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Ethanol Endovascular Repair of AVMs Of The Mandible And Ear
Ethanol Endovascular Repair of AVMs Of The Mandible And Ear
AVM in right lateral deep faceoblitaration of the NIDUS.Oclussion of DOVShobinger stage IV.Yakes type I
Going Rogue: Off The Grid Venous Malformation Sclerotherapeutic Techniques
Going Rogue: Off The Grid Venous Malformation Sclerotherapeutic Techniques
coil embolizationPersisting Venous MalformationsclerotherapyTherapeutic / Diagnostic
Transcript

- [Jose] All right good morning everyone, guess we'll get rolling here. Welcome to New York City and the Veith Symposium. You're in the venous section. I'm Jose Almeda, I'll be one of your course leaders, and I'm joined by Drs. Lowell Cabnik and Tom Wakefield. This venous section started,

Frank had asked Lowell and I about 12 years ago to start this when we were back at the Sheridan, and it started in a small room down in a basement, and quickly has exploded. So we're now, you know yesterday we did the venous workshops in the afternoon which were very well attended,

and I think well received. And then today, tomorrow, and Saturday morning we'll have a venous section. Obviously they are concomitant with the arterial folks. But today we will focus on superficial vein disease. We always start with the basics

and kind of ramp our way up through all the issues. We'll talk about thermal and non-thermal ablation of the saphenous vein, ambulatory phlebectomy, how to work up a patient. And even a section that's become unfortunately important is this venous governance and the problems

that we're having out there with over utilization and overuse. We'll try and tackle with you some of those issues.

- Thank you and thank Dr. Veith for giving me this opportunity to come again and speak to our increasing experience on this difficult sort of angulated area, vasculomimetic stents, the Supera, in the angulated areas other than the SFA. No disclosures.

That's the hospital that I work at. And apart from the SFA there are other areas which allow the Superas to be used across joints, across cavities, across curves. I mean, conforming to the angulations and flowing along the arteries,

the flexibility of the arteries, and avoiding kinks and fractures for the stents. So these ares challenges which are in the other non-SFA territories that one has to actually try and you are set up against. The Supera mimics the natural structure

and the movement of the anatomy fairly well. It has high radial strength as we all know. It is relatively kink resistant. And it stands up to the calcium. So the properties of the Supera that we've utilized in the non-fempop regions

are the, it's ease of conformability, its flexibility, and the mobility that it offers. So we've actually used the Supera off label in a number of non-SFA territories, the first being the brachial artery. This was gentleman who actually had a fractured elbow

and he had, subsequent to that, was someone had actually placed in a stent for continuity of his brachial artery. He had very poor overlying skin, and this stent occluded after about two years or so and we just did not want to enter the surgical option,

and here we actually outlined and endolined it with a Supera with a very, very good results distally, and that stood the, it's been there, it's been working for the last almost two and a half years. Superas have also been used across the AV fistulas in the arm.

We've just had experience of placing them on two occasions, and they seem to be doing fairly well. But the actual challenge that we actually, which we are up against is in the subclavian and in the iliac areas where the stents have to withstand the pulsatility,

the external compressive forces of calcium, and the bending fatigue. No single stent is ideal in all these indications. And the external iliac stents are more prone to fractures up to almost 5% as has been reported, and so there's a real need for a flexible, compliant,

self-expanding stent with a very high radial resistive force. In the subclavian arteries you can see if we place, for an ostial lesion we placed a balloon expandable stent. It tends to occlude at the level of the angulation, at the angulation, and we've endolined that

with a Supera coming up the arm with a very, very good result. As you can see, there's another stent which we've placed in the axillary artery, which is actually also held out. Now this is actually the area of interest. We've done almost about 25 such cases in the iliac artery.

You can see that the iliac has multiple turns and tortuosities and these actually is what results in all the fractures. And so this was a study which was done in the Acta Biomaterialia which was reported in July 2018 when they studied the extension, inflation, and torsion

for all these arteries and showed that there was a distinctly stiffer behavior in the circumferential than in axial direction of both the arteries, and the stiffness increased with age, especially in the iliac arteries.

So here's a patient who had actually a fractured stent, which was successfully endolined with a Supera coming up from the brachial root, and that encouraged us to actually use these for the aortoiliac occlusive disease. We came down from the brachial transbrachial approach,

both the right and the left side, and endolined them with Superas after placing aortoiliac self-expanding stents at the ostium and that is the final completion angiogram and there's another case in which this complete, almost near total occlusion,

and we managed to reline these with Superas and two aortoliliac stents beyond the, I mean, at the aortic bifurcation. So there's one Supera and one self-expanding stent on each side which actually gave us very good results. So this is exactly what our experience has been

for the last almost three years. We've done about 35 cases, 25 of them being in the aortoiliac segment. And of course, there's followup. And I must, there've been no fractures to date, and all the arteries,

all the stents placed have been patent. Obviously we looking at experience of other centers and of course long-term followup is something that really needs to be looked at. So thank you very much for the privilege of the podium. After placing aortoiliac

self-expanding stents at the ostium. And that is the final completion angiogram, and there's another case in which there's complete almost near total occlusion and we managed to reline these with Superas and two aortoiliac stents beyond the, I mean, at the aortic bifurcation.

So there's one Supera and one self-expanding stent on each side which actually gave us very good results. So this is exactly what our experience has been for the last almost three years. We've done about 35 cases, 25 of them being in the aortoiliac segment.

And of course there's followup, and there have been no fractures to date, and all the arteries, all the stents placed have been patent. Obviously we looking at experience of other centers, and of course long-term followup

is something that really needs to be looked at. So thank you very much for the privilege of the podium.

- [Moderator] Anybody have any burning questions? So Enrico, who do you not do duplex-guided interventions on? - [Enrico] Ah that's a very good question. When I don't have somebody adept to help me. If I'm doing it by myself, I'm not going to do it at this point. Hopefully there's a couple of companies

that are working on devices where you'll be able to do it by yourself. But at this point, you need someone that's going to handle the probe while you handle the catheter so. And the second contraindication

would be a severely calcified, sicofriend calcified vessel. If you have this calcification for about two centimeters and the rest you can see, segmentally it's okay, but if it's a long calcified occlusion

where you cannot see anything, of course it's not going to be acceptable to do on the ultrasound guidance. - [Panelist] I have a question for Dr. Rico. But is the problem here is that so many of those groins have been used and abused forever

with closure devices and all that. So when you go back to that groin, it looks like it been operated four times. There's a lot of inflammation around. I realized that my fellow is staying away from those groins now.

He call in sick when I tell him tomorrow we have a groin to do. So do you think that the results just, I understand first time around, but for those patient with much pulled sticks before and devices.

Should we consider a stand instead? - I have no scientific argument to answer to you, because what we have done these of novel groin incision. If you have a patient with a very fat weave of free producent divention of the groin.

This could be a problem, but in this case I mean if you have a careful surgical technique I mean you kind of already have a complication growing infection (mumbling) like this. I think it's alright if you're really safe even.

But you have to take time and to do everything right. I think to put a (mumbles). When you see oh important is deep feminal aheartery. I think it's quite dangerous. And if it jail. And if he trembles.

I mean you are really in a bad situation. - Okay I think that wraps it up.

- [Instructor] Thank you, Dr. Ratchman. Dr. Veith gave me a title longer than my talk. These are my potential, but not real conflicts. So Coral concluded that renal artery stenting did not confer a significant benefit when added to comprehensive, multifactorial medical therapy in people, whatever that means,

with atherosclerotic renal artery stenosis and hypertension or chronic kidney disease. Neither Astral nor Coral bothered to measure pressure gradients and most of the patients included had stenosis less than 60%, so you can figure out what that means.

We do know that pressure gradients are significant and a mean 10% arterial pressure gradient is the minimum for renal production and therefore, a hemodynamically significant stenosis. This was an 84 year-old who presented with an elevated serum creatinine chronic hypertension

chronic lung disease, and the day after admission looked like this with severe congestive failure. Our clinical course she was admitted to the CCU became oliguric then anuric. Jumped to a creatinine of 4.6.

Right kidney was 6.8. Blood pressure 180 over 80. And her BNP was 2000. She failed diuretics, decompensated CHF, pulmonary edema, respiratory failure, intubation, and so she had a diagnosis of both acute and chronic

kidney disease and secondary cardiac dysfunction. I got called in on a Saturday emergently to look at her, and I will just summarize her clinical history. She had essential hypertension beginning in 2000. An Echo in 2001 was normal. In 2011, still normal, and the right kidney was 9.8.

The blood pressures are indicated below. And her kidney was 9.3 in 2012. And you can see that they sort of watched her blood pressure on medications as she drifted along, and then for a while nobody was bothering to take blood pressures until she presented in July

as I showed you before. And had an ejection fracture of less than 40%, and the right kidney was now 6.8 centimeters. So I got called in to do the emergency renal artery stent. This is what she looked like. Severe heavily calcified aorta.

Occluded right. Severely calcified occluded left. And you can see the calcium and you can also see no progression of contrast in the left kidney. This is before stent and here it is after stent. And this is one day after,

6 hours later, 24 hours later, and for comparison. Most importantly, immediately afterwards autodiuresis in the lab on the table, she was extubated and her blood pressure as of this week is still 130 over 70. And her creatinine is below two.

In conclusion, Coral stated that renal artery stenting did not confer a significant benefit. I think Coral results apply only to a population studied where most had hemodynamically insignificant or uncertain stenosis, and without confirmatory blood pressure gradients.

Coral, Astral, and Star proved that stenting hemodynamically non-significant renal artery stenosis, which is not and cannot be the cause of the disease does not and cannot cure it. So the clinical criteria to evaluate a patient for suspected renal artery stenosis

should be renal dysfunction, recent onset or progressive, and moderate to severe. Hypertension, which is difficult to control, severe or recent onset. And finally pulmonary edemas, especially in the absence of significant coronary artery disease

and jeopardized renal parenchyma. Anatomically, bilateral or solitary kidney disease greater than 70% diameter stenosis, collaterals, post-stenotic dilatation, reduction in renal size judged by those criteria. And so our algorithm at Cornell is what it was

believe it or not, 20 years ago. Clinical suspicion and plasma renal activity with ace inhibition in hypertensives. Renal vend, and you can pick one of these tests, but don't do all of them. And if they are positive, in spite of the NSF

I think MRA is the best. You go onto a cath and if there's a gradient, you fix it. If there is no gradient, patient goes on medical therapy. In ischemic nephropathy, it's very simple. Clinical suspicion based on the criteria I already gave. And no history of medical nephropathy,

you do an ultrasound or an MRA for renal size asymmetry, renal artery stenosis, and increased resistive index perhaps. Again if there's a gradient, you fix it. If there's no gradient, patient goes on medical therapy. Thank you very much.

- I think it's unfair to have Wayne here with all his expertise and knowledge and throwing all these combative comments, vulgar attack, et cetera. But the bottom line is all these types, no matter how you define them, they are mixed.

They are mixed, they are not, with the exception for HDT. You have Type 1 in a midst of Type 2. You have Type 2A and then 3B, type something. I don't even know what they are, except that you say venous predominance, yes. Can be multiple venous predominance, yes.

Then you can have Type 4, these are the major groups. But to have a filler that occupies a space, can be Onyx, it's fine. It doesn't cure. You have to do something to these cells. You have to compress them.

