HEART Score Zero. Computer Normal ECG. Troponin Undetectable. Speckle Tracking Echo normal.

A completely healthy 30-something year old woman with no cardiac risk factors had sudden onset of bilateral trapezius pain that radiated around to her throat.  It resolved after about 5 minutes, but then recurred and was sustained for over an hour.  She called 911.

EMS recorded these ECGs:

Time 0:

In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 mm at the J-point, relative to the PQ junction.  But there are also unusually Large T-waves

Called Normal by computer
This is the Zoll algorithm

I sent this to the Queen of Hearts:

Check out our recent article on the Queen of Heart's performance among ECGs manifesting OMI but which were interpreted as normal by the conventional algorithm:

Artificial Intelligence Detection of Occlusive Myocardial Infarction from Electrocardiograms Interpreted as “Normal” by Conventional Algorithms

Time = 13 min

T-wave in V2 is now taller and fatter, the ST segment is more straight.
T-wave in V3 is no taller, but it is fatter due to a straighter ST segment
This is highly suspicious for early LAD occlusion

Not identified as STEMI, but not normal either
This is the Zoll algorithm

Time = 24 min

No significant change
Zoll did not recognize acute MI, but did not call it normal

These prehospital ECGs were not seen.

The patient arrived in the ED.

The pain completely resolved after nitroglycerine 

Moments later, the this ECG was recorded in the ED when she had been pain free for moments only:

Computer read: Normal ECG.

This was by the Veritas algorithm

The ECG is diagnostic of LAD OMI

However, T-waves are still unusually large; the computer almost never sees this.

The T-wave in V2 is smaller. 
QTc is 444 ms.
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm, QRSV2 = 8.5
Formula value is 19.38, which indicates LAD occlusion 

(The most accurate cutpoint is 18.2 -- a value greater than 18.2 has high probability of LAD Occlusion).  

This patient has a nondiagnostic ECG by most rules.  

However, with attention to subtleties, especially when compared with the unseen prehospital ECGs, it is very worrisome.

And to my expert pattern recognition it is definitely LAD OMI

Since I taught the Queen of Hearts, she knows that it is OMI:

The first troponin was below the level of detection (LoD).

If you use something like the HEART score:
1. H  History: She has atypical pain (trapezius) (score = 0)
2. E  EKG: a negative ECG (score = 0)
3. A  Age: = 0
4. R  Risk factors = 0
5. T:  Troponin = 0 [first troponin (contemporary, not high sensitivity) was less than the level of detection). 
Total HEART score = 0.  Risk of 30-day adverse events is less than 1.7%.   Some might send her home.

But maybe she has an acute LAD occlusion that will get even worse. 

The providers did a bedside echo and even used speckle tracking to look for strain:

I think maybe there is an anterior wall motion abnormality, but this is very difficult.  They read it as normal.

Here are a couple shots with strain, or "speckle tracking" on ED Echo:

To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this.

She said:

This is a tough one. I see what you mean, initially when I looked at the image, I also thought there was an anterior wall motion abnormality.  But then on closer inspection, I suspect that maybe the anterior wall is just not being tracked well. In systole, you can see the anterior wall come down and outside of the area that is being tracked (more so than the other tracked walls). Even though the strain values are a little off in the graph (so is the posterior wall) it is still a value range (about -18) that would be considered non-ischemic by the cardiology literature, I believe.  I have been wrong before though! So it is possible that I am misinterpreting the clip. If it were me, I would get values at the level of the mitral valve, papillary muscles, and apex (all in PSS axis). Also, narrowing the area being tracked helps the walls get recognized much better.


As I wrote, the first troponin was below the Level of Detection.

She remained pain free, and was admitted without further serial ECGs.  

When in doubt, one should always get serial ECGs.  Bedside echo is not enough.


At time = 240 minutes (4 hours), the second troponin returned at 1.15 ng/mL.  That prompted recording of this ECG:

Back to normal for this patient.  This demonstrates that all ST elevation of the previous ECGs was ischemic, not normal.  She was having a transient STEMI, briefly.

It is very lucky that she spontaneously reperfused her LAD.  It did not progress to full STEMI with loss of the anterior wall, as in this case.

Also, persistence of a pain free state does not guarantee an open artery.  See this case.

A formal contrast echo was done at this point:

Normal estimated left ventricular ejection fraction, 65%.

Regional wall motion abnormality-distal septum and apex.

She was treated medically for NonSTEMI, pending next day cath, which showed  ulcerated plaque and a 60% thrombotic stenosis in the LAD distal to the first diagonal.  It was stented.

Learning Points:
1. Always get serial ECGs when there is any doubt about what is going on.

2. Use the 4-variable formula!!

12 Example Cases of Use of 3- and 4-variable formulas, plus Simplified Formula, to differentiate normal STE from subtle LAD occlusion

3. Always find and look at prehospital ECGs.  They give extremely valuable information.
4. Hyperacute T-waves remain for some time after reperfusion of an artery.  I always say that "you get hyperacute T-waves both 'on the way up' (before ST segment elevation) and 'on the way down' (as ST elevation is resolving).
5. Wall motion abnormalities are very hard to see, even with advanced Speckle Tracking technology.  They require a great contrast exam and expert interpretation.
6.  This case does not demonstrate it, but a wall motion abnormality may disappear after spontaneous reperfusion (see this case).
7. Patients with transient occlusion may manifest only transient STEMI on ECG.  Subsequent troponins may be all negative and subsequent formal echo may be normal.  See this case. 

