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V-block Assisted Sclerotherapy VBAS NTNT
V-block Assisted Sclerotherapy VBAS NTNT
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Sclerotherapy For Telangiectasia
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anastomosisangiogrambailbypasscarotidCarotid bypassCEACFAdurableembolicendarterectomygoregrafthybridHybrid vascular graftinsertedlesionnitinolpatencypatientperioperativeproximalPTAptferestenosisstenosistechniquetransmuralvascular graft
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aneurysmaorticchimneyChimney EVARChimney graftdisappearedendograftendoleakendoleaksgraftsnitinoloccludeoversizingparallelpatternscansealingshrinkageskeletonSnorkelstenttherapeuticthoracoabdominaltreattypezone
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Boston ScientificMedtronicParadise (ultrasound ballon)Peregine (Chemical denervation system)Renal denervation systemSymplicity SpyraltherapeuticVessix (RDS
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brachialC-GuardcarotidCASCovered stentcumulativedemographicdeviceembolicembolic protection deviceenrolledexternalInspire MDminormyocardialneurologicneurologicalocclusionongoingpatientsproximalratestenosisstenttiastranscervicaltransfemoral
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adjudicatedanticoagulationarmsbioabsorbableBioconvertible IVC filterBTG Interventional MedicinecavalclinicalcomparescomplicationscontraindicationdeviceDVTendpointfavorablyfilterfilteringfiltersfracturehydrolysisimagedimplantocclusionorthopedicovinepatientspercentperforationretrievalriskSentrysymptomatictherapeuticthrombosistransientvenogramvenograms
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Aorto-Renal BypassAspiration SystemGore Viabahn VBX (Gore Medical)PenumbraPenumbra’s Indigotherapeutic

ok vblock assistant sclerotherapy always

called the bass another non-thermal non-domestic not available in the u.s. it's think of it as an inverted vena caval filter with a PTFE coding it's basically a plug that you put up at the subpoena formal junction and then

there's a dual catheter system here that as you inject sclerosis and liquids frozen it sucks blood out through the other luminous two lumens here so you're injecting a collapse Fame compared to injecting a dilated vein with blood in

it and it's a disposable system this is it being done you inject one syringe and the blood gets sucked out of the other one and you pull back relatively quickly as Pope a crate is really not such a big deal very early things

Ralph come back in Germany has the longest experience with this there's some experience in Israel actually went in and did four cases with him it's very relatively simple to do so in conclusion

- I think there'll be a little bit of duplication here cuz he talked about a lot of things that I put in here. I've no disclosures. The Goals of Sclerotherapy is damage of the endothelium with vascular fibrosis and obliteration. The idea is to use the minimal dose of sclerosant and minimal concentration and avoid injury

to the surrounding normal vessels and tissue. Of course, I won't go into a lot of detail about the history and physical, but what is very important is trying to get some realistic expectations. I saw some incredible results just now.

I don't know if I get that all the time, and so I do want my patients to be aware that perfection is I usually don't seem to really get that. So the consent's very important and photographic documentation is extremely important

because you really do want to show em what it looked like beforehand cuz many times they forget where they started. Just like Dr. Miyake said determine the source of the spider vein's very important. If there's axial vein problems,

I'm not suggesting you have to do a duplex on everybody, but if you have evidence of varicosities, venous insufficiency you might you're not going to get very good results if you have axial vein reflux particularly in line with where

the spider veins and telangiectases are. Same with perforator veins, you may have an issue there, and if you're just treatin' the spiders and not gettin' the source. Dr. Dillavou is going to talk about reticular veins next, but I do emphasize the importance of treating

the feeding veins that are feeding into the spider complex. The equipment, well these are now absolutely required for me and use to be I may not have had to have em, but now I do. I have to have magnification, course you need sclerosants, syringes, needles, and cotton balls.

I like the butterfly needle for the larger veins and 30 gauge for the spiders. There are these polarized lights or vein lights which sometimes come in handy. You've seen the infrared imaging now in the last two talks. I'll show you a little bit of that.

I personally don't use it, but I do think there are probably some cases where it come in very handy, and of course compression stockings and cotton balls and tape even though I don't compress routinely for just spider veins.

Basic Principles, treat the large to small, proximal to distal which you do with varicose veins. The most important though is what Dr. Miyake just mentioned. You want the lowest effective concentration, but in particular, you want to minimize the plunger pressure.

Sometimes you can get a little frustrated when you're trying to get into a vein, you don't want to really inject hard at all or you will get an ulceration. And post-op compression, again is somewhat controversial, at least in my mind, but ambulation of course

is very, very helpful. Contraindications, course allergies, acute DVT, PAD, acute SVT, most of the things you would an active infection in the extremity, you're not going to treat that. The Sclerosants are divided into detergents,

osmotics, and chemical irritants. The main detergents are sodium tetradecyl sulfate and polidocanol. These are primarily what I use in my practice cuz they're FDA-approved and I tend to like to have that when I'm treating patients,

and the concentrations listed here which are in line with what you just saw. There is this study of Sclerotherapy of Telangiectases comparing tetradecyl and polidocanol to a control of isotonic saline and of course there was a significant difference

between the sclerosants and isotonic saline thank goodness. The only thing I'm not real think this study's that helpful cuz it compared one percent STS to .5 polidocanol. I don't think that's a fair comparison

usually I use .1 to .2, and I think STS and tetradecyl are fairly equivalent. The osmotic agents you just heard about, but you know about saline probably, hypertonic saline but also hypertonic dextrose, or there's the combination of saline and dextrose which is a sclerodex.

Again, not really available here. Chemical irritants are glycerin and chromate glycerin. Again, very viscous, low ulcerative capabilities, but again not FDA-approved for this. I don't really use it routinely. There are other sclerosants out there,

but I don't know of anybody using them for telangiectases. Technique, lowest effective concentration again, results determined by the concentration and contact time so that's why I'll say use a low concentration but when you inject, let it sit there a second as you're injecting, just for a few seconds,

maybe 10 seconds even. That contact time helps a lot. I'm already out of time, and I still have quite a bit here, but here's some videos. That's me using a polarized light source. We'll skip through all that.

Here's treating the reticular vein that feeds the spider veins, lower cartoon to kind of show you what I was talking about there. I think you'll probably got the concept but again, if you don't treat the feeder vein,

you're probably not going to get very good results. Here's that infrared technology. Now, I can't seem to skip, okay Complications, well you just actually heard a very good talk on that, so I'll probably stop here since I'm already out of time.

So, I was going to run through that but basically you've already seen it well covered, so I'll stop here.

- 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.

- Like to thank Dr. Veith and the committee for asking me to speak. I have no conflicts related to this presentation. Labial and vulvar varicosities occur in up to 10% of pregnant women, with the worst symptoms being manifested in the second half of the pregnancy.

Symptoms include genital pressure and fullness, pruritus, and a sensation of prolapse. These generally worsen with standing. Management is usually conservative. Between compression hose, cooling packs, and exercise, most women can make it through to the end of the pregnancy.

When should we do more than just reassure these women? An ultrasound should be performed when there's an early presentation, meaning in the first trimester, as this can be an unmasking of a venous malformation. If there are unilateral varicosities,

an ultrasound should be performed to make sure that these aren't due to iliac vein thrombosis. If there's superficial thrombosis or phlebitis, you may need to rule out deep venous extension with an ultrasound. When should we intervene?

You may need to intervene to release trapped blood in phlebitis, or to give low molecular weight heparin for comfort. When should a local phlebectomy or sclerotherapy be performed? Should sclerotherapy be performed during pregnancy?

We know very little. Occasionally, this is performed in a patient who is unknowingly pregnant, and there have been no clear complications from this in the literature. The effectiveness of sclero may also

be diminished in pregnancy, due to hormones and increased venous volume. Both polidocanol and sodium tetradecyl sulfate say that there is no support for use during pregnancies, and they advise against it. So what should you do?

This following case is a 24 year old G2P1, who was referred to me at 24 weeks for disabling vaginal and pelvic discomfort. She couldn't go to work, she couldn't take care of her toddler, she had some left leg complaints, but it was mostly genital discomfort and fullness,

and her OB said that he was going to do a pre-term C-section because he was worried about the risk of hemorrhage with the delivery. So this is her laying supine pre-op, and this is her left leg with varicosities visible in the anterior and posterior aspects.

