- [Dr. Vikram Kashyap] Thanks to Dr. Viets for the kind invitiation. Dr. Hotze and Dr. Calgoro, and thank you Dr. Escobar for that great introduction. Obviously, percutaneous mechanical thrombectomy's something that we all use. It hastens treatment, and we use it regularly
for both venous and arterial thrombosis. However, PMT has been linked to cases of reversible post-operative acute kidney injury. It's thought to be due to either the hemolysis and the deposition of red corpuscle elements into the kidney parenchyma, and it may actually also
potentiate contrast-induced nephrotoxicity. Clearly, PMT leads to mechanical breakdown, but the intravascular hemolysis is perhaps the concern. And as Dr. Escobar illuminated, clearly can reduce the time for catheter-directed thrombolysis
or overall thrombectomy, period. Catheter-directed thrombolysis on the other hand, chemical breakdown through, usually, the plasminogen system, with converting to plasma, and then fibrinolysis. But clearly, because of the risk of bleeding, we think about using PMT to decrease the CDT time.
Our hypothesis was that there is an increased incidence of renal dysfunction in patients undergoing PMT for treatment of an acute thrombus, compared to patients undergoing CDT alone. So this is a report- a single-center, retrospective study. 227 patients were reviewed.
145 patients were included into the study analysis. The excluded patients included patients that had acute kidney injury before their intervention, patients that were already end-stage renal patients on dialysis, and patients who that either inadequate or no follow-up data.
So of those 145-odd patients, one-third had arterial thrombosis, two-thirds had venous thrombosis, and as you can see in this pie graph, about half the patients had combination catheter directed thrombolysis
and percutaneous mechanical thrombectomy. 12 percent had CDT alone. 10 percent had PMT alone. And then 29 percent had PMT with pulse spray tPA in a single-setting intervention. We used the RIFLE Criteria to characterize
the severity of renal dysfunction after intervention. And in the RIFLE Criteria, you can see in these rows risk, injury, and failure. There's an increase in creatinine or a decrement in GFR and Loss and ESRD are obviously patients that go on to either temporary or permanent dialysis.
This was the incidence of renal dysfunction in this group. 20 percent in the patients that had PMT alone. With power pulse PMT TPA - 21 percent. With the combination PMT and catheter-directed thrombolysis - 14 percent. And with catheter-directed thrombolysis alone - zero percent
These were highly significantly different between these two groups and the CDT group with values as you can see here on the lower right. If we look at the RIFLE Criteria, none of these patients went on to permanent dialysis. They all had risk, injury, or failure,
which were decrements in GFR, or escalations in creatinine. In fact, all the patients were covered to their baseline renal function, but it took an average of 5.1 days. This lengthened their hospitalization. And all 22 patients that had renal dysfunction
had either PMT alone or PMT combination therapy. If you look at the procedural of variables in this table, you can see that the length of admission's actually fairly similar. Importantly, the total TPA dose was similar, and the total contrast volume
between these two groups was also similar. If you look at other post-procedure outcomes, luckily, none of these patients that had renal dysfunction had long-term harm. There was similar six month mortality, six percent versus five percent.
Other complications were very similar. Limb salvage was 92 and 95 percent and there was no increased readmission rate for DVT or arterial thrombosis. So, ladies and gentlemen, in conclusion, the use of PMT as a treatment for venous
or arterial thrombosis is associated with acute renal dysfunction, but is not associated with adverse six month clinical outcomes. We still use this to hasten thrombolysis time and decrease time in the hospital,
but I think it necessitates that we have post-operative, post-procedure vigilance, and renal protective measures as much as possible to decrease the likelihood of renal dysfunction. Thank you very much.
- Good afternoon to everybody. Thank you very much, Linio and Frank, for the invitation to the great session. First, the main problem is to define who is a no-option CLI patient? So I want to use, this is a young male, with a long history of diabetes, on hemodialysis.
This is the baseline angio. As you can see, the big vessel are absolutely open. We have an open spot of femoral artery, popliteal artery, and then also below the knee vessel are quite open, and we can see that the blood is going very well to the distalis, but in the foot,
we have a disease of all the foot vessel, which is a calcific disease. You can see here, this is the plain x-ray. I think that the plain x-ray of the foot is one of the most important information that we can get on the patients.
For every patient, I want to have this plain x-ray. You can see the medial artery calcification spreading everywhere, dorsalis pedis artery is occluded. We have a small, thin, tortuous, tarsal artery giving some blood to the forefoot. Medial plantar artery is occluded.
The lateral plantar artery is occluded. We have no any clear identification of the metatarsal vessels. This is the forefoot of this patient, and the majority of this patient, with a long history of diabetes and on hemodialysis,
have this medial artery calcification spreading to the tiptoe, and the first toe is totally avascular. This is the reason why this patient developed critical limb ischemia. So who is a no-option CLI patient?
I think that today, a no-option CLI patient is a patient without a target foot vessels. Today, SAD is the most common cause of no-option CLI patient because the SAD is correlated to the age, to diabetes, and end-stage renal disease. We have an epidemic of all of these three vascular factors
in our societies. In the majority of the cases, SAD is actually associated with medial artery calcification, in at least 25% of CLI patients, but today, I think that we are close to 40% present some degree of SAD-MAC.
So in this patient, how to create and master the hybrid foot vein arterialization circuit. This is the patient. My friend, Andrea Casini, vascular surgeon, has done a bypass with the proximal anastomosis of the great saphena vein on the distal P3 segment
of popliteal artery, and here we have this (mumbles) to give him blood to the medial marginal vein. Now, these are very good images, but we must learn how to read these images first. This is an arterialization on the superficial dorsal system of the foot,
so we have an inflow represented from, by the great saphena vein, and an outflow represented fundamentally by the medial marginal vein. We have other collaterals in the superficial system. For example, this is an ancillary superficial vein, and we see a faint shadow of the small saphena vein.
Then we have the deep dorsal system. We have a connection here, a perforant vessel, because it perforates the fascia, and goes from the superficial vein system to the deep dorsalis vein system. Here we have the two anterior tibial veins,
and the dorsalis pedis veins. Then we have the plantar system, the deep plantar system. We have these two plantar veins, the medial plantar vein, these are the two lateral plantar veins, and the deep plantar arch, and the two posterior tibial veins.
Now we have the last system, vein system of the foot represented by the superficial plantar systems, the Lejar's sole, and you can see here, this network, a network without valves, very thin veins, in all of the superficial plantar sole. We have a lot of connection
between these four systems of the foot. This is, for example, the perforator that I have dilated to give blood not only on the superficial dorsal system, but also to the deep dorsal system. We have many collaterals. I have embolized, for example, the anterior,
proximal anterior tibial veins, in order to avoid a precautious still of blood at the ankle level. I have embolized these collaterals that are perforator coming from the superficial dorsal system to the deep plantar system,
and stilling blood precautiously, and here we have the forefoot cross, which is the main cross between the three system, the superficial dorsal, the deep dorsal, and the deep plantar. Now, we can see that the arterialization was able to fill all the forefoot vein system,
and this is very important. When we get the direct blood flow through this collateral to the Lejar's sole, we know that the arterialization can really function. So I asked to my foot surgeon to do a non-geography guided surgery, wait for swelling,
wait for arterialized network expansion, respect the arterialized circuit, respect the forefoot cross, because we think that after foot vein arterialization, the foot is still ischemic, the arterialized circulation has not the same function of the standard circulation.
We must use a tension-free surgery to avoid focal ischemia. This is the tension-free surgery. I know that a transmetatarsal amputation could have been maybe more structurally stable, but I prefer to use this minimal surgery, and the patient has a complete healing
in two months, in two months. Now, the main problem of foot vein arterialization is to understand why this arterialization functions. Now, I propose you two hypotheses. The first is the mechanical hypothesis. Arterial and hydrostatic pressure force vein valves
leading to progressive valve incompetence, distal vein recruitment, and finally, direct issue nutrition by reverse blood flow. In 1906, Alexis Carrel made some experiments on dog, connecting with an anastomosis, the common femoral artery with the common femoral vein,
and he observed that there was the need of three hours at least to force by blood pressure the valves of the vein. Final, he said that practically complete reversal of the circulation is established about three hours after the operation. I want to prepare you this patient.
Observe, this is the acute phase immediately after treatment of foot vein arterialization with some leaking of blood on this vein that I have dilated. Eight days later, three months later, observe this geometry. Are impressive in my opinion.
Can we think that this geometry of vein, pure veins, can feed tissues like a normal standard geometry of artery? When I see these images, I answer, yes, I believe it. I believe it because we know that the venular plexus have a very thin vessel wall like capillaries, so it's a way, when we see these images,
we can really think about a complete reversal blood flow or something that is able to get the tissues and to feed the tissues. The second hypothesis is a biological hypothesis. Vein wall shear stress promotes a global remodeling and/or neoangiogenesis of the vascular system of the foot,
creating a new distribution system, and it was in hypothesis proposed by Languar. This is a LimFlow procedure on a patient like the first one, completely calcified, and this is the evolution, baseline, acute result, 45 days, 90 days after transmetatarsal amputation.
Look at this, 90 days, three months after the LimFlow procedure, the percutaneous deep vein arterialization, and about two months after the transmetatarsal amputation. This is really impressive. Look at these images.
What type of geometry, this one. Look at the baseline angio, and now we have all this vessel connecting with the veins. I am injecting blood contrast dye, so here in the distal stent of the LimFlow procedure, so we have no any blood flow coming
from the previous diseased arteries. This is the patient some months later. This is another patient baseline. An arterialization and after the occlusion of this arterialization, you can see this new neoangiogenesis.
Our results in 36 patients. We're able to get a 69% of limb salvage at 10 months, and I think that in highly selected no-option CLI patient, foot vein arterialization can be the only solution to avoid major amputation. Thank you very much for your attention.
- [Man] Bert, what some magnificent imaging and congratulations. When, just so that I'm clear, I mean, I've done, been lucky enough to have done a couple of LimFlow cases, and we are performing valve, using a valve at the time to perform valvotomies.
Are you suggesting that the pressure alone is enough to do something for the valves of the foot or how extensive do you think valvotomy needs to be in these cases? - [Man] This is our major limit because our limb salvage was correlated to the patency of the bypass,
and our patency was very poor, and it was very poor because we have not the reverse antegrade valvulotome, which is a part of the LimFlow kit. It's not sold alone, so we used some artisanal ways, like high pressure inflation of an oversized balloon. This is very effective but you have a restenosis rate,
very high reocclusion, thrombosis, and every failure, precautious failure of the graft of the bypass was correlated to a major amputation. - [Man] Yeah, okay. Any other questions or comments? - [Man] Is there any difference in your opinion
between a (mumbles) a total percutaneous? - [Man] I think that a total percutaneous procedure is a procedure with a target, which is the posterior system, essentially, because very few cases were done on the anterior system and the anterior deep system, in my opinion, is not a good target for the arterialization
because it is the poorest system, base system of the foot. The hybrid procedure can be done on both, the superficial dorsal system and the deep system. Obviously, you must choose according to the imaging of the baseline imaging or the vein system. Every patient is very different,
so you need to choose the proper target, vein target, into the foot. - [Man] Good. - [Man] Yeah, Roberto, this is very exciting stuff, and Rico and Asher and I tried to do this with primitive valvular destruction back in the 90s.
We had some incredible successes, but we also had some very bad failures. Patients got big, very much edema, one got into heart failure, one actually died, we felt, because of the AV fistula, and so we stopped, but can you talk about the mode of failure.
The successes are brilliant, and I think you definitely have something. We had some good cases but we had, our failures were all with the patent graft, and did you, you said I thought that you only failed when the graft closed.
- [Man] I read all your paper regarding this before starting, so I know that it's not easy. First of all, the key problem either the selection of patient. One of the key factor is heart function. We selected only patient with good heart function,
and second, the procedure is not a single procedure, standalone procedure. We had to follow the patient for months. Healing needs months, maybe repeat intervention, so you need a patient with an acceptable life expectancy and acceptable quality of life expectancy,
and acceptable working capacity, a salvageable foot, so a patient that can really cope with you in this long process of healing. The selection is a key factor. - [Man] Second question, why didn't you use the LimFlow exclusively?
- [Man] Because the LimFlow procedure is very costly, obviously, and in Italy, it is not reimbursed absolutely. This is the main reason.
- [Andrew] It was said that, "There is nothing new under the sun, but there is something old we do not know" and I think we can say this about the use of compliant balloons in aortic intervention. Really, since the early days of EVAR, we've been using compliant balloons to mold endografts and prevent or treat endoleaks.
