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The Altura Double D Endograft Device For EVAR: Advantages, Limitations And 4-Year Results
The Altura Double D Endograft Device For EVAR: Advantages, Limitations And 4-Year Results
Altura stent graft systemEndovascular stent graftLombard medicaltherapeutic
Transcript

- [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.

- Yeah, thank you very much. Unfortunately Dierk Scheinert couldn't come, so thankfully he's allowed me here to take this presentation over so thanks a lot for this. So these are the latest 5-year results of the INCRAFT device from Cordis Devices currently under FDA review not yet approved

in the US, but in Europe. These are the conflict of interests, this is (mumbles). So this device is a three-piece modular system, low porosity polyester. You can bilaterally in-situ length adjust it up to 3cm. And the main feature I think with this device

is it's a low-profile device, 13 Fr inside 14 Fr outside except the biggest body which has an outer diameter of 16 Fr. The innovation study that was 60 patients, you can see here some objectives. So the question was whether you could deploy it

accurately where you wanted to have it without any type I, III, and IV endoleaks and of course there were also some other primary and secondary endpoints and again follow-up had to be done up to five years. This is a busy slide just showing you,

please look to the right side, to show you that there were quite some violations of the recommendations in which kinds of anatomies to implant this craft. Here for example neck lengths less than 10mm, here were some patients implanted.

Also angulations over 60 degrees, three patients, there were some thrombus in the neck, and here you can see aortic bifurcation smaller than 18mm, there were quite some patients and especially the iliac sealing length was shorter than 10mm in nearly 50% of the patients

and also the diameter of the external iliac arteries were nearly 50% lower than 7mm. Here the freedom from endoleaks type I was one at 30 days which has been resolved and another one developed after 30 days which also has been involved. No type III.

Stent graft patency after 30 days also 100% and otherwise also no other adverse events with this device at thirty days. So to answer the question with this device to the first question of (mumbles) will lighter fabrics and stent material decrease EVAR durability?

Will there be more endoleaks I, III, or IV? You can see here the long-term data so no Ia endoleak developed over four and five years, there was one Ib endoleak which developed at four years which also was apparent at five years. No type III endoleak.

One graft patency failure with a (mumbles) occlusion here at four years which also was here at five years. No migration, one fraction of the (mumbles) proximal third graft, otherwise it was very safe. You can see here once again the Kaplan-Meier curve for type I endoleaks through five years here

with type Ib here later on, and this is the patency Kaplan-Meier curve also showing here the good patency at five years, and this is freedom from second large vent. Here I don't have any data whether this is type II endoleak or not so this still has to be reported and clarified.

So to conclude the INCRAFT performed well on long-term while overcoming more difficult access morphologies. The endograft can be utilized in patients with demanding access and vessel morphology, and there are more studies ongoing.

There is one in the US and Japan where we wait for long-term data, 190 patients and also from Europe's 180 patients also there we still wait for long-term data. 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.

- I'd like to thank Dr. Veith for allowing me to come back to present here. I have no disclosures. A recent large study, retrospective study from Canada looked at the bleeding complications associated with oral anticoagulants, and they identified that there were

significant differences in the patterns of bleeding when compared to the DOACs with Warfarin. Patients receiving Warfarin had a slightly higher rate in intercranial hemorrhage and hematuria, whereas patients receiving DOACs had a significantly higher rate

of gastrointestinal bleeding. In their review of the treatment patterns for these bleeding complications, the patients receiving Warfarin had a significantly higher rate of a Vitamin K administration as would be assumed

and prothrombin complex concentrate administration significantly higher than in the DOAC group. The DOAC group did because they had a higher rate of GI bleeding. Probably had higher rate of packed red blood cells transfusion as well.

Their treatment patterns were in general agreement with generally accepted practice guidelines for Vitamin K antagonist-associated bleeding and that includes for non-major bleeding Vitamin K administration, transfusion of blood components as necessary

for red cells and platelets as necessary but for major bleeding a slightly higher rate of Vitamin K administration, and then the Kcentra, or the 4-factor prothrombin complex concentrates which are administered on a dosing

which depends on the patient's initial presenting INR. The cost of a 4-factor prothrombin complex concentrate's average wholesale price is about $1.20 to $1.60 per unit which equates to about $2200 to over $5000 per treatment for patients receiving Kcentra. This is in contrast to patients receiving FFP

with a cost of about $1600 per patient. We, in our institution, tend to underutilize the 4-factor prothrombin complex concentrates despite their advantages. The advantages of the 4-factor PCCs for reversing Vitamin K antagonist-associated bleeding

include much more effective hemostasis, much more rapid INR correction, 62% versus 9% for plasma, and then median total volume which was significantly lower with the 4-factor PCCs compared to a much higher volume needed to resuscitate and to reverse the INR, fairly ineffectively, in the patients receiving plasma.

Now moving a little bit on to the direct thrombin inhibitors and the factor Xa inhibitors. They are ubiquitous in our practices in vascular surgery and cardiology. That's just going to increase even more with the recent FDA approved indication

for major cardiovascular event reduction in the patients with PAD. Fortunately, the patients receiving DOACs have a somewhat lower rate of bleeding complications compared to the Vitamin K antagonists, although that's not zero.

I'll go a little bit into the specific reversal agents for the DOACs. The first of these being Idarucizumab which is an antibody fragment directed against Dabigatran. It has a dosing, which is fairly simply, of five grams of intravenous bolus

with an additional five gram intravenous bolus which can be administered if there's ongoing bleeding. It's a fairly short half-life, 47 minutes. The cost of this medication is fairly similar. $3600 to $3800 dollars per dose for these patients. The benefit of this is that it actually

irreversibly binds to the Dabigatran and increases the illumination of that medication. I will just very briefly go into the clinical studies that led to the approval of Andexanet. Patients, basically 67 patients, who had major bleeding, gastrointestinal bleeding, intracranial hemorrhage,

and there was, in brief, just a very significant robust reduction in the factor Anti-Xa activity approved in May of 2018. It is used to treat Rivaroxiban and Apixaban. It has a fairly complex dosing protocol which is dependent on the type of

DOAC which is being administered. The last dose and the last timing for the last dose. The cost of this medication is way out of the ball park compared to the other medications. $3300 per 100 milligram vial equating to a low dose infusion of $26000

and a high dose infusion of $59000. CMS does allow for additional payment of $14 to $15000 per patient, but that still does not counteract that significant cost. There is also the problem with regard to the rebound activity which occurs at

four to six hours later. So I'll briefly go into the CHEST guidelines which just came out in August of this year saying that for minor bleeding, NOAC, and Vitamin K bleeding you just reduce the dose or decrease it. For moderate bleeding, transfusion as necessary

and consider charcoal for Dabigatran, and for severe, life-threatening bleeding consider the specific anticoagulant reversal agents. However, I predict that our hospitals over the next year are going to be grappling with who will be doing the approval for these medications

and how many will be administered at any one time point. Thank you.

- Thank you Mr. Chairman. Thank you, Dr. Veith for you kind invitation. Okay, there we go. Excuse me. DEVASS stands for Dutch EVAS study Group. We all know that women have a twofold, increased risk frequency of rupture.

The average aortic size at rupture is five millimeters smaller. They have a higher rate of undiagnosed cardiovascular diseases. They have smaller ileofemo

more concomitant iliac aneurysms They have a more challenging aortic neck. Smaller proportion is eligible for EVAR and, therefore less likely to meet EVAR IFU. They have a longer length of hospital stay after EVAR, a higher re-admission rate, more major complications,

a higher mortality rate. So, women and AAA is a challenging combination. The rationale behind EVAS is known to you all, I think. The DEVASS cohort is from three high volume centers in The Netherlands. It's a retrospective cohort of 355 patients,

included from April, 2013 to December 2015. So I have two years of result data. If you look at the baseline characteristics, 45 females were in this cohort, with the age of 76 and with some known comorbidities. They were within the instructions for use of 2013, at 28.9%

and even less in the IFU of 2016. These are some more anatomical characteristics with the AAA outer diameter 5.6 centimeters. This is the procedure, most of the patients were under general anesthesia, with the cutdown and the procedure time

was about 100 minute. Straight forward procedure 33 cases out of these 45. Let's have a quick look at the clinical outcomes. The re-intervention's done in the first 12 month. One patient had to conversion to open repair at month 11 due to type 1A Endoleak, and the others were not directly

related to the procedure itself. Although, there was thrombus in approximate stand. In the second month we saw, in the second year we saw some more type 1A migrations and a Stenosis that needed relining, and two out of these patients were within IFU.

If you look at the total cohort of type 1A Endoleak, one patient was not operated on and the other were, either open conversion or relining, and one patient was within IFU. A quick look at the death characteristics. Only one patient was within IFU,

and died after open procedure. So the re-interventions, once again, the first year four patients, in the second year five patients. Conversion to open repair, in total three patients. Endovascular re-intervention was performed

in the first year in two patients and in the second year there were three relinings performed. Endoleak 1A, in total six as stated before. No type two Endoleak reported, and in the first year five patients died, which one was aneurisym related, as in the second year, two patients died,

which one was aneurysm related. If we compare this data with the EVAS Global data, of two years not the three year data, this is the freedom from all persistent Endoleak, close to 98% which is good. Freedom from type 1A Endoleak is within IFU, 97% in the global and outside IFU 85%,

and remind these patients 71% were outside IFU. Freedom from secondary interventions, we had to re-intervene in nine patients and its comparable with outside IFU. Freedom from mortality at two years, a bit higher, aneurism related mortality is 95% which is higher, and also the all cost mortality is higher in women.

So to conclude, this is the first cohort that focuses on women after EVAS. The majority of the patients was outside IFU, and as in EVAR women do not that very good in result, appear to be very much like an EVAR. Thank you.

