ECG Blog #523 — Is there a "Culprit"?

The ECG in Figure-1 was obtained from an older woman — who presents to the ED (Emergency Department) with CP (Chest Pain) that began ~2 hours earlier.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Would you activate the cath lab?

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

MY Thoughts on Today's CASE:

Given the history of new CP — this is an extremely worrisome ECG:

• The  rhythm is sinus at ~80/minute. Regarding intervals — the PR interval and QRS duration are both normal, with the QTc no more than of borderline duration. Regarding chamber enlargement — the S wave of >20 mm in lead V2 is consistent with voltage for LVH (See Figure-7 in the Addendum of ECG Blog #73).

Regarding Q-R-S-T Changes:

• A small and narrow Q wave is seen in lead aVL.
• R wave progression — is normal (Small but definite initial r waves are seen in both leads V1,V2 — with transition occurring normally between leads V3-to-V4).

The remarkable findings relate to ST-T waves:

• My attention was immediately drawn to the ST-T waves in the 3 inferior leads — which show eyecatching straightened and downsloping ST segments (RED arrows in leads II,III,aVF in Figure-2). Each of these leads show terminal T wave positivity (upright YELLOW arrows) — with this down-up T wave appearance in a patient with new CP being an especially worrisome sign of hyperacuity.
• Support for our concern is forthcoming from the hyperacute ST-T wave appearance in lead aVL (with ST segment straightening, subtle-but-real ST elevation given small size of the QRS — and a disproportionately "fattened" T wave with wide base).

In the Chest Leads: 

• Lead V1 is notable for ST segment straightening — which is especially remarkable in light of the distinctly abnormal 1-2 mm of flat ST segment depression in leads V3,V4,V5,V6 (BLUE arrows in these leads). Each of these 4 chest leads show significant terminal T wave positivity — which in this patient with new CP strongly suggests hyperacuity.
• I found lead V2 especially interesting as a "transition" lead — in that it shows neither J-point depression or elevation. This is most probably because lead V2 is situated between lead V1 (which is remarkable for its hyperacute-looking ST segment straightening) — and leads V3,V4,V5,V6 (each of which show unmistakeable ST segment flattening and depression with terminal T wave positivity).
• Finally — there is slight-but-real ST elevation in lead aVR.

Figure-2: I've labeled today's initial ECG.

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Putting It All Together:

• I'd immediately activate the cath lab. The history of new-onset CP in this older woman whose initial ECG shows significant ST-T wave abnormalities in no less than 11/12 leads indicates an acute cardiac event until proven otherwise.

The question arises as to what the "culprit" artery might be? 

• The only lead showing ST elevation is lead aVL. In the absence of ST elevation in other lateral leads — I thought acute LCx (Left Circumflex) occlusion to be less likely.
• ST elevation is commonly seen in multiple chest leads with proximal LAD (Left Anterior Descending) occlusion — but there is no anterior lead ST elevation in today's initial ECG..
• Instead, we see the ST segment straightening in lead V1 — with the predominant findings in Figure-2 being the very acute-looking ST depression with terminal T wave positivity in 7 leads (leads II,III,aVF — and in V3,V4,V5,V6) — with transition lead V2 — and with ST elevation in lead aVR.
• 
  
• PEARL #1: The most logical explanation for this series of acute-looking ST-T wave abnormalities without suggestion of a specific "culprit" artery — is that there is severe multi-vessel disease.
• I suspected acute LAD occlusion given findings of ST straightening in V1 + transition lead in V2 with lateral chest lead ST depression suggesting a Precordial "Swirl" pattern in a patient with significant multi-vessel disease (See ECG Blog #380). Supportive findings of ST elevation in aVL with reciprocal inferior lead ST depression is consistent with proximal LAD occlusion — with the diffuseness of the ST depression reflecting impossible-to-account-for attenuation effects from multi-vessel involvement.
• Bottom Line: None of this matters. What counts is simply that prompt cath with PCI is needed. Specific anatomy to be revealed by cardiac cath.

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The CASE Continues:

• Cardiac cath was performed — and revealed severe multi-vessel disease (with an 80% ostial LMain lesion — a 95% "culprit" mid-LAD lesion + RCA disease).
• The initial hs-Troponin-I came back with borderline elevation. The repeat Troponin was clearly elevated.

PEARL #2: It does not matter what Troponin shows in today's case. This is because regardless of what the 1st and 2nd Troponin assays show — prompt cath with PCI will be needed given the history of new-onset CP and today's initial ECG showing diffuse acute-looking ST-T wave changes in 11/12 leads!