And more recently, we've been using compliant balloons for hemodynamic control during EVAR for ruptured aneurysms and of course, in the last few years, there's been an explosion of interest in compliant balloons to provide hemostasis and a range of other conditions, the so-called REBOA, resuscitative endovascular balloon
occlusion of the aorta, for a whole lot of indications. What's also happened is that these compliant balloons, that were very bulky devices originally, are now much lower in profile, and because of this we can start to think of using these balloons in other indications. Here's a very interesting paper, and you'll see that
Tilo Kolbel was a co-author here, where there was a secular aneurysm of the posterior arch. Obviously, they had problems delivering a stent graft that tended to go into the aneurysm, so they inflated a compliant balloon to deflect the endograft and then treat the aneurysm.
I want to talk about aortic branch artery entry and the use of compliant balloon assistance. We call that a C-BABE technique. Really, we've often had problems with cannulation of aortic branches. We can often get a wire into these branches,
but often trying to deliver catheters, sheaths and stents, et cetera, are problematic because these tend to prolapse. The key components of this C-BABE technique are these compliant balloons. It's also very important to have a long, supportive sheath immediately below or above the balloon,
to prevent this balloon displacement. We can use this technique with the balloon placed either above or below the branch artery we're going to access, and I'm going to show you examples in both cases. So, let's first of all use the C-BABE technique. We will use the occlusion balloon below the branch
that we want to cannulate. And this really clinically is relevant in chimney EVAR and chimney EVAS procedures. So here, for example, this is a 76-year-old male patient with an aneurysm. The renal arteries are offset,
and the lowermost left renal artery also had a stenosis. We planned to form chimney EVAS with Nellix with a stent in the left renal artery. We couldn't even get a stable catheter position from above in this renal artery, so I ended up going from below, passing a guidewire from below and then I tried to
"buddy" wire a wire from above. And this video just shows you just how unstable this situation. I'm sure all of you who have tried to do these kind of procedures run into this problem where you've got a lot of support, but it tends to do that,
and it repeatedly does that. In the end, I ended up having to stent the renal artery from below, and then I used the C-BABE technique with a compliant balloon that's inflated from below, really so that this catheter could not push down quarterly, and could not prolapse and we could perform the procedure.
One of the key things, therefore, you'll see is that the sheath is just below the balloon to prevent it from being displaced. You've got to actually often pull these balloons up quite a lot higher than you think. And it's a dynamic process that you can do.
You can be inflating the balloon more or less as you need to. And you'll see this balloon inflating and you may need to change this, but essentially, it's providing resistance for the catheter that you saw prolapsed before, but essentially you can see it pushing against the balloon
and there's really only one way for that catheter to go. And you can use that balloon during all the stages of the procedure to deliver the covered stent and various steps to facilitate success in that particular procedure. Here's another example where we've used the balloon below the branch.
This was a patient who developed a late type-one A endoleak after an endograft, and we decided to use Nellix to repair this particular problem. And again, we used this C-BABE technique. Here, you can see we're having difficulty delivering the catheter into the right renal artery.
We're keeping that balloon up, and delivering that catheter out through the catheter past it to the ostium. And you can do that in all the steps. For example, here now we needed to deliver a sheath so that we could deliver a covered stent and really, it kept prolapsing until we used a compliant balloon, which we
delivered through, in this case, a tin French sheath from the left side to deliver that sheath and catheter out into the artery. So, and completed that particular procedure. We found that Nellix is, a very nice indication for Nellix is for repairing these
endoleaks from endografts. See the type 1A or type three and you can see we got a good result. So what about using C-BABE really with the balloon above the branch that you're wanting to access. And really, we've already learned this technique during
fenestrated repairs, where for example we can push a catheter around the constrained top cap of a cook graft. And that really is the same thing. It's providing constraint to allow us to deliver balloons and wires. Here's an example of ours where we had
to really get the wire right around the top of the graft in order to deliver this. We can do exactly the same thing with a compliant balloon. And now, these are very low profile. And I want to show you multiple examples in our clinical practice where we've used this technique over and above
the use of cannulating fenestrations in endografts. One is particular is cannulating the contralateral gate of a standard graft. This case was very difficult because one of the limbs of this gore graft was compressed against the aortic wall and we just couldn't get up from below.
And every time we tried to pass the catheter across the bifurcation, it prolapsed up. The patient had had thoracic surgery which meant that we couldn't use an upper loom approach. But what we could do is have a compliant balloon sitting above the aortic bifurcation of the graft
and then we could deliver a wire. This catheter has nowhere to prolapse. It's very stable and we could deliver a wire and snare it, and provide through and through access that we could complete the procedure. So you can see this compliant balloon, now a very low
profile above the branch we want to cannulate, has enabled us to facilitate this procedure. Here's another example of a patient with an unusual secular aneurysm of a pararenal aorta. The patient was in renal failure so we're able to cover the renal arteries, but they had an ECMA stenosis, so we wanted
to put a parallel graft from below to a so-called "snorkel graft" from below to keep the IMA patent. And actually, cannulating the IMA, the steeper IMA was very difficult. But we can use the C-BABE technique. And here you can see that you do need to be able to inflate,
deflate, and be prepared to move this around. The wire just kept on wanting to prolapse, but until we actually got the balloon into an appropriate position, that really helped us follow. So I think you'll see in this movie that I've deflated the balloon, taken it up a little bit higher so really,
the catheter really does push off the balloon and inflate that. And you can vary the amount that you inflate. And then really, there's only one place then that that catheter could go. It had to go and follow into the inferior mesenteric artery.
And then that allowed us to successfully do a parallel graft and complete the procedure. Finally, here's another example where you keep the balloon above the branch you want to cannulate. Here's a patient with a graft limb that's pulled out and a type 1B endoleak.
We wanted to put a limit stent down and we needed to embolize the hypogastric artery in this patient. Pretty tough to do it across the bifurcation or from above but a relatively simple way to do this is to use the C-BABE technique with a parallel compliant graft and then, you can push off that
and get into an iliac or hypogastric artery. And really, it's a very simple procedure. You can keep that balloon up and down all the time through the various stages to deliver that catheter. You can see that we could only get a wire in there, but really using the C-BABE technique,
we can get a catheter to follow. Then you can exchange for a stiff wire and you can advance there. And really, it can't prolapse because it's got nowhere to prolapse against. And we can complete this procedure using that intermittently
at the various stages that we needed to to plug the hypogastric artery and put a stent graft extension and treat the patient. So the use of a compliant balloon to facilitate arterial branch cannulation, the C-BABE technique, has really been facilitated by the fact that these devices are now
low in profile, and really I think it's a process you need to use dynamically. Be prepared to inflate, deflate, reposition to get the job done. But it has multiple new applications and I encourage you to think about using them.
Thanks very much.
- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company
for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.
The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the
middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,
which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up
in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.
Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,
embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,
we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,
which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.
We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,
excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success
just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and
no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.
We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,
and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.
We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,
post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch
blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it
through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,
we actually have several publications out, demonstrating safety and ethicacy. Thank you.
- Thanks, Stefan and Frank for having me back again this year. These are my disclosures as it pertains to the renal topics here. We all know that renal dysfunction severely impacts survival, whether we're doing open or endovascular aortic repair,
as you see by these publications over the past decade, patients with no dysfunction have a significant advantage in the long term, compared to those patients who suffer acute kidney injury, or go on to be on new hemodialysis. When you look at the literature,
traditionally, through open repair, we see that the post-operative rate of acute kidney injury ranges anywhere from 20 to almost 40 percent, and it doesn't seem to vary whether it's a suprarenal or infrarenal type
of clamp or repair. Chronic renal replacement therapy in this population ranges somewhere between 0 and 3 percent. That really forms a baseline when we want to compare this to the newer techniques such as chimney and fenestrated or branched EVAR.
Now, if you look at the results of the ZFEN versus Zenith AAA trials, and this is published by Gustavo, the acute kidney injury rate is approximately at 25%, acute kidney injury rate being defined as patients, excuse me, greater than 25% change in GFR,
but in one month acute kidney injury rate is 5% for FEVAR and about 9% for EVAR in this study. There's no difference in these rates at two years or five years between the Zenith AAA and the ZFEN devices. What about the progression of patients
with Stage 4 or Stage 5? At two years, it's about the same, 2% versus 3% for EVAR, and at five years, 7 and 8% respectively. Overall, progression to renal failure occurs in about 1.5% of patients in this cohort.
Well, how does that compare to chimney cases, if you look at the Pythagoras and PERICLES studies, there are a limited number of patients, you see in Pythagoras, 128 patients, 92% of them had either one or two chimneys, meaning generally addressing renal arteries in this case,
patency of those grafts was about 96% and there is no real discussion in that manuscript of the degree of acute kidney injury. And in PERICLES registry, however, they report a 17.5% incidence of acute kidney injury post-op,
and a 1.5% incidence of temporary or permanent dialysis. What about if you compare them? This is a publication in 2017, if you look at both of these studies, very similar, 17.8% for acute kidney injury in FEVAR, and about 19% for a chimney.
You have to realize, though, there are more complete repairs in the FEVAR group, and there are more symptomatic patients in the ChEVAR group, so these aren't completely comparable, but you get some idea that they're probably in the general range of one another.
So the real questions, I think, that come up, is, which arteries can you sacrifice? Are renal embolizations impacting patients' overall function? And what is the mid-term impact of branch and fenestrate on volume of your kidneys
and patients' eGFR. We've studie we looked at the incidence and clinical significance of renal infarcts, whether we actually embolized these pre-procedure,
or whether we accidentally covered or intentionally covered an accessory renal artery, what was the outcome of those patients? We see over time, the average renal volume loss, calculated by a CT scan and VAT volume, is about 2.5% if you embolize it
and if you just cover an accessory renal, about 6.4%. But overall, about 4%, didn't change significantly, overall the GFR changed over the lifespan of the first two years of the patient of 0.1, so it wasn't a significant clinical impact on the patient's overall renal function.
Now what about looking at it specifically of what happens when you do branch and fenestrate cases with respect to eGFR and volume of those? We presented this at this past year's SABS, and it is in submission. If you look at the changes of eGFR,
you notice that in the first six months, the patient declines, but not significantly, and then you see in the graph there, it tends to come back up by a year, year and a half. Very similar to what Roy Greenberg published in his initial studies,
but what we did in this study was actually compare it to the age match publications, and you see that eGFR over time was similar to what happens in age-related changes, but we also noticed that 16% of the patients, 9 of 56, had improvement of their eGFR
to greater than 60. Now whether this is just related to the inaccuracy of the eGFR and its variance, or whether we actually improved some renal stenosis, is difficult to tell in this small study. In conclusion, open, fenestrated,
and chimney EVAR procedures are associated with acute kidney injury in approximately 20% of patients. Causes of deterioration are likely multifactorial and may be different for each technique used. Renal infarcts from covering accessory renal arteries
and embolization occur in about a quarter of the patients, and is a small contributor to renal decline over time. Renal decline made after FEVAR is similar to associated with age. Thank you.
- Speaking about F/EVAR and Ch/EVAR, and try to prove that the evidence of Ch/EVAR is solid, especially in some circumstances also better than the evidence about F/EVAR. Well, let's try to define this title. Durability of Ch/EVAR is solid if the procedure is done right.
And I think this is very, very crucial. We heard and we know the PERICLES Registry tried to evaluate this technique, collecting the worldwide experience from 13 US and European university centers, and published in annals of surgery.
And also, the PROTAGORAS study focused exactly on the performance of the Endurant device in order to avoid this heterogeneity which we had in the study (mumbling) published literature up to now. Focusing exactly on the Endurant device
in combination with balloon expandable covered stent. And based on these two registries and studies, we identified four key points, four key factors, which we'd like to give you as take home message in context to have the Ch/EVAR technique as solid procedure. So, we learned that the technique performs very well
if we use the technique for single or maximum double chimney grafts. We highlighted how important it is for this technique to use suitable combinations between aortic stent-graft and chimney devices. And we learned also, how important is the oversizing.
We have to have enough fabric material to wrap up the chimney grafts of 30% of the aortic stent-grafts. And in this context, we highlighted also the importance of creating a new sealing zone of 20 millimeter in order to have durable results.
Which is also very important is to know when we should probably avoid to perform the technique, and I would like also to highlight these points. So, we learned in case of excessive thrombus formation in the thoracic, especially also LSA, we have to be very, very careful with this technique,
because of course, we have the risk of cerebral vascular events. We learned also that performance of this technique in a neck diameter of more than 30 millimeter is associated with high risk of Type 1A endoleaks, which will be persistent, and which probably
lead to failure of the treatment. Which also learned is to evaluate very carefully the morphology of the renal arteries, especially focus of the calcification of the stenosis, and also of the diameter. And last but not least, it's very important to
have access to the suitable materials for renal cannulations, and also experience. So, if we consider these key points of doing and not doing chimneys, I think we have a very good base to have durable and good results over the time. And we have seen that.