- So I'll be talking about different bio-chemical profiles in both, inflammatory or non-healing and granulating wounds. Specifically venous leg ulcers. So, you've heard a lot about venous leg ulcers and there's a lot of treatments but, were going to look at some of the molecular differences that you can actually see in these wounds,

when we actually analyze some of the fluid. (clicking) Nothing to disclose. (clicking) Oop, I'm not going forward. Oh, there we go. So, actually, well go back to Bill Martson's work

with Stephanie Beidler and actually showed very early on that before compression there's a significant inflammatory component within these venous leg ulcers. This is by biopsies and then when these wounds are compressed, after four weeks

of compression, they actually reduce significantly a number of these cytokines and chemokines. As, well as increase the growth factor TGF-Beta. Indicating that, certainly, there's an inflammatory component but with compression, you actually change this to a healing component.

(clicking) We also evaluated work with Ferdinando Mannello in both inflammatory wounds and non-inflammatory wounds or non-healing wounds or granulating wounds in 32 patients and 16 granulating patients. These are all venous leg ulcers,

this is the demographics here. We analyze a number of factors cytokines, chemokines, growth factors and metalloproteinase. All by multiplex immunoassay. This is what the wounds look like before in the inflammatory phase.

I think you're very familiar with that. Then after debridement and after compression as well as interventions of the superficial system, this is what the wounds were looking afterwards. This is where we collected the wound fluid in these two different states.

We find the number of differences that were significant. And other individuals have also seen this. The red circles are actually the significant changes for inflammatory wounds, demonstrating the increase in interleukins. Interleukin-10,

which is actually an anti-inflammatory cytokine, but this is overly expressed in the inflammatory wounds over the granulating wounds. A chemokine IL-8, they're calling it Stimulating Factor Granulocyte Monocyte and also VEGF also consistent with what's

written in the literature, the VEGF's overexpressed in non healing wounds. What we did find actually in granulating wounds, that they expressed other things, specifically RANTES, which is very important in centralizing a number of these pathways

that's overexpressed in the granulating wounds as well as PDGEF factor BB, which is actually consistent again with the literature that PDGEF is actually a predictor of wounds that go on to heal. (clicking)

We then went on to also look at TGF-Beta, there's three different types of TGF-Beta. Three isoforms. And what we found that was significant is that TGF-Beta 3, which is not written too much about in the literature,

is significantly higher in inflammatory wounds. And why is this important? Because this is actually an antagonist to TGF-Beta 1. It actually causes significant inflammatory responses to take place, increases cytokines, increases metalloproteinase 9 and causes

the degradation of wounds leading to actually non healing. And we see that this was significantly elevated. Importantly, we found that endoglin is which is actually a co-factor for the TGF-Beta receptor was significantly elevated in granulating wounds. And that's significant because it has

significant anti-inflammatory properties by inhibiting the monocyte-endothelial activation. So, we found that this were significant changes. In looking at the proteases, we found that MMP-1, MMP-7 and MMP-13,

which are collagenases, and the stromelysin, were significantly elevated in the granulating wounds as opposed to seeing the degrading enzymes, such as, MMP-2 and MMP-9 and metalloelastase being higher in the inflammatory wounds.

Again, consistent with the literature, MMP-2 and '9,' which are the gelatinases, if you look at the literature, these are consistently higher in non-healing wounds. Oop, sorry, I think I went back there for a second. (clicking)

In looking at the TIMPs, TIMP-1 and '2,' are overly expressing in the inflammatory, which would be expected since they have a significant amount of protease activity. In TIMP-4 which is novel,

was overly expressed in the granulating wounds. Again, this could be a potential marker. Now, there's also the cytokines and the TAM/ligands, these are tyrosine kinase receptors and, the ligands for innate immunity. And just showing that there's actually difference,

both in inflammatory and non-healing wounds and granulating, or healing, wounds, both from the receptor standpoint as well as the ligands. Which again, shows that there's differences in innate immunity,

which could be a significant factor. Furthermore, like if you look at toll-like receptor 2, which again, also codes for innate immunity. In healing wounds all of these are decreased versus non-healing wounds. So, in conclusion,

there's significant expression of different cytokines and chemokines of growth factors in venous leg ulcers and wound fluid. The cytokines and proteinases have different signatures with in the healing state of a venous leg ulcer.

An innate immunity is also involved in a venous leg ulcer inflammation and healing. These could be specific, potential markers, but also pathways and possible targeted therapy for venous leg ulcers. Thank you.

- [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.

- Bill outlined why some of these trials fail. And there's so many pathways that are involved in the pathophysiology of venous leg ulcers. And I'm going to just talk about the proteins and the degradomes involved. And certainly you can talk about free radicals, you can talk about map kinases,

you can talk about TGF beta pathways, there's a lot. First some definitions. Proteomics, large scale study of proteins particularly their structure and function. The proteome is the entire set of proteins produced

or modified by an organism. In humans, just to give you an example, there's 27,000 proteins, that does not even include the ones that are actually post-translationally modified by glycosylation and phosphorylation and other mechanisms. The degradome, degradomics, aims to identify proteases

and protease substrates, the repertoires or degradomes of an organism wide-scale, identifying new roles for proteases in vivo. The study of degradome is directly related to measurement of enzymatic activities and will facilitate the identification of new

pharmaceutical targets to treat disease. So we actually did a review of analysis back in 2016, just to see what has been found in the venous leg ulcer, whether it was biopsied or whether it was wound fluid. And these are all the different types of

cytokines and proteins. There's ferritin, there's transferrin, there's hyaluronic acid, lactate, lactotransferrin, monoperoxidase, you go on and on and on. And of course, as I've mentioned, there's a number of cytokines and growth factors

that have been identified. And these are, whether they're cause and effect we don't know. But certainly we know they're present, they definitely have an influence, they've been measured,

and they've been associated with healing and non healing wounds. To go on, you can actually see some of these other proteins and proteases both serine proteases and metalloproteinase, and some of these things we don't even know what their function is, or what they're

doing in the venous leg ulcers, and that's really important. And again, here's further showing cathepsins and caspases and kallikrein, and different TIMPs. So all of these things have actually be found in venous leg ulcer wound, whether fluid or biopsy. This actually, probably a seminal article

that looked at, for the first time, the proteomics in patients with both healing and non healing venous leg ulcers. This was collected by wound fluid, it was analyzed by liquid chromatography and mass spectroscopy.

And what they identified was 149 proteins that had differential detection. In the healing there was 23 that were identified, in non healing 26. And actually they then looked at three proteins and analyzed a series of patients,

and these are the number of patients that they've analyzed, to evaluate. And this is what they found, a lactotransferrin S100A9 and the annexins have different expression whether you're healing or non healing. And that's important because these proteins

have some significance, and this is what their significance. Lactotransferrin is important in iron scavenging. And we know that free iron, if it's in the wounds, it's actually very toxic leading to different types of peroxides that are developed, and also cellular pathways that can be disrupted.

So annexins are also important in inflammatory response, and they play a significant role not in just wound healing, but also in the detriments of venous leg ulcers. And S100A9 is actually a calcium binding protein that has significance in wound healing also. So in conclusion it's actually very complex,

the proteomics and degradomics. But they provide an opportunity to study novel proteins, function, and activity in venous leg ulcer. They do provide some proof of concept and possible mechanisms of venous leg ulcer pathology. They identify possible biomarkers, both for

identification of wounds that go on to heal versus the ones that don't go on to heal, as well as treatment and prognosis. And obviously possible targets for therapy. Thank you very much.

- Good morning, I want to thank Professor Vitta for the privilege of presenting on behalf of my chief, Professor Francesco Speziale, the result from the EXTREME Trial on the use of the Ovation stent graft. We know that available guidelines recommend to perform EVAR in patient presenting at least a suitable

aortic neck length of >10mm, but in our experience death can be a debatable indication because it may be too restrictive, because we believe that some challenging necks could be effectively managed by EVAR. This is why when we published our experience 2014,

on the use of, on EVAR, on the use of different commercially available device on-label and off-label indication, we found no significant difference in immediate results between patient treated in and out IFU, and those satisfactory outcomes were maintained

during two years of follow-up. So, we pose ourself this question, if conventional endografts guarantee satisfactory results, could new devices further expand EVAR indication? And we reported our experience, single-center experience, that suggests that EVAR by Ovation stent-graph can be

performed with satisfactory immediate and mid-term outcomes in patient presenting severe challenging anatomies. So, moving from those promising experiences, we started a new multi-center registry, aiming to demonstrate the feasibility of EVAR by Ovation implantation in challenging anatomies.

So, the EXTREME trial was born, the expanding indication for treatment with standard EVAR in patient with challenging anatomies. And this is, as I said, a multi-center prospective evaluation experience. The objective of the registry was to report the 30-day and

12 month technical and clinical success with EVAR, using the Ovation Stend-Graft in patient out of IFU for treatment by common endograft. This is a prospective, consecutively-enrolling, non-randomized, multi-center post market registry, and we plan to enroll at least 60 patients.

We evaluated as clinical endpoints, the freedom from aneurysm-related mortality, aneurysm enlargement and aneurysm rupture. And the technical endpoint evaluate were the access-related vascular complications, technical success, and freedom from Type I and III endoleaks, migration,

conversion to open repair, and re-interventions. Between March 17 and March 18, better than expected, we enrolled 122 patients across 16 center in Italy and Spain. Demographics of our patient were the common demographic for aneurysm patients.

And I want to report some anatomical features in this group. Please note, the infrarenal diameter mean was 21, and the mean diameter at 13mm was 24, with a mean aortic neck length of 7.75mm. And all grafts were released accorded to Ovation IFU. 74 patients out of 122

presented an iliac access vessel of <7mm in diameter. The technical success reported was 98% with two type I endoleak at the end of the procedure, and 15 Type II endoleaks. The Type I endoleak were treated in the same procedure

by colis embolization, successfully, and at one month, we are no new Type Ia endoleaks, nine persistent Type II endoleaks, and two limb occlusion, requiring no correction. I want to thank my chief for the opportunity of presenting and, of course, all collaborators of this registry,

and I want to thank you for your attention, and invite you, on behalf of my chief, to join us in Rome next May. Thank you.

