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Rifampin Soaked Endografts For Treating Prosthetic Graft Infections: When Can They Work And What Associated Techniques Are Important
Rifampin Soaked Endografts For Treating Prosthetic Graft Infections: When Can They Work And What Associated Techniques Are Important
2 arch homograftsOpen Ilio-Celiac bypassSacular TAA ; Endograft AbscessTAAA repair with left heart bypassTEVARtherapeutic
Octopus Technique To Treat Urgent Or Ruptured TAAAs With OTS Components: What Is It, Technical Tips And Results
Octopus Technique To Treat Urgent Or Ruptured TAAAs With OTS Components: What Is It, Technical Tips And Results
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Terumo Aortic Relay Thoracic Endograft For TEVAR In Complex Aortic Pathology With Angles >90°: Advantages And Results
Terumo Aortic Relay Thoracic Endograft For TEVAR In Complex Aortic Pathology With Angles >90°: Advantages And Results
Gore Tag (Gore Medical) / Valiant (Medtronic) / Zenith Alpha (Cook Medical)RelayPlusstent graft systemTerumo Aortictherapeutic
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
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- I don't have any relevant conflicts. Thank you, Frank, for inviting me again. So there are big problems with cognitive testing. And it is simply not valid to assume that testing cognitive function before and after a procedure without strict controls is going to provide

any useful information whatsoever. The Mini-Mental State and the MOCA are easy to administer, but they're not comprehensive and they're not sensitive at all. There are improvements in scores with retest. So just testing before and after a procedure is invalid.

There are improvements in cognitive function with placebo and there's a very powerful effect, placebo effect of surgery. So you can't just go and test cognitive function before and after procedure and say yeah, it got better, it's a good thing to do.

There are practice effects and the practice effects are bigger in patients with milder cognitive impairment. Placebo scores in this case, it was study of polyunsaturated fatty acids, the placebo was actually better

than the active therapy in this study. There are important placebo effects in cognitive testing. And there's a huge placebo effect of surgery, so you may remember the Vineburg procedure. That's ancient history. A more recent sham-controlled trial

of percutaneous coronary intervention for angina showed very clearly that intervention was no better than placebo. So this was the paper that was in Lancet 2018. You look at all these different ways of assessing outcomes.

So there was exercise time, time to one minute ST depression, peak oxygen uptake which looks like, you know it's a pretty objective test, no better. Cognitive testing is too simply usually.

It is subject to learning effects and placebo effects. Surgery has powerful placebo effects. So the only valid way to determine if revascularization improves cognitive function is to do a sham trial, sham surgery or sham stenting.

And belief, no matter how strongly held, does not qualify as evidence. Thank you.

- 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.

- Thank you, and thanks to Dr. Veith for the opportunity to share some of our data. These are my disclosures, some devices presented here are investigational and I want to acknowledge my friend Gustavo, who actually shared some of the slides that we'll show. And I want to reference some of his papers. So a spinal cord ischemia has been presented here

as a devastating complication, after both open and endovascular repair of thoracoabdominal aortic aneurysms. The spinal drains are routinely used to ameliorate the frequency and also the severity of spinal cord ischemia, the problem with this trains is that they may result inherent morbidity and mortality.

Now, intraoperative neuromonitoring has been used to not only monitor, but also to manage potential cases of spinal cord ischemia, this is a study by the group at the Mayo Clinic, led by Gustavo. 49 patients, of which 90% had thoracoabdominal aortic aneurysms, all these patients have spinal drain splice,

spinal cord ischemia was seen in six patients. But interestingly, 63% of the patients had significant decrease in the amplitude of both motor and somatosensory evoked potentials. And interestingly all of these changes came back to baseline except in one patient once

their lower legs were reperfused. However, and despite all of these papers that have, you know, talk about the use of spinal drains for endovascular reparative thoracoabdominal aortic aneurysms against the effectiveness of the spinal drains has not been shown.

And the aim of our study was to assess the outcomes of spinal cord protection without the routine use of spinal drains. We actually has some complications in this report, we decided that we were going to use only selectively in our series, the device is used for this in patients

were all part of a physician-sponsored investigational device exemption, demonstrating branch devices were used including the drainage device. We use a similar protocol as the one described by the Mayo Clinic group, which rely on permissive hypertension maintaining the maps above 90 or 100,

and the systolic pressures above 140. However, as mentioned, we did not place spinal drains routinely, the spinal drains were only considered in those patients that had persistent motor evoked potential deficits, at the end of the procedure. Once the legs have been reperfused, we did not use

conduits, we did percutaneous access in all patients. But of note, we did use endo conduits in all patients that have significant iliocclusive disease, not only to be able to deliver the device, but also to maintain flow to the lower extremities, to avoid distal ischemia. So 34 patients were enrolled in this study,

all patients had intraoperative neuromonitoring, and select spinal drains were placed. 10 patients, 29%, were extent 4 thoracoabdominal repairs, and 24 were extent type one to three. Important all patients with type one and three thoracoabdominal aneurysms underwent a staged repair.

We use in 20% of the cases off-the-shelf device is specifically the debranch, and 80% underwent custom made devices, all these devices were pre-loaded with wires. So, of these patients, 73 were male, 9% Type I, 38% Type II, 24% were Type III,

and 29% were Type IV. We saw significant changes in the evoked potentials in 80% of the patients. In all of them those changes came back to baseline except in one patient, who actually had a spinal drain at the end of the procedure.

30-day mortality in two patients, spinal drain was required eventually in only four patients, that's 12%. One because of sustained changes in the motor evoked potentials, spinal cord ischemia occurred in four patients, in all cases secondary to hypertension. After a procedure, in these cases two were permanent,

the cases had spinal drain splice, however, the deficit persisted, two had transient paraplegia, one resolved with permissive hypertension, and one resolved with a spinal drainage, I mean, the spinal drain was only effective in half of those patients. We did have two cases of intracranial bleeding,

associated with hypertension. So in conclusions, we don't believe that the spinal drains are necessary in all patients. A standard protocol that relies on perioperative maintenance of adequate blood pressure in intraoperative neuralmonitoring is however required.

And we believe that tight blood pressure control is mandatory to avoid possible complications related to uncontrolled hypertension, thank you.

- Thank you, Mr. Chairman. Good morning ladies and gentleman. I have nothing to disclose. Reportedly, up to 50 percent of TEVARs need a left subclavian artery coverage. It raises a question should revascularization cover the subclavian artery or not?

It will remain the question throughout the brachiograph available to all of us. SVS guidelines recommend routine revascularization in patients who need elective TEVAR with the left subclavian artery coverage. However, this recommendation

was published almost ten years ago based on the data probably even published earlier. So, we did nationwide in patient database analysis, including 7,773 TEVARs and 17% of them had a left subclavian artery revascularization.

As you can see from this slide, the SVS guideline did affect decision making since it was published in 2009, the left subclavian artery revascularization numbers have been significantly increased, however, it's still less than 20%.

As we mentioned, 50% of patient need coverage, but only less than 20% of patient had a revascularization. In the patient group with left subclavian artery revascularization, then we can see the perioperative mortality and morbidities are higher in the patient

who do not need a revascularization. We subgroup of these patient into Pre- and Post-TEVAR revascularization, as you can see. In a Post-TEVAR left subclavian revascularization group, perioperative mortality and major complications are higher than the patient who had a revascularization before TEVAR.

In terms of open versus endovascular revascularization, endovascular group has fewer mortality rate and major complications. It's safer, but open bypass is more effective, and durable in restoring original profusion. In summary, TEVAR with required left subclavian artery

revascularization is associated with higher rates of perioperative mortality and morbidities. Routine revascularization may not be necessary, however, the risks of left subclavian artery coverage must be carefully evaluated before surgery.

Those risk factors are CABG using LIMA. Left arm AV fistula, AV graft for hemodialysis. Dominant left vertebral artery. Occluded right vertebral artery. Significant bilateral carotid stenosis.

Greater than 20% of thoracic aorta is going to be or has been covered. And a history of open or endovascular aneurysm repair. And internal iliac artery occlusion or it's going to be embolized during the procedure. If a patient with those risk factors,

and then we recommend to have a left subclavian artery revascularization, and it should be performed before TEVAR with lower complications. Thank you very much.

- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.

Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates

an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.

You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't

or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.

CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,

we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.

She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.

So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.

Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.

It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign

and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there

but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?

Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy

and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.

So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,

a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,

gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection

it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible

before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains

in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low

or cut out the super renal fixations so you can take them out a little easier. Thank you.

- Well thank you and um, it's kind of a how to do it, how to tie your shoes type talk. And clearly now that these venous assessment tools have been present for more than two decades. It has created a common landscape for communication, for comparing outcomes.

