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Technical Tips For Maintaining Carotid Flow During Branch Revascularization When Performing Zone 1 TEVARs
Technical Tips For Maintaining Carotid Flow During Branch Revascularization When Performing Zone 1 TEVARs
anastomosisanterioraorticarteriotomyarterybordercarotidcarotid arterycommoncreateddissectiondistalendograftflowhemostasisincisioninnominateleftlooploopsLt Subclavian RetrosmiddlepreferredprostheticproximalproximallyrestoredsecuredshuntstentsubclavianSubclavian stentsuturesystemicallyTAVRtechniquetherapeutictransversetunnelingvesselwish
Use Of Indirect Access Sites For AV Intervention
Use Of Indirect Access Sites For AV Intervention
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Italian National Registry Results With Inner Branch Devices For Aortic Arch Disease
Italian National Registry Results With Inner Branch Devices For Aortic Arch Disease
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Estimation Of Long-Term Aortic Risk After EVAR: The LEAR Model: How Can It Guide And Modulate Surveillance Protocols
Estimation Of Long-Term Aortic Risk After EVAR: The LEAR Model: How Can It Guide And Modulate Surveillance Protocols
Indications And Advantages Of Antegrade In Situ Fenestration For F/EVAR: How To Do It
Indications And Advantages Of Antegrade In Situ Fenestration For F/EVAR: How To Do It
aneurysmantegradeaorticaxillarybailoutbrachialbridgingceliacCutting BalloonendoleakendovascularevarfenestratedfenestrationgraftischemiclaserLaser Atherectomy CatheterLaser ProbelfEVARmidtermprobeproximalrenalretrogradesitusteerablestentingsubclaviantechniquethoracicthoracoabdominalTurbo-Eliteunfitvisceral
Advantages Of Cook Zenith Spiral Z Limbs For EVARs Landing In The External Iliac Artery
Advantages Of Cook Zenith Spiral Z Limbs For EVARs Landing In The External Iliac Artery
aneurysmarterybuttockclaudicationCook ZenithdeployedendograftendoleaksevarevarsexcellentfinalgrafthelicalhypogastriciliacjapaneselandinglimbobservationalocclusionoperativepatencypatientspercentrenalrequiredspiralSpiral Z graftstenosisstentStent graftstentsstudytripleVeithzenith
Percutaneous Pharmaco-Mechanical Intervention For PE: Is There A Rationale
Percutaneous Pharmaco-Mechanical Intervention For PE: Is There A Rationale
Angiodynamicsangiovaccannulacircuit for thrombiemboli removalFlowTriever (Infusion aspiration system - Inari) / Penumbra CAT8 (Thromboaspiration system - Penumbra) / AngioJet (Peripheral thrombectomy system - Boston Scientific)therapeutic
Panel Discussion (Session 59a) 2018
Panel Discussion (Session 59a) 2018
BeGraftBentley InnomedGore Viabahn VBX (Gore Medical)stent graft systemtherapeutic
Successes And Limitations Of Endograft Treatment Of Aortic Infections: When Can It Be Effective Definitive Treatment And When It Can Only Be A Bridge To Definitive Open Treatment
Successes And Limitations Of Endograft Treatment Of Aortic Infections: When Can It Be Effective Definitive Treatment And When It Can Only Be A Bridge To Definitive Open Treatment
What Morphological Changes On CT After EVAR Predict The Need For Re-Interventions: From The DREAM Trial
What Morphological Changes On CT After EVAR Predict The Need For Re-Interventions: From The DREAM Trial
Gutter Endoleaks On Completion Angiography With Ch/EVAR: When To Ignore; How To Prevent; When And How To Treat
Gutter Endoleaks On Completion Angiography With Ch/EVAR: When To Ignore; How To Prevent; When And How To Treat
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Ascending Aortic TEVAR: Where Is It And What Is Its Future Potential
Ascending Aortic TEVAR: Where Is It And What Is Its Future Potential
Ascending SGCombined Ascending + Branched Graft / Valved ConduitMedtronicStent grafttherapeutic
Single Branch Carotid Ch/TEVAR With Cervical Bypasses: A Simple Solution For Some Complex Aortic Arch Lesions: Technical Tips And Results
Single Branch Carotid Ch/TEVAR With Cervical Bypasses: A Simple Solution For Some Complex Aortic Arch Lesions: Technical Tips And Results
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Testing For Cancer And Other Hypercoagulable States In PE
Testing For Cancer And Other Hypercoagulable States In PE
CVD thrombectomydiagnosticlysisUnprovoked VTE / Ovarian cancer
Non-Invasive 24/7 Flow Augmentation In Deep Venous Pathology
Non-Invasive 24/7 Flow Augmentation In Deep Venous Pathology
With Complex AAAs, How To Make Decisions Re Fenestrations vs. Branches: Which Bridging Branch Endografts Are Best
With Complex AAAs, How To Make Decisions Re Fenestrations vs. Branches: Which Bridging Branch Endografts Are Best
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Why Indications For Invasive Treatment Of Carotid Stenosis Is Much Less In Women Than Men
Why Indications For Invasive Treatment Of Carotid Stenosis Is Much Less In Women Than Men
Status Of Aortic Endografts For Occlusive Disease: Indications, Precautions, Technical Tips And Value
Status Of Aortic Endografts For Occlusive Disease: Indications, Precautions, Technical Tips And Value
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Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
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Results Of A Multicenter Italian Registry Of Real World CAS With The C-Guard Mesh Covered Stent: The IRONGUARD 2 Study
Results Of A Multicenter Italian Registry Of Real World CAS With The C-Guard Mesh Covered Stent: The IRONGUARD 2 Study
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Why The Differences In RCT And Registry Results For CAS Are Important In Determining Who Benefits From CAS And Who Does Not
Why The Differences In RCT And Registry Results For CAS Are Important In Determining Who Benefits From CAS And Who Does Not
Selective SMA Stenting With F/EVAR: When Indicated, Value, Best Bridging Stent, Technical Tips
Selective SMA Stenting With F/EVAR: When Indicated, Value, Best Bridging Stent, Technical Tips
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Value Of Statins In CAS Patients: What Drug, What Dose And When: How Do They Help
Value Of Statins In CAS Patients: What Drug, What Dose And When: How Do They Help
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- I don't have any relevant conflicts. Thank you, Frank, for inviting me again. So there are big problems with cognitive testing. And it is simply not valid to assume that testing cognitive function before and after a procedure without strict controls is going to provide

