Is OMI an ECG Diagnosis?

Written by Jesse McLaren

 

A 70 year old with prior MIs and stents to LAD and RCA presented to the emergency department with 2 weeks of increasing exertional chest pain radiating to the left arm, associated with nausea. The pain recurred at rest 90 minutes prior to presentation, felt like the patient’s prior MIs, and was not relieved by 6 sprays of nitro. Paramedics provided another 3 sprays of nitro, and 6mg of morphine, which reduced but did not resolve the pain.  What do you think of the ECG, and does it matter?

There’s normal sinus rhythm, LAFB, old anterior Q waves, and no diagnostic sign of OMI. I sent this to the Queen of Hearts

So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. But does this matter?

 

The ECG is just a test: a Bayesian approach to acute coronary occlusion

 

If a patient with a recent femur fracture has sudden onset of pleuritic chest pain, shortness of breath, and hemoptysis, the D-dimer doesn’t matter: the patient’s pre-test likelihood for PE is so high that they need a CT.  Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram.  Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]  European guidelines add "regardless of biomarkers".

 

But only 6.4% of such ‘high risk Non-STEMI’ patients get angiography within 2 hours.[2] This is because, contrary to Bayesian reasoning, the STEMI paradigm is named after and defined by one part of one test: ST elevation on ECG. Emergent cath lab activation is also named after this test (code STEMI), so patients whose ECGs don’t meet STEMI criteria don’t get emergent angiograms, despite guidelines. 

 

The sensitivity of STEMI criteria for acute coronary occlusion is much worse than the sensitivity of D-dimer for PE: a recent meta-analysis of the only three studies that have assessed STEMI criteria found sensitivity of only 43.6%”[3] Expert ECG interpretation for subtle ECG signs of Occlusion MI, and AI trained to identify these signs, have twice the sensitivity of STEMI criteria with preserved specificity.[4] This is a major improvement, but it means that the ECG at its best is still only 80% sensitive for OMI. This is why the OMI paradigm is not named after the ECG or any other test - all of which have their limitations, including angiography - but rather the pathology in the patient. The OMI paradigm shift both maximizes the test characteristics of the ECG, while putting them in context of the patient – using Bayesian reasoning.[5]

 

Back to the case

 

The patient had serial ECGs over the next hour with no significant change:

The first troponin came back at 1,400 ng/L (normal <26 in males and <16 in females), confirming MI – and the patient’s refractory ischemia indicated this was an Occlusion MI. But no ECG met STEMI criteria so the patient was referred to cardiology as Non-STEMI.

 

Cardiology started a nitropatch (ACC/AHA guidelines specifically state that they are ineffective and should not be used), with a plan for nitro infusion (rather than emergent cath) if the pain worsened. But when the repeat troponin two hours later rose to 9,000 ng/L,  the patient was transferred for urgent angiogram. Door-to-cath time was 7 hours, and found a complex 99% ostial LAD lesion and 80% OM lesion. Echo showed new anterior regional wall motion abnormality and decrease EF from 60% to 45%.

 

The patient was transferred to CCU to consider surgical options. Refractory ischemic chest pain continued and trop increased to 160,000ng/L, with subtle convex anterior ST elevation:

The patient was brought back to cath lab for stenting of LAD and balloon angioplasty to OM. Peak troponin was 225,000 ng/L and discharge ECG showed anterior reperfusion T wave inversion

This was a massive infarct from an acutely occluded coronary artery, yet no ECG met STEMI (or OMI) criteria. And because there was no Code STEMI, the discharge diagnosis was “non-STEMI”, so this case will not be flagged as an opportunity for improvement. If instead this was considered an OMI with delayed reperfusion, then there could be steps towards improvement. For example, the patient could have been identified at triage (or even earlier, by EMS) as having a high likelihood of OMI, so despite a non-diagnostic ECG there could have been a stat cardiology consult with bedside echo, and cath lab activation before waiting for serial troponins to rise. But the only way to actually meet 'high risk NSTEMI' guidelines is to shift the paradigm to Occlusion MI.

 

 

Take away

1.     STEMI criteria miss the majority of OMI, and ‘high risk NSTEMI’ guidelines are not followed because both the disease (STEMI) and the treatment protocol (code STEMI) are named after the poor surrogate marker of STE

2.     OMI is a clinical diagnosis that incorporates advanced ECG interpretation, complementary echo, and treatment for refractory ischemia regardless of the ECG

3.     Queen of Hearts can double the sensitivity of STEMI criteria with preserved specificity, but needs to be applied in clinical context and doesn’t rule out OMI if there is high pre-test likelihood.

