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Theres ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. Lets see what happens in the current STEMI paradigm. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. What do you think?
However, whether immediate blood glucose and FIB levels affect coronary blood flow during primary percutaneous coronary intervention (PCI) remains unclear.ObjectiveTo explore the correlation between admission blood glucose (ABG), fibrinogen (FIB) and slow blood flow during primary PCI for acute ST segment elevation myocardial infarction (STEMI).MethodsA
This ECG was texted to me with the implied question "Is this a STEMI?": I responded that it is unlikely to be a STEMI. Septal STEMI often has ST depression in V5, V6, reciprocal to V1. Then combine with clinical presentation and low pretest probability 2 Saddleback STEMIs A Very Subtle LAD Occlusion.T-wave wave in V1??
Meyers, Weingart and Smith published their OMI Manifesto — in which they extensively document the critically important concept that management of acute MI by separation into a “STEMI” vs “non-STEMI” classification is an irreversibly flawed approach.
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]
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?
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. years old ± 13.7
mmm ECG Blog #193 — Reviews the concept of why the term “OMI” ( = O cclusion-based MI ) should replace the more familiar term STEMI — and — reviews the basics on how to predict the " culprit " artery. The importance of the new OMI ( vs the old STEMI ) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
IMPRESSION: In this patient who presents with severe, new-onset CP — today's ECG is diagnostic of an extensive, ongoing antero-lateral STEMI. ECG Blog #193 — Reviews the basics for predicting the " culprit " artery ( as well as reviewing why the term "STEMI" — should be replaced by "OMI" = O cclusion-based MI ).
If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate at least accurate enough to not miss STEMI, and that physicians should not be interrupted to interpret it, because there would be no change in patient management. What is the gold standard for ECG interpretation: patient outcome!!!
Background Early recognition of ST-segment elevation myocardial infarction (STEMI) is needed for timely cardiac monitoring and reperfusion therapy. Results Of 5465 patients with STEMI, 73% were transported to hospital by ambulance. and non-ACS diagnosis in 29.7%.
Methods Clinical data from patients admitted to the cardiology division between 2018 and 2022, who were diagnosed with AMI and underwent an IPF testing. Results Among the 277 patients diagnosed with AMI who underwent IPF testing, 113 had (STEMI) and 164 had (NSTEMI). Notably, among STEMI patients, those with IPF ≥ 4.2%
Here they are: Patient 1, ECG1: Zoll computer algorithm stated: " STEMI , Anterior Infarct" Patient 2, ECG1: Zoll computer algorithm stated: "ST elevation, probably benign early repolarization." He diagnosed anterior "STEMI" and activated the cath lab. 25 minutes later, EMS called back with this new ECG: Super obvious STEMI(+) OMI.
P utting I t A ll T ogether : After correcting for LA-LL lead reversal — ECG # 1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement. PEARL # 3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx ( L eft C ircumfle x ) coronary occlusion.
Purpose Construction of a prediction model to predict the risk of major adverse cardiovascular events (MACE) in the long term after percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI).
There is an obvious inferior posterior STEMI(+) OMI. Methods Retrospective study of consecutive inferior STEMI , comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. For review — GO TO: The June 4, 2018 post ( LA-LL reversal ).
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 In the 500+ Comments I have written on Dr. Smith's ECG Blog since becoming an Associate Editor in 2018 — I do not believe we have had a case of RA-LL lead reversal. For review — GO TO: The June 4, 2018 post ( LA-LL reversal ).
We present the cumulative percutaneous coronary intervention (PCI) data of all comers (stable angina and acute coronary syndromes [ACS]) who presented to Hadi Clinic between January 2018 and December 2020. A total of 567 patients underwent coronary catheterisation for the three-year period between January 2018 and December 2020.
Unfortunately you can see that the conventional Zoll algorithm sees nothing even to suggest AMI, let alone STEMI. KEY Point: The best way to confirm acute RV MI — is with use of right -sided leads ( See My Comment in the July 19, 2020 and July 11, 2018 posts). During EMS transport, the pain suddenly resolved.
The Non-STEMI, which was an OMI, was diagnosed much faster with AI on the ECG than with troponin. The door to balloon time was incredibly short and there was a 100% circumflex occlusion that was opened and stented. Then the high sensitivity troponin T returned at 1400 ng/L.
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?
At this point — I learned a bit more about today's patient: The patient is a man who had an inferior STEMI in 2010. 2 prior ECGs were found in his medical record — the latest of which was done circa 2018 ( which would be ~8 years after his inferior MI — and ~5 years before ECG #1 ).
