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

Abstract

Brugada syndrome (BrS) is a primary electrical disease associated with increased risk of sudden cardiac death due to polymorphic ventricular arrhythmias. The prognosis, risk stratification, and management of asymptomatic individuals remain the most controversial issues in BrS. Furthermore, the decision to manage asymptomatic patients with an implantable cardioverter‐defibrillator should be made after weighing the potential individual risk of future arrhythmic events against the risk of complications associated with the implant and follow‐up of patients living with such devices, and the accompanying impairment of the quality of life. Several clinical, electrocardiographic, and electrophysiological markers have been proposed for risk stratification of subjects with BrS phenotype, but the majority have not yet been tested in a prospective manner in asymptomatic individuals. Recent data suggest that current risk factors are insufficient and cannot accurately predict sudden cardiac death events in this setting. This systematic review aims to discuss contemporary data regarding prognosis, risk stratification, and management of asymptomatic individuals with diagnosis of Brugada electrocardiogram pattern and to delineate the therapeutic approach in such cases.

Tpeak‐Tend, Tpeak‐Tend/QT ratio and Tpeak‐Tend dispersion for risk stratification in Brugada Syndrome: A systematic review and meta‐analysis

“…In the Mugnai study, the largest study to date, the percentage of patients with adverse events were the lowest at 13% . Male gender, a spontaneous Type 1 Brugada pattern and SCN5a mutation positive status were significantly associated with ventricular arrhythmias . Therefore, the lower percentage of patients with adverse events can be explained by the lower percentage of Type 1 Brugada patients (21% vs 28%‐100% in the remaining studies) and lower percentage male patients (61% vs 72%‐100%) despite similar percentage with SCN5a positive status (22% vs 13%‐50%).…”

“…This would suggest as a single measurement, T peak ‐T end is unlikely to be useful in its own right. Indeed, accurate risk stratification will require a composite scoring system assessing not only dispersion of repolarization, but that of conduction, clinical symptoms, family history, the type of Brugada pattern, genetic background, electrical and drug provocation testing as well as electrophysiological mapping …”

Should all individuals with suspected arrhythmias but initially nondiagnostic electrocardiogram be ordered routinely higher intercostal space ECG?

“…Therefore, the transient normalization of the ECG does not make the diagnosis with standard 12‐lead ECG possible in many cases. Moreover, beyond the Brugada phenocopies, sometimes it is difficult to diagnosis BrS with standard 12‐lead ECG when the leads V1 and V2 are placed in the standard position of the right and left fourth intercostal spaces in a patient with suspected cardiac arrhythmias in daily practice …”

The dividing line of arrhythmogenic right ventricular cardiomyopathy and Brugada syndrome at epicardial ablation era: Limited to or beyond RVOT?

“…Although Brugada syndrome (BrS) has been described 30 years ago, it remains one of the most debated among channelopathies with several open questions on its genetic substrate, arrhythmia mechanisms (depolarization versus repolarization, trigger vs substrate), and clinical management (the role of electrophysiological testing and implantable cardiac defibrillator in asymptomatic patients) . Despite that it was initially described as a purely electric condition in structurally normal hearts, today it is now recognized that structural changes, especially at the right ventricular outflow tract (RVOT), are present in some patients .…”

“…Therefore, the presence of isolated subepicardial RVOT scar shares a broad differential diagnosis including BrS, cardiac sarcoidosis, exercise‐induced arrhythmogenic remodeling of athletes, ARVC/D, and post inflammatory cardiomyopathy . Although there is no clear dividing line between BrS and ARVC/D, it is believed that both are different clinical entities with respect to the clinical presentation and the genetic predisposition . Whereas the continuous administration of low‐dose isoproterenol may be effective for the suppression of repetitive ventricular arrhythmia occurrence in patients with BrS, the isoproterenol appears to have potential added diagnostic value in the setting of patients with suspected ARVC …”