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Transcript

left foot. He has no tissue loss, no sensory or motor loss. And he does have a history of a previous SFA stent

and a below-knee pop to posterior tibial vein bypass. So he was last seen in 2014. So he's been doing well for about two years until he presented with a cold foot. So here is the left lower extremity arteriogram. It shows a patent SFA proximally

with occlusion of the distal SFA stent. Here is the little nub end and the large collateral bypassing it. There're multiple collaterals crossing the knee. And here is the calf showing multiple clips. This is where the proximal anastomosis of the below-knee pop to distal PT bypass is. Based on prior imaging we know that's where it is. And here you can see collateral vascular

of the ankle with some filling of that reconstituted PT going across the ankle. So we crossed that thrombosis with cathether and wire and we got our catheter down to where we knew the proximal anastomosis was. And were able to get an Ekos in and performed overnight thrombolysis. So the next day you can see here, this may have been inciting lesion

here. We have a stenosis in the proximal edge of the stent. And then you've got continued thrombosis of the distal portion of the stent and really no reconstitution of the pop here. So this is the picture of how we started, the occlusion here. So in this case we did angioplasty of that proximal lesion and then we went old school and

put a 6 French guide catheter actually down into the popliteal and aspirated the remaining thrombus. And here you can see this is the image after that. Now you can see the hood of the bypass here, with the by pass still occluded, a few collateral vessels going around it.

So at this point, the decision wise do we discontinue thrombolysis or try to get the bypass open or do we try to be more aggressive and try to recanalize the bypass on the table? In 2014, the by pass was widely opened, he's been fine up until this point.

So we presume this is an acute occlusion of the by pass. >> This is a different bypass right, not the three week old one? >> Right, this is >> The distal one. >> Yeah this is our below-knee pop to PT pop vein bypass so >>

Vein grafts are different from synthetic grafts in that when they thrombose they are not necessary get opened up, cause they get atretic and stuff. So you can balloon and stent all that but at the end of the day, what I found with those is after wasting all this time and money on the vein graft I just go after the native vessel

anyway. So just do that from the start. >> Right. Well, in this one, I don't think we really had a target to go after, but we decided to send this guy back for overnight thrombolysis and doing it proximally. Cause we didn't wanna cross into the bypass because we knew the size

of the bypass was small. And one thing you have to be careful with when you're dealing with thrombosed tibials if you're thinking about doing overnight thrombolysis, you are putting like a five and sometimes six French catheter into very small vessels.

And I have seen several times where when you try to lysis a distal pop or a tibial, you have no flow around the catheter and just because you are infusing high powered lytic medication, if you don't have flow you're not going to get it open. And you could even make the situation worse with propagation of the thrombosis retrograde up into the popliteal and SFA.

So in that case what we did here is we just dripped it from above the occlusion and- >> Question. >> Go ahead. >> I noticed that you are using Ekos again. >> Yes. >> What's the rational

for using Ekos and endhall/g infusion? >> That's a great question. Actually this is not the, I just had to put a picture in here for thrombolysis. This is not actually the- >> [LAUGH] >> Yeah. [LAUGH] Sorry .

>> How many people are using Ekos in the arterial system? Some people do, okay. I'm surprised cause I don't see it that much. To me if I use it it's venous and even there not that much. >> Why not just put an infusion wire down? >> We don't have it.

>> [INAUDIBLE] >> That's- >> That's the answer here. >> Absolutely yeah. >> [INAUDIBLE] >> Cause you don't wanna be called on that, about the infusion wire not working. >> [LAUGH] >> [INAUDIBLE] >> I haven't used those in a long time. >> [INAUDIBLE] >> Yeah exactly. >> [INAUDIBLE]

>> So as you guys could probably predict this does not work. And this is basically the identical picture that we had prior to the lysis. And this is what it looked like before. So this is kind of goal that we're going after. So in this case we did get,

on that day we did get more aggressive. Got across the occlusion with a catheter and wire and performed aspiration thrombectomy with an over-the-wire device. And we did probably three passes to get it to look like this. Which revealed multiple stenoses in the proximal aspect of the bypass. Distally it looked reasonable.

And here's the distal anastomosis here. So we then performed a PTA of the proximal part of the bypass. And looks a lot better here. But the problem is down here in the distal anastomosis, we've actually lost a large branch coming off distally which back in 2014 was patent and supplied the PT below the ankles.

So we then introduced the cocktail of thrombolytics, heparin, and Nitrocine to see if that would help, it did not. And so then we, what's the definition of insanity? Doing the same thing?

So we did overnight thrombolysis and actually, again this is in-hole thrombolysis. This is just a picture to tell you that we did that. And the next day actually that bit of thrombus did melt away. Again most of the times if you're not across the thrombosis you are not gonna be successful, but in the distal arterial beds,

I've seen this this a couple of times where if you do in-hole thrombolysis you do actually get lysis of the clot, the near the ankle or near the hand if you have embolic disease in the hands. >> I agree. That's how I do it these days. Used to do like infusion wires and stuff. But even with those you see a lot of pericardial thrombus in my

experience. And I'd say in general I just do it in-hole. >> Yeah. >> For the pop. >> And that's 2014. And this is where we started from on this presentation.

>> Persistence pays. >> Yes persistence pays. [LAUGH] >> How long would either of you continue lysis? Like what's your limit? Number of hour -

>> 72 hours. >> Yeah. Me too. Don't let it go beyond three days. >> Yeah. >> What do you guys think?

[LAUGH]. >> How many milligrams an hour do you give them for three days? >> One milligram. >> To go three days? >> There's a problem. >> You didn't jot that down? >> [INAUDIBLE] >> [INAUDIBLE]

>> Right right. This guy was 55 I think. >> And is everyone checking fibrinogen, and all that jazz. >> Yeah, we do Q. 8 hours fibrinogen, cut the dose in half if it's below 150 and turn

off if it's below 100. >> So you're giving one milligram an hour for two days? >> Mm-hm. I mean it's not 72 hours consistently, we've got breaks during the procedures and -

>> [INAUDIBLE]. >> 500 units per hour through the sheath. So it's not systemic heparinization. It's basically just to keep the sheath open. >> You are able to consider dropping that down to [INAUDIBLE] >> That's what I would do.

Actually I think my standard does these days is half a milligram >> [INAUDIBLE]. >> Is anyone using anything other than TPA for thrombolysis. >> [INAUDIBLE]

>> Nice. >> Yeah, very good. >> [LAUGH] >> With your [UNKNOWN] it can go longer than three days. >> What about tenecteplase? [BLANK_AUDIO]

Anybody using that? >> [INAUDIBLE] A lot of patients dropped their fibrinogen in the first 12 to 48 hours [INAUDIBLE]. We started dropping routinely after 12 hours to half a milligram. And we've seen no difference in our success.

Half a milligram in the [INAUDIBLE], and it's been just fine. >> And have you seen a difference in the fibrinogen levels? >> Well, fibrinogen levels are much easier to manage. >> Right. >> You almost always see them stop dropping [INAUDIBLE]

[INAUDIBLE] >> I agree. >> [INAUDIBLE] [INAUDIBLE] >> You're worried [INAUDIBLE] [INAUDIBLE] or if we don't get desired results after first night,

we add an infusion of [UNKNOWN] through the sheath, and I tell you what, if I ever have an ichemic arm I start right away because I feel like it really changes the game. >> When you say infusion- >> So we use cardiac dos. So we don't give the bolus but we

give the cardiac 12-hour infusion through the sheath or through the infusion catheter directly into the site. >> With a TPA? >> With TPA. And I well you that it's a game changer in these cases that you're on the edge, really worried that they're not gonna be reversal in the arm to get a lot more digital arteries back

>> That's a good

- Thank you for asking me to speak. Thank you Dr Veith. I have no disclosures. I'm going to start with a quick case again of a 70 year old female presented with right lower extremity rest pain and non-healing wound at the right first toe

and left lower extremity claudication. She had non-palpable femoral and distal pulses, her ABIs were calcified but she had decreased wave forms. Prior anterior gram showed the following extensive aortoiliac occlusive disease due to the small size we went ahead and did a CT scan and confirmed.

