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VANISH-2 Trial - One-Year Results
VANISH-2 Trial - One-Year Results
2016BTG-IMClariVeinClosureFastCovidieneCloseeventsMedtronicneurologicnoindexpatientpatientsResearchsbvSIRsymptomsV-blockVANISH-2VarithenaVascular InsightsVeCloseVenaSealVenefitVVSymQVVT Medical
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Transcript

patients they were followed for first 48 weeks and then at at one year but here's

where all these things came up this is the vcm q this is an independent physician review panel looked at pictures and said gee this patient get better or not and this was the patient said hey do I think my legs look better

or not so this is all the patient driven how did it affect the patient and this was one of the great things about this trial it really brought to our attention that that's where we need to to be going and here's your initial baseline of ECM

q-ball the patients and you notice that at one year everybody is down to almost no symptoms at all so again you close this afternoon saying patients feel better think and improve their quality of life so that one year

results everything improve symptoms improved appearance reproved disease severity got better as measured by V CSS and the they also correlated this with the veins quality of life so it's a good thing i'm giving my talk after we we

heard the talk from before so you understand here that they're looking at how did it affect the patient minimal complications more importantly they'll I am blind and with foam you have this idea you're going to get some

neurological events no neurologic events were seen so it's relatively safe and this is a really nice thing here and one year but was going to show pictures that patient didn't get better right

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

- Mister Chairman, ladies and gentlemen. Good morning. I am excited to present some of the data on the new device here. These are my disclosure. There are opportunities to improve current TEVAR devices. One of that is to have a smaller device,

is a rapid deployment that is precise, and wider possibilities to have multiple size matrix to adapt to single patient anatomy. The Valiant device actually tried to meet all these unmet needs, and nowadays the Navion has been designed on the platform

of the Valiant Captivia device with a completely different solution. First of all, it's four French smaller than the Valiant Captivia, and now it's 18 French in outer diameter for the smallest sizes available.

The device has been redesigned with a shorter tip and longer length of the shaft to approach more proximal diseases, and the delivery system deploys the graft in one step that is very easy to accomplish and precise.

The fabric has been changed with nowadays the Navion having the multi-filament weave of the Endurant that already demonstrates conformability, flexibility, and long-term durability of the material. It's coming with a wide matrix of options available. In terms of length, up to 225 mm.

Diameters as small as 20 mm, and tapered device to treat particular anatomical needs. But probably the most important innovation is the possibility to have two proximal configuration options: the FreeFlo and the CoveredSeal.

Both tied to the tip of the device with the tip-capture mechanism that ensures proximal deployment of the graft that is very accurate. This graft is being under trial in a global trial

that included 100 patients all over the world. The first 87 patients have been submitted for primary endpoint analysis. 40% of the patients were females. High risk patients showed here by the ASA class III and IV. Most of the patients presented

with a fusiform or saccular aneurysm, and the baseline anatomy is quite typical for these kinds of patients, but most of the patients have the very tortuous indices, both at the level of the access artery tortuosity and the thoracic aorta tortuosity.

Three-fourths of the patients had been treated with a FreeFlo proximal end of the graft, while one-fourth with the CoveredSeal. Complete coverage of the left subclavian occurred in one-fifth of the patients. Almost all had been revascularized.

Procedure was quite short, less than one and half hour, percutaneous access in the majority of cases. There were no access or deployment failures in this series. And coming to the key clinical endpoints, there were two mortality reported out of 87 patients.

One was due to the retrograde type A dissection at day one, and one was not device related almost at the end of the first month. Secondary procedures were again two. One was in the case of retrograde type A dissection, and the second one in a patient

that had an arch rupture due to septicemia. Type 1a endoleak was reported in only one case, and it was felt to be no adverse event associated so was kept under surveillance without any intervention. Major Adverse Events occurred in 28% of the cases. Notably four patients had a stroke

that was mild and not disabling, regressing in two weeks. Only one case of spinal cord ischaemia that resolved by drainage and therapy in 20 days. In summary, we can say that the design enhancement of Valiant Navion improved upon current generation TEVAR.

Acute performance is quite encouraging: no access or deployment failure, low procedural and fluoro times, low rate of endoleaks, Major Adverse Events in the range expected for this procedure.

Nowadays the graft is USA FDA approved as well as in Europe CE mark. And of course we have to wait the five years results.

- 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 very much, Professor Torsello, dear Chairmen, ladies and gentlemen. After the publication of the PERICLES Registry, collecting the published world-wide experience from 13 US and European centers, a nonindustry founded project, we focused on several appealing topics,

which have to do with the chimney technique, and I would like to present you a nice overview of these new findings. Here is a flowchart, you see. After the publication of the PERICLES Registry, five new topics and publications,

and let's start and speak about the gutters. So regarding gutters, this is always a nice topic to be discussed after ch-EVAR, also presented as Achilles' heel of the technique, we classified the phenomenon of gutters based on causative mechanisms,

so we found three, as you see here, patterns, which are responsible for the persistence gutters type 1A endoleak, so two of them have to do with the oversizing, so we have seen cases with excessive oversizing of more than 30% of the aortic stent graft,

leads to this enfolding of the device, and this is a reason for our persistent endoleak as we see here. Another crucial causative mechanism is the undersized aortic endograft, which is often to be seen in case of large neck diameters or multiple chimneys,

so you see that in these cases, we have a gap. We don't have enough fabric material to wrap up the chimney grafts, and we have a persistent type 1 endoleak, and third reason for these phenomenon is a very short sealing zone.

The next key point, or the next appealing topic, was the incidence and factors for several vascular events after ch-EVAR. We published that in JVS. We analyzed this phenomenon, and actually we found a really low incidence of clinical relevant

cerebrovascular events of almost 2%. What we have seen in a very nice analysis is that the bilateral axis from the upper extremity seems to have a significant association with cerebrovascular events, and this is how we perform and administer a double chimney, so we avoid the exposure of the right

and the left upper extremity artery. We prefer the exposure of the axillary artery and double puncture, avoiding the bilateral access from above. Another nice topic is the treatment of type 1A endoleaks after EVAR.

