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Phlebolymphedema: Hallmark Of Combined Insufficiency Of Venous-Lymphatic System
Phlebolymphedema: Hallmark Of Combined Insufficiency Of Venous-Lymphatic System
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Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
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TIPS: Techniques- Stent Grafts | TIPS & DIPS: State of the Art
TIPS: Techniques- Stent Grafts | TIPS & DIPS: State of the Art
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Case- May Thurner Syndrome | Pelvic Congestion Syndrome
Case- May Thurner Syndrome | Pelvic Congestion Syndrome
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Angiographic Predictors of Successful Revascularization | Determining the Endpoints of CLI Interventions
Angiographic Predictors of Successful Revascularization | Determining the Endpoints of CLI Interventions
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Introduction to Imaging Lymphatics | Lymphatic Imaging & Interventions
Introduction to Imaging Lymphatics | Lymphatic Imaging & Interventions
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Diagnosis | Pelvic Congestion Syndrome
Diagnosis | Pelvic Congestion Syndrome
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Venous Insufficiency- Imaging | Pelvic Congestion Syndrome
Venous Insufficiency- Imaging | Pelvic Congestion Syndrome
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Ideal Stent Placement | TIPS & DIPS: State of the Art
Ideal Stent Placement | TIPS & DIPS: State of the Art
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Protein Losing Enteropathy | Lymphatic Imaging & Interventions
Protein Losing Enteropathy | Lymphatic Imaging & Interventions
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Background to Pelvic Venous Congestion | Pelvic Congestion Syndrome
Background to Pelvic Venous Congestion | Pelvic Congestion Syndrome
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Carotid Artery Stenting- Case | Carotid Interventions: CAE, CAS, & TCAR
Carotid Artery Stenting- Case | Carotid Interventions: CAE, CAS, & TCAR
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Results | Pelvic Congestion Syndrome
Results | Pelvic Congestion Syndrome
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Percutaneous Biliary Drainage  | Biliary Intervention
Percutaneous Biliary Drainage | Biliary Intervention
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C. Cope and Access | Lymphatic Imaging & Interventions
C. Cope and Access | Lymphatic Imaging & Interventions
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MR Angiography | Determining the Endpoints of CLI Interventions
MR Angiography | Determining the Endpoints of CLI Interventions
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Treatment Case 2 | Pelvic Congestion Syndrome
Treatment Case 2 | Pelvic Congestion Syndrome
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Pedal Lymphangiography | Lymphatic Imaging & Interventions
Pedal Lymphangiography | Lymphatic Imaging & Interventions
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Rad Aid- IR Nursing in Tanzania | Advancing Radiology and Nursing through Global Health Outreach
Rad Aid- IR Nursing in Tanzania | Advancing Radiology and Nursing through Global Health Outreach
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Algorithm for Treatment | Pelvic Congestion Syndrome
Algorithm for Treatment | Pelvic Congestion Syndrome
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Case- Brain Infarction | Brain Infarct After Gastroesophageal Variceal Embolization
Case- Brain Infarction | Brain Infarct After Gastroesophageal Variceal Embolization
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Transcript

- Thank you Tom. Good morning ladies and gentlemen. I like to thank, too, the organizing committee and Doctor Veith for the invitation. No conflict of interest. Venous and lymphatic system are mutually dependent dual outflow system of the circulation

we all know. When one of these two mutually interdepdent should fail, it gives additional burdening to the other system. When this additional loading should exceed its limit such a condition would precipitate a fail

of other system as well resulting in total fail of these two inseparable system all together resulting in so-called phlebolymphedema. Hence phlebolymphedema represent the combined condition of chronic venous as well as a lymphatic insufficiency as the outcome of simultaneous fail

of dual outflow veno-lymphatic system. Primary phlebolymphedema represent combined condition of venous insufficiency caused by the venous malformation and they vary in severity by the lymphatic malformation simultaneously. Most common venous malformations cause

the venous insufficiency in this group is a marginal vein with a venous reflux and hypertension. Lymphatic insufficiency for this group is mostly due to primary lymphedema by truncular malformation. These two vascular malformations together to cause a primary phlebolymphedema too

as the most common vascular disorder of the Klippel-Trenaunay Syndrome you are all familiar with. Chronic venous insufficiency of secondary phlebolymphedema however, is mostly due to the sequellac of post-thrombotic syndrome following deep vein thrombosis.

The venous insufficiency of secondary phlebolymphedema is generally secondary outcome of regional lymphedema following steady progress of the local tissue damage by recurrent infection. Secondary phlebolymphedema therefore developed along the end stage of CVI caused the local condition

more complicated with local lymphedema often as a newly added condition. For the diagnosis. Assessment of the phlebolymphedema should start with proper diagnosis of etiology to differentiate two different types.

Non-invasive tests alone is generally sufficient for the basic assessment of the extent severity of the chronic venous insufficiency. However, secondary phlebolymphedema phlebography is infrequently indicated. Lymphoscintigraphy in general is essential

for the chronic lymphatic insufficiency assessment. Full investigation of the venous malformation and lymphatic malformation is mandated before proceeding to any individual assessment of venous and the lymphatic insufficiency based on the non-invasive tests.

Marginal vein assessment for the reflux to cause the venous insufficiency should be done with simultaneous deep vein assessment the for the possible coexisting venous dysplasia. Baseline therapy for the phlebolymphedema is the compression therapy reinforced

with decongestive lymphatic therapy to control venous as well as lymphatic insufficient all together. Marginal vein as the cause of venous insufficiency can be treated with resection or embolo-sclerotherapy as long as deep vein system is fully developed

to be able to handle diverted blood influx. Deep vein reconstruction to relieve venous insufficiency caused by deep vein dysplasia can be beneficial only when there is a clear evidence for the hemodynamic gain. Secondly phlebolymphedema with CVI by PTS

should be treated more aggressively to relieve the cause of obstruction with various forms of open surgical endovascular therapy. When the CVI is caused by a multilevel DVT sequellac even minimum correction is able to assist tremendous improvement efficacy.

As the conclusion, phlebolymphedema can be managed more effectively when open or endovascular therapy is added to the basic compression therapy. Primary phlebolymphedema with CVI caused by reflux of marginal vein can be treated successfully with a marginal vein resection.

And secondary phlebolymphedema with venous insufficiency caused by PTS can be further improved with correction of venous outflow obstruction with angioplasty stent. Thank you for your attention.

quick I did want to mention t-carr briefly and try to get you guys closer to back on time this is a hybrid procedure this is combining the surgical procedure we talked about first and carotid stenting it takes combined

carotid exposure at the base of the clavicle or just above the clavicle and reverses blood flow just like we talked about but tastes slightly different technique or approach to doing this and then you put the stent in from a drug

carotid access here's the components of the device right up by the neck there is where the incision is made just above the clavicle and you have this sheet that's about eight French in size that only goes in about us to 2 cm or 1 and a

half cm overall into the vessel and then that sheath is sutured to the the chest wall and then it's got a side arm that goes what's labeled number six here is this flow reversal urn enroute neuroprotection kit it reverses the

blood flow and then you get a femoral sheath in the vein right in the common femoral vein and you reverse the blood flow so this is a case a picture from our institution up on the right is the patient's neck and that's the carotid

exposure and the initial sheath is in place so the sidearm of that sheath is the enroute protection system which is going up up at the top of the image there we're gonna back bleed that let that sidearm of that sheath continue to

bleed up to the very top and then connect that to the common femoral venous sheet that we have in place there's a stepwise of that and then ultimately what we see at the end of the procedure is that filter inside that

little canister can be interrogated after and you can see the debris this is in the box D here on the bottom left the debris that we captured during the flow reversal and this is a what we call a passive and then active flow reversal

system so once the system is in place the direct exposure carotid sheath in place the flow controller and AV shunt in place you see the direction of blood flow so now all that blood flow in that common carotid artery is going reverse

direction and so when you place a sheath or wire and and ultimately through that sheath up by the carotid artery there's no risk for distal embolization because everything is flowing in Reverse here's a couple

case examples ferns from our institution this is a patient who had a symptomatic critical greater than 90% stenosis has tandems to nose he's so one proximal at the origin and one a little bit more distal we you can see the little

retractors down at the base of the image there in the sheath that's essentially the extent of the sheath from the bottom of that image into the vessel only about a cm or two post angioplasty instant patient tolerated that quite well here's

another 71 year-old asymptomatic patient greater than 90% stenosis pretty calcified lesion a little more extensive than maybe with the CT shows there's the angiography and then ultimately a post stent placement using the embolic

protection device and overall the trials have shown good good safety met profile overall compared to carotid surgery so it's a minimum minimal exposure not nearly as large the risk of stroke is less because you're not mucking around

up there you're using the best of a low profile system with flow reversal albeit with a mini surgical exposure overall we've actually have an abstract or post trip this year's meeting this is just a snapshot of that you can check it out

this is our one year experience we've had comparable low complication rates overall in our experience so in summary

- [Dr. Vikram Kashyap] Thanks to Dr. Viets for the kind invitiation. Dr. Hotze and Dr. Calgoro, and thank you Dr. Escobar for that great introduction. Obviously, percutaneous mechanical thrombectomy's something that we all use. It hastens treatment, and we use it regularly

for both venous and arterial thrombosis. However, PMT has been linked to cases of reversible post-operative acute kidney injury. It's thought to be due to either the hemolysis and the deposition of red corpuscle elements into the kidney parenchyma, and it may actually also

potentiate contrast-induced nephrotoxicity. Clearly, PMT leads to mechanical breakdown, but the intravascular hemolysis is perhaps the concern. And as Dr. Escobar illuminated, clearly can reduce the time for catheter-directed thrombolysis

or overall thrombectomy, period. Catheter-directed thrombolysis on the other hand, chemical breakdown through, usually, the plasminogen system, with converting to plasma, and then fibrinolysis. But clearly, because of the risk of bleeding, we think about using PMT to decrease the CDT time.

Our hypothesis was that there is an increased incidence of renal dysfunction in patients undergoing PMT for treatment of an acute thrombus, compared to patients undergoing CDT alone. So this is a report- a single-center, retrospective study. 227 patients were reviewed.

145 patients were included into the study analysis. The excluded patients included patients that had acute kidney injury before their intervention, patients that were already end-stage renal patients on dialysis, and patients who that either inadequate or no follow-up data.