She had a very small aorta measuring 14 millimeters in outer diameter and circumferential calcium of her aorta as well as proximal common iliac arteries. Due to this we treated her with a right common femoral artery cutdown and an antegrade approach to her SFA occlusion with a stent.

We then converted the sheath to a retrograde approach, place a percutaneous left common femoral artery access and then placed an Endologix AFX device with a 23 millimeter main body at the aortic bifurcation. We then ballooned both the aorta and iliac arteries and then placed bilateral balloon expandable

kissing iliac stents to stent the outflow. Here is our pre, intra, and post operative films. She did well. Her rest pain resolved, her first toe amputation healed, we followed her for about 10 months. She also has an AV access and had a left arterial steel

on a left upper extremity so last week I was able to undergo repeat arteriogram and this is at 10 months out. We can see that he stent remains open with good flow and no evidence of in stent stenosis. There's very little literature about using endografts for occlusive disease.

Van Haren looked at 10 patients with TASC-D lesions that were felt to be high risk for aorta bifem using the Endologix AFX device. And noted 100% technical success rate. Eight patients did require additional stent placements. There was 100% resolution of the symptoms

with improved ABIs bilaterally. At 40 months follow up there's a primary patency rate of 80% and secondary of 100% with one acute limb occlusion. Zander et all, using the Excluder prothesis, looked at 14 high risk patients for aorta bifem with TASC-C and D lesions of the aorta.

Similarly they noted 100% technical success. Nine patients required additional stenting, all patients had resolution of their symptoms and improvement of their ABIs. At 62 months follow up they noted a primary patency rate of 85% and secondary of 100

with two acute limb occlusions. The indications for this procedure in general are symptomatic patient with a TASC C or D lesion that's felt to either be a high operative risk for aorta bifem or have a significantly calcified aorta where clamping would be difficult as we saw in our patient.

These patients are usually being considered for axillary bifemoral bypass. Some technical tips. Access can be done percutaneously through a cutdown. I do recommend a cutdown if there's femoral disease so you can preform a femoral endarterectomy and

profundaplasty at the same time. Brachial access is also an alternative option. Due to the small size and disease vessels, graft placement may be difficult and may require predilation with either the endograft sheath dilator or high-pressure balloon.

In calcified vessels you may need to place covered stents in order to pass the graft to avoid rupture. Due to the poor radial force of endografts, the graft must be ballooned after placement with either an aortic occlusion balloon but usually high-pressure balloons are needed.

It usually also needs to be reinforced the outflow with either self-expanding or balloon expandable stents to prevent limb occlusion. Some precautions. If the vessels are calcified and tortuous again there may be difficult graft delivery.

In patients with occluded vessels standard techniques for crossing can be used, however will require pre-dilation before endograft positioning. If you have a sub intimal cannulation this does put the vessel at risk for rupture during

balloon dilation. Small aortic diameters may occlude limbs particularly using modular devices. And most importantly, the outflow must be optimized using stents distally if needed in the iliac arteries, but even more importantly, assuring that you've

treated the femoral artery and outflow to the profunda. Despite these good results, endograft use for occlusive disease is off label use and therefor not reimbursed. In comparison to open stents, endograft use is expensive and may not be cost effective. There's no current studies looking

into the cost/benefit ratio. Thank you.

- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations

related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,

and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be

a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation

of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest

as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher

patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.

The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence

that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization

versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,

in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,

one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients

who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored

superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months

for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.

But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear

to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.

Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.

- Talk to you a little bit about again a major paradigm shift in AVMs which is the retrograde vein approach. I mean I think the biggest benefit and the biggest change that we've seen has been in the Yakes classification the acknowledgment

and understanding that the safety, efficacy and cure rate for AVMs is essentially 100% in certain types of lesions where the transvenous approach is not only safer, but easier and far more effective. So, it's the Yakes classification

and we're talking about a variety of lesions including Yakes one, coils and plugs. Two A the classic nidus. Three B single outflow vein. And we're talking now about these type of lesions. Three A aneurysmal vein single outflow.

Three B multiple outflows and diffuse. This is what I personally refer to as venous predominant lesions. And it's these lesions which I think have yielded the most gratifying and most dramatic results. Close to 100% cure if done properly

and that's the Yakes classification and that's really what it's given us to a great degree. So, Yakes one has been talked about, not a problem put a plus in it it's just an artery to vein.

We all know how to do that. That's pulmonary AVM or other things. Yakes two B however, is a nidus is still present but there is a single outflow aneurysmal vein. And there are two endovascular approaches. Direct puncture, transarterial,

but transvenous retrograde or direct puncture of the vein aneurism with the coil, right. You got to get to the vein, and the way to get to the vein is either by directly puncturing which is increasingly used, but occasionally transvenous. So, here's an example I showed a similar one before,

as I said I think some of these are post phlebitic but they represent the archetype of this type of lesion a two B where coil embolization results in cure, durable usually one step sometimes a little more. In the old days we used to do multiple

arterial injections, we now know that that's not necessary. This is this case I showed earlier. I think the thing I want to show here is the nature of the arteriovenous connection. Notice the nidus there just on this side of the

vein wall with a single venous outflow, and this can of course be cured by puncture, there's the needle coming in. And interestingly these needles can be placed in any way. Wayne and I have talked about this.

I've gone through the bladder under ultrasound guidance, I've gone from behind and whatever access you can get that's safe, as long as you can get a needle into it an 18 gauge needle, blow coils in you get a little tired, and you're there a long time putting in

coils and guide wires and so on. But the cures are miraculous, nothing short of miraculous. And many of these patients are patients who have been treated inappropriately in the past and have had very poor outcomes,

and they can be cured. And that a three year follow-up. The transcatheter retrograde vein is occasionally available. Here's an example of an acquired but still an AVM an acquired AVM

of the uterus where you see the venous filling on the left, lots of arteries. This cannot be treated with the arterial approach folks. So, this one happened to be available

and I was having fun with it as well, which is through the contralateral vein in and I was able to catheterize that coil embolization, cured so. Three A is a slightly different variant but it's important it is different.

Multiple in-flow arteries into an aneurysmal vein wall. And the important identification Wayne has given us is that the vein wall itself is the nidus and there's a single out-flow vein. So, once again, attacking the vein wall by destroying the vein, packing

and thrombosing that nidus. I think it's a combination of compression and thrombosis can often be curative. A few examples of that this was shown earlier, this is from Dr. Yake's experience but it's a beautiful example

and we try to give you the best examples of a singular type of lesion so you understand the anatomy. That's the sequential and now you see single out-flow vein. How do you treat this?

Coil embolization, direct puncture and ultimately a cure. And that's the arteriogram. Cured. And I think it's a several year follow-up two or three year follow-up on this one.

So a simple lesion, but illustrative of what we're trying to do here. A foot AVM with a single out-flow vein, this is cured by a combination of direct puncture right at the vein. And you know I would say that the beauty of

venous approach is actually something which it isn't widely acknowledged, which is the safety element. Let's say you're wrong, let's say you're treating an AVM and you think okay I'm going to attack

from the vein side, well, if you're not successful from the vein side, you've lost nothing. The risk in all of these folks is, if you're in the artery and you don't understand that the artery is feeding significant tissue,

these are where all the catastrophic, disastrous complications you've heard so much about have occurred. It's because the individuals do not understand that they're in a nutrient artery. So, when in doubt direct puncture

and stay on the venous side. You can't hurt yourself with ethanol and that's why ethanol is as safe as it is when it's used properly. So, three B finally is multiple in-flow arteries/arterioles shunting into an aneurysmal vein

this is multiple out-flow veins. So direct puncture, coils into multiple veins multiple sessions. So, here's an example of that. This is with alcohol this is a gentleman I saw with a bad ulcer,

and this looks impossible correct? But look at the left hand arteriogram, you can see the filling of veins. Look at the right hand in a slight oblique. The answer here is to puncture that vein. Where do we have our coil.

