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Paraganglioma|Embolization|23|Female
Paraganglioma|Embolization|23|Female
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Transcript

The second case is about a 20 year old female patient, she presented

with resistant hypertension, dyspnea. The chest x-ray showed enlargement of the mediastinum. Further investigation with MRI showed a paravertebral mass, as in here in T1, one way to the image T2 [INAUDIBLE] with intense enhancement, post contrast enhancement

so which would be the diagnosis? Any idea? [BLANK_AUDIO]. Oh yeah, that's it. [BLANK_AUDIO]. Let's go ahead so the surgeon didn't want to perform any pre-operative embolizations, so he took the patient to the operating

room. However the surgery has to be interrupted due to intense bleeding and vascular collapse and interpretive biopsy showed confirmed paraganglioma. Then pre-operative embolization was requested, this is just a distraction in angiography can show this hypervascular mass supplied mainly by intercostal branches. And now, which would be the embolic agent which you would

prefer to use for this case? [BLANK_AUDIO] Okay onyx and particles [BLANK_AUDIO] Let's come back here [BLANK_AUDIO] So we decided to embolize the

patient using onyx and liquid embolic agent instead of particles, which I'll explain in a few moments. The anatomy of the spine is very, very complex and we have to be always aware of the potential complications due to reflex into the spinal arteries and so here's the selective categorization

of the intercostal branch. So here just the skin when we perform embolization with particles, our main concern is to, I don't know if it's working this, is above the reflex that can

come back and embolize to the spinal arteries. [BLANK_AUDIO] With onyx, we know that we have to stop once we obtain reflux so that the pressure surrounding the microcatheter can act as a plug. The material can act as a plug and provide forward feeling of the material. And today with the advent of the detachable deep microcatheter,

we can perform the initial injection of onyx, we'll also have the reflux. We can come here with another catheter, inject NBCA and continue injecting the onyx forward. So this NBCA would act as a barrier for the reflux which will allow you to get more valium injections and more complex feeling of the tumor, protecting against any reflux.

And at the end we can simply detach the catheter. So we decided to perform the embolization with onyx and here's the final control. The CT scan after embolization. And the success was surgery.

- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations

related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,

and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be

a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation

of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest

as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher

patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.

The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence

that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization

versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,

in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,

one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients

who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored

superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months

for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.

But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear

to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.

Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.

- 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, thanks for the opportunity to present. I have no disclosures. So, we all know that wounds are becoming more prevalent in our population, about 5% of the patient population has these non-healing wounds at a very significant economic cost, and it's a really high chance of lower extremity amputation

in these patients compared to other populations. The five-year survival following amputation from a foot ulcer is about 50%, which is actually a rate that's worse than most cancer, so this is a really significant problem. Now, even more significant than just a non-healing wound

is a wound that has both a venous and an arterial component to it. These patients are about at five to seven times the risk of getting an amputation, the end patients with either isolated venous disease or isolated PAD. It's important because the venous insufficiency component

brings about a lot more inflammation, and as we know, this is associated with either superficial or deep reflux, a history of DVT or incompetent perforators, but this adds an increasing complexity to these ulcers that refuse to heal.

So, it's estimated now about 15% of these ulcers are more of a mixed etiology, we define these as anyone who has some component of PAD, meaning an ABI of under point nine, and either superficial or deep reflux or a DVT on duplex ultrasound.

So we're going to talk for just a second about how do we treat these. Do we revascularize them first, do we do compression therapy? It has been shown in many, many studies, as with most things, that a multi-disciplinary approach

will improve the outcome of these patients, and the first step in any algorithm for these patients involves removing necrotic and infected tissue, dressings, if compression is feasible, based on the PAD level, you want to go ahead and do this secondary, if it's not, then you need to revascularize first,

and I'm going to show you our algorithm at Michigan that's based on summa the data. But remember that if the wounds fail to heal despite all of this, revascularization is a good option. So, based on the data, the algorithm that we typically use is if an ABI is less than point five

or a toe pressure is under 50, you want to revascularize first, I'll talk for a minute about the data of percutaneous versus open in these patients, but these are the patients you want to avoid compression in as a first line therapy.

If you have more moderate PAD, like in the point five to point eight range, you want to consider compression at the normal 40 millimeters of mercury, but you may need to modify it. It's actually been shown that that 40 millimeter of mercury

compression actually will increase flow to those wounds, so, contrary to what had previously been thought. So, revascularization, the data's pretty much equivocal right now, for these patients with these mixed ulcers, of whether you want to do endovascular or open. In diabetics, I think the data strongly favors

doing an open bypass if they have a good autogenous conduit and a good target, but you have to remember, in these patients, they have so much inflammation in the leg that wound healing from the surgical incisions is going to be significantly more difficult

than in a standard PAD patient, but the data has shown that about 60% of these ulcers heal at one year following revascularization. So, compression therapy, which is the mainstay either after revascularization in the severe PAD group or as a first line in the moderate group,

is really important 'cause it, again, increases blood flow to the wound. They've shown that that 40 millimeters of mercury compression is associated with a significant healing rate if you can do that, you additionally have to be careful, though,

about padding your bony areas, also, as we know, most patients don't actually keep their compression level at that 40, so there are sensors and other wearable technologies that are coming about that help patients with that, keeping in mind too, that the venous disease component

in these patients is really important, it's really important to treat the superficial venous reflux, EVLT is kind of the standard for that, treatment of perforators greater than five, all of that will help.

