Open AccessInhibition of Cardiac Ca 2+ Release Channels (RyR2) Determines Efficacy of Class I Antiarrhythmic Drugs in Catecholaminergic Polymorphic Ventricular Tachycardia
Author(s) -
Hyun Seok Hwang,
Can Hasdemir,
Derek R. Laver,
Divya Mehra,
Kutsal Turhan,
Michela Faggioni,
Huiyong Yin,
Björn C. Knollmann
Publication year - 2011
Publication title -
circulation arrhythmia and electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.684
H-Index - 102
eISSN - 1941-3149
pISSN - 1941-3084
DOI - 10.1161/circep.110.959916
Subject(s) - flecainide , catecholaminergic polymorphic ventricular tachycardia , propafenone , ryanodine receptor 2 , medicine , pharmacology , mexiletine , procainamide , quinidine , afterdepolarization , cardiology , ryanodine receptor , calcium , atrial fibrillation , electrophysiology , repolarization
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is caused by mutations in the cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) and can be difficult to treat. The class Ic antiarrhythmic drug flecainide blocks RyR2 channels and prevents CPVT in mice and humans. It is not known whether other class I antiarrhythmic drugs also block RyR2 channels and to what extent RyR2 channel inhibition contributes to antiarrhythmic efficacy in CPVT.
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