Tuesday, March 21, 2023

Watch what happens when you teach others how to find OMI

 Submitted by Dr. Caio Aguiar from Brazil, written by Pendell Meyers

It is immensely rewarding to receive these emails, like I received from Dr. Aguiar last week:

"Last year I had a couple of lessons with you while on my internship.

I finished my residency of Emergency Medicine and I’m working at a great Emergency Department here in Brazil.

Since then, I started looking for OMI EKG findings and not just STEMI.

So, I'm a follower of your blog, and I think I have a interesting case that I attended yesterday."


"Male, 43yo, come to ED with Epigastric Pain started 3 hours ago. Risk Factors: High Cholesterol. Vitals Signs: Normal."

Here is his initial ECG:

PM Cardio standardized version below:
What do you think?

Here we have enlarged it for easier viewing, with limb leads on the left and precordial leads on the right:

Dr. Aguiar diagnosed posterolateral OMI based on hyperacute T waves and slight STE in aVL, with its reciprocal STD and reciprocal negative hyperacute T waves in II, III, aVF, as well as the STD proportionally maximal right on the border of V4/V5.

Here is PM Cardio's Queen of Hearts interpretation of the ECG. Confidently diagnoses OMI.

He contacted the interventional cardiologist who was not convinced and cancelled the cath lab, stating that he wanted to see the first troponin result.

Meyers note: In a case like this, when the cardiologist cannot see the posterior OMI, posterior leads may have shown STE, which might be more understandable for them. Remember: these findings above are included as STEMI equivalent findings in the 2022 ACC Expert Consensus Decision Pathway on ACS Patients in the ED.

The troponin I resulted at about 2-3 hours after arrival (I am not sure why it took this long), at 700 ng/L (upper reference limit 40 ng/L).

A repeat ECG at this time is below:

The repeat ECG shows more STE (but still not 1.0 mm in lead I, thus not STEMI criteria) and was finally understood by the cardiologist.

Angiogram soon after (around 4 hrs after presentation) showed multi vessel CAD, with culprit lesion total occlusion of the first obtuse marginal branch (OM1), which was stented.

No more troponins were obtained.

Unfortunately the echo was not available.


Here is his ECG several hours after reperfusion:

Resolving HATW/STE/STDmaxV1-V4, and new terminal T wave inversion in aVL, all suggesting effective reperfusion.

Learning Points:

To take optimal care of ACS patients, the initial providers who see the patient (hopefully assisted by AI soon) must be able to recognize subtle OMI findings. If only the cardiologist also had such training in this case, the 3-4 hour delay could have been avoided. If Dr. Aguiar hadn't seen it, the patient might have been labelled "NSTEMI" and forced to wait until the next day.

Speed and frequency of repeat ECGs and troponins can help distinguish some OMIs that are not yet understood.

Teaching is rewarding! Go teach some OMI findings.

My Comment by KEN GRAUER, MD (3/21/2023):
Today's case provides one more example of an acute OMI not initially recognized by the On-Call interventionist. The OMI was immediately recognized by the emergency physician who was trained by Dr. Meyers

  • Dr. Meyers' suggestion for when the interventionist does not initially recognize a posterior OMI because "there is not enough ST elevation" — is a good one: Do posterior leads.

  • To EMPHASIZE (as we have previously done in Dr. Smith's ECG Blog — as per My Comment at the bottom of the page in the September 21, 2022 post) — QRST amplitudes (and therefore the amount of ST-T wave elevation) in posterior leads is often modest at best — simply because posterior placement of leads V7,V8,V9 situates these leads in a position from which electrical activity must pass through the thick musculature of the back before being recorded on the ECG. That said — sometimes there will be ST elevation in posterior leads. This may be beneficial if it serves to convince an interventionist who otherwise was not going to cath the patient.

MY Suggestion:
It is difficult to understand why so many clinicians still have difficulty recognizing acute posterior OMI. As noted above — Even when there is posterior OMI, the amount of ST elevation that is seen in posterior leads is most often modest.
  • In contrast to posterior leads — the amplitude of ST-T wave deviations that is seen in anterior chest leads is not attenuated by the thick musculature of the back before being recorded on the ECG. As a result — the mirror-image of anterior chest leads provides a more readily visible picture of ongoing ST-T wave deviations in the posterior wall of the left ventricle.

  • I've called application of this principle the "Mirror Test". This is simply a visual aid that I've used for decades to facilitate recognition of acute posterior OMI(I've added LINKS to a series of other cases in this September 21, 2022 post that illustrate the utility of the Mirror Test)

  • As Drs. Smith and Meyers have emphasized on many occasions — ST depression that is maximal between leads V2-to-V4 in a patient with new chest pain should be assumed to be posterior OMI until proven otherwise. The shape of this ST-T wave depression indicative of posterior OMI is often quite distinctive — in that its mirror-image "looks like" an acute STEMI.

Application to Today's CASE:
The patient in today's case is a 43-year old man who presented to the ED with new symptoms (ie, Not chest pain — but epigastric pain, that can be a mimic at times for an acute cardiac event).
  • For clarity in Figure-1 — I've reproduced the initial ECG in today's case, together with the mirror-image of the chest leads to the right in this Figure.

Dr. Meyers has drawn attention to the abnormal limb lead findings in ECG #1. These include: i) Hyperacute T waves with slight ST elevation in lead aVLandii) Equally acute-looking reciprocal ST-T wave depression in each of the inferior leads.

I wanted to focus on Chest Lead findings:
  • Normally, there is gentle upsloping and slight ST elevation in leads V2,V3. Instead — the ST segment is abnormally straightened, with no more than tiny T waves in these leads. Note the distinct shelf-like ST segment in lead V2.
  • ST depression begins in lead V4 — and is maximal in leads V5 and V6.

  • Because of marked overlap of the QRS in multiple leads — I've outlined in RED the QRS complex in leads V4 and V5.

  • LOOK at the mirror-image picture of the chest leads ( = ECG #1ato the right of the initial ECG in Figure-1)Doesn't the mirror-image of the ST-T waves in leads V4,V5 look like an acute MI?

  • Limb lead findings in ECG #1 are strongly suggestive of acute high-lateral OMI.
  • Typically with isolated posterior OMI — ST depression will be maximal between leads V2-to-V4. This is not quite what we see in ECG #1. Instead — we see abnormal ST-T waves beginning with the ST-T wave flattening that begins in leads V2,V3 — with a positive Mirror Test in lead V4.
  • Significant ST depression extends out to leads V5,V6. Of note — there is also ST elevation in lead aVR.

  • IMPRESSION: I thought ECG #1 conveyed a "mixed" picture. The very acute-looking ST-T waves in the limb leads strongly suggests high-lateral OMI. The abnormally straightened ST segments in leads V2,V3 (shelf-like straightening in V2) — with positive Mirror Test in lead V4 suggests posterior OMI — which together with the hyperacute and elevated ST segment in lead aVL, is consistent with acute occlusion of a branch of the LCx. But ST depression is present in multiple leads, with ST elevation in lead aVR — a picture consistent with diffuse subendocardial ischemia from multi-vessel disease. (Alas, this is precisely what cardiac cath showed = multi-vessel disease with a "culprit" vessel in the 1st Obtuse Marginal branch of the LCx).

Figure-1: The initial ECG in today's case — with the mirror-image view of the chest leads to the right. (To improve visualization — I've digitized the original ECG using PMcardio).

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