And I'm not going to go into any details of wound dressings, but there are plenty of new dressings that are available that can be used in conjunction with compression therapy. So, our final algorithm is we have a patient with these mixed arterial venous ulcers, we do woundcare debridement, determine the degree of PAD,

if it's severe, they go down the revascularization pathway, followed by compression, if it's moderate, then they get compression therapy first, possible treatment of venous disease, if it still doesn't heal at about 35 weeks, then you have to consider other things,

like biopsy for cancer, and then also consider revacularization. So, these ulcers are on a rise, they're a common problem, probably we need randomized control trials to figure out the optimal treatment strategies.

Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try

to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.

And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,

secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group

is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted

by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.

And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use

those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,

but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.

For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions

for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,

and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.

But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,

so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at

the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions

at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR

predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive

of iliac limb reinterventions. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Our group has looked at the outcomes of patients undergoing carotid-subclavian bypass in the setting of thoracic endovascular repair. These are my obligatory disclosures, none of which are relevant to this study. By way of introduction, coverage of the left subclavian artery origin

is required in 10-50% of patients undergoing TEVAR, to achieve an adequate proximal landing zone. The left subclavian artery may contribute to critical vascular beds in addition to the left upper extremity, including the posterior cerebral circulation,

the coronary circulation if a LIMA graft is present, and the spinal cord, via vertebral collaterals. Therefore the potential risks of inadequate left subclavian perfusion include not only arm ischemia, but also posterior circulation stroke,

spinal cord ischemia, and coronary insufficiency. Although these risks are of low frequency, the SVS as early as 2010 published guidelines advocating a policy of liberal left subclavian revascularization during TEVAR

requiring left subclavian origin coverage. Until recently, the only approved way to maintain perfusion of the left subclavian artery during TEVAR, with a zone 2 or more proximal landing zone, was a cervical bypass or transposition procedure. As thoracic side-branch devices become more available,

we thought it might be useful to review our experience with cervical bypass for comparison with these newer endovascular strategies. This study was a retrospective review of our aortic disease database, and identified 112 out of 579 TEVARs

that had undergone carotid subclavian bypass. We used the standard operative technique, through a short, supraclavicular incision, the subclavian arteries exposed by division of the anterior scalene muscle, and a short 8 millimeter PTFE graft is placed

between the common carotid and the subclavian arteries, usually contemporaneous with the TEVAR procedure. The most important finding of this review regarded phrenic nerve dysfunction. To exam this, all pre- and post-TEVAR chest x-rays were reviewed for evidence of diaphragm elevation.

The study population was typical for patients undergoing TEVAR. The most frequent indication for bypass was for spinal cord protection, and nearly 80% of cases were elective. We found that 25 % of patients had some evidence

of phrenic nerve dysfunction, though many resolved over time. Other nerve injury and vascular graft complications occurred with much less frequency. This slide illustrates the grading of diaphragm elevation into mild and severe categories,

and notes that over half of the injuries did resolve over time. Vascular complications were rare, and usually treated with a corrective endovascular procedure. Of three graft occlusions, only one required repeat bypass.

Two pseudoaneurysms were treated endovascularly. Actuarial graft, primary graft patency, was 97% after five years. In summary then, the report examines early and late outcomes for carotid subclavian bypass, in the setting of TEVAR. We found an unexpectedly high rate

of phrenic nerve dysfunction postoperatively, although over half resolved spontaneously. There was a very low incidence of vascular complications, and a high long-term patency rate. We suggest that this study may provide a benchmark for comparison

with emerging branch thoracic endovascular devices. Thank you.

- 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 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.

- 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.

- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing

renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is

near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital

pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency

and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,

except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward

endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac

endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.

The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open

conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small

accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited

incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,

but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis

and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.

- So this is what I've been assigned to do, I think this is a rich topic so I'll just get into it. Here are my disclosures. So I hope to convince you at the end of this talk that what we need for massive PE when we're talking about catheter based therapy is a prospective registry. And what we need for catheter based therapy for

submassive PE is a randomized controlled trial. So we'll start with massive PE and my rational for this. So you know, really as you've heard, the goal of massive PE treatment is to rescue these patients from death. They have a 25 to 65% chance of dying

so our role, whatever type of physician we are, is to rescue that patient. So what are our tools to rescue that patient? You've heard about some of them already, intravenous thrombolysis, surgical embolectomy, and catheter directed therapy.