And with that common language we really have a good guide of what to use. So. From a favorable standpoint you know the CEAP. And this is the revision from 2004. Really established good classification

across the clinical, etiologic, anatomic, pathophysiologic categories. And certainly with the clinical side of things, that really has taken off. Where the EAP has been more on the research side. But with this common language has come the ability

to communicate like versus like. And clearly if you look at the clinical classifications system. There's a clear line drawn really from C4 and greater, and some would include C3. Versus the C 1&2 in terms of disease severity.

And I think we're all familiar with classifications. But these are very categorical type classifications. And you know if you look at population based studies, certainly the c1 2 category counts for most. Where C3 is about 15% of population, and C4 grade are anywhere from 3-5% of the population.

You know the upsides of CEAP it's really proven to be effective in assisting in evaluation of various treatment modalities. Allows comparison of results from different institutions using universal language. It's really enhanced our understanding with these categories

of potential etiologic factors. And by doing so it's improved the scientific standards in the evidence. And allows for meaningful research and comparison of cohorts. Bu there's certainly some limitations to CEAP.

There's a degree of complexity that makes utilization difficult across all spectrums of clinical care. It's limited as a severity classification system, in that it's relatively static. And then even with improvement there's sometimes a little change that happens within the categories.

There's lack of reversibility. There's some problems with differentiation especially when you look at the clinical categories. Varicose veins, edema, and such. Clinical use of C category has been widely adapted. Where there's more limited use of EAP.

And really has raised the need and question to freshen up CEAP with reclassification. So over the last year or so, there's an American VF formed task force. Which has been tasked with revising CEAP. And I apologize I can't present the information just yet.

Because it's still under modification and maybe next year we'll have the revised CEAP classification to promote. With that in mind the Venous Clinical Severity Scoring came in behind CEAP. As a more sensitive scale to determine changes in treatment,

and it's really meant as a compliment to CEAP. And it has both clinical utility and research applications most recently revised in 2010. And again most of us are familiar with VCSS. In that it's several attributes that are rated across the spectrum of severity from 0-3.

From the standpoint of the revised system. It has been studied and it has been shown to have good inter and intra user reproducibility. Which is important in that it makes it consistent across users. And if you look at Michael Vasquez's publication here.

It shows a good practical use of both CEAP and VCSS. And that in this particular patient with some hemosiderin, a pigment change, a C4 category. When you plug in the VCSS it's a 15. And then after treatment there's still a C4,

but there VCSS fell to 11. And similarly the same patient here who starts with a CEAP of six and VCSS of 27. And then across the spectrum of treatment, still is a V6 about mid-treatment, but has improved to VCSS of 19.

And then after completion of treatment the best they can get is going from a C6 to a C5. But they're VCSS is now 5. And most of the benefit comes with pain, varicosity, and edema.

That's where you see most of the change in VCSS. And certainly the guidelines support the use of CEAP. This is varicose vein guidelines where the basic of more for clinical practice than the full CEAP for research. And same thing with the venous ulcer guidelines.

And I'll just leave you with this app which you can pull up on your phone. SVS iPG. Which actually has CEAP and VCSS embedded so you can have it at the bedside. Or you can embed it in your clinical templates.

So in conclusion yes they're helpful. There is no one universal tool but certainly both CEAP and VCSS used together, do achieve the needs of what they're intended to do. There's certainly some improvements that will be forthcoming with CEAP.

And I thank you.

- Thank you, honored to present this work on behalf of our group at the VA, the Michael E. DeBakey VA in Houston, led by Dr. Kougias. Disclosures are here, Dr. Kougias does consultation for Cook Medical. So compared to EVAR, FEVAR has greater lower extremity ischemic times due to larger sheaths,

visceral cannulation, complexity of procedures. And lower extremity complications have been reported as high as 15%, but there's not been a careful analysis of this. So we decided to look at the incidence of lower extremity sensory or motor deficit

after FEVAR, and to look specifically at lower extremity ischemic time, iliac artery occlusive disease, and lower extremity neurologic impairment after FEVAR. So this is a retrospective study over a four-year period. Early experience with our FEVAR cases was included,

and we generally used bilateral femoral access. Iliac stenotic lesions were dilated when required to allow an 18 or 20 French sheath to be placed. Graft alignment was achieved by centering the graft over at least two sheaths in the visceral arteries

before releasing the diameter-reducing wire. Visceral stents were used for all fenestrations and selectively for some scallops. We used perfusion adjunct techniques selectively, such as antegrade 7 French sheath placement into the FSA or sometimes a Dacron conduit into the common

femoral artery, which allows you to retract the sheath. A primary outcome was neurologic impairment. Secondary outcomes were major amputations and ability to ambulate at 30 days after surgery. We measured continuous lower extremity ischemic time from the time of the large sheath insertion into

the femoral artery until it was removed. If we used perfusion adjuncts, we measured the time from the sheath insertion to the perfusion initiation via the adjunctive modality, and the longest ischemic time for each extremity was recorded. We measured common iliac artery lumen diameters.

It was the distance of inner wall to inner wall, the narrowest segment of each common iliac artery. And we entered this as a binary variable based on eight millimeters. Statistics, we did both uni- and multivariate analysis, and I'll just run through that here quickly.

And we did an interaction model looking at the association between lower extremity ischemic time, size of the residual patent common iliac artery lumen versus neurologic impairment in the lower extremities. So there was 101 FEVAR patients with 202 limbs.

Percutaneously done in 16% of cases, we used perfusion adjuncts based on understanding of the case and how long it was going to take. Conduit in eight cases, and antegrade SFA sheath placement in three cases. The configurations are shown here.

Majority were one scallop and two fens, and the ischemic times are shown there. Operative time was about three hours was the average, but the standard deviation was 122 minutes. You can see the fluid requirements there. We looked at intra- and postoperative transfusions.

Then we looked at patients with neurologic impairment. So there were 18 patients who had some neurologic impairment postoperatively. 12 of these patients has mild sensory loss, eight has complete sensory loss, and only two had motor dysfunction.

The deficits tended to resolve within four days, almost all within 14 days. But we had four limbs with persistent sensory deficits, and only one with a persistent motor deficit. Two patients could not ambulate normally at 30 days. No patient underwent an amputation.

If you look at the univariate analysis, limb ischemic time, common iliac lumen less than eight millimeters, intraoperative blood loss, change in hemoglobin, and total transfusion all seem to indicate lower extremity motor dysfunction or sensory dysfunction.

But on multivariate analysis, there are only two factors: limb ischemic time and common iliac artery diameter less than eight millimeters. If you looked at the interaction model we prepared, if the common iliac artery diameter was less than eight millimeters after about two and

a half hours of continuous ischemia, the incidence of neurologic impairment went up. This went up more slowly if it was more than three hours if the iliac artery diameter is greater than eight millimeters. So, in conclusion, lower extremity permanent

neurologic impairment is very low after FEVAR, but there is a relatively high instance of reversible neurologic impairment associated with two things: extremity ischemic time and the presence of pre-existing occlusive disease in the common iliac artery.

We acknowledge this was a single center study. We weren't able to look at extent of aortic coverage or associated spinal cord ischemia, but we conclude that when you anticipate long ischemic times based on the iliac artery diameter, you should consider adjunctive perfusion techniques.

Thank you.

- Well, if fenestrated EVAR is so great, why isn't everyone doing it? And I would submit it has to do with the planning. If you have a perfectly planned procedure, the procedure will go perfectly. These are my disclosures, which are directly related to this presentation.

This is a case that was planned using AortaFit software and it was a case that we identified as being a perfect plan. We went back and looked at our fellow and resident in our training program who we trained to plan these procedures and asked them to plan this case.

Our first trainee submitted the following plan. And when we line up the SMA, we lose the left renal on this plan. We then asked our fellow to plan the case and she provided this plan.

When we line up the SMA on this case we lose the right renal. So, it tells us that there is tremendous variability in human planning. We participate in the VQI in the Pacific Northwest Regional group,

and we perform 88% of the complex EVAR in our region. And we have the lowest procedure times, the lowest estimated blood loss compared to the rest of the nation, the lowest in post-operative complications, excluding death, and the lowest in composite outcomes to include major cardiac events.

We also have the highest rate of return of our patients to a pre-surgical care setting. So how have we achieved this? Using AortaFit software, we are able to take a standard DICOM data set of a juxtarenal aneurysm patient and create a volume rendering.

We can then display the images in an axial, sagittal, and coronal view for the user. All that the user needs to do is to identify the target vessels and to plant seed points into those target vessels, the target vessels that are selected to be preserved.

