- 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.
- Thanks very much, and thanks Frank for the invitation to join us once again at this excellent meeting. These are my disclosures. Now, it's well documented and all of you are fully aware that the periprocedural risk of stroke and death following transfemoral CAS
has been shown to be twice that of when compared with CEA in the important non-industry supported trials of EVA3s, ICSS, and CREST. The increase in the rate of events with CAS however,
is front loaded and occurs, certainly within the first 30 days, and more often than not within the first day or two, after that the subsequent event rates and durability parallel that of CEA. And this is nicely shown in the four-year data from EVA 3S, where we can see that the big jump in event rates
between CAS and CEA occurs upfront, after which, these two curves become entirely parallel. The 10-year data from CREST has been published, and the same phenomenon occurs here, and that is that the higher event rate with stenting compared with carotid endarterectomy occurs right here,
after which the two curves become entirely parallel. So, one has to ask what are the potential causes for periprocedural events with transfemoral CAS and it's already been discussed, a diseased aortic arch, a Type 3 aortic arch making catheterization of the right carotid artery more challenging,
and finally the need to traverse the lesion in order to place a distal embolic protection device. Obviously the embolic protection device doesn't work until it's in place, and when you pass it over the lesion the possibility of knocking free embolic debris is quite high.
I don't expect anybody to read this from the back of the room, but in 2004 there were two seminal papers that were published looking at the possibility of a direct approach to carotid artery stenting, thus avoiding the aortic arch and using flow reversal
by clamping the common carotid artery and diverting blood flow in a reverse direction back to the venous system and were showed excellent results. Along comes industry to provide us with the hardware with which to do this,
these are the components from Silk Road, and basically a small cutdown over the common carotid artery, the placement of the sheath clamping the carotid artery with reversal of flow, thus carrying any embolic material before the placement of a stent is neuroprotective.
One other thing that wasn't mentioned this morning and one of the advantages of flow reversal and the possibility of encouraging all of the release of the embolic material initially is to carry out predilatation of the lesion before placing the stent and not postdilate.
The first-in-man data on the use of this technique was published in Germany and in the proof study, in the proof study there were 44 patients undergoing TCAR, no deaths, no strokes, silent brain infarction rate of 16%, which was entirely comparable to that of carotid endarterectomy.
Along comes the ROADSTER trial at ROADSTER 141 pivotal patients deemed to be high risk by either anatomic or medical criteria, carried out in 20 US sites, there was no major strokes, there were two minor strokes, two deaths, no permanent cranial nerve injuries. And if we compare the TCAR data with CREST data,
here's the transfemoral CAS data out of CREST, 4.1%, 2.3% with carotid endarterectomy, 1.4% with TCAR. And here are the ROADSTER 2 data, if we look at stroke and death in asymptomatic patients in ROADSTER 1, 1.3% dropping to .9%,
stroke and death, ROADSTER 1 in symptomatic patients 2.2% dropping to an astonishing 0.8%. So, from my personal perspective I can offer patients either TCAR or CEA based upon selection criteria with a high degree of comfort that
both of these are going to result in excellent results. How about CREST-2, as you know this is two studies in one, comparing CAS with intensive medical therapy alone and CEA with intensive medical therapy versus intensive medical therapy alone. The future of invasive intervention
to treat asymptomatic carotid stenosis will really depend upon the results of this trial. What are the possible outcomes? Intensive medical management may be equal to or better than either, carotid endarterectomy and CAS may be better than intensive medical management,
or CEA but not CAS may be better than intensive medical management alone, those are the possible possibilities To date, half of the patients have been enrolled, so stay tuned, and thanks very much for your attention.
- 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.
- Yeah, thank you Mr. Chairman. These are my disclosures. Well, we know that the Heli-FX EndoAnchor System provide fixation and seal in aortic necks, and it can prevent or resolve migration or endoleaks. It's important to have an even spacing around aortic circumference and
to resolve type 1A endoleaks, you need successful, of course, deployment of EndoAnchors and adequate penetration into the aortic wall. The objectives for this study was to quantify the EndoAnchor penetration into the aortic wall in patients undergoing EVAR
and to assess the predictors of successful penetration and to associate that with postprocedural type 1A endoleaks. We searched in the ANCHOR database, and we included patients that has been treated for a type 1A endoleak, and we had to have a good quality
first postprocedure contrast-enhanced CT scan without any artifacts due to metal or glue, and without implantation of adjuvant aortic extension cuffs or stents. And then we selected two patient cohorts, patients with successful treatment
after the implantation of EndoAnchors for a type 1A endoleak, and patients with a persistent type 1A endoleak after the EndoAnchor implantation. Well, this is to show how we determined the position of the EndoAnchors, this is a good penetrating EndoAnchor
more than two millimeters in the aortic wall. This is borderline, and this means there is still a gap between the endograft and the aortic wall or the EndoAnchor itself is penetrating less than two millimeters. And this of course, a non-penetrating EndoAnchor.
