ECG Blog #522 — What is the "Other" Diagnosis?

The ECG in Figure-1 is from a middle-aged man who presented to the ED with new-onset severe CP (Chest Pain). His symptoms lasted ~30 minutes — but his CP had totally resolved by the time this ECG was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from middle-aged man with new CP. His CP had resolved by the time this ECG was recorded (To improve visualization — I've digitized the original ECG using PMcardio).

CASE Follow-Up:

Providers on the case interpreted the ECG in Figure-1 as consistent with Brugada Phenocopy (ie, a BrugadaType-1 ECG pattern as a result of "something else" — but not a true Brugada Syndrome).

• Because providers were certain ECG #1 was a manifestation of Brugada Phenocopy — serum Troponin was not ordered.

QUESTION: 

• Do you agree with the above approach?

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NOTE: I review Brugada ECG Patterns in the ADDENDUM below:

• A summary of Brugada Syndrome vs Phenocopy appears in Figure-6 — with more depth exploration in the 2-part ECG Video below (Total view time ~17 minutes).
• For more of an update on Brugada Syndrome — See below!

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MY Thoughts on the CASE:

As is often the case — today's History is KEY ==> a middle-aged man who presents with new CP — but who was asymptomatic by the time today's initial ECG was recorded.

My interpretation of the ECG in Figure-1:

• The rhythm is sinus.
• The QRST complex in lead V1 (within the RED rectangle in Figure-2) — is diagnostic of a Brugada-1 ECG pattern.
• That said — the shape of the ST segment coving in neighboring leads V2,V3,V4 differs from the very steep downsloping ST segment seen in lead V1.  
• Deep, symmetric T wave inversion persists in leads V3 and V4.
• More subtle ST-T wave changes are seen in the limb leads (ST segment straightening in leads I,II,III,aVF — and ST segment coving with slight elevation and T wave inversion in lead aVL). Given small size of the QRS in the limb leads (especially tiny in leads III and aVL) — these changes are subtle indeed!
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• BOTTOM Line for Figure-2: Although the QRST complex in lead V1 is typical for a Brugada-1 ECG pattern — the other findings described above are not expected with Brugada Phenocopy in the absence of ongoing ischemia. Instead, in this patient who presents for new-onset CP — We have to suspect that in addition to the typical Brugada-1 ECG pattern that we see in lead V1 — the neighboring chest leads also suggest there may be an ongoing acute infarction!

Figure-2: I've labeled KEY findings in ECG #1 (and added an insert with illustration of Brugada-1 and Brugada-2 ECG patterns).

The CASE Continues:

As noted above — serum Troponins were not obtained because the provider attributed all ECG findings in Figure-2 to Brugada "Phenocopy".

• A short while later — the ECG in Figure-3 was recorded. 

HINT: The changes in the chest leads of ECG #2 are extremely subtle.

• Do you see them?

Figure-3: Repeat ECG done a short while after ECG #1.

Comparison of the ECGs in Figure-3:

As noted above — the changes between the 2 ECGs in Figure-3 are extremely subtle:

• The R' that was seen in ECG #1 has thinned out — with subtle-but-real reduction in the ß-angle in ECG #2 (See the insert in the upper right of Figure-2 regarding calculation of the ß-angle).
• In neighboring leads V2,V3,V4 of ECG #2 — the ST segment coving is less pronounced, and there is narrowing with slight reduction in the depth of T wave inversion that was seen in the initial ECG.
• Bottom Line: Although subtle indeed — ECG #2 suggests ongoing evolution of reperfusion T waves.

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Figure-4 shows the final ECG done the next day ( = ECG #3):

• Unfortunately — I lack details on this case beyond knowing that the patient had no more chest pain — that Troponins were never done — and that there was no cardiac catheterization.

QUESTION:

• How would you explain the ECG changes seen in Figure-4?

Figure-4: Comparison between the initial and the final ECGs that were recorded in today's case. How best to explain these changes?

MY Thoughts on the ECGs in Figure-4:

Whereas the changes in Figure-3 (between ECGs #1 and #2) were extremely subtle — the changes now seen in Figure-4 (between ECGs #1 and the final ECG #3) are obvious.

• The Brugada-1 ECG pattern in lead V1 of ECG #1 has now almost completely resolved in ECG #3.
• ST segment coving without ST elevation persists in neighboring chest leads of ECG #3 — with marked deepening of symmetric T wave inversion.
• In the limb leads of ECG #3 — there has been slight axis shift, with marked increase in the now widened and tall inferior T waves (essentially the reciprocal opposite ST-T wave picture that is now seen for leads V2 and V3 in ECG #3).
• Deep, widened T wave inversion is now seen in leads I and aVL of ECG #3.
• Bottom Line: Even without Troponin values and without cardiac catheterization — the ECG evolution that is now obvious in ECG #3 confirms reperfusion changes following extensive infero-antero MI (presumably following acute LAD occlusion in a patient with multi-vessel disease).

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Final Editorial NOTE:

I initially hesitated using today's case because I lacked follow-up. Efforts to contact today's patient were unsuccessful. He lived remotely, away from health care facilities — and apparently flew back to the island where he lived without returning calls.