You saw it very nicely (mumbling) the changes of the diameter pre and postoperative, but you forgotten to highlight that there was highly significant in the PERICLES and in the PROTAGORAS Registry. Also, what we have seen is that
more than 90% of the patients had stable or shrinkage of the sac after a CT follow up of two years. And here's a very nice overview of the Kaplan-Meier curves, highlighting that the technique performs very well in this specific combination of the Endurant devices,
abdominal device, and abdominal chimney grafts like the Advanta. Having a very nice chimney graft patency of almost 96%, and a freedom from chimney graft later interventions of 93%. Very important is also if we create these very good sealing zone of two centimeters.
We have a very, very low incidence of new Type 1A endoleaks needed reintervention. And here is an example of a case which had a very short sealing after the previous treatment with chimney for the left renal artery, and over the time was necessary to extend the sealing zone,
creating these durable solution and transformating from single to triple chimney, as we can see here. So, this is very important to know and to highlight. In context of the better or not better for F/EVAR, we can see now the results, and we've compared with meta analysis of F/EVAR.
We see that the results are similar. Keeping in mind also that in F/EVAR, we involve the SMA either as scallop or as bridging device, and we don't have evidence about the SMA outcomes and the SMA patency because most of the patient probably who will die, and will not perform autopsy
for each patient if it has an SMA occlusion or not, so I believe it is underestimated the really incidence of survival after F/EVAR. And also, regarding the patency, we have also in this context, similar results after chimney compared to the patency of the bridging device after F/EVAR.
So, ladies and gentlemen, I believe we've considered these key points. We can achieve very good results performing Ch/EVAR, having as a solid and valuable procedure for our patients. Thank you very much.
- [Boonprasit] I'd like to thank Dr. Veith for the preface to be here. It's my disclosure. One of the most challenging issues for AAA patients is severely angled neck, particularly those who are not candidates for open surgery. Let me start with these two cases.
This 71-year-old gentlemen presented with a tenderness on his right side of his aneurysm with this kind of the neck. This 77-year-old gentlemen had a rapidly enlarged, over nine centimeters, AAA with also this kind of the neck. Open surgery should be the first choice
to treat these patients. However, it's not an option because of the significant comorbidities. So what's next? We wait until it's ruptured before do anything, or can endovascular repair
is a safe and effective option for us? There are three questions to answer. Can we successfully deploy the device? Will we provide a good long-term results? What are the limits? Angled neck.
I will come back to answer these three questions later on. We reviewed our experience of treating AAA patients with neck over 60 degrees in these 8 1/2 years period with Endurant stent graft. And there were 154 patients we treated with neck over 60 degrees, with the average neck length
of almost three centimeters. We categorized these patient into five groups according to their neck angle, started from over 60 all the way up to over 120 degrees. You can see here, 3/4 of the patient had neck over 75 degrees.
That's outside of the IFU. But these are all high-risk patient for open surgery. This is the longest follow-up case that we have, up to eight years. You can see, we started with quite a long neck, in this case, four centimeters neck.
And you can see that up to eight years aneurysm, kind of stable, a little bit slightly decreased in size, but not significant. This lady had up to five years good results aneurysm shrunk, no migration, no endoleak. This twisted neck with empty aneurysm, also good results,
no migration, aneurysm shrunk, no endoleak. Altogether, we've got, of these 154 patients, they get 95% technical success. We got eight proximal endoleak. 30-day mortality was 2.6%. Two died from MIs.
One died from stroke, and one from ruptured aneurysm because of this proximal endoleak. Of these eight proximal endoleaks, four sealed, one spontaneously, three with some adjunct procedures, proximal extension cuff, EndoAnchor, or chimney. Three ruptured, though, and one patient
still doesn't want to have any second procedure done. We follow him very closely. When you put these unwanted complications in the chart together with those complications that we were able to fix there. This patient, we see in this proximal endoleak
at one-year followup, actually, we missed that small endoleak here at one month. We treat this patient with EndoAnchor to quite a good success. Our followup average of around two years, surprisingly, we've got only two late proximal endoleaks.
And most of these patients are from neck dilatation, and both had persistent type II endoleak. Only once did migration of seven millimeter occur in this hostile group. And you can see, this device migration case, and even though seven millimeters migrated at three years,
aneurysm shrunk anyhow. This patient had a neck dilatation at five years, causing proximal endoleak. We fixed it with a proximal extension with a chimney up through the right renal artery. Up to eight years now, the patient is doing well.
So we put these two delayed endoleak into the chart. You can see which group we have the problem. So there are some technical difficulties with a tortuous angled anatomy when we put a stent wire. The anatomy will be shortened. Can be a problem.
And we have to make sure that our stent won't occlude the renal arteries. And belly pushing seems to be quite a helpful maneuver to help to remove this delivery system in some cases. Chimney procedure is needed in 6% of the cases. Aortic cuff is needed in 25% of the cases.
So we put together all these adjust procedures needed in the chart. We're a little bit too busy. Let's put it this way. The red bars are unwanted complication, mortality. The yellow bars are the problems that we can fix.
And the blue line is those adjunct procedure, either cuff or chimney. So where is the limit, 75, 90s, 100? So I'm sure that you know that the answer for these three questions would be yes. So back to, finally, back to our case.
The first case, we did a sandwich to the left renal artery for the patient. After four years, aneurysm shrunk, no migration, no endoleak. The second case, only EVAR, no adjunct procedure needed. At one year, aneurysm shrunk, no migration, no endoleak.
So Mr. Chairman, ladies and gentlemen, we believe that endovascular repair can be offered safely for AAA patients with severely angled neck who are not candidates for open repair. We may need longer neck lengths. The procedure can be difficult.
And adjunct procedures may be needed. What is the limit? Well, this is quite a bold statement. We believe that we may be able to push the boundaries a little bit. Thank you very much for your attention.
- [Dr. de Vries] Thank you for the kind introduction. These are my disclosures. It's why do endografts sometimes need additional fixation with EndoAnchors? Well first, patients with multiple hostile neck parameters still suffer a substantial risk for type I endoleak and endoleak related mortality.
The second reason is that our deployment accuracy of the endograft is not as good as we think. We reviewed 85 consecutive cases in our own hospital and we saw that mainly do the slope of the endograft in the aortic neck, we lose some important apposition,
especially in the outer curve. So the preoperative neck length is not the same as our post-EVAR seal. And the third reason is that some other techniques, like FEVAR do have their limitations and some people are declined because of the branch arteries.
There are also some physiological conditions which is are not good enough for FEVAR. And of course open surgery, well per definition is more invasive and also patients will sometimes have their aneurysm repaired by endovascular means. So EndoAnchors really creates the stability
of a surgical anastomosin shown by David Dietz, and it really rivals the migration resistant of a hand sewn anastomosis. Of the global Anchor registry is captured real-world usage of the EndoAnchors and nowadays 770 patients have been enrolled worldwide.
The Primary Arm represents the majority of the patients in the Anchor Registry, 437 patients in the patients in the Primary Arm. It's not exclusive the Anchor Registry for the Medtronic devices, but also the workhorses like Gore and the Zenith endograft.
Of the prophylactic arm, the patients treated without any endoleak it carries 314 patients in this data slide. And you can see that the majority of those patients will hostile neck parameters. It's true in 91 percentage of the patient cohort.
The median neck length is 11 plus millimeters and also conicity substantial in more than 40% of the cases. What about procedural success? It's high, it's almost 95%. You need an average of around 5.5 EndoAnchors and the time to implant those EndoAnchors is 15 minutes,
and of course there is a learning curve. Core Lab adjudicated outcome, the two years outcomes, there is no new type Ia endoleak in this cohort and no endograft migration. In the Kaplan-Meier Estimates, especially the freedom from
aneurysm related mortality is 98.4% and freedom from secondary procedures at two years timeframe is 92%. There are no serious adverse events related to the implantation of the EndoAnchors itself. No aneurysm rupture and the aneurysm-related mortality
is due to cardiopulmonary comorbidity and not due to aneurysm rupture itself. There's one patient with a surgical conversion in this cohort. And the short neck indication that are patients in the Primary, 70 patients,
only placed with an Endurant in combination with the EndoAnchors and in a prophylactic setting or a patients with a type Ia endoleak. But the median neck length is now less than seven millimeters, so really challenging necks
and also conicity is substantial. It's also a clinical challenging patients cohort. A lot of patients with notable comorbidities and what is important to mention, 17% are patients with symptomatic aneurysm and also one patient with a ruptured aneurysm.
And the well the main treatment is then for prophylactic use but also 21% of the patient do have type Ia endoleak. Procedural results are 31 minutes fluoro time, but only 17 minutes to implant the EndoAnchors. This is the one year outcome. I think it's excellent.
Only one patient with a type I endoleak and he needed a secondary intervention. We had two other patients with a secondary intervention but it was due to a false aneurysm in the groin and a distal extension. No conversion to open surgery and no ruptures.
What about the cost effectiveness? Well you have to consider, it's not only the device cost, but also the level of resource utilization, and also clinical outcomes. And when you compare the short neck cohort, here the 70 patients to the fenestrated IDE study,
there's a cost differential of more than 5,000 U.S. dollars in benefits of the use of the EndoAnchors in those short and hostiles necks. So we can conclude that the Endurant stent graft in combination with the EndoAnchors for short neck indication is easy to use.
It's an off the shelf solution. It gives greater flexibility versus the alternatives. There is no need for renal arterial catheterization and it's really efficient. Thank you very much.
- [Narrator] Thank you, thank you Dr. Veith and the committee for the kind invitation. No related disclosures. Carotid webs are rare, noninflammatory arteriopathy that are also known as pseudovalvular folds, as well as other pseudonyms for this. They are small, shelf-like linear filling defects,
arising posteriorly from the posterior proximal-most ICA and project superiorly into the lumen. They're generally regarded as a developmental anomaly of the brachiocephalic system, and histopathology lacks atheromatous changes and inflammation of the tunica intima.
They may be associated with FMD, or be considered an atypical form of intimal fibroplasia, and generally arise from dysplasia within the media. They will as we will see, carry a considerable stroke risk based on laminar flow disruption and irregular shear profile.
This is the mechanism by which they produce strokes, seen clockwise from the top upper-left. There are areas of stasis in which thrombus can develop behind the web. The thrombus can enlarge and eventually embolize. Operative findings and pathologic findings include
these webs seen here behind this nerve hook, and generally smooth muscle with extensive myxoid degenerative changes. Over the last several years we have treated 10 patients with carotid endarterectomy for symptomatic webs. The mean age of these patients
is generally quite young, in the 40s. The majority are female, one patient had a bilateral web and 70% of these patients had no atherosclerotic risk factors whatsoever. The mean maximum peak systolic velocity on duplex was 77 centimeters,
and five of the cases were closed primarily without a patch. There were no strokes perioperatively in this group, no mortalities, and there have been no new neurological events nor restenosis. Several other groups have looked at this phenomenon as well,
this is a case series of which 7 patients were identified prospectively having had an ischemic stroke. Again, the mean age was young. Of note, five of these patients had a recurrent ipsilateral stroke to the web. No FMD was seen throughout the other vascular beds
and four out of five of these patients, the recurrent patients had CEAs with no recurrence at approximately a year. Another review identified 33 patients who had excellent CAT scan imaging. These were younger patients over a six year period,
with cryptogenic stroke. The prevalence of webs within that group was 21%. Symptomatic patients within that group with webs were 7 patients out of 33 and again you see a young age, predominance of women,
in this study of predominance of African American patients 3 bilateral webs, all patients had MCA infarcts. And oh, 1.6% of the webs in the control group were without a stroke. Another case-control study looked at 62 cases over four years.