The good ones are green, the borderlines are orange, and the non-penetrating are flagged red. Here are results, the anatomical criteria to predict type 1A endoleaks, as you can see here, at the left, in the type 1A endoleak patients, there is a larger aortic diameter
with a median of 30 millimeters, and neck length is shorter, less than one centimeter, compared to the patients with no endoleak. Then about the EndoAnchor penetration, in the patients with a persistent type 1A endoleak, there are significantly more EndoAnchors
which are borderline or non-penetrating. What are the predictors for a successful EndoAnchor penetration. Well, protective factors, oversizing of the endograft compared to the diameter of the infrarenal aortic neck, and the use of the endurant stents.
Independent risk factors are the aortic diameter at the lowest renal artery, and five and 10 millimeters below more than 30 millimeters, a significantly neck thrombus and calcium around the circumference and also a more than two millimeter thickness.
Predictors for a type 1A endoleak, protective factors is the neck length more than one centimeter, and good penetrating EndoAnchors and risk factors for a type 1A endoleak is, again, the aortic diameter five millimeters
below the lowest renal artery more than 30 millimeters, and also boerderline and non-penetrating EndoAnchors and in this logistic regression model, a non-penetrating EndoAnchor is really predictive for a type 1A endoleak, or a persistent type 1A endoleak. A few cases, this is an excellent job,
there are four EndoAnchors placed, and they all penetrate well, although they are not circumferentially divided around the circumference. The majority of the problems in the patients in the ANCHOR database, if a persistent type 1A endoleak
is mainly due to an incorrect indication, these are EndoAnchors red and orange, non-penetrating and borderline. That is because they are above the fabric, or they are in a no-neck aneurysm, so the indication is not correct.
This is again, a patient with an undersized endograft, of course, the EndoAnchors will never penetrate the aortic wall at a post-serial part of the aorta. This is another example of misdeployment, a huge load of calcium and thrombus, and again, to defined a no-neck aneurysm,
and again, well it's obvious that the EndoAnchors will not do their job. These are then the EndoAnchor distribution in successfully treated type 1A endoleaks at the left, 332 EndoAnchors, but if you select only the patients
with an EndoAnchor which are inside recommended use at the right, you can see that more than 90% of those EndoAnchors are good penetrating. Here are the patients at the left with a persistent type 1A endoleak, 248, and you can see the majority is red or orange,
and that means that majority of those patients had an EndoAnchor deployment beyond the recommended use. So to conclude, good EndoAnchor penetration is less likely when there is large aortic diameter, the EndoAnchor is not perpendicular to the stentgraft during deployment,
and it's beyond the recommended use, more than two millimeters of thrombus, not in the infrarenal neck, or a gap more than two millimeters. And in borderline or non-penetrating EndoAnchor, it's predictive for a type 1A endoleak.
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.
- Okay, thank you. We know that inflammatory AAA have quite low incidence. The main problem is related to the thickness of the aortic wall and to the retroperitoneal fibrosis that involves the organs that are close to the aorta. Open surgery is quite difficult for these reasons. And these imply a higher mortality rate
that is threefold the one for standard AAA. And the higher morbidity related to the surgical dissection in fibrosis with risk of iatrogenic injury of the involved organs. So that some authors suggest the supraceliac clamping. That of course have some other issues.
A recent paper suggests that a pre-op treatment with a cortical steroid therapy can be useful to reduce inflammatory signs and so minimize the operative risk for these patients. On the other hand, endovascular treatment has been proposed since 1997 with different outcomes.
