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Duration Of Anticoagulation For DVT: The Forgotten Trifecta
Duration Of Anticoagulation For DVT: The Forgotten Trifecta
Anti-coagulantsanticoagulateanticoagulationclotcumulativedatafactormodalitiesnormalpoplitealrecurrenceresidualscansynergisticveinvenousviii
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
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Treatment Case 2 | Pelvic Congestion Syndrome
Treatment Case 2 | Pelvic Congestion Syndrome
chapterembolizationgonadaliliacinternalocclusionvaricositiesveinveinsvenavenous
Classification of PE | Management of Patients with Acute & Chronic PE
Classification of PE | Management of Patients with Acute & Chronic PE
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Case- Severe Acute Abdominal Pain | Portal Vein Thrombosis: Endovascular Management
Case- Severe Acute Abdominal Pain | Portal Vein Thrombosis: Endovascular Management
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Algorithm for Treatment | Pelvic Congestion Syndrome
Algorithm for Treatment | Pelvic Congestion Syndrome
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Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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CME
Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Angio jet (Zelante)Angiojet (Solent)Catheter-directed thrombolysisConvatecDrain-fixev3 guidewire (Nitrex- Medtronic)IF DVTtherapeutic
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
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Case Example | Management of Patients with Acute & Chronic PE
Case Example | Management of Patients with Acute & Chronic PE
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Transcript

- Thank you very much indeed, and, first of all, I'd like to thank you for allowing me to come to the show and speak about these things. It's a great pleasure and of course to Frank Veith, who has a marvelous, created a marvelous thing

for all of us over the years to interact. Here are my disclosures. VTE is mostly a chronic inflammatory disease that is often not cured with short anticoagulation. Thrombosis is inextricably linked to inflammation and immunologic changes,

and I believe we should discard the simplistic notion that we can decide how long to anticoagulate the patients based upon this simplistic criteria of provoked versus unprovoked. As we all know, life is complicated. We know that Factor VIII is a potent

predictor for first venous thrombosis. Levels are constant, unaffected by anticoagulation. Three months of anticoagulation, after three months off anticoagulation, the vitamin K levels are not affected. And this was a study follow-up of 6.9 years,

and the recurrent VTE was 1.6 for each increase of 10 deciliters of Factor VIII. Cumulative index rates for both provoked and unprovoked are seen, and those with a level of over 200, sorry about that, Factor VIII... Those with the level of greater than 200

had a three-fold higher risk compared to those with a Factor VIII equal to or less than 100 international units. And here you can see on this chart as you go up above 200, 9.5% one year, 30% at five years, 4.4% at one year, and almost 20% at five years,

and so that is significant. But what's more significant and has not been carefully looked at, is the synergistic effect between Factor VIII and vita--. Factor VIII and D-dimer. And if one is abnormal,

the recurrence rate in this study was 6.4% And if both were normal, it was 6.4%. If one was abnormal, it was almost up to 18%. And if both were abnormal, it was 34%. And here, you can see the curves clearly for that. And here, we have a look at--and this is the latest data

and most compelling data about the lack of differences between provoked and unprovoked in cancer patients. And you can see if you look, provoked is the red line. Unprovoked is the black, dark line, and green is cancer-related VTE. So that you can see how similar these are, and

talking about residual obstruction, which I think is very important and I have studied for years. The presence of residual venous obstruction, which, you know, after a while, is not clot but it turns into fibrous material. And the cumulative recurrence rate,

according to Prandoni, was 40%, with a provoked rate of 22 and an unprovoked of 52. And these data force us to question the notion that time-limited anticoagulation is an effective strategy because the rate of recurrence is high, even among those with provoked VTE.

Now I don't totally subscribe to what he said about this compression and 40% of the diameter. You have to take a look at the overall vein and if the overall vein there is significant changes in it, then I think that that influences whether or not you should continue your anticoagulation.

The Achilles heel of this, is that nobody knows for sure how to quantify these changes. And if you take a look, for example, this was a CAT Scan of somebody after three months of a provoked, simple clot. And I always scan them and I would not stop

the anticoagulation in this patient, and you would see because of the reflex and so forth, eventually this patient is going to show signs of post-embolic syndrome, venous insufficiency, but also, I think, has an increase risk of thrombosis. Again, here's another one with significant clot

in the popliteal facet, after what was thought to be a very minor insult. And here we go again on cross sections. So these are the kind of images, once you start looking at them, and I'd encourage you, in some of these patients, to take a look at them

because I think it's very important that these with these changes about continuing anticoagulation. Now, I'm sorry about this, but this is really important. If somebody has a normal D-dimer, a normal Factor VIII, and a normal scan, on anticoagulation, we'll stop it. And then 30 days, 90 days, and 180 days later,

repeat the Factor VIII and D-dimer. And that's assuming that their scan is clean. If they're normal throughout that whole period, then we would consider them to stay off of anticoagulation. And the other thing is that, one of the things that I think is really good about this,

is that now we have very effective modalities for long term anticoagulation, so that I think you ought to take a look at much more beyond time-related criteria. Thank you very much.

CT scan frequently or they actually show up with a CT scan so I want to highlight the fact that this is different these images are different than the patients

who had acute pulmonary embolism I will say that it's very hard to kind of get this into your brain but they're very different so first of all they'll have a VQ scan that'll show that they have mismatch defects after that when you

look at the scan the clot has a different appearance before it was in the middle of the vessel it was surrounded by a rim of normal contrast here it's actually wall adherent it's irregular it's got weird weird angles to

it weird margins and then distally the vessels are very small in acute PE the proximal pulmonary arteries are enlarged because they're hitting they're enlarging because they're hitting a roadblock in here in chronic PE the

vessels shrink down and shrivel beyond it because there's chronic clot they're a lot like patients who have chronic DVT in their legs when you look at that sagittal view kind of think back to the original case that I showed you

you saw that sort of with clot there's a thin lines floating in the middle of the vessel here it's irregular it looks serrated it's gotten really weird angles so this is another example of chronic PE from the literature that believe it or

not is not mediastinal adenopathy it's not a patient with cancer it's a patient with chronic PE all that thrombus sort of lines the inner walls of the pulmonary arteries you can even have calcification just like you would have

in atherosclerosis also the vessels distal to the clot become shriveled down and that's a way to tell if that's chronic PE versus acute here's another example of a patient of the image on the left is the patient years or before and

then the image on the right is a patient with chronic thromboembolic pulmonary hypertension and then a few more examples showing you that it's usually on the side of the blood vessel rather than in the middle of the blood vessel

so if you want to know just an easy way if you see clot in the middle of a blood vessel it's probably acute if you see it on the side and along the walls it's chronic more pictures kind of just to put in your brain so the diagnostic

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

- [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.

original classification of PE is important to know because it man it helps dictate treatment so it used to be classified as massive which is about 5% of PE patients these are the ones that

we all know how to treat they're usually coding essentially when they show up to the ER or to the angio suite or in the ICU they have a 58% ninety day mortality rate so these patients are doing very poorly they're in hemodynamic collapse

which is the diagnostic factor there that sort of makes that diagnosis because of cardiogenic shock sub massive PE is the biggest group that we'll talk about last I'm sorry the most important group we'll talk about last so

minor PE are about 55% of PE patients those are the ones that show to the ER that just don't feel right and they turns out that they have PE so it was really not even anyone's differential diagnosis and most of these patients do

just fine with outpatient anticoagulation monitoring and monitoring so the main group that matters in that most of the talks about PE are about are the sub massive group which is about 40% of patients and these

are the ones that show up with a moderate amount of clot and some right ventricular strain these are the patients who are able to tolerate their PE but they're not doing very well so they come in with shortness of breath

some chest pain and although they're not in hemodynamic collapse they are the ones who require inpatient monitoring or their good it goes to an ICU and that's really the patients that we worry about those are the ones that we're going to

do an intervention on or systemic TPA so that was the sort of the old way of classifying PE and this is the new way of classifying PE so this is the Europeans Society of Cardiology they had a

consensus in 2014 talking about PE and what we look at now and the way we stratify these are high risk PE intermediate which is intermediate high and intermediate low and then low risk PE so this is

important because it in fact it utilizes patients actual biomarkers imaging as well as their clinical symptoms all in one and so what we look at if you look at a patient with high risk PE they have to be in shock or hypotension that is

one factor that has to be there and actually everything else doesn't matter but the things that we look at are the PE severity index or the PES e score if you google PES e PE SI it's basically a bunch of things it asks for the

patient's age whether they have cancer what their heart rate is if what they're owed to sat and on what oxygen content they're on and it gives you a score and that classifies it in 1 through 5 and basically 5 is really bad which means

