- I want to thank Dr. Veith for the invitation to present this. There are no disclosures. So looking at cost effectiveness, especially the comparison of two interventions based on cost and the health gains, which is usually reported
through disability adjusted life years or even qualities. It's not to be really confused with cost benefit analysis where both paramaters are used, looked at based on cost. However, this does have different implications from different stakeholders.
And we look, at this point, between the medical center or the medical institution and as well as the payers. Most medical centers tend to look at how much this is costing them
and what is being reimbursed. What's the subsequent care interventions and are there any additional payments for some of these new, novel technologies. What does the payers really want to know, what are they getting for the money,
their expenditures and from here, we'll be looking mainly at Medicare. So, background, we've all seen this, but basically, you know, balloon angioplasty and stents have been out for a while and the outcomes aren't bad but they're not great.
They do have continued high reintervention rates and patency problems. Therefore, drug technology has sort of emerged as a possible alternative with better patency rates. And when we look at this, just some, some backgrounds, when you look at any sort of angioplasty,
from the physician's side, we bill under a certain CPT code and it falls under a family of codes for reimbursement in the medical center called an APC. Within those, you can further break it down to the cost of the product.
In this situation, total products cost around 1400 dollars and the balloons are estimated to be 406 dollars in cost. However, in drug-coated balloons, there was an additional payment, which average, because they're such more expensive devices than the allotments and this had an additional payment.
However, this expired in January of this year. When you look at Medicare reimbursement guidelines, you'll see that on an outpatient hospital setting, there's a reimbursement for the medical center as well as for the physican which is, oops sorry, down eight percent from last year.
And they also publish a geometric mean cost, which is quite higher than we expected. And then the office based practice is also the reimbursement pattern and this is slated to go down also by a few percentage points.
When you look at, I'm sorry, when you look at stents, however, it's a different family of CPT codes and APC family also. Here you'll see the supply cost is much higher in the, I'm sorry, the stent in this category is actually 3600 dollars.
The average cost for drug-eluting stents, around 1500 dollars and the only pass through that existed was on the inpatient side of it. Again, looking at Medicare guidelines, the reimbursement will be going down 8 percent
for the outpatient setting and the geometric mean cost is 11,700. So, what we want to look at really is what is the financial impact looking at primary patency, target lesion revascularization based on meta analysis. And the reinterventions are where the real cost
is going to come into effect. We also want to look at, when it doesn't work and we do bailout stenting, what is the cost going to happen there, which is not often looked at in most of these studies. So looking at a hypothetical situation,
you've got 100 patients, any office based practice, the payee will pay about 5145. There's a pass through payment which averages 1700 dollars per stent. Now, if you look at bailout stenting, 18.5 percent at one year,
this is the additional cost that would be associated with that from a payer standpoint. Targeted risk for revascularization was 12 percent of additional costs. So the total one year cost, we estimated, was almost a million dollars
and the cost per primary patency limb at one year was 13 four. In a similar fashion, for drug-eluting stents, you'll see that there's no pass through payment, but although there is a much higher payer expenditure. The reintervention rate was about 8.4 percent
at one year for the additional cost. And you'll see here, at the one year mark, the cost per patent limb is about 12,600 dollars. So how 'about the medical center, looking at Medicare claims data, you'll see the average cost for them is 745,000,
the medical center. Additional costs listed at another 1500. Bailout renting, as previously, with relate to a total cost at one year of 1.2 million or at 16,900 dollars per limb. Looking at the drug-eluting stents,
we didn't add any additional costs because the drug-eluting stents are cheaper than the current system that is in there but the reinterventions still exist for a cost per patent limb at one year of 14 six. So in essence, a few other studies have looked
at some model, both a European model and in the U.S. where the number of reinterventions at two to five years will actually offset the additional cost of drug-eluting stents and make it a financially advantageous process.
And in conclusion, drug-eluting stents do have a better primary patency and a decreased TLR than drug-coated balloons or even other, but they are more expensive than conventional treatment such as balloon angioplasty and bare-metal stents.
There is a decreased reintervention rate and the bailout stenting, which is not normally accounted for in a financial standpoint does have a dramatic impact and the loss of the pass through makes me make some of the drug-coated balloons
a little more prohibitive in process. Thank you.
