior lead can be an expression of ER or J-wave caused by transient outward current (Ito)-mediated transmural differences in early phases of the action potential. Haïssaguerre et al. (1) defined inferolateral ERS as a disease characterized by J waves only in inferolateral lead and excluded patients with type 1 (coved) ST-segment elevation in leads V1 to V3 from this syndrome. However, patients with non-type 1 ST-segment elevation or J waves showing notching or slurring in the anterior leads can be theoretically included in this syndrome. Therefore, we investigated the significance of the non-type 1 anterior ER (NT1-AER) excluding coved ST-segment elevation in inferolateral ERS by comparing the clinical profile and long-term prognosis in patients with and without NTI-AER.
The study population consisted of 84 consecutive patients who were admitted to our hospital between 1992 and 2011 due to spontaneous idiopathic VF. Patients exhibited 3 distinct ECG patterns as follows: 31 had inferolateral ERS (ERS-group, 27 men, mean age: 42.0 ± 14.1 years); 40 had type 1 BS (BS-group, 40 men, mean age: 43.0 ± 12.2 years); and 13 had idiopathic VF without J waves (IVF-group, 8 men, mean age: 46.1 ± 12.7 years). None of the patients had structural heart disease, including arrhythmogenic right ventricular (RV) cardiomyopathy, which was confirmed by noninvasive studies (physical examination, 12-lead ECG, 87-lead body surface ECG, exercise stress test, signal-averaged ECG, echocardiography, and cardiac magnetic resonance imaging or computed tomography) and invasive studies consisting of coronary angiography including ergonovine/acetylcholine injection and right or left ventricular (LV) cineangiography. Patients with coronary artery spasm, long QT syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia, commotio cordis, drug-induced VF, and hypothermia were excluded in all groups. Abnormal QTc interval was defined as ≥460 ms and <340 ms during sinus rhythm.
Classification of inferolateral ERS, BS, and IVF groups
We divided the 31 patients with inferolateral ERS and a prior episode of VF into 2 groups according to their baseline ECGs and the results of the drug provocation tests with a sodium channel blocker. One group consisted of patients with an inferolateral ER combined with NT1-AER (ERS[A]-group) (i.e., anterior ER consisting of notching or saddleback ST-segment elevation in any of the right precordial leads). The other group consisted of a pure inferolateral ER without anterior ER (ERS[B]-group).
The presence of inferolateral ER, which was defined as an elevation of the J point in at least 2 leads, was evaluated by baseline 12-lead ECGs (25 mm/s and 10 mm/mV). The amplitude of the inferolateral J-wave or J-point elevation had to be at least 1 mm or 0.1 mV above the baseline level, either as QRS slurring or notching in any of the inferior (II, III, and aVF), lateral (V4, V5, and V6), and high lateral (I and aVL) leads (1) in at least 1 ECG recording.
The NT1-AER was defined as upward/downward notching or downward slurring with an amplitude ≥1 mm at the end of QRS to early ST segment in any of the anterior leads (V1, V2, and V3) in the baseline standard or high costal (second and third) ECG recordings or in those ECGs after drug provocation tests, which includes type-2 and type-3 Brugada-pattern ECG (4). The upward/downward notch in the anterior leads should have appeared between the late QRS and early ST period in the same timeframe as J waves in other leads in the same 12-lead ECG.
Coved AER was defined as type 1 Brugada ECG (4) or coved ST-segment elevation ≥2 mm followed by a positive or flat T-wave in any of anterior leads, either occurring spontaneously or after challenge with a sodium channel blocker. Patients with coved-AER were excluded from the ERS-group and included in the BS-group, although patients in the BS-group should have shown type 1 ECG with a negative T-wave spontaneously or after drug test according to consensus reports (4,5). The ERS-group excluded patients with bundle branch block of QRS duration ≥110 ms on the standard ECG. The IVF-group also excluded patients with J waves or ER in any leads (inferolateral ER, NT1-AER, and coved–AER) in the standard and high costal recordings even after drug provocation test.
Clinical profiles, electrocardiographic characteristics, and VF recurrences during follow-up were compared among the patients in the ERS(A), ERS(B), BS, and IVF groups.