The answer is to puncture here, and this is thin tissue, but we're injecting there. See we're right at the vein, right here and this is a combination arteriogram. Artery first, injection into the vein.

Now we're at the (mumbles), alcohol is repeatedly placed into this, and you can see that we're actually filling the nidus here. See here. There's sclerosis beginning destruction of the vein

with allowing the alcohol to go into the nidus and we see progressive healing and ultimately resolution of the ulcer. So, a very complex lesion which seemingly looks impossible is cured by alcohol in an out-flow vein.

So the Yakes classification of AVMs is the only one in which architecture inform treatment and produces consistent cures. And venous predominant lesions, as I've shown you here, are now curable in a high percentage of cases

when the underlying anatomy is understood and the proper techniques are chosen. Thanks very much.

- Great, thank-you very much, a pleasure to be here. My disclosures. So, we've talked a little bit about obviously percutaneous and thrombectomy techniques. Obviously we have catheter-directed thrombolysis with TPA, but what happens when we can't use TPA

mechanical techniques? We've discussed several of them already in this session, I'm going to try to kind of bring them together and note the differences and how they evolved. And really look at fragmentation, rheolytic therapy, vacuum assisted devices, and vacuum and suction devices.

So when do we need these? Patients that can't tolerate thrombolysis, can't get TPA, that have a high risk of TPA, or maybe there is a situation we need a rapid response. We're trying to create flow and establish flow as much as possible and a lot of times we use this

in combination therapy if we've already hurt. What's the ideal device? I think there are multiple different characteristic's that could define the ideal device. Obviously we want it simple to use, We want it to be reproducible,

we want it to remove a lot of thrombus, but minimize blood loss and trauma to the vessels and to the blood cell. These are just some of them. There's a lot of mechanical thrombectomy devices right now on the market continuing to grow,

both in the arterial and venous system so I think this is going to be an evolution. We started really using mechanical fragmentation with a pig tail and spinning a pig tail. We used that. A lot of times the patient with severe massive pulmonary embolism.

These we're really small antidotes, small case reports. Will Kuo, looked at these in the 2009 and basically saw over all clinical success, about 86% using these mechanical devices. Then we had some that were even more automated.

All these did was break up the clot. So you have the Trerotola Device , Cleaner Device, really almost in the dialysis space. Rheolytic Throbectomy, we've already heard about. Some of how it works and the advantages. Really I think this is the first time we've saw

a system which would try to aspirate and remove some of that thrombus as it got broken up. The PEARL registry really showed for the first time, maybe we can get this done within 24 hours, can we get this done in one session? Unfortunately in this registry only about three or

four percent of patients actually had just rheolytic therapy alone without any TPA. We've discussed a little bit about the use of Ango and this type of device in terms of bradyarrhythmia's and that may be a limitation. But I think we can still use it particularly

outside of the chest. So What about suction devices? You can have a catheter, I think a catheter suction device is very limited. We use that in the arterial tree when there is a small thrombus, a small embolus, I think

we're very limited, not only in the amount of thrombus we can remove but the amount of suction we can apply. Other types like almost mechanical, very simple to use systems is the aspire device. Well you can basically create and suction a

limited area and then help you aspirate the thrombus. And then to the other extreme. We're going to hear my next speaker talk about Angiovac, again a different system, a different system requires a patient on bypass large 26 french devices.

Where we can actually go in and deal with a large amount of thrombus, like this patient had a thrombus cave on both iliac veins. And to be able to basically come with this vacuum aspiration system over wires and kind of pulling them out and you get these little canisters,

seeing what you've actually removed. Very gratifying. But takes a lot of work to get it going. We've heard a little bit about vacuum assisted with the Indigo system. With a system of creating a constant continuous vacuum.

We now have eight french catheters with incredible aspiration volume, almost 20cc's, I'm sorry you can get up to 140cc's of thrombus in a minute can be aspirated quickly. Here is a patient, 80 years old, colorectal CA. You can see the thrombus in the right leg.

There was actually a mass invading this vein. That is where we wanted to use thrombolysis, really went a head and you can see the amount of thrombus. Cleared this out with some passage. You can see this here, the separator. You started seeing thrombus especially when

its acute it kind of looks like this. It's kind of gelatinous, things that we've already seen, and then went ahead and placed a stent, dilated that stent. Had to clean up some more with the device

on top of the stent, but with a good result without needing any TPA. Other types of extraction devices we've seen the Inari device, again this is like a stent Triever device, a nitinol ring we can use this in the pulmonary arteries.

And we've already seen previous and talked about the ClotTriever device Again remove that thrombus, put it into a bag and remove it. So again, capture and removal of thrombus. And this is a solution without the need of TPA. New kid in the block the JETi device

Again very similar to aspiration Indego device, but at the same time it has a jet to macerate the clot and kind of break up the clot a little to smaller areas so we can able to thromb and take more out. I think really here what I've seen and Dr. Razavi

showed me this case. Being able to treat a patient quickly, treat that patient very quickly you can see the amount of thrombus being able to, within about an hour and 15 minutes, get all that thrombus, then create patency in that vein and he showed

some early initial good data. Over the last year we did have a paper that was presented here and published this year in the Journal of Vascular Surgery, venous and lymphatic disorders and again pulled multiple patient's, again showing that

it affective and safe. We still need better data. We need to figure out which patients are best treated with which devices and which again will be affective. Thank-you very much.

- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first

before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.

We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column

from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.

Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,

which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied

and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal

amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,

but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced

from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,

organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC

seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.

You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.

So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these

biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...

Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be

most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.

We have to work that out, I hope. Calcification is generally a very late feature in this process. Thank you very much.

- You already heard about different devices which can finish the treatment of acute DVT in the lab and I would like to add one of the devices which is quite widespread in Europe. And share the first study on this device. This is called the Aspirex device. So what is the objective?

Post traumatic syndrome after proximal DVT, I think that's clear. 25% of the patient are at risk for developing post traumatic syndrome. I think that is clear and some of these patient even expect severe post traumatic syndrome.

We already saw this ATTRACT trial outcome and we learned that especially patient with Iliofemoral DVT might benefit from treatment, invasive treatment of Iliofemoral DVT but of course, we need to know that is catheter-directed thrombolysis causes issues

and therefore our way should be to go away from thrombolytic therapy to a pure mechanical thrombectomy approach. This is a typical case example of a patient, 20 year old female patient who came to the emergency room with that leg on the left side in the morning,

back pain in the evening and this is clear that it is a descending Iliofemoral DVT in that patient caused by May-Thurner syndrome. So, with modern devices like this Aspirex, mechanical thrombectomy device, the 10 French device is able to aspirate up to 130 millimeter,

ml per minute of clots. You see that this can be effectively treated and then stinted within the May-Thurner syndrome within one session approach. So, but, what is clear of course that we need to get data

for these modern Mechanical Thrombectomy devices and therefore, we conducted clinical follow-up study to evaluate safety and efficiency of that Aspirex Mechanical Thrombectomy device. This device is based on the Archimedic principle which you can see here it comes with six up

to 10 French systems and with that you are able, as I already showed to sac 130ml of thrombus per minute. So these are the study details I want to show you. We treated 50 psychs, 56 patients with acute, subacute and acute on chronic which means up to 3 months of symptoms patients with Iliofermal DVT.

