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A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
This case was posted on the [link] ultrasound site, of which this ECG blog is a part. In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI. However, only the first ECG was shown, and it was recorded before the patient became ill.
What do you think the echocardiogram shows? I have posted previous such cases, but in searching my own blog, I could not find them. Here is the ED ECG on arrival: Less STE/STD Provider's Clinical Impression: "findings concerning for myocardial infarction, likely proximal LAD or Left main." NTG drip started. Pain better still.
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. It is a known OMI mimic that we have shown on the blog many times.
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral But at least it does not call it "Normal." Formal echocardiogram: Systolic function is at the lower limits of normal. Learning Points: You cannot trust conventional algorithms even to find STEMI(+) OMI, even when they say "normal ECG."
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock.
This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI. Could it be acute (vs.
He visited an outpatient clinic for it and an echocardiogram and exercise stress test was normal. In the meantime, cardiology consultant sees the patient and performs a bedside echocardiogram which revealed no major wall motion abnormalities. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. 2021.21026.
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. Is this acute STEMI? Is this an acute STEMI? -- Unlikely! He had no chest pain. Medications were aspirin, clopidogrel, metoprolol, and simvastatin.
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, a bedside echocardiogram showed no wall motion abnormality and normal LV function. He wrote most of it and I (Smith) edited.
Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. the presence of such well developed, wide, anterior Q-wave suggests completed transmural STEMI. Could it be acute (vs.
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria. Do you think we discussed this patient's 2-3 hour delay to reperfusion in our quarterly "STEMI meeting"?
Written by Bobby Nicholson What do you think of this “STEMI”? Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching). Echocardiogram was obtained and showed mild LVH without regional wall motion abnormality.
He has a history of STEMI and heart failure. link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics. And then a slightly more remote past ECG Old inferior MI The patient's previous echocardiogram report was viewed: Decreased LV systolic performance, estimated left ventricular ejection fraction is 35%.
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? A 49 year old woman with h/o COPD only presented with sudden dyspnea. She had acute pulmonary edema on exam.
The cardiologist agreed that the ECG was suggestive of STEMI, but the facility's cath lab was apparently not available and he therefore recommended emergent transfer to a cath capable facility. This would have been fairly easy and much more expedient to diagnose with bedside echocardiogram.
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." Her contrast enhanced echocardiogram is shown below in the parasternal short axis view. The case continues. link] Milosevic, A.,
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.
See this post: What do you think the echocardiogram shows in this case? 20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later. Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present.
EKG initially negative but repeat shows a few T wave abnormalities… There is a chance this could be non-cardiac pain” At 1518, an echocardiogram showed normal LV size and systolic function with hypokinesis of the mid and distal anterior wall and the mid and distal septum. At 1605, another repeat troponin resulted at 5.271 ng/mL.
The cath lab was activated for STEMI, but the patient had clean coronaries. This is highly suspicious for acute anterior STEMI. Echocardiogram showed an anteroapical wall motion abnormality. These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns. This 81 yo was found comatose.
So we activated the Cath Lab Angiogram: Impression and Recommendations: Culprit for the patient's anterior ST segment myocardial infarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD The first troponin returned barely elevated at 36 ng/L (URL = 35) In our study of initial troponin in STEMI, 26.8%
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." No prior echocardiogram was available for comparison. Can you diagnose an ACO (STEMI) when you also have LVH?
A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. As per Dr. Aslanger — a number of medical providers were initial confused by what initially appears as marked ST elevation with reciprocal ST depression, indicative of an acute STEMI. That was also my initial concern.
A stat echocardiogram would have helped to make this diagnosis and facilitate timely reperfusion. Possibilities include: serial ECGs (which were done but still nondiagnostic), stat echocardiogram, or posterior ECG. By definition, this is a non-STEMI because there is not 1 mm of ST elevation in 2 consecutive leads.
His echocardiogram showed normal wall motion. From My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog: A subject well worth periodic review — is the concept of Terminal QRS Distortion ( T-QRS-D ). The patient did well afterward without any recurrence of symptoms. There are no further EKGs or troponin measurements.
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 echocardiogram shows a preserved left ventricular ejection fraction (LVEF) of 55% with marked basal and mid inferolateral and basal anterolateral hypokinesia.
An echocardiogram confirmed aortic stenosis with a large pressure gradient. Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI. The next day, and angiogram showed normal coronary arteries. He awoke and did well.
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." Echocardiogram showed severe RV dilation with McConnell’s sign and an elevated RVSP. If this EKG were handed to you to screen from triage without any clinical information, what would you think?
Precordial ST depression may be subendocardial ischemia or posterior STEMI. If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. So there was 3-vessel disease, but with an acute posterior STEMI. There is no ST elevation. See the list below.
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.
An echocardiogram showed: Left ventricular hypertrophy concentric. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580).
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. See this case: what do you think the echocardiogram shows in this case?
His ECG was repeated at this point: This shows a well developed anterior STEMI. On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. the result is 23.9,
Later, I found old ECGs: 5 month prior in clinic: V5 and V6 look like OMI 9 months prior in clinic with no chest symptoms: V5 and V6 look like OMI 1 year prior in the ED with chest pain: V5 and V6 sure look like a STEMI For this ECG and chest pain in the ED, the Cath lab activated. But the angiogram was clean. There was no OMI.
Echocardiogram: The estimated left ventricular ejection fraction is 34% Regional wall motion abnormality-lateral, akinetic. OMI that are not STEMI can be very subtle and difficult to diagnose even though the findings are very specific. A massive acute OMI. Regional wall motion abnormality-inferior base ( this is the posterior wall ).
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 This T-wave inversion morphology is very specific for Wellens' waves. Computerized QTc = 417.
Technically, the STE meets STEMI criteria because there is greater than 2.5 On this blog, the warning is this : It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. These kinds of cases were excluded from the study as obvious anterior STEMI. mm in V2 3.0 - 3.5 mm in V3 2.0
Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. From Gue at al. Circulation.
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. Formal echocardiogram showed normal EF, no wall motion abnormalities, no pericardial effusion. So maybe she is better than I am. No more troponins were done.
Despite ongoing chest discomfort and an uptrending troponin, he never meets STEMI criteria. No further echocardiograms were available after cath. As has been mentioned numerous times on this site and is redemonstrated here: expert, subjective ECG interpretation is superior to STEMI criteria. This picture truly tells 1,000 words!
Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. examined SCAD presenting as STEMI (unlike Hassan et al. Lobo et al.
EMS recorded these ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 She was having a transient STEMI, briefly. It did not progress to full STEMI with loss of the anterior wall, as in this case. Patients with transient occlusion may manifest only transient STEMI on ECG.
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