Certainly mortality rate is lower when compared to open surgery, and even the one year mortality is lower. But we have a problem with periaortic fibrosis that does not decrease as well as with open surgery. And there is some progression, in some cases, with higher nephrosis that leads
to other types of complication. This is not a standard. You see in this paper that there is no problem with periaortic fibrosis after endovascular treatment. But in other papers, the situation is different. There is a worsening fibrosis and even the development
of fibrosis after standard EVAR in patients with no history of inflammatory AAA. And certainly the phenotype eg4 seems to be related to a worse outcome after EVAR. So, based on this situation, what we have done in the last year is to use a systemic steroid protocol
for our patients with inflammatory AAA that is the same that is used for arteritis and retroperitoneal fibrosis. And you see how impressive is the situation in this case. We had only four days of therapy, and we have a decrease in periaortic fibrosis of 28%.
We studied all our patients with PET/CT. We made a comparison with the patient with standard AAA, and we observed an increased level of captation that was really significant. This is our population. All of the patients had immunological screening,
and the evaluation of the inflammatory level. This is the operative situation. All the patients had a good result with no mortality at 30 days. Only one patient died three months later for other reasons. And what we observed is that in almost all cases,
the periaortic fibrosis reduced significantly with the, even with PET/CT. All the patients were asymptomatic. And all the patients with hydronephrosis have a release of the situation. You see that the diameter of the aorta decreased
of 9.76 millimeters, and there was a decrease in periaortic fibrosis of more or less one centimeters. So this is really significant, as you can see. And there was a reduce in the uptake for all the patients but one. We don't know exactly, he had a type two endoleak.
Don't know if this can be a correlation because it's a single patient. And another patient stopped corticosteroid therapy, and so there was a recurrence of this problem. The CRP reduced globally, but of course, it's not specific. So in some patients we had an increase for other reasons.
But our policy now is that we do EVAR, when feasible, associated to steroid therapy. That, in our practice, is effective. We use open surgery in patients unfit for standard EVAR, and probably, even for these patients, steroid therapy can be a choice.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- We are to have a distinction between acute stroke at level of distal small vessels, in which we can see the core infarct in the penumbra around the infarct. And for the treatment of acute stroke, it's important to establish the eligible patient who will receive the
intravenous tissue plasminogen activator. It remains the only proven effective intervention for acute ischemic stroke. But what about the acute stroke for large vessel intra-arterial thrombolysis? What alternatives?
Mechanical revascularization strategies or stent-assisted revascularization. But, in the past, the earliest periods studied was anecdotal cases and no selection of the patients so bad results were recorded.
We have some exclusion criteria for the urgent treatment. Internal major stoke, cerebral ischemic lesion greater than 2.5 centimeter and CT scan, loss of consciousness,
signs of intracranial hemorrhage. But the real goal of early intervention is to stop the plaque embolization. So should we remove this plaque, or we can stent it. So, as what said Rothwell in 2004, time is brain.
And the benefit from CEA is maximal in symptomatic patients operated on within two weeks of the index event. But it's better after 48 hours. In 2010, I published Siena Carotid Artery Stenting Score
for elective patients. And in Italian registry, in order to evaluate that the field urgency of carotid emergency stenting of a symptomatic patient, we have noticed some clinicians had biomarkers spotted from a prospective registry.
And we have studied the Brain ischemia biomarkers such as PAPP-A, hs-CRP, and Interleukin six. But in the (mumbles) published only in European journal of Vascular and Endovascular Surgery said,
that the most effective management is the quickest one. So in this publication, I say that this closed cell stent design would be benefit for the treatment of urgent patients. In this same publication in the Annals of Vascular Surgery.
And in this year, we studied the early carotid artery stenting after onset of neurological symptoms. So we know very well that we are some cerebral protection devices in order to better protect the procedure,
and we had the necessity to obtain a better protection device with proximal absolute devices. So what about new carotid stent design? In order to better approach the symptomatic patients. This is an example at Terumo Roadsaver, with the control with optical cord and tomography.
This is an example of C-Guard with the control optical cord and tomography. We established some cases related to the study with OCT, and the slice-based analysis say that compared with conventional stents,
the incidence of plaque prolapse was lower. So how to choose in emergency. Carotid artery or carotid endarterectomy stenting, my personal opinion, carotid endarterectomy is still the gold standard. Or if we had the space for carotid stenting
in patients with severe comorbidities, in patients with anatomic complex situations, in case of tandem intracranial lesions, but requires correct expertise and plaque evaluation and correct stent and cerebral protection. So in conclusion,
the most effective management is the quickest one, according to a correct selection that allows recognition of those who can really take advantage for early treatment. And how to perform CAS safely in emergency with an appropriate knowledge of
anatomy, anomalies, and equipment. And with growing experience and the use of dedicated CAS technology, CAS can now be performed safely and efficiently by skilled operators even in urgent cases. Thank you for your attention.
