COPY of ECG Blog #499 — on Oct. 2, 2025

I was shown the ECG in Figure-1, obtained from a previously healthy, middle-aged man — who presented to the ED (Emergency Department) with new, severe CP (Chest Pain).

• Of note — the patient is an active endurance athlete.

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 — from a middle-aged man with CP. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Today's CASE:

The history in today's case is worrisome. In this context — I would interpret the ECG in Figure-1 as suggestive of acute proximal LAD occlusion until proven otherwise.

• The rhythm in ECG #1 is sinus at ~65/minute. All intervals (PR-QRS-QTc) and the axis are normal. No chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• There appear to be tiny (probably insignificant) Q waves in leads III and aVF.
• 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).
• ST-T wave changes — The most remarkable finding on this tracing is the disproportionate increased size of T waves in the chest leads (See RED arrows in Figure-2). Especially given modest size of the QRS complex in leads V2,V3,V4 — the T waves in these leads clearly appear larger-than-expected — which in the context of a patient with new CP — qualifies these T waves as hyperacute until proven otherwise!
• In isolation, I probably would not have interpreted the T waves in leads V5,V6 as abnormal. However, in the context of new CP and hyperacute-appearing T waves in neighboring leads V2,V3,V4 — I thought the T waves in leads V5,V6 represented an extension of this process (BLUE arrows in Figure-2).

PEARL #1: When I have any doubt about the clinical implications of chest lead ST-T wave findings in a patient with symptoms — I look extra closely at ST-T wave appearance in the limb leads.

• To Emphasize: Not all cases of acute LAD occlusion manifest abnormal limb lead findings. Most often — it is those proximal LAD occlusions that are most likely to manifest at least some ST elevation in lead aVL and/or reciprocal ST depression in the inferior leads.
• Therefore: If you do not see ST-T wave abnormalities in the limb leads — this does not rule out the possibility of acute LAD occlusion. BUT — IF you do see clear ST-T wave abnormalities in the limb leads — this strongly supports that what you may be questioning in the chest leads — is a valid indicator of an acute ongoing process.

QUESTION:

Take another LOOK at the ECG in Figure-2:

• How would you assess ST-T wave findings in the limb leads?

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

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PEARL #2: It's important to recognize the difficulty in assessing the validity of what you are seeing when there is as much variability in ST-T wave appearance as we see for beats #1,2,3 in leads II,III; and in leads aVL,aVF in Figure-2 (within the broken-lined PURPLE rectangles).

• Which of these first 3 beats in the limb leads reflects the "true" appearance of the ST-T waves in these leads? If it is beat #3 (that shows marked ST depression in the inferior leads with subtle ST elevation in aVL) — then there is no doubt about the hyperacuity of the T waves in the chest leads! 
• BUT — Our assessment might be less certain if beats #1 and #2 reflect the true ST-T wave appearance in leads II,III; and aVL,aVF.

Fortunately — The ST-T waves for the last 2 beats in the limb leads of Figure-2 look to be more consistent in appearance — so I made my assessment largely based on what I see for beats #4 and #5 in Figure-2:

• The ST segment in leads III and aVF for beats #4 and 5 looks straightened.
• Given tiny size of the QRS in lead aVL — the upright T wave for beats #4 and 5 in this lead looks disproportionately large.
• And — all 5 beats in lead I look consistent in appearance — all showing some ST segment straightening with a more "voluminous"-than-expected T wave.
• 
  
• Impression: In this patient with new severe CP — I interpreted this ECG as suggestive of acute proximal LAD occlusion until proven otherwise. My thoughts when I was shown this tracing were to activate the cath lab.
• If providers on the scene had any doubts about the need to activate the cath lab — quick search for a prior ECG on this patient or repeat ECG within 10-15 minutes mght be helpful options.

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The CASE Continues:

• The initial Troponin came back normal.
• The patient was given IV paracetamol — which significantly reduced his pain. 
• Feeling better, the patient was convinced his CP was the result of an intense endurance session the day before. As a result — he left the ED after 30 minutes (such that no repeat ECG or repeat Troponin was done).

MY Thoughts:

When told the above — I wrote back the following:

• I would have activated the cath lab on the basis of the initial ECG that we see in Figure-1.
• 
  
• It would have been really helpful to see a follow-up ECG recorded within 15-to-30 minutes of the 1st tracing. IF the ECG in Figure-1 truly represents an acute evolving MI — it is very likely that a 2nd ECG done within the next 30 minutes would have shown "dynamic" ST-T wave changes (ie, deflation of the hyperacute chest lead T waves) — and that would have been diagnostic!
• 
  
• PEARL #3: A normal initial Troponin does not rule out an acute MI (because up to 25% of STEMI+ infarctions fail to satisfy "rule-in" values on the initial Troponin — Wereski et al — JAMA Cardiology, 2020). Thus, although elevation of the initial Troponin would have been helpful to confirm an ongoing acute event — a normal initial Troponin would not have changed my impression that the cath lab should be activated.
• 
  
• PEARL #4: In patients with new CP, in whom you are suspicious of an acute cardiac event — it is best not to administer analgesics (ie, IV Morphine) — until a decision is made to either activate the cath lab or that an acute OMI has been definitely ruled out. This is because partial (or total) CP relief with IV Morphine may produce a false sense of security — when it reality what it does is delay the diagnosis of acute coronary occlusion in need of definitive treatment = prompt cath with PCI ( = this CASE, and many others in Dr. Smith's ECG Blog).
• 
  
• I asked if it would be possible to get follow-up on this patient.

Final Follow-Up:

Medical providers reached out and were able to contact the patient by phone a few days later.

• The patient was actually doing fine after leaving the hospital. He was convinced that his CP was a result of a muscular injury from his intense endurance training.
• Several weeks later — the patient came in for a follow-up visit. He reported being able to continue his endurance training — albeit with intermittent pain that seemed now to be related to torso movements.
• The was no previous ECG in this patient's file.
• Repeat ECG was essentially the same as the ECG in Figure-1!
• Echo in the office was completely normal (normal chamber size and normal cardiac function).
• CT coronary angiography was performed — and was without significant disease. Normal LV function.

MUST write a conclusion !!!! The initial ECG must have been a normal repol variant in this endurance athlete.

Must ADD a FINAL PEARL #5 = the patien now has an image of his "baseline" ECG that he keep in his cell phone! just in case he ever returns to the ED with new CP.

PEARL #6: Sometimes the cath will be normal. This does not mean cath should not have been done. The normal qtc and normal r wave progression are against acute omi - but esp the size of t wave in v2,3 even in retrospect in this pt with new severe cp to me still indicates a need for cath to define the anatomy

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Acknowledgment: My appreciation to Lorenzo Kapetis (from Lamaca, Cyprus) for the case and this tracing.

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ADDENDUM #1 (8/30/2025):

• 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 earlier) was 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.
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• KEY Clinical Reality: Many of the acute coronary occlusions that we see never develop ST elevation (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.