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HCC with arterioportal Shunt|TACE |68|Male
HCC with arterioportal Shunt|TACE |68|Male
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Surgical Creation Of A Moncusp Valve
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How To Treat By EVAR Complex Aorto-Iliac AAAs In Patients With Renal Transplants, Horseshoe Or Pelvic Kidneys: Technical Tips
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What Morphological Changes On CT After EVAR Predict The Need For Re-Interventions: From The DREAM Trial
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Thrombo-Embolic Complications Of Inflammatory Bowel Disease: Nature, Etiology And Significance
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Challenges And Solutions In Complex Dialysis Access Cases
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Duration Of Anticoagulation For DVT: The Forgotten Trifecta
Duration Of Anticoagulation For DVT: The Forgotten Trifecta
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Single Branch Carotid Ch/TEVAR With Cervical Bypasses: A Simple Solution For Some Complex Aortic Arch Lesions: Technical Tips And Results
Single Branch Carotid Ch/TEVAR With Cervical Bypasses: A Simple Solution For Some Complex Aortic Arch Lesions: Technical Tips And Results
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Long-Term Results Of AV Fistulas And Grafts
Long-Term Results Of AV Fistulas And Grafts
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Endoscopic vs. Open Vein Harvest For Bypasses: What Are The Advantages And Disadvantages Of Each
Endoscopic vs. Open Vein Harvest For Bypasses: What Are The Advantages And Disadvantages Of Each
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Routine Use Of Ultrasound To Avoid Complications During Placement Of Tunneled Dialysis Catheters: Analysis Of 2805 Cases
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Does The ATTRACT Trial Result Change How You Manage Patients With Acute DVT
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Estimation Of Long-Term Aortic Risk After EVAR: The LEAR Model: How Can It Guide And Modulate Surveillance Protocols
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New Developments In The Management Of Blunt Aortic Injuries Using A Practical Grading System: Why It Matters
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Transcript

This is a good case of mine,

hes' a 68 year old male. He has alcohol cirrhosis and esophageal varices, he's not a prisoner. But he doesn't speak English, so just putting that out there. He's a child Pugh A5, he had a total bilirubin of 0.7 his AFP was 43

so not indicative, and his ECOG was 0-1 when he saw me for the first time in clinic and this is what his initial CT scan showed, to from my clinic, he had not been followed up appropriately and just came in with a belly ache and they noted this very large mast in his right hepatic lobe.

Further down you can see that the tumor extends more inferiority and you are getting a very avid enhancement of the portal vein and you can see there's some portal vein thrombosis in there. So the arrow is really pointing at what I was reading as an arterial portal shunt. So knowing that this is what you are going to face ahead of time

sort of can help you plan. So arterial portal shunting diagnosis can very often be made on multiphasic CT scans so you know I'm sure you all get those patients that come from an outside hospital with HCC diagnosis and they have one phase of imaging so it's really important to get that multi phase imaging

CT or MRI because you can make these diagnosis. So this group showed that about 15% of patients can be or actually have this and the diagnosis can be made on CT scan and then they just talked about where these arterial portal shunts are about half of them essential or 24 from a peripheral and then 22 of them are mix. So you can't really tell if they're central or peripheral on the CT

imaging. And then how severe are they, 35% are severe. Severe means that on that arterial phase imaging your portal vein is as bright as your aorta. And 41 or about moderate which is you know.

You can imagine what moderate is and then 24 are mild so you just saying it's within the peripheral areas. Interestingly about half of these patients that do have arterial portal shunting also have portal vein thrombus so even if you just have single phase image and you have portal vein thrombus you can sort of start thinking in your head that these patients may have an arterial portal shunt and they actually

went on to get hepatic and angiography, 22 of these patients went on to get hepatic and angiography and of those patients 86% had arterial portal shunting the author said that they probably all had it they just missed it on angiography. So what's the prevalence really there is not a lot of great data on there you see I went all the way back to 97 to see if I could

actually get a prevalence but overall arterial venous shunting. They said it was about 31%. If you had arterial portal shunting or arterial venous shunting of that, 31% of patients that HCC 92% had arterial portal shunting. So what's the treatment?

So as you can imagine we've all come up with creative things we've been at this meeting all week. And, you go into a room and you can imagine everyone's doing these different things. So, if you can find a single feeding vessel, a coil is a great choice

if you can find it. Glue, if you have a network of vessels and you don't think that glue is gonna get stuck proximally to prevent you from treating the tumor eventually. And particle embolization is a good option. You can use large particles if they don't cross over into the shunting

I had a patient that had a large, we'll get to them in a minute, but it was a very bad complication from outside the hospital. And the other thing is you can try lipidol based embolization and that's not well supported in literature but there are case reports talking about it.

So for my treatment planning, because he had portal vein thrombosis I decided that I was gonna go ahead and do a 190 based on the literature. And so, he showed up to the suites and we had planned for the shunt study. So the initial angiography you can see,

as soon as I'm seeing the arterial phase of imaging. And this is seconds after the injector goes. you can see filling that portal vein, the main portal vein.

And you can see, the filling defect within the main portal vein indicating that he had portal vein thrombus. So, this severe arterial portal shunting was noted. I couldn't find a single vessel, it's just this huge network of vessels that was supplying or communicating with

the portal vein I didn't think I could do glue because I was worried that the glue would embolize the proximal artery and I'll never be able to go back in treat it, and because the tumor was in the right hepatic lobe I just wanted to see is there, I have

had a pulmonary shunt as well as the ulterior portal shunt and so I went ahead and infused the MIA. The lung shunt fraction as is very typical was 20%. And so that brings us to hepatopulmonary shunting. How common is this?

