Why the study?
Although flecainide effectively prevents life-threatening arrhythmias in CPVT, RyR2 inhibition as its principal antiarrhythmic mechanism remains highly debated.
What are the antiarrhythmic mechanisms of flecainide in catecholaminergic polymorphic ventricular tachycardia?
What are the antiarrhythmic mechanisms of flecainide in catecholaminergic polymorphic ventricular tachycardia?
This review summarizes the ongoing debate regarding the exact antiarrhythmic mechanism of flecainide in CPVT, focusing on RyR2 inhibition versus sodium channel blockade.
The mechanism of flecainide in CPVT remains unresolved; leaves open whether RyR2 inhibition or sodium channel blockade predominates.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe yet rare inherited arrhythmia disorder. The cornerstone of CPVT medical therapy is the use of β-blockers; 30% of patients with CPVT do not respond well to optimal β-blocker treatment. Studies have shown that flecainide effectively prevents life-threatening arrhythmias in CPVT. Flecainide is a class IC antiarrhythmic drug blocking cardiac sodium channels. RyR2 inhibition is proposed as the principal mechanism of antiarrhythmic action of flecainide in CPVT, while it is highly debated. In this article, we review the current progress of this issue.
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Li et al. (2022) studied this question.
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