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Hepatic Ischaemia, Necrosis | Splenic Embolization | 35 | Female
Hepatic Ischaemia, Necrosis | Splenic Embolization | 35 | Female
2016angiographicarterialarteriogramarterybranchesceliacembolizedfindingshepaticimprovementischemicliveroperativelyparenchymalperfusionperipheralrobustSIRsplenicsplenomegalytransjugular
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
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Role Of Endovascular Treatments For Pediatric Vascular Trauma
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4 branch CMD TAAA deviceacuteAscending Graft Replacementcardiac arrestRelayBranchRepair segment with CMD Cuffruptured type A dissection w/ tamponadestent graft systemTerumo Aortictherapeutic
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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
Panel Discussion (Session 62) 2018
Panel Discussion (Session 62) 2018
Aspiration SystemPenumbraPenumbra’s Indigotherapeutic
Sail Valve
Sail Valve
Sail ValveVeno ValveVenous Valve
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
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Transcript

So here's my first case. This is a 35 year old female with PSC and went on liver transplant and post operatively developed increased LFT's and underwent a transjugular liver biopsy

found that she had extensive necrosis, lobular necrosis consistent with ischemic ideology. Here's her CT scan as we can see we've got kinda heterogeneous perfusion, we've got splenomegaly which is

not well appreciated here, there is some periportal edema. So this celiac arteriogram is pretty classic for the findings for what's got to be this hepatic arterial hypoperfusion. So what do we have? We have sluggish hepatic arterial flow as you can see here.

We've all done many hepatic arterial grams and this is pretty slow. The arteries are not robust looking. We don't see much in the way of peripheral hepatic enhancements. We see this is going up far enough that we see very robust splenic parenchymal enhancement that really nothing in the liver. The splenic artery is clearly hypertrophied and we clearly have

splenomegaly. So this constellation of angiographic findings is supportive of this syndrome. Obviously not diagnostic based on the imaging alone. Now for this patient, we basically just coil embolized the splenic artery

relatively proximally. Tor/g mentioned that he likes to do this with particles and I think that makes perfect sense. The literature and I know that South Carolina have one of the largest areas and it was very successful. They have about a 100% success rate,

if I recall correctly with this treatment in terms of the improvement in liver function within a couple of days. [BLANK_AUDIO] Post-embolization, we see basically stasis of flow that in the splenic artery. There's actually much improved perfusion of the liver,

hard to appreciate here are the images set side by side with the same frame rate. So I think you can see that the subtle finding is that the artery is slightly increased in size if you look at it closely. And clearly there's improved perfusion. So now we are seeing perfusion way out peripherally.

We see a lot of branches peripheral branches that we don't see in the original hepatic angiogram. So this is compatible with improvement in hepatic arterial flow. This patient actually did quite well.

- Good morning. Happy to discuss with you some of the issues of the currently available stents. Nutcracker Syndrome patients most frequently present with left flank pain, pelvic pain, hematuria, usually due to a significant narrowing in front of the aorta between the aorta and the superior mesenteric artery.

Open surgical treatment has been kind of a gold standard. Left renal vein transposition done most frequently followed by gonadal vein procedures or even renal auto-transplantation. Renal vein stenting, in this country, has been done using Wallstents or SMART stents.

In our experience, where we reported 37 surgical patients. We used stents only for secondary procedures. Three of the six stents had problems of either migration or in-stent restenosis. There is a systematic review in the JVS-VL, recently published, 180 patients, 7 series.

Interestingly, 175 were treated in China with good clinical results in 6-126 months. Stent migration was observed from 0 to 6.7%, depending on the series. We have seen stent migration, sometimes it's immediately during t

and that's obviously the easiest to take care of. Or immediately after, before any healing, that is also a more favorable situation. The problem is when it travels to the heart. It is not frequent, but it happens.

This is the largest series, 75 patients, stented, 5 of them had migration. Two of them to the right atrium, one of them required a medium sternotomy to remove it. Stents not only migrate, although again it's rare,

but even one patient is too frequent in this series that usually involves young, female patients. Stents in this position unfortunately can also fracture. If they don't fracture, they can thrombos. If they don't thrombos, they can be compressed.

If they don't compress, that's a stiff stent, it practically always will perforate their renal vein because of the arching configuration of the renal vein and because the unavailability of less than four centimeter long stance. So it is a problem.

