- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want
in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis
is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied
and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple
aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention
adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,
the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that
there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions
a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.
In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure
with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle
and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis
needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.
Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.
In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,
regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate
without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.
An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis
and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.
This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more
in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.
But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.
The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.
Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion
because I have a flight in a few hours. Thank you very much.
- Thank you, thanks to Dr. Veith and the program committee for allowing me to present this morning. My disclosure. So, uh, I think that there's been an abundance of literature over the years that is suggested that venography may have poured diagnostic sensitivity for identifying iliac and, and
common femoral vein obstruction. Uh, in uh published literature, 34% of patients who have chronic venous symptoms of a severe degree had iliac vein obstruction on imagining techniques other than venography such as IVUS with normal venograms and often times
patients have significant outflow obstruction and there are no pelvic collaterals present so this is not a reliable though maybe specific indicator of outflow obstruction. The video study was designed to prospectively compare multiplanar venography vs. IVUS
to address the question if you do enough views on venogram do you find the same lesions that you might detect with IVUS. And we also wanted to look, does the imaging that you do to look for iliac and common femoral vein outflow track obstruction
effect your clinical decision about intervention. These are the patients in the video trial CEAP 4 through CEAP 6. And so 100 patients were randomized in this or not randomized, but rather entered entered this prospective multi-center single-arm study
at 14 sites in the US and Europe. This was half CEAP 6 patients and the remainder were CEAP 4 and 5. The patients underwent multiplanar venography. The site investigator was asked to make a decision about whether there was a significant lesion
and how they would treat that lesion and then once that was recorded IVUS was preformed and then again after the pull back the investigator was asked to make a decision about whether there was a significant lesion and how they would treat it.
We standardized venography with a hand injection in 3 views as noted. A 30 degree RAO and LAO and an AP view and the catheter was placed at the cranial portion of the femoral vein we adopted the standards and the literature
of a 50% diameter stenosis. And venography in a 50% CSA reduction on IVUS as a significant lesions. The uh, study cohort was approximately 43 women. The left leg was the index limb and 2 to 1 ratio to uh, to the right.
The age average 62 and you can see the majority of the patients were CEAP 4 and CEAP 6. What we identified with IVUS is a 21% greater (mumbling) identification of outflow obstruction. Venography was a lot less sensitive
at identifying these lesions and therefor suggesting that IVUS is a more sensitive imaging modality for identifying outflow obstruction vs. multiplanar venography. And when you looked at the core lab over read
this was for both the IVUS imaging and for the venography. And we at first calculated the diameter stenosis for both modalities we saw that with the multiplanar venography you tended to underestimate
the degree of diameter stenosis compared to IVUS and this resulted in missing about a quarter of the lesions that were greater than 50% diameter stenosis. And in part IVUS intended to score the lesions more severe for the same lesions compared to venography and this was statistically significant.
When we looked at CSA measurements from the IVUS system and also calculated off the venography in the core lab we saw again that venography missed about 18% of the significant greater than 50% CSA lesions even with reviews.
And this resulted in a change of procedure in about 60% of the patients there was a change in the decision about whether to treat of not and in 50 of the patients the number of stents changed from either no stent to 1 stent or 1 stent to 2 stents.
So without IVUS your likely under treating iliac and common femoral vein obstruction. This was the uh, rVCSS scores after treatment in this group. On the right here in green is the improvement on the left worsening.
And you can see in large part these patients all improved uh, expect for this outlier here and then some patients there was no improvement and when you looked at a score a VCSS score greater than 4 as being significant at 1 and 6 months there was a significant improvement post intervention.
And we see here in this receiver operating curve that IVUS best predicted clinical improvement at 6 months. And so we see that IVUS was more sensitive accurate for identifying significant lesions and the iliac and common femoral vein segments. It was the best guide for stent intervention
and it appears that if use a 50% cut off either diameter or CSA reduction it best predicts that intervention will lead to an improved clinical outcome at 6 months. Thank you.
- 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.
- Dear Chairman, dear ladies and gentlemen, thank you for the chance to present these data here. As opposed to United States, this is not first-line therapy in Germany. And I would like to show you some results with the Omega-3-enriched matrix, which is a little bit special.
It's made from fish skin from Atlantic cod, and it's an acellular matrix, which can be used as a xenogeneic skin graft for hard-to-heal wounds in different locations. Some advantages of using fish skin as opposed to a porcine skin or even human skin
is it's a gentle processing possible, it preserves the lipids, which is very important. I think the Omega-3 is a very important feature of this and it preserves the structure. And there's also very little risk of disease transmission, which is
always a matter of concern in xenogeneic materials. And how does it work? The Omega-3 fatty acid has some anti-inflammatory effect by mediating an inhibitor, a new inhibitor. It's called the NLRP3 inhibition,
which is necessary for IL-1 beta activation of cytokine, which is used for inflammation. And so this fish skin is also reducing general inflammation in the surface. So how is this application done? So you see a hard-of-heal wound,
which has to be a little bit clean and infection-free if possible, but it doesn't heal completely. So the fish skin is applied, and it can be covered with polyurethane foam, or even with NWPT with vacuum therapy.
And it takes several treatments. The advantage is it's weekly dressing changes. That means it's possible to do it on an outpatient basis, and I think this is the way it's done mostly in United States. So these are inpatients with very complicated wounds.
23 patients with 25 vascular wounds in different locations. Two in the thigh, seven in the distal calf, 14 in the foot, and two even in the hand. And the time to heal took nine to 41 weeks, so we have to be a little bit patient and stubborn to really wait for the effect of this fish skin.
And in average, you can see here, in some patients, three are enough, but in some patients 26 treatment cycles were necessary. This is just to show you the spectrum of patients treated in the last four years. Not very many, 15 out of 25 only, was complete healing.
This is from three hospitals in Germany, from Hamburg, Mainz, and our hospital in Karlsruhe. And you see here the rate of complete healing is only almost half of them. Here, this is an example, typical example of what we see. This wound became necrotic and dehiscent, and then
after debridement and some cleaning it looks like this. And then it can be treated with the fish skin. It looks a little bit strange if you do the first dressing change, but this is the way it should look. And after a while, this took 33 weeks, but then this foot healed, and there was
no major amputation necessary in this patient, which is the aim of this therapy, actually. This is a very terrible example of steal syndrome in a dialysis patient with a necrotic hand which had to be amputated in an emergency procedure.
And the question was: could this hand be saved somehow? So this was also treated with Omega-3 matrix, and this is the final result, but this hand is not functional, so it needs some additional plastic surgery. But I think after these wounds are healed,
before that no plastic surgeon would do anything with an extremity like this. These are some more examples of the healing. And you see here the curve, how long it takes to heal for these wounds: up to 12 or 14 weeks. This is kind of the average, three months.
There was a publication before with a few similar, even less cases, 18 cases, from United States, which showed complete healing only in three of 18 patients, which is a little bit disappointing, but the primary goal is to get a stable wound
and to avoid amputation, actually. You get a really significant decrease of wound surface, so our results actually were even more successful than this first publication, that there is no much more data available from literature. This is a very special example here,
from presternal necrotic skin flap, which was also treated with Kerecis Omega3 and with mesh graft in the end. So this was a very special case which also was healing. Here you see the time to heal again. It takes a long time, up to 100 days for the healing.
And you see the Hamburg cases here, the wound reduction to 20%, but with some cases 60-80%, and only half of the occasions really complete healing. So in summary, in the shortness of time, summarize that Omega-3 wound matrix is,
for us at least, a innovative biological decellularized wound dressing from cod skin, which works in complicated wounds, in the lower limbs especially. And before they are applicated, there needs to be an effective debridement,
adequate tissue perfusion, and infection control. And weekly dressing changes are absolutely sufficient, so this means that outpatient treatment is possible. Thank you very much for your attention.
So I'm a consultant for both of those. Okay, so repair of coarctations. So surgical repair is effective, has a low procedural mortality and morbidity, and so does stent implantation. But the mortality is very, very low with stents, and the morbidity is also lower in general.
Whatever method you choose, though, both methods are going to be complicated by hypertension, re-intervention for stenosis and aneurysm formation, which is normally just a question of time if you follow up the patient for long enough because the post-stenotic dilatation,
cystic medial necrosis, calcification, it's a sick wall. So the potential advantages of using a covered versus a bare stent versus angioplasty is that the angioplasty just tears, and we don't do angioplasty on native coarctations. But you put a stent in and you get this creation
of a longitudinal framework, and if you have a covered stent you're going to control the integrity of the vessel at the coarctation and below it, which is normally a very dangerous area, the poststenotic dilatation area. And they're particularly useful using covered stents
when there's an aneurysm which is present. However, there's no good studies to say that's really the right thing to do. So recently Tretter and McElhinney, they looked at all the reports that had been done for endovascular therapy for aortic coarctation,
and they noted that aortic rupture was particularly rare, less than 1%. Acute aneurysm formation, when intervening for endovascular therapy, was about up to 13% for angioplasty, up to 5% for bare metal,
and less than 1% after covered stents. But it depends on the reporting bias and there's a lot of inconsistent definitions. And overall, the acute wall injury seems to be going down for coarctation due to better delivery systems, more use of covered stents.
And there are really only three covered stents, which are balloon expandable, and the CP covered stent, which comes bare and covered, and it's stuck on quite loosely, the Atrium V12LD which is not available for the last two years,
which goes up to 22 millimeters, and the aortic BeGraft which comes in a whole range of sizes and covered. This is the Atrium V12LD with stainless steel covering the inside and the outside, and the BeGraft is chromium cobalt
and it's covered on just the outside. So, when you're doing the covered stents, you need to consider the vascular access damage that can be done because you need a relatively large delivery system, and I'm a pediatric cardiologist,
so using these in small kids you have to be very careful, and the CP stent can take even 11 to 12-French system. The stent integrity, because the CP Platinum-Iridium stents tend to fracture, the Atrium has a problem of infolding, and the Bentley is quite a strong stent and I've had no problems with it,
but it's early days yet. And the other thing is the covering integrity. The CP is incomplete while the Atrium and the Bentley seem to have a better cover. So looking at the COAST I study, which was a look at the CP stent,
which was a bare stent, they did 105 patients underwent attempted implantation, and just looking at sort of the aneurysm, the aortic wall injury, they did balloon dilatations just for some compliance testing, which I never do, and they generated some small
aortic aneurysms showing that that area is a problem. And in intermediate followup when they put in bare stents, they had a total of six aortic aneurysms, five were successfully treated with a covered stent placement and one resolved without intervention,
and they had some stent fractures. Then what they did, they did a COAST II study, which was looking at the CP covered stent, which was used, and they used it in a total of 158 patients. 83 had had previous intervention and had some aortic wall injury.
And when they were using that stent, complete coverage of the pre-existing aortic wall injury was achieved only in 92% of the patients, and seven patients had minor endoleaks. The other thing is, so that shows that the covering wasn't that good.
The other thing was is it takes a large delivery system four patients experienced important vascular site injury. In the Advanta trial the covered stents were very good, in general, for getting the blood pressure down, getting the gradient down, and increasing the diameter. And also, comparing sort of the long-term followup,
we followed the blood pressure for three years, the blood pressure stayed down and we had a very good result. The major problem was they had very small problems with femoral artery occlusion only in one patient compared to the four in the CP stents.
So there was one small aortic hematoma treated with a second stent, but the major problem was the stent wasn't robust enough in the aorta and had infolding. Two of which required urgent reintervention. The Bentley, which is a relative,
and we've had it since January 2017, so this is, let's say, a complex native coarctation. So we treated that with a BeGraft. And here you can see this is another patient, a little Bedouin girl, that had an endovasculitis and a coarctation,
and she was treated with a CP stent, which was covered, but you can see the aneurysm stayed. We put the, another Bentley stent in there. So you can see that the covering, even when using covered stent, is not necessarily always the right thing.
We've done now 22 patients with a Bentley BeGraft. You can see the median age and all different types of coarctations which have been previously treated or native. Overall, it gets down the gradient and the coarctation diameter stays up.
We had no acute wall injury and no other immediate complications. Patients that had pre-existing aneurysms, ones which you saw, was successfully treated, and at median followup things look good. So in conclusion, surgery, in my institution,
is the primary choice of intervention in patients who endovascular stenting is not possible. So infants and small children we won't do a balloon angioplasty because it tears the intima and they have aneurysms afterwards. If we can put in a covered stent,
that's our first choice. Safe and effective acute treatment of coarctation and associated with less aortic wall injury than bare metal and balloon angioplasty, but you need a lot of reintervention. The choice of the covered stent,
you need to consider delivery system, the maximum diameter of the stent, the stent integrity, whether it's going to fracture or infold, and the covering integrity. And when all is said and done we still need to have long-term followup imaging.
Thank you very much.
- Jim, thanks so much, and thanks to Doctor Veith for the opportunity to get involved. Here's my disclosure. So, certainly you don't want to be an expert on limb thromboses, however, it happens. And so, when you see these patients, no longer are we looking at fem-fem,
or even lytics, catheter-directed lytics. So how do we get from screen left to screen right in a single session therapy? Well, as we know, when these patients present, there's several different management options. You can do open thrombectomy with or without
a fem-fem, pharmacomechanical thrombectomy. There's catheter delytic and ultrasound accelerated thrombolytics, and then now, today, we have vacuum-assisted thrombectomy, as we've heard throughout this session, or continuous aspiration thrombectomy,
however you want to mention it. Regardless, when you end up with lytics, this is exactly what you're dealin' with. You're playing with fire, and if we do it long enough, you're going to see this complication. So we've really adopted a clot extraction
instead of a clot dissolution policy at our institution. I think Jim just showed you this technique that is afforded to us by the Indigo thrombectomy system, as you can see here in a Vivo model, this catheter actually does work extremely well.
It'll remove this soft thrombus, as you can see here. My first experience with this was actually for an occluded popliteal stent, as you can see here. We had a occlusion of the standard nitinol stent. This aspiration power was incredibly surprising to me. As you can see, it collapsed the standard nitinol stent.
So at that point, several years ago, we realized how good this device was, and how we want to minimize lytics for our folks. So we started in 2014 and recently this year at the Midwest Vascular forum in Saint Louis, we presented our data.
