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The PREPIC Trial: Fact Or Fiction
The PREPIC Trial: Fact Or Fiction
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Transcript

- Afternoon. It's a privilege to be presenting this today. I have no disclosures. If you look at this, this is a picture of the last 10 IVC filters approved by the FDA. You'll notice that they all have some mechanism of removal most commonly hooks.

You may ask yourself, why is that? And the reason for this is basically one or two studies. Basically the PREPIC study which was originally published in 1998 with two-year data, followed by a publication in Circulation with eight-year data.

Now the PREPIC itself, the study itself was the first prospective, randomized trial comparing anticoagulation to IVC filters. It was performed from 1991 to 1995 in France. 400 patients with DVT that were considered at risk for PE were enrolled.

And they were randomized at first either unfractionated versus fractionated heparins, and then IVC filter versus no IVC filter. And the filters used are demonstrated here, the Greenfield, the Cardinal, LGM, and Bird's Nest. And all patients were anticoagulated with warfarin

at the time of discharge whenever possible. Primary outcome was pulmonary embolism. The secondary outcomes were DVT, death, major filter complications, and major bleeding. And again, the data was published at two and eight years. So the two-year results, the PREPIC study,

they presented first some data on unfractionated versus fractionated heparin, but then this table. And this table shows basically that there was no difference in symptomatic PE between groups. But there was a difference in recurrent DVT

with patients having a filter in place having a higher incidence of DVT than those that did not. And the thought was that this presence of the filter increased the risk of DVT. Now the data at eight years, published in Circulation, did show a difference between symptomatic pulmonary embolism

with patients having a filter having a lower incidence of recurrent PE. However, the symptomatic DVT remained elevated in patients that had filters in place. And this was statistically significant. Of note, there was a fairly significant number of patients

that had cable thrombosis in the group that had filters that may have contributed to this number. So if you want to be critical about the study, there are a few things that are a little bit unperfect I guess you could say. It's now thought as a study of filter randomization

in patients with DVT, but it was actually also a study looking at unfractionated and low molecular weight heparins. And this lends itself to be a fairly weak study designed to make conclusions on IVC filters, the performance of IVC filters, and it's underpowered really to make a definitive conclusion.

The other problem with this study is that there's a wide variety of filters, I mean a Bird's Nest and the Greenfield, they're very different filters. And that lack of standardization I think is problematic. These filters both can have different rates

of IVC thrombosis, which can affect the data. So the statistical analysis was less than perfect. They should have corrected for multiple comparisons which they did not. And it also showed that PE can occur remotely, and if you don't have a filter in place,

it's probably not protective, obviously. So a PREPIC study was recently published, the PREPIC 2 in 2015. And this asks the question, do patients with acute PE at high risk of recurrence benefit from IVC filter in addition to anticoagulation?

So it was a multicenter trial in France. They had about 400 patients that were randomized, half into filters, half into no filters. Their risk factors are listed, and they're quite broad. And all filters were removed at three months. And they had follow up at three and six months.

And this is the data. The data at three months shows that there was no difference in recurrent PE between the patients with filters and the patient without filters. And at six months this remained the same. And there was no difference in DVT

between groups at six months. So fact or fiction? Well I think the PREPIC studies are mostly fact with maybe a little bit of fiction thrown in. The data from PREPIC suggests that patients with IVC filters have an increased risk of DVT long term,

but a decreased risk of PE long term. PREPIC 2 suggests that IVC filters may not decrease the risk of PE in high-risk patients, and did not show an association between filters and recurrent DVT at six and three months. Thank you.

- [Tarek] Good morning. First of all I would like to thank Professor Yakes who allowed me to be with you for the second year. I'm getting used to, for something different, which is a story, how we build our Vascular Malformation Program with a 13-year experience in Cairo's International Medical Center.

This my disclosures. Always we have another diagnostic and treatment dilemma with vascular malformation in Egypt. They usually misdiagnose, for one case, you seen someone did a foreign lesions, the neck, many investigation unnecessary,

duplex ultrasound, MR with contrast, CT angio, direct angiography and venography, ending with the same result, probably vascular malformation. But after discussion with Wayne, he told me, "I realize now that "every country in the world has

"the same problem, not only Egypt." They usually left untreated infantile hemangioma, told by the doctor, leave it alone, it will disappear, and never happen. Or, in this 30-year gentleman, extensive venous malformation, left it untreated because

there is no hope for treatment. Or, mistreated, just laser repair for a capillary malformation, mark left alone. This one was a terrible case as we noted that having a misdiagnosis intranatally as an enteratoma mistreated in his first day of life

with extensive surgery, complete facial denervation. When you do the MRI and clinically it is just venolymphatic and need to treatment and you don't know to treat the lesion or treat the complication. So even cases were sent to some centers abroad

with no valuable outcomes. So my dream was to having a new treatment strategy based on a multidisciplinary approach with full integration of the endovascular therapy to improve the patient outcome. So this came true with Professor Yakes in 2005

with a dedicated team and a patient database following the ISSVA classification. We started with patient and family teaching and counseling. They are happy now. And spread of the knowledge to the vascular surgeon of Egypt by publication of Professor Yakes in our

Egyptian Journal for Vascular and Endovascular Surgery. In 2008 we have the first case in Egypt treated with propranolol. As the same year was the discovery for treatment of the infantile angioma. And then nine-months age child

treated with propranolol for two years and then for six year follow-up with good result. We also published this for the knowledge spreading. We picked this case from her neurosurgeon before undergoing an heroic operation at the age of three months age

treated with propranolol oral for one year and with very good recovery. Also publication for spreading the knowledge. Then we start to do that but increase the public awareness by some TV program. On that was Professor Yakes that he shared

in this program also shows that normal people in Egypt can now know that how we diagnose, how we pick the cases and what is the way of treatment. Also spreading of the knowledge between the vascular surgeon in Egypt

and I acknowledge Professor Rahmat Saad is here and he is with us. So most of the vascular surgeon in Egypt now knows that how we pick and how we treat the cases. Also getting Professor Yakes in these meetings. We attracted Professor Vogelzang

all we know, well published in the literature, Professor Evan Seev, the father of EVAR and directed the beginning of the vascular malformation treatment in Sweden, Hamburg and London. I don't know why he's feeling sick.

(audience laughs) Okay, they have been interesting to visit our developing center. But also active, very active, sorry I'll get one, very active, one of the cases he came to us with history of some bleeding from the skull ligation of the external carotid artery

before we put in his sleep. We need six hands to stop the bleeding until all the three professors worked on him with six hours to stop the bleeding and to embolize him. Right carotid venous was shown to some stage. Making of coils from just simple wires

at 2 a.m. in the morning, we done everything. This is a left vertebral using these coils and directional injections and this I the end of the one-hour stage of the treatment until in the morning we can see at least now the scalp itself, now we can see.

And this, four days before he go home for follow-up treatment. At one of the occasion we seen 17 new cases in the outpatient clinic, seven and a half p.m. after a long day we start the clinic to see 70 cases.

Our center now is known as a center of excellence in Egypt for diagnosing and treating the vascular malformation, picking the cases not only from Cairo, Egypt but also from the surrounding countries. We seen patient from everywhere around us. This is vascular malformation workload since 2005

starting only with four cases with Professor Yakes and after proper spread of the knowledge to the public and the doctors in Egypt we, in last September, we treated 110 cases in continuous three and a half days working. This is the distribution of the case.

We see now, at least between three and four cases every week. Now the current situation in Egypt is that, misdiagnosis and mistreated are avoided, early pick up of de-novo case, we have one center of excellence

engaged with the larger malformation patient population and a full experienced expert attending on regular basis which allow for a faster ramp-up experience and, decreasing the complication rates. Now I would like you to come and visit Egypt so you can see the pyramids, Sphinx,

you may go up to Abu Simbel, Luxor, see Ramses temple but if you come closer, you might see Yakes and Radwan. Thank you. (audience laughter)

- Thank you Clem. These are my disclosures, so why single session? Why, Steve did an unbelievable job discussing pharmacomechanical techniques but why have we moved there? I think the answer is inherent. We don't want the cases to go as long as CAVENT

for numerous reasons, the long procedure investment, the costs, the bleeding risks. So there's a number of devices that allow us to perform rapid clot removal, single session therapy. Many of them are listed here, and again,

the advantages are intrinsic. It's going to make the clot go away faster, it's going to reduce the cost, reduce the need for escalated care in this patient population. The disadvantages, again,

Steve had really touched upon this, you don't need to pay for a thrombectomy device, you're clearly going to be more liberal with the use of balloons and stents, and we've clearly seen that in our practice here in New York as well.

A larger sheath, you may leave some clot behind. We don't know whether that's disadvantageous, could that lead to poor outcomes? Is there more trauma to the valvular system leading to venous, deep venous insufficiency? So this is not a new concept.

This is a case series from Hopkins over 10 years ago which show with the introduction of mechanical techniques, you can reduce the procedure time by 50% as well as the lytic dose, and that leads to actually greater technical success rate and reduced cost.

Peter Lin in Texas echoed these outcomes as well with reduced ICU stay, reduced hospital stay, reduced bleeding complications, and again, reduced costs. Tony Comerota answered the question, I think fairly well, about whether or not there's valvular damage done by these mechanical devices

by specifically demonstrating that there were actually more cases with normal valvular function following angiojet thrombectomy than with actually just CDT, suggesting that angiojet in fact can be safe and not lead to deep venous valvular insufficiency. We obviously know that 70% of patients treated medically

at five years will have some degree of the post-thrombolic syndrome and so the ability to maintain an open vein and alleviate a patients symptoms is intuitive. And with the introduction of endovascular techniques with a modicum of cost,

you seem to be able to achieve significant patient quality of life. I was honored to serve on a multi-center U.S. feasibility study looking at the injuries of thrombectomy for DVT clearance where we were able to reduce the time by over 50% as compared to the CAVENT data,

or to the historic venous registry, also reducing the bleeding complications at the same time. That registry used the six french catheter and this is just a representative case using the six french catheter, sort of classic iliofemoral DVT here.

And then eight hours later this required two sessions in a lab. We were able to get complete patency to the entire iliofemoral segment. This was done as outpatient therapy. The patient was put on Lomoh-lequit Heparin

and discharged home the same day. We now have an eight french catheter which has introduced us into the single session realm of therapy. I'm not going to belabor the point about the technical nuances but it is a much more powerful mechanical technique.

And so here's a recent case that we've performed using the eight french catheter, the eight french technology, again, acute iliofemoral popliteal vein, DVT with complete obstruction to outflow in the symptomatic leg.

Again you have the eight french catheter. This is now being used to infuse a thrombolytic agent with a standardized protocol where we use so called power pulse techniques introducing a bow less of a thrombolytic agent in our center. It's ulta placed into the thrombosed vein

and then the catheter is used in a more traditional form used in it's so called thrombectomy mode. And this is just an hour later. And you can see the entire segment is completely cleared of all clot and if you can tell based on the picture here, there appears to be

a narrowing in the common iliac vein which we interrogated with intravascular ultrasound. This was the patients right leg so we were a little bit surprised it was a problem here but this is the pullback from the IVC, and you'll see there's going to be circumferential wall

thickening and a narrowing right when we get down to here, and that's the common iliac vein that was showing up on the veno gram. This was a young patient, we didn't feel it was appropriate to leave this untreated and so we placed an open cell Nitinol Stent here

and you can see that there's a waste clearly at the iliac vein confluence. This was successfully post-dilated. And this is two hours after the procedure was initiated where again we have complete patency to the entire segment. So to conclude,

I would say that rapid flow restoration is now technically feasible. It's a safe method of endovascular treatment of DVT. It results in shorter thrombolytic infusion times, now as low as two hours compared to standard DVT rated between 55 and 60 hours.

This leads to decreased bleeding risks due to lower duration of the thrombolytic agent, decreased costs due to the elimination of the patient going to a monitored care setting, and improved patient satisfaction with faster recovery and less morbidity.

Thank you for your attention.

- 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.

- Thanks again. So I've been charged with talking about drug drug interactions with statins and I have no disclosures. (reads on screen definition) Using that definition, statins have very little, if any,

chemical interactions with other drugs However, what the intent I think of the title is looking at statin levels. How statin levels are affected by drugs which alter the enzmyatic pathways of statin metabolism.

And we know that statins are HMG CoA reducatase is responsible for the rate limiting step of cholesterol synthesis and drugs that inhibit HMG CoA reduce cholesterol.

(reads slide) P-glycoprotein is a transporter protein that moves substances across cell membranes. And this is a list of the common statins and how they interact with P450 substrates. We have the CYP3A4 substrate

and atorvastatin is a major example there and the CYP2C9 substrates and Rosuvastatin. And I'll call you attention to the fact that the most commonly used and most effective statins, Atorvastatin and Rosuvastatin,

are both long half lives compared to the other statins. Now another thing I want to call your attention to 'cause it has clinical implications is the variation in breast cancer resistant protein (BCPR) gene but it alters the absorption

and it significantly increases the absorption of statins from the GI tract. And you can see that Asians are particularly affective and that's why recommendations for beginning statins in Asians are to start at a lower dose and then ramp up rather than start

at the typically maximal dose for most of our arthoscopic patients. Now risk factors thought to be due to interactions are advanced age, frailty, hepatic dysfunction, those with alcohol abuse, renal dysfunction, hyperthyroidism, woman and Asians.

And if they have any of these, we want to dose adjust but that's for risk factors. (reads on screen definition) Now grapefruit juice is often talked about and its due to its interactions with furocoumarins

and Atorvastatin has a large effect and Rosuvastatin very little effect when grapefruit juice is taken. If a patient want to drink six or seven ounces of grapefruit juice a day or every other day, that's fine, we don't want them

drinking a quart of grapefruit juice a day. Simvastatin is particularly a risky statin. It's at higher risk for drug interactions. It's at high risk for being involved with genetic polymorphisms. It has a dose related toxicity

unlike Rosuvastatin and Atorvastatin. And I told you about the FDA warnings. So lets make it easy on how to manage the patients. If a patient has liver disfunction or they're on Niacin, and if they're on Niacin,

I'd rather discontinue the Niacin and keep the statin, treat them with caution. If a patient has renal dysfunction for all statins except for Atorvastatin, adjust the dose.

If a patient is on Digoxin, monitor the dige-level in these patients if they are on a statin because the dige-level can increase. And then we want to avoid statins in patients that need

any of the azol antifungal such as ketoconazole or the mycin antibiotics or cyclosporine. Avoid fibrates and especially genfibrozil and the protease inhibitors if your patient is on an HIV protease inhibitors. (reads on screen information)

Thank you very much.

- I have nothing to disclose. So, just as a matter of background, you've heard a lot about catheter-directed thrombolysis as a means to improve RV function in patients with acute pulmonary embolism. I think there's a lot of limitations to a catheter-directed thrombolytic strategy,

including need for ICU stay for catheters, need for thrombolytics, which even at low dose do carry a finite risk of intracerebral hemorrhage, and other cost related issues. And so, again, to reiterate the last two speakers, a single session, non-lytic based therapy

that's definitive for pulmonary embolism certainly could have a lot of use. And so, I don't really need to outline the importance of the RV to LV ratio as a marker for high risk in pulmonary embolism other than to say that it is very difficult to do a randomized prospective

clinically blinded study in pulmonary embolism for this fact that in the submassive population we're used, unfortunately, used to having surrogate markers for clinical improvement, such as improvement in RV LV ratio. Nevertheless, it is a good outcome

in that it is very reproducible. CT scanning has been shown to be the best way to really get reproducible results with RV to LV ratio. I will talk about the FlowTriever System, which in its original design consisted of an aspiration catheter which is a 20 French catheter

directed from the femoral vein typically into the pulmonary arteries and then the FlowTriever Device which is these nitinol disks that can grasp the clot and help it withdraw and then the retraction aspiration system which is a manual suction based system to withdraw the nitinol frame

as well as to aspirate the clot. So, this procedure and device were studied in the FLARE Study. We wanted to evaluate the safety and efficacy of this device. We looked at 106 patients in 18 sites.

It was prospective single arm multi-center, and we looked at outcomes at 48 hours and 30 days, primarily looking at efficacy with the primary outcome being reduction in RV to LV ratio at 48 hours as well as safety which was a composite major adverse event rate, including device related death, major bleeding

according to the VARC-2 definition, as well as treatment related adverse events such as clinical deterioration, pulmonary vascular injury, cardiac injury, all of the things, the dreaded complications that we worry about when instrumenting these patients who are acutely ill.

