MY Comment, by KEN GRAUER, MD (2/1/2024):
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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
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
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]
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, 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
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-
5. McLaren and Smith. A Bayesian approach to acute coronary occlusion. J Electrocardiol 2023