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

Acta Physiologica

Volumn 218, Issue 4, 2016, Pages 234-235

  Tse, G ^a   Wong, S T ^b   Tse, V ^c   Yeo, J M ^b  

^a UNIVERSITY OF HONG KONG   (Hong Kong)

^b IMPERIAL COLLEGE LONDON   (United Kingdom)

^c MCGILL UNIVERSITY   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

SODIUM CHANNEL;

ACTION POTENTIAL; BRUGADA SYNDROME; COMPARATIVE STUDY; ENDOCARDIUM; EPICARDIUM; HAPLOINSUFFICIENCY; HEART DEPOLARIZATION; HEART REPOLARIZATION; HEART VENTRICLE ARRHYTHMIA; LATENT PERIOD; LETTER; MEMBRANE POTENTIAL; MOUSE; NONHUMAN; PRIORITY JOURNAL; WILD TYPE; ANIMAL; GENETICS; HEART ARRHYTHMIA; HEART MUSCLE CONDUCTION SYSTEM; HUMAN;

ACTION POTENTIALS; ANIMALS; ARRHYTHMIAS, CARDIAC; HAPLOINSUFFICIENCY; HEART CONDUCTION SYSTEM; HUMANS; MICE; SODIUM CHANNELS;

EID: 84994399990     PISSN: 17481708     EISSN: 17481716     Source Type: Journal    
DOI: 10.1111/apha.12694     Document Type: Letter

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