IndraLab

Statements


| 2

sparser
"Most NaV1.5 mutations associated with LQT3 promote a mode of sodium channel gating in which some channels fail to inactivate, contributing to increased late sodium current (INaL), which is directly responsible for delayed repolarization and prolongation of the QT interval."

sparser
"Mutations in the SCN5A gene, which encodes the Nav1.5 protein forming the α subunit of the sodium channel, are common in BrS, accounting for approximately 20% to 25% of cases.[ xref ]In our case, no abnormity in the SCN5A gene was detected."