The group from Rome published that in JEVT, and here is an example showing the utility of this technique in type 1A endoleaks. We have mainly migration of the device due to undulated necks as we see here, and for these anatomies the chimney technique performs well

because we use flexible tubes. As here you can see the Endurant device with single chimney for the right renal artery, so we create a new sealing zone, and we treat the challenging pathology like that, or here a ruptured triple A due to type 1A endoleak,

which treated also here again with tube and single chimney for the right renal artery, and we see here no evidence of type 1 endoleak in the follow-up. Another important point was the identification of optimal device combination.

The group from Florida published this topic in JVS in 2018, and we identified that the combination of the Endurant and the Advanta, a combination of a nitinol endoskeleton with a stainless steel, balloon-expandable copper stents, have a significant better performance

regarding mortality and patency as we see here in these very nice overview of the Kaplan-Meier curves. Last but not least, the impact of the technique in gender is also important. We know from the published literature from the group from Professor Timaran that female patients have

a greater risk for more renal function deterioration, reintervention, if they be treated by FEVAR. So we sought to analyze these phenomenon or these option with the chimney technique, and here is an overview between male and female patients. You see that the female patients underwent mostly placement

of flexible self-expanding covered stent, probably due to the tortuosity of the renal arteries, and if we see the outcomes, we didn't observe significant differences between female and male patients regarding the 30-day mortality renal failure late type 1A endoleaks, but also regarding

the chimney graft patency and reintervention, and this is probably to be explained due to the fact that we use devices with a low profile, flexible devices which probably fits better in the anatomy of the female patients as we see here. So in summary, we have seen that the use of chimneys

for juxtarenal pathologies has benefits for female patients showing no statistical differences regarding mortality, renal failures, patency and complications rate. So the new findings about ch-EVAR from the PERICLES Registry cohort were based in the classification of gutter-related endoleaks.

We have seen low incidence of clinical-driven cerebrovascular events, and it looks that the bilateral access as in case of multiple chimneys has a high risk of increased MACE rate, and successful use of this approach in excessive type 1A endoleaks and also female patients with triple A with short necks.

Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

- Dear Chairman, dear ladies and gentlemen, thank you for the chance to present these data here. As opposed to United States, this is not first-line therapy in Germany. And I would like to show you some results with the Omega-3-enriched matrix, which is a little bit special.

It's made from fish skin from Atlantic cod, and it's an acellular matrix, which can be used as a xenogeneic skin graft for hard-to-heal wounds in different locations. Some advantages of using fish skin as opposed to a porcine skin or even human skin

is it's a gentle processing possible, it preserves the lipids, which is very important. I think the Omega-3 is a very important feature of this and it preserves the structure. And there's also very little risk of disease transmission, which is

always a matter of concern in xenogeneic materials. And how does it work? The Omega-3 fatty acid has some anti-inflammatory effect by mediating an inhibitor, a new inhibitor. It's called the NLRP3 inhibition,

which is necessary for IL-1 beta activation of cytokine, which is used for inflammation. And so this fish skin is also reducing general inflammation in the surface. So how is this application done? So you see a hard-of-heal wound,

which has to be a little bit clean and infection-free if possible, but it doesn't heal completely. So the fish skin is applied, and it can be covered with polyurethane foam, or even with NWPT with vacuum therapy.

And it takes several treatments. The advantage is it's weekly dressing changes. That means it's possible to do it on an outpatient basis, and I think this is the way it's done mostly in United States. So these are inpatients with very complicated wounds.

23 patients with 25 vascular wounds in different locations. Two in the thigh, seven in the distal calf, 14 in the foot, and two even in the hand. And the time to heal took nine to 41 weeks, so we have to be a little bit patient and stubborn to really wait for the effect of this fish skin.

And in average, you can see here, in some patients, three are enough, but in some patients 26 treatment cycles were necessary. This is just to show you the spectrum of patients treated in the last four years. Not very many, 15 out of 25 only, was complete healing.

This is from three hospitals in Germany, from Hamburg, Mainz, and our hospital in Karlsruhe. And you see here the rate of complete healing is only almost half of them. Here, this is an example, typical example of what we see. This wound became necrotic and dehiscent, and then

after debridement and some cleaning it looks like this. And then it can be treated with the fish skin. It looks a little bit strange if you do the first dressing change, but this is the way it should look. And after a while, this took 33 weeks, but then this foot healed, and there was

no major amputation necessary in this patient, which is the aim of this therapy, actually. This is a very terrible example of steal syndrome in a dialysis patient with a necrotic hand which had to be amputated in an emergency procedure.

And the question was: could this hand be saved somehow? So this was also treated with Omega-3 matrix, and this is the final result, but this hand is not functional, so it needs some additional plastic surgery. But I think after these wounds are healed,

before that no plastic surgeon would do anything with an extremity like this. These are some more examples of the healing. And you see here the curve, how long it takes to heal for these wounds: up to 12 or 14 weeks. This is kind of the average, three months.

There was a publication before with a few similar, even less cases, 18 cases, from United States, which showed complete healing only in three of 18 patients, which is a little bit disappointing, but the primary goal is to get a stable wound

and to avoid amputation, actually. You get a really significant decrease of wound surface, so our results actually were even more successful than this first publication, that there is no much more data available from literature. This is a very special example here,

from presternal necrotic skin flap, which was also treated with Kerecis Omega3 and with mesh graft in the end. So this was a very special case which also was healing. Here you see the time to heal again. It takes a long time, up to 100 days for the healing.

And you see the Hamburg cases here, the wound reduction to 20%, but with some cases 60-80%, and only half of the occasions really complete healing. So in summary, in the shortness of time, summarize that Omega-3 wound matrix is,

for us at least, a innovative biological decellularized wound dressing from cod skin, which works in complicated wounds, in the lower limbs especially. And before they are applicated, there needs to be an effective debridement,

adequate tissue perfusion, and infection control. And weekly dressing changes are absolutely sufficient, so this means that outpatient treatment is possible. Thank you very much for your attention.

