Review ArticlesSudden Cardiac Death in Brugada SyndromeKabra, Nitin MD; Gupta, Rahul MD; Aronow, Wilbert S. MD; Frishman, William H. MDAuthor Information From the Cardiology Division, Department of Medicine, Westchester Medical Center/New York Medical College, Valhalla, NY. Disclosure: The authors have no conflicts of interest to report. Correspondence: Wilbert S. Aronow, MD, Cardiology Division, Department of Medicine, Westchester Medical Center and New York Medical College, Macy Pavilion, Room 141, Valhalla, NY 10595. E-mail: email@example.com. Cardiology in Review: July/August 2020 - Volume 28 - Issue 4 - p 203-207 doi: 10.1097/CRD.0000000000000259 Buy Metrics Abstract The Brugada syndrome is an inherited channelopathy that alters the main transmembrane ion currents that constitute the cardiac action potential. These changes not only modify the resting electrocardiogram but also predispose patients to develop malignant ventricular tachyarrhythmias that can lead to syncope, cardiac arrest, and sudden cardiac death. This syndrome is responsible for nearly 20% of all sudden cardiac deaths in patients with structurally normal hearts and up to 12% of all sudden cardiac deaths. Brugada syndrome is diagnosed by its characteristic electrocardiogram consisting of a coved-type ST-segment elevation of at least 2 mm followed by a negative T wave in either one of the right precordial leads. These changes can be observed spontaneously or after administration of a sodium channel blocker. While our understanding of this disease has increased tremendously since its first description in 1992, the primary therapeutic option remains implantation of an implantable cardioverter-defibrillator to avoid sudden cardiac death. Therefore, tremendous effort is being made to effectively risk stratify patients to determine who would benefit from implantable cardioverter-defibrillator implantation. Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.