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 (4/19/2024):

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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).
• 
  
• 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).
• 
  
• 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.