- 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.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- Good morning. I'd like to thank everybody who's in attendance for the 7 A.M. session. So let's talk about a case. 63 year old male, standard risk factors for aneurismal disease. November 2008, he had a 52 mm aneurism,
underwent Gore Excluder, endovascular pair. Follow up over the next five, relatively unremarkable. Sac regression 47 mm no leak. June 2017, he was lost for follow up, but came back to see us. Duplex imaging CTA was done to show the sac had increased
from 47 to 62 in a type 2 endoleak was present. In August of that year, he underwent right common iliac cuff placement for what appeared to be a type 1b endoleak. September, CT scan showed the sac was stable at 66 and no leak was present. In March, six months after that, scan once again
showed the sac was there but a little bit larger, and a type two endoleak was once again present. He underwent intervention. This side access on the left embolization of the internal iliac, and a left iliac limb extension. Shortly thereafter,
contacted his PCP at three weeks of weakness, fatigue, some lethargy. September, he had some gluteal inguinal pain, chills, weakness, and fatigue. And then October, came back to see us. Similar symptoms, white count of 12, and a CT scan
was done and here where you can appreciate is, clearly there's air within the sac and a large anterior cell with fluid collections, blood cultures are negative at that time. He shortly thereafter went a 2 stage procedure, Extra-anatomic bypass, explant of the EVAR,
there purulent fluid within the sac, not surprising. Gram positive rods, and the culture came out Cutibacterium Acnes. So what is it we know about this case? Well, EVAR clearly is preferred treatment for aneurism repair, indications for use h
however, mid-term reports still show a significant need for secondary interventions for leaks, migrations, and rupture. Giles looked at a Medicare beneficiaries and clearly noted, or at least evaluated the effect of re-interventions
and readmissions after EVAR and open and noted that survival was negatively impacted by readmissions and re-interventions, and I think this was one of those situations that we're dealing with today. EVAR infections and secondary interventions.
Fortunately infections relatively infrequent. Isolated case reports have been pooled into multi-institutional cohorts. We know about a third of these infections are related to aortoenteric fistula, Bacteremia and direct seeding are more often not the underlying source.
And what we can roughly appreciate is that at somewhere between 14 and 38% of these may be related to secondary catheter based interventions. There's some data out there, Matt Smeed's published 2016, 180 EVARs, multi-center study, the timing of the infection presumably or symptomatic onset
was 22 months and 14% or greater had secondary endointerventions with a relatively high mortality. Similarly, the study coming out of Italy, 26 cases, meantime of diagnosis of the infection is 20 months, and that 34.6% of these cases underwent secondary endovascular intervention.
Once again, a relatively high mortality at 38.4%. Study out of France, 11 institutions, 33 infective endographs, time of onset of symptoms 414 days, 30% of these individuals had undergone secondary interventions. In our own clinical experience of Pittsburgh,
we looked at our explants. There were 13 down for infection, and of those nine had multiple secondary interventions which was 69%, a little bit of an outlier compared to the other studies. Once again, a relatively high mortality at one year. There's now a plethora of information in the literature
stating that secondary interventions may be a source for Bacteremia in seeding of your endovascular graft. And I think beyond just a secondary interventions, we know there's a wide range of risk factors. Perioperative contamination, break down in your sterile technique,
working in the radiology suite as opposed to the operating room. Wound complications to the access site. Hematogenous seeding, whether it's from UTIs, catheter related, or secondary interventions are possible.
Graft erosion, and then impaired immunity as well. So what I can tell you today, I think there is an association without question from secondary interventions and aortic endograft infection. Certainly the case I presented appears to show causation but there's not enough evidence to fully correlate the two.
So in summary, endograft infections are rare fortunately. However, the incidence does appear to be subtly rising. Secondary interventions following EVAR appear to be a risk factor for graft infection. Graft infections are associated without question
a high morbidity and mortality. I think it's of the utmost importance to maintain sterile technique, administer prophylactic antibiotics for all secondary endovascular catheter based interventions. Thank you.
- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing
renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is
near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital
pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency
and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,
except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward
endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac
endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.
The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open
conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small
accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited
incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,
but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis
and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.
- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old
but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,
and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.
- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,
and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was
revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.
In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat
was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.
Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone
returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.
Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy
with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,
the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.
Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.
So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really
how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017
in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.
Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at
five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery
to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional
independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.
So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,
but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could
help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.
- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.
Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance
between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.
Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.
Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100
consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any
stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria
having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this
on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher
than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of
the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,
you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because
the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity
because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish
this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,
regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. Thank you very much.
- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.
It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.
So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations
of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.
Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.
So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient
who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal
angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near
or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility
was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.
Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal
or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection
or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.
So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump
to prevent hip disarticulation. Thank you for much for your attention.
- Thank you, Tim, and thank you, Frank, for giving me the opportunity to address this specific problem of the gutter endoleaks, which has been described up to 30% after ChEVAR and parallel grafting. But I have to say that in the most papers, not only gutter endoleaks were included,
but also new onset of type Ia endoleak. One paper coming from Stanford addressed specifically the question, how we should deal with the gutter-related type Ia endoleak, and they conclude that in the vast majority of the cases, these gutter endoleaks disappear
and the situation is benign. And based on my own experience, I can confirm this. This is one of the first cases treated with parallel grafts for symptomatic thoracoabdominal aneurysm. And I was a bit concerned as I saw this endoleak at the end of the angiography,
but the lady didn't have any pains and also no option for open or for other type of repair, so we waited. We waited and we saw that the endoleak disappeared after one month. And we saw also shrinkage of the aneurysm after one year.
So now, the next question was how to prevent this. And from the PERICLES registry, but also from the PROTAGORAS, we learned how to deal with this and how to prevent. And it's extremely important to oversize enough the aortic stent graft,
more than treating with the EVAR, normal EVAR. We should reach a sealing zone of at least 15, 20 millimeters. And we should avoid also to use more than two chimney grafts in such patients. The greater the number of the chimney used,
the higher is the risk of type Ia endoleak. And last but not least, we should use the right stent graft. And you see here the CT scan after using a flexible nitinol skeleton endograft on the left, and the gutters if you use a very stiff,
stainless steel skeleton in such situations. The last question was how to treat these patients. And based on the PERICLES, again, we should distinguish three different patterns. One is due to an excessive oversizing of the graft with infolding.
I have only one case, one professor of pathology, treated six years ago now without any endoleak due to this problem. The most are due to an undersized aortic endograft. And in the pattern C, we have an insufficient sealing zone and migration of the graft.
Now, we should consider the pattern B. And with an undersized aortic endograft and if the gutter is small, one possible solution would be to treat this patient with coiling, using coils or Onyx to occlude this gutter endoleaks,
like in this patient. And for the pattern C, if the sealing zone is insufficient, well, we should extend the sealing zone using the chimney parallel technique, as you can see in this case. So in conclusion, ladies and gentle,
gutters are usually benign and more than 95% disappeared in the follow-up. But in case of persistence, we should evaluate the CT scan exactly. And in case of oversizing and not enough oversizing and not enough length,
we should treat this patient accordingly. Thank you very much for your attention.
- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent
flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue
but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using
a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient
and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta
and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once
the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide
and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug
over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect
of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve
and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.
This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft
to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing
in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment
of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
- Thank you Professor Veith. Thank you for giving me the opportunity to present on behalf of my chief the results of the IRONGUARD 2 study. A study on the use of the C-Guard mesh covered stent in carotid artery stenting. The IRONGUARD 1 study performed in Italy,
enrolled 200 patients to the technical success of 100%. No major cardiovascular event. Those good results were maintained at one year followup, because we had no major neurologic adverse event, no stent thrombosis, and no external carotid occlusion. This is why we decided to continue to collect data
on this experience on the use of C-Guard stent in a new registry called the IRONGUARD 2. And up to August 2018, we recruited 342 patients in 15 Italian centers. Demographic of patients were a common demographic of at-risk carotid patients.
And 50 out of 342 patients were symptomatic, with 36 carotid with TIA and 14 with minor stroke. Stenosis percentage mean was 84%, and the high-risk carotid plaque composition was observed in 28% of patients, and respectively, the majority of patients presented
this homogenous composition. All aortic arch morphologies were enrolled into the study, as you can see here. And one third of enrolled patients presented significant supra-aortic vessel tortuosity. So this was no commerce registry.