any useful information whatsoever. The Mini-Mental State and the MOCA are easy to administer, but they're not comprehensive and they're not sensitive at all. There are improvements in scores with retest. So just testing before and after a procedure is invalid.

There are improvements in cognitive function with placebo and there's a very powerful effect, placebo effect of surgery. So you can't just go and test cognitive function before and after procedure and say yeah, it got better, it's a good thing to do.

There are practice effects and the practice effects are bigger in patients with milder cognitive impairment. Placebo scores in this case, it was study of polyunsaturated fatty acids, the placebo was actually better

than the active therapy in this study. There are important placebo effects in cognitive testing. And there's a huge placebo effect of surgery, so you may remember the Vineburg procedure. That's ancient history. A more recent sham-controlled trial

of percutaneous coronary intervention for angina showed very clearly that intervention was no better than placebo. So this was the paper that was in Lancet 2018. You look at all these different ways of assessing outcomes.

So there was exercise time, time to one minute ST depression, peak oxygen uptake which looks like, you know it's a pretty objective test, no better. Cognitive testing is too simply usually.

It is subject to learning effects and placebo effects. Surgery has powerful placebo effects. So the only valid way to determine if revascularization improves cognitive function is to do a sham trial, sham surgery or sham stenting.

And belief, no matter how strongly held, does not qualify as evidence. Thank you.

- Thank you. Here are my disclosures. Our preferred method for zone one TAVR has evolved to a carotid/carotid transposition and left subclavian retro-sandwich. The technique begins with a low transverse collar incision. The incision is deepened through the platysma

and subplatysmal flaps are then elevated. The dissection is continued along the anterior border of the sternocleidomastoid entering the carotid sheath anteromedial to the jugular vein. The common carotid artery is exposed

and controlled with a vessel loop. (mumbling) The exposure's repeated for the left common carotid artery and extended as far proximal to the omohyoid muscle as possible. A retropharyngeal plane is created using blunt dissection

along the anterior border of the cervical vertebra. A tunneling clamp is then utilized to preserve the plane with umbilical tape. Additional vessel loops are placed in the distal and mid right common carotid artery and the patient is systemically anticoagulated.

