Create an account and get 3 free clips per day.
Chapters
Portal Vein Thrombosis, Varices | Splenorenal Shunt, Stenting | 21 | Female
Portal Vein Thrombosis, Varices | Splenorenal Shunt, Stenting | 21 | Female
2016accessadrenalanchorarterybluntcavernousembolizationepisodesesophagealexpandingfemoralfollowicastnegotiateocclusionPatentpercutaneousportalrenalscanshuntSIRsplenicstentthrombosedtransplantveinvenous
Role Of Endovascular Treatments For Pediatric Vascular Trauma
Role Of Endovascular Treatments For Pediatric Vascular Trauma
Blunt Thoracic Aortic TraumacookendograftEndovascular StentingZenith Endograft
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
Vacuum Assisted Thrombectomy With The Penumbra Indigo System For Visceral And Lower Limb Artery Occlusions
Vacuum Assisted Thrombectomy With The Penumbra Indigo System For Visceral And Lower Limb Artery Occlusions
Aorto-Renal BypassAspiration SystemGore Viabahn VBX (Gore Medical)PenumbraPenumbra’s Indigotherapeutic
Panel Discussion (Session 62) 2018
Panel Discussion (Session 62) 2018
Aspiration SystemPenumbraPenumbra’s Indigotherapeutic
Oh My: The Stent Got Away, Now What
Oh My: The Stent Got Away, Now What
Endovascular StentingLt IF DVT
Terumo Aortic Relay Thoracic Endograft For TEVAR In Complex Aortic Pathology With Angles >90°: Advantages And Results
Terumo Aortic Relay Thoracic Endograft For TEVAR In Complex Aortic Pathology With Angles >90°: Advantages And Results
Gore Tag (Gore Medical) / Valiant (Medtronic) / Zenith Alpha (Cook Medical)RelayPlusstent graft systemTerumo Aortictherapeutic
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
GORE MedicalGORE VIABAHNL EIA-IIA bypassleft carotid subclavian bypassstent graft systemTBAD with TAAAtherapeutic
Octopus Technique To Treat Urgent Or Ruptured TAAAs With OTS Components: What Is It, Technical Tips And Results
Octopus Technique To Treat Urgent Or Ruptured TAAAs With OTS Components: What Is It, Technical Tips And Results
6.8 cm TAAAGORE MedicalGore Viabahn VBXOctopus Endovascular Techniquestent graft systemtherapeuticviabahn
Which Stent Would I Use In: Malignancy, Across Inguinal Ligament, IVC, Into Profunda Femoris Vein
Which Stent Would I Use In: Malignancy, Across Inguinal Ligament, IVC, Into Profunda Femoris Vein
Bardo Venovo / Medtronic ABRE / Optimed SInus oblique / Veniti ViciCook Zilver VenaMedtronicstent
Going Rogue: Off The Grid Venous Malformation Sclerotherapeutic Techniques
Going Rogue: Off The Grid Venous Malformation Sclerotherapeutic Techniques
coil embolizationPersisting Venous MalformationsclerotherapyTherapeutic / Diagnostic
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
Transcript

vein thrombosis, portal hypertension, esophageal variceas. She's got ulcerative colitis, ITP, SLE, so she's got a lot of disease process going on. She's had multiple episodes of upper GI bleed with transfusions and endoscopic banding and she had a subselective splenic artery particle embolization four years earlier at age 17.

Despite this whole slew of medical issues, she is sitting across from me in a concert room, with a perfectly normal 21-year-old going to college, and she's just socially adept, the whole nine yards

so she really didn't match as opposed to, Tim s talking about his case of the worst protoplasm, she looked like she didn't have all these issues going on. So here is some representative images of the CT scan showing the portal venous system which has glued varices. Here's a chronal reconstructions again so these cavernous transformation here but there's really occlusion

of the portal vein. Here is the splenic vein coming around and its sort of blunt here, so we have occlusion of the portal. And as I'm scanning through this again, you look here, here is the left renal vein, and in here is the adrenal vein coming up sitting

right next to the splenic. And again splenic is not knocking on the door just like two cases ago that I showed the vorax/g sort of knocking on the door of the IVC. And having transplenic access in our monitrium, like okay, we can do this, we can just bump into this puppy.

