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This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
Bedside ultrasound with no apparent wall motion abnormalities, no pericardial effusion, no right heart strain. Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). Labs ordered but not yet drawn.
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. Medically refractory angina should have immediate angiography, but this only happens 6.4%
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Bedside cardiac ultrasound with no obvious wall motion abnormalities. . — He had a previous ECG on file: Proving the findings are new The cath lab was activated. He was given aspirin and sublingual nitro and the pain resolved.
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 case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. Takotsubo is a sudden event, not one with crescendo angina.
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. ALL TROPS WERE UNDETECTABLE A formal ultrasound was done: Normal estimated left ventricular ejection fraction at rest. The patient did not report angina with stress. I heard that a prehospital cath lab activation was on its way.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. Therefore this is " Transient ST Elevation Unstable Angina." As there was ruptured plaque, this is NOT Prinzmetal's angina. Values: STE60V3 = 2.0,
The patient was given aspirin, heparin, morphine, and ondansetron and and transferred to a PCI-capable facility for a diagnosis of "unstable angina" with dynamic ECG changes. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? What is the rhythm? Moffat, M.
A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill. There is no acute STEMI. This is diagnostic of recent, reperfused STEMI. This is diagnostic of recent, reperfused STEMI. Acute STEMI would have upright T-waves.
Nevertheless, the operator performed intravascular ultrasound and saw erupted calcium nodule consistent with plaque erosion. Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. In the world of STEMI, we are incapable of recognizing the first ECG as a false negative.
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