- These are my disclosures. So aortic neck dilatation is not a new problem. It's been described even before the era of endovascular repair and it's estimated to occur in about 20% of all patients that undergo EVAR two years after the index procedure.
We're seeing more and more cases where patients that survive long enough after EVAR, they develop aortic neck dilatation beyond the nominal diameter of the endograft and like on this patient, this image, large type 1A endoleaks that are difficult to treat.
There's a number of factors that are contributing to aortic neck dilatation including a continuous outward force that is exerted by the endograft. Progression of aortic wall degeneration. Aneurisymal disease is a degenerative procedure.
The presence of endoleaks, particularly type two endoleaks have been implicated in aortic neck dilatation. And then incomplete seal at the proximal neck in the form of microleaks or positional leaks. HeliFX EndoAnchors as you heard were
designed to stabilize and improve the apposition of the endograft to the aortic neck. And as you saw on this video, their presence even when the super no fixation disengages from the wall of the aorta, may help stabilize the graft onto
the aorta and prevent type 1A endoleaks. About three or four years ago we started looking at the anchor registry data, trying to identify predictors of aortic neck dilatation in patients who are undergoing EVAR with EndoAnchors. We published those results about a year ago.
In terms of the one year mark, we had 267 patients in that cohort. We measured the aortic diameter at four different levels. 20 millimeters proximal to the lowest main renal artery and then at the level of the lowest renal artery, five and 10 millimeters distal to that.
We defined the change in diameter that occurred between the pre-implantation EVAR and the first post-implantation EVAR at about one month. As adoptive enlargement due mainly to the effect of endograaft and the interaction with the aortic wall.
And then we defined this dilatation, what occurred between the one month and the 12 month mark, post EVAR. We used 20 different variables and we ran all these variables at the three levels. And what we found in terms of
post-operative neck dilatation is that it occurred in 3.1% of patients at the level of the lowest renal artery. 7.7% five millimeters distal to it and 4.6% at 10 millimeters distal to it. And this is a dilatation with a threshold
of at least three millimeters. We felt that this was much more clinically relevant. In terms of protective factors for adaptive enlargement, the presence of calcium and the aortic diameter of the level of the lowest renal, both of these are easy to understand.
The stiffer the aorta, the lesser the degree of the immediate dilatation. But then when we looked at the true dilatation, we found out that the aortic neck diameter at the lowest renal artery was a significant risk factor as was Endograft oversizing.
So if you started with a large aorta to begin with, these patients were much more likely to develop neck dilatation and if you significantly oversize the endograft that was also an independent risk factor. On the other hand, the neck length as well as the number of EndoAnchors that
were placed in these patients, both appear to have independent protective effects. So the two year preliminary analysis results is what I'm going to present. The analysis is still ongoing, but now we have a larger number of patients, 674.
We performed the same measurements at the same levels. What we found in terms of time course and location of the aortic neck dilatation is that in the suprarenal site, there is negligible dilatation up to 24 months. The largest dilatation occurs at five millimeters,
but more interestingly, a significant number of patients did not even have endograft present in that location. And then at 10 millimeters distal to the lowest renal artery right where most of the aneurysm changes you would expect to occur,
that change in diameter was again negligible. Indirectly suggesting that EndoAnchors have protective effect. So these are our interesting, some interesting insights. Female sex and graft oversize do play a significant role in the post-operative neck dilatation.
With EndoAnchors implanted at the index procedure neck dilatation 10 millimeters distal to the lowest renal artery appears to be negligible both at 12 and at 24 months. But we're working to see a little bit more finer elements at this analysis.
As where exactly the EndoAnchors were placed and how this was associated with the changes in the aortic neck. We hope to have those results later this year. Thank you.
- These are my disclosures. So we all know the problems with long-term failure of EVAR and TEVAR. Type one endoleak being a particular significant concern. We've heard the results of the three year ANCHOR Registry. We know from this 85% of those cases taken on for type one endoleak were successful
and it's fantastic that these cases are still successful at three years. But I guess it's 15% failures and it's important that we talk about how we get success like this. If we're going to talk about a recipe for success we need to think about first of all the indications
for treatment of endoleaks. This is key. Not all endoleaks are the same. Those endoleaks where there's an inadvertent creation of a leak channel around the graft at the top end because of a hostile landing zone
or excessive oversiding of your graft or noncircular aorta, all can be well treated with endoanchors. Again, migration and loss of seal can also be well treated. But others where there's excessive thrombus or calcium won't work and where there's insufficient apposition between the graft and the aorta, again,
this is not a treatment case for endoanchors. So intraoperative type one endoleaks where there's poor conformability of the graft you can see here this barrel-shaped neck, there's a leak around the aorta, and there's a series of endoanchors
placed in rows circumferentially, do really well to seal up that. You can do the same at the distal end of the thoracic graft as we've just seen in those conical necks when you have a type one endoleak. If you have time to treat your leak channel,
you want to get a CT scan and evaluate where that leak channel is. Or you can do more detailed imaging with triangulation on angiography, but that's difficult. You fix the side away from the endoanchor first,
and then fixing rows of staples along the endoleak channel as you can see here, by moving the C-Arm in 15 degree increments across the aortic wall. This is a good example of a case with a leak channel. This graft is in the angulated aorta
with a channel underneath in the bottom end. There's a big endoleak there. And what we've done is fix the contralateral side first and then you're placing a series or rows of endoanchors underneath the stent graft. You can even zipper that up to change the bird beaking.
And that endoleak stayed sealed for three years. The same is true in the proximal thoracic aorta. This is one of Firas Mussa's cases. There's an endoleak on the underside of the arch and five endoanchors placed on the underside of the arch as we've just seen in JP's talk,
can resolve that endoleak quite successfully. When you are doing it in the arch you do need to plan properly. If you have an endoleak at the end of the case what you can do is put the C-Arm in an LAO position and line up the markers on the graft,
place the superior and inferior endoanchors and then rotate cranially and caudally at 15 degree intervals to put a series of endoanchors at the superior and inferior surfaces. That will fix the graft well. Otherwise, if you've got time and plan the case well,
you can work out dedicated C-Arm angles using one of the CT evaluation softwares. The best example is written by Rousseau, and I would get you to read that article to learn further. And that's how I learnt. There is a learning curve.
And this is necessary for success in treating type one endoleaks. You need some experience to gain good endoanchor placement. That's crucial, we've heard that. Start with the infrarenal segment, doing prophylactic cases,
the conical necks and slightly dilated necks, and then move into the thoracic segment. You need to use different size guides for different parts of the arch. On the upper surface the smaller guide is more useful. On the undersurface a larger guide to place the endoanchors
on the under surfaces of the arch is useful. Place them in rows coming back and have some patience. It's not all as easy as it looks right up there in the arch. For migration it's often an excellent strategy. If you can fix your migrated endograft to the native neck it's a good thing to do.
But remember these grafts have migrated and there's often great tortuosity there. If you can extend to gain a seal zone and then place a series of circumferential endoanchors it will fix that well and usually stay fixed for a good period of time.
There are limitations as I alluded to in the first few slides, excessive thrombus, excessive calcification, and where the aorta is dilated excessively and the endograft has stayed the same size. These will not work with endoanchor placement.
These are my tips, really, for success. There is a learning curve. Start with some easier ones. Think about the endoleak and why you've got an endoleak and don't be tricked into thinking the endoanchors will create a landing zone for you.
It won't. You should treat the type one endoleak immediately if you have it at the end of the case with re-interventions. You need to target that effectively and place multiple rows often cranially and caudally. And if you have one of the 13.4% failures,
remember that the use of endoanchors doesn't preclude you from doing something else so don't be too depressed. Thank you very much.
- Thank you very much, chairman and ladies and gentlemen. The funding of this trial was from The Academy of Medical Sciences and The Royal College of Surgeons of England. AKI due to the influence EVAR is actually more common than we all think. This is being shown by prospective studies and registries.
Why is it important? Well, it's associated with a higher intra or inter hospital mortality, cardiovascular events and also long term cardiovascular events and longterm mortality. As even more common and complex, EVAR, and this can range from 22% up to 32%.
These are some of our cases, some of our first, including FEN astrate EVAR in 2010 Thoraco-Abdominal Branch repair 2016 and Fen astrated TEVAR 2018. These are longer procedures, usually with more contrast and direct ventilation after removing arteries.
What are the mechanisms for acute kidney injuries due to infer-renal EVAR? While this involves use of contrast, systemic inflammatory response syndrome, due to ischemic re-perfusion injury, manipulation of the thrombus, aorta and catheterizations which will ------ alpha
and also from high prophalinemia. There is no high-quality evidence for AKI prevention in EVAR. What about Sodium Bicarbonate? Well it's been well know to reduce what been used commonly to reduce CIN in high risk patients in perrifical and
corona graphy. There are two main mechanisms as to how this works. Firstly, from reducing renal tubular ischemia. Secondly, by reducing oxygen deprived free radical formation in the tubules. What is the evidence?
Well this is a met analysis, comparing Sodium Bicarbonate directly with hydration with normal saline, as shown in the orange box. There is no difference. We can look at the population ll
mostly CKD patients or diabetic patients, certainly Hartmann's patients but they are not EVAR patients. They are coronary patients or peripheral an-graphy patients. In addition, serum bicarbonate and the urine pH was not reported so we do not know how effective the Bicarbonate was in these RCT's.
The authors went on to look other outcomes including needful hemo dialysis, cardiac events, the mortality and they found no difference but they concluded the strength of this evidence was low and insufficient. A further Meta-analysis this time published in BMJ this time comes in favor of bicarbonate
but again this is comparing bicarbonate with saline no use of combination therapy. There are again no use of EVAR patients and these patients all have a low eGFR. The preserved trial, a large trial published earlier this year in the New England Journal again using various
treatments again comparing sodium bicarbonates and saline again no difference. But again this compares bicarbonate direct with saline with no combination therapies. In addition, there were no EVAR patients, and these are low eGFR patients.
The met-analysis also showed that by using bicarbonates as a bolus dose rather than a continuous infusion, which was actually the way they used bicarbonates in most of these patients might be better. And using a higher dose of bicarbonate may also be better as shown in this Japanese paper.
So we come to HYDRA trial. They're using a high dose bicarbonate in combination with hydration to protect renal function. We did a UK wide survey of anesthetists of day to day and they felt the best volume expander they would like to use was Hartmann's solution.
So we randomized patients between standard hydration with Hartmann's solution verses standard hydration Hartmann's plus high dose bicarbonate per operatively and low slow intravenous infusion bicarbonate during the surgery. Importantly, with these patients,
we kept the map within 80% of baseline, 90% of the time in contrary to all the RCT's coronary and angeo-porphyry. We're going to skip that slide. This is the inclusion criteria, any patient undergoing infra EVAR, with any renal disfunction,
the primary area you must look at is recruitment and the second area you must look at is AKI. We screened 109 patients of which, 58% were randomized and there were only 2 crossovers. There was a willingness for patients to participate and there was also a willingness for PET 4 Clinitions to
recruit as well. This is the demographics, which is typical of aortic patients they are all on by a few MRSA patients, have normal renal function. Most of the patients wear statins and anti pace agent, only 13% were diabetic.
