COPY-COPY — ECG Blog #510 — Myocarditis or Acute MI — EXTRA COPY

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You are shown the ECG in Figure-1 — obtained from a young adult with palpitations. Is the ST elevation in the chest leads the result of an acute MI? — of myocarditis? — or is it simply a normal repolarization variant?

Figure-1: The initial ECG in today's case — obtained from a young adult with palpitations. (To improve visualization — I've digitized the original ECG using PMcardio).

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About the ST Elevation …

• For clarity in Figure-2 — RED dotted lines in leads V2-thru-V6 highlight the baseline for assessing chest lead ST elevation in this tracing.
• RED arrows highlight the J-point in leads V4,V5,V6 — which serves as the landmark for judging the amount of ST elevation.

QUESTIONS:

• Did YOU begin your interpretation of today’s initial ECG by assessing the rhythm?
• HINT: Why is assessing the rhythm important for assessing today’s rhythm?

Figure-2: XXX 

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ANSWER:

The reason it is especially important in today’s case to begin by assessing the rhythm in the long lead II rhythm strip at the bottom of the tracing — is that the shape of the P waves is changing, and the amount of ST elevation depends on the shape of the P waves preceding each beat.

• PEARL #1: Today’s case provides a prime example for why it is important to begin interpretation of every ECG you encounter — by spending an educated 2-3 seconds looking in front of each QRS complex to see if there is a P wave. 
• If so — Is the shape of each P wave the same? Is the PR interval constant?
• Depending on parameters in the settings of your ECG machine — one or more long lead rhythm strips may be displayed. I favor systems that display a long lead II — because IF upright P waves are present with a constant PR interval in front of each QRS complex, then normal sinus rhythm is present.

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Take another LOOK at the long lead II rhythm strip in Figure-2.

• QUESTION: Is sinus rhythm present in this tracing?

ANSWER:

Upright P waves with a constant PR interval are present for only 3 beats in today’s tracing. As shown in Figure-3 — beats #6,7,8 are sinus-conducted, albeit with a variable R-R interval.

Figure-3: XXXX

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Figure-4: XXXX

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Figure-5: XXXX

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Figure-6: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Armel Carmona’s ECG Rhythms website).

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Figure-7: XXXX

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Rasheed — FB Messenger (6-28.1-2025)

Rasheed Tamimi — from Sanaa, Yemen, (Sanaa being the largest city in Yemen)

Hi Dr.Ken. I. Hope you are doing well. I would like to share you this trace. I have consulted about this ECG, obtained from a 18 year male patient who presented with history of recurrent palpitation, otherwise he is stable. My opinion about ECG: It's non sinus rhythm, of ventricular rate about 92-97. There is slight irregularities in some R R interval. Narrow QRS complex, P wave of short PR interval different axis, with some gradual transition befor it take different axis completely as noted in strip rythm of lead II in bottom of ECG. My impression about this ECG: 1- it may represent wandering atrial pacemaker( we need long stripe rythm to establish it, and to confirm that p wave wander in more than 3 site) 2-AV dissociation by usurpation, as low atrial or junctional rythm usurp sinus rhythm and takeover sinus rhythm with rate of conduction greater than generated by sinus!. Iam looking forward for your great comment.. Regards Rasheed

Hi Rasheed. GREAT teaching tracing. I thought you were going to ask me about the ST elevation that VERY interestingly we see ONLY when the P wave is negative! This is the Emery phenomenon (See ECG Blog #308 — https://tinyurl.com/KG-Blog-308 ) — and for this reason, I'd love to make an ECG Blog of this case.

 

Otherwise — with a wandering pacemaker, the change in P wave morphology is more gradual than what we see here. So I'd first get an Echo (to make sure this otherwise healthy 18yo does not have underlying heart disease). Otherwise — the abrupt change to a negative P wave in lead II suggests either an ectopic atrial focus or ectopic junctional focus (ie, this looks like a "usurping" rhythm that overtakes the underlying sinus rate. We see atrial fusion beats in transition from sinus to the tachycardia). If the patient has a negative Echo, normal thyroid studies, normal CBC — I'd probably just try a beta-blocker — as his overall heart rate is fairly fast, and this may suppress the ectopic focus. You could give him a small daily dose (sometimes low dose is all that is needed) — and let him take an extra dose if the arrhythmia occurs. You could increase the beta-blocker dose if needed. If this works — great. If not — then maybe further evaluation will be needed.

 

Rasheed — May I have your permission to write up this case for an ECG Blog? If so — please tell me HOW you would like me to acknowledge you — What is your last name — or do you just want me to write my thanks from Rasheed

What city and country are you from?

 

It may be a while before I get to this case — but I'll let you know when I publish it.

 

I hope the above is helpful! — :)

 

RASHEED REPLY:

Hi, Very great and useful comments as usual. Of coures, i pleasure to post it in your great blog, You can acknowledge me; EM specialist Rasheed Tamimi Yemen, Sana'a Thanks a lot.

 

MY REPLY:

THANK YOU — It may be a while, but I'll let you know when I publish this! — :)

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Acknowledgment: My appreciation to Rasheed Tamimi (from Yemen, Sana'a) for the case and this tracing.

=======================

Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
• See ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• For more on distinction between Low Atrial vs Junctional Rhythm — Please see My Comment at the BOTTOM of the page in the January 28, 2019 post in Dr. Smith's ECG Blog.
• 
  
• See ECG Blog #290 and ECG Blog #308 — for more examples of the Emery Phenomenon.
• And for additional cases of the Emery Phenomenon — Please see My Comment at the BOTTOM of the page in the June 3, 2020 post and in the February 23, 2023 post in Dr. Smith's ECG Blog.

AI Summary:

The "Emery phenomenon" is a term for a specific type of junctional tachycardia that can occur after congenital heaart surgery, esp. in children — and is characterized by a gradual "warm-up" and "cool-down" period of the heart rate rather than an abrupt start and stop.

ORIGIN = JET (Junctional ectopic tachycardia) —esp. seen in infants and young children

RX— Fix electrolytes, ß-blocker,Amio, verap/dilt — catheter ablation if resistant to meds.

BELOW from the Feb. 23, 2023 post in SSmith!

The KEY to interpreting today’s case — is to be aware of the Emery Phenomenon. As emphasized in My Comment at the bottom of the page of the June 3, 2020 post in Dr. Smith’s ECG Blog — Almost everyone gets fooled the 1st time they see this phenomenon. Because of its potential for invoking uneeded cardiac catheterization or hospital admission — it is worth periodically reviewing this ECG pattern.

• The 1st Clue in today’s case that cardiac catheterization was probably not needed — is in the History. The patient was a previously healthy man in his 40s, who presented with intermittent epigastric abdominal pain over the past several days. While exceptions always exist — this clinical setting sounds like a lower prevalence presentation for acute coronary disease.
• The 2nd Clue — lies with determination of the rhythm. For clarity in Figure-1 — I’ve put the 2 ECGs in today’s case together. I’ve placed the initial ECG ( = ECG #1) on the BOTTOM of Figure-1. 
• Note the negative P wave in lead II of ECG #1 (BLUE arrow). In view of the normal PR interval with this negative P wave — this suggests there was a low atrial rhythm (rather than a junctional rhythm) in the patient’s initial ECG. Awareness that the presence of a negative P wave in the inferior leads (be this from a low atrial or junctional rhythm) — sets up conditions for the Emery Phenomenon, and serves as the 2nd Clue that there is likely to be some non-ischemic ST elevation.

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ECG Blog #308

https://ecg-interpretation.blogspot.com/2022/05/ecg-blog-308-funny-p-waves-acute-inf.html

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The ECG in Figure-1 was obtained from a 70-year old man with longstanding hypertension. The patient was in for his yearly check-up. He denied symptoms.

• A preliminary diagnosis of an acute inferior STEMI was made on seeing the ECG in Figure-1. Do you agree?

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:

Beginning with Rate & Rhythm — the long lead II rhythm strip shows the rhythm to be regular at ~80-85/minute. The QRS complex is narrow. A P wave is seen before each QRS complex  — but this P wave is negative in lead II. Therefore the rhythm is not sinus. Instead — this is either a low atrial rhythm — or — an accelerated junctional rhythm.

• NOTE: Despite short duration of the PR interval — this does not distinguish been a low atrial vs junctional rhythm because it is speed of conduction (rather than distance from the SA node) that determines PR interval duration.

Continuing with Interpretation of ECG #1:

• Intervals: The QRS and QTc intervals are normal.
• Chamber Enlargement: None.
• Q-R-S-T Changes: There is an isolated but large Q wave in lead III. R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4. The principal finding of concern is what appears to be ST elevation in each of the inferior leads — with what appears to be reciprocal ST depression in lead aVL. The rest of the ECG is unremarkable.

