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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. See "Mechanisms of acute coronary syndromes related to atherosclerosis".)
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardial infarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque.
Will evolve into STEMI by prothrombotic trigger of lytic agent ECG will get normalised with clinical stability in some Nothing happens. Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. However by no means, we can say thrombosis do not occur.
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.
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.
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 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. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
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.
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.
As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow). He had multiple cardiac arrests with ROSC regained each time.
Angiography was technically challenging as the patient was receiving CPR, but the cardiologist suspected acute stent thrombosis and initiated cangrelor, although no repeat angiography was able to be obtained. Mechanisms of plaque formation and rupture. Coronary plaque disruption. She was defibrillated perhaps 25 times.
This was attributed to a "Type 2 MI", which is acute MI that is not due to ruptured plaque, but rather due to "supply demand oxygen mismatch". Most MINOCA is due to ruptured plaque with thrombus that lyses and does not leave behind a visible culprit. This is extremely elevated for a type 2 MI and totally consistent with STEMI.
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