You can get the app here:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

 

References

1.     Amsterdam et al. 2014 AHA/ACC guideline for the management of patients with non-ST elevation acute coronary syndromes. Circulation 2014

2.     Alencar et al. Systematic review and meta-analysis of diagnostic test accuracy of ST-segment elevation for acute coronary occlusion. Int J Cardiol 2024

3.     Lupu et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin Cardiol 2022

4.     Herman, Meyers, Smith et al. International evaluation of an artificial-intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digital Health 2024 

5.     McLaren and Smith. A Bayesian approach to acute coronary occlusion. J Electrocardiol 2023

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MY Comment, by KEN GRAUER, MD (4/17/2024):

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Insightful case by Dr. McLaren — that emphasizes the importance of the application of Bayes' Theorem to the clinical history. In other words — "When you hear hoofbeats — Think of horses (not zebras)."

• As per Dr. McLaren — regardless of what the initial ECG in today's case shows, the onus is on us to rule out acute OMI, rather than the other way around. That's because "Time is muscle" — and regardless what the initial troponin and initial ECG show — IF the "pre-ECG likelihood" for acute OMI is high in a patient with new CP (Chest Pain) — then the threshold for performing prompt cath needs to be lowered (if we are to have any hope of lowering door-to-cath time from the unjustifiable 7 hours that it was in today's case).
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• As Drs. Smith and Meyers have so often emphasized — many (perhaps most) "NSTEMIs" end up being OMIs (despite the fact that most of the time the discharge diagnosis remains NSTEMI) — so much so, that the term, "NSTEMI" has in essence become a useless term (See the October 11, 2020 and the September 10, 2023 posts in Dr. Smith's ECG Blog).

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I would add the following PEARL to Dr. McLarens excellent presentation:

• Given the very high pre-ECG likelihood of acute OMI in today's case — I immediately lowered my "threshold" in the assessment of the initial ECG for "suspicious" ECG findings.
• While there is no indication of acute OMI from sinus-conducted beats in today's initial ECG — Even before I looked at the answer, I strongly suspected an acute MI from the appearance of the PVC in lead I of Figure-1 (1st beat in lead I within the BLUE rectangle).
• We have previously shown examples in which acute OMI is only recognized by the appearance of ST-T waves in a PVC, despite no indication of OMI from sinus-conducted beats (See My Comment at the bottom of the page in the October 8, 2018 and September 13, 2022 posts in Dr. Smith's ECG Blog).
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• While specific criteria for when ST-T wave appearance in a PVC is indicative of acute OMI do not exist (probably being impossible to objectively study this phenomenon in random, prospective, controlled trials) — awareness of ST-T wave changes that just-shouldn't-be-there is the subjective criterion that I have found most helpful to me.
• Whereas I would not call the ST-T wave depression of the PVC in leads II and III of Figure-1 diagnostic (even though the relative amount of ST depression in these leads is marked) — the overly tall, "fatter"-at-its-peak and wider-at-its-base T wave in lead I (compared to the tiny QRS of the PVC in this lead) clearly should not be there (BLUE arrow in lead I that suggests a hyperacute T wave for this PVC). Given the history in today's case — even by itself, this PVC appearance in this initial ECG seems strongly suggestive of acute OMI.

Figure-1: I’ve labeled the initial ECG in today's case.

Additional points (Beyond-the-Core) regarding interpretation of today's initial ECG:

• Optimal description of the 12-lead in Figure-1 is challenging. There is sinus rhythm with 1 PVC — slight QRS widening (to 0.11-to-0.12 second) — with marked LAD (Left Axis Deviation).
• The QRS is not wide enough — and QRS morphology lacks the all-upright monophasic R wave in lead V6 — therefore not qualifying as complete LBBB. Instead (as noted by Dr. McLaren) — LAHB (Left Anterior HemiBlock) criteria are satisfied.
• The overly tall R wave (far exceeding 12 mm) qualifies as LVH (supported by an ST-T wave appearance in lead aVL completely typical for LV "strain").
• To NOTE: LVH and LAHB are each estimated to potentially increase QRS duration by 0.01-to-0.02 second (due to slight delay in depolarization of a thicker LV and/or an LV in which the left anterior hemidivision of the conduction system is not functioning). This accounts in Figure-1 for more QRS widening that we might expect with either LVH or LAHB alone.
• While the QS waves in leads V1-thru-V3 in today's initial ECG do represent prior anterior infarction — it is good to appreciate that both LVH and LAHB may result in delayed R wave progression, including the presence of anterior QS waves (LVH by predominance of posterior forces from the large LV that attenuates anterior r wave forces — and LAHB by posterior depolarization via the left posterior hemifascicle that is no longer "opposed" by the blocked left anterior hemifascicle). 
• Despite joint LVH and LAHB — the fragmentation that is clearly seen on the upslope of the S waves in leads V1 and V2 (RED arrows) supports the premise that the anterior QS waves indicate prior anterior infarction. 

The current STEMI paradigm: Because STEMI criteria are not met, let's wait until the myocardium is dead!!

This was sent to me by an inpatient nurse who reads this blog but wants to remain anonymous.

An inpatient rapid response was called for a patient with hypotension.  

The patient was originally admitted for pneumonia and had been transferred out of the ICU a day prior. He had a history of HFrEF, HTN, and AML. 

"When I arrived his blood pressure was 70s/40s and he was pale and profusely diaphoretic." 

"He spoke Spanish but we did deduce that he had 7/10 chest pain radiating to the back." 

"We couldn’t initially get a hold of the primary physician but our hospital allows the rapid response nurses to begin a work-up through protocols/standing orders so I obtained serial EKGs, a high sensitivity trop, and administered aspirin."

Here is the ECG:

The conventional computer read was "Normal sinus rhythm.  Right Bundle Branch Block"

What do you think?

Smith: this ECG with RBBB is diagnostic of proximal LAD Occlusion (OMI).  Absence of ST Elevation is irrelevant.  There is ﹤1 mm of STE in I, aVL, V5 and V6 (no STEMI "criteria", and hyperacute T-waves in I, aVL, V5 and V6.

This nurse, who reads this blog regularly, immediately recognized OMI, in spite of absence of ST Elevation criteria.

Nurse: "I compared it to an admission EKG from four days prior which made me even more concerned." 

Here is that previous ECG:

No RBBB, and no hyperacute T-waves

Finding and viewing this previous ECG should not be necessary to make the diagnosis!

"I called interventional cardiology and sent them pictures of the baseline EKG as well as the serial EKGs during the call, and explained the patient presentation." 

"They replied by saying that the EKG "doesn’t meet STEMI criteria" but that they would come and evaluate at bedside." 

"They agreed with me that the presentation was highly concerning but were initially planning on waiting a few hours (!!) to take the patient for cath later in the afternoon." 

Smith: waiting only makes for more irreversible myocardial loss with attendant heart failure and death.  Why would anyone want to wait??  Don't wait!!

"Luckily, after we moved the patient to the CCU, the critical care team performed a bedside echo that revealed LV hypokinesis and they immediately took the patient to the cath lab."

Delay due to absence of STEMI criteria: The time delay had they not done the echo in the ICU would have been several hours; as it was, there was an extra hour of delay.

Nurse: "They found a thrombotic occlusion of the proximal LAD with TIMI 0 flow and the patient received two stents." 

The initial high sensitivity troponin I was 15 ng/L (below the URL). Depending on troponin would have delayed intervention -- do not use troponin to make the decision when the ECG is diagnostic!.

Smith: I sent the diagnostic ECG to the Queen of Hearts:

And here is the explanation:

You can see that the Queen sees the hyperacute T-waves in I, aVL, V5 and V6.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

Learning points:

1. One's credentials have little to do with one's ability to read an ECG for OMI.  It takes a certain visual talent and lots of practice and, most of all, the ability to free one's mind of the old ways of seeing things.  Some of the best are EKG techs with who have no medical training at all.  Nurses, medics, interns.  All can be expert at this. 

2.  The Queen of Hearts is amazing.

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MY Comment, by KEN GRAUER, MD (4/16/2024):

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Important case for the reasons put forth above by Dr. Smith. I'll add the following thoughts regarding interpretation of the initial ECG in today's case, that I've reproduced and labeled in Figure-1.

• First — to emphasize the presentation of today's patient: This patient had just been discharged from the ICU a day earlier — and now presented with new CP (Chest Pain) and hypo-tension. His past medical history included HFrEF and hyper-tension — and he is tachycardic. It is hard to imagine a more concerning clinical presentation scenario (ergo — our need to rule out rather than rule "in" an acute event).