QUESTION:

• Is the ST elevation in Figure-1 a "real" finding?

ANSWER: The Emery Phenomenon

The appearance of ST elevation in the inferior leads of Figure-1 reflects the Emery Phenomenon — in which the oppositely-directed atrial repolarization wave (ie, the T of the P wave) produces a "pseudo"-ST elevation effect because of the relatively large size of the negative inferior lead P waves, with short PR interval.

• Most of the time — the Tp (also known as the "Ta" or atrial T wave) is hidden within the QRS complex. But on those uncommon occasions when a large negative P wave with short PR interval is seen in the inferior leads — the resultant oppositely-directed Tp may simulate acute inferior infarction (See My Comment in the June 3, 2020 post in Dr. Steve Smith's ECG Blog for discussion of the Emery Phenomenon in the context of a case that went to cath because of this "pseudo"-ST elevation).

To illustrate this phenomenon — I’ve adapted Figure-2, which I’ve taken from a 2015 post on the ECG Rhythms website.

• As suggested in Figure-2 — the atrial repolarization wave (ie, the T of the P wave) is always present — but with sinus rhythm, the timing of the Tp will largely coincide with the timing of the QRS complex, and therefore not be noticed on the ECG (dotted RED half circle, seen to the left in Figure-2).
• As shown in Figure-2 — the Tp will be oppositely directed to the P wave. Therefore, with normal sinus rhythm (in which by definition, the P wave will be upright in lead II) — the TP will be negative.
• IF the P wave in lead II is negative (as may occur with either a low atrial or junctional rhythm) — then the Tp will be upright (dotted RED half circle, seen to the right in Figure-1). If the Tp wave is large in size and upright — it may distort the end of the QRS complex, and produce the false impression of ST elevation.

Figure-2: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Armel Carmona’s ECG Rhythms website).

KEY Points:

• The size of the Tp wave will be proportional to the size of its P wave. A small P wave will produce a correspondingly small Tp wave. A large P wave will produce a much bigger Tp wave.
• Actually, the effect of the oppositely-directed atrial repolarization wave ( = the Tp — also known as the "Ta" or atrial T wave) will be even larger than shown above in Figure-2 — because normal duration of the Ta wave is significantly longer (up to 2-3 times longer) than normal P wave duration (Francis). This may account for an exaggerated effect on the ST segment when the P wave is large.
• That said — I preserved the same relative proportions in Figure-2 as were seen in the original version of this Figure taken from the ECG Rhythms website. Note that the PR interval for the negative P wave in Figure-2 is almost as long as the PR interval for normal sinus rhythm. But IF the PR interval for the negative P wave in lead II is much shorter (as occurs in today’s case) — then the upright Tp wave that will be seen with a low atrial rhythm will be further displaced to the right, which will produce a much greater degree of pseudo-ST-elevation!

The CASE Continues:

10 minutes later in today's case — a repeat ECG was done (Figure-3).

• What has happened in Figure-3?

Figure-3: Comparison between the initial ECG — and the repeat ECG done 10 minutes later.

ANSWER:

The repeat ECG (bottom tracing in Figure-3) — shows return of normal sinus rhythm with an upright P wave in lead II, and an overall slower heart rate than was seen in ECG #1.

• Following this return of the normal upright sinus P wave in lead II (as well as in the other inferior leads) — there is no longer any ST elevation in the inferior leads of ECG #2. In addition — the small amount of J-point ST depression that had been seen in lead aVL of ECG #1 is no longer present.
• 
  
• Since ECG #2 was obtained just 10 minutes after ECG #1, without any change in the patient's clinical condition — this resolution of inferior lead ST elevation (and of the J-point ST depression in lead aVL) — confirms that the ST elevation that had been seen in ECG #1 was not real. Instead — it was simply an effect of the Emery Phenomenon, brought about as a result of the large-amplitude negative inferior lead P waves with short PR interval that were seen in ECG #1.

KEY Point:

• Although there is no longer any ST elevation in ECG #2 — the T waves in the inferior leads still look "hypervoluminous" (ie, each of the inferior lead T waves either equal or exceed amplitude of the R wave in the same lead — and each of these T waves have a broader-than-expected base).
• In addition — despite a QRS complex in lead aVL that is not predominantly negative — the T wave in this lead is still inverted.
• 
  
• PEARL: The importance of the History can not be overstated. IF I was shown ECG #2 and told that the patient with this ECG was complaining of new-onset chest pain — I would interpret this tracing as showing hyperacute T waves in each of the inferior leads, with reciprocal change in lead aVL. My diagnosis would be acute RCA (Right Coronary Artery) occlusion until proven otherwise.
• 
  
• However, the 70-year old man in today's case was completely asymptomatic — with the reason for getting an ECG being "routine", as part of this patient's regular check-up. In view of this information — it is highly likely that nothing acute is going on in ECG #2.
• I suspect that review of this patient's medical record, looking for a previous ECG for comparison would quickly resolve all questions by showing a longstanding similar ST-T wave appearance.

Take-Home MESSAGE:

Be aware of the Emery Phenomenon! All providers whose work entails ECG interpretation will occasionally encounter patients with a low atrial or junctional rhythm (with large negative P waves and a short PR interval in the inferior leads) — that produces inferior lead ST elevation (often with reciprocal change in lead aVL) that simply is not real.

==============================

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AI Summary:

The "Emery phenomenon" is a term for a specific type of junctional tachycardia that can occur after congenital heaart surgery, esp. in children — and is characterized by a gradual "warm-up" and "cool-down" period of the heart rate rather than an abrupt start and stop.

ORIGIN = JET (Junctional ectopic tachycardia) —esp. seen in infants and young children

RX— Fix electrolytes, ß-blocker,Amio, verap/dilt — catheter ablation if resistant to meds.

BELOW from the Feb. 23, 2023 post in SSmith!

The KEY to interpreting today’s case — is to be aware of the Emery Phenomenon. As emphasized in My Comment at the bottom of the page of the June 3, 2020 post in Dr. Smith’s ECG Blog — Almost everyone gets fooled the 1st time they see this phenomenon. Because of its potential for invoking uneeded cardiac catheterization or hospital admission — it is worth periodically reviewing this ECG pattern.

• The 1st Clue in today’s case that cardiac catheterization was probably not needed — is in the History. The patient was a previously healthy man in his 40s, who presented with intermittent epigastric abdominal pain over the past several days. While exceptions always exist — this clinical setting sounds like a lower prevalence presentation for acute coronary disease.
• The 2nd Clue — lies with determination of the rhythm. For clarity in Figure-1 — I’ve put the 2 ECGs in today’s case together. I’ve placed the initial ECG ( = ECG #1) on the BOTTOM of Figure-1. 
• Note the negative P wave in lead II of ECG #1 (BLUE arrow). In view of the normal PR interval with this negative P wave — this suggests there was a low atrial rhythm (rather than a junctional rhythm) in the patient’s initial ECG. Awareness that the presence of a negative P wave in the inferior leads (be this from a low atrial or junctional rhythm) — sets up conditions for the Emery Phenomenon, and serves as the 2nd Clue that there is likely to be some non-ischemic ST elevation.

========================

ECG Blog #308

https://ecg-interpretation.blogspot.com/2022/05/ecg-blog-308-funny-p-waves-acute-inf.html

========================

The ECG in Figure-1 was obtained from a 70-year old man with longstanding hypertension. The patient was in for his yearly check-up. He denied symptoms.

• A preliminary diagnosis of an acute inferior STEMI was made on seeing the ECG in Figure-1. Do you agree?

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:

Beginning with Rate & Rhythm — the long lead II rhythm strip shows the rhythm to be regular at ~80-85/minute. The QRS complex is narrow. A P wave is seen before each QRS complex  — but this P wave is negative in lead II. Therefore the rhythm is not sinus. Instead — this is either a low atrial rhythm — or — an accelerated junctional rhythm.

• NOTE: Despite short duration of the PR interval — this does not distinguish been a low atrial vs junctional rhythm because it is speed of conduction (rather than distance from the SA node) that determines PR interval duration.

Continuing with Interpretation of ECG #1:

• Intervals: The QRS and QTc intervals are normal.
• Chamber Enlargement: None.
• Q-R-S-T Changes: There is an isolated but large Q wave in lead III. R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4. The principal finding of concern is what appears to be ST elevation in each of the inferior leads — with what appears to be reciprocal ST depression in lead aVL. The rest of the ECG is unremarkable.

QUESTION:

• Is the ST elevation in Figure-1 a "real" finding?