At that time, we had 73 patients over the years with acute limb ischemia. And here you can see the breakdown. For this presentation I'm going to focus on this cohort here, which is seven. But as you can see, like my panelists here,
we use it for occlusions, for not only occlusions but emboli as well, and also we had one case of an upper extremity embolism that we were able to successfully treat with this device. At that time, again, looking at all 73 patients,
you can see here that it's a very efficacious device. There were a couple folks who needed transfusion and perhaps the blood loss was a little higher than 300. However, as you can see here, the folks who had a blood loss, all five had open adjunctive interventions as well, and the ones who needed transfusion
all had catheter directed lytics as adjunctive therapy. As far as our efficacy endpoints, what we looked at was antegrade flow. As you can see here, oftentimes with your vacuum system thrombectomy, you're able to get antegrade flow. However, intermittently there's also other
adjunctive therapies that we had to use frequently as well. Going back to what, you know, my topic for today, how do you go from screen left to screen right, where here you can see one of our patients who came in. We did a retrograde ipsilateral stick,
crossed the lesion with the wire, then we delivered our eight french Indigo catheter and were able to get, in a single session, as you can see here, antegrade flow. So here's another, all this in one single session therapy. Here's another patient of ours.
As you can see to the left, one of our Gore Excluder limbs had occluded, and again, with single session therapy we were able to provide patency to that occluded right limb. Another case here, you can see one of our other Medtronic grafts.
And what you'll see here as you're looking to the right, here we are with our eight french Indigo catheter, is the separator, which is like a pipe cleaner. And we were able to clear out this clot and provide patency to this
all in a single session therapy. And again, here you can see from left to right how we were able to thrombectomize that limb. So over the years, the last three years, we do about 80 to 90 EVARs a year. During that time period, we have seven patients
come in with limb occlusions. And as you can see here, four of them were chronic, three claudicants and one res-pain, and three of them were acute limb Rutherford one, two A or two B. As you can see here, 42% of the time for these
occluded limbs, we were able to do it with no lytics, not even a pulse spray, nothing, not one drop of lytics. As you can see here, some of them we did have to do it in a single session. What we do is use a McNamara catheter.
We would squirt out, you know, anywhere from, as you can see, 14 to 18 milligrams of lytics, go get a cup of coffee, go make rounds, come back 20 minutes later, then utilize your device. And again, you can see, in a single session therapy we were able to afford patency.
And then finally, you can see here the blood loss was minimal. So this is a safe device. So in conclusion, I think that single session therapy is safe. It can facilitate achieving antegrade flow
in the management of stent graft limb occlusions. And single session therapy is the future of not only stent graft limb occlusions but all acute limb ischemia. Thanks so much.
- Thank you very much Germano. Thanks to Dr. Veith for inviting us and allowing us to present this here. This is work that we've done in a group in Hamburg together with Nikolaos Tsilimparis. And these are my disclosures. It's been now, more than 15 years ago
that branched endografting has been introduced as a technique for thoracoabdominal aneurysms. And for about five years we have access to the T-Branch device as we've learned from the presentations before. And as we heard from Mark Farber
there's more companies going into that space. In Europe it's also the JOTEC company, which is CryoLife now, and we will, I believe, see more companies going into this space. So, about access, we've been discussing in the past
very much about whether right or left side is the better, or safer, access for branched TEVAR, and at that moment in this publication from our center, we phrased this, the unavoidable use of an upper extremity access. We show you that we've been believing that it's unavoidable.
But is it really unavoidable? In some cases I believe it should be avoided, because we have aortic branch vessels that are occluded, thrombotic, we have AV-fistulas and LIMA Bypasses that we may risk. And we may have antegrade branches
from previous artery repair which we would judge as almost a no antegrade access option here. So what can we do in those cases? And furthermore, upper extremity access has complications and it comes at a cost.
Not only hematoma and nerve damage, plexus damage at the access site, but also stroke is reported being a complication of arm access. We've looked into our experience from two years and found that about 5% of patients needed
some sort of re-operations from complications of upper extremity access, and this is just one of the more severe complications we had with a brachial on the stick due to too small access vessels. Another point is radiation.
Because radiation also as we've shown here, this is unpublished data, is significantly higher if a operator stands at the arm compared to standing at the groin. Is it really unavoidable? If we think about this as our traditional access,
but how about this? I know this has been used a lot in fenestrated endografting. But we started applying this technology also for branched endografting to avoid upper extremity access. First case that we did was a patient
that had an irregular orifice of the right renal artery and it was only one branch that we didn't want to go through all the hassle with upper extremity access. You see here, steerable sheath. You can very well attach that artery without upper extremity access.
Next case, for fenestrated and branched, then have one branch difficult celiac artery, very small stenotic orifice from a large aneurism, but it was attachable from the groin, a good result. Next case, two branches, two fenestrations. As you can imagine,
it also went well for the SMA and for the celiac with a good result without the need of touching arm, without the need going through the arch. This is a more severe one. This is a redo after EVAR patient with an occluded one-sided iliac lack
and a crossover bypass. This is the SMA. This is the right renal artery. You see that we were able to complete this repair from one access side alone, doing a full four-branch thoracoabdominal repair using steerable sheaths.
This series has been recently published as a case series, but we have extended on that experience. I can tell you in all patients that we tried to do it, it was possible to avoid the upper extremity access. Concluding: Endovascular repair has matured over years
and can, in my view, be considered gold-standard for thoracoabdominal repair. Upper extremity access is avoidable if possible. Success rate of femoral access with steerable sheath is safe. And I thank you very much for your attention.
- So this is what I've been assigned to do, I think this is a rich topic so I'll just get into it. Here are my disclosures. So I hope to convince you at the end of this talk that what we need for massive PE when we're talking about catheter based therapy is a prospective registry. And what we need for catheter based therapy for
submassive PE is a randomized controlled trial. So we'll start with massive PE and my rational for this. So you know, really as you've heard, the goal of massive PE treatment is to rescue these patients from death. They have a 25 to 65% chance of dying
so our role, whatever type of physician we are, is to rescue that patient. So what are our tools to rescue that patient? You've heard about some of them already, intravenous thrombolysis, surgical embolectomy, and catheter directed therapy.
The focus of my talk will be catheter directed therapy but let's remember that the fastest and easiest thing to do for these patients is to give them intravenous thrombolysis. And I think we under utilize this therapy and we need to think about this as a first line therapy for massive PE.
However, there's some patients in whom thrombolytics are contraindicated or in whom they fail and then we have to look at some other options. And that's where catheter directed therapy may play a role. So I want to show you a pretty dramatic case and this was an eye-opening case for me
and sort of what launched our PERT when I was at Cornell. It's a 30 year old man, transcranial resection of a pituitary tumor post-op seizures and of course he had a frontal lobe hemorrhage at that time. Sure enough, four or five days after this discovery
he developed hypertension and hypoxia. And then is he CT of the chest, which I still remember to this day because it was so dramatic. You see this caval thrombosis right, basically a clot in transit
and this enormous clot in the right main pulmonary artery. And of course he was starting to get altered, tachycardiac and a little bit hypotensive. So the question is, what to do with this patient with an intracranial hemorrhage? Obviously, systemic thrombolytics are
contraindicated in him. His systolics were in the 90 millimeter of mercury ranged, getting more altered and tachycardiac. He was referred for a CDT and he was brought to the IR suite. And really, at this point,
you could see the multidisciplinary nature of PE. The ICU attending was actively managing him while I was getting access and trying to do my work. So this was the initial pulmonary angiogram you can see there's absolutely no flow to the right lung even with a directed injection
you see this cast of thrombus there. Tried a little bit of aspiration, did a little bit of maceration, even injected a little TPA, wasn't getting anywhere. I was getting a little bit more panicked as he was getting more panicked
and I remembered this device that I had used in AV fistula work called the Cleaner. Totally off label use here, I should disclose that and I have no interest in the company, no financial interest in the company. And so we deployed this thing, activate it a few times,
it spins at 3,000 rpm's, he coughed a little bit, and that freaked us all out also. But low and behold we actually started seeing some profusion. And you can see it in the aortogram actually in this and that's the whole point of massive PE treatment with CDT,
is try to get forward flow into the left ventricle so that you have a systemic blood pressure. Now, you know, when we talk about catheter based therapies we have all sorts of things at our disposal. And my point to you is that you know really, thank you...
You guys can see that, great. So really, the point of these catheter therapies is that you can throw the kitchen sink at massive PE because basically your role is to try to help this patient live. So, if I can get this thing to show up again.
There we go. It's not working very well, sorry. So, from clockwise we have the AngioVac circuit, you have, let's see if this will work again, okay. Nope, it's got a delay. So then you have your infusion catheter,
then you have the Inari FlowTriever, you saw the Cleaner in the previous cast, and you have the Penumbra aspiration device the CAT 8. And some of these will be spoken about in more detail in subsequent talks. But really, you can throw the kitchen sink at massive PE
just to do whatever it takes to get profusion to the left side. So, the best analysis that has been done so far was Will Kuo in 2009. He conducted a meta-analysis of about 594 patients and he found this clinical success rate of 86.5%.
This basically meant these patients survived to 30 days. Well, if that we're the case, that's a much lower mortality than we've seen historically we should basically be doing catheter directed therapy for every single massive PE that comes into the hospital. But I think we have to remember with this meta-analysis
that only 94 of these patients came from prospective studies, 500 came from retrospective, single center studies. So even though it was a very well conducted meta-analysis, the substrate for this meta-analysis wasn't great. And I think my point to you is that
we really are going to have a hard time studying this in a prospective fashion. So what is the data, as far as massive PE tell us and not tell us? Techniques are available to remove thrombus, it can be used if systemic lysis is contraindicated,
but it doesn't tell us whether catheter based therapies are better than the other therapies. Whether they should be used in combination with them and which patients should get catheter based therapy, which should get surgery and which techniques are most effective and safe.
Now, I think something we have to remember is that massive PE has a 5% incidence which is probably a good thing, if this was even higher than that we would have even more of an epidemic on our hand. But this is what makes massive PE very difficult to study.
So, if you looked at a back of the envelope calculation an RCT is just not feasible. So in an 800 bed hospital, you have 200 PE's per year, 5% are massive which means you get 10 per year in that hospital, assume 40% enroll which is actually generous,
that means that 4 massive PE's per year per institution. And then what are you going to do? Are you going to randomize them to IV lytics versus surgery versus interventional therapy, a three arm study, what is the effect size, what difference do you expect between these therapies
and how would you power it? It's really an impossible question. So I do want to make the plug for a Massive PE Prospective Registry. I think something like the PERT consortium is very well-suited to run something like this
especially with this registry endeavors. Detailed baseline characteristics including all these patients, detailing the intervention and looking at both short and long-term outcomes. Moving on to submassive PE. As you've heard much more controversial,
a much more difficult question. ICOPER as you already heard from the previous talk, alerted the world to RV dysfunction which this right ventricular hypokinesis conferring a higher mortality at 90 days than no RV dysfunction. And that's where PEITHO came in as you heard.
This showed that the placebo group met the primary endpoint of hemodynamic decompensation more commonly than the Tenecteplase group. Of course, coming at the risk of higher rate of major bleeding and intracranial hemorrhage. So I just want to reiterate what was just said
which is that systemic thrombolysis has a questionable risk benefit profile and most patients with submassive PE, as seen in the guideline documents as well. So that sort of opens a sort of door for catheter directed therapy.
Is this the next therapy to overcome some of the shortcomings of systemic thrombolysis? Well what we have in terms of CDT is these four trials, Ultima, Seattle II, Optalyse, and Perfect. Three of these trails were the ultrasound assisted catheter, the Ekos catheter.
And only one of them is randomized and that's the Ultima trial. I'm going to show you just one slide from each one of them. The Ultima trial is basically the only randomized trial and it showed that if you put catheters in these patients 24 hours later their RV to LV ratio will be lower
than if you just treat them with Heparin. Seattle II is a single arm study and there was an association with the reduction in the RV to LV ratio at 48 hours by CTA. PERFECT, I found this to be the most interesting figure from PERFECT which is that you're going to start it at
systolic pulmonary artery pressure of 51 and you're going to come down to about 37. Optalyse, a brand new study that was just published, four arms each arm has increasing dose associated with it and at 48 hours it didn't matter, all of these groups had a reduction in the RV to LV ratio.
And there was no control group here as well. What is interesting is that the more thrombolytics you used the more thrombus you cleared at 48 hours. What that means clinically is uncertain at this point. There is bleeding with CDT. 11% major bleeding rate in Seattle II,
no intracranial hemorrhages. Optalyse did have five major bleeds, most of the major bleeds happened in the highest dosed arms. So we know that thrombolytics cause bleeding that's still an issue. Now, clot extraction minus fibrinolytic,
this is an interesting question. We do have devices, you're going to hear about the FLARE trial later in this session. EXTRACT-PE is ongoing which we have enrolled about 75 patients into. What the data does and does not tell us
when it comes to CDT for submassive PE it probably reduces the RV to LV ratio at 24 hours, it's associated with a reduction at 48 hours, major bleeding is seen, we do not know what the short and long-term clinical outcomes are
following CDT for submassive PE. Whether it should be routinely used in submassive PE and in spite of the results of Optalyse this is a preliminary trial, we don't know the optimal dose and duration of thrombolytic drug. And even is spite of these early trials
on these non-lytic techniques, we don't know their true role yet. I'd liked to point out that greater than 1,600 patients have been randomized in systemic lytic trails yet only 59 have been randomized in a single, non-U.S. CDT trial.
So this means that you can randomize patients with submassive PE to one treatment or the other. And we want to get away from this PERT CDT roller coaster where you get enthusiasm, you do more cases, then you have a complication, then the number of cases drops.
You want that to be consistent because you're basing it on data. And that's where we're trying to come up with a way of answering that with this PE-TRACT trial. Which is a RCT of CDT versus no-CDT. We're looking at clinical endpoints
rather than radiographic ones greater than 400 patients, 30 to 50 sites across the country. So in summary I hope I've convinced you that we need a Prospective Registry for massive PE and a Randomized Controlled Trail for submassive PE. Thank you.
