- Thank you Mr. Chairman. Thank you, Dr. Veith for you kind invitation. Okay, there we go. Excuse me. DEVASS stands for Dutch EVAS study Group. We all know that women have a twofold, increased risk frequency of rupture.
The average aortic size at rupture is five millimeters smaller. They have a higher rate of undiagnosed cardiovascular diseases. They have smaller ileofemo
more concomitant iliac aneurysms They have a more challenging aortic neck. Smaller proportion is eligible for EVAR and, therefore less likely to meet EVAR IFU. They have a longer length of hospital stay after EVAR, a higher re-admission rate, more major complications,
a higher mortality rate. So, women and AAA is a challenging combination. The rationale behind EVAS is known to you all, I think. The DEVASS cohort is from three high volume centers in The Netherlands. It's a retrospective cohort of 355 patients,
included from April, 2013 to December 2015. So I have two years of result data. If you look at the baseline characteristics, 45 females were in this cohort, with the age of 76 and with some known comorbidities. They were within the instructions for use of 2013, at 28.9%
and even less in the IFU of 2016. These are some more anatomical characteristics with the AAA outer diameter 5.6 centimeters. This is the procedure, most of the patients were under general anesthesia, with the cutdown and the procedure time
was about 100 minute. Straight forward procedure 33 cases out of these 45. Let's have a quick look at the clinical outcomes. The re-intervention's done in the first 12 month. One patient had to conversion to open repair at month 11 due to type 1A Endoleak, and the others were not directly
related to the procedure itself. Although, there was thrombus in approximate stand. In the second month we saw, in the second year we saw some more type 1A migrations and a Stenosis that needed relining, and two out of these patients were within IFU.
If you look at the total cohort of type 1A Endoleak, one patient was not operated on and the other were, either open conversion or relining, and one patient was within IFU. A quick look at the death characteristics. Only one patient was within IFU,
and died after open procedure. So the re-interventions, once again, the first year four patients, in the second year five patients. Conversion to open repair, in total three patients. Endovascular re-intervention was performed
in the first year in two patients and in the second year there were three relinings performed. Endoleak 1A, in total six as stated before. No type two Endoleak reported, and in the first year five patients died, which one was aneurisym related, as in the second year, two patients died,
which one was aneurysm related. If we compare this data with the EVAS Global data, of two years not the three year data, this is the freedom from all persistent Endoleak, close to 98% which is good. Freedom from type 1A Endoleak is within IFU, 97% in the global and outside IFU 85%,
and remind these patients 71% were outside IFU. Freedom from secondary interventions, we had to re-intervene in nine patients and its comparable with outside IFU. Freedom from mortality at two years, a bit higher, aneurism related mortality is 95% which is higher, and also the all cost mortality is higher in women.
So to conclude, this is the first cohort that focuses on women after EVAS. The majority of the patients was outside IFU, and as in EVAR women do not that very good in result, appear to be very much like an EVAR. Thank you.
- So I'll be talking about different bio-chemical profiles in both, inflammatory or non-healing and granulating wounds. Specifically venous leg ulcers. So, you've heard a lot about venous leg ulcers and there's a lot of treatments but, were going to look at some of the molecular differences that you can actually see in these wounds,
when we actually analyze some of the fluid. (clicking) Nothing to disclose. (clicking) Oop, I'm not going forward. Oh, there we go. So, actually, well go back to Bill Martson's work
with Stephanie Beidler and actually showed very early on that before compression there's a significant inflammatory component within these venous leg ulcers. This is by biopsies and then when these wounds are compressed, after four weeks
of compression, they actually reduce significantly a number of these cytokines and chemokines. As, well as increase the growth factor TGF-Beta. Indicating that, certainly, there's an inflammatory component but with compression, you actually change this to a healing component.
(clicking) We also evaluated work with Ferdinando Mannello in both inflammatory wounds and non-inflammatory wounds or non-healing wounds or granulating wounds in 32 patients and 16 granulating patients. These are all venous leg ulcers,
this is the demographics here. We analyze a number of factors cytokines, chemokines, growth factors and metalloproteinase. All by multiplex immunoassay. This is what the wounds look like before in the inflammatory phase.
I think you're very familiar with that. Then after debridement and after compression as well as interventions of the superficial system, this is what the wounds were looking afterwards. This is where we collected the wound fluid in these two different states.
We find the number of differences that were significant. And other individuals have also seen this. The red circles are actually the significant changes for inflammatory wounds, demonstrating the increase in interleukins. Interleukin-10,
which is actually an anti-inflammatory cytokine, but this is overly expressed in the inflammatory wounds over the granulating wounds. A chemokine IL-8, they're calling it Stimulating Factor Granulocyte Monocyte and also VEGF also consistent with what's
written in the literature, the VEGF's overexpressed in non healing wounds. What we did find actually in granulating wounds, that they expressed other things, specifically RANTES, which is very important in centralizing a number of these pathways
that's overexpressed in the granulating wounds as well as PDGEF factor BB, which is actually consistent again with the literature that PDGEF is actually a predictor of wounds that go on to heal. (clicking)
We then went on to also look at TGF-Beta, there's three different types of TGF-Beta. Three isoforms. And what we found that was significant is that TGF-Beta 3, which is not written too much about in the literature,
is significantly higher in inflammatory wounds. And why is this important? Because this is actually an antagonist to TGF-Beta 1. It actually causes significant inflammatory responses to take place, increases cytokines, increases metalloproteinase 9 and causes
the degradation of wounds leading to actually non healing. And we see that this was significantly elevated. Importantly, we found that endoglin is which is actually a co-factor for the TGF-Beta receptor was significantly elevated in granulating wounds. And that's significant because it has
significant anti-inflammatory properties by inhibiting the monocyte-endothelial activation. So, we found that this were significant changes. In looking at the proteases, we found that MMP-1, MMP-7 and MMP-13,
which are collagenases, and the stromelysin, were significantly elevated in the granulating wounds as opposed to seeing the degrading enzymes, such as, MMP-2 and MMP-9 and metalloelastase being higher in the inflammatory wounds.
Again, consistent with the literature, MMP-2 and '9,' which are the gelatinases, if you look at the literature, these are consistently higher in non-healing wounds. Oop, sorry, I think I went back there for a second. (clicking)
In looking at the TIMPs, TIMP-1 and '2,' are overly expressing in the inflammatory, which would be expected since they have a significant amount of protease activity. In TIMP-4 which is novel,
was overly expressed in the granulating wounds. Again, this could be a potential marker. Now, there's also the cytokines and the TAM/ligands, these are tyrosine kinase receptors and, the ligands for innate immunity. And just showing that there's actually difference,
both in inflammatory and non-healing wounds and granulating, or healing, wounds, both from the receptor standpoint as well as the ligands. Which again, shows that there's differences in innate immunity,
which could be a significant factor. Furthermore, like if you look at toll-like receptor 2, which again, also codes for innate immunity. In healing wounds all of these are decreased versus non-healing wounds. So, in conclusion,
there's significant expression of different cytokines and chemokines of growth factors in venous leg ulcers and wound fluid. The cytokines and proteinases have different signatures with in the healing state of a venous leg ulcer.
An innate immunity is also involved in a venous leg ulcer inflammation and healing. These could be specific, potential markers, but also pathways and possible targeted therapy for venous leg ulcers. Thank you.
- Thanks Stephan, yes I just want to give you five tips and tricks that I've learnt with my experience to this technique, and also then I'll present some results from the Ascend International Trials. I have an obvious disclosure that is important to show.
So, I do think that custom-made devices or phenostate graphs are the gold standard in this area of the difficult neck to aneurysm, but there are constraints with it, both financially and atomically, and of course its not the perfect solution
so we still need to strive to find better solutions for patients and indeed an off the shelf solution is very useful especially in emergency situations. I think we're all quite surprised by the outcomes from parallel grafts.
I certainly, when I saw this originally thought this was never going to work but actually, the results from standard evar with chimneys are really quite good. There is however always the potential for gutter endoleaks when aligning
parallel grafts with conventional EVAR stents which are not really designed for this purpose. So, endovascular sealing with parallel grafts offers a solution to this with the prevention potentially of gutter endoleaks because the polymus bag will seal alongside
the parallel grafts. And in practice this works quite well so you can position two, three or even four parallel grafts alongside the nellix sealing device to give yourself a really good seal and an example is shown here on the CT.
So tips for getting good outcomes from this, well the first is an obvious one, but its to plan very carefully, so do think you need to be very cautious in your planning of these with regard to multiple levels of the technique
including access, the type, length, and the nature of the parallel grafts you're going to use. I'll talk a bit more about the neck lengths but aneurysm lengths as well because there are some restraints with the
nellix device in this regard. You need to take very carefully about seal both proximally and distally and I do think you need to do this in a hybrid theater with experienced operators. I mentioned neck lengths and my Tip two is
you have to not compromise on neck quality and neck length. So you need straight healthy aorta of at least 15mm, of less than 30 diameter and a low thrombus burden. If you do compromise you'll see situations as the one on the photograph shows
where you get migration stents so you must not compromise on the quality and length of your aortic neck and if that means doing more chimneys, do it that's not a major problem but if you compromise on neck,
you will have problems. I mentioned the parallel grafts, again this is part of the planning but we use balloon expandable stents of a reasonable length to ensure that you get at least a centimeter into each of the branches
and you have to be careful to position these above the polymer bags so that they don't become constrained by the polymer bags from the nellix device. You have to be very careful when positioning these so the tip four is watch the parallax in
two different angles to be sure, as in the case here, that you line up all your stents appropriately and that you don't get crushing of any of the individual stents. So parallax is vital. And th
ltiple levels of redundancy in the nellix system which you can use to your advantage to ensure you get a good seal. So here's an example where the bags you can see are not entirely filled using the primary fill.
And it is quite difficult because often you get polymer pressures that are slightly erroneous in the endo bags. So use the redundancy including what's called the secondary fill of these bags so you can adequately fill the bags
right up into the aortic neck and ensure a very good proximal seal. So what are the results, well this is the post-market registry of Ch-EVAS this is an open-label study with no screening and I'll just show you a few slides of the data
on 154 de-novo procedures, which are a combination of single, double triple, and even quadruple chimneys. And if we look firstly at outcomes at 30 days the outcomes are good, that you'd expect in these difficult anatomies,
so 2.6% mortality and stroke, and just two cases of temporary renal failure. And if we look out 12 months, the freedom from aneurysm related and all cause mortality is favorable and comparable with any of the other endovascular techniques
in these difficult anatomies, in the upper 90 percents. And endoleak rates, you pretty much eradicate type two and type three endoleaks, but remember this is only 12 months, and very low levels of type one endoleak
and its really the type one endoleaks that are difficult to fix and if you ensure that proximal neck is adequate this shouldn't occur. And finally just secondary interventions, again this is out 12 months. Secondary Interventions are low and again
I think with the tips that I've shown you, you can reduce this to an absolute minimum. So this does offer an off the shelf alternative I don't think in any way this is to match the current gold standard which to me is the custom-made devices, but it's a very useful
adjunct to the techniques we have, and again provides that off the shelf solution which in emergencies and urgent cases is essential. Don't compromise on your neck, the outcomes I think, in this group are promising, but of course, the long term durability is
absolutely essential so it's important we follow these patients out to at least 5 years. Thank you.
- Yeah, thanks very much. Well, we've already heard that things were going well with the two first EVAS trials in the U.S and Europe predominantly, at one year and then we've seen those events described by both Jeff and Matt at two years. Root cause analysis refined IFU
and then prospectively studying this in the EVAS2 trial in the U.S but also in Europe and in the Asia-Pacific, in the Forward2 trial. I'm going to give you a little bit of an update. As we know there have been some concerning reports on retrospective reviews of experience in the early term,
and we've all heard about the details of the revised IFU, and the useful outcomes or grossly improved outcomes we can expect at two years and now Jeff has just told us at three years. Sorry, we'll just go back. So, as Matt mentioned, there have been several publications
that have retrospectively applied the IFU to center's experience to see if they could replicate the good outcomes that were achieved in the retrospective analysis of the IDE trial. Certainly, what is shown is that if you apply the revised IFU, you significantly reduce
patient applicability with this particular device. It has to be acknowledged that many of the procedures that were performed in these publications were performed, a) with a device that's different to the one that we're now going to use, and b) with a procedure that was very different.