that you have a low or you have a higher mortality as an outpatient and 1 is really low some things like cancer give you a lot of points so that sort of pushes it over to automatically kind of 2 3 then you look at the signs of our V

dysfunction and really with PE that's really the thing that that kills you is your right ventricular dysfunction and if your right heart fails then your left heart fails and then you die and so that's really where the issue is

and then the cardiac laboratory biomarkers are what will sort of give you a blood test that you can figure out and see if that patient is going to do poorly so high risk PE shock or hypotension

low risk Pease the other end where you really don't have any of those things but you do have a PE diagnosed either usually on a CT scan but it could be on an echo as well intermediate high and intermediate low is where we all spend

all the time talking about that's what we kind of do all the studies on is really the intermediate high and low groups and what we should do for them and sort of how we can affect their lives but the main point here that I

want you to see is that they don't have shock or hypotension but they do have positive right ventricular strain either on an echo or a CT scan and they have positive biomarkers if you have positive biomarkers and imaging then you have

intermediate high risk PE and those are the patients who may benefit from some sort of intervention or some sort of further ICU monitoring and anticoagulation so I'm gonna just

so we kind of had a bunch of portal vein cases I think we'll stick with that theme and this is a 53 year old woman who presented to the emergency room with severe abdominal pain about three hours after she ate lunch she had a ruin why two weeks prior the medications were

really non-contributory and she had a high lactic acid so she they won her a tan on consi t scan and this is you can see back on the date which is two years ago or a year and a half ago we're still seeing her now and follow-up and there

was a suggestion that the portal vein was thrombosed even on the non con scan so we went ahead and got a duplex and actually the ER got one and confirmed that portal vein was occluded so they consulted us and we had this kind of

debate about what the next step might be and so we decided well like all these patients we'll put her on some anticoagulation and see how she does her pain improved and her lactate normalized but two days later when she tried to eat

a little bit of food she became severely symptomatic although her lactate remain normal she actually became hypotensive had severe abdominal pain and realized that she couldn't eat anything so then the question comes what do you do for

this we did get an MRA and you can see if there's extensive portal vein thrombus coming through the entire portal vein extending into the smv so what do we do here in the decision this is something that we do a good bit of

but these cases can get a little complicated we decided that would make a would make an attempt to thrombolysis with low-dose lytx the problem is she's only two weeks out of a major abdominal surgery but she did have recurrent

anorexia and significant pain we talked about trying to do this mechanically and I'd be interested to hear from our panel later but primary mechanical portal vein thrombus to me is oftentimes hard to establish really good flow based on our

prior results we felt we need some thrombolysis so we started her decided to access the portal vein trance of Pataca lee and you can see this large amount of clot we see some meds and tera collaterals later i'll show you the SMB

and and so we have a wire we have a wide get a wire in put a catheter in and here we are coming down and essentially decide to try a little bit of TPA and a moderate dose and we went this was late in the afternoon so we figured it would

just go for about ten or twelve hours and see what happened she returned to the IRS suite the following day for a lysis check and at that what we normally do in these cases is is and she likes a good bit but you can see there's still

not much intrahepatic flow and there's a lot of clots still present it's a little hard to catheterize her portal vein here we are going down in the SMB there's a stenosis there I'm not sure if that's secondary to her surgery but there's a

relatively tight stenosis there so we balloon that and then given the persistent clot burden we decide to create a tips to help her along so here we are coming transit paddock we have a little bit of open portal vein still not

great flow in the portal vein but we're able to pass a needle we have a catheter there so we can O pacify and and pass a needle in and here we are creating the tips in this particular situation we decide to create a small tips not use a

covered stent decide to use a bare metal stent and make it small with the hope that maybe it'll thrombosed in time we wouldn't have to deal with the long-term problems with having a shunt but we could restore flow and let that vein

remodel so now we're into the second day and this is you know we do this intermittently but for us this is not something most of the patients we can manage with anticoagulation so we do this tips but again the problem here is

a still significant clot in the portal vein and even with the tips we're not seeing much intrahepatic flow so we use some smart stance and we think we could do it with one we kind of miss align it so we

end up with the second one the trick Zieve taught me which is never to do it right the first time joking xiv and these are post tips and yo still not a lot of great flow in the portal vein in the smv

and really no intrahepatic flow so the question is do we leave that where do we go from here so at this point through our transit pata catheter we can pass an aspiration catheter and we can do this mechanical

aspiration of the right and left lobes you see us here vacuuming using this is with the Indigo system and we can go down the smv and do that this is a clot that we pull out after lysis that we still have still a lot of clot and now

when we do this run you see that s MV is open we're filling the right and left portal vein and we're able to open things up and and keep the the tips you see is small but it's enough I think to promote flow and with that much clot now

gone with that excellent flow we're not too worried about whether this tips goes down we coil our tract on the way out continue our own happened and then trance it kind of transfer over to anti platelets advanced or diet she does

pretty well she comes back for follow-up and the tips are still there it's open her portal vein remains widely Peyton she does have one year follow-up actually a year and a half out but here's her CT the tip shuts down the

portal vein stays widely Peyton the splenic vein widely Peyton she has a big hematoma here from our procedure unfortunately our diagnostic colleagues don't look at any of her old films and call that a tumor tell her that she

probably has a new HCC she panics unbeknownst to us even though we're following her she's in our office she ends up seeing an oncologist he says wait that doesn't seem to make sense he comes back to us this is 11 3 so

remember we did the procedure in 7 so this is five months later at the one year fault that hematoma is completely resolved and she's doing great asymptomatic so yeah the scope will effect right that's exactly right so so

in summary this is it's an interesting case a bit extreme that we often don't do these interventions but when we do I think creating the tips helps us here I think just having the tips alone wasn't going to be enough to remodel so we went

ahead and did the aspiration with it and in this case despite having a hematoma and all shams up resolved and she's a little bit of normal life now and we're still following up so thank you he's

- [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.

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

- [Lars] Thank you again Mr. Chairman. So, here are my disclosures. So the outline of the talk is here. And we need, that the need for radiation protection, it was evident already in 1928 when the ICRP was established. And according the European Union regulation

when it comes to radiation safety, you need practical training and also relevant competence in radiation protection. So in special case of the clinical use of new tecniques training is provided on these tecniques, or should be provided.

So what does that mean? That means, since interventional radiology, we have talked about it already, causes cancer and tissue effects, skin burns. And the new information around health effects has led to increased safety concerns.

We need to think more about this, how to implement this into our daily training for newcomers in radiation and the vascular world. So the comparison of risk in health care with other industries, health care is more like bungee jumping,

while actually the minimal risk is of commercial aviation and nuclear power. And they have a simulation training for years. So we know also that subclinical carotid atherosclerosis and early vascular aging is proposed due to low-dose ionizing radiation exposure.

So in the Cath lab we see that increased subclinical intimal medial thickness. And the telomere length is also shortened so that's essentially evidence that implies an accelerated vascular aging and early atherosclerosis among us.

And we know for sure that cataract especially among the cardiologists is a real problem. Also, many have talked about this, the work from St. George hospitals where radiation exposure during EVAR causes DNA damage in operators.

It's fantastic work by these guys, which actually shows that the lymphocytes have DNA damage. And also that we maybe need to protect our legs in order to be careful with this. So we have together with UKTS, these endovascular fellows who works together in UK

together with the Mentice Company developed some posters to be aligned with radiation safety awareness. Since simulation training is needed. And why is it so? Well is you get better quality.

You get reduced cost. You get better production along this. So simulation-based training is very important for this society and also for the health costs. So we know that we a competence in EVAR tecniques. We have worked with this

in Copenhagen with simulation training. In the upper corner there is the stroke group that we work with also for endovascular simulation training. To be with fast and with stroke, it's couple of new interventions there worldwide. And also we know from this paper here,

how to reduce radiation exposure during EVAR with Stephan Haulon and his friends. That the techniques to reduce radiation dose, it's important to train, not in the Cath lab, but in simulated setting. So you can integrate this to modern than work.

So what you can here can see, what you can do with endovascular simulators like the Mentice simulator, or Simulab simulator. You have a patient, you have an operating heat map. You can work with this, impact of table height and detector position.

You can train this with the fellows to see so they get a real figure immediately on the radiation dose. You can see how much radiation dose when you shoot angio. And you can also make marks on the floor where you get the most heating maps.

And this is even more important to use the shutters when you shoot your angio, which you can see on this as well, while it gets highlighted. And again, decreasing field of view increases also the dose as you can see.

So and also you have to avoid hostile angulation. This gives you a more practical training. Mandatory to have six hours, old PowerPoint presentation in European Union and in Denmark to get your license, but instead working with this in an interactive fashion,

together with a combined Laerdal manikin and a Mentice simulator will give you a much better way to train and you can also assess if they have reached the level of proficiency with this.

