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Occlusion myocardialinfarction is a clinical diagnosis Written by Willy Frick (@Willyhfrick). 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." The case continues. Worrall, C.,
A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. Opiates are associated with worse outcomes in MyocardialInfarction. Abstract 556.
Background Hyperglycemia, characterized by elevated blood glucose levels, is frequently observed in patients with acute coronary syndrome, including ST-elevation myocardialinfarction (STEMI). There are conflicting sources regarding the relationship between hyperglycemia and outcomes in STEMI patients.
See these 2 articles Association between pre-hospital chest pain severity and myocardial injury in ST elevation myocardialinfarction: A post-hoc analysis of the AVOID study Author links open overlay panel [link] 1 Background We sought to determine if an association exists between prehospital chest pain severity and markers of myocardial injury.
BackgroundCurrent research suggests that microvascular obstruction (MVO) following the first percutaneous coronary intervention (PCI) in myocardialinfarction patients is closely related to inflammatory responses. The predictive model incorporating LCR enhances the ability to predict MVO occurrence in patients with STEMI post-PCI.
Introduction Cardiogenic shock (CS) complicates 5%–15% of cases of acute myocardialinfarction (AMI) with inpatient mortality greater than 40%. This prospective registry includes all patients >18 years of age presenting with STEMI with or without CS beginning on 1 February 2023.
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
Primary percutaneous coronary intervention (PPCI) remains the gold-standard treatment for ST-elevation myocardialinfarction (STEMI). We present the case of a man in his 50s, admitted with cardiac arrest secondary to inferolateral STEMI.
BackgroundThere may be variability in willingness to perform percutaneous coronary intervention (PCI) in higherrisk patients who present with STsegmentelevation myocardialinfarction (STEMI). There were 178 984 patients from 582 US hospitals presenting with STEMI who were included. versus 7.4%,P<0.001),
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The article by Aslanger, Smith et al that is featured above in today’s post has just been published.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
BACKGROUND:Microvascular obstruction (MVO) is associated with heart failure (HF) following ST-segmentelevation myocardialinfarction. Circulation: Cardiovascular Imaging, Ahead of Print.
Background:Little is known about the clinical relevance of interleukin (IL)-6 and the severity of patients with acute ST-elevation myocardialinfarction (STEMI). Blood samples for biomarker analyses, including IL-6, were collected.Results:There were 64 consecutive STEMI patients. There was 75% of males.
Background Despite advances in percutaneous coronary intervention (PCI) for ST segment elevation myocardialinfarction (STEMI), in-hospital mortality remains a concern, highlighting the need for the identification of additional risk factors such as serum iron levels. μmol/L) and a control group (Fe ≥7.8 μmol/L).
BACKGROUND:T2-weighted imaging is commonly used to measure myocardial salvage in reperfused myocardialinfarction but is hindered by poor reproducibility and indistinct boundaries. The median MSI was 35.0% (interquartile range, 22.959.5%), with smaller MSI observed in patients with larger infarcts (P<0.001).
This is a value typical for a large subacute MI, n ormal value 48 hours after myocardialinfarction is associated with Post-Infarction Regional Pericarditis ( PIRP ). Mechanical complications secondary to myocardialinfarction are infrequent due to most patients receiving revascularization quite rapidly.
OMI Pocket Guide The OMI Pocket Guide ( [link] ) is a user-friendly online resource designed to help healthcare professionals learn how to recognize subtle signs of acute coronary occlusion on the ECG which represent occlusion myocardialinfarctions (OMI). I’ve accessed this hand OMI Pocket Guide on both my ipad and iphone.
Methods The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed when we extensively searched three electronic databases: PubMed, ScienceDirect, and Web of Science, for studies that compared conservative vs. invasive revascularization treatment outcomes for patients with SCAD from 2003 to 2023.
associated typical MyocardialInfarction therapies such as statins and ACE inhibitors with significantly decreased 1 year mortality in MINOCA patients, which suggests that they do indeed have a similar pathophysiology to MI patients with obstructive coronary disease. MINOCA I do not have the bandwidth here to write a review of MINOCA.
would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic." Can you diagnose an ACO (STEMI) when you also have LVH? The criteria of Armstrong et al. References 1.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardialinfarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque.
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Circulation 2007 2. Khan et al.