Almost in all cases a transfemoral approach was chosen, while also brachial and transcervical approach were reported. And the Embolic Protection Device was used in 99.7% of patients, with a proximal occlusion device in 50 patients.
Pre-dilatation was used in 89 patients, and looking at results at 24 hours we reported five TIAs and one minor stroke, with a combined incidence rate of 1.75%. We had no myocardial infection, and no death. But we had two external carotid occlusion.
At one month, we had data available on 255 patients, with two additional neurological events, one more TIA and one more minor stroke, but we had no stent thrombosis. At one month, the cumulative results rate were a minor stroke rate of 0.58%,
and the TIA rate of 1.72%, with a cumulative neurological event rate of 2.33%. At one year, results were available on 57 patients, with one new major event, it was a myocardial infarction. And unfortunately, we had two deaths, one from suicide. To conclude, this is an ongoing trial with ongoing analysis,
and so we are still recruiting patients. I want to thank on behalf of my chief all the collaborators of this registry. I want to invite you to join us next May in Rome, thank you.
- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations
related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,
and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be
a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation
of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest
as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher
patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.
The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence
that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization
versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,
in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,
one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients
who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored
superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months
for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.
But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear
to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.
Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.
- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.
You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience
the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,
as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.
If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.
We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.
Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.
No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time
of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities
and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice
In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases
due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.
We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.
So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed
with multi-institution trial and longer follow-up
- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,
both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,
and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms
non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches
versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,
that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require
more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage
than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased
due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations
impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion
during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion
after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing
the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials
where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this
from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph
that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents
with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,
whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.
And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent
also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,
and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.
So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,
always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.
Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)
- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.
Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.
Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care
over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.
Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.
And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed
with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better
treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?
That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents
shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,
deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.
Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.
Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.
Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same
that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?
More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article
a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.
- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,
but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody
with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?
And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy
for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,
thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world
for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and
patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt
to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize
what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,
and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,
it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would
ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a
experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,
but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,
it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,
place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,
any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution
using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation
and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology
and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,
it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,
and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a
single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,
and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,
a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at
alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,
and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.
There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,
Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.
Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings
in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?
I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,
you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.
So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,
we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.
- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,
valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction
but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique
to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the
sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness
but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have
smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.
Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse
and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap
we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid
valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility
to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put
in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction
disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. 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.
- 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 Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try
to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.
And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,
secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group
is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted
by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.
And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use
those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,
but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.
For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions
for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,
and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.
But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,
so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at
the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions
at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR
predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive
of iliac limb reinterventions. Thank you very much.
- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery
in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,
but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase
and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,
and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast
in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.
So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,
it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause
of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.
So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes
and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,
and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR
might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement
without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac
Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,
to save our country from a type II endoleak, and I thank you for your attention.
- Thank you, Ulrich. Before I begin my presentation, I'd like to thank Dr. Veith so kindly, for this invitation. These are my disclosures and my friends. I think everyone knows that the Zenith stent graft has a safe and durable results update 14 years. And I think it's also known that the Zenith stent graft
had such good shrinkage, compared to the other stent grafts. However, when we ask Japanese physicians about the image of Zenith stent graft, we always think of the demo version. This is because we had the original Zenith in for a long time. It was associated with frequent limb occlusion due to
the kinking of Z stent. That's why the Spiral Z stent graft came out with the helical configuration. When you compare the inner lumen of the stent graft, it's smooth, it doesn't have kink. However, when we look at the evidence, we don't see much positive studies in literature.
The only study we found was done by Stephan Haulon. He did the study inviting 50 consecutive triple A patients treated with Zenith LP and Spiral Z stent graft. And he did two cases using a two iliac stent and in six months, all Spiral Z limb were patent. On the other hand, when you look at the iliac arteries
in Asians, you probably have the toughest anatomy to perform EVARs and TEVARs because of the small diameter, calcification, and tortuosity. So this is the critical question that we had. How will a Spiral Z stent graft perform in Japanese EIA landing cases, which are probably the toughest cases?
And this is what we did. We did a multi-institutional prospective observational study for Zenith Spiral Z stent graft, deployed in EIA. We enrolled patients from June 2017 to November 2017. We targeted 50 cases. This was not an industry-sponsored study.
