Prolonged QRS Duration in Lead V2 and Risk of Life-Threatening Ventricular Arrhythmia in Patients With Brugada Syndrome

Abstract

SummaryBrugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome. (Int Heart J 2011; 52: 98-102) Key words: Brugada syndrome, Sudden death, Ventricular fibrillation, QRS width B rugada syndrome, which was introduced as a clinical entity in 1992, is a genetic disorder that increases the risk of sudden death secondary to ventricular tachycardia/fibrillation (VT/VF) in patients with structurally normal hearts.1,2) The syndrome is estimated to be responsible for 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts.3) Inheritance of Brugada syndrome occurs via an autosomal dominant mode of transmission with variable penetrance involving several genes. SC-N5A, which codes subunit I Na of sodium channel α, is mutated in 20%-30% of Brugada syndrome patients. 4,5) Mutations in the GPD1L gene 6) and the CACNA1 and CACNB2 genes 7) have also been identified, but these gene variations are infrequent. The typical ST segment elevation in the precordial leads that characterizes Brugada syndrome electrocardiographically can be transitory, vary over time, or be modified by various factors such as vagal tonus, body temperature, and medications. 8,9) This elevation can have a saddleback appearance with a J wave amplitude of ≥ 2 mm and an elevation in the terminal portion of the ST segment of ≥ 1 mm, and then either a positive or biphasic T wave (type 2 electrocardiogram [ECG]) or can be characterized by either a saddleback or coved appearance with an ST segment elevation of < 1 mm (type 3 ECG).10)The vulnerability of individuals with the "Brugada sign" to sudden cardiac death or a life...

Supraventricular tachyarrhythmia in patients with Brugada syndrome: A single‐center study

“…Among our study patients without supraventricular tachyarrhythmia, the prevalence of a spontaneous type 1 Brugada ECG and symptoms were higher and QRS duration was longer than in those with supraventricular tachyarrhythmia. Previous studies have revealed a spontaneous type 1 Brugada ECG and prolonged QRS duration in symptomatic Brugada syndrome patients [24,25]. In addition, the PR and AH intervals were longer in our study patients without supraventricular tachyarrhythmia than in those with supraventricular tachyarrhythmia; however, the differences did not reach statistical significance.…”

SCN5A Genetic Polymorphisms Associated With Increased Defibrillator Shocks in Brugada Syndrome

“…Ohkubo et al also reported prolonged QRS duration of more than 120 ms, as measured on a standard ECG, that is associated with life-threatening ventricular arrhythmia in BrS. 9 These findings occur because of abnormal slow and fragmented epicardial electrograms from reduction in gap junction expression at right ventricular outflow tract evidenced by autopsies. 11 These abnormal electrograms caused by cardiac conduction delay may lead to generate reentry of ventricular arrhythmia, as shown in this study, by appropriate ICD therapy in BrS patients (Table 1).…”

“…The SCN5A mutations may be associated with early and frequent VF recurrence or SCA in BrS patients, which may be related to fibrosis in the right ventricular outflow tract epicardial surface 10, 11. Most studies on SCN5A mutations included both asymptomatic and symptomatic BrS patients 8, 9, 10, 11. This study was aimed to investigate the association of SCN5A mutations and appropriate ICD shock therapy in only symptomatic BrS patients.…”

“…7,8 These SCN5A polymorphisms could decrease expression of sodium-channel proteins and alter gating properties resulting in prolongation of the QRS duration and slow conduction in the heart. 7,9 The SCN5A mutations may be associated with early and frequent VF recurrence or SCA in BrS patients, which may be related to fibrosis in the right ventricular outflow tract epicardial surface. 10,11 Most studies on SCN5A mutations included both asymptomatic and symptomatic BrS patients.…”

Prognosis, risk stratification, and management of asymptomatic individuals with Brugada syndrome: A systematic review

“…More recently, Ohkubo et al. have demonstrated that a QRS prolongation in lead V 2 of more than 120 ms predicts ventricular arrhythmia and/or syncope in BrS patients . We have previously demonstrated that specific ECG markers that reflect ventricular conduction delay in arrhythmogenic right ventricular cardiomyopathy/dysplasia are commonly observed in subjects with spontaneous or drug‐induced type 1 ECG pattern of BrS .…”