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Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The O MI M anifesto.
Cath lab declined as it is not a STEMI." There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves). And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! It is a mass delusion.
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. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
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]
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. ECG Blog #230 — Reviews HOW to c ompare S erial E CGs ( ie, "Are you comparing Apples with Apples or Oranges?" ).
This was a machine read STEMI positive OMI. In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. Written by Willy Frick A 50 year old man with no medical history presented with acute onset substernal chest pain. His ECG is shown below.
Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. What do you think?
These tall T waves are associated with flattening ( straightening ) of the ST segment in the inferior leads — with slight S T elevation in leads V2-thru-V6 ( albeit not enough to qualify as a "STEMI" — Akbar et al, StatPearls, 2023 ). ECG Blog #185 — Reviews the P s, Q s, 3 R Approach to Rhythm Interpretation.
The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves ) will suggest LVH rather than Precordial Swirl ( See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog ). ECG Blog #367 — for another example of acute LCx OMI.
The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. Back to the assessment of ischemia: Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. For national registry purposes, this will be incorrectly classified as a STEMI.) < 0.049).
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.
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 ). ECG Blog #400 — Reviews the concept of " dynamic " ST-T wave changes ( and also DSI = Diffuse Subendocardial Ischemia ). ECG Blog #433 — for another subtle OMI case!
I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease ( ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400 ). ECG Blog #400 — Reviews the concept of " dynamic " ST-T wave changes ( and also Diffuse Subendocardial Ischemia ).
This suggests further severe ischemia. 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. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
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. The ECG only tells you there is ischemia, not the etiology of it. Nevertheless, the clinical situation made other etiologies unlikely.
Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient" , etc. ). To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion ( ie, it is not the pattern of an acute MI ).
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Smith : the profound persistent STE suggests either persistent occlusion or " no reflow " with persistent downstream ischemia. Academic Emergency Medicine 27(S1): S220; May 2020. Abstract 556.
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.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls.
It is due to transmural ischemia not only of the anterior wall and apex, but due to transmural ischemia of the septum, usually due to occlusion proximal to the first septal perforator. As always, LAD OMI need not meet STEMI criteria and usually does NOT! Is this Acute Ischemia? The voltage is high but not huge.
When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI. Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall.
My interpretation was: RBBB with hyperacute T-waves in V4-V6 that are all but diagnostic of LAD occlusion vs. post ROSC ischemia. For more on the application of this Trace-down; Copy-over technique with Shark Fin ST segment deviations — See My Comment in the May 19, 2020 post in Dr. Smith's ECG Blog.
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 days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) I interpret tracings systematically in "real time" ( including my assessment for acute ischemia ).
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. It is often confused with a wide QRS due to conditions such as hyperkalemia. Which artery?
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia.
This blog post also reviews the basics for predicting the " C ulprit" A rtery — and use of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
This blog post reviews the basics for predicting the " C ulprit" A rtery — as well as the importance of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
Here is his ECG: There is no clear evidence of OMI or ischemia. A 40-something male with no previous cardiac disease presented with chest pain. There is a tiny amount of STE in aVL, but it is NOT in the context of a tiny R-wave. There is a tiny amount of STD in lead III, with some non-specific T-wave flattening.
[link] deWinter first reported his unique characteristics of LAD occlusion in 2008, and since the respective ECG changes do not fit the conventional STEMI paradigm (as he even stated – “instead of signature ST-segment elevation” ….) it has been subsequently deemed a STEMI-equivalent.
This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI ( O cclusion-based M yocardial I nfarction ) — most probably with multi -vessel disease ( ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1 ). This patient has new CP — and — he is hypotensive.
If it is STEMI, it would have to be RBBB with STEMI. Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada.
Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia. See My Comment at the bottom of the page in the May 19, 2020 post in Dr. Smith's Blog ). A peak troponin level of 70 ng/L was observed.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] STEMI was activated and the patient went to Cath on arrival.
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. In subendocardial ischemia, cath lab is indicated if the pain persists in spite of medical therapy (aspirin, anticoagulant, IV nitro). At 100 minutes, the above ECG was recorded.
The Queen was not able to see this one: Of course we do not know for certain that the inferior findings represent ischemia. The only way to PROVE that ECG findings are due to the alleged OMI/ischemia is to show evolution in that territory. It could have been a false positive ECG, but if it had been, no harm done. It was not.
Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease.
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. Am J Emerg Med 2020 3. Shin YS, Ahn S, Kim YJ. Bracey A, Meyers HP, Smith SW.
Does this mean that the ST depression in V3 represents "anterior" subendocardial ischemia, and not posterior OMI? This is most consistent with ischemia/infarction in the distribution of the left circumflex coronary artery. non-occlusive ischemia) 2. Thus, they have much less voltage. They have ZERO ST Elevation.
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. Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Lupu L, et al. mg/dL, K 3.5 Abstract 556.
KEY Point: In areas of the heart where an acute STEMI produces ST elevation — reperfusion T waves ( that develop after the "culprit" artery reopens ) will appear as T wave inversion. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
The computer calls it a STEMI. See this case of Type 2 STEMI due to severe hypertension. Here are more Type II STEMI. Any ECG finding that is a manifestation of ischemia will change over time. This ECG was texted to me with the message "A 31 year old with Diabetes and HTN complains of bilateral arm tingling and headache."
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