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The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
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]
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. years old ± 13.7
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
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)]. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia.
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
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. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. Alternatively, it is a variant of diffuse subendocardial ischemia, with STE in V1 reciprocal to ST depression in inferior and lateral leads.
Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" There are very poor R-waves in V1-V4 suggesting old anterior MI. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" All are, however, clearly massive STEMI. Total LM occlusion can present with STE or STD in aVR.
The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. It does not look entirely normal, since there are some nonspecific STT abnormalities, such as flattening of the T waves in aVL.
The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." New ST elevation diagnostic of STEMI [equation value = 25.3 Computerized QTc = 417. Gottlieb SO, et al.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
An initial electrocardiogram (ECG) is provided below. Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia. The patient was promptly admitted to the hospital for further evaluation.
This was just published in JAMA Internal Medicine: The de Winter Electrocardiogram Pattern Evolving From Hyperacute T Waves It reminded me that many believe, due to the assertions in the original de Winter's article, that de Winter's waves are stable. Interventionalist at the Receiving Hospital: "No STEMI, no cath. They are too narrow!
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] STEMI was activated and the patient went to Cath on arrival.
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.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. However, in this context (i.e. is present.
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. Induced Brugada-type electrocardiogram, a sign for imminent malignant arrhythmias. So maybe she is better than I am. Heart Rhythm, 13(7): 1515-1520. [2]:
cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." It does take some time for thrombus to form, but the EKG and the troponin profile show that this was NOT a late presentation STEMI. LV Thrombus , 1.5 0 0 1 95 544 MMRF 4 1 638 14.0 0 0 1 41 238 MMRF 1 1 278 14.0
In other words, the inferior ST segments in the first ECG show more straightening which is more concerning for ischemia. Below is the post -PCI electrocardiogram. Most notably the ST depression in the inferior leads is slightly more upsloping. The QoH interpretation however was the same for both ECGs.
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. The stress electrocardiogram is non-diagnostic. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia. I heard that a prehospital cath lab activation was on its way.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. You will note that it is essentially an unremarkable electrocardiogram except for some PACS. The morphology in V2 is also concerning and it appears that the ST segment is being pushed down, as in ST depression.
3) STEMI criteria failed to identify this acute coronary occlusion, like many others. Background: The value of the 12-lead ECG in the diagnosis of non-ST-elevation myocardial infarction (NSTEMI) is limited due to insufficient sensitivity and specificity of standard markers of ischemia and because ECG confounders may prevent their application.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Induced Brugada-type electrocardiogram, a sign for imminent malignant arrhythmias. Bicarb 20, Lactate 4.2,
A Deep Neural Network learning algorithm outperforms a conventional algorithm for emergency department electrocardiogram interpretation. But lead V2 has a worrisome amount of ST elevation, and in a chest pain patient, I would be worried about STEMI. I do research on Cardiologs' algorithm: Smith SW et al. What an honor.
PCI mid LCx So this is an OMI (Occlusion Myocardial Infarction), but not a STEMI Echo: Decreased left ventricular systolic performance, mild/moderate. This figure comes from the Diamond T study (all type 1 MI were NSTEMI, not STEMI): Notice that the 6 hour value (far right) is very low for type 2 MI. Angiogram: LM 30% ostial.
Even before we have clinical context, this ECG simply does not appear concerning for OMI, notwithstanding the machine's interpretation ** ** ACUTE MI / STEMI ** **. But in the world of STEMI, this is a challenging ECG to most. Artificial intelligence (AI) algorithms show promise to improve electrocardiogram (ECG) interpretation.
The de Winter electrocardiogram pattern is an infrequent presentation, reported to occur in 2% to 3.4% This ECG pattern is my favorite example of how the STEMI criteria are fundamentally flawed. We have a series of 20 TIMI-0 LAD Occlusions that do meet STEMI criteria. Transient ischemia may lead to "stunning".
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