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. Eur Heart J 2018. Is it normal STE? The computer thinks so, and the physician thinks that is quite possible. This is a "Transient OMI".
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? It is often confused with a wide QRS due to conditions such as hyperkalemia. Which artery? There is ST Elevation in every lead except aVR (STD in aVR). Could this be myopericarditis?
Steffen writes this case: "A few weeks ago I was able to recognize a STEMI because of what I had seen on your blog." "I Steffen wrote: " I remembered the ECG from your blog titled: "STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician" from 2013. I also put them side by side: What do you think?
Here it is: The computer reads STEMI What do you think? More from the medic: "LifePak 15 interpretation was STEMI. My response: "I think it is very worrisome for STEMI." It meets STEMI criteria even for a male under age 40, with STE 2.84 No history, meds, or risk factors. Pattern looked to be BER. mm in V2 and 4.08
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. Comment by KEN GRAUER, MD ( 7/11/2018 ): = Insightful blog post by Dr. Smith regarding ECG criteria for recognizing acute RV involvement in patients with inferior STEMI. But which myocardial walls are affected?
This was marked as "Not a STEMI" by the physicians. It is not a STEMI, but it is diagnostic of an LAD OMI (Occlusion MI). has outperformed many cardiologists in its ability to recognize with "high confidence" acute OMIs from ECGs not satisfying STEMI-criteria. Meyers, Weingart and Smith in their 2018 OMI Manifesto.
Discharge ECG showed antero-inferior reperfusion T wave inversion: Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog ).
Another overlooked OMI ( Cardiologist limited by STEMI Definition — OMI evident by Mirror Test ) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog. Smith’s ECG Blog.
It tells us there is an active, ongoing process — and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter-definition of a STEMI has been satisfied. The July 31, 2018 post in Dr. Smith's ECG Blog ( Please scroll down to the bottom of the page to see My Comment ).
He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." See far below for data on 24 troponin T in STEMI and NSTEMI, and correlation with infarct size. This difficulty results in high lateral OMI being the most commonly missed OMIs by the misguided STEMI criteria.
Here is a repeat ECG 45 minutes later with persistent chest pain: Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. Repeat ECGs make difficult decisions easier. -- Comment by K EN G RAUER, MD ( 12/29/2018 ): -- Superb case by Dr. Pendell Meyers, which highlights recognition of subtle acute findings.
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
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. Pacing Clin Electrophysiol.
Angie Lobo ( @aloboMD ) (For open-access reviews of this literature, see Saw 2016 , Saw 2017 , or Hayes 2018.) A recent study found that SCAD causes almost 20% of STEMI in young women. examined SCAD presenting as STEMI (unlike Hassan et al. A study by Hassan et al. Lobo et al. where more than 3/4 of cases were NSTEMI).
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Am J Cardiol 2018; 122(8):1303-1309. Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI.
See these posts for Wellens' mimics: Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH) Anterior STEMI? It even meets STEMI criteria: 2.5 Is it Wellens' Syndrome? This was the first ECG (ECG #1) recorded during pain : This shows ST elevation and hyperacute T-waves in the LAD distribution.
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.
Despite ongoing chest discomfort and an uptrending troponin, he never meets STEMI criteria. As has been mentioned numerous times on this site and is redemonstrated here: expert, subjective ECG interpretation is superior to STEMI criteria. Despite having acute coronary occlusion by cath, his ECGs never met STEMI criteria.
There is a subtle but important difference between OMI and subendocardial ischemia: OMI (that is not STEMI) is due to TIMI 0/1 flow and has any combination of subtle STE, hyperacute T-waves, reciprocal ST depression, decreased QRS amplitude, terminal QRS distortion and other findings. Is this OMI?
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center. As the conversation progressed, another ECG spontaneously printed. 3] Aslanger, E.,
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. I was reading ECGs on the system, and saw this one: What do you think? However, it is difficult to recognize for an interpreter who is does not have special expertise in OMI ECG diagnosis.
There is mixed overlap of ST-segment elevation (STE), ST-segment depression (STD), Hyperacute T waves (HATW), and deWinter pattern (which the ACC regards as a STEMI-equivalent but is better suited under the blanket of OMI). 1] Vitals BP 160/110 HR 90 (trend) RR 24 (BBS CTA) SaO2 92% RA Attached is the Patient's ECG. 2] Costanzo, L.
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