What is then output from the software is a segmentation. And you see the segmented image here, but the magic of the software is that it does the automatic adjustment of the centerline using polynomial equations and goodness of fit. We can superimpose 2D slices over this to check

our orientation of the fenestrations and look at the plugs. And what's output is a graft plan that can either be given to the physician in the form of a 3D printed template or placed on the back of a manufacturing line. Sorry. So, for the physician, an STL file can be produced

to create a 3D printed template to create a physician-modified endograft, but what we really want is to be able to provide the manufacturer with a detailed plan using this software. This is an example of a Terumo Aortic TREO device. We've now done 37 of these cases.

This is a graft that has wide amplitude stents and a large amount of real estate for fenestration. So you can see inserting this 3D printed template that was created using AortaFit software. We can rotate this graft, move it in and out to find the sweet spot

for those fenestrations, and to create a truly customized device for the patient. We then, all that we have to do at that point is to line up the SMA. So you can see, on the panel on the left, we do our first aortogram

prior to deploying the stent graft. We deploy that SMA fenestration, the renals automatically align. We then select our renal arteries and then our fellows know that it's time to call for the next patient because the procedure is essentially done at that point.

This is a cone beam CT of that very first patient that I showed you, showing perfect alignment of all of the fenestrations and target vessels. And here's a 30-day follow-up CT scan, that if you pay attention and look carefully, you can see that all of the fenestrations

are perfectly aligned. There's about four centimeters of seals on length, and lack of endoleak and a successful result in this patient. This, fortunately, is published in this month's Journal of Vascular Surgery as an editor's choice.

And in summary, the long-term durability of fenestrated EVAR has been established, but planning and procedural complexity limits widespread adoption. Automated planning software, we believe, provides efficient and accurate graft plans for the physician

or endograft manufacturer. Well-planned grafts simplify branch access and the procedure and I think will increase fenestrated EVAR utilization. And simplified FEVAR may benefit the majority of patients harboring juxtarenal aneurysms and even standard infrarenal aneurysms and may be the best therapeutic option.

Thank you.

- This is a controversial topic. Basically we have been following standard set-up on the arterial side to grade venous stenosis. But duplex, many people would look at the stenosis either by venogram or duplex and then compare it to the adjacent normal segment.

In arteries the stenosis is usually focal so this approach works well. But in iliac veins particularly, does not work well. On venogram this looks normal but actually on IVUS it's a severe stenosis, 67 square millimeters,

it should be somewhere around 200. So, you are looking at a 70% stenosis. So, just the standard does not work well in veins. You have, does not happen, that type of rokitaskis stenosis does not happen, all the time but is present in varying degrees in about 20% of patients.

Another standard that we have applied, without thinking too much, is so-called critical threshold. Most major arteries, as we know, is not hemodynamically significant until is is somewhere around 70% or so. If the region of resistance is low,

it maybe a little bit low, somewhere around 60%, 70%, 80% depending on local resistance. Why does that happen? It happens because of autoregulation. As increases stenosis there is pressure flow of arterial dilation.

At some point, usually somewhere around 70%, 80% the pressure flow of compensating vasodilation is maxed out. So as increases stenosis the flow goes down and the pressure goes up. I want to point out that the pressure going up is proximal, not downstream.

The pressure goes down downstream. And pressure does go up upstream but is so well compensated on the arterial side by off-load to other areas. Another way to look at it is consider peripheral assistance, as a stenosis in aggregate.

Now there's a fall of blood pressure from 100 mean to somewhere around 30 millimeters post arterial. So that represents a very high-grade stenosis. So any proximal stenosis, by the principle of tandem stenosis, has to exceed

this high value to become hemodynamically significant. So that's why the 70% critical threshold. On the venous side there's no autoregulation. And the only distal downstream stenosis is abdomen. Not very much, about five millimeters of mercury pressure. So, on the venous side, pressure rises

with incremental stenosis. There's no critical threshold, it's nonlinear but no sudden inflection point. So this theory of 70% should not hold on the venous side. As a practical matter, most stenosis are in that range. They are in the 60%, 70% range.

But every once in awhile, say about 10%-15% of cases, where you will come across a 20% or 30% stenosis, which is clinically significant, because the veins are post-thrombotic and they have poor compliance. So even a slight stenosis will increase the pressure.

This is a concept of inflow outflow. If the inflow matches outflow, then the pressure will be normal. So you can calculate from the size of the outflow, we know what is the optimal outflow, you can calculate from the outflow size

whether the stenosis is significant or not. Critics will say this is a morphologic method. Yes and no. It's morphologic but it is tightly connected to flow. So it is a quasi hemodynamic method to measure the outflow size.

And again, calculated by various, by flow femoral size. Thank you.

- Thank you, thanks to Dr. Veith and the program committee for allowing me to present this morning. My disclosure. So, uh, I think that there's been an abundance of literature over the years that is suggested that venography may have poured diagnostic sensitivity for identifying iliac and, and

common femoral vein obstruction. Uh, in uh published literature, 34% of patients who have chronic venous symptoms of a severe degree had iliac vein obstruction on imagining techniques other than venography such as IVUS with normal venograms and often times

patients have significant outflow obstruction and there are no pelvic collaterals present so this is not a reliable though maybe specific indicator of outflow obstruction. The video study was designed to prospectively compare multiplanar venography vs. IVUS

to address the question if you do enough views on venogram do you find the same lesions that you might detect with IVUS. And we also wanted to look, does the imaging that you do to look for iliac and common femoral vein outflow track obstruction

effect your clinical decision about intervention. These are the patients in the video trial CEAP 4 through CEAP 6. And so 100 patients were randomized in this or not randomized, but rather entered entered this prospective multi-center single-arm study

at 14 sites in the US and Europe. This was half CEAP 6 patients and the remainder were CEAP 4 and 5. The patients underwent multiplanar venography. The site investigator was asked to make a decision about whether there was a significant lesion

and how they would treat that lesion and then once that was recorded IVUS was preformed and then again after the pull back the investigator was asked to make a decision about whether there was a significant lesion and how they would treat it.

We standardized venography with a hand injection in 3 views as noted. A 30 degree RAO and LAO and an AP view and the catheter was placed at the cranial portion of the femoral vein we adopted the standards and the literature

of a 50% diameter stenosis. And venography in a 50% CSA reduction on IVUS as a significant lesions. The uh, study cohort was approximately 43 women. The left leg was the index limb and 2 to 1 ratio to uh, to the right.

The age average 62 and you can see the majority of the patients were CEAP 4 and CEAP 6. What we identified with IVUS is a 21% greater (mumbling) identification of outflow obstruction. Venography was a lot less sensitive

at identifying these lesions and therefor suggesting that IVUS is a more sensitive imaging modality for identifying outflow obstruction vs. multiplanar venography. And when you looked at the core lab over read

this was for both the IVUS imaging and for the venography. And we at first calculated the diameter stenosis for both modalities we saw that with the multiplanar venography you tended to underestimate

the degree of diameter stenosis compared to IVUS and this resulted in missing about a quarter of the lesions that were greater than 50% diameter stenosis. And in part IVUS intended to score the lesions more severe for the same lesions compared to venography and this was statistically significant.

When we looked at CSA measurements from the IVUS system and also calculated off the venography in the core lab we saw again that venography missed about 18% of the significant greater than 50% CSA lesions even with reviews.

And this resulted in a change of procedure in about 60% of the patients there was a change in the decision about whether to treat of not and in 50 of the patients the number of stents changed from either no stent to 1 stent or 1 stent to 2 stents.

So without IVUS your likely under treating iliac and common femoral vein obstruction. This was the uh, rVCSS scores after treatment in this group. On the right here in green is the improvement on the left worsening.

And you can see in large part these patients all improved uh, expect for this outlier here and then some patients there was no improvement and when you looked at a score a VCSS score greater than 4 as being significant at 1 and 6 months there was a significant improvement post intervention.

And we see here in this receiver operating curve that IVUS best predicted clinical improvement at 6 months. And so we see that IVUS was more sensitive accurate for identifying significant lesions and the iliac and common femoral vein segments. It was the best guide for stent intervention

and it appears that if use a 50% cut off either diameter or CSA reduction it best predicts that intervention will lead to an improved clinical outcome at 6 months. Thank you.

- Thank you, Mr. Chairman. Ladies and gentleman. I'd also like to thank Dr. Veith for the kind invitation. This presentation really ties to the presentation of Erik Verhoven, I believe. These are my disclosures. So we basically have, obviously, two problems. We treat a dynamic disease by fairly static means.

One of the problems, a local problem, is aortic neck degeneration which is the problem basically of progression of disease. We know in general if you stent them, if you operate them, if you don't treat them they will just dilate and it's a question of time

whether you have a problem or not. So, they will inevitably, if patients live long enough, cause a change of geometry of the aorta and the branch vessels and that cause obviously, that can cause stent fractures and other problems.

