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BackgroundMyocardial ischemia can impair the speed and intensity of myocardial contractility, frequently undetectable by conventional echocardiography in early stages. LVEF1 was independently associated with coronary artery stenosis 50% or 70%. for predicting coronary artery stenosis 70%. A cutoff value of 26.9%
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Or is it a very tight stenosis that does not allow enough flow to perfuse myocardium that has a high oxygen demand from severely elevated BP?
Rescue treatment with stenting, balloon angioplasty, and/or intraarterial thrombolysis or antiplatelets are often required to treat the underlying stenosis. 4 Recent literature has reported clinical benefits associated with rescue stenting in the setting of ICAD‐related MT‐refractory strokes.5
IVUS Measurements Measurements include the measurement of lumen, plaque, calcium, remodeling, stent length and volumetric measurements. In the geometry, the size of the plaque, its relationship to luminal stenosis, arterial remodeling and eccentricity can be evaluated. IVUS can also delineate intramural hematoma and dissection.
2 years prior he had an angiogram which showed 90% proximal stenosis of the circumflex. Left main: no obvious stenosis. LAD: severe in-stent restenosis in the mid (80%) and distal (90%) segment and diffuse disease distally. D1: severe (90%) de-novo stenosis in the mid to distal segment. LCX: non-dominant.
A stent was placed. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. In this case, the duration of ischemia was so brief that there was no such evolution, and there was near-normalization. Ischemia may be so brief that Wellens' waves do not evolve 3. Lessons: 1.
Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. It was opened and stented. Data from stress testing proves that the ST depression of ischemia does not localize.
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Was this: 1) ACS with ischemia and spontaneous reperfusion?
I would expect TIMI-3 flow (normal flow, no persistent ischemia) with a culprit in the RCA (or possibly Circumflex). I would expect that a stent would be placed. The angiogram showed an open artery with 95% stenosis and thrombosis and it was stented. What would I expect the angiogram to show?
It means either a percutaneous coronary intervention with a stent or CABG. Reference : Apart from the heavily quoted classics of COURAGE, BARI-2D, ISCHEMIA, ORBITA 1 etc. You may be. But I am not.You need to undergo some re-vascularisation procedure. What do you mean by that Doctor ? No we can’t.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. It was stented.
More Smith comment: it is true that ST depression (STD) due to subendocardial ischemia does not localize [it is usually diffuse ST depression, in multiple leads and not reciprocal to ST elevation in an opposite territory], this ST depression is different! Both were stented. Notice how useful serial ECGs are! mm ST depression in aVL.
The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia. The red arrow points to a 90% stenosis in the proximal segment of the LAD. RAO Caudal View Post PCI This is the RAO Caudal view after thrombectomy and stent placement.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Normal RV, no valve stenosis or regurgitation.
60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting. The cath lab was activated: Result: Thrombotic 95% stenosis at the ostium of a small LPL2 with 70% stenosis at the LPL2/LPDA bifurcation in the distal/AV groove Cx Tubular 70% stenosis in the mid-circumflex. (In
There is ventricular hypertrophy in the absence of abnormal loading conditions, such as aortic stenosis, or hypertension, for example – of which the most common variant is Asymmetric Septal Hypertrophy. There is LBBB-like morphology with persistent patterns of subendocardial ischemia.
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, This alone could be due to LVH, but V4 could NOT be due to LVH.
This middle aged male with h/o GERD but also h/o stents presented to the ED with chest pain. A 3rd troponin returned before the angiogram was done and was 2956 ng/L Here is the angiogram description: The distal RCA has mild diffuse disease and bifurcates to give a large RPDA which is without significant stenosis.
This is ischemia until proven otherwise. Here I annotate it: This shows 100% occluded circumflex (red arrow) and a 90% stenosis of the LAD (Yellow arrow). The LAD was thought to be not thrombotic, but a chronic tight stenosis. I learned that the patient is on Sotalol for control of PVCs. This explains the long QT.
Angiogram showed a critical LAD thrombotic stenosis. The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow. After many hours, the decided that it was appropriate to do an angiogram and they found a distal LAD occlusion which was opened and stented. He underwent CABG. Male in early 40's with 1.5
The prospective, international, multicenter single-arm observational study evaluated the treatment of de novo, restenotic or occluded iliac lesions in 160 patients with Rutherford Class 2-6 peripheral artery disease using the Dynetic-35 cobalt chromium balloon-expandable stent system. stenosis in the target lesion. At baseline, 12.5%
The goal was to determine whether using FFR to identify functionally significant stenoses (FFR 0.80) for stenting, rather than relying solely on angiographic appearance. FAME series , though never had an intention to compare PCI vs CABG , now we have used the platform to upend it to take on the CABG in multivessel CAD.