Code STEMI was activated by the ED physician based on the diagnostic ECG for LAD OMI in ventricular paced rhythm. This was several months after the 2022 ACC Guidelines adding modified Sgarbossa criteria as a STEMI equivalent in ventricular paced rhythm). LAFB, atrial flutter, anterolateral STEMI(+) OMI.
” R outine nasal Oxygen has little use in the management of STEMI. Now,14 years later, some young researchers reaching out to this concept ,via liquid myocardial oxygen. was presented at the 2023 SCAI meeting in Phoenix. In fact, it can be harmful as it causes vasoconstriction. Circ Cardiovasc Interv.
Triage ECG (no prior for comparison): Computer algorithm read: "Sinus rhythm, low voltage QRS, inferior myocardialinfarction, probably old." Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). He reported a normal stress test a few years ago.
Databases including Embase, PubMed, The Cochrane Library, Web of Science, CNKI, Wanfang Data, VIP, and SINOMED were comprehensively searched for identifying studies published from 1977 to 19 May 2023. The models were mainly constructed using data from individuals diagnosed with ST-segment elevation myocardialinfarction (STEMI).
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
Aslanger's pattern (Smith was co-author on this): A new electrocardiographic pattern indicating inferior myocardialinfarction The next troponin returned at 8822 ng/L. 20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later. Normal left ventricular wall thickness.
Methods:STEMI patients who underwent coronary revascularization therapy and cardiac magnetic resonance (CMR) at about 4 days and 6 months between 2017 and 2023 were included. The patients were divided into groups (Group 1, FSF (-) during procedures with final TIMI-3; Group 2, FSF (+) with TIMI-3; Group 3, final angiogram was non-TIMI-3).
Barely any STE, and thus not meeting STEMI criteria. Read our recent editorial: Hyperacute T-waves Can Be a Useful Sign of Occlusion MyocardialInfarction if Appropriately Defined. Read our recent editorial: Hyperacute T-waves Can Be a Useful Sign of Occlusion MyocardialInfarction if Appropriately Defined.
But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. This confirms these Q waves are caused by an acute infarct. But the ECG still doesn’t meet STEMI criteria. Am J Emerg Med 2023 2. Smith : Normal ST Elevation in V2-V4 never has an associated Q-wave!
It was tested on a large database of known outcomes and was more than twice as senstivity as STEMI criteria and much better than cardiologists. Angiogram Culprit Lesion (s): ST elevation myocardialinfarction due to 99% stenosis of the distal LAD Formal echo: Normal estimated left ventricular ejection fraction, 63%.
So we activated the Cath Lab Angiogram: Impression and Recommendations: Culprit for the patient's anterior ST segment myocardialinfarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD The first troponin returned barely elevated at 36 ng/L (URL = 35) In our study of initial troponin in STEMI, 26.8%
A very large myocardialinfarction. The next day the ECG not unexpectedly shows a completed transmural inferior and posterior wall infarction. The delayed activation of the cath lab would have been avoided had the treating physicians been trained in recognizing occlusion myocardialinfarction.
Angiogram: Culprit for the patient's inferior ECG changes and non-ST elevation myocardialinfarction is a 100% acute thrombotic occlusion of the proximal RCA. The patient was diagnosed with a"Non-STEMI." Here is the main learning point: The infarct was due to an occluded artery (Occlusion MI, OMI).
The ECG is diagnostic of occlusion myocardialinfarction (OMI). It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. The overall read is OMI with HIGH confidence. == Below is the ECG of Patient #2 — as interpreted by the QOH.
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). A New ST-segment elevation myocardialinfarction equivalent pattern? Eur J Emerg Med. 2017;24:236–242. Am J Emerg Med.
I knew that, if the patient had presented with chest discomfort, that this ECG is diagnostic of inferior posterior OMI, even though it is not a STEMI. Unusual and puzzling, as there was a large focal acute MI) Final Diagnosis: Acute MI, Non ST Elevation MyocardialInfarction.
So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardialinfarction.) HsTnI drawn at that time was 9 ng/L (ref. 80%) and definitely too much for hour to hour. And, among our chief goals as medical providers — we want to treat pain when this can be safely done!
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? Physician interpretation: "No STEMI." Physician: "No STEMI." Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia."
ng/mL This single initial troponin at this level, in the context of chest pain, is high enough to be diagnostic of acute myocardialinfarction. Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI. Transient STEMI is at high risk of re-occlusion. Her initial cTnI returned at 0.25
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