- [Dr. Cho] Thank you very much, thank Frank, for the invitation and for the opportunity to speak on the carbon dioxide angiography. Disclosures, none. Here are three images taken, obtained from the carbon dioxide, and MRA, and CTA.

If you look at the CO2 images, it's quite comparable to the MR and CTA, and MR requires gadolinium, which can cause nephrogenic systemic fibrosis. And if you inject the contrast for the CTA there's a risk of the contrast-induced nephropathy.

So, there's many additional advantages using CO2. First of all, CO2: non-allergenic. So, if you have the contrast allergy history of patient, you do not need a sterile preparation. And CO2 is non-nephrogenic,

therefore you can inject the unlimited volume of the procedure, particularly in a complex procedures, and you can use CO2 for both patient, with, without the renal failures. And the CO2 has a very low viscosity.

We talk more about this, this is unique property to allow you to inject CO2 with small pore system, even 25 gauge needle and three French microcatheter. They give a tremendous flexibility when you're doing a procedure. And central reflux,

central reflux, that means, if you inject it distally and CO2 flow backward, the CO2 flow two direction, antegrade as well as retrograde, whereas contrast flow is only antegrade. So that give you additional information

you will see for endovascular interventions. And CO2 is very inexpensive. The tank costs $600, which will last three, four years, but if you use contrast, it may take several million dollars for the contrast budget. And we currently using the plastic bag system.

The bag is filled with CO2 from the tank. You have to have a clean tank, not large, laboratory tanks. CO2 USP, and fill up, then empty several times through the micro filters, and they have connecting system

that have multiple one-way valves. You make two connection between the bag and the collecting system right here, and also here. Those two connections be made by operators, but if you're doing this, you have to make sure these two connections properly connected.

If you have misconnection or disconnection during the procedure, basically you are sucking the air from the room, and then you can get a catastrophe. So it's very important to check them. The way you check, you close the stopper here and aspirate the injection syringe,

you should not be able to fill the syringe. And if you do this, absolutely safe techniques. And there's another device called CO2mmander available on the markets. This is FDA approved and also convenient.

And you can see CO2 floating, called buoyancy. This is CO2, about 20cc in the aorta. You can see, only you'd see about 30% of the ante part of the lumen. Here is the artist's rendition, you can see the renal artery will not fill

because of buoyancy, that's where you turn the patient from side to side depending upon the location of the renal arteries to fill it. And you can take advantage of the buoyancy on the median arcuate ligament compression syndrome,

because celiac SMA originated from the ventral aspect, so the CO2 naturally fills those branches. You need about 10 to 15cc. Here median arcuate ligament compression during expiration, and then inspiration give relief. So CO2 is much better way

to evaluate median arcuate ligament compression syndrome than contrast. We take close-up lateral view. If we inject the contrast in celiac stenoses, you see the flow defect from GDA because reversal, but if you inject the carbon dioxide,

you should get the antegrade flow. That's why the CO2's very (mumbles), and you can see both vessel, antegrade and retrograde. So, when you do CO2 renal angiogram, you already see to some positional change. In this case, you have the left side up

to fill the left renal artery. Sometimes you inject selective injection retrograde flow, but you can do even extreme cases of the left side up, completely, and then take closer lateral view to visualize. When you do CO2 angiogram for the patient

with the aneurysm, the aortic aneurysm, watch out for the trap. Once it's trapped and becomes high, CO2 partial pressure gas exchange takes place between nitrogen and carbon dioxide. You can potentially occlude your diameter

with nitrogen, causing ischemic colitis. In the aortoiliac occlusion, you can see beautiful pictures. CO2 flow backward, antegrade, you can see outflow studies and you can inject the CO2 into the SFA in retrograde so you can see the proximal vessels,

and when you do renal arteriogram, you'd advance the microcatheter more distally and then try reflux back toward the orifice to visualize renal arteries. And when you have motion artifact like this from peristalsis,

you can do a focal new mask, and you can get clean up the vessel with post-processing. When there are multiple irregularities with redundant tortuous (mumbles) to tend to flow more, dependent, non-dependent part, you do stacking technique, you can get beautiful pictures.

If you don't know how to do this, everybody will complain, "the CO2 (mumbles) is bad." And when you have multiple stenoses like this, it looks like a stenosis in frame orientation of the gas, we can do stacking here,

continuous column with the CO2, so you get the post-processing to make a better pictures. And CO2 guided intervention, for the SMA stent is good, renal stentings, and renal transplant, and the femoral artery occlusions

with the CO2 guided intervention, you can do all this with CO2 guided without any contrast. Many of these, at present, high risk. And one of my colleagues doing it at the University of Michigan, you can do a CO2 guided EVAR procedures shows very...

So I'd like to summarize that my presentation is giving the tips and trick for CO2 intervention angiography, you can see all this. Do not use CO2 above diaphragm. Do not inject cerebral coronary in the thoracic aorta.

And use closed system, and CO2, use end-hole catheter for delivering. You don't need a pigtails. And inject more selectively to get a better pictures, and reduce motion and taking fast exposure, get additional mask for the subtraction, using new mask,

and elevate the imaging area, so you can use a vasodilator for the lower extremities, and use the CO2 reflux technique, they will give a much better picture when you inject more antegrade. And the postprocess with new mask and stacking

is very important. Thank you.

- [Dr Heyligers] Thank you, Mr Chairman, I would like to thank Dr. Veet for the opportunity to share our data here in New York. Thank you. Most of us learned medicine by the book, and anatomy on cadavers. And we know that tools cha

how it is educated, and how it is practiced. And if we look at the first x-ray that's performed by Wilhelm Rontgen, like 120 years ago and you compare it to the Hivreal R

that we have right now, a lot of things have changed. This is how, nowadays, medical students can train. By their handheld phone and look at specific stuff like the vasculature, and rotate in different directions to study anatomy. And it's simply by your handheld cellphone.

You can zoom in, and then point out to the structures you're interested in. Simply tap on it, and you'll learn this is the abdominal aorta. What about virtual reality, augmented reality,

and high resolution 3D-3D imaging? These are the tools that now a days are changing medicine. Let's first have a look at virtual reality. What is virtual reality? This is an example of one of our surgical residents who got some work on pelvic fractures,

and you see that when he moves his head, he has a different view on the fracture of this particular patient. And augmented reality is a projected virtual reality in a surrounding like we have here. In this particular case,

he's wearing a Hololens. - You can move it around, you can make it kind of translucent, so you can see through the outside, and that really helped me understand how cardiac anatomy worked.

I actually had a moment where I found the aortic valve, and it was the first time that I actually seen the aortic valve in relation to all the other anatomical structures. You know, it was a way of seeing it that you couldn't do with an actual heart.

- [Dr Heyligers] So this is also the Hololens. Microsoft that offers it. Let's have a look at the High Resolution 3D-3D Imaging of the VPI Reveal. It has patient specific anatomy on the base of CT, and MR images.

It is quick and easy to use software solution, and what you need is a 3D TV and 3D glasses. In the picture you see here, is at our emergency department where different doctors are wearing glasses at the same time, and they're looking at this 3D television.

And this is software solution where you can read CT and MRs instantly. This is an example of a patient I treated with a very hostile abdomen and hostile neck. We did a chimney procedure, and you can appreciate here the vasculature, the liver,

and this is a 2D-3D visualization, but if you put on your 3D glasses and look at the 3D TV, you really appreciate depth. So this is a normal CT scan, just focused on it in a different view. Now you can see the endografting,

and you can see the chimneys in the renals and in the mesenteric artery, from multiple directions. You can fly through, you can helicopter your way, and you can change the settings so when you're interested in bone or,

for example, soft tissue, it will highlight it. So this is an example of the 3D-3D high resolution. But let me stress again that if you put on your 3D glasses, and look at the 3D TV, you really appreciate depth. So what will the value be of all these technologies? First of all, our patients will benefit,

medical students, for sure, will benefit, physicians will, too. And how will it be? Well, patients take their personal anatomy home on hand held devices, on your cell phone. Students will better understand

anatomy, physiology, and pathology. The student and physician simulate invasive treatments on the basis of these technologies. And physicians will increase their, so to speak, interventional confidence. And also, physicians will use

"superposed patient specific anatomy" during the intervention. But not only this, because if we combine and we gather all this data in the cloud, we have cloud solutions and big data, we'll influence patient outcome

because then you start creating artificial intelligence and stuff like self learning capacities in computers, and deep learning will help to diagnose. So these tools and these technologies are here to stay. Thank you.