The patients were matched in terms of hypertension and also fluid hydration pre-operatively measures of via impedance. Here are the results of the trial. The AKI instance in the standard hydration group was like 3% and 7.1% with standard hydration plus bicarbonate. And it was similar in terms of organotrophic support into
and postop and also contrast volume used. It's a safe regime with none of the patients suffering as a result of using bicarbonate. So to conclude, to answer professor Veith's question, about how was this trial different to all the other trials? Well, certainly the previous trials have compared
bicarbonate with saline, there's lack of combination studies that involve mostly coronary an peripheral procedures, not EVAR. And the the most only included patient with low eGFR. HYDRA is different, this is not a regime using high dose bolus of sodium bicarb combined with standard hydration.
It shows promise of reducing AKO. This is an EVAR specific pilot RCT. Again, Unlike previous trials using bicarbonate, 90% of the patients had normal or mild impaired renal function. And unlike previous trials, there's more aggressive management of hypertension intra and postoperatively.
Thank you for listening.
- [Sergio] Good morning everybody. I really do thank you for the opportunity to reason with you about the lower limbs venous kinetics and the consequent impact on drainage direction. I have no conflicts of interest to declare, particularly because this talk is all about physics and about those laws of physics
that rule the venous drainage. We could say that the drainage occurs along our Italian leg, along a deep venous highway, a saphenous freeway and along several tributary and perforated roads.
But we could also say that we could divide the anatomy of our lower limb into three different compartments. So the tributary one's above the fascia, the saphenous one in between the fascia layers, and the deep venous one below the fascia. In this kind of network, talking about physics,
we could apply the Bernoulli's principle which, to make it simple, states that whenever there is an acceleration, a lateral pressure drop occurs. Which introduces the Venturi's effect as a potential aspiration of blood
from a slowest toward a fastest vessel. But actually, up to now, we couldn't say this for sure and say that venous network because we have really few data on the literature about the velocity values that we have in the different segments of the different compartments.
So the aim of this investigation, in the first physiological part, was to evaluate the different velocity values of different segments, understanding if the Venturi's effect could be applied inside this network, and then looking at the pathological cases.
So we have 36 lower limbs of healthy controls, and we assess all the velocity segments in the different segments of the three different compartments, evoking the flow both by active dorsal flection maneuvers of the foot, and by compression/relaxation
of the calf of course. So we compared all the different values of all the different velocities with the two different maneuvers, and we created several tables and we performed several statistical tests to see
how these velocities were behaving in the different compartments. So it's pretty interesting to notice that there are segments of our venous networks in which if we are performing the vocation of the flow with two different maneuvers, we are going to have
significantly different values of velocity. So for example, this happened in the external iliac vein, in the femoral vein, in the posterior tibial vein, and the tributary veins. If you look at the graph, we realize that there is a gradient of velocities
that is decreasing in physiology. While we are moving from the deepest, toward the most superficial compartment. And if we take all these velocities we assess together, we see that there are three different groups of velocities basically, statistically speaking,
that almost totally overlap the anatomical compartments, with some exception. So if you look over here for example, you have the posterior tibial vein that belongs to the deep venous system of course, in terms of anatomy, but not in terms of velocities.
Which means that the velocity we reported were significantly different from the ones belonging to the deep venous compartment. The same thing for the short saphenous vein, which demonstrated to of course belong to the saphenous compartment in terms of anatomy
but not in terms of velocities. If we move toward the pathological part of this, and we look at the 40 chronic venous disease patients we assessed in a model in which we considered incompetent tributary as the segment you see over there, depicted as C.
Compared to the adjacent GSV trunk, A and B. It's interesting to notice how the peak diastolic velocity and the diastolic time average velocity are actually significantly higher in the tributary compared to the GSV in pathological cases.
And if we look at the resistance index, it's interesting to notice how the segment in B, so the GSV trunk below the confluence, is actually higher. Like indicating a sort of preferential road of drainage toward the incompetent tributary.
This introduced the Venturi's effect, so now we can see the Venturi's effect could play a role inside the venous network. In physiology with a gradient that is increasing in terms of velocity, so potential aspiration while we are going toward the deepest compartment.
And the gradient that is subverted in pathology, where we have tributaries that are going faster when they are incompetent, compared to the GSV trunk, so leading to potential aspiration. But our blood is not a newtonian fluid, our vessels are not ideal conduits,
so we have to admit some things we know that we know, and that's of course the newtonian physics. Kn we know that we don't know,
and that's the application of the newtonian physics inside the human body. And then unkn things we don't even know that we don't know. That's the in-vivo validation
of these physical models. Independently by what we know and by what we don't know, I totally agree with profe tters and starting from today we know that Venturi's effect could play a role inside the venous network. Thank you.
- So, here's the dilemma. We have heard that 20% of AAA occur in women. However, 33% of hospitalizations due to rupture of AAAs are in women and 41% of death due to AAA are women and interestingly, 22% are not even smokers. Ruptures occur in women earlier than in men. We heard before, this is because the aorta, naturally,
is smaller in women. So, if you have a threshold of 5 or 5.5 centimeters, it may be too large for women. So, when AAAs are treated in women, the disease is already more advanced, more complex, with more undiagnosed cardiovascular disease.
AAAs go faster and women rupture rate is 4 times in ruptures with smaller diameters. And this is why the aortic surface index was introduced, to better estimate the time when women need to be treated. EVAR is much less suitable in women than in men, shown here in a meta analysis,
and therefore EVAR is much less frequently offered to women than to men. Is open surgery a solution? No, it isn't. If you look here, the mortality is more than double in women compared to men in open surgery for AAA.
In EVAR, the difference is not as big as for open surgeries. Still, less favorable for women. So, in numbers, women are eligible for EVAR in 34% versus 54% in men. Women are declined for intervention 34% versus 19% in men, and the 30-day mortality is 2.3% versus 1.4% overall,
and using all endoprosthesis available. So, why is that? The neck length is not met in women very frequently, and looking at all IFU criteria for AAA neck, it's even worse. Also, looking at the requirement for access arteries,
they are much less met by women compared to men. So, which EVAR, then, should be used in women to meet that problem? The problem is that women are under-represented in trials. You see here that they only comprise 6 to 29% in the IDE trials with the several aortic endoprosthesis.
So, while women comprise for 20% of AAA, only 10% of the populations in trial were women. So, they are under-represented in these trials. So, what is important for endoprosthesis in a woman? We need a small graft profile for small and also diseased access arteries.
And, because they usually are very calcified, we also need good radial force despite the low profile. So, the Ovation procedure. This is a 14-French device which meets that. And because of those polymer rings, it also helps sealing irregular necks,
also more frequent in women, and the legs have a high radial force. We never observed in our institution, kinks, stenosis, or even occlusions of these legs. The LUCY trial is the only trial every dedicated to this gender problem,
with the twin one randomization, women versus men and 225 patients. And we have now 30 days and one year data available. Not surprisingly, the vascular characteristics were less favorable in women regarding neck length,
regarding angulation of necks, and also the size of access arteries. Now, here you can see the size red are the access arteries sizes for women and blue for men. Also, for the other vascular characteristics, 55% of female patients and 35% of males had
one or more challenging baseline anatomic characteristics. Nevertheless, 96% of females, the prosthesis could be offered, compared to 46 to 75% for competitors. The outcomes, very quick. Because there was no difference regarding procedural outcomes, recovery,
major adverse events at 30 days and also at one year. No difference at all regarding mortality, regarding conversion and rupture, and Type 1a Endoleak over 12 months, and also regarding secondary intervention. So, in summary, the 30-day results of the LUCY trial showed
at least 28% more suitability for EVARs in women with AAA. Only 1.3% severe adverse events, the lowest for EVARs described event rate. No deaths. No proximal endoleaks. No leg occlusions.
Low re-hospitalization rate of 3.9%. 100% procedural success, and at one year, similar outcomes regarding conversion rupture, AAA-related mortality, device-related reintervention. What is good in women with difficult anatomy may be also good in men with difficult anatomy.
This is a gentleman we treated just two weeks ago. As you can see here, very calcified access arteries, four stents in place in the iliac arteries, irregular neck, and that was solved also with an Ovation prosthesis and the Type 1a Endoleak was resolved the following post-dilation.
Thank you very much.
- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery
in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,
but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase
and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,
and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast
in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.
So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,
it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause
of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.
So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes
and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,
and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR
might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement
without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac
Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,
to save our country from a type II endoleak, and I thank you for your attention.
- [Bill] Thank you Vikay. I think this is an interesting topic for many reasons but one of the key ones is that if you look at our health care policies by insurers, this tends to define our practice. So I looked at BlueCross BlueShield's policy and they say that treatment of the GSV or SSV
is medically necessary when there is demonstrated saphenous reflux and I looked for more and there was no more. That's all they said so they must think that reflux a time correlates with venous severity. So is this true?
I think, personally, that there are other things that are involved and that volume is really the key. Time, velocity and the diameter of the vein are likely all part of the process and we all know that obstruction
is also critically important as well and probably the worse patients are those that have both reflux and obstruction. Probably reflux is worse in the deep system but we know that large GSV and SSV patients can develop CEAP four to six symptoms
and do very well with saphenous ablations. And I think this is a nice analogy. I love this guy, it looks like he came off of his lawn chair to help the firefighters out but he's probably not going to do so much with his little garden hose now, is he?
So I think size and velocity do matter. What does the literature tell us? Chris Lattimer and his group have done an elegant set of studies looking at how various parameters correlate to air plethysmography and venous filling times. They did show that there is a correlation
between venous filling time and reflux time. However, other things were probably more correlated such as GSV diameter and reflux velocity. And in this nice study of 300 patients they found that there was a relatively weak correlation between reflux time and clinical severity
and their conclusion was that it was a good parameter to identify reflux but not for quantifying the severity. So here's how we use this clinically in my practice. So you see many patients such as this that have mixed venous disease.
53-year-old female, severe edema. You do her studies and she's got reflux in the deep and the superficial system. So how to we decide if saphenous ablation is going to help this patient or not and correct these symptoms, prevent further ulcerations?
So all reflux is not created equal. The top is a popliteal tracing where the maximum reflux velocity is about five centimeters per second versus the bottom one that's about thirty to forty centimeters per second
so these probably aren't going to behave similarly in when we look at them. So we studied this in 75 patients and reported this back in 2008. We look at the maximum reflux velocity in the popliteal vein to tell if these patients
would improve after we ablated their saphenous or not. We found that this was a significant predictor of both improvement in venous filling index and the venous clinical severity score so we think velocity really does matter. And this is where we're seeing this clinically.