We measured these outcomes at 48 hours and followed the data with the typical Data Safety Monitoring Board and Clinical Events Committee that were all independent. So, the inclusion criteria were typical patients aged 18 to 75.

They had to have evidence of proximal pulmonary embolism by CTA. Most of these patients would probably fit into what we would call an intermediate high risk by modern definition. We did exclude patients who were profoundly hypotensive,

patients that had evidence of perhaps chronic pulmonary embolism. They did have to have heart rates less than 130 as well. The exclusion criteria, we didn't want to blur the results with patients who had failed thrombolysis. So that was excluded.

We didn't want to have patients with severe pulmonary hypertension greater than 70, which perhaps might be an indication of chronic pulmonary embolism. Vasopressor requirements, people who had FiO2s greater than six liters per minute to keep their sats up, patients who were profoundly anemic,

patients who had recent cardiac or pulmonary surgery, as well as actively progressive cancer. Of note, patients with a high bleeding risk other than what I had mentioned were included in the trial. We had a very successful enrollment as you can see. We had 106 patients that were enrolled, one of which was

enrolled but unfortunately did not meet eligibility. She had undiagnosed metastatic breast cancer at the time of her enrollment, and so, that was the one patient that ended up resulting in a study related death. We had two patients who received thrombolytics adjunctively

as part of the procedure. That data was analyzed separately. So really the core of the patients were 104 patients who were treated only with the FlowTriever and did not get any adjunctive thrombolytics. As far as baseline characteristics,

we treated 106 patients. The average age was 55.6. The mean BMI was 36.1. I'm based in Louisville, Kentucky and that's below average for our BMI. But unfortunately, DVT and PE is a disease

of obesity, which is only increasing in this country. You had the typical other comorbidities including hypertension, coronary artery disease. 73 patients or 69% had concurrent DVT. Several patients had a history of prior DVT or a prior pulmonary embolism.

As far as the characteristics, we had sPESI score of one in about 45% of the patients, positive troponin in 60%, D-Dimer of 75%, elevated BNP in 73%. Most of these patients had bilateral pulmonary emboli. And as far as prior treatment, most of them got unfractionated heparin.

Some of them got low molecular weight heparin. Almost all of them had femoral access from the right. The other alternative access was from the left. We did not have any patients in this trial that were treated from the internal jugular approach, although that is possible with this procedure.

As far as the devices used, there were a mean of 1.7 devices. We had three sizes, small, medium, and large with an average number of passes of four passes for the treatment, a mean procedure time of one hour and 39 minutes ranging from 39 minutes up to three hours,

and we had zero technical complications in terms of success for delivery, deployment, or retraction of the disks. Here's the example of the delivery of the catheter. You can see in real the advancement of a 20 French catheter from the femoral venous approach over a stiff guide wire into the pulmonary artery.

So, as far as delivery this proved to be quite technically successful and feasible. You can now see that the FlowTriever disks are deployed within the pulmonary artery. You can see that there are two disks deployed. One disk remains retracted into the aspiration guide

catheter and it turns out for our technical point that was the most important thing was to place the aspiration guide catheter close to the clot and then you can see examples of the type of clot removed here. As far as the main efficacy outcome we had

a decrease in the RV LV ratio from 1.5 at baseline to 1.15 with a reduction of .39, which falls in line with all of the other devices and catheter-directed thrombolytic therapies which also seemed to result in a improvement into the RV LV ratio of very similar magnitude.

As far as the clinical outcomes, most patients stayed about one day in the ICU. 44 out of the 106 had zero ICU time. There was three days to discharge on average and we had one patient of all cause mortality, which turned out to be a patient that

died in hospice due to metastatic breast cancer. As far as major adverse events, we had no intracranial hemorrhage, no access site major bleeding, no decide related death, pulmonary injury or cardiac injury. We had one patient with a bleeding event and three patients with treatment

related clinical deterioration. The adverse bleeding event occurred very early in the clinical experience. This patient had hemoptysis and hemothorax after the procedure, and ended up being treated with a lobectomy.

We had three patients with clinical deterioration including worsening PE requiring surgery, cardiogenic shock requiring treatment for cardiogenic shock, and then one patient became agitated and VF-ed prior to actually having the procedure and was treated with defibrillation.

Of note, all four of these patients despite their major adverse clinical outcomes survived to the 30 day end point. I already talked about the relative improvement in RV to LV ratio. Relative to some of the other trails you've seen it falls directly in line and the safety,

I think the big safety note is that the major bleeding rate was quite low in this procedure with no major device related bleeding. So in conclusion, catheter-directed mechanical thrombectomy using the FlowTriever without the use of thrombolysis is safe and effective in improving RV function

in patients with intermediate risk PE. It's associated with a low ICU time, a low total hospital time, and I think it establishes a non-thrombolytic basis for acute, for treatment of acute pulmonary embolism. Certainly there's more investigation needed.

Thank you very much.

- Good afternoon. These are my disclosure. We all know that ectatic common iliac arteries especially in presence of an abdominal aortic aneurysm tend to dilate with time. For example, if you look at the yellow line, in a common iliac artery of 20 millimeters

is growing five millimeters in five years. If this is not important in open repair, it's crucial for endovascular repair, because it represents the landing zone of the procedure. We have already that if you look at the patient for 14 months you don't find any degree of dilation

in patients treated with a bell-bottom. Again, we heard about these long-term results, but actually, only eight patients reached the five year follow up in this paper. So time is crucial. And we, now and then, encounter many patients

following them up along their life, that when we land in short, ectatic iliac sealing zones, then we encounter these type one endoleak for migration of the iliac limb inside the angiograft. Recently reviewed our experience of 610 patients, with a mean follow-up of 99 months

and we found that one-fourth of the patients are still alive after 14 years. So you have to afford very long-term good results. And this is only possible if you have trustable sealing zones. If you want to avoid type one endoleaks and rupture

in case of ectatic iliac arteries, you have to follow them all, and you have to be very aggressive in treating the complication. Two months ago we published this paper, presented at the ESVS meeting.

And we divided our cohort of patients in those with an ectatic iliac artery and those with normal iliac arteries. What we found was that the patient with ectatic iliac arteries, of course, were a little bit at higher risk

in terms of heart disease, cerebrovascular disease, and kidney disease. But in the late outcomes of these patient, was found that Type Ib endoleak was much higher than those in patients with normal iliacs. Reintervention rate was also higher.

In terms of overall mortality, patient with the larger iliacs showed worse survival because of their preoperative risk factors. But in terms of EVAR failure, this patient presented lower success if compared to standard common iliac arteries.

And this is also true in terms of overall reintervention. But coming to the iliac related reintervention, patient with ectatic iliac arteries had a three-fold incidence of reinterention at Type I endoleaks in the long run after 99 months. We have also some iliac-graft failure,

defined as iliac-related reintervention, occlusion, related death, or aneurysm rupture. Patient with ectatic iliacs had 14% risk of failure after 11 years, while patient with ectatic iliacs had only 4% risk of failure in the long run. Is it not known?

No, actually, if you look at the St. George Vascular Institute's risk score, the main determinant of failure is the common iliac diameter. And we have already other experiences reporting the same values.

Is it typical from one graft? Not at all. This is a patient with Talent graft in which one limb migrated into the opposite common iliac aneurysm and we were able to treat it with an extension.

But most of the patient getting old, they don't come back for follow up. They don't come back and we can check the position of the iliac limb in the long run. Is there any other alternative? Yes it is.

We now have the iliac branch endografting that showed that after 10 years, the reintervention needed in only 8% of the patients, so we can afford the durable results in patients like this. So in conclusion we can say that iliac arteries

tend to dilate with time, especially if they are ectatic. EVAR are prone to late failure in these cases, so rigid follow-up protocol is needed for this kind of patients. And probably if you want a long-term result,

you have a consider safer landing zone, like iliac branched device. Thank you for your attention.

- [Interviewer] I mean it's got to be challenging to discuss a graft that none of us have seen but we can start with Jim. Jim can take on anything. What do you think of this new B graft? - [Jim] Well, yeah, I have fortunately been able to see it over in Europe and being teased by it. I guess the concern I have is the thickness of the fabric.

It seems like it is two layer of PTFE and stent sandwiched in between, so you're getting thicker and thicker so if you're using a smaller B Graft Plus, are you concerned about low flow and thrombosis with it? - You may say so.

First of all, it's only the B Graft Plus that has that dull technology and the reason is clearly that it's designed for branches and usually you use, now a days, branches in the larger vessels, mostly the celiac and SMA. We have gone done is using branches for renal arteries

for that precise angle having to reline, because let's be honest, if you use an autograft, you will very much more likely reline it with a self expandable stent to prevent the kinking, so the end result is the same.

So the answer to your question, Jim, is no, I'm not concerned more than with any other bridging stent graft. - And what about the distal flexibility of the B Graft. I mean, that's kind of what's driven me to go to VBX is that, you know, I had a couple patients that came in that

they kind of kinked and you had one in your series there. The VBX tends to be much more flexible distally. - Yeah, I am probably the only guy in this world that is not completely convinced yet by the VBX and I've listened to you, I've listened to Gustave, and to Mark Farmer,

and I hear a few little things here and there. The flexibility is excellent, the tactile feeling of that graft is excellent. I agree that the B Graft Plus feels much harder, but it is very kink resistant and that's why I pointed out

that's the transition though is still important because that indeed is, can in an angle be a problem. So you have to choose it correctly. - So, Jim, in the VBX, and you've done a lot of cases, how often did you have to put an additional stent to fix a kink?

- The only time I've ever had to put another is for length. I've never had to reinforce or put a self expanding end. For like the one that I showed where I went from did it as a parallel graft going all the way down, I had to use two there because they only come in 79 and the one problem we have is when you start,

like any balloon expandable stent, when you start oversizing it and they actually have eight that will go to 16 as Chris pointed out, but it will start for shortening, but I have not had problems where I had to support it with a self expanding stent.

- But also when you enlarge it, you lose some of the radio force, no? Probably the reason you didn't have a kink is because the area that you, actually, the area that could be kinked is not dilated enough. You want to dilate approximately or distant it to fit more

of the the anatomy then you lose of the radio force, I guess. Theoretically at least. - Only the 8L is really expandable beyond two millimeters. So a six you can dilate up to an eight. So I really haven't seen that tremendous for shortening

except with the L, and obviously I'm not going to put an 8L into a renal or a vishal vessel. - The length of the Bridging Stent Graft is interesting though. We are doing far more fenestrations, and if we do Branch Grafts is usually grafts with both

fenestrations and branches, and you have to deploy these grafts based on the position of the fenestrations, and then you plan your branches to be fairly near through the target vessels. Say you end up using more like six centimeters instead of eight centimeters.

We virtually don't use the 79 or the eight millimeters Covera anymore. Having said that, there are new designs, designs from other companies coming out where you are planning even longer Bridging Stent Grafts up to ten 15 centimeters but we will have to see wither that

induces new risks. - I think that was one thing that we found interesting 'cause we also use them for parallel grafts and then you do need longer ones because in the cuffs we never put more than two parallel grafts at any one place, and so if I'm doing it, I'll do like a celiac SMA

and I'll put cuff in there and I'll come down and I'll do the renal so as parallel for torrical abdominal, since we don't have readily available access to the stuff that you have. But then I need longer, so if anything I'd like to see longer than 79,

just for some of these other grafts and the advantage is you go in, you put a six in, and you can flare it to eight to go in the celiac and SMA but you gutters only at a six. - Chris I have a, just one second - Chris the SFA, the VBX for the SFA, when is an over kill and when do you think

it's absolutely decaded? - For the SFA? - SFA. - Yeah, I got to say, I have not used a balloon expandable stent in the SFA very often. I guess if you really had an hospitable reason

that you really needed a stent in precision and short maybe you'd use it. You know, I think the title given here was a misnomer because it was a two year results instead of SFA trial. Truth be told I've used a whole lot of them in the aorta and the iliac and some of the extensions that Jim and

Eric have talked about but I've never used one in the SFA. I think it would be, you know I think if we have other options for the SFA, the viabahn, nitinol stent and then you could reinforce that if you needed to with an interwoven stent if you really needed a pave in graft.

I've not used it in the SFA. - Any question from the audience? We have a couple of extra minutes. - Is the cuffs playing a role for the VBX because in Europe it's clearly more expensive other bridging stent grafts and I heard from the Munster Group,

off the record, when they do chimneys with the VBX the reline it to increase the retinal force. So what about the radio force? - We followed ours going up to two years or as long as VBX has been available for that, we haven't an increase instance of crush or need

for relining. The cost is, and all cost is local, but a 018 viabahn is more expensive in our office than the VBX of equivalent size and length. - And that's the same in our lab as well. - Yes sir.

Introduce yourself and ask the question please. - [Eka] I'm Eka Jaan, so sorry, I'm from Hartford. Question for Doctor Mackenzie regarding the VBX and the fenestrations. Do you have any concerns with the unsupported portion of the VBX at the transition zone with the fenestrations,

it's not supported there so can it collapse or can there be offset between the fenestrations? - That certainly was a concern. I always deploy my stents as 90 degrees the axis so if I've got a four dot fenestration and I turn it to a three dot so I know I'm right perpendicular and I literally will

try and land between the two wire forms so it expands and actually kind of as the grommet seals there, and all the ones we have done we have no had any endoleaks at the approximate aspect of the stent and quiet candidly I'd rather have a leak there than include a stent at distal aspect 'cause I can always come in and put a

balloon expandable which, of course I haven't had to do. - Yes, last question. - [Andy] Hi, Andy Plum, Chicago. Along those lines, yesterday the Munster Group was doing a workshop and they actually favored the Atrium stent over the VBX.

For that reason, they are saying they've seen with the VBX, because the stents are independent without a cross bridge that they've actually seen shortening like accordioning with time with their ChEVARs. Now this was a medtronic presentation, little bit biased towards medtronic,

but they were actually favoring the Atrium stent for their ChEVARs. - My problem is the rigidity of the Atrium stent and it's crushability. Here you've got a little bit more play, David Muino would come out and tell is to do

the eye of the tiger with that and you can do that it but I have not seen for sure accordioning of it especially in a graft that you're using as a parallel graft. Now I guess at the very top you could, it may come down a little bit above the area of where you're

interfacing with the graft but it's going to give it more stability so I'm just not seeing that being a problem, either with implantation or long term follow up. - Thank you.

- So these are my disclosures. So I tried to divide this talk up into four areas that are common that occur in our practice at Mayo. One will cover guidelines. What do the chest guidelines and SIR guidelines show?

And a statement by the AHA, and then patients with PE that are presenting in different phases, and then patients that have a subset of CHF and then obviously special patients such as pulmonary embolectomy.

And so let's talk about the guidelines. And I think it's really important to understand a few factors when you're considering putting filters in. One is obviously the workup of the patient, and what are their anatomical considerations?

Number two the extent of clot burden, and then number three the hemodynamics of the patient for their age and how did they get to you? And then fifth you can look at the guidelines to help you.

So, what is the circumstances that a provoked DVT, unprovoked DVT, with and without malignancy, what is their age? I'm not going to cover that, but that's in the setting of what you should be considering as you think about that.

So these are the guidelines the chest guidelines are on the top, and then the SIR guidelines and there's pretty good uniformity between the two guidelines at least for placement of filters and I've highlighted those.

For example acute proximal DVT if you can't anticoagulate because of risk of bleeding. So that's a 1C recommendation. Part C there is in the treatment of PE acute PE if anticoagulation is not possible because of risk of bleeding.

And then SIR guidelines recommend absolute indication for proven VTE, recurrent VTE despite anticoagulation or contraindication to anticoagulation. So these are really guidelines to help us think about how we would manage these patients

and where we would place filters. And again the other thing that we have to remember is that some of these guidelines were written when we were still doing a fair bit of permanent filters and now with the FDA recommendations

for temporary filters if you put a temporary filter in, or an optional filter you're obligated to schedule the patient for a return to your office to come back for removal. And that creates another set of challenges

for our patient. How do you get em back? How do you schedule em for a return? When do you schedule em for a return? And then obviously does every patient need a filter removal?

