Open AccessMechanistic Links Between Na + Channel (SCN5A) Mutations and Impaired Cardiac Pacemaking in Sick Sinus Syndrome
Author(s) -
Timothy D. Butters,
Oleg Aslanidi,
Shin Inada,
Mark R. Boyett,
Jules C. Hancox,
Ming Lei,
Henggui Zhang
Publication year - 2010
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.110.219949
Subject(s) - sinoatrial node , sick sinus syndrome , sss* , atrium (architecture) , electrical conduction system of the heart , medicine , electrophysiology , sinus (botany) , mutation , sinus rhythm , cardiology , endocrinology , biology , anatomy , heart rate , electrocardiography , gene , atrial fibrillation , genetics , blood pressure , botany , genus
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.
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