Is it a prevalence of overall again arterial venous shunting is 31% and of those hepatopulmonary shunting is much less so it's 8% of those patients. And all patients with HCC they say the prevalence is about 2.4%. Again in my clinic it's probably much higher than that. So the typical shunting in HCC this is Ron Gaver's/g group who talked

about what's the prevalence based on lung shunt fractions they said about 56% of patients are gonna have no lung shunt fractions to less than 10%. 10 to 20% of lung shunt fraction you got 30% of patients with HCC and those higher lung shunt fractions are going to be 14% of your patients that you are treating.

So they also found that there is correlations how can you sort of predict this on imaging sometimes you can't see this hepatic pulmonary shunts on imaging so if you do have an infiltrate of tumor that was correlated with hepatic pulmonary shunting if you had greater than 50% hepatic tumor burden, if you had portal vein thrombosis or

portal vein compression so the tumor is actually pushing on the portal vein you are going to see a higher degree of hepatic pulmonary shunting. If you have arterial portal shunting that's interesting that also correlated with the hepatopulmonary shunting. And if your tumors are hypervascular,

all tumors are hypervascular so that's not gonna be very helpful again how do you treat this? So embolization again if you can see that single feeding vessel that's fantastic and you can do it again glue is possible particle and hepato-based embolization is also then reported. Systemic therapy with Sorafenib has some literature saying that

if you start patients on Sorafenib you can reduce the shunting, this is the case serious with couple of patients, that they showed that the mean shunt fraction in the patients was 26.5 prior to starting Sorafenib therapy, and post sorafenib therapy, went down

to 7.5. But again the time it takes to treat patients with Sorafenib to get those shunts to come down sometimes can be longer than the patient would survive otherwise. And what about if we do the Y90 what if we,

go ahead and do Y90 therapy is there real risk of radiation pneumonitis? So this is out rehabs group and he found that of his 403 patients now these are patients not only with a HCC but all comers 58 of those patients or 14% actually received greater than three gray accumulative lung dose and of those just so I wanted to highlight that HCC population

74% of those patients with those elevated or high lung shunt fractions were actually patients with HCC with sort of a similar to the data that I showed you earlier. And the mean shunt fraction in the HCC patients was 20% and the mean accumulative

of lung dose is 54 Gy to those patients and his report he had no cases of imaging or clinical real issue of pneumonitis. And so you can quote that to your patients that you know a very large series has shown that there's no risk of having any risk issues with the lungs other patients or other series have sort of talked about may be having radiation pneumonitis.

So really the things to consider when I was treating this patient are you have severe arterial portal shunting on the angiogram because we're seeing filling of that main portal vein and now he's also has a hepatic pulmonary shunt which is almost 20% and so do I go on to do Y90? With an arterial portal shunt you have to really think about where

the beads are gonna go so if they cross over into the main portal vein, where are they gonna lodge? So they are gonna lodge any where in the liver and we have started to do or what I've started to do is if you see these large arterial portal shunts you can do CT spect with your MAA and then you can see where the bead is gonna go because that really is a good indicator.

I had a patient a couple of weeks ago that we did that and it actually shunted to the contralateral lobe, so I felt why don't we just treat the whole liver except all of the beads would have got the contralateral lobe not the lobe where the tumor was. So I would have had an effective dose and I would have just cause atrophy of the wrong lobe of the liver.

So that sort of a trick you can think about. With hepatic pulmonary shunting you have to think about can I get a dose high enough to effectively treat the liver without having it just bypass around and go into lungs. And so if that's the case, do I have to worry about this cummulative/g

lung dose? Do I, do I not or can I do some sort of fancy technique in the end of my hepatic vein and do an occlusion during my Y90 administration to get those beads to lodge in, take out the balloon afterwards get an effective treatment.

And really, is it affectatious, do I go ahead and treat and is this gonna affect these patients, appropriately? So again, here's the image this huge tumor. Here's the shunt.

Here's my hepatopulmonary shunt. So, I'll bring my first team question up. [BLANK_AUDIO] So given the clinical and imaging characteristics below, how would you treat the tumor?

Anyone change the words from a monograph. So a, systemic chemotherapy, percutaneous ablation, c, full dose radioembolization d, conventional chemoembolization or e, reduced dose radioembolization.

[BLANK_AUDIO] Good answers. I love it. [LAUGH] I don't think there's a right answer. I chose the answer D,

conventional chemoembolization, and if we can go back to my slide. I said it was incorrect. You can do Sorafenib and I don't think that's the wrong answer it's just a matter of how long are you willing to wait and how often are you gonna re-image these patients to try to shut down their

shunts again. The studies showed that their follow up was up to 270 days, that's almost a year that the patients need to out to be able to get these shunts to shut down. You're never gonna ablate a tumor like this.

It's too big. C. I said is incorrect because the Y90 is gonna disperse throughout the entire liver unless of course you do that spect imaging and then you can sort of determine that it's really gonna go to where you want it to go. So I said I probably wouldn't just go ahead and treat the whole

liver if the patient's is cirrhotic. In the patient that has liver metastasis since they may be willing to or able to tolerate it just depending on how bad your patient's overall liver function is. I thought D was the correct choice,

patient is candidate for conventional chemoembolization. Cuz it really provides treatment while potentially reducing the shunts and allowing the future radioembolization. The other thing I like about lipidal based chemoembolization is you can see it.

So the shunts crosses over, you can see where it's going, so you know if it's going only to the left at the time we can see if it's going only to the right if you're not doing your pre Y90 ahead of time instead of beads where you sort of can't see where they're going and don't really have a good handle on it at the time.