So of those 145-odd patients, one-third had arterial thrombosis, two-thirds had venous thrombosis, and as you can see in this pie graph, about half the patients had combination catheter directed thrombolysis

and percutaneous mechanical thrombectomy. 12 percent had CDT alone. 10 percent had PMT alone. And then 29 percent had PMT with pulse spray tPA in a single-setting intervention. We used the RIFLE Criteria to characterize

the severity of renal dysfunction after intervention. And in the RIFLE Criteria, you can see in these rows risk, injury, and failure. There's an increase in creatinine or a decrement in GFR and Loss and ESRD are obviously patients that go on to either temporary or permanent dialysis.

This was the incidence of renal dysfunction in this group. 20 percent in the patients that had PMT alone. With power pulse PMT TPA - 21 percent. With the combination PMT and catheter-directed thrombolysis - 14 percent. And with catheter-directed thrombolysis alone - zero percent

These were highly significantly different between these two groups and the CDT group with values as you can see here on the lower right. If we look at the RIFLE Criteria, none of these patients went on to permanent dialysis. They all had risk, injury, or failure,

which were decrements in GFR, or escalations in creatinine. In fact, all the patients were covered to their baseline renal function, but it took an average of 5.1 days. This lengthened their hospitalization. And all 22 patients that had renal dysfunction

had either PMT alone or PMT combination therapy. If you look at the procedural of variables in this table, you can see that the length of admission's actually fairly similar. Importantly, the total TPA dose was similar, and the total contrast volume

between these two groups was also similar. If you look at other post-procedure outcomes, luckily, none of these patients that had renal dysfunction had long-term harm. There was similar six month mortality, six percent versus five percent.

Other complications were very similar. Limb salvage was 92 and 95 percent and there was no increased readmission rate for DVT or arterial thrombosis. So, ladies and gentlemen, in conclusion, the use of PMT as a treatment for venous

or arterial thrombosis is associated with acute renal dysfunction, but is not associated with adverse six month clinical outcomes. We still use this to hasten thrombolysis time and decrease time in the hospital,

but I think it necessitates that we have post-operative, post-procedure vigilance, and renal protective measures as much as possible to decrease the likelihood of renal dysfunction. Thank you very much.

craft is basically the only FDA approved stain crafts and I'll show you a

different way of doing it as well besides the Viator especially in countries where the Viator does not does not exist okay the Viator stand sits in the liver just like just like in my hand here the bare

portion is on the portal venous circulation the covered portion is basically on the hepatic vein part of the circulation okay the bare portion is chain-linked and is very flexible that's why kind of cut can crimp like that okay

they're both self expanding the bare portion is self expanding held by the sheath only the covered portion is held by a court okay so they're both self expanding but they're constraints by two different two different two different

methods one's a sheath constraint and one is a is a cord constraint okay these are the measurements the bare portion theoretically allows portal flow to pass if you're in a branch so it doesn't cost from boses of the portal vein branch in

the covered portion is important to cover the parental tract the youth that you've created in the past you had a lot of billary leaks into the tips if it's a bear stance bile is from by genic so it causes thromboses bile also instigates a

lot of reactionary tissue such as pseudo intimal hyperplasia that actually causes the narrowings of the of these tips if you causing bear stance the coverage stance prevents the bile leaks from actually leaking into into the shunt

itself okay and that's why it has a higher patency rate okay ideally this is how it's it's a portal vein and hepatic vein you'll hear people say proximal and distal you'll he'll hear radiologists especially diagnostic

radiologist referring to proximal and distal proximal and distal some people refer to the portal venous and is proximal some people refer to the paddock venous and is proximal and vice versa okay and it

gets confusing nobody knows well what's proximal okay the people that say portal venous and is proximal there they're talking about its proximal to flow so it's basically the first thing that flow hits people that

call the paddock venous and proximal they're talking relatives of the body more central is proximal more peripheral is distal okay so they're using these the same terminology is very confusing so the best thing to use and I we tell

that to radiologists who tell that to IRS is to talk a portal venous and hepatic venous end you don't talk proximal distal everybody knows where the portal venous end is and where everybody knows where the peregrinus end

is and there's no confusion strictly speaking which is the correct one which is proximal for us as IRS tax nurses proximal is always to flow proximal is always anticipate to flow so the correct thing is actually proximal

is the portal venous ends remember P proximal P portal okay proximal is where the expected flow is coming in that's actually the correct one but just to leave e8 the confusion portal venous and hepatic venous end okay there's a new

stents which is the controlled expansion stents it's in my opinion it feels exactly like the old stance the only difference between it is that it's constrained still has the same twenty to twenty millimeter or two centimeter bare

portion chain-linked it still has that four to eight centimeter covered portion but it's constrained in the middle okay and has the same gold ring to actually market the to the to a bare portion and the cover portion self expanding portion

and is constrained down to eight millimeters you can dilate it to eight and nine and ten initially there was a constant there was a misconception that it was like a string like a purse string that you break and jumps from eight

and no this is actually truly a controlled where if you put a nine-millimeter balloon it will dilate to nine only eight balloon little dialect to eight only the only the only key thing is that the atmospheres has to

be ten millimeters at least okay so it has to be a high pressure balloon has to be at least 10 min 10 10 atmospheres okay so when you're passing that that balloon over make sure that it's that that it that at least it's burst is 10

millimeters or or EXA or more on a 10 mil on on 10 atmospheres okay next thing is when you're making a needle pass you got your target now with a co2 you got the portal vein you've got your stank craft and you know how it works okay how

do you make your needle pass okay and how do you know if your needle has hit the portal vein or not there are two schools to do this okay one school is to make a needle pass and aspirate as you pull back and when you get blood back

you basically inject contrast okay before you do all that when you make your needle pass you push saline and especially if you do if you're using a large system so there are several kits out there there is the cook kits that's

a color pinto needle that's a large gauge 14 gauge needle there is the new gore kits which is also 14 gauge needle it's a big system these large systems you need to push out that poor plug that's kind of like a biopsy you have to

push it out with saline first and then as you pull back aspirate okay the other system is a ratio cheetah or a Rocha cheetah it's actually pronounced rasa schita and that's a very small system that there won't be a core that you have

to push out okay so anyway if you're using a large system like a coop into a needle which is the cook system or the gore system you push that plug out and then there are two schools school two aspirates you get blood back you inject

contrast if you're in the hepatic in in the portal vein you basically access it with a wire the other school is to do a ptc style you actually puff contrasts as you pull back you do not ask for H saline you actually puff

contrasts as you pull back okay the latter puffing contrasts as you pull back is the minority I would say less than two percent of operators are gonna puff okay ninety-eight percent of operators at

least are gonna actually aspirate and not puff okay I'm actually in the minority I'm in the 2% and there are advantages and disadvantages like I promised you two different ways and advantages and disadvantage to each to

each one the advantages of puffing contrasts even if you missed the portal vein after a while you actually get contrast around the portal vein and you actually have a visual of the portal vein that's the advantage so when you're

actually injecting contrast and you're missing it you get contrast around the portal vein it actually goes around the portal and you actually see the portal vein and it takes training sometimes this one's easy

okay I'll show you some more difficult ones but this is a beautiful pussy typical portal vein okay in addition to that oh go back in do you see that you see that hole in the middle there see that signal signal you watch that

because you're gonna see it again and again that's usually a posterior portal vein posterior right portal vein heading heading away from you okay that's usually a good target and I'll show you that again here's a little

little bit less obvious to the untrained eye but this is actually where the portal vein sits right there okay so sometimes it needs training right just actually see where the portal vein is and once you've stained the portal vein

then you have a real-time image of where the portal vein is you can actually go go after it and it reduces your needle passes disadvantages of using contrast and puffing away is that it creates a mess okay if you make multiple passes

you and you miss on the multiple passes then you start creating a mess and even with your DSA you can't even see the portal you can't see the portal vein because you've got this great mess another disadvantage of using contrast

is that you have to stomach what you're gonna see okay you make a needle pass and you don't inject contrast you have no proof of where you've been but if you're making a needle pass and you're

injecting contrast you and everybody else is gonna see where you've been that's usually not a good thing sometimes you will see bowel you see gold bladder you'll see arteries you'll see veins you'll see all sorts of stuff

that nobody wants to see and you don't want to document okay so that's another disadvantage so I recommend especially young physicians especially young physicians in places that are not used to this especially young physicians that

are new to hospitals and they're gonna they're gonna make multiple passes not to do this was they're gonna be very they'll be criticized a lot by their texts and by the institution by their colleagues as to what have you done you

know big mass artery you've hit artery but the guys and gals that are just aspirating and not injecting they're actually not documenting what they're going through but they're going through the same stuff okay

okay next up this I think this video yep

now other causes this is a little bit different different scenario here but it's not always just as simple as all

there's leaky valves in the gonadal vein that are causing these symptoms this is 38 year old Lafleur extremity swelling presented to our vein clinic has evolved our varicosities once you start to discuss other symptoms she does have

pelvic pain happiness so we're concerned about about pelvic congestion and I'll mention here that if I hear someone with exactly the classic symptoms I won't necessarily get a CT scan or an MRI because again that'll give me secondary

evidence and it won't tell me whether the veins are actually incompetent or not and so you know I have a discussion with the patient and if they are deathly afraid of having a procedure and don't want to have a catheter that goes

through the heart to evaluate veins then we get cross-sectional imaging and we'll look for secondary evidence if we have the secondary evidence then sometimes those patients feel more comfortable going through a procedure some patients

on the other hand will say well if it's not really gonna tell me whether the veins incompetent or not why don't we just do the vena Graham and we'll get the the definite answer whether there's incompetence or not and you'll be able

to treat it at the same time so in this case we did get imaging she wanted to take a look and it was you know shame on me because it's it's a good thing we did because this is not the typical case for pelvic venous congestion what we found

is evidence of mather nur and so mather nur is compression of the left common iliac vein by the right common iliac artery and what that can do is cause back up of pressure you'll see her huge verax here and here for you guys

huge verax in that same spot and so this lady has symptoms of pelvic venous congestion but it's not because of valvular incompetence it's because of venous outflow obstruction so Mather 'nor like I mentioned is compression of

that left common iliac vein from the right common iliac artery as shown here and if you remember on the cartoon slide for pelvic congestion I'm showing a dilated gonna delve a non the left here but in this case we have obstruction of