You have to ablate them. You have to take them out. And a filler doesn't do that. The filler recolonizes on top of that, as you've put it already, from Molly. Recolonizes.

You can use it as a filler, but the cure, the ablation, has to be something that's powerful. Like a knife, even worse than knife, burn injuries, burn it to the bottom. That's how you achieve a cure. If you don't believe me, just look at ...

Can you play us that clip that was rotating constantly as Walter was talking, here, how Onyx is wonderful? This is the girl that you show on the pictures from Bob. Can you look at that? It's a ton of extras placed into the veins,

arteries, everywhere. She continues to bleed. On top of that, it's horrendous, how to treat it. Wayne managed to stop and control the bleeding, but this is an example.

This is the most scary sample of what Onyx cannot do. So back to the motion. Polymerizing Onyx can cure, and it's the material of choice to use? The answer is no. Alcohol is dangerous, personally,

I say yah, very dangerous, if you drive and you don't know how to use it. But so is everything else. But if you know, you can cure them. Thanks.

- I have nothing to disclose but what I will tell you is that the only way for me to learn the mechanics of treating low-flow malformations has been to learn from Wayne, follow what he's doing, and basically what I've done is I've filmed every single step he's taking,

dissect that, and then present you the way that he's doing it. The best way to do that is not listen to Wayne, but to film him, and just to check that afterwards. And he goes regularly to Cairo, this is the place of Dr. Rodovan sitting here

in front of us, and with Dr. Alaa Roshdy. I've learned a lot there from Wayne. This is Wayne's techniques, so normally if you look at puncture, the low flow malformations here then you get return or you aspirate so this is what happens, they inject contrast then they find volume

and inject whatever agent you prefer to inject. It happens to be alcohol but that is not essential. More often than not, there is no return. What to do then? There is a technique that Wayne has developed. Stab-Inject-Withdraw, just under high modification inject,

identify that you're not outside the vessel, get the vessel, start to fill slowly, and identify that and inject the alcohol. Of course you can do that under exposure just to see the effect of the alcohol thrombosing, et cetera.

Another example of no return is to subcutaneously certainly show that there is a low pressure system, and again, Stab-Inject-Withdrawal, and there is a cyst. Is it extravasation or is the malformation aspirate? And if it collapses, that's the malformation.

And then continue to fill in with contrast, define how big the malformation is, and then accordingly inject the amount of abrasive agent that you're using. Lymphatic malformation is very difficult to treat because the vessel's so small, would say microscopic,

and again, Stab-Inject-Withdraw, identify that it's not extravasating but it is the vessel, and start slowly, slowly to fill and any time in doubt that should there, just do a run, identify, and that is the vessel, or the network of the vessels and

start to fill that with the agent you're using. But there are certain zones that just don't inject anything, and these are the arteries. How often do arteries occur? When you puncture them. I just directly looked at all these 155 patients I've seen Wayne treat there a matter of,

I would say, 100 patients in three days. 30 patients per day, that's about six percent. And you see the artery by pulsating flow depending on the pressure that you apply. And we see again the artery pulsating and we have no doubt about that.

However, it could be difficult to see. Depending on how much you push in the contrast and you see these being ornery so there's a No-Go-Zone, no injection of any agent and again, a tiny bit of lottery there in the foot could be disastrous.

You inject any agent, any, you will have ended up with necrosis of course if you don't inject inhibitors, but not yet. The humorous may not end up with necrosis when all the mysticism with puncture will be gone. So we have extravasation, when you say extravasation

like starting injecting, still good, looking good, but you see how the extravasation even blows up and at the end it bursts, again under pressure they should apply, so pressure is really important to control and then you stop and don't inject any more.

Extravasation, you see how its' leaking in the back there, but you correct the position of the needle, identify all the vessels, the tiny little vessels, just have to be used to identify the pattern and then you start to inject the agent again.

Control is very essential. Here is the emphatic malformation labia and though there is this tiny little bity extravasation you continue because there is you know, run-off, it is filling the system and you can safely inject the alcohol.

Intraarticular could be malformation there and this is definitely safe pla however, if it is in the free space in the the joint, that's again, it's No-Go-Zone. How you see that is just be used to

the pattern recognition and you find that this is free. It's around the condyle there so there is no injection. Compression is again good to note to control by compression where the agents go. This is a normal vein, certainly at risk of getting with alcohol, whatever agent

you're using deep in the system, avoid that by compression. Compression can be applied manually and then that gives you a chance to fill the malformation itself and not strike connection too deep in the system. Intraosseous venous malformation,

low-flow malformations can occur anywhere, here in the spine and the axis is transpedicular patient prone because it's soft. The malformation has softened up the bone. You can just use a 21-gauge needle and identify the malformation and follow

by the agent you're using. Peculiar type of venous malformation called capillary venous malformation. Basically it's a low-flow malformation without any shunt here in the sciatic notch of the patient and geography shows that there is no shunt

there is just big veins and intense pacification. And identify the veins by indirect puncture again, see the pattern of that and inject alcohol and following geography we can see that there has decreased the density but it is a lot more left to be done.

In conclusion, direct puncture is the technique in this low-flow malformation but Stab-Inject-Withdraw is the really helpful technique for successful treatment of microvascular, microcystic lesion. No-Go-Zones for certain when you see arteries

and anytime in doubt you just have to do a run to identify if they're arteries or not. Intraarticular free space and extravasation and normal veins, similarly, No-Go-Zone. Capillary venous, intraosseous malformations can be treated successfully. Thank you.

(audience applause) - [Facilitator] Thank you, Crossey. Excellent talk, very practical and pragmatic. Any comments or questions? Dr. Yakes. - [Dr. Yakes] We have been to many meetings and people have talked about doing

other ultrasound guides, accessing the malformations. You'll never see those arteries by ultrasound. - [Facilitator] That's absolutely correct. I concur. I concur and I think some of the disasters we've seen where suddenly something falls off

have been in these situations because they don't understand or in expansile foam-based therapies, I've seen that. I've seen plenty of these, so it's always present, potentially.

- [Physician] Thank you very much. So this is a venous topic on an arterial arena. A year back, we published a paper defining all the venous symptoms because these are not really well-defined in the literature. One of which was venous claudication. So to start with,

venous claudication is the development of pain or a bursting sensation that occurs when a patient is walking or running. The pain is localized in the leg, thigh, buttock, or in combination of areas. Disappears slowly when the patient rests.

It's facilitated by leg elevation, a finding that allows differentiation from arterial or neurogenic claudication. It's almost exclusively seen in patients with iliofemoral or iliocaval obstruction. A less common type of claudication is neurogenic

from the dilated veins in the spinal canal, and also a rare form of claudication in the calf is due to popliteal vein entrapment. I've seen only two patients, after examining thousands of them. In this claudication, the venous obstruction is so severe,

that during walking the arterial inflow is increased beyond the ability of the venous drainage, leading to swelling and pain. The muscular pressures at rest and during exercise in the calf are much higher compared

with the contralateral unobstructed limb. Unlike arterial claudication, the recovery time to baseline is much longer, taking at least 15 minutes, or even longer. Femoral vein pressures, venous outflow resistance,

arm-foot pressure differentials compared with those having obstruction below the common femoral vein, are significantly elevated. These patients are also more likely to have edema and skin damage.

If you want to look into this more seriously, there's some of papers published in the literature on this topic. Now, how do you evaluate it? Well, in general, evaluation of venous obstruction may be controversial,

because the symptoms are more pronounced, and more often present during standing or walking. Unfortunately, all imaging tests are done in supine position, but the tests we usually use for this condition are venous outflow tests, ultrasound, intravascular ultrasound,

axial imaging with CAT scan or MR, ascending phlebography, and pressure measurements. However, for venous claudication diagnosis is usually easier as chronic venous obstruction is more severe. This first hemodynamic paper

we published in 1997, indicating that the venous outflow resistance is much higher in people having iliofemoral obstruction, and this can explain why these people are more likely to develop a venous claudication. And this is the pressure differential for arm and the leg.

People having iliocaval or iliofemoral obstruction have much higher resting pressures. Also, as you see on this table here, only people with iliocaval or iliofemoral obstruction develop claudication, which is 8% among all patients, or 17% among people with supra-inguinal

chronic venous obstruction. And in the second paper within 2008, we demonstrated that we found no patient with previous DVT on femoropopliteal area, but in people who have iliofemoral obstruction had an instance about 8% of venous claudication.

Now, why the venous claudication? Who cares? Well, when you treat the patient with traditional anticoagulation, because of the large volume of thrombus in the iliofemoral veins, our problematic system,

it fails to lyse the thrombus in the majority of the people, so such patients, they have severe obstruction and they are prone to develop swelling and claudication. Therefore, to prevent this thing, when you have acute iliofemoral DVT, aggressive thrombus removal is necessary

in people having indications. Therefore, this way you'll eliminate the obstruction, the DVT recurrence is reduced, and a chronic venous disease is avoided. And here is a patient with chronic obstruction and claudication.

But in these people if you plant the stent, you make sure have a good inflow, like you see on this image here, but a patient having a comprised inflow like on this panel here, you may consider endo-phlebectomy

and arteriovenous fistula creation prior to stenting. And here is a patient with aortofemoral with chronic iliofemoral obstruction. The IVUS cath, they're much the size of the vein, and it's throughout from the iliac vein all the way down to femoral,

and obviously when you do stenting, you can relieve the obstruction, and the venous claudication as you see on this around here. To finish with, for venous claudication, you need to recognize the symptoms. It is clearly a post-thrombotic event.

Iliac vein compression by itself is not enough to do it, so you're not going to have the claudication by putting a single iliac stent for arterial compression on the vein. Image the iliofemoral veins and the inferior vena cava, aggressive thrombus removal for the femoral DVT, and look for and treat chronic venous obstruction.

Thank you very much.

[Natalie]- Good morning ladies and gentlemen. I want to thank the organizers for the privilege of this invitation. I have no disclosures, and now we are going to treat another animal that is responsible for our cardiovascular death, the hypertension. So the JNC, in 2014 came out with new recommendations, and

they told us how to manage hypertension in our patients. There are a number of drugs. All of them were invented in the last century. We have dozens of groups and hundreds of agents that help us do that. Unfortunately, still 28% of our patients don't know

that they have high blood pressure or 40 are not treated, and up to 65% are not controlled. There are a number of trials worldwide and in the United States, almost a billion people were involved in those trials, and what have we learned? The landmark trials listed here, I am not going to bore

you, the essence is that we can manage hypertension with two or more agents, and the arbs and ACE seem to be doing it a little bit better than others. Again, the same question. How low should we lower the blood pressure in our patient?