- Yeah, thank you Mr. Chairman. These are my disclosures. Well, we know that the Heli-FX EndoAnchor System provide fixation and seal in aortic necks, and it can prevent or resolve migration or endoleaks. It's important to have an even spacing around aortic circumference and

to resolve type 1A endoleaks, you need successful, of course, deployment of EndoAnchors and adequate penetration into the aortic wall. The objectives for this study was to quantify the EndoAnchor penetration into the aortic wall in patients undergoing EVAR

and to assess the predictors of successful penetration and to associate that with postprocedural type 1A endoleaks. We searched in the ANCHOR database, and we included patients that has been treated for a type 1A endoleak, and we had to have a good quality

first postprocedure contrast-enhanced CT scan without any artifacts due to metal or glue, and without implantation of adjuvant aortic extension cuffs or stents. And then we selected two patient cohorts, patients with successful treatment

after the implantation of EndoAnchors for a type 1A endoleak, and patients with a persistent type 1A endoleak after the EndoAnchor implantation. Well, this is to show how we determined the position of the EndoAnchors, this is a good penetrating EndoAnchor

more than two millimeters in the aortic wall. This is borderline, and this means there is still a gap between the endograft and the aortic wall or the EndoAnchor itself is penetrating less than two millimeters. And this of course, a non-penetrating EndoAnchor.

The good ones are green, the borderlines are orange, and the non-penetrating are flagged red. Here are results, the anatomical criteria to predict type 1A endoleaks, as you can see here, at the left, in the type 1A endoleak patients, there is a larger aortic diameter

with a median of 30 millimeters, and neck length is shorter, less than one centimeter, compared to the patients with no endoleak. Then about the EndoAnchor penetration, in the patients with a persistent type 1A endoleak, there are significantly more EndoAnchors

which are borderline or non-penetrating. What are the predictors for a successful EndoAnchor penetration. Well, protective factors, oversizing of the endograft compared to the diameter of the infrarenal aortic neck, and the use of the endurant stents.

Independent risk factors are the aortic diameter at the lowest renal artery, and five and 10 millimeters below more than 30 millimeters, a significantly neck thrombus and calcium around the circumference and also a more than two millimeter thickness.

Predictors for a type 1A endoleak, protective factors is the neck length more than one centimeter, and good penetrating EndoAnchors and risk factors for a type 1A endoleak is, again, the aortic diameter five millimeters

below the lowest renal artery more than 30 millimeters, and also boerderline and non-penetrating EndoAnchors and in this logistic regression model, a non-penetrating EndoAnchor is really predictive for a type 1A endoleak, or a persistent type 1A endoleak. A few cases, this is an excellent job,

there are four EndoAnchors placed, and they all penetrate well, although they are not circumferentially divided around the circumference. The majority of the problems in the patients in the ANCHOR database, if a persistent type 1A endoleak

is mainly due to an incorrect indication, these are EndoAnchors red and orange, non-penetrating and borderline. That is because they are above the fabric, or they are in a no-neck aneurysm, so the indication is not correct.

This is again, a patient with an undersized endograft, of course, the EndoAnchors will never penetrate the aortic wall at a post-serial part of the aorta. This is another example of misdeployment, a huge load of calcium and thrombus, and again, to defined a no-neck aneurysm,

and again, well it's obvious that the EndoAnchors will not do their job. These are then the EndoAnchor distribution in successfully treated type 1A endoleaks at the left, 332 EndoAnchors, but if you select only the patients

with an EndoAnchor which are inside recommended use at the right, you can see that more than 90% of those EndoAnchors are good penetrating. Here are the patients at the left with a persistent type 1A endoleak, 248, and you can see the majority is red or orange,

and that means that majority of those patients had an EndoAnchor deployment beyond the recommended use. So to conclude, good EndoAnchor penetration is less likely when there is large aortic diameter, the EndoAnchor is not perpendicular to the stentgraft during deployment,

and it's beyond the recommended use, more than two millimeters of thrombus, not in the infrarenal neck, or a gap more than two millimeters. And in borderline or non-penetrating EndoAnchor, it's predictive for a type 1A endoleak.

Thank you very much.

- Thank you very much for the opportunity to speak. I will admit that I don't think we've got it all figured out, yet. But we'll go ahead anyway. So, persistent type two endoleaks do occur with some regularity and only about a third of them will resolve spontaneously, but fortunately

rupture is rare. A persistent endoleak with a sac expansion is our most common indication for treatment. We've got multiple treatment modalities, typically with a high initial, technical success, but the overall clinical success is not quite as good.

And so as we've learned the natural history is poorly understood, and there's no real strong evidence to guide our treatments. We tend to use CT image fusion to help us perform transarterial lumbar embolization as well as this is a transarterial from a hypogastric to coil

both lumbars and an IMA as well as the sac. We'll also use a direct sac puncture occasionally from a translumbar approach with the fusion guidance and also use that to guide us in terms of placing our embolic agents and then we'll also perform the transcaval embolization more recently.

This has become preferred over the translumbar approach and we can use that to then guide treatment and we use coils and glue combined typically now. We've performed over 100 procedures in 56 patients averaging two per patient. The average time from the endoleak to the procedure was

37 months and our follow-up is 27 months, about half had their EVAR performed at our institution and then the other half outside and about one in four of those had already had some sort of type two endoleak treatment. At our initial treatment, it's typically a trans, or it's been most commonly, a transarterial lumbar embolization

followed by IMA, followed by transcaval, and then direct sac puncture. Freedom from re-intervention is not perfect, so by one year it's about 50% we'll have a re-intervention for ongoing sac growth. For our secondary procedures, open repair has actually

become more common, followed by transcaval embolization then transarterial lumbar, IMA, direct sac puncture, and then also relining proximal extension with modified graft or anchors or cuffs. We have 10 patients that underwent open repair with a one year freedom from open repair of 94%.

Early on, we performed graft explantation for persistent growth with the type two endoleaks, then we switched to sacotomy initially without a proximal reinforcement. One of these was a patient who did rupture from an isolated IMA type two endoleak. We ligated the IMA, opened the sac, found no other bleeding,

closed the sac, and he's been fine for five years. We've taken to reinforcing the proximal attachment prior to opening the sac. One patient already had a PMEG for a type one and then more recently, we've been placing endoanchors for the proximal attachment prior to opening the sac.

Our clinical success from a single intervention is only 33% with multiple interventions it goes up to 67% and if you include the open repairs with sacotomy it goes up to 88%. This is for sac stabilization or decrease. So, I do still believe that large type two endoleaks

with sac expansion should be treated for lumbars. We will still typically go transarterial for the IMA. We'll go from the SMA. If we can't do those, or we failed, then we'll go transcaval as our next approach followed by translumbar. We like to treat both the nidus and the source feeding

vessel and if we fail with all of those, we proceed to sacotomy then will now place the proximal endoanchors for fixation. What we have been seeing, though, more commonly is this where there's poor attachment at the proximal end or distal end and a patient who we've performed

multiple procedures for type two endoleak and there's ongoing sac growth and even though there's no definitive type one leak, clearly if there were we would just go ahead and treat that, but in those patients who don't have a defined type one or three, but they have poor apposition, then we'll consider relining them,

extending them, anchoring, etc. And then, only then, if they still have problems would we consider treating the small type two endoleak. I'm looking forward to the discussion 'cause I think we've got it all figured out. Thanks.

- Good morning everybody. So first of all let me take note of it for the kind invitation to be here, again. These are my disclosures. So Juxtarenal Aneurysm has been described as those aneurysms very close to or even including in the lower margin of renal artery.

And of course the gold standard at that time was aortic supportive clamping and open surgery. Probably open surgery is still the first choice in this very short and complex aortic neck but what do in case of patients unfit for surgery? Or for patients who are asking for

a minor invasive alternative. Of course, Fenestrated EVAR are the solution, the option two, but they require time, are expensive, so what to in case of patients who have no time or cannot wait for this customization process?

Symptomatic patients, patients with huge aneurysm or patients just unfit for fEVAR because of either access or tortuous proximal neck anatomy. So solution is chimney or ovation VENT. What is ovation VENT? It's a kind of open chimney technique,

it's a combination of ovation with renal bare stent. So you know the the new concept of sealing of this stent graft, the circumferential apposition of polymer-filled ring to the aortic wall, typically at 13mm, so to just translate the length of the neck to a specific point

when a couple of millimeter when in that position of course. And you know with the previous, you have just heard the harder device, but with the standard device, the prime and the IX, we have the device positioned

13mm below the lowest renal artery. So, what to do in case of (unclear) when have no apposition of the ring to the aortic wall, we raise the ring, just very close to the renal artery, and then we place some bare metal stent

at the renal BMS. So here you can see our bench test with the fabric of the collars just moved by the bare metal stents. So, VENT is different from chimney, we don't use the covered stents so

it's a lowered provide bracket approach, and more importantly, chimney and endograft are typically competing for the same room so this the reason for gutters, while with VENT we have a stent and endograft, which are not competing for the same room.

The ring is responsible for the sealing and the stent is just responsible for the ventilation of the renal arteries. So this is a typical example, you can see here, a contained rupture aneurysm, in this point, and with a very short neck, so we decide

to land with the first neck and exactly at that level you can see here the steps of the procedure, the contemporary deployment of the renal stent, and the main graft the injection of the polymer, so the first ring is really in contact with the renal stent,

but they're not competing each other and so you can have a nice sealing of the sack. Another case, conical shaped neck, unfit for standard EVAR, unfit for EVAR, because was a huge aneurysm, much more than 8cm, so we decide again to raise the ring,

13mm and fit for standard ovation. And so here you can see the first ring just at this level, the renal stent, responsible for the patency of the renal artery, and you can see here that the first ring is just touching it in one point, the conical neck.

With good sealing. Again, another case with unfit for fEVAR, because of the small access, tortoise access, and so we plant a double VENT, in this case, you can see here again, prucodanus bracket approach, with five french shift,

contemporaneous deployment of stents, and first ring, again nice sealing, and nice follow up with completed sack screen cage, and another one year follow up. So, up to now we have performed 29 cases. We did the first case in June 2015,

technical success was high, 96.6%, we had just one type one endo-leak fixed introaperticaly with the coil embolization. The follow up is, mean follow up is 19 month, and 100% renal artery patency, no further intervention, no sac enlargement,

the majority of arteries, it's shrinkage more than 5mm. So just in conclusion, this option is in, we believe that in selected measures, it's a nice option. It is safe and effective when you can not wait for fenestration graft, like in case of symptomatic

or huge aneurysm, or just patients are unfit for fenestration because of tortuous anatomy or small iliac vessels. Thank you for your attention.

