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Traditionally, emergency providers looked for signs of ST-segment elevation myocardial infarction (STEMI) to indicate the need for intervention. Emergency physicians have recognized for some time that there are many occlusions of the coronary arteries that do not present with classic STEMI criteria on the ECG.
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
But do they represent acute coronary occlusion? But coronaries were normal, and serial high sensitivity troponin was undetectable. Based on ECG changes and echo findings, the patient was diagnosed as coronary vasospasm. I sent both ECGs to Dr. Smith, with the only information that these were prior vs new ECG.
The ECG shows an inferior ST-Elevated Myocardial Infarction (STEMI). Studies have shown that oxygen can cause vasoconstriction, increase blood pressure and decrease coronary artery blood flow ( Kones et al AM J Med 2011). They felt this would help inform guideline writers on making recommendations in this area.
Posterior leads are unnecessary if anterior leads are diagnostic According to the STEMI paradigm an ECG has to have ST elevation to diagnose acute coronary occlusion, and if there’s no ST elevation on anterior leads you can look for it on posterior leads. Do you need posterior leads? If so, how will they change management?
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." What would you do at this time with this information? But pain is an important signal in MI and informs the clinician of the urgency.
Written by Pendell Meyers Both of these cases were sent to me with no information other than adults with acute chest pain. Thus, this does NOT meet STEMI criteria (though, as of 2022, it is a formal "STEMI equivalent", assuming everyone agrees that this is de Winter morphology, for which there is currently no objective definition).
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. Fortunately the patient did not reocclude while awaiting the angiogram.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. 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. So it can miss some OMI.
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. Additionally, his cardiac telemetry monitor showed runs of accelerated idioventricular rhythm, a benign arrhythmia often associated with coronary reperfusion.
We don’t know any of this information unfortunately and all are key in patient selection The median lactate level before revascularization was 6.9mmol/L (Range 4.6 Control: 53.4% D ECLS: 18.2% Control 8.7% Control 38.0% Control: 49.0% RR 0.98; 95% CI 0.80 to 1.19; p = 0.81 vs 13.9% (RR 0.58; 95% CI 0.33 vs 22.6% (RR 1.03; 95% CI 0.88
This ECG was texted to me with no other information. It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. I assumed the presentation was consistent with acute MI. What did I say? Activate the cath lab." The T-waves in V2-V6 are diagnostic. There is also some non-diagnostic STE in inferior leads.
He has a history of STEMI and heart failure. I read this blinded, with no clinical information, and read it as inferior OMI. The Queen of Hearts interprets it blinded also (no clinical information and no previous ECGs or serial ECGs). link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics.
The chest pain started about 24 hours ago, but there was no detailed information available about whether his pain had come and gone, or what prompted him to be evaluated 24 hours after onset. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Learning Points: 1.
This case was recently posted by Tyron Maartens on Facebook EKG club (he agreed to let me post it here), with the following clinical information: "42 year old male with two weeks of intermittent chest discomfort, awoke 4 hours prior to this ECG with a more severe, heavy chest pain (5/10). Both support acute anterior STEMI. 3.0 = 0.50
Any ST Depression Maximal in V1-V4 is OMI until proven otherwise I sent this ECG with no information to Pendell. 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%. We send each other EKG by the dozens every day.
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?
At this point, with the information above, the patient's overall clinical picture could be consistent with either reperfused OMI, or Non-OMI, since both may have absent pain and inverted T waves. A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD
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.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Learning points: Both patients and other medical providers can report confusing and often contradictory information that obfuscates the diagnosis (in this case, WPW). Serial ECGs enhance the diagnosis of acute coronary syndrome.
Jason was very skeptical of STEMI. Pretest probability: Especially when there is no Chest pain, or there are very atypical symptoms, one should be very suspicious of the diagnosis of coronary occlusion unless the ECG is crystal clear. This also argues against STEMI. He complained of 3 days of diarrhea and abdominal pain.
In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. In other words, the inferior "ST elevation" is due to the abnormal rhythm, and does not signify OMI or STEMI in any way. The angiogram showed completely normal coronary arteries.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. It shows a proximal LAD occlusion, in conjunction with a subtotally occluded LMCA ( Left Main Coronary Artery ). Information is scarce when it comes to what constitutes a toxic dose. The below ECG was recorded. He was taken immediately to the cath lab.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Coronaries were normal, as was serial troponin. Vitals were normal.
If this EKG were handed to you to screen from triage without any clinical information, what would you think? for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." What do you think? In fact, Kosuge et al. Accessed May 28, 2024.
I was reviewing ECGs for a study, and came across this one, and was able to get all the clinical information: What do you think? She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. She went to angio and had normal coronaries. Medics recorded the above ECG and called a STEMI alert.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. His response: “subendocardial ischemia.
I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG. His ECG was repeated at this point: This shows a well developed anterior STEMI. Fesmire et al.
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.
I texted this ECG with no information to Dr. Smith, who immediately said: "If CP, then anterior OMI until proven otherwise." Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). No TIMI flow was listed in the report. Am Heart J. 2005;149:1043–1049.
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. This was sent to me with no information and I immediately replied that it was diagnostic of LAD OMI. Pericarditis?
Is this an anterior STEMI with LBBB? All coronaries were completely normal. Explanation : The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high. He was taken to the cath lab. All troponins were undetectable.
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.
I sent the ECG to Dr. Meyers without any other information. Now let’s compare this with the existing paradigm to identify multiple preventable delays to reperfusion, which can be improved through the paradigm shift from STEMI to OMI. But STEMI criteria has poor sensitivity for acute coronary occlusion.
It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. All coronary arteries were patent without atherosclerotic change. . == Below is the ECG of Patient #2 — as interpreted by the QOH. The ECG is diagnostic of occlusion myocardial infarction (OMI).
ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. The next day, and angiogram showed normal coronary arteries. An echocardiogram confirmed aortic stenosis with a large pressure gradient.
He has had previous angiograms showing "large vessels" and "no significant coronary disease." is very specific for STEMI , and there is some evidence, as well as rationale, that a paced rhythm behaves similarly. Here is one case of anterior STEMI in a paced rhythm. Here is a case of lateral STEMI in a paced rhythm.
Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries). It can only be seen by IVUS.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. Remember that the ECG reports what is happening to the myocytes , then you must use that information to make inferences about what the patient needs. This ECG is highly suspicious for LAD OMI.
Here it is: The computer reads STEMI What do you think? More from the medic: "LifePak 15 interpretation was STEMI. My response: "I think it is very worrisome for STEMI." It meets STEMI criteria even for a male under age 40, with STE 2.84 No history, meds, or risk factors. Pattern looked to be BER. mm in V2 and 4.08
The ED provider ordered a coronary CT scan to assess the patient for CAD. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. The patient started receiving medications for “STEMI” (including heparin!!!)
Dr. Singer sent this to me with just the information: "~40 year old with acute chest pain". Here is the Queen of Heart's interpretation: The cath lab had been activated for concern of STEMI. Other outcome information is not available. Emergent CT coronary angio also likely has a role in such cases. Do you have a prior?
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. Young people can have acute coronary occlusion.
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