It probably impacts on outcomes. I think the major difference with what we'll call the new Nellix device, is that it has the endobag attached firmly, not only to the top of the stent, but also at the bottom. And in our experience this attachment at the bottom
has had a particular impact on aneurysm sac size. The procedure has also evolved, and the procedure now involves steps such as unfurling of the endobags before stent deployment, and also pre-fill of the endobags with saline prior to filling with the polymer,
as well as the importance, as Matt mentioned, of accurately deploying and using all of the infrenal neck and the iliac sealing zones. We also performed a retrospective analysis of our experience in consecutive cases at Aukland Hospital with considerably longer follow-up.
And you can see that the patients on the modified IFU had a significantly different and improved freedom from type 1A endoleak, and also the composite end point of type one endoleak, sac expansion, and freedom from reintervention was highly significantly improved.
So that's a little bit different to the experience reported, possibly because we've been applying the optimized technique and had access to the new Nellix device for some time. So EVAS FORWARD 2 is being performed in Europe and in the Asia-Pacific region.
A 300-patient confirmatory trial with standard parameters. This is the very first case that was done. We did this in Aukland, and you can see something we weren't observing with the earlier Nellix device without the distal seal. We're seeing some cases with significant sac shrinkage.
You can see the earlier, or interim results, I'm just presenting for the first time here today from the FORWARD 2 trial. A very high freedom from type 1A endoleak, and freedom from reintervention, as of July 2018. Just out of interest, we also did a retrospective review
of patients in our own center that has had at least one year of follow-up using the new Nellix device with optimized procedures to see what the outcome would be, and you can see at one year that there's no type one endoleaks. Impressively, absolutely no migration.
We have seen at two years a couple of patients that had some sac growth. Even on IFU we felt that they had degeneration of their iliac arteries with loss of seal. Here you can see a case where you can see the dramatic sac shrinkage we're now seeing
in some cases, and this is the one where we saw some sac growth where we ended up doing a second reintervention to extend the distal seal. Of course, the real driver for us to continue with the Nellix and EVAS technology is this suggestive but very impressive freedom
from all cause in cardiovascular mortality. That really is driving us to use this technology in our patients. So in conclusion, we'll know that, in fact, there's ongoing evolution of this technology, and we're looking forward to being involved
in next generation EVAS that will follow the important EVAS2 and EVAS FORWARD trials sometime later in 2019. Thanks very much. (applause)
- So thank you very much. I would like to acknowledge Suma Devata and Suma Sood, two hematologists who worked with me on this project, and the NIH for support, and the manuscript for this is under review at the moment. No disclosures. If you look at the current drugs that we have available
in yellow, and those in development in blue, they all target the coagulation system, and as such they're all going to have potential for bleeding. If you look for example, at the major bleeding with Enoxaparin, it's around 2%, for VTE prophylaxis and treatment, and even for,
(mouse clicking) it's not moving forward. Okay, I'm sorry, and even for the DOAC's, it's around 10%. And this is important because major bleeding can lead to a case fatality rate of around 10%. This is not moving forward.
There's a remote, okay, thank you, sorry. So if one could target the inflammatory system rather than the coagulation system, one could, theoretically, have a drug that's much safer. So how is inflammation and thrombosis related? When endothelium and platelets get up-regulated,
selectins become present on their surface. There are receptors for selectins on inflammatory cells. This leads to leukocyte endothelial, leukocyte platelet, leukocyte leukocyte interactions, the release of pro-coagulant microparticles, and thrombus amplification.
At the same time, other inflammatory cells come into play, such as activated neutrophils. They bind by other receptors, such as the Mac-1 receptor, leading to fibrin formation, platelet accretion, the release of nuclear material, and further thrombosis. So if you can inhibit that process, theoretically,
you could end up with a drug that is safer, that inhibits thrombosis, and also inhibits the fibrosis that can occur. Now we've been interested in E-selectin as an important regulator of thrombus formation and fibrin content.
We know that endotoxin induced tissue factor mediated coagulation is enhanced in humans carrying an E-selectin allele. And patients homozygous for this allele have an increased risk of VTE recurrence. And from our very early mouse studies we saw in fact that
E-Knockout mice had the least amount of thrombosis. So the compound they were interested in is called GMI-1271. It's an E-selectin antagonist from a company called GlycoMimetics. This drug was being looked at for treatment in sickle cell and cancer.
And we wanted to see if it would be possible to use it for VTE. So we did some initial studies, done by Dan Myers in our laboratory, this is the drug, where we showed that in fact, if you look at 10 and 20 milligrams per kilogram
of this drug, it's equivalent to six milligrams per kilogram of Lovenox in inhibiting thrombosis in our mouse model, without an increase in tail bleeding time. So this led to an application to the VITA Program, which is a program from the NIH to allow investigators to move drugs or other
products through the Valley of Death, so-called Valley of Death. We had three aims of this study. Aim one was to give the drug or Lovenox or saline one time, and then look for safety. Aim two was to give the drug daily for five days,
compared to Lovenox, and look for safety. And then aim three was to treat patients who had calf vein DVT. The reason we chose calf vein DVT is because it's frequent. Complications can occur, but there's clinical equipoise about whether or not you need to treat calf vein DVT.
In fact, the most recent study suggested that you don't need to treat. So the third aim was to give GMI-1271 or Lovenox daily for five days, and then follow the patients with duplex. We had a number of inflammatory coagulation, cell adhesion, and leukocyte and platelet activation biomarkers,
along with hematologic studies. In the first two aims, we found that there were no serious adverse events reported. Lovenox increased some of the TEG values, GMI-71 did not. E-selectin levels tended to be lower in the GMI-1271 treated volunteers,
and there was lower leukocyte and platelet activation in the volunteers. We had two patients before the contract ended that we were able to treat. This is the second patient, he was a 55 year old physician, who had thrombosis in one of his
paired posterior tibial veins. Here is his duplex imaging. You can see at baseline he was thrombosed. At day eight, the vein was still thrombosed. By day 19, the vein was open. And we happened to see him nine months, seven days later.
The non-compression on the left, the compression on the right. The veins were both still patent and open. So in conclusion, VTE is a very common problem. It's the third most common cardiovascular disease behind MI and stroke.
It's the most common cause of in-hospital death. Current drugs all carry significant bleeding complications, and they do not prevent the fibrosis of PTS. Targeting E-selectin is a new strategy to treat VTE, significantly lowering bleeding, and could decrease vein wall fibrosis.
Thank you very much.
- So this talk is similar to Professor Vermossin in that we're trying to establish again the idea that EVAR is really the choice of treatment here, especially for patients who can't undergo an Open Repair. I have no disclosures. So why does this even come up? Well, as we know the DREAM trial very nicely elegantly
show that early on there was a mortality benefit of EVAR over Open Repair, but out to two years that mortality benefit was lost and the curves began to meet and equilibrate. And when you look at the EVAR 1 study, when you get out to eight years,
those curves actually invert and the all cause mortality for Open Repair was actually beneficial as compared to EVAR. And so it becomes a question, based on somebody's RCT or whether or not Open Repair is really the better way to go. But at least for this discussion we're talking about
a select group of patients. Those patients who are unfit for Open Repair. Multiple comorbidities, high frailty index. Totally different population than the overall cohort. And so when you go back to EVAR 1 and you look at it, these patients, these frail patients,
lot of comorbidities. They're the ones who would exactly benefit from that early aneurysm or early all cause mortality benefit from EVAR, 'cause these are the patients that may not life to meet that eight year crossover point.
In addition, there's been a lot of temporal changes in terms of EVAR. There's evolving technology and there's evolving techniques. The devices are lower profile. They have better durability.
It's easier and more precise in terms of delivery and implantation for these devices as well now. Moreover the techniques have evolved significantly. We're doing almost all these percutaneously. There's very rarely a situation where you need to cut down. The procedures are done very quickly now.
A lot of them are done in less than an hour. And there's avoidance at least of major pitfalls, I mean, the last time I've heard about an iliac artery disruption was probably five or six years ago. This type of large complication rarely occurs anymore. And this study from the Mayo Clinic corroborates this.
When they look at their series of patients who had Open Repair and EVAR, the top graph is basically those patients who were treated from 2006 or earlier. The bottom graph is the patients treated from 2005 or later. And you can see the mortality benefit from Open Repair basically disappears in the lower graph
and that cohort that's treated later. Again, kind of corroborating that techniques and devices have changed, improving EVAR's survivability. And this paper looks at the NSQIP database and says basically the same thing. That contemporary 30 day mortality after EVAR
in high risk patients is substantially lower than that reported in EVAR 2 trial. So gain, demonstrating and showing a picture of EVAR with better survivability and the data that's come out from these earlier trials in terms of EVAR mortality is not necessarily translatable to current day.
So, what we are expecting for EVAR? Well, I think really, two things. You want prevention of death from the aneurism and you want a quality of life. I mean, quality of life is important. These patients come in and expect to be able
to be back on their feet shortly after the procedure. And when you look at the EVAR 2 long term survival, aneurism related mortality is improved over Open Repair out to 12 years. And then when you look at the improved data, the quality of life was significantly better
for EVAR versus that of Open Repair. But I wanted to just kind of get you to shift and look at it from a different perspective and not just see it from what EVAR is in terms of beneficial, how it's changed and how the survivability is improved.
But really what are the expectations in terms if Open Repair? What is the patient tolerance? What are the training and what are the volume paradigms in today's day and age? Well clearly, when you look at these two things
percutaneous, especially the access to the groin, is going to be infinitely better tolerated than an open incision, whether it be transperitoneal or retroperitoneal. So clearly there's a benefit of EVAR in terms of that. But more importantly, we know that the,
historically we've shown that high volume centers and high volume surgeons have better results for Open Repair. And without question, the more you do, the better you're going to get at it. And so, when you look at that in conjunction
with these types of data where clearly the numbers of Open Repair through the country are reducing dramatically and continue to decline. We looked at this and this was a slide of EVAR, which was the positive slope, and Open Repair, which is a negative slope,
in terms of trainees graduating. And that ended in 2010. That slope continued to be negative. When you put those two together, you realize that people are coming out with less and less Open training.
Their experience with Open Repair is only declining and when you contrast that with EVAR, which is improving technology and techniques, it becomes obvious that in certain circumstances I think the randomized control data can no longer be looked at and you have really just think about
EVAR as the best treatment for these patients. Thank you.
- Bill outlined why some of these trials fail. And there's so many pathways that are involved in the pathophysiology of venous leg ulcers. And I'm going to just talk about the proteins and the degradomes involved. And certainly you can talk about free radicals, you can talk about map kinases,
you can talk about TGF beta pathways, there's a lot. First some definitions. Proteomics, large scale study of proteins particularly their structure and function. The proteome is the entire set of proteins produced
or modified by an organism. In humans, just to give you an example, there's 27,000 proteins, that does not even include the ones that are actually post-translationally modified by glycosylation and phosphorylation and other mechanisms. The degradome, degradomics, aims to identify proteases
and protease substrates, the repertoires or degradomes of an organism wide-scale, identifying new roles for proteases in vivo. The study of degradome is directly related to measurement of enzymatic activities and will facilitate the identification of new
pharmaceutical targets to treat disease. So we actually did a review of analysis back in 2016, just to see what has been found in the venous leg ulcer, whether it was biopsied or whether it was wound fluid. And these are all the different types of
cytokines and proteins. There's ferritin, there's transferrin, there's hyaluronic acid, lactate, lactotransferrin, monoperoxidase, you go on and on and on. And of course, as I've mentioned, there's a number of cytokines and growth factors
that have been identified. And these are, whether they're cause and effect we don't know. But certainly we know they're present, they definitely have an influence, they've been measured,
and they've been associated with healing and non healing wounds. To go on, you can actually see some of these other proteins and proteases both serine proteases and metalloproteinase, and some of these things we don't even know what their function is, or what they're
doing in the venous leg ulcers, and that's really important. And again, here's further showing cathepsins and caspases and kallikrein, and different TIMPs. So all of these things have actually be found in venous leg ulcer wound, whether fluid or biopsy. This actually, probably a seminal article
that looked at, for the first time, the proteomics in patients with both healing and non healing venous leg ulcers. This was collected by wound fluid, it was analyzed by liquid chromatography and mass spectroscopy.