- Thank you, Mr. Chairman. Thank you, Dr. Veith for inviting again to this great meeting. It's my disclosures. Well, as we know and heard this meeting, there are some certain limitations of current EVAR (mumbles) anatomical procedure and economical reasons,
and I would like to present a relatively new device which may address current EVAR limitations with a simple low profile system, and basically, ALTURA consists of two parallel stent graft systems. ZEUS No Gate Cannulation is needed and unique features include D-shaped proximal stents
and suprarenal fixation. Multi-purpose (mumbles) possibilities as well, and the system of utilize 14 French delivery system. And as aortic components can be deployed offset to accommodate the offset renals, and then the limbs are also unique
because they're deployed retrograde from distal proximally, and this allows precise positioning, both proximally and distally. Well, as the ALTURA clinical experience includes the very first human implants as well as more recent case performed
with a fully commercial device, and a total of 90 patients with a AAA were enrolled between 2011 and 2015, and follow-ups are taken at 30 days, six months, and annually to five years, and this presentation gives a current status of follow-up, and our results with a 12-month follow-up were published earlier this year.
Our clinical data were collected in total of in 11 sites. It includes 90 patients. And you see here, the patient demographics and anatomy do a typical, which are typical for all EVAR patients and the mean follow-up was 2.7 years. And procedure of success was 99%.
Only one patient, one of the first patient was Gen1 was not implanted, and 50% patients were done percutaneously, and majority of them underwent regional or local anesthesia. So when you look into the results, we see that there was only one case of AAA ruptured,
which occurred at three years due to type II endoleak and sac enlargement as the patient, which refused treatment due to type II endoleak. And all other deaths are paired to no original causes, and two patients had device migration at two years. The same patients appear at three-year period,
and basically these were undersized grafts was sort of our learning curve, and there was no any migration later on. Four patients had type I endoleaks visible on CT, and read by independent committee between 30 days and one year.
None have required secondary treatment and have been no aneurysm enlargement observed. And at one year, not surprisingly for this kind of devices, there was 17% type to endoleaks, but only one patient required secondary procedure due significant sac expansion.
Well, wasn't, of course, what we saw, I expected majority of patients has had shrinkage. There was a four-year period. And this is a patient who was recorded with the type IA endoleak at 30 days, caused by the last calcified nodule,
as you he's here probably none of the other device would tolerate that, but the endoleak did not extended into into the sac and had a leak result spontaneously without sac enlargement through a four-year follow-up period, as we're seeing here. Well, here another patient with type IB endoleak,
due to (mumbles) generation was treated with coils and glue an extension with additional stent graft to external iliac artery. What's interesting was the device. Device can tolerate small distal aortas and five patients who were treated
with small distal aortas and the very first patient was not dilated enough and stents were not deployed, simultaneously causing some stenosis which was easily treated with PTA afterwards, so we learned but it's very great, unique feature to treat the small distal aortas for the device.
And of course, sensing what happening with them, septal endoleaks, because everybody being concerned what happening with that, and nevertheless, there were no septal endoleaks observed during the follow-up period. In conclusion, Mr. Chairman, ladies and gentlemen,
I would like to say this Novel Altura endograft concept has potential to play major role in mainstream EVAR cases and potential benefits include predictability, reposition ability to place the device very, very, very precisely, offset renals, to maximize use of the neck, and low profile
overcomes current and anatomic limitations like tortuous iliacs, narrow bifurcation or access vessels and no limbic inhalation is needed, and basically, I truly believe that this offers option for EVAR day surgery and ruptured aneurysms. Of course, first results are very encouraging.
We need more data. Thank you very much.
- One more soft swing, I guess, at EVAR-2 for the afternoon, but this one will be from a slightly different perspective. We'll look at it from a methodological standpoint rather than an analytical standpoint, which I do with some trepidation preceding Phil Goodney on the podium. As we've heard, endovascular techniques have revolutionized
the treatment of abdominal aortic aneurysm, and yet, the EVAR-2 trial published in 2010 provided Level I evidence regarding high-risk patients with abdominal aortic aneurysm. There is no survival advantage of EVAR over observation, as we've heard.
