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Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Angio jet (Zelante)Angiojet (Solent)Catheter-directed thrombolysisConvatecDrain-fixev3 guidewire (Nitrex- Medtronic)IF DVTtherapeutic
Update On The Advantages, Limitations And Midterm Results With The Terumo Aortic 3 Branch Arch Device: What Lesions Can It Treat
Update On The Advantages, Limitations And Midterm Results With The Terumo Aortic 3 Branch Arch Device: What Lesions Can It Treat
4 branch CMD TAAA deviceacuteAscending Graft Replacementcardiac arrestRelayBranchRepair segment with CMD Cuffruptured type A dissection w/ tamponadestent graft systemTerumo Aortictherapeutic
The Altura Double D Endograft Device For EVAR: Advantages, Limitations And 4-Year Results
The Altura Double D Endograft Device For EVAR: Advantages, Limitations And 4-Year Results
Altura stent graft systemEndovascular stent graftLombard medicaltherapeutic
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
New Findings From The PERICLES Registry Shed Light On Ways To Improve Outcomes Of Parallel Grafts To Treat Complex Aneurysms
New Findings From The PERICLES Registry Shed Light On Ways To Improve Outcomes Of Parallel Grafts To Treat Complex Aneurysms
able covered stent / Maquet)Advanta (Ballon expEndurantMedtronicStent grafttherapeutic
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
GORE MedicalGORE VIABAHNL EIA-IIA bypassleft carotid subclavian bypassstent graft systemTBAD with TAAAtherapeutic
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
Mid- And Long-Term Data From The PERICLES Registry Show Mortality, Branch Patency And Freedom From Endoleak For Ch/EVAR To Be Similar To Those Of F/EVAR
Mid- And Long-Term Data From The PERICLES Registry Show Mortality, Branch Patency And Freedom From Endoleak For Ch/EVAR To Be Similar To Those Of F/EVAR
EndurantMedtronicStent grafttherapeuticZenith / Excluder / Jotec / Talent / Viabahn / iCast / Bare Metal
Transcript

- Thanks again. So I've been charged with talking about drug drug interactions with statins and I have no disclosures. (reads on screen definition) Using that definition, statins have very little, if any,

chemical interactions with other drugs However, what the intent I think of the title is looking at statin levels. How statin levels are affected by drugs which alter the enzmyatic pathways of statin metabolism.

And we know that statins are HMG CoA reducatase is responsible for the rate limiting step of cholesterol synthesis and drugs that inhibit HMG CoA reduce cholesterol.

(reads slide) P-glycoprotein is a transporter protein that moves substances across cell membranes. And this is a list of the common statins and how they interact with P450 substrates. We have the CYP3A4 substrate

and atorvastatin is a major example there and the CYP2C9 substrates and Rosuvastatin. And I'll call you attention to the fact that the most commonly used and most effective statins, Atorvastatin and Rosuvastatin,

are both long half lives compared to the other statins. Now another thing I want to call your attention to 'cause it has clinical implications is the variation in breast cancer resistant protein (BCPR) gene but it alters the absorption

and it significantly increases the absorption of statins from the GI tract. And you can see that Asians are particularly affective and that's why recommendations for beginning statins in Asians are to start at a lower dose and then ramp up rather than start

at the typically maximal dose for most of our arthoscopic patients. Now risk factors thought to be due to interactions are advanced age, frailty, hepatic dysfunction, those with alcohol abuse, renal dysfunction, hyperthyroidism, woman and Asians.

And if they have any of these, we want to dose adjust but that's for risk factors. (reads on screen definition) Now grapefruit juice is often talked about and its due to its interactions with furocoumarins

and Atorvastatin has a large effect and Rosuvastatin very little effect when grapefruit juice is taken. If a patient want to drink six or seven ounces of grapefruit juice a day or every other day, that's fine, we don't want them

drinking a quart of grapefruit juice a day. Simvastatin is particularly a risky statin. It's at higher risk for drug interactions. It's at high risk for being involved with genetic polymorphisms. It has a dose related toxicity

unlike Rosuvastatin and Atorvastatin. And I told you about the FDA warnings. So lets make it easy on how to manage the patients. If a patient has liver disfunction or they're on Niacin, and if they're on Niacin,

I'd rather discontinue the Niacin and keep the statin, treat them with caution. If a patient has renal dysfunction for all statins except for Atorvastatin, adjust the dose.

If a patient is on Digoxin, monitor the dige-level in these patients if they are on a statin because the dige-level can increase. And then we want to avoid statins in patients that need

any of the azol antifungal such as ketoconazole or the mycin antibiotics or cyclosporine. Avoid fibrates and especially genfibrozil and the protease inhibitors if your patient is on an HIV protease inhibitors. (reads on screen information)

Thank you very much.

- [Narrator] Thank you, thank you Dr. Veith and the committee for the kind invitation. No related disclosures. Carotid webs are rare, noninflammatory arteriopathy that are also known as pseudovalvular folds, as well as other pseudonyms for this. They are small, shelf-like linear filling defects,

arising posteriorly from the posterior proximal-most ICA and project superiorly into the lumen. They're generally regarded as a developmental anomaly of the brachiocephalic system, and histopathology lacks atheromatous changes and inflammation of the tunica intima.

They may be associated with FMD, or be considered an atypical form of intimal fibroplasia, and generally arise from dysplasia within the media. They will as we will see, carry a considerable stroke risk based on laminar flow disruption and irregular shear profile.

This is the mechanism by which they produce strokes, seen clockwise from the top upper-left. There are areas of stasis in which thrombus can develop behind the web. The thrombus can enlarge and eventually embolize. Operative findings and pathologic findings include

these webs seen here behind this nerve hook, and generally smooth muscle with extensive myxoid degenerative changes. Over the last several years we have treated 10 patients with carotid endarterectomy for symptomatic webs. The mean age of these patients

is generally quite young, in the 40s. The majority are female, one patient had a bilateral web and 70% of these patients had no atherosclerotic risk factors whatsoever. The mean maximum peak systolic velocity on duplex was 77 centimeters,

and five of the cases were closed primarily without a patch. There were no strokes perioperatively in this group, no mortalities, and there have been no new neurological events nor restenosis. Several other groups have looked at this phenomenon as well,

this is a case series of which 7 patients were identified prospectively having had an ischemic stroke. Again, the mean age was young. Of note, five of these patients had a recurrent ipsilateral stroke to the web. No FMD was seen throughout the other vascular beds

and four out of five of these patients, the recurrent patients had CEAs with no recurrence at approximately a year. Another review identified 33 patients who had excellent CAT scan imaging. These were younger patients over a six year period,

with cryptogenic stroke. The prevalence of webs within that group was 21%. Symptomatic patients within that group with webs were 7 patients out of 33 and again you see a young age, predominance of women,

in this study of predominance of African American patients 3 bilateral webs, all patients had MCA infarcts. And oh, 1.6% of the webs in the control group were without a stroke. Another case-control study looked at 62 cases over four years.

They were able to match 53 of these patients with other cerebrovascular pathology, webs were found in 9% of the cases, but only 1% of the controls. And again of the webs, predominance of young patients

and women with two bilateral strokes. So what about diagnosis? Even large webs generally do not meet the velocity criteria for significant stenosis, and while you may see a filling defect, you're generally dependent on B mode imaging,

and having a high level of suspicion, for identifying this process. CTA is the gold standard, it's got rapid, high-resolution imaging, reformatting across planes, makes this an excellent modality

in associated findings of thrombus, and atherosclerosis can also be detected. Angiogram again, as always, gives you a good view of flow dynamics, intra and extra cranial pathology, and in general the finding is of contrast pooling,

which you have to look for behind the web. MRA is one method that's been used to characterize this, in this modality you can see slowed blood flow distal to the web, blood pooling distal to the web, and generally this all leads to an atypical pulsatility, of the carotid wall near the area of the web,

suggesting impaired hemodynamics in this condition. Management is with a carotid endarderectomy which has been the preferred treatment, although some have advocated medical management with formal anticoagulation, patients have had strokes

while on anti platelet therapy, and there are several case series now appearing of acute stroke treated with stents, these are generally delayed following thrombectomy. There's one latrogenic dissection in these groups. These patients have few atherosclerotic risk factors,

in the same demographics as noted above. So in conclusion, these are associated with FMD and intimal fibroplasia. The prevalence is low. The prevalence may be increasing but it's not clear whether this is a true prevalence increase,

or simply increased detection. They're associated with recurrent symptoms even in the setting of adequate medical therapy and is an underappreciated cause of stroke, and are now becoming a recognized, and rather than a cryptogenic cause of stroke.

