Depolarization vs. repolarization: what is the mechanism of ventricular arrhythmogenesis underlying sodium channel haploinsufficiency in mouse hearts?-Reference-Cited by-同舟云学术

Depolarization vs. repolarization: what is the mechanism of ventricular arrhythmogenesis underlying sodium channel haploinsufficiency in mouse hearts?

Published:2016-04-30 Issue:4 Volume:218 Page:234-235
ISSN:1748-1708
Container-title:Acta Physiologica
language:en
Short-container-title:Acta Physiol

Author:

Tse G.¹,Wong S. T.²,Tse V.³,Yeo J. M.²

Affiliation:

1. School of Biomedical Sciences; Li Ka Shing Faculty of Medicine; University of Hong Kong; Hong Kong Hong Kong

2. Faculty of Medicine; Imperial College London; London UK

3. Department of Physiology; McGill University; Montreal QC Canada

Publisher

Wiley

Subject

Physiology

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1111/apha.12694/fullpdf

Reference15 articles.

1. Delayed conduction and its implications in murine Scn5a(+/−) hearts: independent and interacting effects of genotype, age, and sex;Jeevaratnam;Pflugers Arch,2011

2. Frequency distribution analysis of activation times and regional fibrosis in murine Scn5a+/− hearts: the effects of ageing and sex;Jeevaratnam;Mech Ageing Dev,2012

3. Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis;Jeevaratnam;Acta Physiol (Oxf),2016

4. Increased right ventricular repolarization gradients promote arrhythmogenesis in a murine model of Brugada syndrome;Martin;J Cardiovasc Electrophysiol,2010

5. Effects of flecainide and quinidine on arrhythmogenic properties of Scn5a+/− murine hearts modelling the Brugada syndrome;Stokoe;J Physiol,2007

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