So let's unpack a little bit about what we mean by Level I evidence. Level I evidence consists of properly designed randomized controlled trials. They demonstrate the effect size of an intervention, and they're characterized by
strict inclusion/exclusion criteria, are resource intensive and can be difficult to replicate. Keep in mind that enrolled individuals are frequently younger, white, and affluent, receiving care at academic institutions, and clinical scenarios are heavily scripted.
The EVAR and EVAR-2 studies are examples of such trials. By contrast, Level II evidence, and the definition of this varies by region, consists of, for example, use of large administrative and clinical datasets to compare outcomes from different interventions. These are, to be sure, subject to selection bias
and limited granularity, but they're characterized by high power due to large numbers and external validity because they include real life patients in clinical scenarios. Examples of this type of evidence is found in the VQI, NSQIP, NCDB, SEER, and HCUP.
This study, which I'm grateful to have seen referenced in two prior talks, uses the ACS NSQIP database to look at mortality rates after EVAR in high-risk patients. And this is an example of Level II evidence. What we did was look at EVARs
that were performed between 2005 and 2013, and we used the EVAR-2 criteria to define a high-risk cohort and then examined 30-day post-operative outcomes. In that study, we found that the 30-day mortality for these high-risk patients following EVAR and our cohort was 1.9% compared to the EVAR-2 trial in which it was 7.3%.
And we concluded the contemporary mortality following EVAR is substantially lower even in the high-risk group than reported in the EVAR-2 trial. So how do we understand this? I think it's been unpacked a bit by two of the previous speakers,
but our interpretation was that, as I mentioned, randomized controlled trials and Level II evidence are not the same. So randomized controlled trials, again, include and exclude patients for analysis, use selected devices and do often include
a learning curve for new techniques, whereas the use of contemporary cohorts such as our study have an inclusive population, limited granularity, but allows for changing devices and expertise over time. So in conclusion, randomized controlled trials or so-called Level I evidence,
demonstrates effect sizes for new therapies, while large retrospective data analyses augment the findings for these therapies across contemporary practice patterns and devices. Intelligent integration of data across study types leads to improved care of patients
and preserves the role of critical thinking for surgeons. The key points that I would like you to take away are that endovascular techniques and their indications for use are obviously rapidly evolving, and thoughtful assessment of the literature allows surgeons to nimbly integrate evidence into practice.
The bottom line, our analysis of the current literature suggests we should not deny EVAR to high-risk patients. Thank you.
- [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.
- 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)
- 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.
- 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.
- Yeah, thank you very much. Unfortunately Dierk Scheinert couldn't come, so thankfully he's allowed me here to take this presentation over so thanks a lot for this. So these are the latest 5-year results of the INCRAFT device from Cordis Devices currently under FDA review not yet approved
in the US, but in Europe. These are the conflict of interests, this is (mumbles). So this device is a three-piece modular system, low porosity polyester. You can bilaterally in-situ length adjust it up to 3cm. And the main feature I think with this device
is it's a low-profile device, 13 Fr inside 14 Fr outside except the biggest body which has an outer diameter of 16 Fr. The innovation study that was 60 patients, you can see here some objectives. So the question was whether you could deploy it
accurately where you wanted to have it without any type I, III, and IV endoleaks and of course there were also some other primary and secondary endpoints and again follow-up had to be done up to five years. This is a busy slide just showing you,
please look to the right side, to show you that there were quite some violations of the recommendations in which kinds of anatomies to implant this craft. Here for example neck lengths less than 10mm, here were some patients implanted.
Also angulations over 60 degrees, three patients, there were some thrombus in the neck, and here you can see aortic bifurcation smaller than 18mm, there were quite some patients and especially the iliac sealing length was shorter than 10mm in nearly 50% of the patients
and also the diameter of the external iliac arteries were nearly 50% lower than 7mm. Here the freedom from endoleaks type I was one at 30 days which has been resolved and another one developed after 30 days which also has been involved. No type III.
Stent graft patency after 30 days also 100% and otherwise also no other adverse events with this device at thirty days. So to answer the question with this device to the first question of (mumbles) will lighter fabrics and stent material decrease EVAR durability?
Will there be more endoleaks I, III, or IV? You can see here the long-term data so no Ia endoleak developed over four and five years, there was one Ib endoleak which developed at four years which also was apparent at five years. No type III endoleak.