And what they identified was 149 proteins that had differential detection. In the healing there was 23 that were identified, in non healing 26. And actually they then looked at three proteins and analyzed a series of patients,
and these are the number of patients that they've analyzed, to evaluate. And this is what they found, a lactotransferrin S100A9 and the annexins have different expression whether you're healing or non healing. And that's important because these proteins
have some significance, and this is what their significance. Lactotransferrin is important in iron scavenging. And we know that free iron, if it's in the wounds, it's actually very toxic leading to different types of peroxides that are developed, and also cellular pathways that can be disrupted.
So annexins are also important in inflammatory response, and they play a significant role not in just wound healing, but also in the detriments of venous leg ulcers. And S100A9 is actually a calcium binding protein that has significance in wound healing also. So in conclusion it's actually very complex,
the proteomics and degradomics. But they provide an opportunity to study novel proteins, function, and activity in venous leg ulcer. They do provide some proof of concept and possible mechanisms of venous leg ulcer pathology. They identify possible biomarkers, both for
identification of wounds that go on to heal versus the ones that don't go on to heal, as well as treatment and prognosis. And obviously possible targets for therapy. Thank you very much.
- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.
Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates
an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.
You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't
or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.
CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,
we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.
She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.
So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.
Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.
It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign
and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there
but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?
Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy
and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.
So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,
a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,
gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection
it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible
before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains
in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low
or cut out the super renal fixations so you can take them out a little easier. Thank you.
- I think that the most important tip cannot really be summarized in five minutes, which is that these procedures are highly dependent on how well you plan the procedure and how well you really implant the device. That is a fairly long learning curve that I think you need to actually collaborate with people
that they are experienced, and with industry to make sure that you are on the right track on making your measurements to size these devices. But there are a few things to be said about cases that are very difficult, and a few tips that I would highlight on this talk.
First, it's highly important that you build up your inventory so you can get out of trouble. I think you have to have a variety of catheters of your choice, with primary or secondary curves.
The addition of shapeable guides has been a major benefit for these types of procedures. They are fairly expensive, so I would say we don't use them routinely, but they can bail you out. They can allow you to do cases now from the femoral approach that in the past could not be achievable this way.
You have to be able to work on the diffe .035 system, .014 system, .018 system, and know when to apply this. I would like to highlight four maneuvers that we use when vessels don't align.
First, a common maneuver is really not to try to get in a quote/unquote pissing match with the fenestration and the vessel. If you can catheterize the fenestration first, and advance your sheath upwards, and lead a .018 wire into the sheath,
that will basically lock your sheath into the fenestration. Therefore, you don't have to repeatedly catheterize the fenestration and you save a lot of time. You can choose y ose something that has a secondary curve if you have room,
or a Venture 3 catheter, which is one of my choice for catheterization, and you can see here that on this case, the difficulties imposed by a shelf on the ostia of the renal artery, which makes catheterization more difficult. This .018 wire also allows you to bend your sheath
as a guide catheter so that you can achieve a downward curve to catheterize a down-going vessel, like on this renal artery. The second maneuver to highlight is that these devices are constrained posteriorly, and therefore, the fenestrations are naturally moved
posteriorly into the aorta. So one of the first maneuvers is really to try to move the fenestration more anteriorly by rotating the device. Now, some of the companies now have newer constraining mechanisms
that may alleviate some of this, but this is kind of a next maneuver that we do. Finally, rarely nowadays we have to really find more space between the fenestration and the aortic wall, but it is always useful to leave behind a wire when you deploy this device so that in the event
that you need more space, you can perhaps navigate the catheter, inflate, and create some space between the fabric and the aortic wall. Marcelo Ferreira, along with other collaborators, has described a technique that I think is very useful when you have a lot of space.
That's the case, for example, of a directional branch or perhaps if you are using fenestration to target a vessel that is somewhat away from the fabric of the endograft. That's called the snare ride technique. This is summarized on this illustration.
When you see the left renal artery to be up-going, now being targeted from the brachial approach, that was difficult to catheterize, you catheterize that from the femoral approach with an eight French sheath and a snare ride type... You snare the wire from the arm, and then you can
navigate that catheter inwards into the vessel. That can be difficult, sometimes, to actually advance the snare into the vessel. I think that there is some improvement on the profile of these snares that can improve that, but that is a very useful technique,
not only for branches, but also for fenestrations. Finally, sometimes you have too much space. You may seem you are very well aligned on the latitude with the vessel, but in fact, there is so much space the device got displaced on that sac and you cannot simply catheterize the vessel.
It's useful to downsize the system on these cases to a micro-catheter with a micro-wire to find yourself in the sac eventually out through the vessel. Once you achieve that, you would then exchange this micro-wire, usually a glide gold wire, to a .018,
a stiffer wire that is long enough. You advance a balloon that is undersized for that vessel, and with that you can straighten the system and eventually switch that for a wire that is of reasonable strength, such as a rosen wire in this case, and complete the case.
Finally, there is nothing wrong about leaving the battle to be fought another day. It's better to finish a case a little quicker and not end up with leg ischemia and a compartment syndrome and a s the situation
and come back another day. This is a case, for example, that I did a branch endograft. You can see the right renal artery is exceedingly narrowed. I could not find a way in in a reasonable time. I gave myself about half an hour. I decided to quit.
A few days later, I came back through a subcostal incision, got retrograde access, and this literally was a case that didn't take very long and end up doing very well. So in summary, patie select your proper
anticipat stent. To offset these challenges, minimize contrast a master your endovas
it is better to end with a patient alive and fight the battle another day, than to have an excessive long procedure leading to numerous other complications. Thank you very much.
- Thank you for the opportunity to present this arch device. This is a two module arch device. The main model comes from the innominated to the descending thoracic aorta and has a large fenestration for the ascending model that is fixed with hooks and three centimeters overlapping with the main one.
The beginning fenestration for the left carotid artery was projected but was abandoned for technical issue. The delivery system is precurved, preshaped and this allows an easy positioning of the graft that runs on a through-and-through wire from the
brachial to the femoral axis and you see here how the graft, the main model is deployed with the blood that supported the supraortic vessels. The ascending model is deployed after under rapid pacing.
And this is the compilation angiogram. This is a case from our experience is 6.6 centimeters arch and descending aneurysm. This is the planning we had with the Gore Tag. at the bottom of the implantation and these are the measures.
The plan was a two-stage procedure. First the hemiarch the branching, and then the endovascular procedure. Here the main measure for the graph, the BCT origin, 21 millimeters, the BCT bifurcation, 20 millimeters,
length, 30 millimeters, and the distal landing zone was 35 millimeters. And these are the measures that we choose, because this is supposed to be an off-the-shelf device. Then the measure for the ascending, distal ascending, 35 millimeters,
proximal ascending, 36, length of the outer curve of 9 centimeters, on the inner curve of 5 centimeters, and the ascending model is precurved and we choose a length between the two I cited before. This is the implantation of the graft you see,
the graft in the BCT. Here, the angiography to visualize the bifurcation of the BCT, and the release of the first part of the graft in the BCT. Then the angiography to check the position. And the release of the graft by pushing the graft
to well open the fenestration for the ascending and the ascending model that is released under cardiac pacing. After the orientation of the beat marker. And finally, a kissing angioplasty and this is the completion and geography.
Generally we perform a percutaneous access at auxiliary level and we close it with a progolide checking the closure with sheet that comes from the groin to verify the good occlusion of the auxiliary artery. And this is the completion, the CT post-operative.
Okay. Seven arch aneurysm patients. These are the co-morbidities. We had only one minor stroke in the only patient we treated with the fenestration for the left carotid and symptomology regressed completely.
In the global study, we had 46 implantations, 37 single branch device in the BCT, 18 in the first in men, 19 compassionate. These are the co-morbidities and indications for treatment. All the procedures were successful.
All the patients survived the procedure. 10 patients had a periscope performed to perfuse the left auxiliary artery after a carotid to subclavian bypass instead of a hemiarch, the branching. The mean follow up for 25 patients is now 12 months.
Good technical success and patency. We had two cases of aneurysmal growth and nine re-interventions, mainly for type II and the leak for the LSA and from gutters. The capilomiar shows a survival of 88% at three years.
There were three non-disabling stroke and one major stroke during follow up, and three patients died for unrelated reasons. The re-intervention were mainly due to endo leak, so the first experience was quite good in our experience and thanks a lot.
- Good morning everybody. So first of all let me take note of it for the kind invitation to be here, again. These are my disclosures. So Juxtarenal Aneurysm has been described as those aneurysms very close to or even including in the lower margin of renal artery.
And of course the gold standard at that time was aortic supportive clamping and open surgery. Probably open surgery is still the first choice in this very short and complex aortic neck but what do in case of patients unfit for surgery? Or for patients who are asking for
a minor invasive alternative. Of course, Fenestrated EVAR are the solution, the option two, but they require time, are expensive, so what to in case of patients who have no time or cannot wait for this customization process?
Symptomatic patients, patients with huge aneurysm or patients just unfit for fEVAR because of either access or tortuous proximal neck anatomy. So solution is chimney or ovation VENT. What is ovation VENT? It's a kind of open chimney technique,
it's a combination of ovation with renal bare stent. So you know the the new concept of sealing of this stent graft, the circumferential apposition of polymer-filled ring to the aortic wall, typically at 13mm, so to just translate the length of the neck to a specific point
when a couple of millimeter when in that position of course. And you know with the previous, you have just heard the harder device, but with the standard device, the prime and the IX, we have the device positioned
13mm below the lowest renal artery. So, what to do in case of (unclear) when have no apposition of the ring to the aortic wall, we raise the ring, just very close to the renal artery, and then we place some bare metal stent
at the renal BMS. So here you can see our bench test with the fabric of the collars just moved by the bare metal stents. So, VENT is different from chimney, we don't use the covered stents so
it's a lowered provide bracket approach, and more importantly, chimney and endograft are typically competing for the same room so this the reason for gutters, while with VENT we have a stent and endograft, which are not competing for the same room.
The ring is responsible for the sealing and the stent is just responsible for the ventilation of the renal arteries. So this is a typical example, you can see here, a contained rupture aneurysm, in this point, and with a very short neck, so we decide
to land with the first neck and exactly at that level you can see here the steps of the procedure, the contemporary deployment of the renal stent, and the main graft the injection of the polymer, so the first ring is really in contact with the renal stent,
but they're not competing each other and so you can have a nice sealing of the sack. Another case, conical shaped neck, unfit for standard EVAR, unfit for EVAR, because was a huge aneurysm, much more than 8cm, so we decide again to raise the ring,
13mm and fit for standard ovation. And so here you can see the first ring just at this level, the renal stent, responsible for the patency of the renal artery, and you can see here that the first ring is just touching it in one point, the conical neck.