They are generally not identified by current duplex criteria in asymptomatic patients, and duplex may miss them entirely. Axial imaging is essential and currently we don't stratify these based on either legion characteristics or demographics.

So while the optimal management is not completely defined given the recurrent stroke risk CEA seems prudent especially in young, medically fit patients with or without patch angioplasty, which may have some impact on quality metrics

at least in the United States. We've treated patients with three months of antiplatelet therapy, aspirin indefinitely. Right now the role of statins is undefined, and the durability and role for endovascular approaches remains also undefined.

Thank you.

- 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.

- [Gerry] These are my disclosures. When it comes to ilio-femoral deep vein thrombosis, many of us feel that is the most important area to treat. And some of us feel that the inflow is very important, in which case, you've got to worry about it. But if you feel that the inflow doesn't matter at all, then you can forget about it.

So that's for those of you who aren't from New York, that was my Irish accent on a New York, forget it. This is one of the ways to get into the below-knee veins, posterior tibial venous access. It looks quite easy, it's not quite so easy. Although there's two veins side by side,

you typically only get one chance at one vein because the other one goes into spasm. Pardon me, very sensitive mouse, like myself. You choose your wire of choice. I quite like the ED3 Nitrex. And then confirm that you are inside the veins,

because that happens all of the time to me. Those are funny looking veins because I've managed to puncture the artery. And which brings up one of the pitfalls, try not to puncture the artery. If you do manage to get into the vein,

you then insert a catheter and a catheter-directed thrombolysis after that is fairly standard. There's a few little tips and tricks in terms of stitching it in, using a small sheath is possible.

Heparin through the sheath, and then TPA through the infusion catheter. If you are fortunate enough to have the right length of catheter for the thrombus, then you can leave it at that length. Otherwise, you can pull it back

by 10 or 15 centimeters per day. And it typically takes three days to perform catheter-directed thrombolysis in this region. We always put on compression stockings, which sounds fairly basic, but it's important because it means that things don't get pulled.

And curious house officers and doctors don't have a good look at it and pull the whole thing out. Or the patient, for that matter. That's posterior tibial vein access, fiddley, tricky, easy to get into the artery, spasm is coming. You can do it with pharmaco-mechanical thrombectomy

using a 6 French device. The only one that I'm familiar with would be the AngioJet Solent, and not the newer Zelante. Views of the West of Ireland, not from this morning. Then if you want to switch tracks, how else can you get into the deep veins

of the lower extremities? Well, we're talking about improving the inflow, so we're going to now try and go from above and below. This is a patient with massive deep vein thrombosis. You'll see in just a second now. Thrombus starting here,

occlusive thrombus going to the profunda, occlusive thrombus down into the femoral, duplicated femoral vein, and then, most importantly, it goes into the below-knee popliteal. You might say why does this matter? Why do you care about the popliteal at all?

Well, I'm a bit old-school. I do believe that inflow matters quite a lot. Pardon me. So you can see a thrombus starts just here, a rather unusual place for a thrombus to start. Typically it starts much higher in the common iliac vein.

You can see it goes into the profunda femoris here. That's quite important technically, because the profunda is a very important vein in terms of long-term patency of the segment. And you can also see, lordy me, that it goes into the below-knee here as well.

This is what we call criss-cross. Fairly standard, fairly straight-forward, back of the knees, catheters into the popliteal vein from above and below. It sounds very easy, it's actually surprisingly difficult. The problem is that although you start very far apart, your two needles tend to approach

and you tend to puncture the vein in almost identical position, time and time again. So you have to start what feels like an awfully long way apart, in order to get some clearance between the two catheters. This is what you look like

when you're going to start catheter-directed thrombolysis. And what we're doing now, is we start catheter-directed thrombolysis at the bottom end, while working on the top end. The bottom sheath, rather the sheath facing inferiorly, is 6 French, with an infusion catheter

which is typically 20 centimeters long. And then this is a 10 French sheath going north. And through that you can perform AngioJet or whatever your thrombectomy device de jour is. Now this is an initial venogram of the below-knee veins and you can appreciate that there's very little inline flow

going from south to north. And you're seeing a whole lot of collaterals and very little flow going north at all. Pardon me. AngioJet works well here, although there are a variety of thrombectomy devices.

Then I must say I'm a big believer in aspiration. And you can get quite aggressive with a curved 8 French catheter. It sounds very basic, works very well. It's particularly useful, again, to go back to the profunda femoris inflow,

as well as the internal iliac. So this is what it looks like after aspiration. And you can see a rather unusual stenosis. And then, obviously, you need to go on to treat that. We start with our stent at the top to cover the iliac vein compression point,

and then carry on down here, and add a further stent down at the bottom. The inguinal ligament, I don't think is nearly as important as others feel. I think you you have to stent from flow to flow. And you can see that the final flow we've got here

at the end is quite satisfactory. Now this is when I say at the end, this is the end of the above-knee treatment. 'Cause you still haven't dealt with the below-knee veins. So you get your catheters running overnight, and you've got thrombolysis going north and south.

So this is your sort of set-up, your 10 French sheath going north with a catheter through it. A drain fix is quite useful for those of you who have access to that, to keep the catheter in position. And similarly going south, like this.

And this is what it looks like below beforehand, and this is what it looks like afterwards. You might think well, that doesn't really matter very much, but the popliteal vein will guarantee the success of your treatment. If you do not have a patent popliteal vein, in my view,

your success long-term is going to be much more guarded. And then, this is what it looks like from below, and the next morning. You can also appreciate that there's quite significant inflow now from the profunda. You can see the mixing just there, at the top up here.

So you've now guaranteed an inflow from above and below, but it takes two days, typically, because you've got to work one day on the above-knee segment and the second day on the below-knee segment. So could you move it on a bit?

Again, Galway, but not this morning because it was raining. You can do it as a single session criss-cross, so this is very similar to many of the arterial thrombectomies that you perform. I specialize in big, swollen, purple legs,

save the Speedos, they're not mine. But he's got a very, very swollen right leg. Rather unusual when somebody presents with a right leg tense phlegmasia. It starts to get me wondering, why should he have a right leg phlegmasia?

No specific reason. Left, obviously, would be straightforward. A CTV again, heading south here. Nothing really specific there, but you can appreciate this leg is very tense indeed. And there's thrombus in the femoral,

and most importantly, it goes down below-knee again. So you've got no inflow into your popliteal segment. If that popliteal vein is opened, it's a straightforward one hour, one and a half hour procedure. With a thrombosed popliteal vein, it's more difficult.

So here's the view of the external iliac vein, and here's the longitudinal curl reformat, showing A, a very swollen limb, and B, the length of the thrombus. In this case, again, you'd use the same criss-cross technique.

But this time, we were going to attempt a thrombectomy above and below. And starting off, you put a little catheter in here. Niggle it down as far down as you can, and just flush inject five, 10 milligrams of TPA while you're setting up your thrombectomy device.

That usually takes a few minutes. And in that meantime, you then can get to work. And this is just after five to 10 minutes of tissue plasminogen activator. You opened up some segment here. Then you get to work

with, as it happens in this case, the AngioJet. Not perfect, because our puncture points are very close to each other, but you can appreciate that we do have rapid inline flow. And this is over the course of 45 minutes or so. We're now up to about an hour

with, I think that's a Cook Zilver venous stent going from south to north. And this is his CTV, with a filter in situ. At six months, he has a widely patent vein. And the same on the sagittal reformat. You can appreciate that the stent is widely open.