- Thank you very much. Thank you, Frank, for inviting me again. No disclosures. We all know Onyx and the way it comes, in two formulas. We want to talk about presenter results when combining Onyx with chimney grafts. The role of liquid embolization or Onyx is listed here.

It can be used for type I endoleaks, type II endoleaks and more recently for treatment of prophylaxis of gutters. So what are we doing when we do have gutters? Which is not quite unusual. We can perform a watchful waiting policy, pro-active treatment in high flow gutters,

pro-active treatment low flow gutters, or we can try to have a maximum overlap, for instance with ViaBahn grafts 15 centimeters in length or we can use sandwich grafts in order to reduce these gutters in type I endoleaks. Here, a typical example of a type I leak treated with Onyx.

And here we have an example of a ruptured aneurysim treated with a chimney graft. And here is what everybody means when they're talking about gutters. Typical examples, this is what you get. You can try to coil these

or you can try to use liquid embolization. Here's the end result after putting a lot of coils into these spaces. What are these issues of the chimney-technique type I endoleak? Which are not quite infrequent as you see here.

Most of these resolve, but not all of them. So can we risk to wait until they resolve? And my bias opinion is probably not. Here, the incidents of these type endoleaks is still pretty high. And when you go up to the Arch

the results can even be different. And in our own series published here, type I endoleak at the Arch were as high as 28%. A lot of these don't resolve over time simply because it's a very high flow environment. Using a sandwich technique is one solution

which helps in a lot of cases but not all of these simply because you have a longer outlet compared to a straightforward chimney graft. You can't rely on it. So watchful waiting? There are some advocates who

prefer watchful waiting but in high flow gutters this is certainly not indicated. And the more chimneys you have, like in a thoracoabdominal aneurysm with four chimneys, the less you can wait. You have to treat these very actively,

like you see here, in these high flow areas. Here a typical example, again symptomatic aneurysm with sealing. Here Onyx was used but without any success. So what we did is we had to add another chimney and plus polymer sealing and then we had a good result.

Here some results, only small serious primary gutter sealing using Onyx with good results in a type I leak. But again, this is only a small series of patients. Sandwich technique already mentioned. When you use, like we did here for chimney grafts in the arteries, you do need Onyx otherwise you

always get problems with these gutters and they do not seal over time. Another example where liquid polymer was used. And here again, you see the polymer. The catheter in order to inject the polymer is very difficult to see but with a little bit of experience

you know where you are. And again, here it is, the Onyx, a typical example. Here another example of the Arch, bird beacon effect, extension, chimney graft. Again the aneurysm gets bigger. And so a combination of using proximal extensions

plus chimneys plus liquid embolization solves this problem after quite a long period of time. And here typically is what you see when you inject the Onyx. This does not work in all cases. Here we used Onyx in order to seal up the origin of the end tunnel.

This works very nicely but there is so ample space for improvement and in some cases it's probably better to use a fenestrated branch graft or even the opt two stabler instead of using liquid embolization. Thank you very much.

- This is from some work in collaboration with my good friend, Mike Dake. And, a couple of years of experience at Stanford now. First described by Kazy? years ago. This technical note of using multiple main-body endographs in a sandwich formation.

Up at the top but, then yielding multiple branches to get out to the visceral vessels and leaving one branch for a bifurcated graft. We've sort of modified it a little bit and generally either use multiple

grafts in order to create a branch the celiac and SMA. Left the celiac sometimes for a chimney, but the strategy really has been in one of the limbs to share both renals and the limb that goes down to the legs. We noticed early on that this really was not for

non-operative candidates, only for urgent cases and we recognize that the visceral branches were the most important to be in their own limb. I'll just walk you through a case. 6.8 centimeter stent for foraco above

the prior opened repair. The plan drawn out here with multiple main bodies and a second main body inside in order to create the multiple branches. The first piece goes in. It's balloon molded at the level of pulmonary

vein with enough length so that the ipsalateral limb is right next to the celiac. And we then, from above get into that limb and down into the celiac vessel and extend with either a limb or a viabahn. Next, we deploy a second main body inside

of the gate, thus creating now another two limbs to work through. And then through that, extend in its own branch a limb to the SMA. This was an eight by 79 vbx. Then we've got a third limb to go through.

We put a cuff that measures about 14. This is the math so that the double renal snorkle plus the main body fills up this hole. Now, double sheath access from above, looking for both renals. Sheaths out into both renals with viabahns

inside of that. Deployment of the bottom device and then a final angiogram with a little bit of a gutter that we often see when we have any kind of parallel graft configuration. Here's the post-op CT scan wherein

that limb is the two shared renals with the leg. This is the one year post-op with no endo leaks, successful exclusion of this. Here's another example of one of an eight and a half centimeter stent three thorico similar strategy, already with an occluded

celiac. Makes it a little bit easier. One limb goes down to the superior mesenteric artery and then the other limb then is shared again bilateral renals in the lower main body. Notice in this configuration you can get all the way up to the top then by putting a thoracic component

inside of the bifurcated subabdominal component. There's the final CT scan for that. We've spent some time looking at the different combinations of how these things will fill up to minimize the gutters through some more work. In collaboration with some friends in Kampala.

So we've treated 21 patients over the last couple of years. 73 years of age, 48 percent female usual comorbid factors. Oh, I thought I had more data there to show you. O.K. I thought this was a four minute talk.

Look at that. I'm on time. Octopus endovascular strategy is a feasible off the shelf solution for high risk patients that can't undergo open repair. You know obviously, sort of in this forum and coming to this meeting we see what's

available outside of the U.S. and I certainly am awaiting clinical trial devices that will have purpose specific teacher bi-graphs. The end hospital morbidity has still been high, at four percent. The one year survival of 71 percent in this select

group of 21 patients is acceptable. Paraplegia is still an issue even when we stage them and in this strategy you can stage them by just doing the top part plus the viscerals first and leaving the renals for another day. And branch patency thus far has been

in the short term similar to the purpose specific graft as well as with the parallel graft data. 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)

3

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

on a nice, long day.

