Efficacy of Quinidine in Brugada Syndrome: A Literature Review
7 affiliations
- 1Department of Basic and Clinical Sciences, University of Nicosia Medical School, 2417 Nicosia, Cyprus
- 2Department of Cardiology, Larnaca General Hospital, State Health Services Organization, 6301 Larnaca, Cyprus
- 3Arrhythmia Unit, Onassis Cardiac Surgery Center, 17674 Athens, Greece
- 4Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, 300150 Tianjin, China
- 5Kent and Medway Medical School, University of Kent and Canterbury Christ Church University, 927700 Canterbury, Kent, UK
- 6School of Nursing and Health Studies, Hong Kong Metropolitan University, Hong Kong, China
- 7Division of Cardiology, Kingston Health Science Center, Queen’s University, Kingston, ON K7L 3N6, Canada
Abstract
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.
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BibTeX
@article{bazoukis2026efficacy,
title = {{Efficacy of Quinidine in Brugada Syndrome: A Literature Review}},
author = {George Bazoukis and Emmanouil Andreakis and Athanasios Saplaouras and Tong Liu and Gary Tse and Konstantinos P. Letsas and Michael Efremidis and Adrian Baranchuk},
journal = {Reviews in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.31083/rcm51365},
url = {https://doi.org/10.31083/rcm51365},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Efficacy of Quinidine in Brugada Syndrome: A Literature Review
AU - George Bazoukis
AU - Emmanouil Andreakis
AU - Athanasios Saplaouras
AU - Tong Liu
AU - Gary Tse
AU - Konstantinos P. Letsas
AU - Michael Efremidis
AU - Adrian Baranchuk
PY - 2026
DA - 2026/10/12
JO - Reviews in Cardiovascular Medicine
DO - 10.31083/rcm51365
UR - https://doi.org/10.31083/rcm51365
AB - 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.
SN - 1530-6550
SN - 2153-8174
ER -