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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Compensatory enlargement was defined as being present when the total coronary arterial cross-sectional area at the stenotic site was greater than that at the proximal nonstenotic site. Furthermore, if this occurs at all, it is a rare event.
Obvious infero-postero-lateral STEMI(+)OMI, regardless of context Now let’s put them in order: what was the sequence? When the pain recurred the ECG normalized(ECG#2), but this is pseudonormalization : the coronary artery has spontaneously reoccluded, and the T waves are on their way up. What was the outcome and final diagnosis?
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.
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.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). They too have dense white masses consistent with coronary atherosclerosis. The blue circle shows the LCx.
The proof of this is that only 5% of patients enrolled had acute coronary occlusion. 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. This study failed to do so. 5% vs. 58%!!
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).
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.
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." For the same reason, you should not delay coronary angiography because pain resolves with morphine. The case continues. Mukherjee, D.,
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). A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty.
Theres ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. Lets see what happens in the current STEMI paradigm. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. What do you think?
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.
Smith , d and Muzaffer Değertekin a DIFOCCULT: DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction. Coronary arteries cannot be assessed because the scan was not gated, but proximal segments of the coronary arteries seem to be open with some contrast. Again nothing diagnostic.
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.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. This is not the case.
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.
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.
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.
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.) have perfect coronary flow by the time of angiogram. Clinical history is needed.
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?
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?
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). No ECG was ordered on Day #1.
A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD Although a lesion is not visible anatomically on this CT scan, coronary catheter angiography could be considered based on Cardiology evaluation." Transient STEMI is at high risk of re-occlusion.
Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
"Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"." The coronary angiography showed a 100% ostial main (obtuse) marginal occlusion!" Dominant right coronary, atherosclerotic and calcified. Peak troponin: 128,000 ng/L.
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. And dynamic ST-T wave changes between ECG #1 and ECG #2 confirm an acute event in progress. Is it normal STE? This is a "Transient OMI".
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.
This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e STEMI , ST-segment elevation acute myocardial infarction ). I B Ambulance personnel must be trained and equipped to identify STEMI and administer fibrinolysis if necessary.
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. Repeat CT angio chest (not CT coronary, unclear what protocol) showed possible LAD aneurysm and thrombus. Pericarditis?
Takotsubo is a sudden event, not one with crescendo angina. 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. An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
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. References 1.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. Whether this represents a potential acute cardiac event would depend on the history, comparison with prior tracings and serial tracings. Attached is the first ECG.
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.
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial Infarction.
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. No TIMI flow was listed in the report. Am Heart J.
The biphasic T wave is consistent with recent reperfusion of an occluded coronary artery supplying the inferior region. Here’s the angiogram of the RCA : No thrombus or plaque rupture in the RCA (or any coronary artery) was found. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA.
He subsequently had a syncopal event and was down for 1-2 minutes. One might think this represents acute STEMI, or Bundle branch block with discordant ST segments and suspicously concordant T-waves. His wife called 911. EMS found him with an irregular heart rate at 200-250 beats per minute. There is also a wide QRS.
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.
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).
Knowing the patient has a history of coronary disease could be relevant to today's case — as it should add to our suspicion of a new acute event. If this is the case — this size of a Qr wave in lead III, as well as the seemingly wide Q in lead aVF — would seem to suggest prior inferior infarction a t some point in the past.
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. The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. So maybe she is better than I am.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. These include: i ) appreciation of how problematic the definition of “acute STEMI” can be; and , ii ) illustration of how dependence on this definition may result in overlooking acute coronary occlusion.
Here is the post shock ECG: Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm. Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically.
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