Friday, June 17, 2016

Anterior STEMI? Or Benign Early Repolarization?

This was posted a few years ago.  I'm highlighting it again, with comments from Ken Grauer below.

This was sent to me by Jason Winter, of Facebook Clinical Electrocardiology Page

This is a 36 yo m with h/o TBI and epilepsy.  He had a seizure this morning and rolled out of bed unable to get up.   There were no injuries and no chest pain and he appeared well.  He complained of 3 days of diarrhea and abdominal pain.  The medics recorded a prehospital ECG: 
The computerized QTc is 397 ms
Jason writes: "
What's your thoughts Steve?"
Jason was very skeptical of STEMI.
What do you think?

I agree.
V4 especially looks like early repolarization.  There is high R-wave voltage.
The formula for differentiating LAD occlusion from early repolarization requires ST elevation at 60 ms after the J-point (here 5 mm), computerized QTc, and R-wave amplitude.  Unfortunately, the R-wave is cut off on this ECG but it appears as if it would be at least 20 mm.  This results in a value of 22.883.  While one should be suspicious of any value greater than 22.0, this does not indicate LAD occlusion.

Note: In our study, we excluded from analysis cases with 5 mm of ST elevation because they would be "obvious," not subtle, anterior MI.  But this measurement was at the J-point, which on this ECG is 4 mm.  STE at 60 ms after the J-point is substantially higher than at the J-point. 

Pretest probability: Especially when there is no Chest pain, or there are very atypical symptoms, one should be very suspicious of the diagnosis of coronary occlusion unless the ECG is crystal clear.

More analysis: V4 has a high J-point, after which the ST segment is comparatively flat, without a correspondingly massive T-wave.  The T-wave is, in fact, small compared to the large R-wave.  This also argues against STEMI.

What was the outcome?


"I later found out that this is a patient who regularly calls paramedics to c/o chest pains and he had fooled many of them. And the cath lab is alerted most of the time."

So this was the patient's baseline ECG.

Learning point

This is not to suggest that such an ECG should summarily be dismissed, but that in a patient with a low pretest probability and such an ECG may indeed have early repolarization, and further investigation might be undertaken before any cath lab activation.

Look for old ECGs
Do serial ECGs
Do echocardiography

MY Comment by KEN GRAUER, MD (10/1/2020):
From time to time — it's helpful to "resurface" prior cases that convey timeless important lessons. The diagnostic problem posed in today's repost from June 17, 2016 is a perfect example of this. 
  • The ECG in this case was not indicative of acute LAD occlusion. Instead — it represented this patient's "baseline" tracing.

KEY POINTS from this CASE:
  • The presenting history often provides invaluable clues to the likelihood of an acute cardiac event. (The patient is a 36yo man who was seen for a seizure. There was no chest pain. This is a "low prevalence" history for an acute cardiac event.).
  • Always look for prior ECGs for comparison. (Previous ECGs in this case were very similar to the one we were asked to interpret).
  • Check for old records. (Turns out that the patient regularly called EMS for complaints of chest pain that frequently led to cath lab activation.)

When I first looked at the ECG in this case — I was concerned about potential LAD OMI. After all — there is ST elevation in virtually all chest leads, with ST segment straightening in leads V3 and V4 (with no less than 5 mm of J-point ST elevation in lead V3!). In addition — slight ST elevation in lead aVL and T wave inversion in each of the inferior leads looked consistent with reciprocal changes.
  • BUT — This is a prehospital ECG!

For clarity — I have reproduced the ECG in this case in Figure-1, in which I've labeled with RED arrows an important finding seen in 4 KEY leads.

Figure-1: I've labeled today's ECG to show where QRS complexes are cut off.

It’s important to recognize WHY I added the 4 RED arrows to Figure-1:
  • There is a limit to the amount of voltage that prehospital ECGs in most EMS systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit. Careful scrutiny between the 4 RED arrows and the horizontal RED lines reveals the abrupt cutoff from this truncation. Therefore — We have NO idea as to how deep the S waves in leads V2,V3 are — nor how tall the R waves in leads V4,V5 are.

  • Among other examples of this phenomenon (in which prehospital ECGs give a false impression of the relative amount of anterior chest lead ST elevation) — is the case from the February 6, 2020 post in Dr. Smith's ECG Blog (Please see My Comment at the bottom of the page in that post).

