Gating-Dependent Mechanisms for Flecainide Action in SCN5A -Linked Arrhythmia Syndromes | Zendy

Prakash C. Viswanathan | Zendy; Connie R. Bezzina | Zendy; Alfred L. George | Zendy; Dan M. Roden | Zendy; Arthur A.M. Wilde | Zendy; Jeffrey R. Balser | Zendy

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Gating-Dependent Mechanisms for Flecainide Action in SCN5A -Linked Arrhythmia Syndromes

Author(s) -

Prakash C. Viswanathan,

Connie R. Bezzina,

Alfred L. George,

Dan M. Roden,

Arthur A.M. Wilde,

Jeffrey R. Balser

Publication year - 2001

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/hc3501.093797

Subject(s) - flecainide , medicine , gating , cardiac arrhythmia , cardiology , electrocardiography , atrial fibrillation , physiology

Mutations in the cardiac sodium (Na) channel gene (SCN5A) give rise to the congenital long-QT syndrome (LQT3) and the Brugada syndrome. Na channel blockade by antiarrhythmic drugs improves the QT interval prolongation in LQT3 but worsens the Brugada syndrome ST-segment elevation. Although Na channel blockade has been proposed as a treatment for LQT3, flecainide also evokes "Brugada-like" ST-segment elevation in LQT3 patients. Here, we examine how Na channel inactivation gating defects in LQT3 and Brugada syndrome elicit proarrhythmic sensitivity to flecainide.

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