They were able to match 53 of these patients with other cerebrovascular pathology, webs were found in 9% of the cases, but only 1% of the controls. And again of the webs, predominance of young patients
and women with two bilateral strokes. So what about diagnosis? Even large webs generally do not meet the velocity criteria for significant stenosis, and while you may see a filling defect, you're generally dependent on B mode imaging,
and having a high level of suspicion, for identifying this process. CTA is the gold standard, it's got rapid, high-resolution imaging, reformatting across planes, makes this an excellent modality
in associated findings of thrombus, and atherosclerosis can also be detected. Angiogram again, as always, gives you a good view of flow dynamics, intra and extra cranial pathology, and in general the finding is of contrast pooling,
which you have to look for behind the web. MRA is one method that's been used to characterize this, in this modality you can see slowed blood flow distal to the web, blood pooling distal to the web, and generally this all leads to an atypical pulsatility, of the carotid wall near the area of the web,
suggesting impaired hemodynamics in this condition. Management is with a carotid endarderectomy which has been the preferred treatment, although some have advocated medical management with formal anticoagulation, patients have had strokes
while on anti platelet therapy, and there are several case series now appearing of acute stroke treated with stents, these are generally delayed following thrombectomy. There's one latrogenic dissection in these groups. These patients have few atherosclerotic risk factors,
in the same demographics as noted above. So in conclusion, these are associated with FMD and intimal fibroplasia. The prevalence is low. The prevalence may be increasing but it's not clear whether this is a true prevalence increase,
or simply increased detection. They're associated with recurrent symptoms even in the setting of adequate medical therapy and is an underappreciated cause of stroke, and are now becoming a recognized, and rather than a cryptogenic cause of stroke.
They are generally not identified by current duplex criteria in asymptomatic patients, and duplex may miss them entirely. Axial imaging is essential and currently we don't stratify these based on either legion characteristics or demographics.
So while the optimal management is not completely defined given the recurrent stroke risk CEA seems prudent especially in young, medically fit patients with or without patch angioplasty, which may have some impact on quality metrics
at least in the United States. We've treated patients with three months of antiplatelet therapy, aspirin indefinitely. Right now the role of statins is undefined, and the durability and role for endovascular approaches remains also undefined.
- [Presenter] Thank you very much. This is Jordan. It's my pleasure to share this panel with endoanchors believers, I'm one of them. So, there's my disclosures. The scope of the problem about the proximal migration starts
in order to think about the durability of thoracic endografting, because it still is a concern. The cranial migration from the distal attachment is part of this particular concern, especially when the distal neck length is less than three centimeter.
I think this is a under-reported complication in these areas. That is, what has happened, after some kind of follow-up, after four years follow-up, the distal part of the aorta, or the distal part of the endograft is dis-attached from the primary landing zone.
Because all the forces in the ascending thoracic aorta acting in the up cranial fashion. So when you are virtually sure there some kind of migration rate of two years but also have some kind of cranial migration from the distal part of the aorta at the one year is 1.2%
for the VALOR trial and 1% in one year also for the TX2 trial. In our experience, before 2006, for distal neck length, between 1.5 to 3 centimeter in length, 60% of cranial migration rate was registered at five years follow-up. So what's a lot of percent about that we try to perform
a different kind of approach for those particular short or no short, nice distal neck of thoracic aorta. So cranial migration as previously mentioned is under-reported. The upside for the abdominal aorta with the forces acting in the downstream anteriorly in the thoracic one is
posteriorly a cranial and also a cranial migration course. And this kind of phenomenon kind of course in the long run follow-up. These connections and also cranial migration. About the preventative actions there are different kind of creative alternative in order to prevent that,
but let me to focalize my attention and your attention to endoanchors philosophy that is part of our current approach. For a regular neck of more than three centimeters we can use regular endograft but sometimes when it's not so regular it's not so straight, we prefer to use in combination
with endoanchors. When you have a regular straight but between 1.5 and 3 centimeter we prefer to use distal scalloped endograft plus endoanchors as you cam see here. That is what the speakers talk about very extensively but this is just a case in order to see
what happened after two years follow-up in this lady when it has this distal type one endolink we apply the endoanchors and after three years the endoanchors remain in the same position, as you can see here, without any kind of further complications.
So another example, in combination with scalloped devices, scalloped thoracic endograft, just in order to be sure, that the movement in the distal part doesn't occur or even weaken over time. For sure, when you have very short neck length,
that means less than 1.5 centimeter, then we need to switch to another kind of solution like this fenestrated or branched endograft, like you can see here in this example. So in summary, the durability of thoracic endografting remains a concern when cranial migration is a consequence
of biomechanical forces of the thoracic aorta and it is under-reported. The proximal and distal necks deserve equal attention. And many different approaches have been suggested to avoid cranial migration. And endoanchors in combination with the scalloped,
fenestrations and branched endografts should be applied more often. Thank you very much.
- Well, thank you Dr. Veith, and thank you very much for allowing me to speak on the topic. I have no disclosures. This is a nice summary that Dr. Veith is actually second author, that summarize what we know about predicting who will benefit from intervention among the patients with asymptomatic aortic disease.
You look at this eight means that we have, you realize that only one of those related to the fluid deprivation. The rest of them are related to embolic events. And that's very interesting because we know that antiplatelets have very little effect
on prevention of this. That's summarizing that review. Partially because what we focused on is that mechanism of thrombosis which requires platelet activation and attachment to the wall.
And that's where those antiplatelets that we use, act upon. However, you realize if you just look at the any ultrasound, that because of the velocities that we have and the lengths of the stenosis in carotid disease there is no way how the platelets can be attached to that
due to that mechanism. They just fly away too fast and don't have any time to do this. And it's even more because all the studies, basic science, show that at those shear rates that we have in carotid disease
that is more that 70%. There is very little probability of either platelet attachment or Von Willebrand factor attachment, or as a matter of fact even fibrinogen attachment in that particular area. So on the other hand we also know
that at those shear rates that we have, the Von Willebrand factor molecules unfold revealing tens of thousands more adhesive sites that allow them, not only to the platelets but also to the wall at that particular spot. And then the most likely mechanism
of what we dealing with in the carotid disease is this that the Von Willebrand factor attach and this unactivated platelets form conglomerates which can easily, because they don't attach to each other, easily fly. And that is probably one of
the most likely causes of the TIA. So if you look at the antiplatelet that we use on this particular mechanism, is right here. And those aspirin and clopidogrel, and combination of those we usually use, have very little, if any, effect on this particular mechanism.
So if, on the other hand, you can see that, if you specifically address that particular site you may have a much substantial effect. Now, how can we identify it? Well actually, the calculation of near-wall shear rate is quite simple.
All you need is just highest velocity and smallest diameter of the vessel. Of course, it is an estimate and actual shear rate is much higher but that's even more, because you, better than you prevent, more higher rate. Just to demonstrate, you can have the same velocity,
similar velocity, but different diameters. This stenosis technique will give different shear rate, and vice versa. So it's not really duplicating neither one of them. So we decided to look at this. We did a case control study that was published,
still online in the Journal of Vascular Surgery. And what you can see on the ROC curve, that in fact shear rate predicts symptomatic events much better than either velocity or the degree of the stenosis. And we look specifically at this group
with this thresh point of 8,000 per second and you can see that those patients who have those shear rates and the stenosis are 12 times more likely to have ischemic events. We look at the other means like microembolism. It's ongoing study, it's unpublished data that I show you.
And it's a very, very small sample but so far we have the impression that those microemboli that we can decide for, make a decision for intervention, actually happen only in this category of patient that have high shear rate. Based on this, this is our proposed algorithm,
how we deal with this. If you have asymptomatic patients with more than 70% degree of their stenosis and shear rate that exceeds certain level, we think it's about 8,000 per second, that may be an indication for intervention.
On the other hand if you a have lower shear rate then you can use other means. And what we use is microembolis per hour. Then you can duplicate their areas. If TCD on the other hand is normal you can continue best medical therapy and repeat the ultrasound in a year.
It's arbitrary. This is proposal agreed and based on our studies and that's, I'm thankful for the opportunity to share it with you. Thank you very much.
- Thank you friends who have invited me again. I have nothing to disclose. And we already have published that as far as the MFM could be assumed safe and effective for thoracoabdominal aneurysm when used according to the instruction for use at one, three, and four years. Now, the question I'm going to treat now,
is there a place for the MFM? Since 2008, there were more than 110 paper published and more than 3500 patient treated. 9 percent of which amongst the total of published papers relating the use of the MFM for aortic dissections. So, we went back to our first patients.
It was a 40 year old male Jehovah Witness that I operated in 2003 of Type A dissection and repair with the MFM in 2010 because he had 11 centimeter false aneurysm. Due to his dissection, this patient was last to follow up because he was taking care full time off of
his severe debilitated son. When we checked him, the aneurysm seven years later shrunk from 11 to 4 centimeters wide. And he's doing perfectly well. Then the first patient we treated seven years ago, same patient with Professor Chocron
Type A dissection dissection repair in 2006. Type B treated with MFM in 2010. We already published that at one year that the patient was doing fine. But now, at three and seven years, the patient was totally cured.
The left renal artery was perfused retrogradely by aspiration. That's a principle that has been described through the left iliac artery. So what's next? Next there was this registry
that has been published and out of 38 patients 12 months follow up, there were no paraplegia, no stroke, no renal impairment, and no visceral insult. And at 12 month the results looked superior
to INSTEAD, IRAD and ABSORB studies. This is the most important slide to us because when you look at the results of this registry, we had 2.6 percent mortality at 30 days versus 11 30 and 30.7 no paraplegia, no renal failure, and no stroke vessel
13 to 12.5. 33 and 34 and 13 and 11.8 percent. With a positive aortic remodeling occurring over time with diminishing the true lumen increasing the true lumen and increasing the false lumen.
And so the next time, the next step, was to design an international, multicenter, prospective, non-randomized study. To treat, to use the MFM, to treat the chronic type B aortic dissection. So out of 22 patients to date,
we had mainly type B and one type A with no dissection, no paraplegia, no stroke, no renal impairment, no loss of branch patency, no rupture, no device failure, with an increase in true lumen and decrease in false lumen that was true at discharge.
That was true at one, three, and six and 12 month. And in regards with the branch occluded from the parts or the branches were maintained patent at 12 and all along those studies. So, of course these results need to be confirmed in a larger series and at longer follow up,
yet the MFM seems to induce positive aortic remodeling, is able to keep all branches patent during follow-up, has been used safely in chronic, acute, and subacute type B and one type A dissection as well. When we think about type B dissection, it is not a benign disease.
It carries at 20 percent when it's complicated mortality by day 2 and 25 percent by day 30. 30 percent of aortic dissection are complicated, with only 50 percent survival in hospital. So, TEVAR induces positive aortic remodeling, but still causes a significant 30 day mortality,
paraplegia event, and renal failure and stroke. And the MFM has stabilized decreased the false lumen and increase the true lumen. Keeps all the branch patent, favorize positive aortic remodeling. So based on these data, ladies and gentleman,
we suggest that the MFM repair should be considered for patients with aortic dissection. Thank you very much.
- So regarding fenestrated limbs, these are my disclosures. Typical scenario where you have a rather unwelcoming iliac, common iliac artery, you need around 16 millimeters at least to accommodate a branched graft in the iliac artery. You want to preserve the hypogastric flow.
In this case you also see a stenosis, so you need two things, ideally, to accommodate a branched device, which would be the diameter of 16 millimeters and also the angle of the artery. This is very pleasant to put in a branched device.
However, there are patients where you want to preserve the hypogastric blood flow, and in these cases, above the origin of the hypogastric artery, there is not enough room to open up a branched device, or the angle is very unfavorable
to put in a branched device. And here fenestrated iliac limbs come into play. These are usually made to measure, different lengths, different proximal and distal diameters and also you can place the single fenestration where it obviously is positioned best.
There are basically two, I think very useful indications. Here we can see a type 1B endoleak in a 13 millimeter limb. The distance to the hypogastric artery was not enough to have a full expansion
of the iliac limb, and therefore in this case if you want to preserve the hypogastric artery, which I would really strongly always recommend if possible, is to put in a fenestrated limb. But it's also really very helpful in these cases
is that you don't have to come from above, you can come from below and finish the whole procedure from below. So you have a full deployment of the endograft and then you'll put in a connecting stent graft
with obviously a very good seal and result. Most importantly, for complex cases as in this, for instance, patient who's had an open procedure 10 years previously and had further interventions with an over-stenting of the hypogastric on the right side and large thoracoabdominal aortic aneurysm
as well as an anastomotic aneurysm on the left side, you really want to preserve the hypogastric artery. And you can also that actually it's an anastomotic aneurysm at the left side, so here a branched device certainly doesn't work. First, because it doesn't open up,
and second, the angle of the hypogastric is really very unfavorable. So again, you just put in your fenestrated device and then connect it from below with the stent graft in order to preserve the hypogastric blood flow of the last remaining hypogastric artery.
