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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Thus, angiography may be fairly accurate in determining lumen size, but it will not detect the “volume” of atherosclerosis present. The angiographer uses a denominator that is too small, thereby underestimating the degree of stenosis.
There is an area of dense white in the middle of the circle consistent with atherosclerosis. They too have dense white masses consistent with coronary atherosclerosis. The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”.
Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram.
1-4 Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Learning Points: 1.
A "STEMI alert" was called and soon cancelled. This pattern occurs regardless of whether the cause is ACS (decreased supply) or any other cause of decreased supply or increased demand. There is a tiny hint of STE in aVL, but overall I do not think this looks like high lateral OMI. Pain lasted for approximately 45 minutes.
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 had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI. I believe the latter (type II STEMI) is most likely.
We have found in our study comparing inferior STEMI (manuscript in preparation) to inferior early repol several distinguishing characteristics. It showed a 99% stenosis in the RCA, and proximal to a posterolateral branch. Nevertheless, even young people have atherosclerosis and plaque rupture. Not take directly to cath lab.
pre-existing, stable atherosclerosis) amidst any state of global duress – to include hypertension, hypoxia, tachycardia, hypotension, sepsis, and GI bleed, for example. STEMI was activated and the patient went to Cath on arrival. There may even be significant overlap between these factors.
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