Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan

Miyasaka, Yoko; Tsuji, Hisako; Yamada, Koichi; Tokunaga, Shigehiko; Saito, Daiki; Iizawa, Yusuke; Matsumoto, Noriko; Iwasaka, Toshiji

doi:10.1016/s0735-1097(01)01419-x

Cited by 227 publications

(146 citation statements)

References 12 publications

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“…In contrast, Priori et al found no episodes of malignant arrhythmias over a period of 3 years in 30 asymptomatic patients with a Brugada sign 9 . A very low rate of arrhythmic events in this patient group has been confirmed by multiple recent and larger-scale studies 7,[10][11][12][13] . In one study of 14,000 individuals in Japan, the mortality rate of 98 subjects with a Brugada sign was not higher than the rest of the cohort 7 .…”

Section: Introductionsupporting

confidence: 69%

“…A very low rate of arrhythmic events in this patient group has been confirmed by multiple recent and larger-scale studies 7,[10][11][12][13] . In one study of 14,000 individuals in Japan, the mortality rate of 98 subjects with a Brugada sign was not higher than the rest of the cohort 7 . Despite the discrepancy in prognosis among different studies, there is evidence that some asymptomatic individuals with a Brugada-type ECG tend to die suddenly during sleep, a clinical observation characteristic of SUNDS, suggesting that SUNDS may underlie at least a part of Brugada-type ECG.…”

Section: Introductionsupporting

confidence: 69%

“…Recent studies have revealed that the prevalence of a Brugada-type ECG is 0.1-0.7% in the general population in Asia and other countries [5][6][7] .…”

Section: Introductionmentioning

confidence: 99%

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Double SCN5A mutation underlying asymptomatic Brugada syndrome

et al. 2005

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Heterologously expressed mutant Na channels exhibited a negative shift of steady-state inactivation (9.2 mV) and enhanced slow inactivation, suggesting that this individual harbors a subclinical channel dysfunction compatible with symptomatic Brugada syndrome. Conclusions:Asymptomatic individuals with a Brugada-type ECG generally have a better Yokoi et al. page 4 prognosis than their symptomatic counterparts, but there may be a subgroup of these individuals with poor prognosis. Severe Na channel dysfunction due to SCN5A mutations may not be sufficient to cause symptoms or arrhythmias in the Brugada syndrome, suggesting some unknown factors or modifier genes influencing the arrhythmogenesis.

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Section: Introductionsupporting

confidence: 69%

Section: Introductionsupporting

confidence: 69%

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Double SCN5A mutation underlying asymptomatic Brugada syndrome

et al. 2005

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“…Although the prevalence of BS is higher in Asian countries, [28][29][30][31][32] the prevalence of Brugada-type ECGs in Japan is only 0.14-1.22%. [29][30][31][32] All patients in the present study were recruited from only 1 institute. Therefore, further prospective studies using a large number of patients are needed to validate the present findings.…”

Section: Study Limitationsmentioning

confidence: 95%

Bradycardia-Dependent ECG Changes in Brugada Syndrome

Mizumaki

Fujiki

Nishida

et al. 2006

Circ J

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rugada syndrome (BS), a distinct subtype of idiopathic ventricular fibrillation (VF), is characterized by a distinctive ST segment elevation in the right precordial leads. [1][2][3] The mechanism responsible for this ST segment elevation and genesis of VF is still under investigation. Several possible mechanisms have been proposed for the ST segment elevation in BS. Among them are conduction delay, accentuation of the action potential notch and loss of the action potential dome in the right ventricular outflow epicardium. 3,4 In BS, unlike other diseases, VF and sudden death mainly occur in the resting state, predominantly during sleep. 5,6 The typical ECG changes are variable over time and are modulated by exercise or pharmacological interventions that interact with autonomic nervous activities. 5,[7][8][9] We recently reported an inadequate prolongation of the QT interval (short QT interval) at longer RR intervals 10 and an augmentation of the ST elevation through vagal activity in patients with BS. 11 The nighttime onset of VF episodes may be related to both a shorter QT interval and an enhanced ST elevation during bradycardia at night. This could be because of a slow recovery from the inactivation of prominent Ito. 12 However, it is still unclear how the RR intervals affect the ECG changes in BS and whether rate dependent changes in the ECG would be different between symptomatic and asymptomatic patients. The present study was therefore designed to examine the effects of the RR intervals on ECG changes during an electrophysiologic study (EPS) in both symptomatic and asymptomatic patients. Methods Study PopulationTwenty-one consecutive male patients with BS were studied: 9 were symptomatic with either documented VF or episodes of unexplained syncope, and the other 12 were asymptomatic without either spontaneous VF or inducible VF during the EPS. The study protocol was approved by the institutional review board and written informed consent was given by all patients before participation. We diagnosed BS in accordance with recently established ECG criteria. 3 Patients with coved-type ST elevation accompanied by Jwave amplitude ≥2 mm in one of the leads V1-3 were included. 3 For patients with saddle-back-type ST elevation (type 2 or 3), coved-type ST elevation ≥2 mm induced by pilsicainide, a class Ic antiarrhythmic drug, was required. 3 In all patients, physical examination, chest X-ray, 2-dimensional-echocardiography, exercise test and thallium or 99m Tc-tetrofosmin myocardial single photon emission computed tomography failed to disclose apparent evidence of organic heart disease. Patients with diabetes mellitus, long QT syndrome or electrolyte abnormality and patients taking any drugs were excluded from the present study. EPS and Analysis of ECGsEPS was performed in all 21 patients after all antiarrhythmic drugs had been discontinued for at least 5 halflives of the drug. A steerable 6F octapolar catheter with Background In patients with Brugada syndrome (BS), ventricular fibrillation (VF) occurs mainly during ...