- Sam, Louis, thank you very much. I also kind of reduced the title to make it fit in a slide. Those are my disclosures. We've switched to using a hybrid room routinely a couple of years ago and what happened then is that we started using 3D imaging

to guide us during the procedure using a fusion overlay. Obviously this was a huge benefit but the biggest benefit was actually 3D imaging at the end of the procedure so rather than doing an AP fluoro run, we would do a 3D acquisition in a cone beam CT

and have those reconstructions available to check technical success and to fix any issues. We've been using this technique to perform translumbar type 2 endoleak treatment and what we do is we do a cone beam CT non contrast and we fuse the pre-op CT on top of this cone beam CT

and it's actually quite easy to do because you can do it with the spine but also obviously with the endograft so it's a registration on the graft on top of the endograft and then the software is really straightforward. You just need to define a target in the middle

of the endoleak. You need to define where you want to puncture the skin and then the system will automatically generate to you a bull-eye view which is a view where you puncture the back of the patient and the progression view you obviously see the needle

go all the way to your target. And what is interesting is that if you reach the target and if you don't have a backflow so you're not in the endoleak, you have this stereo 3D software which is interesting because you do two lateral fluoro runs

and then you check the position of the needle and then it shows you on the pre-op CT where you are. So here in this specific patient, I didn't advance the needle far enough. I was still in the aortic wall,

that's why I didn't get backflow so I just slightly advanced the needle and I got backflow and I could finish the embolization by injecting contrast, close and then ONYX to completely exclude this type 2 endoleak. So now let's go to our focus today is fenestrated endograft.

You see this patient that were treated with a fenestration and branches. You can see that the selective angio in the left renal looks really good but if on the cone beam CT at the end of the procedure we actually had a kink on the left renal stent

so because I had depicted it right away at the end of the procedure I could fix it right away so this is not a secondary procedure. This is done during the index procedure so I'll go directly to what we did is we reinflated a ballon,

we re-fed the balloon and then had a nice result but what happen if you actually fail to catheterize? This was the case in this patient. You see the left renal stent is completely collapsed. I never managed to get a wire from the aortic lumen and back into the renal artery

so we position the patient in the lateral position, did a cone beam CT and used the same software so the target is now the renal artery just distal to this crushed renal stent and we punctured this patient back in the target and so you can see is right here

and you can see that the puncturing the back. We've reached the renal artery, pushed a wire through the stent now in the artery lumen and snared the wire and over this through and through wire coming out from the back we managed

to reopen this kinked left renal stent. You can see here the result from this procedure and this was published a couple of years, two years ago. Now another example, you can see here the workflow. I'm actually advancing the needle in the back

of the patient, looking at the screen and you can see in this patient that had a longer renal stent I actually punctured the renal stent right away because at the end of the procedure I positioned another covered stent inside

to exclude this puncture site and then, oops sorry, and then, can we go to the, yeah great thank you. And then I advance the wire again through this kinked renal stent into the endograft lumen and this is a snare from the groin

and I got the wire out from the groin. So you see the wire is coming from the back of the patient here, white arrow, to the groin, red arrow and this is the same patient another view and over this through and through wire

we manged to re advance and reopen this stent and we actually kinked the stent by getting the system of branched endograft through a previous fenestrated repair and fortunately my fellow told me at the end of the procedure we should check the FEVAR

with a cone beam CT and this is how we depicted this kink. So take home message, it's a very easy, straightforward workflow. It's a dedicated workflow that we use for type 2 endoleak embolization. We have this intermediate assessment with Stereo 3D

that helps us to check where we are so with 3D imaging after the learning curve it's become routine and we have new workflows like this way of salvaging a kinked renal stent. Thank you very much for your attention.

- 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.

- Thank you, Dr. Moore, and thank you Frank for inviting me back. These are my disclosures. I am a consultant for Silk Road Medical since I ran the first pivotal trial. Now, six years ago I gave a presidential address before the Society for Vascular Surgery

centered on the carotid space and I added this disclaimer, at least in part, because we were due to embark at that point on ROADSTER 1. And further on in that address, I suggested that transfemoral distal filter protection CAS was an experiment that had failed in my view.

And over the years of course in the legacy trials, that seems to be well born out by the data from these trials and yes, over time results with transfemoral CAS improved. Was it related to better technology? Perhaps.

It was certainly highly impacted by better patient selection and one only needs to see, for example, the evolution of the endovascular management committee in cres 2, as to how anatomic features have figured in that clinical decision making. Now, I'm proud to say that vascular surgeons,

first Juan Parodi and then Enrique Criado, pioneered the concept of flow reversal for neuro protection and CAS procedures and CAS procedures and of course, in my view, the TCAR procedure is in fact the ultimate evolution of that.

Now, thank you Frank for framing my debate with my Italian colleagues. Laura Capoccia's conclusion slide perhaps said it all and my worthy opponents and subsequent speakers I'm sure are going to focus on the fact that flow reversal with the MO.MA

can be achieved can be achieved with a totally percutaneous transfemoral approach, but the early data certainly suggested, as you can see here, that things were not much better. No, I'm sure we'll see results from this prospective registry with a lot of well known

Italian interventional cardiologist. Achieving an admirable 30 day major adverse event rate, but in a sense, this is the evolution of patient selection because it represents a cherry picking type of experience compared to low risk patients. Now, the final thing to consider from a technical aspect,

is that flow stagnation with the MO.MA device hardly equals high flow reversal, because although the concepts are similar, of course the actual operations are quite a bit different. And the authors even acknowledge that embolic signals from TCD were often detected during incursion

of this rather bulky transfemoral in to the arch device. And indeed, the steps of the procedures have been studied and as you can see here, there's really no difference between MO.MA and Distal Filter in the critical step of arch manipulation. Obviously a big part of the strategy, of the TCAR procedure

is avoidance of the arch, and when we've studied anatomic exclusions as recently reviewed by, this procedure can be applied to the overwhelming majority of candidates for CAS. Now Dr. Colin Buck showed you that this strategy

has achieved, as assessed by DWI imaging, lesion production rates, equivalent to carotid endarterectomy and when we published ROADSTER 1, it was the lowest stroke risk ever reported for a carotid stent trial.

