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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.
This suggests further severe ischemia. MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. And yet the arteries remain open.
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.
I would expect TIMI-3 flow (normal flow, no persistent ischemia) with a culprit in the RCA (or possibly Circumflex). 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? Jesse McLaren et al.
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.”
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia. Am J Emerg Med.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection. link] We know that most type 1 acute MI due to plaque rupture and thrombosis occurs in lesions that are less than 50% (see Libby reference).
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.
Although the attending crews did not consider the ECG pathognomonic for occlusive thrombosis, they nonetheless considered the patient high-risk for ACS and implored him to reconsider. A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The pathology is now painfully evident.
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. it has been subsequently deemed a STEMI-equivalent. The patient verbalized spontaneous improvement just before 324mg ASA administration. But the lesion is still active!
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits. These include.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. In there ECG evidence of possible ongoing ischemia? (ie,
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. 24 yo woman with chest pain: Is this STEMI? This is not "diffuse", this is simply anterior, lateral, and likely apical.
Smith15, and PERFECT Study Author Group 1 Hennepin County Medical Center, 2 Minneapolis Medical Research Foundation, 3 Background : The Smith-modified Sgarbossa criteria (MSC) are frequently recommended for diagnosing acute coronary occlusion (ACO; STEMI-equivalent) in the setting of ventricular paced rhythm (VPR).
Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. Negative trops and negative angiogram does not rule out coronary ischemia or ACS. This is extremely elevated for a type 2 MI and totally consistent with STEMI.
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! There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ).
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