Here is some chronal reconstruction, showing the same thing. Here is the renal vein coming across, here is the adrenal renal coming up and sitting right next to the splenic vein. So again our options include,

sitting down, again this is where you have to work very closely with your transplant surgeons. I was talking with the small bowel transplant surgeon and we were reviewing this case for a possible TIPS, but what are the options? Surgical spleno-renal shunt here,

follow up is splenic artery embolization, percuteneous spleno-renal shunt. So again after seeing this, okay lets give this a shot. I'm thinking, hey this has never been done before. It's been done before obviously.

So this is a group from Australia that published in the American Journal of Transplantation just last year. They called it a percutaneous retroperitoneal spleno-renal shunt. Do you have any thoughts on the- [LAUGH] We were talking yesterday how Americans

are getting a lot of control here. But nonetheless we said, okay let's give it a shot here. Work for us with going from the IVC to the barracks. Let's give this

to throw. So basically gain percutaneous access to the splenic vein. It did run, and here's the splenic vein, here is the SMV rather, and then there's really no portal venuos system to be seen here. This correlates is very well to the CT images that we saw.

That's why again I love the preprocedural imaging. And here's further on the run this is almost like an abdominal Moyamoya more or less. You see really nothing. All these cavernous transformations and varices going into the liver and all these gastric and esophageal varices.

From the femoral vein we got up into the left renal vein and then the left adrenal. And here is our transsplenic access. You can see how they are crisscrossing here. Here's a run from the splenic venous side. We put up a little GooseNeck Snare into the adrenal vein,

used a Chiba needle to just get across that short distance we saw in the CT scan able to pass an 018 wire, snared it, pulled it through and we have through-and-through access from the splenic vein through the

femoral vein. We placed a 7 x 38 iCAST stent. Here is our run afterwards, widely patent, splenorenal shunt. We did a run. Everything washed through.

Had a talk before a round of high fives all over the place. Here's the spleno-renal shunt again, widely patent, great positioning. This is the CT scan, the follow up CT. And as you can see here is the renal vein and here is the covered

iCAST stent and with the tip of it just sort of against the far wall. So, if you look a little closer here, we were thrombosed so, so much of those high fives. We got back up from the groin,

we got up into the adrenal vein. As you can see we did a run. This is fully thrombosed. Got back in to spleen, got through. We placed a self-expanding

stent to anchor on either side. And therefore it would be up against the wall. We declotted the whole shunt. We did another run, you can see brisk flow through to the IVC. Get a full CT scan a day later, thrombosed again.

We declotted again thrombosed again. So she's got this innate antiphosolipid syndrome, she's got oscholitis. So she's just prone to clot. Unfortunately in this case as I said could we have stented further in a little earlier,

and precluded the first thrombosis? For sure. And that's a horrible lesson to learn there and she's just a case where it might be very difficult to keep this thing open. Long story short, we ended up gluing the spleen. She wanted to avoid that initially after she had very unpleasant experience the first time with her upper [UNKNOWN] embolization.

But in six months follow up, she's had no further bleeding episodes and she's already follow up endoscopy. I think what's key about this case though is it shows you that once you start expanding on certain levels, just gaining transsplenic

access, it opens a door to a whole new school of different procedures that you can do that you never really looked at before. You're looking at now where are these vessels in relation to others, because you're opening up new doors. I mean, just like transrenal access is opening up new doors for doing UVs and TACE/g and Y-90.

I think that transplant approaches really allow us to do a lot more in the portal venous system. >> Great case quick question I didn't catch why you had to go transsplenic the second time around. You already had a stent [INAUDIBLE]. >> Correct so it was fully thrombosed and we could not get back

into the stent. And if you look the CT scan here is the renal vein, and the stent is against the sort of wall renal vein. So we cannot negotiate this,

and I think that's one of the reasons in the addition to her hyper [UNKNOWN] state that this thrombosed to begin with. because despite in the AP projection, this looking great, I think posturally it was against the wall, and we could not negotiate

that. We had hoped to negotiate it from below and that was our goal but it didn't work out. >> Do you think the gut crush between [INAUDIBLE] CT the back end of it [INAUDIBLE]. >>The back end was still why widely patent and you're talking about this stent?

>> The front end. >> I still think that was still patent we got through, and I think this is just, if you look at this, if I could magnify this up, I think that's fine. I think it's just, this is covered, this is covered, and this is

really where the fluid should be, and really didn't recognize it, the old DR thing, I think it was an IVU I think if we had done some [UNKNOWN] maybe we would have appreciated a little bit better.