Clinical data, ECG, genetic, and electrophysiological testing
Clinical data including age at the first episode of VF, sex, family history of sudden cardiac death at <45 years of age, activity of patients at VF, the location of leads showing ER, and prognosis were collected for all patients. We defined the state of patients at VF as “sleep” when VF occurred in a state of sleeping and as “near sleep” when VF occurred in a resting state without physical activity just after waking. During follow-up, patients were considered to have an arrhythmic event if VF was documented by implantable cardioverter-defibrillator (ICD) interrogation. An electrical storm was defined as ≥3 VF episodes within 24 h. The beginning of the follow-up period was at the time of the first VF event. In patients with recurrent arrhythmias, the choice of antiarrhythmic drugs was decided by the physician of the patient.
All ECGs were analyzed by 2 independent cardiologists (T.K., S.K.), and consensus was reached about the diagnosis. The J waves in the extensive lead were considered to be J waves in the inferior and lateral or high lateral leads.
Electrophysiological study was conducted in 59 (ERS[A]: 6; ERS[B]: 10; BS: 32; and IVF: 11) patients, as previously reported (7). Patients with inducible VF were classified as inducible. Genetic testing for mutations in SCN5A gene was also performed in 43 (ERS[A]: 7; ERS[B]: 12; and BS: 24) patients, as previously described (8).
Drug provocation test
Drug provocation tests were conducted with pilsicainide (up to 1 mg/kg body weight at a rate of 5 to 10 mg/min), disopyramide (1.5 mg/kg, 10 mg/min), or flecainide (2 mg/kg, 10 mg/min) in all patients of the ERS and IVF groups during standard and high costal (second and third) ECG recordings. This study was approved by the institutional research board of National Cerebral and Cardiovascular Center.
Data were analyzed with JMP7 software (SAS Institute, Inc., Cary, North Carolina). Numeric values are presented as mean ± SD. The chi-square test, Student t test, or 1-way analysis of variance was performed as appropriate to test for statistically significant differences. Survival curves were constructed by the Kaplan-Meier method and compared by the log-rank test. A probability value of p < 0.05 was considered statistically significant.
ECG findings of ERS(A) and ERS(B) groups
Figures 1 and 2 show typical ECGs at baseline and after drug provocation test, respectively, in patients with inferolateral ERS. Twelve of 31 (39%) patients in the inferolateral ERS group had NT1-AER in the right precordial leads in standard or high costal ECG recordings, spontaneously or after drug provocation tests: 7 ( type 2: 4; type 3: 2; notch: 1) on the baseline standard ECGs; 4 (type 2: 2; type 3: 1; notch: 1) only on the high intercostal ECG recordings before drug provocation (Figs. 1A and 1C); and 1 (type 2: 1) on the high intercostal ECG after pilsicainide injection (Fig. 1B). None of these ECGs of patients including high costal recordings ever revealed the coved-AER pattern during follow-up. By contrast, 19 patients in the ERS(B)-group showed only inferolateral ER pattern spontaneously or after drug provocation test and in follow-up (Fig. 2).
Clinical profiles in each group
Clinical characteristics of the patients in each group are shown in Table 1. Most patients were male. Ventricular fibrillation developed during sleep or near sleep in 10 of 12 (83%) patients in ERS(A) (sleep: 8; near sleep: 2) and in 22 of 40 (55%) patients in the BS-group (sleep: 17; near sleep: 5), in contrast to only 2 of 19 (11%) patients (sleep: 2) in the ERS(B)-group (ERS[A] vs. ERS[B], p < 0.0001; and BS vs. ERS[B] p = 0.0015) and 1 of 13 (8%) patients (sleep: 1) in the IVF-group. Most patients in the ERS(B) and IVF-group had VF during activity.
The J waves were spontaneously noted in the high lateral, lateral, inferior, and extensive leads in 10, 7 ,6, and 5 patients, respectively, in the ERS(A)-group and in 3, 15, 15, and 12 patients, respectively, in the ERS(B)-group. After sodium channel blocker provocation, J waves disappeared or were attenuated with appearance of S waves and slight prolongation of QRS interval in all patients of the ERS(B)-group (Fig. 2); conversely, the J waves were augmented in various leads of the inferior (Fig. 1B), high lateral (Fig. 1C), and anterior leads (Figs. 1A and 1B) in 9 of 12 patients of the ERS(A)-group (Table 1).