Does a 90 year old patient with a optional IVC filter need an aggressive treatment for filter removal than a 50 year old for example. And so these are the guidelines. And these are the relative indications.

If you're not sure, these are sort of on the... Depending on where you're at for example large free-floating proximal DVT ilio clot in transit gets a filter placed as well. So I want to talk about a scientific statement

that Mike, Dr. Jaff co-chaired. And this was a statement from American Heart, and it really also provided some guidelines also for IVC filters in the setting of acute PE, and it listed different scenarios

of when you might place a filter. Adult patients with an acute PE very similar to what the SIR guidelines and AACP were. This was class one level B that could not be contraindicated or anticoagulated

due to excessive bleeding. Number two was anticoagulation should be assumed in patients with an IVC filter once contraindications to anticoagulation or active complications have been resolved. And we're going to talk a little bit about

how they got to this. And then patients who have retrieval filters should be evaluated periodically. That's very important I sort of alluded to this. If you place a filter, you need to somehow have a mechanism in place to bring em back.

In our facility every patient that gets an optional filter placed, has a nurse assigned to making sure once their care has resolved and they're ready for filter removal that they're scheduled for a return with an office visit.

And then number four recurrent acute PE despite therapeutic anticoagulation. It's reasonable to place an IVC filter very similar to the chest guidelines, and I won't repeat the rest. So how did we get here?

So this is the first paper that I'm going to review. This was a clinical trial of permanent filters in patients with proximal DVT. So permanent filter this was 200 patients randomized to permanent filters for preventing clots.

And what this paper showed was that if you had an iliofemoral DVT and a clot and you got a filter, that it put you at a higher risk for filters and really didn't prevent PE. And so this is number one paper that's

very important that we should recognize. So this is again permanent filters four different types of filters that are basically not used that often. One of them is the Bird's Nest. And this was a New England Journal paper

a PREPIC 1 trial, and this is what the age group were and the filters are very well matched. This was the gender as you can see the baseline characteristics very well matched. And this is table two this was the endpoint

within the first 12 days. And if you look at the filter group, you'll see that there was PE: two symptomatic in the filter group, five in the non-filter group P value 0.03, major bleeding was about the same

nine in the filter group versus six. So again, filter plus anticoagulation versus filter alone. And then there's death no difference in death. And so this really helped set the stage in the early or late 90s early 2000s

of how to manage permanent filters. And this is principle endpoints at two-year follow-up in the filter group versus non-filter group. And you can see symptomatic PE no difference. Recurrent DVT there was a difference,

and this sort of changed the way we managed filters and our temporary filters. We used this data set to help us with iliofemoral DVTs for example, and this is major bleeding and death. So again, no difference between

filter and no filter. And this is within 12 days. This is the principle endpoint within first 12 days after randomization. Between Heparin and Unfractionated Heparin because patients were treated with either

of the therapy again showing no difference. And this is the last table from that paper which is endpoints during the two-year follow-up of Low-Molecular Weight Heparin again showing no differences between Low-Molecular Weight Heparin

and Unfractionated Heparin. How about retrievable filters? The French group the same set of authors looked at the same problem, but looked at it with retrievable IVC filters. And what they wanted to do is evaluate

the efficacy and safety of retrievable IVC filters plus anticoagulation versus anticoagulation alone for preventing PE. In patients who were at risk for acute PE and a high risk for, or had acute PE and were at a high risk.

So this is retrievable IVC filters, and what is this study shows. So this was a study again done outside the US. It was randomized, open label, blinded endpoint, PREPIC2 with a six-month follow-up. Took seven years to enroll 400 patients.

Patients had to have an acute symptomatic PE with a lower limb DVT, and have at least one criteria for severity. They were assigned to retrievable IVC filter implantation plus anticoagulation or anticoagulation alone,

and they had to have a planned retrieval of filter at three months, six month follow-up data. The primary endpoint was symptomatic recurrent PE at three months and secondary outcomes were recurrent PE

at six months, symptomatic DVT, major bleeding, death at three and six months and filter complications. And the results showed that in the filter group the filter they had a few patients that couldn't get the filter so they

could have placed 193 filters out of 200, and they were retrieved 153 were retrieved of the 164 in which retrieval was attempted. So again you're seeing patients not getting filters retrieved. By three months recurrent PE had occurred

in six patients in the filter group versus three. So you saw a prevention of recurrent PE in patients with a filter, and the results were very similar at six months. So you see the confidence intervals there. There was no difference observed among

the two groups regarding the other outcomes. And filter thrombosis occurred again in three patients. So what about IVC filter and PE plus or minus thrombolysis? So I'm going to show you a couple of studies

that suggest that patients that are with PE and thrombolysis may do better with a filter. And these are large databases. The first one was alluded to by our previous speaker is Paul Stein

Paul Stein's group. And they looked at in hospital all-cause fatality rate according to the use of vena cava filters as determined using the nationwide in-patient sample, and patients across the US.

And this is very interesting. As I was getting ready for this talk, this was an interesting observation that they made. So this is all-cause mortality in patients with PE across the country,

and patients were either categorized according to unstable or stable and you can see that across the X axis, and whether or not they got lytic therapy or not. And on the Y axis you can see fatality, in the hospital fatality based on filter

and non filter. And as you look across the different groups if you had an unstable patient who did not get lytic therapy, patients with filters did better than patients without filters.

If you had an unstable patient who had planned lytic therapy, unstable patients did better with filters than not. And even in the stable lytic group there was a difference in the groups.

So this suggests that there is a treatment benefit for patients with PE that are stable or unstable that are getting planned lytic therapy or not getting planned therapy. There is no difference if you are stable

with no lytic therapy. So it's implying that there may be an effect from the lower extremity or clot outside of where you're treating that may be contributing to the fatality. Here's another paper from the same group.

And this is using a premier health care database over 2010 to 2014, and they classified patients into similar groups based on ICD 9 codes and whether they were unstable or stable. So these were patients with PE

and an admitting diagnosis of PE, as well as a primary diagnosis of PE. And they used a time-dependent analysis according to the date of insertion of the IVC filter to control for the immortal time bias.

I don't understand all that but this is what the authors showed. So they had 266,000 patients with PE. 4,200 were unstable, PE admitting and primary diagnosis was down to 479 and those were divided

into thrombolytics versus non thrombolytics and if you saw if you got a filter eight patients died versus in the first group in thrombolytic group versus 42. Again in the non thrombolytic group, less patients died 27 versus 80.

So again showing a protection in patients with PE who are getting, who are unstable and who are getting admitted with filters. So there are other subsets, I'm not going to speak about them.

But I want the audience to understand there's patients with heart failure that may be that filters may be protective for. So if you present with heart failure in the setting of PE, that there is a large paper

large data set showing that patients should receive filters. And another sub special group patients undergoing pulmonary embolectomy that filters may also be protective for. So I want to be cognizant of the time,

and I'm going to stop there. Thank you.

So I'm a consultant for both of those. Okay, so repair of coarctations. So surgical repair is effective, has a low procedural mortality and morbidity, and so does stent implantation. But the mortality is very, very low with stents, and the morbidity is also lower in general.

Whatever method you choose, though, both methods are going to be complicated by hypertension, re-intervention for stenosis and aneurysm formation, which is normally just a question of time if you follow up the patient for long enough because the post-stenotic dilatation,

cystic medial necrosis, calcification, it's a sick wall. So the potential advantages of using a covered versus a bare stent versus angioplasty is that the angioplasty just tears, and we don't do angioplasty on native coarctations. But you put a stent in and you get this creation

of a longitudinal framework, and if you have a covered stent you're going to control the integrity of the vessel at the coarctation and below it, which is normally a very dangerous area, the poststenotic dilatation area. And they're particularly useful using covered stents

when there's an aneurysm which is present. However, there's no good studies to say that's really the right thing to do. So recently Tretter and McElhinney, they looked at all the reports that had been done for endovascular therapy for aortic coarctation,

and they noted that aortic rupture was particularly rare, less than 1%. Acute aneurysm formation, when intervening for endovascular therapy, was about up to 13% for angioplasty, up to 5% for bare metal,

and less than 1% after covered stents. But it depends on the reporting bias and there's a lot of inconsistent definitions. And overall, the acute wall injury seems to be going down for coarctation due to better delivery systems, more use of covered stents.

And there are really only three covered stents, which are balloon expandable, and the CP covered stent, which comes bare and covered, and it's stuck on quite loosely, the Atrium V12LD which is not available for the last two years,

which goes up to 22 millimeters, and the aortic BeGraft which comes in a whole range of sizes and covered. This is the Atrium V12LD with stainless steel covering the inside and the outside, and the BeGraft is chromium cobalt

and it's covered on just the outside. So, when you're doing the covered stents, you need to consider the vascular access damage that can be done because you need a relatively large delivery system, and I'm a pediatric cardiologist,

so using these in small kids you have to be very careful, and the CP stent can take even 11 to 12-French system. The stent integrity, because the CP Platinum-Iridium stents tend to fracture, the Atrium has a problem of infolding, and the Bentley is quite a strong stent and I've had no problems with it,

but it's early days yet. And the other thing is the covering integrity. The CP is incomplete while the Atrium and the Bentley seem to have a better cover. So looking at the COAST I study, which was a look at the CP stent,

which was a bare stent, they did 105 patients underwent attempted implantation, and just looking at sort of the aneurysm, the aortic wall injury, they did balloon dilatations just for some compliance testing, which I never do, and they generated some small

aortic aneurysms showing that that area is a problem. And in intermediate followup when they put in bare stents, they had a total of six aortic aneurysms, five were successfully treated with a covered stent placement and one resolved without intervention,

and they had some stent fractures. Then what they did, they did a COAST II study, which was looking at the CP covered stent, which was used, and they used it in a total of 158 patients. 83 had had previous intervention and had some aortic wall injury.

And when they were using that stent, complete coverage of the pre-existing aortic wall injury was achieved only in 92% of the patients, and seven patients had minor endoleaks. The other thing is, so that shows that the covering wasn't that good.

The other thing was is it takes a large delivery system four patients experienced important vascular site injury. In the Advanta trial the covered stents were very good, in general, for getting the blood pressure down, getting the gradient down, and increasing the diameter. And also, comparing sort of the long-term followup,

we followed the blood pressure for three years, the blood pressure stayed down and we had a very good result. The major problem was they had very small problems with femoral artery occlusion only in one patient compared to the four in the CP stents.

So there was one small aortic hematoma treated with a second stent, but the major problem was the stent wasn't robust enough in the aorta and had infolding. Two of which required urgent reintervention. The Bentley, which is a relative,

and we've had it since January 2017, so this is, let's say, a complex native coarctation. So we treated that with a BeGraft. And here you can see this is another patient, a little Bedouin girl, that had an endovasculitis and a coarctation,

and she was treated with a CP stent, which was covered, but you can see the aneurysm stayed. We put the, another Bentley stent in there. So you can see that the covering, even when using covered stent, is not necessarily always the right thing.

We've done now 22 patients with a Bentley BeGraft. You can see the median age and all different types of coarctations which have been previously treated or native. Overall, it gets down the gradient and the coarctation diameter stays up.

We had no acute wall injury and no other immediate complications. Patients that had pre-existing aneurysms, ones which you saw, was successfully treated, and at median followup things look good. So in conclusion, surgery, in my institution,

is the primary choice of intervention in patients who endovascular stenting is not possible. So infants and small children we won't do a balloon angioplasty because it tears the intima and they have aneurysms afterwards. If we can put in a covered stent,

that's our first choice. Safe and effective acute treatment of coarctation and associated with less aortic wall injury than bare metal and balloon angioplasty, but you need a lot of reintervention. The choice of the covered stent,

you need to consider delivery system, the maximum diameter of the stent, the stent integrity, whether it's going to fracture or infold, and the covering integrity. And when all is said and done we still need to have long-term followup imaging.

Thank you very much.

- Dear Chairman, dear ladies and gentlemen, thank you for the chance to present these data here. As opposed to United States, this is not first-line therapy in Germany. And I would like to show you some results with the Omega-3-enriched matrix, which is a little bit special.

It's made from fish skin from Atlantic cod, and it's an acellular matrix, which can be used as a xenogeneic skin graft for hard-to-heal wounds in different locations. Some advantages of using fish skin as opposed to a porcine skin or even human skin

is it's a gentle processing possible, it preserves the lipids, which is very important. I think the Omega-3 is a very important feature of this and it preserves the structure. And there's also very little risk of disease transmission, which is

always a matter of concern in xenogeneic materials. And how does it work? The Omega-3 fatty acid has some anti-inflammatory effect by mediating an inhibitor, a new inhibitor. It's called the NLRP3 inhibition,

which is necessary for IL-1 beta activation of cytokine, which is used for inflammation. And so this fish skin is also reducing general inflammation in the surface. So how is this application done? So you see a hard-of-heal wound,

which has to be a little bit clean and infection-free if possible, but it doesn't heal completely. So the fish skin is applied, and it can be covered with polyurethane foam, or even with NWPT with vacuum therapy.

And it takes several treatments. The advantage is it's weekly dressing changes. That means it's possible to do it on an outpatient basis, and I think this is the way it's done mostly in United States. So these are inpatients with very complicated wounds.

23 patients with 25 vascular wounds in different locations. Two in the thigh, seven in the distal calf, 14 in the foot, and two even in the hand. And the time to heal took nine to 41 weeks, so we have to be a little bit patient and stubborn to really wait for the effect of this fish skin.

And in average, you can see here, in some patients, three are enough, but in some patients 26 treatment cycles were necessary. This is just to show you the spectrum of patients treated in the last four years. Not very many, 15 out of 25 only, was complete healing.

This is from three hospitals in Germany, from Hamburg, Mainz, and our hospital in Karlsruhe. And you see here the rate of complete healing is only almost half of them. Here, this is an example, typical example of what we see. This wound became necrotic and dehiscent, and then

after debridement and some cleaning it looks like this. And then it can be treated with the fish skin. It looks a little bit strange if you do the first dressing change, but this is the way it should look. And after a while, this took 33 weeks, but then this foot healed, and there was

no major amputation necessary in this patient, which is the aim of this therapy, actually. This is a very terrible example of steal syndrome in a dialysis patient with a necrotic hand which had to be amputated in an emergency procedure.

And the question was: could this hand be saved somehow? So this was also treated with Omega-3 matrix, and this is the final result, but this hand is not functional, so it needs some additional plastic surgery. But I think after these wounds are healed,

before that no plastic surgeon would do anything with an extremity like this. These are some more examples of the healing. And you see here the curve, how long it takes to heal for these wounds: up to 12 or 14 weeks. This is kind of the average, three months.

There was a publication before with a few similar, even less cases, 18 cases, from United States, which showed complete healing only in three of 18 patients, which is a little bit disappointing, but the primary goal is to get a stable wound

and to avoid amputation, actually. You get a really significant decrease of wound surface, so our results actually were even more successful than this first publication, that there is no much more data available from literature. This is a very special example here,

from presternal necrotic skin flap, which was also treated with Kerecis Omega3 and with mesh graft in the end. So this was a very special case which also was healing. Here you see the time to heal again. It takes a long time, up to 100 days for the healing.

And you see the Hamburg cases here, the wound reduction to 20%, but with some cases 60-80%, and only half of the occasions really complete healing. So in summary, in the shortness of time, summarize that Omega-3 wound matrix is,

for us at least, a innovative biological decellularized wound dressing from cod skin, which works in complicated wounds, in the lower limbs especially. And before they are applicated, there needs to be an effective debridement,

adequate tissue perfusion, and infection control. And weekly dressing changes are absolutely sufficient, so this means that outpatient treatment is possible. Thank you very much for your attention.

- I'd like to thank Dr. Veith, program committee, and the moderators for the honor of presenting on this topic. Here's my disclosures, not relevant to this topic. One fairly large randomized trial, and a handful of retrospective studies have shown benefit to anticoagulation

and the patency of either prosthetic or high risk vein bypasses. And this data's formed the primary basis for what is common, but not universal surgical practice which is aspirin for standard vein bypasses or prosthetic to the above knee popliteal artery.

And then the addition of warfarin for prosthetic bypass below the knee or high risk conduits or poor outflow. But really, guidelines for medical therapy after low extremity bypass are weak and high variable. SVS guidelines recommend only antiplatelet therapy

and specifically say that evidence is inadequate to comment on anticoagulation. And guidelines from other important societies are largely silent on this topic as well. Of course we know that our bypass patients have other indications for anticoagulation.

