Efficacy of Quinidine in Brugada Syndrome: A Literature Review

Brugada syndrome (BrS) is an inherited arrhythmogenic disorder associated with an increased risk of ventricular fibrillation (VF) and sudden cardiac death. Quinidine and hydroquinidine are currently used to prevent ventricular arrhythmias in BrS. This review summarizes the available evidence on the efficacy, safety, and clinical applications of these drugs in BrS. Ten studies involving more than 300 patients with BrS were analyzed. Quinidine or hydroquinidine therapy prevented VF inducibility in 42.9–90% of cases and reduced recurrent arrhythmic events by approximately 60–70%. Among patients with implantable cardioverter-defibrillators (ICDs), reductions in both appropriate and inappropriate shock counts were observed. Gastrointestinal intolerance was the most common side effect, occurring in 20–30% of patients, with drug discontinuation in up to 26%. QT prolongation was infrequent, and serious proarrhythmic events were rare. Despite these benefits, quinidine remains unavailable or difficult to access in many regions, limiting its widespread clinical use. In conclusion, quinidine and hydroquinidine exert antiarrhythmic effects in BrS and reduce the recurrence of ventricular arrhythmias, particularly among ICD-treated or high-risk patients. Although therapy is constrained by gastrointestinal intolerance and limited availability, low-dose regimens may be better tolerated while maintaining efficacy. These agents can be considered, in selected patients, as adjuncts or alternatives to device therapy; meanwhile, further multicenter studies are warranted to confirm long-term safety, determine optimal dosing, and improve global accessibility.