Brugada syndrome without mutation of the cardiac sodium channel gene in a Taiwanese patient.

Article Details

Citation

Copy to clipboard

Chen SM, Kuo CT, Lin KH, Chiang FT

Brugada syndrome without mutation of the cardiac sodium channel gene in a Taiwanese patient.

J Formos Med Assoc. 2000 Nov;99(11):860-2.

PubMed ID

11155778 [ View in PubMed

]

Abstract

We describe a 45-year-old Taiwanese man with specific features of Brugada syndrome but no clinical features of structural heart disease. He was successfully treated with an implantable cardioverter-defibrillator. His electrocardiogram (ECG) patterns changed intermittently. Alpha-adrenoceptor stimulation and beta-adrenoceptor blockade augmented the characteristic ST-segment elevation, whereas alpha-adrenoceptor blockade and beta-adrenoceptor stimulation mitigated the ST-segment elevation. Intravenous procainamide administration did not aggravate ST-segment elevation when ECG had shown coved ST elevation in the right precordial leads. Molecular study did not reveal the same mutations in the cardiac sodium channel gene (SCN5A) as previously reported in Brugada syndrome. This case demonstrates the genetic heterogeneity of SCN5A in Brugada syndrome.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Procainamide	Sodium channel protein type 5 subunit alpha	Protein	Humans	Unknown	Inhibitor	Details