It can actually cause significant, severe migration, completely occluding the inferior vena cava together with perforation of the renal vein. Obviously these cases require open surgical repair,

and have a chance to remove a few of these stents. Percutaneous retrieval, fortunately, is possible in about 90% of the cases, and sometimes, if it doesn't cause significant cardiac injury even from the heart or the pulmonary artery and

we had several case reports, of stents, especially after the TIPS procedure, early on, that migrated into the central circulation that would be removed with different types of techniques, of snaring and pulling the lost stent into a large sheath,

whether you snare it at the end or you snare it in the middle. There are good case reports. This patient that we had, we could use a balloon, pull it down to the vena cava, and then from above and below, we could remove it

with a large sheath. Current stents, if you really don't want it to migrate, the only option we see is transposition patch and using hybrid procedure to fix the stents in the renal vein.

So, in general, open surgery remains the first line of intervention. Stents have a reported high mid-term success rate but migration, fracture, perforation, thrombosis, restenosis are problems and if you go to the FDA website, you see that there are much more cases than

those that are reported. So what do we need? We need dedicated renal vein stents that are short, flexible, resist fracture and migration, and we need them urgently. 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.

- 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.

- 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, 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.

- Symptomatic post-thrombotic disease affect at least 30-50% of patients with deep vein thrombosis. Regular wearing of individually selected compression garments with regular follow-up alleviate symptom in many patients. However, compression therapy doesn't eliminate chronic structural post-thrombotic changes,

implies lifelong treatment, ineffective of many cases, and low overall patient compliance remain a serious challenge. Raju S. Et., alia Asia. Percutaneous balloon angioplasty and stenting of iliofemoral venous segment have recently improved

the outcomes for patients with severe PTS, related to venous outflow obstruction. Postinflammatory vein wall remodeling and destruction of the venous value is considered to be the morphological substrate for PTS. Auto transplantation of valve-containing venous segment

demonstrated good five year results of half of patients, 50%. Maletti., Perrin., 10 years ago. However, there is currently low correlation between hemodynamic effect and clinical success of deep vein surgery in published literature.

The main goal of this study is to develop a novel surgical technique on venous neo-valve formation to correct deep axial reflux and improve venous outflow in post-thrombotic disease We perform the first series of in vitro experiments

using methods of mathematical modeling to develop a novel surgical technique on venous neo-valve formation. Five macroscopically intact common femoral veins were taken out autopsies from individuals without history of venous thrombosis.

And five common femoral veins were taken off autopsies from individuals with PTS. It was very difficult. The surgical technique involves complete transection of the common femoral vein, eversion of the proximal end of the vessel

with simultaneous endo-phlebectomy and creation of neo-leaflets from the inverted vein wall by interrupted sutures. Transection of the femoral vein and eversion of the approximal end of the vessel. During mathematical modeling appropriate dimensions

of the neo-valve were determined to resemble morphology of a native valve. An optimal vein wall thickness for neo-leaflets was determined to enable appropriate elasticity and coaptation. The hydraulic probe demonstrated good competency

of the neo-valve at 1.5 atmospheric in vitro. The absence of outflow obstruction was predicted as less than 20% stenosis during the maximal valve leaflets separation. In conclusion: A novel experiment model was autologous deep

venous neo-valve was created and evaluated in vitro. In vivo experiments to evaluate hemodynamic effect, thrombosis risk, and long term hemodynamic effect. Thank you very much.

- 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.

- 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.

- [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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you.

- Thank you 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.

- Thanks, so we've talked about open techniques, and as Marsham mentioned, wouldn't it be nice if we could develop some type of endovascular valve replacement or any reflux procedure. There are a subset of patients that require this, as we get out in these more severe disease severity, is when start seeing more

of a higher prevalence of deep venous incompetence. This tends to be a mix of primary deep venous incompetence and post-thrombotic, which also gives you a mix of the pathology of reflux and obstruction along the axial vein tree. And really, it's to find the most critical

site of disease for repair. As you've heard, the open surgical techniques have been the mainstay now, conservative would be compression, and we're now going to talk about implantable valves. Kistner, as we know, has been the father of this,

and really, his concept has been that in the deep axial system, that we have the, really, the external iliac, 25% percent of the time, has one valve. But, in general, the iliac system is valveless. But, we're choosing the common femoral vein,

the femoral vein profunda, or popliteal, that we need one competent valve somewhere along those axial segments to get the control of venous hypertension. That's really the goal. We've heard about external repair, or reefing,

that's available if the valve is intact. However, if the valve is not intact, and destroyed, then you need to bring in a new valve, either transplanted from the axillary, or transposing from good valve, to an axial segment. And really, this has been the data with open repair.

