Ventricular arrhythmogenesis: insights from murine models.
Ventricular arrhythmias are the key underlying cause of sudden cardiac death, a common cause of mortality and a significant public health burden. Insights into the electrophysiological basis of such phenomena have been obtained using a wide range of recording techniques and a diversity of experimental models. As in other fields of biology, the murine system presents both a wealth of opportunities and important challenges when employed to model the human case. This article begins by reviewing the extent to which the murine heart is representative of that of the human. It then presents a novel physiological classification of mechanisms of arrhythmogenesis, critically assessing the extent to which the study of murine hearts has offered worthwhile insights.
Sabir
Ian N
IN
Physiological Laboratory, University of Cambridge, Downing Street, Cambridge, UK.
Killeen
Matthew J
MJ
Grace
Andrew A
AA
Huang
Christopher L-H
CL
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D004195:Disease Models, Animal; D004562:Electrocardiography; D055724:Electrophysiological Phenomena; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009124:Muscle Proteins / Q000235:genetics / Q000502:physiology; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel; D015222:Sodium Channels / Q000235:genetics / Q000502:physiology; D013045:Species Specificity; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology
D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; C568321:Scn5a protein, mouse; D015222:Sodium Channels