- [Interviewer] I mean it's got to be challenging to discuss a graft that none of us have seen but we can start with Jim. Jim can take on anything. What do you think of this new B graft? - [Jim] Well, yeah, I have fortunately been able to see it over in Europe and being teased by it. I guess the concern I have is the thickness of the fabric.
It seems like it is two layer of PTFE and stent sandwiched in between, so you're getting thicker and thicker so if you're using a smaller B Graft Plus, are you concerned about low flow and thrombosis with it? - You may say so.
First of all, it's only the B Graft Plus that has that dull technology and the reason is clearly that it's designed for branches and usually you use, now a days, branches in the larger vessels, mostly the celiac and SMA. We have gone done is using branches for renal arteries
for that precise angle having to reline, because let's be honest, if you use an autograft, you will very much more likely reline it with a self expandable stent to prevent the kinking, so the end result is the same.
So the answer to your question, Jim, is no, I'm not concerned more than with any other bridging stent graft. - And what about the distal flexibility of the B Graft. I mean, that's kind of what's driven me to go to VBX is that, you know, I had a couple patients that came in that
they kind of kinked and you had one in your series there. The VBX tends to be much more flexible distally. - Yeah, I am probably the only guy in this world that is not completely convinced yet by the VBX and I've listened to you, I've listened to Gustave, and to Mark Farmer,
and I hear a few little things here and there. The flexibility is excellent, the tactile feeling of that graft is excellent. I agree that the B Graft Plus feels much harder, but it is very kink resistant and that's why I pointed out
that's the transition though is still important because that indeed is, can in an angle be a problem. So you have to choose it correctly. - So, Jim, in the VBX, and you've done a lot of cases, how often did you have to put an additional stent to fix a kink?
- The only time I've ever had to put another is for length. I've never had to reinforce or put a self expanding end. For like the one that I showed where I went from did it as a parallel graft going all the way down, I had to use two there because they only come in 79 and the one problem we have is when you start,
like any balloon expandable stent, when you start oversizing it and they actually have eight that will go to 16 as Chris pointed out, but it will start for shortening, but I have not had problems where I had to support it with a self expanding stent.
- But also when you enlarge it, you lose some of the radio force, no? Probably the reason you didn't have a kink is because the area that you, actually, the area that could be kinked is not dilated enough. You want to dilate approximately or distant it to fit more
of the the anatomy then you lose of the radio force, I guess. Theoretically at least. - Only the 8L is really expandable beyond two millimeters. So a six you can dilate up to an eight. So I really haven't seen that tremendous for shortening
except with the L, and obviously I'm not going to put an 8L into a renal or a vishal vessel. - The length of the Bridging Stent Graft is interesting though. We are doing far more fenestrations, and if we do Branch Grafts is usually grafts with both
fenestrations and branches, and you have to deploy these grafts based on the position of the fenestrations, and then you plan your branches to be fairly near through the target vessels. Say you end up using more like six centimeters instead of eight centimeters.
We virtually don't use the 79 or the eight millimeters Covera anymore. Having said that, there are new designs, designs from other companies coming out where you are planning even longer Bridging Stent Grafts up to ten 15 centimeters but we will have to see wither that
induces new risks. - I think that was one thing that we found interesting 'cause we also use them for parallel grafts and then you do need longer ones because in the cuffs we never put more than two parallel grafts at any one place, and so if I'm doing it, I'll do like a celiac SMA
and I'll put cuff in there and I'll come down and I'll do the renal so as parallel for torrical abdominal, since we don't have readily available access to the stuff that you have. But then I need longer, so if anything I'd like to see longer than 79,
just for some of these other grafts and the advantage is you go in, you put a six in, and you can flare it to eight to go in the celiac and SMA but you gutters only at a six. - Chris I have a, just one second - Chris the SFA, the VBX for the SFA, when is an over kill and when do you think
it's absolutely decaded? - For the SFA? - SFA. - Yeah, I got to say, I have not used a balloon expandable stent in the SFA very often. I guess if you really had an hospitable reason
that you really needed a stent in precision and short maybe you'd use it. You know, I think the title given here was a misnomer because it was a two year results instead of SFA trial. Truth be told I've used a whole lot of them in the aorta and the iliac and some of the extensions that Jim and
Eric have talked about but I've never used one in the SFA. I think it would be, you know I think if we have other options for the SFA, the viabahn, nitinol stent and then you could reinforce that if you needed to with an interwoven stent if you really needed a pave in graft.
I've not used it in the SFA. - Any question from the audience? We have a couple of extra minutes. - Is the cuffs playing a role for the VBX because in Europe it's clearly more expensive other bridging stent grafts and I heard from the Munster Group,
off the record, when they do chimneys with the VBX the reline it to increase the retinal force. So what about the radio force? - We followed ours going up to two years or as long as VBX has been available for that, we haven't an increase instance of crush or need
for relining. The cost is, and all cost is local, but a 018 viabahn is more expensive in our office than the VBX of equivalent size and length. - And that's the same in our lab as well. - Yes sir.
Introduce yourself and ask the question please. - [Eka] I'm Eka Jaan, so sorry, I'm from Hartford. Question for Doctor Mackenzie regarding the VBX and the fenestrations. Do you have any concerns with the unsupported portion of the VBX at the transition zone with the fenestrations,
it's not supported there so can it collapse or can there be offset between the fenestrations? - That certainly was a concern. I always deploy my stents as 90 degrees the axis so if I've got a four dot fenestration and I turn it to a three dot so I know I'm right perpendicular and I literally will
try and land between the two wire forms so it expands and actually kind of as the grommet seals there, and all the ones we have done we have no had any endoleaks at the approximate aspect of the stent and quiet candidly I'd rather have a leak there than include a stent at distal aspect 'cause I can always come in and put a
balloon expandable which, of course I haven't had to do. - Yes, last question. - [Andy] Hi, Andy Plum, Chicago. Along those lines, yesterday the Munster Group was doing a workshop and they actually favored the Atrium stent over the VBX.
For that reason, they are saying they've seen with the VBX, because the stents are independent without a cross bridge that they've actually seen shortening like accordioning with time with their ChEVARs. Now this was a medtronic presentation, little bit biased towards medtronic,
but they were actually favoring the Atrium stent for their ChEVARs. - My problem is the rigidity of the Atrium stent and it's crushability. Here you've got a little bit more play, David Muino would come out and tell is to do
the eye of the tiger with that and you can do that it but I have not seen for sure accordioning of it especially in a graft that you're using as a parallel graft. Now I guess at the very top you could, it may come down a little bit above the area of where you're
interfacing with the graft but it's going to give it more stability so I'm just not seeing that being a problem, either with implantation or long term follow up. - Thank you.
Thank you, Mr Chairman. In order to avoid unnecessary repetition, I'm going to try to move forward with some of my slides. There we go. And, again, in order to avoid that, we're just going to move through the cases. I have some cases that are different
to the ones presented before. It seems that everybody's happy with this technology. This is a CTO recanalization of a patient with subacute total occulsion of the SFA that previously had a stent in place,
in the distal SFA. And here you can see how we are able to reopen the vessel and look at the clot in the entire length at the end of the catheter there. So, this technology really works.
Let me show you now an acute bowel ischemia case. A patient that comes with abdominal pain. A CTA shows that the patient has an occlusion of the proximal SMA. We put a catheter there,
we do a diagnostic angiogram confirming the occlusion, then we cross the lesion and we inject distali showing that the branches are patent. And then we put in place
an oscar directional sheath that will give us great stability to work and through that one we use a Cat Eight, from Penumbra. As you can see here, advancing the catheter in combination with the separator,
and this is the final angiogram showing complete opening of the main SMA and you can see very clearly the elements that were occluding the MSL. We are also using this technology in DVT, acute DVT, with proprietal access
and here you can see the before, and then, sometimes we use it alone, sometimes we use it in combination with angiojet and with the bull spray, followed by this technology for the areas that did not respond.
But this is usually a technology that is helping us to get rid of most of the clot. Like here, you see there is some residual clot. And after Penambra, you can direct the catheter and you can really clean the entire vein. Same here, before and after.
We are also using it for PE. I know that you guys in Miami are doing the same and we are happy with the results. And then, just to finish, I think this is a really nice case that was done by one of our partners in vascular surgery.
A patient with an occluded carotid subclavial bypass. So you see access from the brachial artery on one side. And this person, the person who did this, was smart enough to also came from the groin
and put the filter in the internal carotid artery, just in case. So then he starts to manipulate that occluded subclavial carotid bypass. As you can see here. And at a certain point,
he does a follow-up angiogram showing that the entire carotid, including the internal and external, is totally occluded. So, because he was prepared, he had a filter,
he didn't panic, he went and used the indigo device, and he was able to get all that clot out and re-establish nice anterial flowing in the carotid artery,
completely clean. The carotid subclavial bypass. And he did a final angiogram in AP and lateral view, confirming that there is no distimbolisation at the intercranial level. So, this technology really works.
I think that we all agree. And these are good examples on how we can help patients with that technology. Thank you for your attention.
- Thanks (mumbles) I have no disclosures. So when were talking about treating thoracoabdominal aortic aneurysms in patients with chronic aortic dissections, these are some of the most difficult patients to treat. I thought it would be interesting
to just show you a case that we did. This is a patient, you can see the CT scrolling through, Type B dissection starts pretty much at the left subclavian, aneurysmal. It's extensive dissection that involves the thoracic aorta, abdominal aorta,
basically goes down to the iliac arteries. You can see the celiac, SMA, renals at least partially coming off the true and continues all the way down. It's just an M2S reconstruction. You can see again the extent of this disease and what makes this so difficult in that it extends
from the entire aorta, up proximally and distally. So what we do for this patient, we did a left carotid subclavian bypass, a left external to internal iliac artery bypass. We use a bunch of thoracic stent grafts and extended that distally.
You can see we tapered down more distally. We used an EVAR device to come from below. And then a bunch of parallel grafts to perfuse our renals and SMA. I think a couple take-home messages from this is that clearly you want to preserve the branches
up in the arch. The internal iliac arteries are, I think, very critical for perfusing the spinal cord, especially when you are going to cover this much. And when you are dealing with these dissections, you have to realize that the true lumens
can become quite small and sometimes you have to accommodate for that by using smaller thoracic endografts. So this is just what it looks like in completion. You can see how much metal we have in here. It's a full metal jacket of the aorta, oops.
We, uh, it's not advancing. Oops, is it 'cause I'm pressing in it or? All right, here we go. And then two years post-op, two years post-op, you can see what this looks like. The false lumen is completely thrombosed and excluded.
You can see the parallel grafts are all open. The aneurysm sac is regressing and this patient was successfully treated. So what are some of the tips and tricks of doing these types of procedures. Well we like to come in from the axillary artery.
We don't perform any conduits. We just stick the axillary artery separately in an offset manner and place purse-string sutures. You have to be weary of manipulating around the aortic arch, especially if its a more difficult arch, as well as any thoracic aortic tortuosity.
Cannulating of vessels, SMA is usually pretty easy, as you heard earlier. The renals and celiac can be more difficult, depending upon the angles, how they come off, and the projection. You want to make sure you maintain a stiff wire,
when you do get into these vessels. Using a Coda balloon can be helpful, as sometimes when you're coming from above, the wires and catheters will want to reflux into that infrarenal aorta. And the Coda balloon can help bounce that up.
What we do in situations where the Coda doesn't work is we will come in from below and a place a small balloon in the distal renal artery to pin the catheters, wires and then be able to get the stents in subsequently. In terms of the celiac artery,
if you're going to stent it, you want to make sure, your wire is in the common hepatic artery, so you don't exclude that by accident. I find that it is just simpler to cover, if the collaterals are intact. If there is a patent GDA on CT scan,
we will almost always cover it. You can see here that robust collateral pathway through the GDA. One thing to be aware of is that you are going to, if you're not going to revascularize the celiac artery you may need to embolize it.
If its, if the endograft is not going to oppose the origin of the celiac artery in the aorta because its aneurysmal in that segment. In terms of the snorkel extent, you want to make sure, you get enough distal purchase. This is a patient intra-procedurally.
We didn't get far enough and it pulled out and you can see we're perfusing the sac. It's critical that the snorkel or parallel grafts extend above the most proximal extent of your aortic endograft or going to go down. And so we take a lot of care looking at high resolution
pictures to make sure that our snorkel and parallel grafts are above the aortic endograft. This is just a patient just about a year or two out. You can see that the SMA stent is pulling out into the sac. She developed a endoleak from the SMA,
so we had to come in and re-extend it more distally. Just some other things I mentioned a little earlier, you want to consider true lumen space preserve the internals, and then need to sandwich technique to shorten the parallel grafts. Looking at a little bit of literature,
you can see this is the PERCLES Registry. There is a number of type four thoracos that are performed here with good results. This is a paper looking at parallel grafting and 31 thoracoabdominal repairs. And you can see freedom from endoleaks,
chimney graft patency, as well as survival is excellent. This was one looking purely at thoracoabdominal aneurysm repairs. There are 32 altogether and the success rates and results were good as well. And this was one looking at ruptures,
where they found that there was a mean 20% sac shrinkage rate and all endografts remained patent. So conclusion I think that these are quite difficult to do, but with good techniques, they can be done successfully. Thank you.
- Here are my disclosures. Okay, so I'm going to start things as well with an unknown case. This is a 29 year old Caucasian male with severe shortness of breath, diaphoresis, low blood pressure, worsening fatigue and was recently seen to be subtherapeutic on his warfarin dosing.
His history included antiphospholipid antibody syndrome, lupus anticoagulant positive and what test do we start with? A CT, a VQ scan, ultrasound, MRI, what additional tests might we get? So, you know, I'm going to quote the man sitting next to me here and it's important to remember
and this will come up throughout our discussion here. Is the yield of a CT pulmonary angiogram is actually relatively low, that's because of, as Dr. Calori just mentioned, if you suspect it, you should get it off the table. And it's Gestalt really does matter, especially, expertise,
I think doesn't always factor into these published studies, but if you're Gestalt tells you, you should look, you should look, we should really lower the burden, the bar to looking. If you look, when there's no thromboembolic risk factors, that's exceedingly low, so something like two percent.