We performed IVIS on all these patients. We found May-Thurner syndrome in at least half of these patients as a reason for the Iliofermal DVT. You see the patient demographics. Some of the patients had even malignancy condition. A lot of patients were on oral contraceptives.

Here are the clinical symptoms within our cohort. Most of the patients came with swelling and rest pain. The rVCSS at the beginning was 4.5 within this cohort. Most of the traumatic lesions were on the left side involving even the profunda and the common femoral vein in this cohort.

You see here the excess which we used for treating these Iliofermal DVT, we used in the main part of the cohort, the left popliteal vein access or left femoral vein access. 84% were treated with 10 French system, the Aspirex device. As I mentioned we used IVIS

to analyze underlying pathologies. We found in most of the patients underlying pathologies and this explains why we implanted stents in 100% of the patients. You see the treatment duration which was in mean 94 minutes within this treatment cohort.

These are the patency analysis within one year. You see patency at 12 months, 87% percent in these patients, which we could follow up after 12 months. Here you see the Post-thrombotic syndrome analysis after 12 months so only low PTS

and some kind of moderate PTS were seen in these patients. There were no severe Post-thrombotic syndrome. Most of the patients just had a little bit of swelling after that procedure. Of course, it's important to mention safety and those end points.

There were just some small punctures associated, site being complicationS. Of course re-hospitalization is a severe adverse event which you can see here. But there were of course no bleeding events in this cohort. And to follow up

on this much more multicentric perspective trial, we just started a multicenter trial on this and we'll follow up patients up to five years within this just initiated multicenter registry. And I think we can show some preliminary data next year. Thank you very much.

- Thank you Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try

to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.

And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,

secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group

is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted

by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.

And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use

those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,

but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.

For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions

for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,

and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.

But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,

so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at

the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions

at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR

predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive

of iliac limb reinterventions. Thank you very much.

- Thanks Frank, for inviting me again. We know very well that CAS and CEA are, and will remain, emboli-generating. This is an algorithm in which we can see the microembolic profile during unprotected carotid stenting. But I am a vascular surgeon, oriented to an endovascular approach, and I believe strongly

in carotid artery stenting renaissance, when we use tips, tricks and new devices. So the real difference between the two procedures are between 0 and 30 days, and this is demonstrated by the result of 10 year by CREST and by ACT 1. So, but the procedure must be protected.

Because as the Kastrup metanalisys said, the unprotected procedure are three, four-fold increase for cerebral protection embolic. And these are the recommendations from European Society of Cardiology and American Heart Association, regarding

the use of embolic protection devices. But what kind of embolic protection device? We know very well that the cerebral distal protection have some strengths and some weaknesses. And the same is for the cerebral proximal protection with the strengths and weaknesses.

So, but this is rarely used, both in the rest of Europe and in Italy. But what about dissent? We are four studies with only prospective, including a population cohort larger than 100 patients. From Italy, from Germany, from Piotr Michalik,

from Poland, again from Italy. As these are the results that are near with the rod centered stent, with very satisfactory results. With very low rate of... This is the CLEAR-ROAD study, with very low rate of complication.

This is a total of 556 patients who underwent stenting with the new generation of stent. This is the incidence of adverse events at 30 days. So, how we can apply the benefit to our procedures with OCT? And OCT demonstrated the safety of new stent design. And why I use OCT in carotids?

With two main issues. A high definition of carotid plaque, and the correct interaction between plaque and stent. With the high definition of carotid dark in order to identify the plaque type. The degree and area of stenosis,

the presence of ulceration, and the thrombus. I study the interaction between plaque and stent. In order to study the stent apposition, the stent malapposition, the fibrous cap rupture, and the plaque micro-prolaps. So this data I published last year on

EuroIntervention, with the conclusion that in relation to the slice-based analysis, we have the correct comparison with conventional stents, and the incidence of plaque prolapse was absolutely lower. So in conclusion, why I strongly believe in a reinvigoration of carotid stenting?

For the use of better embolic protection device. For the use of newer mesh covered stents, and definitively, OCT proves it as shown. Thank you for your attention.

- Oh, thank you, dear colleague, that's a very long title. This is my disclosure, this. We are all very efficient for treating all those patient, but sometimes, especially on the very long recanalization, we may fail to reenter into the very precise distal landing zone,

and that's when we fail, please do not panic. That's how to perfectly reenter into the distal lumen and I think that's the retrograde approach. Distal puncturing is very useful and very efficient, very safe technique to increase the long recanalization. And it needs to be consider very, very rapidly,

very quickly, usually in my daily practice this is in less than 10 minutes after failure to rentry into the distal zone. Thus, we have many site of puncture, of distal punctures, and what is also very important,

this is to have the very dedicated devices. Usually I use a 16-gauge needle, and also this is quite always a sheathless technique. Thus, let me share with you this case and answer to all the question. This is a case with an long occlusion

of on the right side of the SFA. This I've used, as maybe many of us, the crossover technique. The crossing was really not a problem. It was quite difficult, we have used many guidewires

and also many support catheter but we crossed finally to the distal zone, but it was impossible to reenter very precisely and very safely into the distal SFA into the P1 popliteal artery. That's once again no hesitation.

We do a direct puncture into the P1 popliteal artery zone. The patient have been always prepared before, and, as you may see, this is an 16-gauge needle. That's after, once again, we inserts the guidewires and note this is a sheathless technique and directly thereafter the support catheter

and this is so very important to inject to be sure that we are very precise for the punctures. After this is a two team work, one from below and one from above,

and this is the mix between two 3D dissection and the main goal, this is to connect one dissection with the other and also thereafter is to insert one guidewire into the other support catheters to have at the end only one guidewires. And after we use a telepherique technique

by pulling the balloon for the predilitation of the first opening of the SFA by pulling on the guidewires that is exiting on the proximal popliteal arteries. And only at the end you may exchange the way of the guidewires to move it distally

and thereafter you push on the balloon that is inflated during at least three minutes for the distal sealing. And this is the initial control that is quite, very, very bad. By the way, I'm answer

to the other question, "When is it important to stent?" And especially I know that we are into a less metal left behind era, but it's a very, very good indication for sustaining these recanalized long lesion,

especially flow limiting dissection and residual stenosis. And this is what we have made for obtaining this by the end very, very good result. Thus, in conclusion, for the long recanalization, especially if it's very, very calcified,

experience is definitely required. And we needs to be familiar with a lot of guidewire and support catheter of a very good portfolio. The retrograde access that made, this is very safe, and that may increase technically the success rate and the stenting, I mean the scaffolding is quite

always necessary on the long recanalization. And keep in mind that the patience is really the key of all those procedures. Thank you.

- Good afternoon, Dr. Veith, organizer. Thank you very much for the kind invitation. I have nothing to disclose. In the United States, the most common cause of mortality after one year of age is trauma. So, thankfully the pediatric vascular trauma

is only a very small minority, and it happens in less that 1% of all the pediatric traumas. But, when it happens it contributes significantly to the mortality. In most developed countries, the iatrogenic

arterial injuries are the most common type of vascular injuries that you have in non-iatrogenic arterial injuries, however are more common in war zone area. And it's very complex injuries that these children suffer from.

In a recent study that we published using the national trauma data bank, the mortality rate was about 7.9% of the children who suffer from vascular injuries. And the most common mechanism of injury were firearm and motor vehicle accidents. In the US, the most common type of injury is the blunt type

of injury. As far as the risk factors for mortality, you can see some of them that are significantly affecting mortality, but one of them is the mechanism of injury, blunt versus penetrating and the penetrating is the risk factor for

mortality. As far as the anatomical and physiological consideration for treatment, they are very similar to adults. Their injury can cause disruption all the way to a spasm, or obstruction of the vessel and for vasiospasm and minimal disruption, conservative therapy is usually adequate.

