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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.
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.
Theres ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. Lets see what happens in the current STEMI paradigm. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. What do you think?
The patient presented to an outside hospital An 80yo female per triage “patient presents with chest pain, also hurts to breathe” PMH: CAD, s/p stent placement, CHF, atrial fibrillation, pacemaker (placed 1 month earlier), LBBB. Most large STEMI have peak troponin I in the 20.0 This was stented with a 2.25 Next trop in AM.
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. The patient had a history of ‘NSTEMI’ a decade prior, with an RCA stent. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion.
A man in his mid 60s with history of CAD and stents experienced sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. It is stented with good angiographic result.
Primary percutaneous coronary intervention (PPCI) remains the gold-standard treatment for ST-elevation myocardial infarction (STEMI). We present the case of a man in his 50s, admitted with cardiac arrest secondary to inferolateral STEMI.
Written by Jesse McLaren A 70 year old with prior MIs and stents to LAD and RCA presented to the emergency department with 2 weeks of increasing exertional chest pain radiating to the left arm, associated with nausea. I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion.
The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI"). I advised that perhaps posterior leads would help to persuade the interventionalist, since the 2022 ACC recommendations include posterior STEMI as a formal STEMI equivalent, but only officially by 0.5
Triage ECG: It was interpreted as lateral STEMI, and he was sent to the cath lab, where the angiogram showed unchanged CAD from known prior, with no acute culprit. His disease included 70% prox LAD, 80% distal LAD, 10% in-stent stenosis in the distal LCX, 70% OM1, 70% OM2, and 60% prox RCA. Described as a dull ache, 6/10 in severity.
The near-immediate or instant feedback learning process by which the heart responds to any new invasive procedural variation facilitates each new change; be it drug-eluting stent, drug-coated balloon, or both in different combinations and permutations.
This is all suggestive of posterior STEMI, but not definitely diagnostic. mm in only one posterior lead is highly sensitive and specific for posterior STEMI). Two stents were placed. ST depression in V1-V4, isolated, may be either posterior STEMI or NSTEMI. The ECG normalized overnight. Maximum troponin was 2.1
There was a 100% proximal LAD occlusion that was opened and stented. Therefore, the provider had appropriately recorded another ECG (but unfortunately unnecessarily delayed by 45 minutes at 0615): Now it is obvious to everyone, not only to an expert. The cath lab was activated. But 45 minutes later than it should have been.
Nature Reviews Cardiology, Published online: 02 April 2024; doi:10.1038/s41569-024-01020-2 In ST-segment elevation myocardial infarction, the role of interventional modification of thrombi in the coronary arteries before stenting is controversial.
While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. Cath lab was activated, and found a 95% proximal LAD occlusion which was stented. It’s unclear if the paramedic ECGs were seen or missed in the ED.
She was treated for NonSTEMI with antiplatelet and antithrombotic agents and went to cath the next day, where an where multiple LAD thrombi were found and the lesion will be stented. Waiting to cath a transient STEMI can be hazardous. See this case in which I made that mistake. Learning Points: 1.
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.
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. An open 90% LAD was stented.
I would expect that a stent would be placed. The angiogram showed an open artery with 95% stenosis and thrombosis and it was stented. Quiz : What percent of full blown STEMI have an open artery with normal flow at angiogram? It too is "normal" and you decide that this is not OMI or STEMI and you just decide to get troponins.
Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI." They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result. Learning Points: STEMI criteria misses 25-40% of OMI, like this case for example. mm of the "required" 1.0
Background Hyperglycemia, characterized by elevated blood glucose levels, is frequently observed in patients with acute coronary syndrome, including ST-elevation myocardial infarction (STEMI). There are conflicting sources regarding the relationship between hyperglycemia and outcomes in STEMI patients. 3.45) and 4.47 (95% CI: 2.54–7.87),
Subtle as a STEMI." (i.e., She was taken to the cath lab, where she was found to have 100% in-stent restenosis of the proximal LAD. In our study, there were 20/53 complete LAD OMI (TIMI-0 flow) which did not meet STEMI criteria. None of the 20 ever evolved to STEMI criteria. This one is easy for the Queen.
The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”. Troponin was elevated and no “STEMI” was seen on the EKG, so if it is acute MI, then “NSTEMI” is the diagnosis (however flawed), not a pathology on the differential.
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”. It was stented. This was a large OMI.
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.
Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. It must have re-occluded between the ED and the cath lab) --Lesion was stented. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.)