the common iliac vein that's causing back up of pressure the blood wants to sort of decompress itself or flow elsewhere and so it backed up into the internal iliac veins and are causing her symptoms along with her of all of our

varicosities and just a slide describing everything i just said so i don't think we have to reiterate that the treatments could you go back one on that I think I did skip over that treatments from a thern er really are also endovascular

it's really basically treating that that compression portion and decompressing the the pelvic system and so here's our vena Graham you can see that huge verax down at the bottom and an occluded iliac vein so classic Mather nur but causing

that pelvic varicosity and the pelvic congestion see huge pelvic laterals in pelvic varicosities once we were able to catheterize through and stent you see no more varicosity because it doesn't have to flow that way it flows through the

way that that it was intended through the iliac vein once it's open she came back to clinic a week later significant improvement in symptoms did not treat any of the gonadal veins this was just a venous obstruction causing the increased

pressure and symptoms of pelvic vein congestion how good how good are we at

- [Jean] Thank you, Will, thank you again, Frank, for inviting me to your symposium. I'm going to talk to you about this concept of the value of EndoAnchors and TEVAR, and if you talk about that, basically, you need to figure out if we can predict TEVAR failure. So we published, last year, the creation of a novel

that makes a severity grading score to assess thoracic aneurysm and see if we can actually predict the patient that will not behave nicely with a simple TEVAR. Here's an example of two scores. Patient with an ASG score of 24

and the other one with an ASG score of 43. And the top of the ASG score is all the way up to 57 if you have all the worst characteristic that is applied to the different region of the thoracic aorta. So we found by doing a ROC Curve analysis

that an ASG score of 24 was actually the cut off, and below 24 was the low score group. And 24 and higher were patients with the really bad, challenging anatomy. And those patients had only a 69% freedom

from postoperative endoleak, requiring re-intervention at two years. So this novel anatomic severity grading score can actually really successfully identify patients that are at increased risk of endoleak requiring re-intervention

and then it would make sense in those patients to potentially apply for prophylactic EndoAnchors. And this is what we did in this next study where we looked at only patients with a high ASG score. So we had 63 patients with those high scores. 40% had only TEVAR and under the 20 patients

had TEVAR and prophylactic EndoAnchors as well. And if you look at those patients that only had TEVAR and bad anatomy, we had a 58% chance of freedom from aortic related re-intervention at three years. The 62% freedom from Type I endoleak at three years.

But when you place prophylactic EndoAnchors you end up with an excellent result with 95 to 100% survival free from any of those two kind of problem. So this would be the value in using EndoAnchors and these are better to me now. The technique for the thoracic EndoAnchor

and compared to the abdominal is that we have the selection of three potential active guide size, 22, 32, 42. And we size it according to the size of the endograft. I say as an example of a patient with challenging anatomy that was the patient with the ASG score of 43. This patient had a hemiarch debranching

and then we went ahead and deployed the endograft and deployed the EndoAnchor at the inner arch. This is the completion angiogram after those prophylactic EndoAnchors. And there is no endoleaks at two years. This patient is now currently at over three year follow-up

no migration and no endoleak, despite an extremely challenging anatomy. You can also have another prophylactic indication is to prevent upward migration. If you look at the tapering of the thoracic endograft right above that celiac artery,

this is really an area that in fact in the Valor II trial, has really showed that a lot of patient have Type 1B endoleak after a few years. And by using circumferential placement of those EndoAnchors at the distal end of the TEVAR,

you can really prevent this upward migration and endoleak 1B formation. Now the technique it's really about the angle of attack. I think if you have a bad angle of attack, you will not be able to deliver properly. But when you have a real 90 degree perpendicular attack

of the endograft this is how you can safely deploy those EndoAnchors in the thoracic aorta. This is a deployment of the ascending aorta in an RAO view, so you can not only deploy at the inner curve, but you can also deploy EndoAnchor on the interior or posterior aspect of the arch

by deploying anchors with these special view with the barrel. When you look at the outer curve of the arch, this is an easy Zone 1 delivery. This is a more tricky Zone 1 delivery, but it also possible to deploy EndoAnchors

in the outer curve. Same thing when we have the sternum open to do a total arch debranching, we can deploy EndoAnchors in an antegrade fashion in Zone 0 and obtain also great result. Top 10 tips for EndoAnchors.

First is take the time for preoperative planning. Second one is wishful thinking will not create the landing zone. Sometimes you have to do some debranching to obtain a landing zone. Deliver the endograft accurately.

Do the aortic balloon molding first. You have to size the Aptus guide according to the endograft size. You have to undersize it when you want to use it at the level of the outer curve of the arch. You deploy two rows in TEVARs.

I always deploy three rows in arch because of the increase in hemodynamics at that level. I think a good place to learn to do TEVAR and EndoAnchors is the distal end near the celiac artery. And never start a challenging TEVAR case without EndoAnchors.

So in summary, EndoAnchors in TEVAR are done in imperfect landing zones, improve outcomes by decreasing Type I endoleaks and the need for aortic reinterventions. Safe and effective deployment of EndoAnchors really relies on simple techniques, device selection,

and the knowledge of the failure modes of doing TEVAR in those challenging zones. Thank you.

predictors of a successful or vascular ization there are several so obviously you know you have a great result Andrew

graphically when you say hey the vessels back that wasn't there before so Payton see if a previously occluded vessel is a good sign but what else improve vessel caliber so after an angioplasty the vessel becomes you know more normal and

caliber the flow velocity increases or the outflow improves you see less collateral so that's a good sign that you've done something good because those collaterals have only gotten large because of increased pressure and the

normal outflow vessel and then increased distal branch opacification Perry procedurally things that you can look at that indicators of success are if the pulses returned or if you have a Doppler signal

that either comes back or goes from a mono phasic I'm not gonna repeat those sounds they were way above my pay grade but go from a mono phasic signal back to a normal triphasic or sometimes even biphasic is pretty close to normal

particularly in diabetics skin discs skin coloration you sit you may see a foot pink up relatively quickly after a good revascularization and actually some patients may develop rube or if they've had prolonged ischemia because their

capillaries are chronically dilated so you now sending flow into chronically dilate a capillary bed and they may get rubriz capillary refill time as you mentioned earlier may decrease to a normal range to less than 5 seconds and

ulcerations I've seen them just begin weeping or bleeding right on the table if you do a really good job upon awaking from sedation patients who have rest paint off and indicate that the pain is gone but you have to remember that

patients with wounds may actually wake up and be in a lot of pain because you're reap refusing an area that's been dead for or dying for a long time so the wound blush is something that I'm always looking for and I'm frustrated if I

don't see it and basically this is analogous to when the when the ulcer begins bleeding after a good revascularization you may see Andrew graphically that there's now a contrast blush in the area of the ulcer and so I

like to mark on the patient usually with a hemostat or something the area of the ulcer and take my final angiogram just to kind of know where it is and to be looking for that it may it not always be visible as it may take time for the

capillary network to adapt to the new flow pathways and for basal spasm to resolve but this is an example of a patient has an ulcer underneath the base of their big toe after revascularize them and you can see

that there's increased perfusion to that area so this is a sign of a good result

it's a pleasure to be here this is the second day vir had the pleasure of speaking at and it's always a treat to get to interact with all the technologies from around the country I did recently make the move to Emory University it's been delighted to have a

few of my technologies in the room as well so quick shout out to Abby and Marcel so we're gonna be talking about lymphatic imaging and interventions is probably my biggest area of research as as well as a passion mostly because this

is yet another area where I think IR can make a tremendous difference in the outcome for patients I certainly remember a patient in my own training who was bed bound for weeks on end in the hospital until we were able to

successfully treat him so we'll talk about the challenges of imaging lymphatics it's not something that isn't necessarily easy though it is getting easier I know probably a lot of the more senior technologist in the room are

probably groaning as soon as they hear lymphatics and they they think of the old lymph angiography pumps the cut downs the methylene blue the 30 gauge needles injecting in the foot and closing down a room all day so we're

gonna talk about how to to get away from all of that and make your life a little bit easier it's not uncommon in a typical day that I can knock out three to four of these cases we'll review the current imaging techniques involved with

lymphatics talk about lymphatic access points I'll show you my setup and how I do it review the current evidence on thoracic lymphatic interventions abdominal lymphatic interventions and overview some of the future

possibilities so just a general overview you know we think of a lymphatics a lot of us really think of just the peripheral lymphatics right somebody has breast cancer they have a mastectomy they have a lymph node dissection etc

they have a swollen arm a swollen leg from some of the lymphedema but that's actually just the smallest component of your entire lymphatic system the predominant the predominant sir lymphatic circulation actually comes

from your liver where a lot of the protein is manufactured and goes through the lymphatics as it returns back to the circulation and the intestines where a lot of the fats are absorbed and go to the lymphatics back to the venous system

the rest of it only 20% of the lymphatic fluid comes from the capillary permeability in the extremities of the legs as well as the arms so when you look at liver lymphatics it's very protein rich you

look at intestinal emphatic so it's very fatty rich and then the stuff on the periphery is really lymphocyte predominant when we look at these

pelvic veins and in the most common scenarios it's the left go nate'll Baine and that's the vein that's circled there

and so when we're evaluating someone for leaky valves in their pelvic venous system you do that through catheter vena Graham and I'll show you exactly how we do it but really there's four pathways at least for the four main ones that you

have to look at and that's the both side gonad all veins for right and left gonna handle vein which are imaged there and then the internal iliac veins on both sides so those are sort of the four pathways that you start with evaluating

on a catheter vena Graham the first sign that there is a leaky valve is by doing a vena Graham in the renal vein so the left gonadal vein communicates with the left renal vein if you want to hit play on that video the if I do a left renal

vena Graham you should not even see the gonna dull vein but if you see reflux down the gonadal vein you'll see it here so renal vein looks great but you should not see any blood flow going against against the

grain there so that's clearly venous insufficiency I think this is just another video showing the same you want to hit the play on that one a different patient again renal vena Graham showing a huge go nate'll Baine so that clearly

has valves that don't work that's how you can specifically test for venous insufficiency on this one you'll hit the play on this video this shows us what a normal renal vena Graham would look like and you're not seeing any part of the

gonadal vein so what are the general

- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company

for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.

The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the

middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,

which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up

in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.

Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,

embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,

we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,

which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.

We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,

excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success

just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and

no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.