Their coronary disease, there's cerebrovascular disease, and so ultimately, about 25 or 30% of bypass patients are discharged on anticoagulation. Enter the NOACs or the Novel Oral Anticoagulants. Instead of working on Vitamin K dependent factors, they either directly inhibit factor 10A or thrombin itself.

And many of the advantages are well known. These are approved for non-valvular AFib, DVT and PE, and I highlight a few of the approval dates here. I highlight dabigatran and rivaroxaban because these are two captured in the VQI data registry

that I'm going to highlight and show some data on. We hypothesize in this analysis that my colleagues and I performed that these are increasingly utilized as off-label anti-thrombotic therapy in PAD, and specifically in bypass patients.

And we wanted to do an analysis to look at the contemporary utilization of NOACs and their impact on graft outcomes and limb outcomes. WE looked at 19,000 bypasses in the VQI over three years. Now, we stared in 2014 because that's when NOACs were first captured in this data.

When you exclude patients who had less than one year follow up, and some other patients, we're left with about 7,100 bypasses, of whom about 3.5% were discharged after bypass on a NOAC, 21% on warfarin, 76% with none.

This graph plots the utilization over time of NOACs and warfarin. We see that warfarin utilization went from 24% on discharge in the beginning, to 15% over the time period and then correspondingly, NOACs increased from 0.6% of discharges to 6%.

We naturally looked at a lot of bypass patient characteristics to figure out which patients had been selected for either warfarin or NOAC, and they were actually similar. Tibial bypasses, prosthetic bypasses, and long operative times, that should be 300 minutes,

were all chosen for, at some form of anticoagulation. When we look at patency of bypasses on warfarin and NOACs, we see that those bypasses that are not placed on anticoagulation have superior primary patency and that bypasses on warfarin and NOACs have inferior and not different between the two.

The same holds true for assisted patency. And the same holds true for secondary patency where bypasses on anticoagulation inferior to those not on anticoagulation and no significant difference between warfarin and NOACs. When we look at freedom from major adverse limb events,

we see that again, a similar trend. Patients on warfarin and NOAC have inferior freedom from major adverse limb events compared to patients on no anticoagulation after their bypass. Naturally, we did multi varied analysis to look and see

if these were independent predictors of failure. And in fact, they were. Both warfarin and NOAC, even when you control for a variety of patient anatomic characteristics, both were independently associated with failed patency at the hazard ratios you see.

Other predictors of patency were things that are commonly described to date. Same thing is true with major amputation and major adverse limb events. Both warfarin and NOAC were independently associated with major adverse limb events after bypass.

Other factors associated with MALE have been described in the literature as well. So certainly, there are a lot of limitations to this sort of analysis. The registry might not capture important factors that influence the selection of patients

who receive NOACs or their outcomes. This is also limited by the fact that the only NOACs captured in this analysis are dabigatran and rivaroxaban, not the more newly approved NOACs. And this follow-ups naturally limited to one year.

But based on this retrospective data, we see that NOACs and warfarin are utilized after infrainguinal bypass in high-risk patients with high-risk graph characteristics. NOAC utilization is definitely increasing while warfarin is decreasing.

At one year, NOACs and warfarin were associated with worse mid-term graft outcomes and limb related outcomes even after controlling for other factors. And there was really no difference in the outcomes between NOACs and Coumadin. There's a lot of ongoing work in this area.

The COMPASS trial does include some patients of small minority who had previous low extremity revascularization, though they certainly were not all bypasses. Upcoming data from the Voyager-PAD trial where low dose rivaroxaban is tested against aspirin alone

may shed some light on optimal management of anticoagulation. But certainly, based on this data, ongoing study of the impact of NOACs on graft-related and limb-related outcomes is warranted. Thank you very much.

- I'd like to thank Dr. Veith, program committee, and the moderators for the honor of presenting on this topic. Here's my disclosures, not relevant to this topic. One fairly large randomized trial, and a handful of retrospective studies have shown benefit to anticoagulation

and the patency of either prosthetic or high risk vein bypasses. And this data's formed the primary basis for what is common, but not universal surgical practice which is aspirin for standard vein bypasses or prosthetic to the above knee popliteal artery.

And then the addition of warfarin for prosthetic bypass below the knee or high risk conduits or poor outflow. But really, guidelines for medical therapy after low extremity bypass are weak and high variable. SVS guidelines recommend only antiplatelet therapy

and specifically say that evidence is inadequate to comment on anticoagulation. And guidelines from other important societies are largely silent on this topic as well. Of course we know that our bypass patients have other indications for anticoagulation.

Their coronary disease, there's cerebrovascular disease, and so ultimately, about 25 or 30% of bypass patients are discharged on anticoagulation. Enter the NOACs or the Novel Oral Anticoagulants. Instead of working on Vitamin K dependent factors, they either directly inhibit factor 10A or thrombin itself.

And many of the advantages are well known. These are approved for non-valvular AFib, DVT and PE, and I highlight a few of the approval dates here. I highlight dabigatran and rivaroxaban because these are two captured in the VQI data registry

that I'm going to highlight and show some data on. We hypothesize in this analysis that my colleagues and I performed that these are increasingly utilized as off-label anti-thrombotic therapy in PAD, and specifically in bypass patients.

And we wanted to do an analysis to look at the contemporary utilization of NOACs and their impact on graft outcomes and limb outcomes. WE looked at 19,000 bypasses in the VQI over three years. Now, we stared in 2014 because that's when NOACs were first captured in this data.

When you exclude patients who had less than one year follow up, and some other patients, we're left with about 7,100 bypasses, of whom about 3.5% were discharged after bypass on a NOAC, 21% on warfarin, 76% with none.

This graph plots the utilization over time of NOACs and warfarin. We see that warfarin utilization went from 24% on discharge in the beginning, to 15% over the time period and then correspondingly, NOACs increased from 0.6% of discharges to 6%.

We naturally looked at a lot of bypass patient characteristics to figure out which patients had been selected for either warfarin or NOAC, and they were actually similar. Tibial bypasses, prosthetic bypasses, and long operative times, that should be 300 minutes,

were all chosen for, at some form of anticoagulation. When we look at patency of bypasses on warfarin and NOACs, we see that those bypasses that are not placed on anticoagulation have superior primary patency and that bypasses on warfarin and NOACs have inferior and not different between the two.

The same holds true for assisted patency. And the same holds true for secondary patency where bypasses on anticoagulation inferior to those not on anticoagulation and no significant difference between warfarin and NOACs. When we look at freedom from major adverse limb events,

we see that again, a similar trend. Patients on warfarin and NOAC have inferior freedom from major adverse limb events compared to patients on no anticoagulation after their bypass. Naturally, we did multi varied analysis to look and see

if these were independent predictors of failure. And in fact, they were. Both warfarin and NOAC, even when you control for a variety of patient anatomic characteristics, both were independently associated with failed patency at the hazard ratios you see.

Other predictors of patency were things that are commonly described to date. Same thing is true with major amputation and major adverse limb events. Both warfarin and NOAC were independently associated with major adverse limb events after bypass.

Other factors associated with MALE have been described in the literature as well. So certainly, there are a lot of limitations to this sort of analysis. The registry might not capture important factors that influence the selection of patients

who receive NOACs or their outcomes. This is also limited by the fact that the only NOACs captured in this analysis are dabigatran and rivaroxaban, not the more newly approved NOACs. And this follow-ups naturally limited to one year.

But based on this retrospective data, we see that NOACs and warfarin are utilized after infrainguinal bypass in high-risk patients with high-risk graph characteristics. NOAC utilization is definitely increasing while warfarin is decreasing.

At one year, NOACs and warfarin were associated with worse mid-term graft outcomes and limb related outcomes even after controlling for other factors. And there was really no difference in the outcomes between NOACs and Coumadin. There's a lot of ongoing work in this area.

The COMPASS trial does include some patients of small minority who had previous low extremity revascularization, though they certainly were not all bypasses. Upcoming data from the Voyager-PAD trial where low dose rivaroxaban is tested against aspirin alone

may shed some light on optimal management of anticoagulation. But certainly, based on this data, ongoing study of the impact of NOACs on graft-related and limb-related outcomes is warranted. Thank you very much.

- I think we have time. If there are any questions, please come up to the microphone and any of the panels have questions for each other. I have a number of questions I could ask but I just see if anyone wants to start out. Claudio?

- I have a question Doctor Mark. He show us very nice utilization of this device for occluded limbs. My question is, do you protect in any way the other side? If not, don't you have, you're not concerned

or you're not afraid of pushing clots from one side to the other one when you're manipulating the device? And the second one, do you do this percutaneously? And if that's the case, do you have any concern about having destabilization?

Because once you start to manipulate the clot that is occupying the entire graft, and there is reestablishment of flow in an antegrade flush, and you may have some of that clot dislodge and embolize distant. - Yeah, as I mentioned,

nobody wants to be the guru of limb occlusions. However, we have seen them and we always go retrograde ipsilateral, not seen emboli once from those seven cases and in fact, the 73 we presented at the midwest there was only two instances of embolization

when we utilized this device. And both times we were able to extract those just by going further down with the cat six and both of them was below the knee popliteal. In particular, the acute ones, it's soft and it's no different than watching it in vivo

or in vitro model, as you know better than I, comes out quite easily. - Let's take our question from the audience. - [Scott] Hi, Scott Tapart from Stuart, Florida. So I'd like to poll the panel there about are you doing every single

acute limb ischemia percutaneously? The pictures are elegant, the techniques are elegant, but the last speaker touched on the profoundly ichemic Rutherford 2B patient, where you're most likely going to have to do a fasciotomy. Are you going to the OR

or are you doing this percutaneously and then watching and waiting and seeing about fasciotomy? Or has this changed your fasciotomy approach? - So since we have a number of people, that's a great question. Why don't we start at the end

and let's just go kind of rapid fire, maybe one or two sentences, how do you choose your patients and what do you do with those 2Bs and we'll try to get through everybody. - Sure, so, to reiterate the last slide of the presentation,

essentially anybody with a significant motor or neutral deficit is somebody I tend to do in an open fashion. And if I'm the least bit concerned about doing a fasciotomy or there's evidence of compartment syndrome I do that patient open.

- We try to start endovascular, and if we can clean and reestablish antegrade flow, that would take care of the problem. And of course, I'm a radiologist, so I always consult with my colleagues in surgery and they decide if a fasciotomy needs to be done or not.

And it's that at the end. - Okay, I have to be honest, we start with the selective indication but now we move maybe to 90% of our patients doing percutaneously. We will adjust patients with probably an embolization,

a huge embolization, into the common femoral artery for open surgery. Of course, in our mind, also in the registry, we have some cases of fasciotomy after percutaneous approach so it's not a limitation. - The advantage of acute arterial protocol,

as they all go to the end of asher suite and they all run along our protocol but you can run the option. You get them to treatment quicker because they don't dilly-dally around in the holding room. But then according to how the patient's doing

you can mop up as much clot as you can with the percutaneous technique and then do the fasciotomy when you're done or press head and drip more if you need to. So I think to have an algorithm where you can treat the full spectrum

is what's best for the patient. - I think it depends on the time as well because I did two weeks ago a patient who needed a fasciotomy directly so I performed that first and then it rules out any traumalitic therapy

or whatever that you want to do. And actually, if I do antivascular techniques I usually give a shot or RTPA or something and then go further with it. But anomerization of this patient's arteries as well so prefer actually if it's really a case

that needs fasciotomy just to perform surgical thrombectomy. - Yeah, percutaneous eight French up and over and almost always, you're going to be done with your thrombectomy within about 30 to 45 minutes. I don't think you're adding that much time

and for us, by the time we get anesthesia in him assuming anesthesia's anesthesia no matter what part of the world you're in, so you can get to the hybrid room quicker and then if it's going to fail then you're going to call in the OR or call an anesthesiologist.

- I wouldn't have much else to add. I do think there is some patient selection, if you have an entire SFA, 30 centimeter clot, that's going to take you hours to do so for these thromboembolic things that are 10 centimeters or shorter

lodged in the popliteal TP trunk, this method works really well. I think for the longer patients, you might think about something else. - But just a comment on the general anesthesia. If a patient is in real or really pain,

he can't lie down for 30 minutes, even. I mean, they are rolling in pain and I would do the fasciotomy first because general anesthesia is needed because there is so much pain or, yes, so yeah.

- So, let me say, does that answer it, Scott? So let's, since we have a number of panelists and we're running out of time, how about if we ask each person going down the room, you heard a whole bunch of different speakers here with a lot of experience

and if you haven't used this, there is a learning curve. The learning curve is pretty shallow. Really, a lot of it has to do with controlling your blood loss. But if we ask each person for just one tip

and we'll see if we can get through everybody. If you telling people who hadn't done a lot of this, one tip or one trick, let's see if we can get seven or eight tips and tricks out. So, I'll go last. Let's start back down at that end

and we'll end up at this end. - Sure. Use the largest catheter that the vessel will comply to. - Amen, brother. - I agree with that.

And the way I do it, in order to avoid too much blood loss, I like to engage with a syringe. So I come with my catheter, I hook a syringe in the bag, 20cc or sometimes even larger, and when I have the fish at the end of my line, then I connect to the pump and I continue.

That way if I'm aspirating, I'm not going to aspirate a large volume so I want to engage the clot. And then I bring the clot out. That's my trick. - Okay.

Very nice comment. Of course, I agree with the previous colleagues but I will say that first the trick is really the largest catheter is better, then my idea that I developed during my learning curve is the use of separate to cut away.

I probably use now in 95% of cases because it just makes everything quicker and faster and better. - I use the perclose device for large-bore catheters often and that allows me to pull the plug out, especially if it's fibrous plugs,

safe from the heart without shearing it off on the end of the catheter. I've got one question for Claudio, on that case of the carotid subclabian with the acute carotid occlusion, do you think the nitroglycerin would have helped?

- For the doctor? - For the surgeon. - Absolutely. - And then, change the diapers. - Well, I would advise if you do a surgical embolectomy do it also on the hybrid room

and try to do it also over the wire. Especially be careful if you do it below the knee. I would suggest do it open below the knee, even. - I would say don't afraid to use an eight French for ALI and that closure devices are your friends here. But you can use an eight all the way down to the pop

and then for us, the tibials, we'll use a six. - Yeah, I would agree with that. So I guess my tip would be, I agree with everything everyone said, although I don't use the separator very often in the arterial side, I do in the veins.

But one tip is, if you're not going to use a separator, if you're going to start without it, let's say you want to give it a try, I don't work through a 2E borst because the angle, the eddy currents that form around that 2E borst

trap clots and you constantly have to clean that 2E out so if you're going to start with a focal embolis in the artery my recommendation is take the 2E off, hook up to the vacuum directly, and you'll get less clot stuck in the 2E. If you want to go to the separator

then you can always add that on at the back end. - So I have a question for Fennel. I used a penumbra like a few weeks ago and it ended up really bad because the surrounding catheter from the penumbra, everything got, you know, clotted

and then I didn't have any outflow did I choose the wrong size or what is it that happened, did you see it ever? - We have not had that problem. We're usually working on heparinized patients and have not seen that happen.

- She was heparinized. No? Okay. - Okay. Any other comments? Otherwise, we'll end one minute early

on a nice, long day.

- Great thank you very much. It's great to be here at Veith and talk to you about optimally deploying the Supera interwoven stent. This is a stent which is very unique and different from other stents. Slotted-tube stents are laser

cut from nitinol tubes with an open cell geometry compared to Supera which incorporates six pairs of elastic nitinol wires into an interwoven helical closed cell geometry.

This design gives it vascular-mimetic like properties in the dynamic vessel that we treat. And it has four times the radial strength of slotted-tube stents so it is resistant to compression from outside. That said its physiologically conformable

and essentially fracture-proof and it has by far the lowest chronic outward force of any of the nitinol-like stents. This just shows the off the-chart radial strength of Supera compared to nitinol and it is this

outward radial force which may generate some of the neoplastic hyperplasia. This gives the clinical advantages. You can use it in flexion points, calcified lesions with no recoil, long lesions with its conformability

and lack of fractures and if you want to convince yourself I encourage you do either intervascular ultrasound or bent-knee angiograms and compare them in this type of stent to the slotted-tube stents.

