We describe a 45-year-old Taiwanese man with specific features of Brugada s
yndrome but no clinical features of structural heart disease. He was succes
sfully, treated with an implantable cardioverter-defibrillator. His electro
cardiogram (ECG) patterns changed intermittently. Alpha-adrenoceptor stimul
ation and beta-adrenoceptor blockade augmented the characteristic ST-segmen
t elevation, whereas alpha-adrenoceptor blockade and beta-adrenoceptor stim
ulation mitigated the ST-segment elevation, intravenous procainamide admini
stration did not aggravate ST-segment elevation when ECG had shown coved ST
elevation in the right precordial leads. Molecular study did not reveal th
e same mutations in the cardiac sodium channel gene (SCN5A) as previously r
eported in Brugada syndrome. This case demonstrates the genetic heterogenei
ty of SCN5A in Brugada syndrome.