We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,

and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.

We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,

post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch

blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it

through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,

we actually have several publications out, demonstrating safety and ethicacy. Thank you.

so what what venous insufficiency is is really leaky valves so if you want to hit the play on that so that's all venous insufficiency that's what we

talked about it's it's leaky valves and so you can see this the valve leaflets there which are paper-thin is allowing blood to go the wrong way if you want to hit play on that one when we looked for valve

insufficiency for sure in the legs we use ultrasound and there's a bunch of different things that we look at an ultrasound you first look if you can augment blood flow so that was that first part we see if it's compressible

to make sure there's not a clot in it that's this part you can see the vein winking at you and then finally we look at valsalva or some type of way to determine if the valves are competent or incompetent and what this figure is

showing is that when a patient valsalva Zoar tenses up their abdominal muscles you see the gray line for the ultrasound crossing the access and going the opposite way all that means is it's got opposite directional flow which you

should not be able to do if your valves work so if your valves work you would not see that ultrasound picture crossing the line here it would just continue right there or would just stop and then flow would start again once you stop fel

salving so that's how we check in a leg but for pelvic venous insufficiency that's kind of hard to ultrasound the deep pelvic veins I could certainly look for varicosities with a an ultrasound of the pelvis but you can't really find the

source of an usually the source veins are the internal iliac veins or the gun at Elaine's and those are tough to ultrasound so secondary evidence of incompetence or leaky valves in those systems is varicosities

and so in the case of pelvic venous insufficiency those varicosities are in the pelvis and you see on the slide here you got varicose veins deep in the pelvis here and here and see some larger ones in that same

area on that CT scan so that'll tell us varicose veins that doesn't necessarily tell you whether the issue is with a gonadal vein or an internal iliac vein it just tells you that there are sequelae of varicosities much like in

the leg you might have varicose veins in the ankle but the problem is really higher up in the leg at this afterno femoral Junction so that gives us secondary evidence but it hasn't really told us the cause of the varicose veins

this is just a CT image that it also may show a large gonadal vein right here so you normally should not see it that big it's right there also secondary evidence that the valve is incompetent but it doesn't really test the valve itself

it's it just gives you the idea that veins enlarge and the valves gonna be leaky this is a cartoon schematic of the

stamp placement we talked a little bit about it I'm gonna talk to you a little

bit more about it and ideal stance is a straight stance that has a nice smooth curve with a portal vein and a nice smooth curve with a bad igneous end well you don't want is it is a tips that T's the sealing of the hepatic vein okay

that closes it okay and if there's a problem in the future it's very difficult to select okay or impossible to select okay you want it nice and smooth with a patek vein and IVC so you can actually get into it and it actually

has a nice hemodynamic outflow the same thing with the portal thing what you don't want is slamming at the floor of the portal vein and teeing that that floor where where it actually portly occludes your shunts okay or gives you a

hard time selecting the portal vein once you're in the tips in any future tips revisions okay other things you need it nice and straight so you do not want long curves new or torqued or kinks in your tips you

a nice aggressive decompressive tips that is nice and straight and opens up the tips shunt okay we talked a little bit you don't want it you don't want to tee the kind of the ceiling of the of the hepatic vein another problem that we

found out you want that tips stance to extend to the hepatic vein IVC Junction you do not want it to fall short of the paddock vein IVC Junction much okay much is usually a centimeter or centimeter and a half is it is acceptable

the problem with hepatic veins and this is the same pathology as the good old graft dialysis grafts what is the common sites of dialysis graft narrowing at the venous anastomosis why for this reason it's the same pathogenesis veins whether

it's in your arm for analysis whether it's in your liver or anywhere are designed for low flow low turbidity flow of the blood okay if you subject a vein of any type to high turbot high velocity flow it reacts by thickening its walls

it reacts by new intimal hyperplasia so if you put a big shunt which increases volume and increased flow turbidity in that area in that appear again the hepatic vein reacts by causing new into our plays you actually get a narrowing

of the Phatak vein right distal to the to the to the Patek venous end of the shunt so you need to take it all the way to the Big C to the IVC okay how much time do I have half an hour huh 17 minutes okay

Viator stents is one way let's say you don't have a variety or stent many countries you don't have a virus then what's an alternative do a barre covered stem combination you put a wall stent and then put a covered stance on the

inside okay so put a wall stent a good old-fashioned you know oldie but a goodie is is a 1094 okay you just put a ten nine four Wahl cent which is the go to walls down so I go to stand for tips before Viator

and then put a cover sentence inside whatever it is it's a could be a fluency it could be a could be a vibe on and and do that so that's another alternative for tips we talked about an ace tips as a central straight tips and it's not out

and fishing out in the periphery okay this is an occlusion with a wall stance this is why we use think this is why now we use stent grafts this is complete occlusion of the tips we're injecting contrast this is not the coral vein this

is actually the Billy retreat visit ptc okay that's a big Billy leaked into the into the tips okay and that's why we use covered stance I'm gonna move forward on this in early and early and experienced

interrupting something else getting back

to a paddock with angiography something that we're starting to look at the group at University of Pennsylvania has a publication out on this as well I looked at the liver lymphatics certainly the livers where we produce a

lot of protein it goes through the lymphatics to be returned to the circulation in patients who have heart failure they tend to have increased lymphatic flow in the liver and they think that protein lost in enteropathy

protein losing a property happens when the liver lymphatic leaks into the intestines just some images from their article you see them looking at the hepatic lymphatics there and once they had a needle in the hepatic lymphatics

they actually put her scope in and they injected blue dye and as a proof-of-concept they saw the blue dye leaking into the intestine so now that they see that the blue dye leaking the intestine they say well we can embolize

that they embolize it with some glue and that's what it looked like at the end and then the algorithm levels and all these patients return to near normal so a new a new frontier and lymphatic intervention so just to summarize

lymphatic imaging the current status you know we have very effective non-invasive as well as in vases imaging in the peripheral and central lymphatics we certainly need to this allows for improved diagnosis and once we have

these diagnostic capabilities we were able to come up with these novel treatments for these diseases that were previously untreatable we still don't have good ways to consistently visualize the paddocks invasively and then and

non-invasively it would be great to be able to see that hepatic and intestine lymphatics cuz that's 80% of lymphatic flow so if we can find a way to image these under mr it could be a game-changer for a lot of diseases in

terms of lymphatic interventions Calla thorax interventions greater than 90% effective technical knowledge you know when I was a trainee was really centered to just a few major medical centers now it's defusing out to more places we've

certainly shown as a proof of concept the plastic bronchitis lymphatic flow disorders cattle societies and protein losing enteropathy are all treatable and we're getting emerging experience so don't be surprised if you start to see

more requests for this more patients at your centers these are uncommon disorders that's not to say that you still won't see them every once in a while the role of lymphatics in pathophysiology is still being studied

particularly in terms of heart failure transplant as well as in different cancers in the spread one of the cool stuff that we're looking at right now is actually sampling different lymphatic fluid in different areas of the body

trying to see how the different cancers may spread and/or possibilities in immunology immuno oncology thank you guys and just something I noticed a couple weeks ago in jeopardy clear body lymph continuing white blood cells body

fluid and you guys know what is limp that's your answer so thank you saying thank you to the avir committee and it's been a pleasure [Applause]

- [Dr. de Vries] Thank you for the kind introduction. These are my disclosures. It's why do endografts sometimes need additional fixation with EndoAnchors? Well first, patients with multiple hostile neck parameters still suffer a substantial risk for type I endoleak and endoleak related mortality.

The second reason is that our deployment accuracy of the endograft is not as good as we think. We reviewed 85 consecutive cases in our own hospital and we saw that mainly do the slope of the endograft in the aortic neck, we lose some important apposition,

especially in the outer curve. So the preoperative neck length is not the same as our post-EVAR seal. And the third reason is that some other techniques, like FEVAR do have their limitations and some people are declined because of the branch arteries.

There are also some physiological conditions which is are not good enough for FEVAR. And of course open surgery, well per definition is more invasive and also patients will sometimes have their aneurysm repaired by endovascular means. So EndoAnchors really creates the stability

of a surgical anastomosin shown by David Dietz, and it really rivals the migration resistant of a hand sewn anastomosis. Of the global Anchor registry is captured real-world usage of the EndoAnchors and nowadays 770 patients have been enrolled worldwide.

The Primary Arm represents the majority of the patients in the Anchor Registry, 437 patients in the patients in the Primary Arm. It's not exclusive the Anchor Registry for the Medtronic devices, but also the workhorses like Gore and the Zenith endograft.

Of the prophylactic arm, the patients treated without any endoleak it carries 314 patients in this data slide. And you can see that the majority of those patients will hostile neck parameters. It's true in 91 percentage of the patient cohort.

The median neck length is 11 plus millimeters and also conicity substantial in more than 40% of the cases. What about procedural success? It's high, it's almost 95%. You need an average of around 5.5 EndoAnchors and the time to implant those EndoAnchors is 15 minutes,

and of course there is a learning curve. Core Lab adjudicated outcome, the two years outcomes, there is no new type Ia endoleak in this cohort and no endograft migration. In the Kaplan-Meier Estimates, especially the freedom from

aneurysm related mortality is 98.4% and freedom from secondary procedures at two years timeframe is 92%. There are no serious adverse events related to the implantation of the EndoAnchors itself. No aneurysm rupture and the aneurysm-related mortality

is due to cardiopulmonary comorbidity and not due to aneurysm rupture itself. There's one patient with a surgical conversion in this cohort. And the short neck indication that are patients in the Primary, 70 patients,

only placed with an Endurant in combination with the EndoAnchors and in a prophylactic setting or a patients with a type Ia endoleak. But the median neck length is now less than seven millimeters, so really challenging necks

and also conicity is substantial. It's also a clinical challenging patients cohort. A lot of patients with notable comorbidities and what is important to mention, 17% are patients with symptomatic aneurysm and also one patient with a ruptured aneurysm.

And the well the main treatment is then for prophylactic use but also 21% of the patient do have type Ia endoleak. Procedural results are 31 minutes fluoro time, but only 17 minutes to implant the EndoAnchors. This is the one year outcome. I think it's excellent.

Only one patient with a type I endoleak and he needed a secondary intervention. We had two other patients with a secondary intervention but it was due to a false aneurysm in the groin and a distal extension. No conversion to open surgery and no ruptures.

