An increased late inward sodium current can delay repolarization if fast 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 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.[ref] The experimental association of sodium-channel abnormalities with inherited disease supports the inward-current mechanism.[ref]

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