It's a unique stent so it has unique deployment. It's a ratchet delivery rather than a conventional mechanisms. The stent length is not at exact and depends on who well you implant it. It's not oversized.

You must aggressively pre-treat all segments that you're going to implant the stent. It is a slower deployment, a two-handed which is kind of an art-from if you will. It's a great stent but you have

more potential for trouble if you don't do it correctly. Here are the three important easy steps you must have documented. Aggressive pre-dilation to all of the segments where you're

going to put the stent. It's got to be one-to-one sizing. And you have to deploy it slowly on high magnification after that pre-treatment. That's it, those three steps. The pre-treatment we usually do

on Roadmap with focal force or regular balloons at least one-to-one what we're going to implant and usually a little bit higher. After that, the stent deployment, we use a Roadmap for the distal edge only.

Once we have the distal edge released, we take the Roadmap off, mag up and go slowly. The right hand throws the ratchet system, the left hand adjusts the tension. If the stent elongates a little bit, you slow down and push forward.

If it packs too much slow down, pull backwards. Here's a typical but illustrative case long disease, CTO, calcified disease in the adductor canal and the popliteal. Here's the pre-treatment with a 6 O ballon before a 5 5 superium

to make sure that it's well-expanded. Here is the mag-ed up slow deployment but you can see how beautiful it looks immediately on delivery and how well it stands up without post-dilation in this heavy calcium in the adductor canal.

Now here's the final AP angiogram. We're used to seeing good angiograms in the AP view but here's a bent-knee angiogram just showing the conformability of this stent and its strength in calcified lesions. It has great data.

Eighty-six point three primary patency in the superb trial with no fractures. Furthermore if you deploy it properly and nominally the primary patency was more than ninety percent. Extremely durable at three years

if you nominally deploy the stent, ninety-four percent freedom from TLR. Some things to remember. Again, pre-treat every vessel segment where you're going to put the stent, not just the tight part.

If you don't get pre-dilation with a longer balloon go to a shorter more aggressive focal force or non-compliant balloon. After you pre-medicate the patient don't use the small Superas.

And I can summarize mag up and slow down when you deploy the stent. We don't post dilate unless there's issues but if it does elongate or pack that's when we post dilate. What not to do with a Supera stent.

Don't use it if precision is needed at the back end for example an ostial SFA lesion from above. Again it's not an exact stent length. If there's a lot of mismatch it's not your stent.

You must adequately pre-treat, if you can't pre-treat it, don't put a Supera or in my opinion and stent. And of course you would never primary stent with this type of stent. So in conclusion the Supera stent

is a unique interwoven design giving it vascular mimetic qualities uniquely suited for the femora-popliteal lesion. Has excellent clinical results that seem to be independent of the stent length. All that said proper lesion preparation

and stent deployment techniques are essential to the success of this device. And I thank you very much for your attention.

- There's a new DCB now on the market just C-marked, and I would like to share you interim data of this brand new Kanshas DCB into the preliminary data so far available. So, as we just heard, DCB is a wide-spread accepted technology, which delivers a durable anti-restenotic efficacy

after single-balloon inflation. I think this is clear, but definitely, as we have just seen from Dr. Vermani, efficacy is not a class effect. It is critical determined by the presence and choice of the excipient of each balloon.

And we know that from different studies like here, from Jopa, we can see that outcome efficacy is different in terms of the different effects of the DCBs. So this new and novel Kanshas Drug-Coated Balloon is covered with a paclitaxel 3.2 micrograms per square millimiter.

There's a unicoat technology, which is a uniform coating with micro-crystal aspects where the Paclitaxel is embedded with micro-crystal, which provides a large surface area, which facilitates a drug transfer to the lesion. It's available up to 200 millimeter.

It is a monorail balloon. You can see that in (mumbles) and some preclinical animal models, the Paclitaxel tissue concentration was definitely different in comparison to other already-established DCB, and of course, this new concept has now

to prove an efficacy and safety in the first human study. So, I can provide you now the six-months primary outcome of that KANSHAS 1 study on behalf of all the investigators. 50 patients were enrolled at six sites in Germany and Belgium. Patients will be followed up up to year, two years.

The primary endpoint is freedom from composite safety at six months. You see all the centers which enrolled patients between April 2017 and January 2018. Main inclusion criteria, Rutherford Clinical Category two to four,

lesion length up to 15 centimeter. Just want to highlight that also popliteal artery segments, could, when moved into study, I will show you also the outcome for the to P3 segment where we planted the balloon. The other baseline and lesion characteristic of the patient.

Typical risk profile, most of the patient had a Rutherford category three. On right side, you see the lesion locations, where the balloon was implanted. I see that 19 patients had a treatment with an popliteal artery.

Cumulative lesion length, 88.6 millimeter. As usual (mumbles) DSB trials classification was more on the lower side. Here the procedural characteristics. DCB per lesion 1.2. Total inflated length 72.1.

(mumbles) 14% of 14 patient, 28%, a little bit more on the higher side for that lesion length. This was due to flow limiting that section and residual stenosis. Here are the six-months outcomes in terms of hemodynamic outcomes

and Rutherford class change from a baseline. As you can see, most of the patients improved during this first six months of followup. Here's the freedom from composite safety and efficacy endpoint within couple of micro curve analyzed. This is a target of 100%,

which means freedom from device and procedure-related deaths through 30 days and freedom from target limb amputation and clinical driven TLR through six months. There were no device and procedure-related Severe (mumbles) during that six months of followup.

So let me conclude the DCB angioplasty for de novo femoropopliteal artery lesions with that new KANSHAS balloon was so far safe and efficient through six months of the procedure. It has a remarkable clinical hemodynamic improvement

at six months, but we have to wait, of course, the further followup 12 and 24 month. Thank you very much.

- Well I'd like to thank everyone for being here, and for Dr. Veith and the committee for inviting me to speak. I am a recipient of research grant funding from Acelity as well a Speakers Fee. However, my study was initiated prior to any arrangement and any award of grant funding.

Acelity was not involved in any aspect of this study design, data collection, analysis, or presentation. So surgical site infections correlate with readmissions, reoperations, and increased healthcare expenditures. SSI's after infrainguinal vascular surgery procedures

range from seven to almost 40% of cases. We hypothesize that these are due to lymphatic disruption, proximity to the perineum, prostetic use, and we all know that these are catastrophic cases and can lead to limb loss and even death. At Duke, we had a bad surgical site infection problem.

To combat this, we crafted a perioperative bundle. This was a multidisciplinary effort that incorporated pre, intra, and postop measures to try to decrease surgical site infections. Use of an incisional wound vacuum, which started in the operating room

and went into the postop period was part of this bundle. The closed-incision negative pressure vacuum, is thought to act in many ways to decrease surgical site infections. It's thought to stabilize wounds,

to protect the wound against contamination, and that leads to early increase in wound strength and a narrower zone of dermal scar. Also it's hypothesized that this device reduces edema, increases blood flow, increases lymphatic flow,

and thereby reduces hematoma and seroma formation. What we found was after we introduced our bundle of infection prevention strategies, we had a much welcomed decrease in our surgical site infection rate. We then started thinking about which one of these factors

was effective and the Prevena device, which had been urged to be used on all groin and infrainguinal incision, was the first target as it is an additional cost to the hospital. We separated our patients into conventional versus negative pressure dressings

and we found that females were more likely to be in the negative pressure group. The negative pressure group had longer operative times, and more active smokers. So these were higher risk wounds. When we looked at outcomes,

we found in the negative pressure group we had the same readmission and return to OR rate, however, we had lower surgical site infections, fewer wound complications, and a lower 90 day mortality. When we did a regression analysis,

looking at different factors, we found the female sex was predictive of infection and that EVAR protected against infection. Negative pressure wound therapy emerged as an independent predictor against wound infection. The current data that's in the literature to date,

has many studies and a few of them are prospective randomized trials. The Gombert study is the latest, this is the AIMS Trial, and this is a prospective, multicenter, randomized trial looking at Prevena versus

standard gauze incisions. They found a significantly decreased rate of surgical site infection with Prevena. The DiMuzio Group at Thomas Jefferson Hospital also looked at cost data. They found that they had fewer reoperations

and fewer readmissions with the Prevena use, although this did not result in an overall decrease in cost. In conclusions, SSI's remain a major source of morbidity in infrainguinal vascular surgery. Efforts to reduce perioperative SSI's

using a care bundle, seems to decrease wound complications in this patient cohort. Prevena appears to add protective effect to decrease SSI in overall wound complications and was an independent predictor

within our bundled SSI reduction package. Data indicating cost savings remain to be elucidated. Thank you.

- Thanks again to the organizing committee for inviting me. There has been an extensive session this morning on ascending endografting. I think almost everything was said and will be repetition, but we'll still do so. What we learned in ascending endografts is that post surgery legions

are probably the best indications when we have pseudoaneurysm or bleeding in the ascending. Type A dissection is a rare indication, and ascending aneurysm actually doesn't work very well due to the fusion form type of these anatomies. Our experience is lended to 24 cases until 2017,

and you will notice that most of those cases were emergent, they were usually referred by a cardiothoracic surgery to our unit in order to treat those patients in a rather emergency situation. And in these cases we have mainly taken transfemoral approaches,

but you see that from transapical and trans subclavian also have been applied. There's some significant mortality tied to this treatment option, and this is due to the emergent character of the treatment. There were a lot of, a few type A dissections,

ruptures, bleedings, et cetera. Our device of choice has been the cook ascent device, which has been first published here, to be used in acute type A dissection, and is not current, not commercially available. We've also used a lot of customized grafts,

which is especially helpful when you need to tapered graft with a different proximal and distal diameters, and there you can use tapered grafts and just cut them to length that is, that fits well. There have been reports with these kind of customized

or off the shelf grafts that are commercially available, and trimmed to the length that is needed and experiences have been mainly very good. Main issue remains in over sizing and that is especially an issue because the type of CT for which they,

which is used for measuring the aorta is quite different. You need to know whether it's native or its graft, its gated or non-gated, systolic, diastolic, gated CT, the age and blood loss play a role in the pulsatility of the vessel, but generally I would like to say

that 20% over sizing's probably the right number, and this is mainly due to that already the pulsatility of this area of the aorta is, within 15%, relatively high. This is a case with the type A aortic dissection, you see that at the greater curvature, how the contrast goes into the dissection.

There's a cook ascent device that is delivered from transfemoral route, and you see here on the completion angiogram it looks quite nicely sealed, but what you also see is a problem that we frequently see is that the bare struts go into the valve

and cause a valvular insufficiency in this patient, so the patient required a TAAD that was done transapically, but the target valve did not stay where it was suppose to so it needed to be snared into a better position, and then again treated with an ascending TEVA. This time from the transapical

because we already had that access. And when this was done the patient could receive his, um, let me go back. Could receive this uh, Edwards, uh valve. Just to show you

that you can put a lot of these materials into one patient and maybe he would have been better off with open surgery, but I'm sure there was a reason why he was preferred for endo treatment. One of the big issues is inner curve apposition,

because the device is proximity, quite often not perpendicular, what is necessary in order to give them the radiant force to seal. And you see this from the, come picture this, images I got from other colleagues,

are about the Gore ARISE Studies. And what Gore is, um, is uh, is using here is a mechanism to meet this problem of the inner curvature, which I think is very helpful. We've been doing similar,

and been presented here ten years ago at the Veith-Symposium. We called it in situ bending, a bowden-cable principle to shorten the curve, the inner curvature. Medtronic has been working, Ali Khoynezhad is in the room.

He's been doing the physician sponsored IDE trial on this with really good results, and we hope to hear more from him. But if I look at the images, there's also the same issue of perpendicularity of the device, the approximate part,

and you see the same in other publications. Here from us, and again you see that the devices don't really deploy well at the inner curvature. I think I jumped over this case, which is about a transapical bridging stent,

because I have run out of time, I apologize for that. This is also imported for Martin Czerny, who has been on the podium showing today, the combination of Bolton NBS ascending graft, because its really what we need

in order to treat those patients, in order to get a safe landing zone. And to summarize, in my belief, the endovascular treatment of the ascending aorta is already beneficial in selected high risk patients, and those surgery lesions are the best aneurysms

will not work without having a valve attached to the ascending graft. Transfemoral delivery may not be the right route, in my belief the transapical was much more promising, and we see a significant process in the device development. Thank you very much.

- Thank you, it's a pleasure to be here. I'll address how the Indigo Thrombectomy technology can expand the reach of what you can do for your patients. It will preserve treatment options, improve patient outcomes, conserve hospital resources,

and perhaps most importantly, improve your day. The old treatment strategy, every time I had someone with acute limb ischemia I felt like I was shopping at this store. When I went to surgery, I wished I could put a drip catheter in, it lasts a little longer,

to mop up some di when I went to the angio suite, I wished I could cut down and remove some more macroscopic debris. I submit that the new Indigo technology

will provide a new strategy for treating acute arterial ischemia. On the same concepts are predicated STEMI, code stroke, Level I trauma alerts, we've instituted acute aorta, and piggybacked on that, an acute arterial ischemia protocol.

So that means when a patient like this presents with acute arterial ischemia, they get an algorithmic, systemic, trained, metered approach. They go past the holding room directly to the endovascular suite,

and all the processes happen in parallel, not in series. The call team is trained and dedicated, and while anesthesia is working up top with labs and lines, we use the duplex ultrasound to pick carefully our access sites. A faster time to reperfusion allows us to

do it and avoid general anesthesia, incision in hostile groins, and the exposure of lytic therapy, resulting in a decreased morbidity and mortality. Being able to treat the full spectrum of the arterial tree allows us to run options.

We preserve options by first mopping up more proximal clot, and then dripping distally when we need to, or, dripping distally to open up distal targets for surgical bypasses. As an example, this was a recent case

on a trauma CT scan, injured inthrelane aorta with emblogenic thrombus confirmed on intravascular ultrasound. We went in with a large bore system, a cath to aspirate the clot, and then used a cover stent to repair the aorta.

We shot an arteriogram the lower extremities, noticed that it embolized distally, and we used a Cat 6 to pluck out this clot and restore flow. Able to work up and down the full arterial tree. A learning curve for me was to understand that debris has to be corked to removal, which means no flow.

And most other worlds in vascular surgery, flow is good. No flow is bad. Also, you have to vacuum the clot out. Which means you have to uncross the lesion, which is counter intuitive for most of the precepts I've learned.

I've learned to use long sheaths to approach the lesion and to use larger catheters to remove more macroscopic debris. I rarely use the separator, I engage it and cork it for 90 seconds. That allows it to get a firm grip and purchase on it.

And I have to remember that no flow is good. This demonstrates how you approach the catheter with a large sheath. Under roadmap guidance you turn the aspiration vacuum on immediately before you cork it to minimize blood loss. And you use it like a vacuum by uncrossing the lesion

and let it slowly engage and aspirate the catheter. Ninety seconds allows it to get a firm grip and purchase so you can extract it without breaking it loose. I rarely use a separator, I use it only for large thrombus burdens, sub-acute clot, adherent debris,

or when the Indigo catheter is clogged. I strip out the catheter with the separator like a pipe cleaner, and then, every once in a while, on a subacute clot, I'll peck and morcellate it with a separator. Typically, in my lab, when I have new technology

I never have the team trained when I have just the right case, so I've learned over time, to train the team first. And with a trained team, they've taught me a lot. I've found with the Indigo catheter it's hard for me to watch the monitor,

work the catheter, handle the on-off switch, and watch the flow in the canister. So, what we do is we have a spotter who's not scrubbed. They taught me to take the on-off switch out, and then mechanically kink the tubing to make and on-off switch.

And they provide me feedback and just say fast, slow, or corked, so I can run the catheter and watch the monitor. I've learned to beware of the Cook Flexor sheaths, because they scuff up the tip. Use a check flow valve that unscrews from the

catheter if possible. I use coaxial catheters whenever possible, and I telescope them. You can telescope large catheters over small catheters. I use large sheaths and catheters whenever possible, using the preclose technique,

and then you can preserve options if you want to press more distally, you can cinch down, remove the large sheath, put in a 4 5 French, and then press ahead. I also, after I use a pulse technique, will occasionally use the Jungle Juice.

The team taught me the Jungle Juice is half strength contrast, some TPA and some nitroglycerine. When I lace the clot with Jungle Juice, I can observe fluoroscopically, the progress I'm making as I'm aspirating the clot. Thank you.

