The Brugada syndrome is characterized by ST segment elevation in the right 
precodial leads V1-V3 on surface ECG accompanied by episodes of ventricular 
fibrillation causing syncope or even sudden death. The molecular and cellular 
mechanisms that lead to Brugada syndrome are not yet completely understood. 
However, SCN5A is the most well known responsible gene that causes Brugada 
syndrome. Until now, more than a hundred mutations in SCN5A responsible for 
Brugada syndrome have been described. Functional studies of some of the 
mutations have been performed and show that a reduction of human cardiac sodium 
current accounts for the pathogenesis of Brugada syndrome. Here we reported 
three novel SCN5A mutations identified in patients with Brugada syndrome in 
Taiwan (p.I848fs, p.R965C, and p.1876insM). Their electrophysiological 
properties were altered by patch clamp analysis. The p.I848fs mutant generated 
no sodium current. The p.R965C and p.1876insM mutants produced channels with 
steady state inactivation shifted to a more negative potential (9.4 mV and 8.5 
mV respectively), and slower recovery from inactivation. Besides, the steady 
state activation of p.1876insM was altered and was shifted to a more positive 
potential (7.69 mV). In conclusion, the SCN5A channel defect related to Brugada 
syndrome might be diverse but all resulted in a decrease of sodium current.