What about the cost effectiveness? Well you have to consider, it's not only the device cost, but also the level of resource utilization, and also clinical outcomes. And when you compare the short neck cohort, here the 70 patients to the fenestrated IDE study,

there's a cost differential of more than 5,000 U.S. dollars in benefits of the use of the EndoAnchors in those short and hostiles necks. So we can conclude that the Endurant stent graft in combination with the EndoAnchors for short neck indication is easy to use.

It's an off the shelf solution. It gives greater flexibility versus the alternatives. There is no need for renal arterial catheterization and it's really efficient. Thank you very much.

thanks everyone thanks for having me appreciate being here certainly as the title suggests here public congestion syndrome is probably something that you've heard of it's a little bit of a misnomer we don't really call it pelvic congestion syndrome anymore but I'll get

into that a little bit certainly have time for questions afterwards but if there's something that I want to talk about as we go I'm certainly happy to do that too no disclosures unfortunately for me so I'll do a little bit of a

background give some historical perspective and then I'll I'll basically just talk about the clinical symptoms and what type of workup that I go through and then how I do procedures for patients that have pelvic venous

insufficiency and then talk a little bit about outcomes so background you know chronic it's it's basically this spectrum of chronic pelvic pain which we'll get into a little bit but pelvic venous venous insufficiency for chronic

pelvic pain is really poorly understood and it's it's under-diagnosed oftentimes the patients that come to clinic to see me have been through a lot of different scenarios to try and find a source for their symptoms that's that's sort of the

most common scenario the second scenario that I find patients coming to me is through our vein clinic when they have symptoms of varicose veins in their legs and then we start talking a little bit further getting into their symptoms a

little bit more it starts to become clear that maybe there's a problem a little higher up than in the legs and so those are sort of the two scenarios but it's certainly under diagnosed at least as a portion or at least as a

contributor to chronic pelvic pain in women by definition it's intermittent or constant pain lasting three to six months duration and it's localized in the abdomen or pelvis not limited to two menstrual cycle and it's not associated

with pregnancy necessarily and like I mentioned a bit ago it's really part of this constellation of symptoms in chronic pelvic pain which there is a really big differential diagnosis for most of the time the patients

that have the significant symptoms range between eighteen and fifty and it's pretty big age range but like I said lengthy differential diagnosis so this is not number one on the list for foreign OB kind doctor to think about oh

yeah maybe this is pelvic venous insufficiency causing their pain and so that's why it goes under diagnosed and I mentioned the term pelvic congestion syndrome but really really what this is is we're talking about pelvic vein

insufficiency that's causing chronic pelvic pain so that's that's really what we're talking about

are in the room here's a case of an 80

year old with a previous mi had a left hand are directing me and it's gonna go for a coronary bypass graft but they want this carotid stenting significant card accenting lesion to be treated first there's the non-invasive blow

through this but there's the lesion had a prior carotid endarterectomy so had that surgery we talked about first but at the proximal and distal ends of that patch has now a stone osis from the surgical fix that's developed so we

don't want to go back in surgically that's a high resolution we want for a transfer Merle approach and from there here's what it looks like an geographically mimics what we saw on the CT scan you can see the the marker and

the external carotid artery on the right that's the distal balloon and then proximally in the common carotid artery and they're noted there and then when you inflate the balloons you can see them inflated in the second image in the

non DSA image that's the external carotid room carotid artery balloon that's very proximal the common carotid balloon is below or obscured by the shoulders and ultimately when you inflate the common carotid balloon you

just have stagnant blood flow then we treat them you can see both balloons now and the external carotid and common carotid in place we have our angioplasty balloon across the lesion and then ultimately a stent and this is what it

looked like before this is what it looks like after and tolerated this quite well and we never had risk of putting the patient for dis Lombok protection or to salamba lusts overall I'm not gonna go over this real

symptoms technical success rate is high so that means are we able to diagnose and treat what we're looking for and yes if we see in a incompetent gonadal vein

almost always we are able to embolize and treat but that doesn't always mean that their symptoms get better so even if you have the right symptoms and pelvic venous insufficiency and you got a gonad a vein the size of a three

car garage it doesn't always mean that the patient's give better and that's what this clinical success slide shows that looking through meta analyses of all the studies patients that have all those things the classic symptoms and

classic venous insufficiency their symptoms don't get better 100% of the times and so that's part of the the patient expectation and management and clinic and follow-up and looking for other causes chronic pelvic pain is

really complicated and venous insufficiency is part of it and you'd love to tell them that we're gonna do this procedure and it's gonna make you feel a hundred percent better but at least takes that element out of the the

scenario complications are our few range from 3 to 9 percent non-target embolization depending on what type of embolic you're using is certainly one thing that you always have to be concerned about but if done carefully

extremely rare there is a small risk of paradoxical emboli and stroke in the case of using a foam sclerostin recurrence as I mentioned earlier can happen in up to 10 percent of patients I think that can happen when you know the

vein wreak analyzes so successful embolization helps decrease that and that's the reason that you treat sort of the whole vein that's that's abnormal

- [Instructor] Thank you very much. So, you saw some of the issues that our, oh, this is the slightest cut, but that's okay. Some of the issues that we've seen with these percutaneous mechanical devices, and, back in the 90's, and perhaps even more than a decade ago, there were a lot of these.

And this space gets hot and cold, and one of the problems is that the level of evidence for doing these is very low, and when it is done, it wasn't done well. And this is a nice registry, a lot of patients enrolled, unfortunately we didn't learn

what we had to learn from these types of registries, because of just the study wasn't done well. So the level of evidence is low, and when we did have them, they didn't really work. And you saw some of the problems, that these devices can cause.

And here's another problem that wasn't discussed. You can see the DVT, iliofemoral DVT in here, and a device is pushed a few times up and down, and sort of aspiration, a Bertoulli, that type of thing. And this looks, oh wow, well this looks good,

maybe the thing is working, except all the clot is up here. So, these devices tend to push the clot around. So the issue is, enter now more recently, these are some of the more recent ones. Note that the AngioVac is not here, I don't consider that a practical thrombectomy device,

and so, it's not here. So, we're going to be talking about JETi. This is a system that is an aspiration system with a jet that comes inside the catheter, therefore the clot is engaged and pulled in and broken down by the jet, therefore there's no hemolysis.

And this demonstrated in this case, which is acute and chronic 17 year old multiple DVTs in the past, the iliofemoral segments are stented, as you can see here, this segment is somewhat fresh clot but these, as you can see, are subacute clot. Look at this, so the system now is designed

for over the wire, but for DVT you can use it without the wire, because it works a lot better. As you can see it can really aspirate the clot, in before your eyes. Now this I have passed the device in here once, and you can see the fresh clot is gone,

we have some residual debris in there, we have not established flow yet, and then I turn the device on... and it pulls the whole thing in, okay? So, very powerful aspiration method. So, and as you can see here, we don't have

a flow establish, outflow established yet. Therefore, when you turn it on, you have a vacuum created right here, and so this tells you how strongly this device can aspirate and work. And this isn't on the table.

After a pass here, two passes here, some residual clot in here, obviously there's residual clot there. So we pass it around these areas once more, and this segment obviously needs to get stented and on the table, re-establish antegrade flow. Since May, we've had 19 patients treated, most of them DVT.

And, based on our assessment, 17 of the 19 patients at a total time of 90 minutes on the table, had better than 90% clot retrieve. We have 30-day patency data on only 16 of those patients, because this is really since this May. And 15 of those were open, one re-thrombosed

and we had to retrieve again. Conclusion, so preliminary experience indicates that this is an effective device. There were no safety issues, we don't see any hemolysis, we don't see any pushing around of the clot, but there is a learning curve to it,

and for best application, thank you.

we do drain the Louie systems we actually do this extremely successfully as interventional radiologists and it's a very high technical success like I said in this sort of supine position

from the mid-axillary line and these things are and you've seen a lot of these how these done really you need to pacify the system you get trans you most post people go trends in to cost Albany because the liver sometimes can be

tucked up way above and we usually want to make sure that the lung and the costophrenic angle doesn't come down low in nothing I take a deep inspiration first to make sure that you're not dealing with and then we now map your

track than you find some people do this with ultrasound guidance frequently with and dilated structures and most of the time it's actually much probably routine to actually do blind passes in the like I said the path of high success and to

pull back when you a passive our blue system is the only structure that doesn't wash away generally portal vein hepatic vein hepatic artery all of those structures are cylindrical

tubule alike are not are going to wash away move away and quite quickly and you can see this PDC and show in fact a left insertion of a right into your ductal system and frequently this will be something that we would have to make

people watch out like I said identification of choosing the right duct thereafter after you've identified you've performed a color angiogram is to identify how you're going to drain this and the most important thing to identify

is a peripheral duct doesn't matter which one there are ones with higher success but then within the lateral position find one market on the table then with a second axis as a to stick axis and I'm sure this is very germane

and common you've seen get into the peripheral duct and the AP fluoroscopy get a wide down you get a tube down and then eventually go it with a coaxial system getting a skinny wire converted to a larger wire and then following that

with a below a tube and your goal is to really get axis that goes transpannic through a perfect century through obstruction or no obstruction if it's just untie elated and through into the small bowel and lock a some type of

locking system it's interesting the size that you choose does make it different so if you go larger than the 12 french-trained initially the risk of bleeding actually goes above 10% for initial axis so the best is to probably

start with a 8 and 10 and that's what we typically do this is what we connect what it ends up looking like left a

and then getting back to really where the rubber hits the road you know we can do all of these fancy techniques why

does it matter well Constantin cope one of the fathers of IR is certainly the pioneer of lymphatic interventions and over subsequent five publications in the mid 90s really showed the the technical

build as well as the feasibility of imaging lymphatics putting a needle into them and then starting to be able to embolize them and functionally curing patients who had Kyle authorities and a potential morbidity or mortality of over

50% and how did he do it well as he did his lymph angiogram and it got up to the retroperitoneum and the structure started dilating into some of the central structures such as the cisterna chyli he would take that 21 gauge needle

and go after that structure put a needle into him pass a wire that wire would pass into the central lymphatic circulation and then he'd be able to put in a micro catheter Neff set machan visa or whatever inner inner

components and then do central and faint geography as well as potential and fame gia embolization so that would be the general antegrade trains abdominal access this was a traditional access that was done for over a decade more

recently a lot of authors have started focusing on doing retrograde trans venous access which you do basically a PICC line axis on the left arm and you take a sauce catheter to where the thoracic duct dumps into the veins and

you catheterize it backwards and just kind of showing you and get your sheath down or you can put a wire from below and then snare and come across it so that's a retrograde transvenous and finally the direct train cervical access

and some patients who you never see another target you can potentially access this under ultrasound or if you have fluoroscopy and some contrast in there in this case we put our wire retrograde and were able

to complete the case and you see of the lymphatic fluid leaking out in this case as well so those are your three main ways to access the central lymphatics

- [Presenter] Thank you very much. This is Jordan. It's my pleasure to share this panel with endoanchors believers, I'm one of them. So, there's my disclosures. The scope of the problem about the proximal migration starts

in order to think about the durability of thoracic endografting, because it still is a concern. The cranial migration from the distal attachment is part of this particular concern, especially when the distal neck length is less than three centimeter.