If you look at, so let's take that six, that low yield and then let's look at those patients and what happens to them. If you look at the positive PE studies, out of the broad number of scans we do, only a very small fraction will have mortality.
So you're talking about, in this highest risk, the massive pulmonary embolism, only five percent of patient qualify as massive PE and just over half of those will actually have a mortal PE. Whereas the submassives, a large number of 40%,
22% morality and then the low risk ones, they do pretty well, it's over less than one percent and that's more than half. You know, when we do a CT scan, just to say we're going to make the diagnosis in the first place, you're going to look for filling defects.
So the whole basis of the exam is just, is there absence of filling of a pulmonary artery with contrast, if it's timed appropriately, we should have no problem doing this. So you can see, in the middle, you've got a central pulmonary embolism, on the right and left branches here,
you can see these are low bar PEs, but they're also peripheral. So they're not central, you can actually see the calcification on the left here. So it's not quite the simple story of just this is a PE, you can see, that the calcification is a mark
of chronic thrombus and the peripheral location chronicity. The appropriate criteria and you can read any one you like, I just picked the ACR from 2016 shows, that short of X ray CTA is the first test you should do. And part of the reason, I think CT and X ray trump the VQ scan is, that you can see alternative diagnosis
and when the yield is low, you can look for other causes. The other thing is, that the VQ scan is a little more cumbersome and a CT scan is much more available in most locations. So we're going to look at the CT scan, we're going to look for filling defects,
the character of the defect, location, the shape of it. The calcification, chronicity, positioning within the pulmonary radially. The burden of the thrombus overall, we have seen, that it's really not going to predict outcomes. And then there's other findings, that are ancillary
regarding pulmonary embolisms, such as bronchial artery hypertrophy and cardiac chamber enlargement, especially the right ventricle. You can see here, when you look at the, on the bottom right image here, that's an invasive angiogram and you can imagine why there's difficulty seeing
what's not there. It's not, that we don't see the filling defect in this large left lower lobe pulmonary embolism, it's that you don't know where the vessel should be and then the CT, it shows the location of the vessel and then the lack of filling within it.
When we're going to look at the chamber enlargement, the first thing you should do is look for right heart enlargement, it's for free. You're probably making this as your initial test, although, if you're highly efficient, like Roger, then you're actually doing the echo in your clinic
and then sending the patient, but the CT scan images the heart anyway, so why not take a look. You know, there's been a bunch of publications, some looking at doing cardiac reformatting to look at the heart the way we would look with an echo. And that's nice, that cost time and energy
and not always available, not already all of us have the skill, not all departments have the workstations. It turns out you don't need to, you can look for RV to LV enlargement. For the purpose of this slide, I just picked on a single image, but you're actually allowed
to look at different slices. And you're looking for ratio to keep it simple, greater than one. So if the intraluminal diameter of the right ventricle is greater than the left ventricle, which, even though, we don't have a great left sided contrast on this image,
you can still see it. That's a ratio greater than one and you can train most radiologists to do that, even if they're not comfortable with doing special processing and reformatting. Now, if you want to get fancy and do a cardiac gated CT
or even an MRI, you can and just starting with CT, since you're already using that as your gold standard diagnostic test, you can do ECG gating in the temporal resolution of CT scans, it's as low as 66 milliseconds. Just a few years ago, it was as high as 200 milliseconds,
so that's the time, the number of projections to acquire enough data to make one image. So when you look at that, you can really see the heart, even when you don't intend to and if you do it with an ECG mapping, you can actually get multiple frames in time and with a price of a little bit
of increased radiation, you can get moving, beating images, like this. But now you've got a lot more data, that's more time to cross over to your data archive, more time to interpretation. And you need to think about the yield.
So basically, for about, you know, a three milli sec at the right and left heart function, the amount of time to analyze that accurately takes time. You can see here, we can also look at the coronary arteries. You'd probably want to give nitro glycerin, if you were doing a full coronary rollout, if possible.
We can look at coronary plaque. You can reformat the images, you can even see there's a volume rendered on the bottom right here. Volume's over the RV at endo diastolic and then endo systolic. So you can actually get the true RV ejection fraction.
Which does have some prognostic significance. Dual energy CT is another way to use modern technology and this is kind of becoming our standard of care at our hospital. One of the reasons is patients like this. This is a very large patient, BMI was 44,
a lot of risk factors and high clinical suspicion and you can see on the single energy reformat is the way of strolling actually here. It's a little difficult to see those filling defects, but what you can do is take that source image and then you can deconstruct it into different energies,
so it's sort of like playing with a bass and a tremble on your stereo and you can bring out the contrast, and so that's what we've done here with a low KEV image. And you can see, on the arrows there, it improves the conspicuity of the contrast filing defects.
Or you can make really fancy pictures, which is great for talks and good for diagnosis. As you can see here, this is a ventilation perfusion map made purely from the CT scan, so we're mapping iodine to be orange, so when you see all the bronchial tree in white, you can see the absence of iodine getting
to the lung in this personal bilateral lower lobe PEs. Excuse me, so back to our case at hand. The 29 year old with a lot of risk factors, and APLS and lupus anticoagulant, and he's subtherapeutic on this meds. We looked at the source images.
Not a dual energy scan, but it's a decent exam. You can see he's a larger individual, we didn't see any filling defects, the right heart doesn't look enlarged, is there anything else we can do, while we have him at making this initial diagnosis. What's the incremental value of a Venus evaluation?
Well, we can do doppler and you can see here, that doppler, you know, has a lot of subtle findings as well as obvious findings, like the presence of a non compressible thrombus. We can also do that with a CT scan, we can just chase the contrast two minutes later
and look at the lower extremities and it basically has a very similar sensitivity. We can look for a filling defect. In our case here, we didn't have that. This is an example of somebody else, that did have a DVT and an abstracting pelvic cancer
creating abdominal waveforms. But this comes out in the guidelines as, you know, sometimes appropriate to look at the lower extremities with the contrast and it's really just the same exam, so it doesn't involve another test. Although, if you have doppler widely available,
it seems, like the obvious thing to do, there's no radiation, that's reproducible, just costs a little bit of time and money. Also important to remember, when we're looking at the CT scan, that the mimics of the pulmonary embolism can actually be more common than actually diagnosis,
when you have a low yield. So all four of these cases were initially called as pulmonary embolism, but they were actually going clockwise on the top left. That's a pulmonary sarcoma, you can see enhancement, it's a very large defect
and presented much more inconspicuously. The top right is a mixing artifact, that's very common, especially, when you have heart failure, as this patient does. The bottom left, that's endocarditis and a patent ductus arteriosus and the tissue
can develop infection. And then the bottom right is probably the most common one you'll see, which is mucus in the bronchi, so this is something, that looks like a filling defect, but you can see it's in the bronchi, if you scroll up and down.
They're next to the pulmonary arteries, not in the pulmonary arteries. Lung cancer patient with pulmonary embolism. Important to remember, that not all filling defects are actually thrombi, this is a patient of Rachel's and she'll probably comment on it more later,
but this is somebody, who kept coming back with on and off PEs and what it actually was was lack of filling, because there's lack of lung. What you'll see here is the patient has a couple of CCs left of normal lung and so you don't have filling and the perfusion with normal lung.
So when we brought the patient back with delayed images, that filled right in, so this is just slow flow in an area, that should have slow flow, because it's not normally perfused. VQ scans have become a coin flip and I think that's probably because it's a lost art, but also, when you're looking at,
you know, a lack of perfusion in a new area and you're not sure what the anatomy is, it's difficult and we never had much more than probability. MRI is not ready for primetime, I don't think it ever will be. This is an image from the PIOPED three study,
you can see, that the exam is really good and you can see the filling defects, when you can see them, but about a quarter of the scans were actually technically inadequate. Also requires getting contrast, which is nobodies favorite. So back to our patient, this is a patient,
who actually did not have a PE, but actually had his hemodynamic collapse due to bilateral, bilateral adrenal hemorrhage. So he had, actually, a scan about a week earlier and you can see the adrenals, that actually hemorrhaged due to the massive hemorrhage causing his hemodynamic
instability and a very scary scenario, that looked a lot like pulmonary embolism and a high risk patient. So anyway, in summary, the CTA is your first line and your second line, VQ scan can be useful, but is really a lost art, MRI is not quite ready
for primetime, MRI can be done for any of these functional tests as well as instead of CT. So it might be a selected test. Don't forget the mimics of pulmonary embolism and remember, the overall low yield of a CTPA and think about the risk factors, and put it in context.
And I would also recommend all outside calls of PE get a local over-read by your radiologist. And you're part of a PERT team, I'm sure we'll hear more about that later, thank you.
- Thank you, it's a pleasure to be here. I'll address how the Indigo Thrombectomy technology can expand the reach of what you can do for your patients. It will preserve treatment options, improve patient outcomes, conserve hospital resources,
and perhaps most importantly, improve your day. The old treatment strategy, every time I had someone with acute limb ischemia I felt like I was shopping at this store. When I went to surgery, I wished I could put a drip catheter in, it lasts a little longer,
to mop up some di when I went to the angio suite, I wished I could cut down and remove some more macroscopic debris. I submit that the new Indigo technology
will provide a new strategy for treating acute arterial ischemia. On the same concepts are predicated STEMI, code stroke, Level I trauma alerts, we've instituted acute aorta, and piggybacked on that, an acute arterial ischemia protocol.
So that means when a patient like this presents with acute arterial ischemia, they get an algorithmic, systemic, trained, metered approach. They go past the holding room directly to the endovascular suite,
and all the processes happen in parallel, not in series. The call team is trained and dedicated, and while anesthesia is working up top with labs and lines, we use the duplex ultrasound to pick carefully our access sites. A faster time to reperfusion allows us to
do it and avoid general anesthesia, incision in hostile groins, and the exposure of lytic therapy, resulting in a decreased morbidity and mortality. Being able to treat the full spectrum of the arterial tree allows us to run options.
We preserve options by first mopping up more proximal clot, and then dripping distally when we need to, or, dripping distally to open up distal targets for surgical bypasses. As an example, this was a recent case
on a trauma CT scan, injured inthrelane aorta with emblogenic thrombus confirmed on intravascular ultrasound. We went in with a large bore system, a cath to aspirate the clot, and then used a cover stent to repair the aorta.
We shot an arteriogram the lower extremities, noticed that it embolized distally, and we used a Cat 6 to pluck out this clot and restore flow. Able to work up and down the full arterial tree. A learning curve for me was to understand that debris has to be corked to removal, which means no flow.
And most other worlds in vascular surgery, flow is good. No flow is bad. Also, you have to vacuum the clot out. Which means you have to uncross the lesion, which is counter intuitive for most of the precepts I've learned.
I've learned to use long sheaths to approach the lesion and to use larger catheters to remove more macroscopic debris. I rarely use the separator, I engage it and cork it for 90 seconds. That allows it to get a firm grip and purchase on it.
And I have to remember that no flow is good. This demonstrates how you approach the catheter with a large sheath. Under roadmap guidance you turn the aspiration vacuum on immediately before you cork it to minimize blood loss. And you use it like a vacuum by uncrossing the lesion
and let it slowly engage and aspirate the catheter. Ninety seconds allows it to get a firm grip and purchase so you can extract it without breaking it loose. I rarely use a separator, I use it only for large thrombus burdens, sub-acute clot, adherent debris,
or when the Indigo catheter is clogged. I strip out the catheter with the separator like a pipe cleaner, and then, every once in a while, on a subacute clot, I'll peck and morcellate it with a separator. Typically, in my lab, when I have new technology
I never have the team trained when I have just the right case, so I've learned over time, to train the team first. And with a trained team, they've taught me a lot. I've found with the Indigo catheter it's hard for me to watch the monitor,
work the catheter, handle the on-off switch, and watch the flow in the canister. So, what we do is we have a spotter who's not scrubbed. They taught me to take the on-off switch out, and then mechanically kink the tubing to make and on-off switch.
And they provide me feedback and just say fast, slow, or corked, so I can run the catheter and watch the monitor. I've learned to beware of the Cook Flexor sheaths, because they scuff up the tip. Use a check flow valve that unscrews from the
catheter if possible. I use coaxial catheters whenever possible, and I telescope them. You can telescope large catheters over small catheters. I use large sheaths and catheters whenever possible, using the preclose technique,
and then you can preserve options if you want to press more distally, you can cinch down, remove the large sheath, put in a 4 5 French, and then press ahead. I also, after I use a pulse technique, will occasionally use the Jungle Juice.
The team taught me the Jungle Juice is half strength contrast, some TPA and some nitroglycerine. When I lace the clot with Jungle Juice, I can observe fluoroscopically, the progress I'm making as I'm aspirating the clot. Thank you.
- Thank you Louie, that title was a little too long for me, so I just shortened it. I have nothing to disclose. So Takayasu's arteritis is an inflammatory large vessel vasculitis of unknown origin. Originally described by Dr. Takayasu in young Japanese females.
The in-di-gence in North America is fairly rare. And its inflammation of the vessel wall that leads to stenosis, occlusion or aneurysmal formation. Just to review, the Mayo Clinic Bypass Series for Takayasu's, which was presented last year, basically it's 51 patients, and you can see
the mean age was 38. And you can see the breakdown based on race. If you look at the early complication rate and we look at specific graft complications, you had two patients who passed away, you had two occlusions, one stenosis, one graft infection.
And one patient ruptured from an aneurysm at a distant site than where the bypass was performed. If you look at the late complications, specifically graft complications, it's approximately 40%. Now this is a long mean follow up: this is 74 months, a little over six years.
But again, these patients recur and their symptoms can occur and the grafts are not perfect. No matter what we do we do not get superb results. So, look at the graft outcomes by disease activity. We had 50 grafts we followed long-term. And if you look at the patency, primary patency
right here of active disease versus non-ac it's significantly different. If you look at the number of re-interventions it's also significantly different. So basically, active disease does a lot worse
than non-active disease. And by the way, one of our findings was that ESR is not a great indicator of active disease. So we're really at a loss as to what to follow for active or non-active disease. And that's a whole 'nother talk maybe for another year.
So should endovascular therapy be used for Takayasu's? I'd say yes. But where and when? And let's look at the data. And I have to say, this is almost blasphemy for me
to say this, but yes it should be used. So let's look at some of the larger series in literature and just share them. 48 patients with aortic stenosis fro all were treated with PTA stenting.