With good sealing. Again, another case with unfit for fEVAR, because of the small access, tortoise access, and so we plant a double VENT, in this case, you can see here again, prucodanus bracket approach, with five french shift,
contemporaneous deployment of stents, and first ring, again nice sealing, and nice follow up with completed sack screen cage, and another one year follow up. So, up to now we have performed 29 cases. We did the first case in June 2015,
technical success was high, 96.6%, we had just one type one endo-leak fixed introaperticaly with the coil embolization. The follow up is, mean follow up is 19 month, and 100% renal artery patency, no further intervention, no sac enlargement,
the majority of arteries, it's shrinkage more than 5mm. So just in conclusion, this option is in, we believe that in selected measures, it's a nice option. It is safe and effective when you can not wait for fenestration graft, like in case of symptomatic
or huge aneurysm, or just patients are unfit for fenestration because of tortuous anatomy or small iliac vessels. Thank you for your attention.
- Here we go. So, we know that late survival of patients with aortic aneurysms is not as good as matched controls and much of this is related to higher incidents of cardiovascular events. Other factors that impact survival are aneurysm size, as well as antiplatelet and statin therapy.
And we know that EVAR has no long-term survival advantage compared to open repair and, in fact, aneurysm related survival is worse after eight years for EVAR rather than open repair and, yet, 50% of our aneurysm patients are alive eight years after repair.
We've already seen about the differences in the mechanism of EVAR versus EVAS. With EVAR there's sac thrombosis, with or without endoleak, and we've previously shown that with sac expansion there's a significantly worse late survival compared to patients with no sac expansion.
This was a VSGNE study and then a larger VQI study showed that not only is sac expansion have worse survival but, even failure to regress so stable sacs also have worse survival compared to those that have sac regression. And this is independent of whether or not there's
an endoleak or reintervention. So, this prompted us to wonder if EVAS might be associated with a difference in All Cause Mortality compared to EVAR, and we know the act of sac management processed with EVAS involves obliteration of the flow loom and minimizing the chance for
type two endoleaks. This was spurred on by, as Jeff had mentioned previously, the excellent freedom from All Cause and Cardiovascular Mortality seen both in the US IDE but also in the global registry. And, on top of that, in a comparison with the report
from the Mayo Clinic, when looking at the EVAS patients from those two studies broken down by aneurysm diameter there seem to be, again, a difference in a three year survival of the EVAS patients compared to traditional EVAR. Why might this be? Well, several reports have come out demonstrating a
difference in post implant syndrome, various inflammatory markers, major adverse events, cardiac adverse events and endoleaks when comparing EVAS with EVAR. And, CRP levels are elevated in the entire
early post operative period with EVAR relative to EVAS. So, we wanted to compare All Cause Mortality with EVAS to EVAR so we used the 333 patients from the US IDE trial, from 2014 to 2016, and a comparison group we used all the EVAR patients in the US VQI
from the same time period and then applied the same exclusion criteria from the IDE being patients on dialysis or with elevated creatinine or rupture were excluded and then we used propensity weighting to account for differences is baseline characteristics and we did
weighting based on aneurysm characteristics and cardiovascular risk factors and implied inverse probability weighting to compare the risk adjusted long-term survival. Our primary outcome was overall survival and this propensity weighted cohort, and as a secondary analysis
we compared survival when stratified by aneurysm diameter, a small, less than 5.5 or greater than or equal to 5.5. And, in the overall cohort what we found was EVAS survival at three years of 93% compared to 88% for EVAR, a 41% lower hazard for mortality that was statistically significant.
When we looked at the patients with smaller aneurysms, we found no benefit, no difference in survival between the EVAS and EVAR. But in the patients with the larger aneurysms greater than, or equal to, 5.5 we had 92% and 86% three year survival, so double the mortality rate
in the standard EVAR patients. So, in conclusion, EVAS seems to be associated with the higher long-term survival compared to EVAR, and this association was strongest in those with largest aneurysms. We think the biology of the AAA after EVAS plays a role,
and we think that this supports the continued evaluation and iteration of this therapy. Thank you.
- Good afternoon to everybody. Thank you very much, Linio and Frank, for the invitation to the great session. First, the main problem is to define who is a no-option CLI patient? So I want to use, this is a young male, with a long history of diabetes, on hemodialysis.
This is the baseline angio. As you can see, the big vessel are absolutely open. We have an open spot of femoral artery, popliteal artery, and then also below the knee vessel are quite open, and we can see that the blood is going very well to the distalis, but in the foot,
we have a disease of all the foot vessel, which is a calcific disease. You can see here, this is the plain x-ray. I think that the plain x-ray of the foot is one of the most important information that we can get on the patients.
For every patient, I want to have this plain x-ray. You can see the medial artery calcification spreading everywhere, dorsalis pedis artery is occluded. We have a small, thin, tortuous, tarsal artery giving some blood to the forefoot. Medial plantar artery is occluded.
The lateral plantar artery is occluded. We have no any clear identification of the metatarsal vessels. This is the forefoot of this patient, and the majority of this patient, with a long history of diabetes and on hemodialysis,
have this medial artery calcification spreading to the tiptoe, and the first toe is totally avascular. This is the reason why this patient developed critical limb ischemia. So who is a no-option CLI patient?
I think that today, a no-option CLI patient is a patient without a target foot vessels. Today, SAD is the most common cause of no-option CLI patient because the SAD is correlated to the age, to diabetes, and end-stage renal disease. We have an epidemic of all of these three vascular factors
in our societies. In the majority of the cases, SAD is actually associated with medial artery calcification, in at least 25% of CLI patients, but today, I think that we are close to 40% present some degree of SAD-MAC.
So in this patient, how to create and master the hybrid foot vein arterialization circuit. This is the patient. My friend, Andrea Casini, vascular surgeon, has done a bypass with the proximal anastomosis of the great saphena vein on the distal P3 segment
of popliteal artery, and here we have this (mumbles) to give him blood to the medial marginal vein. Now, these are very good images, but we must learn how to read these images first. This is an arterialization on the superficial dorsal system of the foot,
so we have an inflow represented from, by the great saphena vein, and an outflow represented fundamentally by the medial marginal vein. We have other collaterals in the superficial system. For example, this is an ancillary superficial vein, and we see a faint shadow of the small saphena vein.
Then we have the deep dorsal system. We have a connection here, a perforant vessel, because it perforates the fascia, and goes from the superficial vein system to the deep dorsalis vein system. Here we have the two anterior tibial veins,
and the dorsalis pedis veins. Then we have the plantar system, the deep plantar system. We have these two plantar veins, the medial plantar vein, these are the two lateral plantar veins, and the deep plantar arch, and the two posterior tibial veins.
Now we have the last system, vein system of the foot represented by the superficial plantar systems, the Lejar's sole, and you can see here, this network, a network without valves, very thin veins, in all of the superficial plantar sole. We have a lot of connection
between these four systems of the foot. This is, for example, the perforator that I have dilated to give blood not only on the superficial dorsal system, but also to the deep dorsal system. We have many collaterals. I have embolized, for example, the anterior,
proximal anterior tibial veins, in order to avoid a precautious still of blood at the ankle level. I have embolized these collaterals that are perforator coming from the superficial dorsal system to the deep plantar system,
and stilling blood precautiously, and here we have the forefoot cross, which is the main cross between the three system, the superficial dorsal, the deep dorsal, and the deep plantar. Now, we can see that the arterialization was able to fill all the forefoot vein system,
and this is very important. When we get the direct blood flow through this collateral to the Lejar's sole, we know that the arterialization can really function. So I asked to my foot surgeon to do a non-geography guided surgery, wait for swelling,
wait for arterialized network expansion, respect the arterialized circuit, respect the forefoot cross, because we think that after foot vein arterialization, the foot is still ischemic, the arterialized circulation has not the same function of the standard circulation.
We must use a tension-free surgery to avoid focal ischemia. This is the tension-free surgery. I know that a transmetatarsal amputation could have been maybe more structurally stable, but I prefer to use this minimal surgery, and the patient has a complete healing
in two months, in two months. Now, the main problem of foot vein arterialization is to understand why this arterialization functions. Now, I propose you two hypotheses. The first is the mechanical hypothesis. Arterial and hydrostatic pressure force vein valves
leading to progressive valve incompetence, distal vein recruitment, and finally, direct issue nutrition by reverse blood flow. In 1906, Alexis Carrel made some experiments on dog, connecting with an anastomosis, the common femoral artery with the common femoral vein,
and he observed that there was the need of three hours at least to force by blood pressure the valves of the vein. Final, he said that practically complete reversal of the circulation is established about three hours after the operation. I want to prepare you this patient.
Observe, this is the acute phase immediately after treatment of foot vein arterialization with some leaking of blood on this vein that I have dilated. Eight days later, three months later, observe this geometry. Are impressive in my opinion.
Can we think that this geometry of vein, pure veins, can feed tissues like a normal standard geometry of artery? When I see these images, I answer, yes, I believe it. I believe it because we know that the venular plexus have a very thin vessel wall like capillaries, so it's a way, when we see these images,
we can really think about a complete reversal blood flow or something that is able to get the tissues and to feed the tissues. The second hypothesis is a biological hypothesis. Vein wall shear stress promotes a global remodeling and/or neoangiogenesis of the vascular system of the foot,
creating a new distribution system, and it was in hypothesis proposed by Languar. This is a LimFlow procedure on a patient like the first one, completely calcified, and this is the evolution, baseline, acute result, 45 days, 90 days after transmetatarsal amputation.
Look at this, 90 days, three months after the LimFlow procedure, the percutaneous deep vein arterialization, and about two months after the transmetatarsal amputation. This is really impressive. Look at these images.
What type of geometry, this one. Look at the baseline angio, and now we have all this vessel connecting with the veins. I am injecting blood contrast dye, so here in the distal stent of the LimFlow procedure, so we have no any blood flow coming
from the previous diseased arteries. This is the patient some months later. This is another patient baseline. An arterialization and after the occlusion of this arterialization, you can see this new neoangiogenesis.
Our results in 36 patients. We're able to get a 69% of limb salvage at 10 months, and I think that in highly selected no-option CLI patient, foot vein arterialization can be the only solution to avoid major amputation. Thank you very much for your attention.
- [Man] Bert, what some magnificent imaging and congratulations. When, just so that I'm clear, I mean, I've done, been lucky enough to have done a couple of LimFlow cases, and we are performing valve, using a valve at the time to perform valvotomies.
Are you suggesting that the pressure alone is enough to do something for the valves of the foot or how extensive do you think valvotomy needs to be in these cases? - [Man] This is our major limit because our limb salvage was correlated to the patency of the bypass,
and our patency was very poor, and it was very poor because we have not the reverse antegrade valvulotome, which is a part of the LimFlow kit. It's not sold alone, so we used some artisanal ways, like high pressure inflation of an oversized balloon. This is very effective but you have a restenosis rate,
very high reocclusion, thrombosis, and every failure, precautious failure of the graft of the bypass was correlated to a major amputation. - [Man] Yeah, okay. Any other questions or comments? - [Man] Is there any difference in your opinion
between a (mumbles) a total percutaneous? - [Man] I think that a total percutaneous procedure is a procedure with a target, which is the posterior system, essentially, because very few cases were done on the anterior system and the anterior deep system, in my opinion, is not a good target for the arterialization
because it is the poorest system, base system of the foot. The hybrid procedure can be done on both, the superficial dorsal system and the deep system. Obviously, you must choose according to the imaging of the baseline imaging or the vein system. Every patient is very different,
so you need to choose the proper target, vein target, into the foot. - [Man] Good. - [Man] Yeah, Roberto, this is very exciting stuff, and Rico and Asher and I tried to do this with primitive valvular destruction back in the 90s.
We had some incredible successes, but we also had some very bad failures. Patients got big, very much edema, one got into heart failure, one actually died, we felt, because of the AV fistula, and so we stopped, but can you talk about the mode of failure.
The successes are brilliant, and I think you definitely have something. We had some good cases but we had, our failures were all with the patent graft, and did you, you said I thought that you only failed when the graft closed.