Her ultrasound showed open iliac veins and large refluxing varicosities in the left vulvar area. She had no venous malformation or clot, and she had reflux in the saphenofemoral junction and down the GSV. I performed a phlebectomy on her,

and started with an ultrasound mapping of her superficial veins and perforators in the labial region. I made small incision with dissection and tie ligation of all the varicosities and perforators, and this was done under local anesthesia

with minimal sedation in the operating room. This resulted in vastly improved comfort, and her anxiety, and her OB's anxiety were both decreased, and she went on to a successful delivery. So this diagram shows the usual location of the labial perforators.

Here she is pre-op, and then here she is a week post-op. Well, what about postpartum varicosities? These can be associated with pelvic congestion, and the complaints can often be split into local, meaning surface complaints, versus pelvic complaints.

And this leads into a debate between a top down treatment approach, where you go in and do a venogram and internal coiling, versus a bottom up approach, where you start with local therapy, such as phlebectomy or sclero.

Pelvic symptoms include aching and pressure in the pelvis. These are usually worse with menstruation, and dyspareunia is most pronounced after intercourse, approximately an hour to several hours later. Surface complaints include vulvar itching, tenderness, recurrent thrombophlebitis, or bleeding.

Dyspareunia is present during or at initiation of sexual intercourse. I refer to this as the Gibson Algorithm, as Kathy Gibson and I have talked about this problem a lot, and this is how we both feel that these problems should be addressed.

If you have an asymptomatic or minimally symptomatic patient who's referred for varicosities that are seen incidentally, such as during a laparoscopy, those I don't treat. If you have a symptomatic patient who has pelvic symptoms, then these people get a venogram with coils and sclerotherapy as appropriate.

If they are not pregnant, and have no pelvic symptoms, these patients get sclero. If they are pregnant, and have no pelvic symptoms, they get a phlebectomy. In conclusion, vulvar varicosities are a common problem, and usually conservative management is adequate.

With extreme symptoms, phlebectomy has been successful. Pregnancy-related varicosities typically resolve post-delivery, and these can then be treated with local sclerotherapy if they persist. Central imaging and treatment is successful for primarily pelvic complaints or persistent symptoms.

Thank you.

- Thank you, Tim, and thank you, Frank, for giving me the opportunity to address this specific problem of the gutter endoleaks, which has been described up to 30% after ChEVAR and parallel grafting. But I have to say that in the most papers, not only gutter endoleaks were included,

but also new onset of type Ia endoleak. One paper coming from Stanford addressed specifically the question, how we should deal with the gutter-related type Ia endoleak, and they conclude that in the vast majority of the cases, these gutter endoleaks disappear

and the situation is benign. And based on my own experience, I can confirm this. This is one of the first cases treated with parallel grafts for symptomatic thoracoabdominal aneurysm. And I was a bit concerned as I saw this endoleak at the end of the angiography,

but the lady didn't have any pains and also no option for open or for other type of repair, so we waited. We waited and we saw that the endoleak disappeared after one month. And we saw also shrinkage of the aneurysm after one year.

So now, the next question was how to prevent this. And from the PERICLES registry, but also from the PROTAGORAS, we learned how to deal with this and how to prevent. And it's extremely important to oversize enough the aortic stent graft,

more than treating with the EVAR, normal EVAR. We should reach a sealing zone of at least 15, 20 millimeters. And we should avoid also to use more than two chimney grafts in such patients. The greater the number of the chimney used,

the higher is the risk of type Ia endoleak. And last but not least, we should use the right stent graft. And you see here the CT scan after using a flexible nitinol skeleton endograft on the left, and the gutters if you use a very stiff,

stainless steel skeleton in such situations. The last question was how to treat these patients. And based on the PERICLES, again, we should distinguish three different patterns. One is due to an excessive oversizing of the graft with infolding.

I have only one case, one professor of pathology, treated six years ago now without any endoleak due to this problem. The most are due to an undersized aortic endograft. And in the pattern C, we have an insufficient sealing zone and migration of the graft.

Now, we should consider the pattern B. And with an undersized aortic endograft and if the gutter is small, one possible solution would be to treat this patient with coiling, using coils or Onyx to occlude this gutter endoleaks,

like in this patient. And for the pattern C, if the sealing zone is insufficient, well, we should extend the sealing zone using the chimney parallel technique, as you can see in this case. So in conclusion, ladies and gentle,

gutters are usually benign and more than 95% disappeared in the follow-up. But in case of persistence, we should evaluate the CT scan exactly. And in case of oversizing and not enough oversizing and not enough length,

we should treat this patient accordingly. Thank you very much for your attention.

- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent

secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results

in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different

in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,

or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,

PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus

or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk

of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,

but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.

and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.

Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.

So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.

Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.

In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,

and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide

a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.

And an E-portal is being developed for dissemination. Thank you very much.

- 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.

- Thank you Dr. Asher. What an honor it is to be up here with Dr. Veith and Dr. Asher towards the end. You guys are leading by example being at the end of the meetings. So, thank you for allowing me to be up and talking about something

that not a lot of vascular surgeons have experience with, including me. I have no disclosures. On your left, I have listed some of the types of diseases that we most commonly see in the vertebral artery, and there are quite a lot.

And on the right, the standard types of treatment that we pursue in vascular surgery or as a vascular specialist. And often, in the vertebral artery, if we are going to pursue treatment, it's the endovascular route.

But I'll talk a little bit about open surgery. The clinical presentation is often vague. And the things I wanted to point out here in this long list are things like alternating paresthesias, dysphagia, or perioral numbness may be something in the history to look for

that you may not be thinking about when you're thinking about vertebral basilar disease. The anatomy looks straightforward in this picture, with the four segments, as you can see. It gets a little more complicated with just the arterial system,

but then when you start looking at all these structures, that you have to get out of of the way to get to the vertebral artery, it actually can be a difficult operation, particularly even in the V1 segment. The V1 typically is atherosclerotic disease.

V2 is often compression, via osteophyte or musculo-tendon structures. And V3 and V4, at the top, are typically from a dissection injury from sort of stretch or trauma injury. The pathophysiology isn't that well understood.

You have varying anatomy. It's very difficult to access this artery. Symptoms can be difficult to read, and treatment outcomes are not as reliable. But I'm going to take you through a very quick path through history here in the description

of the V1 segment exposure by Dr. Rentschler from 1958. And I love these pictures. Here is a transverse incision over the sternocleidomastoid, just above the clavicular head on the right side. And once you get the sternoclavicular head divided, you can see the longus colli muscle there.

Anteromedial is the carotid. Of course, you surround that with a Penrose drain. And then once you do that, you can separate your longus colli, and deep to that, the vertebral artery just easily slips right up, so you can do your transposition.

It's not quite that easy. I've done one of these operations, and it was difficult finding t e. And, again, here is on the opposite side, you can see the transposition in this cartoon.

Dr. Berguer is the world's expert, and a lot of this open surgical work comes out of the University of Michigan. Here is a study looking at 369 consecutive extracranial vertebral artery reconstructions. You can see the demographics of clinical presentation.

And note that about 34% of patients are presenting with hemispheric symptoms, with 60% in the vertebral basilar distribution. 300 of these reconstructions were for atherosclerosis. And the outcomes were pretty good. Before 1991, there wasn't really a protocol in place

in assessing and doing these procedures. And you can see the stroke and death rates of 4.1 and 3.2% respectively. And then the outcomes after 1991 are considerably better with a five year patency rate of 80%. So, in summary, vertebral artery disease is,

I think if you review this, is somewhat under diagnosed. Revascularization is a viable option. Most often, it's endovascular. But if you have endo-hostility, then an open, particularly for the V1 segment, may be a better option.

And this requires people with good operative experience. Thank you very much.

Thanks very much, Tom. I'll be talking about thermal ablation on anticoagula is it safe and effective? I have no disclosures. As we know, extensive review of both RF and laser

ablation procedures have demonstrated excellent treatment effectiveness and durability in each modality, but there is less data regarding treatment effectiveness and durability for those procedures in patients who are also on systemic anticoagulation. As we know, there's multiple studies have been done

over the past 10 years, with which we're all most familiar showing a percent of the durable ablation, both modalities from 87% to 95% at two to five years. There's less data on those on the anticoagulation undergoing thermal ablation.