That's just one of many papers Erik also has shown a migrated graft. With his fenestrated grafts showing that the problem is also prevalent in M stents and Z stents, and obviously also in

as in the Fenestrated Anaconda. So I'll talk briefly about our experience. In Vienna where we have treated so far 179 patients with either double, triple, or quadruple fenestrated grafts. Majority nowadays are quadruple in our series

where we have also treated patients with extensions of thoracic stent grafts or extensions further down to the iliac arteries. In these patients we've had relevant neck degenerations in five cases. Where either the branches had issues

or the graft had migrated relevantly. And these basically represent three different faces of the problem. So one is neck degeneration with migration and loss of seal. Certainly the biggest problem that can cause ruptures. That's one of the cases in 2015

what is certainly important is to have a look at the super celiac area of the aorta and you see it's degenerated, it's dilated. So we have a nice ring of aorta at the visceral segment but above it wasn't. And it was a

you see the saddle of the stent graft and one and a half years later the saddle (cough) has flattened out. We've had a stent fracture of the left renal stent.

We screwed it with anchors and fixed the stent graft. We believe that's going to be the solution. We were wrong. Yet anothe leak and a further migration of the case.

So we had to put in a thoracic endograft and bring in a 4 fen and a mono-iliac crossover solution. The other problem would be neck degeneration or progression of disease without migration or loss of seal. As in this case where we have implanted a 4 fen case and you can see here that there is

a diseased proportion of the thoracic aorta. Could look like a penetrating ulcer. And again we had to put in a thoracic stent graft and a 4 fen solution with a mono-iliac ending and a crossover. What's more important, I believe,

is the progression of general, generalized aortic disease. So there is no real migration, as in this case in 2013. You can see a nice saddle and very straight iliac limbs. 2018 you can see that the saddle is actually flattened out. Renal arteries look upwards, so you would actually believe in

a migration of the stent graft. Also if you look at the iliac limbs you can see that they have actually compressed somewhat. But if you look closely at the difference between the ring and the SMA, so that's lateral view, you can see that there is no difference.

The stent graft actually has not migrated. What happened is that the patient developed a thoracic aneurysm of 7.5cm and the whole aorta is not only increased in diameter but also in length. So the whole thing has moved its confirmation without basically a migration of the

not yet. So, Mr Chairman, Ladies a lessons we have learned is- and I could also repeat wh

seal in the healthiest proportion of the aorta. So if you see a nice visceral ring and above that you see a diseased proportion of the aorta, as in this case, where you have already a degenerated thoracic aorta.

You should really treat this as well and not go for a 2 or 3 fen case. And also the progressio the general progression of disease is an issue. So even if you have no migrations

you may end up with real problems and target vessel occlusions or stent graft fractures. Thank you very much

- I find it very difficult to get into an argument with one of my mentors, Dr. Raju, and I apologize for going off on a little tangent. And I will submit to you that when we look at this, this may be a better way of looking at it because we're taking an instance of non-flow dynamics as well as collapsible tubes

and everything's not perfect. So I have no real disclosures with this. And with the emergence of dedicated venous stents and understanding the role of individual design elements, cell architecture, radial strength, flexibility, and the performance of stents,

and more importantly how this therapy improves patients outcomes is critical in continuing the treatment pathway and continued improvement in stents. My take home message are very clear. For a given perimeter, lumen shape impacts area,

lumen shape impacts pressure, aspect ratio is a better predictor of flow and patient outcomes versus area. So, what is aspect ratio? It's the Degree of Roundness. And if you look at aspect ratio is equal to

the maximum diameter to the minimal diameter and if keep the change the keep the perimeters the same, you see what happens to the area, it actually decreases.

And you can see what happens to the aspect ratio. So the perfect aspect ratio is one. As we get to a more elliptical area, or an oval, it changes to four. So, if we look at this again, when we look at the whole area here,

even keeping the perimeters the same, you can see what happens to the area. The area shrinks. As the aspect ratio also changes. But more importantly, as we look at a mathematical calculation of shape and area,

round equals more area and less drag and thus better flow. Remember we're dealing not with arteries, we're dealing with veins and collapsible tubes. And increasing the flatness as you go across the X axis equals less area and more drag and thus less flow. And we always look at Poiseuille's Law,

but Poiseuille's Law's only important for perfect circles. And what I'm trying to submit to you, is that vein's are certainly not perfect circles, but as we get to figuring out what a perfect circle is and using a stent then this does apply.

And so, shape impacts on flow and pressure for a given perimeter summary. Shape directly impacts area. Area has an indirect impact on flow and pressure. The greater the aspect ratio the smaller the area. And shape becomes flatter

flow decreases and pressure increases. So, if we look at this publication by Dr. Cho, he looked at a better accuracy, patency associated with a rounder lumen. And he took 48 patients with iliac compression and acute DVT followed for an average of 20 months.

Stent compression considered significant if lumen compression was greater than 50 percent. And significant stent compression was inversely correlated with stent patency. And so, healthy veins are not round. What shape results in better outcomes?

So, if look at the VIRTUS trial, and looking at the feasibility trial, we looked at aspect ratios, and I would submit to you that if you look at the pre-stent aspect ratio, you can see it starting at 2.51

and then as over the 12 months, it was figured at 1.23. So as we get closer to one, it becomes more oval. And the same thing, the areas improved as well. But if you look at this scattergram, the relationship between post-stent vessel change

and 12-month patient outcome, this being a change in VCSS scores, so anything greater than a VCSS score of change of 2, there was no correlation in terms of Pearson coefficient here, but there was a mild correlation here,

with looking at aspect ratio. One would expect a positive correlation with area if we went with Dr. Raju, however just for this limited trial, there was none. And if we're looking at the graphs, there was no clear pattern for area change,

well the change in aspect ratio is clear. Moderately positive relationship between decreased ellipticity and clinical improvement. And patients with greatest luminal change oval to round most likely to exhibit clinical improvement. And I submit to you that aspect ratio is something

that we should consider as we go forward. Thank you very much.

- Well, thank you Dr. Veith, and thank you very much for allowing me to speak on the topic. I have no disclosures. This is a nice summary that Dr. Veith is actually second author, that summarize what we know about predicting who will benefit from intervention among the patients with asymptomatic aortic disease.

You look at this eight means that we have, you realize that only one of those related to the fluid deprivation. The rest of them are related to embolic events. And that's very interesting because we know that antiplatelets have very little effect

on prevention of this. That's summarizing that review. Partially because what we focused on is that mechanism of thrombosis which requires platelet activation and attachment to the wall.

And that's where those antiplatelets that we use, act upon. However, you realize if you just look at the any ultrasound, that because of the velocities that we have and the lengths of the stenosis in carotid disease there is no way how the platelets can be attached to that

due to that mechanism. They just fly away too fast and don't have any time to do this. And it's even more because all the studies, basic science, show that at those shear rates that we have in carotid disease

that is more that 70%. There is very little probability of either platelet attachment or Von Willebrand factor attachment, or as a matter of fact even fibrinogen attachment in that particular area. So on the other hand we also know

that at those shear rates that we have, the Von Willebrand factor molecules unfold revealing tens of thousands more adhesive sites that allow them, not only to the platelets but also to the wall at that particular spot. And then the most likely mechanism

of what we dealing with in the carotid disease is this that the Von Willebrand factor attach and this unactivated platelets form conglomerates which can easily, because they don't attach to each other, easily fly. And that is probably one of

the most likely causes of the TIA. So if you look at the antiplatelet that we use on this particular mechanism, is right here. And those aspirin and clopidogrel, and combination of those we usually use, have very little, if any, effect on this particular mechanism.

So if, on the other hand, you can see that, if you specifically address that particular site you may have a much substantial effect. Now, how can we identify it? Well actually, the calculation of near-wall shear rate is quite simple.

All you need is just highest velocity and smallest diameter of the vessel. Of course, it is an estimate and actual shear rate is much higher but that's even more, because you, better than you prevent, more higher rate. Just to demonstrate, you can have the same velocity,

similar velocity, but different diameters. This stenosis technique will give different shear rate, and vice versa. So it's not really duplicating neither one of them. So we decided to look at this. We did a case control study that was published,

still online in the Journal of Vascular Surgery. And what you can see on the ROC curve, that in fact shear rate predicts symptomatic events much better than either velocity or the degree of the stenosis. And we look specifically at this group

with this thresh point of 8,000 per second and you can see that those patients who have those shear rates and the stenosis are 12 times more likely to have ischemic events. We look at the other means like microembolism. It's ongoing study, it's unpublished data that I show you.

And it's a very, very small sample but so far we have the impression that those microemboli that we can decide for, make a decision for intervention, actually happen only in this category of patient that have high shear rate. Based on this, this is our proposed algorithm,

how we deal with this. If you have asymptomatic patients with more than 70% degree of their stenosis and shear rate that exceeds certain level, we think it's about 8,000 per second, that may be an indication for intervention.