- [Man] I read all your paper regarding this before starting, so I know that it's not easy. First of all, the key problem either the selection of patient. One of the key factor is heart function. We selected only patient with good heart function,
and second, the procedure is not a single procedure, standalone procedure. We had to follow the patient for months. Healing needs months, maybe repeat intervention, so you need a patient with an acceptable life expectancy and acceptable quality of life expectancy,
and acceptable working capacity, a salvageable foot, so a patient that can really cope with you in this long process of healing. The selection is a key factor. - [Man] Second question, why didn't you use the LimFlow exclusively?
- [Man] Because the LimFlow procedure is very costly, obviously, and in Italy, it is not reimbursed absolutely. This is the main reason.
- Speaking about F/EVAR and Ch/EVAR, and try to prove that the evidence of Ch/EVAR is solid, especially in some circumstances also better than the evidence about F/EVAR. Well, let's try to define this title. Durability of Ch/EVAR is solid if the procedure is done right.
And I think this is very, very crucial. We heard and we know the PERICLES Registry tried to evaluate this technique, collecting the worldwide experience from 13 US and European university centers, and published in annals of surgery.
And also, the PROTAGORAS study focused exactly on the performance of the Endurant device in order to avoid this heterogeneity which we had in the study (mumbling) published literature up to now. Focusing exactly on the Endurant device
in combination with balloon expandable covered stent. And based on these two registries and studies, we identified four key points, four key factors, which we'd like to give you as take home message in context to have the Ch/EVAR technique as solid procedure. So, we learned that the technique performs very well
if we use the technique for single or maximum double chimney grafts. We highlighted how important it is for this technique to use suitable combinations between aortic stent-graft and chimney devices. And we learned also, how important is the oversizing.
We have to have enough fabric material to wrap up the chimney grafts of 30% of the aortic stent-grafts. And in this context, we highlighted also the importance of creating a new sealing zone of 20 millimeter in order to have durable results.
Which is also very important is to know when we should probably avoid to perform the technique, and I would like also to highlight these points. So, we learned in case of excessive thrombus formation in the thoracic, especially also LSA, we have to be very, very careful with this technique,
because of course, we have the risk of cerebral vascular events. We learned also that performance of this technique in a neck diameter of more than 30 millimeter is associated with high risk of Type 1A endoleaks, which will be persistent, and which probably
lead to failure of the treatment. Which also learned is to evaluate very carefully the morphology of the renal arteries, especially focus of the calcification of the stenosis, and also of the diameter. And last but not least, it's very important to
have access to the suitable materials for renal cannulations, and also experience. So, if we consider these key points of doing and not doing chimneys, I think we have a very good base to have durable and good results over the time. And we have seen that.
You saw it very nicely (mumbling) the changes of the diameter pre and postoperative, but you forgotten to highlight that there was highly significant in the PERICLES and in the PROTAGORAS Registry. Also, what we have seen is that
more than 90% of the patients had stable or shrinkage of the sac after a CT follow up of two years. And here's a very nice overview of the Kaplan-Meier curves, highlighting that the technique performs very well in this specific combination of the Endurant devices,
abdominal device, and abdominal chimney grafts like the Advanta. Having a very nice chimney graft patency of almost 96%, and a freedom from chimney graft later interventions of 93%. Very important is also if we create these very good sealing zone of two centimeters.
We have a very, very low incidence of new Type 1A endoleaks needed reintervention. And here is an example of a case which had a very short sealing after the previous treatment with chimney for the left renal artery, and over the time was necessary to extend the sealing zone,
creating these durable solution and transformating from single to triple chimney, as we can see here. So, this is very important to know and to highlight. In context of the better or not better for F/EVAR, we can see now the results, and we've compared with meta analysis of F/EVAR.
We see that the results are similar. Keeping in mind also that in F/EVAR, we involve the SMA either as scallop or as bridging device, and we don't have evidence about the SMA outcomes and the SMA patency because most of the patient probably who will die, and will not perform autopsy
for each patient if it has an SMA occlusion or not, so I believe it is underestimated the really incidence of survival after F/EVAR. And also, regarding the patency, we have also in this context, similar results after chimney compared to the patency of the bridging device after F/EVAR.
So, ladies and gentlemen, I believe we've considered these key points. We can achieve very good results performing Ch/EVAR, having as a solid and valuable procedure for our patients. Thank you very much.
- Thank you, I have no disclosure for this presentation. Aorotopathy is a different beast as oppose to patients with dissections that we normally see in the elderly population, but we have the same options open surgery, endovascular, and hybrid. If they all meet the indications for surgery so why not open surgery?
We know in high volumes centers the periprocedural mortality acceptable in especially high volume centers. The problem is the experience surgeons are getting less and less as we move into more and more prevalence of endovascular. And this is certainly more acceptable in lower or
moderate high risk patients. So why not be tempted by endovascular in these patients? (to stage hand) Is there a pointer up here? So the problem with aorotopathy is the proximal and distal seal zones and we've already heard some talks today about possible retrograde dissection,
we've also heard about nuendo tear distally and aorotopathy is certainly because of the fragile aorta lend itself to these kinds of problems. But it is tempting because these patients often do very well in the very short term. The other problem with aorotopathy is they often have
dissection with have problems for branch unfenestrated technology and then of course if these dissection septum are near the proximal and distal seal zones, you're going to have a lot of difficulty trying to break that septum with a ballon and possibly causing new
entry tears proximally or distally. Doctor Bavaria and his colleagues from Italy were one of the first ones to do a systematic review and these are not a large number of patients but they combined these articles and they have 54 patients. Again, the very acceptable low operative risk, 1.9%.
But they were one of the first ones to conclude and cation that TEVAR in these patients, especially Marfan's patients in this series carries a substantial risk of early and late complications. They actually cautioned the routine use of endovascular stent grafts.
One of the largest series, again stress, these are not large numbers but one of the largest series was just 16 patients and look at this alarming rate of primary failure. 56% treated successfully, 40% required conversion to open operation and interestingly enough
43% of those patients had mortality. My friend and colleague at the podium, doctor Azizzadeh was given the unbeatable task of arguing for endovascular therapy in Marfan syndrome and the best he can come up with was that midterm follow up demonstrates sizeable numbers of complications but,
he identify area where probably it was acceptable in patients with rupture, reintervention for patch aneurysms and elective interventions in which landing zone was in a synthetic graft. So why not hybrid? Well this seems to be the more acceptable version
of using TEVAR, if you can, in these aorotopathy patients. But this is not a great option because in this particular graft that you see this animation, we're landing in native aortic tissues. So really, what you have to do is you have to combine this and try to figure out a way to create a landing zone,
either proximally or distally and this is a patient and not with Marfan's this time but with Loeys-Dietz, who we had presented recently, previous ascending repair but then presented with horticultural abdominal aneurysm as a result of aneurysm habilitation of a previous dissection and here
you see a large thoracal abdominal aneurysm on the axial and coronal and as many of these patients with aorotopathy express other problems with their multisystem diseases and you can see the patients left lung is definitely not normal there, left lung is replaced with bullae and this is a patient who would not do well
with an open thoracal abdominal repair. So what do you do? You have to create landing zones and in this particular patient, he had a proximal landing zone so we were able to just use a snorkel graft from the mnemonic but distally we had to do biiliac debranching grafts to to all his vistaril arteries
and then land his stent-graft in the created distal zone and as you can see, we had an endoleak approximately and thank goodness that was just from a type II endoleak from the subclavian artery which we were able to take care of with embolization and plugs.
And there is his completion C.T. So not all aorotopathy is the same, this is a patient who presented with a bicuspid aortic valve and a coarctation and I would submit to you, this is not a normal aorta. This is probably a variant of some sort of aorotopathy,
we just don't have a name for it necessarily, and do these patients do well or do worst with endovascular stent-graft, I just don't think we have the data. This particular patient did fine with a thoracic stent-graft but this highlights the importance of following these patients and being honest with the patients family and the
patient that they really do have to concentrate on coming back and having closer follow up in most patients. So in summary, I think endovascular is acceptable in aorotopathy if you're trying to save a life, especially in an acute rupture or in an emergency situation, but I think often we prefer to land these
endovascular stent-graft in synthetic. Thank you very much.
- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --
- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.
But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,
is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy
in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.
The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation
so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later
that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low
and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse
even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean
as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques
different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between
pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients
are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system
you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because
this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out
now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference
between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing
a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is
the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories
and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here
again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result
and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not
fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again
look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as
the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here
This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you
- Thank you very much for the opportunity to speak. I will admit that I don't think we've got it all figured out, yet. But we'll go ahead anyway. So, persistent type two endoleaks do occur with some regularity and only about a third of them will resolve spontaneously, but fortunately
rupture is rare. A persistent endoleak with a sac expansion is our most common indication for treatment. We've got multiple treatment modalities, typically with a high initial, technical success, but the overall clinical success is not quite as good.
And so as we've learned the natural history is poorly understood, and there's no real strong evidence to guide our treatments. We tend to use CT image fusion to help us perform transarterial lumbar embolization as well as this is a transarterial from a hypogastric to coil
both lumbars and an IMA as well as the sac. We'll also use a direct sac puncture occasionally from a translumbar approach with the fusion guidance and also use that to guide us in terms of placing our embolic agents and then we'll also perform the transcaval embolization more recently.
This has become preferred over the translumbar approach and we can use that to then guide treatment and we use coils and glue combined typically now. We've performed over 100 procedures in 56 patients averaging two per patient. The average time from the endoleak to the procedure was
37 months and our follow-up is 27 months, about half had their EVAR performed at our institution and then the other half outside and about one in four of those had already had some sort of type two endoleak treatment. At our initial treatment, it's typically a trans, or it's been most commonly, a transarterial lumbar embolization
followed by IMA, followed by transcaval, and then direct sac puncture. Freedom from re-intervention is not perfect, so by one year it's about 50% we'll have a re-intervention for ongoing sac growth. For our secondary procedures, open repair has actually
become more common, followed by transcaval embolization then transarterial lumbar, IMA, direct sac puncture, and then also relining proximal extension with modified graft or anchors or cuffs. We have 10 patients that underwent open repair with a one year freedom from open repair of 94%.
Early on, we performed graft explantation for persistent growth with the type two endoleaks, then we switched to sacotomy initially without a proximal reinforcement. One of these was a patient who did rupture from an isolated IMA type two endoleak. We ligated the IMA, opened the sac, found no other bleeding,
closed the sac, and he's been fine for five years. We've taken to reinforcing the proximal attachment prior to opening the sac. One patient already had a PMEG for a type one and then more recently, we've been placing endoanchors for the proximal attachment prior to opening the sac.
Our clinical success from a single intervention is only 33% with multiple interventions it goes up to 67% and if you include the open repairs with sacotomy it goes up to 88%. This is for sac stabilization or decrease. So, I do still believe that large type two endoleaks
with sac expansion should be treated for lumbars. We will still typically go transarterial for the IMA. We'll go from the SMA. If we can't do those, or we failed, then we'll go transcaval as our next approach followed by translumbar. We like to treat both the nidus and the source feeding
vessel and if we fail with all of those, we proceed to sacotomy then will now place the proximal endoanchors for fixation. What we have been seeing, though, more commonly is this where there's poor attachment at the proximal end or distal end and a patient who we've performed
multiple procedures for type two endoleak and there's ongoing sac growth and even though there's no definitive type one leak, clearly if there were we would just go ahead and treat that, but in those patients who don't have a defined type one or three, but they have poor apposition, then we'll consider relining them,
extending them, anchoring, etc. And then, only then, if they still have problems would we consider treating the small type two endoleak. I'm looking forward to the discussion 'cause I think we've got it all figured out. Thanks.
- Thank you very much, Frank, for the opportunity to be part of this fantastic panel. So, I'm no more a part of the debate, and I will not show the differences, but if we look on the arch, on the literature addressing the different types of repair, we can see that the result are in the same range, approximately.
