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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?
Written by Jesse McLaren A 70 year old with prior MIs and stents to LAD and RCA presented to the emergency department with 2 weeks of increasing exertional chest pain radiating to the left arm, associated with nausea. I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of 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.
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.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. It was stented. My Comment , by K EN G RAUER, MD ( 10/24/2018 ): = Important teaching points are made in this post by Dr. Smith. Here is his triage ECG: There is massive STE in V3-V6, and also STE in II, III, aVF. There was good flow.
There is an obvious inferior posterior STEMI(+) OMI. Angiogram: Culprit Lesion (s): Thrombotic occlusion of the proximal RCA -- stented. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not. What is the atrial activity? Is it sinus arrest with junctional escape? How would one tell?
The door to balloon time was incredibly short and there was a 100% circumflex occlusion that was opened and stented. The Non-STEMI, which was an OMI, was diagnosed much faster with AI on the ECG than with troponin. Then the high sensitivity troponin T returned at 1400 ng/L.
One stent was deployed with restorative TIMI-0 flow. 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.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. The case was reviewed by all parties, and it was stated correctly that the ECG does not meet the STEMI criteria. The LAD lesion was acute and required 3 stents to restore flow.
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.
Submitted and written by Alex Bracey with edits by Pendell Meyers and Steve Smith Case A 50ish year old man with a history of CAD w/ prior LAD MI s/p LAD stenting presented to the ED with chest pain similar to his prior MI, but worse. Despite ongoing chest discomfort and an uptrending troponin, he never meets STEMI criteria.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. He did, found the true culprit, and went back in to stent it. 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.
One would not expect wall motion to recover so quickly after stenting, so this is good evidence that the POCUS echo was indeed accurate. Angiogram: Severe diffuse left main disease, up to 80% at the ostial left main. Post cath ECG: Normal or near normal Peak troponin I was 15 ng/mL. Is this OMI?
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. He was rushed to the Cath Lab where an LAD culprit lesion was stented. Here is the LAD after stent placement. As the conversation progressed, another ECG spontaneously printed. The pathology is now painfully evident.
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. A mid-LAD culprit lesion was identified and stented. Smith comment : V5 and V6 are excessively discordant!!!! Pacing Clin Electrophysiol.
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.
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.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. A 99% LAD occlusion was stented. Attached is the first ECG.
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). Troponin I returned 80 ng/mL, and the Cath Lab was then reactivated where a 100% LAD occlusion was found and stented.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. Is that an obvious STEMI underneath that rhythm? Is this inferor STEMI? Atrial Flutter with Inferior STEMI? If I fix the rhythm will the ST changes resolve?
The patient was then taken to the cath lab an found to have a proximal RCA 100% thrombotic occlusion which was successfully stented. 3) STEMI criteria failed to identify this acute coronary occlusion, like many others. J Electrocardiology January–February, 2018; Volume 51, Issue 1, Pages e5–e6.
It is equivalent to a transient STEMI. Not much, but studies of STEMI and NonSTEMI show that about 70% of those diagnosed with STEMI have a peak troponin I above 10 ng/mL and that about 70% of those diagnosed with NonSTEMI have a peak troponin I below 10 ng/mL. The lesion was stented. Again, cath lab was not activated.
Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused. To our knowledge, the patient did well.
The culprit lesion was opened and stented. For more on this mirror-image opposite ST-T wave relation in leads III vs aVL — See My Comment in the March 8, 2019 and August 9, 2018 posts in Dr. Smith's ECG Blog ). The QoH now recognizes the OMI with mid confidence. Below is the post -PCI electrocardiogram.
STEMI was activated and the patient went to Cath on arrival. Advanced multi-vessel disease was found with stents deployed to the mid-LCx (80% stenosis), D1 (90% stensosis), and the pLAD (95% stenosis). The ECG’s were sent to the PCI center, and the providers in the respective ED identified the T wave characteristics mentioned above.
It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. He was found to have a 100% occlusion of the proximal anastomotic portion of a prior SVG from the aorta to the OM1 which in turn had a vein graft to the distal RCA. There was initially TIMI 0 flow. THANK YOU Dr. Lee!
Compare to the anatomy after stenting: The lower of the 2 now easily seen branches is the circumflex, now with excellent flow. Here is his angiogram: This shot shows that the left circumflex (LCx) is occluded at the ostium (origin). This is seen just millimeters beyond the tip of the catheter. The patient recovered well.
Note: according to the STEMI paradigm these ECGs are easy, but in reality they are difficult. Theres inferior STE which meets STEMI criteria, but this is in the context of tall R waves (18mm) and relatively small T waves, and the STD/TWI in aVL is concordant to the negative QRS. This was false positive STEMI with an ECG mimicking OMI.
Written by Jesse McLaren An 80 year old with a history of CHF, ESRD on dialysis, and multiple prior cardiac stents presented to the emergency department with 3 days of intermittent chest pain and shortness of breath that resolved after nitro, which felt like prior episodes of angina. Discharge diagnosis was Non-STEMI.
After stent deployment, we often see improvement in the ST-T within seconds or minutes. Here is the final angiogram following placement of a stent in the ostial RCA. 2:04 PM, post stent deployment You can see that even after complete restoration of flow, the ECG still looks terrible, V most of all. link] Chatzidou, S.,
It is diagnostic of OMI, but this is SUBACUTE OMI I sent this ECG to my "EKG Nerdz" friends, without any clinical info at all and they answered "OMI" The Queen said: "STEMI-Equivalent with High Confidence:" Notice she sees findings in both normal beats and PVCs. It was opened and stented. The January 30, 2018 post — for PTA.
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