The proximal and distal vessel loops are tightened and a transverse arteriotomy is created between the middle and distal vessel loops. A flexible shunt is inserted and initially secured with the proximal and middle vessel loops. (whistling)

It is then advanced beyond the proximal vessel loop and secured into that position. The left common carotid artery is then clamped proximally and distally, suture ligated, clipped and then transected. (mumbling)

The proximal end is then brought through the retropharyngeal tunnel. - [Surgeon] It's found to have (mumbles). - An end-to-side carotid anastomosis is then created between the proximal and middle vessel loops. If preferred the right carotid arteriotomy

can be made ovoid with scissors or a punch to provide a better shape match with the recipient vessel. The complete anastomosis is back-bled and carefully flushed out the distal right carotid arteriotomy.

Flow is then restored to the left carotid artery, I mean to the right carotid artery or to the left carotid artery by tightening the middle vessel loop and loosening the proximal vessel loop. The shunt can then be removed

and the right common carotid artery safely clamped distal to the transposition. The distal arteriotomy is then closed in standard fashion and flow is restored to the right common carotid artery. This technique avoids a prosthetic graft

and the retropharyngeal space while maintaining flow in at least one carotid system at all times. Once, and here's a view of the vessels, once hemostasis is assured the platysma is reapproximated with a running suture followed by a subcuticular stitch

for an excellent cosmetic result. Our preferred method for left subclavian preservation is the retro-sandwich technique which involves deploying an initial endograft just distal to the left subclavian followed by both proximal aortic extension

and a left subclavian covered stent in parallel fashion. We prefer this configuration because it provides a second source of cerebral blood flow independent of the innominate artery

and maintains ready access to the renovisceral vessels if further aortic intervention is required in the future. Thank you.

- I'm going to be speaking about indirect access sites for access intervention. I'm going to be focusing on the transjugular approach. So access interventions, typically we perform them through a direct puncture of the fistula. Sometimes you place two introducers. There are some disadvantages to the direct approach.

The crossing catheters technique that we generally use for declots is awkward and cumbersome. The introducers can obstruct flow, there's dead space behind the introducers that can trap clot, and there's radiation exposure or the direct exposure

or scatter radiation from hands near the field. Admit it, we've all had access-site complications, suture-site necrosis and infection, as well as pseudoaneurysms. There's also prolonged procedure time related to needing to obtain hemostasis

in the high-pressure segment. There are also problems particularly to immature fistulas, such as hematoma formation, spasm at the introducer site causing pseudo-stenosis, decreased flow, and fistula thrombosis. Now, the good news is that we do have options

for alternative access sites. I'm sure many of you here use arterial access for immature fistulas in particular. Brachial access can be used to, this can be used for diagnostic or therapeutic purposes. We can also utilize radial or ulnar access.

Rarely, femoral access is used, as we saw in the last presentation. But there's also pendula venous access sites. You can sometimes, as a fortuitous tributary, what I call a target of opportunity, and also, the internal jugular vein.

Now, the transjugular approach was first reported in 1998. It does have some definite advantages over direct puncture technique. You can avoid the cumbersome access, you can keep your hands away from the beam, and there's no dead space as compared

to crossing sheaths for your declot. And if the intervention is unsuccessful, you can convert your IJ access to a catheter if you already have a wire in it. There are some technical challenges associated with this technique.

You do have to overcome the valves. It can be difficult to access the cephalic vein, but you can get around this by using a snare. And there's possibly a risk of IJ thrombosis if you're using large introducers. When to use this technique?

Well, when direct puncture's going to be difficult or cumbersome, when there's a short cannulation segment, when it's an extensively stented access, and when there's inflow pathology requiring a retrograde approach or arterial empathalogy, and it's a good option for clotted access.

The technique, micropuncture access of the jugular vein, ipsilateral or contralateral, place a sheath, and an important thing to use is a reverse-curve catheter, followed by glidewire. So here, we've cannulated the jugular vein going down,

glidewire out into the arm. If you're unable to cross into the cephalic vein, you can use that snare technique. And you can get a long, stable access in this way. It's been reported about, there's about 10 publications on transjugular approach, seven retrospective studies.

There's a large study that's reported thrombectomy. Also a large study looking at immature fistulas. Smaller studies looking at dysfunctional access and pseudoaneurysms. Two case reports, one review article, but there's of course no randomized studies.