In summary, there's pros and cons to both. First of all, you have to believe that the popliteal vein matters in terms of inflow. I do, I believe that inflow matters in terms of most vascular procedures. CDT is less labor intensive but costs more,

and there are the risks of thrombolysis. Pharmaco-mechanical thrombectomy is faster, and you can do all of your work in one go. But it certainly takes two hours of your time. Posterior tibial vein is more difficult than it it looks. There's lots of ways to skin this particular cat

and Fabritzio and I wrote a little book last year. If you're interested, you can learn more. Thank you so much.

- 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.

- Thank you very much, Gustavo, you read the abstract so now my task is to convince you that this very counter-intuitive technique actually works, you are familiar with Petticoat, cover stent to close a proximal entry tear and then uncover stents, bear stents, downstream. This what it would look like when we open up

the bare stent, you know dissect the aorta. So here's a case example, acute type B with malperfusion, the true lumen is sickle shaped, virtually occluded. So we use Petticoat, and we end up with a nice reopening of the true lumen, it is tagged here in green, however if you look more closely you see that here

wrapping around the true lumen there is a perfused false lumen. This is not an exception, not a complication, this is what happens in most cases, because there are always reentries in the celiac portion of the aorta.

So the Stablise concept was introduced by Australian group of Nixon, Peter Mossop in 2012, after you do the Petticoat, you are going to voluntarily balloon inside both the stent graft and the bare stents in order to disrupt, to fracture the lamel, obtain a single-channeled aorta.

This is what it looks like at TEE, after deployment of the stent graft, you see the stent graft does not open up completely, there is still some false lumen here, but after the ballooning, it is completely open. So the results were immediately very, very good, however technique did not gain a lot of consensus,

mainly because people were afraid of rupturing the aorta, they dissect the aorta. So here's a Stabilise case, once again, acute setting, malperfusion, we do a carotid subclavian bypass because we are going to cover the subclavian artery, we deploy

the cover stent graft, then with one stent overlap, we deploy two bare stent devices all the way down to the iliacs and then we start ballooning from the second stent down, so you see Coda balloon is used here, but only inside the cover stent with fabric.

And then more distally we are using a valvuloplastic balloon, which is noncompliant, and decides to be not larger than the aorta. So, I need probably to go here, this is the final result, you can see from the cross-sections that the dissection is completely gone and

the aorta is practically healed. So you might need also to address reentries at the iliac levels, attention if you have vessels that only come from the false lumen, we want to protect them during the ballooning, so we have a sheath inside this target vessel, and we are

going to use a stent afterwards to avoid fragments of the intima to get into the ostium of the artery. And this is a one-year control, so as you can see there is a complete remodeling of the aorta, the aorta is no longer dissected, it's a single channel vessel, here we can see stents in two vessels that came

from the false lumen, so very satisfactory. Once again, please remember, we use compliant latex balloons only inside the the cover stent graft, and in the bare stents we use non-compliant balloons. We have published our first cases, you can find more details in the journal paper, so in conclusion,

dear colleagues, Stabilise does work, however we do need to collect high-quality data and the international registry is the way to do this, we have the Stabilise registry which is approved by our ethical committee, we have this group of initial friends that are participating,

however this registry is physician initiated, it's on a voluntary base, it is not supported by industry, so we need all the possible help in order to get patients as quickly as possible, please join, just contact us at this email, we'd be more than happy to include everybody who is

doing this technique according to this protocol, in order to have hard data as soon as possible, thank you very much for your attention.

- Thank you Louie, that title was a little too long for me, so I just shortened it. I have nothing to disclose. So Takayasu's arteritis is an inflammatory large vessel vasculitis of unknown origin. Originally described by Dr. Takayasu in young Japanese females.

The in-di-gence in North America is fairly rare. And its inflammation of the vessel wall that leads to stenosis, occlusion or aneurysmal formation. Just to review, the Mayo Clinic Bypass Series for Takayasu's, which was presented last year, basically it's 51 patients, and you can see

the mean age was 38. And you can see the breakdown based on race. If you look at the early complication rate and we look at specific graft complications, you had two patients who passed away, you had two occlusions, one stenosis, one graft infection.

And one patient ruptured from an aneurysm at a distant site than where the bypass was performed. If you look at the late complications, specifically graft complications, it's approximately 40%. Now this is a long mean follow up: this is 74 months, a little over six years.

But again, these patients recur and their symptoms can occur and the grafts are not perfect. No matter what we do we do not get superb results. So, look at the graft outcomes by disease activity. We had 50 grafts we followed long-term. And if you look at the patency, primary patency

right here of active disease versus non-ac it's significantly different. If you look at the number of re-interventions it's also significantly different. So basically, active disease does a lot worse

than non-active disease. And by the way, one of our findings was that ESR is not a great indicator of active disease. So we're really at a loss as to what to follow for active or non-active disease. And that's a whole 'nother talk maybe for another year.

So should endovascular therapy be used for Takayasu's? I'd say yes. But where and when? And let's look at the data. And I have to say, this is almost blasphemy for me

to say this, but yes it should be used. So let's look at some of the larger series in literature and just share them. 48 patients with aortic stenosis fro all were treated with PTA stenting.

All were pre-dilated in a graded fashion. So they started with smaller balloons and worked up to larger balloons and they used self expanding stents in all of them. The results show one dissection, which was treated by multiple stents and the patient went home.

And one retro-paret-tin bleed, which was self limiting, requiring transfusion. Look at the mean stenosis with 81% before the intervention. Following the intervention it was 15%. Systolic gradient: 71 milligrams of mercury versus 14. Kind of very good early results.

Looking at the long term results, ABI pre was .75, increased to .92. Systolic blood pressure dropped significantly. And the number of anti-hypertensive meds went from three to 1.1. Let's look at renal arteries stenosis.

All had a renal artery stenosis greater than 70%. All had uncontrolled hypertension. They were followed with MRI or Doppler follow up of the renal arteries. So, stents were used in 84% of the patients. Restenosis occurred in 50% of them.

They were, all eight were treated again, two more developed restenosis, they ended up losing one renal artery. So at eight years follow up, there's a 94% patency rate. What about supra-aortic lesions? And these are lesions that scare me the most for endovascular interventions.

Carotids, five had PTA, two had PTA plus stent. Subclavian, three PTA, two PTA. One Innominate, one PTA plus stent. One early minor stroke. I always challenge what a minor stroke is? I guess that's one that happens to your ex mother-in-law

rather than your mother, but we'll leave it that way. Long term patency at three years, 86%. Secondary patency at three years, 76%. Fairly good patency. So when Endo for Takayasu's, non-active disease is best. The patient is unfit for open surgery.

I believe short, concentric lesions do better. In active disease, if you have to an urgent or emergent, accept the short term success as a bridge to open repair. If you're going to do endovascular, use graded balloons or PTAs, start small. Supra-aortic location, short inflation times

I think are safer. And these three, for questions for the future. I guess for the VEITHsymposium in three years. Thank you.

- The only disclosure is the device I'm about to talk to you about this morning, is investigation in the United States. What we can say about Arch Branch Technology is it is not novel or particularly new. Hundreds of these procedures have been performed worldwide, most of the experiences have been dominated by a cook device

and the Terumo-Aortic formerly known as Bolton Medical devices. There is mattering of other experience through Medtronic and Gore devices. As of July of 2018 over 340 device implants have been performed,

and this series has been dominated by the dual branch device but actually three branch constructions have been performed in 25 cases. For the Terumo-Aortic Arch Branch device the experience is slightly less but still significant over 160 device implants have been performed as of November of this year.

A small number of single branch and large majority of 150 cases of the double branch repairs and only two cases of the three branch repairs both of them, I will discuss today and I performed. The Aortic 3-branch Arch Devices is based on the relay MBS platform with two antegrade branches and

a third retrograde branch which is not illustrated here, pointing downwards towards descending thoracic Aorta. The first case is a 59 year old intensivist who presented to me in 2009 with uncomplicated type B aortic dissection. This was being medically managed until 2014 when he sustained a second dissection at this time.

An acute ruptured type A dissection and sustaining emergent repair with an ascending graft. Serial imaging shortly thereafter demonstrated a very rapid growth of the Distal arch to 5.7 cm. This is side by side comparison of the pre type A dissection and the post type A repair dissection.