What is the ideal number? The HOPE Study was hoping to answer this question, and with the mindset in is lower better? And the answer was really it wasn't because even if a patient with the intermediate risk of no cardiovascular disease, the combination of arb and diaretic failed

to lower the rate of major cardiovascular events. The SPRINT Trial that was published a couple of years ago randomized patients with increased cardiovascular risk but no diabetes to intensive goal of 120 versus standard recommended goal by JNC of 140, and it showed that there was benefits for primary outcome of

cardiovascular events and cardiovascular related death. However, the trade-off was more syncope, hypotension, AKI, HyperNa in intensive treatment group. As we know, our patients of high risk (mumbles) disease, diabetes in the ACCORD Trial that was published in 2010 again tight control less than 120 was implemented

and showed that in diabetic patients with higher cardiovascular risk lower goal of 120, did not reduce the rate of major cardiovascular events. Many of our patients have chronic kidney disease, and the tighter blood pressure control did not improve the renal outcome nor did it make a difference

for cardiovascular outcomes. Where should we measure the pressure, what would recommend? And the latest study by Japanese group of over 20,000 subjects, HONEST showed that when the patients measure pressure at home, lower hypertension level of 145 or more was better predictive of insidence

of cardiovascular events. Then the pressure measured in the clinic of 160. This book was published in Jack last year. We all know that we get older as a population of people on this planet, and should we treat hypertension in the elderly?

HYVET Trial included almost 4,000 of older patients over 80, and it showed when we treat them to achieve 150/80 goal, there were benefits of primary endpoint of fatal and nonfatal stroke as well as death from any cause. And the SPRINT investigators recently published in JAMA in 2016.

Their study of patients who were 75 years and older with the same criteria, and they found for ambulatory adults over 75 years old, the systolic pressue of 120 was resulting in significantly lower rates of major cardiovascular events. It reduced it by 33% and death by 32%.

JNC and SPRINT investigators just this year and last month published that the greatest decline in cognitive status was when patients were not controlled with a blood pressure of 150, and the least cognitive decline occurred in patients with systolic pressure less than 120, and this goal was more benefitial

for black patients. In the summary, all the patients blood pressure goal is still elusive. It seems to be that lower goals, a tighter control of 120/80 provided better cognitive outcome, and the home blood pressure reported by patients may

be superior to clinic blood pressure to predict cardiovascular death and stroke death. In the news, even though you are a surgeon, but if you are to follow MACRA requirements for our patients in our electronic medical record, you have to now monitor blood pressure, and you have to make sure that our

pressure in the patients is well controlled. And whether it is the art of the science, you have to decide for yourself. Thank you.

- [Tarek] Good morning. First of all I would like to thank Professor Yakes who allowed me to be with you for the second year. I'm getting used to, for something different, which is a story, how we build our Vascular Malformation Program with a 13-year experience in Cairo's International Medical Center.

This my disclosures. Always we have another diagnostic and treatment dilemma with vascular malformation in Egypt. They usually misdiagnose, for one case, you seen someone did a foreign lesions, the neck, many investigation unnecessary,

duplex ultrasound, MR with contrast, CT angio, direct angiography and venography, ending with the same result, probably vascular malformation. But after discussion with Wayne, he told me, "I realize now that "every country in the world has

"the same problem, not only Egypt." They usually left untreated infantile hemangioma, told by the doctor, leave it alone, it will disappear, and never happen. Or, in this 30-year gentleman, extensive venous malformation, left it untreated because

there is no hope for treatment. Or, mistreated, just laser repair for a capillary malformation, mark left alone. This one was a terrible case as we noted that having a misdiagnosis intranatally as an enteratoma mistreated in his first day of life

with extensive surgery, complete facial denervation. When you do the MRI and clinically it is just venolymphatic and need to treatment and you don't know to treat the lesion or treat the complication. So even cases were sent to some centers abroad

with no valuable outcomes. So my dream was to having a new treatment strategy based on a multidisciplinary approach with full integration of the endovascular therapy to improve the patient outcome. So this came true with Professor Yakes in 2005

with a dedicated team and a patient database following the ISSVA classification. We started with patient and family teaching and counseling. They are happy now. And spread of the knowledge to the vascular surgeon of Egypt by publication of Professor Yakes in our

Egyptian Journal for Vascular and Endovascular Surgery. In 2008 we have the first case in Egypt treated with propranolol. As the same year was the discovery for treatment of the infantile angioma. And then nine-months age child

treated with propranolol for two years and then for six year follow-up with good result. We also published this for the knowledge spreading. We picked this case from her neurosurgeon before undergoing an heroic operation at the age of three months age

treated with propranolol oral for one year and with very good recovery. Also publication for spreading the knowledge. Then we start to do that but increase the public awareness by some TV program. On that was Professor Yakes that he shared

in this program also shows that normal people in Egypt can now know that how we diagnose, how we pick the cases and what is the way of treatment. Also spreading of the knowledge between the vascular surgeon in Egypt

and I acknowledge Professor Rahmat Saad is here and he is with us. So most of the vascular surgeon in Egypt now knows that how we pick and how we treat the cases. Also getting Professor Yakes in these meetings. We attracted Professor Vogelzang

all we know, well published in the literature, Professor Evan Seev, the father of EVAR and directed the beginning of the vascular malformation treatment in Sweden, Hamburg and London. I don't know why he's feeling sick.

(audience laughs) Okay, they have been interesting to visit our developing center. But also active, very active, sorry I'll get one, very active, one of the cases he came to us with history of some bleeding from the skull ligation of the external carotid artery

before we put in his sleep. We need six hands to stop the bleeding until all the three professors worked on him with six hours to stop the bleeding and to embolize him. Right carotid venous was shown to some stage. Making of coils from just simple wires

at 2 a.m. in the morning, we done everything. This is a left vertebral using these coils and directional injections and this I the end of the one-hour stage of the treatment until in the morning we can see at least now the scalp itself, now we can see.

And this, four days before he go home for follow-up treatment. At one of the occasion we seen 17 new cases in the outpatient clinic, seven and a half p.m. after a long day we start the clinic to see 70 cases.

Our center now is known as a center of excellence in Egypt for diagnosing and treating the vascular malformation, picking the cases not only from Cairo, Egypt but also from the surrounding countries. We seen patient from everywhere around us. This is vascular malformation workload since 2005

starting only with four cases with Professor Yakes and after proper spread of the knowledge to the public and the doctors in Egypt we, in last September, we treated 110 cases in continuous three and a half days working. This is the distribution of the case.

We see now, at least between three and four cases every week. Now the current situation in Egypt is that, misdiagnosis and mistreated are avoided, early pick up of de-novo case, we have one center of excellence

engaged with the larger malformation patient population and a full experienced expert attending on regular basis which allow for a faster ramp-up experience and, decreasing the complication rates. Now I would like you to come and visit Egypt so you can see the pyramids, Sphinx,

you may go up to Abu Simbel, Luxor, see Ramses temple but if you come closer, you might see Yakes and Radwan. Thank you. (audience laughter)

- Thanks a lot for again for inviting me because you know, (laughs) I'm in very hostile territory, (audience laughs) but, I will tell you the truth now, (audience laughs) and being in hostile territory and telling the truth can

be totally different things and I, I'm also never in any way, you know I'm totally scientific type, I will never be polemic, like you are. (audience laughs) Okay, so let's start with the truth, start with the truth, I show you two typical cases, this is a typical ethanol case

here with couple of, it was successful, at least in losing it's toes, and I'll show you another example again, a foot AVM, this is one session, one session, in fact its 14 vials of squid in this case, and it's done. so, this is not statistic, but I always

see, and I've seen it today in a couple of talks, Onyx used as glue. And that doesn't work, you have, if you start to treat a patient, you have to really treat him and it's not something you inject, and that it's gone, you have to fill all the AV shunts, you have to fill the whole lesion.

And if you don't do it, of course you see a lot of failed on ex-patients and if its used improperly, and that's the only thing I, I wouldn't say I agree with you, I would say I'm thinking in the same direction, yeah, that's if you use Onyx in the wrong way, you have a very good chance to make thing worse.

So, its a technical thing, and if people start to use Onyx, and they inject something, and then its something like putting in some coils, that's not worthwhile, it makes no sense to include some arterial feeders, we know this since, I think more than 20 years, it's like making a surgical ligation of the feeding

artery, it's totally senseless. You have to completely occlude the area of the arteriovenous shunting, apart from the predominantly venous one, where you can just occlude the venous outflow, by whichever thing you use, and the area of arteriovenous shunting is always bigger than you see it in a normal DSA,

because the blood does the same as the contrast medium does, it flows along the route of the least flow resistance. And so, at the end, if you want to be sure that you have to completely occluded the AVM, you will end up with a cast which is much bigger than what you see at the beginning of a DSA, yep, it was agreed, see.

- [Audience Member] You know I'm shaking my head as you talk. - Yeah, yeah, your getting tired. (laughs) Here we go, So, and this is only the really scientific slide in my talk, because when people die when you inject ethanol

in vascular malformation treatment, its something, its banal, all of us have seen it many times, but there was a scientific question, why do people die on the table if you inject ethanol in AVM treatment on vascular malformation treatment? And there's one scientific publication here, because we

all thought do they die because of complete vasoconstriction in the pulmonary arterial system, or is it, are they dying due to the thrombi? That, you know ethanol, it uses small slatch or big thrombi and they go to the pulmonary circulation and they die. So, is it the vasospasm, induced by ethanol, or is it the

thrombi induced by ethanol, that they die is clear. So, there was a very nice publication out there in 2012, was presented in Malibu, at the IFSA meeting, it was about four patients, which three of them died, two were just after injecting of between five and 12 milliliters of ethanol, one was a direct puncture pelvic AVM, and it was caused,

that this was nicely stated there, it was caused by multiple small peripheral emboli. So it's not vasospasm that kills the people, it's the thrombus, and I think this was a very very worthwhile contribution to all our knowledge and really thank you Bob for this paper, thank you

very much, now we know why they died. I haven't, unfortunately I can't contribute to this discussion with Onyx because there wasn't any patient dying on the table during my embolization's and I've done now, we're preparing the paper of 160 AVM patients with I don't know, 400 sessions and well maybe if we wait

40 years more, 50% will have died but, (audience laughs) from natural cause, so I can tell you again this is the truth, we will talk about the truth here, and this is, ethanol can be worthwhile even in AVM's, I don't deny that and maybe it will have its place for a couple of more years

before we do Onyx and MEK1-Inhibitors, so there is for couple of more years, this is a role for ethanol, but it's somewhere deep down there, and this is a slide I show for the third time now just for you Wayne, please and I show it because you should start to publish your classification.

I didn't use it because there is no paper there, please publish it then I will always classify according to your classification. - [Audience Member Cheers] - Thank you for your attention, thank you for giving me the chance to talk about the truth here in this seminary

and please don't do anything stupid with ethanol.

- [Dr. Kim] Good morning, ladies and gentlemen. It's my great pleasure and honor to be here again. First of all, I would like to give my big thanks to professor Frank Veith and (mumbles) for inviting me. Today, my talk is about what is the future for stem cell therapy in vascular disease, especially in ischemic vasculopathy.

First of all, let's think about why do we need the stem cell therapy in ischemic vasculopathy. As you know, where there are many unmet needs in intervention was surgery for ischemic vasculopathy. Low patency, limitation of target artery for treatment. Some patients had a high risk issue for surgery.

So, to solve this unmet need, we have been studying the stem cell research for several years. I also have been studying the stem cell research from 2002, and I found the stem cell has potential to differentiate and newly develop the vessels, (mumbles) angiogenesis. And also, I found the stem cells

secrete many kinds of cytokines. With (mumbles) chemical standing message, we prove the angiogenic vessel differentiated from the (mumbles) stem cells like shown in this slide. As you can see in this slide, the capillary number was increased with stem cell therapy.