So we asked for friends to participate, and in the end, we had 24 hospitals from all over Japan participate in this trial. And the board collected 65 patients, a total of 74 limbs, and these are the results. This slide shows patient demographics. Mean age of 77,
80 percent were male, and mean triple A diameter was 52. And all these qualities are similar to other's reporting in these kinds of trials. And these are the operative details. The reason for EIA landing was, 60 percent had Common Iliac Artery Aneurysm.
12 percent had Hypogastric Artery Aneurysm. And 24 percent had inadequate CIA, meaning short CIA or CIA with thrombosis. Outside IFU was observed in 24.6 percent of patients. And because we did fermoral cutdowns, mean operative time was long, around three hours.
One thing to note is that we Japanese have high instance of Type IV at the final angio, and in our study we had 43 percent of Type IV endoleaks at the final angio. Other things to notice is that, out of 74 limbs, 11 limbs had bare metal stents placed at the end of the procedure.
All patients finished a six month follow-up. And this is the result. Only one stenosis required PTA, so the six months limb potency was 98.6 percent. Excellent. And this is the six month result again. Again the primary patency was excellent with 98.6 percent. We had two major adverse events.
One was a renal artery stenosis that required PTRS and one was renal stenosis that required PTA. For the Type IV index we also have a final angio. They all disappeared without any clinical effect. Also, the buttock claudication was absorbed in 24 percent of patients at one month, but decreased
to 9.5 percent at six months. There was no aneurysm sac growth and there was no mortality during the study period. So, this is my take home message, ladies and gentlemen. At six months, Zenith Spiral Z stent graft deployed in EIA was associated with excellent primary patency
and low rate of buttock claudication. So we have most of the patients finish a 12 month follow-up and we are expecting excellent results. And we are hoping to present this later this year. - [Host] Thank you.
- Thank you for asking me to speak. Thank you Dr Veith. I have no disclosures. I'm going to start with a quick case again of a 70 year old female presented with right lower extremity rest pain and non-healing wound at the right first toe
and left lower extremity claudication. She had non-palpable femoral and distal pulses, her ABIs were calcified but she had decreased wave forms. Prior anterior gram showed the following extensive aortoiliac occlusive disease due to the small size we went ahead and did a CT scan and confirmed.
She had a very small aorta measuring 14 millimeters in outer diameter and circumferential calcium of her aorta as well as proximal common iliac arteries. Due to this we treated her with a right common femoral artery cutdown and an antegrade approach to her SFA occlusion with a stent.
We then converted the sheath to a retrograde approach, place a percutaneous left common femoral artery access and then placed an Endologix AFX device with a 23 millimeter main body at the aortic bifurcation. We then ballooned both the aorta and iliac arteries and then placed bilateral balloon expandable
kissing iliac stents to stent the outflow. Here is our pre, intra, and post operative films. She did well. Her rest pain resolved, her first toe amputation healed, we followed her for about 10 months. She also has an AV access and had a left arterial steel
on a left upper extremity so last week I was able to undergo repeat arteriogram and this is at 10 months out. We can see that he stent remains open with good flow and no evidence of in stent stenosis. There's very little literature about using endografts for occlusive disease.
Van Haren looked at 10 patients with TASC-D lesions that were felt to be high risk for aorta bifem using the Endologix AFX device. And noted 100% technical success rate. Eight patients did require additional stent placements. There was 100% resolution of the symptoms
with improved ABIs bilaterally. At 40 months follow up there's a primary patency rate of 80% and secondary of 100% with one acute limb occlusion. Zander et all, using the Excluder prothesis, looked at 14 high risk patients for aorta bifem with TASC-C and D lesions of the aorta.
Similarly they noted 100% technical success. Nine patients required additional stenting, all patients had resolution of their symptoms and improvement of their ABIs. At 62 months follow up they noted a primary patency rate of 85% and secondary of 100
with two acute limb occlusions. The indications for this procedure in general are symptomatic patient with a TASC C or D lesion that's felt to either be a high operative risk for aorta bifem or have a significantly calcified aorta where clamping would be difficult as we saw in our patient.
