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Traditionally, emergency providers looked for signs of ST-segment elevation myocardial infarction (STEMI) to indicate the need for intervention. Emergency physicians have recognized for some time that there are many occlusions of the coronary arteries that do not present with classic STEMI criteria on the ECG.
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. Fortunately the patient did not reocclude while awaiting the angiogram.
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.
But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Cardiac arrest #3: ST depression, Is it STEMI? Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI. The April 8, 2022 post by Drs.
It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. What lowered my confidence in calling ECG #1 a definite OMI — was the finding of somewhat similar-appearing , upright T waves with slight-but-real J-point ST elevation in so many leads ( ie, leads I,II,aVF; V2-thru-V6 ). What did I say?
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.
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral But at least it does not call it "Normal." Learning Points: You cannot trust conventional algorithms even to find STEMI(+) OMI, even when they say "normal ECG." It is clearly missed by the conventional algorithm.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. 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. So it can miss some OMI.
Smith , d and Muzaffer Değertekin a DIFOCCULT: DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction. Coronary arteries cannot be assessed because the scan was not gated, but proximal segments of the coronary arteries seem to be open with some contrast. Again nothing diagnostic.
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. Thanks in part to rapid bedside diagnosis, the patient was able to avoid emergent coronary angiography. When EMS found her, she was dyspneic and diaphoretic.
Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) have perfect coronary flow by the time of angiogram. Clinical history is needed.
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.
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 reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. 1, 2] The most clinically useful definition to account for this entire constellation is intraventricular conduction delay. Attached is the first ECG. Isn’t VT ALWAYS “wide”?
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.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Serial ECGs enhance the diagnosis of acute coronary syndrome. Is there STEMI? About one hour later his high sensitivity troponin I resulted at 3,000 ng/L (reference 3-54 ng/L). The patient continued having chest pain.
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?
A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD Although a lesion is not visible anatomically on this CT scan, coronary catheter angiography could be considered based on Cardiology evaluation." Transient STEMI is at high risk of re-occlusion.
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.
This ECG is highly concerning for LAD occlusion despite it not showing a STEMI criteria. You can find the variables used to calculate the value on MD calc here: [link] Utilizing Dr. Smith’s Subtle Anterior STEMI Calculator (4-Variable), the value is greater than 18.2 which is concerning for LAD occlusion.
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. This is not the case.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. It shows a proximal LAD occlusion, in conjunction with a subtotally occluded LMCA ( Left Main Coronary Artery ). There is no definite evidence of acute ischemia. (ie, The below ECG was recorded. He was taken immediately to the cath lab.
This is my response: "This is definitely acute or subacute. See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Both support acute anterior STEMI. It is not chronic. There is no question that this benefits from immediate PCI. 3.0 = 0.50
"Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"." The coronary angiography showed a 100% ostial main (obtuse) marginal occlusion!" Dominant right coronary, atherosclerotic and calcified. Peak troponin: 128,000 ng/L.
Thus, there are some suspicious abnormalities, but no definite signs of ischemia. This abnormality in V3 was apparently not seen by the treating MD, who is a nationally recognized expert in STEMI care (showing how difficult these diagnoses can be). But the definition misses the point. There are thin and normal inferior Q-waves.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). No ECG was ordered on Day #1.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. They are definitely high in amplitude and, intermittently, appear to disproportionately tower over the respective QRS. Closer inspection will show that it is Sinus, after all.
He has a history of STEMI and heart failure. link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics. A Coronary angiogram from 8 years prior revealed that he had had an inferior posterior STEMI at the time due to 100% occlusion of the proximal RCA. He was belted and it was low speed.
20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later. Angiogram: Severe two-vessel coronary artery disease with possible co-culprits (90% proximal circumflex, 70% mid/distal RCA) in the setting of non-ST elevation myocardial infarction.
In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. In other words, the inferior "ST elevation" is due to the abnormal rhythm, and does not signify OMI or STEMI in any way. The angiogram showed completely normal coronary arteries.
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.
In the context of remote rural communities, this can help emergency physicians advocate for their patients, and reduce reperfusion delays by days for STEMI(-)OMI == MY Comment , by K EN G RAUER, MD ( 9/8 /2023 ): == Today’s case is distinguished by its occurrence in a remote rural community ( where the nearest cath lab is a plane ride away ).
It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. All coronary arteries were patent without atherosclerotic change. Only after troponin returned elevated was an Echo was done, revealing a definite wall motion abnormality.
Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. So there is a definite inferior and lateral MI. We looked at serial ECGs on patients with acute coronary occlusion ACO) who underwent reperfusion and compared to serial ECG on patients without ACO. Limkakeng AT.
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.
There is sinus rhythm with minimal STE in V1-V3, not meeting STEMI criteria. However, this STE is definitively abnormal in the setting of a normal QRS complex and hyperacute T-wave morphology in V2. The delay between OMI and STEMI sometimes causes unacceptable loss of myocardium or worse.
She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. She went to angio and had normal coronaries. Medics recorded the above ECG and called a STEMI alert. No d-dimer or CT pulmonary angiogram was done when they discovered that she had normal coronary arteries. Her troponin I returned at 900 ng/L.
Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient ’ s oxygen saturation. More recent evidence, however, demonstrates that too much oxygen could be harmful ( AVOID Trial ) by causing coronary vasoconstriction and increasing oxidative stress. Low O2 protocol: 3.1%
Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries). It can only be seen by IVUS.
Angiography showed normal coronaries. This is a troponin I level that is almost exclusively seen in STEMI. A followup ECG was recorded 2 days later: No definite evidence of infarction. So this is either a case of MINOCA, or a case of Type II STEMI. I believe the latter (type II STEMI) is most likely.
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.
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