In this slide of animal study, you can see many of angiogenic vessels in stem cells treated in here, compared to the control limb. We did several numbers of clinical trials from 2004, as shown in this slide. In clinical trial, actually, this is Buerger's disease,

called thromboangiitis obliterans. We found there are many newly developed angiogenic vessels in stem cell treated limbs. Especially, look at the pictures E and F. Picture E means the pre-stem cell status, and Picture F was the post-stem cell's angiogram.

We can see many of the angiogenic vessels in Picture F's post-stem cell angiogram. This slide shows my current technique for stem cell therapy in critical limb ischemia. The stem cell was obtained from the iliac bone, and the autologous whole bone marrow stem cell was injected

into the ischemic muscle directly. The ischemic pain score decreased from 5.4 to 3.5 and 2.5 in one month, and 3 months after stem cell therapy. This decreasing score was statistically significant. Also, the clinical ischemic score improved

after stem cell therapy. But, there was no major or minor complications related with this stem cell therapy. During the (mumbles), there was so many stem cell articles for the treatment of ischemic vasculopathy. As I am a vascular surgeon, I also published

many of my stem cell articles to the several numbers of international journals shown in this slide, such as Stem Cells, considered as the most top ranking international journal in the stem cell research field, and Scientific Reports, one of the nature publishing group journals.

So ladies and gentlemen, take home message from my (mumbles) If someone asked me, "Will the stem cell "be effective for the treatment of" "peripheral arterial disease in the future?" My answer will be always definitely. Yes, it will be.

Currently, I am a president of the Korean Society for Stem Cell Research, and I was the editor in chief of International Journal of Stem Cells during the last 80 years. Thank you for your attention. (applause)

- [Dr. Veith] Thank you very much, Dr. Kim. We're going to move to imaging. Image Based Coronary Computational Flow Analysis (FFRCT). Can it reduce peri-operative myocardinal infraction and improve outcomes in vascular patients with AAAs and occlusive disease?

How does it work? Dr. Zarins, welcome. - [Dr. Zarins] Thank you very much, I'd like to thank Dr. Veith for the privilege of updating you on this new technology. I have a significant financial interest in HeartFlow.

So, CT image based coronary flow analysis is really non-invasive fractional flow reserve. Fractional flow reserve is measured in the cath lab with a pressure wire placed across the lesion and provides one value of FFR at one single point in the vascular tree.

With non-invasive computational analysis of FFR, you get a three-dimensional map of FFR values throughout the coronary tree, and here, you see such a map, and you see a significant lesion in the LAD with an FFR value of 0.43. Also, in the right corner, we have an FFR value of 0.81.

This technology has been evaluated over the years, and I've had an opportunity to tell you about that with validation of FFRCT against measured FFR, a number of clinical utility studies... There's a large body of published literature, and there's regulatory approval by CE mark and Europe,

FDA clearance in the US, and PMDA in Japan. Recently, since last year's VEITH meeting has been evidence reviews by NICE in the UK, and the Blue Cross and Blue Shield with positive reviews from Evidence Street. So now, there's a building momentum

of activity of this technology. Since the 1st of the year, there's been approval on coverage for over 90 million lives by insurance companies in the United States. We have collaboration agreements with Siemens, GE, and Philips to help further bring out this technology.

And, most important, on November 1st, Medicare granted a new technology, APC, and there will be a reimbursement for Medicare patients for this technology starting January 1st of 2018. There's been clinical adoption in US, Europe, Canada,

and Japan with over 15,000 patients now being evaluated with this technology. So, how does this technology work? Well, you use a standard 64 slice or greater cardiac CT scan, upload it to our servers by Amazon web service from anywhere in the world.

We do the computational analysis, and then we return the results to you, within usually six to eight hours. In the emergency room on stat procedures, we can do it as quickly as two to three hours. The physicians then interrogate the model, then plan a treatment plan for the patient.

Most important now, there's a CPT code for physicians to now submit a bill for interpretation of the... FFRCT report. So, each year that I've been here, Frank has asked the question, "When will this be available for "patients with peripheral vascular disease?"

Well, I can tell you it's available now. And, can it reduce peri-operative myocardial infractions and improve outcome? Well, I think so, but the data's not in yet, but this is something that we 'ought to be investigating. One thing that we have to remember is that

our patients with peripheral vascular disease die of coronary disease. They do not die of their peripheral vascular disease. Patients with critical limb ischemia, in one year, 20% mortality. In four years, it's 50%.

Interestingly, when we evaluate new therapies with critical limb ischemia, the end point is amputation-free survival. We're worrying about the amputation, but not the survival of the patients with peripheral vascular disease. The disease is unrecognized, and

from our perspective, not really treated. Look at this evidence from the Danish National Registry. Patients with PAD and no history of coronary disease have a higher death rate than patients with MIs. Is that because patients with MIs are treated by cardiologists and cared for, and patients

with peripheral vascular disease have unrecognized coronary disease and die of that disease? So, what can we do to improve the treatment of patients with peripheral vascular disease? Well, we can diagnose their coronary disease, and we can do that by getting a coronary CT, and

if there is plaque there, we can evaluate that with FFRCT. Here's an example from Latvia. Patient admitted with ischemic rest pain scheduled for fem-pop bypass. Pre-op coronary CT reveals the severely critical right coronary stenosis.

Here's another patient: 61 year old diabetic woman. She has an occluded stent of SFA, an ischemic ulcer. She also has a severely critical LAD stenosis. More than 50% of all patients admitted for peripheral vascular reconstruction have these kinds of lesions.

A lot of them don't. Here's a patient of only 49 years old. He's already got a plaque in the LAD in the right coronary artery. This man needs to be on aggressive medical therapy. So in conclusion, patients with PAD had high risks

for MI and cardiovascular events. You can perform pre-op evaluation of these patients to identify clinically significant coronary disease, and this will allow treatment planning, not only of their peripheral vascular disease, but also of their coronary disease.

Thank you.

- The proposition is polymerizing agents can and do cure AVMs and are now the agents of choice, ethanol is too dangerous. When I saw what Wayne had asked me to talk about, I immediately called him. And I said there are two words in this proposition

which are giving me some trouble. The first word is dangerous. In IR we do dangerous every day, especially in July. And with respect to cure in IR, mostly we just try to fix things.

Nonetheless, there are proper uses of ethanol. There are, however, some risks to the use of ethanol in medicine. First off, ethanol is a sclerosing agent and it is toxic to tissue. It denatures the proteins

of the endothelium, activates the coagulation system and produces blood clots. While we are trying to do that, when we're trying to control an AVM, it does also generate acetaldehyde and reactive oxygen species

which damage healthy tissue. It can result in endotoxin leakage, inflammatory cytokine release, and modification of signal transduction in the cell membrane and when we deliver alcohol, unless we dilute it with contrast,

we really cannot see where it goes. There are some other issues with ethanol. The first is that it's known to impair wound healing. If ulcers occur with ethanol use, they are difficult to heal. If you place skin grafts on these lesions,

they typically fail. And if you use ethanol in an area of prior surgical scar, there is a high risk of skin injury. In addition, the use of ethanol is associated with pain, it's a painful procedure.

If you deliver ethanol in proximity to a nerve, you will develop nerve injury and if you have sciatic nerve injury, that can be devastating which can take months if it all to heal. The other issue relates to the dosing

and the volume of ethanol that's delivered. If you deliver high doses of ethanol at one sitting, you can get systemic effects. Now, a slightly tipsy patient post-embolization is not necessarily a big problem, however, if the patient develops hemoglobinuria,

that can be significant. If you use low volumes of ethanol with each treatment, it requires multiple treatments. You can also get cardiopulmonary problems with ethanol. The ethanol can induce arrhythmias, it can induce bronchiospasm,

it can precipitate pulmonary emboli because of the sludge that migrates up to the lungs and you can get cardiovascular collapse with the use of ethanol. Fortunately that is rare. Other polymers such as the cyanoacrylates

or liquid embolics and their viscosity can be altered. The downside in our experience with the cyanoacrylates is that they're difficult to control, they tend to spatter.

And our long-term experience with the cyanoacrylate shows that it is not permanent and it does degrade. The ethanol vinyl alcohol copolymer or Onyx behaves as a filler. It induces a mild inflammatory reaction.

It's associated with minimal pain post-procedure and skin injury is infrequent and it is in our experience a permanent agent. There may be difficulty getting it to travel deep into the nidus and that can be a big problem,

if you just deliver the Onyx in just a push away, it will not go very far and you will leave your nidus untreated which can lead to recanalization. So, we dilute our Onyx 18 with DMSO

which makes it more easier to spread out into the distal portion of the malformation. It is somewhat harder to see when it is diluted. We also use a glue roadmap. This will reduce our radiation dose

and we don't deliver the Onyx the way the neuro-interventionalists do, we tend to deliver it much faster than the neuro people do. And if you have obscuration of your vessels by prior Onyx placement, the glue roadmap can help.

When we use Onyx without operative resection, it is an off label use. But nonetheless, when used, it does facilitate operative resection and you just have to remind your surgeons to use a bipolar bovie otherwise you will get sparking.

With respect to cure. I think cure, when we talk about it, it really depends upon our definition of cure. Polymer occlusion will result in relief of AVM symptoms. And it can cure some lesions.

Whether we are able to remove all shunting in large lesions I think is doubtful, but nonetheless, Onyx copolymer is associated with lower morbidity than alcohol. And when we look at ethanol versus polymers, the ethanol is a one-generation agent.

Whereas if we look at polymers, if we consider cyanoacrylate as a first generation and Onyx as a second generation, and squid maybe as a third, the future is pretty much unlimited for us because you can prepare polymers which will contain drugs

or other agents. So, I think the choice is you have to determine whether you want to use ethanol, or whether you want to use a polymer. Thank you.

- Good afternoon. I have no disclosures. I was going to say that the bulk of this work was done by Johnston Moore who's a 3rd-year medical student with us and my partner, Ben Pearce does the novel work that's in this. As you all know there are a number of risk factors

for peripheral vascular disease and diabetes is certainly one of the more important ones. And that's what I'm going to talk about in this talk. This image here shows you the odds ratio increase for peripheral vascular disease with each of these risk factors.

Why should we care? If you look at this map in 1995, it was all yellow, in the 0-6.5% rate of diabetes and now much of the country is getting to look like Alabama, where we say we're in the heart of the biscuit belt.

This is the increasing rate of diabetes diagnosed in the country over a 50-year time span, over 50 years, and you can see that it seems to be ever increasing. The importance of limb preservation, I don't need to tell this group for patients

that get a higher level of amputation more often go to nursing homes and more often end up in a wheelchair. So limb preservation is very important. This slideshow is a functional outcome after amputation, which decreases with a higher level of amputation. And diabetes is known to be associated

with higher levels of amputation. As you may know, Hemoglobin A1C has been linked to lower extremity amputation in diabetic patients and worsened Hemoglobin A1C increases the risk of amputation and higher level of amputation. This is a nice meta analysis that shows multiple papers

that demonstrated that an increasing Hemoglobin A1C over 7 increases the risk of amputation by 26% for every 1% rise in A1C level. Another interesting paper about insulin-sensitizers. So these are the glitazone drugs and Metformin. There is some suggestion that patients

that are on a sensitizing agent in addition to insuin have a lower risk of amputation. They also have a lower risk of peripheral arterial disease in general. Comparison to patients that are on insulin only they have a lower risk of requiring revascularization

and a lower risk of amputation as I said. So we did a project at UAB, looking at these questions about A1C and a choice of diabetic control regimen, and thus impact on amputation and amputation-free survival. When we pulled patients who had A1C levels within three months of their procedure

we ended up with 306 limbs. And we looked at patients that had amputation and/or death, both endo and open revascularization. And what we found was a simple diagnosis of diabetes, and this is not new, increased the risk of amputation pretty significantly.