I've mentioned previously that it has achieved neuro protection equivalent to carotid endarterectomy and here are some of the ROADSTER data. I won't read the data. Vic Kashif showed it to you. Now, in the most recent MO.MA experience of course,

we see the anatomic exclusions. And the anatomic exclusions in the lower right corner are not exclusions for TCAR. You've seen this data previously and our host, Frank Vees, in his most recent meta analysis, indicated that there was no positive

impact of the MO.MA strategy versus Distal Filter protection. This is a graph of the rapid adoption of TCAR by North American vascular surgeons in the TCAR surveillance project. Mul mentioned to you that the beginning data

from these registries and projects have now been presented. Just this week, I saw the updating of the TCAR surveillance project with sustained excellent result, now at over 3,000 patients. So in conclusion.

In my opinion TCAR is the technical evolution of CAS. Avoiding the arch and superior neuro protection with high flow reversal indicated the procedure of choice and transfemoral CAS should go in to the history books. Thank you for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

- Thank you very much, thank you Cees, that was really interesting, it's um, it's a topic close to my heart and I think that there's a great deal of work about pneumatic compression that we can learn from. These are my disclosures. Your stent choice, well,

we talk an awful lot about stents, but it is really only one part of the entire spectrum of factors that get it right. And when you get it right, you have an open vein and we believe that the open vein works, although the open vein hypothesis

seems somewhat compromised, considering where it came from in terms of open arteries. But your stent choice is just one of the factors that goes into it, and your inflow, and your outflow generally we can improve upon. Your muscle pump we'd like to improve

by using pneumatic compression boots, and then obviously getting your anti-coagulation right, as Dr. Weinberg explained, is really really key afterward. So, stent choice is one of the aspects, but it's certainly not the only aspect. You're familiar, and probably sick of these diagrams

showing the differences between radial force, crush resistance, and the trade-offs between stent flex, strengths, rather, and when I use strength it's a fairly generic term, and flexibility. And obviously in Europe, we have access to a wide variety of stents.

The Cook Zilver Vena first came out in 2010. Bard Venovo was, I think, 2016. The ABRE was just last December, but it's commercially available. The Optimed Sinus-Venous has been around for quite some time, I'm going to say 2011 if I'm correct.

And the Sinus Obliquus, then it was a little bit later, maybe 2014, 2015, and for those of you who haven't seen this before, this has got a, a closed-cell design at the top which is quite rigid, if I may, and then a very flexible sinus,

or rather open-cell design at the inferior portion, the top portion is angled to address the IVC confluence. And then the Veniti Vici, which is, (coughs) excuse me, was extensively studied in the VIRTUS trial, and this is a more closed-cell, but there's still a considerable flexibility.

So, like everything else in life, you know, you can go for the old broad who's got loads of money, or you can go for the young hot chick, and you know, she's broke. And you know, life is like that, and stents are like that too.

You know, what you get in one you lose in the other. And like a lot of the other things, you have to get everything right to make the stent work. That analogy certainly does not apply to women. But the closed-cells generally have higher force but they're slightly more rigid.

The open-cells are, perhaps, slightly weaker, but there's infinite varieties of imaginations and changes that can be made to those two very generic statements. For instance, in the newer stents, if you cut off a larger, laser cut a Nitinol tube,

you will intrinsically get thicker struts, and therefore slightly larger sheath size, but ultimately slightly more strength at the expense of slightly less flexibility. I think for me, the thing that I've learned the most about the newest venous stents,

or using the newer venous dedicated stents, is that you must do very aggressive balloon dilatation pre and post, that's absolutely essential. Regardless of what stent you use. And I'm horrified to see some of the Twitter handles of people using pre-dilatation

with an eight millimeter balloon, then putting in a 20 millimeter Wallstent and then ballooning it again to 14. Absolutely no logic to any of that. So I think you should balloon to the nominal diameter of the stent.

And it is interesting that you get a much higher force when you get that stent to the nominal diameter. The actual physical properties of the stent change when it hits that diameter. So not getting to the diameter of the stent is a huge mistake.

Now, do fractures really matter? We've been looking extensively at this in a variety of the different trials, and it's hard to know. Certainly, luminal reduction does. Fractures, not so sure about. Fractures sound like they're easy to diagnose.

They're actually very difficult. And compression at the inguinal ligament, is it real? It seems to be real. It seems to be more real than I certainly believed, in a certain proportion of patients. Typically skinnier ones, in my experience,

again, skinny females. Flexibility is obviously a big, big issue, and when you think of where your knee goes in relation to your shoulder if you're doing your yoga class, or anything else for that matter, tying your shoelaces,

there's a lot of bend required. And if you think of where we are now in aortic stent grafting compared to where we were when I last had hair, everything has changed. All of the devices have changed.

We went from Ancure, which had 64 steps, through AneuRx, and now, you know, things have moved on way past 2010 as well. So, in terms of my choices, in the USA you've got two choices, you got Wallstent and Z stent.

And if you got a rupture, use a Gore or something like that. In Europe, it's a much more, nuanced and challenging to try and figure out which ones you do. And these are just my choices. Is there any evidence to back them up?

None whatsoever. Have I had problems with most of the stents? Yes. Most of those problems were probably self-induced. I've certainly learned that pre-dilatation and post-dilatation are the essentials.

And flexibility is a lot more important than I would've thought if you had asked me five years ago. 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.

- 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.

- Thanks (mumbles) I have no disclosures. So when were talking about treating thoracoabdominal aortic aneurysms in patients with chronic aortic dissections, these are some of the most difficult patients to treat. I thought it would be interesting

to just show you a case that we did. This is a patient, you can see the CT scrolling through, Type B dissection starts pretty much at the left subclavian, aneurysmal. It's extensive dissection that involves the thoracic aorta, abdominal aorta,

basically goes down to the iliac arteries. You can see the celiac, SMA, renals at least partially coming off the true and continues all the way down. It's just an M2S reconstruction. You can see again the extent of this disease and what makes this so difficult in that it extends

from the entire aorta, up proximally and distally. So what we do for this patient, we did a left carotid subclavian bypass, a left external to internal iliac artery bypass. We use a bunch of thoracic stent grafts and extended that distally.

