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A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. This was sent to me by an undergraduate name Hans Helseth, who is an EKG tech, but who is an expert OMI ECG reader. He wrote most of it and I (Smith) edited.
The paramedic called the EM physician ahead of arrival and discussed the case and ECGs, and both agreed upon activating "Code STEMI" (even though of course it is not STEMI by definition), so that the acute LAD occlusion could be treated as fast as possible. So the cath lab was activated. Long term outcome is unavailable.
She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. Here is the EM decision making: "The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. Back to the case: Unfortunately, the ECG was not understood by the provider.
It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. As discussed above in Dr. Smith's excellent discussion — serial ECGs, correlated to severity of patient symptoms soon confirmed the acute event in today's patient. This ECG was texted to me with no other information. What did I say?
Subtle as a STEMI." (i.e., Here is the bottom line of the article: It is widely believed that hyperacute T-waves are a transitional state preceding ST Elevation 1–4 Thus, it is tempting to postulate that early cases of OMI will eventually evolve to STEMI; yet, our data contradicts that notion. This one is easy for the Queen.
Jason was very skeptical of STEMI. This also argues against STEMI. KEY POINTS from this CASE: The presenting history often provides invaluable clues to the likelihood of an acute cardiac event. ( This is a "low prevalence" history for an acute cardiac event.). He complained of 3 days of diarrhea and abdominal pain.
Major adverse cardiac events 40 minutes after giving the antiarrhythmic. Major adverse cardiac events 40 minutes after giving the antiarrhythmic. The following table shows their results, take a look: Note that procainamide leads with less adverse cardiac events. His initial EKG is the following: What do you think?
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Furthermore, if this occurs at all, it is a rare event. He does have a recently diagnosed PE, and has not been taking his anticoagulation due to cost. He had a previous ECG on file: Proving the findings are new The cath lab was activated.
Obvious infero-postero-lateral STEMI(+)OMI, regardless of context Now let’s put them in order: what was the sequence? With serial ECGs that are ‘STEMI negative’ the physician could have waited for serial troponin levels or referred the patient as “non-STEMI”. 2 Normal ECG #3. What was the outcome and final diagnosis?
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. There was no association between moderate to severe chest pain on arrival and major adverse cardiac events at 6 months (20% vs. 14%, p=0.12).
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”. Troponin was elevated and no “STEMI” was seen on the EKG, so if it is acute MI, then “NSTEMI” is the diagnosis (however flawed), not a pathology on the differential.
COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab. N Engl J Med [Internet] 2019;Available from: [link] Should all patients with shockable arrest be taken to angiography regardless of STEMI or No STEMI?
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The more leads with suspicious findings — the greater the concern for an acute ongoing event.
Discharge ECG showed antero-inferior reperfusion T wave inversion: Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. A healthy 45-year-old female presented with chest pain, with normal vitals. What do you think? But which one is it?
This was a machine read STEMI positive OMI. The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury. What would you guess is the culprit artery?
Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".) It is not yet available, but this is your way to get on the list.
They wanted to know if I would like them to activate the outside hospital's "STEMI alert." But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."
This is a very subtle change but cannot be anything other than an acute coronary event. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. Comment by K EN G RAUER, MD ( 12/22 /2022 ): = Brilliant post by Dr. Aslanger — with emphatic illustration of "the difference in OMI vs STEMI philosophy" — in action!
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI.
Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." She seems a little concerned about some very subtle depression in the high lateral leads, but otherwise sees a pretty benign tracing.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
This patient could have very easily been overlooked, both because the ECG was STEMI negative and because the Q waves were attributed to an “old infarct”. Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. OMI or STEMI? As cardiology documented, “possible STEMI.
Quiz : What percent of full blown STEMI have an open artery with normal flow at angiogram? It too is "normal" and you decide that this is not OMI or STEMI and you just decide to get troponins. So despite the artifact — and even without any history — this initial ECG has to be interpreted as an acute event until proven otherwise.
Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). large ASD, partial anomalous pulmonary venous return, significant tricuspid regurgitation, carcinoid valvular disease, etc,) 2) Conditions causing pressure overload of the RV. Any cause of pulmonary hypertension. At this point an old ECG on file was found for comparison.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria). But I'd be less certain about an acute event without more information and prior and/or serial tracings.
Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) We send each other EKG by the dozens every day. Most are OMI look alikes (mimics).
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Potassium was normal. This is not unusual.
There’s mild inferior ST elevation in III that doesn’t meet STEMI criteria, but it’s associated with ST depression in aVL and V2 that makes it diagnostic of infero-posterior Occlusion MI (from either RCA or circumflex)– accompanied by inferior Q waves of unknown age. Are there any signs of occlusion or reperfusion?
Here is a repeat ECG 45 minutes later with persistent chest pain: Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. There is a small amount of STE in V2 and V3, with a very small amount of STD in V4-V6. The T-waves are not definitively hyperacute. There was no prior for comparison. The patient did well.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). As far as I can tell, there is only one randomized trial of immediate vs. delayed intervention for transient STEMI. Labs ordered but not yet drawn.
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. Is it normal STE? The computer thinks so, and the physician thinks that is quite possible. However , there is terminal QRS distortion in lead V3.
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. Written by Pendell Meyers A man in his 70s with no cardiac history presented with acute weakness, syncope, and fever. He denied chest pain or shortness of breath. There was a 0.9%
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? Physician interpretation: "No STEMI." Physician: "No STEMI." Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia."
STEMI , ST-segment elevation acute myocardial infarction ). 1 Initial diagnosis of STEMI ECG Management Recommendation Level of evidence A 12-lead ECG should be interpreted immediately (within 10 minutes) at first medical contact. I C Pain Titrated i.v. IIa C Anxiety Tranquillizer (e.g benzodiazepine) is considered.
It was tested on a large database of known outcomes and was more than twice as senstivity as STEMI criteria and much better than cardiologists. These are identical to Wellens' waves because Wellens' syndrome is a transient OMI (or transient STEMI) Learning Points 1. Has never had this before. Takes metoprolol for HTN.
Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"." And Olivier finishes with this commentary: "Yet another example in favor of abandoning STEMI criteria for diagnosing OMI. Peak troponin: 128,000 ng/L. Every 15 minutes!
But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. But the ECG still doesn’t meet STEMI criteria. It was therefore interpreted as “no STEMI” and the patient was treated with dual anti-platelets and referred to cardiology as “NSTEMI.” the cardiologist 5.
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. Whether this represents a potential acute cardiac event would depend on the history, comparison with prior tracings and serial tracings.
Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern.
That's because this patient has clinical, ECG and Troponin evidence that an acute event did in fact occur ( ie, a more than doubling of Troponin in the context of a changing pattern of CP that correlates temporally with "dynamic" ECG changes — therefore strongly suggesting transient acute occlusion regardless of cath findings in today's case ).
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria. Of note, there is arguably terminal QRS distortion in V4-V6. I sent this to our group without information and Dr. Smith responded: "Not OMI. Pericarditis maybe."
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Day 12 ECG: FINAL DIAGNOSIS: "NSTEMI" Despite the fact that his day 4 ECG easily meets STEMI criteria, the patient is diagnosed as NSTEMI.
would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic." Can you diagnose an ACO (STEMI) when you also have LVH? The criteria of Armstrong et al.
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