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Background: Primary PCI is the recommended reperfusion strategy in patients with STEMI and should be initiated within 2 hours after first medical contact. Paper: Van de Werf, F et al. In non-PCI-capable hospitals this goal is not always achievable due to delays in transfer. Primary PCI: 95.7% Primary PCI: 95.7% Primary PCI: 78.4%
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).
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]
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]
So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion. First trop was 7,000ng/L (normal 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion.
Unknown algorithm The Queen gets it right Case 4 How unreliable are computer algorithms in the Diagnosis of STEMI? The patient's prehospital ECG showed that there was massive STEMI and these are hyperacute T-waves "on the way down" as they normalize. Pain was resolving. Diagnosed as Normal by the computer. Troponin negative.
This was a machine read STEMI positive OMI. Readers of this blog can easily appreciate the hyperacute T waves in the precordium, clearest in V1-V4. 118.007305) from Heitner et al. , Written by Willy Frick A 50 year old man with no medical history presented with acute onset substernal chest pain. His ECG is shown below.
The latest is Langlois-Carbonneau et al. If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate at least accurate enough to not miss STEMI, and that physicians should not be interrupted to interpret it, because there would be no change in patient management.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. de Winter et al in N Engl J Med 359:2071-2073, 2008. Cath attending is aware. Abstract 556.
This patient does not show up in the STEMI registry, and the time to reperfusion will likely not be identified as the problem that it was. The STEMI registry will show very high sensitivity of the ECG for STEMI, obscuring the fact the STEMI has low sensitivity for OMI Queen of Hearts sees it easily, like readers of the blog would.
COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab. Lemkes JS, Janssens GN, van der Hoeven NW, et al. These physicians did not want a patient with an OMI that was not a STEMI to be randomized to no angiogram.
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. She was out walking her dog when she developed sudden dizziness and light-headedness. When EMS found her, she was dyspneic and diaphoretic.
Meyers, Weingart and Smith published their OMI Manifesto — in which they extensively document the critically important concept that management of acute MI by separation into a “STEMI” vs “non-STEMI” classification is an irreversibly flawed approach.
They wanted to know if I would like them to activate the outside hospital's "STEMI alert." But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Deutch et al. Fortunately the patient did not reocclude while awaiting the angiogram.
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.
Dr. Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al. Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. In such cases — radiofrequency ablation of ectopic beats triggering malignant ventricular arrhythmias was needed for control of arrhythmic storm because the antiarrhythmic medications tried were ineffective ( Marrouche et al — JACC 5;43(9): 1715-20, 2004 ).
Lindahl et al. From Gue at al. 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. References: 1.
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. Herzog et al. Khan et al. Circulation 2007 2.
STEMI was activated and the patient went to Cath on arrival. From Smith ECG Blog LCx occlusion There is aVR STE with broad STD, appreciable in both Leads II and V5. Readers interested in a more robust discussion of STD vectors, and their implications in OMI, are encouraged to read this phenomenal post at the Smith ECG Blog.
This has been discussed many times before on this blog. In-depth discussion is beyond the scope of this blog. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Bigger et al. Is there STEMI? Sadowski ZP, Alexander JH, Skrabucha B, et al. Leave it alone.
Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.) [and Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
A Short Comment on PIRP and T Waves: Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery.
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. Lemkes JS, et al.
You can see how V1, V2, aVR, and V4R would have ST elevation in either a right ventricular STEMI or with a septal STEMI, and how lateral leads, and even posterior leads, would have reciprocal ST depression. In a 1999 study by Engelen et al. of patients with anterior STEMI, ST elevation of greater than or equal to 3.0
Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.), Raitt et al.), Armstrong et al.), 3) Oliva et al. (4) Armstrong PW et al.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Studies such as those by Moise et al 14 and Ellis et al 39 have shown that the relative risk of developing an acute myocardial infarction in the territory supplied by an artery with a 70%. He was started on nitro gtt.
for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." In fact, Kosuge et al. Stein et al. This is a paper worth reading : Marchik et al. Kosuge et al. Witting et al. of patients with PE and 3.3% of patients without PE.
There is mixed overlap of ST-segment elevation (STE), ST-segment depression (STD), Hyperacute T waves (HATW), and deWinter pattern (which the ACC regards as a STEMI-equivalent but is better suited under the blanket of OMI). link] [1] Zachary et al. Western Journal of Emergency Medicine, 18 (4), 752-760. [2] 2] Costanzo, L. Physiology.
link] Hughes KE et al. The cath lab was activated, as it should be with transient STEMI. See this case of transient STEMI: Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death. Computer algorithms are completely unreliable at diagnosing STEMI, with both poor sensitivity and poor specificity.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
Zeymer HT et al. References: Zeymer HT et al. PMID: 37634145 Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami ) The post The ECLS-SHOCK Trial: ECPR in Infarct-Related Cardiogenic Shock appeared first on REBEL EM - Emergency Medicine Blog. bleeding, stroke, limb ischemia, and hemolysis). Control: 53.4%
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. Claeys MJ, Bosmans J, Veenstra L, et al.
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 Armstrong et al. The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria. Instead we discussed 5 minute delays for the STEMI(+) OMI patients.
So we activated the Cath Lab Angiogram: Impression and Recommendations: Culprit for the patient's anterior ST segment myocardial infarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD The first troponin returned barely elevated at 36 ng/L (URL = 35) In our study of initial troponin in STEMI, 26.8%
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. 4] Baranchuk, A, et al.
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%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) The cath lab was activated prehospital But imagine if the patient had walked in.
Evidence regarding intervention to non-culprit plaques is mixed and beyond the scope of this blog post. Heitner et al. We have on many occasions in Dr. Smith's ECG Blog, highlighted the downside of indiscriminate use of morphine in patients who present with new ischemic CP ( C hest P ain ). DOI:10.1161/CIRCINTERVENTIONS.118.007305),
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%
The Queen of Hearts agrees: Here the Queen explains why: However, it was not interpreted correctly by the providers: ED interpretation of ECG: "paced rhythm, LBBB but no STEMI pattern." Most large STEMI have peak troponin I in the 20.0 There are hyperacute T-waves in V5 and V6. Next trop in AM. Peak trop 257.97 ng/mL - 80.0
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 In the 500+ Comments I have written on Dr. Smith's ECG Blog since becoming an Associate Editor in 2018 — I do not believe we have had a case of RA-LL lead reversal. What do you think? mm STE in V2).
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