You can see we tapered down more distally. We used an EVAR device to come from below. And then a bunch of parallel grafts to perfuse our renals and SMA. I think a couple take-home messages from this is that clearly you want to preserve the branches

up in the arch. The internal iliac arteries are, I think, very critical for perfusing the spinal cord, especially when you are going to cover this much. And when you are dealing with these dissections, you have to realize that the true lumens

can become quite small and sometimes you have to accommodate for that by using smaller thoracic endografts. So this is just what it looks like in completion. You can see how much metal we have in here. It's a full metal jacket of the aorta, oops.

We, uh, it's not advancing. Oops, is it 'cause I'm pressing in it or? All right, here we go. And then two years post-op, two years post-op, you can see what this looks like. The false lumen is completely thrombosed and excluded.

You can see the parallel grafts are all open. The aneurysm sac is regressing and this patient was successfully treated. So what are some of the tips and tricks of doing these types of procedures. Well we like to come in from the axillary artery.

We don't perform any conduits. We just stick the axillary artery separately in an offset manner and place purse-string sutures. You have to be weary of manipulating around the aortic arch, especially if its a more difficult arch, as well as any thoracic aortic tortuosity.

Cannulating of vessels, SMA is usually pretty easy, as you heard earlier. The renals and celiac can be more difficult, depending upon the angles, how they come off, and the projection. You want to make sure you maintain a stiff wire,

when you do get into these vessels. Using a Coda balloon can be helpful, as sometimes when you're coming from above, the wires and catheters will want to reflux into that infrarenal aorta. And the Coda balloon can help bounce that up.

What we do in situations where the Coda doesn't work is we will come in from below and a place a small balloon in the distal renal artery to pin the catheters, wires and then be able to get the stents in subsequently. In terms of the celiac artery,

if you're going to stent it, you want to make sure, your wire is in the common hepatic artery, so you don't exclude that by accident. I find that it is just simpler to cover, if the collaterals are intact. If there is a patent GDA on CT scan,

we will almost always cover it. You can see here that robust collateral pathway through the GDA. One thing to be aware of is that you are going to, if you're not going to revascularize the celiac artery you may need to embolize it.

If its, if the endograft is not going to oppose the origin of the celiac artery in the aorta because its aneurysmal in that segment. In terms of the snorkel extent, you want to make sure, you get enough distal purchase. This is a patient intra-procedurally.

We didn't get far enough and it pulled out and you can see we're perfusing the sac. It's critical that the snorkel or parallel grafts extend above the most proximal extent of your aortic endograft or going to go down. And so we take a lot of care looking at high resolution

pictures to make sure that our snorkel and parallel grafts are above the aortic endograft. This is just a patient just about a year or two out. You can see that the SMA stent is pulling out into the sac. She developed a endoleak from the SMA,

so we had to come in and re-extend it more distally. Just some other things I mentioned a little earlier, you want to consider true lumen space preserve the internals, and then need to sandwich technique to shorten the parallel grafts. Looking at a little bit of literature,

you can see this is the PERCLES Registry. There is a number of type four thoracos that are performed here with good results. This is a paper looking at parallel grafting and 31 thoracoabdominal repairs. And you can see freedom from endoleaks,

chimney graft patency, as well as survival is excellent. This was one looking purely at thoracoabdominal aneurysm repairs. There are 32 altogether and the success rates and results were good as well. And this was one looking at ruptures,

where they found that there was a mean 20% sac shrinkage rate and all endografts remained patent. So conclusion I think that these are quite difficult to do, but with good techniques, they can be done successfully. Thank you.

- Doctor Dangas, congrats on really putting this all together and being the champion for this technique. 13 Centers, 517 patients in the original report. We've talked about this, the follow up and some of the limitations at 17 months, primary patency 94%, Gutter Endoleak 2.9%.

What about late outcomes? That's what everybody keeps wanting to know. We've put this series together so that hopefully by next year we'll be in the, some printed literature. Two and half years follow up,

a subset analysis of patients that have had that follow up. 244 patients, 387 snorkel/chimney grafts, nearly four years mean follow up in this cohort. Mean diameter, 64 milimeters. The neck diameter, 26. And the infrarenal neck length of 4.6.

Obviously then after the chimney strategy that increases as most of them generally have gone then above the, both renal arteries. 38% right renal. 46% left renal. A couple of accessory renals. A small number of SMA and Celiac snorkels in this group.

More than half of the Endurant Graft and the rest are of mix of Zenith, Excluder, Jotec, Talent that's no longer being used. And a couple of thoracic proximal pieces. About half Viabahn. 38% iCAST or Advant of E12. And a handful of Bare Metal very early in the series.

Half with one graft, more than a third with two, 10 percent with three and a small number with four. Pre-op Mean Sac Diameter from the entire 244 sub-cohort, 64 millimeters. The latest follow up with now four years Mean follow up 55, Mean Sac Regression per patient

in the 244 eight millimeters. This is an example of one of ours. Loss of Branch Patency. Look at the Kaplan-Meier number at risk even out to four years, 136 of the 368, not the typical Kaplan-Meier where out to four years

there's like five patients left, or five renals left. Out of 48 months, 92.5% patency. Univariate analysis, no predictors including the use of different types of chimney balloon-expandable versus self-expanding, total number of chimney grafts

did not seem to have an affect. Obviously, the problem with this technology or with this strategy has still been persistent or Late Type-1a Endoleaks and Gutter Endoleaks. We found in a couple of different series individual case series many of these do resolve

by the six or 12 month follow up. In this longer term cohort, now up from 3.7 is at 48 months Mean Follow Up time at 5.9% Gutter Endoleak, needing re-interventions in half of them. What are the risk factors for developing a persistent Gutter Endoleak?

