Quinidine in Brugada Syndrome: Still a Long Way to Go….

Abstract

Since Brugada syndrome was identified in 1992, its therapeutic management of patients has presented a great challenge for clinicians.1 Article see p 1393 In this issue of Circulation Arrhythmia and Electrophysiology , Belhassen et al2 suggest both risk stratification of arrhythmia and therapeutic improvements using electrophysiological study (EPS) and quinidine. Although gradual progress in risk stratification at the population level has been reached through the creation of large databases,3–5 we must admit that >30 years after its first description, arrhythmic risk assessment and, therefore, the best treatment choice in a patient affected by Brugada syndrome still remain a real challenge for clinicians. There are many factors that come into play in the treatment of Brugada syndrome. First, clinical diagnosis of Brugada syndrome is sometimes difficult and usually overestimated because it is based on the ECG aspect.6 After diagnosis, the main feature is the risk of ventricular fibrillation. However, events can be distant from each other—sometimes >20 years between 2 arrhythmic events.6 Moreover, although a trigger can be found in most arrhythmic diseases, it is rare in Brugada syndrome patients, making the prediction of such an event uncertain.6 In fact, the main challenge in evaluating patients affected with Brugada syndrome is the relatively low incidence of events. For instance, in the FINGER registry, patients who experienced cardiac arrest had a 7.7% event rate per year, patients with syncope had 1.9%, and asymptomatic patients had 0.5%.3 This risk seems to be cumulative over time and reaches a 12% risk at 10 years in asymptomatic patients with a spontaneous aspect …