ECG Blog #497 — Nonspecific ST-T Wave Changes

I was sent the ECG shown in Figure-1 — and told that it was from a previously healthy older man who had a witnessed collapse.

• This ECG was interpreted as showing, “nonspecific" ST-T wave changes. 

QUESTIONS:

• Do you agree with this interpretation?
• Any other concerns?

Figure-1: The initial ECG in today's case — from an older man with witnessed collapse. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on the ECG in Figure-1:

Given the concerning circumstances of a "witnessed collapse" — the ECG in Figure-1 is not normal.

• The rhythm in ECG #1 is sinus at ~85/minute. Intervals (PR-QRS-QTc) are normal. The frontal plane axis is horizontal (about zero degrees — given the isoelectric QRS in lead aVF). There is no chamber enlargement.

Regarding Q-R-S-T wave changes:

• My "eye" was immediately drawn to leads V2 and V3 (within the RED rectangle in Figure-2). Normally there is slight, upward-sloping ST elevation in these 2 leads. Instead — the ST segments are flat without any ST elevation at all (RED arrows in these leads). This abnormal finding, when seen in a patient with new symptoms — should suggest the possibility of recent or acute posterior OMI (Occlusion-based MI ) — as explained by the "Mirror Test" in ECG Blog #351.

Given the common blood supply of the inferior and posterior walls of the left ventricle — I next focused on the inferior leads.

• There is subtle-but-real ST segment coving in lead III, and to a lesser extent in lead aVF — in association with shallow-but-real terminal T wave inversion (BLUE arrows in these leads).
• Reciprocal changes are seen in lead aVL (ST segment straightening — with terminal T wave positivity).
• ST segment straightening, albeit without ST depression — is also seen in leads I, II; and in leads V5,V6.

KEY Point: The ECG in Figure-2 is not normal. While true that the above ECG findings are subtle, and might be described as "nonspecific" — given the clinical setting of a patient who had a "witnessed collapse" — there are ECG abnormalities in no less than 9/12 leads. 

• My concern was that ECG #1 could indicate a recent infero-postero OMI in a patient with significant underlying coronary disease. Additional evaluation was essential.

Figure-2: I've labeled today's ECG.

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Follow-Up of Today's CASE:

It turns out that this patient’s collapse was associated with no pulse and no respiration ==> cardiac arrest! The arrest was witnessed — and CPR was promptly initiated. EMS was quickly on the scene — and found the patient to be in VFib (Ventricular Fibrillation).

• EMS immediately defibrillated the patient — with prompt ROSC (Restoration Of Spontaneous Circulation).
• The patient arrived in the ED a short while later — sitting up, alert and oriented (albeit with no memory of what had just happened).
• At no time did the patient have any chest pain. He did not feel ill prior to collapsing, and had no specific symptoms that he could recall.
• The ECG in Figure-2 was recorded within minutes after achieving ROSC.

In the ED — the initial Troponin was normal.  

• Cardiology was consulted. Plavix, heparin and IV infusion of Amiodarone were all started — and the patient was transferred in timely fashion to a center with 24/7 access to cardiology services.
• Cardiac cath revealed multi-vessel coronary disease (I don't know further details of this patient's cath report).
• The patient's condition stabilized — and arrangements were made for CABG (Coronary Artery Bypass Grafting). The patient did extremely well — and was subsequently discharged from the hospital without neurologic deficit.

Additional Thoughts:

Today's case is a success story. Cardiac arrest was witnessed — CPR was promptly started — and, EMS was quickly on the scene to defibrillate the patient, with restoration of sinus rhythm.

• This patient never had chest pain.
• While I don't have access to all data on the case — the initial Troponin was negative. This is not uncommon. As per references in the ADDENDUM below — there will often be spontaneous reopening (reperfusion) of the "culprit" artery, even before any medical treatment is given. If the period of time that the "culprit" artery was occluded is brief — then even high-sensitivity Troponin may not be elevated (or only minimally elevated).
• If the moment in time that the initial ECG was recorded occurred in between the period of ST elevation — and the period of ST depression with the T wave inversion that is commonly seen with reperfusion of the occluded vessel — then the ECG may show pseudo-normalization, with no more than minimal ST-T wave abnormalities (consistent with the ECG picture seen in Figure-2 of today's case).
• Subtle signs in Figure-2 of reperfusion in today's case include: i) Terminal T wave inversion in leads III, aVF; — ii) Terminal T wave positivity in lead aVL; — and, iii) The flat, non-elevated ST segments in leads V2,V3 — with somewhat peaked and upright T waves in these leads.
• Today's patient had no symptoms prior to his sudden arrest. This older man was unaware that he had longstanding underlying coronary disease. The hint on his ECG to underlying multivessel disease is the presence of ST-T wave flattening in so many leads (ie, in leads I,II; V5,V6 — in addition to the abnormal findings in the infero-postero lead distribution). Presumably — this patient's arrest was the result of acute infero-postero OMI, that then promptly reperfused.

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Acknowledgment: My appreciation to Michael Moore (from Kansas, USA) for this case and this tracing.

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ADDENDUM (9/20/2025):

• 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.