ECG Blog #474 — "Please Believe Me & My ECGs"

The ECG in Figure-1 is from a man in his 60s — who presented to the ED (Emergency Department) for new-onset CP (Chest Pain).

• The patient reported intermittent CP for the past 2-3 days prior to this episode.
• Tonight's epsiode began ~1 hour prior to arrival in the ED. His CP severity =10/10 at the time the ECG in Figure-1 was recorded.

QUESTION:

In view of the above history:

• How would you interpret the initial ECG in Figure-1?

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

MY Initial Thoughts on Today's CASE:

New-onset CP of 10/10 severity in a man in his 60s is a worrisome clinical scenario that immediately places this patient in a higher-risk group for an acute event. As a result — the onus of "proof" is on us to rule out an acute event (rather than having to "rule in" an acute event). KEY Points include the following:

• Given the above history — any ECG abnormalities on this patient's initial tracing should be concerning.
• And, if no diagnostic ECG findings are seen on this patient's initial ECG — then especially since this patient's acute episode of CP began just 1 hour prior to arriving in the ED, the ECG should be repeated within 15-30 minutes.
• The fact that this patient has had intermittent CP over the previous 2-3 days may complicate interpretation of the initial ECG. This is because an event could have occurred 2-3 days ago (when this patient's CP began) — which if followed by spontaneous reperfusion of the "culprit" artery — might result in an initial ECG with no more than subtle abnormalities (ie, if the initial ECG was recorded during the period of pseudo-normalization).

PEARL #1: Many emergency providers still do not appreciate the clinical reality that the process of acute coronary occlusion (ie, acute OMI) — is often not a single fixed event. 

• Instead of a single fixed event — what often happens is that the "culprit" coronary artery occludes (with resultant acute CP and ST elevation) — but then minutes-to-hours later, there is spontaneous reopening of the culprit vessel (with a decrease or even resolution of CP that occurs in association with a return of ST segments toward normal). 
• What then follows is development of "reperfusion T waves" — in the form of ST depression or T wave inversion that ensues in the minutes, hours or sometimes 1-2 days after reestablishment of coronary flow.
• Because the above process may occur more than once (ie, the "culprit" artery may spontaneously close — then reopen — then reocclude again) — the ultimate state of the "culprit" artery might be anything at the time the initial ECG is recorded.

The Initial ECG in Figure-1:

With the above considerations in mind — I thought the initial ECG in today's case manifested a number of concerning findings that I have labeled in Figure-2.

• Of note — the very low amplitude P wave in lead II, with small negative P wave in lead III and positive P wave in lead aVL — suggests that there may be a low atrial rhythm. This can be a normal variant rhythm — that does not alter our assessment of potential acute ST-T wave changes.
• Beyond the rhythm — my "eye" was immediately drawn to high-lateral leads I and especially aVL (within the RED rectangles in Figure-2). In this patient with new CP — there is no doubt that the straightened, downsloping ST segment in lead aVL and the shelf-like flattened ST depression in lead I are abnormal.
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• PEARL #2: Given the "magic" mirror-image opposite ST-T wave relationship between lead III and lead aVL that exists with acute inferior OMI — I always scrutinize with extra attention the 2nd member of this lead III-aVL tandem when the 1st member looks abnormal.
• Although subtle — there is ST segment straightening with slight ST elevation in lead III — that presents the mirror-image opposite appearance to the downsloping, straightened ST segment we see in lead aVL (See ECG Blog #171 — for more on this "magic" leads III-aVL relationship).
• Support that this subtle ST segment straighening with a hint of slight ST elevation in lead III is "real" — is forthcoming from the similar ST segment appearance in the other 2 inferior leads ( = leads II and aVF — within the BLUE rectangles).

Figure-2: I've highlighted abnormal ST-T wave findings in today's initial ECG. What about the chest leads?

What about the Chest Leads in Figure-2?

Additional confirmation regarding concern for an ongoing acute inferior OMI — is forthcoming from the appearance of leads V2 and V3 in Figure-2:

• PEARL #3: Because of the common blood supply in most patients between the inferior and posterior walls of the left ventricle — seeing a suggestion of acute posterior OMI adds support that uncertain limb lead findings are likely to be "real".
• This is precisely what we see in Figure-2. As is often emphasized in this ECG Blog — there normally is slight, upward sloping ST elevation in leads V2 and V3. However, the BLUE arrows in these leads show, if anything — that there is slight ST depression in leads V2,V3 in association with ST segment flattening.
• Abnormal ST segment flattening continues in lead V4 — with in addition, slight ST depression in leads V5 and V6.

