Monday, March 6, 2023

What do you think of this ECG?? Is this during pain, or after pain resolution? Also, see the CT image of the heart.

If you saw this ECG only knowing that it is an acute chest pain patient, what would be your interpretation?

This is a trick question, as you will see below.  But you can make a diagnosis here, and Pendell and I do this all the time when reading ECGs from databases. 

I sent this to Pendell without any information at all, and he replied "Postero-lateral Reperfusion."

The T-waves in V2-V4 appear hyperacute, suggesting LAD occlusion, BUT there is also T-wave inversion that is typical morphology for reperfusion in V5 and V6.

Thus, one must think of reperfusion.  When there is reperfusion and there are large T-waves in V2 and V3 along with inverted T-waves in lateral leads, one must think of a posterolateral OMI that is reperfused.   

These large T-wave are "Posterior Reperfusion T-waves: Wellens' syndrome of the posterior wall."

Here is the case in total.  

62 yo with severe (10/10) CP of 3.5 hours duration.  BP is 186/106.  The patient had this ECG recorded at 7 minutes after registration at triage as a walk-in (not by EMS):

What do you think?

This is diagnostic of posterolateral OMI.  There is ST depression maximal in V2-V4.  Contrary to popular knowledge, the T-wave need not be upright!! It can be upright, inverted, or biphasic (we proved this fact in this paper)  In V2, it is entirely inverted.   V5 and V6 have hyperacute T-waves.

There was high suspicion of OMI, so patient was brought to critical care area and another ECG was recorded just 7 minutes later as the pain had diminished to 4/10.

If seen by itself, this is non-specific, but the T-wave inversion in V2 is a typical sign of active (not reperfusing) posterior OMI.  Suspicious but not diagnostic.

However, in the context of the first ECG and the waning chest pain, this is diagnostic of reperfusion.

At this point, the cath lab was activated.  

It was night time and so it would take a while for the cath team. 

Due to the severity of the pain and the high BP, they obtained an aortic dissection CT.  This exam was negative, but did have one interesting finding:

The lateral wall is dark (not perfused with contrast).  The radiologist blindly read this as acute transmural MI.  

This is more support for the OMI paradigm; the OMI paradigm not only does not depend on ST Elevation, it does not depend on the ECG!

Study idea: We should look at all OMIs who had a chest CT and compare to all patients with Non-OMI pathology who had a contrast chest CT and have radiologists blindly interpret the perfusion of the myocardium

The cardiology fellow came down to the ED and said: "What are you worried about?  This ST depression?"

This is a very common refrain from cardiologists, who often do not recognize the significance of ST depression maximal in V1-V4.  STD in V1-V4 has high specificity for posterior OMI;  Many cardiologists do not accept posterior OMI with ST depression only as a real entity, even though the ACC recently named it a reason for cath lab activation (see reference below).

After return from CT, the patient's pain was severe again.  Here is the repeat ECG at 52 minutes after arrival to triage:

Obvious posterolateral STEMI

Angiographic findings:

1. Left main: no significant stenosis.

2. LAD: proximal 60% eccentric stenosis the hemodynamic significance of

which is indeterminate. It supplies a small diagonal branch.

3. LCX: Thrombotic occlusion in the mid segment after a small OM1 (TIMI 0

flow). It supplies a very large OM2 that feeds the posterolateral wall.

The distal LCX is small and has diffuse disease.

4. RCA: Dominant: Mid 50-60% stenosis. It supplies an RPDA and two RPLAs

that have luminal irregularities.

Trops returned at these times and levels

Drawn at t = 17 minutes, resulted at t = 72 minutes (after cath lab activation),  = 221 ng/L

The 2 hour troponin returned at 30,919 ng/L

The 4 hour troponin returned at >50,000 ng/L


The T-waves in V2, V3 are enlarging (reperfusion T-waves)

9 hours after arrival:

32 hours after arrival (this is the one I showed you at the top of the page):

Posterior Reperfuson T-waves and Lateral inverting T-waves of Posterolateral Reperfusion.

Formal contrast echo:

The estimated left ventricular ejection fraction is 44%.

Regional wall motion abnormality-anterolateral.

Regional wall motion abnormality-inferolateral (this is the formal ultrasound location of a posterior wall motion abnormality).

Is the ability to diagnose posterior reperfusion a useful skill?

Here is a case from a while back.  I am sure that I posted it, but don't know when or where:

This patient arrived to the ED by ambulance with chest pain that had resolved.  This is the initial ED ECG

I knew immediately that these were posterior reperfusion T-waves.  There are also inverted reperfsuion T-waves in inferior leads, which strongly supports that interpretation.

  I knew they were not hyperacute T-waves because the chest pain was resolved, just like in Wellens' syndrome.

So I asked the medics if they had a preshospital ECG.  They did, but had not recognized it.  Here it is:
Obvious inferior posterior lateral OMI.

This of course made cath lab activation easy.


Writing Committee, Kontos MC, de Lemos JA, et al.
2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: A report of the American college of cardiology solution set oversight committee.
J Am Coll Cardiol 2022;80(20):1925–60.
Available from:

Section 5.2.2, page 1932
“The application of STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion.(21)
“Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion, such as hyperacute T waves or ST-elevation<1 mm.”

