ECG Blog #506 — What did the Repeat ECG Show?

This case was sent to me by an anonymous follower.

• If told that this patient was having new CP (Chest Pain) — How would YOU interpret this tracing?

Figure-1: The initial ECG in today's case — obtained from a patient with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

In view of the history of new CP — I was extremely concerned by this tracing. To emphasize — that the ECG findings are extremely subtle, but they often are on an initial tracing.

• In Figure-2 — I have highlighted within the RED rectangle the single lead that most caught my "eye".
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• Why do I say this?

Figure-2: I've highlighted the lead that most caught my "eye".

My Concern about Lead V1:

The QRS complex in lead V1 is tiny.

• Normally — the ST-T wave in this lead is isoelectric, or slightly negative. In a patient who does not have LVH or QRS widening — the ST-T wave in lead V1 should virtually never show the amount of disproportionate ST segment coving and elevation that we see in Figure-2.
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• Given the history of new CP — the abnormal appearance of the ST-T wave in lead V1 prompted me to look extra carefully at the other 11 leads on this tracing.

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MY Thoughts on the Other 11 Leads:

As stated earlier — the ECG findings on today's tracing are extremely subtle. But they often are on the initial tracing of an acute cardiac event. I've labeled KEY findings below in Figure-3.

• The rhythm is sinus arrhythmia at a rate slightly over 60/minute. Intervals (PR-QRS-QTc) and the frontal plane axis are normal. There is no chamber enlargement.
• There is low voltage in the limb leads (None of the 6 limb leads exceed 5 mm in amplitude).
• Transition occurs early (ie, The R wave in lead V2 is already equal to the S wave in this lead — whereas "transition" usually does not occur until later).
• There is ST segment straightening in lead V3. Given my heightened concern about anterior ST elevation, prompted by the history of new CP and the abnormal ST-T wave appearance in lead V1 — I thought the ST-T wave in lead V3 looked "bulkier" than-it-should-be (ie, "fatter"-at-its-peak and wider-at-its-base than I'd expect given modest R wave amplitude in this lead).
• I was uncertain what to make of the ST-T wave appearance in neighboring leads V4,V5 — but there is definite ST segment flattening and subtle-but-real ST depression in lead V6.
• That the above-noted ST-T wave findings in leads V1,V3,V6 are "real" — is supported by the subtle ST segment flattening and depression in each of the inferior leads (BLUE arrows in these leads).

MY Impression of Today's Tracing:

Based on the above findings (and before I was told what happened in this case) — I wrote back that my concern was that the ECG picture in Figure-3 could represent the early appearance of Precordial "Swirl".

• As described in detail in ECG Blog #380 — the colorful term, "Swirl" facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.
• KEY features of "Swirl" are: i) Abnormal ST elevation and an usual ST-T wave appearance in lead V1 (especially when there is no LVH and no QRS widening); — and ii) Reciprocal ST depression in lead V6 (if not also in lead V5) — with the shape of this lateral chest lead ST depression being flatter than that seen with simple LV "strain" from LVH (Check out ECG Blog #380 for a much more detailed description!).
• To emphasize — that other anterior leads in addition to lead V1 often manifest hyperacute T waves with "Swirl" — but that in an early pattern, ST-T wave abnormalities in other chest leads might not be obvious. It is for this reason that my concern regarding leads V1,V3,V6 was heightened in today's case because this patient had new CP — and especially because each of the inferior leads showed definite ST segment flattening and depression (as they often do with a proximal site of LAD occlusion).

Figure-3: I've labeled KEY findings on today's tracing.

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CASE Follow-Up:

Today's patient died suddenly — a short while after today's ECG was recorded (before a repeat tracing could be recorded). Providers were appropriately concerned about abnormal findings on the initial ECG.

• Presumably — the ECG in Figure-3 is the result of a very proximal acute LAD occlusion that rapidly evolved into an extensive acute infarction with cardiogenic shock before treatment to open the "culprit" vessel could be initiated.

Learning Points:

Sometimes the evolution of acute infarction is extremely rapid — with dramatic ECG changes and clinical deterioration of the patient occurring over a period of minutes (See ECG Blog #459 — as well as many other cases in this ECG Blog).

• Today's case serves as reminder that: i) A history of worrisome new chest pain immediately places your patient at increased risk of an acute evolving event — therefore the need for close attention to subtle ECG findings that might not otherwise be important in an asymptomatic patient; — ii) When we see 1 or 2 leads that clearly manifest abnormal ECG findings in a higher-risk patient with new CP (as was the case for leads V1 and V6 in today's tracing) — We need to pay extra close attention to other leads that may show subtle supportive findings (as per the inferior lead ST depression in today's tracing); — and, iii) When there is any doubt about whether an acute process is evolving — Repeat the ECG within 10-20 minutes of the 1st tracing (which in today's case was not possible given the rapid demise of this patient).

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P.S.: And the Patient had Low Voltage ...

As I've often noted in this ECG Blog — there are many potential causes of low voltage (See ECG Blog #272 — for full discussion of this entity).

• The above said — among the potentially relevant causes of low voltage in today's case is myocardial "stunning" — that may be the result of a large acute infarction associated with cardiogenic shock that presumably resulted in the sudden demise of today's patient.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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ADDENDUM (11/22/2025): 

• 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.