And also, obviously do something else to the rest of the patient, so this was a five branched endograft in a patient with two left kidneys. And also another case, you see actually on the angiography already the shaggy aorta,
so occlusion or seal at the distal origin of the common iliac just above the hypogastric is not really a good option, so we've re-over stented, or you do something about it. Now this is the case with a thoracic endograft
and a full-fen extension. So again, we really opt to preserve these hypogastrics as much as possible. So in conclusion, Mr. Chairman, (coughs) sorry ladies and gentlemen, fenestrated limbs are a good tool to preserve
hypogastric arteries. Now just to put it into perspective, is it common? No, we have around 30 branched iliac devices a year we implant, and we had all in all five fenestrated during the last two years.
So this is really a rare anatomical solution, but I believe it really is helpful. It's not an off-the-shelf device, so it takes around four weeks to produce, and the company's still not really decided how to price it, so we really can nicely negotiate it.
Thank you very much.
- I wanted to discuss this topic because some of us are more sensitive to DNA damage than others. And it's a complicated ethical issue. I have a disclosure in that I developed a formulation to premedicate patients prior to CT and x-ray. We all know that we stand in fields of radiation for most of our careers,
and we also know that many of us have no hair for example on the outside of our left leg. This is a picture that a bunch of us took for fun demonstrating this. But this is in fact radiation dermatitis. We know that the founders of our field
suffered consequences from the chronic high doses that they received in the 1920's. And they lost digits, they lost ears, they lost noses any many of them died of cancers or cardiovascular disease. The mechanism of injury is the x-rays
impinge upon water molecules in our cells. They create free radicals. These free radicals bind with our DNA and then Oxygen binds with that site resulting in an oxidative injury which can be reduced by the use of anti-oxidants.
I studied this over the last eight or nine years and I looked at the issue of chronic low dose radiation. Now this is different from the data that we collect from Nagasaki and Hiroshima and from Chernobyl and elsewhere. There are cancer risks but there
are also cardiovascular risks. And there are risks from chronic inflammation from increased reactive Oxygen species circulating with our system. I've been in touch with the IAEA recently about this and they didn't actually
realize that we don't wear our badges. So they thought the data they were getting on the doses that we were receiving were accurate. So that was a very interesting conversation with them. So cardiologists have been known
to get lifetime doses of of over one Gray. There's a lot of literature on this in public health literature. For example for every 10 milliSieverts of low dose ionizing radiation and received by patients with acute MI's,
there's a 3% increase in age and sex adjusted cancer risk in the follow-up five years. There's an excellent paper from Kings College London demonstrating that when endovascular surgeons were studied with two specific immunofluorescence tests, P53 and H2 alpha,
they were able to demonstrate that some endovascular surgeons are more sensitive to radiation dose than others. So why would that be? Well it's interesting if you look at this genetically and you look at the repair mechanisms
and in this whole thing I think in fact the lens is kind of the canary in the coal mine. When you get radiation induced cataracts, it's in the posterior chamber of the lens not the middle or anterior, which is where age-related injury occurs.
And this is the germinal layer or reproductive layer. The growth layer in the lens itself. And this is where cataracts develop. And this is really kind of a harbinger I think of injury that occurs elsewhere in our system. We know that when we wear DLDs on our chest,
on our bodies, on our arms, that the dose to the left side of our head is six times higher than to the right. In fact they dosed the left lens as higher than the right. And most of us who have lens replacements have it of the left eye.
This literature from adjacent fields that we may no be aware of. In the flight safety literature for pilots and stewardesses. There's extensive literature on cosmic radiation to flight crews who's doses annually are in the same range as ours.
So when you look at medical staff, you have to look at the overall context of the human in the Angio suite. Many of our medical staff will not be well. They may have chronic cardiac disease. They may be on say drugs for auto
immune disease or Methotrexate. They may have other illnesses such as Multiple Myeloma. They may have antibiotics on board that alter the DNA repair ability like Tetracycline. And they have chronic stress and sleep dysfunction. Cigarettes and alcohol use.
All of these things decrease their ability to repair DNA damage. If you look at DNA repair mechanisms, there are constantly the terms BRCA1 and two, PARP, P53, and ATM that show up. And deficiencies in these,
I'm going to skip all this to show you, can result in increased injury from a same dose being received by two different individuals. Now who is at risk from this is well understood in adjacent fields.
Here are 37 references from the public health literature related to mutations and SNPs or polymorphisms in DNA structure known to cause increased sensitivity to radiation. So I would propose that in, and here are papers on that topic
in adjacent fields that we don't read. So when we talk about personalized medicine for our patients, we need to also think about personalized career choices based on our DNA repair ability when we decide what we do. This has to be done in the context
of empathetic compassionate approach. It may begin with screening based on family history and personal history, and then advance in the right context to genetic screening through mutations and SNPs that can decrease their ability
to repair DNA damage from our occupational exposure. I'll skip all this because I'm out of time. But one other issue to think about, mitochondrial DNA is inherited purely maternally. So maternal DNA damage, mitochondrial DNA damage could be transmitted across generations
in female interventionalists. Also screening is important. It's emotionally complex. It's ethically complex. But it's an important conversation to begin to have. Thank you.
- [Martin] Dear chairman, dear ladies and gentlemen, sorry for the long title which was given to me. It was not my idea. It's enough for three presentations, but I will try to answer within the given time. These are my conflict of interests. Traditionally, and there's a lot of literature,
also very recent literature. EVAR treatment has limitations in women because first of all, they are less eligible than men for EVAR trials. For instance in the EVAR One trial it was about nine to 10% even though the incidence of aneurysms is higher.
This is due to some specific anatomical restrictions like small iliacs, kinked iliacs, and special necks. Also they have more complications, axis related complications due to these iliacs are shown an example. So lower profile devices are needed
to go through these iliacs and enable their eligibility for female patients. That might improve outcomes. So this is probably one factor, so that's data here showing that in-hospital deaths after EVAR is
even over time not going down, but actually going up a little bit. It might be due to more broad indications, but this is some matter of concern. There are some low-profile devices available. This device, probably all familiar with this,
is approved in the United States, is a 14-F ultra low-profile, it's called ultra low, so it's actually low-profile, it can be placed percutaneously and has very kink-resistant limbs. It has a very good suprarenal fixation
and is polymer fitting with custom seal of the neck. This device is measuring the neck diameter 30 millimeters below the renals. A new Ovation Alto, which is now under IDIE trial in the United States, has only seven millimeters distance
from the renal arteries. So this is one example of one of our first patients which we did. 64 year old, aneurysm size 55 millimeters, very short neck, tortuous, narrow and calcified iliacs. And can still be done with this device.
And you'll see the one year picture without any endoleak. So after the pivotal trial in the United States there was a European post-market registry with prospective data collection. 501 patients with monitoring, so this is not a prospective randomized trial.
And this did not really have the end-point for a gender-specific error variation. But we still did this evaluation. The first patient was enrolled in May 2011 and follow-up was done annually, it's planned up to five years.
And I'll show you the four-year results today. And gender sub-analysis showed a percentage of 14% females. As you can here see, female patients were a little bit older than men. And men had a higher other classification but you can see his neck diameter
was lower in female patients and minimal iliac diameter especially was a big problem in these patients. So in this registry trial, these patients were all included. Anyway, you can see here the numbers of the 432 men and 69 women.
There's no specific EVAR trial so far designed for women, except the LUCI trial, which is now ongoing, actually finished in the United States. And European registry also ongoing. There was no real difference in the early procedure analysis.
Also you can see here, in four years this is the results. At four years the only difference was limb occlusion was a little bit higher, maybe due to the low diameter. But all the other aspects, I'll show you the graphs in a moment.
Freedom from mortality, all-cause mortality. In endoleak there was no difference. Also no conversion rate differences in freedom from rupture. You see reinterventions, this is also an issue. There were a little bit higher
percentage here, but this was not significant. Only more Type Two endoleaks in women. We don't the exact reason, it must be anatomical specific differences in the patient population. Here you see the freedom from mortality is very recent data extracted in October 24.
Freedom from aneurysm related mortality and all-cause mortality was not a significant difference. Type One endoleak and Type Three endoleak, no difference in occlusion. There was a difference because more female patients had limb occlusions,
which could be of course repaired. Freedom from rupture and freedom from conversion was no statistic difference of within four years. And freedom from aneurysm growth, also a matter of concern, if there is Type Two endoleak or persistent Type Two endoleak, there was no difference.
But 10% of the patients developed this problem. So in conclusion, the message would be women, in the past at least, had limited eligibility for, and worse outcomes after EVAR, not only because of anatomical reasons, but because of the management.
Ovation Prime and Ovation IX and other low-profile grafts, if they are available, expand eligibility. And in our prospective data collection we could demonstrate it's possible, indeed possible to derive similar benefits
using such a graft which is maintained over four years. Thank you very much.
- One more soft swing, I guess, at EVAR-2 for the afternoon, but this one will be from a slightly different perspective. We'll look at it from a methodological standpoint rather than an analytical standpoint, which I do with some trepidation preceding Phil Goodney on the podium. As we've heard, endovascular techniques have revolutionized
the treatment of abdominal aortic aneurysm, and yet, the EVAR-2 trial published in 2010 provided Level I evidence regarding high-risk patients with abdominal aortic aneurysm. There is no survival advantage of EVAR over observation, as we've heard.
So let's unpack a little bit about what we mean by Level I evidence. Level I evidence consists of properly designed randomized controlled trials. They demonstrate the effect size of an intervention, and they're characterized by
strict inclusion/exclusion criteria, are resource intensive and can be difficult to replicate. Keep in mind that enrolled individuals are frequently younger, white, and affluent, receiving care at academic institutions, and clinical scenarios are heavily scripted.
The EVAR and EVAR-2 studies are examples of such trials. By contrast, Level II evidence, and the definition of this varies by region, consists of, for example, use of large administrative and clinical datasets to compare outcomes from different interventions. These are, to be sure, subject to selection bias
and limited granularity, but they're characterized by high power due to large numbers and external validity because they include real life patients in clinical scenarios. Examples of this type of evidence is found in the VQI, NSQIP, NCDB, SEER, and HCUP.
This study, which I'm grateful to have seen referenced in two prior talks, uses the ACS NSQIP database to look at mortality rates after EVAR in high-risk patients. And this is an example of Level II evidence. What we did was look at EVARs
that were performed between 2005 and 2013, and we used the EVAR-2 criteria to define a high-risk cohort and then examined 30-day post-operative outcomes. In that study, we found that the 30-day mortality for these high-risk patients following EVAR and our cohort was 1.9% compared to the EVAR-2 trial in which it was 7.3%.
And we concluded the contemporary mortality following EVAR is substantially lower even in the high-risk group than reported in the EVAR-2 trial. So how do we understand this? I think it's been unpacked a bit by two of the previous speakers,
but our interpretation was that, as I mentioned, randomized controlled trials and Level II evidence are not the same. So randomized controlled trials, again, include and exclude patients for analysis, use selected devices and do often include
a learning curve for new techniques, whereas the use of contemporary cohorts such as our study have an inclusive population, limited granularity, but allows for changing devices and expertise over time. So in conclusion, randomized controlled trials or so-called Level I evidence,
demonstrates effect sizes for new therapies, while large retrospective data analyses augment the findings for these therapies across contemporary practice patterns and devices. Intelligent integration of data across study types leads to improved care of patients
and preserves the role of critical thinking for surgeons. The key points that I would like you to take away are that endovascular techniques and their indications for use are obviously rapidly evolving, and thoughtful assessment of the literature allows surgeons to nimbly integrate evidence into practice.
The bottom line, our analysis of the current literature suggests we should not deny EVAR to high-risk patients. Thank you.
- Thank you very much, Frank, for the opportunity to be part of this fantastic panel. So, I'm no more a part of the debate, and I will not show the differences, but if we look on the arch, on the literature addressing the different types of repair, we can see that the result are in the same range, approximately.