Sometimes you can use papevrin or nitroglycerin. Of significant concern in children is traumatic AV fissure that needs to be repaired as soon as possible. For hard signs, when you diagnose these things, of course when there is a bleeding, there is no question that you need to go repair.

When there are no hard signs, especially in the blunt type of injuries, we depend both on physical exams and diagnostic tools. AVI in children is actually not very useful, so instead of that investigators are just using what is called an Injured Extremity Index, which you measure one leg

versus the other, and if there is also less than 0.88 or less than 0.90, depending on the age of the children, is considered abnormal. Pulse Oximetry, the Duplex Ultrasound, CTA are all very helpful. Angiography is actually quite risky in these children,

and should be avoided. Surgical exploration, of course, when it's needed can give very good results. As far as the management, well they are very similar to adults, in the sense that you need to expose the artery, control the bleeding, an then restore circulation to the

end organ. And some of the adjuncts that are using in adult trauma can be useful, such as use of temporary shunts, that you can use a pediatric feeding tube, heparin, if there are no contraindications, liberal use of fasciotomy and in the vascular technique that my partner, Dr. Singh will be

talking about. Perhaps the most common cause of PVI in young children in developed countries are iatrogenic injuries and most of the time they are minimal injuries. But in ECMO cannulation, 20-50% are injuries due to

ECMO have been reported in both femoral or carotid injuries. So, in the centers are they are doing it because of the concern about limb ischemia, as well as cognitive issues. They routinely repair the ECMO cannulation site.

For non-iatrogenic types, if is very common in the children that are above six years of age. Again, you follow the same principal as adult, except that these arteries are severely spastic and interposition graft must accommodate both axial and radial growths of these arteries, as well as the limb that it's been

repaired in. Primary repair sometimes requires interrupted sutures and Dr. Bismuth is going to be talking about some of that. Contralateral greater saphenous vein is a reasonable option, but this patient needs to be followed very, very closely.

The most common type of injury is upper extremity and Dr. McCurdy is going to be talking about this. Blunt arterial injury to the brachial artery is very common. It can cause ischemic contracture and sometimes amputation.

In the children that they have no pulse, is if there are signs of neurosensory deficit and extremity is cold, exploration is indicated, but if the extremity is pulseless, pink hand expectant treatment is reasonable. As far as the injuries, the most common, the deadliest injuries are related to the truncal injuries and the

mechanism severity of this injury dictates the treatment. Blunt aortic injuries are actually quite uncommon and endovascular options are limited. This is an example of one that was done by Dr Veith and you can see the arrow when the stent was placed and then moved.

So these children, the long-term results of endovascular option is unknown. So in summary, you basically follow many tenets of adult vascular trauma. Special consideration for repair has to do with the fact that you need to accommodate longitudinal

and radial growth and also endovascular options are limited. Ultimately, you need a collaborative effort of many specialists in taking care of these children. Thank you.

- Good morning. I'd like to thank Dr. Veith and Symposium for my opportunity to speak. I have no disclosures. So the in Endovascular Surgery, there is decrease open surgical bypass. But, bypass is still required for many patients with PAD.

Autologous vein is preferred for increase patency lower infection rate. And, Traditional Open Vein Harvest does require lengthy incisions. In 1996 cardiac surgery reported Endoscopic Vein Harvest. So the early prospective randomized trial

in the cardiac literature, did report wound complications from Open Vein Harvest to be as high as 19-20%, and decreased down to 4% with Endoscopic Vein Harvest. Lopes et al, initially, reported increase risk of 12-18 month graft failure and increased three year mortality.

But, there were many small studies that show no effect on patency and decreased wound complications. So, in 2005, Endoscopic Vein Harvest was recommended as standard of care in cardiac surgical patients. So what about our field? The advantages of Open Vein Harvest,

we all know how to do it. There's no learning curve. It's performed under direct visualization. Side branches are ligated with suture and divided sharply. Long term patency of the bypass is established. Disadvantages of the Open Vein Harvest,

large wound or many skip wounds has an increased morbidity. PAD patients have an increased risk for wound complications compared to the cardiac patients as high as 22-44%. The poor healing can be due to ischemia, diabetes, renal failure, and other comorbid conditions.

These can include hematoma, dehiscense, infection, and increased length of stay. So the advantages of Endoscopic Vein Harvest, is that there's no long incisions, they can be performed via one or two small incisions. Limiting the size of an incision

decreases wound complications. It's the standard of care in cardiac surgery, and there's an overall lower morbidity. The disadvantages of is that there's a learning curve. Electro-cautery is used to divide the branches, you need longer vein compared to cardiac surgery.

There's concern about inferior primary patency, and there are variable wound complications reported. So recent PAD data, there, in 2014, a review of the Society of Vascular Surgery registry, of 5000 patients, showed that continuous Open Vein Harvest

was performed 49% of the time and a Endo Vein Harvest about 13% of the time. The primary patency was 70%, for Continuous versus just under 59% for Endoscopic, and that was significant. Endoscopic Vein Harvest was found to be an independent risk factor for a lower one year

primary patency, in the study. And, the length of stay due to wounds was not significantly different. So, systematic review of Endoscopic Vein Harvest data in the lower extremity bypass from '96 to 2013 did show that this technique may reduce

primary patency with no change in wound complications. Reasons for decreased primary patency, inexperienced operator, increased electrocautery injury to the vein. Increase in vein manipulation, you can't do the no touch technique,

like you could do with an Open Harvest. You need a longer conduit. So, I do believe there's a roll for this, in the vascular surgeon's armamentarium. I would recommend, how I use it in my practices is, I'm fairly inexperienced with Endoscopic Vein Harvest,

so I do work with the cardiac PA's. With increased percutaneous procedures, my practice has seen decreased Saphenous Vein Bypasses, so, I've less volume to master the technique. If the PA is not available, or the conduit is small, I recommend an Open Vein Harvest.

The PA can decrease the labor required during these cases. So, it's sometimes nice to have help with these long cases. Close surveillance follow up with Non-Invasive Arterial Imaging is mandatory every three months for the first year at least. Thank you.

- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update

about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures

and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.

So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy

and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.

As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura

off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image

of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures

including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut

because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein

are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,

I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.

23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,

first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious

about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,

and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases

of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged

on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required

in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.

- Thank you very much. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,

12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end

or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three

now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing

that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,

they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.

The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal

and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients

were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.

That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.

Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known

that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage

for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available

in about a month, thank you.

- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide

and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter

is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues

that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement

of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side

and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,

then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,

coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,

and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques

with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation

of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.

We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go

so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side

or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.

Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.

On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded

and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.

Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.

Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,

despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients

to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,

and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,

and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.

- Thank you very much, so my disclosures, I'm one of the co-PIs for national registry for ANARI. And clearly venous clot is different, requires different solutions for the arterial system. So this is a device that was built ground up to work in the venous system. And here's a case presentation of a 53 year old male,

with a history of spondylolisthesis had a lumbar inner body fusion, he had an anterior approach and corpectomy with application of an inner body cage. And you can see these devices here. And notably he had application of local bone graft and bone powder

and this is part of what happened to this patient. About seven days later he came in with significant left leg swelling and venous duplex showed clot right here, and this extended all the way down to the tibial vessels. And if you look at the CT

you can see extravasation of that bone powder and material obstructing the left iliac vein. And had severe leg swelling so the orthopedic people didn't want us to use TPA in this patient so we considered a mechanical solution. And so at this day and age I think goals of intervention

should be to maximize clot removal of course and minimize bleeding risk and reduce the treatment or infusion time and go to single session therapy whenever possible. Our ICUs are full all the time and so putting a lytic patient in there

reduces our ability to get other patients in. (mouse clicks So this is the ClotTriever thrombectomy device. It has a sheath that is a 13 French sheath and they're developing a 16 French, that opens up with a funnel

after it's inserted into the poplitiel. So the funnel is in the lower femoral vein and this helps funnel clot in when it's pulled down. The catheter has this coring element that abuts the vein wall and carves the thrombus off in a collecting bag

that extends up above to allow the thrombus to go into the bag as you pull it down. So you access the popliteal vein, cross the thrombosed segments with standard techniques and you need to then put an exchange length wire up into the SVC

or even out into the subclavian vein for stability. And then the catheter's inserted above the clot and is gradually pulled down, sort of milking that stuff off of the wall and into the bag that is then taken down to the funnel and out of the leg.