There's a recent study from this year from Ferral and Alonzo. This was a retrospective study. Over two years they performed 30 transjugular AV access interventions. This accounted for 5% of their access experience

and this series was all fistulance. Indications for the procedure, 43% were declots, 43% were arterial and fistual pathology, there were two immature fistulas and two bleeding pseudoaneurysms. The access approach was 29 for ipsilateral,

only one contralateral. The results, 97% technical success, a snare was required in 4 cases, a catheter was inserted in two of the cases. There were no episodes of jugular vein thrombosis. In the remaining time, I'd like to show

a couple of case studies. Again, from Ferral and Alonzo. This is a case of an immature fistula. This was a partially occluded, immature left upper arm fistula. The initial fistulagram shows outflow stenosis

with a multiple stenosis in thrombus, and there's an arterial in stenosis that's distal to the access point, so you're not going to be able to treat that. They performed four millimeter angioplasty. Follow-up fistulagram shows a small, but patent vein

and the arterial end could not be treated. They brought the patient back in two weeks for a staged transjugular approach. And you can see the jugular catheter coming down. The vein diameter's improved, but there's still the untreated arterial end stenosis,

which is easily treated through the jugular approach. This is a study from, a case from Dr. Rabellino, ruptured pseudoaneurysm. This is a basilic transposition with a ruptured pseudoaneurysm at an infiltration site. Pretty ugly arm, swollen, skin necrosis.

I don't think we want to be sticking that arm. They initially went with a femoral approach for the fistulagram, demonstrated the pseudoaneurysm. As you can see here, tandem outflow stenoses. Coming up from below with the femoral artery diagnostic catheter.

Down and into the arm through the jugular approach. And here, you can see the venous outflow after angioplasty, covered stent deployed through the jugular access. So in summary, the transjugular approach is a useful but underutilized technique. The advantages include single-puncture intervention,

does not involve the outflow vein directly, simplified hemostasis, it's a low pressure system. It does have the advantage that you can use large introducers, there's less radiation for the operator, and you can convert to a catheter easily if needed. It is a useful technique for fistula maturation,

thrombectomy, and access maintenance. I say go for the jugular.

- Thank you Mr Chairman, ladies and gentlemen. These are my disclosure. Open repair is the gold standard for patient with arch disease, and the gupta perioperative risk called the mortality and major morbidity remain not negligible.

Hybrid approach has only slightly improved these outcomes, while other off-the-shelf solution need to be tested on larger samples and over the long run. In this scenario, the vascular repair would double in the branch devices as emerging, as a tentative option with promising results,

despite addressing a more complex patient population. The aim of this multi-center retrospective registry is to assess early and midterm results after endovascular aortic arch repair. using the single model of doubling the branch stent graft in patient to fit for open surgery.

All patient are treated in Italy, with this technique. We're included in this registry for a total of 24 male patient, fit for open surgery. And meeting morphological criteria for double branch devices.

This was the indication for treatment and break-down by center, and these were the main end points. You can see here some operative details. Actually, this was theo only patient that did not require the LSA

re-revascularization before the endovascular procedure, because the left tibial artery rising directly from the aortic arch was reattached on the left common carotid artery. You can see here the large window in the superior aspect of the stent graft

accepting the two 13 millimeter in the branches, that are catheterized from right common carotid artery and left common carotid artery respectively. Other important feature of this kind of stent graft is the lock stent system, as you can see, with rounded barbs inside

the tunnels to prevent limb disconnection. All but one patient achieved technical success. And two of the three major strokes, and two retrograde dissection were the cause of the four early death.

No patient had any type one or three endoleak. One patient required transient dialysis and four early secondary procedure were needed for ascending aorta replacement and cervical bleeding. At the mean follow-up of 18 months,

one patient died from non-aortic cause and one patient had non-arch related major stroke. No new onset type one or three endoleak was detected, and those on standard vessel remained patent. No patient had the renal function iteration or secondary procedure,

while the majority of patients reported significant sac shrinkage. Excluding from the analysis the first six patients as part of a learning curve, in-hospital mortality, major stroke and retrograde dissection rate significant decrease to 11%, 11% and 5.67%.

Operative techniques significantly evolve during study period, as confirmed by the higher use of custom-made limb for super-aortic stenting and the higher use of common carotid arteries

as the access vessels for this extension. In addition, fluoroscopy time, and contrast median's significantly decrease during study period. We learned that stroke and retrograde dissection are the main causes of operative mortality.

Of course, we can reduce stroke rate by patient selection excluding from this technique all those patient with the Shaggy Aorta Supra or diseased aortic vessel, and also by the introduction and more recent experience of some technical points like sequentIal clamping of common carotid arteries

or the gas flushing with the CO2. We can also prevent the retrograde dissection, again with patient selection, according to the availability of a healthy sealing zone, but in our series, 6 of the 24 patients

presented an ascending aorta larger than 40 millimeter. And on of this required 48-millimeter proximal size custom-made stent graft. This resulted in two retrograde dissection, but on the other hand, the availability on this platform of a so large proximal-sized,

customized stent graft able to seal often so large ascending aorta may decrease the incidence of type I endoleak up to zero, and this may make sense in order to give a chance of repair to patients that we otherwise rejected for clinical or morphological reasons.