- So this talk is similar to Professor Vermossin in that we're trying to establish again the idea that EVAR is really the choice of treatment here, especially for patients who can't undergo an Open Repair. I have no disclosures. So why does this even come up? Well, as we know the DREAM trial very nicely elegantly

show that early on there was a mortality benefit of EVAR over Open Repair, but out to two years that mortality benefit was lost and the curves began to meet and equilibrate. And when you look at the EVAR 1 study, when you get out to eight years,

those curves actually invert and the all cause mortality for Open Repair was actually beneficial as compared to EVAR. And so it becomes a question, based on somebody's RCT or whether or not Open Repair is really the better way to go. But at least for this discussion we're talking about

a select group of patients. Those patients who are unfit for Open Repair. Multiple comorbidities, high frailty index. Totally different population than the overall cohort. And so when you go back to EVAR 1 and you look at it, these patients, these frail patients,

lot of comorbidities. They're the ones who would exactly benefit from that early aneurysm or early all cause mortality benefit from EVAR, 'cause these are the patients that may not life to meet that eight year crossover point.

In addition, there's been a lot of temporal changes in terms of EVAR. There's evolving technology and there's evolving techniques. The devices are lower profile. They have better durability.

It's easier and more precise in terms of delivery and implantation for these devices as well now. Moreover the techniques have evolved significantly. We're doing almost all these percutaneously. There's very rarely a situation where you need to cut down. The procedures are done very quickly now.

A lot of them are done in less than an hour. And there's avoidance at least of major pitfalls, I mean, the last time I've heard about an iliac artery disruption was probably five or six years ago. This type of large complication rarely occurs anymore. And this study from the Mayo Clinic corroborates this.

When they look at their series of patients who had Open Repair and EVAR, the top graph is basically those patients who were treated from 2006 or earlier. The bottom graph is the patients treated from 2005 or later. And you can see the mortality benefit from Open Repair basically disappears in the lower graph

and that cohort that's treated later. Again, kind of corroborating that techniques and devices have changed, improving EVAR's survivability. And this paper looks at the NSQIP database and says basically the same thing. That contemporary 30 day mortality after EVAR

in high risk patients is substantially lower than that reported in EVAR 2 trial. So gain, demonstrating and showing a picture of EVAR with better survivability and the data that's come out from these earlier trials in terms of EVAR mortality is not necessarily translatable to current day.

So, what we are expecting for EVAR? Well, I think really, two things. You want prevention of death from the aneurism and you want a quality of life. I mean, quality of life is important. These patients come in and expect to be able

to be back on their feet shortly after the procedure. And when you look at the EVAR 2 long term survival, aneurism related mortality is improved over Open Repair out to 12 years. And then when you look at the improved data, the quality of life was significantly better

for EVAR versus that of Open Repair. But I wanted to just kind of get you to shift and look at it from a different perspective and not just see it from what EVAR is in terms of beneficial, how it's changed and how the survivability is improved.

But really what are the expectations in terms if Open Repair? What is the patient tolerance? What are the training and what are the volume paradigms in today's day and age? Well clearly, when you look at these two things

percutaneous, especially the access to the groin, is going to be infinitely better tolerated than an open incision, whether it be transperitoneal or retroperitoneal. So clearly there's a benefit of EVAR in terms of that. But more importantly, we know that the,

historically we've shown that high volume centers and high volume surgeons have better results for Open Repair. And without question, the more you do, the better you're going to get at it. And so, when you look at that in conjunction

with these types of data where clearly the numbers of Open Repair through the country are reducing dramatically and continue to decline. We looked at this and this was a slide of EVAR, which was the positive slope, and Open Repair, which is a negative slope,

in terms of trainees graduating. And that ended in 2010. That slope continued to be negative. When you put those two together, you realize that people are coming out with less and less Open training.

Their experience with Open Repair is only declining and when you contrast that with EVAR, which is improving technology and techniques, it becomes obvious that in certain circumstances I think the randomized control data can no longer be looked at and you have really just think about

EVAR as the best treatment for these patients. Thank you.

- Thank you, Mr. Chairman. Thank you, Dr. Veith for inviting again to this great meeting. It's my disclosures. Well, as we know and heard this meeting, there are some certain limitations of current EVAR (mumbles) anatomical procedure and economical reasons,

and I would like to present a relatively new device which may address current EVAR limitations with a simple low profile system, and basically, ALTURA consists of two parallel stent graft systems. ZEUS No Gate Cannulation is needed and unique features include D-shaped proximal stents

and suprarenal fixation. Multi-purpose (mumbles) possibilities as well, and the system of utilize 14 French delivery system. And as aortic components can be deployed offset to accommodate the offset renals, and then the limbs are also unique

because they're deployed retrograde from distal proximally, and this allows precise positioning, both proximally and distally. Well, as the ALTURA clinical experience includes the very first human implants as well as more recent case performed

with a fully commercial device, and a total of 90 patients with a AAA were enrolled between 2011 and 2015, and follow-ups are taken at 30 days, six months, and annually to five years, and this presentation gives a current status of follow-up, and our results with a 12-month follow-up were published earlier this year.

Our clinical data were collected in total of in 11 sites. It includes 90 patients. And you see here, the patient demographics and anatomy do a typical, which are typical for all EVAR patients and the mean follow-up was 2.7 years. And procedure of success was 99%.

Only one patient, one of the first patient was Gen1 was not implanted, and 50% patients were done percutaneously, and majority of them underwent regional or local anesthesia. So when you look into the results, we see that there was only one case of AAA ruptured,

which occurred at three years due to type II endoleak and sac enlargement as the patient, which refused treatment due to type II endoleak. And all other deaths are paired to no original causes, and two patients had device migration at two years. The same patients appear at three-year period,

and basically these were undersized grafts was sort of our learning curve, and there was no any migration later on. Four patients had type I endoleaks visible on CT, and read by independent committee between 30 days and one year.

None have required secondary treatment and have been no aneurysm enlargement observed. And at one year, not surprisingly for this kind of devices, there was 17% type to endoleaks, but only one patient required secondary procedure due significant sac expansion.

Well, wasn't, of course, what we saw, I expected majority of patients has had shrinkage. There was a four-year period. And this is a patient who was recorded with the type IA endoleak at 30 days, caused by the last calcified nodule,

as you he's here probably none of the other device would tolerate that, but the endoleak did not extended into into the sac and had a leak result spontaneously without sac enlargement through a four-year follow-up period, as we're seeing here. Well, here another patient with type IB endoleak,

due to (mumbles) generation was treated with coils and glue an extension with additional stent graft to external iliac artery. What's interesting was the device. Device can tolerate small distal aortas and five patients who were treated

with small distal aortas and the very first patient was not dilated enough and stents were not deployed, simultaneously causing some stenosis which was easily treated with PTA afterwards, so we learned but it's very great, unique feature to treat the small distal aortas for the device.

And of course, sensing what happening with them, septal endoleaks, because everybody being concerned what happening with that, and nevertheless, there were no septal endoleaks observed during the follow-up period. In conclusion, Mr. Chairman, ladies and gentlemen,

I would like to say this Novel Altura endograft concept has potential to play major role in mainstream EVAR cases and potential benefits include predictability, reposition ability to place the device very, very, very precisely, offset renals, to maximize use of the neck, and low profile

overcomes current and anatomic limitations like tortuous iliacs, narrow bifurcation or access vessels and no limbic inhalation is needed, and basically, I truly believe that this offers option for EVAR day surgery and ruptured aneurysms. Of course, first results are very encouraging.

We need more data. Thank you very much.

- Good afternoon to everybody. Thank you very much, Linio and Frank, for the invitation to the great session. First, the main problem is to define who is a no-option CLI patient? So I want to use, this is a young male, with a long history of diabetes, on hemodialysis.

This is the baseline angio. As you can see, the big vessel are absolutely open. We have an open spot of femoral artery, popliteal artery, and then also below the knee vessel are quite open, and we can see that the blood is going very well to the distalis, but in the foot,

we have a disease of all the foot vessel, which is a calcific disease. You can see here, this is the plain x-ray. I think that the plain x-ray of the foot is one of the most important information that we can get on the patients.

For every patient, I want to have this plain x-ray. You can see the medial artery calcification spreading everywhere, dorsalis pedis artery is occluded. We have a small, thin, tortuous, tarsal artery giving some blood to the forefoot. Medial plantar artery is occluded.

The lateral plantar artery is occluded. We have no any clear identification of the metatarsal vessels. This is the forefoot of this patient, and the majority of this patient, with a long history of diabetes and on hemodialysis,

have this medial artery calcification spreading to the tiptoe, and the first toe is totally avascular. This is the reason why this patient developed critical limb ischemia. So who is a no-option CLI patient?

I think that today, a no-option CLI patient is a patient without a target foot vessels. Today, SAD is the most common cause of no-option CLI patient because the SAD is correlated to the age, to diabetes, and end-stage renal disease. We have an epidemic of all of these three vascular factors

in our societies. In the majority of the cases, SAD is actually associated with medial artery calcification, in at least 25% of CLI patients, but today, I think that we are close to 40% present some degree of SAD-MAC.

So in this patient, how to create and master the hybrid foot vein arterialization circuit. This is the patient. My friend, Andrea Casini, vascular surgeon, has done a bypass with the proximal anastomosis of the great saphena vein on the distal P3 segment

of popliteal artery, and here we have this (mumbles) to give him blood to the medial marginal vein. Now, these are very good images, but we must learn how to read these images first. This is an arterialization on the superficial dorsal system of the foot,

so we have an inflow represented from, by the great saphena vein, and an outflow represented fundamentally by the medial marginal vein. We have other collaterals in the superficial system. For example, this is an ancillary superficial vein, and we see a faint shadow of the small saphena vein.

