DSAE STEMI Review, Mod 2: Brugada Syndrome

The tracing below is from a 51-year-old male who presents with complaints of recurring syncopal episodes.


 The Brugada Syndrome


This is a classic example of the Brugada Syndrome.  You can easily see why one might interpret the tracing as one of an acute ST-elevation MI or STEMI (Anteroseptal).  Note particularly the ST elevation and T-wave inversion in Lead V3.  Of note is that the computer interpretation of this tracing was incorrectly stated as “Acute MI”.  This is an example of many to remind you to not practice medicine according to the computer interpretation of the cardiogram!


This cardiac abnormality is a genetic disorder (autosomal dominant transmission).  It is characterized by an electrical abnormality with a structurally normal heart.  The syndrome proper is characterized as follows (without symptoms it is referred to as the Brugada Sign):

1.  Clinical episodes of near syncope, syncopal episodes, seizures or sudden death.

2.  Structurally normal heart.

3.  Characteristic ECG pattern displaying ST elevation and T-wave inversion/biphasic T’s in Leads
V1, V2 and V3 (pattern resembles RBBB).


For emphasis, I have magnified Lead V2.  Please note that I have labeled and color-coded, red, the ST segment.  The ST segment assumes a peculiar ramp-like elevation at an angle of nearly 45 degrees.  The T-wave is inverted (negative) and is color-coded blue.  These ST-T changes are the hallmark of the Brugada Syndrome.


A careful analysis of the tracing above will reveal why it is frequently misdiagnosed as

a.  Atypical RBBB

This tracing demonstrates RSR’ in Lead V2 with a biphasic Lead I and small terminal S-wave.  The QRS duration is slightly prolonged.

b.  Acute Anteroseptal MI

ST elevation (concave down) in Leads V1, V2 and V3.

T-wave inversion or biphasic T-waves in Leads V1, V2, and V3.


This syndrome has been recognized virtually worldwide, less common in the United States and most common in southeast Asia (Thailand and Laos).  It is stated to be responsible for five deaths per year per 10,000 population in these areas where it is endemic.  The arrhythmia leading to sudden death is Polymorphic Ventricular Tachycardia
(Torsades de Pointes) with degeneration to ventricular fibrillation.


If treatment is indicated, please know that the objective would be directed to the prevention of Ventricular Tachycardia and sudden death.  Some patients with electrocardiographic changes of Brugada Sign might be negative for sudden death and the patient’s history might be negative for syncope, pre-syncope or seizures.  However ALL  patients you encounter in your practice with these classic ECG findings should be referred to the cardiologist for a work-up and treatment recommendation.  (Choose a cardiologist who has a familiarity with this disorder.)

If the patient is experiencing symptoms related to transient Ventricular Tachycardia, antiarrhythmic drugs including beta blockers and amiodarone are ineffective to prevent Ventricular Tachycardia and sudden death.  The only effective treament mode is the automatic implantable defibrillator.


* Characterized by ST-segment elevation in Leads V1, V2, V3 with a peculiar slant at approximately 45 degrees and T-wave inversion or biphasic T-waves.
* Disorder occurs world-wide but most common in Southeast Asia.
* QT interval is usually normal.
* Only treatment to avoid Ventricular Tachycardia and Ventricular Fibrillation and sudden death is the automatic implantable defibrillator.
* Incidence of male:female is approximately 8:1.
* Death commonly occurs during rest or sleep (in Thailand, it is known as “lai tai” aka “death during sleep”).
* It is a genetic disorder.
* Medications such as amiodarone or Beta blockers do NOT prevent sudden death.
* With no known cardiac disease, Brudaga is the most common cause of sudden death age < 50 years in South Asia.
* This disorder may be the leading cause of natural death among young men in poverty-stricken Northeast Thailand.


 The Brugada Syndrome