And despite the fact that we didn't spoke about this, probably, there is a bias of selection where else the best patient will be addressed by open surgery, patient that fits for branched and FEVAR will be treated by those technology, and the remaining of the patient
is addressed by parallel grafts. There is a second point I would like to address and this is one part of my talk, is that the results for the endovascular options are not good, are not so long described in the literature. There are some papers with longer follow-up,
but in the mean, the follow-ups are rather short. So, let's go to our expanse that is a little bit longer. In the arch, we treated 94 patients. We had a mortality of 14% stroke, or neurological complication 8%, endoleak, primary, 18%, but we addressed 40% of acute patients,
and 50 patient with redo thoracic surgery. So, an example: 75 years old patient, he had complicated type B dissection with malperfusion, did get the TEVAR with a sandwich for the LSA. In the follow-up, he showed an aortic enlargement with the dissection extending proximal to the LSA,
and he had, again, and antegrade perfusion of the sur-lumen. He refused general anesthesia because he had severe delire when he was treated first. So we address this with periaortic grafts. We put one chimney for the brachiocephalic trunk in the aorta, one chimney for
the left carotid artery in the ascending aorta, then we deployed a TAG in the aorta then, to match the diameter of the BCT we extended the first viable, which is 13 mm, and you can see here, the six month follow-up with a nice result. So, if we want to go to long-term results,
we freezed a cohort of patient we treated 2009 to 2014. These are 41 patients with an Euroscore II of 28%, 68 years the mean age, 30 day mortality was 12%, so half of the predicted. You see here 42 months follow-up of this cohort. There is this typical mortality of 10% a year
following the procedure, due to the comorbidity cardiac pulmonary renal functions, freedom of branch occlusion is nice and the branch behaved stable. There have been reintervention during the follow-up, mainly to treat endoleaks, branch issues,
or other problems on this patient, but you see there is a three and a half year follow-up and the rate of reintervention is the same than for other endovascular options. Looking now at the more complex patients, the free vessel in the arch, you see
that the results here are good too, for the parallel grafts. Here down, we see one patient dying, no stroke, no endoleak. If we go to the visceral patient, here the literature review shows a mortality of 4.7%, with an endoleak type 1A of 7% for the parallel grafts. If we do compare now CHIMPS with FEVAR and open repair,
you can see that maybe the difference is more redo, but it's not really much more than for the FEVAR/BEVAR, and here is particularly due to the gutters. We treated here also for the long-term follow-up, we freezed a cohort of patient, 127 patient, 40% symptomatic, 11% ruptured patient.
Hostile chest, 37%, hostile abdomen, 26%. Most of the proximal landing was above the renal artery, mostly chimneys, but also reversed grafts and sandwich. Here a case, patient that was rejected after rupture from two centers to one because he was unfit for surgery, the other because he qualified not for FEVAR/BEVAR.
He had a challenging anatomy with an occluded left renal artery and celiac trunk, a shaggy arch and LSA, so we treated him transfemorally with two parallel grafts and you see the outcome of this patient. So, there are reinterventions. The mortality in this cohort is 2.4%, endoleak is 7%.
Reintervention, chimney-related, mainly gutter endoleaks. These are the curves in the follow-up, and you see that the results are similar than the patient in the arch with a need for reintervention, but that's the same for any kind of endovascular procedure in the arch.
18% at three years of reintervention. This has been for branch thrombosis or endoleak cages. So, in conclusion, the results are good for parallel grafts in the arch and in the visceral types, and selected patient, they need an appropriate anatomy, a life expectancy of two years.
They behave durable up to more than three years mean follow-up, taking into account the number of reintervention. The unsolved issue with the parallel graft is the gutter, so this technique can improve, and you can see here that they may be solution for the future.
This is an anti-gutter design from Endospan that really eliminates any kind of gutter endoleak and wandering, and this will be the patient cohort that we will compare with other repair technique in the future. Thank you very much for your attention.
- Well, if fenestrated EVAR is so great, why isn't everyone doing it? And I would submit it has to do with the planning. If you have a perfectly planned procedure, the procedure will go perfectly. These are my disclosures, which are directly related to this presentation.
This is a case that was planned using AortaFit software and it was a case that we identified as being a perfect plan. We went back and looked at our fellow and resident in our training program who we trained to plan these procedures and asked them to plan this case.
Our first trainee submitted the following plan. And when we line up the SMA, we lose the left renal on this plan. We then asked our fellow to plan the case and she provided this plan.
When we line up the SMA on this case we lose the right renal. So, it tells us that there is tremendous variability in human planning. We participate in the VQI in the Pacific Northwest Regional group,
and we perform 88% of the complex EVAR in our region. And we have the lowest procedure times, the lowest estimated blood loss compared to the rest of the nation, the lowest in post-operative complications, excluding death, and the lowest in composite outcomes to include major cardiac events.
We also have the highest rate of return of our patients to a pre-surgical care setting. So how have we achieved this? Using AortaFit software, we are able to take a standard DICOM data set of a juxtarenal aneurysm patient and create a volume rendering.
We can then display the images in an axial, sagittal, and coronal view for the user. All that the user needs to do is to identify the target vessels and to plant seed points into those target vessels, the target vessels that are selected to be preserved.
What is then output from the software is a segmentation. And you see the segmented image here, but the magic of the software is that it does the automatic adjustment of the centerline using polynomial equations and goodness of fit. We can superimpose 2D slices over this to check
our orientation of the fenestrations and look at the plugs. And what's output is a graft plan that can either be given to the physician in the form of a 3D printed template or placed on the back of a manufacturing line. Sorry. So, for the physician, an STL file can be produced
to create a 3D printed template to create a physician-modified endograft, but what we really want is to be able to provide the manufacturer with a detailed plan using this software. This is an example of a Terumo Aortic TREO device. We've now done 37 of these cases.
This is a graft that has wide amplitude stents and a large amount of real estate for fenestration. So you can see inserting this 3D printed template that was created using AortaFit software. We can rotate this graft, move it in and out to find the sweet spot
for those fenestrations, and to create a truly customized device for the patient. We then, all that we have to do at that point is to line up the SMA. So you can see, on the panel on the left, we do our first aortogram
prior to deploying the stent graft. We deploy that SMA fenestration, the renals automatically align. We then select our renal arteries and then our fellows know that it's time to call for the next patient because the procedure is essentially done at that point.
This is a cone beam CT of that very first patient that I showed you, showing perfect alignment of all of the fenestrations and target vessels. And here's a 30-day follow-up CT scan, that if you pay attention and look carefully, you can see that all of the fenestrations
are perfectly aligned. There's about four centimeters of seals on length, and lack of endoleak and a successful result in this patient. This, fortunately, is published in this month's Journal of Vascular Surgery as an editor's choice.
And in summary, the long-term durability of fenestrated EVAR has been established, but planning and procedural complexity limits widespread adoption. Automated planning software, we believe, provides efficient and accurate graft plans for the physician
or endograft manufacturer. Well-planned grafts simplify branch access and the procedure and I think will increase fenestrated EVAR utilization. And simplified FEVAR may benefit the majority of patients harboring juxtarenal aneurysms and even standard infrarenal aneurysms and may be the best therapeutic option.
- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --
- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.
But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,
is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy
in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.
The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation
so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later
that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low
and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse
even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean
as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques
different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between
pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients
are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system
you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because
this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out
now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference
between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing
a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is
the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories
and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here
again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result
and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not
fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again
look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as
the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here
This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you
- [Presenter] I have nothing to disclose. The incidence of limb thrombosis after EVAR is reported with a percentage between three and 7% of cases. A narrow distal aorta is a well-recognized risk factor for this complication, especially if calcified, with possible limb kink and compression at the level of the bifurcation at subsequent thrombosis.
Historically, aorto-uniiliac reconstruction has been proposed as the treatment of choice to address this problem. Nevertheless, it should be, it is a more invasive approach and today should be considered the last-resort option. The unibody design stent graph
is an appealing concept in this scenario. We have a single-lumen main body stent graft with no iliac limbs at the level of the aortic bifurcation and a reported low rate of reintervention in the followup. Last but not least, a possible solution to address the problem of a small distal aorta
is to implant a standard modular stent graft and reinforce the radial strength of the stent graft limbs at the level of the bifurcation, implanting two high radial force kissing stents. And several papers have been published that confirm the effectiveness of an aggressive policy
of primary stenting to prevent limb complications in the presence of a small distal aorta. We reviewed our experience with endoluminal repair of triple As in the last four years, with 343 patients treated since January 2014. We approved five cases of reintervention
for limb complications that were all fixed by the secondary procedure. Considering only the anatomies with a real small distal aorta, we identified 17 patients with an aortic bifurcation equal or less than 16 millimeter in diameter.
Among these patients, seven were treated with a unibody bifurcated stent graft, and 10 received the modular stent graft with the adjunctive primary stenting. - Just repeat. - One out of seven patients in the unibody stent graft group was reoperated
two years after the first intervention and required the relining with kissing stents. In contrast, none of the patients who were treated with the modular stent graft with adjunctive primary stenting was reoperated, and all limbs are patent at mean followup of 14 months.
I'm going to show you some images from our experience. Here we have a male patient with an aneurysm of the distal portion of the aorta and then a real narrow aortic bifurcation. This patient was treated with a unibody Endologix AFX device with ballooning of the aortic bifurcation.
Had a nice final result that is maintained 30 months after the procedure at CT scan followup. This is the case that was reoperated in the unibody stent graft group. She was a lady with a large aortic aneurysm
and highly calcified aortic bifurcation. Her first treatment was the implant of an Endologix AFX device, but the patient was readmitted two years later for symptoms of the left side due to compression of the left main body prosthesis
at the level of the bifurcation. And the problems were fixed, implanting two kissing stent with a good final result. This is another case of triple A with a small distal aorta. In this patient, we used the standard modular stent graft.
At the end of the procedure, we implanted two kissing stents to reinforce the radial strength of the stent graft at aortic bifurcation, and you see that the post-operative CT scan confirms the good expansion of the stent graft limbs. This is the last case I'm going to show you,
a patient with a sacral aortic aneurysm along distal aortic neck and an aneurysm of both common iliac arteries. This patient was treated with a GORE EXCLUDER Device with adjunctive iliac branch device on both sides to preserve the epigastric arteries.
At in the end of the procedure, we implanted two kissing stent to reinforce the stent graft limbs. - [Man] It's back. (faint speaking) - Not to worry. - [Man] Yeah, there's nobody else.
- [Presenter] Okay. (faint speaking) (laughing) And this was the case I was showing to you. The patient with aneurysm of the abdominal aorta, both common iliac arteries,
the implant of a modular GORE EXCLUDER Device with iliac branch on both sides, and then the end of the procedure reinforce the strength of the iliac limbs implanting two kissing stents. And you see the nice final result
that is confirmed at the post-operative CT scan. In conclusion, ladies and gentlemen, a narrow distal aorta carries a high risk of limb complications after EVAR. The unibody design stent graft may be a good option in this anatomical setting.
Nevertheless, according to our experience, in the presence of a real small aorta, implant of a standard modular stent graft with adjunctive primary stenting is the most rational and effective approach. I thank you very much for your attention.
- The only disclosure is the device I'm about to talk to you about this morning, is investigation in the United States. What we can say about Arch Branch Technology is it is not novel or particularly new. Hundreds of these procedures have been performed worldwide, most of the experiences have been dominated by a cook device
and the Terumo-Aortic formerly known as Bolton Medical devices. There is mattering of other experience through Medtronic and Gore devices. As of July of 2018 over 340 device implants have been performed,
and this series has been dominated by the dual branch device but actually three branch constructions have been performed in 25 cases. For the Terumo-Aortic Arch Branch device the experience is slightly less but still significant over 160 device implants have been performed as of November of this year.
A small number of single branch and large majority of 150 cases of the double branch repairs and only two cases of the three branch repairs both of them, I will discuss today and I performed. The Aortic 3-branch Arch Devices is based on the relay MBS platform with two antegrade branches and
a third retrograde branch which is not illustrated here, pointing downwards towards descending thoracic Aorta. The first case is a 59 year old intensivist who presented to me in 2009 with uncomplicated type B aortic dissection. This was being medically managed until 2014 when he sustained a second dissection at this time.
An acute ruptured type A dissection and sustaining emergent repair with an ascending graft. Serial imaging shortly thereafter demonstrated a very rapid growth of the Distal arch to 5.7 cm. This is side by side comparison of the pre type A dissection and the post type A repair dissection.
What you can see is the enlargement of the distal arch and especially the complex septal anatomy that has transformed as initial type B dissection after the type A repair. So, under FDA Compassion Use provision, as well as other other regulatory conditions
that had to be met. A Terumo or formerly Bolton, Aortic 3-branch Arch Branch device was constructed and in December 2014 this was performed. As you can see in this illustration, the two antegrade branches and a third branch
pointing this way for the for the left subclavian artery. And this is the images, the pre-deployment, post-deployment, and the three branches being inserted. At the one month follow up you can see the three arch branches widely patent and complete thrombosis of the
proximal dissection. Approximately a year later he presented with some symptoms of mild claudication and significant left and right arm gradient. What we noted on the CT Angiogram was there was a kink in the participially
supported segment of the mid portion of this 3-branch graft. There was also progressive enlargement of the distal thoracoabdominal segment. Our plan was to perform the, to repair the proximal segment with a custom made cuff as well as repair the thoracoabdominal segment
with this cook CMD thoracoabdominal device. As a 4 year follow up he's working full time. He's arm pressures are symmetric. Serum creatinine is normal. Complete false lumen thrombosis. All arch branches patent.