Coronary angiography gives a visual impression about the severity of the stenosis. But it need not imply the actual functional significance of the stenosis in terms of flow physiology. indicates inducible ischemia while an FFR above 0.80 excludes ischemia in 90% of cases. Normal FFR is 1.0 and an FFR below 0.75
Objective:To compare the 1-month stroke, myocardial infarction (MI), and/or death rates among symptomatic patients undergoing either CAS or CEA according to the timing of the procedure in Carotid Revascularization Endarterectomy versus Stenting Trial (CREST).Methods:We
Background:Patients with atrial fibrillation were excluded from clinical trials evaluating carotid artery stent(CAS) or carotid endarterectomy (CEA).We Background:Patients with atrial fibrillation were excluded from clinical trials evaluating carotid artery stent(CAS) or carotid endarterectomy (CEA).We
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] STEMI was activated and the patient went to Cath on arrival.
Background Untreated multivessel disease (MVD) in acute myocardial infarction (AMI) has been linked to a higher risk of recurrent ischemia and death within one year. The immediate non-IRA PCI is associated with a significantly lower occurrence of unplanned ischemia-driven PCI (OR 0.60; confidence interval [CI] 0.44–0.83)
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. Angiogram showed a culprit lesion of 100% stenosis to the right coronary artery and 100% stenosis of the right posterior descending artery, both with TIMI 0 flow.
A middle-aged male with h/o CAD and stents presented with typical chest pressure. The so-called "ST Elevation" is really the end of the QRS of Right Bundle Branch block. --Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was This is a very common misread.
RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. He was taken to the cath lab and underwent emergent intervention: Thrombotic stenosis of the proximal RCA (95% with evidence of plaque rupture) is the culprit for the patient's inferoposterior STEMI. He was successfully stented.
This ECG is all but diagnostic of subepicardial ischemia of the anterior, lateral, and inferior walls, most likely due to Occlusion MI (OMI), probably of the LAD. They found an acute lesion of the LAD at the site of the prior stents, including 70% proximal LAD lesion and 95% mid-LAD stenosis with TIMI 3 flow at the time of cath.
So the patient was taken for emergent cath, showing: Culprit artery: LAD (100% stenosis, TIMI 0) requiring thrombectomy and stent. EKG shown here: LAFB with no clear signs of OMI or ischemia. Queen of Hearts interpretation: Now the cardiologist considered it "STEMI"! No labs were performed. EKG and CT head were performed.
Marked differences can be seen in the prevalence of coronary artery stenosis at autopsy by age and gender. In 30-39 year old women the rate of coronary stenosis at autopsy was 5/1,545 (0.3%) while 60-69 year old men had a prevalence of 12%, almost 40 times higher. The results of this dataset by age and gender follow. This happens.
She underwent angiogram within a few hours and was found to have mid-RCA culprit lesion, 99% stenosis, TIMI 3 flow. 1) The ECG with active ischemia or reperfusion or subendocardial ischemia or nonspecific (no ischemia) 2) presence or absence of symptoms. (A Initial troponin (high sensitivity trop I): 212 ng/L.
It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued. The proximal and mid LAD stenoses were stented and the OM 2 was left alone. Subendocardial ischemia does not localize.
Here is the angiogram: Very tight stenosis in circumflex, but with TIMI-3 flow, thanks to thrombolytics. Here is the circumflex after stenting: Wide open The cardiologist called Dr. Lufkin back and said "Great call!!" Later, the first troponin I returned at 0.057 ng/mL (4th generation, not high sensitivity).
In a 90% LAD lesion with compromised flow, this can worsen ischemia, outweighing any flow benefit from higher pressure. This can lead to ischemia, especially in the subendocardium, which is most vulnerable due to higher oxygen demand. Hypertension increases left ventricular afterload, raising myocardial oxygen demand.
The therapeutics of coronary stenosis has become a technogical wonder, interwoven with statistical wordplay in the last few decades. otherwise, if you keep getting even the slightest doubt and anxiety over the hidden blocks, go for a stent immediately at a good Institution. (My What is the big deal to analyze suboptimal PCI vs OMT?
August 2024 Approvals Minima Stent System (P240003) (Approval Date: August 28, 2024) The Minima Stent System is an expandable cobalt-chromium metal mesh tube to reopen blood vessels in neonates, infants, and children with Coarctation of the Aorta and Pulmonary Artery Stenosis, specifically designed to expand as younger patients grow.
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