The largest study with any long-term follow up was by Sharifi in 2011, and that was 88 patients and follow-up at one year. Both RF and the EVLA had 100% durable ablation with minimal bleeding complications. The other studies were all smaller groups

or for very much shorter follow-up. In 2017, a very large study came out, looking at the EVLA and RF using 375 subjects undergoing with anticoagulation. But it was only a 30-day follow-up, but it did show a 30% durable ablation

at that short time interval. Our objective was to evaluate efficacy, durability, and safety of RF and EVLA, the GSV and the SSV to treat symptomatic reflux in patients on therapeutic anticoagulation, and this group is with warfarin.

The data was collected from NYU, single-center. Patients who had undergone RF or laser ablation between 2011 and 2013. Ninety-two vessels of patients on warfarin at the time of endothermal ablation were selected for study. That's the largest to date with some long-term follow-up.

And this group was compared to a matched group of 124 control patients. Devices used were the ClosureFast catheter and the NeverTouch kits by Angiodynamics. Technical details, standard IFU for the catheters. Tumescent anesthetic.

And fiber tips were kept about 2.5 centimeters from the SFJ or the SPJ. Vein occlusion was defined as the absence of blood flow by duplex scan along the length of the treated vein. You're all familiar with the devices, so the methods included follow-up, duplex ultrasound

at one week post-procedure, and then six months, and then also at a year. And then annually. Outcomes were analyzed with Kaplan-Meier plots and log rank tests. The results of the anticoagulation patients, 92,

control, 124, the mean follow-up was 470 days. And you can see that the demographics were rather similar between the two groups. There was some more coronary disease and hypertension in the anticoagulated groups, and that's really not much of a surprise

and some more male patients. Vessels treated, primarily GSV. A smaller amount of SSV in both the anticoagulated and the control groups. Indications for anticoagulation.

About half of the patients were in atrial fibrillation. Another 30% had a remote DVT in the contralateral limb. About 8% had mechanical valves, and 11% were for other reasons. And the results. The persistent vein ablation at 12 months,

the anticoagulation patients was 97%, and the controls was 99%. Persistent vein ablation by treated vessel, on anticoagulation. Didn't matter if it was GSV or SSV. Both had persistent ablation,

and by treatment modality, also did not matter whether it was laser or RF. Both equivalent. If there was antiplatelet therapy in addition to the anticoagulation, again if you added aspirin or Clopidogrel,

also no change. And that was at 12 months. We looked then at persistent vein ablation out at 18 months. It was still at 95% for the controls, and 91% for the anticoagulated patients. Still not statistically significantly different.

At 24 months, 89% in both groups. Although the numbers were smaller at 36 months, there was actually still no statistically significant difference. Interestingly, the anticoagulated group actually had a better persistent closure rate

than the control group. That may just be because the patients that come back at 36 months who didn't have anticoagulation may have been skewed. The ones we actually saw were ones that had a problem. It gets harder to have patients

come back at three months who haven't had an uneventful venous ablation procedure. Complication, no significant hematomas. Three patients had DVTs within 30 days. One anticoagulation patient had a popliteal DVT, and one control patient.

And one control patient had a calf vein DVT. Two EHITs. One GSV treated with laser on anticoagulation noted at six days, and one not on anticoagulation at seven days. Endovenous RF and EVLA can be safely performed

in patients undergoing long-term warfarin therapy. Our experience has demonstrated a similar short- and mid-term durability for RF ablation and laser, and platelet therapy does not appear to impact the closer rates,

which is consistent with the prior studies. And the frequency of vein recanalization following venous ablation procedures while on ACs is not worse compared to controls, and to the expected incidence as described in the literature.

This is the largest study to date with follow-up beyond 30 days with thermal ablation procedures on anticoagulation patients. We continue to look at these patients for even longer term durability. Thanks very much for your attention.

- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing

renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is

near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital

pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency

and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,

except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward

endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac

endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.

The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open

conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small

accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited

incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,

but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis

and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.

- Thank you, Ulrich. Before I begin my presentation, I'd like to thank Dr. Veith so kindly, for this invitation. These are my disclosures and my friends. I think everyone knows that the Zenith stent graft has a safe and durable results update 14 years. And I think it's also known that the Zenith stent graft

had such good shrinkage, compared to the other stent grafts. However, when we ask Japanese physicians about the image of Zenith stent graft, we always think of the demo version. This is because we had the original Zenith in for a long time. It was associated with frequent limb occlusion due to

the kinking of Z stent. That's why the Spiral Z stent graft came out with the helical configuration. When you compare the inner lumen of the stent graft, it's smooth, it doesn't have kink. However, when we look at the evidence, we don't see much positive studies in literature.

The only study we found was done by Stephan Haulon. He did the study inviting 50 consecutive triple A patients treated with Zenith LP and Spiral Z stent graft. And he did two cases using a two iliac stent and in six months, all Spiral Z limb were patent. On the other hand, when you look at the iliac arteries

in Asians, you probably have the toughest anatomy to perform EVARs and TEVARs because of the small diameter, calcification, and tortuosity. So this is the critical question that we had. How will a Spiral Z stent graft perform in Japanese EIA landing cases, which are probably the toughest cases?

And this is what we did. We did a multi-institutional prospective observational study for Zenith Spiral Z stent graft, deployed in EIA. We enrolled patients from June 2017 to November 2017. We targeted 50 cases. This was not an industry-sponsored study.

So we asked for friends to participate, and in the end, we had 24 hospitals from all over Japan participate in this trial. And the board collected 65 patients, a total of 74 limbs, and these are the results. This slide shows patient demographics. Mean age of 77,

80 percent were male, and mean triple A diameter was 52. And all these qualities are similar to other's reporting in these kinds of trials. And these are the operative details. The reason for EIA landing was, 60 percent had Common Iliac Artery Aneurysm.

12 percent had Hypogastric Artery Aneurysm. And 24 percent had inadequate CIA, meaning short CIA or CIA with thrombosis. Outside IFU was observed in 24.6 percent of patients. And because we did fermoral cutdowns, mean operative time was long, around three hours.

One thing to note is that we Japanese have high instance of Type IV at the final angio, and in our study we had 43 percent of Type IV endoleaks at the final angio. Other things to notice is that, out of 74 limbs, 11 limbs had bare metal stents placed at the end of the procedure.

All patients finished a six month follow-up. And this is the result. Only one stenosis required PTA, so the six months limb potency was 98.6 percent. Excellent. And this is the six month result again. Again the primary patency was excellent with 98.6 percent. We had two major adverse events.

One was a renal artery stenosis that required PTRS and one was renal stenosis that required PTA. For the Type IV index we also have a final angio. They all disappeared without any clinical effect. Also, the buttock claudication was absorbed in 24 percent of patients at one month, but decreased

to 9.5 percent at six months. There was no aneurysm sac growth and there was no mortality during the study period. So, this is my take home message, ladies and gentlemen. At six months, Zenith Spiral Z stent graft deployed in EIA was associated with excellent primary patency

and low rate of buttock claudication. So we have most of the patients finish a 12 month follow-up and we are expecting excellent results. And we are hoping to present this later this year. - [Host] Thank you.

- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.

Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.

Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care

over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.

Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.

And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed

with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better

treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?

That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents

shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,

deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.

Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.

Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.

Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same

that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?

More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article

a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.

Thank you.

- This one is an easier publication we did, but I do think it's interesting because there are no data for real in the use of the aquatic environment for our lymphedema patients. I have no conflicts of interest to declare, but I declare that I'm really interested in this topic because if you look at the Global Spa & Wellness Summit report,

every single year this is the amount of money that are spent in the business of the aquatic environment and of the spa centers. And we are not behaving so well as vascular specialists because what you're looking at over here is a vision of the literature showing that muscle skeleton system data

are out there in the literature for the benefits of the effects of the aquatic environment, but we as vascular specialists are not producing so much data. Before the publication we put on Phlebology on this topic, just these six papers were dealing with the use

of the aquatic environment for lymphedema patients, and all of them are basically on quality of life measurements, not really on objective data of drainage, so every single day in nice hotels also like this one, you have people going inside the pool

and doing all of these activities, not really knowing what's going on inside their venous system, and something cool could actually happen because if you really think about that every single centimeter of water is performing 0.7 millimeters of mercury in terms of standing load,

so when I have a patient standing up inside the pool at 120 centimeters of depth, his feet is actually over one by 88 millimeters of mercury, so four times the stockings we are usually prescribing. We also know that, of course, activating the muscle pump is fundamental, so what we did was activating

the muscle pump inside the aquatic environment, creating a standardized protocol of exercises that we tested on 32 lower limbs of 16 patients affected by bilateral lymphedema. These patients went inside the pool for doing the standardized protocol:

50 minutes per session, twice per week, for a total of five sessions. The protocol is published on Phlebology, so you can download that for free. Basically it's an activation of all the joints of the lower limb.