The focus of my talk will be catheter directed therapy but let's remember that the fastest and easiest thing to do for these patients is to give them intravenous thrombolysis. And I think we under utilize this therapy and we need to think about this as a first line therapy for massive PE.

However, there's some patients in whom thrombolytics are contraindicated or in whom they fail and then we have to look at some other options. And that's where catheter directed therapy may play a role. So I want to show you a pretty dramatic case and this was an eye-opening case for me

and sort of what launched our PERT when I was at Cornell. It's a 30 year old man, transcranial resection of a pituitary tumor post-op seizures and of course he had a frontal lobe hemorrhage at that time. Sure enough, four or five days after this discovery

he developed hypertension and hypoxia. And then is he CT of the chest, which I still remember to this day because it was so dramatic. You see this caval thrombosis right, basically a clot in transit

and this enormous clot in the right main pulmonary artery. And of course he was starting to get altered, tachycardiac and a little bit hypotensive. So the question is, what to do with this patient with an intracranial hemorrhage? Obviously, systemic thrombolytics are

contraindicated in him. His systolics were in the 90 millimeter of mercury ranged, getting more altered and tachycardiac. He was referred for a CDT and he was brought to the IR suite. And really, at this point,

you could see the multidisciplinary nature of PE. The ICU attending was actively managing him while I was getting access and trying to do my work. So this was the initial pulmonary angiogram you can see there's absolutely no flow to the right lung even with a directed injection

you see this cast of thrombus there. Tried a little bit of aspiration, did a little bit of maceration, even injected a little TPA, wasn't getting anywhere. I was getting a little bit more panicked as he was getting more panicked

and I remembered this device that I had used in AV fistula work called the Cleaner. Totally off label use here, I should disclose that and I have no interest in the company, no financial interest in the company. And so we deployed this thing, activate it a few times,

it spins at 3,000 rpm's, he coughed a little bit, and that freaked us all out also. But low and behold we actually started seeing some profusion. And you can see it in the aortogram actually in this and that's the whole point of massive PE treatment with CDT,

is try to get forward flow into the left ventricle so that you have a systemic blood pressure. Now, you know, when we talk about catheter based therapies we have all sorts of things at our disposal. And my point to you is that you know really, thank you...

You guys can see that, great. So really, the point of these catheter therapies is that you can throw the kitchen sink at massive PE because basically your role is to try to help this patient live. So, if I can get this thing to show up again.

There we go. It's not working very well, sorry. So, from clockwise we have the AngioVac circuit, you have, let's see if this will work again, okay. Nope, it's got a delay. So then you have your infusion catheter,

then you have the Inari FlowTriever, you saw the Cleaner in the previous cast, and you have the Penumbra aspiration device the CAT 8. And some of these will be spoken about in more detail in subsequent talks. But really, you can throw the kitchen sink at massive PE

just to do whatever it takes to get profusion to the left side. So, the best analysis that has been done so far was Will Kuo in 2009. He conducted a meta-analysis of about 594 patients and he found this clinical success rate of 86.5%.

This basically meant these patients survived to 30 days. Well, if that we're the case, that's a much lower mortality than we've seen historically we should basically be doing catheter directed therapy for every single massive PE that comes into the hospital. But I think we have to remember with this meta-analysis

that only 94 of these patients came from prospective studies, 500 came from retrospective, single center studies. So even though it was a very well conducted meta-analysis, the substrate for this meta-analysis wasn't great. And I think my point to you is that

we really are going to have a hard time studying this in a prospective fashion. So what is the data, as far as massive PE tell us and not tell us? Techniques are available to remove thrombus, it can be used if systemic lysis is contraindicated,

but it doesn't tell us whether catheter based therapies are better than the other therapies. Whether they should be used in combination with them and which patients should get catheter based therapy, which should get surgery and which techniques are most effective and safe.

Now, I think something we have to remember is that massive PE has a 5% incidence which is probably a good thing, if this was even higher than that we would have even more of an epidemic on our hand. But this is what makes massive PE very difficult to study.

So, if you looked at a back of the envelope calculation an RCT is just not feasible. So in an 800 bed hospital, you have 200 PE's per year, 5% are massive which means you get 10 per year in that hospital, assume 40% enroll which is actually generous,

that means that 4 massive PE's per year per institution. And then what are you going to do? Are you going to randomize them to IV lytics versus surgery versus interventional therapy, a three arm study, what is the effect size, what difference do you expect between these therapies

and how would you power it? It's really an impossible question. So I do want to make the plug for a Massive PE Prospective Registry. I think something like the PERT consortium is very well-suited to run something like this

especially with this registry endeavors. Detailed baseline characteristics including all these patients, detailing the intervention and looking at both short and long-term outcomes. Moving on to submassive PE. As you've heard much more controversial,

a much more difficult question. ICOPER as you already heard from the previous talk, alerted the world to RV dysfunction which this right ventricular hypokinesis conferring a higher mortality at 90 days than no RV dysfunction. And that's where PEITHO came in as you heard.