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“…A type I Brugada ECG pattern is found rarely in the European population, but it appears more commonly in Southeast Asia, with an estimated prevalence of 0.12% in Japan. 9,10 No apparent structural heart disease can be found in BrS, at least macroscopically. Some microscopic myocardial alterations have been reported, suggesting that the channelopathy may induce cardiomyopathic changes in some patients.…”

Section: Clinical Diagnosis Diagnostic Criteriamentioning

confidence: 99%

Brugada syndrome: clinical and genetic findings

Sarquella-Brugada

Campuzano

Arbelo

et al. 2016

Genetics in Medicine

125

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Review ARticleMore than 20 years ago, eight individuals were resuscitated from sudden cardiac death (SCD) caused by documented ventricular fibrillation (VF); all showed a characteristic ST segment elevation in the right precordial leads and a structurally normal heart. 1 In 1996, the term "Brugada syndrome" (BrS) was used to describe what was previously known as "right bundle branch block, persistent ST segment elevation, and sudden death syndrome. " 2 A year later, BrS was reported to be the same disease as sudden unexplained nocturnal death syndrome (SUNDS). In other countries, BrS has different names: Lai Tai (Thailand), Pokkuri (Japan), and Bangungut (Philippines). Currently, the prevalence of BrS is estimated at ~3-5 in 10,000 people, and it is higher in young men of Southeast Asian origin. It is the main cause of death among young healthy men in Southeast Asia. 3 Recent reports suggest that BrS could be responsible for 4% of all SCD and up to 12% of sudden death in patients with structurally normal hearts. The clinical phenotype manifests in adulthood, at a mean age of 41 years, and it is 8-to 10-times more frequent in males. Frequently, sudden death can be the first manifestation of the disease. 4 In 1998, the genetic basis of BrS was established when the sodium channel protein type V subunit α gene (SCN5A), which encodes the α-subunit of the voltage-gated Na v 1.5 cardiac sodium channel responsible for regulating rapid sodium current (I Na ), was associated with the disease. 5 Currently, BrS is recognized as a rare, inherited cardiac channelopathy caused by an alteration of ionic currents that leads to ventricular arrhythmias and SCD. It is clinically characterized by ST segment elevation in leads V1-V3 of the electrocardiogram, but incomplete penetrance and variable expressivity confound the diagnosis. 6 Despite the identification of 18 associated genes, 65-70% of clinically diagnosed cases remain without an identifiable genetic cause. 4 CLINICAL DIAGNOSIS Diagnostic criteriaThe clinical diagnosis of BrS requires the identification of the ST segment elevation in the right precordial leads at baseline or after the use of sodium blockers. Three different electrocardiographic (ECG) patterns can be often observed in families with BrS: type I, which consists of a coved-type ST segment elevation greater than 2 mm followed by a descending negative T wave in at least two right precordial leads (V1 to V3); type II ST elevation, saddleback-shaped patterns with a high initial increase followed by an ST elevation greater than 2 mm; and saddleback-shaped patterns with a high initial increase followed by an ST elevation less than 2 mm (Figure 1). The second Brugada Consensus Report proposed that only type I is diagnostic for BrS 7 and, in 2013, it was proposed that a definitive diagnosis of BrS considers both spontaneous type I pattern and a provoked type I pattern (with a baseline type II or III pattern) in at least one right precordial lead (V1 or V2). 8 The diagnosis of BrS is currently accepted in those patients ...

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Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan

Cited by 227 publications

References 12 publications

Double SCN5A mutation underlying asymptomatic Brugada syndrome

Double SCN5A mutation underlying asymptomatic Brugada syndrome

Bradycardia-Dependent ECG Changes in Brugada Syndrome

Brugada syndrome: clinical and genetic findings

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