All were pre-dilated in a graded fashion. So they started with smaller balloons and worked up to larger balloons and they used self expanding stents in all of them. The results show one dissection, which was treated by multiple stents and the patient went home.
And one retro-paret-tin bleed, which was self limiting, requiring transfusion. Look at the mean stenosis with 81% before the intervention. Following the intervention it was 15%. Systolic gradient: 71 milligrams of mercury versus 14. Kind of very good early results.
Looking at the long term results, ABI pre was .75, increased to .92. Systolic blood pressure dropped significantly. And the number of anti-hypertensive meds went from three to 1.1. Let's look at renal arteries stenosis.
All had a renal artery stenosis greater than 70%. All had uncontrolled hypertension. They were followed with MRI or Doppler follow up of the renal arteries. So, stents were used in 84% of the patients. Restenosis occurred in 50% of them.
They were, all eight were treated again, two more developed restenosis, they ended up losing one renal artery. So at eight years follow up, there's a 94% patency rate. What about supra-aortic lesions? And these are lesions that scare me the most for endovascular interventions.
Carotids, five had PTA, two had PTA plus stent. Subclavian, three PTA, two PTA. One Innominate, one PTA plus stent. One early minor stroke. I always challenge what a minor stroke is? I guess that's one that happens to your ex mother-in-law
rather than your mother, but we'll leave it that way. Long term patency at three years, 86%. Secondary patency at three years, 76%. Fairly good patency. So when Endo for Takayasu's, non-active disease is best. The patient is unfit for open surgery.
I believe short, concentric lesions do better. In active disease, if you have to an urgent or emergent, accept the short term success as a bridge to open repair. If you're going to do endovascular, use graded balloons or PTAs, start small. Supra-aortic location, short inflation times
I think are safer. And these three, for questions for the future. I guess for the VEITHsymposium in three years. Thank you.
- Good afternoon. These are my disclosure. We all know that ectatic common iliac arteries especially in presence of an abdominal aortic aneurysm tend to dilate with time. For example, if you look at the yellow line, in a common iliac artery of 20 millimeters
is growing five millimeters in five years. If this is not important in open repair, it's crucial for endovascular repair, because it represents the landing zone of the procedure. We have already that if you look at the patient for 14 months you don't find any degree of dilation
in patients treated with a bell-bottom. Again, we heard about these long-term results, but actually, only eight patients reached the five year follow up in this paper. So time is crucial. And we, now and then, encounter many patients
following them up along their life, that when we land in short, ectatic iliac sealing zones, then we encounter these type one endoleak for migration of the iliac limb inside the angiograft. Recently reviewed our experience of 610 patients, with a mean follow-up of 99 months
and we found that one-fourth of the patients are still alive after 14 years. So you have to afford very long-term good results. And this is only possible if you have trustable sealing zones. If you want to avoid type one endoleaks and rupture
in case of ectatic iliac arteries, you have to follow them all, and you have to be very aggressive in treating the complication. Two months ago we published this paper, presented at the ESVS meeting.
And we divided our cohort of patients in those with an ectatic iliac artery and those with normal iliac arteries. What we found was that the patient with ectatic iliac arteries, of course, were a little bit at higher risk
in terms of heart disease, cerebrovascular disease, and kidney disease. But in the late outcomes of these patient, was found that Type Ib endoleak was much higher than those in patients with normal iliacs. Reintervention rate was also higher.
In terms of overall mortality, patient with the larger iliacs showed worse survival because of their preoperative risk factors. But in terms of EVAR failure, this patient presented lower success if compared to standard common iliac arteries.
And this is also true in terms of overall reintervention. But coming to the iliac related reintervention, patient with ectatic iliac arteries had a three-fold incidence of reinterention at Type I endoleaks in the long run after 99 months. We have also some iliac-graft failure,
defined as iliac-related reintervention, occlusion, related death, or aneurysm rupture. Patient with ectatic iliacs had 14% risk of failure after 11 years, while patient with ectatic iliacs had only 4% risk of failure in the long run. Is it not known?
No, actually, if you look at the St. George Vascular Institute's risk score, the main determinant of failure is the common iliac diameter. And we have already other experiences reporting the same values.
Is it typical from one graft? Not at all. This is a patient with Talent graft in which one limb migrated into the opposite common iliac aneurysm and we were able to treat it with an extension.
But most of the patient getting old, they don't come back for follow up. They don't come back and we can check the position of the iliac limb in the long run. Is there any other alternative? Yes it is.
We now have the iliac branch endografting that showed that after 10 years, the reintervention needed in only 8% of the patients, so we can afford the durable results in patients like this. So in conclusion we can say that iliac arteries
tend to dilate with time, especially if they are ectatic. EVAR are prone to late failure in these cases, so rigid follow-up protocol is needed for this kind of patients. And probably if you want a long-term result,
you have a consider safer landing zone, like iliac branched device. Thank you for your attention.
- Thank you and good morning. I have no relevant financial disclosures. At Mayo, we have long been proponents of in-situ replacement of infected, both open and endografts with good results, both in terms of mortality and limb salvage. Our approach to graft infection involves
draining abscesses prior to the operation. Completely removing the infected graft and debriding the periaortic tissues, and replacement in-situ with a new graft sewn to help the aorta. Covering the graft 360 degrees
with omentum and long term suppressive antibiotic therapy. Rifampin-soaked conduits work well for low grade infections and aortaonteric fistula, but for patients with large abscesses we prefer cryopreserved allografts. Naturally para and suprarenal aortic graft infections
add another measure of challenge in the form of need for preservation of renal and visceral blood flow and sometimes presence of large abscesses around the grafts create further challenges to in-situ repair requiring creative
positioning and tunneling of the grafts. Dr.Milina mentioned the Swedish registry and yes, there are encouraging early results of EVAR for infected aortas, but mind you, these were all primary mycotic aortic aneurysms
and not infected grafts which are a different level of infection as he pointed out as well. So, we still prefer in this situation as well, in-situ reconstruction for most patients, but periaortic abscess may dictate the need for remote reconstruction,
and treatment needs to be customized to each patient's different anatomy. And it's important to have a multidisciplinary team. Our treatment strategy includes a single stage procedure with sequential visceral and aorto-iliac reconstruction. We like to have several plans for reconstruction ready
as CT often underestimates the amount of periaortic inflammation. And we like to perform separate bypasses for the renal or visceral arteries prior to the aortic reconstruction to reduce the physiologic stress.
This is one example of antegrade debranching of the viscerals and renals, and a synthetic graft replacement. And here, one for an infected endograph with cryopreserved aorta. This is a gentleman who presented
with an infected infrarenal opening aortic graft and a suprarenal mycotic aneurysm. Osteomyelitis extensively in the spine. He was status post lumber decompression and suffered a post operative myocardial infection as well. PCR demonstrated Q fever and he
had a large paraspinal abscess that had been drained preoperatively. He underwent a decompressing axillofemoral graft temporarily to offload the heart. And then an intra-abdominal exposure of the supraceliac aorta,
And debranching of the viscerals and the right renal artery. Tunneling these grafts to the foramen of Winslow, to the right side of the abdomen. And then tunneling similarly, an aortic replacement graft
in the right paracolic gutter and down into the pelvis, followed finally by a left medial visceral rotation and dealing with the left-sided paraspinal abscess debridement of the periaortic tissues as well as the vertebral bodies. And this is the final result with a post operative CT.
Another patient with an infected endograft and a aortoenteric fistula, who underwent a similar reconstruction tunneled on to the left side of the abdomen in the paracolic gutter, and appropriate pre-debranching of the visceral and renal arteries
to reduce that physiologic stress. In this patient we used saphenous vein grafts to perform the renal artery bypasses in a similar fashion. Sometimes you do have to go to the thoracic aorta to do the debranching to the viscerals and renals,
to stay away from the infected tissue. And lastly, this is a patient with an infected Carrel patch aneurism after the thorocoabdominal repair previously debranched in this fashion, preserving part of the patch and then wrapping the whole graft with omentum.
So, thus far we have experience with 16 such patients with paravisceral graft infection. Just over half were dealt with in a trans-abdominal manner, about two-thirds with in-situ reconstruction using Dacron and majority underwent Omentoplasty. About half of them underwent only renal,
and the other half renal and visceral reconstruction concomitantly. Majority with rifampin-soaked polyester. 30 day mortality was zero, however these are very sick patients, and three patients did succumb within the next 90 days, from multisystem organ failure
and just overall debility. Major renal and respiratory complications were of the order of about 15% but there was no further mortality over a median clinical follow-up of six years. And no graft thrombosis or reinfections.
So, although challenging single stage infected aortic graft excision with visceral and aortic reconstruction can be safely performed. Sequentially to decrease the physiologic stress. The new grafts can be successfully routed away from areas of major sepsis.
Early mortality and morbidity are significant but complete graft excision results in low risk of reinfection in survivors. I thank Dr.Veith for the kind invitation.
- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.
Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates
an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.
You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't
or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.
CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,
we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.
She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.
So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.
Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.
It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign
and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there
but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?
Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy
and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.
So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,
a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,
gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection
it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible
before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains
in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low
or cut out the super renal fixations so you can take them out a little easier. Thank you.
- Okay, thank you very much. I appreciate the invitation from Dr Veith to discuss this technique and really, this is a how to do it technique. These are my disclosures. So we know that if you're doing a type B dissections that are chronic and you're going to use a fenestrated
device often times you have vessels that are on the false lumen that are not easily accessible. You can see in this picture up above, here's you're flap, this is the right renal artery across the fenestration and you can't really see the actual original fenestration.
There can also be some misalignment between the natural fenestration and where you want to put your fenestration. So this technique allows us to create a neo-fenestration at your site of choice. So here's our stent graft planning in this particular patient.
Here's the dissection flap, here's our graft in the true lumen with the SMA and celiac and the right renal. We've placed the fenestration for the left renal right opposite the left renal artery. And this is a schematic representation of
our in press article. Basically once you've accessed the bottom of the graft you can use a steerable directional sheath and put it right at the level of your fenestration. Use the power wire from Baylis, and what you do is put it right up against the graft.
It's like a cautery, you step on the pedal, it gives a one second burst and that goes across the flap. You can then widen it and then connect your stent graft. This is an example of one of our early cases. Here you can see injection in the true lumen with the right renal, you can't see the left renal,
that's bowel gas and another one of the true lumen branches. You can see with the fusion imaging we've now been able to put the graft, the right renal and the graft expanded. Here you can see an injection and we've got our catheter right up against the left renal fenestration. And here you can next see, the power wire,
the tip of the power wire is just at the edge of the catheter. And if you step on the pedal you can see that the power wire goes across into the false lumen right near here, you can inject your false lumen, you can see your renal
and after that you can see that we've now accessed the artery. We balloon it and then stent it. So these are the tools that are required. You need the power wire generator, you need the power wire itself,
you need a pad on the patient just like a cautery pad, and an Oskar or other steerable sheath is very effective in helping you. A short pulse in one second is usually enough to cross the lumen. Here's a second example.
A patient again with a false lumen, the right renal artery is the one this particular time. You can see the dissection flap is here. We planned the fenestration right opposite the renal artery.
And you can see here similar technique with the catheter. The power wire is already actually been deployed across the channel and then put in place. So this is a relatively simple technique that you can use to access false lumen branches. It allows planning the fenestration on your pre-op plan
close to the target vessel, and it assists you when the natural fenestration is not visible, or misaligned. And it uses an existing technique that we've used for left subclavian in situ fenestration and for some aortic dissection acute cases where you need to fenestrate the false lumen.
- Thank you, Dr. Moore, and thank you Frank for inviting me back. These are my disclosures. I am a consultant for Silk Road Medical since I ran the first pivotal trial. Now, six years ago I gave a presidential address before the Society for Vascular Surgery
centered on the carotid space and I added this disclaimer, at least in part, because we were due to embark at that point on ROADSTER 1. And further on in that address, I suggested that transfemoral distal filter protection CAS was an experiment that had failed in my view.
And over the years of course in the legacy trials, that seems to be well born out by the data from these trials and yes, over time results with transfemoral CAS improved. Was it related to better technology? Perhaps.
It was certainly highly impacted by better patient selection and one only needs to see, for example, the evolution of the endovascular management committee in cres 2, as to how anatomic features have figured in that clinical decision making. Now, I'm proud to say that vascular surgeons,
first Juan Parodi and then Enrique Criado, pioneered the concept of flow reversal for neuro protection and CAS procedures and CAS procedures and of course, in my view, the TCAR procedure is in fact the ultimate evolution of that.
Now, thank you Frank for framing my debate with my Italian colleagues. Laura Capoccia's conclusion slide perhaps said it all and my worthy opponents and subsequent speakers I'm sure are going to focus on the fact that flow reversal with the MO.MA
can be achieved can be achieved with a totally percutaneous transfemoral approach, but the early data certainly suggested, as you can see here, that things were not much better. No, I'm sure we'll see results from this prospective registry with a lot of well known
Italian interventional cardiologist. Achieving an admirable 30 day major adverse event rate, but in a sense, this is the evolution of patient selection because it represents a cherry picking type of experience compared to low risk patients. Now, the final thing to consider from a technical aspect,
is that flow stagnation with the MO.MA device hardly equals high flow reversal, because although the concepts are similar, of course the actual operations are quite a bit different. And the authors even acknowledge that embolic signals from TCD were often detected during incursion
of this rather bulky transfemoral in to the arch device. And indeed, the steps of the procedures have been studied and as you can see here, there's really no difference between MO.MA and Distal Filter in the critical step of arch manipulation. Obviously a big part of the strategy, of the TCAR procedure
is avoidance of the arch, and when we've studied anatomic exclusions as recently reviewed by, this procedure can be applied to the overwhelming majority of candidates for CAS. Now Dr. Colin Buck showed you that this strategy
has achieved, as assessed by DWI imaging, lesion production rates, equivalent to carotid endarterectomy and when we published ROADSTER 1, it was the lowest stroke risk ever reported for a carotid stent trial.