ANSWER: The Emery Phenomenon

The appearance of ST elevation in the inferior leads of Figure-1 reflects the Emery Phenomenon — in which the oppositely-directed atrial repolarization wave (ie, the T of the P wave) produces a "pseudo"-ST elevation effect because of the relatively large size of the negative inferior lead P waves, with short PR interval.

• Most of the time — the Tp (also known as the "Ta" or atrial T wave) is hidden within the QRS complex. But on those uncommon occasions when a large negative P wave with short PR interval is seen in the inferior leads — the resultant oppositely-directed Tp may simulate acute inferior infarction (See My Comment in the June 3, 2020 post in Dr. Steve Smith's ECG Blog for discussion of the Emery Phenomenon in the context of a case that went to cath because of this "pseudo"-ST elevation).

To illustrate this phenomenon — I’ve adapted Figure-2, which I’ve taken from a 2015 post on the ECG Rhythms website.

• As suggested in Figure-2 — the atrial repolarization wave (ie, the T of the P wave) is always present — but with sinus rhythm, the timing of the Tp will largely coincide with the timing of the QRS complex, and therefore not be noticed on the ECG (dotted RED half circle, seen to the left in Figure-2).
• As shown in Figure-2 — the Tp will be oppositely directed to the P wave. Therefore, with normal sinus rhythm (in which by definition, the P wave will be upright in lead II) — the TP will be negative.
• IF the P wave in lead II is negative (as may occur with either a low atrial or junctional rhythm) — then the Tp will be upright (dotted RED half circle, seen to the right in Figure-1). If the Tp wave is large in size and upright — it may distort the end of the QRS complex, and produce the false impression of ST elevation.

Figure-2: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Armel Carmona’s ECG Rhythms website).

KEY Points:

• The size of the Tp wave will be proportional to the size of its P wave. A small P wave will produce a correspondingly small Tp wave. A large P wave will produce a much bigger Tp wave.
• Actually, the effect of the oppositely-directed atrial repolarization wave ( = the Tp — also known as the "Ta" or atrial T wave) will be even larger than shown above in Figure-2 — because normal duration of the Ta wave is significantly longer (up to 2-3 times longer) than normal P wave duration (Francis). This may account for an exaggerated effect on the ST segment when the P wave is large.
• That said — I preserved the same relative proportions in Figure-2 as were seen in the original version of this Figure taken from the ECG Rhythms website. Note that the PR interval for the negative P wave in Figure-2 is almost as long as the PR interval for normal sinus rhythm. But IF the PR interval for the negative P wave in lead II is much shorter (as occurs in today’s case) — then the upright Tp wave that will be seen with a low atrial rhythm will be further displaced to the right, which will produce a much greater degree of pseudo-ST-elevation!

The CASE Continues:

10 minutes later in today's case — a repeat ECG was done (Figure-3).

• What has happened in Figure-3?

Figure-3: Comparison between the initial ECG — and the repeat ECG done 10 minutes later.

ANSWER:

The repeat ECG (bottom tracing in Figure-3) — shows return of normal sinus rhythm with an upright P wave in lead II, and an overall slower heart rate than was seen in ECG #1.

• Following this return of the normal upright sinus P wave in lead II (as well as in the other inferior leads) — there is no longer any ST elevation in the inferior leads of ECG #2. In addition — the small amount of J-point ST depression that had been seen in lead aVL of ECG #1 is no longer present.
• 
  
• Since ECG #2 was obtained just 10 minutes after ECG #1, without any change in the patient's clinical condition — this resolution of inferior lead ST elevation (and of the J-point ST depression in lead aVL) — confirms that the ST elevation that had been seen in ECG #1 was not real. Instead — it was simply an effect of the Emery Phenomenon, brought about as a result of the large-amplitude negative inferior lead P waves with short PR interval that were seen in ECG #1.

KEY Point:

• Although there is no longer any ST elevation in ECG #2 — the T waves in the inferior leads still look "hypervoluminous" (ie, each of the inferior lead T waves either equal or exceed amplitude of the R wave in the same lead — and each of these T waves have a broader-than-expected base).
• In addition — despite a QRS complex in lead aVL that is not predominantly negative — the T wave in this lead is still inverted.
• 
  
• PEARL: The importance of the History can not be overstated. IF I was shown ECG #2 and told that the patient with this ECG was complaining of new-onset chest pain — I would interpret this tracing as showing hyperacute T waves in each of the inferior leads, with reciprocal change in lead aVL. My diagnosis would be acute RCA (Right Coronary Artery) occlusion until proven otherwise.
• 
  
• However, the 70-year old man in today's case was completely asymptomatic — with the reason for getting an ECG being "routine", as part of this patient's regular check-up. In view of this information — it is highly likely that nothing acute is going on in ECG #2.
• I suspect that review of this patient's medical record, looking for a previous ECG for comparison would quickly resolve all questions by showing a longstanding similar ST-T wave appearance.

Take-Home MESSAGE:

Be aware of the Emery Phenomenon! All providers whose work entails ECG interpretation will occasionally encounter patients with a low atrial or junctional rhythm (with large negative P waves and a short PR interval in the inferior leads) — that produces inferior lead ST elevation (often with reciprocal change in lead aVL) that simply is not real.

COPY-ECG Blog 509- Brugada Info (12-11.21-2025)- EXTRA COPY

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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!
• Given that this 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.The management plan for this patient should include full investigation for potential precipitating factors of his cardiac arrest (including genetic testing and family history assessment). 
• Bottom Line: Given the occurrence cardiac arrest in association with the Brugada-1 pattern on ECG — an ICD (Implantable Cardioverter-Defibrillator) will almost certainly be recomended.

Follow-Up of Today's CASE: 

• It turns out that today's patient is of southeast Asian descent. As noted in the ADDENDUM below (See Figure-5) — this geographic area of the world has by far, the highest prevalence of Brugada Syndrome. 
• Work-Up of this 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: 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).

================================

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.

================================

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.

================================

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. 
• 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.

======================

What then is Brugada Syndrome?

Full discussion of Brugada Syndrome is beyond the scope of this ECG Blog. Instead — I include below selected concepts relevant to emergency providers.

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

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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. 

==================================

 

ADDENDUM (12/13/2025): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

==================

BELOW is FROM ECG Blog #238

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-238-53-what-is-phenocopy.html

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The ECG shown in Figure-1 was obtained from an elderly woman, who presented to the ED (Emergency Department) with an acute febrile illness (40°C).

• How would you interpret her initial ECG?
• Clinically — Could this be an early acute antero-septal STEMI?

 

Figure-1: ECG obtained from an elderly woman with an acute febrile illness (See text).

 

 

The Case Continues:

The ECG was repeated (Figure-2) — this time with anterior leads placed 1 interspace higher.

 

Figure-2: Repeat ECG of the tracing shown in Figure-1, with anterior leads placed 1 interspace higher (See text).

 

QUESTION:

• Do these serial tracings suggest an acute evolving anterior STEMI?

 

 

 

=======================================

NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #53 before reading My Thoughts regarding the ECGs in Figure-2. This 2-part ECG Video (9 minutes and 8 minutes) — reviews the ECG recognition and clinical significance of Brugada-1 and Brugada-2 ECG patterns + it clarifies the concept of Brugada Phenocopy.

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018).
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• For brief summary of this material — Please refer to Figures-5, -6 and -7 in the Addendum below.

My THOUGHTS on this Case:

Looking first at the ECG in Figure-1 — The rhythm is sinus — all intervals (PR, QRS, QTc) and the axis are normal — and there is no chamber enlargement.

 

Regarding Q-R-S-T Changes in Figure-1:

• There are no Q waves.
• R Wave Progression is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
• Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1, V2 and V3, with "double-hump" upward concavity in lead V3.
• ST segments are noticeably flattened in several limb leads — as well as in lateral chest leads (that also show slight ST depression).

 

My Impression of ECG #1: There is no denying the presence of anterior ST elevation with ST segment flattening and slight ST depression in other leads.

• That said — Against these ST-T wave changes in ECG #1 representing an acute cardiac event — is the clinical history of acute febrile illness in this elderly woman, with no mention in the history of associated chest pain.

 

QUESTION:

What happened in ECG #2 (bottom tracing in Figure-2)?

 

 

ANSWER:

The main difference between ECG #1 and ECG #2 is the appearance of the ST-T waves in leads V1, V2 and V3:

• The R' peak in leads V1 and V2 is higher in ECG #2, with sharp downsloping that leads into a more noticeably inverted T wave.
• The "double-hump" upward ST segment concavity that was seen in lead V2 of ECG #1 — is now seen in lead V3 of ECG #2.