The VF inducibility in the ERS(A)-group was similar to that in the BS-group (ERS[A]: 50%; BS: 81%, p = 0.13). Mutations of SCN5A were identified in 8 of 24 patients in the BS-group but in no patients in the ERS group.
Mean follow-up period for ERS(A), ERS(B), BS, and IVF groups was 90 ± 57, 76 ± 46, 104 ± 63, and 82 ± 50 months, respectively. Seventy-eight of 84 patients received an ICD. One patient in the ERS(B)-group, 2 patients in the BS-group, and 3 patients in the IVF-group were followed without ICD implantation. No patients died during the follow-up period.
Ventricular fibrillation recurred in 7 of the 12 (58%) patients in the ERS(A)-group and in 22 of the 40 (55%) patients in the BS-group. These groups had significantly higher recurrence rates of VF compared with the ERS(B)-group (2 of 19 [11%]) and IVF-group (2 of 13 [15%]) (ERS[A] vs. ERS[B]: p = 0.012; and BS vs. ERS[B]: p = 0.002). Electrical storm was also significantly higher in the ERS(A)-group (5 of 12 [42%]) and BS-group (10 of 40 [25%]), compared with the ERS(B)-group (0 of 19 [0%]) and IVF-group (0 of 13 [0%]) (ERS[A] vs. ERS[B]: p = 0.0047; and BS vs. ERS[B]: p = 0.022). Among 7 patients in the ERS(A)-group with VF recurrences, 6 had J waves in the high lateral lead. One patient with a VF recurrence in the ERS(B)-group showed J waves in the extensive lead.
Kaplan-Meier curves of the 4 groups are illustrated in Figure 3. Patients in the ERS(A) and BS groups exhibited significantly higher arrhythmic events than those in the ERS(B)-group (log-rank, p = 0.0038). Patients in ERS(B) and IVF groups without known disease showed a more favorable prognosis. Figure 4 illustrates Kaplan-Meier analyses for time free of VF for the ERS(A)-group, BS with inferolateral ER group, and BS without inferolateral ER group. Eleven patients (28%) in the BS-group had J waves in inferolateral leads. Eight of them (73%) had recurrence of VF, and 3 (27%) of them had VF storm in the follow-up. Although BS with inferolateral ER group tended to develop VF recurrences, there was no statistically significant difference between the ERS(A)-group and BS with inferolateral ER group (log-rank, p = 0.38). Patients in the BS with inferolateral ER group showed significantly worse outcome compared with those in the BS without inferolateral ER group (log-rank, p = 0.026), consistent with a previous report (7).
Medical treatment during follow-up
Quinidine (9) was started after the initial VF episode in 2 patients in the BS-group and in 1 patient in the ERS(A)-group without recurrent VF attack. None of the patients in the ERS(B)-group and IVF-group took antiarrhythmic drugs.
After the second VF attack or electrical storm, bepridil—a multichannel blocker with a transient outward potassium current-blocking effect (10,11)—was administered in 3 patients in the ERS(A)-group; even so, 2 of the 3 developed VF. Two patients treated with cilostazol, a phosphodiesterase III inhibitor that augments ICa-L current (10), 1 patient treated with quinidine, and 1 patient treated with denopamine, an oral α+β–adrenergic stimulant (10), in the ERS(A)-group had no other recurrences. Among the 22 patients in the BS-group with VF recurrences, 3 patients treated with quinidine, 2 with bepridil, 1 with denopamine, and 1 with cilostazol were followed without subsequent VF recurrences.
Inferolateral ERS consisted of 2 subtypes with heterogeneous clinical profiles. The ERS(A)-group patients were composed of patients with NT1-AER, who comprised 39% of the ERS patients, had clinical profiles similar to BS with high recurrence rates of VF and electrical storm and tended to show J waves in the high lateral leads. In contrast, ERS(B)-group patients, who had a predominant J-wave distribution in the inferior or extensive lead, showed different clinical profiles, such as VF episodes in an awake state and few VF recurrences as observed in IVF patients.
Characteristics of patients with inferolateral ERS
In this patient population, the first VF occurred while sleeping in 32% (10 of 31), VF was induced by programmed electrical stimulation in 38% (6 of 16), and VF recurred in 29% (9 of 31) of all ERS patients; this was in agreement with previous reports by Haïssaguerre et al. (1,12), in which VF attack occurred during sleep, VF inducibility by electrophysiological study, and VF recurrence was observed in 19%, 34%, and 40% of patients, respectively. In addition, that some ERS patients with VF recurrences in the ERS(A)-group responded to quinidine, cilostazol, and denopamine—which were reported to be effective in patients with BS (9–11)—was also consistent with their report. This means that the ERS patients in this study had very similar clinical characteristics to the ERS cohort in the study by Haïssaguerre et al. (1,12).
