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Coronary Intravascular Ultrasound (IVUS) equipment consists of an IVUS catheter, pullback device and the imaging console. IVUS Measurements Measurements include the measurement of lumen, plaque, calcium, remodeling, stent length and volumetric measurements. Incomplete stent apposition can be detected by intravascular ultrasound.
The secondary outcomes included ischemia-driven target lesion revascularization, target vessel myocardial infarction, death, cardiac death, target vessel revascularization, stent thrombosis, and major adverse cardiac events. OCT was associated with a significant reduction of stent thrombosis compared with ICA (OR, 0.49 [95% CI, 0.26–0.92])
No ischemia. A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality. We already know that the ischemia is ongoing, though mild (because of the persistent pain). The culprit was opened and stented.
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. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible.
He underwent coronary stenting (uncertain which artery). Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks n ormal here) , and in a patient with chest pain are nearly diagnostic of ischemia. An emergency cardiac ultrasound could be very useful. Could this have been avoided?
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. This was a point of care ultrasound, not a bubble contrast echo.
I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. Two stents were placed. A posterior ECG was done and showed no ST elevation, not even 0.5 mm in only one posterior lead is highly sensitive and specific for posterior STEMI). The ECG normalized overnight.
Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes. So the RCA was stented. Learning points 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.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. A single DES stent was placed, and the patient did well post-procedure. Abstract 556. You can't use absence of WMA to rule out need for emergent angiography!
A middle-aged male with h/o CAD and stents presented with typical chest pressure. A bedside ultrasound was done by the emergency physician, using Speckle Tracking. RBBB does not affect wall motion by dyssynchrony in the way that LBBB does. --Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was
This proves that the first one was, surprisingly, due to ischemia!! After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. He was successfully treated with one drug eluting stent.
This is an ultrasound (a bit like the type that we use on pregnant women to look at the baby). An ultrasound will allow you to visualise the heart, measure the sizes of the chambers, assess the heart valves and work out how well the heart functions as a pump. It is still possible to have ischemia without coronary disease.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF.
This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. It was stented. This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct. Values: STE60V3 = 2.0, QRS V2 = 10, RAV4 = 15.5, There was good flow. But maybe not.
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. To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing. It was stented.
RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). He was successfully stented. It was about a 7 minute transport time.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. This was stented. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. He appeared to be in shock.
The operator performed intravascular ultrasound and visualized acute plaque rupture with thrombus formation and placed a stent. There was reperfusion ischemia superimposed on benign T-wave inversion. He is very lucky that he spontaneously reperfused and was stented before he had the chance to re-occlude.
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago.
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