- I try to dissect this convoluted title into two questions, basically, when is endovascular treatment of post coarctation aneurysm best, and when is an open surgical intervention required. A couple of years back in time, we looked at predictors

of aneurysmal formation in patients after surgical correction of coarctation, and we found essentially two predictors, which is previous surgical patch repair, and the age at the surgical repair, as predictors for the evolution of

a post coarctation aneurysm. In other words, these two predictors could actually become important for the selection of patient for open surgery. I come to this in a moment.

A year later, we could publish the feasibility of percutaneous endovascular repair of those post coarctation aneurysm, post surgical aneurysm, easily by a customized

or off the shelf stent graft. So that is basically accepted in the community, and reflected in guidelines, that basically come to the conclusion to the question, when is endovascular treatment

of post coarctation aneurysm best. In the case of a risk-benefit ratio high for open surgery, which is in case it's a redo surgery, of course, in presence of extensive collaterals, with a significantly increased bleeding risk,

adult patients above the age of 13.5 years, according to the statistical analysis, and when end to end anastomosis is not feasible, and of course, patients need to be suitable for an endovascular approach.

Patient preference may play a role, most recently, and of course, is conclusion of endo first should be executed in dedicated centers that have options to treat the patient even openly.

The second part of my title, or the second question is basically to the preferred use of open stents or covered stents, and in order to show our recent analysis on this, I had the privilege to compare

a group of patients from my previous institution that used self-expanding open stents, and with my current position in another place, that uses CP stents, or covered balloon expandable stent grafts

in the setting of coarctation as the first and only option. So we have no data from two different hospitals that show similar patient sets, a total of 52 in each group, that do not show any demographic differences

over a time of 10 years, collected over 10 years. Clinical presentation of comorbidities are essentially the same, so we're dealing with a comparable set of patients

and two different concepts of treating primary coarctation. The post interventional vascular events are also similar, no significant differences between the two concepts from two different sites,

with a trend towards more re-stenosis in the setting of ballon expandable stents being used as the first approach, but not significantly more. Even in hospital complications, comparing these two groups of 52 patients,

age didn't show any significant difference, with a trend for longer hospitalization in patients treated with the CP stent or covered stent. Maybe this is only a coincidental finding and a more cultural event

rather than medically driven. If you look at the outcome curves between both groups, with no mortality in either group, there is a similar shape of the Kaplan-Meier curves

over up to 90 months, with an interesting difference in the first post interventional phase, with three asymptomatic localized dissection in the balloon expandable stent graph group, however, no significant difference over time.

This next slide summarizes the ballon expandable procedure with the CP stent. After obtaining lumen and connection between this ectatic aorta, it was possible to stent the segment

with a covered CP stent very nicely. You see the result on the lower right corner. The other concept is a bare self expanding Nitinol stent placed first after recanalization of the coarctation and then potential post ballooning

to obtain an appropriate dimension and the lumen. In summary, comparing those two approaches and answering the question, when is an open operation still required, I think it's fair to say that in adult coarctation,

and endo approach should be chosen first, and bare, self-expanding Nitinol are relatively safe as a concept, and durable solution, without the risk of side branch obstruction, whereas covered ballon expandable CP stents

are also safe, and offer a durable solution, but have to respect the LSA anatomy. An open surgery I think should be reserved for infants and children younger than 13.5 years, only in view of an end-to-end anastomosis.

Thank you very much.

- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --

- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.

But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,

is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy

in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.

The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation

so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later

that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low

and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse

even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean

as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques

different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between

pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients

are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system

you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because

this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out

now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference

between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing

a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is

the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories

and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here

again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result

and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not

fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again

look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as

the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here

This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you

- [Audience Member 1] So I have a question for Dr. Jackson, but maybe everybody else on the panel can chip in, and it just has to do with what your first intervention is going to be for a focal stenosis in a vein graft, and I guess, Ben, my question is, in general, is your first time you intervene going to be a drug-eluding stent?

Our strategy generally has been, to start with, a cutting balloon based on a series, I think it was from Schneider, who compared it and saw pretty good results. Nowadays, I think maybe I'd do that, and at the same time then put a drug-coated balloon in, and that's

increasing the cost, there's no good data to say that's better than just a cutting balloon, but I think I might do that and reserve the drug-eluding stent for the second time or third time. So my question is, what's your intervention the first time you intervene endovascularly

for a focal vein graft stenosis? - [Dr. Benjamin Jackson] So if you're not going to do an open revision, right, we'll preface with that, I'll use a coronary drug-eluding stent first. - [Audience Member 1] Okay. - [Speaker 1] Okay, so, are you happy with that?

- [Audience Member 1] Well, I was hoping to get other opinions, but if you want to move on, that's fine. - [Speaker 1] Alright, so I'll give you my opinion. I don't think there's anything wrong with putting a stent. The idea that the stent is going to be occupying space and is going to mess up your next procedure, I think

that's more out of fear than actually the reality. We have patients that in the SFA popliteal segmentary, we're on the fifth round of stents, and you'd be surprised how you can distend the fifth stent inside the SFA. I never thought it was possible, actually.

We have some IBIS documentation showing at least a five millimeter lumen after you do that thing. So I'm not so concerned about that. The problem with this, and I agree with putting a stent because there's a very rigid lesion sometimes. It's not easy to balloon them, it's not easy to

because usually the cutting balloon probably already got the lumen that you want, but then definitely it increases the cost that way. Again, who knows the other answer. Anybody else? - [Dr. Chris Metzger] Yeah, a brief comment.

I don't think all vein graft lesions are alike, so it depends if it's diffused or focal. The other thing is, I think your response to initial therapy is important, so if you do your balloon, cutting balloon, then it's going to tell you recoil, not recoil,

and the other thing I would say is intravascular ultrasound, if you're in doubt on how large that is, I think helps a lot. So, you know, if it's very focal, very high grade, I think drug-eluding stent is perfect, the question is what size, IBIS helps with that.

Otherwise, I think your strategy for longer disease might be a reasonable strategy as well. - [Dr. George Adams] And the only other comment I'd make is if there is a thrombotic component like Chris was saying, depending on the client morphology I might use laser atherectomy followed by a

biologic therapy such as a drug-coated balloon. - [Speaker 1] Yes, sir? - [Audience Member 2] About that last presentation, are you using any type of anticoagulation when you do these PTFE tibial bypasses, or were the groups comparable where there's only antiplatelet

therapy in the vein grafts and in the prosthetic grafts, or are you putting all of them on factor 10A inhibitor coumadin? - [Dr. Peter Lin] So our patient, we typically put them on aspirin, and for the Propaten we don't add any distal antiplatelet agents.

- [Audience Member 2] Because that's a lot better than historical reports, probably. I wondered, why do you think it shows so much better, even with previous vein cusp patches? - [Dr. Peter Lin] So I think the patch matters, and I also think that over the years, we also learned

a whole lot about the distal anastomotic patch, because time won't let me tell you something and go into great detail. So the patch, you know, we make, is about two to two and a half centimeter long, so that length of the patch is almost twice the length of

the diameter of the graft itself, so I think that's also a significant factor. So it's something that previous literature has not really emphasized on, and the PTFE ideally should be connected to the proximal one-third, instead of distal one-third, so that also may make

some of the same area boost configuration. So the whole idea is you want to make the patch as long distally as possible. So some of the variations, I think, have in part helped, and ideally is that the vein is available, that would be great, if not we also have used a lot

of bovine patch as our patch material, so that thing I think made a lot of difference. So I don't think, all things considered, antiplatelet agents played a huge role, but I think the distal anastomotic compliance mismatch, if we can alleviate that, it will help your outcome.

- [Speaker 1] So Peter, you believe that those grafts have a thrombotic threshold, or you think there's no thrombotic threshold for PTFE? - [Dr. Peter Lin] Oh, I think so. - [Speaker 1] Let me just continue my thought process. So if there is a thrombotic threshold, it doesn't matter

how long you're going to put the vein patch. You can put a 16 millimeter vein patch, it's not going to make any difference, if you reach that thrombotic threshold. So then we come to the criticism that maybe you're selecting the cases

with good runoff, and in the good runoff, it's hard to show a difference between vein and (unintelligible) bonded with the patch, maybe. But if you are to do those terrible cases that have an isolated TPO segment, or they're all the way on the foot or the plantar arteries, that maybe the

saphenous vein will come up much better than this. What do you think? - [Dr. Peter Lin] Well, these are all great points. It's hard to discern based on a single yes or no answer. Saphenous vein has certain limitations, although I believe there's still a standard of care

in terms of conduit choice. Often times the veins are sclerotic, we're limited by vein length, so again, I brought up some points that in some patients we can only connect it to a superficial femoral, even a popliteal bypass because the vein is not long enough.

So PTFE, while it's not perfect in some scenarios, it does have advantages, because I can connect it even to the external iliac artery, I can connect at the common femoral artery, so that's that benefit. I did mention very briefly in our multi-vein analysis, the single vessel runoff is the (unintelligible) runoff.

So in those cases, you're going to have bad outcome no matter what kind of conduit you use, I do believe that, but in general we'd just use aspirin for that patient. But I believe that if we do believe there's an underlying prothrombotic condition, we would add additional anticoagulants, but that's not typical routine practice.

- [Speaker 1] Alright, I just want to add that in poor runoff situations, the vein clearly does better, and it works for a long time. We had published three years ago, on plantar arteries in branches of tibial vessels in the foot, and they did work, only with vein.

Everything else kind of failed, even with the fistulas. Yes, sir? - [Audience Member 3] I have just a quick question about the Phoenix device, a two part question. A, do you use it with a filter, or can you use it with a filter, and two, do you use it as a standalone therapy

or adjunct to a drug-eluding balloon or anything else? - [Dr. George Adams] So, in general, atherectomy is always with adjunct balloon angioplasty. In regards to the filter, especially with the Phoenix device, you have to be careful and very selective with the wire that you use,

you want to use a nitinol wire. So for a filter usually I use a free-floating filter, the NAV-6, and you can't use it over that nitinol wire, you have to use a graduated tip wire, usually a Viper or a Viper Flex. So I would select cases where you would not use

a filter specifically with this device, so if you have a long lesion or if there's any thrombotic component to it, I'd be very conscientious of using this device with that. - [Speaker 1] Thank you. Any questions from the panel?

Because I have a few questions. - [Dr. George Adams] Actually, it was I think very stimulating as to the conversation we just had, in regards to thrombotic or anticoagulants with antiplatelets, you know. Recently the COMPASS trial just came out, as well

as an E-PAD which was more or less a pilot study, showing that just taking peripheral arterial disease regardless of grafts, there seems to be a thrombotic component, and factor 10A inhibitors may have benefit in addition to antiplatelet therapy in regards to all PAD patients.

I think it's a very interesting discussion. - [Speaker 1] I have a question, Dr. Dorigo. Once you identify the high risk group of patients, is there any strategy to modify them to improve them and get them to another category? - [Dr. Walter Dorigo] Most of the perimeters we

examined were not modifiable. Age, extension of disease, coronary artery disease. Maybe one possibility is to improve the runoff status but, in concomitance with the intervention, one can try to improve the runoff score. But four out of five factors were not modifiable.

- [Speaker 1] Thank you, okay. I have one more question. So, do you do distal bypasses? - [Speaker 2] We do distal bypasses, I personally don't. I have a big group, I have three people in my group that only do distal bypasses.

- [Speaker 1] So, it says a patient in your group does not have a saphenous vein, and has a limited runoff. How will you approach there? - [Speaker 2] Well, that was a question I would want to ask both Walter and Peter.

Is there a role for composite bypasses? Because we do it quite a lot where we only have shorter parts of vein available, shorter lengths of vein available, we would do the above-knee PTFE, and then cross the knee with the vein. But I remember that last year at this meeting,

the Americans said that it's worse results, but we still do it. - [Dr. Walter Dorigo] Yes, in the registry are a crude amount, so about one, 150 composite bypasses with the short or long segmental vein and the part of PTFE graft, we use it.

And the results are not particularly better than those with the grafts, but it's likely better. - [Speaker 1] Right, I want to ask the panel, if you have the use the common femoral artery as an in-flow, and this vessel has been used

a few times before, what do you prefer to use? The external iliac, redo the groin again, or use the deep femoral as an in-flow? We'll start with Peter Lin. - [Dr. Peter Lin] I would probably go to external iliac,

because higher, it's got proximal better vessels, and it's greater diameter, all things considered. If you go deep femoral, you still got to navigate across a stenotic plaque common femoral artery. - [Speaker 1] No, it's not stenotic, it's a normal vessel. - [Dr. Peter Lin] So, I would, if all had been equal,

obviously common femoral might be better, but if common femoral's highly disease, stented and treated, and so there's a lot of scar tissue, I'd probably go with external iliac. - [Speaker 1] Okay, anybody else want to make a comment on what they preferentially use for in-flow?

- [Speaker 2] It depends what material you're going to use. If we use the vein, we go back to the common femoral, if we use prosthetic material, we would prefer to have a site where it's easier to go in and lower the risk of infection. - [Speaker 1] Right. I'll say that it depends on

the length, if I have enough length just to go deep femoral, I'll go deep femoral preferentially, but I have gone to the external iliac with a vein and have had no problem with kinking or anything, it would just make a tunnel lateral to the artery. We don't go medially because there are too many

branches there, but laterally, and you can do the anastomosis vein, and it only adds about two, three centimeters of length when you get it just above the inguinal ligament. With that, I'm going to thank the speakers, it was a great conference, and call the next moderators, please.

- Thank you so much. Thanks Dr. Bies. This my disclosures. Well, the indication all starts having healthy common carotid artery, at least 6mm in diamter, free of calcification, and atherosclerosis,

and you want to have that artery distance between your clavicle and your bifurcation to be at least 5 cm. We define this, or call it, the landing zone. The depth of the artery, the less deep the artery, the better,

the easier the procedure is, and you want a ratio of the common carotid artery depth to the landing zone to be less than one, and likely, like when you get closer to half, where the ease of the procedure is significantly noticeable. Now, the contraindication, again focusing on access,

you don't want to have a severely calcified artery, you don't want to have significant atherosclerotic disease right where you're going to puncture the artery, as you can see here on the ultrasound. Now, the dual antiplatelet therapy here is a must,

you have to have it, you have to start it at least a week prior to, here there's two randomized trials showing the benefit of dual antiplatelet therapy. You have to make sure the patients are on statin, and we've shown on others, the benefit of statin.

You can almost reduce the risk of death for more than 60% in patient who develop severe complication after carotid stenting. Blood pressure here is interesting because on one hand you want to keep the blood pressure as high as possible during the flow reversal,

greater than 140, greater than 160 because you want to maintain that delta between the systolic pressure and the venous pressure. That's how the flow reversal work, and this is how you have a good protection of your patients. But after the procedure, you want to treat it like

any other carotid stent, and you want to maintain the blood pressure less than 140 because you want to avoid a stroke. We've shown as well here, that you can reduce that risk by 70% if you put patient on beta blockers, preventing them from having severe

hypertension after stenting. The exposure's going to be between the two head of the clavicles. A small incision, 3 to 4 centimeter, but you can get about 5 centimeter almost, of the carotid, and you want to put a

vessel loop proximally, or an umbilical tape just to cause a gentle traction on the artery, and purse string stitch, or u-stitches very helpful here at the end of the case, you can tie it down when you pull your sheath. This is essential here to prevent dissection.

You want to have the needle to be parallel to the artery, so with a gentle traction, you don't want the needle to invaginate the anterior wall or to go into the back wall, and then you start a dissection. So if you can get the wire, the microwire,

into the lumen at this point, that's essentially preventing dissection. Once you're in with the microsheath few centimeter, you just do an angiogram, and if you see disease here at the bifurcation, you stay short, so you advance your microwire followed by

a sheath with a dilator, in exchange over an O55 to your stiff or six French sheath, 8 French sheath. Now, if you have a healthy looking external carotid artery, I highly recommend that you engage the external carotid artery by advancing the microwire

into it, followed by the microsheath, and then your stiff wire, because you going to get at least couple a more centimeter of purchase, and having a purchase I think is essential again in avoiding dissection. So if you have your wire in and you can

dilate just the anterior wall with sequential six and nine French, that allow your sheath to go very smoothly into the common carotid artery, and once your sheath is in there, you're basically done with the procedure, as far as my concern.