And then C, they've talked about in a literature doing a load of stuff that guys at Stanford published trying to decrease your dosing when you do Y90 and they actually show that it had decreased efficacy of treatment. So that's probably not the best choice according to the literature that we have now.

So I went ahead and I proceeded with TACE I did the lipiodol based TACE. We don't have any support in Wisconsin I think that's probably universal in the United States these days. So I used Doxorubicin and mitomycin I mix my lipiodol thicker so it would get stuck into those blood

vessels so it would trap it so it wouldn't cross over into the portal veins so I did a two to one and sometimes I'll even do a three to one just to get that lipiodol thicken and sludging in instead of just crossing over into the portal vein,

and now embolized into the back end with 3 to 5 PVA. So this is what my angio looked like at the end. It was sort of shocking that we had shut down that shunt with the lipiodol based TACE. We always get CT scans the day following.

I would show you the picture but really, you can't appreciate where the lipiodol is because it's so defused throughout the entire liver, I thought this is never gonna work. I called the medical oncologist and I said can we start the Sorafenib?

And I told the patient and his family I didn't have very good hope that this was going to work but we were gonna try to take care of him. On follow up imaging about a month later, this is what it looked like so you can see that that huge mass is gone,

I thought I had the wrong patient. Study pulled up and then, did you scan the wrong patient? I looked at the other anatomical structures, those were his kidneys,

no, this is this guy. It really melted away that tumor. You can see some residual lipiodol there and he did have a residual viable tumor that you could see. His portal vein thrombus had melted away so that was no longer there and on the arterial phase imaging there was no longer any appreciable

or arterial coral shunting. So we decided why don't we go ahead and repeat the shunt study and see what's happened to the hepatopulmonary shunt and see if that was also effectively treated. This is the second study. I took these pictures and I told my fellow this was the most traumatic

case that I had ever seen in my life and everyone should go back and look at the pre-images because I've never seen this that you have zero arterial portal shunting after one session of TACE, is a very dramatic change in his imaging. I did a CT spin just to

see if I could figure out the distribution of was there anything going to that left hepatic lobe you can see this is residual viable tumor enhancing here and nothing is going to that left hepatic lobe again we did hepato pulmonary, a lung shunt fraction calculations and

it came down to 7.4%. We went on to do a Y90 radio embolization of the right hepatic artery and on seven month follow up the patient is disease free, he has no residual viable tumor he has no portal vein thrombus and he tells me that he prayed and I told him to tell me to whom he prayed

cuz I wanna give that to all of my other patients.

- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.

And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.

Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.

Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.

It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,

if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?

You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you

about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,

and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may

be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.

A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased

the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,

and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.

But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history

or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?

Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because

more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.

Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.

They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.

To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history

in various degrees of relatives. So with that, thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

- 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.

- 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.

- I'd like to thank Larry and John for the opportunity to speak today. This really is kind of an exciting time in Vascular Access 'cause you know this whole session's devoted to all the new tools and technologies, and they're really a lot of different options

that are available to us now to create functioning fistulas in patients. Those are my disclosures. I just want to mention one thing, when I was asked to give this talk, the name of the device was the Everlink device then,

and that was first developed by TBA Medical at Austin, Texas. Eventually the company was bought by Bard, and then Beckett Dickinson bought Bard, and then they changed the name of the device to the WaveLinq device,

just so that we're all on the same page here. The basic gyst of this system basically it's a two-catheter system, it involves punctures in the brachial artery and brachial vein above the elbow over wires, the catheters are then aligned

in the ulnar artery and ulnar vein. The venous catheter has an RF electrode on it, the arterial component has a ceramic foot plate, and there's rare earth magnets in the catheters that help them align in the artery and vein. They'll coapt, you deploy the foot plate,

and then you fire the RF energy from the RF generator, and the RF energy then creates a four millimeter hole between the artery and vein. This is just what it looks like under fluoroscopy, this is the arterial catheter going in here's the footplate here

this is the venous catheter then being directed and you can see the magnets on these they look like Lincoln Logs they'll kind of line up. You rotate the catheters 'til the foot plate aligns, you do some flyovers with the II make sure everything's lined up,

and then you create the fistula with the RF energy. Then this is just what Fistulagram looks like once the fistula's created. At the completion of that, for this device we then place coils, occluding coils, in the deep vein which was just beyond the sheath

where we accessed the brachial vein. And by putting those plugs in there, coils in there, It helps to direct the flow up to through the superficial veins which we cannulated for dialysis, and much like the other device

that Dr. Malia was talking before, this creates essentially a split vein fistula, it's going to mature both the cephalic and basilic if those veins are available through that from the perforator coming on out. This is just what it looks like you know,

this was in some early studies in the animal model, you can see that it creates exactly a four millimeter hole between the artery and vein. Eventually this will re-endothelialize they had endothelialization at 30 days. So really the nice thing about it is

it standardizes the size of the arteriotomy because it makes exactly a four millimeter fistula. Now, as I mention this is created at the level of the ulnar artery and ulnar vein, so the requirements basically to do this you need a adequate size obviously ulnar artery and vein,

but the big component is to have that adequate perforator vein that's going to help feed the superficial veins to mature that fistula. And then it's just creating a side to side fistula between the ulnar artery and vein.

This is just a composite of all the data that's been collected on the device so far so this is what the global registry looks like. The FLEX study was kind of the first studies in man. The NEAT trial was run in the Canada and the UK, that was one of the earlier trials.

