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 https://www.facebook.com/EKG.ECG/

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?

Jason,

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?

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

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MY Comment by KEN GRAUER, MD (10/1/2020):

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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.)

ACKNOWLEDGMENT:

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.

My THOUGHTS on ECG #1: 

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!