Even before looking at this patient's prior ECG, done just 4 days earlier — We see the following in Figure-1:

• Sinus tachycardia (in association with new CP and hypotension) = a very worrisome finding!
• Bifascicular block (RBBB/LPHB).
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• ST-T wave abnormalities in multiple leads — which as per Dr. Smith (even before comparing with the ECG from 4 days earlier) is diagnostic of acute proximal LAD OMI.

Looking closer at the specific ECG findings I have labeled in Figure-1:

• Typically with simple RBBB — there is ST-T wave depression in at least several anterior leads. There should not be the ST segment coving seen in ECG #1 (which I highlight with the "frowny"-shape coved BLUE curved lines that I've drawn in leads V1,V2,V3).
• I've superimposed with a dotted BLUE line in leads V1,V2 the approximate depth I'd expect to see for the ST depression in these leads with uncomplicated RBBB (especially given the surprisingly tall R' deflection in lead V1). The absence of any ST-T wave depression in lead V2 (and to a lesser extent, the less-than-expected amount of ST-T depression in V1) is almost certainly the result of attenuation by what would otherwise probably be anterior ST elevation.
• RED dotted lines in leads I, aVL; V4,V5,V6 are drawn at the ST segment baseline. Because of the ST segment coving in each of these leads (which as per Dr. Smith — clearly reflects hyperacute ST-T waves in these leads) — it is difficult with these smooth ST segments to know where the "J-point" truly lies — but although not great in terms of amount — I interpreted the ST segments in each of these 5 leads as elevated (especially in lead V4).
• RED dotted lines in inferior leads III and aVF are also drawn at the ST segment baseline. I interpreted the ST-T wave depression in these 2 inferior leads as consistent with reciprocal changes in acute proximal LAD OMI. 
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• BOTTOM Line: If we add in the abnormal ST-T wave flattening in lead II — then, in addition to sinus tachycardia and bifascicular block (RBBB/LPHB) in this patient with a very worrisome clinical presentation — there are worrisome, acute-looking ST-T wave changes in 11/12 leads (ie, in all leads except aVR).
• As per Dr. Smith — it's hard to imagine why anyone would want to delay immediate cardiac cath and PCI in this patient who by all evidence, appears to be in the throes of progressing to cardiogenic shock.

Figure-1: The initial ECG in today's case.

56 year old male had 5/10 chest pain for several hours, then presented to the ED in the middle of the night with 1/10 pain.

A 56 year old male with PMHx significant for hypertension had chest pain for several hours, then presented to the ED in the middle of the night.

He reported chest pain that developed several hours prior to arrival and was 5/10 in intensity.  The pain was located in the mid to left chest and developed after riding his bike.   There was associated fatigue when symptoms developed and mild shortness of breath at onset of chest pain however that has since resolved.  

The patient states he experienced similar 7/10 chest pain 2 days prior when he had to hurry to catch the bus.  He states he experienced shortness of breath and chest pain with exertion and once he sat on the bus his symptoms slowly resolved. 

He presented on this day because it did not go away.

Here is his first ECG (1/10 pain):

Smith: sinus rhythm with RBBB and normal ST-T.  No ischemia.

An ECG from 4 years prior was the same.

The Queen of Hearts interpreted "OMI with Low confidence".  This surprises me, but the Queen often sees things that I cannot see.  On the other hand, I have also seen quite a few false positive Queen interpretations in the presence of RBBB.

The explainability map is here:

It seems that part of the diagnosis of OMI is due to T-wave inversion in V4 and V5.  In RBBB, the T-wave should be normally upright, so this is indeed abnormal.

Case Continued

The first hs troponin I returned at 139 ng/L.

Management: The clinical scenario with a troponin of 139 makes the diagnosis of acute MI.  However, I would not activate the cath lab immediately.  Rather, I would manage medically.  If that did not resolve the symptoms, then I would activate the cath lab.  In the absence of clear ECG signs of OMI, one should always start with aspirin and NTG, perhaps intravenous NTG, and see if the pain can be managed.  Do not give opiate analgesics!!  They only mask the underlying pathology.

Aspirin and heparin were given, but no NTG.

