Risk Stratification of Individuals with the Brugada Electrocardiogram: A Meta‐Analysis

Gehi, Anil K.; Duong, Truong D.; Metz, Louise D.; Gomes, J. Anthony; Mehta, Davendra

doi:10.1111/j.1540-8167.2006.00455.x

Cited by 296 publications

(249 citation statements)

References 75 publications

(91 reference statements)

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“…The PR prolongation could differentiate between SCN5A and non ‐SCN5A BrS patients 19, 20. The study herein also showed longer PR intervals in BrS patients with either R1193Q or H558R SCN5A polymorphisms (Tables 2, 3 through 4).…”

Section: Discussionsupporting

confidence: 57%

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

Makarawate

Chaosuwannakit

Vannaprasaht

et al. 2017

JAHA

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BackgroundBrugada syndrome (BrS) is an inherited primary arrhythmia disorder leading to sudden cardiac arrest. SCN5A, encoding the α‐subunit of the cardiac sodium channel (Nav1.5), is the most common pathogenic gene of BrS. An implantable cardioverter defibrillator (ICD) is the standard treatment for secondary prevention. This study aimed to evaluate association of the SCN5A variant with this cardiac conduction disturbance and appropriate ICD shock therapy in Thai symptomatic BrS patients with ICD implants.Methods and ResultsSymptomatic BrS patients diagnosed at university hospital were enrolled from 2008 to 2011. The primary outcome of the study was an appropriate ICD shock defined as having non‐pacing‐associated ICD shock after the occurrence of ventricular tachycardia or ventricular fibrillation. Associations between SCN5A polymorphisms, cardiac conduction disturbance, and potential confounding factors associated with appropriate ICD shock therapy were analyzed. All 40 symptomatic BrS patients (median age, 43 years) with ICD implantations were followed for 24 months. There were 16 patients (40%) who had the appropriate ICD shock therapy after ICD treatment. An independent factor associated with appropriate ICD shock therapy was SCN5A‐R1193Q with an adjusted hazard ratio of 10.550 (95% CI, 1.631–68.232).Conclusions SCN5A‐R1193Q is associated with cardiac conduction disturbances. It may be a genetic marker associated with ventricular arrhythmia leading to appropriate ICD shock therapy in symptomatic BrS patients with ICD treatment. Because of the small sample size of study population and the appropriate ICD shock outcome, further large studies are needed to confirm the results of this study.

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Section: Discussionsupporting

confidence: 57%

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

Makarawate

Chaosuwannakit

Vannaprasaht

et al. 2017

JAHA

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“…Recent meta-analysis, which included, in most of the studies, all BrS ECG patterns, revealed that worldwide BrS ECG patterns prevalence is 0.4% and it is 9 times higher in men than in women (0.9% vs. 0.1%) [13]. This result is consistent with other reports which indicate that the BrS occurrence may be even eight times higher in men than in women [6,14]. The trends in incidence of spontaneous type 1 BrS ECG pattern are changing.…”

Section: Epidemiologysupporting

confidence: 86%

Brugada syndrome: current diagnostics, epidemiology, genetic data and novel mechanisms (RCD code: V-1A.1)

Matusik

Pudło

Rydlewska

et al. 2017

Journal of Rare Cardiovascular Diseases

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Brugada syndrome (BrS) is a cardiac channelopathy associated with ventricular arrhythmias and sudden cardiac death. Diagnosis of BrS is based on type 1 BrS electrocardiogram (ECG) pattern (coved pattern) presence, observed spontaneously or after provocation test. The worldwide prevalence of BrS ECG patterns is estimated to reach 0.4% and strongly depends on the population studied. BrS results from various genetic mutations of sodium, calcium and potassium channels and/or associated proteins affecting ion currents. SCN5A mutations are the most prevalent in BrS. Pathogenesis of BrS is explained by the depolarization theory, the repolarization theory and the neural crest theory, which seem to be complimentary, at least partially. This review summarizes current diagnostic criteria of BrS and epidemiology of BrS ECG patterns. We also discuss the recent understanding of BrS pathophysiology and the role of genetic testing in BrS. JRCD 2017; 3 (3): 73-80

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“…Zespół Brugadów jest dziedziczony jako cecha dominująca i charakteryzuje się penetracją zależną od wieku i płci. Objawy kliniczne choroby są częstsze u osób dorosłych, a u mężczyzn występują 8-krotnie częściej niż u kobiet [450]. Częstoskurcz komorowy występuje w średnim wieku 41 ± 15 lat, ale może się ujawnić w dowolnym wieku, zwykle w spoczynku lub podczas snu [451].…”

Section: Definicje I Epidemiologiaunclassified

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Priori

Blomström‐Lundqvist²,

Mazzanti³

et al. 2015

Kardiol Pol

233

337

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Risk Stratification of Individuals with the Brugada Electrocardiogram: A Meta‐Analysis

Cited by 296 publications

References 75 publications

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

Brugada syndrome: current diagnostics, epidemiology, genetic data and novel mechanisms (RCD code: V-1A.1)

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

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