So this is the patient we had, we had thrombus in the femoral and up into the IVC. Extensive, you can see the hardware here. And it was very obstructed right at that segment where it was, had the bone material pushing on the vein it was quite difficult to get through there

but finally we did and we ballooned that to open a channel up large enough to accommodate ClotTriever catheter. We then did multiple passes and we extracted a large amount of thrombus. Some looking like typically acute stuff

and then some more dense material that may have been a few days worth of build up on the wall there. We then stinted with an 18 by 90 across the obstructed segment and this was our completion run.

It's not perfect but it looks like a pretty good channel going through. This is the hardware not obstruction at that level. Hospital course, the patient had significant improvement in their swelling by post-op day one. Was discharged on compression and anti-coagulation.

He returned about two months ago for his three month follow-up and really had very minimal symptoms in the left leg. Venous duplex showed that the left common femoral was partially compressible but did have phasic flow and the stent appeared to be open through it's course.

So of course this is an anecdote, this is early in the experience with this catheter. There have been numerous improvements made to ease the use of it and do it in fewer steps. And so we're starting a ClotTriever outcomes registry

to enroll up to 500 patients to begin to define outcomes with this device. It does offer the promise of single session therapy without lytic administration and we'll see how it performs and which patients it works best in through the registry.

Thank you very much.

- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries

that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations

on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th

how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.

Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.

It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.

The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.

So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this

with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,

placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,

this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous

catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm

coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.

And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,

and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,

nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot

in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area

and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.

Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.

Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,

endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)

- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.

The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,

however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,

defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought

to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.

I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have

right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.

This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,

small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have

SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented

five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.

The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by

a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of

atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for

inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries

are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.

- Thank you very much for the kind introduction and thank you very much to you Frank for being here once again to this outstanding symposium. So I have to report a rather rear technique, it's a revival of a technique, and to be honest it's a technique which originally comes from Cardiology. Cardiologist intervented the technique of Crush-Stenting.

Combining balloon expandable stents and we do this also in endovascular therapy for the reconstruction for example of the aortic bifurcation. Combining self expanding stents and balloon expandable stents. We do this sometimes in complications

or for complication management in emergency situations, combining balloon expandable stents, each other. And sometimes we use it if we have malplaced a stent in the distal SFA, we have crush with self expanding stent with another one and we've reported these kind of complications in one of our booklets.

But how to deal with occluded self expanding stents we implanted previous many months ago in the distal popliteal artery or in the SFA, usually we use standard debulking techniques. We use DCBs if we can pass the lesion intraluminally. But if this fails, then we might come into trouble

and then probably we have to go around the stent. That means we have to perform the so called pier technique and probably we have to trespassing pier wise the subintimal space to create a neo-lumen. This was almost reported 10 year ago with one case report but probably it was not that recognized.

There was another case report in Japan some years ago and it was called the |Double-Barrel Restenting technique. We nowadays use this called crush stenting technique with for example Hydrophilic Guide Wires with support catheters, we combine them. Very often we have to use the so called re-entry technique

and then once we have created the neo-lumen, we use balloon angioplasty. Then we implant a stent and we mainly use self expanding stent probably the interwoven nitinol stent. We feel this might be the most appropriate stent to overcome this situation.

But we need to use dual antiplatelet immediately in these cases and this is necessary for the use of self expanding stents, nitinol stents, for carbon stents for example, like the Viabahn as mentioned earlier for the interwoven nitinol stent. Once again dual antiplatelet therapy is of utmost importance

in order to avoid any re-occlusion of these things, you see we always perform different planes of the file angiogram, and at least one plane with the bended knee for 90 degree. And while doing that we can see how the stent works and if we need probably another stent proximally or distally

in order to support this technique for technical successful outcome. So my conclusions are rather clear, crush stenting is really a rear exception, it is a challenge, it can be a challenge. You need to dedicate to technique,

you need dedicated devices, you have to go for the pier technique, you have to be ready for re-entry devices and you need then an aggressive re-stenting of the neo-lumen and we call it crush stenting combined with intermediate dual antiplatelet therapy.

And probably the advantages are clear, you have a high technical success endovascular means. You have high intermediate term patency rates in these small patient populations. And the stents which are required for this are self expanding stents and I probably would go for

interwoven nitinol stent. Thank you very much for your attention high appreciate it. (audience applauds)

- Yeah, thank you Dr. Asher, and again, I want to give credit to Dr. Zheng, one of our fellows who put together this work. So duplex surveillance for lower extremity revascularization, I think we all do that for vein grafts. It's less well accepted for prosthetic grafts. It's controversial for peripheral stent grafts,

and it's very controversial for peripheral stents. If we had time, I'd like to poll all of you and ask how many of you do a duplex scan after you put in a peripheral arterial stent, but more importantly, how many would intervene if you find the velocities are increasing.

So why do it? Well, revision of failing stents may yield better patency rates than if you intervene after the stent has occluded. You may not be able to restore patency if the stent has already occluded, I mean,

some of you may think you can always do that, I know I can't always do that. And performing endovascular treatment is obviously easier than converting to open surgery. So we reviewed 172 stents in 30 iliac and 89 fempop arteries.

Some were overlapping stents, so we kind of said there were 119 segments that we analyzed. The treated length for the iliac artery was about seven and a half centimeters, and for fempop, was about 12 centimeters. And we did duplex surveillance

in our accredited vascular lab in our office. We measured the peak systolic velocity, and the PSV ratios, every two centimeters within the stent but also in the adjacent proximal and distal arteries. We considered it an abnormal duplex finding, I think pretty much consistent

with what you would do for a vein graft, also, if you had a focal PSV over 300, uniform PSVs throughout the stent less than 45, or a ratio more than three, we would say that probably corresponds with more than a 75% stenosis

and generally we would intervene. We did the duplex one week after we put in a peripheral stent, and then about every six months. The follow up averaged about two years. So of these 119 stented segments, about half of 'em stayed normal.

All of the duplex criteria stayed normal during the entire follow up, nothing needed to be done. But interestingly, of the other half, they developed at least one abnormal duplex criterion. 40 of the 57 cases we intervened on, but of the 17 other cases we did not intervene,

either due to patient refusal, or the surgeon felt, well, let's just keep an eye on it, five did remain patent for a short follow up, but 12 of the 17 went on to occlude. Of the 12 occluded segments, we found that if there was more than one

abnormal duplex finding and you did not treat, 70%, again the numbers are small, but 70% occluded, compared to if you had the normal duplex findings, only 3% occluded, and this was highly significant. So of the 12 occluded stents, what happened? Well six we didn't do anything,

they were just for claudication, and the patients chose not to have open surgery. But four, we did try to open 'em and could not, and they needed a bypass, mainly for limb salvage. But two, we couldn't do anything, and they ended up with amputations.