Then we have the deep dorsal system. We have a connection here, a perforant vessel, because it perforates the fascia, and goes from the superficial vein system to the deep dorsalis vein system. Here we have the two anterior tibial veins,

and the dorsalis pedis veins. Then we have the plantar system, the deep plantar system. We have these two plantar veins, the medial plantar vein, these are the two lateral plantar veins, and the deep plantar arch, and the two posterior tibial veins.

Now we have the last system, vein system of the foot represented by the superficial plantar systems, the Lejar's sole, and you can see here, this network, a network without valves, very thin veins, in all of the superficial plantar sole. We have a lot of connection

between these four systems of the foot. This is, for example, the perforator that I have dilated to give blood not only on the superficial dorsal system, but also to the deep dorsal system. We have many collaterals. I have embolized, for example, the anterior,

proximal anterior tibial veins, in order to avoid a precautious still of blood at the ankle level. I have embolized these collaterals that are perforator coming from the superficial dorsal system to the deep plantar system,

and stilling blood precautiously, and here we have the forefoot cross, which is the main cross between the three system, the superficial dorsal, the deep dorsal, and the deep plantar. Now, we can see that the arterialization was able to fill all the forefoot vein system,

and this is very important. When we get the direct blood flow through this collateral to the Lejar's sole, we know that the arterialization can really function. So I asked to my foot surgeon to do a non-geography guided surgery, wait for swelling,

wait for arterialized network expansion, respect the arterialized circuit, respect the forefoot cross, because we think that after foot vein arterialization, the foot is still ischemic, the arterialized circulation has not the same function of the standard circulation.

We must use a tension-free surgery to avoid focal ischemia. This is the tension-free surgery. I know that a transmetatarsal amputation could have been maybe more structurally stable, but I prefer to use this minimal surgery, and the patient has a complete healing

in two months, in two months. Now, the main problem of foot vein arterialization is to understand why this arterialization functions. Now, I propose you two hypotheses. The first is the mechanical hypothesis. Arterial and hydrostatic pressure force vein valves

leading to progressive valve incompetence, distal vein recruitment, and finally, direct issue nutrition by reverse blood flow. In 1906, Alexis Carrel made some experiments on dog, connecting with an anastomosis, the common femoral artery with the common femoral vein,

and he observed that there was the need of three hours at least to force by blood pressure the valves of the vein. Final, he said that practically complete reversal of the circulation is established about three hours after the operation. I want to prepare you this patient.

Observe, this is the acute phase immediately after treatment of foot vein arterialization with some leaking of blood on this vein that I have dilated. Eight days later, three months later, observe this geometry. Are impressive in my opinion.

Can we think that this geometry of vein, pure veins, can feed tissues like a normal standard geometry of artery? When I see these images, I answer, yes, I believe it. I believe it because we know that the venular plexus have a very thin vessel wall like capillaries, so it's a way, when we see these images,

we can really think about a complete reversal blood flow or something that is able to get the tissues and to feed the tissues. The second hypothesis is a biological hypothesis. Vein wall shear stress promotes a global remodeling and/or neoangiogenesis of the vascular system of the foot,

creating a new distribution system, and it was in hypothesis proposed by Languar. This is a LimFlow procedure on a patient like the first one, completely calcified, and this is the evolution, baseline, acute result, 45 days, 90 days after transmetatarsal amputation.

Look at this, 90 days, three months after the LimFlow procedure, the percutaneous deep vein arterialization, and about two months after the transmetatarsal amputation. This is really impressive. Look at these images.

What type of geometry, this one. Look at the baseline angio, and now we have all this vessel connecting with the veins. I am injecting blood contrast dye, so here in the distal stent of the LimFlow procedure, so we have no any blood flow coming

from the previous diseased arteries. This is the patient some months later. This is another patient baseline. An arterialization and after the occlusion of this arterialization, you can see this new neoangiogenesis.

Our results in 36 patients. We're able to get a 69% of limb salvage at 10 months, and I think that in highly selected no-option CLI patient, foot vein arterialization can be the only solution to avoid major amputation. Thank you very much for your attention.

- [Man] Bert, what some magnificent imaging and congratulations. When, just so that I'm clear, I mean, I've done, been lucky enough to have done a couple of LimFlow cases, and we are performing valve, using a valve at the time to perform valvotomies.

Are you suggesting that the pressure alone is enough to do something for the valves of the foot or how extensive do you think valvotomy needs to be in these cases? - [Man] This is our major limit because our limb salvage was correlated to the patency of the bypass,

and our patency was very poor, and it was very poor because we have not the reverse antegrade valvulotome, which is a part of the LimFlow kit. It's not sold alone, so we used some artisanal ways, like high pressure inflation of an oversized balloon. This is very effective but you have a restenosis rate,

very high reocclusion, thrombosis, and every failure, precautious failure of the graft of the bypass was correlated to a major amputation. - [Man] Yeah, okay. Any other questions or comments? - [Man] Is there any difference in your opinion

between a (mumbles) a total percutaneous? - [Man] I think that a total percutaneous procedure is a procedure with a target, which is the posterior system, essentially, because very few cases were done on the anterior system and the anterior deep system, in my opinion, is not a good target for the arterialization

because it is the poorest system, base system of the foot. The hybrid procedure can be done on both, the superficial dorsal system and the deep system. Obviously, you must choose according to the imaging of the baseline imaging or the vein system. Every patient is very different,

so you need to choose the proper target, vein target, into the foot. - [Man] Good. - [Man] Yeah, Roberto, this is very exciting stuff, and Rico and Asher and I tried to do this with primitive valvular destruction back in the 90s.

We had some incredible successes, but we also had some very bad failures. Patients got big, very much edema, one got into heart failure, one actually died, we felt, because of the AV fistula, and so we stopped, but can you talk about the mode of failure.

The successes are brilliant, and I think you definitely have something. We had some good cases but we had, our failures were all with the patent graft, and did you, you said I thought that you only failed when the graft closed.

- [Man] I read all your paper regarding this before starting, so I know that it's not easy. First of all, the key problem either the selection of patient. One of the key factor is heart function. We selected only patient with good heart function,

and second, the procedure is not a single procedure, standalone procedure. We had to follow the patient for months. Healing needs months, maybe repeat intervention, so you need a patient with an acceptable life expectancy and acceptable quality of life expectancy,

and acceptable working capacity, a salvageable foot, so a patient that can really cope with you in this long process of healing. The selection is a key factor. - [Man] Second question, why didn't you use the LimFlow exclusively?

- [Man] Because the LimFlow procedure is very costly, obviously, and in Italy, it is not reimbursed absolutely. This is the main reason.

- [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.

- Thank you friends who have invited me again. I have nothing to disclose. And we already have published that as far as the MFM could be assumed safe and effective for thoracoabdominal aneurysm when used according to the instruction for use at one, three, and four years. Now, the question I'm going to treat now,

is there a place for the MFM? Since 2008, there were more than 110 paper published and more than 3500 patient treated. 9 percent of which amongst the total of published papers relating the use of the MFM for aortic dissections. So, we went back to our first patients.

It was a 40 year old male Jehovah Witness that I operated in 2003 of Type A dissection and repair with the MFM in 2010 because he had 11 centimeter false aneurysm. Due to his dissection, this patient was last to follow up because he was taking care full time off of

his severe debilitated son. When we checked him, the aneurysm seven years later shrunk from 11 to 4 centimeters wide. And he's doing perfectly well. Then the first patient we treated seven years ago, same patient with Professor Chocron

Type A dissection dissection repair in 2006. Type B treated with MFM in 2010. We already published that at one year that the patient was doing fine. But now, at three and seven years, the patient was totally cured.

The left renal artery was perfused retrogradely by aspiration. That's a principle that has been described through the left iliac artery. So what's next? Next there was this registry

that has been published and out of 38 patients 12 months follow up, there were no paraplegia, no stroke, no renal impairment, and no visceral insult. And at 12 month the results looked superior

to INSTEAD, IRAD and ABSORB studies. This is the most important slide to us because when you look at the results of this registry, we had 2.6 percent mortality at 30 days versus 11 30 and 30.7 no paraplegia, no renal failure, and no stroke vessel

13 to 12.5. 33 and 34 and 13 and 11.8 percent. With a positive aortic remodeling occurring over time with diminishing the true lumen increasing the true lumen and increasing the false lumen.

And so the next time, the next step, was to design an international, multicenter, prospective, non-randomized study. To treat, to use the MFM, to treat the chronic type B aortic dissection. So out of 22 patients to date,

we had mainly type B and one type A with no dissection, no paraplegia, no stroke, no renal impairment, no loss of branch patency, no rupture, no device failure, with an increase in true lumen and decrease in false lumen that was true at discharge.

That was true at one, three, and six and 12 month. And in regards with the branch occluded from the parts or the branches were maintained patent at 12 and all along those studies. So, of course these results need to be confirmed in a larger series and at longer follow up,

yet the MFM seems to induce positive aortic remodeling, is able to keep all branches patent during follow-up, has been used safely in chronic, acute, and subacute type B and one type A dissection as well. When we think about type B dissection, it is not a benign disease.

It carries at 20 percent when it's complicated mortality by day 2 and 25 percent by day 30. 30 percent of aortic dissection are complicated, with only 50 percent survival in hospital. So, TEVAR induces positive aortic remodeling, but still causes a significant 30 day mortality,

paraplegia event, and renal failure and stroke. And the MFM has stabilized decreased the false lumen and increase the true lumen. Keeps all the branch patent, favorize positive aortic remodeling. So based on these data, ladies and gentleman,

we suggest that the MFM repair should be considered for patients with aortic dissection. Thank you very much.