So far, ERS and BS patients have been considered to share a similar genetic background and to represent a continuous spectrum of phenotypic expression termed J-wave syndrome, which is thought to be mediated by repolarization abnormality due to the transient outward current in the ventricular myocardium (13). However, some clinical manifestations reportedly differ between ERS and BS, whereby VF occurs less frequently at night, originates mainly from the LV, and is inducible to a lesser degree by programmed electrical stimulation in the inferolateral ERS (1,4,5,7,12). Besides, several findings contradicting the repolarization abnormality have been reported. Kawata et al. (14) and Roten et al. (15) separately indicated that sodium channel blockers, pilsicainide and ajmaline, showed a different response in patients with inferolateral J waves (i.e., these drugs led to attenuation or disappearance of J waves), contrary to augmentation of those in Brugada patients. Another was the report by Abe et al. (16), who suggested that circadian changes of signal-averaged ECG parameters in patients with inferolateral J waves implied an association with depolarization abnormalities.
These clinical features are inconsistent with the theoretical basis that ERS should resemble BS, and have caused confusion and difficulty in understanding ERS. This study showed that ERS is a mixture of different ER subtypes—1 (ERS[A]-group) with features similar to BS, and the other (ERS[B]-group) without Brugada features—and that the coexistence of anterior ER determines the clinical characteristics that are partially similar to BS and an unfavorable prognosis in inferolateral ERS.
Prognosis of patients with ERS(A) and ERS(B)
With regard to the outcome of patients with clinical features consistent with NT1-AER, Kamakura et al. (7) had already reported in a Japanese Brugada registry with standard 12-lead ECG that patients with a history of VF, no inferolateral ER, and non-type 1 ST-segment elevation even after drug provocation test show poor prognosis, just as ln patients with type 1 BS. They also indicated that patients with inferolateral ER and type 1 Brugada ECG have a poorer outcome. In this study, we demonstrated that VF patients with inferolateral ER and NT1-AER also show poor outcome, even though none of the patients in the previous study (7) were included in the ERS group of this study. However, we would like to point out that approximately one-half of NT1-AER could not be detected on the standard ECG (Figs. 1A to 1C) but were only detected on ECGs during high costal recording or after drug provocation test. Besides, the ECGs showed nonspecific ER morphology, just as saddleback ST-segment elevation or upward/downward notching. In this sense, this NT1-AER might be designated a latent ER that is far from previous understanding of the anterior ER, supposedly showing coved-pattern ECG in the right precordial lead (8,13).
Few VF recurrences and VF attacks during activity in patients with pure inferolateral ER (ERS[B]-group) is another novel finding in this study. These clinical characteristics of the ERS(B)-group were very similar to that of the IVF-group, which excluded VF caused by already-known diseases or anterior ER. Thus far, the precise clinical characteristics of this kind of IVF have not been fully understood, although Haïssaguerre et al. (1) reported that the outcome of IVF patients was better, compared with patients with inferolateral ERS.
Relationship between prognosis of patients and localization of J waves
Antzelevitch and Yan (13) proposed the classification of inferolateral ERS into 3 subtypes, depending on the location of J waves, and suggested that there was a risk of life-threatening arrhythmias as ER grade increases stepwise from 1 to 3, although they did not clearly define ECG morphology of anterior J waves. Tikkanen et al. (2) reported that ER pattern in the inferior lead was associated with the risk for VF. They also stressed the significance of a horizontal or descending ST-segment after J waves as an indicator of poor prognosis in patients with inferolateral ER (17). In our study, J waves were preferentially located in the inferior and extensive leads in the ERS(B)-group, with few VF recurrences in the long-term follow up. Furthermore, no significant difference in VF recurrence was observed between patients with horizontal/descending ST-segment (6 of 17 [35%]) and those with ascending ST-segment elevation (3 of 14 [21%]) in the ERS group (p = 0.46). Sixty percent of patients in the ERS(A)-group in whose ECGs J waves were noted in the high lateral leads (I and aVL) had recurrence of VF. This means that VF is likely to recur in patients with anterior and high lateral J waves, irrespective of ST-segment characteristics and the number of leads with J waves, although initial arrhythmic events mainly occur in ER patients with inferior or extensive-global J waves. The close relationship between anterior ER and high lateral J waves can be explained by the anatomical proximity of precordial or upper precordial leads to the lead positions of the left upper chest area where ECG morphology resembles that of I and aVL leads (18).
