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Because the most severe LAD OMIs can cause ischemic failure of the RBB and LAF, any patient with ACS symptoms and new RBBB and LAFB with any concordant STE has LAD OMI until proven otherwise. There is no recognition of STEMI equivalency in this setting in the USA guidelines currently. Long term outcome is unavailable.
I simply texted back: "Definite posterior OMI." The person I was texting knows implicitly based on our experience together that I mean "Definite posterior OMI, assuming the patient's clinical presentation is consistent with ACS." The patient was a middle-aged female who had acute chest pain of approximately 6 hours duration.
There were zero patients in this study with a "normal" ECG who had any kind of ACS! So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Deutch et al.
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. Do NOT give it unless you are committed to the cath lab!! Cath attending is aware. It is a mass delusion.
I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form Then I learned that a Code STEMI was activated for concern of anterior "STEMI" in V1-V2. High sensitivity troponin I was 23 ng/L.
Then assume there is ACS. Cardiac arrest #3: ST depression, Is it STEMI? Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit ( as the patient's condition improves ) — allowing clearer definition between the T and P waves. This may or may not be true, but it should give you pause.
Based on recent studies, current guidelines recommend that O2 should not be given to non-hypoxemic patients with STEMI or NSTEMI [2,3]. REBEL Cast Ep114 – High Flow O2, Suspected ACS, and Mortality? 4159 patients (10% of total population) had STEMI 30d Mortality: High O2 protocol: 8.8% Low O2 protocol: 3.1%
Angiogram No obstructive epicardial coronary artery disease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. Therefore, this does not meet the definition of myocardial infarction ( 4th Universal Definition of MI ), which requires at least one troponin above the 99% reference range. You can see the deficiency of the definition of MI.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. This is diagnostic of ACS; it appears to be a reperfused acute inferior OMI. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria). So it can miss some OMI.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Similarly, the OMI paradigm respects ACS as a dynamic process in which ECG changes reflect the phase of myocardial injury and risk stratify which patients may benefit from emergent PCI. Is there STEMI? Leave it alone.
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). But because the patient had no chest pain or shortness of breath, it was not deemed to be from ACS. This is not unusual. Take home 1.
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. 1, 2] The most clinically useful definition to account for this entire constellation is intraventricular conduction delay.
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Day 12 ECG: FINAL DIAGNOSIS: "NSTEMI" Despite the fact that his day 4 ECG easily meets STEMI criteria, the patient is diagnosed as NSTEMI. No TIMI flow was listed in the report. Am Heart J.
This patient could have very easily been overlooked, both because the ECG was STEMI negative and because the Q waves were attributed to an “old infarct”. Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. OMI or STEMI? As cardiology documented, “possible STEMI.
Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it. Obvious inferoposterior STEMI. J ACC 61(4):e78-140; page e83.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? This is the response he got: Interventionist: "No STEMI, no cath. After stabilizing the patient and recording more ECGs, he tried again: Interventionalist: "It isn't a STEMI." It is a STEMI equivalent. We don't know how many though.
He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI." Learning Points: STEMI criteria misses 25-40% of OMI, like this case for example. mm of the "required" 1.0
The cardiologists decided to overrule the STEMI criteria and the cath lab activation was NOT cancelled, and she was taken immediately to the cath lab and found to have an acute thrombotic distal LAD occlusion (TIMI 0). At triage she stated her pain is still persistent, but it is mildly improved compared to when she decided to come to the ED.
80%) and definitely too much for hour to hour. However, the Definition of MI requires at least one value above the 99th percentile, which for a male is 34 ng/L (16 ng/L for women). Thus, these troponins are very concerning for ACS, and subsequent ones will probably be diagnostic of acute MI. of the time.
Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern.
There is perhaps a tiny J-wave in several of the QRS complexes in V3, but it would not be enough to definitively say there is a J-wave. Lead aVL, for example, has a definite J-wave. link] He was admitted to the cardiology unit for serial troponin measurements and concern for possible ACS. Stat echo would also be helpful.
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). In our opinion it should not be given in ACS unless you are committed to the cath lab.
Here is an article I wrote: Updates on the ECG in ACS. The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present.
Because there was proven thrombus (ACS) but the troponin never went above the 99% reference range (and therefore cannot be called MI -- definition of MI requires rise and/or fall of troponin with at least one value above the 99% reference range), this is UNSTABLE ANGINA with ST Elevation.
Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). 3) RV Failure leads to hypotension but NOT pulmonary edema (unlike LV failure) 4) Repeat ECGs, right sided ECG and bedside echo may be helpful in making a diagnosis of ACS. Lead aVL is definitely not normal. The LV EF was 57% at formal echo.
Findings: - Sinus tachycardia - Poor R wave progression - STD in leads V3 and V4 - there is almost an appearance of STE in V6, but it is not definite - there is also slight STE in aVL with slight reciprocal STD in inferior leads Impression: Diagnostic of posterior OMI [and the subtle lateral involvement (aVL) supports this] until proven otherwise.
The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery.
Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. Kurkciyan et al.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
This pattern occurs regardless of whether the cause is ACS (decreased supply) or any other cause of decreased supply or increased demand. A "STEMI alert" was called and soon cancelled. You must understand that this pattern does not differentiate ACS from other causes of supply/demand mismatch.
If it is maximal in V1-V4, and the patient's presentation in consistent with ACS (as this certainly is), then it is DIAGNOSTIC of Occlusion with 90% specificity (We have an upcoming article that proves this). Angiogram: "ACS - Non ST Elevation Myocardial Infarction. Because we are hypnotized the STEMI paradigm. "If
SCAD isn’t rare, especially in women Historically SCAD had been identified in 22% of ACS cases in women. A recent study found that SCAD causes almost 20% of STEMI in young women. Pregnancy is not a common cause of SCAD When ACS occurs in the peripartum period, SCAD is responsible in 43% of cases. A study by Hassan et al.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. One must always be careful when looking for "baseline" ECGs, because the prior ECG on file may have been during another ACS event, as this one clearly was. This ECG is highly suspicious for LAD OMI.
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. Limkakeng AT.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion).
Had the cardiologists followed NSTEMI or transient STEMI guidelines, which recommend non-urgent cath, the patient could have redeveloped an OMI and had a worse outcome. But this foresight will not be recorded, because the patient was diagnosed as "transient STEMI", even though no ECG ever met STEMI criteria. Take home 1.
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. Sensitivity of POCUS even for definite wall motion abnormalities is far from perfect. The ECG only tells you there is ischemia, not the etiology of it.
He had no symptoms of ACS. 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)? His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS." Physician: "No STEMI."
There’s mild inferior ST elevation in III that doesn’t meet STEMI criteria, but it’s associated with ST depression in aVL and V2 that makes it diagnostic of infero-posterior Occlusion MI (from either RCA or circumflex)– accompanied by inferior Q waves of unknown age. Are there any signs of occlusion or reperfusion?
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
There is definite STE inferior and lateral but it just doesn't look like true positive STE to me. I wouldn't activate the lab for this EKG alone, but if the patient is clinically compatible with ACS you could call a heart alert. If I had known there was no definite chest pain or pressure this would have been slightly more confident.
Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI.
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