- [Germano] Thank you very much Mr. Chairman. Let me please thank Dr. Veith for his invitation, for his great hospitality and for being my friend and the mentor for many, many years. Thank you Frank. So, I also would like to thank Mario

for making a very interesting point that the EVAR is very appropriate unless it's not appropriate. And I certainly do acknowledge the value of EVAR. It's a great technique when it's appropriate. However, the problem is,

should it be considered the only choice? And this could be the case if it offered better results, if it was always feasible and maybe cheaper. So, as far as better results are concerned, we've already heard about all the randomized trials not significant.

There's a meta-analysis on over 80,000 patients that also showed no significant difference in mortality. And regarding feasibility, I think we all agree that there are anatomic limitations of EVAR and cases that are really tough with EVAR are really straightforward with surgery.

And this also applies to access vessels. And it also applies to anomalies of the kidneys, for example, saw a pelvic kidney here with its surgical solution. A horseshoe kidney here. And also there are clinical limitations,

are not many common, but certainly we don't want to treat an infection or a fistula with EVAR. And we know that large hematomas are a problem if we don't open the belly and raise a surgical solution for this.

And then there are logistic limitations, of course especially if you tried to treat most of the cases you need advanced techniques for at least a quarter of these cases, as shown by Mario (mumbles), and to do so you need

of course round the clock availability of highly trained endo team and everything else. Including, a large warehouse of gadgets. This is Mario's warehouse for all his wires and things. And actually this debate has been going on

for several years now. So, I've been trying to search the literature a little bit to see if there's anything new about it. And there's actually a couple of interesting, a few interesting new papers. Such as this one from Sweden,

from Anders and his colleagues, that show that very interesting change in the epidemiology of triple A's. Which is related to the introduction of EVAR, to the screening of the population, to the reduced prevalence of triple A's.

And we also saw these from the data that Mario showed in the first years of his cases. It was 30, 20, and now in the last years he's showing about 10 cases per year. We've all been seeing this. And this results, of course, in increased incidence

of intact triple A's, reduced incidence in ruptured triple A's and improved survival for both. And Warner and co-workers show that regionalizations of emergent ruptured aneurysms repaired to tertiary centers decreased the mortality by 20%. And transfer did not impact the mortality.

I think that Bam showed to us very beautifully how this can be achieved in a very scientific and sophisticated way. And we do have an update. This year update of the Cochrane Review that includes all four randomized trials.

And once again, there's no difference in 30-days mortality shown and neither there's a difference in 6 and 12 months outcomes. This last literature paper from Siracuse and co-workers, on behalf of the American College of Surgeons,

showed the registries of over 400 patients treated by open repair in the United States, so it shows that this is still commonly done. And the overall mortality was 35%, which is somehow lower than previous historic data. So regarding training, I think we should consider

that if a center does 90% or more of the elective case endovascularly there is very little or no chance to train new generations to open surgeries. So, for these kind of centers the boat has sailed already and this ability has been lost for the future generations.

So, we should consider this very carefully when we decide what we want to do with our patients. In conclusion, dear colleagues, Chairman, Mario, I believe that the present evidence is that EVAR for ruptured aneurysm is not superior, feasibility is not 100% and therefore,

there is still a justification to have a selective approach for these patients. Thank you.

- [Narrator] Thank you, I'd like to thank Doctor Veith for the privilege of the podium and the long title of my talk. I have nothing to disclose financially but I will say that one of my disclosures is that I've actually never implanted an Endologix device but I have

removed a large number of them and treated a large number of type three endoleaks as a result of them. The AFX graft is a unibody stent design. It is a single component designed to sit on the aortic bifurcation.

The company calls that anatomic fixation. It has an endoskeleton which is a unique design compared to many of the other devices available. And it is coated in a second generation PTFE polymer. The advantage is that it avoids a need for contralateral gate cannulation

and the goal is to place the device at the aortic bifurcation and then gradually build up to the infrarenal neck. Over time the device was used for broader and broader indications with larger and larger proximal cuffs being placed

to treat wider infrarenal necks. Even to the point that a whole generation of cases called Topper cases was developed where very large aortic cuffs were crammed down into the main body of the device and even thoracic endograft proximal cuffs

were placed within this device to achieve a seal and relatively large necks. Our experience is that two large tertiary hospitals here in New York, these are both 800 bed hospitals and we looked at our experience from a period of 2013 to 2015 when we implanted

approximately 80 of these devices. Over that period of time we encountered 11 type three endoleaks, four of those patients presented ruptured and three of those patients had died from aneurysm-related deaths. As is evident in many of these published pictures

the problem occurs at the connection point between the main body of the device and the upper proximal component leading to a type three endoleak. In a fantasy world where all the aneurysms are perfectly vertical, up and down,

the force vector of the blood flow is transmitted along the center-line of the device down to the aortic bifurcation. So conceptually placing the device on the aortic bifurcation makes a lot of sense. However in the real world most aneurysms

are angulated, usually to the left, resulting in a different vector of force leading toward the blood being pushed toward the outer wall of the aorta. My argument is that if you are sitting on the aortic bifurcation that acts as a fulcrum point

because the vector of force is now off to the side of the aneurysm, the lower part of the device has nowhere to go and is basically seated on the aortic bifurcation. So the idea is that if you have good proximaL fixation and now you have good,

a distal fulcrum, the only area where the device can then relieve that pressure is in the mid-component between the proximal cuff and the distal component. And as you add larger and larger sac diameters the room for that disconnection becomes larger.

And this was evident in some later papers. Furthermore in these Topper cases where a very large cuff is being sandwiched inside of a smaller device, you see this instability in this junction where you have a watermelon seeding effect where

this large device which is being crammed down there actually will pop out. This we see when there are different manufactured components for the proximal device as well as these large thoracic cuffs. I would argue that this is a danger zone.

Here you can see two examples. Here on the left side you can see a very large cuff being crammed down into a very small main body device. In the second panel you can see the similar situation, you can expect

that this is not a long-term stable situation. This was published by Gary Lemmon in 2016 where they did a retrospective review of their experience with a variety of devices, not just the Endologix device. But they were specifically looking at type three endoleaks.

They divided the cohort into two groups, Endologix and everybody else. And there was a substantially increased risk of post-implant rupture and the need for re-interventions in the Endologix group. Ultimately concluding that the uncoupling

of these components is a big problem and that you should not use these oversized aortic cuffs. Once these disconnections do happen there are significant challenges to secondary intervention. These devices have internal wireframes which make negotiation difficult

and the severe angulation that you can see evident in this picture here makes bridging the gap very challenging. Duplex ultrasound is not adequate for following these devices because as the disconnections occur there's not much to see of duplex.

So I believe that serial radiography needs to occur. The IFU was changed in 2015 to recommend not placing proximal devices that are significantly enlarged in this device. So in conclusion, I would say, should we prophylactically reline these devices?

I believe to some degree many of these devices out there are essentially ticking time bombs. The devices don't present themselves until a rupture has already occurred in many instances, and these are the patients that are significantly at risk.

So in summary, component separation remains a significant problem with this device. It's associated with a significant risk of rupture and death especially in patients with large aortic sacs. Vigilant surveillance is definitely

required and prophylactic relining of the device should be considered. Thank you.

few different devices and techniques to do this so that everyone sort of again understands what are the different options available to us so you can of course do catheter directed thrombolysis

this can be any of a few different types of catheters so this is an example of a unifier when I talk to the residents and fellows and I just tell them it looks kind of like a garden hose that you poke a bunch of holes in right and you turn

it on and so that's what that looks like you're gonna give delivery of thrombolytic right into the pulmonary arteries ideally you're bathing the pulmonary arteries and you have a catheter on both sides usually on with

two N's one on normal throught normal vessel and the other on the normal vessel in the holes basically embedded in the clot the benefit of this is that you get the drug to the clot very quickly very directly

and you can do it in lower doses than systemic therapy alone the drawbacks are that there are actually no control studies for this there's no randomized control trials that have started everything is a case control series

maybe one institution versus another or within your own institution looking at several things or a registry which I'll show you a few of examples of different types of catheters our unify our Craig McNamara being the two most commonly

used another main mainstay and PE

- [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.

- [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.