- Yeah, thanks very much. Well, we've already heard that things were going well with the two first EVAS trials in the U.S and Europe predominantly, at one year and then we've seen those events described by both Jeff and Matt at two years. Root cause analysis refined IFU

and then prospectively studying this in the EVAS2 trial in the U.S but also in Europe and in the Asia-Pacific, in the Forward2 trial. I'm going to give you a little bit of an update. As we know there have been some concerning reports on retrospective reviews of experience in the early term,

and we've all heard about the details of the revised IFU, and the useful outcomes or grossly improved outcomes we can expect at two years and now Jeff has just told us at three years. Sorry, we'll just go back. So, as Matt mentioned, there have been several publications

that have retrospectively applied the IFU to center's experience to see if they could replicate the good outcomes that were achieved in the retrospective analysis of the IDE trial. Certainly, what is shown is that if you apply the revised IFU, you significantly reduce

patient applicability with this particular device. It has to be acknowledged that many of the procedures that were performed in these publications were performed, a) with a device that's different to the one that we're now going to use, and b) with a procedure that was very different.

It probably impacts on outcomes. I think the major difference with what we'll call the new Nellix device, is that it has the endobag attached firmly, not only to the top of the stent, but also at the bottom. And in our experience this attachment at the bottom

has had a particular impact on aneurysm sac size. The procedure has also evolved, and the procedure now involves steps such as unfurling of the endobags before stent deployment, and also pre-fill of the endobags with saline prior to filling with the polymer,

as well as the importance, as Matt mentioned, of accurately deploying and using all of the infrenal neck and the iliac sealing zones. We also performed a retrospective analysis of our experience in consecutive cases at Aukland Hospital with considerably longer follow-up.

And you can see that the patients on the modified IFU had a significantly different and improved freedom from type 1A endoleak, and also the composite end point of type one endoleak, sac expansion, and freedom from reintervention was highly significantly improved.

So that's a little bit different to the experience reported, possibly because we've been applying the optimized technique and had access to the new Nellix device for some time. So EVAS FORWARD 2 is being performed in Europe and in the Asia-Pacific region.

A 300-patient confirmatory trial with standard parameters. This is the very first case that was done. We did this in Aukland, and you can see something we weren't observing with the earlier Nellix device without the distal seal. We're seeing some cases with significant sac shrinkage.

You can see the earlier, or interim results, I'm just presenting for the first time here today from the FORWARD 2 trial. A very high freedom from type 1A endoleak, and freedom from reintervention, as of July 2018. Just out of interest, we also did a retrospective review

of patients in our own center that has had at least one year of follow-up using the new Nellix device with optimized procedures to see what the outcome would be, and you can see at one year that there's no type one endoleaks. Impressively, absolutely no migration.

We have seen at two years a couple of patients that had some sac growth. Even on IFU we felt that they had degeneration of their iliac arteries with loss of seal. Here you can see a case where you can see the dramatic sac shrinkage we're now seeing

in some cases, and this is the one where we saw some sac growth where we ended up doing a second reintervention to extend the distal seal. Of course, the real driver for us to continue with the Nellix and EVAS technology is this suggestive but very impressive freedom

from all cause in cardiovascular mortality. That really is driving us to use this technology in our patients. So in conclusion, we'll know that, in fact, there's ongoing evolution of this technology, and we're looking forward to being involved

in next generation EVAS that will follow the important EVAS2 and EVAS FORWARD trials sometime later in 2019. Thanks very much. (applause)

- (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.

- Here we go. So, we know that late survival of patients with aortic aneurysms is not as good as matched controls and much of this is related to higher incidents of cardiovascular events. Other factors that impact survival are aneurysm size, as well as antiplatelet and statin therapy.

And we know that EVAR has no long-term survival advantage compared to open repair and, in fact, aneurysm related survival is worse after eight years for EVAR rather than open repair and, yet, 50% of our aneurysm patients are alive eight years after repair.

We've already seen about the differences in the mechanism of EVAR versus EVAS. With EVAR there's sac thrombosis, with or without endoleak, and we've previously shown that with sac expansion there's a significantly worse late survival compared to patients with no sac expansion.

This was a VSGNE study and then a larger VQI study showed that not only is sac expansion have worse survival but, even failure to regress so stable sacs also have worse survival compared to those that have sac regression. And this is independent of whether or not there's

an endoleak or reintervention. So, this prompted us to wonder if EVAS might be associated with a difference in All Cause Mortality compared to EVAR, and we know the act of sac management processed with EVAS involves obliteration of the flow loom and minimizing the chance for

type two endoleaks. This was spurred on by, as Jeff had mentioned previously, the excellent freedom from All Cause and Cardiovascular Mortality seen both in the US IDE but also in the global registry. And, on top of that, in a comparison with the report

from the Mayo Clinic, when looking at the EVAS patients from those two studies broken down by aneurysm diameter there seem to be, again, a difference in a three year survival of the EVAS patients compared to traditional EVAR. Why might this be? Well, several reports have come out demonstrating a

difference in post implant syndrome, various inflammatory markers, major adverse events, cardiac adverse events and endoleaks when comparing EVAS with EVAR. And, CRP levels are elevated in the entire

early post operative period with EVAR relative to EVAS. So, we wanted to compare All Cause Mortality with EVAS to EVAR so we used the 333 patients from the US IDE trial, from 2014 to 2016, and a comparison group we used all the EVAR patients in the US VQI

from the same time period and then applied the same exclusion criteria from the IDE being patients on dialysis or with elevated creatinine or rupture were excluded and then we used propensity weighting to account for differences is baseline characteristics and we did

weighting based on aneurysm characteristics and cardiovascular risk factors and implied inverse probability weighting to compare the risk adjusted long-term survival. Our primary outcome was overall survival and this propensity weighted cohort, and as a secondary analysis

we compared survival when stratified by aneurysm diameter, a small, less than 5.5 or greater than or equal to 5.5. And, in the overall cohort what we found was EVAS survival at three years of 93% compared to 88% for EVAR, a 41% lower hazard for mortality that was statistically significant.

When we looked at the patients with smaller aneurysms, we found no benefit, no difference in survival between the EVAS and EVAR. But in the patients with the larger aneurysms greater than, or equal to, 5.5 we had 92% and 86% three year survival, so double the mortality rate

in the standard EVAR patients. So, in conclusion, EVAS seems to be associated with the higher long-term survival compared to EVAR, and this association was strongest in those with largest aneurysms. We think the biology of the AAA after EVAS plays a role,

and we think that this supports the continued evaluation and iteration of this therapy. Thank you.

- Well Mr. Chairman, dear friends, last year was here on the same stage for discussion of the results of the EVAR 1 trial and trying to tell you that the results of the EVAR 1 trial were no longer valid and this year I'll try to do the same for the EVAR 2 trial. The EVAR 2 trial was a randomized control trial

conducted in the UK in 33 centers with enrollment between 1999 and 2004. It was a randomized trial in which the patients were randomized between conservative treatment and open treatment and the common ground for the study was that these patients were unfit for open repair.

What is unfit for open repair in the EVAR 2 trial? Well the decision was made from three criteria. Cardiac reasons were the main reasons to consider patients as being unfit. Respiratory and renal reasons are the criteria that were used.

There have been several publications on this trial showing a design of the trial, the preliminary results, the final results in our recently last year, the very long results with this trial. And what are the results? Well as you can see here, it was a statistically

significant difference in aneurysm related mortality between the patients treated with EVAR and those treated conservatively but there was no difference in overall total mortality and this led us to the conclusion that indeed there was not really a place in those EVAR in those patients unfit for open repair.

However, we might look more closely to these results. The first thing in this trial is that almost 10% or more than 10% of the 197 patients that were randomized for EVAR actually did not receive the EVAR procedure because they died prior to the intervention and what was the reason for this?

Well the mean time between randomization and EVAR in this study was two months and in a quarter of the patients, it was even three months. The nine ruptures that occurred before the intervention had taken place. Actually it'd be more than half of

the aneurysm related mortality in this group. Another striking observation was that those patients that had no intervention, 1/3 of these actually were treated with EVAR in the followup period. And when we look at the results, whether it's observation-influenced results,

well you see when we perform a vertical analysis, the difference in aneurysm related mortality was even bigger and also there was a clear trend towards improved overall survival. Although this was not significant and therefore, the author still remains to the conclusion

that there was no place for EVAR in these patients. Looking again closer to the results and looking specifically at the patients with no intervention, already in 2009, there was more than half of these patients in this group actually were patients that already had EVAR.

And even worse, in 2015, of the 13 patients in this group that still survived, there was only one, yes only one, that did not have an EVAR procedure. So it's clear for me that only patients with EVAR actually survive.

Why are the results no longer valid either? Well this study was performed in 1999 up to 2004 and it's clear from further studies, just one example, that the results in the meantime have clearly improved from 1999 to 2004. While it wasn't the Stone Age for EVAR,

it was not more than Middle Ages. Plus mortality clearly improved with time and then when you look at the results of this trial, the 5.7% operated mortality in the EVAR group are actually at this moment no longer standard of care when you compare to these three other studies

which actually use the same criteria for considering patients that's unfit for open repair. Also we've got longer term survival. The mortality of 40% after, no, no, 60% after 40 as in 80% off of JVS can no longer be considered really as up to date results and probably the reason for that

is also the fact that medical treatment upstream in these optimal patients as only 40% statins. So are EVAR 2 results still valid? I think it's clear they are not. It's an old study with old devices. The mortality is not conform to actual standards.

Medical treatment was not optimal. The delay in treatment caused preventable deaths. More than 1/3 of the patients crossed over and the statistical analysis does not reflect the actual treatments of the patients. Does this mean that we should operate on all patients?

Well, maybe not. This is a very recent study published earlier this year in logical patients and you see that when some, certainly once several of the risk factors were considered being unfit patients were present, that results were indeed worse,

especially when there is renal insufficiency. The IR for the SVS guidelines correctly state that it is just to inform high risk patients over their risk status and their mortality score and then making an informed decision whether we should proceed with aneurysm repair or not.

It's my personal opinion though that clinical judgment is probably the most important factor in this decision making process. Thank you for your attention.

- Okay, thank you. We know that inflammatory AAA have quite low incidence. The main problem is related to the thickness of the aortic wall and to the retroperitoneal fibrosis that involves the organs that are close to the aorta. Open surgery is quite difficult for these reasons. And these imply a higher mortality rate

that is threefold the one for standard AAA. And the higher morbidity related to the surgical dissection in fibrosis with risk of iatrogenic injury of the involved organs. So that some authors suggest the supraceliac clamping. That of course have some other issues.

