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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. This confirms that the pain was ischemia and is now resovled. He does have a recently diagnosed PE, and has not been taking his anticoagulation due to cost. He was given aspirin and sublingual nitro and the pain resolved.
There may be ischemia present, but it is not evident on the ECG. LVH and the diagnosis of STEMI - how should we apply the current guidelines? This one mimics inferior STEMI (Figure 4): Concentric LVH, NO wall motion abnormality Case 5. How about diagnosing anterior STEMI in the setting of LVH? All troponins were negative.
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]
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. This rules out subendocardial ischemia and is diagnostic of posterior OMI. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
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). ST depression in V1-V4, isolated, may be either posterior STEMI or NSTEMI. A posterior ECG was done and showed no ST elevation, not even 0.5 The ECG normalized overnight.
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. Circulation 1999;99(15):1972-7.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
This suggests further severe ischemia. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
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.
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?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Circulation 2007 2. Khan et al.
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
This ECG is diagnostic of diffuse subendocardial ischemia. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. Circulation 122:Abstract 101. Kurkciyan et al. Chicago November 2010.
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 receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. Circulation Research , 56 (2), 184–194. Circulation , 63 (2), 333–340. What is the rhythm?
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 Circulation 1991;84:1454-1455.
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 patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. On arrival, GCS was 13 and the patient complained of ongoing chest pain.
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 rapidly regained consciousness, reporting no residual pain. A peak troponin level of 70 ng/L was observed.
This blog post reviews the basics for predicting the " C ulprit" A rtery — as well as the importance of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think? The ECG is consistent with high lateral STEMI. Called 911.
It is equivalent to a transient STEMI. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. It they are static, then they are not due to ischemia. This is better evidence for ischemia than any other data point. Again, cath lab was not activated.
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. Circulation 1993; 88:896-904. Circulation 1995; 91:1659-1668.
STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. Circulation [Internet] 2017;135(16):1481–9. Circulation.
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. Circulation, 117, 1890–1893. [3]: So maybe she is better than I am. Smith comment: the ECG in question could be due to Brugada, even though there is a change from baseline.
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. Circulation, 117, 1890–1893. [3]: See additional image at the bottom of this post. Bicarb 20, Lactate 4.2,
Of course this depends on many factors: 1) duration of occlusion, 2) whether full or near occlusion with zero flow or some flow -- the flow in the artery is the critical factor, measured by "TIMI" flow, 3) presence of collateral circulation and others.
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). In this case, the vessel supplied a portion of the posterior LV circulation. J Am Heart Assoc. 2021 Dec 7;10(23):e022866. doi: 10.1161/JAHA.121.022866. 121.022866.
If you still have not read it, I strongly recommend that you read the following article on the diagnosis of "posterior" MI: Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia), by Meyers HP et al. Circulation 2002; 105(4): 539-42.
This doesn’t meet STEMI criteria so in the current paradigm there’s no urgency to getting an angiogram. Even though they were passed the 12 hour mark traditionally associated with reperfusion benefits, ongoing ischemia requires emergent angiogram On assessment, the patient appeared uncomfortable, leaning forward in his chair.
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.
50% of LAD STEMI have Q-waves by one hour. Smith : In limb leads, the ST vector is towards lead II (STE lead II STE lead III, which is more likely with pericarditis than with STEMI). There were no other causes of dyspnea apparent and thus we can assume that myocardial ischemia started 6 days prior. See Raitt et al.:
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Circulation Research , 114 (12), 18521866. Circulation , 92 (3), 657671. Circulation , 125 (3), 491496.
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