ECG Blog #485 — 30 Minutes Later

Today's patient is a previously healthy middle-aged man who reported a brief episode of CP (Chest Pain) while walking, relieved by rest — followed a day later by recurrence of CP, that now was occurring at rest.

• Additional details about the timing and duration of this patient's CP — as well as the relative severity of his CP at the time the ECG in Figure-1 was recorded — are uncertain.
• Initial hs-Troponin was negative. 

QUESTIONS:

• In view of this history — How would you interpret ECG #1?

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

MY Initial Thoughts:

A history of new CP that is severe enough to prompt a visit to the ED (Emergency Department) — is always of concern. That said — it's hard to draw conclusions as to the likelihood of an acute event from the history we are given. That said:

• The initial ECG is not normal.
• The rhythm is sinus at ~90/minute. All intervals and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves — absent (There is a small initial positive deflection = an r wave in lead III).
• R Wave Progression — probably appropriate (although the finding of an initial R wave that is taller in lead V2 than in V3 suggests that there may be some anatomic misplacement of these 2 electrode leads).

Regarding ST-T Wave Changes — This is concerning! (See Figure-2):

• In this patient with a history of new CP — I interpreted the ST-T wave in lead V2 as hyperacute until proven otherwise (ie, disproportionately enlarged with respect to modest size of the QRS in this V2 lead).
• In the context of new CP + a hyperacute ST-T wave in lead V2 — I interpreted neighboring lead V3 as also hyperacute (ie, "fatter"-at-its-peak and wider-at-its-base than expected, given modest size of the QRS in this V3 lead).
• PEARL #1: In cases like this — I begin my interpretation by looking for the 1 or 2 leads which I know are clearly abnormal (that being leads V2 and V3, which are clearly hyperacute!). My "threshold" for interpreting other leads in this tracing as abnormal is then lowered, especially for neighboring leads (in this case — for leads V1 and V4!).
• PEARL #2: In a patient who shows no sign of LVH on ECG — the slight-but-real ST elevation with surprisingly tall positive T wave in lead V1 is definitely abnormal! Given new CP + hyperacute T waves now in leads V1,V2,V3 (with this ST elevation beginning in lead V1) — this suggests a proximal LAD "culprit" until proven otherwise.
• PEARL #3: The final "neighboring lead" — is lead V4. If I were to see lead V4 in isolation — I might not necessarily call it "abnormal". BUT — in the context of new CP + hyperacute T waves in leads V1,V2,V3 — I interpreted neighboring lead V4 as also hyperacute (the base of this T wave being wider-than-what-I'd-expect for a normal ST-T wave).
• KEY Point: I find it helpful to always try to tell a "story" when interpreting an ECG. As a result, given the clinical history of new CP + hyperacute T waves in leads V1,V2,V3 — my "threshold" for assessing neighboring lead V4 needs to be lowered. Considering this context — I interpreted the wider-than-expected T wave base that we see in lead V4 as abnormal (ie, making for a 4th consecutive hyperacute T wave from lead V1-thru-to-lead V4).
• PEARL #4: Given the above context — the ST segment straightening and slight-but-real ST depression that we see in lead V6 of Figure-2 is real! This most probably represents Precordial "Swirl" (ie, hyperacute anterior lead ST-T waves with ST elevation beginning in lead V1 + ST depression in lead V6 — as discussed in detail in ECG Blog #380).
• Finally — subtle-but-definitely-present ST segment flattening with slight J-point ST depression is also seen in lead V5. I suspect the reason this lead V5 finding is so subtle — is that this is a "transition lead" that falls in between the hyperacute ST-T waves from leads V1-thru-V4 and the ST depression we see in lead V6.

QUESTION:

What about the limb leads in Figure-2? 

• Take another LOOK at ECG #1. Do YOU see any abnormalities in any of the limb leads that support my suspected diagnosis of proximal LAD OMI?

Figure-2: I've labeled today's initial ECG.

ANSWER:

In the absence of a history of new CP and the above-described ST-T wave findings that we see in the chest leads of ECG #1 — I would probably have called the ST-T wave findings that we see in the limb leads of this tracing "nonspecific". BUT — in the context of today's case — there are definitely abnormal ST-T wave findings in a number of limb leads:

• The most remarkable finding in Figure-2 is in lead aVF. Although the QRS complex is tiny in this lead — there should be no doubt that the ST segment is abnormally flat. There is also subtle-but-real terminal T wave positivity in this lead aVF.
• To a lesser extent — similar ST segment flattening with terminal T wave positivity is also seen in the other 2 inferior leads ( = leads II and III).
• To Emphasize: In isolation — I would have called these inferior lead ST-T wave findings "nonspecific". But in the context of clearly abnormal chest lead findings — these reciprocal ST-T wave changes in the inferior leads support the likelihood of ongoing acute proximal LAD occlusion.
• PEARL #5: Once you identify one or two definitely abnormal leads in a patient with new CP (such as leads V2 and V3) — the more additional leads that manifest abnormal ST-T wave findings — the more this supports the premise of acute OMI. In Figure-2 — at least 9/12 leads manifest an abnormal ST-T wave appearance.

