The worst thing you can be when you have this ECG is to be a young woman

This was contributed by a great paramedic, Drew Williams.  He now is his agency's "Clinical Improvement Analyst for STEMI performance and quality assurance.”

A 30-something woman called 911 for chest pain.  Medics report this:

They recorded a prehospital ECG:

What do you think?

To me, this is an obvious proximal LAD occlusion.  However, I am always surprised at how what is obvious to me, is completely missed by many other physicians.

There is a hyperacute T-wave in V2 and aVL, STE in V1, and ST depression in I, inferior leads, and V3-V6.  This should never be missed.

This is a classic "Swirl" pattern, which we described for the first time in a recent publication in the Journal of Electrocardiology.

"When defined as a narrow QRS plus STD in V5/V6 plus T wave to S wave amplitude ratio > 0.40 in V2, precordial swirl pattern yielded PPV 70 %, sensitivity 9 %, specificity 98 %. Of the 23 Occlusion MI patients correctly identified by precordial swirl sign, 19 (83 %) had LAD culprit lesions, and 16 (70 %) were missed by STEMI criteria."

Here is the PMCardio Queen of Hearts AI Model's interpretation:

And here is the explainability "heat map" (notice that she sees the hyperacute T-wave in V2 and the inferior ST depression.

Interesting that she does not highlight the ST depression in V3-V6

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But the providers in EMS and in the ED did not see it.  

I do not have any ED ECG.  But it is likely that they never developed diagnostic ST Elevation, since this is very common.  

We have a paper In Press at the Eur Ht Journal Acute Cardiovascular Care in which we show that 20/53 TIMI-0 LAD Occlusions did not have diagnostic ST Elevation.  17/20 had hyperacute T-waves.  Both a blinded expert (Smith) and the Queen identified OMI in 20/20 cases.  NONE of the cases with hyperacute T-waves ever developed diagnostic ST Elevation.  Compared with the 33 with STEMI criteria (diagnostic STE), they had longer door to balloon times.

Case continued

3 hours after arrival in the ED she arrested in ventricular fibrillation.

She went to the cath lab:

So, this unfortunate 30-something woman lost half of her heart, had a cardiac arrest, required a balloon pump and vasopressors, all because no one could read her "Non-STEMI" EKG that was a total coronary occlusion.

She will probably have permanent heart failure, if she lives.

Literature

1. If you don't know about this topic, read this recent article we wrote in JACC Advances:

From ST-Segment Elevation MI to Occlusion MI: The New Paradigm Shift in Acute Myocardial Infarction

Full text: https://www.jacc.org/doi/epdf/10.1016/j.jacadv.2024.101314

2.  Here is the seminal article on the Queen of Hearts: 

International evaluation of an artificial intelligence–powered electrocardiogram model detecting acute coronary occlusion myocardial infarction 

3.  There are now reams of data showing that the Queen will identify almost all acute coronary occlusions (and identify mimics).  See the list of publications here.

Learning points:

1. Use The Queen of Hearts, if allowed, to help you recognize acute coronary occlusion.

2. Young Women often have their OMI missed.  "Nah, couldn't be an MI in a young woman!"

3. If you don't have the Queen, you need to spend a lot of time learning this extremely difficult skill of reading the ECG for subtle OMI.

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MY Comment, by KEN GRAUER, MD (6/5/2025):

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Today's case will be frustrating, not only for medical providers familiar with the concept of acute OMI (Occlusion-based Myocardial Infarction) — but even for those who have only been trained in the basics of ECG interpretation for evaluation of the patient with new CP (Chest Pain). This type of case should not be missed.

• Today's CASE: Paramedics were called to the scene where a 30-something woman reported new CP persisting since she awakened in the morning. Regardless of the younger age of this patient — the history of new and persistent CP severe enough to prompt contacting 911 — automatically places this patient in a higher risk group for having an acute event.
• This history in today's case — should by definition mean that the role of EMS and ED providers is to rule out an acute event rather than the other way around.

For clarity in Figure-1 — I've reproduced and labeled the initial EMS ECG.

• Without entering into the more advanced findings of the specific ECG diagnosis in Figure-1 — the basics that have to be appreciated by even less experienced emergency providers are: i) That the QRS is narrow and the rhythm in Figure-1 is sinus (upright P waves with a constant and normal PR interval in lead II ); and, ii) That there is ST depression in multiple leads (ie, in the 8 leads highlighted by BLUE arrows in Figure-1).
• Regardless of whether or not one ascribes to strict millimeter-based criteria of ST elevation ( = the STEMI-paradigm) — or — whether one has embraced the ever-increasing body of literature that we continually document in support of the newer and more comprehensive OMI paradigm (See the OMI Literature Timeline and OMI Facts and References TABS in the upper MENU on the top of every page in Dr. Smith's ECG Blog) — the combination of new and persistent CP, severe enough to prompt notification of 911 and today's ECG showing ST depression in multiple leads — needs to initiate an expeditious evaluation that leads to prompt cath before the ventricular fibrillation episode that this patient developed because these basic concepts were not appreciated.

Looking Closer at ECG #1:

As per Dr. Smith's above discussion — ECG #1 represents an obvious acute proximal LAD OMI. Our "eye" should be immediately captured by leads V1 and V2 (within the RED rectangle):

• In a patient with new CP — it is the disproportionately increased "bulk" of the ST-T wave in lead V2 (with respect to the relatively small S wave in this lead) that indicates hyperacuity.
• In a patient with a narrow QRS and no LVH — the ST-T wave in Lead V1 should never be more than minimally (if at all) positive. Instead, especially in the the context of the disproportionate ST-T wave in lead V2 — the ST coving and elevation that we see in lead V1 in Figure-1 is an equally hyperacute change as the overly "bulky" ST-T wave in V2.
• We've highlighted the concept of Precordial "Swirl" on multiple occasions in Dr. Smith's ECG Blog (See the October 15, 2022 post — with 20 illustrative ECGs by Drs. Smith and Meyers — and with "My Take" at the bottom of the page on some Pearls for quick recognition of a "Swirl" pattern).
• ECG #1 fits perfectly with this Oct. 15, 2022 description of "Swirl" because: i) In this patient with new CP and a narrow QRS and no LVH on ECG — The ST-T waves in leads V1,V2 are clearly hyperacute; and, ii) There is flat ST depression in leads V5,V6.

Additional ECG findings in Figure-1 include:

• Sinus tachycardia (at ~105-110/minute) — which is unusual in a simple MI unless something else is going on (extensive infarction in this case — that shortly thereafter evolved into VFib).
• A hyperacute T wave in lead aVL (which supports the hyperacute ST-T waves that we see in leads V1,V2 — as indication of a proximal LAD location for this "culprit" artery).
• ST elevation in lead aVR — which in association with this Precordial "Swirl" pattern showing ST depression in 8/12 leads, suggests either multivessel disease and/or an extensive ongoing infarction.

Figure-1: I've reproduced and labeled today's initial EMS ECG.