Then there's a post-market registry, uh, in Europe that's being run now. The EASE trial is the trial with the Four French device and I'll share a little bit about that at one of the slides at the end. But basically pull all the data from this

there's almost 157 patients that they collected data on. And, you can see that with this the primary patency, or the primary patency's on at 75 percent, and the accumulative patency's almost 80 percent, and then the number of fistulas that were cannulated at six months successfully with two needles was 75 percent.

If you look at some of the interventions that've had to be done it really seems to be a lower number of interventions that have to be done to get a mature functioning fistula, uh, using this device. I just want to point out a couple things on this slide,

there was never any requirement for angioplasty at the uh, the ulnar artery the ulnar vein anastomosis, and there was, you know, with these embolizations that were performed, 12 of these were performed on patients prior to incorporating that into the procedure itself,

so right now in the IFU it says that the deep veins should be coiled to help direct that flow up into the superficial veins. Now as, uh, was alluded to earlier with the Ellipsys device this kind of falls somewhere between, uh, the radiocephalic fistula and a brachiocephalic fistula,

and again comparing these two devices basically you're creating, this is the Ellipsys device is radial-radial, and this device is really ulnar-ulnar, but again you're creating that split-flow fistula it's going to allow flow both up

into the basilic and cephalic veins. So, where can this be used? It can be used for primary access creation so that's the first option to provide a patient with a functioning fistula. It can be a secondary option to radiocephalic fistula,

or those that have failed the radiocephalic fistula, and it also is an alternative to surgery so there are patients that may not want to have open surgery to have a fistula created, and this obviously provides an option for those patients. In the UK now they're using it to condition veins,

so they'll create the fistula hoping to condition the cephalic and basilic veins to allow them to become usable for dialysis, and they're also using it in patients that have no superficial veins actually using it to mature the brachial vein

or the deeper veins, uh, and then superficializing the brachial vein to create a native fistula for patients who don't have adequate superficial veins. Now I mentioned the Four French device and what the Four French device allows is basically access

from a lot of different points. So now because it's a smaller device, we can place it, if the vein and artery are large enough, it can be placed at the wrists, so radial-radial fistula, so you come in from the wrist, put both catheters up, create the fistula at the radial-radial,

you can do it from the ulnar-ulnar, so it's just two catheters up from the wrist. And these cases are nice, the other option is you can come arterial from the wrist and you can come from the vein at the top, match up the catheters in a parallel

and create that fistula at the ulnar-ulnar level. And the nice thing about this is it really makes managing the puncture very easy you just put a TR band on 'em, and then you're good to go. So it really kind of opens up a lot of different options for creating fistulas.

So in summary this device seems to create a functional fistula without the need for open surgery. It has very good primary and cumulative patencies and seems to take fewer interventions to maintain and mature the functioning fistula, and this may add another tool that we have to create

functioning fistulas in patients who are on dialysis. So thank you very much.

- Thank you, Dr. Ascher. Great to be part of this session this morning. These are my disclosures. The risk factors for chronic ischemia of the hand are similar to those for chronic ischemia of the lower extremity with the added risk factors of vasculitides, scleroderma,

other connective tissue disorders, Buerger's disease, and prior trauma. Also, hemodialysis access accounts for a exacerbating factor in approximately 80% of patients that we treat in our center with chronic hand ischemia. On the right is a algorithm from a recent meta-analysis

from the plastic surgery literature, and what's interesting to note is that, although sympathectomy, open surgical bypass, and venous arterialization were all recommended for patients who were refractory to best medical therapy, endovascular therapy is conspicuously absent

from this algorithm, so I just want to take you through this morning and submit that endovascular therapy does have a role in these patients with digit loss, intractable pain or delayed healing after digit resection. Physical examination is similar to that of lower extremity, with the added brachial finger pressures,

and then of course MRA and CTA can be particularly helpful. The goal of endovascular therapy is similar with the angiosome concept to establish in-line flow to the superficial and deep palmar arches. You can use an existing hemodialysis access to gain access transvenously to get into the artery for therapy,

or an antegrade brachial, distal brachial puncture, enabling you treat all three vessels. Additionally, you can use a retrograde radial approach, which allows you to treat both the radial artery, which is typically the main player in these patients, or go up the radial and then back over

and down the ulnar artery. These patients have to be very well heparinized. You're also giving antispasmodic agents with calcium channel blockers and nitroglycerin. A four French sheath is preferable. You're using typically 014, occasionally 018 wires

with balloon diameters 2.3 to three millimeters most common and long balloon lengths as these patients harbor long and tandem stenoses. Here's an example of a patient with intractable hand pain. Initial angiogram both radial and ulnar artery occlusions. We've gone down and wired the radial artery,

performed a long segment angioplasty, done the same to the ulnar artery, and then in doing so reestablished in-line flow with relief of this patient's hand pain. Here's a patient with a non-healing index finger ulcer that's already had

the distal phalanx resected and is going to lose the rest of the finger, so we've gone in via a brachial approach here and with long segment angioplasty to the radial ulnar arteries, we've obtained this flow to the hand

and preserved the digit. Another patient, a diabetic, middle finger ulcer. I think you're getting the theme here. Wiring the vessels distally, long segment radial and ulnar artery angioplasty, and reestablishing an in-line flow to the hand.

Just by way of an extreme example, here's a patient with a vascular malformation with a chronically occluded radial artery at its origin, but a distal, just proximal to the palmar arch distal radial artery reconstitution, so that served as a target for us to come in

as we could not engage the proximal radial artery, so in this patient we're able to come in from a retrograde direction and use the dedicated reentry device to gain reentry and reestablish in-line flow to this patient with intractable hand pain and digit ulcer from the loss of in-line flow to the hand.

