ECG Blog #481 — New, Old — or in Between?

You are given the ECG shown in Figure-1 — and told that it was obtained from a middle-aged man who presented with epigastric pain and "faints" over the previous 4 days.

• There was no CP (Chest Pain).
• No prior tracing — and no additional information is available at the time you are given this tracing.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
•    — Should the cath lab be activated?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today’s CASE:

There are a lot of ECG findings on the tracing shown in Figure-1. As a result, I favor spending the first ~30 seconds of my assessment of ECG #1 on the basic parameters of Rate & Rhythm, Intervals, Axis and Chamber Enlargement — before focusing on acute Changes (See ECG Blog #205 for review of my Systematic Approach).

• To Emphasize: Making today's case especially challenging — is the lack of CP and duration of 4 days.
• The rhythm in ECG #1 is sinus at 80-85/minute.
• All intervals (PR, QRS, QTc) are normal.
• The frontal plane axis is markedly leftward — consistent with LAHB (Left Anterior HemiBlock) given the predominantly negative QRS in each of the inferior leads.
• There is no chamber enlargement.

And now — a look for acute Changes (as I'll be assessing all leads for Q waves, R wave progression — and ST-T wave changes).

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What Caught My "Eye" ...

• My "eye" was immediately drawn to lead V2 (within the RED rectangle in Figure-2). The amount of J-point ST elevation, and especially the size and "volume" of the ST-T wave in this lead is clearly disproportionate to the modest size of the S wave in this lead.
• NOTE #1: There is some variation in ST-T wave morphology between the 4 beats that we see in lead V2. The 2nd complex in this lead (to which I’ve added the RED arrow, that highlights the amount of J-point ST elevation) — manifests the most concerning ST segment morphology. This raises the question as to which of these 4 beats in V2 is the most accurate reflection of true ST-T wave morphology in this lead?
• KEY Point: The way that I instantly knew that my concern about the ST-T wave in lead V2 was real — is by the clear ST segment straightening that we see in leads V4,V5,V6 (RED lines in these leads). These are all hyperacute T waves.
• There is also ST elevation in these 3 lateral chest leads that should not be there (especially in lead V4).
• Similar abnormal ST segment straightening is seen in lead II.
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• NOTE #2: At this point, despite the lack of CP — I knew there has been infarction at some point in time, perhaps beginning ~4 days earlier when this patient’s symptoms began. But there is much more going on in this ECG (See below in Figure-3).

Figure-2: My "eye" was immediately drawn to lead V2.

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Reperfusion T Waves?

In Figure-3 — I've added BLUE arrows to highlight subtle-but-real T wave inversion in lead V3 and lead III (and probably also in lead II ).

• I found lead V3 particularly interesting, in that it is placed in between chest leads with much more remarkable ST-T wave findings (ie, hyperacute ST-T waves in lead V2 — and in leads V4,V5,V6). The terminal T wave inversion that the BLUE arrow highlights in this lead V3 (as well as the cardiac cath findings below) — explain why.

Figure-3: Subtle T wave inversion (BLUE arrows).

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Putting It All Together:

I highlight a series of additional important findings that next caught my "eye" in Figure-4.

• There has been inferior infarction at some point in time. While difficult to determine if we are seeing QS waves or a tiny initial r wave in leads III and aVF — there clearly does appear to be an initial small q wave in lead II (See magnified insert of this lead in Figure-4).
• PEARL #1: It is sometimes difficult to distinguish LAHB from inferior MI — as well as from the possibility that there is both LAHB and inferior infarction. The "pseudo-Q" wave that we see here in this lead II magnified insert — indicates that there is more than simple LAHB (which by itself does not produce an inferior Q wave).
• It is hard to determine the age of the inferior MI in Figure-3 — given the hyperacute T wave in lead II — potential reperfusion T waves in leads II and III (subtle terminal T wave inversion) — but no more than minimal (at most) ST elevation in leads III and aVF.

Q waves and R Wave Progression in the Chest Leads:

With regard to the chest leads — We know there has been anterior infarction at some point in time because:

• Assuming no electrode lead misplacement — there has been “loss of R wave” from lead V2-to-V3 (There may or may not be a tiny initial r wave in lead V3).
• There is a definite QS complex in lead V4.
• PEARL #2: It is difficult to “date” this anterior infarction. Perhaps the acute process began ~4 days earlier (ie, at the time the patient developed epigastric pain and began having syncopal spells?). Perhaps the inferior and/or anterior infarction(s) are old — with a superimposed new event? 
• Although it is possible that this patient has a left ventricular aneurysm from prior infarction — the hyperacute-looking ST-T waves clearly suggest that something more is going on.
• NOTE: Finding a prior ECG on this patient might be enlightening as to what may be "new" vs "old" vs "new superimposed on old". 
• BOTTOM Line: Given this patient’s history and the above ECG findings — promp cardiac cath is indicated to clarify the anatomy (since reperfusion with PCI may be needed).

Figure-4: Q waves and R wave progression in today's case.

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Follow-Up in Today's CASE:

• Troponin came back significantly elevated.
• Cardiac cath revealed complete occlusion of both the LAD and the LCx artery (which probably explains the relatively modest ST-T wave morphology in transition lead V3 — which is situated in between more marked ST-T wave changes in neighboring leads V2 and V4,5,6). PCI was accomplished.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ADDENDUM (5/10/2025):

• For More Material — regarding 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).
• In 'My ECG Videos" — Check out near the top of that page 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.
• The Clinical Reality: Many acute coronary occlusions 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.

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