The Antiarrhythmic Mechanisms of Flecainide in Catecholaminergic Polymorphic Ventricular Tachycardia

Yukun Li; Xiaodong Peng; Rong Lin; Xuesi Wang; Xinmeng Liu; Rong Bai; Changsheng Ma; Ribo Tang; Yanfei Ruan; Nian Liu

doi:10.3389/fphys.2022.850117

The Antiarrhythmic Mechanisms of Flecainide in Catecholaminergic Polymorphic Ventricular Tachycardia

Front Physiol. 2022 Mar 9:13:850117. doi: 10.3389/fphys.2022.850117. eCollection 2022.

Authors

Yukun Li^{1

2}, Xiaodong Peng^{1

2}, Rong Lin³, Xuesi Wang^{1

2}, Xinmeng Liu^{1

2}, Rong Bai⁴, Changsheng Ma^{1

2}, Ribo Tang^{1

2}, Yanfei Ruan^{1

2}, Nian Liu^{1

2}

Affiliations

¹ Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
² National Clinical Research Center for Cardiovascular Diseases, Beijing, China.
³ North China Medical and Health Group XingTai Hospital, Xingtai, China.
⁴ Banner - University Medical Center Phoenix, University of Arizona College of Medicine, Phoenix, AZ, United States.

Abstract

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.

Keywords: antiarrhythmic mechanism; catecholaminergic polymorphic ventricular tachycardia; flecainide; ryanodine receptor; sodium channel.

Publication types

Review