 

My Impression of ECG #2: The ECG picture in Figure-2 stongly suggests we are seeing Brugada ECG patterns.

• The "double-hump" upward ST segment concavity in lead V2 of ECG #1 — is consistent with a Brugada-2 (ie, "Saddleback" ) pattern.
• The higher-rising, steeper downsloping ST-T wave appearance in leads V1 and V2 of ECG #2 — now meets criteria for a Brugada-1 ECG pattern, with a Brugada-2 pattern now seen in lead V3.
• In view of the clinical history — this is unlikely to represent an acute anteroseptal STEMI.

 

PEARL #1: It turns out that ECG #2 was repeated soon after ECG #1. This illustrates how the simple measure of placing anterior leads 1 or 2 interspaces higher on the chest may serve to bring out a Brugada ECG pattern!

 

 

The Case Continues:

The patient was treated for her acute febrile illness. Her ECG was repeated after her fever had resolved (Figure-3).

Figure-3: Repeat ECG following resolution of this patient's fever — compared to the initial ECG in this case (See text).

 

QUESTION:

Does the patient in today's case have Brugada Syndrome?

 

 

 

WHAT is Brugada Syndrome?

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 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 of age).
• PEARL #2: 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).
• PEARL #3: 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 during the past 10 years, in which I've closely followed numerous international ECG internet forums — I've seen countless cases, especially of transient Brugada ECG patterns similar to today's case. 

• Once a clinical entity is "discovered" — it begins to get noticed with increasing frequency.

 

 

Regarding BRUGADA Syndrome vs Phenocopy: 

I reference an excellent state-of-the-art Review article on Brugada Syndrome (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). I've synthesized key aspects of this article:

• A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-4).
• A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or 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 after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
• NOTE: 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 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria).
• Panel B in Figure-2 illustrates the Brugada Type-2 or "Saddleback" ECG pattern. This pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome (See Figure-4).

 

Figure-4: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (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°).

 

PEARL #4: 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.

• The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, the acute febrile illness in today’s case) may result in resolution of the Brugada-1 ECG pattern — with a much better longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD may not be needed, as it probably would be if true Brugada Syndrome was present!).
• 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.

 

==================================

Final Comment on Today's Case:

Assuming the elderly woman in today's case had otherwise been healthy (without a personal history of syncope, serious arrhythmias, seizures or nocturnal agonal respiration) — the fact that the Brugada-1 ECG pattern we initially saw completely resolved so soon after fever resolution, strongly suggests she has Brugada Phenocopy (and not Brugada Syndrome) — and that her longterm prognosis is likely to be good.

• Whether she needs to undergo a negative sodium channel-blocker challenge test at her advanced age (and what impact her family history might have at her age) — are issues for her informed consent and medical providers to decide.

 

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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.

==================================

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

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ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 thn 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).

 

Figure-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

==============================================

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 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 110/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). 
• 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 slight ST elevation seen in neighboring lead V3 reflects a continuation of the Brugada-1 pattern). This is not the ECG of acute infarction!
• Given that this 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.The management plan for this patient should include full investigation for potential precipitating factors of his cardiac arrest (including genetic testing and family history assessment). 
• Bottom Line: Given the occurrence cardiac arrest in association with the Brugada-1 pattern on ECG — an ICD (Implantable Cardioverter-Defibrillator) will almost certainly be recomended.

Follow-Up of Today's CASE: 

• Today's patient is of southeast Asian descent. As noted in the ADDENDUM below (See Figure-5) — this geographic area of the world has by far, the highest prevalence of Brugada Syndrome. 
• Work-Up of this 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: 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 I favor — and as I show in this Figure). Both Type-2 and Type-3 look similar — but a Type-3 Brugada Pattern manifests less ST elevation (less than 2 mm of J-point elevation — and less than 1 mm of ST elevation).

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What about the QT Interval in Today's ECG?

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

• Is the QTc too short? 

ANSWER: Is the QTc too short?

Among 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.

As implicit in its name, identification of SQTS depends on finding a short QTc — 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 in this situation.

• To faciliate XXXX

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• 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.

================================

For my discussion of a case — Please check out My Comment in the Sept 2, 2019 post in Dr. Smith's ECG Blog.

BEGIN HERE!

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Figure-4: Estimation of the QTc in today's case.

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BEGIN HERE !!!!!

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El Sayed et al — StatPearls, 2023

— this goes over Brugada Syndrome

https://www.ncbi.nlm.nih.gov/books/NBK519568/

Adytia and Sutanto — Current Prob in Cardiol 49(6), 2024

https://www.sciencedirect.com/science/article/abs/pii/S0146280624002056

— this goes over Brugada Syndrome vs Phenocopy

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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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MUBARAK AL-HATEMI <mubarakhatmi88@gmail.com>

— The computer says "Acute MI"—

Good Afternoon Prof. Ken. 9/25/2025 —

I send you this nice case of Brugada syndrome. This ECG belongs to a 35 years old male from southeast Asia. No past medical history witnessed cardiac arrest in the hotel , initiated CPR by security personnel for nearly 5 minutes , when EMS arrived he was in ventricular fibrillation with successful one DC shock and ROSC achieved. Fully recovered.

Plan: ICD insertion.

 

— Me to check QTc to see if this is SHORT QTc Syndrome? —

NOTE: Mubarak is from Doha, Qatar —

MY REPLY:

Hi. GREAT case that I most probably will use for an ECG Blog — THANK YOU!

I will acknowledge you and let you know when I publish this (may be a little while …).

 

QUESTION — Was cardiac cath done on this patient? If so — WHEN with respect to his cardiac arrest? (ie, Was it emergent or done after a couple of days).

 

Again — Excellent teaching case — and very fortunate for this 35yo that he had his arrest where others witnessed it and were able to promptly shock him! — : ) Ken

 

MY THOUGHTS — Note the ST elevation in V3 and ST coving in aVL — so this patient should have cardiac cath, since acute MI is one of the causes of a Brugada-1 Phenocopy!

 

REFERENCES:

Batchvarov — Eur Cardiol 9(2):82-87, 2014

https://pmc.ncbi.nlm.nih.gov/articles/PMC6159405/

 

Netsere et al — BMC Cardiovasc Dis 25, 638, 2025

https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-025-05102-y

 

Nakano and Shimizu — JACC Asia 19:2(4):412-421, 2022

https://pmc.ncbi.nlm.nih.gov/articles/PMC9627855/

SSmith — September 2, 2019 post —

https://drsmithsecgblog.com/what-is-differential-of-this-very/

==================================

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

==================================

ADDENDUM (12/13/2025): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

==================================

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

==================

BELOW is FROM ECG Blog #238

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-238-53-what-is-phenocopy.html

========================

The ECG shown in Figure-1 was obtained from an elderly woman, who presented to the ED (Emergency Department) with an acute febrile illness (40°C).

• How would you interpret her initial ECG?
• Clinically — Could this be an early acute antero-septal STEMI?

 

Figure-1: ECG obtained from an elderly woman with an acute febrile illness (See text).

 

 

The Case Continues:

The ECG was repeated (Figure-2) — this time with anterior leads placed 1 interspace higher.

 

Figure-2: Repeat ECG of the tracing shown in Figure-1, with anterior leads placed 1 interspace higher (See text).

 

QUESTION:

• Do these serial tracings suggest an acute evolving anterior STEMI?

 

 

 

=======================================

NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #53 before reading My Thoughts regarding the ECGs in Figure-2. This 2-part ECG Video (9 minutes and 8 minutes) — reviews the ECG recognition and clinical significance of Brugada-1 and Brugada-2 ECG patterns + it clarifies the concept of Brugada Phenocopy.

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018).
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• For brief summary of this material — Please refer to Figures-5, -6 and -7 in the Addendum below.

My THOUGHTS on this Case:

Looking first at the ECG in Figure-1 — The rhythm is sinus — all intervals (PR, QRS, QTc) and the axis are normal — and there is no chamber enlargement.

 

Regarding Q-R-S-T Changes in Figure-1:

• There are no Q waves.
• R Wave Progression is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
• Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1, V2 and V3, with "double-hump" upward concavity in lead V3.
• ST segments are noticeably flattened in several limb leads — as well as in lateral chest leads (that also show slight ST depression).

 

My Impression of ECG #1: There is no denying the presence of anterior ST elevation with ST segment flattening and slight ST depression in other leads.

• That said — Against these ST-T wave changes in ECG #1 representing an acute cardiac event — is the clinical history of acute febrile illness in this elderly woman, with no mention in the history of associated chest pain.

 

QUESTION:

What happened in ECG #2 (bottom tracing in Figure-2)?

