Key result
Quinidine prevents arrhythmogenesis in Brugada syndrome when ICDs are not indicated or sufficient.
Why the study?
Does pharmacological therapy prevent arrhythmogenesis in patients with Brugada syndrome?
Does pharmacological therapy prevent arrhythmogenesis in patients with Brugada syndrome?
Pharmacological therapy, particularly quinidine, plays a crucial role in preventing arrhythmias in Brugada syndrome, especially when ICDs are insufficient or contraindicated.
May support quinidine consideration when ICDs are insufficient in Brugada syndrome; leaves open need for prospective trials.
Brugada syndrome (BrS) is a cardiac disease caused by an inherited ion channelopathy associated with a propensity to develop ventricular fibrillation. Implantable cardioverter defibrillator implantation is recommended in BrS, based on the clinical presentation in the presence of diagnostic ECG criteria. Implantable cardioverter defibrillator implantation is not always indicated or sufficient in BrS, and is associated with a high device complication rate. Pharmacological therapy aimed at rebalancing the membrane action potential can prevent arrhythmogenesis in BrS. Quinidine, a class 1A antiarrhythmic drug with significant Ito blocking properties, is the most extensively used drug for the prevention of arrhythmias in BrS. The present review provides contemporary data gathered on all drugs effective in the therapy of BrS, and on ineffective or contraindicated antiarrhythmic drugs.
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Brodie et al. (2018) conducted a review in Brugada syndrome. Pharmacological therapy (e.g., Quinidine) was evaluated. Pharmacological therapy, particularly quinidine, can prevent arrhythmogenesis in Brugada syndrome when implantable cardioverter defibrillators are not indicated or sufficient.
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