Long QT and Brugada syndromes are two hereditary cardiac diseases. Brugada 
syndrome has so far been associated with only one gene, SCN5A, which encodes the 
cardiac sodium channel. However, in long QT syndrome (LQTS) at least six genes, 
including the SCN5A, are implicated. The substitution (D1790G) causes LQTS and 
the insertion (D1795) induces both LQTS and Brugada syndromes in carrier 
patients. hH1/insD1795 and hH1/D1790G mutant channels were expressed in the 
tsA201 human cell line and characterized using the patch clamp technique in 
whole-cell configuration. Our data revealed a persistent inward sodium current 
of about 6% at -30 mV for both D1790G and insD1795, and a reduction of 62% of 
channel expression for the insD1795. Moreover, a shift of steady-state 
inactivation curve in both mutants was also observed. Our findings uphold the 
idea that LQT3 is related to a persistent sodium current whereas reduction in 
the expression level of cardiac sodium channels is one of the biophysical 
characteristics of Brugada syndrome.