History and Physical Examination

History

Syncope and cardiac arrest are the most common clinical manifestations leading to the diagnosis of Brugada syndrome. Nightmares or thrashing at night may occur. However, some patients remain asymptomatic, and the diagnosis of Brugada syndrome is suggested by a routine electrocardiogram (ECG) showing ST-segment elevation in leads V₁ through V₃.

A family history of sudden cardiac death is common, though not universal, as the syndrome can occur sporadically. In about 20% of patients, atrial fibrillation is an associated arrhythmia.^[1]

The context of the cardiac event is important. In many cases, cardiac arrest occurs during sleep or rest. Cases occurring during physical activity are rare. Fever is often reported to trigger or exacerbate the clinical manifestations of Brugada syndrome.

A 2012 study suggested that the quality of symptoms prior to syncope can predict a benign or malignant cause in patients with Brugada syndrome. Specifically, the lack of a prodrome was more common in patients with ventricular fibrillation documented as the cause of syncope.^[2]

Physical examination

The physical examination is usually normal in patients with Brugada syndrome. Nevertheless, physical examination is required to rule out other possible cardiac causes of syncope or cardiac arrest in an otherwise healthy patient (eg, heart murmurs from hypertrophic cardiomyopathy or from a valvular or septal defect).

Differential Diagnoses

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Media Gallery

Schematics show the 3 types of action potentials in the right ventricle: endocardial (End), mid myocardial (M), and epicardial (Epi). A, Normal situation on V2 ECG generated by transmural voltage gradients during the depolarization and repolarization phases of the action potential. B-E, Different alterations of the epicardial action potential that produce the ECG changes observed in patients with Brugada syndrome. Adapted from Antzelevitch, 2005.
Three types of ST-segment elevation in Brugada syndrome, as shown in the precordial leads on ECG in the same patient at different times. Left panel shows a type 1 ECG pattern with pronounced elevation of the J point (arrow), a coved-type ST segment, and an inverted T wave in V1 and V2. The middle panel illustrates a type 2 pattern with a saddleback ST-segment elevated by >1 mm. The right panel shows a type 3 pattern in which the ST segment is elevated < 1 mm. According to a consensus report (Antzelevitch, 2005), the type 1 ECG pattern is diagnostic of Brugada syndrome. Modified from Wilde, 2002. Image courtesy of Richard Nunez, MD, and EMedHome.com (http://www.emedhome.com/).

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Author

Jose M Dizon, MD Professor of Clinical Medicine, Clinical Electrophysiology Laboratory, Division of Cardiology, Columbia University College of Physicians and Surgeons; Attending Physician, Department of Medicine, New York-Presbyterian/Columbia University Medical Center

Jose M Dizon, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society

Disclosure: Nothing to disclose.

Coauthor(s)

Tamim M Nazif, MD Fellow, Division of Cardiology, Columbia University College of Physicians and Surgeons

Tamim M Nazif, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, American Thoracic Society

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Actelion, Bayer, Gilead, United Therapeutics<br/>Received research grant from: Actelion, Arena, Gilead, GSK, Liquidia, Reata, United Therapeutics<br/>Received income in an amount equal to or greater than $250 from: Actelion, Complexa, Gilead, Medtronic, Reata, United Therapeutics.

Chief Editor

Mikhael F El-Chami, MD Associate Professor, Department of Medicine, Division of Cardiology, Section of Electrophysiology, Emory University School of Medicine

Mikhael F El-Chami, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Medtronic; Boston Scientific, Biotronik<br/>Received research grants (as part of Multicenter studies) from Medtronic and Boston Scientific.

Additional Contributors

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Chair of Institutional Review Board, University of California, Los Angeles, David Geffen School of Medicine

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, International Society for Magnetic Resonance in Medicine, American College of Physicians, American Federation for Medical Research, Radiological Society of North America

Disclosure: Nothing to disclose.

Characteristic	Type 1	Type 2	Type 3
J wave amplitude	≥2 mm	≥2 mm	≥2 mm
T wave	Negative	Positive or biphasic	Positive
ST-T configuration	Cove-type	Saddleback	Saddleback
ST segment, terminal portion	Gradually descending	Elevated by ≥1 mm	Elevated by < 1 mm

Brugada Syndrome Clinical Presentation

History and Physical Examination

History

Physical examination

References

Tables

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