What you can have after five sessions of this protocol is a significant reduction of the lower limb volume, that by more than 300 mils. The circumferences of the leg and the subcutaneous thickness measured by ultrasound is significantly decreasing, but the interesting part is this one, I think.

You see over there Michael Jackson with the Moonwalk because we were having patients walking backward because you have the biggest activation of the ankle at that point, and it was interesting to notice that the range of motion of the ankle was increase of up to four degrees, and if you put that into statistics,

it's really interesting to notice that the volume reduction was directly related with a 0.4 correlation to the increase in the ankle motion. The evidence of feeling of the leg was decreased from 7.3 to 5.5 out of ten as a score. The functional ambulation classification,

which is a score for debility of walking, was not significantly changed. Again, everything is on Phlebology if you want to download it, and now we are doing other investigations because of course we could bring some about not just the physical property

of the aquatic environment, but also the chemical properties of the kind of water we are using and on the temperature that we want to use over that. So at the current moment I cannot discuss that. We are under a grant of investigation, but for sure I do think this is a way to go

because it's like killing two birds with one stone because indeed you can have patients that are hypomobile or that are, for example, obese that can perform exercises inside the aquatic environment that they could not perform outside the pool, but I have to say that we didn't find anything new because the guy you see

over there is Conrad Jobst. There is a nice quote by van der Stricht. He was saying we should know the history so to avoid wasting our time trying to open doors that were already opened by others, and the door was already opened by Jobst

because as you know he was an engineer. He was affected by an ulcer and in reality he noticed that when he was standing inside his pool, his ulcers was getting better. Being an engineer he understood that it was related to the standing though and so he created the concept

of the graduated pressure that you have inside the water in the stockings we are now prescribing that are then son of the aquatic environment.

- Now we all have seen one thing. We have to treat AVM's according to their classification angio anatomy. If you have something like, direct arterial venous communications, like pulmonary HHT patients, like the rare patients with inborn arterial venous fistulas,

you will never use ethanol. That's my opinion. That's an opinion. But I think most of us will agree on that. Will you? - [Audience] Yes.

- I think many of us will agree. So would you just do it for a HHT pulmonary patient, you would inject ethanol? - [Audience] No. - So, okay. And the direct arterial venous communications inborn,

they are very rare and they can be beautifully treated with plugs and whatever. These are one part on the AVM patients. Second part is predominantly venous outflow. However you say it's 2B, 3A or whatever. It's a dominant venous outflow

and you can cure them and I say cure, even in my paper there is imaging of follow up, but it's not in the abstract bar. (smiling) So you just, - (laughing)

- So you just occlude the venous outflow, as close to the nidus as you can. So I don't need ethanol for that. I don't need to take the risk for my patient. And so that leaves the type 4 small vessel AVM's. They are, even in my opinion,

not treatable with a polymerizing agent. There is a real place for ethanol. And then you you go to these difficult, more net-like, type 3 or whatever, AVM's, then my opinion is, I do it as long as possible,

with a safe agent. Like pushing in tons of onyx. And if there is something left over, or if there comes something in follow up, because we all need follow up for these patients, then you can finish it with ethanol.

That's my statement. Thank you.

- I think we have time. If there are any questions, please come up to the microphone and any of the panels have questions for each other. I have a number of questions I could ask but I just see if anyone wants to start out. Claudio?

- I have a question Doctor Mark. He show us very nice utilization of this device for occluded limbs. My question is, do you protect in any way the other side? If not, don't you have, you're not concerned

or you're not afraid of pushing clots from one side to the other one when you're manipulating the device? And the second one, do you do this percutaneously? And if that's the case, do you have any concern about having destabilization?

Because once you start to manipulate the clot that is occupying the entire graft, and there is reestablishment of flow in an antegrade flush, and you may have some of that clot dislodge and embolize distant. - Yeah, as I mentioned,

nobody wants to be the guru of limb occlusions. However, we have seen them and we always go retrograde ipsilateral, not seen emboli once from those seven cases and in fact, the 73 we presented at the midwest there was only two instances of embolization

when we utilized this device. And both times we were able to extract those just by going further down with the cat six and both of them was below the knee popliteal. In particular, the acute ones, it's soft and it's no different than watching it in vivo

or in vitro model, as you know better than I, comes out quite easily. - Let's take our question from the audience. - [Scott] Hi, Scott Tapart from Stuart, Florida. So I'd like to poll the panel there about are you doing every single

acute limb ischemia percutaneously? The pictures are elegant, the techniques are elegant, but the last speaker touched on the profoundly ichemic Rutherford 2B patient, where you're most likely going to have to do a fasciotomy. Are you going to the OR

or are you doing this percutaneously and then watching and waiting and seeing about fasciotomy? Or has this changed your fasciotomy approach? - So since we have a number of people, that's a great question. Why don't we start at the end

and let's just go kind of rapid fire, maybe one or two sentences, how do you choose your patients and what do you do with those 2Bs and we'll try to get through everybody. - Sure, so, to reiterate the last slide of the presentation,

essentially anybody with a significant motor or neutral deficit is somebody I tend to do in an open fashion. And if I'm the least bit concerned about doing a fasciotomy or there's evidence of compartment syndrome I do that patient open.

- We try to start endovascular, and if we can clean and reestablish antegrade flow, that would take care of the problem. And of course, I'm a radiologist, so I always consult with my colleagues in surgery and they decide if a fasciotomy needs to be done or not.

And it's that at the end. - Okay, I have to be honest, we start with the selective indication but now we move maybe to 90% of our patients doing percutaneously. We will adjust patients with probably an embolization,

a huge embolization, into the common femoral artery for open surgery. Of course, in our mind, also in the registry, we have some cases of fasciotomy after percutaneous approach so it's not a limitation. - The advantage of acute arterial protocol,

as they all go to the end of asher suite and they all run along our protocol but you can run the option. You get them to treatment quicker because they don't dilly-dally around in the holding room. But then according to how the patient's doing

you can mop up as much clot as you can with the percutaneous technique and then do the fasciotomy when you're done or press head and drip more if you need to. So I think to have an algorithm where you can treat the full spectrum

is what's best for the patient. - I think it depends on the time as well because I did two weeks ago a patient who needed a fasciotomy directly so I performed that first and then it rules out any traumalitic therapy

or whatever that you want to do. And actually, if I do antivascular techniques I usually give a shot or RTPA or something and then go further with it. But anomerization of this patient's arteries as well so prefer actually if it's really a case

that needs fasciotomy just to perform surgical thrombectomy. - Yeah, percutaneous eight French up and over and almost always, you're going to be done with your thrombectomy within about 30 to 45 minutes. I don't think you're adding that much time

and for us, by the time we get anesthesia in him assuming anesthesia's anesthesia no matter what part of the world you're in, so you can get to the hybrid room quicker and then if it's going to fail then you're going to call in the OR or call an anesthesiologist.

- I wouldn't have much else to add. I do think there is some patient selection, if you have an entire SFA, 30 centimeter clot, that's going to take you hours to do so for these thromboembolic things that are 10 centimeters or shorter

lodged in the popliteal TP trunk, this method works really well. I think for the longer patients, you might think about something else. - But just a comment on the general anesthesia. If a patient is in real or really pain,

he can't lie down for 30 minutes, even. I mean, they are rolling in pain and I would do the fasciotomy first because general anesthesia is needed because there is so much pain or, yes, so yeah.

