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I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. The RCA was opened with POBA ("plain old balloon angioplasty") and eptifibatide was started. His pain was intermittent and he was vague about when it was present and when it was resolved.
Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis] 2 more days later, this was recorded: ST elevation is still present. The LAD has reperfused early. This was recorded 2.5
Is primary PCI superior to thrombolysis in the first hour of STEMI ? Steg PG, Bonnefoy E, Chabaud S, Lapostolle F, Dubien PY, Cristofini P, Leizorovicz A, Touboul P; Comparison of Angioplasty and Prehospital Thrombolysis In acute Myocardial infarction (CAPTIM) Investigators. No, it is not. Circulation. 2003 Dec 9;108(23):2851-6.
The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1).
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.
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. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
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"." Successful primary angioplasty of the mid-circumflex artery towards the main marginal branch with the implantation of a drug-eluting stent. Good angiographic result.
Here are three more dramatic cases that illustrate RBBB + LAFB Case 1 of cardiac arrest with unrecognized STEMI, died. Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAH) on the admission ECG.
Barely any STE, and thus not meeting STEMI criteria. Annals of Emergency Medicine Cardiology was called to evaluate the patient immediately for emergent cath, but they stated that the ECG did not meet STEMI criteria and elected to wait for further information before proceeding with cath. He was given 6mg IV morphine for ongoing pain.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
For example — We would not normally expect to see more ST elevation after PCI ( as we do in ECG #3 ) — unless reperfusion of the "culprit" artery with the procedure was not successful — or — unless additional ECGs done prior to PCI showed additional ST elevation occurred before angioplasty opened the occluded vessel.
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 Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI.
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. Type B waves are deeper and symmetric. When the patient had chest pain, prior to nitroglycerine, what do you think the ECG showed ? A stent was placed.
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."
Inferior ST Depression does NOT mean there is inferior subendocardial ischemia; it is generally reciprocal to high lateral (aVL) subepicardial ischemia (OMI/STEMI) == MY Comment by K EN G RAUER, MD ( 2/10/2023 ): == There are certain patterns in ECG interpretation that experienced providers are able to immediately recognize.
See these posts for Wellens' mimics: Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH) Anterior STEMI? It even meets STEMI criteria: 2.5 A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J.
Spontaneous coronary artery dissection Dissection of a coronary artery may occur in the context of atherosclerosis, or be iatrogennic during angiography or angioplasty. A recent study found that SCAD causes almost 20% of STEMI in young women. examined SCAD presenting as STEMI (unlike Hassan et al. A study by Hassan et al.
Code STEMI was activated. A man in his 80s with chest pain What, besides large anterior STEMI, is so ominous about this ECG? Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy?
The lesion was intervened on with balloon angioplasty and had subsequent TIMI 3 flow. He was found to have a 100% occlusion of the proximal anastomotic portion of a prior SVG from the aorta to the OM1 which in turn had a vein graft to the distal RCA. There was initially TIMI 0 flow. His troponin I peaked at 97 ng/mL (very large MI!).
STEMI negative : the EMS automated interpretation read, “STEMI negative. According to the STEMI paradigm, the patient doesn’t have an acute coronary occlusion and doesn't need emergent reperfusion, so the paramedics can bring them to the ED for assessment, without involving cardiologists. Inferior infarct, age undetermined.
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