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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.
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.
Thus, the patient does not (yet) get a formal diagnosis of MI and must be called unstable angina unless further troponins return above the 99th percentile. On the basis of unresolved angina, cardiology decided to perform rescue PCI. Although it is statistically unlikely, multiple plaque ruptures are possible. Heitner et al.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Patient is pain free and clearly has Wellens' syndrome: 1) pain free episode following an episode of angina, typical Pattern A (biphasic, terminal T-wave inversion with an initial upsloping ST Segment) findings, preserved R-waves. Aspirin given.
This has important clinical significance , as many successfully lysed STEMI patient might have minimal segments of dissection/deep plaque fissures. , may be misdiagnosed as post infarct angina. Kim N Engl J Med 2020; 383:2358-2370 Next query What is the difference between plaque fissure and coronary arterial dissection?
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. Therefore this is " Transient ST Elevation Unstable Angina." As there was ruptured plaque, this is NOT Prinzmetal's angina. There was good flow.
Will evolve into STEMI by prothrombotic trigger of lytic agent ECG will get normalised with clinical stability in some Nothing happens. In addition, the criteria require the absence of precordial Q waves, the presence of history of angina, and normal or slightly elevated cardiac serum markers. ECG will remain same.
Takotsubo is a sudden event, not one with crescendo angina. To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! I need to innoculate you against the subsequent opinions below. It can only be seen by IVUS. MINOCA has many etiologies.
LAD plaque with 0-25 percent stenosis. Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The A CT Coronary angiogram was ordered.
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.
It is equivalent to a transient STEMI. Not much, but studies of STEMI and NonSTEMI show that about 70% of those diagnosed with STEMI have a peak troponin I above 10 ng/mL and that about 70% of those diagnosed with NonSTEMI have a peak troponin I below 10 ng/mL. Again, cath lab was not activated. Int J Cardiol. 2016;207:341–348.
Nevertheless, the operator performed intravascular ultrasound and saw erupted calcium nodule consistent with plaque erosion. Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. In the world of STEMI, we are incapable of recognizing the first ECG as a false negative.
The fear comes built in with the diagnosis often amplified by young felllows on call (& often times by senior consultants as well) It may appear real, from a clinical angle, but trust, when we deal with the whole gamut of so-called ACS (other than STEMI), there is indeed a benign face in many of them.
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