This showed that the placebo group met the primary endpoint of hemodynamic decompensation more commonly than the Tenecteplase group. Of course, coming at the risk of higher rate of major bleeding and intracranial hemorrhage. So I just want to reiterate what was just said

which is that systemic thrombolysis has a questionable risk benefit profile and most patients with submassive PE, as seen in the guideline documents as well. So that sort of opens a sort of door for catheter directed therapy.

Is this the next therapy to overcome some of the shortcomings of systemic thrombolysis? Well what we have in terms of CDT is these four trials, Ultima, Seattle II, Optalyse, and Perfect. Three of these trails were the ultrasound assisted catheter, the Ekos catheter.

And only one of them is randomized and that's the Ultima trial. I'm going to show you just one slide from each one of them. The Ultima trial is basically the only randomized trial and it showed that if you put catheters in these patients 24 hours later their RV to LV ratio will be lower

than if you just treat them with Heparin. Seattle II is a single arm study and there was an association with the reduction in the RV to LV ratio at 48 hours by CTA. PERFECT, I found this to be the most interesting figure from PERFECT which is that you're going to start it at

systolic pulmonary artery pressure of 51 and you're going to come down to about 37. Optalyse, a brand new study that was just published, four arms each arm has increasing dose associated with it and at 48 hours it didn't matter, all of these groups had a reduction in the RV to LV ratio.

And there was no control group here as well. What is interesting is that the more thrombolytics you used the more thrombus you cleared at 48 hours. What that means clinically is uncertain at this point. There is bleeding with CDT. 11% major bleeding rate in Seattle II,

no intracranial hemorrhages. Optalyse did have five major bleeds, most of the major bleeds happened in the highest dosed arms. So we know that thrombolytics cause bleeding that's still an issue. Now, clot extraction minus fibrinolytic,

this is an interesting question. We do have devices, you're going to hear about the FLARE trial later in this session. EXTRACT-PE is ongoing which we have enrolled about 75 patients into. What the data does and does not tell us

when it comes to CDT for submassive PE it probably reduces the RV to LV ratio at 24 hours, it's associated with a reduction at 48 hours, major bleeding is seen, we do not know what the short and long-term clinical outcomes are

following CDT for submassive PE. Whether it should be routinely used in submassive PE and in spite of the results of Optalyse this is a preliminary trial, we don't know the optimal dose and duration of thrombolytic drug. And even is spite of these early trials

on these non-lytic techniques, we don't know their true role yet. I'd liked to point out that greater than 1,600 patients have been randomized in systemic lytic trails yet only 59 have been randomized in a single, non-U.S. CDT trial.

So this means that you can randomize patients with submassive PE to one treatment or the other. And we want to get away from this PERT CDT roller coaster where you get enthusiasm, you do more cases, then you have a complication, then the number of cases drops.

You want that to be consistent because you're basing it on data. And that's where we're trying to come up with a way of answering that with this PE-TRACT trial. Which is a RCT of CDT versus no-CDT. We're looking at clinical endpoints

rather than radiographic ones greater than 400 patients, 30 to 50 sites across the country. So in summary I hope I've convinced you that we need a Prospective Registry for massive PE and a Randomized Controlled Trail for submassive PE. Thank you.

- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.

Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.

Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care

over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.

Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.

And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed

with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better

treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?

That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents

shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,

deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.

Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.

Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.

Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same

that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?

More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article

a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.

Thank you.

- [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.

- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,

particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients

have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance

with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,

has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches

of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.

It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,

and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test

using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture

and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.

You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,

and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer

that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,

and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.

Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,

bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old

with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,

although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,

and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,

peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,

partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,

and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.

I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution

of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)

- 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.

3

- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,

but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody

with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?

And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy

for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,

thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world

for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and

patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt

to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize

what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,

and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,

it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would

ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a

experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,

but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,

it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,

place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,

any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution

using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation

and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology

and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,

it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,

and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a

single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,

and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,

a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at

alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,

and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.

There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,

Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.

Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings

in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?

I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,

you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.

So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,

we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.

- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years

of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).

It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,

it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases

that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it

was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.

And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted

inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted

selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.

In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients

stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.

This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,

and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,

and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.

- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.

And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.

Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,

it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized

due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage

of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,

which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal

in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak

which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.

And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success

is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent

Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,

an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,

retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered

balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.

At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed

if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.

