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ObjectiveSpinal cord ischemia due to damage or occlusion of the orifices of aortic segmental arteries (ASA) is a serious complication of open and endovascular aortic repair. Furthermore, it aids in planning and conducting safe aortic intervention and assists in deciding on single- or two-staged stent graft procedures.
BACKGROUNDThe optimal endovascular approach for acutely ruptured wide‐neck intracranial aneurysms remains uncertain, and the use of stent‐assisted coiling or flow diversion is controversial due to antiplatelet therapy requirements and potential risks. Stroke: Vascular and Interventional Neurology, Ahead of Print. versus BAC: 2.8%;P=
5 ICSS‐ MRI study (International Carotid Stenting Study Magnetic Resonance Imaging Study), indicated that patients with periprocedural hemodynamic depression had decreased cerebral blood flow and increased the risk of new lesions in imaging.6 This is secondary to delayed postoperative cerebral ischemia and infarction caused by vasospasm.7
IntroductionThe optimal endovascular approach for wide‐neck intracranial aneurysms (IAs) during the acute phase of bleeding remains uncertain, and the use of stent‐assisted coiling or flow diversion is controversial due to antiplatelet therapy requirements and potential risks (1, 2).
However, old MI w/aneurysm morphology (persistent ST-Elevation) can look just like this. While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. Old MI w/Aneurysm will show moderate ST Elevation, as seen here.
The patient is female in her 80s with a medical hx of previous MI with PCI and stent placement. Are you confident there is no ischemia? Primary VT , and the VT with tachycardia is causing ischemia with chest discomfort (supply-demand mismatch/type 2 MI)? These are all findings that can be expected with left ventricular aneurysm.
Of the 32 patients, 9(28.1%) had dissection with diagnostic angiograms, 6(18.8%) endovascular thrombectomy, 15(46.9%) aneurysm treatment, and 2(6.3%) angioplasty with or without stenting. Only 4(12.5%) were treated with hyperacute stenting. One patient was symptomatic with neck pain.
Normal RBBB, no evidence of ischemia. It was opened and stented. This may be permanent and may be associated with echocardiographic dyskinesis (aneurysm). LV aneurysm is common in completed, full thickness (transmural) MI, which is what we have here. Here is the patient's previous ECG (Figure 2): Previous ECG.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. The EKG is diagnostic of acute inferior, posterior, and lateral OMI superimposed on “LV aneurysm” morphology. It was stented. He wrote most of it and I (Smith) edited.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. A CT was completed to rule out dissection, PE, or aneurysm, and this was unremarkable. A single DES stent was placed, and the patient did well post-procedure.
Persistent ST elevation 3 days after a nearly transmural MI portends possible LV aneurysm. It is very unlikely to be LV aneurysm morphology when the ST elevation is so high and the T-Wave inversion is so deep. An open 90% LAD was stented. This 42 yo diabetic male presented with cough and foot pain. The LAD has reperfused early.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. QS waves from V2-V5 consistent with LV aneurysm morphology.
A middle-aged male with h/o CAD and stents presented with typical chest pressure. An elderly patient with a ruptured abdominal aortic aneurysm: Formal ECG Interpretation (final read in the chart!) : "Inferior ST elevation, lead III, with reciprocal ST depression in aVL." This is a very common misread. What do you think?
This ECG is all but diagnostic of subepicardial ischemia of the anterior, lateral, and inferior walls, most likely due to Occlusion MI (OMI), probably of the LAD. They found an acute lesion of the LAD at the site of the prior stents, including 70% proximal LAD lesion and 95% mid-LAD stenosis with TIMI 3 flow at the time of cath.
This transmural ischemia, but not necessarily completed infarction (yet). See more images of this case at Gopal's Spectral CT Blog: It's all about confidence With continued symptoms, an elevated troponin, and no other explanation, this is acute MI with ongoing ischemia until proven otherwise.
All these factors, again, support an ECG diagnosis of LVH The patient was nonetheless taken for emergency angiography, and a 99% mid-LAD lesion was found and stented. However, the ST segments in patients with LVH may show significant variation over time in the absence of ischemia. Is LVH like left ventricular aneurysm?
It was treated with and dual "kissing balloons" and drug eluting stents. Here is the post stent ECG: There is greater than 50% resolution of ST elevation (all but diagnostic of successful reperfusion) and Terminal T-wave inversion (also highly suggestive of successful reperfusion). Perhaps she will not develop an LV aneurysm.
Compare to the anatomy after stenting: The lower of the 2 now easily seen branches is the circumflex, now with excellent flow. Post-myocardial infarction (MI) ventricular septal defects are frequently seen in mid-anteroseptal and apical septal segments, whereas apex and the basal inferior segment are prone to aneurysm formation.
His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained. ECG at time 82 minutes: What do you think?
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