I think this is a under-reported complication in these areas. That is, what has happened, after some kind of follow-up, after four years follow-up, the distal part of the aorta, or the distal part of the endograft is dis-attached from the primary landing zone.

Because all the forces in the ascending thoracic aorta acting in the up cranial fashion. So when you are virtually sure there some kind of migration rate of two years but also have some kind of cranial migration from the distal part of the aorta at the one year is 1.2%

for the VALOR trial and 1% in one year also for the TX2 trial. In our experience, before 2006, for distal neck length, between 1.5 to 3 centimeter in length, 60% of cranial migration rate was registered at five years follow-up. So what's a lot of percent about that we try to perform

a different kind of approach for those particular short or no short, nice distal neck of thoracic aorta. So cranial migration as previously mentioned is under-reported. The upside for the abdominal aorta with the forces acting in the downstream anteriorly in the thoracic one is

posteriorly a cranial and also a cranial migration course. And this kind of phenomenon kind of course in the long run follow-up. These connections and also cranial migration. About the preventative actions there are different kind of creative alternative in order to prevent that,

but let me to focalize my attention and your attention to endoanchors philosophy that is part of our current approach. For a regular neck of more than three centimeters we can use regular endograft but sometimes when it's not so regular it's not so straight, we prefer to use in combination

with endoanchors. When you have a regular straight but between 1.5 and 3 centimeter we prefer to use distal scalloped endograft plus endoanchors as you cam see here. That is what the speakers talk about very extensively but this is just a case in order to see

what happened after two years follow-up in this lady when it has this distal type one endolink we apply the endoanchors and after three years the endoanchors remain in the same position, as you can see here, without any kind of further complications.

So another example, in combination with scalloped devices, scalloped thoracic endograft, just in order to be sure, that the movement in the distal part doesn't occur or even weaken over time. For sure, when you have very short neck length,

that means less than 1.5 centimeter, then we need to switch to another kind of solution like this fenestrated or branched endograft, like you can see here in this example. So in summary, the durability of thoracic endografting remains a concern when cranial migration is a consequence

of biomechanical forces of the thoracic aorta and it is under-reported. The proximal and distal necks deserve equal attention. And many different approaches have been suggested to avoid cranial migration. And endoanchors in combination with the scalloped,

fenestrations and branched endografts should be applied more often. Thank you very much.

very helpful these patients the calcium this and the vessels can be

seen through with the MRA it doesn't it doesn't cause as much artifact so it could be easier to see what's going on in calcified vessels additionally you saw an image in Marc's talk as well of this is an example of a time-resolved

image of an MRA or you can basically recreate exactly what you're seeing in an angiogram and this could be very helpful to kind of determine what kind of TVL disease you're getting yourself into

newer MRI techniques that we're using in the evaluation patients with PID functional MRI which compares the ratio of how much oxygen versus deoxygenated hemoglobin we have in a tissue so we can apply this to a pre and post exercise

scenario in patients to have claudication as well although it's not it's only approved in research protocols this is an example of what you see for that so pre intervention here's the CTA image reconstruct

in 3d with a long segment an iliac occlusion and then post intervention you can see there's a standard reconstructed vessel and the you can both chart this out and do it and superimpose it on the MRA image and you're gonna get an actual

quantitative amount of tissue reperfusion but studies are still ongoing to determine just how much increasing the amount of red that's in that image is important we don't know the answer to that yet here's just

another example a patient underwent an anterior tibial artery recanalization and you can see the improvement in the t2 star which is just one of the one of the measurements that you can use on these images so what's on the horizon

you see again renal Dena Graham you can see a hint of the gonad of Ain selective

vena Graham again showing us the large gonadal vein and that's my post so charcoal with the occlusion balloon and then treat I showed the cartoon slide before that we look at all four of those territories so I always start with the

left but then I'm gonna look at the right gonadal vein as well as the internal iliac veins on both sides in this case the right go Natalie was normal as were the internal iliac veins so not seeing any varicosities

normal venous outflow so this patient it was only treated with a left gonadal vein embolization

- [Lu Qingsheng] I have no disclosures. We know for indication of EVAR we need favorable proximal neck anatomy but if it not unfavorable maybe we are some Type 1a endoleak it's a serious complication for EVAR. So for prevent and treat Type 1a endoleak

especial for some juxtarenal aneurysm maybe we use the chimney fenestration branch and some sac bag. Could we find a simple safe cheap and effective method? So we find from open surgery we were introduced this fibrin glue

means its complex of thrombin and fibrinogen, it's used hemostasis in open surgery so we put that into inject that into the sac, we call it fibrin glue sac embolization. I will show you some cases.

For this case is very short neck and not quality of deck and after deploy the stent graft, of course very serious Type 1a endoleak. But fortunately, we put a catheter before we deploy the stent graft so this catheter is into the sac of the aneurysm

then we use up a long controlled blood flow and we inject from the catheter into the sac of the aneurysm and we inject the fibrin glue. And you can find the contrast not moved after we withdraw balloon. Then we do the angiogram.

We find no any endoleak. Another case showed is angulated neck as this patient. Of course after we deployed stent graft have a lot of endoleak. And we do again this technique. And control the balloon, control the blood flow,

then inject the fibrin glue, and we check all that and withdrew the balloon, there are no any movement about the sac. And we do the angiogram and no any endoleak. Till now, we did, we begin this technique 2002, so we follow long time that we can show it's safe.

So till now we treat 156 cases and proximal less then short proximal neck is 75 cases even some of less than 10 millimeters. And angulation more than 60 degree even some cases more than 75 degree.

Most of them more than 98% of patients' endoleak was resolved. And during our follow up, the mean time more than 100 months, only three patients died of aneurysm related sac enlargement.

The mean maxim aneurysm diameter decreased and no recurrent Type 1 endoleak so we have confidence that it's safe and no any sealant-related complication for example renal failure and aplasia other things. So we discuss the mechanism

it's not only embolization for endoleak but also coagulating all sac of aneurysm like this in shows how it worked. And we also measure the pressure in the sac. Intrasac pressure decreased significantly in treated cases. And how about that technique we need occlusion

proximal blood flow and protect branch ateliers and prevent distal embolization. And we also treated into the rupture aneurysm and it can treat any type of endoleak as these cases it's a rupture aneurysm we do the EVAR emergency.

And after we deploy this devices, we find this endoleak. We don't make sure which kind of endoleak but anyway we just do that, control the blood flow use the balloon then inject the fibrin glue in that.

And all the sac of aneurysm. Then we do the angiogram and endoleak disappeared. We'll be treat any type endoleak of the rupture EVAR we prevent rupture post-EVAR and we decreased abdominal compartment syndrome. So the conclusion is

fibrin glue sac embolization is a simple and effective treatment method. And this method could expand the current indication of EVAR. For selective the length maybe can to the 5 millimeters, angle maybe can to the 90 degree,

and for emergency we seen it should be into the older EVARs for rupture aneurysms. Thank you very much.

- [Narrator] Thank you, thank you Dr. Veith and the committee for the kind invitation. No related disclosures. Carotid webs are rare, noninflammatory arteriopathy that are also known as pseudovalvular folds, as well as other pseudonyms for this. They are small, shelf-like linear filling defects,

arising posteriorly from the posterior proximal-most ICA and project superiorly into the lumen. They're generally regarded as a developmental anomaly of the brachiocephalic system, and histopathology lacks atheromatous changes and inflammation of the tunica intima.

They may be associated with FMD, or be considered an atypical form of intimal fibroplasia, and generally arise from dysplasia within the media. They will as we will see, carry a considerable stroke risk based on laminar flow disruption and irregular shear profile.

This is the mechanism by which they produce strokes, seen clockwise from the top upper-left. There are areas of stasis in which thrombus can develop behind the web. The thrombus can enlarge and eventually embolize. Operative findings and pathologic findings include

these webs seen here behind this nerve hook, and generally smooth muscle with extensive myxoid degenerative changes. Over the last several years we have treated 10 patients with carotid endarterectomy for symptomatic webs. The mean age of these patients

is generally quite young, in the 40s. The majority are female, one patient had a bilateral web and 70% of these patients had no atherosclerotic risk factors whatsoever. The mean maximum peak systolic velocity on duplex was 77 centimeters,

and five of the cases were closed primarily without a patch. There were no strokes perioperatively in this group, no mortalities, and there have been no new neurological events nor restenosis. Several other groups have looked at this phenomenon as well,

this is a case series of which 7 patients were identified prospectively having had an ischemic stroke. Again, the mean age was young. Of note, five of these patients had a recurrent ipsilateral stroke to the web. No FMD was seen throughout the other vascular beds

and four out of five of these patients, the recurrent patients had CEAs with no recurrence at approximately a year. Another review identified 33 patients who had excellent CAT scan imaging. These were younger patients over a six year period,

with cryptogenic stroke. The prevalence of webs within that group was 21%. Symptomatic patients within that group with webs were 7 patients out of 33 and again you see a young age, predominance of women,

in this study of predominance of African American patients 3 bilateral webs, all patients had MCA infarcts. And oh, 1.6% of the webs in the control group were without a stroke. Another case-control study looked at 62 cases over four years.