One graft patency failure with a (mumbles) occlusion here at four years which also was here at five years. No migration, one fraction of the (mumbles) proximal third graft, otherwise it was very safe. You can see here once again the Kaplan-Meier curve for type I endoleaks through five years here
with type Ib here later on, and this is the patency Kaplan-Meier curve also showing here the good patency at five years, and this is freedom from second large vent. Here I don't have any data whether this is type II endoleak or not so this still has to be reported and clarified.
So to conclude the INCRAFT performed well on long-term while overcoming more difficult access morphologies. The endograft can be utilized in patients with demanding access and vessel morphology, and there are more studies ongoing.
There is one in the US and Japan where we wait for long-term data, 190 patients and also from Europe's 180 patients also there we still wait for long-term data. Thank you.
- 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.
- 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.
- 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.
- I have no disclosures that are relevant to this discussion. What I would start off with is, maybe you don't do it at all. Be careful what you ask for. This is very unforgiving work and know that going into it. The technical considerations a
absence of arteriosclerosis, it's a small vessel diameter and as we heard Dr. Eslami talk about, very high risk of vasospasm. The local clinical experience, I'm going to credit Dr. Jeff Friedman
who's one of our local reconstructive plastic surgeons, 10 patients underwent open surgery for repairs, eight arterial, two venous injuries. The age range 36 weeks of gestation to 12 months, Eight of the nine patients, 13 weeks of age or less. 90% of the injuries,
and we saw that again in Dr. Eslami's talk, are injuries that are iatrogenic as a result of invasive procedures performed on the effe cardiac catheterizations, arterial line placement,
direct arterial ligation, femoral vein injury, intra-arterial infusion or trauma. Most of these are like I menti femoral arterial lines, any sort of umbilical catheterizations,
femoral catheterizations and so on. One of the most important things is to do a real thorough evaluation, so in 70% of these cases they had a color flow doppler examination. Six patients had operative intervention. Doppler results verified intraoperative results
or ultrasound results in all cases and in one patient with preoperative arteriogram demonstrating accuracy of the diagnosis as well. No significant limb loss in these 10 patients, of course a small series despite prolonged ischemia times and I think that's probably one of the primary lessons
to take home is that kids tolerate ischemia fairly well and so to follow these would kind of be expectant treatment. Only one patient had toe amputations. Seven of the 10 patients survived, one early postop mortality, one late postop mortality and one nonoperative mortality.
Functional results were good, two with limb growth discrepancies. This is just to identify what you're looking at, make sure you're doing a good intraoperative ultrasound exam and know what you're getting into. This is just some examples of one child,
with obviously an ischemic limb there, this was from access from catheterization. You can see what the arm looks like, the hematoma down around the brachial artery and a microvascular repair there as you see. Going down and a little fasciotomy
all the way down into the hand, with a reasonable result. Of course, a nasty scar but a functional hand. The diagnosis am, doppler evaluation we place heavy weight on, the color doppler examination,
real time assessment of vessel patency, determine the level of occlusion. And then acutely the treatme acute intervention if obvious injury, discontinue the local catheter that's caused the injury,
anticoagulation with heparin, if possible, and really wait about six to eight hours before going unless the limb is totally threatened, warm packs, elevation, intervention if no improvement. And so, the operati
wide proximal and distal control, as you saw in that one case that I presented, complete division of the affected vessel, usually it's severely injured from the catheterization, proximal and distal thrombectomy using a #2 Fogarty, direct vascular repair if possible, vein grafts rarely.
I think Dr. Singh also mentioned that primary repair is better and we certainly believe the same way. And then fasciotomy is used liberally, postoperative anticoagulation again if possible.
suture usually with a microscope, interrupted sutures are a mainstay, papavarin and nitroglycerin generally work fairly well for vasospasm, again back to the ultrasound and then determine the appropriateness for operative intervention. You kind of need to know that going into it.
Operative intervention only in the case of no improvement and venous injuries are usually a little more difficult to treat and often surgical intervention gives poor results. If you just look at t am and doppler, suspected spasm or thrombosis,
conservative management first, if fails, six to eight hours eventually go to the operating room, if it resolves, obviously no care after that. In the future I think development of a team approach with plastic surgery, pediatric cardiology, pediatric surgery and neonatology is important,
establish early intervention program, and determine the possibility avoiding long term sequelae. 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.
- 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.
- 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.
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