- So, let me say, does that answer it, Scott? So let's, since we have a number of panelists and we're running out of time, how about if we ask each person going down the room, you heard a whole bunch of different speakers here with a lot of experience

and if you haven't used this, there is a learning curve. The learning curve is pretty shallow. Really, a lot of it has to do with controlling your blood loss. But if we ask each person for just one tip

and we'll see if we can get through everybody. If you telling people who hadn't done a lot of this, one tip or one trick, let's see if we can get seven or eight tips and tricks out. So, I'll go last. Let's start back down at that end

and we'll end up at this end. - Sure. Use the largest catheter that the vessel will comply to. - Amen, brother. - I agree with that.

And the way I do it, in order to avoid too much blood loss, I like to engage with a syringe. So I come with my catheter, I hook a syringe in the bag, 20cc or sometimes even larger, and when I have the fish at the end of my line, then I connect to the pump and I continue.

That way if I'm aspirating, I'm not going to aspirate a large volume so I want to engage the clot. And then I bring the clot out. That's my trick. - Okay.

Very nice comment. Of course, I agree with the previous colleagues but I will say that first the trick is really the largest catheter is better, then my idea that I developed during my learning curve is the use of separate to cut away.

I probably use now in 95% of cases because it just makes everything quicker and faster and better. - I use the perclose device for large-bore catheters often and that allows me to pull the plug out, especially if it's fibrous plugs,

safe from the heart without shearing it off on the end of the catheter. I've got one question for Claudio, on that case of the carotid subclabian with the acute carotid occlusion, do you think the nitroglycerin would have helped?

- For the doctor? - For the surgeon. - Absolutely. - And then, change the diapers. - Well, I would advise if you do a surgical embolectomy do it also on the hybrid room

and try to do it also over the wire. Especially be careful if you do it below the knee. I would suggest do it open below the knee, even. - I would say don't afraid to use an eight French for ALI and that closure devices are your friends here. But you can use an eight all the way down to the pop

and then for us, the tibials, we'll use a six. - Yeah, I would agree with that. So I guess my tip would be, I agree with everything everyone said, although I don't use the separator very often in the arterial side, I do in the veins.

But one tip is, if you're not going to use a separator, if you're going to start without it, let's say you want to give it a try, I don't work through a 2E borst because the angle, the eddy currents that form around that 2E borst

trap clots and you constantly have to clean that 2E out so if you're going to start with a focal embolis in the artery my recommendation is take the 2E off, hook up to the vacuum directly, and you'll get less clot stuck in the 2E. If you want to go to the separator

then you can always add that on at the back end. - So I have a question for Fennel. I used a penumbra like a few weeks ago and it ended up really bad because the surrounding catheter from the penumbra, everything got, you know, clotted

and then I didn't have any outflow did I choose the wrong size or what is it that happened, did you see it ever? - We have not had that problem. We're usually working on heparinized patients and have not seen that happen.

- She was heparinized. No? Okay. - Okay. Any other comments? Otherwise, we'll end one minute early

on a nice, long day.

- [Presenter] Thanks again, Laurel, for this kind invitation. We're going to discuss about how I do the treatment for varicose veins for the foot. And we're going to show you our experience for that. I have no disclosure. I came from Natal, Brazil.

There's our wonderful beach that we have there, but we don't have time to go there, unfortunately. This is our hospital, and these are the people that worked with us. To do this treatment we have to pay attention of the history and the physical examination.

It's very important to decide what you can do to these patients, because we have to associate some tools to do this kind of treatment. So phleboscopy, transillumination is very important to define the feeder veins,

so it's very important in this case to show us where is the veins that we feed these spider veins to treat that. And of course, the ultrasound associated with all the physical examinations of course and then the black scan. You can see in this case, a patient does not have any

varicose veins on the thigh, of the leg. They have only varicose veins by the foot. If you can see, the reflux of there, comes from the junction to the foot. If you don't have the good ultrasound

or duplex scan it can have a mistake and treat wrong way these patients. So, what are the tools we have to do to treat these patients? A lot of tools, you can see the liquid sclerotherapy with a low concentration of 75%.

Foam polidocanol for these two concentrations. Of course, transdermal laser, hooks that we can apply in the surgery and polidocanol laser. How about this procedure? This paper from the Netherlands, show us patient satisfaction after ambulatory phlebectomy

of varicose veins, what they conclude about that. The most important factors that influence the patient satisfaction is: discoloration, persistent pain, and the perception of varices after surgery. This last one is very important for us,

because the patient comes to us to be cleaning off veins of the foot, if we miss that everything we did, the patient will complain about after their surgery. We have two kinds of treatment, ambulatory treatment being the option

and the hospital we can do the procedures. We have separate patients with CO grade, CEAP classifications and C2 classifications. When we have a C1 grade classification we use transdermal laser and liquid sclerotherapy. You can see one case is a cosmetic

and one is a severe one. A C2 case we have ambulatory treatment, we have transdermal laser and we associate all this with foam sclerotherapy. But the concentrations are 0.5% and 0.25%, you can see its low concentrations.

At the hospital we have can do almost everything nearly in the same day. Transdermal laser, liquid sclerotherapy, foam sclerotherapy. Yes, we can associate liquid sclerotherapy, sometimes the people say that you cannot do that, but we do that.

In case like this, we also say transdermal laser in spider veins, phlebectomy and you can see in this case we have a use for sclerotherapy and is this is the result of 60 days. This other case that we use phlebectomy and we have to be careful because you

can take nerves, the patient will complain about after surgery. And these are the results. Polidocanol with laser tool, yes, but it's not our routine to use that. In conclusion:

Physical exam and a precise diagnosis of the feet varicose veins is essential to do a good surgery. With all these tools, that we have, the treatment of varicose veins of the foot is safe and effective. This is my fugu in Natal, Brazil.

Thank you.

- Hello, thank you again for the invitation. I have the disclosure here is kind of funny because I'm going to talk about CLaCS but I don't profit on that. Those are the most frustrating result on sclerotherapy and obviously death. These are very frustrating result. Sorry.

And this is not like funny but it's unfortunately the worst part is that all those cases are not published and that's less change from frustrating to devastating, the death cases. Let's talk about the less common, sorry,

the most common problems, skin ulcer. Like skin ulcer. Skin ulcer may be also terrible. Those are slides from my father's collection from the 60s probably. And I suggest you to read this paper.

It took me 20 years to get published with the help of Ted King of this hypothesis from the 70s and he studied on rabbit ears and I cannot have time to explain all that but he simulated the skin ulcer and showed that the causes the reflux to the arterial venous system

and how to avoid it, CLaCS is a great solution and by using the extra 75% due to its high viscosity, you avoid 100% of reflux to the arterial system. Matting is another problem.

Those are theories of my father as well. He said divided in two types of angiogenic where you inject on the telangiectasia and you destroy veins that you wanted to close or you didn't want to touch. And then you have reflux a new reflux and

a lot of telangiectasia. There would be occlusive, where you destroy too much, you destroy the drainage of those telangiectasias. And then how to avoid? Is to be less aggressive or to be more focal. That means treat only the feeder vein

and the telangiectasia and avoid injecting a lot of volume and because those sclerotic agents will reach another vein that you don't want to touch. Pigmentation is another problem. And to control pigmentation of course

you have to have less thrombus and once again ClaCS would be very nice idea because the transdermal lazer causes vein wall edema and contraction and then you inject the Dextrose 75%. And then you have less internal diameter

in the vein, that means you have less outflow, the Dextrose will stay there it's a synergy, and you have less clot, less pigmentation. Also Dextrose is a medium power sclerosing agent that doesn't cause too much pigmentation as the other agents.

Well once again my father, and my father is at the hospital right now, and he probably will not survive, but here is a tribute for him. And he developed this surgical treatment of the telangiectasia by removing

the feeder veins. And, sorry. Here a study with phlebography showing a double perforant insufficient vein, and these telangiectasia wouldn't respond. And that's a complex telangiectasia, not a simple telangiectasia.

Like here another example, the phlebectomy showing the result of the treatment of telangiectasia. Well, diagnosis is very important if you are a skipper of a boat, if you have a special device to diagnose you certainly will have a better result.

And here are very tricky, looks simple to treat but as you compress you see there is a reflux, and this reflux is going have five feeder veins and one is going to the reflux in saphenous vein and patient the patient is CEAP1. Well, I also.