The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR

combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,

and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.

- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,

valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction

but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique

to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the

sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness

but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have

smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.

Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse

and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap

we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid

valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility

to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put

in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction

disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.

Thank you.

- Thank you very much again. Thank you very much for the kind invitation. The answer to the question is, yes or no. Well, basically when we're talking about pelvic reflux, we're talking really, about, possibly thinking about two separate entities. One symptoms relate to the pelvis

and issues with lower limb varicose veins. Really some time ago, we highlighted in a review, various symptoms that may be associated with the pelvic congestion syndrome. This is often, either misdiagnosed or undiagnosed. The patients we see have had multiple investigations

prior to treatment. I'm not really going to dwell on the anatomy but, just really highlight to you it is incompetence in either the renal pelvic and ovarian veins. What about the patterns of reflux we've heard from both Mark and Nicos what the pattern are

but, basically if you look a little more closely you can see that not only the left ovarian vein is probably effected in a round-about 60%. But, there is incompetence in many of the other veins. What does this actually have implication for with respect to treatment.

Implications are that you probably, if you only treat an isolated vein. There is a suggestion, that the long term outcomes are not actually as good. Now this is some work from Mark Whiteley's group because, we've heard about the diagnosis

but, there is some discussion as to whether just looking at ovarian vein diameter is efficient and certainly the Whiteley group suggests that actually diameter is relatively irrelevant in deciding as to whether there is incompetence in the actual vein itself.

That diameter should not be used as a single indicator. You may all well be aware, that there are reporting standards for the treatment of pelvic venous insufficiency and this has been high-lighted in this paper. What of the resuts, of pelvic embolization and coiling? The main standard is used, is a visual analog scale

when you're looking at pelvic symptoms to decide what the outcome may be. This is a very nice example of an article that was... A review that was done in Niel Khilnani's group and you can see if you look at the pre

and post procedural visual analog scales there is some significant improvement. You can see that this is out at one year in the whole. Now, this is a further table from the paper. Showing you their either, there's a mixture

of glue, coils, scleroses and foam. The comments are that, there are significant relief and some papers suggest its after 100% and others up to 80%. If you look at this very nice review that Mark Meissner did with Kathy Gibson,

you will see that actually no improvement in worse. There's quite a range there for those patients 53% of patients in one study, had no improvement or the symptoms were potentially worse. We know that those patients who have coil embolization will have reoccurrence of symptomatology

and incompetence up to about a quarter of the patients. What about varicose veins? The answer is there is undoubtedly evidence to suggest that there is physiological/anatomical incompetence in some of the pelvic veins in patients

who have recurrent varicose veins. Whether this is actually a direct cause or an association, I think it's something we need to have some further consideration of. As you know, there are many people who now would advicate actually treating

the pelvic veins prior to treating the leg veins. You can maybe discuss that in the question time. If we then look at a comparative trial. Comparing coils and plugs, you can see over all there really isn't no particular difference. If we then look again to highlight this,

which comes again from the Whiteley group. You can see that 20% of patients will have some primary incompetence but, it'll go up to around 30% if they are re-current. There is no randomized control data looking at this. What are the problems with coils?

Actually, a bit like (mumbling) you can find them anywhere. You can find them in the chest and also you can find that there are patients now who are allergic to nickel and the very bottom corner is a patient who's coils I took out by open laparotomy because they were allergic to nickel.

So, ladies and gentlemen I would suggest to you certainly, for continuing with pelvic embolization when doubtedly it needs some more RCT data and some much better registry data to look where we're going. Thank you very much.

- Thank you Professor Veith. Thank you for giving me the opportunity to present on behalf of my chief the results of the IRONGUARD 2 study. A study on the use of the C-Guard mesh covered stent in carotid artery stenting. The IRONGUARD 1 study performed in Italy,

enrolled 200 patients to the technical success of 100%. No major cardiovascular event. Those good results were maintained at one year followup, because we had no major neurologic adverse event, no stent thrombosis, and no external carotid occlusion. This is why we decided to continue to collect data

on this experience on the use of C-Guard stent in a new registry called the IRONGUARD 2. And up to August 2018, we recruited 342 patients in 15 Italian centers. Demographic of patients were a common demographic of at-risk carotid patients.

And 50 out of 342 patients were symptomatic, with 36 carotid with TIA and 14 with minor stroke. Stenosis percentage mean was 84%, and the high-risk carotid plaque composition was observed in 28% of patients, and respectively, the majority of patients presented

this homogenous composition. All aortic arch morphologies were enrolled into the study, as you can see here. And one third of enrolled patients presented significant supra-aortic vessel tortuosity. So this was no commerce registry.

Almost in all cases a transfemoral approach was chosen, while also brachial and transcervical approach were reported. And the Embolic Protection Device was used in 99.7% of patients, with a proximal occlusion device in 50 patients.