• Today's case is insightful — because it illustrates that among the causes of a transient Brugada-1 ECG pattern are acute LAD occlusion, which may superimpose on the ST-T wave changes of acute infarction.
• In my experience — the most common precipitants of a Brugada-1 ECG pattern in patients who do not have Brugada Syndrome (ie, Brugada "Phenocopy" ) — are acute febrile illness and hyperkalemia. I've seen cases in which there is complete resolution of the Brugada-1 ECG pattern after resolution of the febrile illness and hyperkalemia.
• But — acute ischemia and/or infarction and/or S/P cardiac arrest may also be causes of a Brugada-1 ECG pattern, as was seen in today's patient whose presenting complaint was new chest pain.

 

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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Johore, Malaysia) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (3/13/2026): 

I've added below material relating to Brugada ECG Patterns — beginning with my 2-part ECG Video:

• NOTE: Although I recorded this 2-part ECG Video in 2021 ( = 5 years ago) — with the exception of a few changes in approach (that I highlight below) — this 2-part video remains current, and hopefully facilitates recall of Brugada ECG patterns.
• I introduced the concept of Brugada Phenocopy in my ECG Blog #238 (published in July, 2021). This distinction between true Brugada Syndrome — vs a transient Brugada ECG pattern attributable to some other precipitating condition (ie, febrile illness; hyperkalemia; acute ischemia/MI, etc.) with resolution of the ECG pattern once the precipitating condition resolves — remains critical for risk assessment, as well as for optimal management (Adytia and Sutanto — Current Prob in Card 49(6), 2024).  

What's NEW?

I'll preface the 2-part Video below with select updates from the following comprehensive newer references:

• Xu et al — Brugada Syndrome Update- 2025 —
• Krahn et al — JACC: Clinical EP 8(3):386-405, 2022 —

Brugada ECG Patterns: 

• As per the above JACC Review — for practical purposes, the only ECG pattern that is diagnostic of BrS (Brugada Syndrome) is Type-1 (as shown below for A in Figure-5 — when this ECG pattern is present in ≥1 of the anterior leads = V1,V2,V3).
• I had not been distinguishing between a Type-2 vs Type-3 pattern (as per my illustration in Figure-2 above). For investigators who do favor distinction between Type-2 ( = B in Figure-5) and Type-3 ( = C in Figure-5) — the shape of the ST-T wave is similar, with the difference being that with Type-3, there is <2mm of ST elevation. 
• My Preference: I still favor use of only 2 Types ( = Brugada Types-1 and -2) — but whatever your preference, it’s good to be aware that some investigators employ the use of 3 Types (as shown below in Figure-5).
• Neither Type-2 nor Type-3 Brugada ECG patterns alone are diagnostic of BrS. That said — BrS can be diagnosed in these patients IF provocative testing with a SCB (Sodium Channel Blocker) converts a Type-2 or Type-3 pattern into a Brugada-1 ECG. 

Figure-5: The 3 Brugada ECG Patterns (Adapted from Krahn et al — JACC: Clin Electrophys 8(3):386-405, 2022).

Additional Considerations:

The KEY to optimal management of BrS lies with Risk Assessment (To Emphasize: Risk assessment is best performed by cardiologists well versed in the many manifestations of BrS — with current accepted concepts explored in the above 2 references).

• SAEs (Serious Arrhythmic Events) — are rarely the 1st symptom in patients with BrS (which emphasizes the importance of identifying Brugada ECG Patterns — and determining which of these patients are at highest risk for SAEs, and therefore in need of preventive treatment).
• Aside from a malignant arrhythmia — highest risk of SAEs are in: i) Patients with a history of cardiogenic syncope; — ii) The presence of a spontaneous Brugada-1 ECG; — and/or, iii) Association with Other Factors (ie, Excessive alcohol consumption — hypo-/hyperKalemia — Acidosis — Febrile Illness — have all been shown to facilitate Brugada-1-induced SAEs).
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• The sensitivity for ECG recognition of a Brugada-1 pattern is increased by ~50% including high-lead positions (ie, Recording of leads V1 and V2 not only in the 4th IC space — but also in the 2nd and 3rd IC spaces, so as to account for anatomic variation in the position of the vulnerable RV Outflow Track).
• Be aware of intermittent, spontaneous fluctuations in the presence and potential sudden resolution of a Brugada-1 ECG pattern, especially in response to potential precipitating factors such as febrile illness, hyperkalemia, and/or certain drugs. As a result — Provocative Testing with a SCB (Sodium-Channel Blocking agent), is an important adjunct in risk assessment of the patient with a Brugada-1 ECG pattern (NOTE: Not all SCBs used in provocative testing are created equal — but this concept extends well beyond the scope of this ECG Blog).
• Genetic Testing is an important part of Brugada-1 risk assessment (especially since such testing may facilitate identifying family members at risk).

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In Part 1 of this ECG Video (9 minutes) — the essentials of Brugada Syndrome are reviewed.

Int Part 2 (8:00 minutes) — these essentials are applied clinically. 

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Figure-6: 2-page Summary of the essentials of Brugada Syndrome (from Grauer K: ECG-2014-ePub, KG/EKG Press, 2014).

 

Figure-7: World prevalence map of Brugada Syndrome. The overall worldwide prevalence of Brugada Syndrome is ~0.5/1,000 in the population. This prevalence is highest in Southeast Asia (at least 5 times more common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence than for 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-8: Summary of KEY concepts reviewed in the above ECG Video.