A native neck diameter of greater than 30 and the absence of Infrarenal on univariate, and on multi-variate, only the native neck diameter greater than 30. Again, suggesting this theme that I think has been throughout the meeting of larger,

of needing more proximal fixation for things. Obviously, a lot of work going into trying to prevent or find optimal strategies for Gutter Type-1a Endoleaks. Mortality for the entire cohort now with the extended follow up at four years, 71%.

Costache already went over the optimal combinations of devices, which I think this contributed to the approval CE mark, at least of the enduring graft with a balloon-expandable chimney for that. Interestingly and what, you know, I think many of us have been proposing,

one to two is obviously better than three or four, and I don't think that aligning it is necessary. So in summary, compared to meta-analysis of real world data for fenestrated, which I understand in the room there are obviously single center experts

that have better numbers than what's out there listed in the literature in terms of number of grafts, mortality Type-1a Endoleak, branch patency and need for 2nd intervention similar between these strategies. Thanks for your time.

- 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.

- Thank you, I have no disclosure for this presentation. Aorotopathy is a different beast as oppose to patients with dissections that we normally see in the elderly population, but we have the same options open surgery, endovascular, and hybrid. If they all meet the indications for surgery so why not open surgery?

We know in high volumes centers the periprocedural mortality acceptable in especially high volume centers. The problem is the experience surgeons are getting less and less as we move into more and more prevalence of endovascular. And this is certainly more acceptable in lower or

moderate high risk patients. So why not be tempted by endovascular in these patients? (to stage hand) Is there a pointer up here? So the problem with aorotopathy is the proximal and distal seal zones and we've already heard some talks today about possible retrograde dissection,

we've also heard about nuendo tear distally and aorotopathy is certainly because of the fragile aorta lend itself to these kinds of problems. But it is tempting because these patients often do very well in the very short term. The other problem with aorotopathy is they often have

dissection with have problems for branch unfenestrated technology and then of course if these dissection septum are near the proximal and distal seal zones, you're going to have a lot of difficulty trying to break that septum with a ballon and possibly causing new

entry tears proximally or distally. Doctor Bavaria and his colleagues from Italy were one of the first ones to do a systematic review and these are not a large number of patients but they combined these articles and they have 54 patients. Again, the very acceptable low operative risk, 1.9%.

But they were one of the first ones to conclude and cation that TEVAR in these patients, especially Marfan's patients in this series carries a substantial risk of early and late complications. They actually cautioned the routine use of endovascular stent grafts.

One of the largest series, again stress, these are not large numbers but one of the largest series was just 16 patients and look at this alarming rate of primary failure. 56% treated successfully, 40% required conversion to open operation and interestingly enough

43% of those patients had mortality. My friend and colleague at the podium, doctor Azizzadeh was given the unbeatable task of arguing for endovascular therapy in Marfan syndrome and the best he can come up with was that midterm follow up demonstrates sizeable numbers of complications but,

he identify area where probably it was acceptable in patients with rupture, reintervention for patch aneurysms and elective interventions in which landing zone was in a synthetic graft. So why not hybrid? Well this seems to be the more acceptable version

of using TEVAR, if you can, in these aorotopathy patients. But this is not a great option because in this particular graft that you see this animation, we're landing in native aortic tissues. So really, what you have to do is you have to combine this and try to figure out a way to create a landing zone,

either proximally or distally and this is a patient and not with Marfan's this time but with Loeys-Dietz, who we had presented recently, previous ascending repair but then presented with horticultural abdominal aneurysm as a result of aneurysm habilitation of a previous dissection and here

you see a large thoracal abdominal aneurysm on the axial and coronal and as many of these patients with aorotopathy express other problems with their multisystem diseases and you can see the patients left lung is definitely not normal there, left lung is replaced with bullae and this is a patient who would not do well

with an open thoracal abdominal repair. So what do you do? You have to create landing zones and in this particular patient, he had a proximal landing zone so we were able to just use a snorkel graft from the mnemonic but distally we had to do biiliac debranching grafts to to all his vistaril arteries

and then land his stent-graft in the created distal zone and as you can see, we had an endoleak approximately and thank goodness that was just from a type II endoleak from the subclavian artery which we were able to take care of with embolization and plugs.

And there is his completion C.T. So not all aorotopathy is the same, this is a patient who presented with a bicuspid aortic valve and a coarctation and I would submit to you, this is not a normal aorta. This is probably a variant of some sort of aorotopathy,

we just don't have a name for it necessarily, and do these patients do well or do worst with endovascular stent-graft, I just don't think we have the data. This particular patient did fine with a thoracic stent-graft but this highlights the importance of following these patients and being honest with the patients family and the

patient that they really do have to concentrate on coming back and having closer follow up in most patients. So in summary, I think endovascular is acceptable in aorotopathy if you're trying to save a life, especially in an acute rupture or in an emergency situation, but I think often we prefer to land these

endovascular stent-graft in synthetic. Thank you very much.

- [Lu Qingsheng] I have no disclosures. We know for indication of EVAR we need favorable proximal neck anatomy but if it not unfavorable maybe we are some Type 1a endoleak it's a serious complication for EVAR. So for prevent and treat Type 1a endoleak

especial for some juxtarenal aneurysm maybe we use the chimney fenestration branch and some sac bag. Could we find a simple safe cheap and effective method? So we find from open surgery we were introduced this fibrin glue

means its complex of thrombin and fibrinogen, it's used hemostasis in open surgery so we put that into inject that into the sac, we call it fibrin glue sac embolization. I will show you some cases.

For this case is very short neck and not quality of deck and after deploy the stent graft, of course very serious Type 1a endoleak. But fortunately, we put a catheter before we deploy the stent graft so this catheter is into the sac of the aneurysm

then we use up a long controlled blood flow and we inject from the catheter into the sac of the aneurysm and we inject the fibrin glue. And you can find the contrast not moved after we withdraw balloon. Then we do the angiogram.

We find no any endoleak. Another case showed is angulated neck as this patient. Of course after we deployed stent graft have a lot of endoleak. And we do again this technique. And control the balloon, control the blood flow,

then inject the fibrin glue, and we check all that and withdrew the balloon, there are no any movement about the sac. And we do the angiogram and no any endoleak. Till now, we did, we begin this technique 2002, so we follow long time that we can show it's safe.