What you can see is the enlargement of the distal arch and especially the complex septal anatomy that has transformed as initial type B dissection after the type A repair. So, under FDA Compassion Use provision, as well as other other regulatory conditions

that had to be met. A Terumo or formerly Bolton, Aortic 3-branch Arch Branch device was constructed and in December 2014 this was performed. As you can see in this illustration, the two antegrade branches and a third branch

pointing this way for the for the left subclavian artery. And this is the images, the pre-deployment, post-deployment, and the three branches being inserted. At the one month follow up you can see the three arch branches widely patent and complete thrombosis of the

proximal dissection. Approximately a year later he presented with some symptoms of mild claudication and significant left and right arm gradient. What we noted on the CT Angiogram was there was a kink in the participially

supported segment of the mid portion of this 3-branch graft. There was also progressive enlargement of the distal thoracoabdominal segment. Our plan was to perform the, to repair the proximal segment with a custom made cuff as well as repair the thoracoabdominal segment

with this cook CMD thoracoabdominal device. As a 4 year follow up he's working full time. He's arm pressures are symmetric. Serum creatinine is normal. Complete false lumen thrombosis. All arch branches patent.

The second case I'll go over really quickly. 68 year old man, again with acute type A dissection. 6.1 cm aortic arch. Initial plan was a left carotid-subclavian bypass with a TEVAR using a chimney technique. We changed that plan to employ a 3-branch branch repair.

Can you advance this? And you can see this photo. In this particular case because the pre-operative left carotid-subclavian bypass and the extension of the dissection in to the innominate artery we elected to...

utilize the two antegrade branches for the bi-lateral carotid branches and actually utilize the downgoing branch through the- for the right subclavian artery for later access to the thoracoabdominal aorta. On post op day one once again he presented with

an affective co arctation secondary to a kink within the previous surgical graft, sustaining a secondary intervention and a placement of a balloon expandable stent. Current status. On Unfortunately the result is not as fortunate

as the first case. In 15 months he presented with recurrent fevers, multi-focal CVAs from septic emboli. Essentially bacteria endocarditis and he was deemed inoperable and he died. So in conclusion.

Repair of complex arch pathologies is feasible with the 3-branch Relay arch branch device. Experience obviously is very limited. Proper patient selection important. And the third antegrade branch is useful for later thoracoabdominal access.

Thank you.

- Thank you Mr. Chairman. Thank you, Dr. Veith for you kind invitation. Okay, there we go. Excuse me. DEVASS stands for Dutch EVAS study Group. We all know that women have a twofold, increased risk frequency of rupture.

The average aortic size at rupture is five millimeters smaller. They have a higher rate of undiagnosed cardiovascular diseases. They have smaller ileofemo

more concomitant iliac aneurysms They have a more challenging aortic neck. Smaller proportion is eligible for EVAR and, therefore less likely to meet EVAR IFU. They have a longer length of hospital stay after EVAR, a higher re-admission rate, more major complications,

a higher mortality rate. So, women and AAA is a challenging combination. The rationale behind EVAS is known to you all, I think. The DEVASS cohort is from three high volume centers in The Netherlands. It's a retrospective cohort of 355 patients,

included from April, 2013 to December 2015. So I have two years of result data. If you look at the baseline characteristics, 45 females were in this cohort, with the age of 76 and with some known comorbidities. They were within the instructions for use of 2013, at 28.9%

and even less in the IFU of 2016. These are some more anatomical characteristics with the AAA outer diameter 5.6 centimeters. This is the procedure, most of the patients were under general anesthesia, with the cutdown and the procedure time

was about 100 minute. Straight forward procedure 33 cases out of these 45. Let's have a quick look at the clinical outcomes. The re-intervention's done in the first 12 month. One patient had to conversion to open repair at month 11 due to type 1A Endoleak, and the others were not directly

related to the procedure itself. Although, there was thrombus in approximate stand. In the second month we saw, in the second year we saw some more type 1A migrations and a Stenosis that needed relining, and two out of these patients were within IFU.

If you look at the total cohort of type 1A Endoleak, one patient was not operated on and the other were, either open conversion or relining, and one patient was within IFU. A quick look at the death characteristics. Only one patient was within IFU,

and died after open procedure. So the re-interventions, once again, the first year four patients, in the second year five patients. Conversion to open repair, in total three patients. Endovascular re-intervention was performed

in the first year in two patients and in the second year there were three relinings performed. Endoleak 1A, in total six as stated before. No type two Endoleak reported, and in the first year five patients died, which one was aneurisym related, as in the second year, two patients died,

which one was aneurysm related. If we compare this data with the EVAS Global data, of two years not the three year data, this is the freedom from all persistent Endoleak, close to 98% which is good. Freedom from type 1A Endoleak is within IFU, 97% in the global and outside IFU 85%,

and remind these patients 71% were outside IFU. Freedom from secondary interventions, we had to re-intervene in nine patients and its comparable with outside IFU. Freedom from mortality at two years, a bit higher, aneurism related mortality is 95% which is higher, and also the all cost mortality is higher in women.

So to conclude, this is the first cohort that focuses on women after EVAS. The majority of the patients was outside IFU, and as in EVAR women do not that very good in result, appear to be very much like an EVAR. Thank you.

- 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.

- Thank you. Thank you again for the invitation, and also my talk concerns the use of new Terumo Aortic stent graft for the arch. And it's the experience of three different countries in Europe. There's no disclosure for this topic.

Just to remind what we have seen, that there is some complication after surgery, with mortality and the stroke rate relatively high. So we try to find some solution. We have seen that we have different options, it could be debranching, but also

we know that there are some complications with this technique, with the type A aortic dissection by retrograde way. And also there's a way popular now, frozen elephant trunk. And you can see on the slide the principle.

But all the patients are not fit for this type of surgery. So different techniques have been developed for endovascular options. And we have seen before the principle of Terumo arch branch endograft.

One of the main advantages is a large window to put the branches in the different carotid and brachiocephalic trunk. And one of the benefit is small, so off-the-shelf technique, with one size for the branch and different size

for the different carotids. This is a more recent experience, it's concerning 15 patients. And you can see the right column that it is. All the patients was considered unfit for conventional surgery.

If we look about more into these for indication, we can see four cases was for zone one, seven cases for zone two, and also four cases for zone three. You can see that the diameter of the ascending aorta, the min is 38,

and for the innominate artery was 15, and then for left carotid was eight. This is one example of what we can obtain with this type of handling of the arch with a complete exclusion of the lesion, and we exclude the left sonography by plyf.

This is another, more complex lesion. It's actually a dissection and the placement of a stent graft in this area. So what are the outcomes of patients? We don't have mortality, one case of hospital mortality.

We don't have any, sorry, we have one stroke, and we can see the different deaths during the follow-up. If we look about the endoleaks, we have one case of type three endoleak started by endovascular technique,

and we have late endoleaks with type one endoleaks. In this situation, it could be very difficult to treat the patient. This is the example of what we can observe at six months with no endoleak and with complete exclusion of the lesion.

But we have seen at one year with some proximal type one endoleak. In this situation, it could be very difficult to exclude this lesion. We cannot propose this for this patient for conventional surgery, so we tried

to find some option. First of all, we tried to fix the other prosthesis to the aortic wall by adjusted technique with a screw, and we can see the fixation of the graft. And later, we go through the,

an arrangement inside the sac, and we put a lot of colors inside so we can see the final results with complete exclusion. So to conclude, I think that this technique is very useful and we can have good success with this option, and there's a very low

rate of disabling stroke and endoleaks. But, of course, we need more information, more data. Thank you very much for your attention.

- I wanted to discuss this topic because some of us are more sensitive to DNA damage than others. And it's a complicated ethical issue. I have a disclosure in that I developed a formulation to premedicate patients prior to CT and x-ray. We all know that we stand in fields of radiation for most of our careers,

and we also know that many of us have no hair for example on the outside of our left leg. This is a picture that a bunch of us took for fun demonstrating this. But this is in fact radiation dermatitis. We know that the founders of our field

suffered consequences from the chronic high doses that they received in the 1920's. And they lost digits, they lost ears, they lost noses any many of them died of cancers or cardiovascular disease. The mechanism of injury is the x-rays

impinge upon water molecules in our cells. They create free radicals. These free radicals bind with our DNA and then Oxygen binds with that site resulting in an oxidative injury which can be reduced by the use of anti-oxidants.