Here this is one year amputation-free survival, 78% of non-diabetics and 61% in diabetics. As I said, just a simple diagnosis of diabetes was actually the more important risk factors. But an insulin only diabetic was the most significant risk factor for amputation and increasing level of A1C

was approaching statistical significance. A multivariate logistic regression, Creatinine, insulin-only management, and age were associated with amputation. So in summary, the diagnosis of diabetes increases overall mortality, that's known.

Decreases amputation free survival and in a small cohort there was a trend towards higher amputation rates for poor glucose control measured by Hemoglobin A1C. The glycemic control strategy was significantly associated with amputation free survival. So those patients with only insulin control

had higher rates of amputation. The strongest predictor of poor amputation free survival, as I mentioned, is diabetes, but the modality of glycemic control does impact the outcome and insulin sensitizers may improve patient outcomes over time.

Thank you.

- Alright, that's our beautiful city by our inland freshwater ocean. I'm against the proposal because, in my opinion, ONYX and the polymerizing agents don't do what they're supposed to do, which is cure. You know, we could talk about this, but in preparation for this, I looked at the

relatively sparse, but available, literature on ONYX, and the fact of the matter is, repeatedly when one looks at what is in the literature, ONYX does not cure with a few exceptions. For example, this is the curative exception. This is a mandibular AVMs, three of them cured

at one year angiographic followup. Now, I consider cure a very simple metric: is it gone at one year followup angiography or imaging? And this meets that criteria, but again, we know that mandibular AVMs, as Dr. Fannis has so nicely shown, this is a bone cyst, essentially,

fill it with anything, it'll get cured. All venous predominant legions, three A. So, yes, cure is possible in isolated circumstances. I think Walter has acknowledged that. But, all the other data, including Dr. Loglos' own data, is that there is no angiographic

followup, short clinical followup. Other papers, Embolization of peripheral high-flow AVMs by Kilani et. al, surgical excision in nine out of 19. Right, that's not the same thing, but it is one aspect of doing it, and there's no angiographic followup. And we see this again and again and again.

Very short clinical followup. So paper after paper refused to tell us that we don't really know what the behavior of ONYX is, as defined by the very simple metric of cure. Although complete, in this paper for example, although complete angiographic exclusion of the nidus

is obtained in a minority, 36 percent, of cases, there's no angiographic followup, so the exclusion is presumably based on immediate post-embolization angiography. In other words, ONYX looks good, acts bad. Other embolization agents in this paper also used,

probably some of them ethanol, which actually got the job done. And then finally, another paper with zero clinical or angiographic followup. So the answer is obvious: ONYX, while it is used copiously by some of the participants in this debate, does not cure,

and I, as my Chinese friends said, think ONYX is garbage. I don't think it works. Few examples of that, here's a young woman, a patient of Dr. Yakes, who, 12 years old, extensive facial maxillary scalp AVM, nine ONYX embolizations, left blind in the right eye

with persistent massive oral and nasal hemorrhage, and after appropriate embolizations, patient was stabilized clinically, and the ONYX was resected. She's stable now, not cured, but she's actually had an excellent clinical result. And you can see that's what it looks like.

Now that's hideous, that's not going to work. And it also, I think, points out what Dr. Walgramuth has actually admitted to, which is it's very difficult to see through this stuff. Radiation dose is increased, and identifying what to do and where to go is a real challenge.

Another such example, I think, suffice it to say a picture is worth a thousand words is this illustrative case of an extensive pelvic AVM, treated with what appeared to be gallons of ONYX, with very little benefit, and an enlarging ulcer. This was later treated by direct alcohol injection

with cure and improvement resolution of that ulcer. So, in summary, it's real simple, folks. There's no evidence in the literature that polymerizing agents have cured AVMs with an exception of a few venous predominant legions. And as I said, you could probably put Jello

in the outflow of those things and it'd work. My own personal experience is repeatedly had ONYX failures, and importantly, many patients are worsened by this treatment, and actually, their subsequent curative treatments are hampered. Thanks very much.

- This work has been done by in my hospital with collaboration of the University of Bologna in Italy. We have no financial disclosures. So all starts from the result of a new TECCO study, but it was published last year showing that stenting was equivalent or even be better in surgery for the de novo common femoral and deep femoral arterial stenosis.

This was a small randomized study of around 117 patients with common femoral artery stenosis. Interestingly enough, 86% of his patients were claudicants, so the applicability of a randomized control trial should be limited to claudicant. The primary outcome was on the patency,

but it was with complication. The combined rate of morbidity and mortality that was 26% in the open surgical arm, and 12.5% in the stent population, and this was just significant. After a median follow up of 24 months, the rates of primary

patency target lesions and system clinical improvement were similar in the two groups. There was no mortality in every group, but one stroke in the endovascular arm. Minor complication were more often seen in the surgical arm with hematoma, delayed wound healing, temporary lymphatic

leakage, paresthesia, but no infection of a graft. The follow up in this small study was not powered enough to assess secondary endpoint, and only 46 patients were available at 24 months for analysis. And the length of stay in the stent group were three days, and six days in the surgical group.

So if you go through the Vascular Quality Initiative published by (mumbling) last year, we find that the 30-day mortality was 1.6%. And the access site hematoma was 5.2%, with a risk of arterial dissection. We have a total rate of complication of nearly 10%.

And interestingly enough in this Siracuse study, was where mostly claudicants were taken care of. You see that the result depends on the symptomatology. If you have a patient with critical infracting ischemia, you have real operation and bad result with the endo first technique.

We have studied our result. In a retrospective study of nearly 150 open revascularizations, half claudicants, half rest pain, and our 30-day result we had 98% of primary patency, three occlusion, 1.7% of mortality at 30 days, 1.4% of cardiovascular complication MI,

groin wound complication was seen in five percent of cases, and in multivariate analysis, only tissue loss and infection, wifi three-four was a predictive factor for wound complication at the groin. This is perhaps the most important aspect of the study. This is what we're seeing in these patients.

As you see here, most of the lesion were at the orifice of a deep femoral artery in more than 73% of the cases. So if you do endo in this application, you can jail or covered the deep femoral artery. Inside of this by open surgery you can clean both artery and leave a good vascularization.

In our practice result in claudicants are excellent, are shown here. They are not so good in patient with rest pain and gangrene because obviously these patients with CLTI and occlusion of the popliteal and infrapopliteal artery needs a popliteal or tibial revascularization

in addition to that of a deep femoral artery to save a foot. So we think that until now open surgery is still the best option in most cases. Thank you.

3

3

- I am not Walter's enemy. I can tell you that. I am against the motion. (man laughing) I will stick to the truth, to the facts. I don't like polemic, like you. I don't like to play, let's say games

of undermining what my opponent is saying. I'm just showing what I believe in because it is the truth, okay? (quiet laughter) I have nothing to disclose. Let's stick to the definition of 'cure.'

We all know that 'cure' means 'at least one year follow-up, angiographic follow-up after the, so-called, final angiography, that shows that malformation is gone.' Call it whatever you want.

Technical success, obliterated, trombosed, concluded, ablated, gone. Then at least one year follow-up on that. Angiographic to prove it's gone. The rest is just a scale on how you can evaluate the results.

Angiographically and clinically. The only way, for me, to speak to the truth is to find in a material where there is a chance to compare.

Hat to hat. Both type of treatments. Polymerizing versus alcohol. And, the only way to find such a place is to go to Wayne's place, because he's also constantly called

talking about salvaging this and salvaging that. I am very critical about what Wayne does. You can be assured about that. He's had 16 patients, I dig out there, and polymerizing agents they were failed.

Definitely, failed. Actually, they were salvaged, by Wayne. And, I'll show that to you. These are the patients. This is the time to which they've been treated. The usual type of distribution.

Young patients. All of them extensive. There is no, for a lack of an effort. There is no, for a lack of knowing how to use

the polymer. Onyx. How we can tell that, most of those is Onyx, some of them are glue. Or a combination. The median number of sessions

with this polymerizing agent is 8.5. Range from one to thirty. The other radiologists, the other experts, besides my honorable opponent, Doctor, Professor Wolgemuth,

they also know how to use Onyx. I can assure that. Sixteen patients, all symptomatic. They are all decompensated, showing three, four tier symptomatically. They have high cardiac output,

they have required repeated, repeated blood transfusions, infections, ulcers, disarticulation. To have disarticulation of vascular malformation means, oh, horrible bleeding, infected. There is no doubt,

they are symptomatic. Couple of examples. This is a young woman, extensive AVM in the foot, type four. Been treated five times with Onyx. And they know what they've done.

They've treated well. Yet, worsening symptoms, wheelchair bound, infected ulcer. Seventy-one session. Now, pay attention. Seventy-one sessions of ethanol/coils embolization. And, this woman is now running with her friends

after her amputation of couple of necrotic toes. Not because of the alcohol. Because of the malformation. Angiographically, not cured. Example of that. Okay.

This is malformation. This is not something in a tiny, little bitty thing. It's a malformation, no question about that. Before treatment. And, this is after treatment. We can all agree that,

this is not completely cured. It is a grade three it is 80 to 99 percent still left. But, clinically, she's running. She continues to be treated. Another example.

One year old girl with bleeding malformation from the lip. Admittedly only one Onyx being used because we didn't know what to do. Luckily, the little girl was close by so she came to Wayne and after,

it's intravenous predominant lesion. It's a type two lesion. Only after a six month treatment sessions, cured. This is before start of ethanol treatment. No question there is recurrence. We can not close that only by pushing

polymerizing agents somewhere in something called 'nidus.' But if you ablate the cells, ablate the nidus. You achieve cure.

And it's cured in one year angiographic follow-up. This is time and time and again. I will show these examples. This is the outcome. The outcome tells you six cured angiographically. Eight considerably improved, they improved.

None of them is failed in this. All failed polymerizing agent treatment. Then we can move on. Complication because that's where talking about how dangerous. Alcohol is very dangerous,

but so is knife in operating room. Take a knife and stab it somewhere in some artery, or in a pressurized vein, you'll have all this blood in your face and a shoot of blood doesn't taste very good in your mouth. So it's dangerous.

But, if you use it carefully, that's what you achieve, as a result. Where do we stand with these patients? Ongoing treatment, five. Cured, five, by summation.

One still waiting for a follow-up on angiographic follow-up. Improved on watchful observation is two. Lost to follow-up because schizophrenia. Lost to follow-up because of unknown reason, after two years of follow-up.

He's been doing well throughout these two years. One clinical failure. I will tell you that Wayne have, he's seen this person. Not clinical failure. Yeah, it's clinic.

By definition, is clinical failure. Angiographically, improved. Clinically, improved. The little boy was wheelchair bound, didn't want to continue with that and, therefore, went for amputation.

So it's a clinical failure. One. To summarize that, I highlight on this, venous predominant lesions. These are the ones these create.