A recent paper suggests that a pre-op treatment with a cortical steroid therapy can be useful to reduce inflammatory signs and so minimize the operative risk for these patients. On the other hand, endovascular treatment has been proposed since 1997 with different outcomes.

Certainly mortality rate is lower when compared to open surgery, and even the one year mortality is lower. But we have a problem with periaortic fibrosis that does not decrease as well as with open surgery. And there is some progression, in some cases, with higher nephrosis that leads

to other types of complication. This is not a standard. You see in this paper that there is no problem with periaortic fibrosis after endovascular treatment. But in other papers, the situation is different. There is a worsening fibrosis and even the development

of fibrosis after standard EVAR in patients with no history of inflammatory AAA. And certainly the phenotype eg4 seems to be related to a worse outcome after EVAR. So, based on this situation, what we have done in the last year is to use a systemic steroid protocol

for our patients with inflammatory AAA that is the same that is used for arteritis and retroperitoneal fibrosis. And you see how impressive is the situation in this case. We had only four days of therapy, and we have a decrease in periaortic fibrosis of 28%.

We studied all our patients with PET/CT. We made a comparison with the patient with standard AAA, and we observed an increased level of captation that was really significant. This is our population. All of the patients had immunological screening,

and the evaluation of the inflammatory level. This is the operative situation. All the patients had a good result with no mortality at 30 days. Only one patient died three months later for other reasons. And what we observed is that in almost all cases,

the periaortic fibrosis reduced significantly with the, even with PET/CT. All the patients were asymptomatic. And all the patients with hydronephrosis have a release of the situation. You see that the diameter of the aorta decreased

of 9.76 millimeters, and there was a decrease in periaortic fibrosis of more or less one centimeters. So this is really significant, as you can see. And there was a reduce in the uptake for all the patients but one. We don't know exactly, he had a type two endoleak.

Don't know if this can be a correlation because it's a single patient. And another patient stopped corticosteroid therapy, and so there was a recurrence of this problem. The CRP reduced globally, but of course, it's not specific. So in some patients we had an increase for other reasons.

But our policy now is that we do EVAR, when feasible, associated to steroid therapy. That, in our practice, is effective. We use open surgery in patients unfit for standard EVAR, and probably, even for these patients, steroid therapy can be a choice.

Thank you.

- [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.

- So regarding fenestrated limbs, these are my disclosures. Typical scenario where you have a rather unwelcoming iliac, common iliac artery, you need around 16 millimeters at least to accommodate a branched graft in the iliac artery. You want to preserve the hypogastric flow.

In this case you also see a stenosis, so you need two things, ideally, to accommodate a branched device, which would be the diameter of 16 millimeters and also the angle of the artery. This is very pleasant to put in a branched device.

However, there are patients where you want to preserve the hypogastric blood flow, and in these cases, above the origin of the hypogastric artery, there is not enough room to open up a branched device, or the angle is very unfavorable

to put in a branched device. And here fenestrated iliac limbs come into play. These are usually made to measure, different lengths, different proximal and distal diameters and also you can place the single fenestration where it obviously is positioned best.

There are basically two, I think very useful indications. Here we can see a type 1B endoleak in a 13 millimeter limb. The distance to the hypogastric artery was not enough to have a full expansion

of the iliac limb, and therefore in this case if you want to preserve the hypogastric artery, which I would really strongly always recommend if possible, is to put in a fenestrated limb. But it's also really very helpful in these cases

is that you don't have to come from above, you can come from below and finish the whole procedure from below. So you have a full deployment of the endograft and then you'll put in a connecting stent graft

with obviously a very good seal and result. Most importantly, for complex cases as in this, for instance, patient who's had an open procedure 10 years previously and had further interventions with an over-stenting of the hypogastric on the right side and large thoracoabdominal aortic aneurysm

as well as an anastomotic aneurysm on the left side, you really want to preserve the hypogastric artery. And you can also that actually it's an anastomotic aneurysm at the left side, so here a branched device certainly doesn't work. First, because it doesn't open up,

and second, the angle of the hypogastric is really very unfavorable. So again, you just put in your fenestrated device and then connect it from below with the stent graft in order to preserve the hypogastric blood flow of the last remaining hypogastric artery.

And also, obviously do something else to the rest of the patient, so this was a five branched endograft in a patient with two left kidneys. And also another case, you see actually on the angiography already the shaggy aorta,

so occlusion or seal at the distal origin of the common iliac just above the hypogastric is not really a good option, so we've re-over stented, or you do something about it. Now this is the case with a thoracic endograft

and a full-fen extension. So again, we really opt to preserve these hypogastrics as much as possible. So in conclusion, Mr. Chairman, (coughs) sorry ladies and gentlemen, fenestrated limbs are a good tool to preserve

hypogastric arteries. Now just to put it into perspective, is it common? No, we have around 30 branched iliac devices a year we implant, and we had all in all five fenestrated during the last two years.

So this is really a rare anatomical solution, but I believe it really is helpful. It's not an off-the-shelf device, so it takes around four weeks to produce, and the company's still not really decided how to price it, so we really can nicely negotiate it.

Thank you very much.

- One more soft swing, I guess, at EVAR-2 for the afternoon, but this one will be from a slightly different perspective. We'll look at it from a methodological standpoint rather than an analytical standpoint, which I do with some trepidation preceding Phil Goodney on the podium. As we've heard, endovascular techniques have revolutionized

the treatment of abdominal aortic aneurysm, and yet, the EVAR-2 trial published in 2010 provided Level I evidence regarding high-risk patients with abdominal aortic aneurysm. There is no survival advantage of EVAR over observation, as we've heard.

So let's unpack a little bit about what we mean by Level I evidence. Level I evidence consists of properly designed randomized controlled trials. They demonstrate the effect size of an intervention, and they're characterized by

strict inclusion/exclusion criteria, are resource intensive and can be difficult to replicate. Keep in mind that enrolled individuals are frequently younger, white, and affluent, receiving care at academic institutions, and clinical scenarios are heavily scripted.

The EVAR and EVAR-2 studies are examples of such trials. By contrast, Level II evidence, and the definition of this varies by region, consists of, for example, use of large administrative and clinical datasets to compare outcomes from different interventions. These are, to be sure, subject to selection bias

and limited granularity, but they're characterized by high power due to large numbers and external validity because they include real life patients in clinical scenarios. Examples of this type of evidence is found in the VQI, NSQIP, NCDB, SEER, and HCUP.

This study, which I'm grateful to have seen referenced in two prior talks, uses the ACS NSQIP database to look at mortality rates after EVAR in high-risk patients. And this is an example of Level II evidence. What we did was look at EVARs

that were performed between 2005 and 2013, and we used the EVAR-2 criteria to define a high-risk cohort and then examined 30-day post-operative outcomes. In that study, we found that the 30-day mortality for these high-risk patients following EVAR and our cohort was 1.9% compared to the EVAR-2 trial in which it was 7.3%.

And we concluded the contemporary mortality following EVAR is substantially lower even in the high-risk group than reported in the EVAR-2 trial. So how do we understand this? I think it's been unpacked a bit by two of the previous speakers,

but our interpretation was that, as I mentioned, randomized controlled trials and Level II evidence are not the same. So randomized controlled trials, again, include and exclude patients for analysis, use selected devices and do often include

a learning curve for new techniques, whereas the use of contemporary cohorts such as our study have an inclusive population, limited granularity, but allows for changing devices and expertise over time. So in conclusion, randomized controlled trials or so-called Level I evidence,

demonstrates effect sizes for new therapies, while large retrospective data analyses augment the findings for these therapies across contemporary practice patterns and devices. Intelligent integration of data across study types leads to improved care of patients

and preserves the role of critical thinking for surgeons. The key points that I would like you to take away are that endovascular techniques and their indications for use are obviously rapidly evolving, and thoughtful assessment of the literature allows surgeons to nimbly integrate evidence into practice.

The bottom line, our analysis of the current literature suggests we should not deny EVAR to high-risk patients. Thank you.

- [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.

- Folks always ask if you can do saphenous vein ablation in the presence of Deep Venous Obstruction. So, we'll talk about that a little bit. So, deep vein thrombosis, as we know, acutely, the danger, or the pulmonary embolus

is what we worry about anti-coagulation is the standard for that, but the longer fate of a DVT may be the post-thrombotic syndrome of which this is from scarring and valve damage, as we know. Mark Meissner showed us in this study back in '97

that more proximal DVT, femoral DVT fares worse than calf vein DVT as far as symptoms, and that goes out to about four years in this study. And we know that the worse actor of all is probably ileo femoral DVT,

so the more progressable the deep vein thrombosis, the greater the obstruction, the greater the symptoms. So, I always show, I like this study by Lois Killewich that she did back in 1989 basically showing the recanalization of deep vein thrombosis on a timeline.

And the message here is, that around three months, 86% of the recanalization has occurred. So, that's kind of my trigger as far as the earliest that I would even consider doing intervention on a post-thrombotic, would be at least three months to allow recanalization to occur.

We know that folks with, post thrombotic folks, do worse as far as receipt scores at five years if you compare primary deep veinous disease with post thrombotics, the post thrombotics fare poorly. And that's really the rationale between these

clot removal strategies in the ileo femoral segment to try and mitigate post-thrombotic syndrome. So, when you have a patient in front of you, the way I kind of line these things up, there going to be either obstruction dominant or reflux dominant.

You're not going to get a limb assymetry. A big, you know, one leg just clearly, larger than the other from saphenous vein reflux. It's just not going to happen. So, if you got true limb assymetry, and a saphenous vein that's 10mm and incompetent,

you're not going to improve their limb assymetry from saphenous vein ablation. So, you got to look at your indications. This patient should be looking for something ileo femoral that you can stent, but I don't think the saphenous is going to be much of a contribution.

