Brugada Syndrome: Current Perspectives

  • Apichai Khongphatthanayothin
  • Koonlawee NademaneeEmail author
Part of the Cardiac and Vascular Biology book series (Abbreviated title: Card. vasc. biol.)


Brugada syndrome was first reported as a distinct entity in 1992. It is diagnosed by signature EKG changes including at least 2-mm J-point elevation with coved-type ST elevation and T-wave inversion in at least one right precordial leads (type I Brugada marker). Initially thought of as a rare entity, Brugada syndrome is now widely recognized as a common cause of natural death among young men as a result of ventricular arrhythmia occurring at rest, particularly during sleep. The etiology of this disease is likely multifactorial, with genetic predisposition playing an important role in the pathogenesis. Mutation in the sodium channel gene SCN5A is seen in up to 20–25% of patients with at least 17 additional genes were reported to be associated with the disease. However, mutation in a single gene could be implicated in less than 30% of patients with Brugada syndrome, and a recent study showing association of this disease with common single nucleotide polymorphism of SCN5A, SCN10A, and HEY2 pointed toward polygenic or oligogenic pattern of inheritance rather than a single gene defect. Despite initial reports of normal structural heart in majority of patients, recent reports showed frequent minor structural abnormalities, especially in the right ventricular outflow tract (RVOT) in these patients. Brugada syndrome is now viewed as a spectrum of cardiomyopathy as well as channelopathy. The pathophysiologic underlying cardiac arrhythmia in Brugada syndrome is still unresolved with continued debate on depolarization versus repolarization defect. Treatment is largely dependent on the symptom with implantable cardioverter-defibrillator (ICD) implantation indicated in patients with severe symptoms. Avoiding medications and/or conditions that predispose the patient to ventricular arrhythmia is advised in all patients. Quinidine, by blocking transient outward current, has been used with some success. RF ablation of the epicardial substrate in the RVOT has been shown to prevent recurrence of ventricular arrhythmia in severe cases.



The authors would like to thank the National Research Council of Thailand (NRCT) for support on the study of Brugada syndrome.

Compliance with Ethical Standards

Conflict of Interest

Author Apichai Khongphatthanayothin declares that he has no conflict of interest. Author Koonlawee Nademanee declares that the following conflict of interests: Research grants from Medtronic Inc & Royalty from Biosense Cordis Webster Inc.

Ethical Approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Inform consent was obtained from all individual participants included in the study.


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Apichai Khongphatthanayothin
    • 1
  • Koonlawee Nademanee
    • 1
    • 2
    Email author
  1. 1.Chulalongkorn UniversityBangkokThailand
  2. 2.Pacific Rim Electrophysiology Research InstituteLos AngelesUSA

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