This is a patient that was referred to me for a second opinion concerning whether she would need ablation of her great saphenous vein. And this is the reflux tracing and you can see the scale here is turned up so that this is a measurement of reflux at about two centimeters per second.
This was used to document abnormal reflux and to justify ablation of the saphenous. So I checked one of our tracings. This is what it looks like.
- The FLEX Scoring Catheter is one of the new tools, which is dedicated to vessel preparation, either as a stent, as a therapy followed by plain balloon angioplasty, or preparing the vessel for drug-eluting balloons and stents. So, the background basically is that
we're more and more tackling chronic total occlusions, and these kind of lesions, they have an increased risk of being calcium-containing, creating dissections, perforations, embolization, and poor luminal gain. And for that purpose, this device, which is more or less
a kind of surgical device, was developed. It's a interventional tool which can be introduced via a six-French sheath. It's an over-the-wire system, running over a 14 or 18 thousandths guide wire. It's common in shaft lengths of
40 centimeters dedicated to AV, fistula treatment and 120 centimeters, and the device is exposed to the vessel wall with three atherotomes, with the indication for femoropopiliteal and AV fistula excess treatment. One size fits all is really the right description
of this device, except having two different shaft lengths, the device itself is coming in one size only. What does it result in? Well, it results in micro-incisions, as you can see it over here, also over here in an OCT image, and the depths of these incisions
is about 0.5 millimeters, the pressure which is applied to the surface is about one atmosphere, independent on the vessel size. So, the idea and the rationale for this device is to facilitate and increase the vessel compliance and to create an controlled environment for angioplasty.
There are, just recently, some specimen analysis performed by CBSET, what you can see over here, marked by arrows, these arrows indicate the FLEX-induced micro-incisions, and you can see that these incisions are really circumferential with controlled,
uniform depths of those incisions into the plaque or the vessel wall. This is a 150 times magnification and you can see these longitudinal micro-incisions, which are very much parallel, it's like using a cutting balloon,
the advantage, however, is that this device can be applied to even longer lesions, the limitation of a cutting balloon is the balloon length of 20 centimeters only. So what are the early results? I can present you the acute outcomes
of 100 patients' sample size, with chronic total femoropopliteal occlusions. We can see that the average lesion length was really significant, 191 millimeters, the range was up to 35 centimeters, and there was moderate to severe calcification
in almost 50% of those cases. The luminal gain post FLEX application was about 31%, and the following balloon opening pressure, which was documented within this registry, was four atmospheres only, which is a signal that really the vessel compliance
is significantly improved, considering the almost 50% of moderate to severe calcification of those lesions. There had been no emboli, there had been no flow-limiting dissections, nevertheless, the provisional stent use was still high with 19%.
This is one of two case examples I would like to share with you. This was an instant re-occlusion of the popliteal artery, 10 centimeters in length, this was passed with an 18 thousandths guide wire, three passes with the FLEX catheter had been performed,
as you can see over here. And this was then, this was the result after FLEX catheter application and this is post additional drug-coated balloon angioplasty, there was no dissection, there was no significant residual stenosis.
Another case example, unfortunately, the video will not run, this was a long distance flush occlusion of the SFA, and you can see the calcium here in the entire length of the lesion, this lesion was treated, again, with the FLEX catheter, here, the video is not running,
this is the final result after DCB application. So, in summary, there's a high degree of technical success in achieving consistent luminal gain post FLEX, there's a low opening balloon pressure, and the re-canalization of CTOs was possible with a low rate, zero rate of significant dissections
and the low provisional stent rate. Thank you very much.
- Now we are delighted that there's apparently two things that we came up with years ago proved useful. This is the Near-Infrared Spectroscopy slide by Joe Bavaria from UPENN providing patient data on delayed paraplegia. That's a problem that we see in open NN (mumbles) very frequently.
How does the NIRS work? And again to this illustrative picture and now imagine the spinal cord sitting here in the spine canal and there's no more blood flow and this is the end result. When you know the oxygenation in the collateral network
and there was the problem with this technology that had been attempted 12 years back already, in Houston, I bet they put the NIRS optodes in the midline and the light cannot penetrate bone so it didn't work. But if you put it on the collateral network
and you measure the oxygen in this area, you obviously know it in the spinal canal. Dorsal view, again, so this is position of the optodes and this is oxygen content way interested in it. This is another cast just to illustrate
how these segmentals are regionally connected into the spinal canal, obviously. Experimental validation and pilot series in the next two minutes. Experimental cross clamping, this is the setup so years mentoring Laser Doppler Flow
to a real time evaluation of what you measure with your infrared setup in the animal lab and we see here, correlation is very nice between the lumbar NIRS, optodes, and the actual lumbar spinal cord oxygenation measured by Laser Doppler which is evaluated
with other techniques. Very nice to see the corelation between the two. So lumbar collateral network NIRS directly reflects spinal cord tissue oxygenation. After we have proven that step, next step was serial segmental artery occlusion.
As this is a technology that we or the strategy that we using, obviously want to know with our monitoring works for that. You see here, experimental setup basically the same. Starts with anesthesia, exposure of the segmentals. Now an open approach
and then you get 120 minutes surveillance period. You got a drop or dip in the NIRS measurements. Interestingly in the experimental setup in the recovery group, you see here that the new logical function comes back after the procedure and the NIRS comes back after the procedure.
Paraplegic group, all segmentals sacrificed NIRS, drops after the procedure in the first couple days, and the neurologic function does not recover. So experimental evidence that actually works. Nice corelation, again, so the experimental validation proves that lumbar NIRS
reflects lumbar spinal cord oxygenation and reacts to occlusion, of segmental arteries in real-time, but careful it's only regional so where ever you put your optodes, this is the area where you can monitor
your collateral network associated dip when you coil or include the segmental arteries. First clinical results published a couple years ago, I think you have all seen this video. Optodes are putting in the back of the patient, same setup for endo and open
and then we take the monitors theory and we have real-time monitoring on oversights midline here, this is (mumbles). Concept validation from 2016 with the first clinical data and now we're working on the clinical evaluation
of the use of this technology in EVAR and in clinical coil-embolization. 11 patients have been included so far for the EVAR group and you see here, it is very sensitive when you put stent in, stent deployment, but we have to still work so to speak
on the area that we have to monitor. There's a lot of work to do and probably also device modifications are necessary. MISACE, last couple words, on this you see pretty stable, NIRS all over the time course and actually this is nothing we wouldn't have expected
because the patient obviously were protected from spine cord anesthesia. So also here but sometimes we see a significant drop and this is when you should be careful and that's when you usually stop the procedure. So in conclusion, minor changes
in Collateral Network oxygenation have been seen in EVAR in this preliminary results using the nearest technology and to establish one very nice ... Nicely how clinical practice is already guided at his institution.
There's no immediate complete occlusion of covered segmental arteries and there's ongoing study in very heterogeneous patient group. There's no relevant changes with the chlorine technology so far,
but that, just to remind you, is the purpose of this technology, that we do not harm the patient during the preparation period. Thank you very much for your attention.
- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,
it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.
And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication
what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies
to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging
that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,
with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures
to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit
in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is
based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,
and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.
Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system
that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress
and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform
a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.
I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient
before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.
But we hope to present on that more solid data next year. Thank you very much.
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- I'd like the thank Doctor Veith for inviting me back to speak. I have no disclosures, we will be discussing some slight off-label use of the anitcoagulants. As we all know, acute limb ischemia occurs as a result of acute thrombosis of a native artery or bypass graft or embolism from a proximal
source, dissection, or trauma. The incidence is not insignificant, 15 cases per 100 000 persons per year, or interestingly about 10 to 16% of our vascular workload. Despite the relative frequency of this condition, there are relatively few guidelines to
guide us for anticoagulation therapy. The last set of guidelines for the American College of Chest Physicians regarding PAD gives some very brief, generic recommendations from 2012. They state, suggest immediate systemic anticoagulation with unfractionated heparin.
We suggest reperfusion over no reperfusion, which seems pretty obvious to an audience of vascular specialists. One of the challenges with acute limb ischemia is that it is a fairly heterogenous group. It can be thrombosis or embolism to the aorticiliac segments to the infrainguinal segments, and
there's also the patients who develop ALI from trauma. So we actually looked at the various phases of anticoagulation for acute limb ischemia and then we do, as with many institutions, utilize intravenous heparin at the time of the diagnosis, as well as obviously at the time of surgery,
but we found that there was a significant variation with regard to the early, post-operative anticoagulation regimens. One option is to give therapeutic intravenous heparin on an adjusted dose, but what we found in a significant minority of patients across the country actually,
is that people are giving this fixed mini-dose 500 unit an hour of heparin without any standardization or efficacy analysis. Then, obviously you go the long-term anticoagulation. We reviewed 123 patients who had ALI at our institution, who underwent surgical revascularization.
And they had the typical set of comorbidities you might expect in someone who has PAD or atheroembolism. In these patients, the Rutherford Classification was viable or marginally threatened in the majority, with about 25% having immediately threatened limb.
Various procedures were performed for these patients, including thromboembolectomy in the majority, bypass operations, angioplasty and stenting was performed in the significant minority and then primary amputation in the various selects few. We divided these patients into
the first four days of anticoagulation. Therapeutic with unfractionated heparin early on versus subtherapeutic or this mini-dose unfractionated heparin and we found that 29% of our patients were receiving the mini-dose unfractionated heparin, again without much efficacy analysis.
We used the International Society for Thrombosis and Haemostasis Anticoagulation Outcome Guidelines to look at the ischemic complications, as well as major and minor bleeding for these patients, and we identified actually not a significant rate of difference between the
subtherapeutic category and the therapeutic category of patients, with regard to mortality, with regard to recurrent limb ischemia, MI, VTE, or stroke, major amputation, and we actually didn't find because it's a fairly small study, any significant difference in major or minor bleeding for these patients.
So, we do feel that this small study did justify some efficacy of mini-dose unfractionated heparin because we didn't find that it was causing recurrent lower extremity thromboembolsim in these patients. Now on to long-term anticoagulation, for these patients, after that first three or four days
after the surgery, the options are long-term vitamin K antagonists, the DOAC's or vitamin K antagonists if you have atrial arrhythmia, or in the patients who had no other comorbidities, there really is not much guidance until recently. The compass trial was recently published in 2018
in stable PAD and carotid disease patients, identifying that rivaroxaban plus aspirin had a significant benefit over aspirin alone in patients who had stable PAD. And then, an upcoming trial, which is still ongoing currently in patients who underwent recent
revascularization, whether open or endo, is hopefully going to demonstrate that rivaroxaban, again has a role in patients with lower extremity ischemia. So in conclusion, there is relatively a scarcity of clinical data to help guide anticoagulation after acute limb ischemia.