- [Julio] And I appreciate the invitation from Dr. Veith. Those are my disclosures. The first time that I use a aortic occlusive balloon, it was actually not for endoluminal repair, it was done for a open repair, and that's important to know, because for those that believe that open repair is the way

to deal with ruptures, then this a tool that you can use to avoid decompensation on a patient. In my case, it was a life-saving technique. So the scenario of a rupture is really a challenging one. It demands quick and precise steps to avoid decompensation, and if you're planning

on using a aortic occlusion balloon, that might be time-consuming. So some tips to a streamlined decision and technique might be helpful here. Now, the first question is, since sometimes the placement of the balloon could turn into a difficult

and time-consuming task, a time to deal with small, calcified or tortuous iliac, we need to know who really need it. There is no guidelines available to assist you in that determination. However, we like to use the coronal view

of the CT scan because it give you immediately a glance of the magnitude of the retroperitoneal bleeding. We did a study in which we want to correlate this hematoma with the probability of survival and also to look into incidence of decompensation during the procedure, so we take this coronal view

and we divide this abdominopelvic region in nine segment. A line above the sac of the aneurysm, one at level of the bifurcation, and two vertical lines just crossing the psoas, a very quick determination that can be done. So we defined the small hematoma every time

the less than four segments of the bleeding is presented, and we found 20 patients with that category. The medium-size hematoma, four to six segment, and those we found 22 patient. The large hematoma was defined by seven to nine segments, and we included 15 patients in that category.

So besides that, we look into the condition of the patient, hemodynamically speaking at arrival, what was their response to the induction of anesthesia, and what kind of events we have during the procedure, talking about hypotension, shock, or even arrest. Although I don't have time enough to go in details

of the whole study, but I can forward to you the conclusion. The small hematoma, we don't see or witness any particular events of hypotension, so our conclusion is no balloon support is needed for this group. However, the large hematoma, we have events

that goes from hypotension to code arrest, so those patients always has to be supported, and I recommend that you use the balloon even from the very beginning. The medium-size hematoma, however, was an unpredictable group.

However, those that came with a hematocrit of less than 24, even though it seems to be hemodynamically stable and has no adequate volume resuscitation prior, I'm talking about here blood transfusion, those need to be supported as well. So once your determination on who should get the balloon,

the access has been presented before can be done under local anesthesia. And even though the ultrasound-guided technique becoming very popular, one of the technique that I use for many years is just do a small cut-down, a blunt dissection with my finger

getting to the anterior surface of the artery at puncture the vessel, but I can get to know that many patient with hypotension without palpable pulses, you can use ultrasound very well with those cases. The decision of going brachial versus common femoral

should be done beforehands by looking at the CAT scan. But in any case, a quick angiogram can be done in doubtful iliacs. Consider for those patients with the small iliacs, place the aortic occlusive balloon over the stiff wire. Never use a floppy or hydrophilic wire

because you will have your balloon pushed down by the pressure. The best iliac should be reserved for the EVAR unless the decision was made to open the patient. Immediately exchange for a quick stiff wire like the Lunderquist wire, and I believe

the long, stiff sheath should be at level of the visceral branches. That allow you for support and prevent the balloon to being pushed down by the aortic pressure. We believe that the preferred location for the balloon is the supraceliac position.

That allows for quick stabilization, and also it give you adequate room for the completion of the endografting. Once you've deployed the main body, a quick maneuver of moving the balloon from contralateral to ipsilateral side can be done.

In those that doesn't tolerate the deflation of the balloon because become unstable, avoid decompensating by using double balloon technique. A second puncture can be done in the groin to introduce a new balloon as well. Make sure that the patient is hemodynamically stable

before removal of the balloon, and having the sheath beyond the top of the graft is advantageous because prevent the endograft can get cuts by the hooks, the barbs of the bare metal of the endograft. Remember, the best outcome occurs

when the institution has in place an algorithm to deal with rupture aneurysms. Thank you very much.

[Mark] - Thanks Evan, thanks Dr. Veith for inviting me again this year. These are my disclosures as it pertains really to this talk, a major one being Centerline Biomedical. You know, what's all the really talk about why is there a whole session dedicated to this? Well this really has come about, this is a paper about

brain tumors for cardiologists that came up and there's really a call of an alarm. What is our exposure as interventionalists and what is our risk? If you look at things that have gone on, you can look at the explosion of endovascular procedures done by

vascular specialists. Those of us that do it a very wide, varied practice, are going to be different than those who do disease specific practices, and you can see there the amount of EVAR change has grown significantly over the years, not only for EVAR but also for Thoracic disease.

But really what we're talking about is what is our exposure risk, and you heard Lars talk to us about exposure in the operating room. The biggest portion of that exposure is scatter radiation from the beam as it comes off the patient. And you need to learn how to protect yourself and consider

its importanty. Obviously as the complexity of the procedure increases, that will increase as the body habitus of the patient changes that number increases. The more you get to an angled radiation exposure, that matters.

Now you can do some things to protect yourself. Obviously, the further you're away from the radiation source the lower it's going to be. But also the proper imaging can make a difference if you have your imaging intensifier upside down, and yes it does happen, I've been at places where this is.

You see how much significantly in the middle panel there, it increases your exposure. Not having the image collector down as far on the patient is a difference, and having appropriate lead shielding on the ground as you see on the far right, hanging all the way to the floor makes a difference in your exposure.

Now there are protective strategies, whether that's protective equipment, drapes or shielding. In the last session, you can see in the bottom middle, the red pad which are fairly inexpensive compared to some, that makes a difference. The anesthesiologist having a full lead shield there all

the way in front of them, makes a significant difference for them. In our institution, I do use a zero gravity suit. But what people also don't understand is that even not using the appropriate equipment the right way makes a difference. If you do not have side shields on your glasses, about 21%

of the exposure is going to come around the sides of those glasses, and in. And you can consider that a window into your brain, in terms of potential exposures. So you need to make sure that you have appropriate fitted glasses, and there are side shields on your glasses,

to protect yourself. Not only against cataracts, but also radiation exposure the the brain. Now as there have been studies on zero gravity, we actually had two zero gravities, one for myself and one for my partner which is typically the fellow on the other side

of the table when we do complex procedures. But they've looked at the 122 procedures here in zero gravity versus lead apron. And those people not familiar with zero gravity suit, it's a 75 pound lead suit suspended from a boom above you, so you're not wearing any lead when you don't need it,

and there's no weight on your neck and shoulders for the case, and it's much more extensive protection that covers you all the way from above your head, down to your ankles. And you can see here the decrease in exposure in the middle panel. The fold is anywhere from two to about five fold decrease

in radiation exposure. The problem if you talk to physicists, it's hard to prove because they make us wear our badges on the outside of the zero gravity suit, and if you do a double badge situation, it's 11% of your inner badge and 89% of your outer badge, so the most you could prove from a physicist is

a reduction of 11%. Now what about modern day badges? We are in the habit of not knowing about our radiation exposures until a month later, so what were you doing wrong, and when were you doing it wrong, gets to be a problem. Now with modern day badges that detect an early warning,

this is what happens. You can track your cases over time, you can see which day you had a higher exposure rate, and so these real time dose monitorings, allow you to adjust what you're doing in the operating room that can give you direct feedback, in terms of standing too close, standing on the foot pedal

too long for the radiation exposure, and changing your angle or not coning out your images makes a difference. But also we need to consider about a better way to do things. Center line imaging or center line biomedical has now a new system which they're developing.

Our current paradigm is ionizing radiation in 2d visualization. We need to consider moving to intraoperative positioning system, with a 3d interactive image and electromagnetic navigation. Catheters and wires will have censors on them, will allow

you to locate your wires and catheters inside the patient by using electomagnetic panel that sits below the patient. This is a porcine model where you take your CT scan preoperatively, fuse it just like you currently do with technology, but you take that image and you place it into a display imaging system.

This display imaging system connects in with electromagnetic navigation, and you can then track your catheters throughout the body and look at any view you want. In this case we're catheterizing the left renal artery, in a porcine model. From that, you can then do a final conformation angiogram

as you see here, to prove that you're in your left renal artery. So in conclusion, current advancements in vascular therapy significantly increase the exposure of aortic specialist to the harmful effects of ionizing radiation. Maximal efforts should be employed by proceduralists to

protect themselves. And future research should be directed at identifying non-ionizing methods for navigation and device implantation. Thank you.

- [Doctor] Mr. Chairman, dear colleagues, I have nothing to disclose. My only disclosure is that I might be recognized as being ambassador of one of the most beautiful region of the world. So ruptures of abdominal aortic aneurysms into the vena cava or into the iolaco veins

are rare clinical entities. The symptoms are those of ruptured aneurysms together with signs of congestive heart failure, or leg swelling. The diagnosis is often made clinically or confirmed by CT scan, as in this example.

The reported results of treatment were earlier more focused on open repair. During the last years, more and more papers advocated endovascular treatment showing lower mortality, but all these studies performed as cohort analyzers or in case reporters have poor evidence level.

