Increased right ventricular repolarization gradients promote arrhythmogenesis in a murine model of brugada syndrome

Journal of Cardiovascular Electrophysiology

Volumn 21, Issue 10, 2010, Pages 1153-1159

  Martin, Claire A ^a   Zhang, Yanmin ^a,b   Grace, Andrew A ^a   Huang, Christopher L H ^a  

^a UNIVERSITY OF CAMBRIDGE   (United Kingdom)

^b XI'AN JIAOTONG UNIVERSITY   (China)

Author keywords

action potentials; antiarrhythmic drugs; arrhythmia; Brugada syndrome; conduction velocity; ion channels; repolarization; sodium channels; sudden death; ventricular tachycardia

Indexed keywords

FLECAINIDE; QUINIDINE; SODIUM CHANNEL NAV1.5;

ACTION POTENTIAL; ANIMAL TISSUE; ANTIARRHYTHMIC ACTIVITY; ARRHYTHMOGENESIS; ARTICLE; BRUGADA SYNDROME; CONTROLLED STUDY; DRUG EFFECT; ELECTROSTIMULATION; ENDOCARDIUM; EPICARDIUM; GENETIC MODEL; HEART CONDUCTION; HEART LEFT VENTRICLE; HEART PACING; HEART REPOLARIZATION; HEART RIGHT VENTRICLE; ISOLATED HEART; MOUSE; NONHUMAN; PRIORITY JOURNAL;

ACTION POTENTIALS; ANIMALS; BRUGADA SYNDROME; DISEASE MODELS, ANIMAL; HEART CONDUCTION SYSTEM; HEART VENTRICLES; HUMANS; MICE;

EID: 78649301999     PISSN: 10453873     EISSN: 15408167     Source Type: Journal    
DOI: 10.1111/j.1540-8167.2010.01767.x     Document Type: Article

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