They were able to match 53 of these patients with other cerebrovascular pathology, webs were found in 9% of the cases, but only 1% of the controls. And again of the webs, predominance of young patients

and women with two bilateral strokes. So what about diagnosis? Even large webs generally do not meet the velocity criteria for significant stenosis, and while you may see a filling defect, you're generally dependent on B mode imaging,

and having a high level of suspicion, for identifying this process. CTA is the gold standard, it's got rapid, high-resolution imaging, reformatting across planes, makes this an excellent modality

in associated findings of thrombus, and atherosclerosis can also be detected. Angiogram again, as always, gives you a good view of flow dynamics, intra and extra cranial pathology, and in general the finding is of contrast pooling,

which you have to look for behind the web. MRA is one method that's been used to characterize this, in this modality you can see slowed blood flow distal to the web, blood pooling distal to the web, and generally this all leads to an atypical pulsatility, of the carotid wall near the area of the web,

suggesting impaired hemodynamics in this condition. Management is with a carotid endarderectomy which has been the preferred treatment, although some have advocated medical management with formal anticoagulation, patients have had strokes

while on anti platelet therapy, and there are several case series now appearing of acute stroke treated with stents, these are generally delayed following thrombectomy. There's one latrogenic dissection in these groups. These patients have few atherosclerotic risk factors,

in the same demographics as noted above. So in conclusion, these are associated with FMD and intimal fibroplasia. The prevalence is low. The prevalence may be increasing but it's not clear whether this is a true prevalence increase,

or simply increased detection. They're associated with recurrent symptoms even in the setting of adequate medical therapy and is an underappreciated cause of stroke, and are now becoming a recognized, and rather than a cryptogenic cause of stroke.

They are generally not identified by current duplex criteria in asymptomatic patients, and duplex may miss them entirely. Axial imaging is essential and currently we don't stratify these based on either legion characteristics or demographics.

So while the optimal management is not completely defined given the recurrent stroke risk CEA seems prudent especially in young, medically fit patients with or without patch angioplasty, which may have some impact on quality metrics

at least in the United States. We've treated patients with three months of antiplatelet therapy, aspirin indefinitely. Right now the role of statins is undefined, and the durability and role for endovascular approaches remains also undefined.

Thank you.

- Thank you very much. I'd like to thank Dr. Veith for the opportunity to be here and give a quick smattering in four minutes and a quarter. I have no disclosures. So despite the well-documented benefits of straightforward catheter-directed thrombectomy, it remains slow. It can several days and we need speed.

So, devices for physical removal of clots, disruption of clot, large volume removal, and/or combinations of above have certainly been developed. So, with regards with physical removal, aspiration devices, the number of which we'll have several speakers following, the CAT series is by far the

best example of it, if you will. Suction device connected to a continuous pump. Unfortunately, if offers poor transition into the wire. You have to advance in bare. Particularly when you're doing arteries, this can be concerning.

As you advance the thing, you can't tell if the clot is actually removed or not removed, so sometimes you can push it forward. If you've ever used the device, you've seen this. And clogging requires the entire remov

and thus, and you have to put it back through the artery and start all over again. And the concept of continuous removal with a pump is good for suction, but unfortunately, you can remove up to 160 cc's with just 20 seconds of using the device, as it doesn't have a reperfusion system.

The Aspire Mechanical is sort of a low-tech version, a manual aspiration device, where you have a pump that you manually pump up to start negative pressure. You can advance the catheter. The nice thing, you can connect it to literally anything.

If you can get a catheter in there, you screw it in and away you go. You're less likely to have extreme blood loss. You're unable to adjust the suction, unfortunately. And it's not really clear if the suction is actually working or not working.

The pump is on, you know that. But if you pumped it two or three times, is it sucking or not sucking? There's no actual feedback. The AngioVac is the most powerful or large-volume aspiration system.

It's filtered through a veno-veno extracorporeal pump. You can get a big circuit in there. You can do vena cavas, you can do iliacs, it's great. But you have to set up this very complex system. You require, what I'm going to put here as massive sheaths. So if you ever think about doing this in arteries,

you really can't do it. You need a 24-french sheath to put the device in, and then you need at least an 18 or a 20 to put the volume back in. So unfortunately, for arteries, you're going to have to put a conduit in,

and you're going to have to advance it bare through an artery. The extracorporeal filter pump is very expensive and it's not reimbursed. A lot of institutions will either let you use it a few times until they realize how much it costs, and then you're only going to be reimbursed for a thrombectomy.

With regards with mechanical, the Arrow-Trerotola is probably the most powerful and classic mechanical clot disrupter. It's got a spinning cable that looks like this, the new version. And it can damage native vessels,

so it's designed only for grafts. However, it can also get entangled in wires and stents, so even though the black box warning says don't do it, it doesn't keep people from trying it and having multiple attempts. And this is something that we had to remove once

from a graft because it was all entangled in the wire, and it could neither be pushed in or pulled out. It causes embolic materials. It spins inside, and we've never really manned up or womanned up and looked at what happens to the lungs when we fracture all this stuff.

Combination systems, like the Angiojet, is nice 'cause it can shoot out TPA and spray out a saline and break things up. And also, it has a negative pressure, which causes Bernoulli effect to extract clot. The upside is that it removes soft clot

through small side holes. We love it. It's fast, it sprays saline. However, it can also damage vessel walls. At some point, we've read and/or done ruptured in a thin vessel.

And of course, there's a black box warning against pulmonary. But also, if you've ever used it in a cadaveric graft, you'll do it once, and then they'll come back a month later, and now you have this diffused aneurysmal destruction of your bypass.

It also causes hemolysis. Typically, if you look at a Foley catheter, this is what your urine starts with at the bottom and what your urine ends with at the end. And both my group and Dr. Kashyap, who will be following, have assumed that it may not be good for the kidney.

I'll let him continue with that. So in summary, be judicious when you're choosing your approach. Continue to consider the potential downsides of each product. Risk/benefit ratio based on the patient.

Patient has renal dysfunction, limited outflow, sheath size. Old school lysis may be the way to go. Just look at it and maybe you don't have to do a fancy device every time. Or, actually, go with an open thrombectomy.

Mechanical thrombectomy is thus not like a car. When you're looking at these different options and say, "Gosh. You know, maybe it is faster, but perhaps I should think about it." But if somebody offers you this, there's no conceivable downside.

I would go with it. Thank you very much.

one pain geography as we know it was first described in 1955 by Kenneth in

the UK and I always find it interesting that you know we sit here we talk about how not fun it used to be but he said well lymphatic vessels at least the normal ones are much smaller than our deserve Eanes they're hard to see they

contain colorless lengths etc so this is something that has not been a state secret for for a long time but in this case he actually I used the microscope you see a needle he's doing hand injection and he did a surgical incision

across the foot and when he did that he was able to generate these images so one of them is a normal empathic you see a very fine vessel with a hemostat at the bottom of the image and the other one that has his tortuous winding vein or

vein appearance or varicose vein appearance is actually an abnormal lymphatic so this technique was described in fifty five seven years later was described in Pediatrics very similar about

much more difficult as well and they were able to get some very nice images you see these examples of abnormal lymphatics and these pediatric patients so in my fellowship at Brigham we were still doing PETA limp angiography during

my training and usually whenever we started and sat around talk with our text and nurses in the morning you could hear the groans and you could see the frowns but basically we knew that we closed down a room for one day and it

would start by us injecting a freezing solution in the inners web spaces of the toes and then injecting this methylene blue dye we would then milk the foot up until the dorsum of the foot had a blue streak and that's where we knew the

lymphatic vessel was we'd make this vertical incision and skeletonize the vessel we tie it off with some silk we tape it down and then we would get to work trying to catheterize this little skinny vessel with a 30 gauge needle now

this process alone would usually take a couple hours and a lot of patience and then we'd fix our catheter up and attach it to a pump and it would go at a rate of five to eight CC's an hour it'd take a couple hours to get the pictures

through the leg a couple more hours to go from the leg to the rest of the retroperitoneum etc so now you've talked now you're talking six plus hours and you haven't even really done the case yet elegant images you see how fine and

wispy these vessels are we have many more lymphatics than you do any other vessel in your body we don't really have a good grasp with the distribution of of all the different variants that you have from person to person but there's a lot

of variation obviously a technically challenging procedure to have high-quality peda lymph angiography it's time-consuming invasive to patients you have this incision that would take several mattress sutures and a couple

weeks to heal but the images have good resolution it was diagnostic it was therapeutic in some cases of lymphatic injury leaks as well no to lymph

so let me just be honest you know two things about me when I speak I can't stand still if you've ever heard me talk

before so he always has to make me up but secondly I don't think I'm gonna make it through this without getting emotional I feel like if I can get through this whole spill without it being an ugly cry then I look like it's

a success and if you don't know what that is you can Google Kim Kardashian ugly cry so all right so I had the opportunity to go to Tanzania in October November of this year and be part of the first ground zero nurses on the ground

and the first IR there and let me tell you how this went down the end McNamara was really involved with rad aid before she got off our board and one day I had a wild hair and told Bruce from our management company was like hey I think

I want to do one of those trips can you hook me up with Patti over at Rite Aid and he was like yeah sure so Patti calls and she said you know I think he'd be great for a tanzania project I'm like great let's go and she's like wait now

who are you and how do we how are you even affiliated with Arab and I said no where's Tanzania so that's where it's at and if you know me I'm kinda like eh let's go and I don't even know where we're going and it's a 23 hour flight in

case you're interested but Tanzania is a country of 60 million people for you to get a perspective of what that looks like it's California and New York State's population combined and could you imagine not having an IR we've

have five IR s in Little Rock Arkansas going down one small interstate that looks like no biopsy no drain no just the very basic IR procedures that we take for granted don't exist there or didn't before we got there so in October

of 2017 the Yale read a chapter went down there and they assessed the potential for establishing an ir intends and so based on these findings they decided with went collaboration between the movie and Billy National Hospital

the orthopaedic Institute which you're actually like toothed small hospitals on the same campus or actually excuse me MNH is very large and then mo I is kind of smaller but on the same campus there University and the Rite Aid chapter they

would joint plan to start the first ir so the program consists of three components which is practical training a curriculum development and then finding a way to create some sustainable product development you're probably probably

aware you hear about people donating products to these countries but there's the sustainable how do I create a program in a process where we're not just waiting on someone to donate something where we can keep this our

system going so the program overview so this was we're going on two-week rotations over three years and the teams consist of an IR doc and RN and Artie we were the first group to go over in 2018 and so our goals are in year one to do

basic percutaneous procedures biopsies and drains year to going to vascular access and in year three doing more angio type cases like tase's embolization zan etc and developing a teaching curriculum because while there

is a radiology program for residents there was an IR specific one and they're creating that now so our goal is the first nurses on the ground was to provide this comprehensive nursing assessment to help map the project over

the next three or five years now when they went in the year before you can imagine all of the infrastructure assessment all of the you know the equipment there was so much that went into that but the nursing piece was our

job as the first people on the ground and this was so incredibly well received in Tanzania and they were so excited that we were on the front page of the Guardian you can see our doctors Eric and aza down at the bottom right who are

actually here at SAR this week on what looks like to be Good Morning America in Tanzania and when I arrived I was I found out we were having a first conference and there was a camera in my face so I'm

not sure what's which Swahili speaking news outlet I was on but I think I might have been on one and to the left you can see David Pro logo was the attending that I worked with at the same press conference so what I'm trying to say is

no pressure I was like we got it no pressure we have to create this nursing assessment and we wanted to do a good job because it was very well received in the media and we wanted to make sure this all went off really well I would

- [Clark] Well, dear chairmen, Frank, thanks for the invitation. In this talk, I'd like to focus on the role of calcifications in the aortic wall, and whether we could use it for clinical risk assessment. My disclosures. Well, an aortic calcification is, of course,

a clear anatomical entity. It's not that difficult to visualize it. Obviously, for a meaningful assessment, we need to quantify it. This can be done by a simple, abdominal aortic calcium score, AAC 0.8.