 

 

ANSWER:

The main difference between ECG #1 and ECG #2 is the appearance of the ST-T waves in leads V1, V2 and V3:

• The R' peak in leads V1 and V2 is higher in ECG #2, with sharp downsloping that leads into a more noticeably inverted T wave.
• The "double-hump" upward ST segment concavity that was seen in lead V2 of ECG #1 — is now seen in lead V3 of ECG #2.

 

My Impression of ECG #2: The ECG picture in Figure-2 stongly suggests we are seeing Brugada ECG patterns.

• The "double-hump" upward ST segment concavity in lead V2 of ECG #1 — is consistent with a Brugada-2 (ie, "Saddleback" ) pattern.
• The higher-rising, steeper downsloping ST-T wave appearance in leads V1 and V2 of ECG #2 — now meets criteria for a Brugada-1 ECG pattern, with a Brugada-2 pattern now seen in lead V3.
• In view of the clinical history — this is unlikely to represent an acute anteroseptal STEMI.

 

PEARL #1: It turns out that ECG #2 was repeated soon after ECG #1. This illustrates how the simple measure of placing anterior leads 1 or 2 interspaces higher on the chest may serve to bring out a Brugada ECG pattern!

 

 

The Case Continues:

The patient was treated for her acute febrile illness. Her ECG was repeated after her fever had resolved (Figure-3).

Figure-3: Repeat ECG following resolution of this patient's fever — compared to the initial ECG in this case (See text).

 

QUESTION:

Does the patient in today's case have Brugada Syndrome?

 

 

 

WHAT is Brugada Syndrome?

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 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 of age).
• PEARL #2: 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).
• PEARL #3: 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 during the past 10 years, in which I've closely followed numerous international ECG internet forums — I've seen countless cases, especially of transient Brugada ECG patterns similar to today's case. 

• Once a clinical entity is "discovered" — it begins to get noticed with increasing frequency.

 

 

Regarding BRUGADA Syndrome vs Phenocopy: 

I reference an excellent state-of-the-art Review article on Brugada Syndrome (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). I've synthesized key aspects of this article:

• A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-4).
• A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or 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 after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
• NOTE: 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 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria).
• Panel B in Figure-2 illustrates the Brugada Type-2 or "Saddleback" ECG pattern. This pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome (See Figure-4).

 

Figure-4: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (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°).

 

PEARL #4: 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.

• The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, the acute febrile illness in today’s case) may result in resolution of the Brugada-1 ECG pattern — with a much better longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD may not be needed, as it probably would be if true Brugada Syndrome was present!).
• 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.

 

==================================

Final Comment on Today's Case:

Assuming the elderly woman in today's case had otherwise been healthy (without a personal history of syncope, serious arrhythmias, seizures or nocturnal agonal respiration) — the fact that the Brugada-1 ECG pattern we initially saw completely resolved so soon after fever resolution, strongly suggests she has Brugada Phenocopy (and not Brugada Syndrome) — and that her longterm prognosis is likely to be good.

• Whether she needs to undergo a negative sodium channel-blocker challenge test at her advanced age (and what impact her family history might have at her age) — are issues for her informed consent and medical providers to decide.

 

==================================

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

==================================

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

==================================

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 thn 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).

 

Figure-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

==================================

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

==================

BELOW is FROM ECG Blog #238

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-238-53-what-is-phenocopy.html

========================

The ECG shown in Figure-1 was obtained from an elderly woman, who presented to the ED (Emergency Department) with an acute febrile illness (40°C).

• How would you interpret her initial ECG?
• Clinically — Could this be an early acute antero-septal STEMI?

 

Figure-1: ECG obtained from an elderly woman with an acute febrile illness (See text).

 

 

The Case Continues:

The ECG was repeated (Figure-2) — this time with anterior leads placed 1 interspace higher.

 

Figure-2: Repeat ECG of the tracing shown in Figure-1, with anterior leads placed 1 interspace higher (See text).

 

QUESTION:

• Do these serial tracings suggest an acute evolving anterior STEMI?

 

 

 

=======================================

NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #53 before reading My Thoughts regarding the ECGs in Figure-2. This 2-part ECG Video (9 minutes and 8 minutes) — reviews the ECG recognition and clinical significance of Brugada-1 and Brugada-2 ECG patterns + it clarifies the concept of Brugada Phenocopy.

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018).
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• For brief summary of this material — Please refer to Figures-5, -6 and -7 in the Addendum below.

My THOUGHTS on this Case:

Looking first at the ECG in Figure-1 — The rhythm is sinus — all intervals (PR, QRS, QTc) and the axis are normal — and there is no chamber enlargement.

 

Regarding Q-R-S-T Changes in Figure-1:

• There are no Q waves.
• R Wave Progression is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
• Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1, V2 and V3, with "double-hump" upward concavity in lead V3.
• ST segments are noticeably flattened in several limb leads — as well as in lateral chest leads (that also show slight ST depression).

 

My Impression of ECG #1: There is no denying the presence of anterior ST elevation with ST segment flattening and slight ST depression in other leads.

• That said — Against these ST-T wave changes in ECG #1 representing an acute cardiac event — is the clinical history of acute febrile illness in this elderly woman, with no mention in the history of associated chest pain.

 

QUESTION:

What happened in ECG #2 (bottom tracing in Figure-2)?

 

 

ANSWER:

The main difference between ECG #1 and ECG #2 is the appearance of the ST-T waves in leads V1, V2 and V3:

• The R' peak in leads V1 and V2 is higher in ECG #2, with sharp downsloping that leads into a more noticeably inverted T wave.
• The "double-hump" upward ST segment concavity that was seen in lead V2 of ECG #1 — is now seen in lead V3 of ECG #2.

 

My Impression of ECG #2: The ECG picture in Figure-2 stongly suggests we are seeing Brugada ECG patterns.

• The "double-hump" upward ST segment concavity in lead V2 of ECG #1 — is consistent with a Brugada-2 (ie, "Saddleback" ) pattern.
• The higher-rising, steeper downsloping ST-T wave appearance in leads V1 and V2 of ECG #2 — now meets criteria for a Brugada-1 ECG pattern, with a Brugada-2 pattern now seen in lead V3.
• In view of the clinical history — this is unlikely to represent an acute anteroseptal STEMI.

 

PEARL #1: It turns out that ECG #2 was repeated soon after ECG #1. This illustrates how the simple measure of placing anterior leads 1 or 2 interspaces higher on the chest may serve to bring out a Brugada ECG pattern!

 

 

The Case Continues:

The patient was treated for her acute febrile illness. Her ECG was repeated after her fever had resolved (Figure-3).

Figure-3: Repeat ECG following resolution of this patient's fever — compared to the initial ECG in this case (See text).

 

QUESTION:

Does the patient in today's case have Brugada Syndrome?

 

 

 

WHAT is Brugada Syndrome?

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 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 of age).
• PEARL #2: 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).
• PEARL #3: 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 during the past 10 years, in which I've closely followed numerous international ECG internet forums — I've seen countless cases, especially of transient Brugada ECG patterns similar to today's case. 

• Once a clinical entity is "discovered" — it begins to get noticed with increasing frequency.

 

 

Regarding BRUGADA Syndrome vs Phenocopy: 

I reference an excellent state-of-the-art Review article on Brugada Syndrome (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). I've synthesized key aspects of this article:

• A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-4).
• A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or 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 after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
• NOTE: 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 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria).
• Panel B in Figure-2 illustrates the Brugada Type-2 or "Saddleback" ECG pattern. This pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome (See Figure-4).

 

Figure-4: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (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°).

 

PEARL #4: 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.

• The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, the acute febrile illness in today’s case) may result in resolution of the Brugada-1 ECG pattern — with a much better longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD may not be needed, as it probably would be if true Brugada Syndrome was present!).
• 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.

 

==================================

Final Comment on Today's Case:

Assuming the elderly woman in today's case had otherwise been healthy (without a personal history of syncope, serious arrhythmias, seizures or nocturnal agonal respiration) — the fact that the Brugada-1 ECG pattern we initially saw completely resolved so soon after fever resolution, strongly suggests she has Brugada Phenocopy (and not Brugada Syndrome) — and that her longterm prognosis is likely to be good.

• Whether she needs to undergo a negative sodium channel-blocker challenge test at her advanced age (and what impact her family history might have at her age) — are issues for her informed consent and medical providers to decide.

 

==================================

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

==================================

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

==================================

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 thn 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).

