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Arrhythmias arise from breakdown of orderly action potential (AP) activation, propagation and recovery driven by interactive opening and closing of successive voltage-gated ion channels, in which one or more Na⁺ current components play critical parts. Early peak, Na⁺ currents (I _Na) reflecting channel activation drive the AP upstroke central to cellular activation and its propagation. Sustained late Na⁺ currents (I _Na-L) include contributions from a component with a delayed inactivation timecourse influencing AP duration (APD) and refractoriness, potentially causing pro-arrhythmic phenotypes. The magnitude of I _Na-L can be analysed through overlaps or otherwise in the overall voltage dependences of the steady-state properties and kinetics of activation and inactivation of the Na⁺ conductance. This was useful in analysing repetitive firing associated with …