Sorry. Next slide. If you are a painter and you want to paint this wall, it's not easy you need to find a feeder vein and that's why I've developed this classification where you have three, two questions

and you look for varicosities and telangiectasias and here you have, lets go fast, the ultrasound showing reflux and the augmented reality showing if there is feeder vein or not. And here a good example of a patient that was,

the examination would lead to a CEAP 1, but as we exam, we noticed that she's score nine, where she had a long reflux asymptomatic that was treated with endovenous lazer phlebectomy and CLaCS, and that's how we got the result. Then treatment failure is also can be avoided

by a good classification and then CLaCS. If you want to learn more about that, we have a congress, it's going to be the ninth in IMAP in Saul Paulo next year, and I kindly invite you to participate. 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)

- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.

And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.

Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,

it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized

due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage

of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,

which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal

in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak

which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.

And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success

is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent

Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,

an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,

retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered

balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.

At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed

if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.

The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR

combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,

and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.

- Good morning everybody, and thank you for inviting me again for the same topic since five years now. Every time I have to rebuild my slides, and you will see why. So, you all know this story, renal denervation was almost destroyed by The Earthquake on January 9, 2014, and that was when Medtronic announced that HTN-3

did not make it to primary endpoint. What has been achieved since the earthquake? Better techniques with old devices, positive trials with old devices, new devices, and some positive trials with new devices. So, what about better technique?

More is better, that's what we learned, total number of ablation is important, circumferential ablation is important. Go distal is important in distal vessel segments, the nerves are closer to the vessel wall. We have the DENER-HTN heart trial with the old system

which was positive, and we have new devices, like the Symplicity Catheter, Spyral Catheter, the Vessix, Paradise, and Peregrine. So, what about new trials with new devices? Spyral HTN-OFF MED, HTN-ON MED, REDUCE HTN, RADIANCE HTN SOLO, RADOSOUND-HTN,

and Peregrine PMS - TARGET BP OFF-MED trial. SPYRAL HTN - OFF MED was a trial with patients without medications, or permitting discontinuing the oral drug therapy at that time, and they had to make certain values of blood pressure office and 24 hours, and you can see the results.

There was a significant effect in all parameters in systolic blood pressure ties to the blood pressure. 24-hour blood pressure and all these differences have been significant in favor of innovative denervation, so renal denervation certainly works. What about in those patients who are on meds,

and this has also been reported now. You see the patients had to have one to three anti-hypertensive medications. Again, they had to fulfill certain criteria regarding their blood pressure, and when you look at the result safety, it's very safe procedure,

no adverse events occurred, and office blood pressure changed from baseline to six months, it was a significant decrease systolic and diastolic blood pressure as well as 24-hour blood pressure, so renal denervation also works in patients

who are on anti-hypertensive medication. Reduce HTN was a trial with the Vessix system, which is not really a new system, but this is a new trial, and they used a balloon-based radiofrequency technique. They did an off-med study, the primary endpoint was reduction in 24-hour ambulatory blood pressure,

at eight weeks, which probably was too early, and the trial was stopped early due to slow enrollment and because it was determined that the trial could not achieve its primary endpoint at eight weeks, but when you look at the long-term results with this trial, there was actually a significant rate

of proportion of Vessix patients with office blood pressure below 140 versus control after six months, and this was significant and there was also over six months, systolic blood pressure continued to decrease in the Vassix group with a lesser decrease in the control group, and these differences

also have been significant to the match major part. RADIANCE HTN-SOLO trial is using the Ultrasound Based Renal Denervation using a balloon technology. You can see that these patients responded. There was a clear benefit in favor of the technique compared to a placebo group, significant difference 0.001.

Radiosound HTN was a trial, a randomized blinded trial comparing the different techniques, like ablation of the center part of the renal artery, distal part of renal artery, and ultrasound, and there was a significant benefit of ultrasound compared to the ablation of the proximal renal artery only.

Peregrine is using alcohol injected into the adventitial space, also significant effect of this technique, so now we have multiple randomized blinded renal denervation trials, OFF and ON meds, which are clearly positive. The decrease of blood pressure is, without any question,

clinically relevant, but it is smaller than expected and hoped. Everybody is asking, "Does it justify an invasive procedure? "So better not to do it?" At the same time, no major adverse events occurred, so why not to do it?

Everybody agrees that more research is needed. There are other device based approaches which are either stopped or covered by other talks in this, so I'm going to skip this. Thank you much for your attention.

- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old

but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,

and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.

- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,

and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was

revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.

In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat

was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.

Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone

returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.

Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy

with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,

the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.

Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.

So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really

how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017

in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.

Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at

five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery

to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional

independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.

So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,

but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could

help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.

- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification

for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,

also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of

a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,

and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct

arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,

and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding

the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,

mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from

multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views

on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied

by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?

IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.

This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way

to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,

but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.

Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?

And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,

the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.

So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.

Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.

So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,

and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described

in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,

so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example

50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System

is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.

Thank you very much.


- 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 chairman, ladies and gentlemen. I have no disclosures on this topic. So first, in short, the clinical challenge that we confront, this is course entity. As we all know, the primary extracranial carotid artery aneurysm with various etiologies, and it's very nice intervention to perform on it,

very nice surgery and the vascular techniques, but the main question actually, that we have to answer, do we need to treat it at all? And as there is a lack of natural history, we started in 2014 a web-based international registry in which all patients with an extracranial

carotid aneurysm can be included, and we look for clinical and imaging follow up data from admission to 30 days and longer on. I want to give you today an update on status of the registry. So far we included 371 patients.

If you take in acceleration that in all data published so far is only 3,000 patients of which about the health is case reports, I think this is already a large achievement. We are moving on ahead. In the graph you can see that we are

have increasing inclusion rates, and we are little behind in data management. But this seems very promising. About half the patients are derived from the Netherlands thus far. And about half the patients are from

international contributors. About the patient characteristics, about two thirds is male, age is respectively younger as considered to atherosclerotic disease in the carotid territory, as may be expected. What is important on the other characteristics

is that the data are largely comparable between the national and international cohort. About the characteristics of the aneurysm itself, are also there a large comparison between the two cohorts, national and international. A bit more often in the proximal and common

carotid in the international cohorts, and that's probably related as more international patients have been operated on, I come to that in the next slides. Most relevantly, for a primary goal to report also on the natural course,

about half the patients included so far were asymptomatic and had a natural course follow up. About treatment strategies performed, again, large part of the patients are followed up in a conservative fashion. We have some data on endovascular or hybrid approach,

but the large part of the revascularization is primary surgery. And next, to our analysis of natural course follow up, of course we also report on our long term outcomes of surgical intervention. This is the overview of completion of follow up,

there's some work to do as you can see. We expect to report a preliminary results in early next year when the data on the first year follow up is complete for the current cohort. In the meantime, we have large data sets on imaging, therefore we performed already

some analysis on the exceptional tortuosity as we can often see in these cases. We compared four available software packages using two observers and two rounds to define a tortuosity index. And we actually found that for these four

commercially available packages, have all of them have an excellent intraobserver agreement and also agreement between the observer. So, all four of these can be used to perform further imaging. As also we are looking for semi automated

volume measurements to define a standardized follow up in these patients. So for now, I can confirm that the Carotid Aneurysm Registry is an ongoing and observational registry. I think it's the largest registry on ECAA

so far and still growing. I would advise you all today, also to contribute to this registry and you can see the e-mail address for further information update. Thank you for your attention.

- Good morning. I'd like to thank everybody who's in attendance for the 7 A.M. session. So let's talk about a case. 63 year old male, standard risk factors for aneurismal disease. November 2008, he had a 52 mm aneurism,

underwent Gore Excluder, endovascular pair. Follow up over the next five, relatively unremarkable. Sac regression 47 mm no leak. June 2017, he was lost for follow up, but came back to see us. Duplex imaging CTA was done to show the sac had increased

from 47 to 62 in a type 2 endoleak was present. In August of that year, he underwent right common iliac cuff placement for what appeared to be a type 1b endoleak. September, CT scan showed the sac was stable at 66 and no leak was present. In March, six months after that, scan once again

showed the sac was there but a little bit larger, and a type two endoleak was once again present. He underwent intervention. This side access on the left embolization of the internal iliac, and a left iliac limb extension. Shortly thereafter,

contacted his PCP at three weeks of weakness, fatigue, some lethargy. September, he had some gluteal inguinal pain, chills, weakness, and fatigue. And then October, came back to see us. Similar symptoms, white count of 12, and a CT scan

was done and here where you can appreciate is, clearly there's air within the sac and a large anterior cell with fluid collections, blood cultures are negative at that time. He shortly thereafter went a 2 stage procedure, Extra-anatomic bypass, explant of the EVAR,

there purulent fluid within the sac, not surprising. Gram positive rods, and the culture came out Cutibacterium Acnes. So what is it we know about this case? Well, EVAR clearly is preferred treatment for aneurism repair, indications for use h

however, mid-term reports still show a significant need for secondary interventions for leaks, migrations, and rupture. Giles looked at a Medicare beneficiaries and clearly noted, or at least evaluated the effect of re-interventions

and readmissions after EVAR and open and noted that survival was negatively impacted by readmissions and re-interventions, and I think this was one of those situations that we're dealing with today. EVAR infections and secondary interventions.

