Absolute Event Rate: 16.3% vs 5.4%
p-value: p=<0.01
The T1620M mutation associated with Brugada syndrome enhances intermediate inactivation of sodium channels, providing a biophysical mechanism for reduced sodium current and arrhythmogenesis.
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Wang et al. (2000) studied Brugada syndrome. T1620M SCN5A mutation vs. Wild-type recombinant human heart sodium channels (WT-hH1) was evaluated on Amplitude of intermediate inactivation (IM) after 1 sec prepulse duration (p=<0.01).
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