Unfractionated heparin pre and intraop are standardized, but postop anticoagulation is quite variable. The mini-dose, we consider to be a reasonable option in the first few days to balance bleeding versus rethrombrosis, and fortunately we are having larger randomized clinical trials to help demonstrate the benefit of the DOACs and
aspirin in patients who are stable or post-revascularization for PAD, thank you.
- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans
can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.
But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.
What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?
Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for
all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',
and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.
He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.
So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.
It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,
and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after
you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,
and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.
That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.
How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.
But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.
In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,
the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors
such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants
to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study
because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.
So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist
on maximal protection and assume that all radiation is dangerous. Thank you very much.
- I'm going to take it slightly beyond the standard role for the VBX and use it as we use it now for our fenestrated and branch and chimney grafts. These are my disclosures. You've seen these slides already, but the flexibility of VBX really does give us a significant ability to conform it
to the anatomies that we're dealing with. It's a very trackable stent. It doesn't, you don't have to worry about it coming off the balloon. Flexible as individual stents and in case in a PTFE so you can see it really articulates
between each of these rings of PTFE, or rings of stent and not connected together. I found I can use the smaller grafts, the six millimeter, for parallel grafts then flare them distally into my landing zone to customize it but keep the gutter relatively small
and decrease the instance of gutter leaks. So let's start with a presentation. I know we just had lunch so try and shake it up a little bit here. 72-year-old male that came in, history of a previous end-to-side aortobifemoral bypass graft
and then came in, had bilateral occluded external iliac arteries. I assume that's for the end-to-side anastomosis. I had a history of COPD, coronary artery disease, and peripheral arterial disease, and presented with a pseudoaneurysm
in the proximal juxtarenal graft anastomosis. Here you can see coming down the thing of most concern is both iliacs are occluded, slight kink in the aortofemoral bypass graft, but you see a common iliac coming down to the hypogastric, and that's really the only blood flow to the pelvis.
The aneurysm itself actually extended close to the renal, so we felt we needed to do a fenestrated graft. We came in with a fenestrated graft. Here's the renal vessels here, SMA. And then we actually came in from above in the brachial access and catheterized
the common iliac artery going down through the stenosis into the hypogastric artery. With that we then put a VBX stent graft in there which nicely deployed that, and you can see how we can customize the stent starting with a smaller stent here
and then flaring it more proximal as we move up through the vessel. With that we then came in and did our fenestrated graft. You can see fenestrations. We do use VBX for a good number of our fenestrated grafts and here you can see the tailoring.
You can see where a smaller artery, able to flare it at the level of the fenestration flare more for a good seal. Within the fenestration itself excellent flow to the left. We repeated the procedure on the right. Again, more customizable at the fenestration and going out to the smaller vessel.
And then we came down and actually extended down in a parallel graft down into that VBX to give us that parallel graft perfusion of the pelvis, and thereby we sealed the pseudoaneurysm and maintain tail perfusion of the pelvis and then through the aortofemoral limbs
to both of the common femoral arteries, and that resolved the pseudoaneurysm and maintained perfusion for us. We did a retrospective review of our data from August of 2014 through March of 2018. We had 183 patients who underwent endovascular repair
for a complex aneurysm, 106 which had branch grafts to the renals and the visceral vessels for 238 grafts. When we look at the breakdown here, of those 106, 38 patients' stents involved the use of VBX. This was only limited by the late release of the VBX graft.
And so we had 68 patients who were treated with non-VBX grafts. Their other demographics were very similar. We then look at the use, we were able to use some of the smaller VBXs, as I mentioned, because we can tailor it more distally
so you don't have to put a seven or eight millimeter parallel graft in, and with that we found that we had excellent results with that. Lower use of actual number of grafts, so we had, for VBX side we only had one graft
per vessel treated. If you look at the other grafts, they're anywhere between 1.2 and two grafts per vessel treated. We had similar mortality and followup was good with excellent graft patency for the VBX grafts.
As mentioned, technical success of 99%, mimicking the data that Dr. Metzger put forward to us. So in conclusion, I think VBX is a safe and a very versatile graft we can use for treating these complex aneurysms for perfusion of iliac vessels as well as visceral vessels
as we illustrated. And we use it for aortoiliac occlusive disease, branch and fenestrated grafts and parallel grafts. It's patency is equal to if not better than the similar grafts and has a greater flexibility for modeling and conforming to the existing anatomy.
Thank you very much for your attention.
- So thank you for the kind introduction and thanks for professor Viet for the invitation again this year. So, if we talk about applicability, of course you have to check the eye views from this device and you're limited by few instructions for users. They changed the lengths between the target vessel
and the orifice and the branch, with less than 50 mm , they used to be less than 25 mm. Also keep in mind, that you need to have a distance of more than 67 mm between your renal artery cuff and your iliac bifurcation. The good thing about branch endografts
is that if you have renal artery which comes ... or its orifice at the same level of the SME, you can just advance and put your endorafts a bit more proximally, of course risking more coverage of your aorta and eventually risking high rate
of paraplegia or spinal cord ischemia. Also if your renal artery on one side or if your target vessel is much lower with longer bridging stent grafts which are now available like the VBX: 79 mm or combination of bridging stem grafts, this can be treated as well.
Proximally, we have short extensions like the TBE which only allows 77 or 81 mm. This can also expand its applicability of this device. The suitability has already been proven in.. or assessed by Gaspar and vistas and it came around plus 60%
of all patients with aortic aneurysms. Majority of them are limitations where the previous EVAR or open AAA repair or the narrow diameter reno visceral segment in case of diabetes sections. So, what about the safety of the T-branch device?
We performed an observational study Mister, Hamburg and Milner group and I can present you here the short term results. We looked at 80 patients in prospective or retro prospective manner with the t-branch as instructed for use.
Majority were aneurysms with the type two or type four Crawford tracheal aneurysms, also a few with symptomatic or ruptured cases. Patient characteristics of course, we have the same of the usual high risk cardiovascular profiling,
this group of patients that has been treated. Majority was performed percutaneously in 55%. The procedure time shows us that there is still a learning curve. I think nowadays we can perform this under 200 minutes. What is the outcome?
We have one patient who died post operative day 30, after experiencing multiorgan failure. These are 30 day results. No rupture or conversion to open surgery. We had one patient with cardiac ischemia, seven patients with spinal cord ischemia
and one patient has early branch occlusion. There was both renal arteries were occluded, he had an unknown heparin induced thrombocytopenia and was treated with endovascular thrombectomy and successfully treated as well. Secondary interventions within 30 days were in one patient
stent placement due to an uncovered celiac stent stenosis In one patient there was a proximal type one endoleak with a proximal extension. One patient who had paraplegia or paraparesis, he had a stenosis of his internal iliac artery which stem was stented successfully,
and the paraparesis resolved later on in this patient. And of course the patient I just mentioned before, with his left and right renal artery occlusion. So to conclude, the T-branch has wide applicability as we've seen also before, up to 80% especially with adjuvant procedures.
Longer, more flexible bridging stent grafts will expand the use of this device. Also the TBE proximal extensions allows aortic treatment of diameters for more than 30 mm and I think the limitations are still the diameter at reno visceral segment,
previous EVAR or open AAA repair and having of course multiple visceral arteries. Thank you.
- Good morning. Thank you very much for the invitation, as always, to be here at Veith. It's always a great pleasure to be at this meeting. These are my conflicts, of course. This work that I'm presenting is presented on behalf of this group of people, principally Mr. Justinas Silickas
and Mr. Prakash Saha who've done the majority of the analysis of this MRI data. The point for looking at clot aging with MRI and why we're interested in these techniques is really about how we progress acute DVT lysis. We know that ATTRACT has raised a number of questions for us
and one of the main issues that is not necessarily focused on is when we're trying to select patients for DVT lysis, we don't really know which patients will benefit because we take a history from the patient that suggests clots within an age that may be
suitable for lytic, but we know that history is unreliable. We end up treating a mixture of what we call acute thrombis and chronic clot, which is, of course, a misnomer because chronic clot is really a replacement of thrombis burden with collagen and this will not be receptive to lytic therapies,
and in fact may not be receptive to the devices we try to use in it. So, undeniably, we have a need to select patients better for these treatments. In our center, we've taken a mouse model of clot aging and using the base of this model to understand
that there is a progression from red blood cells, which is the yellow bars, through to thrombin, which are the red bars, and finally replace them with collagen, with the blue bars at the bottom of the screen. We can try and work out where clot is in this aging process.
And from this mouse model, we used a mouse MRI scan as to develop a human imaging protocol technique to look at these various changes in clot, which are based on both MR T1 mapping and various other diffusion weighting schemes. This gives us an image that looks something like this,
with the animal venogram, once we overlay the T1 maps, and these are thought to suggest which clot would be lysable in this particular patient. This was the case with all the clot lysing and no need for stent at the end. In the second patient, we knew that the top part
of the vein and the common iliac segment was likely a chronic lesion and that the external iliac vein and common femerol vein had fresh thrombis in them, and this is what turned out to be. This patient required a stent at the end of the procedure. Then this third patient, the imaging had suggested
the clot would not be lysable, and indeed this was the case. And all three of these patients had relatively similar history and presentation and we got completely different ideas and treatment from them. So based on this initial work,
we've taken now a number of patients through our center who were recruited into a study to look at this in a more structured fashion. They all had the multisequence imaging performed with a collection of a number of imaging modalities and MR. And we generated these sort of images for these patients
to try and predict what the course of lysis would be. So we took the images before, predicted whether they would lyse, and then we looked at that afterwords to see if this was in fact the case. This segmentation sequence is a
manual segmentation sequence to get all these maps out. We had 41 patients go through the process. The most significant was that the T1 is predictive of lysis by itself. The other two sequences did not show a significant difference between
lysis and no lysis if you used them separately. But, if you combine these into multi imaging modality sequence, in particular T1 plus ADC, you get quite a high positive predictive value. Of course, negative predictive value is very good and the accuracy overall is 96 percent.
So the point is taking individual segments of MR don't seem to add as much value as combining these multiple sequences together to predict the role for patients. So essentially where we're going with MRI imaging now is that we do believe that multi-sequence techniques
can be used with combination, of particularly T1 relaxation times, to predict which patients will be suitable for lysis. We are able to identify experimentally thromboarteritis. The sequence is very short and can be performed with a standard MRI machine,
a one and a half Tesla machine, in thirty minutes. However, segmentation is still labor intensive and this particular part needs automation to make this a more reproducible technique that anybody else can use and we do think that further investigation to help guide therapy
based on MRI imaging techniques will be very helpful. Thank you very much.