21. Meyers HP,  Smith SW. Comparison of the ST-Elevation Myocardial Infarction (STEMI) vs. NSTEMI and Occlusion MI (OMI) vs. NOMI Paradigms of Acute MI. J Emerg Med 2020; Volume 60, Issue 3, March 2021, Pages 273-284

My Comment by KEN GRAUER, MD (3/6/2023):
There are many reasons why I love today's case — as it highlights a series of important points brought out in Figure-1, in which I reproduce the first 3 tracings shown above in Dr. Smith's discussion. The important "Take-Home" Points from today's case include the following:
  • The answer to the "trick" question that starts off today's case — in which Dr. Smith asks for an interpretation of ECG #1, revealing only that the patient had new chest pain. As per Dr. Smith — the KEY for distinguishing between hyperacute (hypervoluminous) anterior T waves from acute LAD occlusion — vs postero-lateral reperfusion T waves — lies with recognition of typical reperfusion T wave inversion in all lateral leads (ie, leads I,aVL; V5,V6). With proximal acute LAD occlusion — we expect to see at least some ST elevation in lead aVL, yet there is none in ECG #1.

  • Recognizing within seconds — that in a patient with chest pain, the initial ECG in today's case ( = ECG #2— is diagnostic of acute posterior OMI until proven otherwise!
  • Recognizing from ECG #2 — that the LCx (Left Circumflex) is the likely "culpritartery because of: i) The positive "Mirror Test" for posterior OMI, as seen in leads V3,V4 — that occurs in association with — ii) Subtle ST elevation and hyperacute T waves in lateral chest leads V5,V6; andiii) That occurs in the absence of acute ST elevation in the inferior leads. (For more on the Mirror Test for recognizing posterior OMI — See My Comment in the September 21, 2022 post in Dr. Smith's ECG Blog).

  • Appreciation that in as little as 7 minutes — an ECG that was diagnostic of acute posterior OMI ( = ECG #2) — may largely resolve its diagnostic findings (as occurs in ECG #3).

  • Realization that although ECG findings in ECG #3 are much more subtle than they were 7 minutes earlier — that the ST-T wave appearance in leads V3 and V4 of ECG #3 are still very suspicious of acute posterior OMI (ie, Normally there is a small amount of gently upsloping ST elevation in lead V3 — but instead there is ST segment straightening with slight depression — and — the flat "shelf-like" ST depression in neighboring lead V4 is distinctly abnormal).

  • Appreciation of how important is the specific time correlation of the presence (and severity) of chest pain, in association with each serial ECG. All-too-often this information is not written down — yet without this symptom severity correlation with each serial tracing — optimal clinical interpretation is simply not possible!

  • Recognizing that leads V1 and V2 in ECG #3 have been placed too high on the chest — because: i) The P wave is negative in both leads; ii) Leads V1 and V2 both manifest an rSr' pattern with T wave inversion; andiii) QRST appearance looks very similar in leads aVR, V1 and V2. Given that the KEY to optimal diagnosis in today's case rests with recognizing acute posterior OMI — not to correct this too-high placement of leads V1 and V2 severely handicaps our ability to recognize acute posterior wall ST-T wave changes (For more on recognizing lead V1,V2 misplacement — See My Comment in the April 17, 2022 post in Dr. Smith's ECG Blog).

  • Finally — Reasons why ST-T wave changes of posterior OMI in ECG #3 are much more subtle than they were in ECG #2 (done just 7 minutes earlier) — are: i) The severity of this patient's chest pain has greatly decreased during these 7 minutes (ie, from 10/10 severity — down to 4/10 severity) — suggesting there has been spontaneous reperfusion of the "culprit" artery; andii) ECG #3 was obtained after ECG #2 — but before ECG #1. Therefore — ECG #3 is a "transition" tracing (ie, with an intermediate ST-T wave appearance between the hyperacute postero-lateral OMI phase — and — the reperfusion T wave phase that followed a day later in ECG #1).

  • BONUS: Isn't incidental detection of the non-perfused lateral wall on Chest CT an impressive finding! (especially since this Chest CT was done to rule out aortic dissection). As per Dr. Smith's study proposal for testing the validity and potential applicability of this finding — this accidental "pick-up" might lead to additional use of Chest CT as a way to confirm selected acute OMI cases not yet proven by other parameters.

Figure-1: I've reproduced the first 3 ECGs from today's case that are shown by Dr. Smith in his above discussion. 

P.S. Because of space constraints (from my decision to place 3 ECGs into Figure-1) — I omitted the long lead rhythm strip for ECG #2. Of note — the rhythm in ECG #2 is markedly irregular. Unfortunately — baseline artifact makes visualization of atrial activity challenging. That said — I saw no evidence of extra P waves in ECG #2 (ie, The deflections following the T wave in lead V3 are U waves and not P waves). Therefore, the rhythm in ECG #2 is a marked sinus arrhythmia — which was not clinically important, and which resolved within minutes by the time ECG #3 was recorded. 

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