So in conclusion, endovascular arch repair with double branch devices is a feasible approach that enrich the armamentarium for vascular research. And there are many aspects that may limit or preclude the widespread use of this technology

with subsequent difficulty in drawing strong conclusion. Operative mortality and major complication rates suffer the effect of a learning curve, while mid-term results of survival are more than promising. I thank you for your attention.

- [Physician] Thank you very much. So this is a venous topic on an arterial arena. A year back, we published a paper defining all the venous symptoms because these are not really well-defined in the literature. One of which was venous claudication. So to start with,

venous claudication is the development of pain or a bursting sensation that occurs when a patient is walking or running. The pain is localized in the leg, thigh, buttock, or in combination of areas. Disappears slowly when the patient rests.

It's facilitated by leg elevation, a finding that allows differentiation from arterial or neurogenic claudication. It's almost exclusively seen in patients with iliofemoral or iliocaval obstruction. A less common type of claudication is neurogenic

from the dilated veins in the spinal canal, and also a rare form of claudication in the calf is due to popliteal vein entrapment. I've seen only two patients, after examining thousands of them. In this claudication, the venous obstruction is so severe,

that during walking the arterial inflow is increased beyond the ability of the venous drainage, leading to swelling and pain. The muscular pressures at rest and during exercise in the calf are much higher compared

with the contralateral unobstructed limb. Unlike arterial claudication, the recovery time to baseline is much longer, taking at least 15 minutes, or even longer. Femoral vein pressures, venous outflow resistance,

arm-foot pressure differentials compared with those having obstruction below the common femoral vein, are significantly elevated. These patients are also more likely to have edema and skin damage.

If you want to look into this more seriously, there's some of papers published in the literature on this topic. Now, how do you evaluate it? Well, in general, evaluation of venous obstruction may be controversial,

because the symptoms are more pronounced, and more often present during standing or walking. Unfortunately, all imaging tests are done in supine position, but the tests we usually use for this condition are venous outflow tests, ultrasound, intravascular ultrasound,

axial imaging with CAT scan or MR, ascending phlebography, and pressure measurements. However, for venous claudication diagnosis is usually easier as chronic venous obstruction is more severe. This first hemodynamic paper

we published in 1997, indicating that the venous outflow resistance is much higher in people having iliofemoral obstruction, and this can explain why these people are more likely to develop a venous claudication. And this is the pressure differential for arm and the leg.

People having iliocaval or iliofemoral obstruction have much higher resting pressures. Also, as you see on this table here, only people with iliocaval or iliofemoral obstruction develop claudication, which is 8% among all patients, or 17% among people with supra-inguinal

chronic venous obstruction. And in the second paper within 2008, we demonstrated that we found no patient with previous DVT on femoropopliteal area, but in people who have iliofemoral obstruction had an instance about 8% of venous claudication.

Now, why the venous claudication? Who cares? Well, when you treat the patient with traditional anticoagulation, because of the large volume of thrombus in the iliofemoral veins, our problematic system,

it fails to lyse the thrombus in the majority of the people, so such patients, they have severe obstruction and they are prone to develop swelling and claudication. Therefore, to prevent this thing, when you have acute iliofemoral DVT, aggressive thrombus removal is necessary

in people having indications. Therefore, this way you'll eliminate the obstruction, the DVT recurrence is reduced, and a chronic venous disease is avoided. And here is a patient with chronic obstruction and claudication.

But in these people if you plant the stent, you make sure have a good inflow, like you see on this image here, but a patient having a comprised inflow like on this panel here, you may consider endo-phlebectomy

and arteriovenous fistula creation prior to stenting. And here is a patient with aortofemoral with chronic iliofemoral obstruction. The IVUS cath, they're much the size of the vein, and it's throughout from the iliac vein all the way down to femoral,

and obviously when you do stenting, you can relieve the obstruction, and the venous claudication as you see on this around here. To finish with, for venous claudication, you need to recognize the symptoms. It is clearly a post-thrombotic event.

