ECG Blog #441 — What to Learn from this Case?

The ECG in Figure-1 was obtained from a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with a 1-hour history or new CP (Chest Pain). 

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Should the cath lab be activated?  And, if not — What would you do?

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

MY Thoughts on this CASE:

This is difficult. The ECG findings in Figure-1 are extremely subtle. That said — the initial ECG in today's case is not normal!

• It's important to start with the premise that since this middle-aged woman presented for emergency care with new-onset CP — she is automatically in a higher-risk group for an acute cardiac event. As a result — our threshold for interpreting ECG findings as potentially consistent with a recent or ongoing acute is lowered. 
• By way of contrast — our suspicion for an acute event would not be as high if this patient's symptoms were less typical for new-onset chest pain.

As to the ECG in Figure-1: 

• The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes: 

• There are no Q waves (a tiny initial r wave [and not a Q wave] is seen in lead aVL). 
• R wave progression is normal (with Transition, where the R wave becomes taller than the S wave is deep — occurring normally between lead V2-to-V3).

The ECG abnormalities relate to ST-T wave findings:

• In a patient with new CP — my "eye" was immediately drawn to lead V2 (within the RED rectangle in Figure-2). As I often emphasize in this ECG Blog — there should normally be slight, gently upsloping ST elevation in leads V2 and V3. This is clearly missing in lead V2. Instead — the ST segment in lead V2 is flat without any J-point elevation — and with a biphasic T wave showing terminal positivity.
• In the context of the definitely abnormal ST-T wave in lead V2 — neighboring lead V3 (within the BLUE rectangle) is also abnormal because its ST segment shows flattening and no J-point ST elevation.

KEY Point: Although the remaining 10 leads in Figure-2 might understandably be thought of as insignificant — in this patient with new CP — the subtle-but-definitely-abnormal ST-T wave abnormalities in leads V2 and V3 suggest the possibility of acute posterior OMI until proven otherwise.

• By itself — I would not have interpreted the negative ST-T wave in lead V1 as abnormal, since this ST-T wave shape in lead V1 may sometimes be seen normally. But in the context of suspecting posterior OMI (from the appearance of ST-T waves in neighboring leads V2,V3) — the ST-T wave in lead V1 could reflect a continuation of this process.
• Posterior OMI is very commonly associated with inferior OMI — since blood supply to these 2 areas of the heart is similar (arising from either the RCA or LCx). Therefore, the ST segment coving seen in leads III and aVF of Figure-2 (albeit without any ST elevation) could reflect recent inferior OMI.
• The final subtle finding I noted in Figure-2 — relates to straightening of ST segment in lead V6. In the context of the above noted other ST-T wave abnormalities — this could represent a hyperacute T wave in this lateral chest lead.

BOTTOM Line: I don't know that I would have necessarily activated the cath lab on the sole basis of the ECG in Figure-2. That said — in this middle-aged woman with new CP — we need to appreciate the possibility of recent or ongoing infero-postero-lateral OMI.

• Sometimes — "Ya gotta be there." If this patient's CP was severe and persistent in association with the ECG recorded in Figure-2 — this may have been enough to activate the cath lab at that time (ie, unrelieved ischemic CP is an accepted indication for cardiac cath!).
• At the least — a repeat ECG should have been obtained within 15-30 minutes of ECG #1 — with continued frequent serial ECGs being recorded until it can be comfortably determined IF an acute OMI was or was not ongoing (with recording of frequent serial ECGs also serving the goal of convincing a reluctant interventionist on the need for prompt cath).
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• Given the history of new CP and the ECG findings highlighted above — any elevation in Troponin needs to be taken as evidence of an ongoing event until proven otherwise (especially if serial Troponins show a continued increase).
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• Stat Echo in the ED at the time of CP — can provide additional objective evidence of an acute evolving event (ie, If there is a localized wall motion abnormality on Echo). 
• To Emphasize: If the patient is no longer having CP at the time that the Echo is done — then a normal Echo does not rule out anything. The patient must be having CP at the time of the Echo for a normal result to be used as evidence against an acute event.

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

The CASE Continues:

• The ECG was not repeated in the ED ...
• The initial Troponin was slightly elevated. There was slight increase with the 2nd Troponin, though the total level was still under 2.0 ng/mL.
• Echo was not part of initial evaluation.
• Information regarding the status of the patient's CP was not available from chart review.

Cardiac Cath was done the next day — presumably because of slow-rising Troponin levels that attained ~10 ng/mL.

• Cath showed 100% occlusion of the 1st Obtuse Marginal Branch of the LCx (Left Circumflex) coronary artery, which was felt to be the "culprit" artery. PCI was successful in restoring flow.
• Echo done around the time of cardiac cath showed no wall motion abnormality, and an excellent ejection fraction of 72%.
• The patient did well clinically — and was discharged with a diagnosis of "NSTEMI".

The repeat ECG (that was done after cath with PCI) — is shown together with the initial ECG in Figure-3.

Figure-3: Comparison between the 2 ECGs in today's case.

COMMENT:

Putting together the “pieces” of today’s case that we are aware of — it appears that this patient did have an acute OMI. The cath finding of acute coronary occlusion of a branch of the LCx is consistent with the above-noted infero-postero-lateral changes seen in ECG #1.

• A repeat ECG was apparently only done after a successful PCI procedure was completed (shown in comparison to the initial ECG in Figure-3). The principal changes in this post-PCI are seen in the chest leads — and feature: i) A decidedly earlier increase in R wave amplitude, which is now predominant already in lead V2 (consistent with a completed posterior OMI); ii) Return of a more normal-looking appearance to the ST-T waves in leads V2 and V3, which now feature slight J-point ST elevation and upright T waves (consistent with posterior reperfusion T waves); and, iii) T wave “deflation” in lateral chest leads V4,V5,V6 (also consistent with reperfusion).
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• Concluding Thoughts: PCI was “successful” in reperfusing the “culprit” vessel in today’s case. That said — cardiac cath was only performed the following day, whereas the diagnosis of acute OMI could have been made much sooner (potentially salvaging significantly more myocardium). 
• Among the Lessons-to-be-Learned include those noted in interpretation of the subtle findings in the initial ECG and the BOTTOM Line reflections noted in my above discussion. Today’s case covers many similar aspects recently covered in ECG Blog #433.
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• P.S.: As noted above — the final discharge diagnosis in today's case was that "the patient had a NSTEMI". But as happens in all-too-many cases — the history, elevated troponin, cath finding of 100% occlusion of the 1st Obtuse Marginal Branch of the LCX — and the post-cath ECG findings consistent with a completed posterior MI (ie, the predominant R wave seen in lead V2 of Figure-3 — as well as the serial ECG changes consistent with reperfusion T waves) — the "real" diagnosis is that the patient had an infero-postero-lateral OMI that was overlooked by the treatment team (similar in regard to misdiagnosed "NSTEMIs" in ECG Blog #337 and ECG Blog #400).

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Acknowledgment: My appreciation to 張三毛 = JJ (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes (and also Diffuse Subendocardial Ischemia).
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• ECG Blog #337 and ECG Blog #400 — Examples of "NSTEMI" that were really ongoing OMIs.
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• ECG Blog #274 — How to tell if leads V1,V2 are misplaced.
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• ECG Blog #351 — Blog #285 — Blog 246 — Blog #80 — for examples of acute posterior OMI.
• ECG Blog #317 — reviews whether to use Posterior Leads?