ECG Blog #494 — Much to Learn from this Case ...

The ECG in Figure-1 was obtained from an older woman who presents with a history of “indigestion” and CP (Chest Pain). She took 2 Tums, with enough relief of her symptoms to fall asleep — only to be awakened by 10/10 CP.

QUESTIONS:

• How would you interpret ECG #1 — which was recorded on arrival in the ED (Emergency Department)?
• Would you activate the cath lab? (Think to yourself about WHY you would or would not activate the cath lab on the basis of the above history and the ECG in Figure-1).

Figure-1: The initial ECG in today's case — recorded in the ED from an older woman with new CP. (To improve visualization — I've digitized the original ECG using PMcardio).

CASE Follow-Up:

The cath lab was not activated. The concern was that ECG #1 doesn't quite satisfy "STEMI criteria". That is, in this female patient — there is not more than 1.5 mm of ST elevation in leads V2 and V3 (Akbar and Mountfort — StatPearls, Oct. 2024).

• The initial Troponin was slightly elevated.
• The patient’s CP improved with Morphine that was given in the ED.

QUESTION:

• What are your thoughts on the above scenario?

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The Case Continues:

A prior ECG on this patient was found (shown in Figure-2).

QUESTION:

• Does access to this prior ECG in any way alter your impression about this case?

Figure-2: A prior ECG on today's patient.

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MY Thoughts: 

As per material in today's ADDENDUM — strict adherence to millimeter-based STEMI criteria will miss many acute OMIs ( = Occlusion-based Myocardial Infarctions). Simply stated — Whether or not STEMI criteria are satisfied depends more on When during the process the ECG is obtained, rather than whether or not there has been acute occlusion of a major coronary artery.

• This process is not "static". Instead — an OMI typically starts with acute coronary occlusion (accompanied by new-onset CP and ST elevation) — but along the way, the course may be "stuttering" (ie, Even before treatment — the "culprit" vessel may spontaneously reopen — and then spontaneously reclose — sometimes going back-and-forth between open and closed, until ultimately — the final state of the "culprit" artery is reached).
• Clues from the history that spontaneous reperfusion may have occurred at some point — are that the patient's symptoms are not constant — but instead wax and wane. If the initial ECG is obtained at a time after symptoms have lessened (or resolved) — then there may be some degree of "pseudo-normalization" (ie, Elevated ST segments may be returning to the baseline on their way toward ST depression and T wave inversion because the "culprit" artery has now opened).
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• PEARL #1: The history in today's case is potentially consistent with some degree of spontaneous reperfusion — because this patient's "indigestion" and initial CP improved enough for her to go to sleep. The reason it is important to be aware of this aspect in the history — is that it alerts YOU that the presence of subtle, seemingly minimal ST-T wave findings may be significant IF the ECG is in the process of "pseudo-normalizing". It also highlights that frequent serial ECGs may be needed to detect "dynamic" ST-T wave changes that may continue until the acute OMI has completely evolved.
• PEARL #2: The clinical problem — is that what spontaneously reopens — may just as easily spontaneously reclose. It is for this reason that once you recognize an acute OMI has occurred — that definitive treatment (ideally prompt cath with PCI) is still needed even if the patient is now pain-free, in order to prevent the "culprit" artery from reclosing.
• PEARL #3: Morphine should not be given until the decision has been made to perform prompt cath (or if 24/7 cath facilities are not available — until the decision has been made to begin thrombolytic therapy). This is because morphine may mask the patient's CP, giving a sense of false security that the process is over. We know this occurred in today's case — because the decision to perform cardiac catheterization was deferred until the following day.
• PEARL #4: Details in today's case are missing. We know this because: i) Temporal correlation between the presence and relative severity of this patient's CP and the initial ECG was not noted (The easiest way to document this correlation — is to write down on each ECG as it is recorded the patient's symptoms at that time on a scale of 1-to-10); and, ii) Frequent serial ECGs were apparently not done (ie, Repeating the initial ECG within 15-to-30 minutes will often reveal acute "dynamic" ST-T wave changes that confirm an ongoing acute process in need of prompt cath and definitive treatment).
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• PEARL #5: Frequent serial ECGs over the ensuing minutes to the first few hours should be obtained until confidence can be attained as to whether your patient has (or has not) had an acute OMI. That said, in a patient with worrisome new symptoms (as in today's case) — any amount of Troponin elevation is enough to satisfy clear indication for prompt cath.
• PEARL #6: Troponins are far from an ideal indicator of an acute process. Instead, they provide a "rear-view mirror" of myocardial damage that has already occurred (because of the natural delay after acute coronary occlusion until enough Troponin is released to be picked up in a blood test). And sometimes, despite acute OMI — the initial Troponin value may be negative (This may happen if the duration of acute coronary occlusion is very brief — as may be suggested by a history of CP that does not last for long).