Type four. (man speaking off screen) Tough. Couple of examples. Striking examples. This is venous predominant lesion, IIA.

I'm sorry. IIIa, IIIb being treated. Sorry. Can we go back to that? Any way I can go back on that?

This IIIa, IIIb, there's has been five. That's moves forward. Five surgery, Onyx, anything thrown in. Extensive malformation. Shoulder, arm, a no-flow into the lower arm

because of the. And it's moving forward. I'm sorry for that. But it was cured. And there was a follow-up, too. I believe there was something.

Twenty, 15, 17 months follow-up. So we have the next patient. Thirty-two year old female treated with glue in the past.

Twenty procedure including all vessels. Everything that can not be, could be embolized, was emolized. Ended up with the worsening and this is the typical example a IIIa malformation, typical example.

This was way back in the past. This is how Wayne has developed that. It took him, I heard, nine hours and another 100 coils, but he cured that.

- [Male] 298. - Two hundred ninety-eight. This is the follow-up, you know. Eighteen months later. To summarize on that. Nothing to do with my feelings for Wayne.

Nothing to do with Walter being my enemy. (quiet laughter) No, it's just a fact, a truth. Polymerizing agents, by definition, do not cure AVMs. Do not cure.

Sometimes, when used properly, still worsen the patient's symptoms. Ethanol cures AVM. Provided that you do that with precision and skills. How you acquire precision and skills? Ask the surgeons around here.

How do they lift up this face? How Max can lift out, you know, big time metastasis sections in liver? How do you do that? With skills.

How do you acquire skills? Learn. Thank you.

- Thank you, Mr. Chairman. Thank you, Dr. Vieth for the kind invitation to be here. My disclosures, so Angiotomagraphy show us zoozataous To choose the better approach our technical approach to our patients, length, diameters, localization of the aneurism sac, so neck diameters less than 4mm suggest us

that no adjunctive technique could be necessary only embolization. Dome-to-neck ratio less than 1.2 suggest us that stent-assisted technique or remodel technique with balloon probably will be necessary as we do prefer our technical approach so is general anesthesia

to get a panea to get a nice image transfemoral or transbraquial says transaxial says covered stents after heparin initial aortogram to do super selective catheterization of our vessels in coaxial technique to do super selective catheterization

to get the vascular disdel belt road-mapping and scaffolding technique to do the compactation of the coils. Dual Antiplatelet Therapy 5 days before the procedure so the goal of the treatment is to prevent aneurysm expansion by excluding

it from the arterial circulation, saving branches, patency, and freedom from rupture. The radial shows the stent in red deployed, and the microcatheter inside the aneurysm sac in this Intraparenchymal Aneurysm The CT control.

So the materials that we use when necessary The enterprise, solitaire stents, detachable coils-axium 3D to get more volume inside the aneurysm sac and solaris as a new Brazilian stent graft. Another case to explain Intraparenchymal Aneurysms to treat distill one the stent are deployed,

the microcatheter inside the aneurysm sac the stent avoid migration or animation of the coils that's a nice compaction. So the prosmo one Same technique and the normal flow to the spleen. So in seven years, we treated 26 cases

in 21 patients electively. Coiling alone in 65% of experience in wide-neck case coiling with stent, 25% and balloon with remodeling technique in 10% as we are doing more nowadays. Follow up 1-3-12 months with ourdoplar

To show us aneurysm exclusion. So are main results are complete regression of all aneurysm sac, with no evidence of recurrences up to now. No deaths, no secondary interventions and 1 Retroperitoneal Hematoma, our major complication

threethirty consecutively. You use covered stents when we have large arteries, notruousity, youresilitus mojor impact, stent graft available now visible so in this case a large right renal artery aneurysm is treated with covered stent with a nice result.

Another case, you can see the exclusion of the aneurysm sac in the basilar branches. Superormedial aneurysm case is treated with multilayer, the final result show a exclusion of the aneurysm sac and the patency branches inside of the device.

So in conclusion, ladies and gentlemen it's a feasible, safe, and should be done with low risk in our opinion. For the treatment of visceral artery aneurysms planning is necessary to get positive result individualizing all cases.

Endovascular treatment is the first line of option in our opinion to treat our patients, but don't forget we are vascular surgeons and if there are technical or anatomical restrictions do open access those publications about these issues, thank you about your attention

- My rebuttal is short and sweet. I think that those of us who have seen both agents, seen it in a fair comparison, understand that while ethanol has an appearance of difficulty to use, have come to the conclusion that it is actually safe. It has to be applied in the right spot. If it is such it will absolutely cure

and in it's very, very safe fashion. I think Walter mentioned the four deaths that I referred to. I agree, tragic, terrible, but we learn. Haven't had any deaths since, because I understand now the mistake I made and how to use ethanol.

I think the same thing is true. Max will tell you that there were enumerable deaths during the development of transplanting these difficult operations. No longer, all controlled, it's all because of learning. Thanks.

- I've made this agent comparison chart, just sort of summarizing the areas where I think that Onyx is better as compared to ethanol. I think things to come, oops, sorry, I got to go back. I think the items to be commented on are one, that there's less skin necrosis with the polymers.

It's a less painful procedure, and the Onyx, in our experience, is durable. But in the treatment of any type of AVM, you have to get your agent into the nidus of the malformation. If you don't do that,

then you're just doing a proximal occlusion. And we know from the surgical literature that that does not work. They will simply, the angiogenic stimulus, whatever triggers it, will continue. And that gets me to another point.

I really don't think that we really know what stimulates these malformations to grow. We think it may have something to do with a resistance in the flow, but we have some pelvic AVMs who have been stable for 30 years.

We're not touching them, and we have no intention of touching them, whereas we have children who will present with an AVM at age four and then by age seven, they are unable to ambulate. So in any event, I think that

polymers represent the future. And I just want to quote from this old movie, The Graduate. "Plastics," thank you.

- [Mark] Thank you. First of all, I'd like to thank Dr. Veith for inviting me here, as well as Dr. Greg Stone, who's working on the project with me. One of the things we'll talk about initially, because it's not intuitive is the mechanism of action for this device.

Some are calling it carotid expansion. It's really not the true mechanism. If you look on the left of the screen, you see the carotid bulb shape, obviously circular and the radius shown here. What happens with this device is a change

in the architecture of the carotid bulb, such that the, if you look at this part in the window of the carotid sinus, of the carotid bulb, the relative radius increases. Based on the strain equation, then you would expect with each pulse,

then there'll be increased strain and increased stretch in that particular segment of the carotid. Since the carotid is activated, the receptors are activated by stretch and not pressure, then this would be expected to drop blood pressure,

which was shown in preclinical animal studies. The device, I was recruited by Yossi Gross who came up with this idea, to help develop a system or a device that could be implanted. So Yossi deserves the credit for the concept. This what the device looks like today.

It's in three different sizes. It's designed not to migrate through the carotid bulb. It's re-captureable and re-positional and the engineering team that developed this implant was part of a neuro interventional team in the past. The first in man study is a 50 patient trial

that had 30 patients enrolled in Europe and 20 in the U.S. The first 30 patients were reported in European Society of Cardiology two months ago and those patients where published in Lancet. This was a safety trial primarily, but we also did look at 24 hour ambulatory blood pressure.

This is kind of a snapshot of what the baseline characteristics of these patients look like, the 40 that we're reporting here today. The final report of the 50 patients will be forthcoming. Mean 24 hour blood pressure was industrial strength at 165. They're on four and a half meds roughly.

Equally important, nine of the patients had failed renal denervation in the past. The implantations obviously are guided by meticulous imaging looking at or excluding issues of plaque on Duplex as well at CT and MRA looking at the architecture of the arch

and making sure access can be done safely. The safety results of the study looked promising. There were no unexpected adverse device events. We did have the biggest number of adverse events were related to symptomatic hypotension. You'll see an immediate drop in blood pressure

with these patients. This is what the 24 hour ambulatory blood pressure looks like and one of the big concerns about this device is resetting after implant. But what we've seen in some patients now out to three years

is a continued decline in blood pressure. In six months we'll see, again this is not randomized, a 20 millimeter drop in systolic pressure on 24 hour ambulatory blood pressure. These promising safety, this first in man safety study

led to the development of the CALM-2 trial. This is the design of the CALM-2 trial and I think in the introduction I think it was stated we're going to talk about the results of the CALM-2. It's really just getting started. Basically these patients will have

24 hour ambulatory blood pressure analysis. As with any contemporary resistant hypertension study, we'll enroll 300 patients. They'll have imagining studies to exclude carotid plaque or significant disease and then be randomized to get either a sham procedure

or the device implant. What's unique about the CALM-2 trial is that we are doing strict medication compliance adjudication. So before the 24 hour ambulatory blood pressure is placed we will observe them taking their medications.

There also will be urine testing to show that they're taking their medication and being compliant. This is a permanent implant and so they'll be meticulous imaging of the carotid bulb including core lab analysis of

intima-media thickness et cetera. So in conclusion, ladies and gentleman, the pre-clinical and first in man safety data suggests that Carotid Baroreceptor Activation Therapy appears to be safe in carefully selected patients. We were real meticulous about who we enrolled,

and it may reduce blood pressure in patients with resistant hypertension. The CALM-2 trial will provided needed randomized, sham controlled evidence regarding safety and efficacy and we're taking the learnings from issues related to regression to the mean,

the Hawthorn effect, and all the other lessons we've learned from renal stent as well as denervation trials and baking those into this definitive study to improve the accuracy of the results. Thank you for your attention.

- I will be sharing a novel technique of using the ClariVein catheter for declotting thrombosed AV grafts. This technique has been pioneered and utilized in my institution over the past two years. I have no relevant conflicts of interest to declare. As we all know, the outcomes for

vascular access are generally poor, more so for AV grafts than AV fistulas. For AV grafts in particular, the incidence of graft malfunction in the first year ranges anywhere between 60 to 80%. The patency at two years is also poor,

with a primary patency of 40 and secondary patency of 60%. As such, the thrombosed AV graft is a common problem that most vascular surgeons deal with on a regular basis. Over the years, several percutaneous techniques have been described, each with varying costs, time taken, amount of thrombolytics

administered, amongst other considerations. These methods all rely on the principle of first declotting, followed by treatment of the underlying offending lesion. My center generally prefers an endovascular approach whenever feasible.

I'm sure that most of you in the audience already know this, but for the uninitiated, the ClariVein catheter is a catheter system originally designed for the treatment of venous reflux. It achieves this by a combination of mechanical damage to the endothelial cells

by the rotating catheter tip, and chemical damage with a liquid sclerosant. We chose to infuse a thrombolytic agent, which is urokinase in this case, and combined this with the rotating catheter tip to augment the thrombolytic process.

I shall now proceed to demonstrate the technique of pharmacomechanical thrombolysis using the ClariVein catheter. In the video on the right, you can see the graft artery anastomosis with the edge of the thrombus cap clearly visible.

First, the arterial side of the graft is punctured under ultrasound guidance at a distance of about one centimeter from the arterial anastomosis. This serves two purposes: the one-centimeter segment is long enough to prevent

the spontaneous reestablishment of influent in the graft before thrombolysis is complete. But at the same time, it's also short enough to ensure that only a minimal amount of thrombus gets throughout to the central veins later on. A six French Brite Tip sheath is then inserted.