 

Figure-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

Adytia and Sutanto — Current Prob in Cardiol 49(6), 2024

https://www.sciencedirect.com/science/article/abs/pii/S0146280624002056

— this goes over Brugada Syndrome vs Phenocopy

Brugada syndrome (BrS) and Brugada phenocopy (BrP) are conditions that share similar electrocardiogram (ECG) patterns characterized by right bundle branch block and elevated ST segments in the right precordial leads, yet they differ fundamentally in their etiology, diagnosis, management, and prognosis. BrS is a clinical entity first described in 1992, characterized by distinctive ECG abnormalities and an increased risk of sudden cardiac death, particularly in young patients without overt structural heart disease. The hallmark of BrS is a coved-type ST elevation in the right precordial leads (V1-V3) on the ECG, often associated with episodes of ventricular tachyarrhythmias. Genetic studies have identified mutations in the SCN5A gene, which encodes the alpha subunit of the cardiac sodium channel, as a primary cause of BrS, affecting approximately 20-30 % of cases. These mutations lead to a decrease in sodium current (INa), causing imbalance in the transmembrane ion flow during the cardiac action potential, thereby predisposing individuals to arrhythmias.1 In contrast, BrP is a condition presenting with ECG patterns identical to those of BrS but resulting from various reversible external factors rather than genetic abnormalities (Fig. 1). The concept of BrP was introduced to acknowledge instances where Brugada-like ECG patterns are observed in the absence of the congenital syndrome, thereby expanding the diagnostic landscape to include acquired conditions that mimic the ECG manifestations of BrS. BrP can be triggered by a wide array of conditions, including metabolic disorders, mechanical compression, myocardial ischemia, and drug toxicity, among others. Notably, the Brugada-like ECG abnormalities in BrP are transient and resolve once the underlying condition is treated.2,3

Understanding BrP is crucial for several reasons. First, it prevents the misdiagnosis of BrS, which can lead to unnecessary treatments such as the implantation of an implantable cardioverter-defibrillator (ICD), a common and recommended treatment for BrS but not for BrP. Second, recognizing BrP prompts the search for reversible underlying conditions, which, when treated promptly, can resolve the ECG changes and prevent possible adverse outcomes. Third, it highlights the importance of a thorough clinical evaluation and tailored treatment approach based on the specific etiology of the Brugada-like ECG pattern. The distinction between BrS and BrP has significant clinical implications. While BrS requires long-term management strategies focused on the prevention of arrhythmias and sudden death, BrP calls for an etiology-specific treatment approach aimed at reversing the underlying condition. For instance, BrP can be induced by conditions such as hyperkalemia, acute myocardial infarction, pulmonary embolism, or even by mechanical compression from a mediastinal tumor, each requiring a different treatment modality.1,2 The importance of accurate diagnosis cannot be overstated. A misdiagnosis not only exposes the patient to unnecessary risk from inappropriate treatments but also delays the correct treatment for the underlying condition causing BrP. Therefore, healthcare providers need to be aware of the concept of BrP, understand its various causes, and recognize the clinical situations in which it may arise. This awareness will ensure the implementation of appropriate diagnostic evaluations and the initiation of targeted treatments, ultimately improving patient outcomes.

This article on BrP aims to provide a nuanced understanding of this condition, differentiating it from BrS through clear definitions and diagnostic criteria that reflect its unique etiology and clinical presentation. A key objective is to enumerate the diverse underlying conditions that can induce BrP, such as metabolic disturbances, mechanical compression, myocardial ischemia, and others, thereby highlighting its etiological diversity. Another primary goal is to emphasize the importance of accurate diagnosis to prevent the implementation of unnecessary treatments, such as the inappropriate use of implantable cardioverter-defibrillators, which are indicated for BrS but not for BrP. The review also aims to discuss targeted treatment strategies for BrP, focusing on addressing the reversible conditions that give rise to its manifestation and the subsequent resolution of the Brugada-like ECG pattern. Additionally, it seeks to address the prognostic implications of recognizing and effectively treating BrP, contrasting these with the genetic nature of BrS. Lastly, the review identifies gaps in current research and proposes future directions to better understand BrP, with the ultimate goal of enhancing diagnostic accuracy, refining treatment approaches, and improving patient care and outcomes. This comprehensive overview aims to arm clinicians with the necessary knowledge to accurately diagnose and manage BrP, improving patient care through tailored treatment strategies and avoiding interventions designed for BrS.

==================

XXXXXX 

Sayed et al — StatPearls, 2023

— this goes over Brugada Syndrome

https://www.ncbi.nlm.nih.gov/books/NBK519568/

Brugada syndrome is a rare but potentially life-threatening inherited disease that predisposes patients to fatal cardiac arrhythmias. The syndrome is characterized by the ECG findings of a right bundle branch block and ST-segment elevations in the right precordial leads (V1-V3). This activity outlines the evaluation and management of Brugada syndrome and explains the roles of the interprofessional team in caring for patients with patients with Brugada syndrome.

Objectives:

• Describe the etiology and epidemiology of Brugada syndrome.
• Summarize the pathophysiology of Brugada syndrome.
• Outline the typical presentation and evaluation of a patient with Brugada syndrome.
• Explain the importance of improving care coordination among the interprofessional team to improve outcomes for patients affected by Brugada syndrome.

Access free multiple choice questions on this topic.

Go to:

Introduction

Brugada syndrome is a genetic disease that predisposes patients to fatal cardiac arrhythmias. It is named after Josep and Pedro Brugada who first described it in 1992. The syndrome is characterized by the ECG findings of a right bundle branch block and ST-segment elevations in the right precordial leads (V1-V3). [1] 

Go to:

Etiology

The first genetic association with Brugada syndrome discovered was a loss-of-function mutation in the cardiac voltage-gated sodium channel gene SCN5A. It is thought to be found in 15-30% of Brugada Syndrome cases. [2] Mutations in calcium and potassium channels, associated channel proteins, and desmosomal proteins have also been linked with the disease. Brugada syndrome is inherited in an autosomal dominant pattern; however, affected individuals may demonstrate variable expressivity and reduced penetrance. Additionally, many environmental and genetic factors may influence the phenotype, including temperature, medications, electrolyte abnormalities, and cocaine.[3]

Go to:

Epidemiology

The prevalence of Brugada Syndrome is approximately 3 to 5 per 10,000 people. Brugada syndrome is approximately 8 to 10 times more common in males than females. This gender difference, however, is not found in pediatric patients. This has been hypothesized to be due to higher testosterone levels after puberty and different proportions of ionic currents based on sex. Brugada syndrome is also more prevalent in those who are of Southeast Asian descent. The mean affected age is 41 years old. Brugada syndrome accounts for 4% of all sudden cardiac deaths. [3] 

Go to:

Pathophysiology

The exact mechanism for Brugada Syndrome is not clear. There are two main physiologic hypotheses that have been suggested: the repolarization disorder and the depolarization disorder models. According to the repolarization disorder model, the decrease in sodium current secondary to the loss-of-function sodium channel mutation causes the right ventricular epicardium's action potential to have a deeper notch when compared to the action potential of the endocardium. This difference in current can lead to the typical EKG finding of Brugada syndrome and subsequent fatal arrhythmias. The depolarization disorder model, on the other hand, suggests that the EKG findings of Brugada syndrome are secondary to a delay in depolarization due to slow conduction in the right ventricular outflow tract.

Go to:

Histopathology

When Brugada syndrome was first described, it was thought to be only in structurally normal hearts. However, newer research revealed right ventricular outflow tract abnormalities, such as an increase in adipose tissue and fibrosis. These structural abnormalities support the depolarization disorder model as a possible cause of slower conduction in the right ventricular outflow tract. Nonetheless, whether these structural abnormalities account for the arrhythmias caused in Brugada syndrome or that they are the result of the disease and aging process is still a matter of debate. [4]

Go to:

History and Physical

Symptoms of Brugada syndrome range from the absence of any symptoms to sudden cardiac death. Sudden cardiac death typically occurs during sleep, possibly secondary to increased vagal tone. Approximately 80% of Brugada syndrome patients who develop ventricular tachycardia or ventricular fibrillation experience syncope. Palpitations and dizziness have also been described as possible symptoms. History of a febrile illness may be present as fever may precipitate symptoms and arrhythmias. 10 to 30% of Brugada syndrome patients will have an atrial arrhythmia, and supraventricular tachycardia is also more common in Brugada syndrome patients than the general population. However, 72% of those with Brugada syndrome will not show any symptoms, and 28% will not have a family history of sudden cardiac death.