Case continued

Another ECG was recorded 3 hours later, still 1/10 pain:

There is sinus bradycardia with RBBB.  There is minimal STE in I and aVL, but this can be quite normal in RBBB.  There is some minimal reciprocal STD in inferior leads.   There is some STD in V1-V3, but this is normal discordant STD in RBBB.  There is minimal STD in V4-V6, but it does not have an ischemic appearance.  There is some non-specific new T-wave inversion in inferior leads; this could be due to inferior reperfusion.  But there are also new Q-waves, stronly suggesting new infarction.

Overall interpretation: this does not look like OMI to me.  

A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality.

This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia.  An inferior wall motion abnormality does NOT say that there is active ischemia because previous ischemia will result in persistent wall motion abnormality (stunning).  

We already know that the patient is suffering an acute MI.  We already know that the ischemia is ongoing, though mild (because of the persistent pain).

Only the ECG and presence or absence of pain can tell you what is happening right now.

Again, I would give NTG and re-assess.

Case continued:

A 2nd troponin I returned at 744 ng/L.  So we know there is myocardial infarction and the patient has persistent pain, but it is very mild.

A rising troponin does NOT mean that there is active ischemia.  Troponin tells you what was happening hours ago, not what is happening now.  Again, active presence of ischemia (or absence) and the ECG are the only evidence you have of the present ischemic condition of the myocardium.

Sublingual NTG was given and the pain completely resolved, from 1/10 to 0/10.

3rd ECG at 4 hours, pain free:

ECG is dynamic, since the ischemia is dynamic.  Q-waves are even more pronounced.

Troponin profile

See how the troponins rise even after 3 AM when the ischemia is apparently gone.

No further trops were measured, even after PCI

So we don't know how high they would have gone

Echo the next AM showed dense inferior WMA.

Angiogram:

Culprit for the patient's non-ST elevation myocardial infarction is a thrombotic occlusion of the proximal RCA

Incidentally noted mid LAD occlusion that is suspected to be chronic given heavy proximal calcification and relatively well-developed left to left collaterals.

The culprit was opened and stented.

Learning points:

You must remember that if someone has a brief episode of ischemia, or for a few hours, and then it goes away, that the wall motion abnormality will remain (the myocardium is “stunned”).  Of course if there is infarction, there will also be persistent wall motion abnormality.  Similarly, the troponin that was released during the ischemia will keep rising even though the ischemia is now gone.  

ONLY the ECG and presence or absence of pain tells you the ischemic state of the myocardium at any moment.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

A 29 year old male with chest pain, ST Elevation, and very elevated troponin T

By Magnus Nossen

This ECG is from a young man with no risk factors for CAD, he presented with chest pain. How would you assess this ECG? How confident are you in your assessment? What is your next step? Note: lead format is Cabrera

I was sent this ECG in real time. The patient is a young adult male with chest pain. The chest pain was described as pressure like and radiation to both arms and the jaw. Symptoms were on and off. The pain was worse in the night and better when moving. The patient sought medical attention when the pain recurred for a second straight night accompanied by arm numbness as well as radiating pain. The above ECG was recorded. 

It is easy to say pericarditis in such a case. (young male no risk factors and ST-elevation in several leads) As Dr. Smith has emphasized many times you diagnose pericarditis at your patient's and your own peril. The ST segment depression in V1 had me worried, the (inappropriately) almost isoelectric ST segment in V2 worried me even more. In conjunction with the inferior and lateral minimal ST elevation I felt I had to rule out inferoposterolateral OMI as the consequences can be catastrophic. 

I sent this out to our "EKG Nerdz" group and in spite of his usual warning, Dr. Smith texted back: "I am going to go out on a limb and say it is a fake."  

Dr. Smith's top 2 most important features for differentiating OMI from Pericarditis are 1) absence of reciprocal ST depression in any lead except aVR and 2) "flat" ST segments, meaning without large T-waves, perhaps more specifically stated as a low T/ST ratio.

I accepted the patient for transfer to our PCI center. On arrival patient was slightly tachycardic. HR about 90-100/min. Other vital signs normal. No fever. Hand held echo showed overall ejection fraction being normal. With normal EF the tachycardia is not compensatory. ACS then becomes less likely. Before the lab values returned this patient had an emergent coronary CT angiogram done that ruled out CAD. Final diagnosis was myocarditis. Initial Troponin T  returned at 1233ng/L. Myocarditis can be very difficult if not impossible to differentiate from OMI based on ECG changes. The ECG can show ST-elevation with reciprocal changes and myocarditis can have regional WMA on echo, just as OMI. Invasive or non-invasive angiogram should strongly be considered for this group of patients. A false positive cath lab activation is also off course acceptable for this diagnosis if you cannot get an emergent coronary CT angiogram. 

