5 Cardiologists said this is not a STEMI. But was it an OMI?

Written by Pendell Meyers

A male in his early 50s presented with waxing and waning chest pain starting at rest. He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS.

Here is his initial ECG:

What do you think?

Sinus rhythm
-STE in V1-V5, possibly a tiny amount in V6, and small amount in I and aVL, and II
-Reciprocal STD (although perhaps isoelectric at J point, immediate STD after the J point) with very ischemic appearance in lead III (down-up T-wave is strongtly suggestive)
-Large T-waves in V2-V4, which may be either a normal variant or hyperacute
-Very tiny Q wave in lead V2, as well as V6, I, and aVL, which is not seen in normal variant
-STEMI criteria are not formally met; although V2 has sufficient STE (greater than 2.0 mm), neither of it's neighbors have enough STE to meet criteria (V1 is close at 0.5 mm of the "required" 1.0 mm)


This is all highly diagnostic of acute anterior MI, with the most likely etiology being OMI of the proximal-mid LAD.

The formulas would be formally contraindicated because of the Q-wave in V2, but if we use them anyway the results are (using QTc 397 ms):


4 Variable formula: 20.32
3 Variable formula: 24.08

Both formulas predict LAD occlusion.





The physician called the on-call cardiologist immediately to discuss this ECG, but the cardiologist reportedly said not to activate the cath lab because he/she was not convinced by the ECG. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI."


The first troponin I returned elevated at 0.11 ng/mL.

Serial ECGs were obtained, including this one several hours later:

Slightly more STE and longer QT than prior.

Although I do not see much difference between the ECGs, for some reason (perhaps ongoing pain or rising troponins) the case was reevaluated at this time and the decision was made to perform cath.

They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result.


Peak troponin I was greater than 75 ng/mL (the assay does not measure higher than this apparently).

Learning Points:

STEMI criteria misses 25-40% of OMI, like this case for example.

Due to our paradigm which lags far behind the current achievable skill level, cases like this will continue to be missed or delayed until we solve the problem by replacing the paradigm.

This is another case demonstrating OMI with all ST segments concave.

Pay attention to even the tiniest Q-waves in the right context and assume they are new until proven otherwise. New Q-waves during MI are NOT wide ("greater than 40 ms") until later.

Any Q-wave in V2 in the presence of an otherwise normal QRS complex is abnormal.

Repeat ECGs are almost always helpful.

Use of the formulas would have improved recognition of this OMI.

Ongoing ischemia (by symptoms, ECG, or troponin) despite maximal medical management is an indication for emergent cath lab activation.

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MY Comment by KEN GRAUER, MD (8/15/2019):

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Once again, the wrong question was asked in this case. That's because it should not matter IF the initial ECG in this case ( = ECG #1 in Figure-1) represents an acute STEMI or an acute OMI — since initial management should be the SAME:

• Considering that this patient had multiple cardiac risk factors + a good story for ongoing new ischemic-sounding chest pain and, the ECG abnormalities seen in ECG #1 — prompt cath to define the anatomy, with goal of acute reperfusion if acute OMI is confirmed is the treatment of choice.
• Unless a prior ECG on this patient can be found that shows identical findings as we see in ECG #1 — there is NO way to rule out acute OMI. As a result — it’s hard to justify not doing acute cath ...

Figure-1: The 2 ECGs in this case (See text).

MY THOUGHTS on ECG #1: Dr. Meyers has skillfully detailed the abnormal ECG findings. To facilitate visualization — I’ve put both tracings together and labeled the following key points:

• There is loss of the initial r wave in lead V1 — with development of a small-but-real Q wave in lead V2 of ECG #1. Overall QRS morphology in lead V2 is strange, with this qRS complex being “sandwiched in” between an rS complex in lead V1, and an rS complex in lead V3 — so there may be some lead misplacement of lead V2. That said — the small q in V2 is almost certainly a real finding, and clearly abnormal.
• There is more than 2 mm of ST elevation in lead V2 of ECG #1 (Compare the RED horizontal baseline with the RED arrow in this lead). The very wide T wave base, with T wave peak clearly exceeding R wave amplitude in this lead clearly defines the T waves in V2 as being hyperacute.
• Disproportionate T wave amplitude (compared to R wave height) in leads V3 and V4 define those T waves as also being hyperacute.
• Note that there is more ST elevation in lead V4 of ECG #1, than there is in lead V3 (Compare the RED horizontal baseline with the RED arrow in these leads). There shouldn’t be more ST elevation in V4 than in V3.
• Finally (as per Dr. Meyers) — the ST-T wave in lead III is clearly abnormal (curved RED line) — with the scooped ST segment ending in a biphasic (negative-then-positive) T wave.

BOTTOM LINE: Without an identical-looking prior tracing — there is NO way to rule out the possibility (if not probability) of acute ST-T wave findings in at least leads V2-thru-V4 + Q in V2 + reciprocal change in lead III, in this patient with new chest pain. A millimeter definition of acute STEMI should not be needed to justify the need for prompt cardiac catheterization.

• NOTE: With proximal LAD OMI — one typically sees: i) significant ST elevation beginning in leads V1,V2; ii) reciprocal ST depression in each of the 3 inferior leads (II,III,aVF); and, iii) significant ST elevation in lead aVL. Because we only partially see these features in ECG #1 — I would interpret this tracing exactly as Dr. Meyers did = probable “proximal-mid acute LAD occlusion”.

MY THOUGHTS on ECG #2: Several hours later — ECG #2 was obtained. As per Dr. Meyers — for the most part, there has been little change between the 2 tracings. That said:

• I think there is now more ST elevation in lead V2 of ECG #2 than there was in ECG #1 (Compare the BLUE horizontal baseline with the BLUE arrow in this lead).
• Note that there is once again more ST elevation in lead V4 than in lead V3 of ECG #2. This is not a normal finding.

BOTTOM LINE: Given the clinical history — ECG #2 should not have been needed for making the decision to take this patient to the cath lab ...


Our THANKS to Dr. Meyers for this insightful case!