Yes, you can get ulcer healing, but there's a pretty rapid fall off at about three to five years with all these open techniques, with valve fatigue, or scarring, or enamel hyperplasia, or thrombosis. This is really, so Dusan Pavcnik at Dotter Institute

in Oregon, has been working on this for a while, the bioprosthetic valve. The first-generation, he was using sub intestinal submucosa, which basically gave you a collagen skeleton, with growth factors sewn onto a metal frame.

And then that gets implanted, and the idea was that hopefully, it'll repopulate with endothelial cells and mimic a human valve. The problem with this one was mostly tilting of the frame in vivo.

And this is kind of what it looks like, developed, delivered through its delivery system. The second-generation valve, they worked more on the frame, and still, you know, with a prosthetic in here, you do see good incorporation of the bioprosthetic valve in a vein wall with population of endothelial cells.

They've also looked at transplanting native valve to native valve on a frame, so using jugular of one side, taking it out, sewing it onto a frame, and placing it on the other side in sheep.

And that was mixed with a variety of problems, as always enamel hypoplasia and thrombosis are the main two actors that cause these to fail. Then the last thing that I've seen, that I haven't seen any results on, was this idea of the autologous endothelial monolayer

on a valve, which, when you then put it in the circulation, then you've got flow conditions, and then you worry about the sheer and the flow disrupting the populated cells from the valve. So, I asked Tim Liem, who's,

whom you've met earlier, he's out there in Oregon, and knows the Dotter institute, and I wanted to see the fate of these valves that we just talked about, with autologous, and they've implanted some in Korea and Europe. They lasted for about three months

and they all go on to fibrose or thrombose. So, it's been a challenge with the autologous valves. We've heard about neovalves already, which again is open monocusp, and now there's an endovascular system under development, where they use

intra-vasc or ultrasound mounted on a catheter, a blade, and a balloon, to create an endovascular monocusp valve. So, that's been under development for a while. But, in conclusion, a percutaneous valve is an unmet need in a small subset of patients

who come to us with wide open deep venous incompetence, ulceration, and a miserable quality of life, and currently there's not a great option, except for open surgery, which doesn't last more than five years or so. Thank you.

- Thank you again for the opportunity to discuss this topic on acute or chronic vein. Acute or chronic ovarian vein thrombosis. No financial relationships for this particular topic. An etiology is generally obstetric, although even in the obstetric population, it's rare about one in 2000 deliveries.

It's tends to be associated with infectious etiologies including postpartum sepsis, group B strep, ruptured ectopic, hydatidiform mole. There are other potential non-obstetric causes as well. Inflammatory processes that tend to affect the pelvis or the retroperitoneum including pelvic surgery,

certain malignancies, pelvic inflammatory disease, appendicitis, diverticulitis and inflammatory bowel disease. So the pathophysiology in pregnancy and why it occurs is you get significant fluctuations in the ovarian vein itself. The diameter of the ovarian vein

increases up to three times. This corresponds to over 60 fold increase in ovarian blood volume which may lead to ovarian vein incompetence. This incompetence and stasis coupled with Virchow's Triad and pregnancy, particularly in the postpartum period

with stasis in volume contraction, endothelial injury from the delivery itself and just the overall, hypercoagulability of pregnancy, result in this pathology. The clinical features are that, unlike chronic reflux and pelvic congestion syndrome,

this tends to be more frequently right-sided 70 to 90% of the time in the majority of case series. It's bilateral in a small percentage of 11% and left-sided in two to three percent. The reason again being that this is typically a postpartum issue and there was a dextroposition

of the gravid uterus, this results in typical retrograde flow in the left ovarian vein. However, the right ovarian vein which may be compressed and have difficulty draining results and integrated flow stay stasis,

and then this postpartum ovarian vein thrombosis. When it does occur, tends to occur within a week or so within the first 10 days postpartum. And it has a classic triad of where the majority of patients will have fever because there was some infectious component

to what's going on, chills, right lower quadrant pain in more patients than left lower quadrant pain. Again, corresponding with the anatomic distribution of the disease. In certain dramatic instances, it's been described that you can palpate

a sausage shaped tender mass, although this may be challenging in a postpartum patient and in someone, who has an elevated BMI. And if it's asymptomatic, potentially it's not pregnancy related but malignancy related.