Iliac vein compression by itself is not enough to do it, so you're not going to have the claudication by putting a single iliac stent for arterial compression on the vein. Image the iliofemoral veins and the inferior vena cava, aggressive thrombus removal for the femoral DVT, and look for and treat chronic venous obstruction.

Thank you very much.

- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery

in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,

but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase

and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,

and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast

in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.

So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,

it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause

of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.

So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes

and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,

and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR

might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement

without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac

Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,

to save our country from a type II endoleak, and I thank you for your attention.

- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent

secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results

in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different

in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,

or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,

PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus

or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk

of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,

but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.

and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.

Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.

So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.

Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.

In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,

and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide

a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.

And an E-portal is being developed for dissemination. Thank you very much.

- So, my topic today is: Antegrade In Situ Fenestration for Fenestrated EVAR: How To Do It. Here are my disclosures. So, Jean Panneton has shown already the validity of retrograde laser fenestration. That is a feasible technique,

an effective option for acute thoracic pathology, with an excellent midterm patency, which it is very easy to do retrograde laser fenestration compared to an anterograde technique. We have done a lot of bench tests to perform all like this (mumbles).

So, the in situ laser fenestration technique is an off-label procedure. It is a bailout solution, and dedicated to emergent cases, patient unfit to open repair, or unfit to CMD device.

And we use this technique for left subclavian arch, and the anterograde technique for visceral arteries, and in a few cases of TEVAR. This is a technique. I use a Heli-FX 16 French. And I use

a 0.9 laser probe. We don't need to use another laser probe for this technique to avoid any larger hole. This is the steps for the technique. I do a primary stenting of the arteries using your effusion.

And then I do the endovascular exclusion. I position the steerable sheath at the level of the targeted artery and then do laser fenestration. This is a pre-stenting. And then the graft deployment

at the level of the seating zone. This was a type 1A endoleak after EVAR. The next step is to do the laser fenestration. You can see the tip of the laser probe. (Mumbles)

You could see the tip of the laser probe coming in the lumen of the SMA. And, we'll then, after this laser fenestration, quite easy, we'll then do

an enlargement of the ULL, using first a small cutting balloon and then do a progressive dilation using a bigger balloon, four millimeter, and then a six millimeter balloon.

The next step is to do, like, what we do for fenestrated cases, we do the bridging covered stent. Yeah, at the level of the SMA, and then the flairing, to have a good sealer

of the proximal part of the bridging stent. After the SMA, we then do the renal fenestration. And we used to stop with the celiac trunk. Our main indications are juxta para renal aneurysm, or type 1A Endoleak when there is a straight aorta. And in a few cases, thoracoabdominal aortic aneurysms.

This is an example of a type 1A endoleak, as I have presented. This is our first trial with 16 patients, treated on between three years. And we have now 29 patients with laser fenestration EVAR,

66 fenestrations, 5% of aortic aneurysm treated in our center. The median ischemic time is 12 minutes for the SMA, one hour for the renal arteries, and around two hours for the celiac trunk. The fenestration success rate is 95%.

Here are the outcomes. There was no mortality, even for very old patients. 16% of transitory dialysis. No spinal cord ischemia, one case of pneumonia, and the short follow-up of 22 months with 24 re-operations

in seven patients. Here are my conclusion. The laser fenestration EVAR must not be used for elective cases. In our strategy, the best options for urgent thoracoabdominal is to use

an off-the-shelf graft, like the T-branch. If a custom-made device graft is not available, the laser fenestration will be our reference treatment, and you don't need any brachial or axillary approach for this technique. Thank you very much.

- Thank you, Ulrich. Before I begin my presentation, I'd like to thank Dr. Veith so kindly, for this invitation. These are my disclosures and my friends. I think everyone knows that the Zenith stent graft has a safe and durable results update 14 years. And I think it's also known that the Zenith stent graft

had such good shrinkage, compared to the other stent grafts. However, when we ask Japanese physicians about the image of Zenith stent graft, we always think of the demo version. This is because we had the original Zenith in for a long time. It was associated with frequent limb occlusion due to

the kinking of Z stent. That's why the Spiral Z stent graft came out with the helical configuration. When you compare the inner lumen of the stent graft, it's smooth, it doesn't have kink. However, when we look at the evidence, we don't see much positive studies in literature.

The only study we found was done by Stephan Haulon. He did the study inviting 50 consecutive triple A patients treated with Zenith LP and Spiral Z stent graft. And he did two cases using a two iliac stent and in six months, all Spiral Z limb were patent. On the other hand, when you look at the iliac arteries

in Asians, you probably have the toughest anatomy to perform EVARs and TEVARs because of the small diameter, calcification, and tortuosity. So this is the critical question that we had. How will a Spiral Z stent graft perform in Japanese EIA landing cases, which are probably the toughest cases?

