Risk Stratification in Brugada Syndrome

Priori, Silvia G.; Gasparini, Maurizio; Napolitano, Carlo; Bella, Paolo Della; Ottonelli, Andrea Ghidini; Sassone, Biagio; Giordano, Umberto; Pappone, Carlo; Mascioli, Giosuè; Rossetti, Guido; Nardis, Roberto De; Colombo, Mario P.

doi:10.1016/j.jacc.2011.08.064

Cited by 526 publications

(238 citation statements)

References 31 publications

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“…Recent evidence, however, has clearly demonstrated that family history has not been a reliable marker for high risk in patients affected by BrS 2. Moreover, the value of a family history of sudden death in BrS patients has been extensively investigated, and results in that family history of SCA are not predictive for future arrhythmic events 25, 26. Consistent with these studies, present results have also shown that family history of SCA was not associated with recurrent ICD shocks in Thai symptomatic BrS.…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

Makarawate

Chaosuwannakit

Vannaprasaht

et al. 2017

JAHA

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“…In particular, a male patient with Brugada syndrome and CAS alone developed sudden death because of recurrent VF without a cautionary chest pain or preceding ischemic ECG changes, although he was treated with antianginal agents, including CCBs ( Figure 5). Because the role of electrophysiological testing for predicting OHCA remains controversial in Brugada syndrome, 19 dual induction tests might be less reliable in patients with the disorder.…”

Section: Long-term Prognosis According To the Presence Or Absence Of mentioning

confidence: 99%

Usefulness of Testing for Coronary Artery Spasm and Programmed Ventricular Stimulation in Survivors of Out-of-Hospital Cardiac Arrest

Komatsu

Takahashi

Fukuda

et al. 2016

Circ: Arrhythmia and Electrophysiology

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Background-Optimal therapy for patients resuscitated from out-of-hospital cardiac arrest (OHCA) who are not found to have structural heart disease remains to be established, especially regarding the use of implantable cardioverterdefibrillators. Coronary artery spasm (CAS) and lethal ventricular arrhythmias are important causes of OHCA. Methods and Results-In 47 consecutive OHCA survivors without structural heart disease who had fully recovered (M/F 44/3, 43±13 years.), we performed dual induction tests, including acetylcholine provocation test first followed by programmed ventricular stimulation after 1 to 2 weeks. Patients with CAS were treated with calcium channel blockerbased antianginal medications; implantable cardioverter-defibrillators were implanted in all patients. The results of the dual induction tests defined 4 groups: CAS alone (n=7), inducible ventricular arrhythmias alone (n=13), both positive (n=24), and both negative (n=3). During a median follow-up period of 38 months, ventricular fibrillation recurred in all groups except the both-negative group. Of the 16 patients with a type I Brugada ECG, 2 had CAS alone, 8 had ventricular arrhythmias alone, and 6 had both positive. No ventricular fibrillation episodes were observed in the CAS-alone patients who did not also have Brugada syndrome. Kaplan-Meier analysis showed that the CAS-alone group was at lower risk for OHCA recurrence as compared with the Brugada syndrome group (log-rank test; P=0.036). Conclusions-Among OHCA survivors without structural heart disease, provokable CAS and ventricular arrhythmias are common and can be seen in Brugada syndrome. CAS alone without Brugada syndrome who are treated for CAS may be a lower-risk group. (Circ Arrhythm Electrophysiol. 2016;9:e003798.

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“…42 Although large studies agree that electrophysiological study inducibility is greatest among BrS patients, there has been no consensus on the value of the EP study in predicting outcome. 6,43,44 Several consensus documents have addressed this issue and the current recommendation is to implant an ICD in inducible patients (Class IIb indication). …”

Section: -40mentioning

confidence: 99%

Brugada Syndrome and Early Repolarisation: Distinct Clinical Entities or Different Phenotypes of the Same Genetic Disease?

Conte

Caputo

Regoli

et al. 2016

Arrhythmia &Amp; Electrophysiology Review

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General understanding of early repolarisation (ER) has dramatically changed in the last decade. For several years, ER has been considered a benign electrocardiographic (ECG) finding with high prevalence in the general population. Recently different studies have challenged this view and showed a significant association with life-threatening arrhythmias. [1][2][3][4][5] In 2008 Haïssaguerre et al. first reported an increased prevalence of a particular pattern of ER on the resting 12-lead ECG of patients with history of idiopathic ventricular fibrillation (VF) (see Figure 1). 2 In these patients, ER was characterised by elevation of the QRS-ST segment junction of at least 0.1 mV above the baseline level, manifesting as QRS slurring (a smooth transition from the QRS complex to the ST segment) or notching (a positive J deflection of at least 1 mm inscribed on the S wave) in two adjacent inferior (II, III and aVF), lateral (I, aVL, and V4-V6), or infero-lateral leads. The ER pattern was observed in 31 % of patients with idiopathic VF and in 5 % of healthy control subjects.Moreover, patients with idiopathic VF and ER pattern presented a higher risk of experiencing an arrhythmic recurrence during a 5-year follow-up.2 This observation was confirmed by a case-control study showing that J-point elevation in the inferior and lateral leads is more frequent in patients with idiopathic VF than in matched control subjects (27 % versus 8 % in inferior leads; 13 % versus 1 % in lateral leads).3 Conversely, ER localised exclusively in V4 to V6 occurs with similar frequency among patients and healthy subjects.

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Risk Stratification in Brugada Syndrome

Cited by 526 publications

References 31 publications

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

Usefulness of Testing for Coronary Artery Spasm and Programmed Ventricular Stimulation in Survivors of Out-of-Hospital Cardiac Arrest

Brugada Syndrome and Early Repolarisation: Distinct Clinical Entities or Different Phenotypes of the Same Genetic Disease?

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