The severity of calcification is measured in points assigned to the presence of high-density signaling on the anterior and posterior walls of the aorta between the first and the fourth lumbar vetrabra. The cumulative points of both anterior and posterior walls represent the AAC 0.8 score.

This is a cut from (mumbles) for event-free survival in 2 1/2 thousand individuals, and it shows the prognostic value of AAC for cardiovascular outcomes. A high AAC score predicts future events, and it says something about overall survival.

Now, occlusive and aneurysmal disease are not the same, but calcifications also occur in the aneurysmal wall, and they can be assessed with CTA, quite simply. The effects of calcification are unclear, and we don't know whether it's protective or it's generative.

To verify the roles of these calcifications, patients with an aneurysm confirmed by CT in a six-year period were included. Three groups were distinguished on the likelihood of rupture. The elective group were patients,

who had received elective surgery. Acute aneurysms were either symptomatic, nonruptured, or ruptured confirmed CTA. Doing so, significant differences in diameter and calcification were found between ruptured and elective patients.

Using the AAC score, symptomatic patients were significantly more calcified than elective ones. Then after logistic regression, comparing elective versus nonelective aneurysms, female gender came out as the most important risk factor. Compared to diameter, the AAC was better able to distinguish

acute from elective aneurysms. Now, it's obvious that the conclusions of the few studies we have on the prognostic value of calcification in triple A, directly linked to reliability of the methods of measuring the extent of calcification.

Fully quantitative measurements are considered to be best. Mass and volume and several software tools are currently being used, but without exact knowledge on accuracy or, ultimately, use of these tools. This one, we used the Phantom with calcium rods

of pre-established, massive volumes, which were scanned with the specifics D protocol for coronary arteries and one for the abdominal aorta. This was done to see whether calcification tools tested on coronary arteries can be directly applied to the aorta without adjustments.

Five CT scans for each protocol were performed, and the Phantom was moved two to five millimeters in a random direction between each scan to mimic patients' movement. For each measurement tool and for both scanning protocols, the mass and volume were greatly overestimated.

It appears that the error and the variability of the results increased, when the size and the mass of the calcium element decreased. Also, the presence of contrast has a significant effect on aortic calcification's course. To assess the size of this effect

on the clinical conditions, 50 four-phased liver CT scans were retrospectively collected and analyzed in patients over 65 years of age. The first phase was with contrast, followed by three... No, without contrast followed by three contrast

and have phases of different intensity. Here we saw that measuring calcifications under contrast-enhanced conditions overestimated the calcium volume by a significant margin, yet it underestimated the mass of calcification significantly.

As the results, there's no provision factor to adjust for the error. Clinically-relevant small calcifications are most erroneously measured. Tools validated for coronary arteries that can now be extrapolated to the abdominal aorta,

and patients will need two instead of one CT scan, so, with and without contrast. Most striking, I believe, the previous research using calcification scoring tools on the abdominal aorta, especially with contrast, should be highly scrutinized. As a final conclusion, I think it's clear

that before future studies are implemented, we should first harmonize protocols and software packages to get reliable calcium measurement results. Thank you for your attention.

typical symptoms if you want to hit the play on this I think this is one we've probably already seen but it's it's the the algorithm that I go through for treatment so we do my renal vena Graham

there we go it's classic definitely has reflux and so next I will selectively catheterize the gonadal vein and here you see very large pelvic varicosities and so my standard is to actually treat the varicose veins with a sclerostin

much like I would sclerosis a varicose vein in the leg and there's a few reasons that I do that and so here's how I do it I'll put an occlusion blown up you see the picture on the left of the screen has an occlusion balloon it's the

same occlusion balloon we use for a tips procedure and I'll temporarily block the gonadal vein and fill up the system or the varicosities with contrast so that I get a sense for the volume of sclerosis and I would use then the picture on the

right is a venogram after I've injected the sclerostin so I've evaluated the volume and then I've replaced all that contrast by forcing it through the system to drain out the pelvic veins and filling the varicosities with

soldier column I do that because I believe and there's no data to prove it that it helps prevent superficial phlebitis in those varicosities so if we're just gonna block off the gonna dull vein then we have stagnant blood in

all the pelvic varicosities and stating that blood wants to clot and when blood clots on its own it'll stretch and expand the vein and cause pain and so in my own personal experience that has created a little bit worse post

procedural symptoms for patients compared to the patients that I use so TRADOC all to actually treat the varicosities so that's what I start out with and then since I'm kind of an old-fashioned guy I still go with the

coils and so I coiled the whole going a ttle vein and you can use sort of whatever you want you know that's the simplest thing for me are using nester coiours coils and and fill it up some people use the long detachable shaping

coils kind of an expensive way to do it if it saves you radiation then then that's that's one of the reasons to do it but the point is in in the venous system you have to be able to and I show this slide because you can see a

collateral vein or at least a branch there a confluence point that we've coiled off too if you do not treat the entire length there's a there's a lot higher chance for recurrence and veins have a way to find their way around if

they can communicate back up then patient gets recurrent symptoms and that can happen in about ten percent of cases so in order to prevent that you treat the whole gun out of vein and that's sort of why I think some people like to

use liquid sclerosis because then they will be able to sort of profuse all those branch points that would have a chance for recurrence case number two

I like to talk about brain infarc after Castro its of its year very symbolic a shoe and my name is first name is a shorter and probably you cannot remember my first name but probably you can remember my email address and join ovation very easy 40 years old man presenting with hematemesis and those coffee shows is aphasia verax and gastric barracks and how can i use arrow arrow on the monitor no point around yes so so you can see the red that red that just a beside the endoscopy image recent bleeding at the gastric barracks

so the breathing focus is gastric paddocks and that is a page you're very X and it is can shows it's a page of Eric's gastric barracks and chronic poor vein thrombosis with heaviness transformation of poor vein there is a spline or inertia but there is no gas drawer in urgent I'm sorry tough fast fast playing anyway bleeding focus is gastric barracks but in our hospital we don't have expert endoscopist

for endoscopy crew injections or endoscopic reinjection is not an option in our Hospital and I thought tips may be very very difficult because of chronic Peruvian thrombosis professors carucha tri-tips in this patient oh he is very busy and there is a no gas Torino Shanta so PRT o is not an option so we decided to do percutaneous there is your embolization under under I mean there are many ways to approach it

but under urgent settings you do what you can do best quickly oh no that's right yes and and this patience main program is not patent cameras transformation so percutaneous transit party approach may have some problem and we also do transit planning approach and this kind of patient has a splenomegaly and splenic pain is big enough to be punctured by ultrasonography and i'm a tips beginner so I don't like tips in this difficult

case so transplanting punch was performed by ultrasound guidance and you can see Carolus transformation of main pervane and splenorenal shunt and gastric varices left gastric we know officios Castries bezier varices micro catheter was advanced and in geography was performed you can see a Terrell ID the vascular structure so we commonly use glue from be brown company and amputee cyanoacrylate MBC is mixed with Italy

powder at a time I mixed 1 to 8 ratio so it's a very thin very thin below 11% igloo so after injection of a 1cc of glue mixture you can see some glue in the barracks but some glue in the promontory Audrey from Maneri embolism and angiography shows already draw barracks and you can also see a subtraction artifact white why did you want to be that distal

why did you go all the way up to do the glue instead of starting lower i usually in in these procedures i want to advance the microcatheter into the paddocks itself and there are multiple collateral channels so if i in inject glue at the proximal portion some channels can be occluded about some channels can be patent so complete embolization of verax cannot be achieved and so there are multiple paths first structures so multiple injection of glue is needed

anyway at this image you can see rigid your barracks and subtraction artifacting in the promenade already and probably renal artery or pyramid entry already so it means from one area but it demands is to Mogambo region patient began to complain of headache but american ir most american IRS care the patient but Korean IR care the procedure serve so we continue we kept the procedure what's a little headache right to keep you from completing your

procedure and I performed Lippitt eight below embolization again and again so I used 3 micro catheters final angel officio is a complete embolization of case repair ax patients kept complaining of headache so after the procedure we sent at a patient to the city room and CT scan shows multiple tiny high attenuated and others in the brain those are not calcification rapado so it means systemic um embolization Oh bleep I adore mixtures

of primitive brain in park and patient just started to complain of blindness one day after diffusion-weighted images shows multiple car brain in park so how come this happen unfortunately I didn't know that Porter from Manila penis anastomosis at the time one article said gastric barracks is a connectivity read from an airy being by a bronchial venous system and it's prevalence is up to 30 percent so normally blood flow blood in the barracks drains into the edge a

ghost vein or other systemic collateral veins and then drain into SVC right heart and promontory artery so from what embolism may have fun and but in most cases in there it seldom cause significant cranker problem but in this case barracks is a connectivity the promontory being fired a bronchial vein and then glue mixture can drain into the rapture heart so glue training to aorta and system already causing brain in fog or systemic embolism so let respectively

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