Friday, November 28, 2025

EXTRA COPY- Blog #508 — Tall, Pointed T Waves- EXTRA COPY


The ECG in Figure-1 was obtained from a middle-aged man who presented to the ED (Emergency Department) with severe, new-onset CP (Chest Pain).
  • BP = 130/90 mm Hg.
  • Initial hs-Troponin was normal.

QUESTIONS:
  • How would you interpret this ECG?
    • Should you activate the cath lab?



Figure-1: The initial ECG in today's case — obtained from a patient with new chest pain.


My Thoughts on This CASE:
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Figure-2: XXXX





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Figure-3: XXXX


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==================================
Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.
================================== 

Related ECG Blog Posts to Today’s Case:
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 

  • ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
  • ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
  • ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
  • ECG Blog #461 — Another example of the differential diagnosis between LVH vs acute anterior MI vs LV aneurysm.
  • ECG Blog #380 and Blog #482 — on Precordial "Swirl".
  •  
  • For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020  March 31, 2019  March 29, 2019 — and the December 27, 2018 post.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 



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


ADDENDUM (11/15/2025):
  • For More Material — regarding the ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).


Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.


  • In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion)NOTE: The timed-contents of this Podcast #2 facilitate quickly finding whatever key concepts you wish to review.
  • Check out near the top of the "My ECG Videos" page, those videos from my MedAll ECG Talks that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).

  • Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.
  • As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
  • BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlierwas clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
  • The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.

  • KEY Clinical Reality: Many of the acute coronary occlusions that we see never develop ST elevatio(or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.





陳俊宏 drumbeater1978@gmail.com

Tall, Pointed T Waves

 

Dear Dr. Grauer — I hope this message finds you well. I am writing to seek your expert opinion on a clinical case that presented some diagnostic uncertainty regarding ECG interpretation.

Case summary:
A 54-year-old male presented to our emergency department with acute chest pain and cold sweating starting at 6:00 AM. Vital signs on arrival: BP 129/92 mmHg, HR 49 bpm, RR 22/min, BT 34.2°C. Initial high-sensitivity troponin I was 0.0023 ng/mL.

The ECG was interpreted as possibly showing hyperacute T waves, prompting emergent coronary angiography for suspected STEMI. The angiographic findings revealed:

  • LM: normal
  • LAD: middle LAD atherosclerosis with severe coronary spasm and TIMI 0 flow, which improved after intracoronary nitroglycerin; IVUS showed mild atherosclerosis without significant stenosis (final TIMI 3 flow)
  • LCX/RCA: normal or mild atherosclerosis
  • SYNTAX score: 0

Final diagnosis: coronary spasm with insignificant CAD; managed medically.

Given these findings, I wonder whether the initial ECG changes should instead be interpreted as early repolarization rather than true hyperacute T waves of STEMI.

If possible, I would be most grateful for your thoughts on this ECG pattern — specifically how to distinguish hyperacute T waves from early repolarization in such cases where troponin is normal and angiography reveals no significant obstruction.

initially EKG

Thank you very much for your time and teaching. Your educational work on ECG interpretation has been invaluable to clinicians like me.

Warm regards,
Chun-Hung Chen, MD

MY REPLY: 

Hi. Fascinating case. I’m attaching a 2018 article on Coronary Spasm — that I find helpful. I remember the 1980’s when Carl Pepine was studying coronary spasm at the University of Florida (which is the institution where I taught for 30 years). Coronary spasm is not that common — but is still problematic …

 

So your investigations PROVE this patient has coronary spasm with minimal underlying coronary disease.

 

I really wonder what a TRUE BASELINE ECG on this patient looks like? I see little difference between the 8:13 vs 10:37 tracings that you sent me. These ECGs are totally consistent with coronary spasm (diffuse ST elevation and very hyperacute looking T waves,  but without localization and without any reciprocal ST depression!).

 

Can you get that ECG after IV NTG relieved symptoms ???

 

Can you get a true baseline ECG?

 

I would never call this ECG “normal”. I suspect this patient may have a “baseline” ECG that still shows ST elevation and peaked T waves — but I doubt his true “baseline” ECG will look like this.

 

So “early repolarization” (or a “repolarization variant” ) is a diagnosis of exclusion, after you rule out underlying disease (and rule out ongoing coronary spasm). I do not believe we yet have a “true baseline” ECG on this patient.

 

KEY POINTS:

— Is this patient a smoker ????? If so — absolutely EVERY cigarette must be stopped!

— I would make a copy of this patient’s ECG — and either a paper copy or scanned for his smart phone, I’d suggest that he carry this along with him so that if ever he has to go to an emergency department — he can show this ECG to medical providers.

 

IF you can find a true “baseline” for this patient — or if you can find his ECG after the IV NTG relieved symptoms — then I’d love to make an ECG Blog on this case.

 

I hope the above (and the attached article) are helpful!

 

BEST — :) Ken

 

CHEN REPLY:

Dear Dr. Grauer, Thank you very much for your detailed and insightful reply — it’s truly an honor to receive your comments.

Regarding your questions:

1.    Unfortunately, there is no previous (baseline) ECG available for this patient.

2.    The patient was sent directly for coronary angiography immediately after the initial ECG, so we did not obtain an ECG after IV nitroglycerin relief at that time.

3.    However, we did record a third ECG after the catheterization, which is attached as the third tracing in the file.

In addition, follow-up laboratory data showed a significant rise in cardiac biomarkers:

·       At 6 hours after symptom onset, hs-Troponin-I was 6.2373 ng/mL (abnormal ≥ 0.0875; reference ≤ 0.0175).

·       At 12 hours, hs-Troponin-I increased to 66.1647 ng/mL (abnormal ≥ 0.0875; reference ≤ 0.0175).

Thank you again for your generous guidance and for sharing the 2018 article on coronary spasm — it was very helpful. I will continue to follow up with this patient and will send you any further ECGs if available.

Warm regards — Chun-Hung Chen, MD

MY REPLY:

Thanks for the followup. I think i will write this case up! As usual - I will acknowledge you, and let you know when i publish it! Thank you! — : ) Ken

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

Me to write Chun back — there IS a difference between ECG-1 and -2 !!!! ECG-2 looks more benign, less symmetric — so more like early repol! Wish we had an ECG right after IV NTG and wish we had a baseline ECG !!!!

SSmith — Hyperacute T waves are more symmetric. The T waves of early repol have a slower upstroke than downstroke, and thus more cocavity!



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Thursday, November 20, 2025

COPY of ECG Blog #509 — Computer said, "Acute MI" - COPY of 599

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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 


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 (TOPthe ß-angleBOTTOMA 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°).


XXXXXXX



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

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/



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

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 deepoccurring normally between leads V3-to-V4.
  • Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1V2 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:

  • 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 (TOPthe ß-angleBOTTOMA 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; andiv) 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 유영준 (from Seoul, Korea) 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).