I studied this over the last eight or nine years and I looked at the issue of chronic low dose radiation. Now this is different from the data that we collect from Nagasaki and Hiroshima and from Chernobyl and elsewhere. There are cancer risks but there

are also cardiovascular risks. And there are risks from chronic inflammation from increased reactive Oxygen species circulating with our system. I've been in touch with the IAEA recently about this and they didn't actually

realize that we don't wear our badges. So they thought the data they were getting on the doses that we were receiving were accurate. So that was a very interesting conversation with them. So cardiologists have been known

to get lifetime doses of of over one Gray. There's a lot of literature on this in public health literature. For example for every 10 milliSieverts of low dose ionizing radiation and received by patients with acute MI's,

there's a 3% increase in age and sex adjusted cancer risk in the follow-up five years. There's an excellent paper from Kings College London demonstrating that when endovascular surgeons were studied with two specific immunofluorescence tests, P53 and H2 alpha,

they were able to demonstrate that some endovascular surgeons are more sensitive to radiation dose than others. So why would that be? Well it's interesting if you look at this genetically and you look at the repair mechanisms

and in this whole thing I think in fact the lens is kind of the canary in the coal mine. When you get radiation induced cataracts, it's in the posterior chamber of the lens not the middle or anterior, which is where age-related injury occurs.

And this is the germinal layer or reproductive layer. The growth layer in the lens itself. And this is where cataracts develop. And this is really kind of a harbinger I think of injury that occurs elsewhere in our system. We know that when we wear DLDs on our chest,

on our bodies, on our arms, that the dose to the left side of our head is six times higher than to the right. In fact they dosed the left lens as higher than the right. And most of us who have lens replacements have it of the left eye.

This literature from adjacent fields that we may no be aware of. In the flight safety literature for pilots and stewardesses. There's extensive literature on cosmic radiation to flight crews who's doses annually are in the same range as ours.

So when you look at medical staff, you have to look at the overall context of the human in the Angio suite. Many of our medical staff will not be well. They may have chronic cardiac disease. They may be on say drugs for auto

immune disease or Methotrexate. They may have other illnesses such as Multiple Myeloma. They may have antibiotics on board that alter the DNA repair ability like Tetracycline. And they have chronic stress and sleep dysfunction. Cigarettes and alcohol use.

All of these things decrease their ability to repair DNA damage. If you look at DNA repair mechanisms, there are constantly the terms BRCA1 and two, PARP, P53, and ATM that show up. And deficiencies in these,

I'm going to skip all this to show you, can result in increased injury from a same dose being received by two different individuals. Now who is at risk from this is well understood in adjacent fields.

Here are 37 references from the public health literature related to mutations and SNPs or polymorphisms in DNA structure known to cause increased sensitivity to radiation. So I would propose that in, and here are papers on that topic

in adjacent fields that we don't read. So when we talk about personalized medicine for our patients, we need to also think about personalized career choices based on our DNA repair ability when we decide what we do. This has to be done in the context

of empathetic compassionate approach. It may begin with screening based on family history and personal history, and then advance in the right context to genetic screening through mutations and SNPs that can decrease their ability

to repair DNA damage from our occupational exposure. I'll skip all this because I'm out of time. But one other issue to think about, mitochondrial DNA is inherited purely maternally. So maternal DNA damage, mitochondrial DNA damage could be transmitted across generations

in female interventionalists. Also screening is important. It's emotionally complex. It's ethically complex. But it's an important conversation to begin to have. Thank you.

- Thank you Dr. Melissano for the kind interaction. TEVAR is the first option, or first line therapy for many pathologies of the thoracic aorta. But, it is not free from complications and two possible complications of the arch are the droop effect and the bird-beak. I was very interested as Gore came up with the new

Active Control System of the graft. The main features of this graft, of this deployment system are that the deployment is staged and controlled in putting in the graft at the intermediate diameter and then to the full diameter. The second important feature is that we can

optionally modify the angulation of the graft once the graft is in place. Was very, very interesting. This short video shows how it works. You see the graft at the intermediate diameter, we can modify the angulation also during this stage

but it's not really used, and then the expansion of the graft at the full diameter and the modification of the angulation, if we wished. This was one of the first cases done at our institution. A patient with an aneurysm after Type B dissection. You see the graft in place and you see the graft after

partial deployment and full deployment. Perhaps you can appreciate, also, a gap between the graft and the lesser curvature of the arch, which could be corrected with the angulation. As you can see here, at the completion angiography we have an ideal positioning of the graft inside the arch.

Our experience consisted only on 43 cases done during the last months. Mostly thoracic aneurysm, torn abdominal aneurysm, and patients with Type B aortic dissection. The results were impressive. No mortality, technical success, 100%,

but we had four cases with problems at the access probably due to the large bore delivery system as you can see here. No conversion, so far and no neurological injury in this patient group. We have some patients who came up for the six months follow-up and you see here we detected one Type 1b endoleak,

corrected immediately with a new graft. Type II endoleak which should be observed. This was our experience, but Gore has organized all the registry, the Surpass Registry, which is a prospective, single-arm, post market registry including 125 patients and all these patients

have been already included in these 20 centers in seven different countries in Europe. This was the pathology included, very thorough and generous, and also the landing zone was very different, including zone two down to zone five. The mean device used per patient were 1.3.

In conclusion, ladies and gentlemen, the Active Control System of the well known CTAG is a really unique system to achieve an ideal positioning of the graft. We don't need to reduce the blood pressure aggressively during the deployment because of the intermediate diameter

reached and the graft angulation can be adjusted in the arch. But, it's not reversible. Thank you very much for your attention.

- Thank you, Mr. Chairman. Thank you, Dr. Veith for inviting again to this great meeting. It's my disclosures. Well, as we know and heard this meeting, there are some certain limitations of current EVAR (mumbles) anatomical procedure and economical reasons,

and I would like to present a relatively new device which may address current EVAR limitations with a simple low profile system, and basically, ALTURA consists of two parallel stent graft systems. ZEUS No Gate Cannulation is needed and unique features include D-shaped proximal stents

and suprarenal fixation. Multi-purpose (mumbles) possibilities as well, and the system of utilize 14 French delivery system. And as aortic components can be deployed offset to accommodate the offset renals, and then the limbs are also unique

because they're deployed retrograde from distal proximally, and this allows precise positioning, both proximally and distally. Well, as the ALTURA clinical experience includes the very first human implants as well as more recent case performed

with a fully commercial device, and a total of 90 patients with a AAA were enrolled between 2011 and 2015, and follow-ups are taken at 30 days, six months, and annually to five years, and this presentation gives a current status of follow-up, and our results with a 12-month follow-up were published earlier this year.

Our clinical data were collected in total of in 11 sites. It includes 90 patients. And you see here, the patient demographics and anatomy do a typical, which are typical for all EVAR patients and the mean follow-up was 2.7 years. And procedure of success was 99%.

Only one patient, one of the first patient was Gen1 was not implanted, and 50% patients were done percutaneously, and majority of them underwent regional or local anesthesia. So when you look into the results, we see that there was only one case of AAA ruptured,

which occurred at three years due to type II endoleak and sac enlargement as the patient, which refused treatment due to type II endoleak. And all other deaths are paired to no original causes, and two patients had device migration at two years. The same patients appear at three-year period,

and basically these were undersized grafts was sort of our learning curve, and there was no any migration later on. Four patients had type I endoleaks visible on CT, and read by independent committee between 30 days and one year.

None have required secondary treatment and have been no aneurysm enlargement observed. And at one year, not surprisingly for this kind of devices, there was 17% type to endoleaks, but only one patient required secondary procedure due significant sac expansion.