Pre-dilatation was used in 89 patients, and looking at results at 24 hours we reported five TIAs and one minor stroke, with a combined incidence rate of 1.75%. We had no myocardial infection, and no death. But we had two external carotid occlusion.

At one month, we had data available on 255 patients, with two additional neurological events, one more TIA and one more minor stroke, but we had no stent thrombosis. At one month, the cumulative results rate were a minor stroke rate of 0.58%,

and the TIA rate of 1.72%, with a cumulative neurological event rate of 2.33%. At one year, results were available on 57 patients, with one new major event, it was a myocardial infarction. And unfortunately, we had two deaths, one from suicide. To conclude, this is an ongoing trial with ongoing analysis,

and so we are still recruiting patients. I want to thank on behalf of my chief all the collaborators of this registry. I want to invite you to join us next May in Rome, thank you.

- Good morning. I'd like to thank everybody who's in attendance for the 7 A.M. session. So let's talk about a case. 63 year old male, standard risk factors for aneurismal disease. November 2008, he had a 52 mm aneurism,

underwent Gore Excluder, endovascular pair. Follow up over the next five, relatively unremarkable. Sac regression 47 mm no leak. June 2017, he was lost for follow up, but came back to see us. Duplex imaging CTA was done to show the sac had increased

from 47 to 62 in a type 2 endoleak was present. In August of that year, he underwent right common iliac cuff placement for what appeared to be a type 1b endoleak. September, CT scan showed the sac was stable at 66 and no leak was present. In March, six months after that, scan once again

showed the sac was there but a little bit larger, and a type two endoleak was once again present. He underwent intervention. This side access on the left embolization of the internal iliac, and a left iliac limb extension. Shortly thereafter,

contacted his PCP at three weeks of weakness, fatigue, some lethargy. September, he had some gluteal inguinal pain, chills, weakness, and fatigue. And then October, came back to see us. Similar symptoms, white count of 12, and a CT scan

was done and here where you can appreciate is, clearly there's air within the sac and a large anterior cell with fluid collections, blood cultures are negative at that time. He shortly thereafter went a 2 stage procedure, Extra-anatomic bypass, explant of the EVAR,

there purulent fluid within the sac, not surprising. Gram positive rods, and the culture came out Cutibacterium Acnes. So what is it we know about this case? Well, EVAR clearly is preferred treatment for aneurism repair, indications for use h

however, mid-term reports still show a significant need for secondary interventions for leaks, migrations, and rupture. Giles looked at a Medicare beneficiaries and clearly noted, or at least evaluated the effect of re-interventions

and readmissions after EVAR and open and noted that survival was negatively impacted by readmissions and re-interventions, and I think this was one of those situations that we're dealing with today. EVAR infections and secondary interventions.

Fortunately infections relatively infrequent. Isolated case reports have been pooled into multi-institutional cohorts. We know about a third of these infections are related to aortoenteric fistula, Bacteremia and direct seeding are more often not the underlying source.

And what we can roughly appreciate is that at somewhere between 14 and 38% of these may be related to secondary catheter based interventions. There's some data out there, Matt Smeed's published 2016, 180 EVARs, multi-center study, the timing of the infection presumably or symptomatic onset

was 22 months and 14% or greater had secondary endointerventions with a relatively high mortality. Similarly, the study coming out of Italy, 26 cases, meantime of diagnosis of the infection is 20 months, and that 34.6% of these cases underwent secondary endovascular intervention.

Once again, a relatively high mortality at 38.4%. Study out of France, 11 institutions, 33 infective endographs, time of onset of symptoms 414 days, 30% of these individuals had undergone secondary interventions. In our own clinical experience of Pittsburgh,

we looked at our explants. There were 13 down for infection, and of those nine had multiple secondary interventions which was 69%, a little bit of an outlier compared to the other studies. Once again, a relatively high mortality at one year. There's now a plethora of information in the literature

stating that secondary interventions may be a source for Bacteremia in seeding of your endovascular graft. And I think beyond just a secondary interventions, we know there's a wide range of risk factors. Perioperative contamination, break down in your sterile technique,

working in the radiology suite as opposed to the operating room. Wound complications to the access site. Hematogenous seeding, whether it's from UTIs, catheter related, or secondary interventions are possible.

Graft erosion, and then impaired immunity as well. So what I can tell you today, I think there is an association without question from secondary interventions and aortic endograft infection. Certainly the case I presented appears to show causation but there's not enough evidence to fully correlate the two.

So in summary, endograft infections are rare fortunately. However, the incidence does appear to be subtly rising. Secondary interventions following EVAR appear to be a risk factor for graft infection. Graft infections are associated without question

a high morbidity and mortality. I think it's of the utmost importance to maintain sterile technique, administer prophylactic antibiotics for all secondary endovascular catheter based interventions. Thank you.

