Role of signal-averaged electrocardiograms in arrhythmic risk stratification of patients with Brugada syndrome: A prospective study

Huang, Zhengrong; Patel, Chinmay; Li, Weihua; Xie, Qiang; Wan, Rong; Zhang, Lijuan; Tang, Rong; Wan, Xiaoquen; Ma, Yuanfang; Zhen, Wuyang; Gao, Lei; Yan, Gan‐Xin

doi:10.1016/j.hrthm.2009.05.007

Cited by 86 publications

(70 citation statements)

References 34 publications

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“…Noninvasive markers of arrhythmic risk have been assessed in risk stratification, focused on the presence of late potentials on a signal-averaged ECG, which increases the risk of arrhythmic episodes. 24 In 2012, Priori et al 25 published the PRELUDE (programmed electrical stimulation predictive value) registry, a prospective registry designed to assess the predictive accuracy of sustained VT or VF inducibility and to identify additional predictors of arrhythmic events in BrS patients without history of VT/VF. 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.…”

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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“…The filtered QRS duration (fQRS), the root mean square voltage of the terminal 40 msec in the filtered QRS complex (RMS40), and the duration of lowamplitude signals (< 40 μV) in the terminal filtered QRS complex (LAS40) were measured using the SA-ECG system in both groups. Late potentials were considered as positive when two criteria were met (RMS40 < 20 μV and LAS40 > 38 msec) (Tatsumi et al 2006;Huang et al 2009). …”

Section: Signal-averaged Ecgmentioning

confidence: 99%

“…On the other hand, the mechanisms of developing late potentials in Brugada syndrome are considered as being based on both repolarization and depolarization abnormality theory (Antzelevitch 2002;Huang et al 2009). In general, it is known that action potential duration in endocardial cells is longer than that in epicardial cells and that epicardial cells show a notch on the first phase of action potential, which was not observed in endocardial cells (Antzelevitch 2006).…”

Section: Late Potentials By Sa-ecgmentioning

confidence: 99%

“…Depolarization abnormalities noted in these studies may contribute to the development of late potentials in patients with Brugada syndrome. It was previously reported that late potentials detected by SA-ECG play some roles in risk stratification for patients with type 1 ECG, in whom especially measurement of RMS40 in late potentials is useful to predict their arrhythmic events (Kuchar et al 1987;Ikeda et al 2000;Ajiro et al 2005;Huang et al 2009). However, the risk stratification strategy for patients with type 2 ECG remains to be established (Ikeda et al 2001;Ajiro et al 2005;Huang et al 2009).…”

Section: Late Potentials By Sa-ecgmentioning

confidence: 99%

“…Late potentials are also frequently seen in patients with Brugada syndrome, especially among those with type 1 ECG, and they also could be associated with their arrhythmic risk stratification (Huang et al 2009). However, their roles in patients with type 2 ECG remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Prognostic Significance of Late Potentials in Outpatients with Type 2 Brugada Electrocardiogram

Fukuda

Kondo

Segawa

et al. 2016

Tohoku J. Exp. Med.

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Brugada syndrome is characterized by distinguishing electrocardiogram (ECG) patterns (coved and saddleback types with day-to-day variation) and occurrence of lethal tachy-arrhythmias. The appearance of coved type ECG (type 1) is required for the diagnosis of Brugada syndrome, whereas the significance of saddleback type ECG (type 2), which is inadequate for the diagnosis, has not been fully established. We enrolled 34 consecutive patients with type 2 ECG on outpatient-clinic. Among them, 7 patients were ventricular fibrillation (VF) survivors who were diagnosed as Brugada syndrome with transient appearance of type 1 ECG, and showed type 2 ECG on their first outpatient-clinic visit after the VF event (VF group). The remaining 27 were asymptomatic and never showed type 1 ECG on repeated ECG examinations (control group). The VF group showed significantly longer RJ intervals in leads V1 and V2 and QTc intervals in lead V2 compared with the control group (P < 0.030, P < 0.017, and P < 0.030, respectively). Late potentials, detected on the signal-averaged ECG (SA-ECG), reflect conduction abnormalities and are known as one of the risk markers of arrhythmic events. Among the 34 patients, late potentials were negative in 12 patients belonging to the control group. In conclusion, the SA-ECG could be helpful to identify high-risk patients for its high negative predictive value as the first step, and ECG parameters, including RJ intervals in leads V1 and V2 and QTc interval in lead V2, could be useful for further risk stratification in patients with type 2 Brugada ECG.

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Inherited Heart Diseases

2017

Clinical Arrhythmology

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Role of signal-averaged electrocardiograms in arrhythmic risk stratification of patients with Brugada syndrome: A prospective study

Cited by 86 publications

References 34 publications

Brugada syndrome: clinical and genetic findings

Brugada syndrome: clinical and genetic findings

Prognostic Significance of Late Potentials in Outpatients with Type 2 Brugada Electrocardiogram

Inherited Heart Diseases

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