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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).
BUT — Cardiac catheterization done a little later did not reveal any significant stenosis. Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI ( presumably from acute LAD [ L eft A nterior D escending ] coronary artery occlusion).
I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form Then I learned that a Code STEMI was activated for concern of anterior "STEMI" in V1-V2. High sensitivity troponin I was 23 ng/L.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Because the pathologist determines the degree of stenosis by dividing the lumen area by the total area, the degree of stenosis will be overestimated. He was given aspirin and sublingual nitro and the pain resolved.
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.
Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram. From Gue at al.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI. The April 8, 2022 post by Drs.
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. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He wrote most of it and I (Smith) edited. It was stented.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain.
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. aVR ST segment elevation: acute STEMI or not? His response: “subendocardial ischemia.
Unfortunately you can see that the conventional Zoll algorithm sees nothing even to suggest AMI, let alone STEMI. Angiogram showed no significant disease of the left main, LAD, or LCX, but acute culprit lesion of the proximal RCA with "99% stenosis" and TIMI 2 flow. During EMS transport, the pain suddenly resolved.
J Electrocardiol [Internet] 2022;Available from: [link] Cardiology opinion: Takotsubo Cardiomyopathy (EF 30-35%) V Fib Cardiac arrest Prolonged QTC NSTEMI (Smith comment: is it NSTEMI or is it Takotsubo? -- these are entirely different) Moderate single-vessel CAD. Reference on Troponins: Xenogiannis I, Vemmou E, Nikolakopoulos I, et al.
Cath at approximately 0945: "The LAD had a 90% proximal stenosis with TIMI 3 flow which corresponds to his ECG although LV function remains preserved. With nitroglycerin there is improvement in the 90% stenosis but still persistent stenosis consistent with the dynamic nature of his presentation. When is it anterior STEMI?
Code STEMI was activated by the ED physician based on the diagnostic ECG for LAD OMI in ventricular paced rhythm. This was several months after the 2022 ACC Guidelines adding modified Sgarbossa criteria as a STEMI equivalent in ventricular paced rhythm). LAFB, atrial flutter, anterolateral STEMI(+) OMI. Limkakeng AT.
Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. Left main: no significant stenosis. LAD: proximal 60% eccentric stenosis the hemodynamic significance of which is indeterminate. RCA: Dominant: Mid 50-60% stenosis. It supplies a small diagonal branch.
LAD plaque with 0-25 percent stenosis. Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The A CT Coronary angiogram was ordered.
There is clearly sufficient STE for STEMI criteria in leads V2 and aVL, but lead I has less than 1.0 mm of STE - thus, technically this ECG does not meet STEMI criteria, although it is a quite obvious OMI. This ECG was immediatel y discussed with the on-call cardiologist who said the ECG was "concerning but not a STEMI."
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."
Here is the South African Flag sign ( Figure by Ken Grauer — with the original 12-lead from Patient 1 attached below — See his Comment from the April 8, 2022 post in Dr. Smith's ECG Blog for more on this sign ). ECG read as: "Shows T wave inversions in the inferior leads and less than 1mm STE in V2, without STEMI criteria."
I knew that, if the patient had presented with chest discomfort, that this ECG is diagnostic of inferior posterior OMI, even though it is not a STEMI. Angiogram at 4 hours after ECG 1 (and approximately 6 hours after pain onset): Culprit is 100% stenosis in the mid RCA. No wall motion abnormality.
Discharge Diagnosis was STEMI (The STE did not meet "criteria," so "OMI" would be better, but "STEMI" is far better than what this could have been called: NonSTEMI) Quotes from a note written by a really fine and knowledgable physician: "12-lead EKG was obtained initial 1 at time zero. Chest pain is squeezing or tight in nature.
90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. An EKG from a year prior was available for comparison: The ED physician noted Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. See reference and discussion below.
At 1210, the case was discussed with a cardiologist at a PCI capable facility, who accepted the patient for transfer, noting the ST depression in anterior leads as consistent with ischemia but not a STEMI. As a result, the diagnostic utility of posterior leads is limited ( See My Comment in the September 21, 2022 post).
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". First obtuse marginal also had an 80% stenosis and was stented. 2022;Available from: [link] Click here to sign up for Queen of Hearts Access. == MY Comment, by K EN G RAUER, MD ( 10/27/2024 ): == I view today's case as unfortunate.
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