The recommendation, however, seem to favorize clearly the endoscopic option showing lower mortality rates overall. If you treat an aortic AV fistula as in this example, with a shunt into the left iliac vein using a first step, a unilateral left sided

bifurcated scent craft. Here you see the case. And then the reconstruction after two days with the contralateral bifurcated graft, and an aortal biolextent graft, and the postop CT scan, then shows no evidence of Type I endoleak,

and no persistent AV fistula. The problem of course, seems to be resolved. You have no persistent AV fistula. But not in all cases, as shown in this example, the eventual Type II endoleak are isolated from the AV fistula, so if you have

the situation with the successfully fixed aneurysm on one hand, but a Type II endoleak in combination with the fistula in the cable vein or in the aortic vein on the other hand, what are you doing now? In the persistent AV fistula,

for Type II endoleak, in this very special situation, really is this really a bad thing or is it eventually helpful for aneurysm shrinking, and what about the clinical evidence of ongoing AV shunt? This is such an example of a patient with chest pain having had a syncope

with a CT scan showing the contrast media in the vein already in the early phase, as shown in this picture. In the lateral view and also in the transverse section, you see the fistula, obviously, despite very kinked aortic arteries in this example.

This was all done by IVAR pEVAR, and beside these very kinked arteries on both sides, the intervention could be done successfully by percutaneous approaches on both side. The intraoperative angiography, as you might see on the next slide,

showed initially the fistula in the vena cava and finally the Type II endoleak is still visible. Ilioac and lumber arteries, and the inferior mesenteric artery were responsible for the endoleak, as you can see here, but the patient showed an immediate relief

of all symptoms, and he could be discharged. After three months, the aneurysm sack shrinking was remarkable, and this continued also after nine months. It was shown that still the endoleak was obvious and the fistula was persistent, but the patient had no symptoms.

So what about these persistent AV fistulas? Should we treat them, for example, by venous sealing, as recommended by a few authors? No complication of strombosis of the venous stent grafts are reported, and together with other groups, we recommend clearly not to do this,

and to make any effort and not to make any efforts to close the fistula when it's in combination with an endoleak Type II. The same observation was made here by Ferhaugae, a few years ago, and in this further study by Malina, one year ago.

They all stated despite, you could also say, it was rather mean, thanks to the AV fistula that was shrinking. So in conclusion, Mr. Chairman, after own experience, and after studying the literature. Can you go back, sorry?

And studying the literature, we are all convinced that EVAR as the preferred option in ruptured triple a with AV fistula, venous ceiling on treating the endoleak Type II should not be aimed. In contrary, in endoleak Type II persistent AV fistula might be helpful for aneurysm sack shrinking,

and peak pressurization of the aneurysm. Thank you.

- [Gerry] These are my disclosures. When it comes to ilio-femoral deep vein thrombosis, many of us feel that is the most important area to treat. And some of us feel that the inflow is very important, in which case, you've got to worry about it. But if you feel that the inflow doesn't matter at all, then you can forget about it.

So that's for those of you who aren't from New York, that was my Irish accent on a New York, forget it. This is one of the ways to get into the below-knee veins, posterior tibial venous access. It looks quite easy, it's not quite so easy. Although there's two veins side by side,

you typically only get one chance at one vein because the other one goes into spasm. Pardon me, very sensitive mouse, like myself. You choose your wire of choice. I quite like the ED3 Nitrex. And then confirm that you are inside the veins,

because that happens all of the time to me. Those are funny looking veins because I've managed to puncture the artery. And which brings up one of the pitfalls, try not to puncture the artery. If you do manage to get into the vein,

you then insert a catheter and a catheter-directed thrombolysis after that is fairly standard. There's a few little tips and tricks in terms of stitching it in, using a small sheath is possible.

Heparin through the sheath, and then TPA through the infusion catheter. If you are fortunate enough to have the right length of catheter for the thrombus, then you can leave it at that length. Otherwise, you can pull it back

by 10 or 15 centimeters per day. And it typically takes three days to perform catheter-directed thrombolysis in this region. We always put on compression stockings, which sounds fairly basic, but it's important because it means that things don't get pulled.

And curious house officers and doctors don't have a good look at it and pull the whole thing out. Or the patient, for that matter. That's posterior tibial vein access, fiddley, tricky, easy to get into the artery, spasm is coming. You can do it with pharmaco-mechanical thrombectomy

using a 6 French device. The only one that I'm familiar with would be the AngioJet Solent, and not the newer Zelante. Views of the West of Ireland, not from this morning. Then if you want to switch tracks, how else can you get into the deep veins

of the lower extremities? Well, we're talking about improving the inflow, so we're going to now try and go from above and below. This is a patient with massive deep vein thrombosis. You'll see in just a second now. Thrombus starting here,

occlusive thrombus going to the profunda, occlusive thrombus down into the femoral, duplicated femoral vein, and then, most importantly, it goes into the below-knee popliteal. You might say why does this matter? Why do you care about the popliteal at all?

Well, I'm a bit old-school. I do believe that inflow matters quite a lot. Pardon me. So you can see a thrombus starts just here, a rather unusual place for a thrombus to start. Typically it starts much higher in the common iliac vein.

You can see it goes into the profunda femoris here. That's quite important technically, because the profunda is a very important vein in terms of long-term patency of the segment. And you can also see, lordy me, that it goes into the below-knee here as well.

This is what we call criss-cross. Fairly standard, fairly straight-forward, back of the knees, catheters into the popliteal vein from above and below. It sounds very easy, it's actually surprisingly difficult. The problem is that although you start very far apart, your two needles tend to approach

and you tend to puncture the vein in almost identical position, time and time again. So you have to start what feels like an awfully long way apart, in order to get some clearance between the two catheters. This is what you look like

when you're going to start catheter-directed thrombolysis. And what we're doing now, is we start catheter-directed thrombolysis at the bottom end, while working on the top end. The bottom sheath, rather the sheath facing inferiorly, is 6 French, with an infusion catheter

which is typically 20 centimeters long. And then this is a 10 French sheath going north. And through that you can perform AngioJet or whatever your thrombectomy device de jour is. Now this is an initial venogram of the below-knee veins and you can appreciate that there's very little inline flow

going from south to north. And you're seeing a whole lot of collaterals and very little flow going north at all. Pardon me. AngioJet works well here, although there are a variety of thrombectomy devices.

Then I must say I'm a big believer in aspiration. And you can get quite aggressive with a curved 8 French catheter. It sounds very basic, works very well. It's particularly useful, again, to go back to the profunda femoris inflow,

as well as the internal iliac. So this is what it looks like after aspiration. And you can see a rather unusual stenosis. And then, obviously, you need to go on to treat that. We start with our stent at the top to cover the iliac vein compression point,

and then carry on down here, and add a further stent down at the bottom. The inguinal ligament, I don't think is nearly as important as others feel. I think you you have to stent from flow to flow. And you can see that the final flow we've got here

at the end is quite satisfactory. Now this is when I say at the end, this is the end of the above-knee treatment. 'Cause you still haven't dealt with the below-knee veins. So you get your catheters running overnight, and you've got thrombolysis going north and south.

So this is your sort of set-up, your 10 French sheath going north with a catheter through it. A drain fix is quite useful for those of you who have access to that, to keep the catheter in position. And similarly going south, like this.

And this is what it looks like below beforehand, and this is what it looks like afterwards. You might think well, that doesn't really matter very much, but the popliteal vein will guarantee the success of your treatment. If you do not have a patent popliteal vein, in my view,

your success long-term is going to be much more guarded. And then, this is what it looks like from below, and the next morning. You can also appreciate that there's quite significant inflow now from the profunda. You can see the mixing just there, at the top up here.

So you've now guaranteed an inflow from above and below, but it takes two days, typically, because you've got to work one day on the above-knee segment and the second day on the below-knee segment. So could you move it on a bit?

Again, Galway, but not this morning because it was raining. You can do it as a single session criss-cross, so this is very similar to many of the arterial thrombectomies that you perform. I specialize in big, swollen, purple legs,

save the Speedos, they're not mine. But he's got a very, very swollen right leg. Rather unusual when somebody presents with a right leg tense phlegmasia. It starts to get me wondering, why should he have a right leg phlegmasia?

No specific reason. Left, obviously, would be straightforward. A CTV again, heading south here. Nothing really specific there, but you can appreciate this leg is very tense indeed. And there's thrombus in the femoral,

and most importantly, it goes down below-knee again. So you've got no inflow into your popliteal segment. If that popliteal vein is opened, it's a straightforward one hour, one and a half hour procedure. With a thrombosed popliteal vein, it's more difficult.

So here's the view of the external iliac vein, and here's the longitudinal curl reformat, showing A, a very swollen limb, and B, the length of the thrombus. In this case, again, you'd use the same criss-cross technique.

But this time, we were going to attempt a thrombectomy above and below. And starting off, you put a little catheter in here. Niggle it down as far down as you can, and just flush inject five, 10 milligrams of TPA while you're setting up your thrombectomy device.

