Brugada syndrome is a hereditary cardiac disease causing abnormal ST segment 
elevation in the ECG, right bundle branch block, ventricular fibrillation and 
sudden death. In this study we characterized a new mutation in the SCN5A gene 
(T1620M), causing the Brugada syndrome. The mutated channels were expressed in 
both Xenopus leavis oocytes and in mammalian tsA201 cells with and without the 
beta-subunit and studied using the patch clamp technique. Opposite phenotypes 
were observed depending on the expression system. T1620M mutation led to a 
faster recovery from inactivation and a shift of steady-state inactivation to 
more positive voltages when expressed in Xenopus oocytes. However, using the 
mammalian expression system no effect on steady-state inactivation was observed, 
but this mutation led to a slower recovery from inactivation. Our finding 
supports the idea that the slower recovery from inactivation of the cardiac 
sodium channels seen in our mammalian expression system could decrease the 
density of sodium channels during the cardiac cycle explaining the in vivo 
arrhythmogenesis in patients with Brugada syndrome.