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Nature Reviews Cardiology, Published online: 02 April 2024; doi:10.1038/s41569-024-01020-2 In ST-segment elevation myocardial infarction, the role of interventional modification of thrombi in the coronary arteries before stenting is controversial.
Bi-phasic scan showed no dissection or pulmonary embolism. The lesion was successfully stented. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. --In summary, some subtle findings which do not fit into a pattern, therefore may be nonspecific ECG changes which are encountered everyday. doi: 10.5543/tkda.2021.21026.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
This ECG is highly concerning for LAD occlusion despite it not showing a STEMI criteria. You can find the variables used to calculate the value on MD calc here: [link] Utilizing Dr. Smith’s Subtle Anterior STEMI Calculator (4-Variable), the value is greater than 18.2 The culprit mid LAD lesion was stented.
There is inferior STEMI. He took another look and realized that the culprit was indeed in the proximal RCA and that the thrombus had embolized distally. And so he put the stent in the proximal RCA. See down below for explanation if you don't want to watch the video. But there is also ST elevation in leads V1 and V2.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had been on a long drive, suggesting possible pulmonary embolism (this was unlikely given absence of tachyardia, hypoxia, or any other feature of PE), so we sent a d dimer. The troponin I returned at 4.1 mm STE in one lead. This includes: 1.
It was opened and stented. It is uncommon in the age of reperfusion therapy, as most STEMI get treated reasonably early, before transmural infarct. LV aneurysm puts them at risk for a mural thrombus, which puts them at risk for embolism, especially embolic stroke. Patient course The first troponin returned at 200 ng/mL!!
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.
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.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. However, by the time of the angiogram it had embolized distally, and had only done so after the right sided ECG was recorded. He did, found the true culprit, and went back in to stent it. But which myocardial walls are affected?
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). TIMI flow is 0. Door to balloon time was 51 minutes.
You may see a filling defect in distal LAD, most probably due to an embolization from proximal lesion. The lesion was successfully stented, but it was unfortunately done after a significant myocardial loss. Also note that LAD does not extensively wrap-around apex and supply inferior wall. Aslanger as one of the co-authors ).
The emergency medicine physician documented, "His initial EKG is riddled with artifact and difficult to interpret but does not look like a STEMI." The ECG remains positive for STEMI by GE. The true AV groove LCx was "jailed" by the stent and appears occluded in the post PCI image. The emergency physician consulted cardiology.
He reports this was similar to how he felt when he had his heart attack 4 years prior, now s/p 4 stents. Note: the 2022 ACC Expert consensus Chest pain guidelines state that "posterior STEMI-Equivalent" is a sign of acute coronary occlusion. 2/3 of STEMI have a peak 4th generation troponin I greater than 10.0 NSTEMI-OMI").
After stent deployment, we often see improvement in the ST-T within seconds or minutes. Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. Here is the final angiogram following placement of a stent in the ostial RCA.
His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained. ECG at time 82 minutes: What do you think?
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". No pulmonary embolism is identified. First obtuse marginal also had an 80% stenosis and was stented. Pt received 324 ASA and 2 sprays of nitro with improvement. Cath lab was activated by EMS and transported emergent."
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