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t is acknowledged that mutations in the cardiac sodium channel gene, SCN5A, are associated with various arrhythmia syndromes such as long QT syndrome type 3 (LQT3), Brugada syndrome (BrS), conduction disease, sick sinus syndrome, atrial fibrillation, atrial standstill, and sudden infant death syndrome (SIDS).1,2 Mixed phenotypes can be frequently observed as “cardiac sodium channel overlap syndrome”. In 1999, Bezzina et al reported that a single Na+ channel mutation (SCN5A-1795insD) can lead to overlap syndrome with symptoms of LQT3 and BrS in combination.3 Grant et al reported another Na+ channel mutation (SCN5A-∆K1500) showing a mixed phenotype of LQT3 and BrS.4 In addition, Makita et al have recently reported that the E1784K mutation in SCN5A is associated with the phenotypic overlap of type LQT3 syndrome and BrS.5 Thus, several SCN5A mutations are reported to produce a mixed phenotype of LQT3 and BrS (Figure 1). Article p 1136

<i>SCN5A </i>Mutations Associated With Overlap Phenotype of Long QT Syndrome Type 3 and Brugada Syndrome