Brugada syndrome was first described in 1992 as a novel clinical-electrocardiographic entity associated with ventricular arrhythmias and sudden death in patients without evident structural heart disease. It is classified within the group of channelopathies – conditions resulting from alterations in transmembrane ion channels involved in cellular action potentials, which confer a predisposition to arrhythmia development. Implantation of an implantable cardioverter-defibrillator (ICD) is recommended for symptomatic patients with Brugada syndrome who have survived a cardiac arrest or have documented sustained ventricular arrhythmia. Moreover, in cases of recurrent ICD discharges due to ventricular fibrillation, the use of quinidine or catheter ablation has demonstrated efficacy in reducing the frequency of such discharges. Genetic mutations associated with Brugada syndrome result in dysfunctional myocardial sodium channels, leading to a reduction in sodium inflow currents and consequently shortened action potentials. A prominent Ito current in the right ventricular epicardium further abbreviates the action potentials. Some studies suggest that quinidine may exert its therapeutic effects in Brugada syndrome through inhibition of the Ito current, thereby restoring electrical homogeneity.
This study outlines the experience with quinidine as a therapeutic agent to prevent arrhythmic events following ICD implantation in patients with Brugada syndrome at the Central University Hospital of Asturias. The drug was administered to two patients, both diagnosed with type I Brugada syndrome, induced with a flecainide test. Each patient had an ICD implanted for primary prevention. One patient commenced quinidine therapy thirteen years post-ICD implantation following hospital admission for an arrhythmic storm. In the second case, quinidine treatment began one year after ICD implantation due to the occurrence of multiple arrhythmic episodes. One of the patients died four years later of non-cardiovascular causes; the other patient continues to receive quinidine therapy. The mean duration of treatment with quinidine was 2,071 ± 832 days. During this period, neither patient experienced further arrhythmic events. In conclusion, based on our experience, the use of quinidine in patients with Brugada syndrome and ICD implants appears to be both safe and effective in preventing the recurrence of arrhythmic episodes.
