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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. Remember, pericarditis is the thing you say and write down when youre actively trying to miss an OMI.
His disease included 70% prox LAD, 80% distal LAD, 10% in-stent stenosis in the distal LCX, 70% OM1, 70% OM2, and 60% prox RCA. Triage ECG: It was interpreted as lateral STEMI, and he was sent to the cath lab, where the angiogram showed unchanged CAD from known prior, with no acute culprit. Three troponins were undetectable.
These latter findings are typical of pericarditis, but pericarditis never has reciprocal ST depression. This led to immediate cath lab activation — which revealed total occlusion of a large 1st diagonal branch that was stented. == Below is the ECG of Patient #3 — recorded from a 35-year old man with sudden, new-onset CP.
It was treated with and dual "kissing balloons" and drug eluting stents. Here is the post stent ECG: There is greater than 50% resolution of ST elevation (all but diagnostic of successful reperfusion) and Terminal T-wave inversion (also highly suggestive of successful reperfusion). Myocardial Rupture and Postinfarction Pericarditis.
Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." Here is the angiogram after stent placement. Is there anything else on the tracing to corroborate inferior OMI? link] Bischof, J.
On day 3 of hospitalization she underwent coronary angiography, revealing a 95% lesion in the mid-LAD which was stented. Repeat ECG the next morning: Resolution of findings above, as well as new deep T-wave inversions in V3-V6 and inferior leads, consistent with reperfusion.
Both were stented. In patients with suspicion of acute MI who have any ST elevation, aVL is also a very useful lead to differentiate between pericarditis and MI. Among 49 patients with pericarditis who had inferior ST elevation, zero of 49 had ST depression in aVL (though there are always rare exceptions such as this case ).
Of course the patient was saddled with the erroneous "pericarditis" diagnosis after CTs ruled also ruled out PE and dissection. The patient was found to have total "mid" LAD occlusion which was stented: Pre-PCI. Serial ECGs remained unchanged. Echo showed normal EF and no wall motion abnormalities, and no pericardial effusion.
You can easily imagine this patient getting one of several diagnoses -- vasospasm, MINOCA , pericarditis, or maybe even no diagnosis at all beyond "non-obstructive coronary artery disease." The operator documented thoughtful consideration of risks and benefits of stent placement.
The patient was referred immediately for cath which revealed RCA occlusion that was stented. There is some down sloping ST-segment and T wave inversion in lead aVL. The findings are diagnostic of inferior and posterior wall OMI. How did the Queen of Heart AI model perform? True Positive ECG#2 : Also sinus rhythm.
60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting. Pericarditis? It was stented. A straight ST segment virtually never happens in inferior ST elevation that is NOT due to OMI (normal variant, pericarditis) 4. The patient had a p rior h istory of MI + stents.
This is a bad ST vector orientation, because it causes widespread STE and one of the most important mistakes that needs to be avoided here is thinking of the diagnosis of pericarditis. Such an out-of-proportion STE is virtually never seen in pericarditis. Look at the STE in lead II, aVF.
It was opened and stented. Patients with completed, transmural infarct are also at risk for post-infarction regional pericarditis and myocardial rupture. One can now see that these large R-waves are Q-waves and the ST depression, as seen from the posterior wall, is really ST elevation! The cath lab was activated.
The 50-something patient with history of coronary stenting and slightly reduced LV ejection fraction. In the setting of prior stenting and reduced left ventricular ejection fraction, would pursue a heart team revascularization approach Syntax score 28.5, Pericarditis would be even more unlikely in someone without chest pain.
Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". The cath lab was now activated. He was found to have 100% mid LAD occlusion.
First Troponin I was <2 and peak was 8, echo showed subtle apical lateral hypokinesis, CRP was elevated, and patient was discharged with a diagnosis of regional pericarditis. In this case, there would be evolution, but the evolution would be typical of pericarditis (if the diagnosis of pericarditis was accurate!!
Despite apparently hearing the above history together with two diagnostic ECGs and a troponin compatible with OMI, the cardiologist thought the ECG represented pericarditis and recommended echocardiogram. The true AV groove LCx was "jailed" by the stent and appears occluded in the post PCI image. The OM is a much larger vessel.
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