That usually takes a few minutes. And in that meantime, you then can get to work. And this is just after five to 10 minutes of tissue plasminogen activator. You opened up some segment here. Then you get to work

with, as it happens in this case, the AngioJet. Not perfect, because our puncture points are very close to each other, but you can appreciate that we do have rapid inline flow. And this is over the course of 45 minutes or so. We're now up to about an hour

with, I think that's a Cook Zilver venous stent going from south to north. And this is his CTV, with a filter in situ. At six months, he has a widely patent vein. And the same on the sagittal reformat. You can appreciate that the stent is widely open.

In summary, there's pros and cons to both. First of all, you have to believe that the popliteal vein matters in terms of inflow. I do, I believe that inflow matters in terms of most vascular procedures. CDT is less labor intensive but costs more,

and there are the risks of thrombolysis. Pharmaco-mechanical thrombectomy is faster, and you can do all of your work in one go. But it certainly takes two hours of your time. Posterior tibial vein is more difficult than it it looks. There's lots of ways to skin this particular cat

and Fabritzio and I wrote a little book last year. If you're interested, you can learn more. Thank you so much.

- [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.

- [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.

- [Narrator] I'd like to thank Dr. Veith and this symposium for being able to talk on this subject. I have no disclosures. When it was discussed in the last section, when we get this, preferentially in our institution, we attempt to repair ruptured aneurysms endovasucularly. And, as we all know, ruptured triple A's are,

they're a surgical emergency and a fatal surgical emergency at that with a overall mortality of approximately 80%. In the U.S., it ranks 12th to 15th, depending on the year, as the overall cause of death. Traditional treatment of ruptured aneurysms

has been open surgical repair, but over the last decade EVAR has become the preferred treatment modality. EVAR, as we all know, was introduced in the late 80s. Evolution of endovascular technology and increased surgeon comfort with EVAR

has made it the treatment of choice for ruptured triple A's in many institutions. Studies suggest that patients with EVAR for ruptured triple A's have higher secondary intervention rates both early and late. So, type two endoleaks after elective EVAR,

management is somewhat unclear. And the natural history is not all that well known. We don't know which type two endoleaks will go on to cause problems and which will not. The management of type two endoleaks is generally determined by the behavior of the aneurysm sac.

In the elective setting, delayed rupture of EVAR is rare. Approximately 80% of all type two endoleaks will spontaneously resolve in elective EVAR within six to twelve months. Type two endoleaks in a setting of an intact aneurysm are treated, generally, if the sac enlarges 5 millimeters

or if it persists for more than six months. Type two endoleak after EVAR for ruptured aneurysm is somewhat different. The aneurysm sac is disrupted in this situation and the blood is not contained within the aneurysm itself. The lack of aneurysm sac integrity can result

in expansion of a retroperitoneal hematoma in the presence of a type two endoleak. This can result in continued hemorrhagic shock or abdominal compartment syndrome. About 30% of EVARs ruptured triple A will have associated with them

a type two endoleak on completion angiography. Most type two endoleaks are treated at the time of repair or shortly after EVAR for ruptured aneurysms. Approximately one quarter of type two endoleaks will not be seen on completion angiogram, but would rather be visualized later on CT follow-ups.

We're missing a good 20% of them on completion 25% of them on completion angiogram. Treatment of type two endoleaks in EVAR for ruptured aneurysms prolongs operating time in the generally unstable, hypothermic, and coagulopathic patient.

These patients might be better served, rather than spending the extra time to embolize the type two endoleak, they might be better served in the ICU being rewarmed and resuscitated. Treatment of type two endoleaks should be reserved

for patients who deteriorate or have expansion of retroperitoneal hematoma or expansion of the excluded aneurysm sac. But, how often does this occur? We noted that practice is widely variable even in our own group as what we do

with type two endoleaks after ruptured aneurysm. So we decided to take a look at this. We did a retrospective review of EVARs ruptured aneurysms from two larges tertiary centers, the University of Michigan and Dartmouth. We took a look at comorbidities, anatomic variables,

and operative details and our primary outcomes were the presence of a type two endoleaks, reintervention, delayed aneurysm rupture, and aneurysm-related death. We had 56 patients over a 13 year period. The mean follow-up was 634 days. We found 21% had type two endoleaks on completion angiogram,

with an additional 7% detected on CTA later. The Iliolumbars were the source in the vast majority of cases. And of the 14 patients that went in immediate postop CTA, 43% had already sealed their type two endoleak and 36% underwent surgical embolization

upon surgeon preference. Only one patient for ongoing anemia. But in this group, there were no sac enlargement, delayed rupture, or the need for graft explantation in the entire cohort. These are our patient demographics

for patients with endoleaks and patients without endoleaks. There's no difference except for BMI. The larger the BMI the more likely you were to have a type two endoleak. Anatomic variables such as concurrent iliac aneurysm, thrombus at the IMA or at the level of the aorta,

or device did not correlate with the presence of endoleak after ruptured aneurysm. And the post operative variables, the only variable that came out was associated with type two endoleak after ruptured EVAR was pneumonia.

And the overall mortality was not different over the entire timeline of the cohort. Conclusions, type two endoleaks after EVAR is relatively common. The natural history of these appear to be surprisingly benign.

Early CTA prior to discharge may identify type two endoleaks that you may not see on completion angiogram. 50% of type two endoleaks for EVAR will spontaneously seal in the postoperative period and those that remain do not appear to increase the risk of sac expansion or rupture.

And, a conservative approach to type two endoleaks in ruptured EVAR may be warranted. Thank you very much.

- [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.

- (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.

PE the first one of course is

anticoagulation so heparin and bridging the patient to coumadin or now aid a direct oral anticoagulant is really the mainstay of treatment most patients again 55 percent of patients with PE have low risk PE all of those patients

should be on according to the chest guidelines three months of anticoagulation so they're gonna get heparin as an inpatient if they even need it and they're gonna get sent home on lovenox bridge to coumadin or they're

gonna get the one of the new drugs like Xarelto or Eliquis but here's all the other things that we do so these patients that are in the intermediate high risk so I'm gonna try to keep saying those terms to try to kind of put

that in everyone's brain because I think the massive and sub massive PE is what everyone used to talk about but we want to keep up with our colleagues in cardiology who are using the correct terminology we're gonna say high risk

and an intermediate but in those patients - intermediate high risk or Matt or the high risk PE patients we're gonna be treating them with systemic thrombolysis catheter directed thrombolysis ultrasound assisted

thrombolysis and maybe some real lytic and elected me or thrombectomy there's other techniques that we can use for one-time removal of clot like rotational and electa me suction thrombus fragmentation and then of course

surgical mblaq t'me so when anticoagulation is not enough so I like to show this slide because it shows the difference between anticoagulation and thrombolysis they are very different and sometimes I think everybody in this room

understands the difference but I think our referring providers don't and so when we when we get consulted and we recommend anticoagulation they're like yeah TPA well that's not the right thing so anticoagulation stops the clotting

process so when you start a patient on a heparin drip they should theoretically no longer before new thrombus on that thrombus so when you have thrombus in a vessel you get a cannon you get a snowball effect more

and more thrombus is gonna want to form heparin stops that TPA however for thrombolysis actually reverses the clouding process so that tissue plasminogen activator or streptokinase or uro kindness will actually dissolve

clot so there you're stopping new clot forming versus actually dissolving clot anticoagulation allows for natural thrombolysis so your body has its own TPA and so when you put a patient on heparin you're allowing your natural

body defenses to work you're giving it more time TPA accelerates that process so you give TPA either systemically or through a catheter you're really speeding up that process anticoagulation on its own has a

lower bleeding risk you're putting a patient on heparin or Combe it in it's it is less but it is still real thrombolysis however is a very very high bleeding risk patients when I when I consult a patient for thrombolysis I

tell them that we are about to do give them the absolute strongest blood clot thinning agent or an reversal agent which is the TPA and we're gonna just run it through your veins for hours and hours

um and that sort of gives them an idea of what we're doing anticoagulation in and of itself is really not invasive you just give it through an IV or even a pill thrombolysis however is given definitely through an IV through

systemic means and a large volume there thereafter or catheter directed so again

- [Timothy K. Liem] Thank you, I wanted to thank Doctor Veith for inviting me back. This a low-tech solution, I have no high-tech things on radiation or imaging or anything like that. I would like to describe for you our experience with regard to our attempts over the last several years to reduce our rate of postoperative hemorrhage and hematoma.