- Good afternoon, Dr. Veith, organizer. Thank you very much for the kind invitation. I have nothing to disclose. In the United States, the most common cause of mortality after one year of age is trauma. So, thankfully the pediatric vascular trauma

is only a very small minority, and it happens in less that 1% of all the pediatric traumas. But, when it happens it contributes significantly to the mortality. In most developed countries, the iatrogenic

arterial injuries are the most common type of vascular injuries that you have in non-iatrogenic arterial injuries, however are more common in war zone area. And it's very complex injuries that these children suffer from.

In a recent study that we published using the national trauma data bank, the mortality rate was about 7.9% of the children who suffer from vascular injuries. And the most common mechanism of injury were firearm and motor vehicle accidents. In the US, the most common type of injury is the blunt type

of injury. As far as the risk factors for mortality, you can see some of them that are significantly affecting mortality, but one of them is the mechanism of injury, blunt versus penetrating and the penetrating is the risk factor for

mortality. As far as the anatomical and physiological consideration for treatment, they are very similar to adults. Their injury can cause disruption all the way to a spasm, or obstruction of the vessel and for vasiospasm and minimal disruption, conservative therapy is usually adequate.

Sometimes you can use papevrin or nitroglycerin. Of significant concern in children is traumatic AV fissure that needs to be repaired as soon as possible. For hard signs, when you diagnose these things, of course when there is a bleeding, there is no question that you need to go repair.

When there are no hard signs, especially in the blunt type of injuries, we depend both on physical exams and diagnostic tools. AVI in children is actually not very useful, so instead of that investigators are just using what is called an Injured Extremity Index, which you measure one leg

versus the other, and if there is also less than 0.88 or less than 0.90, depending on the age of the children, is considered abnormal. Pulse Oximetry, the Duplex Ultrasound, CTA are all very helpful. Angiography is actually quite risky in these children,

and should be avoided. Surgical exploration, of course, when it's needed can give very good results. As far as the management, well they are very similar to adults, in the sense that you need to expose the artery, control the bleeding, an then restore circulation to the

end organ. And some of the adjuncts that are using in adult trauma can be useful, such as use of temporary shunts, that you can use a pediatric feeding tube, heparin, if there are no contraindications, liberal use of fasciotomy and in the vascular technique that my partner, Dr. Singh will be

talking about. Perhaps the most common cause of PVI in young children in developed countries are iatrogenic injuries and most of the time they are minimal injuries. But in ECMO cannulation, 20-50% are injuries due to

ECMO have been reported in both femoral or carotid injuries. So, in the centers are they are doing it because of the concern about limb ischemia, as well as cognitive issues. They routinely repair the ECMO cannulation site.

For non-iatrogenic types, if is very common in the children that are above six years of age. Again, you follow the same principal as adult, except that these arteries are severely spastic and interposition graft must accommodate both axial and radial growths of these arteries, as well as the limb that it's been

repaired in. Primary repair sometimes requires interrupted sutures and Dr. Bismuth is going to be talking about some of that. Contralateral greater saphenous vein is a reasonable option, but this patient needs to be followed very, very closely.

The most common type of injury is upper extremity and Dr. McCurdy is going to be talking about this. Blunt arterial injury to the brachial artery is very common. It can cause ischemic contracture and sometimes amputation.

In the children that they have no pulse, is if there are signs of neurosensory deficit and extremity is cold, exploration is indicated, but if the extremity is pulseless, pink hand expectant treatment is reasonable. As far as the injuries, the most common, the deadliest injuries are related to the truncal injuries and the

mechanism severity of this injury dictates the treatment. Blunt aortic injuries are actually quite uncommon and endovascular options are limited. This is an example of one that was done by Dr Veith and you can see the arrow when the stent was placed and then moved.

So these children, the long-term results of endovascular option is unknown. So in summary, you basically follow many tenets of adult vascular trauma. Special consideration for repair has to do with the fact that you need to accommodate longitudinal

and radial growth and also endovascular options are limited. Ultimately, you need a collaborative effort of many specialists in taking care of these children. Thank you.

- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent

flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue

but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using

a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient

and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta

and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once

the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide

and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug

over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect

of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve

and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.

This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft

to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing

in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment

of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)

- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%

in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.

They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.

If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.

And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.

If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.

The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis

greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,

including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,

the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,

at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft

rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.

We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.

And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.

And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.

Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,

cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered

earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.