And this is what we did. We did a multi-institutional prospective observational study for Zenith Spiral Z stent graft, deployed in EIA. We enrolled patients from June 2017 to November 2017. We targeted 50 cases. This was not an industry-sponsored study.

So we asked for friends to participate, and in the end, we had 24 hospitals from all over Japan participate in this trial. And the board collected 65 patients, a total of 74 limbs, and these are the results. This slide shows patient demographics. Mean age of 77,

80 percent were male, and mean triple A diameter was 52. And all these qualities are similar to other's reporting in these kinds of trials. And these are the operative details. The reason for EIA landing was, 60 percent had Common Iliac Artery Aneurysm.

12 percent had Hypogastric Artery Aneurysm. And 24 percent had inadequate CIA, meaning short CIA or CIA with thrombosis. Outside IFU was observed in 24.6 percent of patients. And because we did fermoral cutdowns, mean operative time was long, around three hours.

One thing to note is that we Japanese have high instance of Type IV at the final angio, and in our study we had 43 percent of Type IV endoleaks at the final angio. Other things to notice is that, out of 74 limbs, 11 limbs had bare metal stents placed at the end of the procedure.

All patients finished a six month follow-up. And this is the result. Only one stenosis required PTA, so the six months limb potency was 98.6 percent. Excellent. And this is the six month result again. Again the primary patency was excellent with 98.6 percent. We had two major adverse events.

One was a renal artery stenosis that required PTRS and one was renal stenosis that required PTA. For the Type IV index we also have a final angio. They all disappeared without any clinical effect. Also, the buttock claudication was absorbed in 24 percent of patients at one month, but decreased

to 9.5 percent at six months. There was no aneurysm sac growth and there was no mortality during the study period. So, this is my take home message, ladies and gentlemen. At six months, Zenith Spiral Z stent graft deployed in EIA was associated with excellent primary patency

and low rate of buttock claudication. So we have most of the patients finish a 12 month follow-up and we are expecting excellent results. And we are hoping to present this later this year. - [Host] Thank you.

- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,

but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody

with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?

And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy

for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,

thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world

for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and

patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt

to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize

what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,

and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,

it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would

ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a

experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,

but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,

it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,

place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,

any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution

using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation

and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology

and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,

it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,

and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a

single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,

and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,

a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at

alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,

and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.

There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,

Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.

Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings

in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?

I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,

you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.

So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,

we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.

- [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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. These are my disclosures. So, infected aorta, in terms of the primary infected aorta and secondary infected stent grafts is a difficult problem, and its instance is probably increasing the more we treat. These patients present late, they're often very malnourished,

and they have significant comorbidity. One place where endovascular therapy is definitely effective is in the emergency situation, both the primary infected aortas, like this case on the right hand side, and also for primary aorto-enteric fistula in an emergency.

This is a young man who had obesity surgery and leaked from his gastric anastomosis. He had an esophageal stent, which then caused a significant infection in the mediastinum and eroded through his aorta. He came in in extremis bleeding

and a short stent to cover that saves his life and gives you an opportunity for later on. It's also effective in secondary infections. This is a young lady who had an aortobifemoral bypass, who is bleeding in the retroperitoneum, and you can cover that with a stent graft

and think about further treatment later. Certainly in the short term, endovascular results from treating primary mycotic aneurysms are good. Our series on the left hand side, we had only one death in our endovascular group. In further case series and in systematic reviews,

the 30 day mortality is consistently somewhere between 10% and 15% in the early stage. Long term results from primary mycotic aneurysm treatment are not that bad. This is the biggest paper, I think, in circulation, showing the three, four, five year results

which are acceptable, but you have to remember that success was gained in this group. In those without persistent sepsis, in those without aortoenteric fistula, and probably in some bacterial types, particularly salmonella, which can be treated

well before the endograft is implanted. The secondary graft infection we have to remember, though, has a significant early mortality. This is our series from Imperial, our open graft excision surgery, for urgent and emergency cases included, is 25%,

but for that you swap an excellent five year mortality. Only a few patients die in that long period. If you're putting an endograft in for secondary graft infection and aortoenteric fistula, we can look to this systematic review which I was good to join in with Steve Kakkos.