Fortunately infections relatively infrequent. Isolated case reports have been pooled into multi-institutional cohorts. We know about a third of these infections are related to aortoenteric fistula, Bacteremia and direct seeding are more often not the underlying source.

And what we can roughly appreciate is that at somewhere between 14 and 38% of these may be related to secondary catheter based interventions. There's some data out there, Matt Smeed's published 2016, 180 EVARs, multi-center study, the timing of the infection presumably or symptomatic onset

was 22 months and 14% or greater had secondary endointerventions with a relatively high mortality. Similarly, the study coming out of Italy, 26 cases, meantime of diagnosis of the infection is 20 months, and that 34.6% of these cases underwent secondary endovascular intervention.

Once again, a relatively high mortality at 38.4%. Study out of France, 11 institutions, 33 infective endographs, time of onset of symptoms 414 days, 30% of these individuals had undergone secondary interventions. In our own clinical experience of Pittsburgh,

we looked at our explants. There were 13 down for infection, and of those nine had multiple secondary interventions which was 69%, a little bit of an outlier compared to the other studies. Once again, a relatively high mortality at one year. There's now a plethora of information in the literature

stating that secondary interventions may be a source for Bacteremia in seeding of your endovascular graft. And I think beyond just a secondary interventions, we know there's a wide range of risk factors. Perioperative contamination, break down in your sterile technique,

working in the radiology suite as opposed to the operating room. Wound complications to the access site. Hematogenous seeding, whether it's from UTIs, catheter related, or secondary interventions are possible.

Graft erosion, and then impaired immunity as well. So what I can tell you today, I think there is an association without question from secondary interventions and aortic endograft infection. Certainly the case I presented appears to show causation but there's not enough evidence to fully correlate the two.

So in summary, endograft infections are rare fortunately. However, the incidence does appear to be subtly rising. Secondary interventions following EVAR appear to be a risk factor for graft infection. Graft infections are associated without question

a high morbidity and mortality. I think it's of the utmost importance to maintain sterile technique, administer prophylactic antibiotics for all secondary endovascular catheter based interventions. Thank you.

- Ladies and gentlemen, I'd like to thank the organizers once again for the opportunity to present at this meeting. And I have no disclosures. As we know the modern option for treating Truncal Varices includes Thermal Ablation. Major Venous Tributaries are treated

with phlebectomies, ligation, and foam sclerotherapy using sodium tetradecyl sulfate and polidocanol. The mechanism of action of these agents includes lysis of endothelium, and it takes a very short time to work. And most people use the Tessari technique,

which induces these agents and uses fibrosis of the veins and obliteration of the lumen. And this is how it's done. One of the risks of sclerotherapy may include deep vein thrombosis.

And as we've just heard, the perforator veins are variable anatomy and function, works in very amazing ways. So, what happens to the below knee veins after sclerotherapy? Well the NICE guidelines does not address this issue, and nowhere really is it addressed.

The NICE guidelines reported one of almost 1000 patients with a pulmonary embolism after Ultrasound Guided Sclerotherapy. So, we'd like to propose the term Deep Vein Sclerosis, or Deep Vein Sclerosae, rather than Deep Vein Thrombosis after Sclerotherapy

because it's caused by Sclerotherapy. The veins that they affected are usually patent, but non-compressible on ultrasound. Thrombus is usually absent, but it may be present, and it resolves quite quickly. We treated 386 legs in 267 patients

with CEAP III-VI disease. They had pre-intervention duplex, marking, and identification of perforators, they were treated with compression stockings and low-molecular weight Heparin, and they had serial ultrasound scanning.

Despite meticulous scanning, we identified deep vein sclerosis in 90 of our patients. So 23, almost a quarter. Perforating veins were identified with ultrasound in only 27 of this group, and forgive the mathematics there.

And perforating vein was seen in the post-intervention scans in almost a half after treatment. This is detailed list of the findings. The perforators alone were affected in 41 of these patients. And in 49% of patients, tibial veins and other

below knee deep veins were affected. Interestingly enough, in 24 of these 44 perforators were unidentified prior to treatment. And of these, a total of 49 patients of DVS involved the tibial veins and/or perforators. And, DVS involved the perforator only in 41 patients,

and this is thought to be adequate treatment of the superficial tributaries. 55% of the patients of previously unidentified perforator veins had DVS involved in the tibial veins. Treatment after we've identified this included compression stockings for at least six weeks,

aspirin for 12 weeks, and surveillance scanning. We found that no lesions actually progressed. They were unchanged in about 27%, completely resolved in 51%, and much smaller in about 22%. So, we'd like to propose that these changes

post-sclerotherapy in the below knee veins are different to deep vein thrombosis. The changes are provoked, there's a limited duration of the insult, most patients are low-risk and ambulant, and the patients are generally asymptomatic.

The veins that are non-compressible on ultrasound usually have no thrombus. In conclusion with the chairman ladies and gentlemen, Deep Vein Sclerosae occurs in almost 25% of patients having ultrasound-guided Foam Sclerotherapy, the lesions are of short length,

the course of these lesions appear fairly benign, and are adequately treated with stockings and aspirin, and the majority of these cases resolved or decreased in length within six to twelve weeks, and no lesions progressed. Thank you very much.

- Thank you so much. I have no disclosures. These guidelines were published a year ago and they are open access. You can download the PDF and you can also download the app and the app was launched two months ago

and four of the ESVS guidelines are in that app. As you see, we had three American co-authors of this document, so we have very high expertise that we managed to gather.

Now the ESVS Mesenteric Guidelines have all conditions in one document because it's not always obvious if it's acute, chronic, acute-on-chron if it's arteri

if there's an underlying aneurysm or a dissection. And we thought it a benefit for the clinician to have all in one single document. It's 51 pages, 64 recommendations, more than 300 references and we use the

ESC grading system. As you will understand, it's impossible to describe this document in four minutes but I will give you some highlights regarding one of the chapters, the Acute arterial mesenteric ischaemia chapter.

We have four recommendations on how to diagnose this condition. We found that D-dimer is highly sensitive so that a normal D-dimer value excludes the condition but it's also unfortunately unspecific. There's a common misconception that lactate is

useful in this situation. Lactate becomes elevated very late when the patient is dying. It's not a good test for diagnosing acute mesenteric ischaemia earlier. And this is a strong recommendation against that.

We also ask everyone uses the CTA angiography these days and that is of course the mainstay of diagnoses as you can see on this image. Regarding treatment, we found that in patients with acute mesenteric arterial ischaemia open or endovascular revascularisation

should preferably be done before bowel surgery. This is of course an important strategic recommendation when we work together with general surgeons. We also concluded that completion imaging is important. And this is maybe one of the reasons why endovascular repair tends to do better than

open repair in these patients. There was no other better way of judging the bowel viability than clinical judgment a no-brainer is that these patients need antibiotics and it's also a strong recommendation to do second look laparotomoy.

We found that endovascular treatment is first therapy if you suspect thrombotic occlusion. They had better survival than the open repair, where as in the embolic situation, we found no difference in outcome.

So you can do both open or endo for embolus, like in this 85 year old man from Uppsala where we did a thrombus, or the embolus aspiration. Regarding follow up, we found that it was beneficial to do imaging follow-up after stenting, and also secondary prevention is important.

So in conclusion, ladies and gentlemen, the ESVS Guidelines can be downloaded freely. There are lots of recommendations regarding diagnosis, treatment, and follow-up. And they are most useful when the diagnosis is difficult and when indication for treatment is less obvious.