The differential diagnosis is all other causes of acute abdomen including appendicitis, adnexal torsion, tube ovarian abscess, pyelonephritis, etc. Imaging is critical. Complications from this include septic emboli,

IVC or renal vein thrombosis. Again, propagation of thrombus into the respective draining veins, pulmonary embolis, ureteral obstruction just from the adjacent inflammatory process and mass effect and chronic pelvic pain in the long run.

So the diagnosis, you have to have a high index of suspicion. A Diagnostic laparoscopy is frequently done by the gynecologist and it may determine the source of abdominal pain and identify this.

And then a duplex ultrasound will identify a hypoechoic, hydrogenous, and it's tube shaped mess with inner echos, again adjacent to the psoas muscle as shown on this diagram. The sensitivity is about 52% of duplex ultrasound. So really the diagnosis ends up getting made

by CT scan or MRI, as seen in the upper right hand corner. The CT scan will show this sausage shaped mass running along the paracolic gutter. MRI is nearly a 100% sensitive and it has the added benefit of determining the acute or subacute of the disease process.

So the treatment it's typically anticoagulation, for a full anticoagulation course for DVT as well as antibiotics. Interventional treatments are kept to a minimum and it can be an IVC filter which would have to be placed suprarenal in these instances,

partIcularly for the right gonadal vein. And then percutaneous thrombectomy and surgical techniques. Again, this is exceedingly rare but retroperitoneal or transparent neal exposures of the gonadal vein are relatively straightforward.

The treatment of chronic tends to be that for refluxing ovarian vein and pelvic congestion syndrome, and that's already been delineated. So to conclude, you have to have a high index of suspicion. MRI is the most sensitive study. It can tell you about acute and subacute.

It's the standard of care anticoagulation with antibiotics and for refractory patients, endovascular versus surgery, and then for chronic, the treatment for pelvic congestion syndrome. 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you Jose and Marcia. No disclosures. So the primary valve incompetence treatment techniques was started by Bob Kistner and the techinique involved a longitudinal internal valvuloplasty by longitudinal incision and tacking of the redundant valve edges.

And the next treatment available was a transverse valvuloplasty which was again under vision and the valves were tacked at the at the commissures but the incision was transverse. And a combination of the two techniques resulted in the technique of Sottiurai, the T internal valvuloplasty

which was later modified by Michel Perrin to be able to evaluate all aspects of the valve. Further to that, we developed the trapdoor internal valvuloplasty in which a trapdoor was created. All these techniques, the mainstay was reefing of the valve commissures.

On the left hand side, you can see a redundant valve, prolapsing cusps, and on the right hand side, a repaired valve after the reefing. But you can see that the commissure is quite heavily placated. So the possible disadvantage of reefing technique

is the resultant heaped up commissural junctions. This creates valvular rugal folds and obviously when healing occurs it will have increased cicatrization, it will occupy the space, and reduction of functional valve area. When we evaluated the various thrombosis results of

supra-valvular technique, modified T technique, and the trapdoor technique, we found that on an average, there was about a 4.5 to 9% incidence of valve thrombosis. And we also found that in another 6.1% patients there, the valve stations resolved. Cumulatively, these two complicates accounted

for almost 13% of all valvuloplasties. We published a new technique of reduction internal valvuloplasty on the lessons that we leared from Dr. Lugli's experience. And we wanted to quantify the repairs that we do by measuring intra valvular distances and

trans-commissural diameters preoperative as well as intra-operative by ultrasound. We used various techniques, we devised measuring forceps and this is how it's done, whereby we are able to excise the redundant valve and stitch it back onto the valve

and have no rugal folds at the end. And this can induce, this can reduce incision in high shear areas as well. And therefore, give you a good result. This is intra-operative result of competence where you can see the patient is doing valsalva

and you can see the two valve leaflets and this is the stripping technique. And a post-operative descending angiogram or venogram shows a competent valve. So when we looked at the relationship of reflux, valve repair, and ulcer healing,

we found that when we did single level repairs, we only found 50% ulcer healing. But when we did multiple level repairs, the healing was 100% in a short period of time. And the valve competency always did not correlate with ulcer healing.