These patients are usually being considered for axillary bifemoral bypass. Some technical tips. Access can be done percutaneously through a cutdown. I do recommend a cutdown if there's femoral disease so you can preform a femoral endarterectomy and
profundaplasty at the same time. Brachial access is also an alternative option. Due to the small size and disease vessels, graft placement may be difficult and may require predilation with either the endograft sheath dilator or high-pressure balloon.
In calcified vessels you may need to place covered stents in order to pass the graft to avoid rupture. Due to the poor radial force of endografts, the graft must be ballooned after placement with either an aortic occlusion balloon but usually high-pressure balloons are needed.
It usually also needs to be reinforced the outflow with either self-expanding or balloon expandable stents to prevent limb occlusion. Some precautions. If the vessels are calcified and tortuous again there may be difficult graft delivery.
In patients with occluded vessels standard techniques for crossing can be used, however will require pre-dilation before endograft positioning. If you have a sub intimal cannulation this does put the vessel at risk for rupture during
balloon dilation. Small aortic diameters may occlude limbs particularly using modular devices. And most importantly, the outflow must be optimized using stents distally if needed in the iliac arteries, but even more importantly, assuring that you've
treated the femoral artery and outflow to the profunda. Despite these good results, endograft use for occlusive disease is off label use and therefor not reimbursed. In comparison to open stents, endograft use is expensive and may not be cost effective. There's no current studies looking
into the cost/benefit ratio. Thank you.
- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.
And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.
Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,
it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized
due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage
of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,
which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal
in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak
which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.
And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success
is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent
Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,
an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,
retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered
balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.
At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed
if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.
The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR
combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,
and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.
- Thank you chairman, ladies, and gentlemen. These are my disclosures. The objective was to asses the prognostic value of a high or immeasurable Ankle-Brachial Index at baseline for major amputation and Amputation Free Survival in patients with CLTI. And, we did this within two randomized control trials,
the PADI trial and the JUVENTAS trial, which I will spend a bit on later. We did a regression analysis of both trials, and had data pooled at a patient level, looking at risk factors such as Diabetes, Cardiovascular Comorbidities,
and Ankle-Brachial-Index. Patients were divided in either low, intermediate, or a high, or immeasurable, ABI. So, in short, the PADI trial was a Multicenter 2-arm randomized clinical trial with controls looking at Rutherford Category over three on
Infrapopliteal Lesions comparing Drug Eluting Stents verses PTA and without bail out stenting, endpoints, patency, major amputation, and mortality. This study was published in 2017. The JUVENTAS Trial, was a stem cells trial with double-blinded placebo controlled giving a
infusion of bone marrow stem cells versus placebo. And again, the endpoints were major amputation and mortality, published in 2015. Overall from these two trials, we were able to collect 260 patients, and this is the baseline table.
You can see that the majority of patients fitted in the Low ABI group, 146 patients. And, 33 patients fitted in the High ABI group. Overall, the prevalence of Diabetes, History of Stroke Coronary Disease, and Impaired Renal Function, was significantly higher in the High ABI group.
Follow-up of these patients with median of 229 weeks, and in this period we observed 59 amputations, and 103 deaths. The majority of this major amputations was performed, actually, in the first year after inclusion within these trials,
which you can see here in this Kaplan Meier Curve, showing that the amputation rate was about double in the High ABI group, as compared to the Low or Intermediate group. Looking at ABI for its Amputation Free Survival, again showed significantly higher rate of amputations
in the High ABI group, as compared to Low or Intermediate. And, at five years, you can see that almost all patients in the High ABI group either had amputation or had died. This was about 50% in the Low or Intermediate group. Looking at the Multivariate Regression Analysis, we observe the Rutherford Category and ABI
in the High or Immeasurable group, related to major amputation, and is same for amputation or death, now adding also age. So, the interrelation between ABI and major events, is J shaped, and actually, there's a higher risk for patients with a high or immeasurable ABI for major events,
as compared to patients with a low ABI. So why is this so? Well, it's not fully elucidated, but it's believed to be related to Medial Arterial Calcifications, being an independent age associated pathway different from Atherosclerosis.
And, the stiffness due to this calcification, may prevent compensatory positive remodeling related to Atherosclerosis when both diseases coincide. And, actually it's coexistence of Medial Calcification Atherosclerosis is not that uncommon, even up to 80%. So, what is the clinical relevance of all this?