And this patient now, two years out, remains patent. Our outcomes at the University of Pennsylvania, typically these have been steal symptoms and/or ulceration and high rates of technical success. Clinical success, 70% with long rates of primary patency comparing very favorably

to the relatively sparse literature in this area. In summary, endovascular therapy can achieve high rates of technical, more importantly, clinical success with low rates of major complications, durable primary patency, and wound healing achieved in the majority of these patients.

Thank you.

- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery

in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,

but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase

and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,

and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast

in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.

So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,

it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause

of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.

So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes

and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,

and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR

might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement

without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac

Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,

to save our country from a type II endoleak, and I thank you for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

of iliac limb reinterventions. Thank you very much.

patient female patient who has the sudden onset of upper abdominal pain here's the CT we did all these cases in one day it was crazy it was terrible so so here's a big hematoma a big peritoneal hematoma you

can see it anterior to the right kidney you can see the white blob of contrast right in the middle of the hematoma that's a pseudoaneurysm or even active extravagance um less experienced people would probably say it's active

extravagant I think most of us would prefer that it be called kind of a pseudoaneurysm this active extrapolation would be much more cloudy and spread out this is more constrained and you can see on the

coronal image you get a sense that there's that hematoma same type of problem all right is there more imaging that we can do to figure out the next step again I said earlier earlier in this lecture

that sometimes we use CTA now sometimes a CTA is worthwhile I do find that for a lot of these patients I think we're getting smarter and we're doing CTAs right at the beginning of this whole thing you know when a trauma

patient comes in we're getting CTAs so we can max out the amount of information that we get on the initial diagnostic imaging here's what we're seeing on the CTA and in this particular case I think it's pretty clear that you can see the

pseudoaneurysm arising from what looks like a branch of the superior mesenteric artery so this is just an odd visceral and Jake visceral aneurysm which looks like it probably ruptured I don't have an explanation for it led to a big

hematoma here's what that is and now we're gonna do an angiogram the neat thing is it just perfectly correlated with a conventional angiogram so here's our super mesenteric angiogram all right the supreme mesenteric artery

on the first image to the left is that vessel going downward towards the right side of the screen all those vessels coming off are really just collateral vessels going up to the liver through the gastroduodenal artery again that

left one looks pretty good it's not until you see the delayed image on the right that you see that area of contrast all right so that's the finding that correlates with the CT scan all right here we're able to get in there you put

a micro catheter in that vessel alright the key next step for this patient as I mentioned earlier is the whole concept of front door and back door so here we're technically in the front door the next thing that we do is we put the

catheter past the area of injury and now we embolize right across the injury because remember once you embolize one thing flow is gonna change we screw it up body the body wants to preserve its flow if we block flow

somewhere the body's gonna reroute blood to get to where we blocked it so we want to think ahead and we want to say okay we're blocking this vessel how's the body going to react and let's let's get in the way of that happening that's what

we did here so we saw the pathology we went past it we embolized all across the pathology and boom now we don't have anymore bleeding and the likelihood of recurrence is gonna be very low for that patient because we went all the way

across the abnormality and I think from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you 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.

- 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.

- 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 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

- 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, thanks for the opportunity to present. I have no disclosures. So, we all know that wounds are becoming more prevalent in our population, about 5% of the patient population has these non-healing wounds at a very significant economic cost, and it's a really high chance of lower extremity amputation

in these patients compared to other populations. The five-year survival following amputation from a foot ulcer is about 50%, which is actually a rate that's worse than most cancer, so this is a really significant problem. Now, even more significant than just a non-healing wound

is a wound that has both a venous and an arterial component to it. These patients are about at five to seven times the risk of getting an amputation, the end patients with either isolated venous disease or isolated PAD. It's important because the venous insufficiency component

brings about a lot more inflammation, and as we know, this is associated with either superficial or deep reflux, a history of DVT or incompetent perforators, but this adds an increasing complexity to these ulcers that refuse to heal.

So, it's estimated now about 15% of these ulcers are more of a mixed etiology, we define these as anyone who has some component of PAD, meaning an ABI of under point nine, and either superficial or deep reflux or a DVT on duplex ultrasound.

So we're going to talk for just a second about how do we treat these. Do we revascularize them first, do we do compression therapy? It has been shown in many, many studies, as with most things, that a multi-disciplinary approach

will improve the outcome of these patients, and the first step in any algorithm for these patients involves removing necrotic and infected tissue, dressings, if compression is feasible, based on the PAD level, you want to go ahead and do this secondary, if it's not, then you need to revascularize first,

and I'm going to show you our algorithm at Michigan that's based on summa the data. But remember that if the wounds fail to heal despite all of this, revascularization is a good option. So, based on the data, the algorithm that we typically use is if an ABI is less than point five

or a toe pressure is under 50, you want to revascularize first, I'll talk for a minute about the data of percutaneous versus open in these patients, but these are the patients you want to avoid compression in as a first line therapy.

If you have more moderate PAD, like in the point five to point eight range, you want to consider compression at the normal 40 millimeters of mercury, but you may need to modify it. It's actually been shown that that 40 millimeter of mercury

compression actually will increase flow to those wounds, so, contrary to what had previously been thought. So, revascularization, the data's pretty much equivocal right now, for these patients with these mixed ulcers, of whether you want to do endovascular or open. In diabetics, I think the data strongly favors

doing an open bypass if they have a good autogenous conduit and a good target, but you have to remember, in these patients, they have so much inflammation in the leg that wound healing from the surgical incisions is going to be significantly more difficult

than in a standard PAD patient, but the data has shown that about 60% of these ulcers heal at one year following revascularization. So, compression therapy, which is the mainstay either after revascularization in the severe PAD group or as a first line in the moderate group,

is really important 'cause it, again, increases blood flow to the wound. They've shown that that 40 millimeters of mercury compression is associated with a significant healing rate if you can do that, you additionally have to be careful, though,

about padding your bony areas, also, as we know, most patients don't actually keep their compression level at that 40, so there are sensors and other wearable technologies that are coming about that help patients with that, keeping in mind too, that the venous disease component

in these patients is really important, it's really important to treat the superficial venous reflux, EVLT is kind of the standard for that, treatment of perforators greater than five, all of that will help.

