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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 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).
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"?
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. Angiography revealed a 30% nonobstructive stenosis of the mid LAD.
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral But at least it does not call it "Normal." Angiogram findings included: 95% mid RCA stenosis with occluded distal right PDA secondary to thrombus (peristent OMI). Formal echocardiogram: Systolic function is at the lower limits of normal.
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.
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.
An echocardiogram showed: Left ventricular hypertrophy concentric. The estimated left ventricular ejection fraction is 58 % Aortic stenosis, mild, 9.0 We found that 38% of out of hospital ventricular fibrillation was due to STEMI. The patient thus did not need immediate angiography. mmHg mean gradient. cm^2 valve area.
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?
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.
Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. Look at the aortic outflow tract.
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.
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.
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).
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.
link] A 62 year old man with a history of hypertension, type 2 diabetes mellitus, and carotid artery stenosis called 911 at 9:30 in the morning with complaint of chest pain. His echocardiogram showed normal wall motion. This is written by Willy Frick, an amazing cardiology fellow in St. Before and after of the LAD shown below.
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.
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.
They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 A repeat ECG was performed and cardiology was re-consulted: Roughly unchanged. No acute culprit. He was admitted to cardiology.
The is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal TWI in aVL, and maximal STD in V2-V3 showing posterior OMI. The cath lab was activated despite lack of STEMI criteria, around 2 am in the morning. 33% of STEMI are reperfused by the time of angiography. Very frustrating.
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.
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