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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 cardiacarrests with ROSC regained each time.
It is apparently fortunate that she had a cardiacarrest; otherwise, her ECG would have been ignored. Then they did an MRI: Patient underwent cardiac MRI on 10/4 that showed mildly reduced BiV systolic function. The degree of stenosis is not a great predictor of thrombosis, and culprits may not be visible.
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?
This is a troponin I level that is almost exclusively seen in STEMI. I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. 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.
It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. Dialysis patients had double the rate of cardiacarrest (11% vs 5%), were less likely to receive reperfusion therapy when eligible (47% vs. 75%), and had an increased odds ratio of death compared to nondialysis patients 1.5 (95%
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