I have no disclosures. Back several years ago in 2012, we came to the recognition that we had a high rate of postoperative hemorrhage and hematoma in our vascular surgery patients when compared to other university hospitals

and other major medical centers around the country. When attempting to identify the potential causes for this Red Dot or high outlier status with regard to postoperative hemorrhage and hematoma, we looked for potential causes. They included capturing the wrong patients

because these are codes and DRGs, or perhaps we are not capturing patient co-morbidities accurately. And lastly, the focus of this presentation, our utilization of postoperative and perioperative anticoagulation for VTE Prophylaxis, bridging anticoagulation, or perhaps overaggressive initiation

of therapeutic anticoagulation during the perioperative period. First looking at our VTE Prophylaxis patterns. When looking to see if we were complying with the best medical evidence, we had to look back at data that was 10 to 30 years old,

and based on this information we came to the conclusion that perioperative low-molecular-weight heparin compared with unfractionated heparin is associated with a lower rate of VTE, but with more bleeding 4 to 11%. Postoperative low-molecular-weight heparin is effective without increased risk of bleeding,

and postoperative low-molecular-weight heparin is as effective as preoperative dosing but with less bleeding. So when we looked at our pattern of VTE Prophylaxis at our institution, we were actually complying with the best medical evidence.

Then, looking at whether or not we were being overaggressive with perioperative bridging anticoagulation for patients who were on chronic anticoagulation. We first looked at the CHEST guidelines which gives us a scheme or a chart which breaks down and categorizes patients

into high risk, moderate risk, and low risk for perioperative arterial and venous thromboembolism and then looking at the common indications for them, such as mechanical heart valves, atrial fibrillation, or venous thromboembolism treatment. The CHEST guidelines basically

didn't have much data to go on, they said basically that for patients at low risk for thromboembolism that you should not give bridging anticoagulation, just stop the Coumadin or the direct anticoagulant. For patients at high risk for venous

and arterial thromboembolism that you should give bridging, but that was not based on much data. The meta-analysis in 2012 of a large number of single-institution studies show that when comparing bridging with no bridging anticoagulation that there was no difference

in perioperative thromboembolism. But perioperative bridging was associated with a three to fivefold higher risk of perioperative bleeding. That was all based on retrospective single-institution studies. Then came in 2015, the first perspective randomized trial

looking at bridging for atrial fibrillation, randomizing patients to receive low-molecular-weight heparin bridging versus placebo. In this study, they identified that forgoing bridging anticoagulation was not inferior to low-molecular-weight heparin for prevention

of thromboembolism, but it was associated with a significant decrease in major and minor bleeding around the time of surgery. The limitations of this study were that only 3% of these patients had CHADS classification of five or six, and only 11% had major surgery.

Then came another study which is currently being conducted, it's called perioperative two, and this is specifically looking at patients who are high risk, prosthetic heart valves or high risk atrial fibrillation or atrial flutter, randomizing patients to receive

either low-molecular-weight heparin or placebo. This study is ongoing, but it should give us more data in the next year or two with regard to these high risk patients. I'm sorry, that was for Vitamin K antagonists, how about our increasing number of patients

who are being put on direct anticoagulants like Dabigatran, Rivaroxaban, and Apixaban? There is no perspective randomized trial looking at how to manage these patients around the time of surgery, but in the retrospective looks at the original trials, heparin bridging in patients did not confer protection

against thromboembolism, but was associated with a higher risk of bleeding. So that gives the authors of the CHEST guidelines some data to basically give us some guidance, and say that for patients who are taking direct anticoagulants, that bridging is not necessary for high risk, moderate,

or low risk individuals, and that warfarin can be used in high risk patients but it is not necessary for moderate and low risk individuals. The dosing guidelines are also being described by the CHEST guideline authors regarding when to discontinue, and when to resume it afterward.

The last situation I'd like to describe is the initiation of postoperative anticoagulation in the absence of bridging. We often were too aggressive at giving anticoagulation too early on on postoperative day zero for patients with lower extremity ischemia. We have since gone toward mini-dose heparin

of 500 units an hour, or prophylactic dosing, and not transitioning to warfarin or a direct anticoagulant for two or three days. What that has allowed us to do is with a significant concerted effort to reduce our perioperative bridging anticoagulation

and reduce our acute postop day one and postop day zero anticoagulation that has then allowed us to significantly reduce our perioperative hemorrhage and hematoma rate and so that makes our hospital administrators very happy since we have no more red dots.

Thank you.

so I'm gonna show an example this is a 57 year old male who presented with a dis neo

he had World Health Organization functional class 3 meaning it's significantly affected his life he can't walk up the flight of stairs really tired walking from the parking lot of his favorite restaurant back to this car

can't really walk around the grocery store he had a history of DVT and PE also had afib he actually went to the ER and was diagnosed with upper respiratory tract infection which many of these patients are they've put him on

antibiotics then for pneumonia he had a VQ after one of his doctors just felt like he just wasn't getting better and it found multiple mismatch defect I'm sorry I don't have those pictures he was actually started on home oxygen after

all of that work up it was found that he had CTF and this required I think three different hospital visits and every time got kicked up to sort of a higher acuity place and then he ended up at our place so these are his pulmonary angiogram

images here I don't know if I can play these but the still images kind of show you that the images on the right show that there's basically no vessels going out distally so I mentioned pruning of vessels there's no branches in the right

upper lobe if you look at the right lower lobe at the tip of the catheter there's areas of stenosis right where the segmental arteries start and on the left you can see that the left pulmonary artery is denuded essentially the entire

left upper low branch is excluded by a rim of thrombus and in the left lower lobe the image on the bottom my bottom right there's actually no branches going to the left lower lobe into the lingula so this is a patient that has had very

bad CTF their main the pulmonary artery pressures are listed there of 77 where the normal high is 25 so three times the normal pulmonary artery pressure so this patient went on to an operation so the image on the right the photograph is

actually the clot that they removed from the operation and that patients pressures improved from 77 to 22 immediately after the operation so they go to the ICU they have a swan-ganz catheter left in place and you can

measure their pressure right afterwards and you can see that that clot they grabbed it it looks like a bunch of fingers well what they do is they crack the chest open like with a mini sternotomy they make an incision in the

pulmonary artery after they put them on bypass and then they basically grab they use they're a little deBakey's the DeBakey forceps and they grab this little elevator and they just start scooping

out the clot and they try to grab it as one big piece take it out and then you get that nice photograph on the side if they break off pieces it's actually worse because that's an area that a pulmonary artery dissection can occur so

it's a very complex operation but you get very nice results and afterwards these patients are sent home usually on lifelong anticoagulation thereafter so

- [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.

- [Dr. Natzi] This is my disclosure. The frequency of neoplasia in triple A patients is reported to vary between 0.5% to 26%. Already 15 years ago, as a Evar Trial Investigators and DREAM study Group, also observed an increase infrequency of the neoplasia in the heart triple A patients.

Currently we are interested in the association of triple A and neoplasia. In our study, we are following 187 consecutive patients referred to our department with confirmed triple A, initial with negative PET-CT for cancer. And it concern also 563 controlled patients

with Coronary Artery Disease. Patients were followed up for 96 months. And, at baseline, all patients were free of cancer. The Primary endpoints of our study were the occurrence of neoplasia within 96 months followup and neoplasia free survival defined as the time difference

between occurrence of neoplasia and baseline. When we look to characteristic of the patients, we found some known differences in triple A group versus control. But, interestingly we found increased level of CRP level in triple A compared to coronary artery disease patients.

The 96 month incidence of neoplasia was significantly higher in the group of triple A compared to Coronary Artery Disease. And the type, the lung, and digestive, and urologic cancer, and the measure of cancer detected during followup. When we look, the incidence of neoplasia

with respect to triple A treatment, there's no differences between patient non-operated and operated patients as well as after EVAR and Open Surgery. When we look after neoplasia free survival in Coronary Artery and triple A patients, we can see

significant difference out of the neoplasia free survival for triple A, and control group as well as Walloon population expected for neoplasia free survival. We obtained these results from Belgium Cancer Registry. When we looked, the relative risk of neoplasia in triple A vs coronary artery disease according to baseline CRP levels,

once again we observed significant incidents of neoplasia in patients with high CRP levels. On the other hand we know that triple A is a Chronic Inflammatory Disease with associated increased metabolic activity in the aneurysmal wall. And more recently, in our paper published a few years ago,

we observed an increase in MMP1 and MMP13 and some chemokine in patients with positive PET-CT in the wall and the serum of the patients. And during this study we also observed increased level of CRP in the serum of the patients, especially with positive PET-CT.

We were interested in the CCL18. CCL18 is a chemokine which is also involved all kind of pathological processes, especially in the cancer. And during this study, we observed an increased level of CCL18 in serum and the aneurysmal aortic wall. We are interested also in microRNA, and during this study we

observed the down regulation and up regulation in some microRNA, which are involved in the development of the aneurysms and rapid growth. But, some of these microRNA also play a major role during the development of the cancer. (reads conclusion verbatim)

Thank you very much for your attention.

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