I've mentioned previously that it has achieved neuro protection equivalent to carotid endarterectomy and here are some of the ROADSTER data. I won't read the data. Vic Kashif showed it to you. Now, in the most recent MO.MA experience of course,
we see the anatomic exclusions. And the anatomic exclusions in the lower right corner are not exclusions for TCAR. You've seen this data previously and our host, Frank Vees, in his most recent meta analysis, indicated that there was no positive
impact of the MO.MA strategy versus Distal Filter protection. This is a graph of the rapid adoption of TCAR by North American vascular surgeons in the TCAR surveillance project. Mul mentioned to you that the beginning data
from these registries and projects have now been presented. Just this week, I saw the updating of the TCAR surveillance project with sustained excellent result, now at over 3,000 patients. So in conclusion.
In my opinion TCAR is the technical evolution of CAS. Avoiding the arch and superior neuro protection with high flow reversal indicated the procedure of choice and transfemoral CAS should go in to the history books. Thank you for your attention.
- After Dr. Mow-knee's excellent review I don't have much to add here, but just go by here. I have no conflict of interest. As he already said, Takayasu arteritis is a systemic disease, affecting entire wall. It's fundamentally different from atherosclerosis. I like to emphasize once again because same principle
to relieve ischemic symptom based on atherosclerosis should not be applied to Takaysu arteritis. That's what we learned for the last three decade. This is a primarily medical condition to need the medical treatment and not a surgical condition until it develops the complication,
hence the primary aim of treatment is to control active inflammation and induce remission just like Dr. Mow-knew gave a thorough review here. The inflammatory nature of TA waxes and wane with active or chronic system inflammation hence strict control of this condition is absolutely warranted before
any surgical or endovascular management is considered. After all, TA is a medical condition and not a surgical one from the outset. TA has a strong nature of the collateral development to provide excellent natural compensation sufficient to relieve the symptoms in general hence not all symptomatic
lesions actually require the intervention, that's what we also learned, for the intervention accompanied with significant morbidity, we already understand, restenosis, thrombosis, and stroke, etc. So intervention should be reserved for specific indication like uncontrolled hypertension, for example.
Open surgery with bypass has been able to relieve most of lesion to cause acute or chronic insufficiency and remain gold standard but it has excellent track record only for its end stage. It does not provide same good result in early stage. Therefore, bypass surgery should not be considered
as a panacea to relieve all the lesion and remains vulnerable through the rest of the life. So surgery should not be undertaken lightly and good only for those in advanced stage. Nevertheless, diffuse, proximal, multifocal involvement make surgical intervention with bypass often difficult
and such lesion would need some other way to try. That is endovascular approach with angioplastent has proven for safety and also effective alternative method. So main indication for the PTA and stent include clinically ischemia involving one or more vascular bed, we just heard.
Intervention gains popularity especially as interim management for the unsettled case, in particular with multiple lesions. Indeed the results of the endovascular intervention are less encouraging, we already heard, compared to open surgery.
The risk of restenosis in TA is significantly higher reaching over 50% at five years just like Mayo data, like ours data here. Our own results on 24 cases almost identical to what Mayo reported, and some other people as we published already.
So a diligent controlled disease activity prior to and following revascularization is crucial to prevent such complications. So as the conclusion, together with a bypass endovascular management with a PTA stent is now well accepted and symptomatic TA inactive chronic state can be managed
safely either by bypass or endovascular surgery. However, endovascular therapy accompanies higher rate of recurrence. Open surgery at present remains the preferred option delivering better long-term outcome and especially in the advanced stage.
Endovascular intervention fulfills its new role as an interim measure especially for the group open surgery carries too high risk like multivessel involvement. Thank you for attention.
- [Audience Member 1] So I have a question for Dr. Jackson, but maybe everybody else on the panel can chip in, and it just has to do with what your first intervention is going to be for a focal stenosis in a vein graft, and I guess, Ben, my question is, in general, is your first time you intervene going to be a drug-eluding stent?
Our strategy generally has been, to start with, a cutting balloon based on a series, I think it was from Schneider, who compared it and saw pretty good results. Nowadays, I think maybe I'd do that, and at the same time then put a drug-coated balloon in, and that's
increasing the cost, there's no good data to say that's better than just a cutting balloon, but I think I might do that and reserve the drug-eluding stent for the second time or third time. So my question is, what's your intervention the first time you intervene endovascularly
for a focal vein graft stenosis? - [Dr. Benjamin Jackson] So if you're not going to do an open revision, right, we'll preface with that, I'll use a coronary drug-eluding stent first. - [Audience Member 1] Okay. - [Speaker 1] Okay, so, are you happy with that?
- [Audience Member 1] Well, I was hoping to get other opinions, but if you want to move on, that's fine. - [Speaker 1] Alright, so I'll give you my opinion. I don't think there's anything wrong with putting a stent. The idea that the stent is going to be occupying space and is going to mess up your next procedure, I think
that's more out of fear than actually the reality. We have patients that in the SFA popliteal segmentary, we're on the fifth round of stents, and you'd be surprised how you can distend the fifth stent inside the SFA. I never thought it was possible, actually.
We have some IBIS documentation showing at least a five millimeter lumen after you do that thing. So I'm not so concerned about that. The problem with this, and I agree with putting a stent because there's a very rigid lesion sometimes. It's not easy to balloon them, it's not easy to
because usually the cutting balloon probably already got the lumen that you want, but then definitely it increases the cost that way. Again, who knows the other answer. Anybody else? - [Dr. Chris Metzger] Yeah, a brief comment.
I don't think all vein graft lesions are alike, so it depends if it's diffused or focal. The other thing is, I think your response to initial therapy is important, so if you do your balloon, cutting balloon, then it's going to tell you recoil, not recoil,
and the other thing I would say is intravascular ultrasound, if you're in doubt on how large that is, I think helps a lot. So, you know, if it's very focal, very high grade, I think drug-eluding stent is perfect, the question is what size, IBIS helps with that.
Otherwise, I think your strategy for longer disease might be a reasonable strategy as well. - [Dr. George Adams] And the only other comment I'd make is if there is a thrombotic component like Chris was saying, depending on the client morphology I might use laser atherectomy followed by a
biologic therapy such as a drug-coated balloon. - [Speaker 1] Yes, sir? - [Audience Member 2] About that last presentation, are you using any type of anticoagulation when you do these PTFE tibial bypasses, or were the groups comparable where there's only antiplatelet
therapy in the vein grafts and in the prosthetic grafts, or are you putting all of them on factor 10A inhibitor coumadin? - [Dr. Peter Lin] So our patient, we typically put them on aspirin, and for the Propaten we don't add any distal antiplatelet agents.
- [Audience Member 2] Because that's a lot better than historical reports, probably. I wondered, why do you think it shows so much better, even with previous vein cusp patches? - [Dr. Peter Lin] So I think the patch matters, and I also think that over the years, we also learned
a whole lot about the distal anastomotic patch, because time won't let me tell you something and go into great detail. So the patch, you know, we make, is about two to two and a half centimeter long, so that length of the patch is almost twice the length of
the diameter of the graft itself, so I think that's also a significant factor. So it's something that previous literature has not really emphasized on, and the PTFE ideally should be connected to the proximal one-third, instead of distal one-third, so that also may make
some of the same area boost configuration. So the whole idea is you want to make the patch as long distally as possible. So some of the variations, I think, have in part helped, and ideally is that the vein is available, that would be great, if not we also have used a lot
of bovine patch as our patch material, so that thing I think made a lot of difference. So I don't think, all things considered, antiplatelet agents played a huge role, but I think the distal anastomotic compliance mismatch, if we can alleviate that, it will help your outcome.
- [Speaker 1] So Peter, you believe that those grafts have a thrombotic threshold, or you think there's no thrombotic threshold for PTFE? - [Dr. Peter Lin] Oh, I think so. - [Speaker 1] Let me just continue my thought process. So if there is a thrombotic threshold, it doesn't matter
how long you're going to put the vein patch. You can put a 16 millimeter vein patch, it's not going to make any difference, if you reach that thrombotic threshold. So then we come to the criticism that maybe you're selecting the cases
with good runoff, and in the good runoff, it's hard to show a difference between vein and (unintelligible) bonded with the patch, maybe. But if you are to do those terrible cases that have an isolated TPO segment, or they're all the way on the foot or the plantar arteries, that maybe the
saphenous vein will come up much better than this. What do you think? - [Dr. Peter Lin] Well, these are all great points. It's hard to discern based on a single yes or no answer. Saphenous vein has certain limitations, although I believe there's still a standard of care
in terms of conduit choice. Often times the veins are sclerotic, we're limited by vein length, so again, I brought up some points that in some patients we can only connect it to a superficial femoral, even a popliteal bypass because the vein is not long enough.
So PTFE, while it's not perfect in some scenarios, it does have advantages, because I can connect it even to the external iliac artery, I can connect at the common femoral artery, so that's that benefit. I did mention very briefly in our multi-vein analysis, the single vessel runoff is the (unintelligible) runoff.
So in those cases, you're going to have bad outcome no matter what kind of conduit you use, I do believe that, but in general we'd just use aspirin for that patient. But I believe that if we do believe there's an underlying prothrombotic condition, we would add additional anticoagulants, but that's not typical routine practice.
- [Speaker 1] Alright, I just want to add that in poor runoff situations, the vein clearly does better, and it works for a long time. We had published three years ago, on plantar arteries in branches of tibial vessels in the foot, and they did work, only with vein.
Everything else kind of failed, even with the fistulas. Yes, sir? - [Audience Member 3] I have just a quick question about the Phoenix device, a two part question. A, do you use it with a filter, or can you use it with a filter, and two, do you use it as a standalone therapy
or adjunct to a drug-eluding balloon or anything else? - [Dr. George Adams] So, in general, atherectomy is always with adjunct balloon angioplasty. In regards to the filter, especially with the Phoenix device, you have to be careful and very selective with the wire that you use,
you want to use a nitinol wire. So for a filter usually I use a free-floating filter, the NAV-6, and you can't use it over that nitinol wire, you have to use a graduated tip wire, usually a Viper or a Viper Flex. So I would select cases where you would not use
a filter specifically with this device, so if you have a long lesion or if there's any thrombotic component to it, I'd be very conscientious of using this device with that. - [Speaker 1] Thank you. Any questions from the panel?
Because I have a few questions. - [Dr. George Adams] Actually, it was I think very stimulating as to the conversation we just had, in regards to thrombotic or anticoagulants with antiplatelets, you know. Recently the COMPASS trial just came out, as well
as an E-PAD which was more or less a pilot study, showing that just taking peripheral arterial disease regardless of grafts, there seems to be a thrombotic component, and factor 10A inhibitors may have benefit in addition to antiplatelet therapy in regards to all PAD patients.
I think it's a very interesting discussion. - [Speaker 1] I have a question, Dr. Dorigo. Once you identify the high risk group of patients, is there any strategy to modify them to improve them and get them to another category? - [Dr. Walter Dorigo] Most of the perimeters we
examined were not modifiable. Age, extension of disease, coronary artery disease. Maybe one possibility is to improve the runoff status but, in concomitance with the intervention, one can try to improve the runoff score. But four out of five factors were not modifiable.
- [Speaker 1] Thank you, okay. I have one more question. So, do you do distal bypasses? - [Speaker 2] We do distal bypasses, I personally don't. I have a big group, I have three people in my group that only do distal bypasses.
- [Speaker 1] So, it says a patient in your group does not have a saphenous vein, and has a limited runoff. How will you approach there? - [Speaker 2] Well, that was a question I would want to ask both Walter and Peter.
Is there a role for composite bypasses? Because we do it quite a lot where we only have shorter parts of vein available, shorter lengths of vein available, we would do the above-knee PTFE, and then cross the knee with the vein. But I remember that last year at this meeting,
the Americans said that it's worse results, but we still do it. - [Dr. Walter Dorigo] Yes, in the registry are a crude amount, so about one, 150 composite bypasses with the short or long segmental vein and the part of PTFE graft, we use it.
And the results are not particularly better than those with the grafts, but it's likely better. - [Speaker 1] Right, I want to ask the panel, if you have the use the common femoral artery as an in-flow, and this vessel has been used
a few times before, what do you prefer to use? The external iliac, redo the groin again, or use the deep femoral as an in-flow? We'll start with Peter Lin. - [Dr. Peter Lin] I would probably go to external iliac,
because higher, it's got proximal better vessels, and it's greater diameter, all things considered. If you go deep femoral, you still got to navigate across a stenotic plaque common femoral artery. - [Speaker 1] No, it's not stenotic, it's a normal vessel. - [Dr. Peter Lin] So, I would, if all had been equal,
obviously common femoral might be better, but if common femoral's highly disease, stented and treated, and so there's a lot of scar tissue, I'd probably go with external iliac. - [Speaker 1] Okay, anybody else want to make a comment on what they preferentially use for in-flow?
- [Speaker 2] It depends what material you're going to use. If we use the vein, we go back to the common femoral, if we use prosthetic material, we would prefer to have a site where it's easier to go in and lower the risk of infection. - [Speaker 1] Right. I'll say that it depends on
the length, if I have enough length just to go deep femoral, I'll go deep femoral preferentially, but I have gone to the external iliac with a vein and have had no problem with kinking or anything, it would just make a tunnel lateral to the artery. We don't go medially because there are too many
branches there, but laterally, and you can do the anastomosis vein, and it only adds about two, three centimeters of length when you get it just above the inguinal ligament. With that, I'm going to thank the speakers, it was a great conference, and call the next moderators, please.
- There's a new DCB now on the market just C-marked, and I would like to share you interim data of this brand new Kanshas DCB into the preliminary data so far available. So, as we just heard, DCB is a wide-spread accepted technology, which delivers a durable anti-restenotic efficacy
after single-balloon inflation. I think this is clear, but definitely, as we have just seen from Dr. Vermani, efficacy is not a class effect. It is critical determined by the presence and choice of the excipient of each balloon.
And we know that from different studies like here, from Jopa, we can see that outcome efficacy is different in terms of the different effects of the DCBs. So this new and novel Kanshas Drug-Coated Balloon is covered with a paclitaxel 3.2 micrograms per square millimiter.
