The Brugada syndrome: pharmacological therapy
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Published on: July 5, 2021
Carla Giustetto1,2, Natascia Cerrato3, Veronica Dusi1,2
1Division of Cardiology, Cardiovascular and Thoracic Department, "Città della Salute e della Scienza" Hospital, C.so Bramante, 88. 10126, Turin, Italy.
Insights
Quinidine effectively prevents ventricular and supraventricular arrhythmias in Brugada syndrome patients, reducing sudden cardiac death risk. However, side effects often limit its use, despite its proven efficacy in preventing dangerous heart rhythms.
Area of Science:
- Cardiology
- Genetics
- Pharmacology
Background:
- Brugada syndrome is an inherited channelopathy increasing risk of sudden cardiac death (SCD) from ventricular arrhythmias (VA).
- Current guidelines recommend implantable cardioverter-defibrillators (ICDs) for SCD prevention, but they do not prevent VA recurrence.
Purpose of the Study:
- To review the literature on pharmacological therapy for Brugada syndrome, focusing on quinidine.
- To evaluate quinidine's efficacy in preventing ventricular and supraventricular arrhythmias in Brugada syndrome.
Main Methods:
- Review of existing literature on quinidine treatment for Brugada syndrome.
- Analysis of studies involving patients with ICDs, recurrent shocks, or inducible ventricular fibrillation (VF).
- Assessment of quinidine's use in preventing supraventricular arrhythmias and in pediatric patients.
Main Results:
- Quinidine demonstrated efficacy in preventing ventricular fibrillation re-induction and spontaneous ventricular arrhythmias in Brugada syndrome patients.
- Studies showed quinidine is effective in preventing supraventricular arrhythmias, including atrial fibrillation/flutter.
- Quinidine proved effective in both adult and pediatric Brugada syndrome patients.
Conclusions:
- Quinidine is an effective pharmacological option for preventing both ventricular and supraventricular arrhythmias in Brugada syndrome.
- Despite its efficacy, quinidine therapy is associated with a high incidence of side effects, potentially leading to treatment discontinuation.
Abstract:
Brugada syndrome is an inherited channelopathy with an increased risk of sudden cardiac death (SCD) due to ventricular arrhythmias (VA) and an increased incidence of supraventricular arrhythmias, as compared with the general population. For the prevention of SCD, the guidelines recommend the implantable cardioverter-defibrillator (ICD); however, ICD does not prevent VA. In this article, we provide a brief review of the literature on the Brugada syndrome pharmacological therapy, mainly focusing on quinidine treatment. The efficacy of quinidine therapy in the prevention of VA in Brugada syndrome has been demonstrated by several small studies in patients with ICD and recurrent shocks or in asymptomatic patients with inducible ventricular fibrillation (VF) at electrophysiological study. Quinidine has also been tested for the prophylaxis of supraventricular arrhythmias, especially atrial fibrillation/flutter, and in paediatric patients. In these studies, quinidine proved highly effective in preventing re-induction of VF and spontaneous recurrences of both ventricular and supraventricular arrhythmias. Unfortunately, this therapy is burdened by a high incidence of side effects, which may lead to drug discontinuation.
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