But it was a prolong case and we thought that it looked great but in retrospect, similar to the case, where we were anchoring down with this self expanding stent and which we ultimately did here. I think that on almost all of this where we were using a covered stent, that's probably gonna be the way to go anchor with self

expanding stent, to make sure that the covered stent doesn't really go to posture wall like in this case. Yes. >> Why did you [INAUDIBLE] >> If you look at the portal venous system it had been out chronically,

so as I said initially she had a partial splenic artery embolization at age 17. So this process had been going on for at least five or six years. And if you look at the CT scan,

again this is blunt here and if you look at the CT, there is really nothing in regards to [UNKNOWN] portal vein essentially. Our goal was to give it a shot we probed around a little bit here but having seen nothing on a CT scan from 4 to 5 years to this, we were very, not confident that's just anything that's you work

to try to get into here. If you look at this is just messier there's really nothing to re-canalize [BLANK_AUDIO] >> Okay thank you. >> Thank you everyone. That brings us up to the end of the session so great questions and

hopefully you'll all leave here with a few more tricks up you sleeve for those challenging TIPS and portal cases.

- Good afternoon. So as we've already heard, traumatic injuries are the leading cause of death and disability in children over the age of one. Fortunately, these types of injuries are relatively infrequent, most commonly involving the lower extremities, for example femur fractures,

causing disruption of the SFA or popliteal artery, or the upper extremities, supracondylar humeral fractures will cause damage to the axial or to the brachial artery. Retrospective review of a children's registry from 1993-2005 with 103 patients all of whom were under the age of 18, most were males.

The majority are penetrating wounds. And most frequently, the extremities were involved. Open surgical repair was favored, primary repair when possible, vein patches for use for those under the age of six, and an interposition graft or bypass was used

for those over the age of 12. Non-operative management was selectively chosen in about 10%, and the outcome in this cohort, 10% mortality, 11 amputations, and limb length discrepancy did become a problem over time, necessitating revascularization in 23%.

A nationwide Swedish registry from 1987-2013 looked at 222 patients, children under 15. In this scenario, 2/3 were male, 2/3 had blunt trauma. Once again, upper extremity injuries were more commonly seen in those under 10. Lower extremity injuries more frequently seen

in those between the ages of 11-15. With that cohort that we talked about, 96% were treated with open surgical repair, similar to what we saw before. Interposition grafts, vein patches for the young, and primary repair whenever possible. However, endo therapy was introduced in this scenario,

with eight patients undergoing intervention for axillary, subclavian artery, iliac, and aortic trauma. A summary of four large series was pooled here, and essentially shows you once again the majority of the injuries are in the extremities. The gold standard to date remains open surgical repair,

either with patch, endo anastomosis, or interposition graft, depending on the age and the location. Lajoie presented this abstract, which is a single center retrospective review, nine years, 60 patients, all under the age of 18. And once again with vascular trauma pediatric group,

majority of treatment is with open, however 16% underwent endovascular intervention with embolization, stents, and stent grafts utilized. None of the stents were implanted in anyone under the age of 13. Follow-up six weeks showed no difference

in the amputation rates or the mortality rates, however reinterventions were certainly higher in those who underwent endovascular therapy. National Trauma Databank from 2007-14 of pediatric trauma under the age of 16. 35,000, so it's a very large cohort.

And you're going to see here, it's not just a trend. This was statistically significant. There is an increase endovascular therapy utilization across the board in that time frame, and specifically for blunt trauma, increasing from 5.8% up to 15.7%.

And what you can take away from this is that the increased endovascular therapy was utilized in children over 12, larger hospitals, level one trauma centers, and those who resided in northeast. In addition to that, those who had a higher

injury severity score also underwent endovascular therapy. The most common procedures, embolization of the internal iliac, and TEVAR for blunt aortic trauma. Unfortunately, despite this, the in-hospital survival failed to improve.

So now there's a plethora of data out there, and multiple single-site institutional reviews of their own experience. Here's what I can say. I think there are some select indications for which endovascular therapy appears to be advantageous.