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MY Comment, by KEN GRAUER, MD (4/27/2025):

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I find it interesting to periodically look back at my ECG interpretations (and at the interpretations of others) from a number of years earlier. I fully acknowledge that doing so provides a number of "cringe moments" for me (in which I find myself thinking "How could I have said that?" ). But that was then — and now is now.

• Today's case is a "repost" from March 28, 2017 — or just over 8 years ago ...
• The "OMI Manifesto" was published by Drs. Meyers, Weingart and Smith shortly after today's repost, in the April 1, 2018 post of Dr. Smith's ECG Blog. 
• In the 8 years since today's repost — Drs. Smith, Meyers, McLaren and others have published an expanding number of relevant references supporting the OMI Paradigm as proving itself to be far superior to the outdated and insensitive STEMI paradigm (over 80 references already included in this listing, with this number continually increasing — and, with all references conveniently linked for you in Dr. Smith's OMI Literature Timeline, which is found in the TOP Menu Tab of every page in this ECG Blog). 

The Initial ED ECG from Today's Case:

As per Dr. Smith — the 3 prehospital ECGs in today's case were "lost", and therefore not seen by ED providers. As a result — initial decision-making was based on the ECG in Figure-1 (which is the 4th ECG shown above in Dr. Smith's discussion — but the 1st ECG that was recorded in the ED). I focus my comments on this initial ED ECG:

• Initial decision-making in the ED was most probably influenced by the younger adult age (30 something) of this previously healthy (without risk factors) woman — who presented with trapezius pain radiating to her throat, but not to her chest.
• The patient's CP (Chest Pain) resolved completely after receiving NTG.
• ECG #4 (in Figure-1) — was obtained very shortly after NTG was given (such that we do not know whether ST-T wave changes might have looked very different after a few more "pain-free" minutes had passed).
• AND — Remember that today's case is a repost from 8+ years ago.

I found today's repost insightful for highlighting what we hope has at the very least improved — since practice patterns in 2017.

Figure-1: The initial ECG that was recorded in the ED.

What We Hope has Improved:

• It's hard to know how the 3 prehospital ECGs got "lost". Hopefully in 2025, among the 1st things EMS providers do on arrival in the ED when transporting a "Rule Out MI Patient" with clearly abnormal prehospital ECGs — is to debrief and directly show those tracings to the ED provider.
• Hopefully in 2025, more providers are aware that as many as 25% of initial Troponin values in STEMI patients may be normal (Wereski, Smith, et al — JAMA Cardiol 5(11): 1302-1304, 2020). As a result, especially in a patient such as in today's case in which the onset of symptoms is so recent and short-lived — it should not be unexpected for the initial Troponin to be normal.
• Hopefully serial ECGs (with repeat of the initial ED ECG occurring within 15-30 minutes, and as frequently as needed thereafter) are now routine in the overwhelming majority of centers (instead of the 4+ hour delay in today's case until an elevated Troponin finally came back as the prompt to repeat the initial ED ECG).
• Hopefully a tracing as abnormal as today's initial ED ECG (especially in a patient with new symptoms) — will be promptly recognized.
• And hopefully emergency providers now realize that although being a younger adult woman without risk factors lowers the risk of an acute cardiac event — it does not eliminate such risk (as today's case conclusively proves). This is all the more true given how abnormal today's initial ED ECG is.

Today's Initial ED ECG:

Recognition of acute LAD OMI until proven otherwise — should occur within seconds of seeing the ECG in Figure-1:

• After identifying normal sinus rhythm — my "eye" was immediately drawn to the hyperacute T wave in lead V3. The height of this T wave is literally twice that of the height of the R wave in this lead — with a prolonged QTc and an extremely wide T wave base. In a patient with new symptoms — there is no way this giant, hypervoluminous T wave is going to be a normal variant.
• My "eye" was next drawn to the ST-T wave in lead V1 — which shows ST segment coving, J-point ST elevation, and terminal T wave inversion. There is no way that this is a normal ST-T wave morphology in lead V1.
• Armed with the knowledge in this patient with new symptoms that leads V1 and V3 are clearly hyperacute — it becomes easy to recognize ST-T wave abnormalities in each of the remaining chest leads.
• The T wave in lead V2 is taller than the R wave in this lead — and this T wave is clearly "fatter"-at-its-peak and much wider-at-its-base than should be expected, given very modest size of the QRS complex in this lead.
• The T wave in lead V4 is still huge (over 10 mm tall). And while relative T wave size is less in leads V5,V6 — I still interpreted these lateral chest lead T waves as overly "bulky" compared to what I would normally expect given QRS appearance in these leads.
• A subtle but additional supportive sign is seen in lead aVL, which clearly shows abnormal ST segment straightening.

Impression: In this patient with new symptoms — this initial ED ECG is alreadly diagnostic until proven otherwise of acute LAD OMI regardless of the lack of risk factors — and regardless of the initial normal Troponin.

• Since this patient's CP has just been relieved by NTG as ECG #4 was being recorded — repeating this initial ED ECG within the next 10-15 minutes would probably remove any doubt one might still have about the diagnosis, since complete relief of symptoms most likely heralds spontaneous reperfusion, that typically is accompanied soon thereafter by resolution of hyperacute ECG changes.
• 
  
• I know that I have learned a lot about the diagnosis of acute OMIs over these past 8 years.