In our case the valve competency levels were 87.5% and ulcer healing was 88.9% but mainly due to the single level repairs, that did not really work. So the Rival Technique in conclusion ladies and gentlemen is a complete departure from the reefing technique which has been the mainstay of valvuloplasties.

At two years, we've had 100% patency and about 87% competency of repaired valves, with a freedom from C6 ulcers at two years about 89%. Rival Technique has now replaced our technique, earlier techniques, and is the preferred technique in our center.

Thank you 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.

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- I like this title because I do think this is probably the final study we're going to see on a large scale for pharmacomechanical thrombectomy and catheter-directed thrombolysis for acute DVT treatment. These are my disclosures. So, the CaVenT trial came on the heels

of a number of smaller single center series and sort of case studies on catheter-directed thrombolysis. And of course this was a randomized study in 24 different Norway hospitals that showed a patency advantage and a reduction in PTS on both early and late term, even out to five years

in patients treated with catheter-directed thrombolysis rather than anticoagulation alone. The ATTRACT trial of course is the follow up to this study in a sense, it was a large US trial, an NIH-funded multicenter trial that used a strategy of thrombus removal with

adjunctive catheter-directed thrombolysis for acute DVT and essentially this accrued over 50 or so hospitals throughout the US. Using either pharmacomechanical thrombectomy and/or catheter-directed thrombolysis versus standard treatment of anticoagulation.

Enrollment completed in 2014 was presented at SIR and has been published in a New England Journal article I show there. Inclusion criteria essentially involved acute DVT's defined as symptomatic DVT of less than 14, or less than or equal to 14 days duration

including the femoropopliteal and iliofemoral segment and I think that's kind of important, these two locations, so you could have isolated femoropopliteal disease. Randomization was a one to one between anticoagulation versus pharmacomechanical thrombectomy plus anticoagulation

and the analysis was stratified by plus or minus common femoral involvement. So you could have a group stratified to no iliac and no common femoral involvement. The PMT treatment was basically infusion first for IVC or popliteal vein thrombosis,

but everything else was treated with an attempt at single session pharmacomechanical thrombectomy followed by lytic therapy if needed to clear residual thrombus for up to 24 hours with adjunctive measures afterward including stunting, et cetera.

No IVIS imaging or any of that was prescribed. These are the primary efficacy and secondary efficacy endpoints, and these are important, I think, because it effects the outcome of our perception of the results of this trial. The primary efficacy endpoint was a binary presence of PTS

at any time point between six and 24 months. Defined as Villalta score of greater than five or a venous ulcer. Whereas secondary endpoints were not binary so much, but continuous, so severity of PTS, proportion of patients with moderate to severe, et cetera.

And then of course there are some quality of life measures, as well as symptoms: leg pain and leg size. These are the primary safety endpoints, primarily episodes of, issues of bleeding, recurrent thromboembolism, and death. So looking at the sort of meat of the study,

or the primary efficacy endpoint, this was considered a negative trial in the sense that this primary endpoint of reduction of the incidents of PTS did not occur in those patients undergoing pharmacomechanical thrombectomy or thrombolysis, and so there's no difference

between these two groups in this regard. On an other hand, there was an unfortunate increase in bleeding risk, both early on as well as any bleeding. So early major bleeding, and any bleeding within the first ten days.

So this was a finding that lead to, or, these two findings lead to the conclusion in the paper, that among patients with acute proximal deep-vein thrombosis, the additional pharmacomechanical catheter-directed thrombolysis to anticoagulation did not result in a lower risk of post-thrombotic syndrome.

And did in fact lead to higher bleeding rates. So this is real and true, but looking deeper into the study, I would say that there are some other important secondary efficacy endpoints, and if you look at this, you see that along the continuous variables, and if you look at severity of PTS,

this was favored in the more aggressively treated arm across all time points. And so, if we're looking at degree of PTS, I think there's quite a difference. It's also true that there was a difference in leg pain severity, so subjective reporting of

pain as well as the actual index limb circumference. If you look at some other secondary endpoints, even though there was no difference in the binary metric of any PTS, across all-comers, if you looked at moderate to severe PTS, there was a significant difference, and this seemed to be more true in the patient

with the proximal iliofemoral DVT, rather than those patients with simply femoropopliteal DVT. So I think there are a lot of criticisms of the ATTRACT trial that we've probably heard and discussed. Large selection bias, large number of patients screened for those who were randomized, devices changed