On the other hand if you a have lower shear rate then you can use other means. And what we use is microembolis per hour. Then you can duplicate their areas. If TCD on the other hand is normal you can continue best medical therapy and repeat the ultrasound in a year.

It's arbitrary. This is proposal agreed and based on our studies and that's, I'm thankful for the opportunity to share it with you. Thank you very much.

- Thanks Stephan, yes I just want to give you five tips and tricks that I've learnt with my experience to this technique, and also then I'll present some results from the Ascend International Trials. I have an obvious disclosure that is important to show.

So, I do think that custom-made devices or phenostate graphs are the gold standard in this area of the difficult neck to aneurysm, but there are constraints with it, both financially and atomically, and of course its not the perfect solution

so we still need to strive to find better solutions for patients and indeed an off the shelf solution is very useful especially in emergency situations. I think we're all quite surprised by the outcomes from parallel grafts.

I certainly, when I saw this originally thought this was never going to work but actually, the results from standard evar with chimneys are really quite good. There is however always the potential for gutter endoleaks when aligning

parallel grafts with conventional EVAR stents which are not really designed for this purpose. So, endovascular sealing with parallel grafts offers a solution to this with the prevention potentially of gutter endoleaks because the polymus bag will seal alongside

the parallel grafts. And in practice this works quite well so you can position two, three or even four parallel grafts alongside the nellix sealing device to give yourself a really good seal and an example is shown here on the CT.

So tips for getting good outcomes from this, well the first is an obvious one, but its to plan very carefully, so do think you need to be very cautious in your planning of these with regard to multiple levels of the technique

including access, the type, length, and the nature of the parallel grafts you're going to use. I'll talk a bit more about the neck lengths but aneurysm lengths as well because there are some restraints with the

nellix device in this regard. You need to take very carefully about seal both proximally and distally and I do think you need to do this in a hybrid theater with experienced operators. I mentioned neck lengths and my Tip two is

you have to not compromise on neck quality and neck length. So you need straight healthy aorta of at least 15mm, of less than 30 diameter and a low thrombus burden. If you do compromise you'll see situations as the one on the photograph shows

where you get migration stents so you must not compromise on the quality and length of your aortic neck and if that means doing more chimneys, do it that's not a major problem but if you compromise on neck,

you will have problems. I mentioned the parallel grafts, again this is part of the planning but we use balloon expandable stents of a reasonable length to ensure that you get at least a centimeter into each of the branches

and you have to be careful to position these above the polymer bags so that they don't become constrained by the polymer bags from the nellix device. You have to be very careful when positioning these so the tip four is watch the parallax in

two different angles to be sure, as in the case here, that you line up all your stents appropriately and that you don't get crushing of any of the individual stents. So parallax is vital. And th

ltiple levels of redundancy in the nellix system which you can use to your advantage to ensure you get a good seal. So here's an example where the bags you can see are not entirely filled using the primary fill.

And it is quite difficult because often you get polymer pressures that are slightly erroneous in the endo bags. So use the redundancy including what's called the secondary fill of these bags so you can adequately fill the bags

right up into the aortic neck and ensure a very good proximal seal. So what are the results, well this is the post-market registry of Ch-EVAS this is an open-label study with no screening and I'll just show you a few slides of the data

on 154 de-novo procedures, which are a combination of single, double triple, and even quadruple chimneys. And if we look firstly at outcomes at 30 days the outcomes are good, that you'd expect in these difficult anatomies,

so 2.6% mortality and stroke, and just two cases of temporary renal failure. And if we look out 12 months, the freedom from aneurysm related and all cause mortality is favorable and comparable with any of the other endovascular techniques

in these difficult anatomies, in the upper 90 percents. And endoleak rates, you pretty much eradicate type two and type three endoleaks, but remember this is only 12 months, and very low levels of type one endoleak

and its really the type one endoleaks that are difficult to fix and if you ensure that proximal neck is adequate this shouldn't occur. And finally just secondary interventions, again this is out 12 months. Secondary Interventions are low and again

I think with the tips that I've shown you, you can reduce this to an absolute minimum. So this does offer an off the shelf alternative I don't think in any way this is to match the current gold standard which to me is the custom-made devices, but it's a very useful

adjunct to the techniques we have, and again provides that off the shelf solution which in emergencies and urgent cases is essential. Don't compromise on your neck, the outcomes I think, in this group are promising, but of course, the long term durability is

absolutely essential so it's important we follow these patients out to at least 5 years. Thank you.

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you Rod and Frank, and thanks Doctor Veeth for the opportunity to share with you our results. I have no disclosures. As we all know, and we've learned in this session, the stakes are high with TEVAR. If you don't have the appropriate device, you can certainly end up in a catastrophe

with a graph collapse. The formerly Bolton, now Terumo, the RelayPlus system is very unique in that it has a dual sheath, for good ability to navigate through the aortic arch. The outer sheath provides for stability,

however, the inner sheath allows for an atraumatic advancement across the arch. There's multiple performance zones that enhance this graph, but really the "S" shape longitudinal spine is very good in that it allows for longitudinal support.

However, it's not super stiff, and it's very flexible. This device has been well studied throughout the world as you can see here, through the various studies in the US, Europe, and global. It's been rigorously studied,

and the results are excellent. The RelayPlus Type I endoleak rate, as you can see here, is zero. And, in one of the studies, as you can see here, relative to the other devices, not only is it efficacious, but it's safe as well,

as you can see here, as a low stroke rate with this device. And that's probably due to the flexible inner sheath. Here again is a highlight in the Relay Phase II trial, showing that, at 27 sites it was very effective, with zero endoleak, minimal stent migration, and zero reported graph collapses.

Here again you can see this, relative to the other devices, it's a very efficacious device, with no aneurism ruptures, no endoleaks, no migration, and no fractures. What I want to take the next couple minutes to highlight, is not only how well this graph works,

but how well it works in tight angles, greater than 90 degrees. Here you can see, compliments and courtesy of Neal Cayne, from NYU, this patient had a prior debranching, with a ascending bypass, as you can see here.

And with this extreme angulation, you can see that proximally the graph performs quite well. Here's another case from Venke at Arizona Heart, showing how well with this inner sheath, this device can cross through, not only a tortuous aorta, but prior graphs as well.

As you can see, screen right, you can see the final angiogram with a successful result. Again, another case from our colleagues in University of Florida, highlighting how this graph can perform proximally with severe angulation

greater than 90 degrees. And finally, one other case here, highlighting somebody who had a prior repair. As you can see there's a pseudoaneurysm, again, a tight proximal, really mid aortic angle, and the graph worked quite well as you can see here.

What I also want to kind of remind everybody, is what about the distal aorta? Sometimes referred to as the thoracic aorta, or the ox bow, as you can see here from the ox bow pin. Oftentimes, distally, the aorta is extremely tortuous like this.

Here's one of our patients, Diana, that we treated about a year and a half ago. As you can see here, not only you're going to see the graph performs quite well proximally, but also distally, as well. Here Diana had a hell of an angle, over 112 degrees,

which one would think could lead to a graph collapse. Again, highlighting this ox bow kind of feature, we went ahead and placed our RelayPlus graph, and you can see here, it not only performs awesome proximally, but distally as well. And again, that's related to that

"S" shaped spine that this device has. So again, A, it's got excellent proximal and distal seal, but not only that, patency as well, and as I mentioned, she's over a year and a half out. And quite an excellent result with this graph. So in summary, the Terumo Aortic Relay stent graph is safe,

effective, it doesn't collapse, and it performs well, especially in proximal and distal severe angulations. Thank you so much.

- Yeah, thank you very much. Unfortunately Dierk Scheinert couldn't come, so thankfully he's allowed me here to take this presentation over so thanks a lot for this. So these are the latest 5-year results of the INCRAFT device from Cordis Devices currently under FDA review not yet approved

in the US, but in Europe. These are the conflict of interests, this is (mumbles). So this device is a three-piece modular system, low porosity polyester. You can bilaterally in-situ length adjust it up to 3cm. And the main feature I think with this device

is it's a low-profile device, 13 Fr inside 14 Fr outside except the biggest body which has an outer diameter of 16 Fr. The innovation study that was 60 patients, you can see here some objectives. So the question was whether you could deploy it

accurately where you wanted to have it without any type I, III, and IV endoleaks and of course there were also some other primary and secondary endpoints and again follow-up had to be done up to five years. This is a busy slide just showing you,

please look to the right side, to show you that there were quite some violations of the recommendations in which kinds of anatomies to implant this craft. Here for example neck lengths less than 10mm, here were some patients implanted.

Also angulations over 60 degrees, three patients, there were some thrombus in the neck, and here you can see aortic bifurcation smaller than 18mm, there were quite some patients and especially the iliac sealing length was shorter than 10mm in nearly 50% of the patients

and also the diameter of the external iliac arteries were nearly 50% lower than 7mm. Here the freedom from endoleaks type I was one at 30 days which has been resolved and another one developed after 30 days which also has been involved. No type III.