The second case I'll go over really quickly. 68 year old man, again with acute type A dissection. 6.1 cm aortic arch. Initial plan was a left carotid-subclavian bypass with a TEVAR using a chimney technique. We changed that plan to employ a 3-branch branch repair.
Can you advance this? And you can see this photo. In this particular case because the pre-operative left carotid-subclavian bypass and the extension of the dissection in to the innominate artery we elected to...
utilize the two antegrade branches for the bi-lateral carotid branches and actually utilize the downgoing branch through the- for the right subclavian artery for later access to the thoracoabdominal aorta. On post op day one once again he presented with
an affective co arctation secondary to a kink within the previous surgical graft, sustaining a secondary intervention and a placement of a balloon expandable stent. Current status. On Unfortunately the result is not as fortunate
as the first case. In 15 months he presented with recurrent fevers, multi-focal CVAs from septic emboli. Essentially bacteria endocarditis and he was deemed inoperable and he died. So in conclusion.
Repair of complex arch pathologies is feasible with the 3-branch Relay arch branch device. Experience obviously is very limited. Proper patient selection important. And the third antegrade branch is useful for later thoracoabdominal access.
- 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.
- Thank you, Mr. Chairman. Thank you, Dr. Veith for inviting again to this great meeting. It's my disclosures. Well, as we know and heard this meeting, there are some certain limitations of current EVAR (mumbles) anatomical procedure and economical reasons,
and I would like to present a relatively new device which may address current EVAR limitations with a simple low profile system, and basically, ALTURA consists of two parallel stent graft systems. ZEUS No Gate Cannulation is needed and unique features include D-shaped proximal stents
and suprarenal fixation. Multi-purpose (mumbles) possibilities as well, and the system of utilize 14 French delivery system. And as aortic components can be deployed offset to accommodate the offset renals, and then the limbs are also unique
because they're deployed retrograde from distal proximally, and this allows precise positioning, both proximally and distally. Well, as the ALTURA clinical experience includes the very first human implants as well as more recent case performed
with a fully commercial device, and a total of 90 patients with a AAA were enrolled between 2011 and 2015, and follow-ups are taken at 30 days, six months, and annually to five years, and this presentation gives a current status of follow-up, and our results with a 12-month follow-up were published earlier this year.
Our clinical data were collected in total of in 11 sites. It includes 90 patients. And you see here, the patient demographics and anatomy do a typical, which are typical for all EVAR patients and the mean follow-up was 2.7 years. And procedure of success was 99%.
Only one patient, one of the first patient was Gen1 was not implanted, and 50% patients were done percutaneously, and majority of them underwent regional or local anesthesia. So when you look into the results, we see that there was only one case of AAA ruptured,
which occurred at three years due to type II endoleak and sac enlargement as the patient, which refused treatment due to type II endoleak. And all other deaths are paired to no original causes, and two patients had device migration at two years. The same patients appear at three-year period,
and basically these were undersized grafts was sort of our learning curve, and there was no any migration later on. Four patients had type I endoleaks visible on CT, and read by independent committee between 30 days and one year.
None have required secondary treatment and have been no aneurysm enlargement observed. And at one year, not surprisingly for this kind of devices, there was 17% type to endoleaks, but only one patient required secondary procedure due significant sac expansion.
Well, wasn't, of course, what we saw, I expected majority of patients has had shrinkage. There was a four-year period. And this is a patient who was recorded with the type IA endoleak at 30 days, caused by the last calcified nodule,
as you he's here probably none of the other device would tolerate that, but the endoleak did not extended into into the sac and had a leak result spontaneously without sac enlargement through a four-year follow-up period, as we're seeing here. Well, here another patient with type IB endoleak,
due to (mumbles) generation was treated with coils and glue an extension with additional stent graft to external iliac artery. What's interesting was the device. Device can tolerate small distal aortas and five patients who were treated
with small distal aortas and the very first patient was not dilated enough and stents were not deployed, simultaneously causing some stenosis which was easily treated with PTA afterwards, so we learned but it's very great, unique feature to treat the small distal aortas for the device.
And of course, sensing what happening with them, septal endoleaks, because everybody being concerned what happening with that, and nevertheless, there were no septal endoleaks observed during the follow-up period. In conclusion, Mr. Chairman, ladies and gentlemen,
I would like to say this Novel Altura endograft concept has potential to play major role in mainstream EVAR cases and potential benefits include predictability, reposition ability to place the device very, very, very precisely, offset renals, to maximize use of the neck, and low profile
overcomes current and anatomic limitations like tortuous iliacs, narrow bifurcation or access vessels and no limbic inhalation is needed, and basically, I truly believe that this offers option for EVAR day surgery and ruptured aneurysms. Of course, first results are very encouraging.
We need more data. Thank you very much.
- [Jean] Thank you, Will, thank you again, Frank, for inviting me to your symposium. I'm going to talk to you about this concept of the value of EndoAnchors and TEVAR, and if you talk about that, basically, you need to figure out if we can predict TEVAR failure. So we published, last year, the creation of a novel
that makes a severity grading score to assess thoracic aneurysm and see if we can actually predict the patient that will not behave nicely with a simple TEVAR. Here's an example of two scores. Patient with an ASG score of 24
and the other one with an ASG score of 43. And the top of the ASG score is all the way up to 57 if you have all the worst characteristic that is applied to the different region of the thoracic aorta. So we found by doing a ROC Curve analysis
that an ASG score of 24 was actually the cut off, and below 24 was the low score group. And 24 and higher were patients with the really bad, challenging anatomy. And those patients had only a 69% freedom
from postoperative endoleak, requiring re-intervention at two years. So this novel anatomic severity grading score can actually really successfully identify patients that are at increased risk of endoleak requiring re-intervention
and then it would make sense in those patients to potentially apply for prophylactic EndoAnchors. And this is what we did in this next study where we looked at only patients with a high ASG score. So we had 63 patients with those high scores. 40% had only TEVAR and under the 20 patients
had TEVAR and prophylactic EndoAnchors as well. And if you look at those patients that only had TEVAR and bad anatomy, we had a 58% chance of freedom from aortic related re-intervention at three years. The 62% freedom from Type I endoleak at three years.
But when you place prophylactic EndoAnchors you end up with an excellent result with 95 to 100% survival free from any of those two kind of problem. So this would be the value in using EndoAnchors and these are better to me now. The technique for the thoracic EndoAnchor
and compared to the abdominal is that we have the selection of three potential active guide size, 22, 32, 42. And we size it according to the size of the endograft. I say as an example of a patient with challenging anatomy that was the patient with the ASG score of 43. This patient had a hemiarch debranching
and then we went ahead and deployed the endograft and deployed the EndoAnchor at the inner arch. This is the completion angiogram after those prophylactic EndoAnchors. And there is no endoleaks at two years. This patient is now currently at over three year follow-up
no migration and no endoleak, despite an extremely challenging anatomy. You can also have another prophylactic indication is to prevent upward migration. If you look at the tapering of the thoracic endograft right above that celiac artery,
this is really an area that in fact in the Valor II trial, has really showed that a lot of patient have Type 1B endoleak after a few years. And by using circumferential placement of those EndoAnchors at the distal end of the TEVAR,
you can really prevent this upward migration and endoleak 1B formation. Now the technique it's really about the angle of attack. I think if you have a bad angle of attack, you will not be able to deliver properly. But when you have a real 90 degree perpendicular attack
of the endograft this is how you can safely deploy those EndoAnchors in the thoracic aorta. This is a deployment of the ascending aorta in an RAO view, so you can not only deploy at the inner curve, but you can also deploy EndoAnchor on the interior or posterior aspect of the arch
by deploying anchors with these special view with the barrel. When you look at the outer curve of the arch, this is an easy Zone 1 delivery. This is a more tricky Zone 1 delivery, but it also possible to deploy EndoAnchors
in the outer curve. Same thing when we have the sternum open to do a total arch debranching, we can deploy EndoAnchors in an antegrade fashion in Zone 0 and obtain also great result. Top 10 tips for EndoAnchors.
First is take the time for preoperative planning. Second one is wishful thinking will not create the landing zone. Sometimes you have to do some debranching to obtain a landing zone. Deliver the endograft accurately.
Do the aortic balloon molding first. You have to size the Aptus guide according to the endograft size. You have to undersize it when you want to use it at the level of the outer curve of the arch. You deploy two rows in TEVARs.
I always deploy three rows in arch because of the increase in hemodynamics at that level. I think a good place to learn to do TEVAR and EndoAnchors is the distal end near the celiac artery. And never start a challenging TEVAR case without EndoAnchors.
So in summary, EndoAnchors in TEVAR are done in imperfect landing zones, improve outcomes by decreasing Type I endoleaks and the need for aortic reinterventions. Safe and effective deployment of EndoAnchors really relies on simple techniques, device selection,
and the knowledge of the failure modes of doing TEVAR in those challenging zones. Thank you.
- Thank you very much. I'd like to thank Dr. Veith for the opportunity to be here and give a quick smattering in four minutes and a quarter. I have no disclosures. So despite the well-documented benefits of straightforward catheter-directed thrombectomy, it remains slow. It can several days and we need speed.
So, devices for physical removal of clots, disruption of clot, large volume removal, and/or combinations of above have certainly been developed. So, with regards with physical removal, aspiration devices, the number of which we'll have several speakers following, the CAT series is by far the
best example of it, if you will. Suction device connected to a continuous pump. Unfortunately, if offers poor transition into the wire. You have to advance in bare. Particularly when you're doing arteries, this can be concerning.
As you advance the thing, you can't tell if the clot is actually removed or not removed, so sometimes you can push it forward. If you've ever used the device, you've seen this. And clogging requires the entire remov
and thus, and you have to put it back through the artery and start all over again. And the concept of continuous removal with a pump is good for suction, but unfortunately, you can remove up to 160 cc's with just 20 seconds of using the device, as it doesn't have a reperfusion system.
The Aspire Mechanical is sort of a low-tech version, a manual aspiration device, where you have a pump that you manually pump up to start negative pressure. You can advance the catheter. The nice thing, you can connect it to literally anything.
If you can get a catheter in there, you screw it in and away you go. You're less likely to have extreme blood loss. You're unable to adjust the suction, unfortunately. And it's not really clear if the suction is actually working or not working.
The pump is on, you know that. But if you pumped it two or three times, is it sucking or not sucking? There's no actual feedback. The AngioVac is the most powerful or large-volume aspiration system.
It's filtered through a veno-veno extracorporeal pump. You can get a big circuit in there. You can do vena cavas, you can do iliacs, it's great. But you have to set up this very complex system. You require, what I'm going to put here as massive sheaths. So if you ever think about doing this in arteries,
you really can't do it. You need a 24-french sheath to put the device in, and then you need at least an 18 or a 20 to put the volume back in. So unfortunately, for arteries, you're going to have to put a conduit in,
and you're going to have to advance it bare through an artery. The extracorporeal filter pump is very expensive and it's not reimbursed. A lot of institutions will either let you use it a few times until they realize how much it costs, and then you're only going to be reimbursed for a thrombectomy.
With regards with mechanical, the Arrow-Trerotola is probably the most powerful and classic mechanical clot disrupter. It's got a spinning cable that looks like this, the new version. And it can damage native vessels,
so it's designed only for grafts. However, it can also get entangled in wires and stents, so even though the black box warning says don't do it, it doesn't keep people from trying it and having multiple attempts. And this is something that we had to remove once
from a graft because it was all entangled in the wire, and it could neither be pushed in or pulled out. It causes embolic materials. It spins inside, and we've never really manned up or womanned up and looked at what happens to the lungs when we fracture all this stuff.
Combination systems, like the Angiojet, is nice 'cause it can shoot out TPA and spray out a saline and break things up. And also, it has a negative pressure, which causes Bernoulli effect to extract clot. The upside is that it removes soft clot
through small side holes. We love it. It's fast, it sprays saline. However, it can also damage vessel walls. At some point, we've read and/or done ruptured in a thin vessel.
And of course, there's a black box warning against pulmonary. But also, if you've ever used it in a cadaveric graft, you'll do it once, and then they'll come back a month later, and now you have this diffused aneurysmal destruction of your bypass.
It also causes hemolysis. Typically, if you look at a Foley catheter, this is what your urine starts with at the bottom and what your urine ends with at the end. And both my group and Dr. Kashyap, who will be following, have assumed that it may not be good for the kidney.
I'll let him continue with that. So in summary, be judicious when you're choosing your approach. Continue to consider the potential downsides of each product. Risk/benefit ratio based on the patient.