Well, wasn't, of course, what we saw, I expected majority of patients has had shrinkage. There was a four-year period. And this is a patient who was recorded with the type IA endoleak at 30 days, caused by the last calcified nodule,

as you he's here probably none of the other device would tolerate that, but the endoleak did not extended into into the sac and had a leak result spontaneously without sac enlargement through a four-year follow-up period, as we're seeing here. Well, here another patient with type IB endoleak,

due to (mumbles) generation was treated with coils and glue an extension with additional stent graft to external iliac artery. What's interesting was the device. Device can tolerate small distal aortas and five patients who were treated

with small distal aortas and the very first patient was not dilated enough and stents were not deployed, simultaneously causing some stenosis which was easily treated with PTA afterwards, so we learned but it's very great, unique feature to treat the small distal aortas for the device.

And of course, sensing what happening with them, septal endoleaks, because everybody being concerned what happening with that, and nevertheless, there were no septal endoleaks observed during the follow-up period. In conclusion, Mr. Chairman, ladies and gentlemen,

I would like to say this Novel Altura endograft concept has potential to play major role in mainstream EVAR cases and potential benefits include predictability, reposition ability to place the device very, very, very precisely, offset renals, to maximize use of the neck, and low profile

overcomes current and anatomic limitations like tortuous iliacs, narrow bifurcation or access vessels and no limbic inhalation is needed, and basically, I truly believe that this offers option for EVAR day surgery and ruptured aneurysms. Of course, first results are very encouraging.

We need more data. 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.

- I have no disclosures. - So the eye lens is a highly radiosensitive tissue. And the radiation damage is a cataract, this is a cancer-like pathology resulting from mutating events. It's a posterior sub-capsular cataract. And in several studies we have seen quite a large number of interventionalists or vascular surgeons or cardiologists

showing this exact type of posterior lens changes, characteristic of radiation exposure. About half of the interventionalists in this study. The risk increases with duration of work years and decreases with regular use of protection. So the conclusion in this paper was

that radiation injuries to the lens can be avoided. By, for example, reducing the dose. So this is obvious that we should do in every way we can do it. And there are many steps shown in this excellent paper published in the European Journal of Vascular Surgery.

And, on top of that, of course, use radiation shields. And I've been focused today on different eye shields. So we tested the eye dose reduction with several commercially-available protection glasses and shields during realistic endovascular procedures in an experimental setting,

using phantoms and dosimeters at the front of the eyes, the left and the right eyes. And this was an EVAR protocol using a Siemens C-arm. So we tested the more modern sports glasses. The reduction to the left eye was only 15 to 50 percent, or in some glasses just 10 to 15 percent.

So much, much lower than what's promised in the brochure. The fit over glasses protected best, especially if you don't use them over personal glasses. So this is because of the, it's if there is just a small gap between the cheek and the glasses, there's scattered radiation pulsing in there.

And it also scatters on your face up to the eye lens. We also tested visors and you can see the effect of having them at a correct angle. They should be downward-angled, and you have a pretty good protection. But the best of all was the ceiling-mounted shield,

if it's properly used with a very high reduction, 90 to 95 percent. So this is an image from our hospital. I'm in the middle with these fit-over glasses that we have all now beginning to use. So in this paper, it was nicely shown that the position

of the shield also is very important. So it should be very tight to the patient and close to the femoral access. Other protective measures like these surgical drapes, we use them and there is a good additive reduction of radiation exposure

to the chest and hands, shown by this paper. But no one has ever related the reduction to the head or the eye. And the latest addition in our center is this zero-gravity suit that has been shown to significantly reduce radiation exposure

to the whole body, including the head and the eyes. So I think this is a very important new device. In this study, from the London group, we can see that adherence to use these kinds of shields is depressingly low. Use of lead-protective glasses was only 36 percent

among the operators and ceiling-mounted leaded shields, no one uses them, at that time at least. So, in conclusion, there are several radiation protection eyeglasses used today. They offer a highly limited dose reduction, giving a false sense of security.

A proper use of ceiling mounted lead shields is essential for adequate protection to the eye lens. And the protection eyeglasses and visors should only be used as a complement. And consider also using additional devices as full-body protection to maximize your protection, 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

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

- 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.

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- I'd like to thank Dr. Veith, program committee, and the moderators for the honor of presenting on this topic. Here's my disclosures, not relevant to this topic. One fairly large randomized trial, and a handful of retrospective studies have shown benefit to anticoagulation

and the patency of either prosthetic or high risk vein bypasses. And this data's formed the primary basis for what is common, but not universal surgical practice which is aspirin for standard vein bypasses or prosthetic to the above knee popliteal artery.

And then the addition of warfarin for prosthetic bypass below the knee or high risk conduits or poor outflow. But really, guidelines for medical therapy after low extremity bypass are weak and high variable. SVS guidelines recommend only antiplatelet therapy

and specifically say that evidence is inadequate to comment on anticoagulation. And guidelines from other important societies are largely silent on this topic as well. Of course we know that our bypass patients have other indications for anticoagulation.

Their coronary disease, there's cerebrovascular disease, and so ultimately, about 25 or 30% of bypass patients are discharged on anticoagulation. Enter the NOACs or the Novel Oral Anticoagulants. Instead of working on Vitamin K dependent factors, they either directly inhibit factor 10A or thrombin itself.

And many of the advantages are well known. These are approved for non-valvular AFib, DVT and PE, and I highlight a few of the approval dates here. I highlight dabigatran and rivaroxaban because these are two captured in the VQI data registry

that I'm going to highlight and show some data on. We hypothesize in this analysis that my colleagues and I performed that these are increasingly utilized as off-label anti-thrombotic therapy in PAD, and specifically in bypass patients.

And we wanted to do an analysis to look at the contemporary utilization of NOACs and their impact on graft outcomes and limb outcomes. WE looked at 19,000 bypasses in the VQI over three years. Now, we stared in 2014 because that's when NOACs were first captured in this data.

When you exclude patients who had less than one year follow up, and some other patients, we're left with about 7,100 bypasses, of whom about 3.5% were discharged after bypass on a NOAC, 21% on warfarin, 76% with none.

This graph plots the utilization over time of NOACs and warfarin. We see that warfarin utilization went from 24% on discharge in the beginning, to 15% over the time period and then correspondingly, NOACs increased from 0.6% of discharges to 6%.

We naturally looked at a lot of bypass patient characteristics to figure out which patients had been selected for either warfarin or NOAC, and they were actually similar. Tibial bypasses, prosthetic bypasses, and long operative times, that should be 300 minutes,

were all chosen for, at some form of anticoagulation. When we look at patency of bypasses on warfarin and NOACs, we see that those bypasses that are not placed on anticoagulation have superior primary patency and that bypasses on warfarin and NOACs have inferior and not different between the two.

The same holds true for assisted patency. And the same holds true for secondary patency where bypasses on anticoagulation inferior to those not on anticoagulation and no significant difference between warfarin and NOACs. When we look at freedom from major adverse limb events,

we see that again, a similar trend. Patients on warfarin and NOAC have inferior freedom from major adverse limb events compared to patients on no anticoagulation after their bypass. Naturally, we did multi varied analysis to look and see

if these were independent predictors of failure. And in fact, they were. Both warfarin and NOAC, even when you control for a variety of patient anatomic characteristics, both were independently associated with failed patency at the hazard ratios you see.

Other predictors of patency were things that are commonly described to date. Same thing is true with major amputation and major adverse limb events. Both warfarin and NOAC were independently associated with major adverse limb events after bypass.

Other factors associated with MALE have been described in the literature as well. So certainly, there are a lot of limitations to this sort of analysis. The registry might not capture important factors that influence the selection of patients

who receive NOACs or their outcomes. This is also limited by the fact that the only NOACs captured in this analysis are dabigatran and rivaroxaban, not the more newly approved NOACs. And this follow-ups naturally limited to one year.

But based on this retrospective data, we see that NOACs and warfarin are utilized after infrainguinal bypass in high-risk patients with high-risk graph characteristics. NOAC utilization is definitely increasing while warfarin is decreasing.

At one year, NOACs and warfarin were associated with worse mid-term graft outcomes and limb related outcomes even after controlling for other factors. And there was really no difference in the outcomes between NOACs and Coumadin. There's a lot of ongoing work in this area.

