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    • arn-509 Clinical genetic electrocardiographic and electrophy

    2019-05-10

    Clinical, genetic, electrocardiographic, and electrophysiological variables did not differ significantly between patients with and without the ER pattern (Table 2).
    Discussion Among our Brugada syndrome patients, the prevalence of the ER pattern was 10.1%, which is high in comparison to the 2%–5% prevalence reported in the general arn-509 [1–4]. But similar to the 10%–12% prevalence reported previously in patients with Brugada syndrome [9–11]. Kui et al. reported a higher prevalence of J waves (7.26%) in apparently healthy Chinese adults [12]. Uberoi et al. reported that the prevalence of J waves in ambulatory clinical population was 2.3%, and J waves were more common in individuals of black ethnicity compared to those of Hispanic, white, or other ethnicities [3]. Therefore, it is possible that the prevalence of J waves may differ among various ethnicities, although Kui et al. adopted a J wave amplitude of >0.05mV and Uberoi et al. adopted a J wave amplitude of >0.1mV [3]. Thus, the prevalence of J waves may be affected by its definition. The clinical implications of Brugada syndrome characterized by ER are controversial. Lantas et al. reported that an ER pattern in inferolateral leads is not an uncommon finding in Brugada syndrome (12%) and found no association between the ER pattern and arrhythmic events during follow-ups in patients with Brugada syndrome (11% with ER vs. 7% without ER, P=0.223) [9]. In contrast, Sarkozy et al. reported that patients with Brugada syndrome and an ER pattern in the inferolateral leads were less likely than those without the ER pattern to be asymptomatic at first presentation (13/32 (41%) patients with ER vs. 156/248 (63%) patients without ER, P=0.02) [10]. Kamakura et al. also reported a significantly higher observed frequency of arrhythmic events in Brugada syndrome patients with ER in the inferolateral leads than in those without (7/33 (21%) patients with ER; vs. 17/297 (6%) patients without ER; P=0.03) [11]. In the present relatively small single-center study, ER was not associated with adverse outcome events in patients with Brugada syndrome. Antzelevitch et al. hypothesized that an outward shift in the repolarizing current due to a decrease in sodium or calcium channel currents or an increase in Ito, IKATP, IKACh, or other outward currents can give rise to J-wave syndromes, including Brugada syndrome, ER syndrome and hypothermia- and ST-segment elevation myocardial infarction-induced VF [14]. The particular phenotype that manifests depends on which part of the heart is principally affected and which ion channels are involved [14]. However, a recent clinical study reported that patients with idiopathic VF and J waves had a high incidence of ventricular late potentials showing circadian variation with night ascendancy, and the authors speculated that J waves may be closely associated with depolarization abnormality and autonomic modulation, rather than a repolarization abnormality [15]. Furthermore, Watanabe et al. reported that a reduced heart rate, longer PR and QRS durations, and loss-of-function mutations in SCN5A were found in patients with idiopathic VF and ER; they hypothesized that decreased a sodium current enhances VF susceptibility [16]. In the present study, QRS duration and the prevalence of late potentials did not differ between Brugada syndrome patients with or without ER. Thus, further large-scale clinical and genetic studies are needed to elucidate the pathogenesis of the J wave and to assess the prognostic significance of the coexistence of J waves in the inferolateral leads of patients with Brugada syndrome.
    Conclusions
    Conflict of interest
    Background Implantable cardioverter-defibrillator (ICD) therapy is the most effective therapy for reducing mortality in patients with a high risk of life-threatening ventricular tachyarrhythmias [1–10]. However, ICDs cannot prevent the occurrence of tachycardia attacks, and this limits the clinical usefulness of ICDs. Several recent clinical trials have shown that patients who received shocks from ICDs for any arrhythmia have a substantially higher risk of death than similar patients who do not receive such shocks [11,12]. Moreover, frequent, repeated shocks from an ICD due to electrical storms (E-storms) have been recognized as an important clinical factor causing deterioration of patient outcomes and quality of life (QOL), but detailed clinical aspects of E-storms after ICD implantation have not yet been investigated.