Now, once spot fluoro before you advance that sheath, because this is where the wire can track back, so if you can avoid the wire tracking back at that point to have the purchase when you get in. And then, from that point, it's just connecting the flow reversal between the arterial and venous.

And then clamping the carotid as they talked about using a atraumatic clamp and then now you have basically an active, but right before you do this, you want to make sure that you have everything on the table, your stent is ready to go to minimize the flow reversal,

your wire, your balloon, everything is ready to go. And you also want to the time out, making sure that the patient is therapeutic under ACT, and the blood pressure is where you need it to be. I'm for not ballooning the stent, so gentle pre-ballooning,

we've shown how ballooning the stent can double the risk of stroke and death, and from there, I think you take one of the most complicated procedure and most dangerous procedure you do to a simple, equivalent to an iliac stent with ipslateral approach,

because you can get your short wire and delivery system and deploy the stent very easily. You've seen here the time can be, as your technique improve, less than an hour, and your clamp time and flow reversal time is about 10 minute.

The technique is published in JVS, if you want to reference to that paper, and then as far as the surveillance project we using the VQI, more than 500 center in the United States now have VQI, so we want to see real world outcome,

to see if the randomized trial or the IDE study apply to real world outcome when people are using it. And you can see the outcome here. We have twice as much neurological complication with transfemoral carotid stent, compared to TCAR. This was presented at VAN and published in JVS.

And essentially, no statistically significant difference in all major adverse events between CEA and TCAR. So the take home points: This is a very promising hybrid procedure with excellent outcome. This outcome that we're seeing now,

is not just in IDE study, but is going in post approval, so we seen it in real world outcome with people who don't have a lot of experience with TCAR, and there are several important techincal points that make this procedure very, very safe, and very easy. Thank you.

- So I don't have to give you any data. I just have to tell you how we do it. So this is the easiest talk of this session. Step-by-step technical tips. Now our definition of pharmaco-mechanical may vary between us so I'll give that as we go along. These are my conflicts.

When to use it. Well certainly as you already heard, Massive PE has contraindication to full dose lytic is one area. Submassive elevated risk may be another. We've already seen multiple people put up

these guidelines so what we're really talking about at this point in time is those patients that we just talked, that those two groups that they just talked about because those are the ones that we're trying to treat. The biggest thing is don't be frozen by indecision.

Majority of patients eligible for thrombolysis do not receive it. It's amazing to me as a referral center to get the call from an outside community hospital or the patient with hypotension, abnormal RV or biomarkers and they've barely given the patient

Heparin and they just want to transfer the patient out of there and you tell them that's a massive PE. Please give them systemic thrombolysis and they go what? And I go you now have 10 times the death rate of an acute myocardial infarction. Would you give this patient lytics for acute MI?

Yes. Then give them the freaking lytics. Save their life. It's amazing what's going on in this country. So the PERT Consortium and everything, we really need to educate the community

because it's ridiculous. If you look at the utilization of thrombolysis, it's going down. Unbelievable and if you look at the in-hospital mortality for these patients that have significant PE, the in-hospital mortality is much higher

if you don't give thrombolysis. You've already seen this indirectly in a bunch of different lectures, but I just wanted to show you very quickly how to do this on an echo or CT. You want to get the center line, get it at the valve and then measure it one centimeter

below that valvular plane. This is something you don't have to depend on radiology just to do. You can just look at the transfer CT. You can look at the echo. You don't have to fight with your echo guy to give you that.

It's also very evident and often times just looking at the images. Why treat submassive elevated risk PE? You know what? I've heard all the mortality stuff. I get it.

It doesn't change mortality that much. It does and we should measure it as a primary endpoint in our trials. Change your discharge time and in this day and age, medicine is so expensive. Time in the hospital, repeat procedures,

elevated your amount of treatment for that patient really has to be looked at as part of that, not just mortality. But there's eight times more recurrent PE and four times a mortality rate if you have a PE and unresolved RV dysfunction at discharge

and that should be looked at prior to discharge, not just say well they look like they're doing okay. Treatment of IVC, higher risk PE. Certainly the other thing we have to look at is there's other things to do. You've already heard a little bit

that there's IVC filters out there. We take out 90 some percent of our IVC filters in our section. We actually as a system now are up to 60% at seven months and it only takes effort. The patients that I see die in our hospital

in the last year that shouldn't have died are patients that should've gotten an IVC filter because they got heroic things to take out their PE and nobody put a filter in even though they had significant DVT left over because they were afraid of the TV commercials?

Oh my gosh. If you look at the 27 extra deaths that we've had from IVC filters that were removable in the United States, and you take our experience and multiply it by the number of tertiary care hospitals in the United States, use them when they're appropriate.

Take them out so the risk is low, but don't go away from them. They've already been shown to be beneficial for the right patient population. But you also have embolectomy and surgery should also be considered.

Step by step. Make the decision and clinically be consistent. PERT team or other consistent mechanisms. We have an app that we use. This is throughout our entire healthcare system so all the vascular specialists have this.

It's an algorithm that's supposed to be used both in the ER and for the different vascular specialties so everybody's being treated very similarly. We have all the different definitions. We have the PESI calculator. All this is in an app

that's readily available to our constituents. Special consideration certainly is the tolerance of thrombolysis, underlying tolerance of pulmonary hypertension. Again, we need to evaluate the patient, not just label them as a PE.

And I also think there's a special population we need to study and that's the socked in pulmonary artery with no perfusion on a CT scan. I think this is a different population long term and we need to study that a little bit more. We got to get the patient back from the edge.

I think I'm opposite of Jeff. I don't want to see them get worse and then treat 'em. I want to prevent them from getting worse as long as I'm selecting that population in a thoughtful matter. We primarily use low dose TNK.

This is nothing I'm going to give you data on. This is an institutional, what do you want to call it, anecdotal experience and we lost our contracts except for TNK so we had to go to this and so we do a lot of catheter-directed. You've already seen all these trials.

There's a ton of different devices out there. The one I want to talk to you about is using a really fancy one called a pigtail catheter and another one called an ethos catheter. This is a patient that had a significant PE. You can see that they've got bilateral main PE.

This is on table. This is what we do for the vast majority of our patients. We sit there, we use ultrasound guided access to the vein so that we cut down our venous complications for access site. The patient is given 20 and 30% of a loading dose

of TNK and then we watch them. If you look at thrombus in a test tube and you give a thrombolytic therapy, it takes about 20 minutes for fibrinolysis. So this is what we do. As you're going to see, this is over 25 minutes

and we see the patient went from a pulmonary pressure of 65 and a heart rate of 115 down to 25 minutes, the patient's pulmonary pressure is about 44 and their heart rate is in the 90's. This patient then has all the catheters removed on the table even though they got lytic

and they're heparinized. This is a venipuncture, so big IV. We send them up to the unit and we typically discharge them the next day. We have an echo B4 discharge to make sure there's been a significant recovery of RV.

If not we'll watch them an extra day and then all these patients get a CT again. I'm sorry an echo again at 30 days to make sure that we're getting good resolution from that. On table results, decrease your complications. Thrombolysis has always been associated with the

duration of thrombolytic therapy and intracranial bleed. Now you can either use a pigtail catheter which is what we use for most of these people because we can measure pressure in it. We spin it around a little bit in the pulmonary arteries and give the dosage.

Again, we give 20-30% of the dose. There is no data for that. If significant improvement does not occur, they'll get dripped overnight in the ICU at usually .5 to 1 milligram per hour. You've already seen the data for EKOS.

We use this if we think we need a little bit quicker Thrombolysis such as in a socked in pulmonary artery 'cause we have no flow. We do think that may help, but we don't have any data for that. It makes us feel good.

We spend a lot more money and so we think that may be reasonable at that point in time. This is just what it looks like when you put in bilateral EKOS catheters. Certainly the patient can be put in the ICU for this. I do think that we should do a trial looking at EKOS

with a little higher dose, do it for 30 minutes, look at those pulmonary pressures right on the table. I think, again, my own opinion is after 25 years, the closer we get to being done on table, catheters out, patients doing well, the better, safer procedure we have,

the less chance of mortality, the less chance of complication and as you decrease complications, your benefit improves. We've already seen the results and you'll see more of these from non-randomized trials such as Seattle 2 which looked at 150 patients,

but they saw very quick recovery of the RV which was very important. If you look at technical success, it was very high. The dosage of thrombolytic exceedingly lower, lower than what we're giving in a PTO catheter, that's for sure.

And if you look at the RV from Ultima Trial which was randomized. There was faster RV recovery utilizing this device. Thank you very much.

- Thanks Gustava, Fred. Thanks Frank for the opportunity. These are my disclosures. So, why are talking about aortic septotomy, and when is it necessary? It's really for treating complicated TADs with malperfusion, planning an EVAR or TEVAR when you don't have

adequate landing zones. So, certainly trying to bail out from a complication or EVAR, TEVAR. This was my first case in 2006. It was an elective case, a clot client who came with an aortic dissection.

And what I ended up doing at the time, was going from true to the false lumen at the aortic bifurcation, marching up the aorta, snaring a stent, snaring a wire from true to false lumen, and then essentially created a place where from the femoral approach, we could just apply

gentle downward traction to tear the septum. I'll show you exactly what this. The two wires come out on the femoral, from the femoral side. You essentially pull down gently and this is simply glide wire,

you could use a variety of wires. So this is something we've implemented in 2006. And of course this experience has grown. We've used it in a lot of different circumstances. Here's a completion angiogram for this case. So, what else can we do?

We can certainly do septotomies. We can put in stentgrafts or just bare metal stents to connect the true to the false lumen. The trouble with this is when aneurysms expand. These stents are really difficult to deal with.

And I'm not a big fan of putting stents in, bare metal stents across a paravisceral aorta. So, for that reason aortic septotemy is very helpful. Certainly can be used when you have infrarenal aortic aneurysms, following up with the thoricoabdominic dissections and you need

to create better landing zones. Once again, true to false lumen snare, gentle downward traction, creating single barrel lumens where you have adequate proximal and distal landing zones to obtain seals. I'll show you through a complication of a TEVAR.

Here's a patient who came in. Sudden onset chest, back pain and left foot rest pain. At the time we went in, and thought just simply getting in through the true lumen, and deploying the stentgraft all the way from the descending thoracic aorta.

From the left subclavian to the descending thoracic aorta would have been sufficient and it seemed like it was. And I think most would treat it this way. The trouble was as soon as the stentgraft was deployed, the paravisceral aorta collapsed. It was an acute dissection and now we have a very

difficult situation where the entire paravisceral aorta has really collapsed from the septum. So in this particular case, we were able to protect the celiac and the SMA with the wires that you see, where the red arrows are. And once again, put a catheter from the true to the false

lumen, snare in the descending thoracic aorta, apply gentle downward traction, to unfold and drag the septum down to the aortic bifurcation, knowing very well, as much as we were going to be able to profuse the visceral arteries, which we were able to,

we now have to deal with an occluded infrarenal aorta. And you have to be ready to do these things, especially if you are using septotomy techniques. And this particular case, we just did kissing stentgrafts, to manage this. Other scenarios could be delayed complications.

This is a patient who initially came in with a thorical dinaric dissection, which expanded into an aneurysm and underwent endovascular repair. Fairly straightforward, the coil embolisation of the false lumen. Everything went uneventful, except the patient

shows up a few days later with saddle paresthesias, bilateral lower extremity weakness, urinary incontinence, only when he ambulated. At rest, he was completely normal. This is, I think, the first case of transient ischemia and cauda conus syndrome following TEVAR.

Of course it was a daunting situation, and what we found is that the obvious dissections extended all the way to the iliac bifurcation. And this particular case, once again, going in from the right and left, true and false lumen from both sides,

I was able to snare wires and catheters into the mid aorta and you'll see this play out in the segment, and once again, gentle downward traction, create a septotomy extending to the left iliac bifurcation and to the right iliac bifurcation, and once again you see that right external iliac artery

has a prolapse septum which we treated with a stentgraft. So, there's a lot of different ways of managing these problems, and this patient's symptoms actually resolved and he recovered immediately. And I think what we need to do is be ready to deal with all sorts of potential complications that occur.

Many others have started to report on these findings as well. And obviously, there's a lot of benefit and right now, Ramon Berguer, Juan Parodi has a septotomy catheter that is currently under trial. So I think, my personal suggestions are,

this is not necessarily simple, but you have to be able to be ready to deal with all potential complications if you do aortic septotomy. And it is a very useful technique in managing complex aortic dissections.

Frank, Jackie, and the team, thank you very much. We love being in New York City at this time.

- These are my disclosures. So I'd like to just highlight first the Einstein PE DVT study. And just to tease out the cancer population, yeah, it this study. So as you can see, the cancer group, small in number with the rivaroxaban

versus the low molecular weight heparin and warfarin. And you can see the incidence of VTE in that population and the hazard ratio. And then bleeding, of course also once again, a small number of patients with a

you can see the incidence of bleeding in this patient population as well. Also like to take the AMPLIFY trial with apixaban and just tease out the cancer population. Little smaller in this group. As you can see, 81 patients in the apixaban group

and 78 in the enoxaparin warfarin group. And you can see the incidence of VTE in this cancer patient population. And I put side by side here the bleeding risk in each of the groups. As you can see, 2.3 and 5.0

in the patients getting enoxaparin and warfarin. The Hokusai study then was published, and this was in New England Journal and Medicine this past year. And this looked at low molecular weight heparin and then edoxaban, and then of course, dalteparin.

200 units per kilogram for the first month and then dalteparin. Clearly showing, looking at this population and looking at outcome. So let's look at recurrence rate in the edoxaban versus dalteparin.

And you can see it's 6.5 versus 10.3% direct comparison. And major bleeding was 6.3% in the edoxaban group and 3.2% in the patients getting dalteparin. The next study that came out looking at the DOACs, this was the SELECT-D trial. And in this trial they looked at rivaroxaban

versus dalteparin once again over a six month period. And what did they find in this study? They found that 11% recurred in the dalteparin group versus 4% in the patients receiving rivaroxaban. The major bleeding incidence was 6%

in the patients getting rivaroxaban and 4% in the patients getting dalteparin. So you can see that the DOACs maybe have a place in this patient population, so that they might be effective. And finally the ADAM study, which will be published soon,

just similar to the rivaroxaban study. Looking at apixaban versus dalteparin. Same model but we don't have any data on this study at this point in time. So the 2018

NCCN Guidelines and the ISTH guidelines of 2018, both show and list now that the DOACs can be part of the process of treating patients with cancer and DVT. So yes, I believe DOACs are ready for prime time. Selection is based on the cancer and cancer is important. Accepting the risk of bleeding as you saw.

We must consider concomitant chemo therapy and the ability to tolerate oral anticoagulants. Thank you very much.

- Well I'd like to thank everyone for being here, and for Dr. Veith and the committee for inviting me to speak. I am a recipient of research grant funding from Acelity as well a Speakers Fee. However, my study was initiated prior to any arrangement and any award of grant funding.

Acelity was not involved in any aspect of this study design, data collection, analysis, or presentation. So surgical site infections correlate with readmissions, reoperations, and increased healthcare expenditures. SSI's after infrainguinal vascular surgery procedures

range from seven to almost 40% of cases. We hypothesize that these are due to lymphatic disruption, proximity to the perineum, prostetic use, and we all know that these are catastrophic cases and can lead to limb loss and even death. At Duke, we had a bad surgical site infection problem.

