ECG Blog #509 — The Computer Says, "Acute MI"

A 35-year old man had a witnessed cardiac arrest in a hotel. 

• EMS was called — and bystander CPR was promptly started. 
• VFib (Ventricular Fibrillation) was documented on arrival by the paramedic team. DC countershock was delivered — with ROSC (Return Of Spontaneous Circulation) and return of the patient to full consciousness.
• The ECG in Figure-1 was obtained following ROSC.

QUESTION:

• How would you interpret the ECG in Figure-1?
• Should the cath lab be activated?

Figure-1: The initial ECG in today's case — obtained following ROSC from witnessed cardiac arrest. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's CASE:

The "good news" about today's case — is that this previously healthy 35-year old man had a witnessed cardiac arrest at a site where bystander CPR was immediately started — and timely defibrillation by emergency responders resulted in restoration of a normal rhythm with full recovery and intact neurological status.

• The post-ROSC ECG shown in Figure-1 shows sinus tachycardia at 115/minute with a narrow QRS complex rhythm.
• My "eye" was immediately drawn to leads V1,V2 (within the RED rectangle in Figure-2). The marked ST elevation in these leads, with downsloping ST segment into terminal T wave inversion — is diagnostic of a Brugada-1 ECG pattern (See Figure-3 below).
• ST segment straightening, with a somewhat limited amount of ST elevation is seen in neighboring lead V3 (hard to define the J-point in this lead for judging the amount of ST elevation). 
• The remainder of this ECG is nonspecific, and surprisingly unremarkable. Small, narrow (and probably insignificant) q waves are seen in the inferior leads. ST segment coving is seen in lead aVL — and minimal J-point depression with an upsloping ST segment is seen in leads V5,V6.

Impression of ECG #1: 

• Sinus tachycardia. 
• Brugada-1 ECG pattern in the anterior leads. (I suspect the ST segment straightening with some ST elevation that is seen in neighboring lead V3 reflects a continuation of the Brugada-1 pattern). 
• This is not the ECG of acute infarction! (Apart than leads V1,V2 that fit perfectly with the Brugada-1 pattern illustrated in Figure-3 — other leads are nonspecific and non-diagnostic for acute MI).
• This is not the ECG of RBBB! (Not only is the QRS not wide enough — but terminal S waves that are wide in lateral leads are missing — and especially because QRS morphology in leads V1,V2 is so typical for the Brugada-1 pattern illustrated in Figure-3).
• Given that today's patient is now fully alert (and that there is no history of chest pain) — there is no indication for immediate activation of the cath lab. Instead, the management plan for this patient who at this moment is completely stable — should include full investigation for potential precipitating factors of his arrest (including genetic testing and family history assessment).
• Bottom Line: Given the occurrence cardiac arrest in association with a Brugada-1 pattern on ECG — an ICD (Implantable Cardioverter-Defibrillator) will almost certainly be recomended.

Follow-Up of Today's CASE: 

• Today's patient turns out to be of southeast Asian descent. As noted in the ADDENDUM below (See Figure-6) — this geographic area of the world has by far, the highest prevalence of Brugada Syndrome. 
• Work-Up of today's patient was negative (including normal CT angiography and normal cardiac MRI).
• An ICD was implanted — and the patient was discharged in excellent condition.

Figure-2: The ST-T wave appearance in leads V1,V2 is diagnostic of a Brugada-1 ECG pattern.  

 

Figure-3: Review of ECG Patterns in Brugada Syndrome (adapted from Brugada et al — in JACC 72(9):1046-1059, 2018) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. 
(B) Brugada-2 ECG pattern ( = the “Saddleback” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave.
(C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: The ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum R’ rise point — the base of the triangle formed is ≥4 mm — as this ensures a ß-angle ≥58°).
= = = = = = = = = = = =
NOTE #1: Traditionally there have be 3 ECG Brugada patterns described. Newer criteria sometimes "combine" Type-2 and Type-3 into a single "Saddleback" classification for simplicity (which is the classification I favor — and which I show in this Figure). ST-T wave morphology looks similar for Type-2 and Type-3 patterns — but Type-3 Brugada manifests less ST elevation than Type-2 ( = less than 2 mm of J-point elevation — and less than 1 mm of ST elevation).
KEY Point: A Brugada-2 (Saddleback) pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome.
= = = = = = = = = = = =
NOTE #2: A Brugada-1 pattern may either be observed spontaneously (with leads V1, V2 positioned normally — or — positioned 1 or 2 interspaces higher than usual) — or — a Brugada-1 pattern may be observed as a response to provocative drug testing (ie, after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide).
= = = = = = = = = = = =
NOTE #3: In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — such that the only thing needed at present to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria as long as there is no reversible cause of the Brugada-1 ECG, as would be the case with Phenocopy [which we describe a little bit further below]).