- Frank, thank you very much for your invitation. This is my disclosure. I think that all vascular surgeons are asking ourself following question. Is diameter of triple A the sole indicator for surgery? To ask for this question since about 20 years, we are interesting with function in aging with a PET CT
using 18F-FDG which allows the evaluation of the regional glucose metabolisms. And shows the presence of an inflammatory reaction at the level of atherosclerotic tissue infiltrated by the inflammatory cells. During our pilot study, we observed that
the uptake of the FDG was also stated with the unstable triple A. And during several studies, we were observed that FDG uptake not only show of predicted rupture but it predict also the site of the rupture
in triple A patients in Thoracic Aortic Aneurysms as well as Aortic Arch Aneurysm as you can see. Here is very easily we are find, you can observe FDG uptake and this patient we performed MRI and you can see here, free iron particles, it's same area of every velope. Starting increase FDG uptake
and this patient refused operation and come back three months later to rupture. Of course FDG is not specific for aneurysm or disease. We can found FDG uptake in cancer disease, infection or arthritis or arthritis and reason why several authors interested with different kind of biomarkers
and sodium fluoride F 18 each one of those one. And it's injections indicated for diagnostic PET imaging of bone to define areas of altered osteogenic activity. The primary clinical use of sodium fluoride PET is in detection of osseous prostate cancer metastasis. But some authors, all of them start to use it for
evaluation of the plaque metabolism in high cardiovascular risk subjects. One group from United Kingdom and leaded by a Dr. Newby from Cambridge, they performed several very nice studies using this marker in coronary artery disease for plaque rupture
and for evaluate aortic stenosis to accumulation of the calcification in the aortic leaflets. And also for carotid stenosis and they, during this several studies, they demonstrated that 18F sodium fluoride, selectively binds to microcalcification coronary
and carotid atherosclerotic plaques and that are associated with plaque vulnerability and rupture. More essentially he interested, they interest also the triple A and they called this study the SoFIA study and it concern about 72 cohort patients
and 20 study population. And it is very nice picture of the patients with positive 18F sodium fluoride uptake. It is specific for one and reason why it is left right in red color here, but anyways, very easy to show the infusion images uptake
at the symptomatic aneurysms. And they divided their cohort study in three levels of Tertile 1, Tertile 2, Tertile 3 according to sodium fluoride uptake from low uptake to increase uptake and they observed that the growth rate,
increased growth rate, aneurysm repair and rupture and aneurysm repair alone, it was significantly higher in the patients in Tertile 3 group. And they concluded that Fluorine-18 sodium PET-CT
is a novel and promising approach to the identification of disease activity in patients with triple A and is an additive predictor of aneurysm growth and future clinical events. My conclusion is 18F-FDG and 18F Sodium Fluoride however,
not specific for inflammation. Therefore, new imaging tracer for a more accurate inflammation detection and therapy evaluation are needed. We need specific markers of angiogenesis and inflammation to predict the triple A evolution and potential rupture.
Thank you very much for your attention.
- Thank you very much and thank you Frank for giving me the opportunity to speak. And I will adapt my talk because I saw some of the slides, I will have to comment of course. So I have no financial disclosures. In many, many papers we know that Endovascular Treatment needs a word
of caution for long-term follow-up and we can see many, many pictures with very good results of viaven or other devices but when you look at the long-term follow-up for this patient, it's quite awful.
So we have late thrombosis just like this, we have curves that goes down and down after 40 or 60 months and much of the patients are very young and so I think it's not a good option. On the contrary, the durability
of open popliteal aneurysm repair has been showed and it's been showed by another of the panelist there and of course I think it's the good way to do and there are several options. The first one, this one, is quite rare
just to make resection with direct anastomosis like this, but it could happen and in this kind of patient, mostly when they are young patients, you don't have to make interposition of any graft.
I mean no vein, no SFA, and no prosthetic grafts. When you have to make some of the conventional open repair just like this, you have to choose between an exclusion graft like this,
I don't like it really much because it can leave a very important aneurysm and it takes a lot of place and it is prone to growing after due to the collaterals
going to the aneurysm sac. Most of the times I like to do something which is a combination of both these two pictures. I mean I like to open the sac to make the aneurysm or if you have the collaterals and then to make a end-to-end
anastomosis at both sides. Of course, when you go to the segment in the gonoral approach you have to make a venous bypass and venous bypass is probably
better when the run-off is awful just like this, but for this patient this was something needing a venous graft and this for me can be treated by synthetic graft because it ends at this level
that mean retroarticular level. So, for the venous graft, I go to venous graft only when I have to make the anastomosis directly on lower-leg vessel just like this and then you mention this
specific paper and if you could read this paper, I'm not one of the first author of this paper because I don't follow this thing because as you say, I think it's not good at all
to section all the muscles and this patient, I know this patient, they can't walk anymore for probably two months, it's not a good option but I'm part of that team and I don't want to defend it for now. Prosthetic bypass is I prefer
because this is very ancient, I agree with you, it's not modern situation, it is very ancient situation but the main thing is that you don't have to cut all the muscles, you have to select patients
with distal neck or retroarticular popliteal artery with good arterial runoff, aminolytic vessels and you have to select the patient and the Angio-CT rather than the angiogram except for
selecting the quality of the run-off. So who should be selected, this kind of patient can be selected because the prosthetic graft will end only here.
And this one could be also, but you can s there is origin of the arteritica artery.
And you have to think at the level of cutting the lower knee popliteal artery. And most of the time you can just externalize the lower knee popliteal artery to make
anastomosis. And then when you make the distal anastomosis, first you can reintegrate after there is the graft. And then the graft in the anastomotic sides goes just below
the level of the endoarticular line just like this. So for me, this is a go even if
you see that it goes just right to the condyles like this. And if you make some pictures with the reflection of the knees, there is no problem for the space. And even when there is a large
length beneath the artery like this. So when (unidentifiable phrase) where there's no vein and no below knee extension. So these are the technique that I expect I already talk about.
This is a small surveys we did I did finally. 20 popliteal arteries, this is the mean diameters. All the patients had good run-off as you can see. And there were only five long bypasses from the common femoral artery.
The other one from the popliteal or distal SFA. This is the mean Length of Stay 4 days only. The limb salvage rate is 100%. Primary patency rates were at one, two and three as 10
and secondary rates were 100% with mean follow-up 2 30 months. So prosthetic bypass is our simple, safe durable options.
I don't cut any muscles for this kind of option. Results compare favorably with our other open and endovascular techniques. And the French survey is going on for now. Thank you very much. (Audience applauds)
- These are our disclosures. We are indebted to the Society for Vascular Surgery and the FDA and others for funding this work. Many patients who undergo endovascular aneurysm repair will also undergo reintervention. How patient-level factors affect the rate of reintervention, however, is poorly described.
Our goal in this project was to identify factors associated with reintervention after EVR in a large real-world cohort. We studied all patients in the Vascular Quality Initiative from 2003 to 2015 who underwent EVR. We linked these patients to their respective Medicare claims
using some patient-level analyses that were highly successful, making sure that we had identified the same patient in the registry, as well as their respective Medicare claim for followup. And we have had about 14000 of these patients.
We then made sure that we could identify the key events, like reintervention or a late rupture. And we were left with about 13000 patients for analysis. It is important to note in this cohort, amongst these 13000 patients, we had essentially 100% followup
for the outcomes of survival, reintervention, or late rupture. How did we measure these? Well, reintervention Medicare claims was measured using some algorithms that detected any procedure related to the aneurysm or the aneurysm repair
that occurred after discharge from the index hospitalization. And we published these algorithms in this JVS recently. This algorithm was found, upon clinical chart review, to be highly sensitive and highly specific in its ability to identify actual clinical events.
A similar algorithm was used to identify late rupture. What did we find amongst these 13000 patients? Well, on average, they were about 76 years old, 20% were female, 4% were black. At the time of initial repair, about 15% had an aneurysm that was small,
less than five centimeters, about 30% were between five and five and a half centimeters, 24% between five and six centimeters, and 30% of the aneurysms were large, greater than six centimeters. 89% were elective, 7% were symptomatic,
and 4% were ruptured. On the X axis we'll show here time, and on the Y axis the rate of reintervention over time. What we found was that the five year rate of reintervention, as by our definitions, was 21% at five years. Amongst elective patients, it was 20%.
It was higher in symptomatic patients at 25%, and ruptured patients had a 27% rate of reintervention at five years. These differences were all statistically significant. We performed similar analyses grouped by aneurysm size, and found that those with the largest aneurysms
had rates of reintervention that were much higher than those with smaller aneurysms. Similarly, these differences were statistically significant. White patients had rates of reintervention of approximately 20%, while African American patients
had rates of reintervention that were also higher. Again, differences that were statistically significant. We did not fine differences by gender. Both males and females had rates of reintervention about 20%. When we stratified our analyses
by the age at which the initial EVR was repaired, we found few differences here as well. Older patients and younger patients had similar rates of reintervention over time. Late rupture, unlike reintervention, was uncommon, just 3% at five years.
Late rupture, when we measured out to 10 years, remained uncommon, still under 5% at 10 years amongst the cohort of surviving patients. Important to know, though, that 70% of our cohort had deceased by 10 years. Our analysis is obviously limited.
It's limited to Medicare patients alone, and may not represent patients who were younger at the time of repair. And, of course, not all reinterventions are of equal magnitude. But, in summary, one in five Medicare patients
will undergo reintervention after EVR within the first five years of their repair. And reinterventions occur at a rate of about 4% per year, and don't appear to plateau over time, and this trend continues out to about a decade. Urgent operations, African American patients,
and those with larger aneurysms have an even higher rate of reintervention and should receive the most diligent surveillance possible. Our study, we believe, has important implications. While reintervention is common, late rupture is not. And how these factors associated with reintervention
also relate to late rupture still remains undescribed. We believe in the future, better describing the factors that are associated with reintervention after EVR may help patients in their decision making when considering abdominal aortic aneurysm repair.
Thank you very much.
- Mr. Chairman and dear friends, I would like to thank Frank Veith for his very kind invitation. I will talk about the value and the limitations of the very rare inflammatory disease. I have no disclosure. You see the list of the inflammatory
and infectious disease which are not very often we are used to make EVAR repair. I would like to show you my cases and some examples from the literature to make and emphasize the limitations and complications while doing EVAR
for those rare cases. Behcet's Disease, as we know, has a 30 to 55% percentage of pseudo-aneurysm after surgery, and we know that EVAR has less wall stress and less cytokine release and causing
inflammatory response. And we know that they need to use immunosuppressive drugs. I have a case 45 years old female, had three times open surgery, but again, she had a pseudoaneurysm rupture here and then we had done the EVAR repair
and put a tubular endograft, and the follow-up we had seen that all the hematoma was absorbed and the retroperitoneal space was clear. This case is 50 years old female, Behcet's Disease, juxta-renal aneurysms
at the orifice of the visceral arteries. We planned to make a bypass and also endograft intraoperatively, but she needed the re-intervention because of the distal endoleak and she also had an occlusion of the left renal artery.