So till now we treat 156 cases and proximal less then short proximal neck is 75 cases even some of less than 10 millimeters. And angulation more than 60 degree even some cases more than 75 degree.

Most of them more than 98% of patients' endoleak was resolved. And during our follow up, the mean time more than 100 months, only three patients died of aneurysm related sac enlargement.

The mean maxim aneurysm diameter decreased and no recurrent Type 1 endoleak so we have confidence that it's safe and no any sealant-related complication for example renal failure and aplasia other things. So we discuss the mechanism

it's not only embolization for endoleak but also coagulating all sac of aneurysm like this in shows how it worked. And we also measure the pressure in the sac. Intrasac pressure decreased significantly in treated cases. And how about that technique we need occlusion

proximal blood flow and protect branch ateliers and prevent distal embolization. And we also treated into the rupture aneurysm and it can treat any type of endoleak as these cases it's a rupture aneurysm we do the EVAR emergency.

And after we deploy this devices, we find this endoleak. We don't make sure which kind of endoleak but anyway we just do that, control the blood flow use the balloon then inject the fibrin glue in that.

And all the sac of aneurysm. Then we do the angiogram and endoleak disappeared. We'll be treat any type endoleak of the rupture EVAR we prevent rupture post-EVAR and we decreased abdominal compartment syndrome. So the conclusion is

fibrin glue sac embolization is a simple and effective treatment method. And this method could expand the current indication of EVAR. For selective the length maybe can to the 5 millimeters, angle maybe can to the 90 degree,

and for emergency we seen it should be into the older EVARs for rupture aneurysms. Thank you very much.

- So thank you to the organizers and to Dr. Veith, and thank you to Dr. Ouriel for giving me the introduction of the expense of an unsuitable procedure for pain patients. We have no disclosures.

I think when you look at MRV or Venous interventions, you can look at it as providing you a primary diagnosis, confirming a diagnosis if there's confusion. Procedural planning, you can use it as a procedural adjunct,

or you can use it as a primary procedural modality. In general, flow-dependent MRI has a low sensitivity and a slow acquisition time, making it practically impractical. Flow-independent MRI has become more popular, with sensitivity and specificities

rounding at 95 to 100%. There's a great deal of data on contrast-enhanced MRI, avoiding adanalenum using the iron compounds, and you'll hear later from Dr. Black about Direct Thrombus Imaging. There has been significant work on Thrombus Imaging,

but I will leave it up to him to talk about it. MR you can diagnose a DVT, either in both modalities, and you can see here with the arrows. It will also provide you data on the least inaccessible areas for duplex and other modalities,

such as the iliac veins and the IVC, as can be seen here. It is also perhaps easier to use than CTV, because at least in my institution CTV always comes out as a CTA, and I can't help that no matter what happens.

MR can also show you collaterals, which may be very important as you are trying to diagnose a patient. And in essence it may show you the smaller vein that you're more interested in, particularly in pelvic congestion syndrome,

such as this patient with an occluded internal iliac vein. It can also demonstrate, for those of you who deal with dialysis access, or it's central line problems, central venous stenosis and Thrombus. But equally importantly

it may show you that a stenosis is not intrinsic to the wall, but it's actually intrinsic to extravascular inflammation, as in this patient with mediastinal fibrosis, and which will give you a different way of what you wish to do and treat.

The European guidelines have addressed MR in it's future with chronic venous disease and they give it a 1C rating, and they recommend that if doesn't work you should proceed to Ibes. It can be used for the diagnoses of pulmonary embolism,

it can eliminate the use of ECHO, one can diagnose both the presence of the Thrombus, the dilatation of the ventricul, and if one is using Dynamic MR Imaging one can also see mcconnell sign or the equivalent on the septum between the two ventricles.

More interestingly it can also be used now in the chronic thrombuc, pulmonary hypertension, where it can show both the legions that are treatable and untreatable, as some of you may have heard from Dr. Roosevelt

earlier in the day, where they're now treating the outlying lesions with balloon angioplasty serial sessions. It can also look at the ventricul and give you some idea of where the ventricul stands with regard to it's performance,

we're looking at and linking this to the lungs. It can also show you the unusual, such as atresia of the IVC or it can help with you the diagnosis of Pelvic Congestion Syndrome. And it is extremely valuable

in dealing with AVM's, although it may take one, two, or three sessions with differing contrast bulosus to identify both the arterial, the intrinsic lesion, and the outflow lesions,

but a very valuable adjunct. In renal carcinoma it has two values, one is that it can may diagnosis venous invasion, and it may also let you understand whether or not you are dealing with bland thrombus or tumor thrombus,

which can change the staging for the patient and also change the actual intervention that you may perform. If you use flash imaging one will get at least an 89% sensitivity of the nature of thrombus,

whether it's bland or tumor thrombus, which may change what you need to do during the procedure. It could also tell you whether there's actual true wall invasion, which will require excision of the IVC

as opposed to the simple thromboendarterectomy. And this can run up to a specificity of 88% to exclude it. In the brain it's commonly used to diagnose the intra tumor vasculature. Diagnosing between veins and arterial systems, which can be helpful

particularly if one is considering percutaneous or other interventions. With regard to central venous stenosis there is some data and most people are now using an onlay technique where they take the MRI,

they develop the lines for the vessels and then use that as guide in one or two dimensions with fusion imaging to achieve access with a wire, catheter and balloon, as opposed to a blind stick technique.

There is data to show that you can image with the correct catheter balloons within the vessels and do serial MR's to show that it works. And finally with guidance catheters EP is now able to guide the catheter further and further in to achieve from the,

either the jugular or the venous access across the septum and to burn the entrium as appropriate. And finally, one can use MR to actually gain access, burn, and then actually use the MR to look at the specific tissue,

to show that you've achieved a burn at the appropriate area within the cardiac system and thus prove that your modality has achieved it. So in summary, we can use it for primary diagnosis, confirmatory diagnosis,

procedural planning, and procedural adjunct, but we're only still learning how to use it as a primary procedural modality. Thank you so 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.

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