Retrospectively one can say that the ST depression in V1 and relative ST depression in V2 is likely reciprocal to diffuse ST elevation. (The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation) 

Below you can find the 3D model of the heart and coronary vessels. Each main coronary artery (LAD, RCA and LCx) are shown in separate images. There are no coronary stenoses.

Description CCTA: Image quality is very good. There are no coronary stenoses. Minimal amount of pericardial effusion. 

Smith: this is an excellent use of CT coronary angiography!

The Queen of Hearts AI model for ECG interpretation is still in its early days. Her interpretation of today’s tracing was OMI high confidence. Maybe eventually she will be able to separate myocarditis from OMI based solely on the ECG. 

Do you think you can outperform the toddler version of the AI model? Keep an eye on the blog as an OMI QUIZ soon will be published where you test yourself vs the Queen!

The QoH groups ECGs into OMI and NOT OMI. Each category is subdivided into three levels of confidence. Thus you can get a reading of NOT OMI (low, mid or high). Or you can get a reading of OMI (low, mid or high). In other words there are six outputs with NOT OMI high confidence on one end and OMI high confidence on the other end. 

How did the Queen do?

The queen was fooled by this one!!

Version 1 was not trained to detect myo- or pericarditis.

Version 2 will do that.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

===================================

MY Comment, by KEN GRAUER, MD (4/11/2024):

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One can never get too much practice in recognizing acute tracings that must be distinguished from OMI mimics. I'll add the following thoughts to the interesting presentation by Dr. Magnus Nossen.

• For clarity in Figure-1 — I've reproduced today's ECG. I highlighted in RED the 3rd lead on the left to remind readers that this is lead -aVR (which corresponds to a frontal axis angle = +30 degrees) — in this ECG that displays the Cabrera Format (See My Comment at the bottom of the page in the October 26, 2020 post of Dr. Smith's ECG Blog for review of the Cabrera format). 
• This case is challenging because of the young age of this patient, who presented with severe chest pain — and because of the fairly subtle abnormalities on ECG. In addition to the V1,V2 leads that concerned Dr. Nossen — I would add that there is straightening of the ST segment takeoff in sequential leads -aVR through to lead III, each of which are associated with subtle-but-real J-point ST elevation. (There is a Q wave in lead III of uncertain significance).
• Support that these ST-T wave findings in the limb leads are real, is forthcoming by the utterly flat ST segment in lead aVL. While not the "mirror-image opposite" picture featured by the "magical" reciprocal lead III-to-lead aVL relationship typically seen when there is acute inferior OMI — I interpreted this uncharacteristic ST-T wave flattening in lead aVL as a reciprocal ST-T wave change.  
• Similar straightening of the ST segment takeoff, with slight ST elevation is also seen in leads V5,V6.
• And the patient has sinus tachycardia ... (at ~100/minute).

BOTTOM Line: There clearly is enough on this initial ECG to support Dr. Nossen's concern that a definitive diagnosis needed to be made on this young man with new, persistent chest pain. The significantly elevated Troponin, Echo showing normal LV function without localized wall motion abnormality — and negative coronary CT angiogram all pointed to acute myocarditis.

• As emphasized many times in Dr. Smith's ECG Blog — it may sometimes not be possible to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and clinical history (See My Comments in the April 25, 2023 —  July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).
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• P.S.: A diagnosis of acute myocarditis (rather than acute OMI ) — is a much better "fit" for this case because: i) The patient is younger than the usual OMI patient — and description of his chest pain is somewhat atypical; and, ii) The ECG is not quite as we'd expect for an acute infero-postero OMI (ie, there is abnormal ST flattening in lead aVL, but not the expected mirror-image opposite picture of ST-T wave changes as seen in lead III — there is no reciprocal ST-T wave change at all in lead I — and lead V1 rather than V2,V3,V4 shows the clearly abnormal ST segment straightening).

Figure-1: The initial ECG in today's case. The insert that I've added in the lower right shows the rationale for limb lead sequencing used in the Cabrera format. (NOTE: To improve visualization — I've digitized the original ECG using PMcardio).