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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.
with ST elevated myocardial infarction (STEMI), 3.41% with unstable angina, 0.56% with stable angina, and 0.11% were diagnosed with various types of arrhythmias. SCAD-PCI revascularization frequently required three or more stents and had residual areas of dissection. Approximately 48.5% and 1.3%, respectively.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Patient is pain free and clearly has Wellens' syndrome: 1) pain free episode following an episode of angina, typical Pattern A (biphasic, terminal T-wave inversion with an initial upsloping ST Segment) findings, preserved R-waves. Aspirin given.
If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”.
Thus, the patient does not (yet) get a formal diagnosis of MI and must be called unstable angina unless further troponins return above the 99th percentile. On the basis of unresolved angina, cardiology decided to perform rescue PCI. RCA and PDA before and after, arrows indicating stented regions. Repeat ECG is shown below.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. It was stented. Therefore this is " Transient ST Elevation Unstable Angina." As there was ruptured plaque, this is NOT Prinzmetal's angina. So Unstable Angina still exists [even with high sensitivity (hs) troponins].
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.
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. and the average number of stents 2.6. The radial approach was used in 544/567 (95.94%), the average SYNTAX score was 34.8 ± 9.6,
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
Types of ACS include stable angina 5.3% (n=8), unstable angina 24% (n=36), NSTEMI 28.7% (n=43), and STEMI 24% (n=36). All patients had interventional PCI with balloon and stent insertion. The mean age of patients was 57.68 (SD= 11.19) years. Rate of MACE as composite outcome 30-days after PPCI as 24.7% (n=37).
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 It was stented. This T-wave inversion morphology is very specific for Wellens' waves. Gottlieb SO, et al.
Here is the prehospital ECG, with pain: Hyperacute anterolateral STEMI The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow. A stent was placed. When the patient had chest pain, prior to nitroglycerine, what do you think the ECG showed ? Lessons: 1. de Zwaan C.,
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.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. The reappearance of de Winter's pattern caused by acute stent thrombosis: A case report. Am J Emerg Med. 2014;32:e5–e8. As per Drs.
A middle-aged woman had intermittent angina for 48 hours, then onset of constant, crushing chest pain for 1.5 It was treated with and dual "kissing balloons" and drug eluting stents. cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." hours when she called 911.
While this ECG is negative for “posterior STEMI”, the resolution of anterior ST depression (accompanied by the troponin elevation) confirms posterior OMI with spontaneous reperfusion. The second opportunity to make the diagnosis and expedite angiography was missed because the ECG never met STEMI criteria and continued to be labeled ‘normal.’
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?
Angiographic and clinical characteristics of patients with unstable angina showing and ECG pattern indicating critical narrowing of the proximal LAD coronary artery. See these posts for Wellens' mimics: Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH) Anterior STEMI? It even meets STEMI criteria: 2.5
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.
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.
The PMCardio Queen of Hearts app asks you, before giving an interpretation of OMI ("STEMI-Equivalent"), whether the patient's clinical presentation is high risk for OMI. Was it unstable angina? Well, really, in this case, there was no angina, only "dizziness") I don't think so. So let's pretend this is acute chest pain.
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.
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