But during the follow-up we had seen that she also is active during all the time, although she had drug use. Another case is referred for us from another center, having a pseudoaneurysm at the distal part. We used AUI endograft, fem-to-fem bypass graft,
and a very good result with the CT examination. And this case is from the literature showed that, had a pseudoaneurysm EVAR technique with tubular endografting, but also another pseudoaneurysm, hidden aneurysm, and they had to make an open surgery repair because of the
polar artery of the right kidney. Systemic lupus erythematosus is a vasculitis involving vaso vasorum, and forming the aneurysm formation, three out of antiphospholipid antibodies, chronic steroid, and cystic medial degeneration caused acceleration of this premature atherosclerosis
and the sharp pain of the chain pest and the abdomen is very important for causing the dissection. These are the cases from the literature. Very good EVAR treatment, but these two cases has a catastrophic result of the rupture and they died.
So it's very important for emergency departments to be aware of the young patients having history of hypertension and using a long steroid using. This is our case, which had the dissection aneurysm and the rupture of the aneurysm,
and she had endografting, so we followed her for a long time. This case is interesting. Because of having a penetrating ulcer, circular aneurysm, during the procedure there's a plaque rupture with the,
left common iliac, external iliac. We put a bare stent and also suture failure. Takayasu is another rare disease. This is the multiple aneurysms of the thoracic and abdominal, and this is our case which had two times rupture,
and the second time we offered him to have a TEVAR and surgery, but he refused and died. This is a rheumatoid arthritis disease patient. We had done EVAR successfully. There's no problem. And tuberculosis is another very important
infectious, mycotic aneurysm. The patient was under immunosuppressive and had an aneurysm treated with EVAR technique. And this patient, our own has, was active tuberculosis. We had to put a AUI endograft,
but it was infected. We have to remove and complete with axillary-femoral bypass. There's a lot of limitations as you hear, and as a conclusion, these rare inflammatory disease, they benefit from EVAR,
but we have to be very careful and be aware of the limitations and complications, and they have to be monitored very closely. Thank you.
- [Narrator] So my assignment is, CMS policy update on non-thermal ablation techniques, and as most of you know, there is not one National CMS policy, so there are a variety of local cover determinations or policies that we're going to look at. I may bore you for a couple minutes
but I found a surprise at the end. So I went to the website, CMS website, and looked up varicose vein LCDs and these seven came up, interestingly Novitas, everybody's favorite, didn't come. So I looked at separately, we're going to look at all these as well.
And here is Novitas, Novitas and their previous LCD had no mention of non-thermal techniques, but in this proposed LCD, which has a lot of people up in arms, they say that the non-thermal techniques are experimental, investigational, and unproven,
and therefore will not be covered. This is next LCDs, this is two from Medicare contractor Noridian, they go on to talk about sclerotherapy and foam sclerotherapy, but they are not going to cover it. And somewhat bizarrely these codes in red here,
which are for Venaseal and Verithena, are listed as indications for RF or laser ablation, which kind of shows you they don't know what they're talking about. And there is no mention of MOCA or Claravein. Wisconsin Physicians Services and other MAC contractor,
and I looked at their LCD, there is no mention of non-thermal techniques. Next up is First Coast Service Options, with these jurisdictions over here on the right. And they get down to the C-classification, VCSS score, and talk about compressive therapy and conservative therapy.
They do mention Clarivein or MOCA. However, they state that it does not meet the Medicare necessity for coverage, and so they won't. And there's absolutely no mention of Verithena or Venaseal in their LCD. Palmetto GBA is another contractor,
with these jurisdictions on the right, and they actually discuss and approve Varithena, microfoam sclerotherapy. They discuss it here in their LCD, they have some restrictions that the physician needs to be competent and experienced with Varithena,
and ultrasound, there is no mention of Clarivein or Venaseal in their LCD. And these are also the folks that tell us how to do stab phlebectomy with 2 mm incisions and a crochet hook. So don't use a 3 mm incision and a hemostat,
it'd probably get denied. Next is CGS Administrators, and this busy slide, they go on to talk about sclerotherapy quite a bit, and all these in the main body, what they are not going to cover for sclerotherapy. They mention that foam sclerotherapy
is basically the same as liquid sclerotherapy, and therefore will not cover it, and again no mention of other treatments of non-thermal techniques. Which brings us to the last LCD, which is National Government Services,
and amazingly they state that the accepted treatments for eliminating reflux and the great saphenous anterior accessory, and small saphenous vein, include RFA, laser, polidocanol, Venaseal, and Verithena. And even more interestingly, they use their Rationale for Determination for MOCA.
The amount and consistency of the data, in addition to the two recent systematic reviews and the strong recommendation of the American Venous Forum, have convinced NGS that Medicare coverage is met. And for PEM, Varithena, the combination of RCTs, meta-analyses, systematic reviews,
the strong recommendation of the AVF, and endorsements from the SVS, ACP, SCAI, and SIR, have convinced them that coverage is appropriate. And the same for Venaseal, same thing. This is craziness. On one Medicare hand,
you have Novitas saying that, treatment is experimental and unproven, and they won't cover it. And on the other Medicare hand, you have this contractor that says, based on the recommendations of the experts,
that it's appropriate, and will be covered. And this is the reason why we need a National Coverage Determination. So, to find out what your policy is, you have to go to the website, you have to find out who your provider is,
or contractor, and see what the policy cause it differs depending upon where you are. Thank you for your attention.
- Thank you very much, Mr. Chairman. Thank you Frank Veith for the invitation, talking about, "SFA lesions can be treated endovascularly: "Should they be?" I do not have any potential conflict of interest for this presentation, and I would like to share with you. We have two ways: Is it technically feasible
to perform always reverse canalization by endovascular technique, and the SFA, and should we do it? And I would like to immediately conclude by it's possible for me to treat all the lesions by endovascular technique in the SFA and popliteal lesion, and for me, I think, for us it's always the first choice.
So, next: What we do to really need an SFA re-canalization and a SFA repair? To be well armed with guides and catheter to perform re-canalization, and it's necessary how to get by unusual ways:
retrograde puncture of each over. And the difficulty is to know if we perform subintimal re-canalization or not, and the success of this technique is always the reentry. So for me, I think it's very important to have a right and clear process when
you perform a re-canalization, and to treat by endovascular therapy, SFA, and popliteal lesion, and I think we can perform a first dilation with POVAR with a balloon superior of 1 mm, compared to the diameter of the SFA.
And it's very important to perform an inflation during three minutes and to follow with a slow deflation and a gentle removal. And stent to the diameter of the SFA, and maybe it's important to use, in certain cases of the DEB.
So the success keys: Is a good experience of re-canalization, a good knowledge of the devices, and a preparation of the vessel. For me, it's very important and the quality of the angiogram tube,
so I would like to share you some example. Here is the example, and a thrombosis occlusion of the whole SFA, and for me you can see on the angiogram the results and it's very important to have a disparation of the decrease of the collateral injection
on the angiogram. This is a case with a total occlusion of SFA in the stent And you can see on the angiogram thrombosis of the stent at the anterior, and I performed for this patient retrograde puncture inside the stent,
and I take the guide wire with the retrograde puncture with the snare and I treat the artery. So, to avoid an hematoma at the puncture it's necessary to inflate before the balloon inside the stent
after the re-canalization, and to remove the introducer and to let the inflation during five minutes. And so, another cases with the total occlusion of the SFA and a very good result, and a very difficult case with a lot of calcification, and it's possible to perform SFA endovascular repair with these techniques.
Okay, and a case, total occlusion SFA, popliteal artery, and the leg artery, and we perform a re-canalization and we use a third-generation stent, Supera, and to have a very good result. And in terms of results, what do the studies say? Analysis of endovascular therapy for femoropopliteal disease
with the Supera stent in Journal of Vascular Surgery shows primary patency is very good, at 90% at one year. Another study, the study with my colleagues, we've used a third-generation of stent with a very good result at 24 months. And open surgery and the estimated
five-year primary patency was 64%. Okay, and in conclusion: For me, "There is no impregna "There are only badly attacked citadels." Thank you very much for your attention.
- Good morning, for all of you who got up early. It's a pleasure to be here, thank you Frank for the invitation. I'm going to talk about a problem that is extremely rare, and consequently can only be investigated by putting together databases from multiple institutions, called adventitial cystic disease.
Okay, I have no conflicts. So adventitial cystic disease is an extremely uncommon problem, but it's important because it occurs often in young people. Virtually all series of adventitial cystic disease have fewer than five patients in it,
so they essentially become case reports. And yet it's a very treatable problem. There are several theories about why it occurs, you can see this picture here. The mucin-assisting material that occurs in the popliteal artery region most commonly.
The etiology of that and the origin of that is debated, whether it comes from the joint space, whether it comes from rest, whatever. But it's not really known. In addition, what's not known is the best treatment. There are several options.
Some would advocate just simple aspiration of the cystic material, although it's very viscous. Others simply excising the cyst and leaving the vessel in place. Some both excising and either doing
an interposition graft or a bypass. Early results with every one of these options have been reported, but they're quite variable as far as the outcome. And therefore, we really don't know not only the optimal approach,
but also the best outcome. For that reason, we did a study with 13 institutions on adventitial cystic disease using a technique called vascular low-frequency disease consortium.
Where everybody uses a standardized database and similar collection to act like a single institution. The aim of this study, which is one of 20 that we've conducted over the last 15 years, was to determine first of all what people were doing
as far as current practice patterns, and then look at the outcomes with the different treatment options. And this was published in the Journal of Vascular Surgery. Adventitial cystic disease of any site was identified using both the CPT ICD-9 physician logbooks,
pathology databases, and procedure codes. And then we collected epidemiologic data as well as operative and follow-up data, with our primary endpoints being vessel patency and the need for re-intervention, since amputation is extremely uncommon and rare.
This is the process for the low-frequency disease consortium. Where not only is a standardized database used, but each institution collects their data after getting IRB approval. And then deidentifies it
before sending it to a central server. So there's no way that there could be a security breach. And then we do an analysis of the data. The results of this study were that in the small number of institutions, 15 institutions, 47 patients were identified.
The majority were male, and the majority were smokers. What was interesting to us was that not all are in the popliteal region. And actually there were several patients as you can see, who had upper-extremity adventitial cystic disease, although it's far more common in the popliteal space.
And also there was actually one patient who had adventitial cystic disease of the femoral vein. The symptoms were typically claudication, and ischemic rest pain or tissue loss were quite rare. If you look at the risk factors, smoking, which was probably a comorbidity
and would not be claimed to be the etiology but was present. Other than that, this is a typical distribution of patients with vascular disease. As far as imaging here, you can see a duplex ultrasound
showing the cystic mass and how it typically looks. The majority of patients had a duplex, but also they often had an MRA or CTA as well as an angiogram. And the angiogram was typically part of the treatment paradigm.
