= Solution
An increased late inward <sodium> current can delay repolarization if fast <Ion-channel inactivation>[inactivation] is incomplete or slowed, if channels reopen excessively, or if the <voltage> range of persistent/window current is enlarged. A larger brief peak current alone is not equivalent to a sustained depolarizing current. Conversely, reduced outward <potassium> current can prolong the <action potential> through fewer functional surface channels, reduced <Electrical conductance>[conductance], slower or less favourable activation, or altered deactivation/availability. Either change shifts the balance towards inward current during repolarization.
These are distinct biophysical routes to <Long QT syndrome>, not claims that every subtype has the same channel defect.https://www.ncbi.nlm.nih.gov/books/NBK1129/[GeneReviews, Long QT Syndrome Overview, updated 2024: sodium gain-of-function and potassium loss-of-function mechanisms]{ref} The experimental association of <Voltage-gated sodium channel>[sodium-channel] abnormalities with inherited disease supports the inward-current mechanism.<Cardiac sodium channel mutations in patients with long QT syndrome, an inherited cardiac arrhythmia by Qing Wang and others>[1995 human genetic study linking cardiac sodium-channel defects to inherited long-QT syndrome]{ref}
Back to article page