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What about the QT Interval?

Take another LOOK at the QT interval in Figure-2.

• Is the QTc too short? 

ANSWER: Is the QTc too short?

Among the potential precipitating etiologies for cardiac arrest in a previously healthy man — is the Short QT Syndrome (SQTS).

• As discussed in the review by Rudic et al (Arrhythm Electrophysiol Rev 3(2):76-79, 2014) — SQTS is an inherited cardiac channelopathy determined by the presence of symptoms (syncope, cardiac arrest), positive family history, and the ECG finding of an abnormally short QTc interval.
• SQTS has only been recognized as a distinct clinical entity since 2000. The disorder is rare — but its importance is as a potential cause of atrial and ventricular arrhythmias, including cardiac arrest. Treatment is by ICD.

NOTE #1: As implied by its name, identification of SQTS depends on finding a short QTc interval — which at times is easier said than done. This is especially true in a symptomatic patient when the heart rate in available ECGs is rapid — because formulas for estimating the QTc (QT interval corrected for rate) are less accurate when the rate is fast.

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What are minimum norms for the QTc?

• Males with a QTc ≤330 msec. (and females with a QTc ≤340 msec.) — are defined as having SQTS, even if they are asymptomatic.
• Males with a QTc ≤360 msec. (and females with a QTc ≤370 msec.) — are said to have a “short” QTc. Such patients may have SQTS if, in addition to the “short” QTc there is a history of cardiac arrest, unexplained syncope or atrial fibrillation at an early age.

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What is the QTc in Today's Case?

To facilitate estimation of the QTc interval at different heart rates — We've added a QTc Calculator in the menu of Tabs that can be found on the top of every page in this ECG Blog.

• In Figure-4 — I show the values instantly arrived at by our QTc Calculator once you plug in the heart rate (115/minute in today's case) — and once you add in the longest QT that you measure (which is 280 msec. in lead V5).
• As is typically seen — there is some variation in measurements by each of the 5 well-known and established formulas for QTc calculation (ie, Some of these formulas perform better at faster or slower heart rates). 
• Whereas in Figure-4 — None of the 5 formulas for QTc calculation come up with an estimated QTc ≤330 msec — both the Fridericia and Framingham methods come up with values below the <360 msec. cutoff for a QTc that is "short" (ie, 348 and 354 msec., respectively).
• Bottom Line: The QTc in today's case is shorter than usual — but is not short enough to qualify as SQTS (keeping in mind the range of QTc values calculated by the different methods — and, that accuracy by any method for QTc estimation is less precise as the heart rate becomes faster).
• P.S.: For discussion of a case of SQTS — Check out My Comment in the Sept 2, 2019 post in Dr. Smith's ECG Blog.

Figure-4: Estimation of the QTc in today's case. 
The GREEN arrow shows where to find my QTc Calculator in the TOP Menu of every page in this ECG Blog.
The lower RIGHT panel shows the values for ECG #1 (given the heart rate = 115/min. — and the measured QT = 280 msec.). Note the range for estimated QTc values (from 348 msec. to 388 msec.) — depending on which of the 5 most commonly used formulas is used.

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What then is Brugada Syndrome?

Full discussion of Brugada Syndrome is beyond the scope of this ECG Blog. Instead — I consider the basics regarding a number of selected concepts relevant to emergency providers.

• Among references I've used in my synthesis are: 
• El Sayed et al (StatPearls, 2023).
• Adytia & Sutanto (Current Prob Cardiol 49(6), 2024). 
• Batchvarov (Eur Cardiol 9(2):82-87, 2014). 
• Netsere et al (BMC Cardiovasc Dis 25, 638, 2025).  
• Nakano, Shimizu (JACC Asia 19:2(4):412-421, 2022).

First described in 1992 — the Brugada Syndrome is important to recognize because of an associated very high risk of sudden death in otherwise healthy young or middle-aged adults who in most cases have structurally normal hearts.

• The prevalence of Brugada Syndrome in the general population is ~1/2,000. The syndrome has become a leading cause of sudden death in young adults (under 40 years old).
• Brugada Syndrome is much more common in Southeast Asia compared to the rest of the world. When considering the possibility of this syndrome — demographics of the patient are important! (See Figure-6 in the Addendum below).
• Although the genetics of Brugada Syndrome are complicated — the gender of the patient is also important. There is a distinct male predominance to this syndrome.

Personal Reflection: I never learned about Brugada Syndrome in medical school (the syndrome had not yet been described). But especially in recent years, in which I've closely followed numerous international ECG internet forums — I've seen countless examples of the Brugada ECG patterns shown above in Figure-3.