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MY Impression of today's Initial ECG:

I thought prompt cath was indicated in today's case as soon as the initial ECG was recorded. For clarity in Figure-3 — I've labeled KEY findings that justify my impression that prompt cath was needed.

• Today's patient is an older woman who presents to the ED with new CP. This immediately places her in a higher-risk category for having an acute cardiac event.
• The rhythm in Figure-3 is sinus tachycardia at a rate just over 100/minute. It's important to be aware of how much less common it is for a patient with an uncomplicated acute MI to present with sinus tachycardia — unless "something else" is also going on (ie, heart failure; shock).
• There is bifascicular block ( = RBBB/LAHB) — which if acute, is an especially worrisome finding when it occurs in association with acute LAD (Left Anterior Descending) occlusion.
• And so, my "eye" was immediately drawn to the leads within the RED rectangle. Small-but-definite initial Q waves are seen in leads V1 and V2. Until proven otherwise — these initial Q waves are not part of an uncomplicated RBBB, but instead serve as a marker that anteroseptal infarction has occurred at some point in time. 
• Normally with RBBB — some amount of ST-T wave depression will be seen in one or more anterior leads. As a result — the small amount of ST elevation seen especially in lead V2 (but also, albeit to a lesser extent — in leads V3,V4,V5) — is significant and suggestive of an acute process. (Insistence on seeing a millimeter-amount of ST elevation in leads V2,V3 in a patient with RBBB, in which some ST depression is normally expected — makes no sense).
• RED arrows in a number of leads in Figure-3 highlight hyperacute ST-T waves (especially in leads V3,V4,V5 — in which these T waves are disproportionately enlarged compared to modest size of S waves in these leads).
• Finally — there is reciprocal ST depression in the inferior leads (especially as highlighted in lead III by the BLUE arrow).

BOTTOM Line: In this older woman with new CP (even without considering the elevated Troponin and availability of the prior ECG) — ECG #1 has to be interpreted as extremely worrisome given sinus tachycardia, bifascicular block (RBBB/LAHB), potentially significant Q waves in leads aVL,V1,V2 — and ST elevation in leads V2,V3 with hyperacute ST-T waves in leads V2-thru-V5 ==> acute proximal LAD occlusion until proven otherwise.

• Waiting until there is more ST elevation (which may or may not ever occur) — or waiting for more troponin results, serial ECGs or an Echo will achieve nothing — because it will not change the fact that prompt cath with PCI is needed.

Figure-3: I've labeled the initial ECG.

What about the Prior ECG?

Despite strong indication for prompt cath on the basis of history and the initial ECG — consultants (and your interventionist) may sometimes be reluctant to so promptly perform cardiac catheterization.

• PEARL #7: If some convincing of your consultant is needed — comparison of your patients initial ECG with either a prior ECG and/or with one or more serial ECGs will often show differences in ST-T wave morphology that prove the findings in the initial ECG are acute.

PEARL #8: All-too-often overlooked is how helpful it can be when comparing one ECG to another — to look lead-by-lead after placing both ECGs together.

• The prior ECG on today's patient was shown above in Figure-2. Isn't it much easier in Figure-4 to compare ECG #1 and ECG #2, now that I have placed both tracings together?
• Which of the ECG findings that I described above have we now proved to be acute in Figure-4 — now that we can compare these 2 tracings looking lead-by-lead?

Figure-4: Comparison of the initial ECG in today's case — with a prior ECG on this patient.

Comparison with the Prior ECG:

The rhythm in both of the tracings in Figure-4 is sinus at a rate close to 100/minute (The heart rate is slightly faster in ECG #1).

• It turns out that the bifascicular block ( = RBBB/LAHB) is not new! Instead, it was present whenever this prior tracing was done. On the one hand — it is good that this patient's acute OMI is not associated with new RBBB/LAHB, as this is an especially severe conduction defect when it occurs as the result of acute  LAD (Left Anterior Descending) occlusion. 
• On the other hand, the longstanding presence of bifascicular block, in association with QRS fragmentation ( = the notching that we see in multiple leads of ECG #2) — strongly suggests significant preexisting coronary disease in this older woman.
• The above said — this means that the ST-T wave changes that I described earlier for today's initial ECG are all new! There was no ST elevation in leads V2,V3 of ECG #2, nor were any of the T waves in leads V2-thru-V5 hyperacute in this prior tracing. In addition, the limb leads in the prior tracing did not show the changes highlighted by the colored arrows in ECG #1.
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• BOTTOM Line: Comparison in Figure-4 between today's initial ECG and this patient's prior tracing — confirms the acuity of diffuse ST-T wave changes in this older woman who now presents with new CP. Any doubt about the presence of acute LAD occlusion (and the need for prompt cath) should have been removed as soon as this prior tracing was found.

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CASE Conclusion:

• Cardiac cath was done a day after this patient came to the hospital. This confirmed the LAD "culprit" artery, which was stented. Unfortunately, by this time — the damage was done.  

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Acknowledgment: My appreciation for the anonymous submission of this 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).
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• 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.