There's a unicoat technology, which is a uniform coating with micro-crystal aspects where the Paclitaxel is embedded with micro-crystal, which provides a large surface area, which facilitates a drug transfer to the lesion. It's available up to 200 millimeter.
It is a monorail balloon. You can see that in (mumbles) and some preclinical animal models, the Paclitaxel tissue concentration was definitely different in comparison to other already-established DCB, and of course, this new concept has now
to prove an efficacy and safety in the first human study. So, I can provide you now the six-months primary outcome of that KANSHAS 1 study on behalf of all the investigators. 50 patients were enrolled at six sites in Germany and Belgium. Patients will be followed up up to year, two years.
The primary endpoint is freedom from composite safety at six months. You see all the centers which enrolled patients between April 2017 and January 2018. Main inclusion criteria, Rutherford Clinical Category two to four,
lesion length up to 15 centimeter. Just want to highlight that also popliteal artery segments, could, when moved into study, I will show you also the outcome for the to P3 segment where we planted the balloon. The other baseline and lesion characteristic of the patient.
Typical risk profile, most of the patient had a Rutherford category three. On right side, you see the lesion locations, where the balloon was implanted. I see that 19 patients had a treatment with an popliteal artery.
Cumulative lesion length, 88.6 millimeter. As usual (mumbles) DSB trials classification was more on the lower side. Here the procedural characteristics. DCB per lesion 1.2. Total inflated length 72.1.
(mumbles) 14% of 14 patient, 28%, a little bit more on the higher side for that lesion length. This was due to flow limiting that section and residual stenosis. Here are the six-months outcomes in terms of hemodynamic outcomes
and Rutherford class change from a baseline. As you can see, most of the patients improved during this first six months of followup. Here's the freedom from composite safety and efficacy endpoint within couple of micro curve analyzed. This is a target of 100%,
which means freedom from device and procedure-related deaths through 30 days and freedom from target limb amputation and clinical driven TLR through six months. There were no device and procedure-related Severe (mumbles) during that six months of followup.
So let me conclude the DCB angioplasty for de novo femoropopliteal artery lesions with that new KANSHAS balloon was so far safe and efficient through six months of the procedure. It has a remarkable clinical hemodynamic improvement
at six months, but we have to wait, of course, the further followup 12 and 24 month. Thank you very much.
- Thank you Dr. Sullivan. It's my pleasure on behalf of the investigators of the Vernacular trial to present the 12 month update on the Venovo Venous Stent Trial. These are my disclosures. Well, the Vernacular study object was to assess the performance of the Venovo Venous Stent
for the treatment of iliac and femoral venous occlusive disease, including acute or chronic DVT and/or May-Thurner Syndrome. The design was a multicenter non-randomized single-arm study that enrolled 170 patients at 22 international sites including the USA, Europe, and Australia.
There was complete independent analysis of all imaging including venography, radiographic assessment of stents, duplex ultrasound. There was of course a clinical events committee and a DSMB. Follow up is presented today is through one year, but there's ongoing follow up for three years
so you'll hear further reports in the future. The stent under evaluation was the Venovo stent which is a self-expanding nitinol stent which has three millimeter flares at each end to enhance wall apposition. It has six radiopaque tantalum markers, three on each end,
and it employs a tri-axial over-the-wire delivery system. These are the stent diameters, 10 to 20 with stent lengths from 40 to 160, and these are the introduction profiles for the various stent diameters. Key inclusion criteria was
symptomatic venous outflow obstruction by venography of greater than 50%, a CEAP clinical score of three or greater, and a VCSS pain score of greater or equal to two. Reference vessel diameters included in this were veins of seven millimeters to 19 millimeters.
Key exclusion criteria were could not have malignant obstruction, could not have contralateral disease in the iliac and femoral veins, or obstruction extending into the IVC or below the lesser trochanter,
could not have a prior stent at the site in the target lesion. The primary efficacy, the primary endpoint was 12-month primary patency by duplex ultrasound. There was also a primary safety endpoint, which is freedom from major adverse events.
As you can see here, that was a composite of all these features. We also had hypothesis-tested secondary endpoints and observations including pre-procedure and 12-month assessment of pain and quality of life. Patient demographics, as you can see a slightly older
in the non-thrombotic iliac vein lesions, or May-Thurners. Both groups, the post-thrombotic and the May-Thurner had a higher preponderance of females that was slightly more exaggerated in the NIVL group. You can notice that that
was represented about 87% of May-Thurner. Lesion characteristics common iliac vein was the site that was most involved, however obviously in the post-thrombotic syndrome where there's more extensive involvement, the external iliac vein was involved in over half of the patients.
Mean lesion length, again, owing to slightly more extensive disease in post-thrombotic syndrome was slightly longer than in May-Thurner. Procedural data, again given the slightly longer mean lesion length there were more stents placed in the post-thrombotic syndrome cohort than in the NIVL cohort.
This represents 45% of the patient population, this represents 55%. In terms of primary patency, you can see compared to a literature-derived performance goal of 74%, the total patency at 12 months was 88.3%, 96.9% in the non-thrombotic iliac vein lesion group,
81.3% in the post-thrombotic syndrome group. This is just a representation in Kaplan-Meier format of what I just presented, again out to 395 days, close to the window for one year, 88.9% patency. Primary safety endpoint, again compared to a literature-derived performance goal
of 89% was 93.5%, again 100% in the NIVL group. Looking at the VCSS pain score, again that's a three point score, mild moderate or severe. You can see the patients started up here at about 2.3 and ended up with no pain or mild pain which was sustained throughout the 12 month followup.
Likewise, the 20 question CIVIQ-20 score looking at quality of life in patients with venous insufficiency you can see a significant drop from baseline to post-procedure which was sustained through 12 months. Secondary observations, there was freedom
from TLR and TVR in 98.6% of the NIVL patients, 87.6% of the post-thrombotic syndrome group, and note that at one year there were zero fractures determined by plain film radiography. In conclusion, this prospective, multicenter trial of the Venovo stent used
to treat obstruction in the iliac and femoral veins demonstrated a high primary patency benefit compared to historical control at 12 months while demonstrating significant improvement from baseline in terms of the VCSS pain score and quality of life. The 12-month patency was 88.3%, and the 12-month freedom
from TLR rate was 7.4%, there were zero fractures and there will be reports at two and three years to follow. Thank you.
- Thank you so much. Thanks Dr. Bies. This my disclosures. Well, the indication all starts having healthy common carotid artery, at least 6mm in diamter, free of calcification, and atherosclerosis,
and you want to have that artery distance between your clavicle and your bifurcation to be at least 5 cm. We define this, or call it, the landing zone. The depth of the artery, the less deep the artery, the better,
the easier the procedure is, and you want a ratio of the common carotid artery depth to the landing zone to be less than one, and likely, like when you get closer to half, where the ease of the procedure is significantly noticeable. Now, the contraindication, again focusing on access,
you don't want to have a severely calcified artery, you don't want to have significant atherosclerotic disease right where you're going to puncture the artery, as you can see here on the ultrasound. Now, the dual antiplatelet therapy here is a must,
you have to have it, you have to start it at least a week prior to, here there's two randomized trials showing the benefit of dual antiplatelet therapy. You have to make sure the patients are on statin, and we've shown on others, the benefit of statin.
You can almost reduce the risk of death for more than 60% in patient who develop severe complication after carotid stenting. Blood pressure here is interesting because on one hand you want to keep the blood pressure as high as possible during the flow reversal,
greater than 140, greater than 160 because you want to maintain that delta between the systolic pressure and the venous pressure. That's how the flow reversal work, and this is how you have a good protection of your patients. But after the procedure, you want to treat it like
any other carotid stent, and you want to maintain the blood pressure less than 140 because you want to avoid a stroke. We've shown as well here, that you can reduce that risk by 70% if you put patient on beta blockers, preventing them from having severe
hypertension after stenting. The exposure's going to be between the two head of the clavicles. A small incision, 3 to 4 centimeter, but you can get about 5 centimeter almost, of the carotid, and you want to put a
vessel loop proximally, or an umbilical tape just to cause a gentle traction on the artery, and purse string stitch, or u-stitches very helpful here at the end of the case, you can tie it down when you pull your sheath. This is essential here to prevent dissection.
You want to have the needle to be parallel to the artery, so with a gentle traction, you don't want the needle to invaginate the anterior wall or to go into the back wall, and then you start a dissection. So if you can get the wire, the microwire,
into the lumen at this point, that's essentially preventing dissection. Once you're in with the microsheath few centimeter, you just do an angiogram, and if you see disease here at the bifurcation, you stay short, so you advance your microwire followed by
a sheath with a dilator, in exchange over an O55 to your stiff or six French sheath, 8 French sheath. Now, if you have a healthy looking external carotid artery, I highly recommend that you engage the external carotid artery by advancing the microwire
into it, followed by the microsheath, and then your stiff wire, because you going to get at least couple a more centimeter of purchase, and having a purchase I think is essential again in avoiding dissection. So if you have your wire in and you can
dilate just the anterior wall with sequential six and nine French, that allow your sheath to go very smoothly into the common carotid artery, and once your sheath is in there, you're basically done with the procedure, as far as my concern.
Now, once spot fluoro before you advance that sheath, because this is where the wire can track back, so if you can avoid the wire tracking back at that point to have the purchase when you get in. And then, from that point, it's just connecting the flow reversal between the arterial and venous.
And then clamping the carotid as they talked about using a atraumatic clamp and then now you have basically an active, but right before you do this, you want to make sure that you have everything on the table, your stent is ready to go to minimize the flow reversal,
your wire, your balloon, everything is ready to go. And you also want to the time out, making sure that the patient is therapeutic under ACT, and the blood pressure is where you need it to be. I'm for not ballooning the stent, so gentle pre-ballooning,
we've shown how ballooning the stent can double the risk of stroke and death, and from there, I think you take one of the most complicated procedure and most dangerous procedure you do to a simple, equivalent to an iliac stent with ipslateral approach,
because you can get your short wire and delivery system and deploy the stent very easily. You've seen here the time can be, as your technique improve, less than an hour, and your clamp time and flow reversal time is about 10 minute.
The technique is published in JVS, if you want to reference to that paper, and then as far as the surveillance project we using the VQI, more than 500 center in the United States now have VQI, so we want to see real world outcome,
to see if the randomized trial or the IDE study apply to real world outcome when people are using it. And you can see the outcome here. We have twice as much neurological complication with transfemoral carotid stent, compared to TCAR. This was presented at VAN and published in JVS.
And essentially, no statistically significant difference in all major adverse events between CEA and TCAR. So the take home points: This is a very promising hybrid procedure with excellent outcome. This outcome that we're seeing now,
is not just in IDE study, but is going in post approval, so we seen it in real world outcome with people who don't have a lot of experience with TCAR, and there are several important techincal points that make this procedure very, very safe, and very easy. Thank you.
- So I don't have to give you any data. I just have to tell you how we do it. So this is the easiest talk of this session. Step-by-step technical tips. Now our definition of pharmaco-mechanical may vary between us so I'll give that as we go along. These are my conflicts.
When to use it. Well certainly as you already heard, Massive PE has contraindication to full dose lytic is one area. Submassive elevated risk may be another. We've already seen multiple people put up
these guidelines so what we're really talking about at this point in time is those patients that we just talked, that those two groups that they just talked about because those are the ones that we're trying to treat. The biggest thing is don't be frozen by indecision.
Majority of patients eligible for thrombolysis do not receive it. It's amazing to me as a referral center to get the call from an outside community hospital or the patient with hypotension, abnormal RV or biomarkers and they've barely given the patient
Heparin and they just want to transfer the patient out of there and you tell them that's a massive PE. Please give them systemic thrombolysis and they go what? And I go you now have 10 times the death rate of an acute myocardial infarction. Would you give this patient lytics for acute MI?
Yes. Then give them the freaking lytics. Save their life. It's amazing what's going on in this country. So the PERT Consortium and everything, we really need to educate the community
because it's ridiculous. If you look at the utilization of thrombolysis, it's going down. Unbelievable and if you look at the in-hospital mortality for these patients that have significant PE, the in-hospital mortality is much higher
if you don't give thrombolysis. You've already seen this indirectly in a bunch of different lectures, but I just wanted to show you very quickly how to do this on an echo or CT. You want to get the center line, get it at the valve and then measure it one centimeter
below that valvular plane. This is something you don't have to depend on radiology just to do. You can just look at the transfer CT. You can look at the echo. You don't have to fight with your echo guy to give you that.
It's also very evident and often times just looking at the images. Why treat submassive elevated risk PE? You know what? I've heard all the mortality stuff. I get it.
It doesn't change mortality that much. It does and we should measure it as a primary endpoint in our trials. Change your discharge time and in this day and age, medicine is so expensive. Time in the hospital, repeat procedures,
elevated your amount of treatment for that patient really has to be looked at as part of that, not just mortality. But there's eight times more recurrent PE and four times a mortality rate if you have a PE and unresolved RV dysfunction at discharge
and that should be looked at prior to discharge, not just say well they look like they're doing okay. Treatment of IVC, higher risk PE. Certainly the other thing we have to look at is there's other things to do. You've already heard a little bit
that there's IVC filters out there. We take out 90 some percent of our IVC filters in our section. We actually as a system now are up to 60% at seven months and it only takes effort. The patients that I see die in our hospital
in the last year that shouldn't have died are patients that should've gotten an IVC filter because they got heroic things to take out their PE and nobody put a filter in even though they had significant DVT left over because they were afraid of the TV commercials?
Oh my gosh. If you look at the 27 extra deaths that we've had from IVC filters that were removable in the United States, and you take our experience and multiply it by the number of tertiary care hospitals in the United States, use them when they're appropriate.
Take them out so the risk is low, but don't go away from them. They've already been shown to be beneficial for the right patient population. But you also have embolectomy and surgery should also be considered.
Step by step. Make the decision and clinically be consistent. PERT team or other consistent mechanisms. We have an app that we use. This is throughout our entire healthcare system so all the vascular specialists have this.
It's an algorithm that's supposed to be used both in the ER and for the different vascular specialties so everybody's being treated very similarly. We have all the different definitions. We have the PESI calculator. All this is in an app
that's readily available to our constituents. Special consideration certainly is the tolerance of thrombolysis, underlying tolerance of pulmonary hypertension. Again, we need to evaluate the patient, not just label them as a PE.
