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

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.

• Authors: S M Chen, C T Kuo, K H Lin, F T Chiang
• Journal: Journal of the Formosan Medical Association = Taiwan yi zhi (J Formos Med Assoc) Vol. 99 Issue 11 Pg. 860-2 (Nov 2000) ISSN: 0929-6646 [Print] Singapore
• PMID: 11155778 (Publication Type: Case Reports, Journal Article)

Chemical References

• Adrenergic beta-Agonists
• Adrenergic beta-Antagonists
• Anti-Arrhythmia Agents
• Propanolamines
• Sodium Channels
• Procainamide
• Isoproterenol
• esmolol

Topics

• Adrenergic beta-Agonists (pharmacology)
• Adrenergic beta-Antagonists (pharmacology)
• Anti-Arrhythmia Agents (therapeutic use)
• Arrhythmias, Cardiac (therapy)
• Autonomic Nervous System (physiopathology)
• Cardiac Pacing, Artificial
• Death, Sudden, Cardiac
• Defibrillators, Implantable
• Electrocardiography
• Humans
• Isoproterenol (pharmacology)
• Male
• Middle Aged
• Mutation
• Procainamide (pharmacology)
• Propanolamines (pharmacology)
• Sodium Channels (genetics)
• Syndrome