Please read the other chapters, too and please come to Hamburg next year for the ESVS meeting. Thank You

- It's my pleasure on behalf of the Sentury Trial investigators to present the two year data on the BTG Novate Sentry filter. These are my disclosures. Well, as we have heard this afternoon, it's no surprise to anyone the topic of IVC filter placement is controversial.

We know that IVC filters can protect patients by preventing PE. We also know that retrievable filters that are not retrieved have been reported to have, be associated with some complications. And we talked about FDA advisory,

obviously that has resulted somewhat in a decrease in filter use in this country. Obviously complication rates we've also heard about increase with implant time and include tilting, migration, fracture, perforation and embolization. And retrieval success reduces with implant time.

What's not controversial, and we have heard also about this, is the frequency of PE in this country and the expense associated with it. Obviously, survival benefits have been shown in appropriate populations, that are selected based on known indications. And existing retrieval technology, unfortunately,

as we've heard from Dr. Askandari, has not met the needs of patients when up to 40 to 50 percent are not coming back for retrieval. That was sort of the impetus behind the design of the Sentry Bioconvertible IVC Filter, which is designed to protect patients at transient risk

from PE and reduce complications of existing technologies. It employs a stable frame with filter arms held together by a bioabsorbable filament and designed to provide PE protection during a transient risk period, reduce IVC filter complications, including tilting, migration, fracture, perforation and embolization.

And this just shows an example in vitro and with a CT scan of the filter in the so-called filtering configuration. The filter then automatically bioconverts after the PE risk period is past. That's guaranteed to be in the

filtering position for at least 60 days. It bioconverts by hydrolysis of the bioabsorbable element, which allows the filter arms to retract to the IVC wall, leaving a patent lumen and reducing the risk for IVC occlusion or thrombosis later on, and obviously, the cost of IFC filter retrieval.

Here you can see filters that are in the bioconverted configuration. This just shows the deployment. It's a simple pin and pull seven French delivery system. These stable arms allow this to be placed almost always without any tilting

and is quite easy and accurate to deploy. This is in an ovine modeled pre-clinical study shows in a bioconverted configuration all of the filter elements become endothelialized and in this angioscopic view, really can't even see any of the filter elements.

This is again sort of predicated on something that I believe we're not all that familiar with and that's when the timing of PE occurs. And you can see here, from the trauma literature, orthopedic literature, other literature, on 500,000 patients and in these groups you can see

that over 90 percent of PEs take place in less than 10 days after an initial event and 99 percent of PEs within 20 days. That led the FDA to write a position decision analysis paper, which recommend filter retrieval between

29 and 54 days after implantation. So, on s, 23 sites, 63 operators. You can see this was a relatively imaging-intense protocol with 24 month CT Venogram and CT Venograms also at one month and six months.

Long term follow up, 94 percent of the eligible subjects were imaged at 24 months. You can see that 67.5 percent of the subjects had current PE and/or DVT at the time of enrollment, and 100 percent had contraindication to anticoagulation for some or all of the protection period.

In terms of the composite primary endpoint, there was a high degree of technical success, 100 percent of the patients received the device. 100 percent freedom from new symptomatic PE to 60 days. Two patients had symptomatic caval thrombosis at 8

by angiojet, one by EKOS. And there was no tilting, migration, embolization, fracture or perforation. At 12 months there were no new symptomatic PEs and there were no device related complications out to 12 months.

And at 24 months, two new symptomatic PEs, days 581 and 632,in patients with fully bioconverted filters. There were no device related out to 24 months. Both of these were adjudicated by a clinical events committee as not being device related.

And again, you can see that the bioconversion rate of 96.5 percent compares favorably to published retrieval rates, and we've talked about that. So, in conclusion, the primary endpoint at six months was met with clinical success of 97.4 percent. No new symptomatic PEs at 12 months.

2.4 new symptomatic PEs at 24 months, but no tilting, migration, perforation, fracture or embolization. And the 96.5 percent bioconversion rate compares favorably to published retrieval rates. Thanks very much.

- Thank you very much Raul and our co-chair and also Frank Veith for inviting me again. I'm going to tell you a little bit about flow augmentation. And I have no disclosures related to this. Well, flow augmentation after venous stenting for venous obstruction potentially improves outcome. That's a statement that is

most of the people will support that. Important characteristic of noninvasive compression device after venous stenting is that they improve blood flow inside the newly stented patient,

they stimulate the calf pump muscle, and they're a synergistic tool along anticoagulation, and to decrease the risk for re-occlusion. Well, there are flow devices. Most of the people I think use intermittent pneumatic calf compression

for a few days after the procedure. That can be done but there are now neuromuscular stimulating devices like the FlowAid and the Geko device to stimulate nerves and then the calf won't contract. The physiologic effects of intermittent

pneumatic compression are there. They had been analyzed significantly. There's a decrease of venous stasis and venous pressure, increase flow, increase fibrinolysis, and the blood volume is better and the venous emptying is better.

There's an increased endothelial shear stress, increased the A-V pressure gradient, and there's a decrease in incidence of thrombosis. Those are already published in several papers. Well, what about the neurostimulation device? We have the FlowAid.

FlowAid is a battery powdered neuromuscular electro-stimulation device designed to increase blood flow in the veins. And again this also shows the sequential pattern of neuromuscular electrical stimulation at the calf and causes the calf muscle pump to expel blood

and increase venous, arterial, and microcirculatory blood flow. While these analyses have all been done with healthy volunteers and they show a better outcome then also in intermittent pneumatic compression.

The same is for the Geko device. It's a device which you put along and you stimulate the peroneal nerve, you get a calf contraction. And this also showed in several papers in healthy volunteers that it improves

venous flow, arterial flow, and microcirculatory flow. But it's all analyzed in healthy volunteers, so we said, well, let's do like a short pilot study and see if for even patient with PTS we get the same results, and we looked at that.

But we did a very short pilot in seven patients. We stopped it because we saw already that we need a bigger study, but I will just explain to you what we found in those seven patients. We measured the flow velocity and volume

before and after stenting in the iliac tract to see if we have the increased flow in the common femoral vein in those PTS patients. These are the seven patients, and as you can see it's important

that they don't have a VCSS of 6.4, and the diseased leg, and less than one in the healthy leg, and the Villalta scores will show above 11 on average. So those patients were analyzed and this is what you see. You see

the velocity in the femoral vein before stenting at baseline is, can I point it, yeah, okay, is here. That you see there's a very low velocity. You can increase the velocity with the neurostimulation but there's a higher velocity increase

with the intermittent pneumatic compression. After stenting you see luckily that the velocity has increased, and the stimulation of the neuromuscular is indeed also higher, but the intermittent

pneumatic compression does better. If you look at the volume flow, of course before the treatment, it's low, 32 cc a minute, and then you get an increase with the Geko and an increase with the intermittent

pneumatic compression which is much higher. And after stenting you see that it also improves, you see luckily the stent procedure was successful because we have a much higher flow rate than before the stent procedure. So in conclusion in the literature and the pilot studies

said that neurostimulatory devices have a proven good augmented blood flow in healthy subjects, even better than IPC devices, but there's no experience in PTS patients yet. So this small pilot study shows that the results obtained in healthy subjects

cannot be extrapolated to PTS patients or patients with post stent situations, therefore we are conducting now two randomized studies to compare FlowAid with IPC and the Geko device with IPC, and to see for if this has use, because why is this important?

A potential benefit of the neurostimulation is that you can use it mobile and 24/7 instead of with the IPC procedure which you can only use in a bedridden patient. So if it is as good as or close to, you can use it for a few weeks after stenting

to get the flow up and running and that you have less early stent occlusions. We are also analyzing for if it can replace AV fistula which we do after end of phlebectomies and to prevent really early re-occlusion. And as I said we need those studies to be done

but that the important message is that we don't go home with the fact that those devices, although in healthy volunteers show a very good outcome, they have to be tested in patients with PTS. Thank you very much.

- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want

in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis

is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied

and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple

aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention

adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,

the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that

there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions

a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.

In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure

with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle

and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis

needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.

Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.

In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,

regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate

without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.

An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis

and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.

This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more

in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.

But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.

The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.

Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion

because I have a flight in a few hours. Thank you very much.

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