Genetic Architecture, Pathophysiology, and Clinical Management of Brugada Syndrome

  • John R. Giudicessi
  • Michael J. AckermanEmail author


Brugada syndrome (BrS) is a genetically complex and heterogeneous disorder characterized by ST-segment elevation in the right precordial leads and an increased risk of syncope and sudden cardiac death in the setting of an otherwise structurally normal heart. Over the last several years, advances at both the bench and the bedside have begun to question existing paradigms surrounding the genetic basis and pathophysiology of BrS as well as usher in novel approaches to the risk stratification and treatment of patients with this potentially fatal disorder. In this chapter, we examine the rapidly evolving understanding of the pathophysiological mechanism(s) underlying BrS, ongoing efforts to reappraise the genetic architecture of BrS, and advances in risk stratification and therapeutic approaches that are redefining how patients with BrS are managed clinically.


Arrhythmia Brugada syndrome Genetics Genetic testing Sudden cardiac death 



American College of Cardiology


American Heart Association


Brugada syndrome


Clinical Genome Resource


European Heart Rhythm Association


Electrophysiology study


European Society of Cardiology


Exome Aggregation Consortium


Genome Aggregation Database


Gene of uncertain significance


Genome-Wide Association Study


Heart Rhythm Society


Implantable cardioverter-defibrillator


Premature ventricular contraction


Right ventricular outflow tract


Sudden cardiac death


Ventricular fibrillation


Ventricular tachycardia


Variant of uncertain significance


Funding Sources

This work was supported by the Mayo Clinic Windland Smith Rice Sudden Comprehensive Sudden Cardiac Death Program (to Dr. Ackerman). Dr. Giudicessi thanks the Mayo Clinic Cardiovascular Diseases Fellowship and Clinician Investigator Training Programs for fostering an outstanding environment for physician-scientist training.

Conflict of Interest Disclosures

Dr. Ackerman is a consultant for Audentes Therapeutics, Boston Scientific, Gilead Sciences, Invitae, Medtronic, MyoKardia, and St. Jude Medical. From 2004 to 2016, M.J.A. and Mayo Clinic received sales-based royalties from Transgenomic for their FAMILION-LQTS and FAMILION-CPVT genetic tests. M.J.A. and Mayo Clinic have an equity/royalty relationship (without remuneration so far) with AliveCor, Blue Ox Health, and StemoniX. However, none of these entities participated in this study. Dr. Giudicessi declares no conflicts.


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Copyright information

© Springer Nature Switzerland AG 2020

Authors and Affiliations

  1. 1.Department of Cardiovascular MedicineMayo ClinicRochesterUSA
  2. 2.Departments of Cardiovascular Medicine, Pediatric and Adolescent Medicine, and Molecular Pharmacology and Experimental TherapeuticsMayo Clinic Genetic Heart Rhythm Clinic and the Windland Smith Rice Sudden Death Genomics LaboratoryRochesterUSA

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