Go to:

Evaluation

A 12-lead electrocardiogram is significant to both diagnose and decide management options of Brugada syndrome. Three different ECG patterns have been described in Brugada syndrome patients: coved ST elevations greater than 2 mm accompanied with an inverted T wave (type I), saddleback-shaped ST elevation greater than 2 mm (type II), and saddle-back shaped ST elevations less than 2 mm (type III). Additionally, patients with a normal ECG and high-risk factors may require a drug challenge test to reveal the typical ECG findings of ST elevations in the precordial leads V1 to V3. These high-risk factors that may require provocative drug testings include having a family history of Brugada syndrome, family history of sudden cardiac death, and symptoms consistent with Brugada syndrome in the setting of questionable ECG abnormalities. [3]

Class IA antiarrhythmics (such as procainamide and ajmaline) and IC antiarrhythmics (such as flecainide and propafenone), which act as sodium channel blockers, are the drugs used in the challenge test. Brugada ECG findings may also be revealed after cocaine use or tricyclic antidepressant toxicity. Electrolyte abnormalities, such as hyperkalemia and hypercalcemia have been known to reveal ST elevations in the right precordial leads.[5]

If a drug challenge test is normal in a pediatric patient, it may require repetition after the child reaches puberty, given the hormonal effects on Brugada syndrome phenotype. Another diagnostic test described to expose the ST elevations of Brugada syndrome is the full stomach test, where ECGs are obtained before and after a large meal, which causes an increase in vagal tone. Other tests that may be useful for some patients include genetic testing for SCN5A mutations and invasive electrophysiology. [3]

Go to:

Treatment / Management

An implantable cardioverter-defibrillator (ICD) is the mainstay of treatment of Brugada syndrome patients. Current recommendations are to perform ICD placement in those who survived cardiac arrest, patients with Brugada ECG abnormalities and syncope, and those who can have Brugada ECG findings on drug challenge tests. Pharmacological treatment with quinidine is also an option. There are conflicting results about using quinidine instead of ICD placement; however, quinidine is useful in Brugada syndrome patients with an ICD who experience multiple shocks and in those who have contraindications for ICD placement. Finally, radio frequency ablation of the anterior part of the right ventricular outflow tract is a new, emerging therapy with a promising prognosis for Brugada syndrome patients. Treatment of asymptomatic individuals with Brugada syndrome ECG findings is more complicated. Personalized risk-stratification is essential in providing the right management for these asymptomatic patients depending on their risk factors using a multi-disciplinary approach and with close and frequent follow-up. [6]

Go to:

Differential Diagnosis

Many of the conditions that may be mistaken for Brugada syndrome also cause syncope as a common symptom. Standard of care for evaluation of syncope is to obtain a 12-lead ECG to evaluate for many of such diseases that may resemble Brugada syndrome. These diseases include QT prolongation, Wolff-Parkinson-White syndrome, pulmonary embolism, sick sinus syndrome, early repolarization syndrome, electrolyte abnormalities, and atrial fibrillation. [3]

Go to:

Enhancing Healthcare Team Outcomes 

Brugada syndrome is not very common, but because it is associated with sudden death, it is important for healthcare workers to be aware of the ECG presentation. The disorder is best managed by an interprofessional team that includes a cardiologist, electrophysiologist and a genetic counselor. The key to diagnosis is a comprehensive medical history of syncopal attacks, chest discomfort or dizziness. Once the diagnosis is made, patients need to be educated about the potential for cardiac arrest. While an ICD is routinely implanted in these patients, it also predisposes them to device-related complications and inappropriate shocks. The actual incidence of death from Brugada syndrome is not known but may account for 3-20% of all sudden deaths in patients with structurally normal hearts. Sudden deaths tend to occur early after the fourth decade of life. The patient, family, and coworkers must be educated about the basics of CPR. Once the diagnosis of Brugada syndrome is made, genetic counseling should be offered to the family.[7][8](Level V)

==========================

BELOW is AI Summary — Should an athlete with Type-2 Brugada pattern be allowed to do sports?

An athlete with a Type-2 Brugada Pattern (BrP) 

can often play sports, especially if asymptomatic, but requires thorough, individualized risk assessment (stress tests, genetics) to rule out higher-risk Type-1 BrP, with guidelines generally allowing participation if low-risk (asymptomatic, no family history, negative electrophysiology study), but requiring ICD/restriction for syncope/cardiac arrest history, always emphasizing hydration, avoiding fever/certain drugs, and having emergency plans. 

Key Considerations for Type-2 BrP Athletes

1. Asymptomatic Status: Being symptom-free (no fainting, palpitations during exertion) is crucial for clearance.
2. Risk Stratification is Key: A cardiologist must conduct tests like exercise stress testing and potentially electrophysiology (EP) studies to differentiate low-risk Type-2 from potentially dangerous Type-1 patterns.
3. Type 2 vs. Type 1: Type-2 patterns (which often disappear with higher heart rates) are generally considered lower risk than Type-1, but a spontaneous Type-1 appearing during stress testing can indicate high risk.
4. Family History: A history of sudden cardiac death (SCD) in the family raises the risk significantly.
5. American Heart Association/ESC Guidelines: Allow competitive sports for asymptomatic individuals with Type 2/3 patterns, provided no other risk factors exist. 

When Sports May Be Allowed (Low-Risk Profile)

• Asymptomatic athlete.
• Type 2 or 3 pattern on ECG.
• No personal history of fainting (syncope) or cardiac arrest.
• No family history of SCD.
• Negative or inconclusive EP study (if performed). 

When Sports May Be Restricted (High-Risk Profile)

• History of syncope or cardiac arrest.
• Spontaneous Type-1 pattern.
• Presence of other risk factors or a positive EP study. 

Essential Safety Measures for All BrS Athletes

• Avoid Triggers: Stay hydrated, avoid fever, and stay cool during exercise.
• Medication Avoidance: Know and avoid drugs that can trigger BrS (refer to resources like BrugadaDrugs.org).
• Emergency Plan: Have an Automated External Defibrillator (AED) accessible and an emergency action plan in place with team officials

===========================

BELOW — CITE this GREAT AJC article !!!!

Sciarra et al — Am J Cardiol 244:9-17, 2025

https://www.ajconline.org/article/S0002-9149(25)00114-6/fulltext

Brugada syndrome (BrS) is a genetic disorder marked by a characteristic electrocardiogram (ECG) pattern of ST-segment elevation and T-wave inversion in right precordial leads, which is associated with an increased risk of ventricular fibrillation in the absence of structural heart disease. Despite advancements in understanding its epidemiology, pathophysiology, and treatment, there is considerable variability in how sports cardiologists approach BrS. This expert opinion by the Italian Society of Sports Cardiology (SICSPORT) aim to review the current definition, diagnosis, epidemiology, genetics, risk stratification, and treatment of BrS and provide guidance for sport eligibility provides guidance for sports doctors and cardiologists in assessing competitive sports eligibility in athletes with BrS. A multiparametric approach to diagnosis and risk stratification is recommended, noting that the presence of a Brugada ECG pattern (BrP) does not confirm a BrS diagnosis. The risk of sudden cardiac death (SCD) is low in asymptomatic individuals with type 1 BrP, especially those with a drug-induced pattern. Pharmacological testing is not required for type 2 or 3 patterns without other risk factors. Low-risk individuals do not require therapy, while intermediate or high-risk patients may need pharmacological treatment, ICD implantation, or ablation. Asymptomatic individuals with type 2 or 3 BrP, no family history of SCD, and no other risk factors may be eligible for competitive sports, as well as asymptomatic type 1 BrP without risk factors and negative electrophysiological study. Conversely, sports eligibility should be denied in patients with BrS who have a history of syncope or cardiac arrest (high-risk subjects), regardless of ICD presence.

KEY POINT: The presence of a Type 2/3 BrP is not diagnostic alone for BrS and it has been described as highly prevalent as 12% in the athletic population, especially in endurance athletes, partially linked to the extreme exercise-induced right ventricular (RV) enlargement.¹⁹ Common features for BrP and early repolarization are the male prevalence, vagal influence and normalization with quinidine. Moreover, improper recording of the ECG with high pass filtering and high placement of the precordial lead can cause a rSr' pattern, but not a baseline Type 1 BrP, in athletes and in the general population.²⁰Misplaced leads can generate the need of additional exams and unnecessary sport restriction, especially in tall endurance athletes.