And I'm not going to go into any details of wound dressings, but there are plenty of new dressings that are available that can be used in conjunction with compression therapy. So, our final algorithm is we have a patient with these mixed arterial venous ulcers, we do woundcare debridement, determine the degree of PAD,

if it's severe, they go down the revascularization pathway, followed by compression, if it's moderate, then they get compression therapy first, possible treatment of venous disease, if it still doesn't heal at about 35 weeks, then you have to consider other things,

like biopsy for cancer, and then also consider revacularization. So, these ulcers are on a rise, they're a common problem, probably we need randomized control trials to figure out the optimal treatment strategies.

Thank you.

- I think by definition this whole session today has been about challenging vascular access cases. Here's my disclosures. I went into vascular surgery, I think I made the decision when I was either a fourth year medical student or early on in internship because

what intrigued me the most was that it seemed like vascular surgeons were only limited by their imagination in what we could do to help our patients and I think these access challenges are perfect examples of this. There's going to be a couple talks coming up

about central vein occlusion so I won't be really touching on that. I just have a couple of examples of what I consider challenging cases. So where do the challenges exist? Well, first, in creating an access,

we may have a challenge in trying to figure out what's going to be the best new access for a patient who's not ever had one. Then we are frequently faced with challenges of re-establishing an AV fistula or an AV graft for a patient.

This may be for someone who's had a complication requiring removal of their access, or the patient who was fortunate to get a transplant but then ended up with a transplant rejection and now you need to re-establish access. There's definitely a lot of clinical challenges

maintaining access: Treating anastomotic lesions, cannulation zone lesions, and venous outflow pathology. And we just heard a nice presentation about some of the complications of bleeding, infection, and ischemia. So I'll just start with a case of a patient

who needed to establish access. So this is a 37-year-old African-American female. She's got oxygen-dependent COPD and she's still smoking. Her BMI is 37, she's left handed, she has diabetes, and she has lupus. Her access to date - now she's been on hemodialysis

for six months, all through multiple tunneled catheters that have been repeatedly having to be removed for infection and she was actually transferred from one of our more rural hospitals into town because she had a infected tunneled dialysis catheter in her femoral region.

She had been deemed a very poor candidate for an AV fistula or AV graft because of small veins. So the challenges - she is morbidly obese, she needs immediate access, and she has suboptimal anatomy. So our plan, again, she's left handed. We decided to do a right upper extremity graft

but the plan was to first explore her axillary vein and do a venogram. So in doing that, we explored her axillary vein, did a venogram, and you can see she's got fairly extensive central vein disease already. Now, she had had multiple catheters.

So this is a venogram through a 5-French sheath in the brachial vein in the axilla, showing a diffusely diseased central vein. So at this point, the decision was made to go ahead and angioplasty the vein with a 9-millimeter balloon through a 9-French sheath.

And we got a pretty reasonable result to create venous outflow for our planned graft. You can see in the image there, for my venous outflow I've placed a Gore Hybrid graft and extended that with a Viabahn to help support the central vein disease. And now to try and get rid of her catheters,

we went ahead and did a tapered 4-7 Acuseal graft connected to the brachial artery in the axilla. And we chose the taper mostly because, as you can see, she has a pretty small high brachial artery in her axilla. And then we connected the Acuseal graft to the other end of the Gore Hybrid graft,

so at least in the cannulation zone we have an immediate cannualation graft. And this is the venous limb of the graft connected into the Gore hybrid graft, which then communicates directly into the axillary vein and brachiocephalic vein.

So we were able to establish a graft for this patient that could be used immediately, get rid of her tunneled catheter. Again, the challenges were she's morbidly obese, she needs immediate access, and she has suboptimal anatomy, and the solution was a right upper arm loop AV graft

with an early cannulation segment to immediately get rid of her tunneled catheter. Then we used the Gore Hybrid graft with the 9-millimeter nitinol-reinforced segment to help deal with the preexisting venous outflow disease that she had, and we were able to keep this patient

free of a catheter with a functioning access for about 13 months. So here's another case. This is in a steal patient, so I think it's incredibly important that every patient that presents with access-induced ischemia to have a complete angiogram

of the extremity to make sure they don't have occult inflow disease, which we occasionally see. So this patient had a functioning upper arm graft and developed pretty severe ischemic pain in her hand. So you can see, here's the graft, venous outflow, and she actually has,

for the steal patients we see, she actually had pretty decent flow down her brachial artery and radial and ulnar artery even into the hand, even with the graft patent, which is usually not the case. In fact, we really challenged the diagnosis of ischemia for quite some time, but the pressures that she had,

her digital-brachial index was less than 0.5. So we went ahead and did a drill. We've tried to eliminate the morbidity of the drill bit - so we now do 100% of our drills when we're going to use saphenous vein with endoscopic vein harvest, which it's basically an outpatient procedure now,

and we've had very good success. And here you can see the completion angiogram and just the difference in her hand perfusion. And then the final case, this is a patient that got an AV graft created at the access center by an interventional nephrologist,

and in the ensuing seven months was treated seven different times for problems, showed up at my office with a cold blue hand. When we duplexed her, we couldn't see any flow beyond the AV graft anastomosis. So I chose to do a transfemoral arteriogram

and what you can see here, she's got a completely dissected subclavian axillary artery, and this goes all the way into her arterial anastomosis. So this is all completely dissected from one of her interventions at the access center. And this is the kind of case that reminded me

of one of my mentors, Roger Gregory. He used to say, "I don't wan "I just want out of the trap." So what we ended up doing was, I actually couldn't get into the true lumen from antegrade, so I retrograde accessed

her brachial artery and was able to just re-establish flow all the way down. I ended up intentionally covering the entry into her AV graft to get that out of the circuit and just recover her hand, and she's actually been catheter-dependent ever since

because she really didn't want to take any more chances. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