- Mr Chairman, dear colleagues. I've nothing to disclose. We know that aneurysm or dilation of the common iliac artery is present in almost 20% of cases submitted to endovascular repair and we have a variety of endovascular solution available. The first one is the internal iliac artery

embolization and coverage which is very technically easy but it's a suboptimal choice due to the higher risk of thrombosis and internal iliac problems. So the flared limbs landing in the common iliac artery is technically easy,

however, the results in the literature are conflicting. Iliac branch devices is a more demanding procedure but has to abide to a specific anatomical conditions and is warranted by good results in the literature such as this work from the group in Perugia who showed a technical success of almost 100%

as you can see, and also good results in other registries. So there are unresolved question about this problem which is the best choice in this matter, flared limbs or iliac branch devices. In order to solve this problem, we have looked at our data,

published them in Journal Vascular Interventional Neurology and this is our retrospective observational study involving treatment with either flared limbs or IBD and these are the flared limbs devices we used in this study. Anaconda, Medtronic, Cook and Gore.

And these are the IFU of the two IBD which were used in this study which were Gore-IBE and Cook-ZBS. So we looked at the 602 EVAR with 105 flared limbs which were also fit for IBD. And on the other side, we looked at EVAR-IBD

implanted in the same period excluding those implanted outside the IFU. So we ended up with 57 cases of IBD inside the IFU. These are the characteristics of the two groups of patients. The main important finding was the year age which was a little younger in the IBD group

and the common iliac artery diameter which was greater, again in the IBD group. So this is the distribution of the four types of flared limbs devices and IBD in the two groups. And as you can see, the procedural time and volume of contrast medium was significantly

higher in the IBD group. Complications did not differ significantly however, overall there were four iliac complication and all occurred in the flared limbs group. When we went to late complications, putting together all the iliac complication, they were significantly

greater in the flared limbs group compared with the IBD with zero percent complication rate. Late complications were always addressed by endovascular relining or relining and urokinase in case of infusion, in case of thrombosis. And as you can see here, the late outcome

did not differ significantly in the two groups. However, when we put together all the iliac complication, the iliac complication free survival was significantly worse in the flared limbs group. So in conclusion, flared limbs and IBD have similar perioperative outcomes.

IBD is more technically demanding, needs more contrast medium and time obviously. The complications in flared limbs are all resolvable by endovascular means and IBD has a better outcome in the long term period. So the take-home message of my presentation

is that we prefer IBD in young patients with high life expectancy and in the presence of anatomical risk factors of flared limbs late complications. Thank you for your attention.

- Thank you so much. I have no disclosures. These guidelines were published a year ago and they are open access. You can download the PDF and you can also download the app and the app was launched two months ago

and four of the ESVS guidelines are in that app. As you see, we had three American co-authors of this document, so we have very high expertise that we managed to gather.

Now the ESVS Mesenteric Guidelines have all conditions in one document because it's not always obvious if it's acute, chronic, acute-on-chron if it's arteri

if there's an underlying aneurysm or a dissection. And we thought it a benefit for the clinician to have all in one single document. It's 51 pages, 64 recommendations, more than 300 references and we use the

ESC grading system. As you will understand, it's impossible to describe this document in four minutes but I will give you some highlights regarding one of the chapters, the Acute arterial mesenteric ischaemia chapter.

We have four recommendations on how to diagnose this condition. We found that D-dimer is highly sensitive so that a normal D-dimer value excludes the condition but it's also unfortunately unspecific. There's a common misconception that lactate is

useful in this situation. Lactate becomes elevated very late when the patient is dying. It's not a good test for diagnosing acute mesenteric ischaemia earlier. And this is a strong recommendation against that.

We also ask everyone uses the CTA angiography these days and that is of course the mainstay of diagnoses as you can see on this image. Regarding treatment, we found that in patients with acute mesenteric arterial ischaemia open or endovascular revascularisation

should preferably be done before bowel surgery. This is of course an important strategic recommendation when we work together with general surgeons. We also concluded that completion imaging is important. And this is maybe one of the reasons why endovascular repair tends to do better than

open repair in these patients. There was no other better way of judging the bowel viability than clinical judgment a no-brainer is that these patients need antibiotics and it's also a strong recommendation to do second look laparotomoy.

We found that endovascular treatment is first therapy if you suspect thrombotic occlusion. They had better survival than the open repair, where as in the embolic situation, we found no difference in outcome.

So you can do both open or endo for embolus, like in this 85 year old man from Uppsala where we did a thrombus, or the embolus aspiration. Regarding follow up, we found that it was beneficial to do imaging follow-up after stenting, and also secondary prevention is important.

So in conclusion, ladies and gentlemen, the ESVS Guidelines can be downloaded freely. There are lots of recommendations regarding diagnosis, treatment, and follow-up. And they are most useful when the diagnosis is difficult and when indication for treatment is less obvious.

Please read the other chapters, too and please come to Hamburg next year for the ESVS meeting. Thank You

- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old

but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,

and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.

- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,

and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was

revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.

In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat

was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.

Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone

returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.

Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy

with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,

the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.

Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.

So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really

how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017

in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.

Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at

five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery

to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional

independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.

So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,

but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could

help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.

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