So the bottom line in this relatively small series was if a stent occluded, they didn't necessarily do well and you couldn't open 'em up. So in conclusion, duplex surveillance for lower extremity stents, and that's what we're talking about,

can significantly predict stent occlusion based on these criteria, and the absence of any criteria strongly predicted stent patency. We even have a little disagreement, frankly, in my own group about how aggressive to be for these.

I tend to be pretty aggressive and intervene. Maybe during the discussion we can talk about this. Thank you.

- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,

valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction

but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique

to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the

sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness

but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have

smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.

Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse

and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap

we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid

valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility

to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put

in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction

disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.

Thank you.

So I think when it comes to distal bypasses and ultra-distal bypasses it's all about how we make our decision. We know now that early intervention these patients have better outcome. We use waveform analysis to make our decision about how critical their skin is

we use different topical anesthesia depending the patient's fitness. I think this is just one important point that patient's with dark skin did not show all the full range of skin changes and patients get this dark foot sign

even before they start necrosing their skin. It's very important how we give our anesthetics we use vascular anesthesia with special interest prevascular disease because these patients are quite labile. We use even sometimes inotropes during the procedure

and post operative to maintain a good blood pressure. We believe that short bypasses have got better outcomes. Dr. Veith, have already published in the 80s about short bypasses also doing now the Tibiotibial bypasses on the look anesthetic. Some patients with very high risk for general anesthesia.

And our study we showed that the majority of our patients, who had ultra-distal bypasses had the bypasses from either popliteal or SFA artery. We use different techniques to improve on how to take our bypasses from the proximal anastomosis distally. So we use hybrid revascularization, we use drug-eluting

balloons, and stenting of the SFA and popliteal artery, so we can perform our bypass from the popliteal level. We even use Remote Endarterectomy to improve on our length of the inflow. So by doing remote endarterectomy of the SFA

and popliteal artery, we can take the bypass quite distally from the popliteal artery to the foot level. This is a patient who got critical leg ischaemia on the right side limited, venous conduit. We did remote endarterectomy of her SFA and popliteal artery. And then we can

easily take the bypass from the popliteal artery down to the foot level. On the left side, she had hybrid revascularization with SFA stenting and ultra-distal bypass. We use venous conduit in almost all our patients with ultra-distal bypass.

In distal bypasses we can PTFE but the majority of our patients have long saphenous veins or even arm veins. We started using Omniflow in our infected patients for distal bypasses with quite good results. We scan all our veins prior to the procedure

to make sure that we got good quality vein and amount to perform the procedure. We have published in our small veins series less than 3mm, we still have a very good outcome in distal bypasses. Especially when we do tibial bypasses

or dorsalis pedis bypasses we turn the grafts anatomically. You can see in this angiogram the graft going through the interosseous membrane down to the foot level. We put our incision a bit immediately on the foot level so if there is necrosis of the wound on the foot level that we don't expose the graft, especially when we

knew the patient was coming from the lateral aspect through the interosseous membrane. We select our bypasses especially in the foot level using the duplic scanogram, angiogram or CT angiogram. During the procedure we don't clamp our arteries we use the Flo-Rester and Flo-Through prothesis

to stop patients from bleeding while we're doing it. And we've never used tourniquet before all this has been published. Hand held doppler is the only quality control that we do we don't do on-table angiograms and we find this quite useful for our patients.

We can do the debridement and at the same time while we're doing the bypass at the ankle level. As for anticoagulation and antiplatelet therapy We do antiplatelet therapy for all patient with distal and ultra-distal bypass. And we use heparin and warfarin for patients

who have got redo surgery. Graft surveillance for all our patients Unfortunately, we can only afford it in the NHS for one year, but if the patient get an intervention they go for another full year. Salvage angioplasty is essential for these patients

and we treat these patients as quite as a emergency when they present. So, conclusion, Mr. Sherman, ladies and gentlemen, distal and ultra-distal bypasses require good planning. We use veins for all our bypasses when it comes to the foot level and ultra-distal bypasses,

and of course selecting the target vessel in the foot is very important. Graft Surveillance is essential to maintain quality and outcome for these patients. Thank you very much.

- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed

is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome

is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement

and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.

So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.

We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy

which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures

that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.

As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.

So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,

and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.

So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.

It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,

'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula

and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.

It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically

a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.

Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal

vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.

Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding

the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody

who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test

confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,

so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,

although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.

It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get

a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.

And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,

immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.

We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.

So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,

and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.

DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,

when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.

- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.

And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,

as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,

presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,

as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.

So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.

Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,

and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.

Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there

in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,

but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,

but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,

but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion

that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer

and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.

And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.

And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,

treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.

And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.

We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat

with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,

and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.

So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.

Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen

and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.

(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.

Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.

And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily

arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,

it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this

florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.

We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation

in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,

which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen

of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.

- [Narrator] Okay, very interesting hypothesis.

- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.

And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.

And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,

but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.

The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.

And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,

or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.

And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome

occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity

Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,

such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.

When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.

We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.

And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.

Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.

Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial

And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05

and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options

that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.

- Thank you Professor Veith. Thank you for giving me the opportunity to present on behalf of my chief the results of the IRONGUARD 2 study. A study on the use of the C-Guard mesh covered stent in carotid artery stenting. The IRONGUARD 1 study performed in Italy,

enrolled 200 patients to the technical success of 100%. No major cardiovascular event. Those good results were maintained at one year followup, because we had no major neurologic adverse event, no stent thrombosis, and no external carotid occlusion. This is why we decided to continue to collect data

on this experience on the use of C-Guard stent in a new registry called the IRONGUARD 2. And up to August 2018, we recruited 342 patients in 15 Italian centers. Demographic of patients were a common demographic of at-risk carotid patients.

And 50 out of 342 patients were symptomatic, with 36 carotid with TIA and 14 with minor stroke. Stenosis percentage mean was 84%, and the high-risk carotid plaque composition was observed in 28% of patients, and respectively, the majority of patients presented

this homogenous composition. All aortic arch morphologies were enrolled into the study, as you can see here. And one third of enrolled patients presented significant supra-aortic vessel tortuosity. So this was no commerce registry.

Almost in all cases a transfemoral approach was chosen, while also brachial and transcervical approach were reported. And the Embolic Protection Device was used in 99.7% of patients, with a proximal occlusion device in 50 patients.

Pre-dilatation was used in 89 patients, and looking at results at 24 hours we reported five TIAs and one minor stroke, with a combined incidence rate of 1.75%. We had no myocardial infection, and no death. But we had two external carotid occlusion.

At one month, we had data available on 255 patients, with two additional neurological events, one more TIA and one more minor stroke, but we had no stent thrombosis. At one month, the cumulative results rate were a minor stroke rate of 0.58%,

and the TIA rate of 1.72%, with a cumulative neurological event rate of 2.33%. At one year, results were available on 57 patients, with one new major event, it was a myocardial infarction. And unfortunately, we had two deaths, one from suicide. To conclude, this is an ongoing trial with ongoing analysis,

and so we are still recruiting patients. I want to thank on behalf of my chief all the collaborators of this registry. I want to invite you to join us next May in Rome, thank you.

- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,

both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,

and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms

non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches

versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,

that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require

more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage

than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased

due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations

impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion

during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion

after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing

the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials

where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this

from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph

that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents

with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,

whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.

And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent

also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,

and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.

So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,

always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.

Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)

- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro

or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire

because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,

or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,

very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D

in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--

radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about

to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.

So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where

the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist

to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here

to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric

reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I

mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic

close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to

understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.

Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use

Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.

We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.

You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.

Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial

phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,

the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,

very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone

and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.

In other words can offer higher value in patient care. Thank you.

- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years

of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).

It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,

it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases

that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it

was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.

And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted

inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted

selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.

In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients

stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.