The other thing, these folks don't have a lot of vericose veins they have more advanced skin damage. Whereas with reflux dominant, saphenous vein incompetent patient will usually present with vericose veins,

they won't have the limb assymetry, and that's why the C-3 gets a little hazy. It's swelling from superficial vein disease. It's usually just some fullness in the malleolus, maybe around the ankle, but you're not going to get full-blown edema

from saphenous vein incompetence. So, know why you're doing saphenous vein ablation. Not all refluxing saphenous veins need to be treated. Can you do saphenectomy in the presence of deep vein obstruction? We've shown this before.

This old Raju study that he did saphenectomy stripping in two groups, those with and without previous thrombosis, and they both did fairly well, did not seem to be impaired by the presence of obstruction.

This study by Puggioni on RFA ablation. She looked at some patients with DVT in a larger group that were all treated with RF ablation, and the bottom-line of her study was that RF ablation in patients with previous DVT is safe. Again, I wouldn't do it until after three months.

Does prophylactic anti-coagulation have any effect on post-thrombosis rates after saphenous vein ablation? Well, not in the study by Knipp. They used low molecular-weight heparin in folks going saphenous vein ablation, and it just increased the risk of bleeding,

and it had no effect on thrombosis. Can you do combined iliac vein stenting and saphenous vein ablation in the same setting? This is another iconic study by Neglen showed that, yes, you can. Patients with advanced disease

that underwent iliac vein stenting and saphenous vein ablation in the same operation had good symptom relief and very few complications. So, in conclusion, saphenous vein ablation may benefit

patients with previous DVT. Clearly, you're not going to do this in the acute phase of the DVT. When is it safe? I'd say the earliest you would do it, or even consider it is three months

because that's when recanalization starts to peak out. Limbs with concomitant superficial vein reflux and deep vein obstruction can be safely treated by combined treatment, at least in the Neglen series, and the DVT prophylaxis should be

administered at the surgeon's discretion. Thanks.

- I think that the most important tip cannot really be summarized in five minutes, which is that these procedures are highly dependent on how well you plan the procedure and how well you really implant the device. That is a fairly long learning curve that I think you need to actually collaborate with people

that they are experienced, and with industry to make sure that you are on the right track on making your measurements to size these devices. But there are a few things to be said about cases that are very difficult, and a few tips that I would highlight on this talk.

First, it's highly important that you build up your inventory so you can get out of trouble. I think you have to have a variety of catheters of your choice, with primary or secondary curves.

The addition of shapeable guides has been a major benefit for these types of procedures. They are fairly expensive, so I would say we don't use them routinely, but they can bail you out. They can allow you to do cases now from the femoral approach that in the past could not be achievable this way.

You have to be able to work on the diffe .035 system, .014 system, .018 system, and know when to apply this. I would like to highlight four maneuvers that we use when vessels don't align.

First, a common maneuver is really not to try to get in a quote/unquote pissing match with the fenestration and the vessel. If you can catheterize the fenestration first, and advance your sheath upwards, and lead a .018 wire into the sheath,

that will basically lock your sheath into the fenestration. Therefore, you don't have to repeatedly catheterize the fenestration and you save a lot of time. You can choose y ose something that has a secondary curve if you have room,

or a Venture 3 catheter, which is one of my choice for catheterization, and you can see here that on this case, the difficulties imposed by a shelf on the ostia of the renal artery, which makes catheterization more difficult. This .018 wire also allows you to bend your sheath

as a guide catheter so that you can achieve a downward curve to catheterize a down-going vessel, like on this renal artery. The second maneuver to highlight is that these devices are constrained posteriorly, and therefore, the fenestrations are naturally moved

posteriorly into the aorta. So one of the first maneuvers is really to try to move the fenestration more anteriorly by rotating the device. Now, some of the companies now have newer constraining mechanisms

that may alleviate some of this, but this is kind of a next maneuver that we do. Finally, rarely nowadays we have to really find more space between the fenestration and the aortic wall, but it is always useful to leave behind a wire when you deploy this device so that in the event

that you need more space, you can perhaps navigate the catheter, inflate, and create some space between the fabric and the aortic wall. Marcelo Ferreira, along with other collaborators, has described a technique that I think is very useful when you have a lot of space.

That's the case, for example, of a directional branch or perhaps if you are using fenestration to target a vessel that is somewhat away from the fabric of the endograft. That's called the snare ride technique. This is summarized on this illustration.

When you see the left renal artery to be up-going, now being targeted from the brachial approach, that was difficult to catheterize, you catheterize that from the femoral approach with an eight French sheath and a snare ride type... You snare the wire from the arm, and then you can

navigate that catheter inwards into the vessel. That can be difficult, sometimes, to actually advance the snare into the vessel. I think that there is some improvement on the profile of these snares that can improve that, but that is a very useful technique,

not only for branches, but also for fenestrations. Finally, sometimes you have too much space. You may seem you are very well aligned on the latitude with the vessel, but in fact, there is so much space the device got displaced on that sac and you cannot simply catheterize the vessel.

It's useful to downsize the system on these cases to a micro-catheter with a micro-wire to find yourself in the sac eventually out through the vessel. Once you achieve that, you would then exchange this micro-wire, usually a glide gold wire, to a .018,

a stiffer wire that is long enough. You advance a balloon that is undersized for that vessel, and with that you can straighten the system and eventually switch that for a wire that is of reasonable strength, such as a rosen wire in this case, and complete the case.

Finally, there is nothing wrong about leaving the battle to be fought another day. It's better to finish a case a little quicker and not end up with leg ischemia and a compartment syndrome and a s the situation

and come back another day. This is a case, for example, that I did a branch endograft. You can see the right renal artery is exceedingly narrowed. I could not find a way in in a reasonable time. I gave myself about half an hour. I decided to quit.

A few days later, I came back through a subcostal incision, got retrograde access, and this literally was a case that didn't take very long and end up doing very well. So in summary, patie select your proper

anticipat stent. To offset these challenges, minimize contrast a master your endovas

it is better to end with a patient alive and fight the battle another day, than to have an excessive long procedure leading to numerous other complications. Thank you very much.

- Thanks Stephan, yes I just want to give you five tips and tricks that I've learnt with my experience to this technique, and also then I'll present some results from the Ascend International Trials. I have an obvious disclosure that is important to show.

So, I do think that custom-made devices or phenostate graphs are the gold standard in this area of the difficult neck to aneurysm, but there are constraints with it, both financially and atomically, and of course its not the perfect solution

so we still need to strive to find better solutions for patients and indeed an off the shelf solution is very useful especially in emergency situations. I think we're all quite surprised by the outcomes from parallel grafts.

I certainly, when I saw this originally thought this was never going to work but actually, the results from standard evar with chimneys are really quite good. There is however always the potential for gutter endoleaks when aligning

parallel grafts with conventional EVAR stents which are not really designed for this purpose. So, endovascular sealing with parallel grafts offers a solution to this with the prevention potentially of gutter endoleaks because the polymus bag will seal alongside

the parallel grafts. And in practice this works quite well so you can position two, three or even four parallel grafts alongside the nellix sealing device to give yourself a really good seal and an example is shown here on the CT.

So tips for getting good outcomes from this, well the first is an obvious one, but its to plan very carefully, so do think you need to be very cautious in your planning of these with regard to multiple levels of the technique

including access, the type, length, and the nature of the parallel grafts you're going to use. I'll talk a bit more about the neck lengths but aneurysm lengths as well because there are some restraints with the

nellix device in this regard. You need to take very carefully about seal both proximally and distally and I do think you need to do this in a hybrid theater with experienced operators. I mentioned neck lengths and my Tip two is

you have to not compromise on neck quality and neck length. So you need straight healthy aorta of at least 15mm, of less than 30 diameter and a low thrombus burden. If you do compromise you'll see situations as the one on the photograph shows

where you get migration stents so you must not compromise on the quality and length of your aortic neck and if that means doing more chimneys, do it that's not a major problem but if you compromise on neck,

you will have problems. I mentioned the parallel grafts, again this is part of the planning but we use balloon expandable stents of a reasonable length to ensure that you get at least a centimeter into each of the branches

and you have to be careful to position these above the polymer bags so that they don't become constrained by the polymer bags from the nellix device. You have to be very careful when positioning these so the tip four is watch the parallax in

two different angles to be sure, as in the case here, that you line up all your stents appropriately and that you don't get crushing of any of the individual stents. So parallax is vital. And th

ltiple levels of redundancy in the nellix system which you can use to your advantage to ensure you get a good seal. So here's an example where the bags you can see are not entirely filled using the primary fill.

And it is quite difficult because often you get polymer pressures that are slightly erroneous in the endo bags. So use the redundancy including what's called the secondary fill of these bags so you can adequately fill the bags

right up into the aortic neck and ensure a very good proximal seal. So what are the results, well this is the post-market registry of Ch-EVAS this is an open-label study with no screening and I'll just show you a few slides of the data

on 154 de-novo procedures, which are a combination of single, double triple, and even quadruple chimneys. And if we look firstly at outcomes at 30 days the outcomes are good, that you'd expect in these difficult anatomies,

so 2.6% mortality and stroke, and just two cases of temporary renal failure. And if we look out 12 months, the freedom from aneurysm related and all cause mortality is favorable and comparable with any of the other endovascular techniques

in these difficult anatomies, in the upper 90 percents. And endoleak rates, you pretty much eradicate type two and type three endoleaks, but remember this is only 12 months, and very low levels of type one endoleak

and its really the type one endoleaks that are difficult to fix and if you ensure that proximal neck is adequate this shouldn't occur. And finally just secondary interventions, again this is out 12 months. Secondary Interventions are low and again

I think with the tips that I've shown you, you can reduce this to an absolute minimum. So this does offer an off the shelf alternative I don't think in any way this is to match the current gold standard which to me is the custom-made devices, but it's a very useful

adjunct to the techniques we have, and again provides that off the shelf solution which in emergencies and urgent cases is essential. Don't compromise on your neck, the outcomes I think, in this group are promising, but of course, the long term durability is

absolutely essential so it's important we follow these patients out to at least 5 years. Thank you.

- [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.

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