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Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." Here is the angiogram after stent placement. Immediate versus delayed invasive intervention for non-stemi patients. Marinkovic, J.,
The primary efficacy objective was to demonstrate superiority of PPA to reduce the primary efficacy end point of all-cause death, nonfatal myocardial infarction, nonfatal stroke, stent thrombosis (definite), or urgent revascularization (any vessel) within 30 days.
There is an obvious inferior posterior STEMI(+) OMI. We recorded an ECG in which V1-V3 were put in the position of V4R-V6R, and V4-6 were placed in V7-9 to (academically) confirm posterior OMI. I say academically because the STD in V2 is diagnostic -- posterior leads are NOT necessary. What is the atrial activity? What to do?
This is diagnostic of inferior MI, though does not meet millimeter criteria for "STEMI." He was worried for inferior MI and ordered another, which was recorded 15 minutes later: Now clearly and obviously diagnostic of inferior STEMI. He was found to have a 100% circumflex lesion for which a bare metal stent was placed.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. No appreciable skin pallor. Is this OMI?
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. The reappearance of de Winter's pattern caused by acute stent thrombosis: A case report. Am J Emerg Med. 2014;32:e5–e8. As per Drs.
There is mixed overlap of ST-segment elevation (STE), ST-segment depression (STD), Hyperacute T waves (HATW), and deWinter pattern (which the ACC regards as a STEMI-equivalent but is better suited under the blanket of OMI). Troponin I returned 80 ng/mL, and the Cath Lab was then reactivated where a 100% LAD occlusion was found and stented.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. Is that an obvious STEMI underneath that rhythm? Is this inferor STEMI? Atrial Flutter with Inferior STEMI? If I fix the rhythm will the ST changes resolve?
Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Academic Emergency Medicine 27(S1): S220. A single DES stent was placed, and the patient did well post-procedure. Unfortunately, they follow their own guidelines only 6% of the time!! Lupu L, et al. mg/dL, K 3.5
He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. At the time of this initial ED ECG, his symptoms were improving ECG #1 on admission to the ED The patient was not seen quickly in the ED as it was a busy shift and the ECG did not meet STEMI criteria. The below ECG was recorded.
It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. Academic lessons from this patient. What is the big deal to analyze suboptimal PCI vs OMT?
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