Stent graft patency after 30 days also 100% and otherwise also no other adverse events with this device at thirty days. So to answer the question with this device to the first question of (mumbles) will lighter fabrics and stent material decrease EVAR durability?

Will there be more endoleaks I, III, or IV? You can see here the long-term data so no Ia endoleak developed over four and five years, there was one Ib endoleak which developed at four years which also was apparent at five years. No type III endoleak.

One graft patency failure with a (mumbles) occlusion here at four years which also was here at five years. No migration, one fraction of the (mumbles) proximal third graft, otherwise it was very safe. You can see here once again the Kaplan-Meier curve for type I endoleaks through five years here

with type Ib here later on, and this is the patency Kaplan-Meier curve also showing here the good patency at five years, and this is freedom from second large vent. Here I don't have any data whether this is type II endoleak or not so this still has to be reported and clarified.

So to conclude the INCRAFT performed well on long-term while overcoming more difficult access morphologies. The endograft can be utilized in patients with demanding access and vessel morphology, and there are more studies ongoing.

There is one in the US and Japan where we wait for long-term data, 190 patients and also from Europe's 180 patients also there we still wait for long-term data. Thank you.

- [Neil] Thanks Tom and thanks Jose and Lowell for inviting me to participate in this great symposium. And I have no relevant disclosures to this talk. Clinical decision making, communication amongst ourselves, in the literature, and to some extent prognosis of patients is dependent a bit on the pattern of reflux in a given patient.

So that's the topic of today's talk for me. Those can be categorized into three rough bins, great saphenous vein reflux, small saphenous vein reflux, and non-saphenous vein or non-truncal reflux. More than one pattern can exist in a given patient, and that obviously has implications

in terms of what needs to be done in recurrence. Even great saphenous vein reflux can be divided into different components based on a variety of elements such as the source of the reflux, which we typically think of

as saphenofemoral junction derived. But the source can be below the junction, either from perforating veins or tributary veins. Sometimes those tributary veins are pelvic derived as in the image on the right. The extent of reflux is obviously very variable.

Sometimes it ends in varicose veins in the thigh and calf and obviously those patients are different than those that have reflux going all the way down to the malleolus or reflux that would be segmental, where it involves the trunk, leaves the trunk into tributaries,

and then comes back into the trunk. The anterior accessory great saphenous vein and saphenofemoral junction can be a cause of great saphenous vein reflux as well as depicted in this diagram where varicose veins shunt the flow from the anterior accessory great saphenous vein

to the great saphenous vein, leading the saphenous vein reflux. Some of the co-panelists for today's session, Dr. Chastanet and Dr. Pitaluga have looked at 1800 patients and categorized their ultrasounds to look at the patterns that exist

in great saphenous vein reflux and identified five different types. The most common type was great saphenous vein reflux with saphenofemoral junction incompetence leading to varicose veins. The second most common type was great saphenous vein

tributary reflux alone. And the third most common type was great saphenous vein reflux with varicose veins without saphenofemoral junction incompetence. This is more than just an academic exercise because if we look at these two types,

type three and type four we'll see that there's a difference in these patients in terms of the phenotypes that they present with their venous disease, specifically in the absence of saphenofemoral junction incompetence,

although, the great saphenous vein and varicose veins are both reflux in the incidence of advanced C4 through C6 venous disease is only 1%. But if you add the saphenofemoral junction component to that patient, the incidence of C4 through C6 disease is 10%.

So that's where the prognosis comes in. Small saphenous vein reflux can be categorized as well. The typical form is derived from the saphenofemoral, sorry, saphenopopliteal junction and leads to sapheno, sorry small saphenous vein reflux and varicose veins.

But that reflux can begin at a higher level, in this case in a perforating vein on the posterior thigh involving the thigh extension and then the small saphenous vein with downward reflux. And it could also begin even in the pelvis with varicose veins leading

to thigh extension reflux downward into the small saphenous vein. Or even at the saphenofemoral junction with reflux through the posterior circumflex vein into the thigh extension and down into the small saphenous vein.

A unique form of what we might call paradoxical reflux that involves the posterior circulation of the venous system superficially would be saphenopopliteal junction where that reflux, in essence, decompresses upward and leads to great saphenous vein reflux and varicose veins.

So all of these different patterns likely have different means to treat, but certainly also may have different long-term prognoses. And then finally varicose veins can be coming from non-saphenous veins. Up to 30% of patients have

non-saphenous related varicose veins. The majority of these patients are female and a lot of these are pelvic-derived varicose veins as you see in the diagram on the right. And many of these are also related to incompetent perforating veins in a number of locations,

particularly the mid thigh, lateral thigh, and popliteal fossa. So in conclusion categorizing reflux in patterns

- Dear chairman, dear colleagues and friends, it's my pleasure to be again with you. Nothing to declare. In our experience of CCSVI and angioplasty we have more than 1,300 patients with different neurological disorders. Not only MS, but also migraine,

lateral amyotrophic sclerosis, Parkinson's disease, left sided amaurosis. We published our data with an emphasis on the safety of the procedure. We had virtually zero percent of serious complication. What about the clinical improvement?

In fact, we noticed function improvement in more than 62.5% of these patients. And in fact, the group of Pierfrancesco Veroux showed similar between 50 and 60% of the patients restoring the normal blood venous flow. In fact, in their work was shown that the type

of anatomic disturbance, anatomic feature is very important predictor if the flow will be restored by the simple PTA. And the most important into the brave dream trial was also that, in fact, the restoration of the flow was achieved in around 70% of the patients.

And exactly in these 70% of the patients with restored flow like Paulo emphasized already, there were lesion, 91% of them were lesion-free on the MRI, and 77% of them were lesion-free on the six-month. We performed a substudy regarding the hypercapnia

and hypoxaemia of the jugular veins in the CCSVI-positive patients. And what we have described in this 178 patients with CCSVI and 50 healthy control group. In fact, we established that the patients CCSVI-positive the venous sample by the jugular veins was typical

with hypercapnia and hypoxaemia in desaturation, huge desaturation with improvement after the balloon angioplasty in all three parameters. What was the reason for that? In fact, in nine patients of our group we examined, the perfusion, the nuclear perfusion of the brain

before and after the treatment. I'm here presenting non-positive for MS young patient without MRI demyelization. And but on the brain perfusion he had deep hyperperfusion on the left side, and the patient was complaining with deep fatigue.

And we saw practically full occlusion of the enominate vein. And after the recanalization using first coronary and after it peripheral balloons, and in this particular case we had to stent finally. And you see still persistence of a huge crossover collateral even after ballooning.

But after stenting we saw practically full restoration of the flow. You see in less than three to four seconds it was very interesting to see on the perfusion imaging, nuclear perfusion, full restoration of the flow of this gentleman.

So this is very important to emphasize that there is direct relationship between the blood gas disturbances on the brain level, and demyelinization process. What about the PTA? It's probably not the optimal treatment.

We have to establish reliable clinical and anatomical predictors for vascular and clinical success in order to answer the important questions: who will be vascular responders, or MRI responders, and finally the clinical responders in this group of patients?

And concluding, ladies and gentlemen, the CCSVI is a real vascular pathologic entity and is probably a trigger for more than one neurologic degenerative disorder. Endovascular treatment, balloon, PTA, and stenting of CCSVI is feasible and safe.

Methods and strategies improving the early and late patency rate have to be elaborated because the good clinical result is strongly dependent on the vascular patency and flow restoration. And thank you very much for your attention.

- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.

They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression

if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.

Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.

This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,

and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients

who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,

and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,

symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.

There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,

again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,

six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,

it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse

if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective

in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.

This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent

because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common

in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.

So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,

those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,

like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.

And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,

get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.

If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners

over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,

it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,

look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.

That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,

then I would do something endovascular. Thank you.

- 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.

- 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 think that the most important tip cannot really be summarized in five minutes, which is that these procedures are highly dependent on how well you plan the procedure and how well you really implant the device. That is a fairly long learning curve that I think you need to actually collaborate with people

that they are experienced, and with industry to make sure that you are on the right track on making your measurements to size these devices. But there are a few things to be said about cases that are very difficult, and a few tips that I would highlight on this talk.

First, it's highly important that you build up your inventory so you can get out of trouble. I think you have to have a variety of catheters of your choice, with primary or secondary curves.

The addition of shapeable guides has been a major benefit for these types of procedures. They are fairly expensive, so I would say we don't use them routinely, but they can bail you out. They can allow you to do cases now from the femoral approach that in the past could not be achievable this way.

You have to be able to work on the diffe .035 system, .014 system, .018 system, and know when to apply this. I would like to highlight four maneuvers that we use when vessels don't align.