• Clinical Irony: Once a medical entity is "discovered" — it begins to get noticed with increasing frequency (such that I always wonder how "common" it was before finally being recognized in the medical literature).

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What is PHENOCOPY? 

A number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. A partial list includes the following:

• Certain drugs (antiarrhythmics; calcium channel blockers; ß-blockers; antianginals; psychotropic medications; alcohol; cocaine; other drugs).
• Acute febrile illness.
• Variations in autonomic tone.
• Hypothermia.
• Electrolyte imbalance (hypokalemia; hyperkalemia).
• Ischemia/infarction.
• Cardioversion/defibrillation.
• Bradycardia. 

 

KEY Point: Development of a Brugada-1 or Brugada-2 ECG pattern as a result of one or more of the above factors — with resolution of this Brugada ECG pattern after correction of the precipitating factor(s) — is known as Brugada Phenocopy.

• By far, the most common clinical situations I've encountered that are prone to induce Brugada Phenocopy are acute febrile illness and hyperkalemia (Acute ischemia, infarction and cardiac arrest are also common causes of Phenocopy — which is why it was important in today's case to make sure that the reason for this patient's Brugada-1 pattern was not underlying coronary disease).
• KEY Point: The importance of being aware of Phenocopy — is that correction of the underlying condition may result in resolution of the Brugada-1 ECG pattern — with usually an excellent longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD is unlikely to be needed — as it would be with true Brugada Syndrome).
• NOTE: To ensure a diagnosis of Brugada Phenocopy — the patient should have: i) A negative family history of sudden death; ii) Lack of a Brugada-1 ECG pattern in 1st-degree relatives; iii) No history of syncope, serous arrhythmias, seizures or nocturnal agonal respiration; and, iv) A negative sodium channel-blocker challenge test.
• P.S.: For more on Brugada Phenocopy with links to clinical case examples — Please scroll down to the bottom of the page for My Comment in the January 13, 2025 post in Dr. Smith's ECG Blog.

 

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Regarding the Need for Genetic Study: 

The reason for genetic study of patients suspected of having Brugada Syndrome — is the finding that certain gene mutations (the most common of which is the SCN5A gene) — may be responsible for altering transmembrane ion flow in a way that predisposes to malignant cardiac arrhythmias. This is in contrast to Phenocopy — in which there is no congenital abnormality — but instead a triggering condition (ie, fever, hyperkalemia) that if successfully treated, usually results in resolution of the Brugada-like ECG pattern without longterm predisposure to malignant ventricular arrhythmias.

• A positive genetic study in a patient with a Brugada-1 ECG pattern — makes the diagnosis of Brugada Syndrome!
• A negative genetic study however, does not rule out the possibility of Brugada Syndrome (since many patients do not have an identifiable gene pattern).

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Should an Athlete with a Type-2 Brugada Pattern play Sports? 

Clearly beyond the scope of this ECG Blog is the question of what to do when "routine" ECG screening of high school, college and/or professional athletes results in the incidental finding of a Brugada-2 (or Brugada-3) ECG pattern?

• Much (most) of the time — these highly conditioned, asymptomatic athletes can be allowed to safely participate in rigorous athletic activity — BUT — they should first be carefully assessed by clinicians experienced in the field to rule out increased risk. 
• Editorial Note: As primary care faculty responsible for interpreting the ECGs of 30+ medical providers — I was happy to send these occasional abnormal screening ECGs to my friendly cardiologists for their final decision.
• KEY Considerations: For clearance to actively participate in sports activities — the individual must be completely asymptomatic (ie, No syncope, presyncope, palpitations during exercise) — and have a negative family history. 
• Assessment Tools: Commonly used assessment tools may include provocative pharmacologic stress testing (to see if this induces a Brugada-1 pattern with exercise) — genetic testing — as well as testing to rule out underlying structural heart disease (consideration of Echo, cardiac MRI, etc.).

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Doha, Qatar) for making me aware of this case and allowing me to use this tracing. 

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ADDENDUM (12/13/2025): Some extra material ...

 

 

Figure-5: 2-page Summary of the essentials of Brugada Syndrome (from my ECG-2014-ePub).

 

Figure-6: World prevalence map of Brugada Syndrome. The overall worldwide prevalence of Brugada Syndrome is ~0.5/1,000 in the population. This prevalence is highest in Southeast Asia (at least 5 times more common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence than the worldwide average. Brugada-2 patterns (ie, "Saddleback") are also much more prevalent in Southeast Asia than elsewhere in the world. (Excerpted from Vutthikraivit et al: Acta Cardiol Sin 34:267-277, 2018).