The COMPASS trial does include some patients of small minority who had previous low extremity revascularization, though they certainly were not all bypasses. Upcoming data from the Voyager-PAD trial where low dose rivaroxaban is tested against aspirin alone

may shed some light on optimal management of anticoagulation. But certainly, based on this data, ongoing study of the impact of NOACs on graft-related and limb-related outcomes is warranted. Thank you very much.

- Thank you so much for having me here. I must confess it's not my talk. It's Professor Veroux's talk. Veroux couldn't join us, so I hope you will forgive me if I cannot read it properly as he would have done. It's just a friendship act of being here.

Talking with you about the potential of these treatment of ventricular veins for relief symptoms, headache like. Professor Veroux published on PlosOne Single-center open label observational study was conducted from January 2011 to December 2015.

Basically focused on 113 headache positive patients. As you see there were different kinds of MS patients involved. 82 were relapsing emitting. 22 were secondary progressive. Nine were primary progressive.

Basically the including criteria included headache resistant to the best medical therapy. There was a bilateral internal jugular vein with a stenosis bigger than 50% of moderate to severe insufficiency of the flow. The stenosis of course were suitable for treatment

and they were followed up at least for 12 months. Basically the followup included a variation of the MIDAS, Migraine Disability Assessment Score. It was preformed the day before angioplasty. Then three months after angioplasty and then at the end of the follow-up.

As it was appears,. Of curse we can add the different kinds of lesions of the juvenile level. As it was previously reported, the Professor Veroux ended selection. It is mandatory in these kinds of procedures.

Adding the transversal defect the single most important criteria for determining if the PTA would be successful or not. Of course, again, transversal rather than longitudinal defects are preferred in the treatment of

this kind of patients. The exclusion criteria were the possibility of hypoplasia or extreme muscle compression. In particular, as you know there is the omohyoid possibility of compression.

Looking at a followup that is significantly of three years or more. The clinical results in these patients affected by headaches lead to significant reduction. And 86% of them with an improvement of the MIDAS scores in the three months following up.

At the same time, the improvement was maintained throughout the followup period up to three years. Mainly in the relapse remitting and the secondary progressive patients. So the conclusion of the investigation you can again (mumbles)

is that patient selection is mandatory, of course, again, on the transverse lesion mainly. Balloon valvuloplasty is feasible in these patients and has succeeded with a good result at three years followup in the MIDAS score. Of course, these findings are suggesting

that it could be a useful intervention for selected MS patients with persistent headaches and of course, non-thrombosis stenosis of the IJVs. Thank you so much.

- And I'll think I'll take just the next presentation or few minutes to describe the military's experience with and some of the rational and processes by which the military has developed this concept of resuscitative endovascular balloon occlusion of the aorta.

And maybe give some examples of how this is now being implemented into the military's more forward practice of causality care down range. So I have no relative disclosures to make as it pertains to this topic.

But I would say for context and I think we often overlook this, is this is really the first war, prolonged period of war, combat operation which was been concurrent with an endovascular revolution. We really describe this, the beginning of implementation of endovascular techniques

downrange in Iraq in the early 2000s. In this manuscript in the Journal of Trauma. And if you think about it as well, this is the first prolonged period of combat in which we have had endovascular trained surgeons So, many of the technologies and then the skill set

just didn't exist in previous long periods of conflict. During the Vietnam war or prior to that. So this is a major impetuous behind this. Both for research and innovation and application of skills that you've heard today. Whether it's stent grafts, coil embolization plugs

or other endovascular approaches. So this war experience coupled with the explosion of endo technologies in the civilian settings for age related disease has really lead the DoD now from our perspective to explore these new approaches and technologies including REBOA.

So it was an initiative path for us to look for control of noncompressible torso hemorrhage. We appraised and redefined balloon occlusion of the aorta as Tao and others have said, this isn't necessarily a new concept, but we did frame it in the concept of hemorrhagic shock and from trauma and injury

from the military standpoint in this 2011 Journal of Trauma procedures and techniques paper we really defined it as a strategy the military wanted to explore for torso hemorrhage and in this paper defined these zones of occlusion in a setting of trauma and hemorrhagenic shock.

We needed of course new and emergency amenable technology a lot of the existing endovascular technology is designed to be used in endovascular suites by highly skilled endovascular specialist and that's great when available, but certainly from our standpoint, we wanted

technology change to make this more amenable for forward situations. We described this in this Journal of Trauma manuscript and sort of show and depict the new technologies, trying initially to downside the catheter, make the balloon

inclusion catheter smaller, perhaps make them not dependent upon fluoroscopy and make them put the nitinol wire inside the catheter so that it does not need an accompany over the wire long over the wire for insertion. So this is a design in this case

for a one pass quick insertion of a ER-REBOA catheter shown or depicted here. We also had markers on the catheter which is fairly simple, but really remarkably was not present on any of our catheters to tell the depth of insertion

because they were all dependent up on fluoroscopies so these are some examples of new technologies that the military has pushed in this area of endovascular balloon inclusion. This has resulted in a commercialized device. The ER-REBOA catheter as one example by PryTime Medical.

This catheter is now been approved in a dozen or more countries world wide. And it has now more than 5,000 patient uses. For Hemorrhagic shock and in the emergency setting. It's now being used by US and other militaries in austere or forward settings

under protocol and under clinical practice guidelines that I'll mention in the next slide. So this technology and making balloon occlusion more amenable for the emergency use setting for hemorrhagic shock has evolved to this point. This is an example of what we would refer

to as rapid-cycle research development translation within a five or six year period, we now have this new device into our clinical practice guideline, this is public domain you can Google JTS CPGs for REBOA and you'll see here

this is actually the second clinical practice guideline the military has done rapid cycle evolution of its CPGs for REBOA and this is as described in the CPG as a resuscitative adjunct to blood resuscitation and other maneuvers, that Tao nicely described. We do have this deployed and it is

under CPG sort of guidance This is an example of a publication from just this last summer on the use of REBOA as a resuscitative adjunct by our special operations surgical teams or SOST teams, you see a typical operating room

or maybe it's at least one example of a far forward operating room. In which the special operation surgical teams are using not only low titer, type O whole blood transfusion as part of damage control resuscitation and damage control surgery, DCS and DCR.

But also REBOA, they've implemented now the use of these balloon catheters as an adjunct in more than 20 cases down range. We have now clinical registry data coming back from the use of this device. As a resuscitative adjunct, mostly as a perioperative

to enter hemoperitoneum in a patient that's shocked when you're in an austere setting without a lot of blood or surgical assistance. So it is being used now down range and that use is described in this reference. It's been described, REBOA's been

described by the Royal Navy. Actually in this Royal Army Medical Core journal paper from 2018. Where they talk about the use of this adjunct Afloat in a type of Role 2 type of setting. So not just by the US military,

but by many international militaries as well. And then finally we are extending this REBOA training paradigm, this is a Journal of Special Operations Medicine, a JSOM paper where many of our young surgeons are describing bringing REBOA closer to the point of injury and training

highly capable special forces medics and arterial access and this procedure. So in summary, you know we've written in this War on the Rocks commentary I refer you to for more descriptions of these topics. You know, we learn from but we don't plan for the past wars

in order to keep our national strategic edge of a sub-10% case fatality rate. We've got to try these new approaches, these new technologies. REBOA is one example of those. And now we have the need to gather clinical data

from this and other technologies to determine their optimal use. And requirements for future technologies. Thank you very much.

- Thank you for the opportunity to present this arch device. This is a two module arch device. The main model comes from the innominated to the descending thoracic aorta and has a large fenestration for the ascending model that is fixed with hooks and three centimeters overlapping with the main one.

The beginning fenestration for the left carotid artery was projected but was abandoned for technical issue. The delivery system is precurved, preshaped and this allows an easy positioning of the graft that runs on a through-and-through wire from the

brachial to the femoral axis and you see here how the graft, the main model is deployed with the blood that supported the supraortic vessels. The ascending model is deployed after under rapid pacing.

And this is the compilation angiogram. This is a case from our experience is 6.6 centimeters arch and descending aneurysm. This is the planning we had with the Gore Tag. at the bottom of the implantation and these are the measures.