This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,

and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,

and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.

- Thank you very much both. It was a great pleasure to see you. I continue to be grateful for the guidance you have given me over the years. Thank you to the organizers for advising me to speak. These are my disclosures. So really there are two questions posed by this topic.

One is, is the patent popliteal vein necessary? I would assume from this is it necessary for patency and symptom relief to be achieved in treating patients with both acute DVT and potentially chronic. And has the evolution formic mechanical therapy

led to over stenting. Which means we have to ask the question what is an appropriate rate for stenting. I am not sure we know the answer to that. So being able to answer over stenting requires us to know how many patients

actually need the stent in the first place in acute DVT treatments. The problem is essentially this. Is that when we form lithic therapies and this is a classic case of treatment formed with formic and mechanical device

but without a follow up using lithic in the patient for whom lithic was not feasible. You end up opening up a vessel but you can see from the image on the left hand side that there is a degree still of luminol contrast deficit suggesting some cult left behind

in the external iliac vein. Well there is obviously a May-Thurner legion at the top. The question of over stenting is one of do we just stent the May-Thruner and extend it down into the external iliac vein to trap that thrombus

or would a period of time of lithic have resulted in this clot resolving and not needed a stent at the end of it. To get to the question of how many people should be stented. The only way we can really do this

is try and exstipulate from the literature to some extent. This is the short and long term outcome from the Kevin study. Where there is ultrasound follow up of patients underwent standard treatment only.

And a additional group in the patients had catheter-directed thrombolysis. We can see there that the patients did six months in catheter-directed thrombolysis group is around 60%. And the patency seen with the non treated group

is around 40%. If we kind of use these numbers as a guide we probably expect therefore that the stent rate would be somewhere between 40 and 60 percent. To account for treating the outflow structure that presumably patients see at six months.

But this is clearly not a very rebost method of being absolutely clear on who needs stents. Additional method is we don't really have and answer for who should be stented at the end of a procedure. So if you look at the massive variability

in the other studies. We see that attract stent rate is approximately 28% for the study. Which is obviously a operative discretion and has been criticized for that reason. But there is no comment on the Popliteal vein

or Popliteal vein patency. Cavent did an stent rate of 15% again with no real comment on whether the Popliteal vein was open and it wasn't a prerequisite for treatment in the study. This contrast with the Ansberg Aspirex Registry.

Which is a registry of a purely mechanical device to aspirex clot and the stent rate is 100%. Baekgaard Copenhagen used a catered-directed thrombolysis with a mandated open popliteal vein for purpose to be in the study. He has a stent rate of 60%.

My own personal experience of 160 odd patients is that were stenting around 80% of patients with outflow legion at the end of treatment. And were not really bothered by whether the popliteal vein is clear or not. But that doesn't necessarily answer the question

whether it makes a difference in the long run. So its very difficult even looking at the data we have because there is no standard definition of what a outflow stenosis is. There is no objective measure for an outflow stenosis. So stenting becomes and operative discretion decision.

But you would have to say that if your taking purely mechanical devices and the stent rates are going up to 100% that the inclination would be that there is potential for formic mechanical therapy to lead to overstenting and increase use

for stents for sure. In our experience then we had 81 patients who had CDT alone verse 70 patients who had AngioJet Thrombectomy. The basic characteristics of the group are pretty much identical.

With similar ages and no difference between whether the thrombus with left side or right side of body or so on. And these are the patency curves for the different groups with equivalent primary, primary assisted and secondary patency over two yeas.

We had no difference in stent rates with the median stenting of 80% in both groups with two stents used in average for each of those patients. However in our practice AngioJet is rarely used alone. So we had 70 patients for whom AngioJet was used. 24 of those where AngioJet was used up front

as the first line of treatment followed by some CDT. We have tended find that if we wanted full clock clearance. We have always had omit to some extent. And single stage therapy is quite difficult to achieve unless you spent a lot of time in it.

Patency in the popliteal vein is clearly affected by some extent. These are our follow up results if we don't have a patent popliteal vein at the end. It does drop off in stent patency. So the conclusions then I think.

Is that patent popliteal vein is necessary for long term results. But you can still treat patients that have acute popliteal vein for larsons that is not a contraindication. Pure mechanical therapies may well lead to higher stent rate.

But is this a bad thing or a good thing? We don't really know this at this stage as to what the long term outcomes will be. Thank you very much.

- This is a little bit more detailed explanation of the pathophysiology behind Type IV AVM's. Medical disclosures are none. And this is the Yakes classification and this is Type IV lesion we are going to talk about now. So, this angioarchitecture has not been described before, and was first described in the Yakes classification.

What is so unique? It has multiple arteries, arterioles, but these arterioles form innumerable fistulas that are of a microsize, and they infiltrate the affected tissue. So, this is, this can affect every kind of tissue,

skin involvement and muscle involvement, and other than brain AVM, bleeding occurs if mucosa involvement is present or if an ulcer is present. So, we have to think about the definition of an AVM, which is an artery to vein connection

without an intervening capillary bed. But, what applies in Type IV? As you can see here, very nice example of this infiltrating type is that the tissue where the AVM is located is also viable, so the assumption is that

normal capillary beds are interspersed into these innumerable AVMs existing next to the malformed AVM fistulas, and this is a new definition of AVM. So, how to access this lesion? Of course, transarterial is possible

with a catheter or micro catheter. If anatomy doesn't allow transarterial approach, direct puncture is an option. Also, as you can see, in the direct puncture in the lower video, you can see the venus drainage of these fistulas,

and direct puncture of the vein compressed to reflux ethanol into the fistulas is also an approach. But, what is the challenge here? If you want to treat this lesion, you have to keep in mind

that you don't want to occlude the capillaries that are supplying the tissue. So, to find the right treatment approach, the physiologic concept is often important to understand that the arteriovenous fistulas drain into multiple veins and arterialize these veins

so we have a high pressure on this venus outflow site. The normal capillaries have a normal outflow too but this is of lower pressure, and this comes to competition between the arterialized veins and the normal venus outflow, which is, which is inferior to the normal capillary outflow.

So, what follows is a restriction of normal tissue flow with back-up to the capillaries, and backing up into the arterial inflow. So, we have the situation that the arterial venus fistulas have a lower pressure, lower resistance, and an increased arterial flow

compared to the normal capillaries, and this has to be taken into advantage for treatment. How can this be achieved? Thicken the fluid and dilute the ethanol by creating a mixture of 50/50 contrast and ethanol. So, this mixture will follow the preferential flow

into the arteriovenous fistulas in transarterial injections bearing the normal capillaries. So, if it's possible to puncture into the fistulas, pure ethanol can be used, but especially in transarterial access where normal nutrient vessels can be filled,

50:50 mixture contrast is the key to treat a Type IV AVM, Type IV Yates AVM, and here, you can see, using this approach, how this AVM can partly be treated in many several treatment sessions. And here you can see the clinical result. So, this huge ulcer, after seven treatments, healed

because of the less venus hypertension in the lesion. So the additional benefit of 50/50% ethanol contrast mixture is that your injection is visible on flouroscopy so you can see if which vessels you are including. You can react and adjust the pressure you're injecting. So, it also has to be considered

that the more you give diluted, the more total ethanol can be needed, but it's not efficient in larger vessels. This is also the advantage that you just treat the microfistulas. It's of importance that you use non-ionic contrast

as ionic contrast precipitates in the mixture. So here, you can see again, see the Type IV AVM of the arm and hand, which I already showed in my first talk, and here, you see the cured result after multiple sessions showing good arterial drum without fistulas remaining.

So, the conclusion is that Yakes Type IV is a new entity. It's crucial to understand the hemodynamics and the concept of 50/50 contrast ethanol mixture to treat this lesion with also a curative approach. Thank you very much.

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