Genetic testing for Brugada syndrome (BrS) is currently recommended in subjects with (1) spontaneous or (2) pharmacologically induced type I pattern, in association with clinical features (such as polymorphic ventricular tachycardia, ventricular fibrillation, arrhythmic syncope) or family history, to support the diagnosis.1 It should be requested by a cardiologist or a physician with specific knowledge in BrS, particularly after excluding phenocopies and known confounding factors.²¹

=================

XXXXXXX

Figure-1: The initial ECG in today's case — obtained from a patient XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

XXXXXXX 

El Sayed et al — StatPearls, 2023

— this goes over Brugada Syndrome

https://www.ncbi.nlm.nih.gov/books/NBK519568/

Adytia and Sutanto — Current Prob in Cardiol 49(6), 2024

https://www.sciencedirect.com/science/article/abs/pii/S0146280624002056

— this goes over Brugada Syndrome vs Phenocopy

XXXXXX

Figure-2: XXX

XXXXXXX

 

Figure-3: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (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: 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 I favor — and as I show in this Figure). Both Type-2 and Type-3 look similar — but a Type-3 Brugada Pattern manifests less ST elevation (less than 2 mm of J-point elevation — and less than 1 mm of ST elevation).

XXXXXXX 

Figure-4: Estimation of the QTc in today's case.

What is the "Short QT Syndrome" ?

A nice review by Rudic et al of Short QT Syndrome (SQTS) appears in Arrhythm Electrophysiol Rev 3(2):76-79, 2014. For my discussion of a case — Please check out My Comment in the Sept 2, 2019 post in Dr. Smith's ECG Blog.

• As emphasized in this article — 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 is a relatively new diagnosis that 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 (implantable cardioverter defibrillator).

================================

• 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.

================================

XXXXX

================================

MUBARAK AL-HATEMI <mubarakhatmi88@gmail.com>

— The computer says "Acute MI"—

Good Afternoon Prof. Ken. 9/25/2025 —

I send you this nice case of Brugada syndrome. This ECG belongs to a 35 years old male from southeast Asia. No past medical history witnessed cardiac arrest in the hotel , initiated CPR by security personnel for nearly 5 minutes , when EMS arrived he was in ventricular fibrillation with successful one DC shock and ROSC achieved. Fully recovered.

Plan: ICD insertion.

 

— Me to check QTc to see if this is SHORT QTc Syndrome? —

NOTE: Mubarak is from Doha, Qatar —

MY REPLY:

Hi. GREAT case that I most probably will use for an ECG Blog — THANK YOU!

I will acknowledge you and let you know when I publish this (may be a little while …).

 

QUESTION — Was cardiac cath done on this patient? If so — WHEN with respect to his cardiac arrest? (ie, Was it emergent or done after a couple of days).

 

Again — Excellent teaching case — and very fortunate for this 35yo that he had his arrest where others witnessed it and were able to promptly shock him! — : ) Ken

 

MY THOUGHTS — Note the ST elevation in V3 and ST coving in aVL — so this patient should have cardiac cath, since acute MI is one of the causes of a Brugada-1 Phenocopy!

 

REFERENCES:

Batchvarov — Eur Cardiol 9(2):82-87, 2014

https://pmc.ncbi.nlm.nih.gov/articles/PMC6159405/

 

Netsere et al — BMC Cardiovasc Dis 25, 638, 2025

https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-025-05102-y

 

Nakano and Shimizu — JACC Asia 19:2(4):412-421, 2022

https://pmc.ncbi.nlm.nih.gov/articles/PMC9627855/

SSmith — September 2, 2019 post —

https://drsmithsecgblog.com/what-is-differential-of-this-very/

==================================

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

==================================

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

==================================

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

Figure-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

==================

BELOW is FROM ECG Blog #238

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-238-53-what-is-phenocopy.html

========================

The ECG shown in Figure-1 was obtained from an elderly woman, who presented to the ED (Emergency Department) with an acute febrile illness (40°C).

• How would you interpret her initial ECG?
• Clinically — Could this be an early acute antero-septal STEMI?

 

Figure-1: ECG obtained from an elderly woman with an acute febrile illness (See text).

 

 

The Case Continues:

The ECG was repeated (Figure-2) — this time with anterior leads placed 1 interspace higher.

 

Figure-2: Repeat ECG of the tracing shown in Figure-1, with anterior leads placed 1 interspace higher (See text).

 

QUESTION:

• Do these serial tracings suggest an acute evolving anterior STEMI?

 

 

 

=======================================

NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #53 before reading My Thoughts regarding the ECGs in Figure-2. This 2-part ECG Video (9 minutes and 8 minutes) — reviews the ECG recognition and clinical significance of Brugada-1 and Brugada-2 ECG patterns + it clarifies the concept of Brugada Phenocopy.

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018).
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• For brief summary of this material — Please refer to Figures-5, -6 and -7 in the Addendum below.

=======================================

In Part 1 of today's ECG Media Pearl #53 (9:00 minutes Video) — the essentials of Brugada Syndrome are reviewed.

Int Part 2 of today's ECG Media Pearl #53 (8:00 minutes Video) — these essentials are applied clinically.

My THOUGHTS on this Case:

Looking first at the ECG in Figure-1 — The rhythm is sinus — all intervals (PR, QRS, QTc) and the axis are normal — and there is no chamber enlargement.

 

Regarding Q-R-S-T Changes in Figure-1:

• There are no Q waves.
• R Wave Progression is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
• Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1, V2 and V3, with "double-hump" upward concavity in lead V3.
• ST segments are noticeably flattened in several limb leads — as well as in lateral chest leads (that also show slight ST depression).

 

My Impression of ECG #1: There is no denying the presence of anterior ST elevation with ST segment flattening and slight ST depression in other leads.

• That said — Against these ST-T wave changes in ECG #1 representing an acute cardiac event — is the clinical history of acute febrile illness in this elderly woman, with no mention in the history of associated chest pain.

 

QUESTION:

What happened in ECG #2 (bottom tracing in Figure-2)?

 

 

ANSWER:

The main difference between ECG #1 and ECG #2 is the appearance of the ST-T waves in leads V1, V2 and V3:

• The R' peak in leads V1 and V2 is higher in ECG #2, with sharp downsloping that leads into a more noticeably inverted T wave.
• The "double-hump" upward ST segment concavity that was seen in lead V2 of ECG #1 — is now seen in lead V3 of ECG #2.

 

My Impression of ECG #2: The ECG picture in Figure-2 stongly suggests we are seeing Brugada ECG patterns.

• The "double-hump" upward ST segment concavity in lead V2 of ECG #1 — is consistent with a Brugada-2 (ie, "Saddleback" ) pattern.
• The higher-rising, steeper downsloping ST-T wave appearance in leads V1 and V2 of ECG #2 — now meets criteria for a Brugada-1 ECG pattern, with a Brugada-2 pattern now seen in lead V3.
• In view of the clinical history — this is unlikely to represent an acute anteroseptal STEMI.

 

PEARL #1: It turns out that ECG #2 was repeated soon after ECG #1. This illustrates how the simple measure of placing anterior leads 1 or 2 interspaces higher on the chest may serve to bring out a Brugada ECG pattern!

 

 

The Case Continues:

The patient was treated for her acute febrile illness. Her ECG was repeated after her fever had resolved (Figure-3).

Figure-3: Repeat ECG following resolution of this patient's fever — compared to the initial ECG in this case (See text).

 

QUESTION:

Does the patient in today's case have Brugada Syndrome?

 

 

 

WHAT is Brugada Syndrome?

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 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 of age).
• PEARL #2: 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).
• PEARL #3: 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 during the past 10 years, in which I've closely followed numerous international ECG internet forums — I've seen countless cases, especially of transient Brugada ECG patterns similar to today's case. 

• Once a clinical entity is "discovered" — it begins to get noticed with increasing frequency.

 

 

Regarding BRUGADA Syndrome vs Phenocopy: 

I reference an excellent state-of-the-art Review article on Brugada Syndrome (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). I've synthesized key aspects of this article:

• A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-4).
• A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or 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 after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
• NOTE: 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 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria).
• Panel B in Figure-2 illustrates the Brugada Type-2 or "Saddleback" ECG pattern. This pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome (See Figure-4).

 

Figure-4: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (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°).

 

PEARL #4: 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.

• The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, the acute febrile illness in today’s case) may result in resolution of the Brugada-1 ECG pattern — with a much better longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD may not be needed, as it probably would be if true Brugada Syndrome was present!).
• 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.

 

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Final Comment on Today's Case:

Assuming the elderly woman in today's case had otherwise been healthy (without a personal history of syncope, serious arrhythmias, seizures or nocturnal agonal respiration) — the fact that the Brugada-1 ECG pattern we initially saw completely resolved so soon after fever resolution, strongly suggests she has Brugada Phenocopy (and not Brugada Syndrome) — and that her longterm prognosis is likely to be good.

• Whether she needs to undergo a negative sodium channel-blocker challenge test at her advanced age (and what impact her family history might have at her age) — are issues for her informed consent and medical providers to decide.

 

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.

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References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

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ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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).

 

Figure-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).