The plan was a two-stage procedure. First the hemiarch the branching, and then the endovascular procedure. Here the main measure for the graph, the BCT origin, 21 millimeters, the BCT bifurcation, 20 millimeters,

length, 30 millimeters, and the distal landing zone was 35 millimeters. And these are the measures that we choose, because this is supposed to be an off-the-shelf device. Then the measure for the ascending, distal ascending, 35 millimeters,

proximal ascending, 36, length of the outer curve of 9 centimeters, on the inner curve of 5 centimeters, and the ascending model is precurved and we choose a length between the two I cited before. This is the implantation of the graft you see,

the graft in the BCT. Here, the angiography to visualize the bifurcation of the BCT, and the release of the first part of the graft in the BCT. Then the angiography to check the position. And the release of the graft by pushing the graft

to well open the fenestration for the ascending and the ascending model that is released under cardiac pacing. After the orientation of the beat marker. And finally, a kissing angioplasty and this is the completion and geography.

Generally we perform a percutaneous access at auxiliary level and we close it with a progolide checking the closure with sheet that comes from the groin to verify the good occlusion of the auxiliary artery. And this is the completion, the CT post-operative.

Okay. Seven arch aneurysm patients. These are the co-morbidities. We had only one minor stroke in the only patient we treated with the fenestration for the left carotid and symptomology regressed completely.

In the global study, we had 46 implantations, 37 single branch device in the BCT, 18 in the first in men, 19 compassionate. These are the co-morbidities and indications for treatment. All the procedures were successful.

All the patients survived the procedure. 10 patients had a periscope performed to perfuse the left auxiliary artery after a carotid to subclavian bypass instead of a hemiarch, the branching. The mean follow up for 25 patients is now 12 months.

Good technical success and patency. We had two cases of aneurysmal growth and nine re-interventions, mainly for type II and the leak for the LSA and from gutters. The capilomiar shows a survival of 88% at three years.

There were three non-disabling stroke and one major stroke during follow up, and three patients died for unrelated reasons. The re-intervention were mainly due to endo leak, so the first experience was quite good in our experience and thanks a lot.

- Good morning everybody. So first of all let me take note of it for the kind invitation to be here, again. These are my disclosures. So Juxtarenal Aneurysm has been described as those aneurysms very close to or even including in the lower margin of renal artery.

And of course the gold standard at that time was aortic supportive clamping and open surgery. Probably open surgery is still the first choice in this very short and complex aortic neck but what do in case of patients unfit for surgery? Or for patients who are asking for

a minor invasive alternative. Of course, Fenestrated EVAR are the solution, the option two, but they require time, are expensive, so what to in case of patients who have no time or cannot wait for this customization process?

Symptomatic patients, patients with huge aneurysm or patients just unfit for fEVAR because of either access or tortuous proximal neck anatomy. So solution is chimney or ovation VENT. What is ovation VENT? It's a kind of open chimney technique,

it's a combination of ovation with renal bare stent. So you know the the new concept of sealing of this stent graft, the circumferential apposition of polymer-filled ring to the aortic wall, typically at 13mm, so to just translate the length of the neck to a specific point

when a couple of millimeter when in that position of course. And you know with the previous, you have just heard the harder device, but with the standard device, the prime and the IX, we have the device positioned

13mm below the lowest renal artery. So, what to do in case of (unclear) when have no apposition of the ring to the aortic wall, we raise the ring, just very close to the renal artery, and then we place some bare metal stent

at the renal BMS. So here you can see our bench test with the fabric of the collars just moved by the bare metal stents. So, VENT is different from chimney, we don't use the covered stents so

it's a lowered provide bracket approach, and more importantly, chimney and endograft are typically competing for the same room so this the reason for gutters, while with VENT we have a stent and endograft, which are not competing for the same room.

The ring is responsible for the sealing and the stent is just responsible for the ventilation of the renal arteries. So this is a typical example, you can see here, a contained rupture aneurysm, in this point, and with a very short neck, so we decide

to land with the first neck and exactly at that level you can see here the steps of the procedure, the contemporary deployment of the renal stent, and the main graft the injection of the polymer, so the first ring is really in contact with the renal stent,

but they're not competing each other and so you can have a nice sealing of the sack. Another case, conical shaped neck, unfit for standard EVAR, unfit for EVAR, because was a huge aneurysm, much more than 8cm, so we decide again to raise the ring,

13mm and fit for standard ovation. And so here you can see the first ring just at this level, the renal stent, responsible for the patency of the renal artery, and you can see here that the first ring is just touching it in one point, the conical neck.

With good sealing. Again, another case with unfit for fEVAR, because of the small access, tortoise access, and so we plant a double VENT, in this case, you can see here again, prucodanus bracket approach, with five french shift,

contemporaneous deployment of stents, and first ring, again nice sealing, and nice follow up with completed sack screen cage, and another one year follow up. So, up to now we have performed 29 cases. We did the first case in June 2015,

technical success was high, 96.6%, we had just one type one endo-leak fixed introaperticaly with the coil embolization. The follow up is, mean follow up is 19 month, and 100% renal artery patency, no further intervention, no sac enlargement,

the majority of arteries, it's shrinkage more than 5mm. So just in conclusion, this option is in, we believe that in selected measures, it's a nice option. It is safe and effective when you can not wait for fenestration graft, like in case of symptomatic

or huge aneurysm, or just patients are unfit for fenestration because of tortuous anatomy or small iliac vessels. Thank you for your attention.

- Thank you very much for the presentation. Here are my disclosures. So, unlike the predecessor, Zenith Alpha has nitinol stents and a modular design, which means that the proximal component has this rather gentle-looking bear stents and downward-looking barbs.

And the distal part has upward-looking barbs. And it is a lower-profile device. We reported our first 42 patients in 2014. And now for this meeting we updated our experience to 167 patients operated in the last five years.

So this includes 89 patients with thoracic aneurysms. 24 patients in was the first step of complex operations for thoracoabdominals. We have 24 cases in the arch, 19 dissections, and 11 cases were redos. And this stent graft can be used as a single stent graft,

in this case most of the instances the proximal component is used or it can be used with both components as you can see. So, during the years we moved from surgical access to percutaneous access and now most of the cases are being done percutaneously

and if this is not the case, it's probably because we need some additional surgical procedures, such as an endarterectomy or in cases of aorto-iliac occlusive disease, which was present in 16% of our patients, we are going to need the angioplasty,

this was performed in 7.7% of cases. And by this means all the stent grafts were managed to be released in the intended position. As far as tortuosity concerned, can be mild, moderate, or severe in 6.6% of cases and also in this severe cases,

with the use of a brachio-femoral wire, we managed to cross the iliac tortuosity in all the cases. Quite a challenging situation was when we have an aortic tortuosity, which is also associated with a previous TEVAR. And also in this instances,

with the help of a brachio-femoral wire, all stent grafts were deployed in intended position. We have also deployed this device both in chronic and acute subacute cases. So this can be the topic for some discussion later on. And in the environment of a hybrid treatment,

with surgical branching of the supoaortic tranch, which is offered to selected patients, we have used this device in the arch in a number of cases, with good results. So as far as the overall 30-day results concerned, we had 97.7% of technical success,

with 1.2% of mortality, and endoleaks was low. And so were reinterventions, stroke rate was 1.2%, and the spinal cord injury was 2.4%. By the way we always flash the graft with CO2 before deployment, so this could be helpful. Similar results are found in the literature,

there are three larger series by Illig, Torsello, and Starnes. And they all reported very good technical success and low mortality. So in conclusion, chairmen and colleagues, Zenith Alpha has extended indications

for narrow access vessels, provide safe passage through calcified and tortuous vessels, minimize deployment and release force, high conformability, it does retain the precision and control of previous generation devices,

however we need a longer term follow up to see this advantages are maintained over time. Thank you very much.

- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans

can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.

But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.

What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?

Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for

all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',

and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.

He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.

So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.

It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,

and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after

you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,

and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.

That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.

How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.

But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.

In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,

the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors

such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants

to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study

because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.

So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist

on maximal protection and assume that all radiation is dangerous. Thank you very much.

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