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral But at least it does not call it "Normal." Successful drug-eluting stent placement opening up 95% mid RCA stenosis to 0% residual Nonobstructive left system disease. At this point — a STEMI was diagnosed, and cardiac cath with PCI was performed.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
The cath lab was activated, and then not cancelled, and the angiogram showed 99% TIMI 2 flow proximal LAD culprit lesion, stented in less than 90 minutes of arrival. Cath days later showed complete occlusion of the LAD, stented. Another missed OMI by the False STEMI-NonSTEMI Dichotomy Don't miss them!!! Normal vitals.
These tall T waves are associated with flattening ( straightening ) of the ST segment in the inferior leads — with slight S T elevation in leads V2-thru-V6 ( albeit not enough to qualify as a "STEMI" — Akbar et al, StatPearls, 2023 ). ECG Blog #185 — Reviews the P s, Q s, 3 R Approach to Rhythm Interpretation.
Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. There is no ST depression in lead I, which suggests a circumflex lesion The cath lab was activated and a circumflex occlusion was opened and stented, with a door to balloon time of 3 hours. Limkakeng AT. Theiling BJ.
Here they are: Patient 1, ECG1: Zoll computer algorithm stated: " STEMI , Anterior Infarct" Patient 2, ECG1: Zoll computer algorithm stated: "ST elevation, probably benign early repolarization." He diagnosed anterior "STEMI" and activated the cath lab. 25 minutes later, EMS called back with this new ECG: Super obvious STEMI(+) OMI.
reports MI in 2001 with a stent placed in the "marginal" artery. First, this patient had a known stent in the "marginal" artery and thought he was having a heart attack. By definition, this is a non-STEMI because there is not 1 mm of ST elevation in 2 consecutive leads. Pain is similar, but associated with less SOB.
This is documented as a STEMI in the clinical notes and in the cath report, but certainly does not meet STEMI criteria and is therefore an NSTEMI by definition. For national registry purposes, this will be incorrectly classified as a STEMI.) Most STEMI have peak cTnI greater than 10.0. Large STEMI are approximately 30-80.
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." Can you diagnose an ACO (STEMI) when you also have LVH? The criteria of Armstrong et al. References 1.
On the combined basis of angiography and IVUS, this patient received stents to his mid RCA, proximal PDA, and OM. RCA and PDA before and after, arrows indicating stented regions. OM before and after, arrow indicating stented region.
Intra-procedural data included access route, coronary anatomy, lesion complexity, number of stents deployed, door-to-balloon time for primary PCI, and any intra-procedural complications. and the average number of stents 2.6. The radial approach was used in 544/567 (95.94%), the average SYNTAX score was 34.8 ± 9.6,
This is typical for subendocardial ischemia, not STEMI, and often means left main ischemia or 3 vessel ischemia. Right sided ECGs are best recorded in the context of inferior STEMI. Because of precordial ST depression, clinicians were also worried about posterior STEMI. A right sided ECG was recorded 3 minutes later.
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.
Another ECG was recorded while awaiting the cath team: Now there is STEMI Let's look at that first (prehospital ECG) again: Very subtle! It was opened and stented. I wondered the next day what the Queen would have said: OMI with high confidence!! Peak trop was 7000 ng/L (since the intervention was so fast)!!
They do not study whether this wave differentiates between MI and non-MI, between STEMI and NonSTEMI, or between OMI and NOMI. Another ECG was recorded: Obvious inferior, posterior, lateral STEMI What is the infarct artery? Of all inferior STEMI, 85% are due to RCA. This is hard to tell. The cath lab was activated.
Submitted and written by Alex Bracey with edits by Pendell Meyers and Steve Smith Case A 50ish year old man with a history of CAD w/ prior LAD MI s/p LAD stenting presented to the ED with chest pain similar to his prior MI, but worse. Despite ongoing chest discomfort and an uptrending troponin, he never meets STEMI criteria.
These elevations meet STEMI criteria ( ≥ 1mm in 2 contiguous leads). While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. In STEMI, they are generally upright and large in proportion to the QRS. This case is tough.
Just as hyperacute T-waves can be reciprocal to T-wave inversion ( last case ),T-wave inversion can be reciprocal to STEMI of opposite wall! An 80% thrombotic RCA was stented. This case was sent by Arthur Lee. Case : A 50 yr old woman presented after a syncopal episode, with sweating and left arm numbness.
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