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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. Thus, intracoronary imaging modalities are crucial in this setting. From Gue at al.
This has important clinical significance , as many successfully lysed STEMI patient might have minimal segments of dissection/deep plaque fissures. , Kim N Engl J Med 2020; 383:2358-2370 Next query What is the difference between plaque fissure and coronary arterial dissection? Is plaque fissure painful ?
EKG from triage: Here is his previous ECG: Normal ST Elevation Resident's interpretation: Reperfusion pattern/Wellens' with biphasic T waves in V2 and V3, and in comparison to an EKG in 2020 this is new. Patient still not having chest pain however this is more concerning for OMI/STEMI. Labs ordered but not yet drawn. Aspirin given.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. It is not rare.
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. I believe the latter (type II STEMI) is most likely. Troponin I rose to 44.1 FFR can be useful.
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.
To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! One of the most common is rupture of a non-obstructive plaque, with thrombus formation and OMI that spontaneously lyses and leaves a wide open artery. It can only be seen by IVUS.
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? Mild Plaque no angiographically significant obstructive coronary artery disease. A 49 year old woman with h/o COPD only presented with sudden dyspnea.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion). Is there STEMI?
I am going to code this as an acute STEMI as he had transient ST elevation which started to evolve in the emergency department but I think this is most appropriately termed STEMI." When is it anterior STEMI? No formal echo was done, and EF was normal on ventriculogram during cath, with no obvious wall motion abnormalities.
The ECG was read as "No STEMI" and the patient was treated like an average chest pain patient (despite the fact that a chest pain patient with active pain and active subendocardial ischemia is very high risk). Therefore it means acute type 1 ACS plaque rupture with impeded flow and impending full occlusion until proven otherwise.
EMS recorded these prehospital ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 She was having a transient STEMI, briefly. It did not progress to full STEMI with loss of the anterior wall, as in this case. Patients with transient occlusion may manifest only transient STEMI on ECG.
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.
They recorded this ECG: Obvious inferior STEMI/OMI What else? Provocative testing is very helpful for this Coronary Thrombus with lysis (one must do optical coherence tomography or at least intravascular ultrasound to find thes non-obstructive plaques that ruptured. He called 911. Medics recorded a BP of 79/52 with pulse of 47.
Influenza-like illness can also trigger plaque rupture. STEMI criteria are only 43% sensitive for OMI. Beware confusing the diagnosis of posterior STEMI by using posterior leads. 7 steps to missing posterior Occlusion MI, and how to avoid them Interventionalist at the Receiving Hospital: "No STEMI, no cath.
Note: the 2022 ACC Expert consensus Chest pain guidelines state that "posterior STEMI-Equivalent" is a sign of acute coronary occlusion. 2/3 of STEMI have a peak 4th generation troponin I greater than 10.0 Comment: The first ECG is diagnostic of OMI that does not meet STEMI criteria. NSTEMI-OMI").
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