Next, using a Berenstein II support catheter in conjunction with an 0.035 Terumo Glidewire, the occluded graft is easily crossed, and the wire is sent into the central veins. A central venogram is first performed to evaluate the patency of the central veins,

as well as the extent of thrombus extension. A catheter pullback is then performed to identify the venous anastomosis of the graft. This was found to be the problematic area in a majority of cases in our case series. At this point of time, IV Heparin and

prophylactic antibiotic of choice are administered. Now, the first video on top shows the ClariVein catheter setup. It is made up of two main components: the catheter assembly unit and the motor drive unit. The rotating tip can be sheathed and unsheathed.

The second video below shows the sheath catheter tip being judiciously maneuvered up the graft. Once the catheter reaches the desired position at the end of the graft, it is unsheathed and fitted on. The ClariVein catheter is then activated and

urokinase is infused through the spinning wire tip. This urokinase is mixed with contrast in a roughly 70 to 30% ratio. The addition of contrast actually allows direct visualization of the adequacy of clot breakdown, which in turn

guides the number of passes of the ClariVein catheter I need. The catheter is pulled back at a speed of one centimeter every three seconds. After the first pass, this is what the catheter tip will look like.

It is important to pluck out the thrombus stuck to the catheter tip, or it may be difficult to inject urokinase in subsequent passes. This is the appearance of the graft after two passes of the ClariVein catheter.

A total of 90,000 units of urokinase was administered in this instance. As you can see, the graft now look pretty clean, with most of the thrombus already broken down. Remember that at this point of time,

both the inflow thrombus cap and outflow offending lesions have not been dealt with as of yet. Keeping the outflow stenosis is actually beneficial, because this serves as a natural embolic filter,

trapping any large thrombus within the graft to allow adequate thrombolysis to first finish. Once thrombolysis is complete, microclots are aspirated by the sheath, and this is the usual appearance of the microclots. It is at this point of time that

the offending lesion, which is usually the venous outflow anastomosis, as well as any other concomitant graft lesions, are plastied. The post-thrombolysis angiogram now shows a clean graft, devoid of any remnant thrombus. Note that the inflow to the graft hasn't been

reestablished yet at this point of time. After the V side of the graft has been treated, the sheath is removed, and the puncture site closed with a simple figure-of-eight stitch. And the V side of the graft is then punctured and a six French sheath inserted.

And now, using the same Berenstein II catheter and Terumo Glidewire, the wire is sent past the remnant thrombus cap, and a 5.5 French over-the-wire Fogarty used to trawl the remnant arterial cap and reestablish arterial inflow.

This is the completion angiogram showing a nice, clean graft with good flow. Post-operatively, I routinely give my patients a shot of subcutaneous Enoxaparin two hours post-op, and another dose the next morning. This is usually not continued on discharge.

The AV graft can be cannulated immediately post-op, and patients are usually sent home after one session of inpatient dialysis. Some time last year, we wrote up and published our center's initial experience with the ClariVein catheter for this purpose.

We have been using this method to perform the bulk of our AV graft declotting over the past two years. As at the end of last year, there were a total of 37 such procedures performed, and we achieved 100% technical and clinical success rate. Looking at the patient demographic

and based on characteristics, most of the offending lesions were located at the venous anastomosis and graft cannulation sites. The mean urokinase dose administered was 87,000 units, and the mean procedure time was about an hour. Our primary patency rates at one and three months

were 78 and 62%, respectively. And other than minor, self-limiting graft perforations, there were no other complications of note. And if anything, I believe that these complications were from aggressive high-pressure balloon angioplasty, rather than the process of declotting.

As you can see, our results are well within the guideline targets. As you can recall, we achieved 100% clinical success rate and 62% patency at three months. Comparing our results to previously published studies, our mean procedure time was generally faster

or comparable, and we utilized a significantly lower dosage of thrombolytic agent. Patency rates were also comparable. While I believe that the adequacy of the clotting effect's short-term patency may be at one month, I'm not fully convinced that

a patency at three months is related to the method of thrombolysis, barring any severe graft damage from the declotting procedure itself. In summary, pharmacomechanical thrombolysis with the ClariVein catheter is a safe and efficacious method. It is relatively simple to perform,

with no additional installation or bulky equipment required, and other benefits include a short procedure time and low dose of urokinase. Thank you.

- Ladies and gentlemen I'm extremely excited to share with you some new technology that's being developed in Seattle. These are my disclosures. The use of central venous catheters for hemodialysis remains high, and the greatest threat to the safety of these patients

is through catheter-related bloodstream infection. In the United States alone, there are over 50,000 new cases of catheter-related infections diagnosed each year. And studies have shown that these patients require hospitalization for up to 13 days on average,

with a cost of 24,000 dollars per infection and high mortality rates. So, we think that we have developed a graft that has improved patency and resists infection. That's the holy grail of dialysis access graft implantation. This is a simple cartoon that shows blood flow

from an AV graft into a venous outflow and we know that when we implant a graft, that scar tissue forms on the outside of the graft and that reduces compliance of the graft and causes Neointimal hyperplasia at the venous outflow. This eventually leads to thrombosis,

and solving this problem would obviously have high impact for our our patients. The material that I'm going to present to you is called the STAR material. It's a silicone-based material but is solves this occlusion problem

by allowing no scar tissue to form on the outside of the graft, and maintain the compliance. I'm going to show you some exciting images about this. What happens is the venous outflow stays open, and allows the STAR graft to remain patent. When we have a close-up view of this STAR biomaterial,

it's not just silicone that you buy at Home Depot, this is silicone biomaterial that has specific pore structures that allow for macrophage infiltration and resistance of infection. It's made of medical-grade silicone which is used in many commercial implants

and it's actually already FDA approved for ophthalmologic surgery and lens implants. The unique geometric structure prevents both scarring and infection, and the 3D scaffold is what allows for the tightly-controlled dimensions. This is an example of intravascular ultrasound

in AV grafts that were implanted in sheep three months after implantation, and you can see the control on the left is stiff it doesn't allow for any expansion or contraction of that graft material, whereas the STARgraft material, which is depicted to the right

shows maintenance of compliance. When we look at six-month arteriograms again in sheep models. These are animal models. We look at the conventional ePTFE graft and we see that classic narrowing at the venous outflow of the sheep models.

But when we look at STARgraft, those remain widely patent at six months. This has been demonstrated consistently in multiple sheep studies and pulled results show 80% reduction in occlusion with the STARgraft material. On your left is the percent diameter

occluded, and then intravascular ultrasound confirms this with near occlusion of the control grafts, but the STARfgrafts that have been coated with this silicone biomaterial remain widely patent at six months. What about infection resistance?

STARgraft prevents biofilm from developing and therefore prevents a biomaterial that bacteria are easily able to colonize. You can see that the blue clusters here are clusters of Staph aureus in sheep implants at two months. Whereas there's minimal fibrotic capsule in the STARgraft.

When we do culture analysis, the bacteria concencentration are dramatically reduced, 1000 times reduced in the STARgraft material. These are ports that have been coated with STARgraft. And if you can imagine this material actually resisting infection, we should be

coating every implantable device with this material to include stent grafts and infusion catheters. If you look at a port that is coated with the STAR material on day number 21 this is in a pig skin model, nearly all of the ports remain infection-free at 21 days, versus the control.

Virtually all of the control devices that are uncoated with STAR material become infected. That's demonstrated here in this graft. And then if you look at the actual pigs, these are pigs. Pigs don't have the cleanest of conditions. These are demanding conditions but at six weeks

all of the ports that had been not coated with the STAR material had to be removed the four controls because they became infected within three weeks. Whereas the STAR coated ports remained uninfected. So this is exciting new technology. This is my last slide and I think that

the value of the STARgraft in an AV model is that it's expected to reduce cost, illness and death among dialysis patients. And it could prevent less frequent infections an alternative to a fistula and avoids the extended use of infection-prone catheters.

We expect our first human trial to begin in the first quarter of 2019 and if any of you are interested in being a part of this trial, please contact Mike Connolly. Mr. Chairman I apologize for both my attire and the fact that I'm not going to be able

to participate in the panel discussion because I have a plane to catch in exactly two hours. And Andrew Marshall is in the audience the chief technical officer, he can answer any questions. Thank you very much.

- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --

- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.

But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,

is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy

in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.

The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation

so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later

that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low

and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse

even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean

as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques

different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between

pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients

are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system

you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because

this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out

now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference

between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing

a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is

the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories

and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here

again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result

and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not

fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again

look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as

the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here

This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you

- Good morning, ladies and gentlemen. Thank you Dr. Kabnick for the kind introduction, and thank you to the Veith Symposium for the opportunity to be here. I have no disclosures. Superficial thrombophlebitis is uncommon, but certainly more common than DVT.

And it used to be thought of as quite a benign entity that could be treated with antibiotics and, oh sorry. Antibiotics and analgesia, apologies for that. However, it is been found to be a wolf in sheep's clothing. And actually, there is a significant risk of DVT,

and of asymptomatic and symptomatic pulmonary embolism. Particularly important for individuals with truncal involvement, and particularly if close to the junction. And actually anything that is less than three centimeters from the junction,

should be treated as a deep venous thrombosis, and requires anti-coagulation. Management sent us on to symptom, sort of addressment, prevention of SVT extension and recurrence, and prevention of venous thromboembolic complications. There've been a number of studies that have been produced

and summarized in different guidelines. The CHEST ACCP guidelines suggest that if you have a superficial vein thrombosis of at least five centimeters in length and more than three centimeters from the junction, you can treat it with prophylactic Fondaparinux

or low molecular weight Heparin for 45 days. And that is superior to no anticoagulation with a grade 2B recommendation. However, Fondaparinux is actually been found to be of higher level than low molecular weight heparin, and that should be used.

Importantly, patient choices also mentioned in these guidelines and the risk-benefit ratio as to whether to take anticoagulation or whether it's run the risk of getting a DVT, must be discussed with the patient. The Cochrane Review was published in February of this year,

and this is the latest summary of the evidence on this topic. They also suggest as per the CALISTO trial which was the largest randomized study on this topic, to give Fondaparinux, 2.5 milligrams for 45 days. And this was found, in this study it was found

that VT development, SVT extension and symptomatic recurrence were lower in the Fondaparinux group as opposed to placebo. Low molecular weight Heparin can also be used. There is some evidence for this, however as graded by the Cochrane library, this was found to be low evidence.