This is just the typical appearance of an MRA showing what some people would call the scimitar sign, which is that it's not a typical plaque. And this is a picture of a CT angiogram showing a similar view of a vessel. The results,
so there were some that did not treat only the cyst, but also resected the artery. And either bypassed it, as you can see here, or did an interposition graft,
here's just a picture of one of those. And there were others that just treated the cyst, and either aspirated it alone or resected the cyst and patched the artery. Or did cyst drainage and nothing else to the vessel. If you look at the typical incision of these patients,
this is a posterior approach of the popliteal region. And the small saphenous vein as you can see is marked, and uses the conduit for bypass. The outcomes of these patients were similar as far as length of stay, complications. The one you'll notice is that
two of the five with cyst resection had a complication, so that's a little bit higher. But otherwise they're quite similar as far as the short-term outcomes and results. The main problem, and also if we look at the improvement in ABI,
although cyst resection with bypass had a higher increase in ABI, the rest of the treatments were similar. In other words, the initial outcome was similar with any of those different options.
The one thing you can see circled in red is the patients who had simple cyst aspiration. It was not durable, and consequently they often had to have a second procedure. And the resection of the artery was generally, or bypass of the artery,
generally had better long-term outcomes. The follow-up was 20 months, and here you can see the recurrence and the types of modality of follow-up. So I just conclude by saying that our experience from multiple institutions
is that this is an uncommon problem, that cyst recurrence is very high if aspiration alone is used, and either interposition or bypass is the optimal treatment. Thanks very much for your attention.
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
- The committee asked me to give an update on the Cook p-Branch device which is in a clinical trial in the United States. This is the disclosures as it relates to this talk. I'm going to discuss the feasibility as well as the pivotal study as you see on this slide. Now these two studies, as you can imagine,
have a different number of patients. The feasibility study was done in 30 patients and, as all studies in the U.S., required a five-year follow-up. And the p-Branch pivotal study is involving 82 patients with also a five-year follow-up, with the objectives really to assess the device's
safety and effectiveness and primary endpoints, treatment at one year. Now, the feasibility study enrolled 30 patients at 10 U.S. sites over a two and a half year period, roughly. So here the mean age was 73 years and maximum aneurysm diameter's 65 millimeters
and proximal neck length with the enrolled patients was 21 millimeters. The distribution of A configuration where the two renal pivot fenestration's are at the same level is 57% and the B configuration which is an offset was 43% of the patients.
About 226 mean operative time, slightly more or close to 70 minutes of fluoro time and about one day in the ICU, and three, four days in the hospital. There were two technical problems, the first two patients enrolled at the same site for the trial,
had the p-Branch deployed below the renal arteries due to difficulty with the cannulation and the case done the following day also had a technical failure by not being able to get in a renal. This prompted an update and some physician training and proctoring so that we actually sent proctors to sites,
and the next 28 cases were all successful. Overall, in the feasibility study, 30 day mortality is 0%. Three deaths in the late phase, after 30 days from a cerebral aneurysm. Dissection at slightly less than a year of a proximal
thoracic aneurysm and cardiomyopathy. Freedom from all-cause mortality was 93% in one year, and 89% at 2 years. No ruptures or surgical conversion to date as of last year, when we locked the data. 28 mean follow-up.
Now, if you look at the renal artery patency, which is what all of us are looking at for these types of studies, you see primary patency of stinted renal arteries for this study is on the left. And if you compare that to the initial p-Branch, a single study that was published last year, very similar.
As well as the ZFEN multicenter trial, you see the patencies are quite similar. What about secondary interventions? If you look at this table, we've plotted out secondary interventions at 30 days, and overall, you see the p-Branch feasibility study
slightly higher, but not statistically significant between that and the p-Branch single-center. And the ZFEN is quite low with the 1%. Overall, the secondary interventions were about a third of the patients in most of these studies. Well, what about the pivotal studies?
They said this is an ongoing trial, it's been going on for about three years, we've had about three quarters of the patients enrolled after three years, and we have 28 active sites. We have data on the first 51 patients enrolled, and you see the high enrollers there on the far right.
The mean age is very similar to the feasibility study. 71 years of age, most patients are male, slightly over six centimeters for the diameter, and approximately one millimeter longer at 22 versus 21. The distribution of A and B is also quite similar, as you see here, slightly more A than B,
anywhere from the 55 to 60% range for most all of these studies. Procedures time with the 28 cites now is very similar, 258 minutes, slightly less than the prior study. And you see the fluro time and days in the ICU and discharge very similar.
At 30 days in those 51 patients, no deaths, no renal or bowel ischemia, no neurologic complications or rupture. There had been 3 occlusions of fenestrated vessels, left and renal artery occlusion at day 23, 23, and 30, so these are most likely technical issues
that the stint is crushed. And we've look at that and we'll continue to monitor that. Two patients had re-intervention subsequently, and no patients developed renal insufficiency renal failure at the time of this analysis. So, overall, patient selection, physican technical
abilities, and proper device training will continue to be important for p-Branch implementation and implantation. The feasibility study, early and intermediate results support its safety and feasibility of off-the-shelf device. Follow-up through five years is ongoing. Enrolled is going to continue for the pivotal study
and currently we need less than 20 cases to complete. Thank you.
- So I'm going to be talking about allografts for peripheral graft infections. This is a femoral artery that's been replaced after a closure device infection and complication, and we've bypassed to the SFA and profunda femoris. These are my disclosures. So peripheral arterial infectious processes,
well the etiology either is primary or secondary. Primary can be from bacteremic states and seeding of ulcerated plaque or thrombus. Secondary reasons for infections can be the vast usage of percutaneous closure devices that really have flooded the market these days.
Prosthetic graft infections after either a bypass or patch in the femoral artery. So early onset infections usually are from break in sterility. Secondary infections can be from either wound breakdowns or late seeding of the prosthetic graft.
The presentation for these patients can be relatively minor such as cellulitis or draining sinus, or much more dramatic, such as sepsis or pseudoaneurysm or mycotic aneurysm. On the CT scan we can see infected mycotic aneurysm after infected closure device and bleeding complications.
The treatment is broad in range. Ligation is obviously one option, but it leads to a very high risk of major limb amputation. So ideally some form of reconstruction, either extra-anatomic through clean planes,
antibiotic graft as we heard from the previous speaker, the use of autologous replacement with deep vein, or we become big proponents of the use of cryopreserved arterial allografts for reconstruction. And much of this stems from our work from about 10 years ago, where we looked
at the use of aortic cryopreserved grafts for aortic graft infections. This was published about 10 years ago but we looked at a small series of patients with aortic infections. You can see the CT scan of an infected stent graft
and associated aneurysm. And then the intraoperative photo after we've resected the stent graft and replaced that segment of the aorta with a cryopreserved aortic segment. So using that as a springboard,
we then decided to look at the outcomes using these types of conduits, arterial conduits, for peripheral arterial reconstructions in contaminated or infected surgical fields. So retrospective review at our tertiary care center, we looked at roughly 60 patients over a 15-year period
and excluded any aortic-based reconstructions. So these are all peripheral reconstructions. Mean follow-up was 28 months. As you would expect, the distribution of treatment zones were primarily in the lower extremities, so 51 cases.
As you can see, there's a list of all the different types of cases that we treated. But then there were a few upper extremity visceral and then carotid. I've shown this slide before at this meeting in the past, with a carotid patch infection
that was treated after it had a blow-out, and it's obviously a infected aneurysm, and this was treated with resection and a cryopreserved arterial segment. Looking at our outcomes, the 30-day outcome showed a mortality rate of 9%.
The 30-day conduit-related complication rate was surprisingly low at 14%. We had four patients that had bleeding complications, four patients with recurrent infectious complications. All eight of those patients required a return back to the operating room for correction.
The late conduit-related complication rate was only 16%. As listed here, you can see there's only one case of reinfection, three cases of graft thrombosis, surprisingly only one major limb amputation, two pseudoaneurysms and one late bleeding complication.
And graphically depicted, you can see here, this area here is looking at the less than 30 days, this is primarily when the complications occur. When you get to six months, fewer complications, and then beyond six months, the primary complications that we would see are either thrombosis of the graft
or the development of late pseudoaneurysms, again relatively low. So in summary, I think peripheral arterial infectious complications can be treated with a cryopreserved arterial allografts. The advantage is it's a single stage operation,
maintains in-line flow, there's a low incidence of repeat infection. I think it's also important to mention that the majority of these patients had adjunctive muscle flap coverage to cover the large soft tissue defect
at the time of the operation. So I think that this is a valuable alternative conduit in a setting of peripheral arterial infections. Thank you.
- I will approach the subject slightly differently and leave the EVAR trial alone since it seems to be pretty heavily on trial here today. So a large abdominal aortic aneurism, it's like a time bomb, and the thing you probably want to know first is what is the time left on the clock, meaning what is the rupture risk of the aneurism?
It's been said that unfit patients usually die of other reasons than aneurism rupture, so I want to remind you of our study from Helsinki, on unfit patients from some years ago. We had 154 patients who were declined from elective operative treatment.
They had significant comorbidities, which were also the reasons for exclusion from treatment. As was expected, majority of them died during the little less than two years of a follow up. Looking at the reasons of death, somewhat unexpectedly, aneurism rupture was the leading cause of death
in all three size groups and taking a closer look on the determination of causes of death, indeed, aneurism rupture deaths were confirmed either at autopsy or in the hospital at the time of rupture. Whereas for the other causes, the accuracy was not as solid and this could mean that even some
of the rupture deaths have been missed. The risk for rupture increased with aneurism size and the medium time to rupture was the shorter, the larger the aneurism, and there was not so much difference between the two biggest groups, over 60 and over 70 millimeters.
So therefore, for unfit patients, probably the threshold for treatment should be slightly higher, like 60 millimeters. When further considering treatment, you probably want to know the physical condition and the functions of the vital organs.
Respiratory, cardiac and kidney functions are something to consider, and, of course, the brain. Today, standard EVAR can easily be done under local anesthesia, so for the procedure, these really are not reasons for exclusion. So the thing left to consider is the brain
and the patients mental and overall condition. When assigning and especially when declining treatment, it is required to have a discussion with the patient and possibly their relatives. These unfit patients are often elderly and sort of on their final road trip. The challenge is to weigh the patient's life expectancy
and what is more important, the quality of life. We nowadays know that age is not the issue, but rather the prospects of the future. Is it a clear view with significance and purpose, or a gloomy view that would rather end sooner than later. Of course the decision is not this clear cut.
But, EVAR should definitely be considered for the patients on the sunny road. On the other hand, if by preventing rupture, you're not preserving quality of life, conservative treatment should be chosen. Then also the possibility of rupture
should be considered, for at the time of rupture, the starting point should be to think that is it possible to return to the sunny road? If not, maybe then palliative care is the way to go. If yes, it should be also considered is laparotomy needed and possibly ICU care, because this would mean
that general anesthesia and possibly open abdomen and then it's a whole different procedure than EVAR under local anesthesia. If the answer is yes, this would favor palliative care. If not, if you, for example, have a stable patient with a contained rupture and you can treat him or her
with EVAR under local anesthesia, I'd say, why not? So my conclusions are the decision should always be done individually. But, in general, an unfit patient should undergo EVAR when the aneurism is over 60 millimeters and there is quality of life to preserve,
and at the time of rupture, when recovering to quality life can be considered possible. Thank you.
