Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans

Hiroshi Watanabe; Nagesh Chopra; Derek Laver; Hyun Seok Hwang; Sean S. Davies; Daniel E. Roach; Henry J. Duff; Dan M. Roden; Arthur A. M. Wilde; Björn C. Knollmann

doi:https://doi.org/10.1038/nm.1942

Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans

Hiroshi Watanabe, Nagesh Chopra, Derek Laver, Hyun Seok Hwang, Sean S. Davies, Daniel E. Roach, Henry J. Duff, Dan M. Roden, Arthur A. M. Wilde, Björn C. Knollmann

Research output: Contribution to journal › Article › Academic › peer-review

493 Citations (Scopus)

Abstract

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal inherited arrhythmia syndrome in which drug therapy is often ineffective. We discovered that flecainide prevents arrhythmias in a mouse model of CPVT by inhibiting cardiac ryanodine receptor-mediated Ca2+ release and thereby directly targeting the underlying molecular defect. Flecainide completely prevented CPVT in two human subjects who had remained highly symptomatic on conventional drug therapy, indicating that this currently available drug is a promising mechanism-based therapy for CPVT

Original language	English
Pages (from-to)	380-383
Journal	Nature medicine
Volume	15
Issue number	4
DOIs	https://doi.org/10.1038/nm.1942
Publication status	Published - 2009

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https://doi.org/10.1038/nm.1942

Cite this

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title = "Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans",

abstract = "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal inherited arrhythmia syndrome in which drug therapy is often ineffective. We discovered that flecainide prevents arrhythmias in a mouse model of CPVT by inhibiting cardiac ryanodine receptor-mediated Ca2+ release and thereby directly targeting the underlying molecular defect. Flecainide completely prevented CPVT in two human subjects who had remained highly symptomatic on conventional drug therapy, indicating that this currently available drug is a promising mechanism-based therapy for CPVT",

author = "Hiroshi Watanabe and Nagesh Chopra and Derek Laver and Hwang, {Hyun Seok} and Davies, {Sean S.} and Roach, {Daniel E.} and Duff, {Henry J.} and Roden, {Dan M.} and Wilde, {Arthur A. M.} and Knollmann, {Bj{\"o}rn C.}",

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AU - Watanabe, Hiroshi

AU - Chopra, Nagesh

AU - Laver, Derek

AU - Hwang, Hyun Seok

AU - Davies, Sean S.

AU - Roach, Daniel E.

AU - Duff, Henry J.

AU - Roden, Dan M.

AU - Wilde, Arthur A. M.

AU - Knollmann, Björn C.

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AB - Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a potentially lethal inherited arrhythmia syndrome in which drug therapy is often ineffective. We discovered that flecainide prevents arrhythmias in a mouse model of CPVT by inhibiting cardiac ryanodine receptor-mediated Ca2+ release and thereby directly targeting the underlying molecular defect. Flecainide completely prevented CPVT in two human subjects who had remained highly symptomatic on conventional drug therapy, indicating that this currently available drug is a promising mechanism-based therapy for CPVT

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DO - https://doi.org/10.1038/nm.1942

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