Impression of ECG #1:

In this patient with intermittent symptoms for 2-3 days, who now presents with new 10/10 CP — it should be apparent on seeing this initial ECG, that prompt cath is almost certain to be needed:

• The diagnosis of acute infero-postero OMI should be strongly suspected from this initial ECG. The lack of sufficient ST elevation to fulfill STEMI criteria may be the result of some pseudo-normalization following some spontaneous reperfusion of the "culprit" artery.
• Additional ST flattening with slight depression extending out to lateral chest leads V5,V6 might reflect multi-vessel disease.
• Repeating this initial ECG in short order may yield a more definitive ECG picture.
• A right-sided ECG may also prove insightful (ie, Given our strong suspicion of acute RCA occlusion — acute RV involvement could be attenuating the amount of anterior ST depression that would otherwise be seen with posterior OMI).

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The CASE Continues:

ASA was given and the consulting cardiologist was called.

• The initial ECG was repeated — and is shown in Figure-3. The patient continued to have 10/10 CP.
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•   — How would YOU interpret this repeat ECG?

Figure-3: This is the repeat ECG — recorded ~10 minutes after the initial tracing. Patient still with 10/10 CP.

The Repeat ECG:

Significant change between ECG #2 and ECG #1 was not noted.

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PEARL #4: It is exceedingly EASY to overlook subtle changes between serial tracings if each ECG is viewed separately. This apparently is what happened in today's case.

• To illustrate this point — I've put the repeat ECG just below the initial tracing in Figure-4.
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•    — Doesn't this placement in Figure-4 make it easier to see subtle-but-real differences between these 2 tracings?  

Figure-4: To facilitate assessment of the first 2 ECGs in today's case — I've put the initial and repeat ECGs together.

Comparison between the Initial and Repeat ECGs:

As a reminder — the 1st thing to do when comparing serial tracings for acute changes — is to compare the frontal plane axis and QRS morphology in the chest leads. This is because a change in either the axis and/or in chest lead QRS morphology may contribute to a difference in ST-T wave appearance that is not the result of increasing ischemia.

• Fortunately in Figure-4 — Both the frontal plane axis and QRS morphology in ECG #2 are essentially unchanged from what they were in ECG #1. This means that even minimal ST-T wave differences that might be seen between these 2 tracings are likely to be "real".
• Regarding the chest leads, other than slightly deeper T wave inversion in lead V2 of ECG #2 — there has been no significant ST-T wave difference in the other 5 chest leads.
• In contrast, there has been a change in ST-T wave appearance in the limb leads, in that: i) The ST-T waves in leads III and aVF look more hyperacute than they did in ECG #1 (the ST-T wave looks "bulkier" in these leads — with a taller T wave peak and more J-point ST elevation); — and, ii) The reciprocal ST depression in leads I and aVL of ECG #2 is deeper, and looks more "acute".

PEARL #5: I interpreted the ST-T wave changes that we see between the 2 tracings in Figure-4 as "real" — because they are present in at least 5 leads. In this patient with 10/10 CP — these findings qualify as a "dynamic" ST-T wave change. This solidifies the diagnosis of acute infero-postero OMI until proven otherwise.

• BOTTOM Line: At this point in today's case (ie, as soon as I saw ECG #2 — which was recorded just over 10 minutes after arrival in the ED) — I thought clear indication for prompt cath with PCI was now established.

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The CASE Continues:

The severity of this patient's CP waxed and waned over the next few minutes — but then returned to a level of 10/10.

• As shown in Figure-5 — a 3rd ECG was obtained in the ED, about 20 minutes after ECG #2. Severity of this patient's CP at the time ECG #3 was recorded was uncertain.
• All 3 tracings were reviewed by cardiology which concluded, "treat as a NSTEMI" — with plan to transfer to a cath-capable center that morning. That transfer was accomplished over 6 hours after the patient arrived in the ED.

QUESTION:

• Your thoughts on the case after seeing ECG #3?

Figure-5: Comparison beween the 2nd and 3rd ECGs.

Assessment of ECG #3 in Figure-5:

There has been further progression of the acute infero-postero OMI in ECG #3.

• All 3 inferior leads show an increase in hyperacuity of the ST-T waves in Figure-5. This is best appreciated in lead III — in which the hypervoluminous ST-T wave now exceeds the height of the R wave in this lead.
• A similar increase in hyperacuity is seen in the depth of the reciprocal ST depression in leads I,aVL — and in the T wave inversion in lead V2. There is also more ST depression in leads V4,V5,V6.
• BOTTOM Line: There is no longer any doubt about the diagnosis. This is not a "NSTEMI". Instead — the history and progressive "dynamic" ST-T wave changes on serial ECGs is diagnostic of an acute OMI resulting in ongoing infero-postero OMI.

Final Follow-Up:

• Cardiac Cath was performed later that morning at the referral hospital. It confirmed that the 99% RCA occlusion seen on cath was indeed the "culprit" vessel.
• Unfortunately — Failure to recognize acute coronary occlusion from the 3 serial ECGs performed in the ED resulted in a 6+ hour delay until cardiac cath and PCI were finally performed.

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Acknowledgment: My appreciation to Frank Maggio (from Florida, USA) for the case and this tracing. 

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For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-6: 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).
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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.
• 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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