Risk Stratification in Patients With Brugada Syndrome Without Previous Cardiac Arrest

Okamura, Hideo; Kamakura, Tsukasa; Morita, Hiroshi; Tokioka, Koji; Nakajima, Ikutaro; Wada, Mitsuru; Ishibashi, Keiichiro; Miyamoto, Koji; Noda, Takashi; Aiba, Takeshi; Nishii, Nobuhiro; Nagase, Satoshi; Shimizu, Wataru; Yasuda, Satoshi; Ogawa, Hisao; Kamakura, Shiro; Ito, Hiroshi; Ohe, Tohru; Kusano, Kengo

doi:10.1253/circj.cj-14-1059

Cited by 62 publications

(29 citation statements)

References 23 publications

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“…The authors concluded that VT/VF inducibility is not sufficient to identify high-risk patients, whereas the presence of a spontaneous type I ECG, history of syncope, ventricular effective refractory period less than 200 ms, and QRS fragmentation are useful for identification of candidates for a prophylactic ICD. Recently, Okamura et al 26 published a retrospective study regarding BrS patients. The authors concluded that syncope, spontaneous type I Brugada ECG, and positive programmed electrical stimulation are important risk factors for SCD and VF in patients with BrS but without previous cardiac arrest.…”

Section: Risk Stratificationmentioning

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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Section: Risk Stratificationmentioning

confidence: 99%

Brugada syndrome: clinical and genetic findings

Sarquella-Brugada

Campuzano

Arbelo

et al. 2016

Genetics in Medicine

125

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“…8, 33 Putatively, the diurnal change of T-wave morphology in patients with hypertrophic cardiomyopathy 34 might explain the inappropriate shock due to T-wave oversensing, which cannot be detected on screening ECG alone. Patients with Brugada syndrome at high risk of VF should also be considered for S-ICD implantation (give their young age), 35 but the clinician should be aware that a positive ST-T segment change in precordial leads during class I blockade has been reported to indicate failure for S-ICD on screening ECG. 36 Careful when infections occur in patients with S-ICD, they have not resulted in sepsis (a particularly threatening condition in congenital patients with conduits and/or prosthetic valves), because the entire system is extravascular.…”

Section: Inverted T Wave In Precordial Lead As Predictor Of Screeningmentioning

confidence: 99%

Right Parasternal Lead Placement Increases Eligibility for Subcutaneous Implantable Cardioverter Defibrillator Therapy in Adults With Congenital Heart Disease

Okamura

McLeod

DeSimone

et al. 2016

Circ J

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Background:The subcutaneous implantable cardioverter defibrillator (S-ICD) provides an attractive option for patients with congenital heart disease (CHD) in whom a transvenous defibrillator is contraindicated. Given the unusual cardiac anatomy and repolarization strain, the surface electrocardiogram (ECG) is frequently abnormal, potentially increasing the screen failure rate. Methods and Results:We prospectively screened 100 adult CHD patients regardless of the presence of clinical indication for ICD utilizing a standard left sternal lead placement, as well as a right parasternal position. Baseline patient and 12-lead ECG characteristics were examined to assess for predictors of screen failure. Average patient age was 48±14 years, average QRS duration was 134±37 ms, and 13 patients were pacemaker dependent. Using the standard left parasternal electrode position, 21 patients failed screening. Of these 21 patients with screen failure, 9 passed screening with the use of right parasternal electrode positioning, reducing screening failure rate from 21% to 12%. QT interval and inverted T wave anywhere in V2-V6 leads were found to be independent predictors of left parasternal screening failure (P=0.01 and P=0.04, respectively). Conclusions:Utilization of both left and right parasternal screening should be used in evaluation of CHD patients for S-ICD eligibility. ECG repolarization characteristics were also identified as novel predictors of screening failure in this group. (Circ J 2016; 80: 1328 -1335

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“…We excluded cases with syncope that was likely due to vasovagal events, such as those that occurred during abrupt postural changes, exposure to heat and dehydration, or emotional reactions. 10) A family history of syncope was defined as an episode of sudden death that was judged as likely being caused by ventricular arrhythmia.…”

Section: Methodsmentioning

confidence: 99%

Low Serum Levels of Eicosapentaenoic Acid and Docosahexaenoic Acid are Risk Factors for Cardiogenic Syncope in Patients with Brugada Syndrome

et al. 2017

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SummaryThe n-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have antiarrhythmic effects, possibly via modulation of the cardiac ion channels. Nevertheless, it is unknown whether low serum levels of n-3 PUFAs are risk factors for ventricular fibrillation in patients with Brugada syndrome (BrS). We retrospectively reviewed data from 62 men with BrS and evaluated their serum levels of EPA and DHA, and the risk factors for sudden cardiac death, including a history of cardiogenic syncope. Nineteen patients had a history of cardiogenic syncope, and their EPA and DHA levels were significantly lower than those of the patients without syncope. Multivariate logistic regression analysis revealed that low EPA and DHA levels were associated with the incidence of syncope. The receiver-operator characteristic curve showed the area under the curves of EPA and DHA for history of syncope were 0.84 and 0.72, respectively. In conclusion, low levels of EPA and DHA are risk factors for cardiogenic syncope in patients with BrS, which suggests that n-3 PUFAs play important roles in preventing ventricular fibrillation in BrS.(Int Heart J 2017; 58: 720-723)

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Risk Stratification in Patients With Brugada Syndrome Without Previous Cardiac Arrest

Abstract: 310OKAMURA H et al.

Cited by 62 publications

References 23 publications

Brugada syndrome: clinical and genetic findings

Brugada syndrome: clinical and genetic findings

Right Parasternal Lead Placement Increases Eligibility for Subcutaneous Implantable Cardioverter Defibrillator Therapy in Adults With Congenital Heart Disease

Low Serum Levels of Eicosapentaenoic Acid and Docosahexaenoic Acid are Risk Factors for Cardiogenic Syncope in Patients with Brugada Syndrome

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