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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardialinfarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. MINOCA I do not have the bandwidth here to write a review of MINOCA.
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). A comparison of electrocardiographic changes during reperfusion of acute myocardialinfarction by thrombolysis or percutaneous transluminal coronary angioplasty.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). Smith comment : Is the ACS (rupture plaque) with occlusion that is now reperfusing? Murakami MM.
So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardialinfarction.) Although it is statistically unlikely, multiple plaque ruptures are possible. The PDA plaque was also bulky, but was not described as inflamed or ulcerated. Heitner et al.
To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! Such cases are classified as MINOCA (MyocardialInfarction with Non-Obstructed Coronary Arteries). It can only be seen by IVUS. MINOCA has many etiologies. Learning Points: 1.
This is a troponin I level that is almost exclusively seen in STEMI. In this case, profound shock for 1 hour would result in the same degree of infarction. A followup ECG was recorded 2 days later: No definite evidence of infarction. So this is either a case of MINOCA, or a case of Type II STEMI. Troponin I rose to 44.1
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
Both of these patterns together suggest Aslanger's pattern , recently published in J Electrocardiology: A new electrocardiographic pattern indicating inferior myocardialinfarction. Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), These suggest inferior OMI with possible RV involvement.
The ECG was read as "No STEMI" and the patient was treated like an average chest pain patient (despite the fact that a chest pain patient with active pain and active subendocardial ischemia is very high risk). Therefore it means acute type 1 ACS plaque rupture with impeded flow and impending full occlusion until proven otherwise.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. But which myocardial walls are affected? Comment by KEN GRAUER, MD ( 7/11/2018 ): = Insightful blog post by Dr. Smith regarding ECG criteria for recognizing acute RV involvement in patients with inferior STEMI.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion). What is it?
It is equivalent to a transient STEMI. This is diagnostic of myocardialinfarction. 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.
Here’s the angiogram of the RCA : No thrombus or plaque rupture in the RCA (or any coronary artery) was found. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. A study by Hassan et al. Lobo et al.
Of course, it is actually clearly an acute inferior MI, even though (as is so frequent) it does not meet "STEMI criteria." It was actually a dissection, not an atherosclerotic plaque rupture. I activated the cath lab and brought her to our stabilization room. I called the cardiologists to tell them that we have 2 acute MIs in the ED.
ng/mL This single initial troponin at this level, in the context of chest pain, is high enough to be diagnostic of acute myocardialinfarction. LAD plaque with 0-25 percent stenosis. Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI. Transient STEMI is at high risk of re-occlusion.
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. As there was ruptured plaque, this is NOT Prinzmetal's angina. First, the name (MyocardialInfarction or Not) is not important. It was stented.
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. EKG is pictured below: What do you think?
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. Is that an obvious STEMI underneath that rhythm? Is this inferor STEMI? Atrial Flutter with Inferior STEMI? If I fix the rhythm will the ST changes resolve?
They recorded this ECG: Obvious inferior STEMI/OMI What else? Here it is annotated in red: Our extremely smart radiologist, Gopal Punjabi , assures me that this finding can only be due to myocardialinfarction, not myocarditis. MyocardialInfarction with Non-Obstructive Coronary Arteries. He called 911.
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.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This was ruptured plaque with thrombus. She was a walk-in at triage.
Influenza-like illness can also trigger plaque rupture. STEMI criteria are only 43% sensitive for OMI. Prevalence and outcome of patients with non-ST segment elevation myocardialinfarction with occluded culprit artery - a systemic review and meta-analysis. But in 34% there is persistent occlusion at next day angiogram.
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 Comment: The first ECG is diagnostic of OMI that does not meet STEMI criteria. NSTEMI-OMI").
This was attributed to a "Type 2 MI", which is acute MI that is not due to ruptured plaque, but rather due to "supply demand oxygen mismatch". Most MINOCA is due to ruptured plaque with thrombus that lyses and does not leave behind a visible culprit. They made a final diagnosis of type II myocardialinfarction.
The authors describe a case with some features in common with our patient -- a stressful event followed by a stress cardiomyopathy/acute myocardialinfarction overlap syndrome. Acute myocardialinfarction: an uncommon complication of takotsubo cardiomyopathy. Mechanisms of plaque formation and rupture. SanzRuiz, R.,
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