Without question, as you've heard already, the blunt thoracic aortic trauma. Here's a 17-year-old, fell from a seven-story building and successfully underwent endovascular intervention. Another case, a 16-year-old gunshot wound to the thigh, injury to the profunda femoris was a large

false aneurysm in the anteromedial thigh, who underwent coil embolization successful exclusion of this area where the pseudoaneurysm happened to be, but maintained perfusion through the SFA and the remaining branches of the profunda. Is there a role here for blunt femoral trauma in the child?

Well, I'm not a big fan of it, doing it in adults, but there is a paper on it. 13-year-old popliteal artery trauma, high ISS score, this occlusion was recanalized and a self-expanding stent placed. And I will note that a bridging technique was utilized.

Once the other injuries were addressed, the patient underwent bypass. 12-year-old with polytrauma, iatrogenic orthopedic screw injury to the SFA, successfully treated with a Jomed stent, and then planned bridging procedure,

who underwent open repair a few days later with an interposition vein graft from the contralateral leg. One more case, 14-year-old polytrauma, self-expanding covered stent placed for an axillary artery injury, and this was a planned procedure as a bridging technique. He, unfortunately expired prior to that opportunity

to perform the bridging technique on him with a bypass. So, in summary, I do think pediatric vascular injuries are uncommon. Open repair, once again, remains the gold standard. Endovascular therapy appears to be increasing, especially TEVAR and embolization.

Endovascular therapy in the extremities is an option as a bridge in older people over 12 who have higher ISS scores. And a nationwide pediatric database for arterial trauma would be beneficial. 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- When stenting are not enough, venoplasty stenting is undoubtedly the treatment of choice in relieving iliocaval obstruction and we have no doubt on what we can technically today obtain with this technique. But open surgery still has a place. The place for the iliocaval segment is today limited

only to oncological patients, their trauma. The disease, given by PTS, is not justifying an open surgery on those segments. But in some cases, at least less than ten percent in our federal center like we are, endovascular technique alone may be not sufficient

to provide durable patency of the iliocaval stenting. An open surgical approach, limited to the common femoral vein, can be required in addition to iliocaval stenting. And I would like to underline that open surgery should not be confused with open access

in event of catheterization failure. It's completely different. At the end, what we apply is endophlebectomy, which is the surgical removal of intraluminal fibrotic tissues. And contrapulizes of the extraluminal damage.

After endophlebectomy, the caliber of the vein is restored by means of bovine pericardium patch. In order to go back to the normal anatomy. Which are the indications for this type of operation? The main indication is to improve the inflow. When the deep femoral system confluence

is inadequate or the axial system is not preserved we have to try to improve the inflow at that level. And it is an essential moment to get a stable patency in the iliocaval segment. The second indication is to provide sufficient room for adequate stent expansion.

If there is lots of rubber and hard tissues that occupies the commofemoral vein, maybe in the long term, the stent can be sufficiently, adequately expanded. And if we remove this tissue we can get a better stent deployment.

The third indication is to reconstruct the vein conduit when it has been lost. This may happen after trauma, after drug injection, and after heterogenic problem. When the vein wall is too damaged, to be treated only by stenting or

only by endophlebectomy, a new conduit can be maybe the better option. What we apply today is a tubulization of bovine pericardium in order to obtain a correct way. And this is probably what we have to underline much more than everything else,

it is a type of hybrid procedure. The operation of endophlebectomy on new oxcilization are rarely performed alone today. We should go down with the stent if required to cover the endophlebectomy area and to treat iliac obstruction in the same moment.

As we listen before, the endophlebectomy limits is to open up the deep femoral conference and the stent usually stop over there. And it is essential because at the present, if we do not apply this, we can say, a kind of protection way to treat

the endophlebectomy segment, its difficult to maintain a long term patency. In this type of operation at the present, we do not apply anymore AV fistula which was limited in our historical work. I would say that today, open surgery

and hybrid procedures are essential in post traumatic treatment strategy. Outcomes in complex cases can be strongly improved. And I would like to underline that it is complex cases. This is not a surgery that is applied in every case of iliocaval stenting.

Its, there has to be attentively, selected because this type of surgery is undoubtedly very delicate, but we can get very good results and despite what we can think, get a good patency over time. It can really today be something

that we can obtain quite attentively. Thank you so much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- My disclosures are not relevant. Joe showed this slide, this is the original SVS guidelines, which really, as he mentioned, is a lesion-based evaluation of what the trauma looks like. And, for the purposes of this discussion, we'll be focusing on grade three injuries. Which really means there's blood outside the aortic wall.