• The initial hs-Troponin may be negative or non-diagnostic in up to 25% of acute STEMI patients (Wereski et al — JAMA Cards 5(11):1302, 2020).
• "Time is Muscle (myocardium)". As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in 60% more myocardium infarcted).
• Serum Troponin values provide a rear-view mirrow of what has already happened — and not of what is about to happen.
• PEARL #3: The decision to perform cardiac cath in today's case can be made as soon as the initial ECG is seen.

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A 2nd ECG was recorded ~3 hours after ECG #1 (shown in Figure-3):

• ECG #2 was obtained prior to cardiac cath — at a time when the patient's symptoms had decreased. Dual antiplatelet therapy (DAPT) and Heparin were ongoing.

QUESTIONS:

• Given that the patient's CP was less at the time ECG #2 was recorded — How would you interpret this repeat ECG?

Figure-3: Comparison between the 2 ECGs in today's case.

MY Thoughts on ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows reperfusion changes in virtually all leads that previously looked acute:

• Most remarkable in ECG #2 is the anterior lead ST segment coving, now with deep, symmetric T wave inversion in lead V2.
• The horizontal ST depression previously seen in leads V3,V4,V5,V6 has essentially resolved.
• Reciprocal reperfusion changes are now seen in the inferior leads — in which downsloping ST depression has been replaced by tall, "bulky" positive T waves.
• Deep symmetric T wave inversion is seen in lead aVL.
• PEARL #4: Especially in view of reduced CP — I interpreted the evolutionary changes in ECG #2 as confirming acute LAD occlusion as the "culprit" artery in this patient with underlying multi-vessel disease.

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

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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!
• 
  
• 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).
• 
  
• 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.

 

 

 

ECG Blog #521 — Inferior MI? — Anything else?

The ECG in Figure-1 was obtained from a middle-aged man with a long history of smoking — who presents with severe new-onset CP (Chest Pain).

• The patient reports having 2 episodes of severe CP — each of which spontaneously resolved. He then presented to the ED (Emergency Department) several hours after the 2nd episode (ie, He was not having CP at the time ECG #1 was recorded).
• The initial Troponin level was negative for acute infarction.

QUESTIONS: 

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

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with CP — but who was asymptomatic at the time this ECG was recorded. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's ECG:

The ECG in Figure-1 shows a regular sinus rhythm at ~80/minute. Intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: There are q waves in the lateral leads (ie, leads I,aVL; and leads V4,V5,V6). These have the appearance of normal septal q waves — in that all of these q waves are narrow and small in size.
• R Wave Progression: Normal (ie, R wave amplitude progessively increases as we move across the chest leads — with transition occurring normally between leads V2-to-V4).

Regarding ST-T Wave Changes:

• In this patient with new CP — My "eye" was immediately drawn to the "scooped" ST depression in lead V2 (within the RED rectangle in Figure-2). 
• This ST depression continues in neighboring leads V3,V4 (RED arrows in these chest leads) — but has largely resolved by lead V5.
• 
  
• ST-T wave changes in the inferior leads are more difficult to evaluate (See below).

Figure-2: I've labeled the ECG in today's case.

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ANSWERS: Putting It All Together . . .

There are a number of reasons why assessment of today's case is challenging. Unfortunately, we lack many details and only have limited follow-up. That said, my purpose in presenting this case — is that the following points can still be made from the brief history we are given, and from today's initial ECG:

• The history of several episodes of new-onset and severe CP in this middle-aged man with a longterm history of smoking immediately place him in a higher-risk group for having an acute cardiac event. Awareness of this clinical situation should lower our threshold for accepting ST-T wave findings as abnormal.
• Availability of a prior ECG for comparison would have made it much easier to determine if the ST-T wave changes that we see in ECG #1 are acute.
• Repeating the ECG within 10-20 minutes of the initial tracing is advisable when symptoms are new and there is uncertainty about whether ST-T wave findings are acute — as diagnostic "dynamic" ST-T wave changes may sometimes be seen within minutes (See ECG Blog #115 — and ECG Blog #459). 
• Obtaining a bedside Echo may sometimes be diagnostic if it shows a localized wall motion abnormality. (While Echo may be diagnostic if positive — a normal Echo does not rule out an acute event if the patient is not having CP at the time the Echo is done).
• The initial normal hs-Troponin in today's case in no way rules out an acute cardiac event (See ECG Blog #508). In addition to infarct size, whether or not Troponin will be elevated depends on how long the "culprit" artery is occluded for — which we do not know in today's case. But if the duration of time that the "culprit" artery is occluded is very brief — there may not be any Troponin elevation at all (and on occasion — the first 2 Troponin values may come back normal despite the patient going on to develop a STEMI).

