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Neutrophils are reported to be critical mediators of to poor outcome after subarachnoid hemorrhage (SAH). Following SAH, neutrophils cause vascular occlusion via neutrophil extracellular traps (NETs) and NETs have been identified as a therapeutic target to prevent delayed cerebral ischemia in mice (DCI) with SAH. nucleosome.
There were many comments that it was too late for thrombolytics or that this signified an LV aneurysm, not acute MI. See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. See my answer below. This is my response: "This is definitely acute or subacute.
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. Of the patients, 60.5%
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). Of the patients, 60.5%
Introduction:Delayed cerebral ischemia (DCI) is a leading cause of morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH). The primary outcome was DCI, defined as an exclusionary change in GCS or new, none-treatment related infarcts on imaging. Stroke, Volume 55, Issue Suppl_1 , Page A114-A114, February 1, 2024.
Neutrophils are reported to be critical mediators of to poor outcome after subarachnoid hemorrhage (SAH). In this study, our hypothesis was that NETs cause vascular occlusion leading to delayed cerebral ischemia (DCI) and worse outcome after SAH. However, degrading NETs only marginally improved outcomes.
Introduction:Elevated levels of Interleukin-6 (IL-6) levels in cerebrospinal fluid (CSF) have been correlated with delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). Further studies are needed to validate findings and refine MAP management for improved outcomes in aSAH patients.
Introduction:Recent randomized control trials suggested that mechanical thrombectomy (MT) was associated with good functional outcomes after acute ischemic stroke (AIS) due to large vessel occlusion (LVO) in patients presenting with low Alberta Stroke Program Early CT Score (ASPECTS) (defined as ASPECTS 2-5). with a score of 2, 17.7%
Introduction:Despite comparable outcomes for different frontline techniques in mechanical thrombectomy (MT) for acute ischemic stroke (AIS), there are sparse data regarding if and when to switch techniques if the first pass is unsuccessful. 3.86, P = 0.002) and 90-day good clinical outcome (adjusted odds ratio 2.10, 95% CI: 1.15-3.85,
Due to the rarity of iatrogenic CeAD, existing literature on management and outcomes is limited. 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.
All of this appears to be consistent with "No Reflow", or small vessel occlusion with persistent ischemia in spite of an open artery. Thus, this ECG predicts poor myocardial perfusion and poor outcome. This ECG is diagnostic of anterior LV aneurysm in the presence of RBBB. See more such cases of RBBB with LV aneurysm here.
T-wave inversion in V2 is inconsistent with early repol, and is typical of posterior ischemia. In addition, there is ST depression, diagnostic of ischemia, in V3-V6. A coronary aneurysm was found. And young women have worse outcomes than other groups with STEMI because of the tendency to say, "Nah, couldn't be!"
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. mg/dL, K 3.5 Another 162mg ASA and heparin were given at this point.
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. The patient continued to have ischemia after PCI, and in fact had an episode of polymorphic VT shortly after while in the ICU.
Full case details and outcomes are below. Repeat ECG at 1624 (shortly before cath): QS waves now present in V2-V3, with slight STE, showing the pattern of left ventricular aneurysm morphology. Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia." Smith's response was: "OMI Mimic."
Background:According to the 2023 guidelines for the management of patients with aneurysmal subarachnoid hemorrhages (SAH), early treatment of ruptured aneurysms reduces the risk of repeated bleeds and facilitates treatment of delayed cerebral ischemia. No differences were noted in the size or location of aneurysm.
BackgroundThe outcome of diffuse angiogram‐negative subarachnoid hemorrhage (dan‐SAH) compared with aneurysmal SAH (aSAH) remains unclear. Propensity score matching resulted in matching 65 patients with dan‐SAH to 260 patients with aSAH, and clinical outcomes were compared between the groups. versus 0%,P=0.027), death (11.2%
BackgroundDelayed cerebral ischemia represents a significant contributor to death and disability following aneurysmal subarachnoid hemorrhage. The lack of standardized experimental setups and outcome assessments, particularly regarding secondary vasospastic/ischemic events, may be partly responsible for the translational failure.
The factors that may affect neuropsychological outcomes after aSAH are not well characterized. Clinical variables, modified Rankin score (mRS) at discharge, hemorrhage volume, and the occurrence of vasospasm or new ischemia during hospitalization were collected. Patients underwent Montreal Cognitive Assessment (MoCA).
Subarachnoid hemorrhage (SAH), commonly caused by a ruptured aneurysm, carries a high rate of disability and death. Preclinical studies demonstrate SAH induces dysregulation of the cerebrovasculature and increases neuroinflammation, which contributes to early brain injury and delayed cerebral ischemia.
This ECG is diagnostic of diffuse subendocardial ischemia. She went for a head CT and had a severe subarachnoid hemorrhage (SAH) due to ruptured aneurysm. Data collected included demographics, initial rhythm, EKG, emergency department (ED) CT and outcomes. Unfortunately, but not surprisingly, the patient died a neurologic death.
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." Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was What do you think? Does he need a stress test? --Is
1,2 ASCVD causes or contributes to conditions that include coronary artery disease (CAD), cerebrovascular disease, and peripheral vascular disease (inclusive of aortic aneurysm).3 mg reduced the risk of cardiovascular death, MI or heart attack, ischemic stroke, or ischemia-driven coronary revascularization by 31% compared with placebo.34
More likely, the patient had crescendo angina, with REVERSIBLE ischemia for 48 hours that only became potentially irreversible (STEMI) at that point in time. During the 48 hours of angina, such reversible ischemia often leads to myocardial stunning with akinesis of the myocardial wall that puts it at risk for thrombus.
Repeat CT angio chest (not CT coronary, unclear what protocol) showed possible LAD aneurysm and thrombus. Finally, coronary angiography was performed (at least 5 days after presentation) which confirmed LAD aneurysm with large thrombus burden, TIMI 0 flow, thrombectomy performed. No further cath details available.
You might think it is "Old MI with persistent ST Elevation" (otherwise known as "LV aneurysm" morphology.") That is a reasonable thought, but we have shown that if there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is STEMI, not LV aneurysm. Pain will resolve with completed infarct or with resolution of ischemia.
Look for Vascular Etiology -- think of these while doing H and P: --Bleeding: ruptured AAA, GI bleed, ruptured ectopic pregnancy, other spontaneous bleed such as mesenteric aneurysms. Cardiac Syncope ("True Syncope") Independent Predictors of Adverse Outcomes condensed from multiple studies 1. Abnormal ECG – looks for cardiac syncope.
There are no Q-waves to suggest old inferior MI, or inferior aneurysm as the etiology of the ST Elevation. The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.) What "initiates" the aortic stenosis cascade?
When there are QS-waves, one should always think about LV aneurysm, but ST to QRS ratio and T-wave to QRS ratio are far too large and not compatible with left ventricular aneurysm. There were no other causes of dyspnea apparent and thus we can assume that myocardial ischemia started 6 days prior.
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