First, a common maneuver is really not to try to get in a quote/unquote pissing match with the fenestration and the vessel. If you can catheterize the fenestration first, and advance your sheath upwards, and lead a .018 wire into the sheath,

that will basically lock your sheath into the fenestration. Therefore, you don't have to repeatedly catheterize the fenestration and you save a lot of time. You can choose y ose something that has a secondary curve if you have room,

or a Venture 3 catheter, which is one of my choice for catheterization, and you can see here that on this case, the difficulties imposed by a shelf on the ostia of the renal artery, which makes catheterization more difficult. This .018 wire also allows you to bend your sheath

as a guide catheter so that you can achieve a downward curve to catheterize a down-going vessel, like on this renal artery. The second maneuver to highlight is that these devices are constrained posteriorly, and therefore, the fenestrations are naturally moved

posteriorly into the aorta. So one of the first maneuvers is really to try to move the fenestration more anteriorly by rotating the device. Now, some of the companies now have newer constraining mechanisms

that may alleviate some of this, but this is kind of a next maneuver that we do. Finally, rarely nowadays we have to really find more space between the fenestration and the aortic wall, but it is always useful to leave behind a wire when you deploy this device so that in the event

that you need more space, you can perhaps navigate the catheter, inflate, and create some space between the fabric and the aortic wall. Marcelo Ferreira, along with other collaborators, has described a technique that I think is very useful when you have a lot of space.

That's the case, for example, of a directional branch or perhaps if you are using fenestration to target a vessel that is somewhat away from the fabric of the endograft. That's called the snare ride technique. This is summarized on this illustration.

When you see the left renal artery to be up-going, now being targeted from the brachial approach, that was difficult to catheterize, you catheterize that from the femoral approach with an eight French sheath and a snare ride type... You snare the wire from the arm, and then you can

navigate that catheter inwards into the vessel. That can be difficult, sometimes, to actually advance the snare into the vessel. I think that there is some improvement on the profile of these snares that can improve that, but that is a very useful technique,

not only for branches, but also for fenestrations. Finally, sometimes you have too much space. You may seem you are very well aligned on the latitude with the vessel, but in fact, there is so much space the device got displaced on that sac and you cannot simply catheterize the vessel.

It's useful to downsize the system on these cases to a micro-catheter with a micro-wire to find yourself in the sac eventually out through the vessel. Once you achieve that, you would then exchange this micro-wire, usually a glide gold wire, to a .018,

a stiffer wire that is long enough. You advance a balloon that is undersized for that vessel, and with that you can straighten the system and eventually switch that for a wire that is of reasonable strength, such as a rosen wire in this case, and complete the case.

Finally, there is nothing wrong about leaving the battle to be fought another day. It's better to finish a case a little quicker and not end up with leg ischemia and a compartment syndrome and a s the situation

and come back another day. This is a case, for example, that I did a branch endograft. You can see the right renal artery is exceedingly narrowed. I could not find a way in in a reasonable time. I gave myself about half an hour. I decided to quit.

A few days later, I came back through a subcostal incision, got retrograde access, and this literally was a case that didn't take very long and end up doing very well. So in summary, patie select your proper

anticipat stent. To offset these challenges, minimize contrast a master your endovas

it is better to end with a patient alive and fight the battle another day, than to have an excessive long procedure leading to numerous other complications. Thank you very much.

- Good morning, I want to thank Professor Vitta for the privilege of presenting on behalf of my chief, Professor Francesco Speziale, the result from the EXTREME Trial on the use of the Ovation stent graft. We know that available guidelines recommend to perform EVAR in patient presenting at least a suitable

aortic neck length of >10mm, but in our experience death can be a debatable indication because it may be too restrictive, because we believe that some challenging necks could be effectively managed by EVAR. This is why when we published our experience 2014,

on the use of, on EVAR, on the use of different commercially available device on-label and off-label indication, we found no significant difference in immediate results between patient treated in and out IFU, and those satisfactory outcomes were maintained

during two years of follow-up. So, we pose ourself this question, if conventional endografts guarantee satisfactory results, could new devices further expand EVAR indication? And we reported our experience, single-center experience, that suggests that EVAR by Ovation stent-graph can be

performed with satisfactory immediate and mid-term outcomes in patient presenting severe challenging anatomies. So, moving from those promising experiences, we started a new multi-center registry, aiming to demonstrate the feasibility of EVAR by Ovation implantation in challenging anatomies.

So, the EXTREME trial was born, the expanding indication for treatment with standard EVAR in patient with challenging anatomies. And this is, as I said, a multi-center prospective evaluation experience. The objective of the registry was to report the 30-day and

12 month technical and clinical success with EVAR, using the Ovation Stend-Graft in patient out of IFU for treatment by common endograft. This is a prospective, consecutively-enrolling, non-randomized, multi-center post market registry, and we plan to enroll at least 60 patients.

We evaluated as clinical endpoints, the freedom from aneurysm-related mortality, aneurysm enlargement and aneurysm rupture. And the technical endpoint evaluate were the access-related vascular complications, technical success, and freedom from Type I and III endoleaks, migration,

conversion to open repair, and re-interventions. Between March 17 and March 18, better than expected, we enrolled 122 patients across 16 center in Italy and Spain. Demographics of our patient were the common demographic for aneurysm patients.

And I want to report some anatomical features in this group. Please note, the infrarenal diameter mean was 21, and the mean diameter at 13mm was 24, with a mean aortic neck length of 7.75mm. And all grafts were released accorded to Ovation IFU. 74 patients out of 122

presented an iliac access vessel of <7mm in diameter. The technical success reported was 98% with two type I endoleak at the end of the procedure, and 15 Type II endoleaks. The Type I endoleak were treated in the same procedure

by colis embolization, successfully, and at one month, we are no new Type Ia endoleaks, nine persistent Type II endoleaks, and two limb occlusion, requiring no correction. I want to thank my chief for the opportunity of presenting and, of course, all collaborators of this registry,

and I want to thank you for your attention, and invite you, on behalf of my chief, to join us in Rome next May. 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.

- Thank you friends who have invited me again. I have nothing to disclose. And we already have published that as far as the MFM could be assumed safe and effective for thoracoabdominal aneurysm when used according to the instruction for use at one, three, and four years. Now, the question I'm going to treat now,

is there a place for the MFM? Since 2008, there were more than 110 paper published and more than 3500 patient treated. 9 percent of which amongst the total of published papers relating the use of the MFM for aortic dissections. So, we went back to our first patients.

It was a 40 year old male Jehovah Witness that I operated in 2003 of Type A dissection and repair with the MFM in 2010 because he had 11 centimeter false aneurysm. Due to his dissection, this patient was last to follow up because he was taking care full time off of

his severe debilitated son. When we checked him, the aneurysm seven years later shrunk from 11 to 4 centimeters wide. And he's doing perfectly well. Then the first patient we treated seven years ago, same patient with Professor Chocron

Type A dissection dissection repair in 2006. Type B treated with MFM in 2010. We already published that at one year that the patient was doing fine. But now, at three and seven years, the patient was totally cured.

The left renal artery was perfused retrogradely by aspiration. That's a principle that has been described through the left iliac artery. So what's next? Next there was this registry

that has been published and out of 38 patients 12 months follow up, there were no paraplegia, no stroke, no renal impairment, and no visceral insult. And at 12 month the results looked superior

to INSTEAD, IRAD and ABSORB studies. This is the most important slide to us because when you look at the results of this registry, we had 2.6 percent mortality at 30 days versus 11 30 and 30.7 no paraplegia, no renal failure, and no stroke vessel

13 to 12.5. 33 and 34 and 13 and 11.8 percent. With a positive aortic remodeling occurring over time with diminishing the true lumen increasing the true lumen and increasing the false lumen.

And so the next time, the next step, was to design an international, multicenter, prospective, non-randomized study. To treat, to use the MFM, to treat the chronic type B aortic dissection. So out of 22 patients to date,

we had mainly type B and one type A with no dissection, no paraplegia, no stroke, no renal impairment, no loss of branch patency, no rupture, no device failure, with an increase in true lumen and decrease in false lumen that was true at discharge.

That was true at one, three, and six and 12 month. And in regards with the branch occluded from the parts or the branches were maintained patent at 12 and all along those studies. So, of course these results need to be confirmed in a larger series and at longer follow up,

yet the MFM seems to induce positive aortic remodeling, is able to keep all branches patent during follow-up, has been used safely in chronic, acute, and subacute type B and one type A dissection as well. When we think about type B dissection, it is not a benign disease.

