Mechanistic links between Na+ channel (SCN5A) mutations and impaired cardiac pacemaking in sick sinus syndrome.

Journal article

RATIONALE: Familial sick sinus syndrome (SSS) has been linked to loss-of-function mutations of the SCN5A gene, which result in decreased inward Na(+) current, I(Na). However, the functional role of I(Na) in cardiac pacemaking is controversial, and mechanistic links between mutations and sinus node dysfunction in SSS are unclear. OBJECTIVE: To determine mechanisms by which the SCN5A mutations impair cardiac pacemaking. METHODS AND RESULTS: Action potential (AP) models for rabbit sinoatrial nod...

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Authors: Butters, T; Aslanidi, O; Inada, S; Boyett, MR; Hancox, J

• Publication status: Published
• Journal: Circulation research
• Volume: 107
• Issue: 1
• Pages: 126-137
• Publication date: 2010-07-01
• DOI: 10.1161/circresaha.110.219949
• EISSN: 1524-4571
• ISSN: 0009-7330
• Language: English
• Keywords: Mutation; Rabbits; Sinoatrial Node; NAV1.5 Voltage-Gated Sodium Channel; Sick Sinus Syndrome; Sodium Channels; Organ Culture Techniques; Heart Conduction System; Animals; Biological Clocks; Male; Computational Biology; Models, Cardiovascular