To combat this, we crafted a perioperative bundle. This was a multidisciplinary effort that incorporated pre, intra, and postop measures to try to decrease surgical site infections. Use of an incisional wound vacuum, which started in the operating room

and went into the postop period was part of this bundle. The closed-incision negative pressure vacuum, is thought to act in many ways to decrease surgical site infections. It's thought to stabilize wounds,

to protect the wound against contamination, and that leads to early increase in wound strength and a narrower zone of dermal scar. Also it's hypothesized that this device reduces edema, increases blood flow, increases lymphatic flow,

and thereby reduces hematoma and seroma formation. What we found was after we introduced our bundle of infection prevention strategies, we had a much welcomed decrease in our surgical site infection rate. We then started thinking about which one of these factors

was effective and the Prevena device, which had been urged to be used on all groin and infrainguinal incision, was the first target as it is an additional cost to the hospital. We separated our patients into conventional versus negative pressure dressings

and we found that females were more likely to be in the negative pressure group. The negative pressure group had longer operative times, and more active smokers. So these were higher risk wounds. When we looked at outcomes,

we found in the negative pressure group we had the same readmission and return to OR rate, however, we had lower surgical site infections, fewer wound complications, and a lower 90 day mortality. When we did a regression analysis,

looking at different factors, we found the female sex was predictive of infection and that EVAR protected against infection. Negative pressure wound therapy emerged as an independent predictor against wound infection. The current data that's in the literature to date,

has many studies and a few of them are prospective randomized trials. The Gombert study is the latest, this is the AIMS Trial, and this is a prospective, multicenter, randomized trial looking at Prevena versus

standard gauze incisions. They found a significantly decreased rate of surgical site infection with Prevena. The DiMuzio Group at Thomas Jefferson Hospital also looked at cost data. They found that they had fewer reoperations

and fewer readmissions with the Prevena use, although this did not result in an overall decrease in cost. In conclusions, SSI's remain a major source of morbidity in infrainguinal vascular surgery. Efforts to reduce perioperative SSI's

using a care bundle, seems to decrease wound complications in this patient cohort. Prevena appears to add protective effect to decrease SSI in overall wound complications and was an independent predictor

within our bundled SSI reduction package. Data indicating cost savings remain to be elucidated. Thank you.

- Jim, thanks so much, and thanks to Doctor Veith for the opportunity to get involved. Here's my disclosure. So, certainly you don't want to be an expert on limb thromboses, however, it happens. And so, when you see these patients, no longer are we looking at fem-fem,

or even lytics, catheter-directed lytics. So how do we get from screen left to screen right in a single session therapy? Well, as we know, when these patients present, there's several different management options. You can do open thrombectomy with or without

a fem-fem, pharmacomechanical thrombectomy. There's catheter delytic and ultrasound accelerated thrombolytics, and then now, today, we have vacuum-assisted thrombectomy, as we've heard throughout this session, or continuous aspiration thrombectomy,

however you want to mention it. Regardless, when you end up with lytics, this is exactly what you're dealin' with. You're playing with fire, and if we do it long enough, you're going to see this complication. So we've really adopted a clot extraction

instead of a clot dissolution policy at our institution. I think Jim just showed you this technique that is afforded to us by the Indigo thrombectomy system, as you can see here in a Vivo model, this catheter actually does work extremely well.

It'll remove this soft thrombus, as you can see here. My first experience with this was actually for an occluded popliteal stent, as you can see here. We had a occlusion of the standard nitinol stent. This aspiration power was incredibly surprising to me. As you can see, it collapsed the standard nitinol stent.

So at that point, several years ago, we realized how good this device was, and how we want to minimize lytics for our folks. So we started in 2014 and recently this year at the Midwest Vascular forum in Saint Louis, we presented our data.

At that time, we had 73 patients over the years with acute limb ischemia. And here you can see the breakdown. For this presentation I'm going to focus on this cohort here, which is seven. But as you can see, like my panelists here,

we use it for occlusions, for not only occlusions but emboli as well, and also we had one case of an upper extremity embolism that we were able to successfully treat with this device. At that time, again, looking at all 73 patients,

you can see here that it's a very efficacious device. There were a couple folks who needed transfusion and perhaps the blood loss was a little higher than 300. However, as you can see here, the folks who had a blood loss, all five had open adjunctive interventions as well, and the ones who needed transfusion

all had catheter directed lytics as adjunctive therapy. As far as our efficacy endpoints, what we looked at was antegrade flow. As you can see here, oftentimes with your vacuum system thrombectomy, you're able to get antegrade flow. However, intermittently there's also other

adjunctive therapies that we had to use frequently as well. Going back to what, you know, my topic for today, how do you go from screen left to screen right, where here you can see one of our patients who came in. We did a retrograde ipsilateral stick,

crossed the lesion with the wire, then we delivered our eight french Indigo catheter and were able to get, in a single session, as you can see here, antegrade flow. So here's another, all this in one single session therapy. Here's another patient of ours.

As you can see to the left, one of our Gore Excluder limbs had occluded, and again, with single session therapy we were able to provide patency to that occluded right limb. Another case here, you can see one of our other Medtronic grafts.

And what you'll see here as you're looking to the right, here we are with our eight french Indigo catheter, is the separator, which is like a pipe cleaner. And we were able to clear out this clot and provide patency to this

all in a single session therapy. And again, here you can see from left to right how we were able to thrombectomize that limb. So over the years, the last three years, we do about 80 to 90 EVARs a year. During that time period, we have seven patients

come in with limb occlusions. And as you can see here, four of them were chronic, three claudicants and one res-pain, and three of them were acute limb Rutherford one, two A or two B. As you can see here, 42% of the time for these

occluded limbs, we were able to do it with no lytics, not even a pulse spray, nothing, not one drop of lytics. As you can see here, some of them we did have to do it in a single session. What we do is use a McNamara catheter.

We would squirt out, you know, anywhere from, as you can see, 14 to 18 milligrams of lytics, go get a cup of coffee, go make rounds, come back 20 minutes later, then utilize your device. And again, you can see, in a single session therapy we were able to afford patency.

And then finally, you can see here the blood loss was minimal. So this is a safe device. So in conclusion, I think that single session therapy is safe. It can facilitate achieving antegrade flow

in the management of stent graft limb occlusions. And single session therapy is the future of not only stent graft limb occlusions but all acute limb ischemia. Thanks so much.

- Thank you, Dr. Moore, and thank you Frank for inviting me back. These are my disclosures. I am a consultant for Silk Road Medical since I ran the first pivotal trial. Now, six years ago I gave a presidential address before the Society for Vascular Surgery

centered on the carotid space and I added this disclaimer, at least in part, because we were due to embark at that point on ROADSTER 1. And further on in that address, I suggested that transfemoral distal filter protection CAS was an experiment that had failed in my view.

And over the years of course in the legacy trials, that seems to be well born out by the data from these trials and yes, over time results with transfemoral CAS improved. Was it related to better technology? Perhaps.

It was certainly highly impacted by better patient selection and one only needs to see, for example, the evolution of the endovascular management committee in cres 2, as to how anatomic features have figured in that clinical decision making. Now, I'm proud to say that vascular surgeons,

first Juan Parodi and then Enrique Criado, pioneered the concept of flow reversal for neuro protection and CAS procedures and CAS procedures and of course, in my view, the TCAR procedure is in fact the ultimate evolution of that.

Now, thank you Frank for framing my debate with my Italian colleagues. Laura Capoccia's conclusion slide perhaps said it all and my worthy opponents and subsequent speakers I'm sure are going to focus on the fact that flow reversal with the MO.MA

can be achieved can be achieved with a totally percutaneous transfemoral approach, but the early data certainly suggested, as you can see here, that things were not much better. No, I'm sure we'll see results from this prospective registry with a lot of well known

Italian interventional cardiologist. Achieving an admirable 30 day major adverse event rate, but in a sense, this is the evolution of patient selection because it represents a cherry picking type of experience compared to low risk patients. Now, the final thing to consider from a technical aspect,

is that flow stagnation with the MO.MA device hardly equals high flow reversal, because although the concepts are similar, of course the actual operations are quite a bit different. And the authors even acknowledge that embolic signals from TCD were often detected during incursion

of this rather bulky transfemoral in to the arch device. And indeed, the steps of the procedures have been studied and as you can see here, there's really no difference between MO.MA and Distal Filter in the critical step of arch manipulation. Obviously a big part of the strategy, of the TCAR procedure

is avoidance of the arch, and when we've studied anatomic exclusions as recently reviewed by, this procedure can be applied to the overwhelming majority of candidates for CAS. Now Dr. Colin Buck showed you that this strategy

has achieved, as assessed by DWI imaging, lesion production rates, equivalent to carotid endarterectomy and when we published ROADSTER 1, it was the lowest stroke risk ever reported for a carotid stent trial.

I've mentioned previously that it has achieved neuro protection equivalent to carotid endarterectomy and here are some of the ROADSTER data. I won't read the data. Vic Kashif showed it to you. Now, in the most recent MO.MA experience of course,

we see the anatomic exclusions. And the anatomic exclusions in the lower right corner are not exclusions for TCAR. You've seen this data previously and our host, Frank Vees, in his most recent meta analysis, indicated that there was no positive

impact of the MO.MA strategy versus Distal Filter protection. This is a graph of the rapid adoption of TCAR by North American vascular surgeons in the TCAR surveillance project. Mul mentioned to you that the beginning data

from these registries and projects have now been presented. Just this week, I saw the updating of the TCAR surveillance project with sustained excellent result, now at over 3,000 patients. So in conclusion.

In my opinion TCAR is the technical evolution of CAS. Avoiding the arch and superior neuro protection with high flow reversal indicated the procedure of choice and transfemoral CAS should go in to the history books. Thank you for your attention.

- So, a little more on this theme that we've been talking about the last couple days, of inflow in the post-thrombotic limb. So, the key to maintaining an iliac-vein stent is good inflow and the key vessel seems to be the profunda, as we've been hearing for the last couple of days. This is the anatomy, the three axial vessels in the thigh,

the saphenous plays a very small role in venous return. We're dependent more on the femoral vein and the profunda. And the femoral vein just seems to be more prone to thrombosis and problems, and the profunda's there to salvage. We like to see good axial transformation of the profunda.

If we see this, you can get an IVUS catheter in these vessels from above usually. You can feel pretty confident the inflow's satisfactory. There's been some enthusiasm now to try and improve inflow, as we've been hearing, by interventions on the femoral vein. And you saw this paper earlier,

where these people had iliac-vein stents, and they we're trying to improve inflow either with femoral-vein stenting or femoral-vein angioplasty alone. And very, very high failure rates. All of them were occluded by a year, in both the angioplasty and stent groups.

My experience, I've probably done a handful of femoral-vein stents. This guy been in the practice for a couple, 15 years, post-thrombotic with iliac vein stents and some reason, his PCP discontinued his Warfarin, and the stent went down. So, this is in the office center,

acutely occluded common iliac, external iliac vein stent, and the confluence. You see thrombus in the confluence and in the profunda, which was obviously, discouraging. I got them open with the AngioJet, including his profunda. So, his symptoms of swollen thigh and calf,

and the thigh markedly improved. And he comes back a couple two year later, he's a UPS worker with complaining that he feels great, but the calf's still a problem, can I do anything else. We had a whole discussion on femoral vein intervention and he wanted to give it a shot.

The femoral vein was occluded beforehand. Here's the profunda open in SFA. So, this is prone on table, we got a good popliteal, we got a good profunda. And, you know, is this going to help him at all? But, he wanted to go for it.

This is with IVUS, the femoral vein's pretty much occluded. The popliteal vein's open. And we put a nitinol stent down, and they key is to try and land above your profunda collateral so you don't jail it. So, this is one if the ones that did well.

I got a couple doing well, and the others, not so well. So, this kid, 31 years old, multiple DVTs at such a young age, in both legs. We want to do something. His common iliac was wide open, this was diseased, so we stented this,

he got a little better, not great, he comes back a year later, can you do anything else. We began the whole discussion of femoral vein intervention doesn't work well. This is on the table prone, and just a harbinger of failure, if I can't get into the popliteal vein,

have to use a gastroc, that's a telling sign. So, I went ahead and stented his femoral vein, tried to preserve the collaterals. You can't see the popliteal that well down here, but it looked decent. He showed up with his INR low and occluded,

the whole thing went down. Here's the tail end of the nitinol stent. You can see the popliteal inflow is horrible. I got him open, but you know, it just doesn't look great. So, he went down and stayed down, reoccurring ulcers, and the poor young guy can't do anything.

In this case, again, the theme is we got iliac stents in place, so we can improve inflow. So, she comes in a couple years later, with new inflow disease on duplex and new symptoms. And you think, well you know, we'll just do a little segment of the femoral vein

where there's a tight lesion, maybe it'll help her inflow. With angioplasty alone, you can see the remain pretty tight, so I went ahead and put a stent there. Looked great afterwards, I was encouraged. But one month later, that segment of femoral vein stent went down.

You've heard of, in the early days, when we were doing thoracic aortic aneurysms iliac artery on a stick, well this is a femoral vein on a stick, so be careful. Conclusion, femoral vein stenting fails often and early. Uncharted waters may be a value in selected cases,

and I also want to see the PTS-XS trial results. Thanks.

- Thank you Dr. Sullivan. It's my pleasure on behalf of the investigators of the Vernacular trial to present the 12 month update on the Venovo Venous Stent Trial. These are my disclosures. Well, the Vernacular study object was to assess the performance of the Venovo Venous Stent

for the treatment of iliac and femoral venous occlusive disease, including acute or chronic DVT and/or May-Thurner Syndrome. The design was a multicenter non-randomized single-arm study that enrolled 170 patients at 22 international sites including the USA, Europe, and Australia.

There was complete independent analysis of all imaging including venography, radiographic assessment of stents, duplex ultrasound. There was of course a clinical events committee and a DSMB. Follow up is presented today is through one year, but there's ongoing follow up for three years

so you'll hear further reports in the future. The stent under evaluation was the Venovo stent which is a self-expanding nitinol stent which has three millimeter flares at each end to enhance wall apposition. It has six radiopaque tantalum markers, three on each end,

and it employs a tri-axial over-the-wire delivery system. These are the stent diameters, 10 to 20 with stent lengths from 40 to 160, and these are the introduction profiles for the various stent diameters. Key inclusion criteria was

symptomatic venous outflow obstruction by venography of greater than 50%, a CEAP clinical score of three or greater, and a VCSS pain score of greater or equal to two. Reference vessel diameters included in this were veins of seven millimeters to 19 millimeters.

Key exclusion criteria were could not have malignant obstruction, could not have contralateral disease in the iliac and femoral veins, or obstruction extending into the IVC or below the lesser trochanter,

could not have a prior stent at the site in the target lesion. The primary efficacy, the primary endpoint was 12-month primary patency by duplex ultrasound. There was also a primary safety endpoint, which is freedom from major adverse events.

As you can see here, that was a composite of all these features. We also had hypothesis-tested secondary endpoints and observations including pre-procedure and 12-month assessment of pain and quality of life. Patient demographics, as you can see a slightly older

in the non-thrombotic iliac vein lesions, or May-Thurners. Both groups, the post-thrombotic and the May-Thurner had a higher preponderance of females that was slightly more exaggerated in the NIVL group. You can notice that that

was represented about 87% of May-Thurner. Lesion characteristics common iliac vein was the site that was most involved, however obviously in the post-thrombotic syndrome where there's more extensive involvement, the external iliac vein was involved in over half of the patients.

Mean lesion length, again, owing to slightly more extensive disease in post-thrombotic syndrome was slightly longer than in May-Thurner. Procedural data, again given the slightly longer mean lesion length there were more stents placed in the post-thrombotic syndrome cohort than in the NIVL cohort.

This represents 45% of the patient population, this represents 55%. In terms of primary patency, you can see compared to a literature-derived performance goal of 74%, the total patency at 12 months was 88.3%, 96.9% in the non-thrombotic iliac vein lesion group,

81.3% in the post-thrombotic syndrome group. This is just a representation in Kaplan-Meier format of what I just presented, again out to 395 days, close to the window for one year, 88.9% patency. Primary safety endpoint, again compared to a literature-derived performance goal

of 89% was 93.5%, again 100% in the NIVL group. Looking at the VCSS pain score, again that's a three point score, mild moderate or severe. You can see the patients started up here at about 2.3 and ended up with no pain or mild pain which was sustained throughout the 12 month followup.

Likewise, the 20 question CIVIQ-20 score looking at quality of life in patients with venous insufficiency you can see a significant drop from baseline to post-procedure which was sustained through 12 months. Secondary observations, there was freedom

from TLR and TVR in 98.6% of the NIVL patients, 87.6% of the post-thrombotic syndrome group, and note that at one year there were zero fractures determined by plain film radiography. In conclusion, this prospective, multicenter trial of the Venovo stent used

to treat obstruction in the iliac and femoral veins demonstrated a high primary patency benefit compared to historical control at 12 months while demonstrating significant improvement from baseline in terms of the VCSS pain score and quality of life. The 12-month patency was 88.3%, and the 12-month freedom

from TLR rate was 7.4%, there were zero fractures and there will be reports at two and three years to follow. Thank you.

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