It carries at 20 percent when it's complicated mortality by day 2 and 25 percent by day 30. 30 percent of aortic dissection are complicated, with only 50 percent survival in hospital. So, TEVAR induces positive aortic remodeling, but still causes a significant 30 day mortality,

paraplegia event, and renal failure and stroke. And the MFM has stabilized decreased the false lumen and increase the true lumen. Keeps all the branch patent, favorize positive aortic remodeling. So based on these data, ladies and gentleman,

we suggest that the MFM repair should be considered for patients with aortic dissection. 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.

- Speaking about F/EVAR and Ch/EVAR, and try to prove that the evidence of Ch/EVAR is solid, especially in some circumstances also better than the evidence about F/EVAR. Well, let's try to define this title. Durability of Ch/EVAR is solid if the procedure is done right.

And I think this is very, very crucial. We heard and we know the PERICLES Registry tried to evaluate this technique, collecting the worldwide experience from 13 US and European university centers, and published in annals of surgery.

And also, the PROTAGORAS study focused exactly on the performance of the Endurant device in order to avoid this heterogeneity which we had in the study (mumbling) published literature up to now. Focusing exactly on the Endurant device

in combination with balloon expandable covered stent. And based on these two registries and studies, we identified four key points, four key factors, which we'd like to give you as take home message in context to have the Ch/EVAR technique as solid procedure. So, we learned that the technique performs very well

if we use the technique for single or maximum double chimney grafts. We highlighted how important it is for this technique to use suitable combinations between aortic stent-graft and chimney devices. And we learned also, how important is the oversizing.

We have to have enough fabric material to wrap up the chimney grafts of 30% of the aortic stent-grafts. And in this context, we highlighted also the importance of creating a new sealing zone of 20 millimeter in order to have durable results.

Which is also very important is to know when we should probably avoid to perform the technique, and I would like also to highlight these points. So, we learned in case of excessive thrombus formation in the thoracic, especially also LSA, we have to be very, very careful with this technique,

because of course, we have the risk of cerebral vascular events. We learned also that performance of this technique in a neck diameter of more than 30 millimeter is associated with high risk of Type 1A endoleaks, which will be persistent, and which probably

lead to failure of the treatment. Which also learned is to evaluate very carefully the morphology of the renal arteries, especially focus of the calcification of the stenosis, and also of the diameter. And last but not least, it's very important to

have access to the suitable materials for renal cannulations, and also experience. So, if we consider these key points of doing and not doing chimneys, I think we have a very good base to have durable and good results over the time. And we have seen that.

You saw it very nicely (mumbling) the changes of the diameter pre and postoperative, but you forgotten to highlight that there was highly significant in the PERICLES and in the PROTAGORAS Registry. Also, what we have seen is that

more than 90% of the patients had stable or shrinkage of the sac after a CT follow up of two years. And here's a very nice overview of the Kaplan-Meier curves, highlighting that the technique performs very well in this specific combination of the Endurant devices,

abdominal device, and abdominal chimney grafts like the Advanta. Having a very nice chimney graft patency of almost 96%, and a freedom from chimney graft later interventions of 93%. Very important is also if we create these very good sealing zone of two centimeters.

We have a very, very low incidence of new Type 1A endoleaks needed reintervention. And here is an example of a case which had a very short sealing after the previous treatment with chimney for the left renal artery, and over the time was necessary to extend the sealing zone,

creating these durable solution and transformating from single to triple chimney, as we can see here. So, this is very important to know and to highlight. In context of the better or not better for F/EVAR, we can see now the results, and we've compared with meta analysis of F/EVAR.

We see that the results are similar. Keeping in mind also that in F/EVAR, we involve the SMA either as scallop or as bridging device, and we don't have evidence about the SMA outcomes and the SMA patency because most of the patient probably who will die, and will not perform autopsy

for each patient if it has an SMA occlusion or not, so I believe it is underestimated the really incidence of survival after F/EVAR. And also, regarding the patency, we have also in this context, similar results after chimney compared to the patency of the bridging device after F/EVAR.

So, ladies and gentlemen, I believe we've considered these key points. We can achieve very good results performing Ch/EVAR, having as a solid and valuable procedure for our patients. Thank you very much.

- I want to talk on managing branch complications. This is my disclosure. We overlook in the Berlin-Brandenburg Helios Vascular Center about 466 patients treated with branched, TVAR and fenestrated EVAR devices. All patients received Zenith stent-grafts, custom made devices, T-Branch, or standard fenestrations

in all cases. The target arteries that we are talking about were renal, SMA, celiac access and internal iliac arteries. We used exclusively bridging stent-grafts that were balloon expandable stent-grafts. This is the differentiation of the patients

so we had EVAR fenestrated grafts in 190, branched TVAR in 138 patients, 93 of them were off the shelf devices and T-branch. EVAR with iliac side branches in 138 patients and all together we treated target arteries of 1270. You see the hospital mortality of these procedures

you can see a clear difference between the EVAR fenestrated graft and the branched T version are much more complex procedure and although overall mortality was 4.9% over these 13 years. What happened in these patients we experienced

in 44 patients, 44 complications in the target arteries so unfortunately one target artery problem per patient in these complicated cases. This means rate of 3.5% problems in the target arteries overall. Involved were renal arteries in 32 cases,

SMA in 10 cases and the celiac artery in two cases. What did we do in these cases? Managed the complications once thrombolysis was different devices for example were Rotorex stenting of the dissected vessels, coiling if unavoidable or occlusion of the side branch if no access was possible.

Show you some examples. This is a very serious complication where we were unable to enter the SMA resulting in occlusion of you see on the right slide that this was solved by laparotomy and retrograde access to the SMA.

This is a stenting of a dissected renal artery which could be managed quite nicely with an extension of the stent. Here we have again a prolonged intraprocedural SMA occlusion. We finally managed to enter the vessel

but it was very, very long and prolonged time. This is an inaccessible celiac artery where we have finally had to skip, not iliac sorry, celiac artery where we had to skip the implantation finally and occlude the branch with Amplatzer plug.

All together if you look at these complications in 34 cases we were successful in clinical point of view. In 9 patients complication was little and majority of these were complications involving the SMA. Eight of nine patients had with severe complication in the SMA and died

and so the SMA complications contribute, compared to the mortality, 40% to the procedural mortality in these branched cases. So in conclusion, injury to target artery in endovascular repair with branched and fenestrated stent-grafts are rare

but may be a serious complication especially damage to the SMA has a high mortality and thus further improvement of endovascular skills, instruments for example moveable sheaths which we had not available in the beginning and troubleshooting devices are mandatory

to avoid these complications. Thank you very much for your attention.

- Ladies and gentlemen, I have nothing to disclose when regarding this topic. We know that TIAs are independent predictors of long-term mortality in the general population, however, they've been left underreported in almost all the randomized clinical trial. And we don't know the effect of TIAs on long-term survival

in patient with carotid disease. So what we have done, we have performed a study, looking at the effect of TIAs in populations submitted to carotid revascularization, either with endarterectomy, or stenting, and we achieved a pretty good long term result.

However, patient's with TIAs had a significantly lower survival compared with the patient without cerebral events. Similarly, patient with stroke, these reduce survival, and TIA behaves exactly like stroke in this population.

So, by multivariate analysis, TIA together with stroke, chronic renal failure, and age were independent predictors for late mortality. So, we have seen that TIAs have this effect in patient with carotid disease, but what about silent cerebral event?

The silent cerebral infarction has small, radiologically detected infarction without a history of acute dysfunction. And they're usually associated with a variety of condition. In the general population, these cerebral infarction are present in almost

one fifth of the population, 21%. And they are associated with significantly reduction in the stroke free survival in this population. For that reason, they are considered a high risk of stroke in patient with carotid disease.

So looking at the series of patient submitted carotid revascularization, we have seen that the presence of these silent brain infarction was significantly associated with either transient ischemic event and stroke. So, the important factors,

we wanted to further expand these experiences just looking at these phenomenon. In another series of 743 patients submitted to endarterectomy are looking at all the preoperative CT scan in this population. And again, we have found that significantly

association between silent cerebral infarcts and stroke. And by logistical regression analysis, this feature was independently associated with postoperative stroke. At long-term, this effect was also present in association with ipsilateral stroke.

And stroke combined stroke and death. Again, these effect was independent from all other feature. So what about their effect in stenting? Actually, there are no papers in the literature looking at this effect. So we perform a retrospective analysis on

420 patient submitted to a stenting procedure. And all patients were selected with preoperative evaluation of the brain. So, again, 30 day outcome, was not significantly affected by the presence of silent cerebral infarcts, however, when we look at the patient

with endarterectomy and stenting, we see that while in the endarterectomy group, there is a clear decrease of the stroke rate in patient without silent cerebral infarction. This effect is less pronounced

in the stenting group. So in conclusion, silent cerebral infarction increases the risk of postoperative events in carotid endarterectomy. This increased risk should be considered when in indication to revascularization is given.

In stenting, the effect is less pronounced, due to the higher overall risk of neurological event. Thank you.

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