Consider the following additional points:

• The patient was not having CP at the time ECG #1 was recorded. This suggests that spontaneous resolution of acute coronary occlusion may have occurred — in which case acute ST-T wave abnormalities that were present during CP may signficantly improve (and even resolve).
• That said — there normally should be slight, gently upsloping ST elevation in leads V2 and V3. This is why in a patient with new CP — the finding of ST depression that is maximal in leads V2,V3,V4 (as is seen in ECG #1) — is diagnostic of acute posterior MI until proven otherwise! (See ECG Blog #351 — and ECG Blog #298, among many others).
• NOTE: Because of a common blood supply to the inferior and posterior walls of the left ventricle — I always look for acute inferior lead changes whenever I suspect acute posterior OMI. Unfortunately, the inconsistent ST-T wave appearance in the inferior leads of ECG #1 makes it all-but-impossible to assess the inferior leads (ie, Whereas complex B within the BLUE rectangle suggests a straightened, hyperacute ST segment with terminal T wave inversion — complexes A and C do not look acute).

BOTTOM Line: Maximal ST depression in leads V2,V3,V4 in this patient with a history of new CP suggests acute posterior OMI until proven otherwise. Knowing that this patient's CP had completely resolved at the time ECG #1 was recorded may account for relatively modest ST-T wave changes in the remaining leads.

• Ideally — the cath lab would be activated on seeing ECG #1.
• If the interventionist was reluctant to catheterize the patient at this point — then the following actions might serve to expedite acceptance to perform this procedure: i) Repeating the ECG within 10-20 minutes — and if this initial repeat tracing failed to show dynamic changes — follow-up with a few more repeat tracings within the hour; — ii) Immediately repeating the ECG if at any time the patient's CP returns; — iii) Searching for a prior ECG on this patient (that most probably would confirm that the ST depression in leads V2,V3,V4 is acute); — iv) Performing bedside Echo, looking for a localized wall motion abnormality; — and, v) Looking for any elevation in the 2nd Troponin value (which in a patient with new worrisome symptoms is indication for prompt cath — even when ECG changes are less than diagnostic).

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CASE Follow-Up: 

My follow-up is limited — but the results that I have reinforce the above clinical points:

• The repeat Troponin was elevated at ~60 (I'm not sure of units or norms — but a value of 60 is clearly elevated).
• A repeat ECG done many hours later seemed to show less acute changes compared to ECG #1.
• Bedside Echo done the next day showed a wall motion abnormality localized to lateral and posterolateral segments.
• Cardiac cath done the next day confirmed the LCx (Left Circumflex) as the "culprit" artery (I do not know about additional cardiac cath findings).

Lessons to Be Learned:

• Waiting for ST elevation before activating the cath lab misses a substantial percentage of acute coronary occlusions. Acute posterior OMI is most easily recognized in a patient with new CP by maximal ST depression in leads V2,V3,V4 — which is much easier to recognize and more reliable than than trying to assess the dampened amplitudes obtained with posterior leads (See ECG Blog #80). Posterior OMI is the best example of how we can make a presumptive diagnosis of acute coronary occlusion without insisting on ST elevation
• The diagnosis of acute OMI could have been made significantly earlier in today's case.
• Delay in diagnosis (and therefore in reperfusion treatment of acute coronary occlusion) comes at a price. The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (Every 2-hour delay results in 60% more myocardium infarcted). Documentation of these Lessons-to-be-Learned is forthcoming in these 3 posts from Dr. Smith's ECG Blog ( = the February 8, 2026 post — the January 15, 2026 post — and the October 23, 2025 post — with My Comment appearing at the bottom of the page in each of these posts).

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Acknowledgment: My appreciation to Hisham Alshamekh (from Egypt) for the case and this tracing.

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ADDENDUM (3/7/2026): 

For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):

• Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
• Consider the 2 Audio Pearls at the bottom of this page.
• Consider Figure-3 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-3: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-3 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Key Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!). Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ] ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).

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How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association), ACC (American College of Cardiology), ESC (European Society of Cardiology), and the WHF (World Heart Federation):

• New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).
• 
  
• In leads V2 and V3:
• ST elevation ≥2 mm for men >40 years of age.
• ST elevation ≥2.5 for men ≤40 years of age.
• ST elevation ≥1.5 mm for women.

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—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.