  • In Figure-1 — I suspect that much of the reason for the seemingly marked ST elevation in lead V3 arises from LVH, with exceedingly deep S waves in leads V2 and V3.
  • A cardiomyopathy with dilated chambers might also explain the RAA (tall, peaked P waves in the inferior leads) — and the ST-T wave depression in the inferior leads (ie, ST-T wave changes of LV "strain" may sometimes be seen in inferior leads in patients with marked LVH).

  • NOTE: The “easy solution” for resolving the problem of excessive QRS amplitude, with resultant truncation of complexes — is to record the ECG at HALF standardization. Unfortunately, this option might not be available for pre-hospital tracings (but it can be done once the patient arrives in the ED for their initial hospital tracing).

FINAL Thoughts on this Case:

Although LVH with extremely deep anterior S waves (in leads V2,V3) may explain the marked ST elevation in lead V3 of Figure-1 — the S wave is not deep in lead V4. In addition — there is ST segment straightening in both leads V3 and V4 — and, at least for the middle complex in lead V5, I thought the ST segment coving looked potentially worrisome.
  • To Emphasize — If I was seeing this patient for the 1st time in the ED without any medical records or prior ECGs available for comparison — and — IF the history was of new-onset cardiac-sounding chest pain — I would not be able to rule out the possibility of an acute cardiac event on the basis of this single ECG alone. But knowing this information (as described above) — allows us to rapidly identify the ECG in Figure-1 as one more manifestation of this patient's baseline ECG. It's worth remembering that this ECG does not represent acute LAD occlusion!



  1. Concave vs Convex, this case is Convex, not concaved i.e., Notch, J hook, Smiley face, etc..

    1. All precordial leads V2-V4 do have a trace of upward concavity, to my eye. There is a bit of inferior ST depression in aVF and, I agree, this is highly suspicious for LAD occlusion. But it goes to show that the two entities can be very difficult to differentiate.

  2. Difficult one

    V3 is especially indicating STEMI

    What about the ST depression and TWI on inferior leads

    Thanks for the case ..

    1. Bashar,
      There is a bit of inferior ST depression in aVF (in addition to inferior T-wave inversion) and, I agree, this is highly suspicious for LAD occlusion. But it goes to show that the two entities can be very difficult to differentiate.

  3. Insightful case! I am curious Steve — How would you have interpreted this tracing if the patient was new to the Emergency Department and presented with new-onset chest pain but no prior tracing was available? This is admittedly a rhetorical question, which I suspect the 3 last lines under your “Learning Point” answers. THANK YOU for presenting this case!

    1. Ken,
      I probably would have activated the cath lab.
      Just goes to show that pretest probability is critical in making decisions based on the ECG!

    2. Thanks Steve — I feel MUCH better hearing your answer — :)

  4. The inferior T-wave inversions are troubling without having a prior ECG for comparison.

    1. Paul,
      Indeed they are. I forgot to point that out and am glad to get comments on that.

  5. Very tough case, Steve. I noticed the P waves in the inferior leads were rather large and gothic-appearing, though the P waves in V1 were unremarkable. It would be interesting to know if there were any history of tricuspid stenosis or anything congenital. Also, the precordial T waves are really very impressive - if not for their height then for their width. Any idea why so wide? It makes me wonder if any of his seizure meds (assuming he is taking some) might have potassium-channel blocking capability, or even if he might be taking a potassium-channel blocker (which could widen the T wave without widening the QRS). I'm not sure how many people who are post-ictal and then have a coronary occlusion or acute spasm react to the pain. If I had never seen this patient before, knew nothing of his history other than he was post-ictal and had no access to a previous ECG, I would activate the cath lab.

    Thanks for a great website!

  6. The exlusion criteria is applied , and the patient is investigated for the need for timely reperfusion. As Jerry highlights findings of prominent P wave got me thinking. With the prodrome days of diarrhoea it had me looking for the potential for hypokaleamia on the ECG. When ischaemia is excluded could the P waves , T wave flattening and inversion , ST depression and U waves indicate this as a co differential ?

    1. I don't think this looks much like hypokalemia. These are typical U-waves for early repolarization, and T-waves are not flattened (some are inverted).


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