Well, we did look at the PREVENT-III prediction model for Amputation Free Survival. You can see on the slide, the included factors in the original PREVENT-III model. We added the I, or Immeasurable ABI to this model, and has lead to an increase in C-statistics from 46% to 72%
Net Reclassification Improvement of 0.38. So, ladies and gentlemen, in conclusion, a high or immeasurable ABI in patients with CLTI and Infrapopliteal Arterial Obstructive Disease is an independent risk factor of major amputation and of poor Amputation Free Survival.
Incorporating this factor in a PREVENT-III prediction model improves its performance. Thank you very much, also to the research groups.
- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent
secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results
in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different
in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,
or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,
PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus
or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk
of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,
but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.
and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.
Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.
So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.
Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.
In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,
and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide
a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.
And an E-portal is being developed for dissemination. Thank you very much.
- Thank you Mr Chairman, ladies and gentlemen. These are my disclosure. Open repair is the gold standard for patient with arch disease, and the gupta perioperative risk called the mortality and major morbidity remain not negligible.
Hybrid approach has only slightly improved these outcomes, while other off-the-shelf solution need to be tested on larger samples and over the long run. In this scenario, the vascular repair would double in the branch devices as emerging, as a tentative option with promising results,
despite addressing a more complex patient population. The aim of this multi-center retrospective registry is to assess early and midterm results after endovascular aortic arch repair. using the single model of doubling the branch stent graft in patient to fit for open surgery.
All patient are treated in Italy, with this technique. We're included in this registry for a total of 24 male patient, fit for open surgery. And meeting morphological criteria for double branch devices.
This was the indication for treatment and break-down by center, and these were the main end points. You can see here some operative details. Actually, this was theo only patient that did not require the LSA
re-revascularization before the endovascular procedure, because the left tibial artery rising directly from the aortic arch was reattached on the left common carotid artery. You can see here the large window in the superior aspect of the stent graft
accepting the two 13 millimeter in the branches, that are catheterized from right common carotid artery and left common carotid artery respectively. Other important feature of this kind of stent graft is the lock stent system, as you can see, with rounded barbs inside
the tunnels to prevent limb disconnection. All but one patient achieved technical success. And two of the three major strokes, and two retrograde dissection were the cause of the four early death.
No patient had any type one or three endoleak. One patient required transient dialysis and four early secondary procedure were needed for ascending aorta replacement and cervical bleeding. At the mean follow-up of 18 months,
one patient died from non-aortic cause and one patient had non-arch related major stroke. No new onset type one or three endoleak was detected, and those on standard vessel remained patent. No patient had the renal function iteration or secondary procedure,
while the majority of patients reported significant sac shrinkage. Excluding from the analysis the first six patients as part of a learning curve, in-hospital mortality, major stroke and retrograde dissection rate significant decrease to 11%, 11% and 5.67%.
Operative techniques significantly evolve during study period, as confirmed by the higher use of custom-made limb for super-aortic stenting and the higher use of common carotid arteries
as the access vessels for this extension. In addition, fluoroscopy time, and contrast median's significantly decrease during study period. We learned that stroke and retrograde dissection are the main causes of operative mortality.
Of course, we can reduce stroke rate by patient selection excluding from this technique all those patient with the Shaggy Aorta Supra or diseased aortic vessel, and also by the introduction and more recent experience of some technical points like sequentIal clamping of common carotid arteries
or the gas flushing with the CO2. We can also prevent the retrograde dissection, again with patient selection, according to the availability of a healthy sealing zone, but in our series, 6 of the 24 patients
presented an ascending aorta larger than 40 millimeter. And on of this required 48-millimeter proximal size custom-made stent graft. This resulted in two retrograde dissection, but on the other hand, the availability on this platform of a so large proximal-sized,
customized stent graft able to seal often so large ascending aorta may decrease the incidence of type I endoleak up to zero, and this may make sense in order to give a chance of repair to patients that we otherwise rejected for clinical or morphological reasons.
So in conclusion, endovascular arch repair with double branch devices is a feasible approach that enrich the armamentarium for vascular research. And there are many aspects that may limit or preclude the widespread use of this technology
with subsequent difficulty in drawing strong conclusion. Operative mortality and major complication rates suffer the effect of a learning curve, while mid-term results of survival are more than promising. I thank you for your attention.