There is loss of integrity of all layers and there's a pseudoaneurysm. We've all transitioned to delayed TEVAR for grade one and two. But, what do we do with these grade three injuries? Where's the boundary between medical therapy

that puts the patient at risk of interval rupture and early repair? Which may, as I'll show, put them at risk of other problems. This is a pretty widely adopted prac the idea of treating traumatic pseudoaneurysms,

at least initially, with some medical therapy. This is a review of 18 studies, almost 1,000 patients. It showed really one in five were managed non-operatively. There is a very low rate of aorta-related mortality which will be a recurring theme on all the data I show you. And, there's a really low rate

of required late interventions. As true for many of our trauma-related literature, there's a really poor long-term follow-up rate. The AAST studies have shown us that delayed repair really can improve outcomes. There's a significant selection bias in

these are non-randomized trials for, I think, exclusively. But the reality is, if a patient can wait until stabilization of their other injuries, they do better if you can wait on repairing the aorta, both mortality and the paraplegia rates are lower.

But, it's not just completely a selection bias. There are maybe some other benefit here. And, one of the things that plays into play is: What are their other injuries like? What is their traumatic brain injury look like? And, we use this as a defining point at Grady

about figuring out whether someone really should be figured for early repair or not. If you look at this series of 300 patients with traumatic aortic injury, 248 had a concomitant brain injury, and those are obviously of a variety of different grades,

from a little blip on the CT scan to a potentially devastating neurologic insult. But, it's not uncommon to have to manage both injuries at the same time. That is the rule rather than the exception. They can be pretty significant

and, again, there's significant selection bias in this series out of Maryland. But, there's about a one third, one third, one third early repair, delayed repair or non-operative strategy. If you look at the non-op patients and the delayed patients, you can see

that we get to that very, very low mortality rate. The early repair patients, as you can imagine, are often associated with a fatal outcome. Now, that fatal outcome is not always a it is usually related to something else

and highlights the selection bias of series like this one, that show us that if you're sick when you come in with an aortic tear, you're going to continue to be sick regardless of whether we fix your tear or not. But, there is some other benefit, potentially. The traumatic brain injury is one piece that I've mentioned,

but it's not uncommon, I think we've all experienced situations like this where the trauma physician and the orthopedic physician and everyone who is taking care of these patients is really focused on a grade three aortic injury. And, it oftentimes allows for neglect

or missing of other injuries that may be more life-threatening. How do we avoid delay? There's a few areas where we can think about intervening. The first thing is getting a good radiographic grade, as Joe alluded to, and there's a variety

of different scoring systems. This ultimately amounts to a simplification of the Harborview scoring system which is the one that I personally have gravitated to over the last two years. Which demonstrates that for the old grade one and two

there is probably no benefit of repeat imaging, there is probably no benefit of intervention, and pseudoaneurysms should be fixed when they are stable and severe ongoing-rupture patients should be fixed right away. That assessment of stability is an important part of this.

Part of Dr. Crawford's interest, in particular, was evaluating the size of the pseudoaneurysm and the size of the hematoma. And so, all of these are things that we've seen before but they all probably behave a little bit differently. So, how do we look and see:

Are there specific types of injury that are more prone to rupture with non-operative therapy? And one of the things that's been assessed is the diameter ratio. I think Joe showed this data a second ago. Another is the size of the periaortic hematoma.

In this large series, if you had two of these three factors: a lactate greater than four, a mediastinal hematoma greater than 10 millimeters or a lesion to normal aortic ratio of greater than 1.4. That was 90% accurate in terms of theoretically predicting early rupture.

Which, if you just look at clinical judgment alone, goes down to 65%. Keeping in mind that clinical rupture, true rupture is very often a fatal event. There is a lot of value in moving that number from 65 to 90. If we can get good modeling that tells us

who is at particularly high risk of rupture in this selected group, there is a lot of potential benefit. Just as importantly, as I've mentioned earlier, if you have a higher aortic grade of injury, you are more likely to die but it does not predict aorta-related mortality.