over the course of time, no IVIS in the protocol, no patency assessment in majority of subjects, and probably the biggest issue is inclusion of femoropopliteal DVT, which is done largely to drive enrollment. And I would argue these issues are common to all

randomized trials, randomized trials do strike a balance between broad applicability to different patient populations while trying to still answer specific questions that are manageable. And so I think these are reasons why we have to look deeper into the trial results with some of the secondary endpoints,

rather than just focusing on that major headline. So I would say that in terms of lessons learned, the ATTRACT trial does confirm that this aggressive strategy of thrombus removal may not be appropriate for all patients with iliofemoral and femoropopliteal DVT

in part because of this increased risk of bleeding. I think this something that we know, and ATTRACT has confirmed that. Finally, this bleeding risk is extraordinarily low overall, so that makes me believe there are some patients who very much warrant it due to their symptoms

and their active status. And I do think it did show that the results in less severe PTS in those patients treated with aggressive strategies of thrombus removal. So this is what we want to avoid, a patient like this, who is very symptomatic,

very young, and very active, who has never had any discussion of thrombolytic therapy offered to him, and then referred only three months later or six months later, when there's really not as much we can do about that patient. So it's in conclusion the ATTRACT trial was well-designed

and rigorous with broad clinical scope. It confirms that decision to offer aggressive strategies of thrombus removal continue to require us to make artful clinical decisions in a patient specific manner. And I think it does illustrate that a certain subset of patients,

especially those younger active patients, probably do warrant thrombolytic therapy, thanks.

- 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.

3

- 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.

- 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.

- Thank you Lowell. - Good morning, and thanks Lowell and Jose, for the invitation to come back this year. I don't have any disclosures. Well, what we're going to talk is imaging the female pelvic veneous system. And the female pelvic venous system is a complex arrangement

of four interconnected venous systems, and really you have to understand the anatomy to understand the keys to imaging it and treating it, and that's the connections between the renal vein, both the left and the right ovarian veins, the tributaries of the internal iliac veins,

and the superficial veins of the lower extremity through the saphenofemeral junction. And central to all of this are the tributaries of the internal iliac vein. Which functions as a gateway between the pelvis and the leg, and really are exactly analogous to perforating veins,

connecting the deep veins of the pelvis to the superficial veins of the leg, and you have to have an intimate knowledge of this anatomy both to image it adequately, as well as to treat it. So classically, the internal iliac vein is thought as the confluence of three tributaries.

That is, the obturator vein anteriorly, tributaries of the internal pudendal vein, sort of in the middle of the pelvis, and the superior and inferior gluteal veins, and these communicate with the legs through four escape points

that the anatomists describe anteriorly as the obturator point or the "O" point, where the round ligament vein comes through the abdominal wall, the "I point. And medially in the thigh, pudendal or the "P" point, and posteriorly the gluteal point,

which communicates both with the posterior thigh as well as with the sciatic nerve and gives rise to sciatic varices. (coughs) From our standpoint today, I'm more interested in atypical, varices, that is, pelvic source lower extremity varices,

arising from the pelvis, anteriorly for the obturator vein, and from the round ligament vein, which communicate with the vulva, branches of the internal pudendal vein, which communicate with the perineum, and the medial thigh, and posteriorly, with branches of the superior and inferior gluteal vein.

So as far as imaging goes, we're interested primarily in two clinical scenarios which the imaging requirements are somewhat different. That is, atypical pelvic source varices without any pelvic symptoms, and atypical varices with pelvic pain, and the way that we study these with venography

are quite different. Although some people do pursue blind sclerotherapy from below, I do think imaging with venography adds substantially to both the control of the sclerosant, as well as how thoroughly you're able to embolize the pelvic tributaries.

And I personally like to do sclerotherapy of the varices with venography, and use direct puncture venography using either a 23 or a 25 gage butterfly needle, that's placed under ultrasound guidance. Contrast is then injected to calibrate both

the variceal bed as well as to track the tributaries, as I'll show a minute, up into the pelvis, and usually you can embolize about to the level of the broad ligament. Simultaneously, foam sclerotherapy is performed, using a combination of Sotradecol,

and Ethiodol as a contrast media, and then is followed both by Flouroscopy, using a reverse road mapping technique to subtract the bone and other things out, and follow the contrast through as well as with ultrasound as shown here.