- Good morning everybody. Here are my disclosures. So, upper extremity access is an important adjunct for some of the complex endovascular work that we do. It's necessary for chimney approaches, it's necessary for fenestrated at times. Intermittently for TEVAR, and for
what I like to call FEVARCh which is when you combine fenestrated repair with a chimney apporach for thoracoabdominals here in the U.S. Where we're more limited with the devices that we have available in our institutions for most of us. This shows you for a TEVAR with a patient
with an aortic occlusion through a right infracrevicular approach, we're able to place a conduit and then a 22-french dryseal sheath in order to place a TEVAR in a patient with a penetrating ulcer that had ruptured, and had an occluded aorta.
In addition, you can use this for complex techniques in the ascending aorta. Here you see a patient who had a prior heart transplant, developed a pseudoaneurysm in his suture line. We come in through a left axillary approach with our stiff wire.
We have a diagnostic catheter through the femoral. We're able to place a couple cuffs in an off-label fashion to treat this with a technically good result. For FEVARCh, as I mentioned, it's a good combination for a fenestrated repair.
Here you have a type IV thoraco fenestrated in place with a chimney in the left renal, we get additional seal zone up above the celiac this way. Here you see the vessels cannulated. And then with a nice type IV repaired in endovascular fashion, using a combination of techniques.
But the questions always arise. Which side? Which vessel? What's the stroke risk? How can we try to be as conscientious as possible to minimize those risks? Excuse me. So, anecdotally the right side has been less safe,
or concerned that it causes more troubles, but we feel like it's easier to work from the right side. Sorry. When you look at the image intensifier as it's coming in from the patient's left, we can all be together on the patient's right. We don't have to work underneath the image intensifier,
and felt like right was a better approach. So, can we minimize stroke risk for either side, but can we minimize stroke risk in general? So, what we typically do is tuck both arms, makes lateral imaging a lot easier to do rather than having an arm out.
Our anesthesiologist, although we try not to help them too much, but it actually makes it easier for them to have both arms available. When we look at which vessel is the best to use to try to do these techniques, we felt that the subclavian artery is a big challenge,
just the way it is above the clavicle, to be able to get multiple devices through there. We usually feel that the brachial artery's too small. Especially if you're going to place more than one sheath. So we like to call, at our institution, the Goldilocks phenomenon for those of you
who know that story, and the axillary artery is just right. And that's the one that we use. When we use only one or two sheaths we just do a direct puncture. Usually through a previously placed pledgeted stitch. It's a fairly easy exposure just through the pec major.
Split that muscle then divide the pec minor, and can get there relatively easily. This is what that looks like. You can see after a sheath's been removed, a pledgeted suture has been tied down and we get good hemostasis this way.
If we're going to use more than two sheaths, we prefer an axillary conduit, and here you see that approach. We use the self-sealing graft. Whenever I have more than two sheaths in, I always label the sheaths because
I can't remember what's in what vessel. So, you can see yes, I made there, I have another one labeled right renal, just so I can remember which sheath is in which vessel. We always navigate the arch first now. So we get all of our sheaths across the arch
before we selective catheterize the visceral vessels. We think this partly helps minimize that risk. Obviously, any arch manipulation is a concern, but if we can get everything done at once and then we can focus on the visceral segment. We feel like that's a better approach and seems
to be better for what we've done in our experience. So here's our results over the past five-ish years or so. Almost 400 aortic interventions total, with 72 of them requiring some sort of upper extremity access for different procedures. One for placement of zone zero device, which I showed you,
sac embolization, and two for imaging. We have these number of patients, and then all these chimney grafts that have been placed in different vessels. Here's the patients with different number of branches. Our access you can see here, with the majority
being done through right axillary approach. The technical success was high, mortality rate was reasonable in this group of patients. With the strokes being listed there. One rupture, which is treated with a covered stent. The strokes, two were ischemic,
one hemorrhagic, and one mixed. When you compare the group to our initial group, more women, longer hospital stay, more of the patients had prior aortic interventions, and the mortality rate was higher. So in conclusion, we think that
this is technically feasible to do. That right side is just as safe as left side, and that potentially the right side is better for type III arches. Thank you very much.
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