Patient has renal dysfunction, limited outflow, sheath size. Old school lysis may be the way to go. Just look at it and maybe you don't have to do a fancy device every time. Or, actually, go with an open thrombectomy.
Mechanical thrombectomy is thus not like a car. When you're looking at these different options and say, "Gosh. You know, maybe it is faster, but perhaps I should think about it." But if somebody offers you this, there's no conceivable downside.
I would go with it. Thank you very much.
- I want to talk on managing branch complications. This is my disclosure. We overlook in the Berlin-Brandenburg Helios Vascular Center about 466 patients treated with branched, TVAR and fenestrated EVAR devices. All patients received Zenith stent-grafts, custom made devices, T-Branch, or standard fenestrations
in all cases. The target arteries that we are talking about were renal, SMA, celiac access and internal iliac arteries. We used exclusively bridging stent-grafts that were balloon expandable stent-grafts. This is the differentiation of the patients
so we had EVAR fenestrated grafts in 190, branched TVAR in 138 patients, 93 of them were off the shelf devices and T-branch. EVAR with iliac side branches in 138 patients and all together we treated target arteries of 1270. You see the hospital mortality of these procedures
you can see a clear difference between the EVAR fenestrated graft and the branched T version are much more complex procedure and although overall mortality was 4.9% over these 13 years. What happened in these patients we experienced
in 44 patients, 44 complications in the target arteries so unfortunately one target artery problem per patient in these complicated cases. This means rate of 3.5% problems in the target arteries overall. Involved were renal arteries in 32 cases,
SMA in 10 cases and the celiac artery in two cases. What did we do in these cases? Managed the complications once thrombolysis was different devices for example were Rotorex stenting of the dissected vessels, coiling if unavoidable or occlusion of the side branch if no access was possible.
Show you some examples. This is a very serious complication where we were unable to enter the SMA resulting in occlusion of you see on the right slide that this was solved by laparotomy and retrograde access to the SMA.
This is a stenting of a dissected renal artery which could be managed quite nicely with an extension of the stent. Here we have again a prolonged intraprocedural SMA occlusion. We finally managed to enter the vessel
but it was very, very long and prolonged time. This is an inaccessible celiac artery where we have finally had to skip, not iliac sorry, celiac artery where we had to skip the implantation finally and occlude the branch with Amplatzer plug.
All together if you look at these complications in 34 cases we were successful in clinical point of view. In 9 patients complication was little and majority of these were complications involving the SMA. Eight of nine patients had with severe complication in the SMA and died
and so the SMA complications contribute, compared to the mortality, 40% to the procedural mortality in these branched cases. So in conclusion, injury to target artery in endovascular repair with branched and fenestrated stent-grafts are rare
but may be a serious complication especially damage to the SMA has a high mortality and thus further improvement of endovascular skills, instruments for example moveable sheaths which we had not available in the beginning and troubleshooting devices are mandatory
to avoid these complications. Thank you very much for your attention.
- [Instructor] Thank you very much. So, you saw some of the issues that our, oh, this is the slightest cut, but that's okay. Some of the issues that we've seen with these percutaneous mechanical devices, and, back in the 90's, and perhaps even more than a decade ago, there were a lot of these.
And this space gets hot and cold, and one of the problems is that the level of evidence for doing these is very low, and when it is done, it wasn't done well. And this is a nice registry, a lot of patients enrolled, unfortunately we didn't learn
what we had to learn from these types of registries, because of just the study wasn't done well. So the level of evidence is low, and when we did have them, they didn't really work. And you saw some of the problems, that these devices can cause.
And here's another problem that wasn't discussed. You can see the DVT, iliofemoral DVT in here, and a device is pushed a few times up and down, and sort of aspiration, a Bertoulli, that type of thing. And this looks, oh wow, well this looks good,
maybe the thing is working, except all the clot is up here. So, these devices tend to push the clot around. So the issue is, enter now more recently, these are some of the more recent ones. Note that the AngioVac is not here, I don't consider that a practical thrombectomy device,
and so, it's not here. So, we're going to be talking about JETi. This is a system that is an aspiration system with a jet that comes inside the catheter, therefore the clot is engaged and pulled in and broken down by the jet, therefore there's no hemolysis.
And this demonstrated in this case, which is acute and chronic 17 year old multiple DVTs in the past, the iliofemoral segments are stented, as you can see here, this segment is somewhat fresh clot but these, as you can see, are subacute clot. Look at this, so the system now is designed
for over the wire, but for DVT you can use it without the wire, because it works a lot better. As you can see it can really aspirate the clot, in before your eyes. Now this I have passed the device in here once, and you can see the fresh clot is gone,
we have some residual debris in there, we have not established flow yet, and then I turn the device on... and it pulls the whole thing in, okay? So, very powerful aspiration method. So, and as you can see here, we don't have
a flow establish, outflow established yet. Therefore, when you turn it on, you have a vacuum created right here, and so this tells you how strongly this device can aspirate and work. And this isn't on the table.
After a pass here, two passes here, some residual clot in here, obviously there's residual clot there. So we pass it around these areas once more, and this segment obviously needs to get stented and on the table, re-establish antegrade flow. Since May, we've had 19 patients treated, most of them DVT.
And, based on our assessment, 17 of the 19 patients at a total time of 90 minutes on the table, had better than 90% clot retrieve. We have 30-day patency data on only 16 of those patients, because this is really since this May. And 15 of those were open, one re-thrombosed
and we had to retrieve again. Conclusion, so preliminary experience indicates that this is an effective device. There were no safety issues, we don't see any hemolysis, we don't see any pushing around of the clot, but there is a learning curve to it,
and for best application, thank you.
- I think that the most important tip cannot really be summarized in five minutes, which is that these procedures are highly dependent on how well you plan the procedure and how well you really implant the device. That is a fairly long learning curve that I think you need to actually collaborate with people
that they are experienced, and with industry to make sure that you are on the right track on making your measurements to size these devices. But there are a few things to be said about cases that are very difficult, and a few tips that I would highlight on this talk.
First, it's highly important that you build up your inventory so you can get out of trouble. I think you have to have a variety of catheters of your choice, with primary or secondary curves.
The addition of shapeable guides has been a major benefit for these types of procedures. They are fairly expensive, so I would say we don't use them routinely, but they can bail you out. They can allow you to do cases now from the femoral approach that in the past could not be achievable this way.
You have to be able to work on the diffe .035 system, .014 system, .018 system, and know when to apply this. I would like to highlight four maneuvers that we use when vessels don't align.
First, a common maneuver is really not to try to get in a quote/unquote pissing match with the fenestration and the vessel. If you can catheterize the fenestration first, and advance your sheath upwards, and lead a .018 wire into the sheath,
that will basically lock your sheath into the fenestration. Therefore, you don't have to repeatedly catheterize the fenestration and you save a lot of time. You can choose y ose something that has a secondary curve if you have room,
or a Venture 3 catheter, which is one of my choice for catheterization, and you can see here that on this case, the difficulties imposed by a shelf on the ostia of the renal artery, which makes catheterization more difficult. This .018 wire also allows you to bend your sheath
as a guide catheter so that you can achieve a downward curve to catheterize a down-going vessel, like on this renal artery. The second maneuver to highlight is that these devices are constrained posteriorly, and therefore, the fenestrations are naturally moved
posteriorly into the aorta. So one of the first maneuvers is really to try to move the fenestration more anteriorly by rotating the device. Now, some of the companies now have newer constraining mechanisms
that may alleviate some of this, but this is kind of a next maneuver that we do. Finally, rarely nowadays we have to really find more space between the fenestration and the aortic wall, but it is always useful to leave behind a wire when you deploy this device so that in the event
that you need more space, you can perhaps navigate the catheter, inflate, and create some space between the fabric and the aortic wall. Marcelo Ferreira, along with other collaborators, has described a technique that I think is very useful when you have a lot of space.
That's the case, for example, of a directional branch or perhaps if you are using fenestration to target a vessel that is somewhat away from the fabric of the endograft. That's called the snare ride technique. This is summarized on this illustration.
When you see the left renal artery to be up-going, now being targeted from the brachial approach, that was difficult to catheterize, you catheterize that from the femoral approach with an eight French sheath and a snare ride type... You snare the wire from the arm, and then you can
navigate that catheter inwards into the vessel. That can be difficult, sometimes, to actually advance the snare into the vessel. I think that there is some improvement on the profile of these snares that can improve that, but that is a very useful technique,
not only for branches, but also for fenestrations. Finally, sometimes you have too much space. You may seem you are very well aligned on the latitude with the vessel, but in fact, there is so much space the device got displaced on that sac and you cannot simply catheterize the vessel.
It's useful to downsize the system on these cases to a micro-catheter with a micro-wire to find yourself in the sac eventually out through the vessel. Once you achieve that, you would then exchange this micro-wire, usually a glide gold wire, to a .018,
a stiffer wire that is long enough. You advance a balloon that is undersized for that vessel, and with that you can straighten the system and eventually switch that for a wire that is of reasonable strength, such as a rosen wire in this case, and complete the case.
Finally, there is nothing wrong about leaving the battle to be fought another day. It's better to finish a case a little quicker and not end up with leg ischemia and a compartment syndrome and a s the situation
and come back another day. This is a case, for example, that I did a branch endograft. You can see the right renal artery is exceedingly narrowed. I could not find a way in in a reasonable time. I gave myself about half an hour. I decided to quit.
A few days later, I came back through a subcostal incision, got retrograde access, and this literally was a case that didn't take very long and end up doing very well. So in summary, patie select your proper
anticipat stent. To offset these challenges, minimize contrast a master your endovas
it is better to end with a patient alive and fight the battle another day, than to have an excessive long procedure leading to numerous other complications. Thank you very much.
- [Lu Qingsheng] I have no disclosures. We know for indication of EVAR we need favorable proximal neck anatomy but if it not unfavorable maybe we are some Type 1a endoleak it's a serious complication for EVAR. So for prevent and treat Type 1a endoleak
especial for some juxtarenal aneurysm maybe we use the chimney fenestration branch and some sac bag. Could we find a simple safe cheap and effective method? So we find from open surgery we were introduced this fibrin glue
means its complex of thrombin and fibrinogen, it's used hemostasis in open surgery so we put that into inject that into the sac, we call it fibrin glue sac embolization. I will show you some cases.
For this case is very short neck and not quality of deck and after deploy the stent graft, of course very serious Type 1a endoleak. But fortunately, we put a catheter before we deploy the stent graft so this catheter is into the sac of the aneurysm
then we use up a long controlled blood flow and we inject from the catheter into the sac of the aneurysm and we inject the fibrin glue. And you can find the contrast not moved after we withdraw balloon. Then we do the angiogram.
We find no any endoleak. Another case showed is angulated neck as this patient. Of course after we deployed stent graft have a lot of endoleak. And we do again this technique. And control the balloon, control the blood flow,
then inject the fibrin glue, and we check all that and withdrew the balloon, there are no any movement about the sac. And we do the angiogram and no any endoleak. Till now, we did, we begin this technique 2002, so we follow long time that we can show it's safe.
So till now we treat 156 cases and proximal less then short proximal neck is 75 cases even some of less than 10 millimeters. And angulation more than 60 degree even some cases more than 75 degree.
Most of them more than 98% of patients' endoleak was resolved. And during our follow up, the mean time more than 100 months, only three patients died of aneurysm related sac enlargement.
The mean maxim aneurysm diameter decreased and no recurrent Type 1 endoleak so we have confidence that it's safe and no any sealant-related complication for example renal failure and aplasia other things. So we discuss the mechanism
it's not only embolization for endoleak but also coagulating all sac of aneurysm like this in shows how it worked. And we also measure the pressure in the sac. Intrasac pressure decreased significantly in treated cases. And how about that technique we need occlusion
proximal blood flow and protect branch ateliers and prevent distal embolization. And we also treated into the rupture aneurysm and it can treat any type of endoleak as these cases it's a rupture aneurysm we do the EVAR emergency.
And after we deploy this devices, we find this endoleak. We don't make sure which kind of endoleak but anyway we just do that, control the blood flow use the balloon then inject the fibrin glue in that.
And all the sac of aneurysm. Then we do the angiogram and endoleak disappeared. We'll be treat any type endoleak of the rupture EVAR we prevent rupture post-EVAR and we decreased abdominal compartment syndrome. So the conclusion is
fibrin glue sac embolization is a simple and effective treatment method. And this method could expand the current indication of EVAR. For selective the length maybe can to the 5 millimeters, angle maybe can to the 90 degree,
and for emergency we seen it should be into the older EVARs for rupture aneurysms. Thank you very much.
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