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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.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. This rules out subendocardial ischemia and is diagnostic of posterior OMI. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
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.
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. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished.
V1 sits over both the RV and the septum, so transmural ischemia of either one with give OMI pattern in V1 and reciprocal STD in V5 and V6. See this post: Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6. However, the pattern is also seen in inferior OMI with right ventricular OMI. (V1
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. and repeat the ECG, to see if the apparent ischemia persists. A third ECG was done about 25 minutes after the first: This shows resolution of all apparent ischemia.
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.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Distinction of PMVT vs VFib is an academic one in this case ). Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. (
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.
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. Academic Emergency Medicine 27(S1): S220.
It does not usually represent subendocardial ischemia, but rather it is usually reciprocal ST depression, reciprocal to inferior ST elevation. Still does not meet STEMI criteria, but it is an obvious OMI And then another one became more obvious: Cath lab was activated and a 100% RCA occlusion was found.
The ECG is diagnostic of LAD occlusion (or even left main occlusion possibly), with the classic pattern of RBBB and LAFB with huge concordant STE in V1-V2, I, and aVL, with reciprocal depression in most other leads (and/or a component of subendocardial ischemia pattern). Code STEMI was activated. This is "shark fin" morphology.
He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. At the time of this initial ED ECG, his symptoms were improving ECG #1 on admission to the ED The patient was not seen quickly in the ED as it was a busy shift and the ECG did not meet STEMI criteria. The below ECG was recorded.
It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. Academic lessons from this patient. What is the big deal to analyze suboptimal PCI vs OMT?
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