- Ladies and gentlemen, I thank Frank Veith and the organizing committee for the invitation. I have no disclosures for this presentation. Dialysis is the life line of patients with end-stage renal failure. Hemodialysis can be done by constructing an A-V fistula, utilizing a graft or through a central venous catheter.

Controversy as to the location of A-V fistula, size of adequate vein and priority of A-V fistula versus A-V graft exists among different societies. Our aims were to present our single center experience with A-V fistulas and grafts. Compare their patency rates,

compare different surgical sites, and come up with preferences to allow better and longer utilization. We collected all patients who underwent A-V fistula or A-V graft between the years 2008 through 2014. We included all patients who had preoperative

duplex scanning or those deemed to have good vessels on clinical examination. Arteries larger than two point five millimeter and veins larger than three millimeter were considered fit. Dialysis was performed three times per week. Follow up included check for a thrill,

distal pulse in the arter non-increased venous pressure or visible effective dialysis and no prolonged bleeding. Any change of one of the above would led to obtaining

fistulogram resulting in either endovascular or open repair of the fistula. We started with 503 patients, 32 of which were excluded due to primary failure within 24 hours. We considered this, of course, the surgeon's blame. So we left with 471 patients with a mean age of 58 years,

51 were older than 60, there was a male predominance of 63%, and over half were diabetics. The type of fistula was 41% brachio-cephalic fistula, 30% radio-cephalic fistula, 16% A-V Graft, and 13% brachio-basilic fistula.

Overall, we had 84% fistulas and 16% grafts. The time to first dialysis and maturation of fistula was approximately six weeks. First use of grafts was after two weeks. 11 patients with A-V fistula needed early intervention prior to or after the first dialysis session.

In sharp contrast, none of the A-V grafts needed early intervention. 68 patients were operated for their first ever fistula without duplex scanning due to clinically good vessels. Their patency was comparable to those who underwent a preoperative scanning.

Looking at complications, A-V grafts needed more reintervention than fistulas. All of them were late. Infection was more prominent in the graft group and pseudoaneurysms were more prominent in the A-V fistula group, some of them occluded

or invaded the skin and resulted in bleeding. Here's a central vein occlusion and you can see this lady is after a brachio-basilic A-V shunt. You can see the swollen arm, the collaterals. Here are multiple venous aneurysms. Here's an ulcer.

When we looked at primary patency of A-V fistulas versus graft, A-V fistulas fared better than grafts for as long as five years. When you looked at 50% patency in grafts, it was approximately 18 months, in Fistula, 13. Here's an assisted primary patency by endovascular technique

and when we looked at the secondary patency for the first 24, two years, months, there was no difference between A-V fistulas and A-V grafts, but there's a large difference afterwards. Comparing radio-cephalic fistula to brachio-cephalic fistula there was really no big difference in maturation.

The time was approximately six weeks. As for primary patency there is a trend towards better patency with brachio-cephalic fistula after six months, one year, and two years, but it didn't reach statistical significance. For patients with diabetes,

differences were statistically significant. Brachio-cephalic fistula showed a trend toward shorter maturation time, needed less reintervention, and had a longer patency rate. In conclusions then, ladies and gentlemen, A-V fistula require a longer maturation time

and have higher pseudoaneurysm formation rate, but better patency rates compared to A-V grafts. A-V grafts have a faster maturation time, but more late interventions are required and infection is more common. Finally, diabetic patients have a better result

with proximal A-V fistulas. Thank you for the opportunity to present our data.

- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper

that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.

Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.

So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.

The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.

And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome

certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups

and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written

and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?

If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.

If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk

of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.

We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,

quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,

but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.

So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.

It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.

And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you to the moderators, thank you to Dr. Veith for having me. Let's go! So my topic is to kind of introduce the ATTRACT trial, and to talk a little bit about how it affected, at least my practice, when it comes to patients with acute DVT.

I'm on the scientific advisory board for a company that makes IVC filters, and I also advise to BTG, so you guys can ask me about it later if you want. So let's talk about a case. A 50-year-old man presents

from an outside hospital to our center with left lower extremity swelling. And this is what somebody looks like upon presentation. And pulses, motor function, and sensation are actually normal at this point.

And he says to us, "Well, symptoms started "three days ago. "They're about the same since they started," despite being on anticoagulation. And he said, "Listen guys, in the other hospital, "they wouldn't do anything.

"And I want a procedure because I want the clot "out of me." so he's found to have this common femoral vein DVT. And the question is should endovascular clot removal be performed for this patient?

Well the ATTRACT trial set off to try and prevent a complication you obviously all know about, called the post-thrombotic syndrome, which is a spectrum from sort of mild discomfort and a little bit of dyspigmentation and up

to venous ulcerations and quite a lot of morbidity. And in ATTRACT, patients with proximal DVT were randomized to anticoagulation alone or in combination with pharma mechanical catheter-directed thrombolysis.