- [Professor Veith] Laura, Welcome. - Thank you Professor Veith, thank you to everybody and good morning. It's a great pleasure, to have the possibility to present the result of this randomized trial we performed near Rome in Italy.
Risk of CAS-related embolism was maximal during the first phases of the second procedure, the filter positioning predilation and deployment and post dilatation. But it continues over time with nithinol expansion so that we have an interaction between the stent struts
and the plaque that can last up to 28 or 30 days that is the so called plaque healing period. This is why over time different technique and devices have been developed in order to keep to a minimum the rate of perioperative neurological embolization.
This is why we have, nowadays, membrane-covered stent or mesh-covered stent. But a question we have to answer, in our days are, "are mesh covered stents able to capture every kind of embolism?" Even the off-table one.
This is why they have been designed. That is to say the embolism that occurs after the patient has left the operating room. This is why we started this randomized trial with the aim of comparing the rate of off-table subclinical neurological events
in two groups of patients submitted to CAS with CGuard or WALLSTENT and distal embolic protection device in all of them. We enrolled patient affected by asymptomatic carotid stenosis more than 70% and no previous brain ischemic lesion
detected at preoperative DW-MRI. The primary outcome was the rate of perioperative up to 72 hour post peri operatively in neurological ischemic events detected by DW-MRI in the two CAS group. And secondary outcome measure were the rise of (mumbles)
neuro biomarker as one on the better protein in NSE and the variation in post procedural mini mental state examination test in MoCA test score We enrolled 29 patients for each treatment group. The study protocol was composed by a preoperative DW-MRI and neuro psychometrics test assessment
and the assessment of blood levels of this two neuro biomarkers. Then, after the CAS procedure, we performed an immediate postoperative DW-MRI, we collect this sample up to 48 hours post operatively to assess the level of the neuro biomarkers
then assess 72 hour postoperatively we perform a new DW-MRI and a new assessment of neuro psychometric tests. 58 patient were randomized 29 per group. And we found one minor stroke in the CGuard group together with eight clinically silent lesion detected at 72 hours DW-MRI.
Seven patient presented in WALLSTENT group silent 72 DW-MRI lesion were no difference between the two groups but interestingly two patients presented immediately postoperatively DW-MRI lesions. Those lesion were no more detectable at 72 hours
this give doubts to what we are going to see with DW-MRI. When analyzing the side of the lesion, we found four ipsilateral lesion in the CGuard patient and four contra or bilateral lesion in this group while four ipsilateral were encountered in WALLSTENT patient and three contra or bilateral lesion
in the WALLSTENT group were no difference between the two groups. And as for the diameter of the lesion, there were incomparable in the two groups but more than five lesion were found in five CGuard patients, three WALLSTENT patient
with no significant difference within the two groups. A rise doubled of S1 of the better protein was observed at 48 hours in 24 patients, 12 of them presenting new DW-MRI lesions. And this was statistically significant when comparing the 48 level with the bars of one.
When comparing results between the two groups for the tests, we found for pre and post for MMSE and MoCA test no significant difference even if WALLSTENT patients presented better MoCA test post operatively and no significant difference for the postoperative score for both the neuro psychometric test between the two groups.
But when splitting patients not according to the treatment group but according to the presence of more or less than 5 lesion at DW-MRI, we found a significant difference in the postoperative score for both MMSE and MoCA test between both group pf patients.
To conclude, WALLSTENT and CGuard stent showed that not significant differences in micro embolism rate or micro emboli number at 72 postoperative hours DW-MRI, in our experience. 72 hour DW-MMRI lesion were associated to an increase in neuro biomarkers
and more than five lesion were significantly associated to a decrease in neuro psychometric postoperative score in both stent groups. But a not negligible number of bilateral or contralateral lesions were detected in both stent groups This is very important.
This is why, probably, (mumbles) are right when they show us what really happened into the arch when we perform a transfer more CAS and this is why, maybe,
the future can be to completely avoid the arch. I thank you for your attention.
- Thank you very much for inviting me here again and I'll be talking about thermal ablation RCTs. My coauthor, Michel Perrin from Lyon, in France, the gourmet capital in the world has collected RCTs on operative treatment of CVD since 1990. Today he has 186 collected RCTs
of the which 84 involve thermal ablation. You can find all this data for free in Phlebolymphology.org. Do we need further RCTs? Well systematic reviews and meta-analyses increasingly important in evidence-based medicine. And this development is well-described
by Gurevitch in Nature this year and criticized by Ioannidis two years earlier. Common sense is a good principle when you try to understand meta-analyses. Do most studies point in the same direction?
Is the effect significant? Are the patient-related outcome measures relevant and what happens if you exclude one study? Since 2008, 10 years back, these are the available meta-analyses and the last came from Ireland earlier this year.
It was published in the JVS, endovenous and in fact this is in March. And they found nine RCTs comparing conventional surgery and endovenous therapy with five years or more follow-up that were selected. Primary outcome was recurrence rate.
There is some sole recurrence rate was that there is no significant difference in laser versus surgery, same for radioactive frequency versus surgery and radioactive frequency versus laser. They found an inferiority
of ultrasound guided foam sclerotherapy versus laser and surgery. Their conclusions were that the quality of evidence is poor therefore more trials that are well-powered to examine long-term outcomes are warranted. The new kids on the block,
steam, MOCA, and Venaseal, are not included in the meta-analyses due to lack of more than five years follow-up in their paper. Obsolete RCTs. Endovenous laser in the presented long-term RCTs
were performed by 810-980 nanometer wavelength using a bare fiber. There is a paucity of RCTs comparing open surgery with novel endovenous laser and new RF techniques. Recent criticism against endovenous ablation, is the pendulum swinging towards high ligation
and stripping again? Olle Nelzen from Sweden in an editorial in British Journal of Surgery reconsidering the endovenous revolution, wrote that neovascularization is a dominant finding following high ligation and stripping
but proximal venous stumps and incompetent anterior accessory saphenous veins are the main factor after endovenous ablation. So long-term follow-up suggests that the recurrence rate after endovenous ablation seem to increase over time. A substantial number of patients who have undergone
endovenous ablation will eventually develop symptomatic recurrence requiring repeat therapy. And such scenario would change the equation regarding patient benefit and costs making endovenous ablation less competitive and challenging current guidelines.
So summary of needs for further RCTs. Quality of present RCTs poor in several meta-analyses, no thermal endovenous technique is superior to open surgery, RCTs rapidly obsolete due to change in technology, and more trials that are well-powered to examine long-term outcomes are warranted.
So final point, apparently we need more RCTs to satisfy the quality requirements for clinically important systematic reviews and meta-analyses. And what about the clinical guidelines? Thank you very much.
- Good afternoon to everybody, this is my disclosure. Now our center we have some experience on critical hand ischemia in the last 20 years. We have published some papers, but despite the treatment of everyday, of food ischemia including hand ischemia is not so common. We had a maximum of 200 critical ischemic patients
the majority of them were patient with hemodialysis, then other patients with Buerger's, thoracic outlet syndrome, etcetera. And especially on hemodialysis patients, we concentrate on forearms because we have collected 132 critical ischemic hands.
And essentially, we can divide the pathophysiology of this ischemic. Three causes, first is that the big artery disease of the humeral and below the elbow arteries. The second cause is the small artery disease
of the hand and finger artery. And the third cause is the presence of an arterial fistula. But you can see, that in active ipsillateral arteriovenous fistula was present only 42% of these patients. And the vast majority of the patients
who had critical hand ischemia, there were more concomitant causes to obtain critical hand ischemia. What can we do in these types of patients? First, angioplasty. I want to present you this 50 years old male
with diabetes type 1 on hemodialysis, with previous history of two failed arteriovenous fistula for hemodialysis. The first one was in occluded proximal termino-lateral radiocephalic arteriovenous fistula. So, the radial artery is occluded.
The second one was in the distal latero-terminal arteriovenous fistula, still open but not functioning for hemodialysis. Then, we have a cause of critical hand ischemia, which is the occlusion of the ulnar artery. What to do in a patient like this?
First of all, we have treated this long occlusion of the ulnar artery with drug-coated ballooning. The second was treatment of this field, but still open arteriovenous fistula, embolized with coils. And this is the final result,
you can see how blood flow is going in this huge superficial palmar arch with complete resolution of the ischemia. And the patient obviously healed. The second thing we can do, but on very rarely is a bypass. So, this a patient with multiple gangrene amputations.
So, he came to our cath lab with an indication to the amputation of the hand. The radial artery is totally occluded, it's occluded here, the ulnar artery is totally occluded. I tried to open the radial artery, but I understood that in the past someone has done
a termino-terminal radio-cephalic arteriovenous fistula. So after cutting, the two ends of the radial artery was separated. So, we decided to do a bypass, I think that is one of the shortest bypass in the world. Generally, I'm not a vascular surgeon
but generally vascular surgeons fight for the longest bypass and not for the shortest one. I don't know if there is some race somewhere. The patient was obviously able to heal completely. Thoracic sympathectomy. I have not considered this option in the past,
but this was a patient that was very important for me. 47 years old female, multiple myeloma with amyloidosis. Everything was occluded, I was never able to see a vessel in the fingers. The first time I made this angioplasty,
I was very happy because the patient was happy, no more pain. We were able to amputate this finger. Everything was open after three months. But in the subsequent year, the situation was traumatic. Every four or five months,
every artery was totally occluded. So, I repeated a lot of angioplasty, lot of amputations. At the end it was impossible to continue. After four years, I decided to do something, or an amputation at the end. We tried to do endoscopic thoracic sympathectomy.
There is a very few number of this, or little to regard in this type of approach. But infected, no more pain, healing. And after six years, the patient is still completely asymptomatic. Unbelievable.
And finally, the renal transplant. 36 years old female, type one diabetes, hemodialysis. It was in 2009, I was absolutely embarrassed that I tried to do something in the limbs, inferior limbs in the hand.
Everything was calcified. At the end, we continued with fingers amputation, a Chopart amputation on one side and below the knee major amputation. Despite this dramatic clinical stage, she got a double kidney and pancreas transplant on 2010.
And then, she healed completely. Today she is 45 years old, this summer walking in the mountain. She sent to me a message, "the new leg prostheses are formidable". She's driving a car, totally independent,
active life, working. So, the transplant was able to stop this calcification, this small artery disease which was devastating. So, patients with critical high ischemia have different pathophysiology and different underlying diseases.
Don't give up and try to find for everyone the proper solution. Thank you very much for your attention.
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