And I also think there's a special population we need to study and that's the socked in pulmonary artery with no perfusion on a CT scan. I think this is a different population long term and we need to study that a little bit more. We got to get the patient back from the edge.
I think I'm opposite of Jeff. I don't want to see them get worse and then treat 'em. I want to prevent them from getting worse as long as I'm selecting that population in a thoughtful matter. We primarily use low dose TNK.
This is nothing I'm going to give you data on. This is an institutional, what do you want to call it, anecdotal experience and we lost our contracts except for TNK so we had to go to this and so we do a lot of catheter-directed. You've already seen all these trials.
There's a ton of different devices out there. The one I want to talk to you about is using a really fancy one called a pigtail catheter and another one called an ethos catheter. This is a patient that had a significant PE. You can see that they've got bilateral main PE.
This is on table. This is what we do for the vast majority of our patients. We sit there, we use ultrasound guided access to the vein so that we cut down our venous complications for access site. The patient is given 20 and 30% of a loading dose
of TNK and then we watch them. If you look at thrombus in a test tube and you give a thrombolytic therapy, it takes about 20 minutes for fibrinolysis. So this is what we do. As you're going to see, this is over 25 minutes
and we see the patient went from a pulmonary pressure of 65 and a heart rate of 115 down to 25 minutes, the patient's pulmonary pressure is about 44 and their heart rate is in the 90's. This patient then has all the catheters removed on the table even though they got lytic
and they're heparinized. This is a venipuncture, so big IV. We send them up to the unit and we typically discharge them the next day. We have an echo B4 discharge to make sure there's been a significant recovery of RV.
If not we'll watch them an extra day and then all these patients get a CT again. I'm sorry an echo again at 30 days to make sure that we're getting good resolution from that. On table results, decrease your complications. Thrombolysis has always been associated with the
duration of thrombolytic therapy and intracranial bleed. Now you can either use a pigtail catheter which is what we use for most of these people because we can measure pressure in it. We spin it around a little bit in the pulmonary arteries and give the dosage.
Again, we give 20-30% of the dose. There is no data for that. If significant improvement does not occur, they'll get dripped overnight in the ICU at usually .5 to 1 milligram per hour. You've already seen the data for EKOS.
We use this if we think we need a little bit quicker Thrombolysis such as in a socked in pulmonary artery 'cause we have no flow. We do think that may help, but we don't have any data for that. It makes us feel good.
We spend a lot more money and so we think that may be reasonable at that point in time. This is just what it looks like when you put in bilateral EKOS catheters. Certainly the patient can be put in the ICU for this. I do think that we should do a trial looking at EKOS
with a little higher dose, do it for 30 minutes, look at those pulmonary pressures right on the table. I think, again, my own opinion is after 25 years, the closer we get to being done on table, catheters out, patients doing well, the better, safer procedure we have,
the less chance of mortality, the less chance of complication and as you decrease complications, your benefit improves. We've already seen the results and you'll see more of these from non-randomized trials such as Seattle 2 which looked at 150 patients,
but they saw very quick recovery of the RV which was very important. If you look at technical success, it was very high. The dosage of thrombolytic exceedingly lower, lower than what we're giving in a PTO catheter, that's for sure.
And if you look at the RV from Ultima Trial which was randomized. There was faster RV recovery utilizing this device. Thank you very much.
- Great thank you very much. It's great to be here at Veith and talk to you about optimally deploying the Supera interwoven stent. This is a stent which is very unique and different from other stents. Slotted-tube stents are laser
cut from nitinol tubes with an open cell geometry compared to Supera which incorporates six pairs of elastic nitinol wires into an interwoven helical closed cell geometry.
This design gives it vascular-mimetic like properties in the dynamic vessel that we treat. And it has four times the radial strength of slotted-tube stents so it is resistant to compression from outside. That said its physiologically conformable
and essentially fracture-proof and it has by far the lowest chronic outward force of any of the nitinol-like stents. This just shows the off the-chart radial strength of Supera compared to nitinol and it is this
outward radial force which may generate some of the neoplastic hyperplasia. This gives the clinical advantages. You can use it in flexion points, calcified lesions with no recoil, long lesions with its conformability
and lack of fractures and if you want to convince yourself I encourage you do either intervascular ultrasound or bent-knee angiograms and compare them in this type of stent to the slotted-tube stents.
It's a unique stent so it has unique deployment. It's a ratchet delivery rather than a conventional mechanisms. The stent length is not at exact and depends on who well you implant it. It's not oversized.
You must aggressively pre-treat all segments that you're going to implant the stent. It is a slower deployment, a two-handed which is kind of an art-from if you will. It's a great stent but you have
more potential for trouble if you don't do it correctly. Here are the three important easy steps you must have documented. Aggressive pre-dilation to all of the segments where you're
going to put the stent. It's got to be one-to-one sizing. And you have to deploy it slowly on high magnification after that pre-treatment. That's it, those three steps. The pre-treatment we usually do
on Roadmap with focal force or regular balloons at least one-to-one what we're going to implant and usually a little bit higher. After that, the stent deployment, we use a Roadmap for the distal edge only.
Once we have the distal edge released, we take the Roadmap off, mag up and go slowly. The right hand throws the ratchet system, the left hand adjusts the tension. If the stent elongates a little bit, you slow down and push forward.
If it packs too much slow down, pull backwards. Here's a typical but illustrative case long disease, CTO, calcified disease in the adductor canal and the popliteal. Here's the pre-treatment with a 6 O ballon before a 5 5 superium
to make sure that it's well-expanded. Here is the mag-ed up slow deployment but you can see how beautiful it looks immediately on delivery and how well it stands up without post-dilation in this heavy calcium in the adductor canal.
Now here's the final AP angiogram. We're used to seeing good angiograms in the AP view but here's a bent-knee angiogram just showing the conformability of this stent and its strength in calcified lesions. It has great data.
Eighty-six point three primary patency in the superb trial with no fractures. Furthermore if you deploy it properly and nominally the primary patency was more than ninety percent. Extremely durable at three years
if you nominally deploy the stent, ninety-four percent freedom from TLR. Some things to remember. Again, pre-treat every vessel segment where you're going to put the stent, not just the tight part.
If you don't get pre-dilation with a longer balloon go to a shorter more aggressive focal force or non-compliant balloon. After you pre-medicate the patient don't use the small Superas.
And I can summarize mag up and slow down when you deploy the stent. We don't post dilate unless there's issues but if it does elongate or pack that's when we post dilate. What not to do with a Supera stent.
Don't use it if precision is needed at the back end for example an ostial SFA lesion from above. Again it's not an exact stent length. If there's a lot of mismatch it's not your stent.
You must adequately pre-treat, if you can't pre-treat it, don't put a Supera or in my opinion and stent. And of course you would never primary stent with this type of stent. So in conclusion the Supera stent
is a unique interwoven design giving it vascular mimetic qualities uniquely suited for the femora-popliteal lesion. Has excellent clinical results that seem to be independent of the stent length. All that said proper lesion preparation
and stent deployment techniques are essential to the success of this device. And I thank you very much for your attention.
- Thank you Clem. These are my disclosures, so why single session? Why, Steve did an unbelievable job discussing pharmacomechanical techniques but why have we moved there? I think the answer is inherent. We don't want the cases to go as long as CAVENT
for numerous reasons, the long procedure investment, the costs, the bleeding risks. So there's a number of devices that allow us to perform rapid clot removal, single session therapy. Many of them are listed here, and again,
the advantages are intrinsic. It's going to make the clot go away faster, it's going to reduce the cost, reduce the need for escalated care in this patient population. The disadvantages, again,
Steve had really touched upon this, you don't need to pay for a thrombectomy device, you're clearly going to be more liberal with the use of balloons and stents, and we've clearly seen that in our practice here in New York as well.
A larger sheath, you may leave some clot behind. We don't know whether that's disadvantageous, could that lead to poor outcomes? Is there more trauma to the valvular system leading to venous, deep venous insufficiency? So this is not a new concept.
This is a case series from Hopkins over 10 years ago which show with the introduction of mechanical techniques, you can reduce the procedure time by 50% as well as the lytic dose, and that leads to actually greater technical success rate and reduced cost.
Peter Lin in Texas echoed these outcomes as well with reduced ICU stay, reduced hospital stay, reduced bleeding complications, and again, reduced costs. Tony Comerota answered the question, I think fairly well, about whether or not there's valvular damage done by these mechanical devices
by specifically demonstrating that there were actually more cases with normal valvular function following angiojet thrombectomy than with actually just CDT, suggesting that angiojet in fact can be safe and not lead to deep venous valvular insufficiency. We obviously know that 70% of patients treated medically
at five years will have some degree of the post-thrombolic syndrome and so the ability to maintain an open vein and alleviate a patients symptoms is intuitive. And with the introduction of endovascular techniques with a modicum of cost,
you seem to be able to achieve significant patient quality of life. I was honored to serve on a multi-center U.S. feasibility study looking at the injuries of thrombectomy for DVT clearance where we were able to reduce the time by over 50% as compared to the CAVENT data,
or to the historic venous registry, also reducing the bleeding complications at the same time. That registry used the six french catheter and this is just a representative case using the six french catheter, sort of classic iliofemoral DVT here.
And then eight hours later this required two sessions in a lab. We were able to get complete patency to the entire iliofemoral segment. This was done as outpatient therapy. The patient was put on Lomoh-lequit Heparin
and discharged home the same day. We now have an eight french catheter which has introduced us into the single session realm of therapy. I'm not going to belabor the point about the technical nuances but it is a much more powerful mechanical technique.
And so here's a recent case that we've performed using the eight french catheter, the eight french technology, again, acute iliofemoral popliteal vein, DVT with complete obstruction to outflow in the symptomatic leg.
Again you have the eight french catheter. This is now being used to infuse a thrombolytic agent with a standardized protocol where we use so called power pulse techniques introducing a bow less of a thrombolytic agent in our center. It's ulta placed into the thrombosed vein
and then the catheter is used in a more traditional form used in it's so called thrombectomy mode. And this is just an hour later. And you can see the entire segment is completely cleared of all clot and if you can tell based on the picture here, there appears to be
a narrowing in the common iliac vein which we interrogated with intravascular ultrasound. This was the patients right leg so we were a little bit surprised it was a problem here but this is the pullback from the IVC, and you'll see there's going to be circumferential wall
thickening and a narrowing right when we get down to here, and that's the common iliac vein that was showing up on the veno gram. This was a young patient, we didn't feel it was appropriate to leave this untreated and so we placed an open cell Nitinol Stent here
and you can see that there's a waste clearly at the iliac vein confluence. This was successfully post-dilated. And this is two hours after the procedure was initiated where again we have complete patency to the entire segment. So to conclude,
I would say that rapid flow restoration is now technically feasible. It's a safe method of endovascular treatment of DVT. It results in shorter thrombolytic infusion times, now as low as two hours compared to standard DVT rated between 55 and 60 hours.
This leads to decreased bleeding risks due to lower duration of the thrombolytic agent, decreased costs due to the elimination of the patient going to a monitored care setting, and improved patient satisfaction with faster recovery and less morbidity.
Thank you for your attention.
- 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
- This is from some work in collaboration with my good friend, Mike Dake. And, a couple of years of experience at Stanford now. First described by Kazy? years ago. This technical note of using multiple main-body endographs in a sandwich formation.
Up at the top but, then yielding multiple branches to get out to the visceral vessels and leaving one branch for a bifurcated graft. We've sort of modified it a little bit and generally either use multiple
grafts in order to create a branch the celiac and SMA. Left the celiac sometimes for a chimney, but the strategy really has been in one of the limbs to share both renals and the limb that goes down to the legs. We noticed early on that this really was not for
non-operative candidates, only for urgent cases and we recognize that the visceral branches were the most important to be in their own limb. I'll just walk you through a case. 6.8 centimeter stent for foraco above
the prior opened repair. The plan drawn out here with multiple main bodies and a second main body inside in order to create the multiple branches. The first piece goes in. It's balloon molded at the level of pulmonary
vein with enough length so that the ipsalateral limb is right next to the celiac. And we then, from above get into that limb and down into the celiac vessel and extend with either a limb or a viabahn. Next, we deploy a second main body inside
of the gate, thus creating now another two limbs to work through. And then through that, extend in its own branch a limb to the SMA. This was an eight by 79 vbx. Then we've got a third limb to go through.
We put a cuff that measures about 14. This is the math so that the double renal snorkle plus the main body fills up this hole. Now, double sheath access from above, looking for both renals. Sheaths out into both renals with viabahns
inside of that. Deployment of the bottom device and then a final angiogram with a little bit of a gutter that we often see when we have any kind of parallel graft configuration. Here's the post-op CT scan wherein
that limb is the two shared renals with the leg. This is the one year post-op with no endo leaks, successful exclusion of this. Here's another example of one of an eight and a half centimeter stent three thorico similar strategy, already with an occluded
celiac. Makes it a little bit easier. One limb goes down to the superior mesenteric artery and then the other limb then is shared again bilateral renals in the lower main body. Notice in this configuration you can get all the way up to the top then by putting a thoracic component
inside of the bifurcated subabdominal component. There's the final CT scan for that. We've spent some time looking at the different combinations of how these things will fill up to minimize the gutters through some more work. In collaboration with some friends in Kampala.
So we've treated 21 patients over the last couple of years. 73 years of age, 48 percent female usual comorbid factors. Oh, I thought I had more data there to show you. O.K. I thought this was a four minute talk.
Look at that. I'm on time. Octopus endovascular strategy is a feasible off the shelf solution for high risk patients that can't undergo open repair. You know obviously, sort of in this forum and coming to this meeting we see what's
available outside of the U.S. and I certainly am awaiting clinical trial devices that will have purpose specific teacher bi-graphs. The end hospital morbidity has still been high, at four percent. The one year survival of 71 percent in this select
group of 21 patients is acceptable. Paraplegia is still an issue even when we stage them and in this strategy you can stage them by just doing the top part plus the viscerals first and leaving the renals for another day. And branch patency thus far has been
in the short term similar to the purpose specific graft as well as with the parallel graft data. Thank you.
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