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    • br Signal averaged ECG Frequency of

    2019-04-29


    Signal-averaged ECG Frequency of late potentials (LP) in the signal-averaged ECG has been reported to be higher in patients with Brugada syndrome than in control subjects. In a single-center study, Ikeda et al. reported a sensitivity of 89%, specificity of 50%, positive predictive value of 70%, and negative predictive value of 77% for LP for risk stratification of life-threatening events [36].
    Fragmented QRS Morita and colleagues reported that fragmented QRS recorded in the standard 12-lead ECGs (with 0- to 150-Hz filters) was more often observed in Brugada patients with VF episodes than in those with syncope or in asymptomatic patients [37]. They also reported that patients who had fragmented QRS frequently experienced recurrence of syncope due to VF within 4 years of the first episode of syncope or VF. More recently, in the PRELUDE study, Priori et al. reported that fragmented QRS was an independent predictor for arrhythmic events in Brugada patients without a history of VF [38].
    Programmed electrical stimulation The usefulness of programmed electrical stimulation (PES) to stratify risk of subsequent arrhythmic events has long been controversial between the Brugada registry and other registries [5,7,10,11,32,33]. To fill this gap, Priori organized a multicenter prospective registry (PRELUDE study) with a uniform protocol in patients with Brugada syndrome without a history of VF [38]. They suggested that arrhythmia inducibility during PES was not a predictor of subsequent events during follow-up but that a ventricular effective refractory order nebivolol hcl <200ms was an independent predictor for arrhythmic events. Makimoto et al. recently reported a significance of the number of extrastimuli at PES as a predictor of arrhythmic events in patients with type-1 Brugada ECG [41]. Multivariate Cox regression demonstrated that the induction of VF with up to double extrastimuli was an independent predictor. Therefore, they suggested that up to double extrastimuli were adequate at PES to stratify risk in patients with Brugada syndrome.
    Cardiac imaging
    Head-up tilt testing Head-up tilt (HUT) testing is recommended to judge an episode of syncope to be likely caused by VF by excluding neurally mediated syncope (NMS). However, NMS may coexist with Brugada syndrome [42]. We conducted HUT testing in 46 patients with type-1 Brugada ECG, 20 healthy control subjects, and 15 patients with suspected NMS [43]. HUT testing was positive in 35% of Brugada patients (16/46), 10% of control subjects (2/20), and 67% of suspected NMS patients (10/15). The HUT-positive rate was significantly higher in Brugada patients with VF (7/14; 50%) than that in control subjects (10%) (P<0.05). Augmentation of ST-segment amplitude (≥0.05mV) in leads V1 through V3 was observed in 69% of the HUT-positive Brugada patients (11/16) during vasovagal responses and was associated with augmentation of parasympathetic tone following sympathetic withdrawal, which was evaluated by the heart rate variability. These data suggested that some Brugada patients have an impaired balance of the autonomic nervous system, which may relate to their syncopal episodes.
    Conflict of interest
    Acknowledgments Dr. Shimizu was supported in part by the Research Grant for the Cardiovascular Diseases (H24-033) from the Ministry of Health, Labour and Welfare, Japan.
    Introduction Brugada syndrome (hereafter referred to as BrS) is characterized by a peculiar ST segment (J point) elevation in the right precordial leads of the electrocardiogram (ECG) as well as idiopathic ventricular fibrillation, occurring particularly during sleep, which often results in nocturnal sudden death. There is a definite male predominance in BrS-related morbidity, and men are ∼10-times more affected than women. Approximately 20% of the phenotype-positive probands have a family history of syncope or sudden death. These clinical features are partially similar to those previously described as “Pokkuri” disease in Japan [1,2] and “Lai Tai” in Thailand [3]. Indeed, its prevalence is higher in Japan and Southeastern Asia, which may be partially related to an Asian-specific sequence in the promoter region of SCN5A[4]. The disease was named after the report in 1992 by the Brugada brothers [5], but several case reports on similar ECG findings and clinical phenotypes from Italy and Japan were published previously [1,2,6]. Some of these reports described an associated structural abnormality, especially in the right-side of the heart, suggesting the coexistence of subclinical arrhythmogenic right ventricular cardiomyopathy [7]. Patients with BrS have been shown to carry SCN5A mutations, which raises the possibility that the specific structural change is caused by SCN5A mutations [8,9]. The inheritance pattern of BrS shows an autosomal dominant mode of transmission. Candidate gene analysis showed that mutations in SCN5A were responsible for the phenotype of BrS in 3 families, and over 300 SCN5A mutations have been reported to date [10].