And just as an example, here's some vulvar varicosities, that communicate both with the obturator vein up here, with the round ligament vein through the "I" point, as well as with the saphenofemoral junction here. And although you could do this blindly, I do think you get a much better understanding

of the anatomy and the volume of sclerosant required, doing it with venography. These are posterior thigh varicosities, that communicate through the "G" point here, and you can actually see the contrast refluxing into the inferior gluteal vein shown here,

and all of this can be treated with sclerosant. The second clinical scenario, is that of atypical varices with pelvic pain, in which case you do want to make sure you treat the pelvic variceal bed completely. And for this, the venography techniques are

balloon occlusion venography performed from above. My preference is right internal jugular vein approach, because it's easier to place the occlusion balloon into the right and left internal iliac veins, which a sequentially selected, and then I use a Berenstein occlusion balloon

and then place it just below the confluence of the internal iliac vein and the external iliac veins, inflate the balloon, inject contrast, which both blocks antegrade flow, and allows reflux into the varices. Most of the time you can't see these varices if you don't have an occlusion balloon,

and then as you see the varices, sequentially select more distal tributaries with a glide wire, put the balloon down, inflate it, and perform sclerotherapy and occasionally, depending on the size of the vein, use coils if you need to. Here is an example of the balloon

in the internal iliac vein, you see the "O" point. We've already sclerosed the contralateral obturator vein, and you see this classical obturator hook here, which is classical for the obturator vein. Here the occulsion balloon is in tributaries of the internal pudendal vein,

you see it communicating through the "P" point with varices in the medial thigh, and then with the great saphenous vein here, with a type two junction. Here the balloon is in the inferior gluteal vein. You see communication with the "G" point here,

as well as communication with sciatic varices, this classic horsetail look shown here. So in conclusion, understanding anatomy is critical to the treatment of pelvic venous disorders, you do clearly have to understand the anatomy of the internal iliac vein, as well as the escape points,

and vary your venographic technique, based on the patient's symptoms. 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.

- Up to the present days, constructive surgery has enjoyed both loyal support and vigorous opposition. The opponents of these operations point to the unproved efficacy of the deep vein reconstruction because the number of patients with primary valve

insufficiency of the deep veins is extremely small, less than 5 percent. These surgical operations are commonly accompanied by corrective procedures, stripping, ligation or perforating veins coagulation and finally,

the use of the idea of reflux circulation the elimination of reflux in the deep veins following standard stripping proves the fact that there is no need for these operations on the whole. It is well known that reflux in the deep veins

is mainly caused by four events: post-thrombotic, primary, congenital hypoplasia and congenital malformation. Total reflux is an axial reflux or it's a segmental reflux of the femoral. Reflux now remember that axial, continuous

reflux from the groin of the lower leg only on the deep vein system and segmental, one segment of femoral or lower leg veins. Two issues remain urgent: Do the patients with primary valve insufficiency of the deep veins need valve correction?

And what is the role of the extra-vasal correction? In our country, the extra-vasal correction of incompetent valves with elastic spirals is the most commonly used procedure, the innovative technique being proposed by Alexander Vedensky in 1979.

Our experience with extra-vasal valve correction comprised of two-hundred and sixty-three patients and includes five stages of development. Now the first stages, the study and development of the technique, the analysis of short-term and long-term results, at the end,

the identification of place and role of extra-vasal correction and valvuloplasty in deep vein valve reconstruction. Long-term results were studied in the follow-up period of five to ten years, aged fifty to sixty years old.

Forty-one patients extra-vasal correction was needed and thirty-seven after valvuloplasty. And satisfactory is related to extra-vasal correction forty-four percent. All persons had segmental reflux before correction. And valvuloplasty satisfactory sixty-seven percent.

What caused these results? We studied morphology of incompetent superficial veins, fifty-four trials and morphology of competent deep vein valves, thirty-eight patients. And five types of valvular valve around the venous valve.

