This is what happened when a hospital implemented the Queen of Hearts

This patient had the onset of chest pain 24 hours before arrival to the ED.  An ECG was recorded immediately at triage and, at this hospital, the Queen of Hearts is routinely used to determine cath lab activation.

Here is that ECG:

Original ECG
What do you think?

There is ST depression maximal in V1-V4, which is diagnostic of posterior OMI.  There is some ST Elevation and slightly hyperacute T-wave in V6.  This is a common finding in posterior OMI because V6 is "almost" around to the back, near where posterior leads would be placed.

These are NOT de Winter's T-waves, which are hyperacute T-waves with depressed ST takeoff due to LAD Occlusion.  What not de Winter's?

Here is the PMcardio version:

Because the Queen diagnosed OMI with High Confidence, the cath lab was activated without bothering a physician.

The door to balloon time was incredibly short and there was a 100% circumflex occlusion that was opened and stented.

Then the high sensitivity troponin T returned at 1400 ng/L.

The Non-STEMI, which was an OMI, was diagnosed much faster with AI on the ECG than with troponin.

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There was also a right sided ECG recorded, I am not sure why:

V3R-V6R are opposite the posterior wall (what would be V7-V9 and opposite V6, and so they all have ST depression).  There is no ST Elevation in these leads, which is what one usually looks for in right sided leads in order to find an RV MI. 

Here was an ECG recorded immediately post PCI:

Notice the T-waves in V2 and V3 are larger.  

These are "Posterior Reperfusion T-waves."    

Reperfusion results in T-wave inversion in leads overlying the affected myocardium.  We do not have leads overlying the posterior wall; the only leads detecting the posterior wall are anterior.  T-wave inversion on the posterior wall shows up as increased T-wave amplitude in the anterior leads.  These are added to the normal upright T-waves of the anterior wall and result in LARGER anterior T-waves than normal.  These are NOT hyperacute T-waves, which are only present when the OMI is active, not reperfused.

I described "Posterior Reperfusion T-waves" in this article.  It had never been described before.

90 minutes later, this ECG was recorded:

There is not a lot of difference between post PCI and 90 minutes later

Here is an overlay of the Median Beats of all 3 ECGs:

Here you can really appreciate the posterior reperfusion T-wave in lead V2, and recovery of the ST segment from depressed to normal.

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MY Comment, by KEN GRAUER, MD (10/6/2024):

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Today's case provides an excellent example of how prompt recognition of acute OMI worked as it should to expedite cardiac cath and coronary reperfusion.

• I focus my comment on the initial ECG — that I've reproduced in Figure-1.

My Thoughts on Today's ECG:

• The rhythm in Figure-1 is sinus at ~85/minute. All intervals (PR-QRS-QTc) are normal. There is no chamber enlargement.
• I wonder if this patient had pulmonary disease? — because: i) Overall, there is relatively low voltage; ii) There is minimal QRS amplitude in lead I (almost a Schamroth Sign — as described in My Comment in the June 17, 2018 post in Dr. Smith's ECG Blog); iii) The frontal plane axis is almost indeterminate (nearly isoelectric complexes in most limb leads); iv) Diffuse S waves are seen (ie, in leads I,II,III — and throughout the chest leads to lead V6); and, v) Criteria are present for incomplete RBBB (rSr' in V1 with terminal s waves in leads I and V6). 
• The relevance of recognizing pulmonary disease on ECG — is that this may sometimes render assessment for acute OMI more difficult — although this was not the case in today's tracing. (For more on ECG findings in pulmonary disease — Check out My Comment in the May 31, 2024 post in Dr. Smith's ECG Blog).
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• Also relevant to today's tracing — is the likelihood that the lead V1,V2 electrodes have been placed too high on the chest — because: i) There are surprisingly deep negative P waves in both leads V1,V2; — ii) There is an rSr' in both V1,V2; — and, iii) The QRST complex in leads V1,V2 resembles the QRST in lead aVR (See My Comment in the November 4, 2018 post). 
• Given the importance of ST-T wave assessment in the anterior leads for today's case — recognizing faulty lead placement of leads V1,V2 may hinder diagnosis of OMI (and may sometimes merit correcting electrode lead placement with repeat ECG).

The above said — in today's patient with a convincing history of chest pain, this initial ECG in Figure-1 was all that was needed for prompt diagnosis of acute postero-lateral OMI.

• There is subtle, nonspecific ST-T wave flattening in most limb leads. I thought this was nondiagnostic. 
• The KEY lead in today's case is lead V3. As often emphasized in Dr. Smith's ECG Blog — there is normally slight, upward sloping ST elevation in leads V2 and V3. Electrode lead misplacement precludes accurate assessment of lead V2 in Figure-1 — but instead of the expected slight, gently upsloping ST elevation in lead V3 — the ST segment in this lead is straightened and clearly depressed (RED arrow in V3).
• Neighboring lead V4 shows less marked, but still clearly abnormal ST segment straightening with slight ST depression (BLUE arrow in V4).
• Lead V6 shows definite ST segment straightening with slight ST elevation. Given the isoelectric ST segment in neighboring lead V5 (with normal upsloping of this V5 ST segment, as it blends with the upright T wave) — I took this as support that the subtle ST segment straightening with slight ST elevation in lead V6 was a lateral lead hyperacute change.
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• BOTOM Line: The medical care team in today's case promptly recognized these findings — as did QOH (Queen Of Hearts). The result was amazingly prompt cath with rapid, successful reperfusion.

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).