And the reason I put proximal in quotes is because it wasn't only common sort of femoral vein clots, but also femoral vein clots including the distal femoral vein were included eventually. And so patients with clots were recruited,

and as I said, they were randomized to those two treatments. And what this here shows you is the division into the two groups. Now I know this is a little small, but I'll try and kind of highlight a few things

that are relevant to this talk. So if you just read the abstract of the ATTRACT trial published last year in the New England Journal of Medicine, it'll seem to you that the study was a negative study.

The conclusion and the abstract is basically that post-thrombotic syndrome was not prevented by performing these procedures. Definitely post-thrombotic syndrome is still frequent despite treatment. But there was a signal for less severe

post-thrombotic syndrome and for more bleeding. And I was hoping to bring you all, there's an upcoming publication in circulation, hopefully it'll be online, I guess, over the weekend or early next week, talking specifically about patients

with proximal DVT. But you know, I'm speaking now without those slides. So what I can basically show you here, that at 24 months, unfortunately, there was no, well not unfortunately,

but the fact is, it did cross the significance and it was not significant from that standpoint. And what you can see here, is sort of a continuous metric of post-thrombotic syndrome. And here there was a little bit of an advantage

towards reduction of severe post-thrombotic syndrome with the procedure. What it also shows you here in this rectangle, is that were more bleeds, obviously, in the patients who received the more aggressive therapy.

One thing that people don't always talk about is that we treat our patients for two reasons, right? We want to prevent post-thrombotic syndrome but obviously, we want to help them acutely. And so what the study also showed,

was that acute symptoms resolved more quickly in patients who received the more aggressive therapy as opposed to those who did not. Again, at the price of more bleeding. So what happened to this patient? Well you know,

he presented on a Friday, obviously. So we kind of said, "Yeah, we probably are able "to try and do something for you, "but let's wait until Monday." And by Monday, his leg looked like this, with sort of a little bit of bedrest

and continued anticoagulation. So at the end of the day, no procedure was done for this particular patient. What are my take home messages, for whatever that's worth? Well I think intervention for DVT

has several acute indications. Restore arterial flow when phlegmasia is the problem, and reduce acute symptoms. I think intervention for common femoral and more proximal DVT likely does have long-term benefit, and again, just be

on the lookout for that circ paper that's coming out. Intervention for femoral DVT, so more distal DVT, in my opinion, is rarely indicated. And in the absence of phlegmasia, for me, thigh swelling is a good marker for a need

for a procedure, and I owe Dr. Bob Schainfeld that little tidbit. So thank you very much for listening.

- 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 so much for the opportunity to present our experience. You are all familiar in this place with the SVS classification for blunt aortic injury, and you all know that it doesn't tell you what to do with each patient,

it doesn't guide treatment. A few years ago we presented a simple, practical grading system based on CAT scan findings for the management of these patients. When a patient has a minimal aortic injury, it's a patient with no aortic contour abnormality,

they have either an intimal flap or a small thrombus less than 10 mm. These patients we don't do any interventions. Patient's that present with an aortic contour abnormality or a large intimal flap or large thrombus have a moderate injury.

These patients get repair in a semi-elective manner once they have stabilized further injuries. One the other hand, persons that present with a severe injury, persons with active extravasation, this patient need to go to the OR because he's dying

and this takes precedence above any other injuries. So, since we implemented this system we took a three years look from 2014 to 2017 to see how are our results. We have 87 patients, 63 percent were moderate, 28 percent minimal, and nine percent severe.

None of the patients underwent open repair, and none of the patients with a minimal got fix. All but three of the patients with a moderate, and all but one of the patients with a severe have TEVAR as a repair method. These are very sick patients, high in the severity scores,

with high rates of intracranial hemorrhages and associated injuries. When we look at the anatomy, the patient with a severe injury are more likely to have a bovine arch anatomy. These are young patients with small aortas,

with a median aortic diameter of 23. The operative timing is the time since the patient hit the door of the emergency room to the patient getting to the OR, was 53 hours for a patient with a moderate injury, and three hours for a patient with a severe.

These are short procedures that can be done in less than 90 minutes with minimal contrast used, and around five minutes of fluoro time. We used intravascular ultrasound very widely. We have covered the subclavian artery

in around 40 percent of the patients. We do all this percutaneously. We are successful in around 86 percent of the cases. We have not had to revascularize any subclavian artery. We had one patient that required a plaque during the index case of the subclavian,

one patient that had a femoral pseudoaneurysm that we treated with thrombin, one patient that was already on a heparin drip for a PE. We took her to the OR more than 24 hours after the heparin drip was started, fixed the TEVAR.

After that the patient had a complete normal CAT scan. More than 12 hours after the heparin drip being restarted for the PE she had a worsening intracranial bleed. We don't know that was related to our procedure. We have no patient with new stroke

or worsening spinal cord injury for the procedure. 30-day followup CT scan had excellent remodeling in every single patient. We have not performed any delay interventions. Our 30-day mortality is very low. There is only one patient with an aortic-related mortality.

This is a patient that presented with a severe injury. She was more than 90 years old and the family elected to don't proceed with any treatment. So in conclusions, we consider the patients with minimal aortic injury do not require surgical treatment or followup imaging.

Patient with a moderate can be safely undergo TEVAR in a semi-elective manner once they are stable from other injuries, but the patient with a severe aortic injury require emergent repair. These procedures are very fast

and can be successfully performed percutaneously. Complications are rare, and the followup reveal excellent remodeling of the aorta that will likely result in longer interval surveillance requirements. Thank you.

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