Mechanism of inferolateral J waves
The mechanism of inferolateral J waves remains unclear and still controversial. There are 2 hypotheses with regard to the origin of J-wave and ST-segment elevation in BS: the repolarization hypothesis and the depolarization hypothesis. In the repolarization hypothesis these are explained by Ito-mediated transmural dispersion of repolarization between the endocardium and epicardium in the RV or LV (13). In the depolarization hypothesis, ST-segment elevation followed by T-wave inversion in the right precordial leads is explained by a potential gradient between the RV outflow tract and RV, which is caused by a significant conduction delay in the RV outflow tract (19). Therefore, the mechanism of ERS(B) does not fit the depolarization hypothesis, because there is no significant ST change in leads V1 to V3, although both hypotheses can be applied to the mechanism of ERS(A).
In this study, J waves in 9 of 12 ERS(A) patients were augmented in the anterior or inferolateral leads by sodium channel blockers, and 10 showed saddleback ST-segment elevation in the anterior lead. In contrast, most J waves in ERS(B) patients were attenuated or disappeared along with QRS prolongation when sodium channel blocking agents were given. The positive J-wave response to sodium channel blockers in ERS(A) patients with frequent VF episodes in the parasympathomimetic status is thought to indicate a repolarization abnormality associated with a depolarization abnormality. By contrast, the negative J-wave response to sodium channel blockers in patients in the ERS(B)-group does not seem to indicate the presence of significant transmural dispersion of repolarization in the ventricle, which is represented by the inferolateral leads. In addition, Nademanee et al. (20) recently reported that the catheter ablation of RV or LV Purkinje network eliminated J waves and VF in selected patients with inferolateral ERS. Taken together, J waves in ERS(B) patients seem to be an expression of a depolarization abnormality in some ventricular areas on the basis of a mechanism unexplained by the previous hypotheses, although subsequent ST-segment elevation is explainable by transmural dispersion of repolarization.
This study demonstrated that inferolateral ERS consisted of heterogeneous ER subtypes with and without NT1-AER. The existence of anterior ER and J waves in the high lateral lead can be useful markers for risk stratification of ERS. In contrast, VF attack during activity or pure inferolateral ER might be predictive of a favorable outcome in ERS patients with VF. A systematic search of the anterior ER with drug challenge test and high costal ECG recording is considered requisite in patients with ERS.
This was a single-center study using retrospective analysis. The small number of patients might limit the interpretation of the results, although it should be pointed out that the number of patients in each group is comparable to that of previous multicenter studies. We had no ERS patients with a coved-AER consisting of coved ST-segment elevation and a flat T-wave, which has already been reported to be linked to various genetic mutations (8,13), although it is possible that such ER might develop type 1 ECG in standard or high costal recordings during follow-up. Further prospective multicenter studies with larger numbers of patients will be needed to confirm these results.
Inferolateral ERS can be divided into 2 heterogeneous groups or subtypes: a pure inferolateral ER group; and a group with inferolateral ER plus non-type 1 anterior ER. Anterior ER seems to be a key predictor of poor outcome in patients with inferolateral ERS.
This work was supported by research grants for the cardiovascular diseases (Grant H23-114, H24-033) from the Ministry of Health, Labor, and Welfare, Japan, and an intramural research fund (22-1-2) for cardiovascular disease of the National Cerebral and Cardiovascular Center. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- Brugada syndrome
- coved anterior early repolarization
- early repolarization
- early repolarization syndrome
- inferolateral early repolarization combined with non-type 1 anterior early repolarization
- pure inferolateral early repolarization without anterior early repolarization
- implantable cardioverter-defibrillator
- idiopathic ventricular fibrillation
- left ventricle/ventricular
- non-type 1 anterior early repolarization
- right ventricle/ventricular
- ventricular fibrillation
- Received April 18, 2013.
- Accepted May 7, 2013.
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