Two mechanisms are generally proposed to explain right-precordial ST-segment elevation in Brugada syndrome: (1) Right-ventricular (RV) subepicardial action-potential shortening and/or loss of dome causing transmural dispersion of repolarization; (2) RV conduction delay. Here we report novel mechanistic insights into ST-segment elevation associated with a Na⁺-current (I_Na) loss-of-function mutation from studies in a Dutch kindred with the C-terminal SCN5A variant p.Phe2004Leu. The proband, a male, experienced syncope at age 22 and had coved-type ST-segment elevations in ECG leads V1 and V2, and negative T-waves in V2. Peak and persistent mutant I_Na were significantly decreased. I_Na closed-state inactivation was increased, slow inactivation accelerated, and recovery from inactivation delayed. Computer-simulated I_Na-dependent excitation was decremental from endo- to epicardium at cycle length 1000 ms, not at cycle length 300 ms. Propagation was discontinuous across the midmyocardial (M) to epicardial transition region, exhibiting a long local delay due to phase-0 block. Beyond this region, axial excitatory current was provided by phase 2 (dome) of the M-cell action potentials and depended on L-type Ca²⁺ current ("phase-2 conduction"). These results explain right-precordial ST-segment elevation on the basis of RV transmural gradients of membrane potentials during early repolarization caused by discontinuous conduction. The late slow-upstroke action potentials at the subepicardium produce T-wave inversion in the computed ECG waveform, in line with the clinical ECG.