And despite the fact that we didn't spoke about this, probably, there is a bias of selection where else the best patient will be addressed by open surgery, patient that fits for branched and FEVAR will be treated by those technology, and the remaining of the patient
is addressed by parallel grafts. There is a second point I would like to address and this is one part of my talk, is that the results for the endovascular options are not good, are not so long described in the literature. There are some papers with longer follow-up,
but in the mean, the follow-ups are rather short. So, let's go to our expanse that is a little bit longer. In the arch, we treated 94 patients. We had a mortality of 14% stroke, or neurological complication 8%, endoleak, primary, 18%, but we addressed 40% of acute patients,
and 50 patient with redo thoracic surgery. So, an example: 75 years old patient, he had complicated type B dissection with malperfusion, did get the TEVAR with a sandwich for the LSA. In the follow-up, he showed an aortic enlargement with the dissection extending proximal to the LSA,
and he had, again, and antegrade perfusion of the sur-lumen. He refused general anesthesia because he had severe delire when he was treated first. So we address this with periaortic grafts. We put one chimney for the brachiocephalic trunk in the aorta, one chimney for
the left carotid artery in the ascending aorta, then we deployed a TAG in the aorta then, to match the diameter of the BCT we extended the first viable, which is 13 mm, and you can see here, the six month follow-up with a nice result. So, if we want to go to long-term results,
we freezed a cohort of patient we treated 2009 to 2014. These are 41 patients with an Euroscore II of 28%, 68 years the mean age, 30 day mortality was 12%, so half of the predicted. You see here 42 months follow-up of this cohort. There is this typical mortality of 10% a year
following the procedure, due to the comorbidity cardiac pulmonary renal functions, freedom of branch occlusion is nice and the branch behaved stable. There have been reintervention during the follow-up, mainly to treat endoleaks, branch issues,
or other problems on this patient, but you see there is a three and a half year follow-up and the rate of reintervention is the same than for other endovascular options. Looking now at the more complex patients, the free vessel in the arch, you see
that the results here are good too, for the parallel grafts. Here down, we see one patient dying, no stroke, no endoleak. If we go to the visceral patient, here the literature review shows a mortality of 4.7%, with an endoleak type 1A of 7% for the parallel grafts. If we do compare now CHIMPS with FEVAR and open repair,
you can see that maybe the difference is more redo, but it's not really much more than for the FEVAR/BEVAR, and here is particularly due to the gutters. We treated here also for the long-term follow-up, we freezed a cohort of patient, 127 patient, 40% symptomatic, 11% ruptured patient.
Hostile chest, 37%, hostile abdomen, 26%. Most of the proximal landing was above the renal artery, mostly chimneys, but also reversed grafts and sandwich. Here a case, patient that was rejected after rupture from two centers to one because he was unfit for surgery, the other because he qualified not for FEVAR/BEVAR.
He had a challenging anatomy with an occluded left renal artery and celiac trunk, a shaggy arch and LSA, so we treated him transfemorally with two parallel grafts and you see the outcome of this patient. So, there are reinterventions. The mortality in this cohort is 2.4%, endoleak is 7%.
Reintervention, chimney-related, mainly gutter endoleaks. These are the curves in the follow-up, and you see that the results are similar than the patient in the arch with a need for reintervention, but that's the same for any kind of endovascular procedure in the arch.
18% at three years of reintervention. This has been for branch thrombosis or endoleak cages. So, in conclusion, the results are good for parallel grafts in the arch and in the visceral types, and selected patient, they need an appropriate anatomy, a life expectancy of two years.
They behave durable up to more than three years mean follow-up, taking into account the number of reintervention. The unsolved issue with the parallel graft is the gutter, so this technique can improve, and you can see here that they may be solution for the future.
This is an anti-gutter design from Endospan that really eliminates any kind of gutter endoleak and wandering, and this will be the patient cohort that we will compare with other repair technique in the future. Thank you very much for your attention.
- I'd like to thank Dr. Veith for allowing me to come back to present here. I have no disclosures. A recent large study, retrospective study from Canada looked at the bleeding complications associated with oral anticoagulants, and they identified that there were
significant differences in the patterns of bleeding when compared to the DOACs with Warfarin. Patients receiving Warfarin had a slightly higher rate in intercranial hemorrhage and hematuria, whereas patients receiving DOACs had a significantly higher rate
of gastrointestinal bleeding. In their review of the treatment patterns for these bleeding complications, the patients receiving Warfarin had a significantly higher rate of a Vitamin K administration as would be assumed
and prothrombin complex concentrate administration significantly higher than in the DOAC group. The DOAC group did because they had a higher rate of GI bleeding. Probably had higher rate of packed red blood cells transfusion as well.
Their treatment patterns were in general agreement with generally accepted practice guidelines for Vitamin K antagonist-associated bleeding and that includes for non-major bleeding Vitamin K administration, transfusion of blood components as necessary
for red cells and platelets as necessary but for major bleeding a slightly higher rate of Vitamin K administration, and then the Kcentra, or the 4-factor prothrombin complex concentrates which are administered on a dosing
which depends on the patient's initial presenting INR. The cost of a 4-factor prothrombin complex concentrate's average wholesale price is about $1.20 to $1.60 per unit which equates to about $2200 to over $5000 per treatment for patients receiving Kcentra. This is in contrast to patients receiving FFP
with a cost of about $1600 per patient. We, in our institution, tend to underutilize the 4-factor prothrombin complex concentrates despite their advantages. The advantages of the 4-factor PCCs for reversing Vitamin K antagonist-associated bleeding
include much more effective hemostasis, much more rapid INR correction, 62% versus 9% for plasma, and then median total volume which was significantly lower with the 4-factor PCCs compared to a much higher volume needed to resuscitate and to reverse the INR, fairly ineffectively, in the patients receiving plasma.
Now moving a little bit on to the direct thrombin inhibitors and the factor Xa inhibitors. They are ubiquitous in our practices in vascular surgery and cardiology. That's just going to increase even more with the recent FDA approved indication
for major cardiovascular event reduction in the patients with PAD. Fortunately, the patients receiving DOACs have a somewhat lower rate of bleeding complications compared to the Vitamin K antagonists, although that's not zero.
I'll go a little bit into the specific reversal agents for the DOACs. The first of these being Idarucizumab which is an antibody fragment directed against Dabigatran. It has a dosing, which is fairly simply, of five grams of intravenous bolus
with an additional five gram intravenous bolus which can be administered if there's ongoing bleeding. It's a fairly short half-life, 47 minutes. The cost of this medication is fairly similar. $3600 to $3800 dollars per dose for these patients. The benefit of this is that it actually
irreversibly binds to the Dabigatran and increases the illumination of that medication. I will just very briefly go into the clinical studies that led to the approval of Andexanet. Patients, basically 67 patients, who had major bleeding, gastrointestinal bleeding, intracranial hemorrhage,
and there was, in brief, just a very significant robust reduction in the factor Anti-Xa activity approved in May of 2018. It is used to treat Rivaroxiban and Apixaban. It has a fairly complex dosing protocol which is dependent on the type of
DOAC which is being administered. The last dose and the last timing for the last dose. The cost of this medication is way out of the ball park compared to the other medications. $3300 per 100 milligram vial equating to a low dose infusion of $26000
and a high dose infusion of $59000. CMS does allow for additional payment of $14 to $15000 per patient, but that still does not counteract that significant cost. There is also the problem with regard to the rebound activity which occurs at
four to six hours later. So I'll briefly go into the CHEST guidelines which just came out in August of this year saying that for minor bleeding, NOAC, and Vitamin K bleeding you just reduce the dose or decrease it. For moderate bleeding, transfusion as necessary
and consider charcoal for Dabigatran, and for severe, life-threatening bleeding consider the specific anticoagulant reversal agents. However, I predict that our hospitals over the next year are going to be grappling with who will be doing the approval for these medications
and how many will be administered at any one time point. Thank you.
- Thanks, Stefan and Frank for having me back again this year. These are my disclosures as it pertains to the renal topics here. We all know that renal dysfunction severely impacts survival, whether we're doing open or endovascular aortic repair,
as you see by these publications over the past decade, patients with no dysfunction have a significant advantage in the long term, compared to those patients who suffer acute kidney injury, or go on to be on new hemodialysis. When you look at the literature,
traditionally, through open repair, we see that the post-operative rate of acute kidney injury ranges anywhere from 20 to almost 40 percent, and it doesn't seem to vary whether it's a suprarenal or infrarenal type
of clamp or repair. Chronic renal replacement therapy in this population ranges somewhere between 0 and 3 percent. That really forms a baseline when we want to compare this to the newer techniques such as chimney and fenestrated or branched EVAR.
Now, if you look at the results of the ZFEN versus Zenith AAA trials, and this is published by Gustavo, the acute kidney injury rate is approximately at 25%, acute kidney injury rate being defined as patients, excuse me, greater than 25% change in GFR,
but in one month acute kidney injury rate is 5% for FEVAR and about 9% for EVAR in this study. There's no difference in these rates at two years or five years between the Zenith AAA and the ZFEN devices. What about the progression of patients
with Stage 4 or Stage 5? At two years, it's about the same, 2% versus 3% for EVAR, and at five years, 7 and 8% respectively. Overall, progression to renal failure occurs in about 1.5% of patients in this cohort.
Well, how does that compare to chimney cases, if you look at the Pythagoras and PERICLES studies, there are a limited number of patients, you see in Pythagoras, 128 patients, 92% of them had either one or two chimneys, meaning generally addressing renal arteries in this case,
patency of those grafts was about 96% and there is no real discussion in that manuscript of the degree of acute kidney injury. And in PERICLES registry, however, they report a 17.5% incidence of acute kidney injury post-op,
and a 1.5% incidence of temporary or permanent dialysis. What about if you compare them? This is a publication in 2017, if you look at both of these studies, very similar, 17.8% for acute kidney injury in FEVAR, and about 19% for a chimney.
You have to realize, though, there are more complete repairs in the FEVAR group, and there are more symptomatic patients in the ChEVAR group, so these aren't completely comparable, but you get some idea that they're probably in the general range of one another.
So the real questions, I think, that come up, is, which arteries can you sacrifice? Are renal embolizations impacting patients' overall function? And what is the mid-term impact of branch and fenestrate on volume of your kidneys
and patients' eGFR. We've studie we looked at the incidence and clinical significance of renal infarcts, whether we actually embolized these pre-procedure,
or whether we accidentally covered or intentionally covered an accessory renal artery, what was the outcome of those patients? We see over time, the average renal volume loss, calculated by a CT scan and VAT volume, is about 2.5% if you embolize it
and if you just cover an accessory renal, about 6.4%. But overall, about 4%, didn't change significantly, overall the GFR changed over the lifespan of the first two years of the patient of 0.1, so it wasn't a significant clinical impact on the patient's overall renal function.
Now what about looking at it specifically of what happens when you do branch and fenestrate cases with respect to eGFR and volume of those? We presented this at this past year's SABS, and it is in submission. If you look at the changes of eGFR,
you notice that in the first six months, the patient declines, but not significantly, and then you see in the graph there, it tends to come back up by a year, year and a half. Very similar to what Roy Greenberg published in his initial studies,
but what we did in this study was actually compare it to the age match publications, and you see that eGFR over time was similar to what happens in age-related changes, but we also noticed that 16% of the patients, 9 of 56, had improvement of their eGFR
to greater than 60. Now whether this is just related to the inaccuracy of the eGFR and its variance, or whether we actually improved some renal stenosis, is difficult to tell in this small study. In conclusion, open, fenestrated,
and chimney EVAR procedures are associated with acute kidney injury in approximately 20% of patients. Causes of deterioration are likely multifactorial and may be different for each technique used. Renal infarcts from covering accessory renal arteries
and embolization occur in about a quarter of the patients, and is a small contributor to renal decline over time. Renal decline made after FEVAR is similar to associated with age. Thank you.
