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This case shows a CT image of subendocardial ischemia. However, there are also Q-waves inferiorly and the inferior T-waves are inverted, suggesting that this is an old MI with persistent ST elevation, or, alternatively, a subacute or partially reperfused, inferior STEMI. This is all but diagnostic of inferior-posterior STEMI.
Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present. They agreed ischemia was likely in the setting of demand given DKA and infection. That this is all demand ischemia is unlikely. Lung exam showed diffuse B lines bilaterally. Aslanger's pattern.
Angiogram No obstructive epicardial coronaryarterydisease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. Detailed coronaryartery evaluation not performed. This suggests further severe ischemia.
Written by Bobby Nicholson What do you think of this “STEMI”? CTA head and neck were obtained and showed no evidence of intracranial hemorrhage, large vessel occlusion stroke (what a helpful and apt name for an acute arterial occlusion paradigm, by the way.), or basilar ischemia. The patient is unconscious and hypoxic.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. The diagnostic coronary angiogram identified only minimal coronaryarterydisease, but there was a severely calcified, ‘immobile’ aortic valve. What do you see?
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. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronaryartery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronaryarterydisease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high).
Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronaryarterydisease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy. An apical OMI has the same ultrasound findings as takotsubo, and thus mimics takotsubo. Lindahl et al. From Gue at al.
The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronaryarterydisease. He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." 418 of these 1788 (23%) had acute coronary occlusion.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronaryarterydisease? Ischemia b. ST depression: is it ischemia? It was a baseline finding in 62% of patients, usually due to LVH. Reference: Knotts RJ , Wilson JM, Kim E, Huang HD, Birnbaum Y.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronaryarterydisease with a near-occlusive culprit lesion in the RCA, possibly reperfused. No significant changes, ongoing pain.
Written by Pendell Meyers A woman in her 70s with known prior coronaryarterydisease experienced acute chest pain and shortness of breath. One could argue or wonder if there is both subendocardial ischemia AND posterior OMI pattern, since the STD in V4 may be equal or possibly slightly worse proportionally than V6.
He has a history of coronaryarterydisease 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.
Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. An EKG from a year prior was available for comparison: The ED physician noted Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. See reference and discussion below.
Severe ischemia can be present even when the chest pain is gone. Learning points: 40% of LAD OMI with TIMI-0 flow do NOT meet STEMI criteria (manuscript under consideration at Eur Ht. 20/53 did not meet STEMI criteria, but all showed OMI diagnosed by both Smith and the Queen of Hearts. But that is not what happened.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Circumstances attending 100 sudden deaths from coronaryarterydisease with coroners necropsies. link] Park, J.,
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