Much of that is the selection bias that people with higher grades of aortic injury are fixed sooner and therefore are not candidates to die from aorta-related mortality. Let's skip through this. And then again, (audience member coughing)

the idea that we need additional information and we need better imaging, better physiologic data that predicts the need for early repair is the take-home message. The answer, as you can imagine, is more information. Part of what the Aortic Trauma Foundation is doing

is going to be evaluating: Are patients really going to do better with non-operative therapy if they have very specific criteria that allows them to be selected out? Are there high-risk criteria that we can figure out besides just eyeballing the CT scan and saying:

This is someone who's not going to do well if we sit on them. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

on a nice, long day.

- This, yeah, I'm not quite sure why I seem to always get this talk. Maybe its because I do have more screw-ups or just show them in a more ridiculous fashion. There's no significant disclosures relative to this, apart from the fact that I'm seriously embarrassed. I'm actually not going to talk about stent migration,

because in the last year or two there's an absolute epidemic of stents being reported in the right atrium, pulmonary artery, floating in the IVC. In one state alone, there's been a 10,000, sorry 1,000% increase in the amount of venous stents placed in the past year,

or past two years. So that is somewhat worrying to me. I'm frankly amazed when iliac stents migrate and I'm always amazed when renal stents don't migrate. And there's a nice image of an echo of, I think that's a wall stent in the right atrium.

That heart doesn't look so good. And here's one being fished out very cleverly out of a pulmonary artery. How they ever got there is kind of amazing. I think patients either with no stenosis or totally mis-sized stents were being used.

No, I'm going to talk about something even worse, and that is, not worse in terms of patient outcome, but it is more embarrassing. So typical patient that we see who was managed conservatively with an iliofemoral deep vein thrombosis and presented about nine months later

with weight gain, venous claudication for which we have no objective measure. But no ulcers and no visible post-thrombotic syndrome. And for reasons that known only to myself and I don't know why I did it, I decided to go up and over from the right groin to try and cross

this left iliofemoral venous obstruction. And I'm not sure how well it projects, but essentially we're getting a TriForce Cook device and a roadrunner wire down here, and in due course we crossed the lesion, and we did a videogram And that looks pretty good.

And so we go on, pardon me, I'll try and go on. And this is a venogram from an oblique view. And again, nothing difficult about this. This is all fairly straightforward. We do a balloon dilatation and there is our final completion stent.

And I'm feeling fairly good. She was feeling quite uncomfortable because the urethral catheter we had difficulty getting in and it's possibly a little bit not concentrating hard enough on that. And so I saw the next day as per standard practice

and was doing my ultrasound. But her leg clinically hadn't improved much at all. And I was, I just wasn't happy with the ultrasound. There wasn't, I couldn't figure out exactly what was wrong. There was certainly flow in the stents and there was flow below.

But it just didn't look right. So I did a CT and admittedly there is a radiation cost here, but just we'll have a little look at this and, yeah, okay. So we'll look at that again, because it isn't quite humiliating enough the first time around. Let's just concentrate just in here, um, yeah.

This is one of these unusual Irish patients where the femoral vein in fact passes posterior to the inferior pubic ramus, otherwise known as the obturator vein. Somewhat embarrassing, and on a sagittal reformatted, it looks just even that bit better. So, you can see it coming in beautifully,

right out the back here. So she was actually incredibly cool about it, I just said, you know, I've screwed up and we've made a mess here. And that's a single shot of it there. You can see that I've placed it into the obturator vein.

And, so then at that stage I go from above and its partially thrombosed. I puncture from below and get access to the stent. And then you can see here we've gone in the correct access here, through the interstices, and now we have actually a straight shot

and then I'm snaring my wires so you're back to first principles and just do things properly after that. And then ballooning here and now this is the only same time you'll see a bifurcated stent of this fashion. And you can see here that we have eventually good flow

in a correct orientation. I've taken out my little sheath here, so there's a small leak here. This is what cone-beam CT looks like. You've got a double stent system here, which then splits right there into the occluded obturator

and the patient common femoral. And she's actually done very, very well since that time. And this her own follow-up and you can see the stent is widely patent. So, although the stent didn't get away, it certainly was misplaced.

Lessons for me, trust your gut. If you think there's something wrong, there is usually is. And I remember Mike Dick years and years ago saying, "Just sit down, take off all your leads, and go into your room, and just think for a few minutes,

before you do the next step." And I wish I had done that at the time. 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.

- 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 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

3

- 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 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 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.

- 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.

Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.