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A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. Here is his ED ECG: There is sinus tachycardia. Is this acute STEMI? Is this an acute STEMI? -- Unlikely! He had no chest pain.
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. The patient had a history of ‘NSTEMI’ a decade prior, with an RCA stent. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion.
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.
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. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. It was stented.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. Notice there is tachycardia. So there was 3-vessel disease, but with an acute posterior STEMI.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. There is widespread ST depression. Figure-1: Comparison of the first 2 ECGs in today's case.
It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. As a result, this 45-year old man did not experince any delay in treatment — and a large diagonal branch of the LAD was stented with good outcome. To the uninitiated — this ECG may appear normal.
There is sinus tachycardia. It was stented. The possibility of anterior STEMI was not noticed during patient care. I saw this as I was reading a large a stack of ECGs: What do you think? The T-waves are slightly peaked, suggesting hyperkalemia. But what is atypical is that the T-wave in V3 towers over the R-wave.
At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”. RAO Caudal View Post PCI This is the RAO Caudal view after thrombectomy and stent placement. RAO Caudal view: This is the RAO Caudal view.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL) , diagnostic of myocardial injury. mm STE in one lead.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. No appreciable skin pallor. Is this OMI?
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.
Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent. C linically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia. In the available view, the RCA appears fully occluded. To our knowledge, the patient did well.
Diagnosis: Acute non-ST segment elevation MI (Non-STEMI, or NSTEMI) Second troponin returned at around 0200: 15,894 ng/L 0245 (unclear if ongoing pain or not) Inferoposterior (and lateral V5-6) reperfusion findings. There is sinus tachycardia at 100-105/minute. Admitted to the hospital service for further evaluation and management."
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? This was stented. Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, 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. 2) Tachycardia to this degree can cause ST segment changes in several ways. Is that an obvious STEMI underneath that rhythm? If I fix the rhythm will the ST changes resolve?
This doesn’t meet STEMI criteria so in the current paradigm there’s no urgency to getting an angiogram. The initial ECG suggested either subacute or reperfused inferoposterior occlusion and clearly does not meet traditional STEMI criteria. Discharge diagnosis was ‘STEMI’, even though no ECG ever met STEMI criteria.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. He was successfully stented.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
pre-existing, stable atherosclerosis) amidst any state of global duress – to include hypertension, hypoxia, tachycardia, hypotension, sepsis, and GI bleed, for example. STEMI was activated and the patient went to Cath on arrival. There may even be significant overlap between these factors.
His first EKG is shown below, with a lead II rhythm strip: EKG 1, 1645 A provisder who is looking for STEMI would not see much in this EKG. It is possible that the T waves in this EKG are of an intermediate morphology between full-blown STEMI and inferior reperfusion. The thrombus was aspirated and the distal RCA was stented.
The CAG showed a 99% thrombotic lesion of the proximal RCA, which was stented. Smith comment: Approximately 33% of cases that everyone would call STEMI reperfuse spontaneously (TIMI-1, 2, 3 flow) before they undergo emergent angiogram (usually under 90 minute door to balloon time) 20% have TIMI-3 flow.
He had undergone stenting of the LAD several weeks ago (unclear whether elective for stable symptoms, or in response to acute coronary syndrome). It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia? It is a wide complex regular tachycardia at a rate of 120. He appeared critically ill.
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.
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