And most of the studies are actually of low quality as opposed to the ones with Fondaparinux. And again, patient choice and patient discussion and need to think about different risk factors for developing SVT. The SURPRISE trial looked at Rivaroxaban

versus Fondaparinux in prophylactic doses and found that Rivaroxaban was non-inferior. And actually this gives us an advantage to give an oral agent for individuals for the treatment of SVT. This is an algorithm that was published

by the British Journal of Hematology, again reminding us that anyone with a DVT or an SVT less than three centimeters away from the junction should be treated as a DVT. If it's more than three centimeters and more than five centimeters in length,

you can give Fondaparinux and I would suggest, also Rivaroxaban. And if the length of the SVT is less than five centimeters, or there's no SVT you don't need to treat. With regards to compression, it's mainly for symptomatic relief and there's very conflicting evidence

as to what the classes or what the length of time is. One study looked at compression versus no compression SVT and they found no additional benefit for compression. And the next pilot randomized study actually had to be halted due to poor recruitment and therefore was underpowered

and couldn't identify any difference between the groups. With regards to follow up, there's no clear guidance. It can be anywhere between eight weeks to six months. In the studies, it's really on a case by case basis based on the risk factors. But what we do know, is that even if we treat SVT,

there is a risk of developing a VT even with treatment dose low molecular weight Heparin. So if you identify thrombus extension, what do you do? Well some studies have looked at different treatment modalities. This randomized control trial by

a professor Nicolaides' team looked at different treatments including compression only, saphenous ligation, saphenous ligation and stripping, and anti-coagulation. And they found that in the stripping group you had less DVT instances or SVT extension. But with respect to newer ways of treating veins,

looking at endovenous saphenous vein ablation in individuals with SVT with refluxing vein this group looked at this and such and they didn't find any inferiority with, or any sort of particular side effects with using endovenous saphenous vein ablation,

however this was a retrospective study and was also underpowered and therefore there is a lack of evidence. So in conclusion, ladies and gentlemen, think SVT is not benign, there is a role for prophylactic Fondaparinux for 45 days,

Rivaroxaban should be considered. Compression is conflicting in evidence and the role of intervention is also unclear. Really we need to assess patients individually with their risk factors, and we need more data. Thank you very much.

- [Lecturer] I thank you, Mr. Chairman, and thank you Dr. Vieth. It is our great pleasure to open our primer endpoint result today in this meeting. I've nothing to disclose. There's been studies of

prospective multicenter registry in Japan, which started at 2012 by vascular surgeons and interventional cardiologists collaboratively. More than 550 CRTI patients were enrolled. More than 70% patients are diabetics and more than half of the patient

are dialysis dependent. So, very high risk patient are including in this observational study. Directing this patient background, so to study the patient while aiming infrapopliteal revascularization.

Taking a look at preoperative QOL, there are some difference between EVT group and surgery group, and the surgical intervention, while frequently selected in a more active or more motivated patient.

In terms of the foot lesion severity, there seemed not difference between two groups by Rutherford classification, but adapting a WIfI classification, so the feet underwent the surgical intervention was significantly similar

in terms of WIfI wound grade, ischemia grade, and foot infection grade. So, adjust this difference and to minimize the bias, we employed a propensity score matching result. Now, I would like to open our primer in the point,

amputation-free survival. As you can see, there are no difference between surgical group and endovascular group, and the AF risk at three years are around 50% for both groups.

There are no difference between the two groups in terms of freedom from MALE, but the freedom from major amputation or any reintervention rate was significantly lower in EVT group. These results came from a sum total of

highly heterogenic population, so it should include patients suitable for EVT and another patient group suitable for surgical intervention, so we have to find out the important factor for selecting intervention procedure.

So therefore, we performed the interaction analysis. This slide shows the impact of the foot lesion severity on selecting revascularization procedure. So, patient with high grade WIfI,

wound grade or infection grade are seemed suitable for bypass surgery, surgical intervention. In terms of general condition, patient who is diabetes, patient who is renal dysfunction

not seem suitable for bypass surgical intervention. So this analysis provides us five factors more favorable for surgical intervention. Each have a +1 point for each, and another five factors

less favorable for surgical reconstruction, which have a -1 point for each. Finally, we propose a favorability score model to select a proper revascularization procedure. If the total point is +2 or more, the patient is suitable

for surgical intervention. On the other hand, the point is -2 or less, the patient is suitable for endovascular treatment. So, the patient risk factor,

as well as foot lesion severity are very important to select the revascularization procedure. In conclusion, ladies and gentlemen, the SPINACH registry explores current clinical outcomes of CLI treatment

in real world setting in Japan, which provides the data recommending how to select adequate revascularization option, in respond to patient's general condition and foot lesion severity, and WIfI system is very useful,

not only assess foot status, but also selecting revascularization procedure. Now, our doctor, analyzing a secondary endpoint is now ongoing. I thank you for your kind attention.

- Thanks, I appreciate the invitation. MR imaging of vascular malformations poses some challenges primarily related to the heterogeneous spectrum of the lesions. The primary distinction to be made with imaging is between low flow and high flow abnormalities. This distinction, however, can often be made clinically

and so the real value in MR is in determining the malformation extent and the associated involvement of adjacent normal structures. The basic MR evaluation of vascular malformations should of course be multiplanar in two or three orthogonal planes, and in each of those planes,

there should be T1 and T2 weighted imaging. There's some debate about the value of contrast-enhanced scans. Certainly contrast-enhanced scanning will show things like arteriovenous shunting and lesion perfusion, but mostly the value of contrast-enhanced scanning

is in making the diagnosis of the abnormality rather than in guiding specific treatment. So let's talk about the various imaging sequences and go through a few examples. On T1 weighted images, we see the anatomy of the limb or of the area in question quite clearly.

But what you notice is that there's a signal similarity between the normal tissues and the adjacent malformation, such that they blend together. That means that assessment of lesion extent is poor on T1 weighted images. Now this is in distinction from T2 weighted imaging

where malformation images tend to stand out quite dramatically from the adjacent surrounding normal tissue, making assessment of lesion extent quite good, with the following caveat that on these bright water-type sequences, edema, when present, especially in high-flow lesions

or in low-flow lesions following embolization, it can result in overestimation of lesion extent. Many people routinely include contrast-enhanced imaging for malformation evaluation. I think it's probably not necessary and doesn't actually provide that much

additional information beyond making the actual diagnosis. Now that said, that's to be distinguished from dynamic time resolved imaging, which is a newer type of contrast-enhanced imaging using faster acquisition. It has what's called a higher temporal resolution and we can clearly differentiate

inflow arteries from draining veins and this can be valuable in treatment planning as well. Here we see pre- and post-contrast images and you'll notice that on the post-contrast images, there's slightly better visualization of the malformation, but the difference between the two is really modest

and probably not clinically relevant. Now that's to be distinguished from time resolved imaging, which will allow us to see arterial, parenchymal, and venous phases, and these can be stitched together to create a movie that really does look quite a bit like a catheter-based angiogram.

The difference between high and low flow malformations is primarily made based on structural characteristics, rather than MR signal abnormalities. So, low flow lesions will usually have minimal mass effect. Here we see signal abnormality with almost no mass effect. When a mass is present, it sometimes has

hamartomatous stromal elements that look like septations running through the mass. When a mass is not present, the lesion tends to be pretty infiltrative. Without any mass effect, sometimes the degree of infiltration is amazingly intimate, as in, case like this.

When we see phleboliths, which are routinely identified on radiographic images, we have confidence that we're dealing with a low flow lesion. But in fact, MRI imaging can identify phleboliths pretty consistently, and here you see they appear as rounder, oval, low signal images

on all imaging sequences, and of course, they don't enhance. Now, these findings are in distinction to high flow lesions, which demonstrate no well-defined mass ever, and in fact, if you see a well-defined mass it should make you think that you're dealing with a tumor rather than a malformation.

But they will demonstrate characteristics of enlarged feeding arteries, enlarged draining veins, and these infiltrative masses will often be riven through with multiple flow voids, and the degree of infiltration can be really, pretty impressive.

There are some signal characteristic differences between the various malformations. It's a long and involved topic, and probably something that doesn't make sense to go into here at this point, but I think the utility of MR in vascular malformations is primarily related to defining the anatomic

characteristics of the malformation, assessing what normal structures are involved or immediately adjacent, and this allows us to mitigate risk and plan the procedures. Now this is different from post-treatment evaluation of MRI, where there's definitely differences between how low flow and high flow lesions respond.

In low flow images, post-embolization we see significant signal changes. In high flow lesions, post-embolization we see anatomic changes. One important caveat to remember is when imaging and malformation within three months of an embolization,

it can be difficult to interpret related to the post-embolization inflammatory reaction. So on T1 weighted imaging post-embolization, we see bright signal, representing thrombus is the treated area as opposed to lack of bright signal, in the non-treated area.

On T2 weighted images, where the malformation generally appears bright, post-embolization we see dark areas in the treated zoned, representing scar. I personally prefer evaluating these with T2 weighted images. I think the distinction between treated and

untreated is greater and more consistent. Another example, scar forming, T2 weighted images. Again, I think the distinction is pretty clear. Although, contrast-enhancement isn't all that valuable in pre-treatment planning. Actually, can I get this video to go?

There we go. Although contrast-enhanced scanning isn't generally valuable in pre-treatment planning, there can be some utility in post-treatment evaluations. Specifically, dynamic time-resolved imaging or virtual angiography can be applicable to high flow malformations.

As you can see here, when the post-treatment evaluation and assessment of residual arteriovenous stunting is an important end point. Thank you. (applauding) - [Announcer] Any questions from the audience?

I think it's important to note, you mentioned the importance of T2 weighted imaging. And it is crucial, particularly for venous and lymphatic, or mixed lesions. But I think it's also important to state with T2 imaging, that you have to have fat suppression,

'cause fat also has bright signal and can be confused with malformation. - [Scott] Yeah, exactly, and there's really a broad range of T2 weighted images. What we rely on mostly is this short towen version recovery which,

- [Announcer] Now that's different, yeah. - [Mark] Yeah that's going to be. - I was going to write next. - [Mark] Yeah, so the, T2 fat suppressed images are, of course, critical, and should be obtained in every plane. We actually also obtain stir imaging in every plane. Yes, question?

- [Audience Member] So is the T2 full, (mumbling) what time do you need. - [Mark] I'm sorry, can you repeat that? - [Audience Member] What time do you need to continue to use of a full of T2 for (mumbling) - [Mark] Well, it depends on what you're looking for.

If you're trying to assess for complications, you can image any time. But, the challenge in interpreting is that the diagnostic radiologist won't necessarily know exactly where you've treated, and the lesion may appear abnormal in ways that aren't understood.

So, as the interventionalist who's doing the procedure, you really need to sit with the radiologist and help them understand what you did within that short timeframe. Now, if you're talking about imaging after three months, it's much easier to interpret signal changes have moderated, and that post-embolization inflammatory

phase has resolved. - [Audience Member] After two or three months? - [Mark] After three months, yeah. - [Announcer] Okay, thank you so much. - [Mark] Thank you.

- Alright-ey, hands put up. Who is for Onyx? Put your arms up. - [Male Audience Member] Who supports the Onyx Motion? - Onyx Motion, that's correct. He should've gone to law school. Who supports the alcohol motion?

Who supports the motion in the ocean? Alright, thank you I think we covered a lot of territory today. We want to have theses things and we are so glad that everybody came. I think this is Tony's first time,

Walter's first time here, Loronze and we really learned a lot today. I'm really glad Pletio Rossi was here because without him and his development of selective catheterization, I mean where would we be

sticking needles in every artery like that, trying to do angiograms, much less advanced sheaths or anything else. Pletio was wonderful having him here, one of my hero's. Anybody like to say anything?

Anybody got any questions or anything? - [Female Audience Member] The HHT scientific meeting's in June in Puerto Rico if you want some more good-- - Do they have electricity there yet? - [Female Audience Member] I hope so, I knew it looked nice before.

- Oh, okay, okay. Alright, well thank ya'll so much and we'll see you next year. (Clapping)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

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

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

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

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

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

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

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

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

That's my statement. Thank you.

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