And the third one, cusp of valve and collagen fibers are very good as you can see and hypertrophy of the intima is the first in the second version. And four and five version, granulated

tissue and loose connective tissue. Valve torus of the deep vein and superficial vein are identical in each case. Two last types are always accompanied by valve insufficiency. Conclusion: segmental reflux is the initial stage

of axial reflux and is due to valve torus incompetence without valve cusps stretching. It is the case of incompetence of the first studied degree according to Bob Kistner after stripping, reflux circulation is possible due to increase of blood flow in the

femoral vein in sixty-five percent of the cases. And axial reflux is accompanied by cusps stretching in the setting of valve torus weakness and requires valvuloplasty and extra-vasal correction. Ultrasound image of anatomy and physiology and

each valve has its own physiologic geometry. Based on the performed trials we made a conclusion about the need in a preoperative stimulation of extra-vasal spiral along the geometry of each individual valve. It's a transposition - excellent transposition of

the vein as you can see a new form of spiral Vedensky it's a competent copied after this procedure. The outcomes of different corrections after technique changes based on the trial's results. Good results, extra-vasal correction eighty-seven

percent of outcomes and valvuloplasty with extra-vasal correction became ninety-three percent. Conclusions: extra-vasal correction should be carried out for all patients with segmental reflux along the whole

length of the femoral vein. Should be the integral part of valvuloplasty. Should be performed after reconstructive surgical operations of the deep veins in post-thrombotic syndrome, different valve transplantation, transposition, Maletti-Lugle

operation, Opi and extra-vasal correction should be carried out using an individual spiral previously simulated by the valve geometry.

- 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.

- [Presenter] Okay, so you've heard two aspects of the valve, so going to give you actually two, what's called the sail valve and also the VenoValve, two other options that are out there. These are my disclosures. So if you look, these are our options in 2017,

but we really talking about these three, Amrit's already spoken about the Neovalve. All these are the indications for secondary venous problems, and usually monocusp, can be bicuspid, usually monocusp, but can be bicuspid also, and this is monocusp as well.

So want you to get the idea, a lot of monocusp is coming around even though we think theoretically, bicuspid works better, but maybe not, in terms of prosthetic valves. So this is what's known as a sail valve.

Its percutaneous is a monocusp valve. It's almost not a valve. It functions in a slightly different way. It does have a physiologic leak and it's a thin piece of PTFE and what happens is if the blood is going from here up,

when it goes up these slits become larger and when the blood wants to reflux back these become smaller slits and it's like a billowing sail so it's a self-cleaning type of valve. You don't get much on the PTFE itself and it's obviously percutaneous.

So they have done 10 pigs placed in their iliac veins. Access is six French, deployment was 100% and it expands to a 10 millimeter diameter which most of us working in this space think you need about an eight to 10 millimeter size of a stent if you're going to use a stent.

Some of the results at four weeks did ascending venography on these pigs, not patients and they were all patent and then they did some descending of venography and eight of them, five were competent, 1 was partially competent, and two were incompetent. That was due to what they said malpositioning

or maybe it's tilting itself. More importantly at least on Histology, in pigs, not humans, there was really no microscopic thrombis on the valves so that was kind of encouraging. That is the sail valve. Then the second one that to complete the whole cycle during this segment is the VenoValve

which is a porcine derived valve. It's monocusp but it is an open insertion and it's based upon heart valve technology. One of the nice things is and that's another nice thing about the Blueleaf, you don't have a size mismatch. The Blueleaf you're doing it in the native vessel

and here you can tailor the inflow and outflow and papers show that that's really clearly important. You can't put a small valve if you have a big inflow and small outflow et cetera. You need a nice tapering so this will allow you to, when you do it open to tailor the size.

This is what it looks like. Here it's a monocusp valve that's mounted on a metal alloy frame. This is placed in the jugular veins of sheep and it's an open insertion. Clearly you suture it closed with some 7-0 sutures and then you affix it to the vein wall so it doesn't migrate also with some 7-0 sutures

and you can test it. This is a decent ascending venogram so head is up here, neck is down here in the jugular vein of the sheep. Then we can do a descending venography as well. So descending injecting from here, and there's not much leak going down.

So the FDA is submittal and hopefully do some sheep. They want to be sacrificed in 30 or 90 days and hopefully start a inhuman trial within the future. So this really goes back to the axillary valve transplant which is where I kind of started, believe it or not, 35 years ago as a, 37 years ago,

as a surgical resident doing axillary valve transplants. This is monocusp. It's an open insertion. It helps you do better inflow and outflow. But the challenges of all these are going to be, as Amrit already said it's a specialized area. And Mike (unintelligible) also.

Who needs this? Is this the first line or the final line of care in these patients and where do we place the valves or where to create the valves? Is it in the popliteal, the femoral region, or the common femoral?

Maybe some of it depends upon the profunda vein status. We've been doing this for 35 years when I was a surgical resident and I'm glad that we're finally getting to the point where we have a lot of nice options and see which ones pan out

because it'd be great for these patients. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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