- I want to talk on managing branch complications. This is my disclosure. We overlook in the Berlin-Brandenburg Helios Vascular Center about 466 patients treated with branched, TVAR and fenestrated EVAR devices. All patients received Zenith stent-grafts, custom made devices, T-Branch, or standard fenestrations
in all cases. The target arteries that we are talking about were renal, SMA, celiac access and internal iliac arteries. We used exclusively bridging stent-grafts that were balloon expandable stent-grafts. This is the differentiation of the patients
so we had EVAR fenestrated grafts in 190, branched TVAR in 138 patients, 93 of them were off the shelf devices and T-branch. EVAR with iliac side branches in 138 patients and all together we treated target arteries of 1270. You see the hospital mortality of these procedures
you can see a clear difference between the EVAR fenestrated graft and the branched T version are much more complex procedure and although overall mortality was 4.9% over these 13 years. What happened in these patients we experienced
in 44 patients, 44 complications in the target arteries so unfortunately one target artery problem per patient in these complicated cases. This means rate of 3.5% problems in the target arteries overall. Involved were renal arteries in 32 cases,
SMA in 10 cases and the celiac artery in two cases. What did we do in these cases? Managed the complications once thrombolysis was different devices for example were Rotorex stenting of the dissected vessels, coiling if unavoidable or occlusion of the side branch if no access was possible.
Show you some examples. This is a very serious complication where we were unable to enter the SMA resulting in occlusion of you see on the right slide that this was solved by laparotomy and retrograde access to the SMA.
This is a stenting of a dissected renal artery which could be managed quite nicely with an extension of the stent. Here we have again a prolonged intraprocedural SMA occlusion. We finally managed to enter the vessel
but it was very, very long and prolonged time. This is an inaccessible celiac artery where we have finally had to skip, not iliac sorry, celiac artery where we had to skip the implantation finally and occlude the branch with Amplatzer plug.
All together if you look at these complications in 34 cases we were successful in clinical point of view. In 9 patients complication was little and majority of these were complications involving the SMA. Eight of nine patients had with severe complication in the SMA and died
and so the SMA complications contribute, compared to the mortality, 40% to the procedural mortality in these branched cases. So in conclusion, injury to target artery in endovascular repair with branched and fenestrated stent-grafts are rare
but may be a serious complication especially damage to the SMA has a high mortality and thus further improvement of endovascular skills, instruments for example moveable sheaths which we had not available in the beginning and troubleshooting devices are mandatory
to avoid these complications. Thank you very much for your attention.
- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company
for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.
The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the
middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,
which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up
in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.
Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,
embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,
we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,
which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.
We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,
excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success
just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and
no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.
We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,
and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.
We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,
post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch
blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it
through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,
we actually have several publications out, demonstrating safety and ethicacy. Thank you.
- Good morning, I want to thank Professor Vitta for the privilege of presenting on behalf of my chief, Professor Francesco Speziale, the result from the EXTREME Trial on the use of the Ovation stent graft. We know that available guidelines recommend to perform EVAR in patient presenting at least a suitable
aortic neck length of >10mm, but in our experience death can be a debatable indication because it may be too restrictive, because we believe that some challenging necks could be effectively managed by EVAR. This is why when we published our experience 2014,
on the use of, on EVAR, on the use of different commercially available device on-label and off-label indication, we found no significant difference in immediate results between patient treated in and out IFU, and those satisfactory outcomes were maintained
during two years of follow-up. So, we pose ourself this question, if conventional endografts guarantee satisfactory results, could new devices further expand EVAR indication? And we reported our experience, single-center experience, that suggests that EVAR by Ovation stent-graph can be
performed with satisfactory immediate and mid-term outcomes in patient presenting severe challenging anatomies. So, moving from those promising experiences, we started a new multi-center registry, aiming to demonstrate the feasibility of EVAR by Ovation implantation in challenging anatomies.
So, the EXTREME trial was born, the expanding indication for treatment with standard EVAR in patient with challenging anatomies. And this is, as I said, a multi-center prospective evaluation experience. The objective of the registry was to report the 30-day and
12 month technical and clinical success with EVAR, using the Ovation Stend-Graft in patient out of IFU for treatment by common endograft. This is a prospective, consecutively-enrolling, non-randomized, multi-center post market registry, and we plan to enroll at least 60 patients.
We evaluated as clinical endpoints, the freedom from aneurysm-related mortality, aneurysm enlargement and aneurysm rupture. And the technical endpoint evaluate were the access-related vascular complications, technical success, and freedom from Type I and III endoleaks, migration,
conversion to open repair, and re-interventions. Between March 17 and March 18, better than expected, we enrolled 122 patients across 16 center in Italy and Spain. Demographics of our patient were the common demographic for aneurysm patients.
And I want to report some anatomical features in this group. Please note, the infrarenal diameter mean was 21, and the mean diameter at 13mm was 24, with a mean aortic neck length of 7.75mm. And all grafts were released accorded to Ovation IFU. 74 patients out of 122
presented an iliac access vessel of <7mm in diameter. The technical success reported was 98% with two type I endoleak at the end of the procedure, and 15 Type II endoleaks. The Type I endoleak were treated in the same procedure
by colis embolization, successfully, and at one month, we are no new Type Ia endoleaks, nine persistent Type II endoleaks, and two limb occlusion, requiring no correction. I want to thank my chief for the opportunity of presenting and, of course, all collaborators of this registry,
and I want to thank you for your attention, and invite you, on behalf of my chief, to join us in Rome next May. Thank you.
- Dear chairman, dear colleagues and friends, it's my pleasure to be again with you. Nothing to declare. In our experience of CCSVI and angioplasty we have more than 1,300 patients with different neurological disorders. Not only MS, but also migraine,
lateral amyotrophic sclerosis, Parkinson's disease, left sided amaurosis. We published our data with an emphasis on the safety of the procedure. We had virtually zero percent of serious complication. What about the clinical improvement?
In fact, we noticed function improvement in more than 62.5% of these patients. And in fact, the group of Pierfrancesco Veroux showed similar between 50 and 60% of the patients restoring the normal blood venous flow. In fact, in their work was shown that the type
of anatomic disturbance, anatomic feature is very important predictor if the flow will be restored by the simple PTA. And the most important into the brave dream trial was also that, in fact, the restoration of the flow was achieved in around 70% of the patients.
And exactly in these 70% of the patients with restored flow like Paulo emphasized already, there were lesion, 91% of them were lesion-free on the MRI, and 77% of them were lesion-free on the six-month. We performed a substudy regarding the hypercapnia
and hypoxaemia of the jugular veins in the CCSVI-positive patients. And what we have described in this 178 patients with CCSVI and 50 healthy control group. In fact, we established that the patients CCSVI-positive the venous sample by the jugular veins was typical
with hypercapnia and hypoxaemia in desaturation, huge desaturation with improvement after the balloon angioplasty in all three parameters. What was the reason for that? In fact, in nine patients of our group we examined, the perfusion, the nuclear perfusion of the brain
before and after the treatment. I'm here presenting non-positive for MS young patient without MRI demyelization. And but on the brain perfusion he had deep hyperperfusion on the left side, and the patient was complaining with deep fatigue.
And we saw practically full occlusion of the enominate vein. And after the recanalization using first coronary and after it peripheral balloons, and in this particular case we had to stent finally. And you see still persistence of a huge crossover collateral even after ballooning.
But after stenting we saw practically full restoration of the flow. You see in less than three to four seconds it was very interesting to see on the perfusion imaging, nuclear perfusion, full restoration of the flow of this gentleman.
So this is very important to emphasize that there is direct relationship between the blood gas disturbances on the brain level, and demyelinization process. What about the PTA? It's probably not the optimal treatment.
We have to establish reliable clinical and anatomical predictors for vascular and clinical success in order to answer the important questions: who will be vascular responders, or MRI responders, and finally the clinical responders in this group of patients?
And concluding, ladies and gentlemen, the CCSVI is a real vascular pathologic entity and is probably a trigger for more than one neurologic degenerative disorder. Endovascular treatment, balloon, PTA, and stenting of CCSVI is feasible and safe.
Methods and strategies improving the early and late patency rate have to be elaborated because the good clinical result is strongly dependent on the vascular patency and flow restoration. And thank you very much for your attention.
- Thank you friends who have invited me again. I have nothing to disclose. And we already have published that as far as the MFM could be assumed safe and effective for thoracoabdominal aneurysm when used according to the instruction for use at one, three, and four years. Now, the question I'm going to treat now,
is there a place for the MFM? Since 2008, there were more than 110 paper published and more than 3500 patient treated. 9 percent of which amongst the total of published papers relating the use of the MFM for aortic dissections. So, we went back to our first patients.
It was a 40 year old male Jehovah Witness that I operated in 2003 of Type A dissection and repair with the MFM in 2010 because he had 11 centimeter false aneurysm. Due to his dissection, this patient was last to follow up because he was taking care full time off of
his severe debilitated son. When we checked him, the aneurysm seven years later shrunk from 11 to 4 centimeters wide. And he's doing perfectly well. Then the first patient we treated seven years ago, same patient with Professor Chocron
Type A dissection dissection repair in 2006. Type B treated with MFM in 2010. We already published that at one year that the patient was doing fine. But now, at three and seven years, the patient was totally cured.
The left renal artery was perfused retrogradely by aspiration. That's a principle that has been described through the left iliac artery. So what's next? Next there was this registry
that has been published and out of 38 patients 12 months follow up, there were no paraplegia, no stroke, no renal impairment, and no visceral insult. And at 12 month the results looked superior
to INSTEAD, IRAD and ABSORB studies. This is the most important slide to us because when you look at the results of this registry, we had 2.6 percent mortality at 30 days versus 11 30 and 30.7 no paraplegia, no renal failure, and no stroke vessel
13 to 12.5. 33 and 34 and 13 and 11.8 percent. With a positive aortic remodeling occurring over time with diminishing the true lumen increasing the true lumen and increasing the false lumen.
And so the next time, the next step, was to design an international, multicenter, prospective, non-randomized study. To treat, to use the MFM, to treat the chronic type B aortic dissection. So out of 22 patients to date,
we had mainly type B and one type A with no dissection, no paraplegia, no stroke, no renal impairment, no loss of branch patency, no rupture, no device failure, with an increase in true lumen and decrease in false lumen that was true at discharge.
That was true at one, three, and six and 12 month. And in regards with the branch occluded from the parts or the branches were maintained patent at 12 and all along those studies. So, of course these results need to be confirmed in a larger series and at longer follow up,
yet the MFM seems to induce positive aortic remodeling, is able to keep all branches patent during follow-up, has been used safely in chronic, acute, and subacute type B and one type A dissection as well. When we think about type B dissection, it is not a benign disease.
It carries at 20 percent when it's complicated mortality by day 2 and 25 percent by day 30. 30 percent of aortic dissection are complicated, with only 50 percent survival in hospital. So, TEVAR induces positive aortic remodeling, but still causes a significant 30 day mortality,
paraplegia event, and renal failure and stroke. And the MFM has stabilized decreased the false lumen and increase the true lumen. Keeps all the branch patent, favorize positive aortic remodeling. So based on these data, ladies and gentleman,
we suggest that the MFM repair should be considered for patients with aortic dissection. Thank you very much.
- Well, if fenestrated EVAR is so great, why isn't everyone doing it? And I would submit it has to do with the planning. If you have a perfectly planned procedure, the procedure will go perfectly. These are my disclosures, which are directly related to this presentation.
This is a case that was planned using AortaFit software and it was a case that we identified as being a perfect plan. We went back and looked at our fellow and resident in our training program who we trained to plan these procedures and asked them to plan this case.
Our first trainee submitted the following plan. And when we line up the SMA, we lose the left renal on this plan. We then asked our fellow to plan the case and she provided this plan.
