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MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. This is in spite of the known proclivity of tighter stenoses to thrombose.
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient had a history of ‘NSTEMI’ a decade prior, with an RCA stent. Deutch et al.
Background Hyperglycemia, characterized by elevated blood glucose levels, is frequently observed in patients with acute coronary syndrome, including ST-elevation myocardial infarction (STEMI). There are conflicting sources regarding the relationship between hyperglycemia and outcomes in STEMI patients. 3.45) and 4.47 (95% CI: 2.54–7.87),
The angiogram showed an open artery with 95% stenosis and thrombosis and it was stented. Quiz : What percent of full blown STEMI have an open artery with normal flow at angiogram? It too is "normal" and you decide that this is not OMI or STEMI and you just decide to get troponins. I would expect that a stent would be placed.
Will evolve into STEMI by prothrombotic trigger of lytic agent ECG will get normalised with clinical stability in some Nothing happens. Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. However by no means, we can say thrombosis do not occur.
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 This T-wave inversion morphology is very specific for Wellens' waves. Computerized QTc = 417.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. It is not small but rather large plaques, which may not be producing significant stenosis, that undergo rupture with acute occlusive thrombosis, resulting in myocardial infarction and other ischemic events. He was started on nitro gtt.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection. link] We know that most type 1 acute MI due to plaque rupture and thrombosis occurs in lesions that are less than 50% (see Libby reference). From Gue at al.
A random-effects model was used for outcomes with high heterogeneity.Results:We included 4 RCTs with 3173 patients comparing FFR-guided CR with culprit-only PCI in patients with STEMI and multivessel coronary artery diseases. vs 13.6%), any stent thrombosis (RR=1.42; 95% CI [0.35, 5.72]; p=0.62; 2.2%
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. it has been subsequently deemed a STEMI-equivalent. The patient verbalized spontaneous improvement just before 324mg ASA administration. But the lesion is still active!
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?
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.
Both these agents never bother to know, which coronary arterial thrombosis its going to work. As a learnt cardiologist, we must realize most of the STEMIs can be managed successfully * without even knowing which is the IRA, forget about the non-IRA.
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. 24 yo woman with chest pain: Is this STEMI? This is not "diffuse", this is simply anterior, lateral, and likely apical.
This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. As it currently stands, an ST/S ratio >15% should raise awareness for new anterior STEMI. Smith comment : V5 and V6 are excessively discordant!!!! Here are two examples of HATW’s in the setting of confirmed LVH. References Naidu, S.
Smith15, and PERFECT Study Author Group 1 Hennepin County Medical Center, 2 Minneapolis Medical Research Foundation, 3 Background : The Smith-modified Sgarbossa criteria (MSC) are frequently recommended for diagnosing acute coronary occlusion (ACO; STEMI-equivalent) in the setting of ventricular paced rhythm (VPR).
The medics were worried about STEMI, as it meets STEMI criteria. The troponins are NOT consistent with STEMI (OMI), which typically has a troponin I of at least 5 ng/mL. Nevertheless, I don't think a thrombosis related type I MI was ruled out here simply because the patient refused further evaluation. What do you think?
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI. I believe the latter (type II STEMI) is most likely.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction.
Although the attending crews did not consider the ECG pathognomonic for occlusive thrombosis, they nonetheless considered the patient high-risk for ACS and implored him to reconsider. A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The pathology is now painfully evident.
The ECG was read as "No STEMI" and the patient was treated like an average chest pain patient (despite the fact that a chest pain patient with active pain and active subendocardial ischemia is very high risk). The reappearance of de Winter's pattern caused by acute stent thrombosis: A case report. Am J Emerg Med. 2014;32:e5–e8.
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 cardiac arrests with ROSC regained each time.
It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. He was found to have a 100% occlusion of the proximal anastomotic portion of a prior SVG from the aorta to the OM1 which in turn had a vein graft to the distal RCA. There was initially TIMI 0 flow.
Andreas Grüntzig, an ardent angiologist crafted an indeflatable sausage-shaped dual-lumen balloon-catheter, designed its delivery to the heart, launched minimally invasive coronary intervention and taught by beaming live demonstration. Subsequent advances are just incremental tweaks and tinkers around this fully formed framework from 1978.
Analysis of feature importance indicated that older age, STEMI, and inflammatory markers were the most important contributing variables. GBC algorithm outscored the RFC and LR models, with area under receiver operating characteristic curve (AUROC) of 0.91 with proposed working point of 83.3% sensitivity and 82.4%
This was most likely acute thrombosis of a coronary artery resulting in OMI: The ECG changes were attributed to hyperkalemia. It is correct that he did not have chest pain, but we must remember that fully 1/3 of full blown STEMI do not present with chest pain. The dye don't lie".except except when it does. Angiogram Negative, or is it?
Angiography was technically challenging as the patient was receiving CPR, but the cardiologist suspected acute stent thrombosis and initiated cangrelor, although no repeat angiography was able to be obtained. There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ).
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