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The CASE Continues:

The initial Troponin in today's case was negative. The decision was made not to activate the cath lab on the basis of the above history, the negative initial Troponin — and the initial ECG shown in Figure-1.

• Over a period of the next ~30 minutes — the patient's CP resolved. At this time — a repeat ECG was obtained (shown below in Figure-3).
• The initial cardiologist contacted did not feel cardiac cath was indicated at this time because: i) Chest lead ST-T wave abnormalities were no longer present in ECG #2; — ii) The patient's CP had resolved; and, iii) The initial Troponin was negative.

QUESTIONS:

• Do YOU agree with the rationale provided by this initial cardiologist for not proceeding with cardiac catheterization?
• How can you explain resolution of the abnormal ST-T wave findings that were seen on the initial ECG?

Figure-3: The repeat ECG — obtained ~30 minutes after ECG #1.

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ANSWERS:

The rationale provided above by the initial cardiologist consulted as the reason not to pursue prompt cath in today's case — highlights a series of KEY points and misconceptions.

• As reviewed by sources noted in the ADDENDUM below — the pathophysiology of acute OMI evolution often includes a period of spontaneous reperfusion that is independent of any treatment measures. This period of spontaneous reperfusion may sometimes only be transient — before spontaneous reocclusion occurs. 
• IF clinicians carefully correlate the presence (and relative severity) of CP with the timing of each serial ECG — we can usually figure out when spontaneous reperfusion has occurred because: i) This is most often accompanied by reduction (if not complete resolution) of CP; and, ii) Acute ECG changes (ie, ST elevation and depression) decrease, if not normalize on the way to developing the typical pattern of reperfusion T waves (ie, T wave inversion in leads that previously showed ST elevation). All the treating clinician(s) need to do — is correlate the presence (and relative severity) of CP symptoms with serial ECGs. Doing so often renders the diagnosis of acute OMI obvious.

Correlating the above concepts to the repeat ECG:

• PEARL #6: To facilitate interpretation of the repeat ECG in today's case ( = ECG #2) — I've placed it next to ECG #1 in Figure-4. The clinical reality is that unless the 2 ECGs you are comparing are reviewed side-by-side — that subtle differences between the 2 tracings will be missed.
• The principal differences between ECG #1 and ECG #2 — are seen in the chest leads. The hyperacute T waves previously seen in the anterior leads have almost completely resolved — with this dramatic improvement in the ECG picture occurring within 30 minutes after ECG #1 was recorded, in association with resolution of CP!
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• PEARL #7: The near complete resolution of hyperacute ST-T wave changes that we see in Figure-4, corresponding to complete resolution of CP: i) Constitutes a "dynamic" ECG change — which provides further support in favor of an acutely evolving cardiac event; and, ii) Strongly suggests that the "culprit" artery was acutely occluded when the patient had CP (ie, at the time ECG #1 was recorded) — but that the culprit artery has now spontaneously opened in association with this dynamic ST-T wave improvement seen at the same time the patient's CP resolves.
• The "good news" — is that the "culprit" artery is now open.
• The "less good news" — is that what spontaneously opens — may at any time spontaneously reclose unless prompt cath with PCI is performed to ensure that the culprit artery remains open.
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• PEARL #8: The fact that the initial Troponin in today's case was negative did not rule out an acute event (as was assumed by the initial cardiologist on the case). More than 25% of patients with an acute STEMI have an initial hs-Troponin value ( = high-sensitivity Troponin) below the threshold for acute infarction (Wereski et al — JAMA Cardiology 5(11):1302, 2020).
• The reason an initial Troponin value may be negative despite an ongoing acute infarction — will in large part depend on the duration of time that the "culprit" artery is occluded. If the culprit artery is only briefly occluded (before spontaneous reperfusion occurs) — then serum Troponin might not rise!
• On occasion — the first and the second hs-Troponin may remain within the normal range despite documented infarction. This is because there may be an ongoing cycle of acute coronary occlusion — followed by spontaneous reperfusion — then spontaenous reocclusion — back-and-forth between culprit vessel closure and spontaneous reopening — until a final state of the culprit artery is reached.
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• KEY PEARL #9: It is precisely because of this potential back-and-forth cycling between spontaneous culprit artery reperfusion and reocclusion — that careful attention to the timing and duration of symptoms, correlated to each serial ECG is so important. For example — IF the initial ECG in today's case had been obtained 30 minutes later than it was (ie, at the time ECG #2 was done) — then providers would have seen a patient whose CP had totally resolved, with an ECG showing no more than minimal nonspecific changes.
• Knowing that your patient's history of symptoms has been stuttering (ie, off-and-on) should prepare YOU to appreciate that a negative initial Troponin and minimal ECG abnormality — might simply reflect spontaneous reperfusion of an acute ongoing infarction. BOTTOM Line: More than 1 Troponin and more than a single ECG may be needed to arrive at the correct diagnosis!

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded ~30 minutes later (after resolution of CP). Unfortunately artifact precludes interpretation of lead V6 in ECG #2.

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Today's CASE Concludes:

Fortunately — today's patient was transferred to a second hospital, where another cardiologist was consulted.

• This 2nd cardiologist did proceed with cardiac catheterization — which revealed 99% occlusion of the LAD, that was stented.

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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 (6/27/2025):

• 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).
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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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