When we line up the SMA on this case we lose the right renal. So, it tells us that there is tremendous variability in human planning. We participate in the VQI in the Pacific Northwest Regional group,
and we perform 88% of the complex EVAR in our region. And we have the lowest procedure times, the lowest estimated blood loss compared to the rest of the nation, the lowest in post-operative complications, excluding death, and the lowest in composite outcomes to include major cardiac events.
We also have the highest rate of return of our patients to a pre-surgical care setting. So how have we achieved this? Using AortaFit software, we are able to take a standard DICOM data set of a juxtarenal aneurysm patient and create a volume rendering.
We can then display the images in an axial, sagittal, and coronal view for the user. All that the user needs to do is to identify the target vessels and to plant seed points into those target vessels, the target vessels that are selected to be preserved.
What is then output from the software is a segmentation. And you see the segmented image here, but the magic of the software is that it does the automatic adjustment of the centerline using polynomial equations and goodness of fit. We can superimpose 2D slices over this to check
our orientation of the fenestrations and look at the plugs. And what's output is a graft plan that can either be given to the physician in the form of a 3D printed template or placed on the back of a manufacturing line. Sorry. So, for the physician, an STL file can be produced
to create a 3D printed template to create a physician-modified endograft, but what we really want is to be able to provide the manufacturer with a detailed plan using this software. This is an example of a Terumo Aortic TREO device. We've now done 37 of these cases.
This is a graft that has wide amplitude stents and a large amount of real estate for fenestration. So you can see inserting this 3D printed template that was created using AortaFit software. We can rotate this graft, move it in and out to find the sweet spot
for those fenestrations, and to create a truly customized device for the patient. We then, all that we have to do at that point is to line up the SMA. So you can see, on the panel on the left, we do our first aortogram
prior to deploying the stent graft. We deploy that SMA fenestration, the renals automatically align. We then select our renal arteries and then our fellows know that it's time to call for the next patient because the procedure is essentially done at that point.
This is a cone beam CT of that very first patient that I showed you, showing perfect alignment of all of the fenestrations and target vessels. And here's a 30-day follow-up CT scan, that if you pay attention and look carefully, you can see that all of the fenestrations
are perfectly aligned. There's about four centimeters of seals on length, and lack of endoleak and a successful result in this patient. This, fortunately, is published in this month's Journal of Vascular Surgery as an editor's choice.
And in summary, the long-term durability of fenestrated EVAR has been established, but planning and procedural complexity limits widespread adoption. Automated planning software, we believe, provides efficient and accurate graft plans for the physician
or endograft manufacturer. Well-planned grafts simplify branch access and the procedure and I think will increase fenestrated EVAR utilization. And simplified FEVAR may benefit the majority of patients harboring juxtarenal aneurysms and even standard infrarenal aneurysms and may be the best therapeutic option.
- So regarding fenestrated limbs, these are my disclosures. Typical scenario where you have a rather unwelcoming iliac, common iliac artery, you need around 16 millimeters at least to accommodate a branched graft in the iliac artery. You want to preserve the hypogastric flow.
In this case you also see a stenosis, so you need two things, ideally, to accommodate a branched device, which would be the diameter of 16 millimeters and also the angle of the artery. This is very pleasant to put in a branched device.
However, there are patients where you want to preserve the hypogastric blood flow, and in these cases, above the origin of the hypogastric artery, there is not enough room to open up a branched device, or the angle is very unfavorable
to put in a branched device. And here fenestrated iliac limbs come into play. These are usually made to measure, different lengths, different proximal and distal diameters and also you can place the single fenestration where it obviously is positioned best.
There are basically two, I think very useful indications. Here we can see a type 1B endoleak in a 13 millimeter limb. The distance to the hypogastric artery was not enough to have a full expansion
of the iliac limb, and therefore in this case if you want to preserve the hypogastric artery, which I would really strongly always recommend if possible, is to put in a fenestrated limb. But it's also really very helpful in these cases
is that you don't have to come from above, you can come from below and finish the whole procedure from below. So you have a full deployment of the endograft and then you'll put in a connecting stent graft
with obviously a very good seal and result. Most importantly, for complex cases as in this, for instance, patient who's had an open procedure 10 years previously and had further interventions with an over-stenting of the hypogastric on the right side and large thoracoabdominal aortic aneurysm
as well as an anastomotic aneurysm on the left side, you really want to preserve the hypogastric artery. And you can also that actually it's an anastomotic aneurysm at the left side, so here a branched device certainly doesn't work. First, because it doesn't open up,
and second, the angle of the hypogastric is really very unfavorable. So again, you just put in your fenestrated device and then connect it from below with the stent graft in order to preserve the hypogastric blood flow of the last remaining hypogastric artery.
And also, obviously do something else to the rest of the patient, so this was a five branched endograft in a patient with two left kidneys. And also another case, you see actually on the angiography already the shaggy aorta,
so occlusion or seal at the distal origin of the common iliac just above the hypogastric is not really a good option, so we've re-over stented, or you do something about it. Now this is the case with a thoracic endograft
and a full-fen extension. So again, we really opt to preserve these hypogastrics as much as possible. So in conclusion, Mr. Chairman, (coughs) sorry ladies and gentlemen, fenestrated limbs are a good tool to preserve
hypogastric arteries. Now just to put it into perspective, is it common? No, we have around 30 branched iliac devices a year we implant, and we had all in all five fenestrated during the last two years.
So this is really a rare anatomical solution, but I believe it really is helpful. It's not an off-the-shelf device, so it takes around four weeks to produce, and the company's still not really decided how to price it, so we really can nicely negotiate it.
Thank you very much.
- [Instructor] Thank you very much. So, you saw some of the issues that our, oh, this is the slightest cut, but that's okay. Some of the issues that we've seen with these percutaneous mechanical devices, and, back in the 90's, and perhaps even more than a decade ago, there were a lot of these.
And this space gets hot and cold, and one of the problems is that the level of evidence for doing these is very low, and when it is done, it wasn't done well. And this is a nice registry, a lot of patients enrolled, unfortunately we didn't learn
what we had to learn from these types of registries, because of just the study wasn't done well. So the level of evidence is low, and when we did have them, they didn't really work. And you saw some of the problems, that these devices can cause.
And here's another problem that wasn't discussed. You can see the DVT, iliofemoral DVT in here, and a device is pushed a few times up and down, and sort of aspiration, a Bertoulli, that type of thing. And this looks, oh wow, well this looks good,
maybe the thing is working, except all the clot is up here. So, these devices tend to push the clot around. So the issue is, enter now more recently, these are some of the more recent ones. Note that the AngioVac is not here, I don't consider that a practical thrombectomy device,
and so, it's not here. So, we're going to be talking about JETi. This is a system that is an aspiration system with a jet that comes inside the catheter, therefore the clot is engaged and pulled in and broken down by the jet, therefore there's no hemolysis.
And this demonstrated in this case, which is acute and chronic 17 year old multiple DVTs in the past, the iliofemoral segments are stented, as you can see here, this segment is somewhat fresh clot but these, as you can see, are subacute clot. Look at this, so the system now is designed
for over the wire, but for DVT you can use it without the wire, because it works a lot better. As you can see it can really aspirate the clot, in before your eyes. Now this I have passed the device in here once, and you can see the fresh clot is gone,
we have some residual debris in there, we have not established flow yet, and then I turn the device on... and it pulls the whole thing in, okay? So, very powerful aspiration method. So, and as you can see here, we don't have
a flow establish, outflow established yet. Therefore, when you turn it on, you have a vacuum created right here, and so this tells you how strongly this device can aspirate and work. And this isn't on the table.
After a pass here, two passes here, some residual clot in here, obviously there's residual clot there. So we pass it around these areas once more, and this segment obviously needs to get stented and on the table, re-establish antegrade flow. Since May, we've had 19 patients treated, most of them DVT.
And, based on our assessment, 17 of the 19 patients at a total time of 90 minutes on the table, had better than 90% clot retrieve. We have 30-day patency data on only 16 of those patients, because this is really since this May. And 15 of those were open, one re-thrombosed
and we had to retrieve again. Conclusion, so preliminary experience indicates that this is an effective device. There were no safety issues, we don't see any hemolysis, we don't see any pushing around of the clot, but there is a learning curve to it,
and for best application, thank you.
- Well Mr. Chairman, dear friends, last year was here on the same stage for discussion of the results of the EVAR 1 trial and trying to tell you that the results of the EVAR 1 trial were no longer valid and this year I'll try to do the same for the EVAR 2 trial. The EVAR 2 trial was a randomized control trial
conducted in the UK in 33 centers with enrollment between 1999 and 2004. It was a randomized trial in which the patients were randomized between conservative treatment and open treatment and the common ground for the study was that these patients were unfit for open repair.
What is unfit for open repair in the EVAR 2 trial? Well the decision was made from three criteria. Cardiac reasons were the main reasons to consider patients as being unfit. Respiratory and renal reasons are the criteria that were used.
There have been several publications on this trial showing a design of the trial, the preliminary results, the final results in our recently last year, the very long results with this trial. And what are the results? Well as you can see here, it was a statistically
significant difference in aneurysm related mortality between the patients treated with EVAR and those treated conservatively but there was no difference in overall total mortality and this led us to the conclusion that indeed there was not really a place in those EVAR in those patients unfit for open repair.
However, we might look more closely to these results. The first thing in this trial is that almost 10% or more than 10% of the 197 patients that were randomized for EVAR actually did not receive the EVAR procedure because they died prior to the intervention and what was the reason for this?
Well the mean time between randomization and EVAR in this study was two months and in a quarter of the patients, it was even three months. The nine ruptures that occurred before the intervention had taken place. Actually it'd be more than half of
the aneurysm related mortality in this group. Another striking observation was that those patients that had no intervention, 1/3 of these actually were treated with EVAR in the followup period. And when we look at the results, whether it's observation-influenced results,
well you see when we perform a vertical analysis, the difference in aneurysm related mortality was even bigger and also there was a clear trend towards improved overall survival. Although this was not significant and therefore, the author still remains to the conclusion
that there was no place for EVAR in these patients. Looking again closer to the results and looking specifically at the patients with no intervention, already in 2009, there was more than half of these patients in this group actually were patients that already had EVAR.
And even worse, in 2015, of the 13 patients in this group that still survived, there was only one, yes only one, that did not have an EVAR procedure. So it's clear for me that only patients with EVAR actually survive.
Why are the results no longer valid either? Well this study was performed in 1999 up to 2004 and it's clear from further studies, just one example, that the results in the meantime have clearly improved from 1999 to 2004. While it wasn't the Stone Age for EVAR,
it was not more than Middle Ages. Plus mortality clearly improved with time and then when you look at the results of this trial, the 5.7% operated mortality in the EVAR group are actually at this moment no longer standard of care when you compare to these three other studies
which actually use the same criteria for considering patients that's unfit for open repair. Also we've got longer term survival. The mortality of 40% after, no, no, 60% after 40 as in 80% off of JVS can no longer be considered really as up to date results and probably the reason for that
is also the fact that medical treatment upstream in these optimal patients as only 40% statins. So are EVAR 2 results still valid? I think it's clear they are not. It's an old study with old devices. The mortality is not conform to actual standards.
Medical treatment was not optimal. The delay in treatment caused preventable deaths. More than 1/3 of the patients crossed over and the statistical analysis does not reflect the actual treatments of the patients. Does this mean that we should operate on all patients?
Well, maybe not. This is a very recent study published earlier this year in logical patients and you see that when some, certainly once several of the risk factors were considered being unfit patients were present, that results were indeed worse,
especially when there is renal insufficiency. The IR for the SVS guidelines correctly state that it is just to inform high risk patients over their risk status and their mortality score and then making an informed decision whether we should proceed with aneurysm repair or not.
It's my personal opinion though that clinical judgment is probably the most important factor in this decision making process. Thank you for your attention.
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