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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).
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.
What do you think the echocardiogram shows? There is a subtle but important difference between OMI and subendocardial ischemia: OMI (that is not STEMI) is due to TIMI 0/1 flow and has any combination of subtle STE, hyperacute T-waves, reciprocal ST depression, decreased QRS amplitude, terminal QRS distortion and other findings.
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.
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"?
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.
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%.
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.
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.
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.
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."
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?
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.
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.
Unfortunately, the ECG was interpreted as no significant change from prior , "no STEMI"!! Approximately 5 minutes after ROSC, this ECG was obtained (about 45 minutes after arrival): Obvious anterolateral OMI, and STEMI criteria positive for those who care or need it. He was sent back to the waiting room, where he suffered a VF arrest.
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.
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.
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.
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,
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.
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.
In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%). This is extremely elevated for a type 2 MI and totally consistent with STEMI.
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?
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 These kinds of cases were excluded from the study as obvious anterior STEMI. mm) Although this was indeed a case of early repolarization, it could be STEMI. In any case, the patient needs at a minimum serial ECGs and perhaps a formal echocardiogram.
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.
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.
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.
The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Here is an article I wrote: Updates on the ECG in ACS. see below).
Here is the prehospital ECG, with pain: Hyperacute anterolateral STEMI The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. Type B waves are deeper and symmetric.
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.
The patient underwent an emergent formal echocardiogram to look for wall motion abnormality: The estimated left ventricular ejection fraction is 63 %. Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma. No wall motion abnormality.
He underwent formal echocardiogram several days later, which confirmed the findings of anterior, and apical wall motion abnormalities. Practice putting the probe on the chest of someone with an obvious STEMI(+) OMI in order to look for regional wall motion abnormalities. Do NOT use them. 1] Wereski, R., Chapman, A. Gray, A., &
Elevated troponins prompted an echocardiogram — which revealed an apical wall motion abnormality (WMA). It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. Patient #1 in today's post did not get expert ECG interpretation. The ECG shows ST depression in lead V3.
Formal Echocardiogram: The estimated left ventricular ejection fraction is 58 %. These include about 60 occlusion MI (OMI) with clear ST segment elevation (none of which would be called “Normal” by the computer) and about 165 Non-STEMI. Of the Non-STEMI in our cohort, about 25% will actually have acute coronary occlusion.
5 years ago Similar Previous formal echocardiogram Inferior posterior with dyskinesis "Dyskinesis" is the technical echo term for LV aneurysm. At this point — I learned a bit more about today's patient: The patient is a man who had an inferior STEMI in 2010. We know today's patient had a documented inferior STEMI in 2010.
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 ).
Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent. To our knowledge, the patient did well.
This appears to be new, as her last formal echocardiogram 2 years ago was relatively normal. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI. Parasternal Long Axis View There is a posterolateral wall motion abnormality. All of this is consistent with an acute postero-lateral MI.
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