The results for endovascular treatment are poor. The rate of current sepsis at two years is 42% in the endovascular group, far worse than that for excisional surgery, so they don't do well. I've got significant concerns for endovascular treatment, and we need to worry about these if we're going to put

endovascular grafts in and leave them in. The first is of antimicrobial resistance, there are more and more resistant bugs occurring in our practice, and it's certainly been our practice in our series. Over the last three years, the number of patients with resistant bugs is up to about 50%.

This is a young man who had infective endocarditis with a fungal disease, a multi-resistant fungus. This is the state of his aorta in the top left hand panel. Of course he needs a deep venous reconstruction, which we then cover with Omentum, and he did well after that.

For aortoenteric fistula, if you're going to put an endograft in, in our experience, these get reinfected and rupture, and they probably do need definitive treatment. In secondary graft infection, aortoenteric fistula, remember, is present in 1/3 of patients,

and you need to consider this. You're only going to find that at surgery if you're placing a stent graft in. Again, we discussed earlier in this session, further interventions: graft infection

is more commonly associated with multiple interventions, and it provides a further nidus for infection. So, when is endovascular therapy effective? Well, endovascular treatments in the emergency cases are life-saving and I think they are effective. For primary aortic infection, it's effective

when there is clearance of sepsis, a low -virulence microorganism, and no fistula. Then, the results are acceptable. For secondary cases treated with Endo techniques, the long term recurrence of sepsis is significant, and they really need definitive graft excision,

or you need to accept they have antibiotics and accept palliation. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- So these are my disclosures. And let's start first of all for the merit to have them, what are the potential benefits? So we'd like to get rid for permanent rigid metallic cage. We'd like to restore vasomotion, angulation, eliminate instant restenosis of metallic stents which is hard to treat.

We also have to keep the ability of late luminal enlargement, preserve the target for CABG and freedom from long-term polymer exposure, inflammation, and it is very appeal to patients and physicians not to have a permanent implant.

But with all these we have seen what is the desire. The desired is to have this absorbed treated artery looks like, very nice healing. Large lumen compared to metallic DES. Does it really happens? And the question was driven initially from data from Europe,

that look on large registries that the results of 30 days and six months with Bioresorbable Scaffolds was acceptable except for one thing, which definite, probable stent thrombosis. 1.5% and 2.1% in the coronary, it is not acceptable. This was also driven or repeated in a similar magnitude

in ABSORB II and ABSORB III which were randomized trials comparing Xience, which was the drug eluting with metallic stents to BVS or Absorb, which showed again over time higher thrombosis rate for both of those randomized trials and this was despite the patients were on DAPT.

As a matter of fact, the recommendations were extended for the Absorb now to three years, for the duration of the absorption time. So the question was whether these were two early studies without implying good technique. And then what is the good technique?

You doing pre-dilatation, you're doing post-dilatation, you're doing imaging. And that was actually implemented later on. So if we look at the latest data that was presented with the Absorb, which was ABSORB IV studies,

now the stent thrombosis are better. They're only 0.7% at one year compared to 0.3% with Xience. It still looks a little bit higher numerically, but these are within the range of what you can expect from drug eluting stent. The other thing that this study showed,

if you look on ABSORB III-like studies, your results are going to be relatively much better that what you have seen with ABSORB III. But nevertheless, this first generation stent, if you can look at the totality of the data was still higher events compared to metallic stent.

Now why did we prolong the DAPT from three years? Because we do know that the three years we still have PLLA that is still there and it could dismantle and cause scaffold thrombosis. Now Abbott pulled out the technology from the market for commercial reasons.

I think the main reason was the fear from thrombosis and patients and physician didn't want to use it. And the ESC guidance just changed their recommendations to Class IIIC, which means you should not use it unless you doing it in clinical trials. So this is really was hampering on the whole field.

And the question, can we resuscitate from this situation. First of all, we need to know how to improve it. We have to improve the technique, PSP, imaging, prolonged DAPT, and also we have to improve the technology with thinner struts, improved mechanical properties.

Are these coming along? Definitely yes. We have a array of second generation BRS with 80 micron, 99 micron, 100 micron compared to 228, 170, 150 in the first generation. So we are going to see secondary generation scaffolds

that perhaps will solve all those issues which we have seen with the thrombosis. And indeed, if it's not going to come from the U.S., probably not very soon, it's coming from China. And look at the number of programs right now. Five programs completed First In Man,

two of them in randomized clinical trials, two already completed registries. So the data from China which is randomized, will come and we'll see how that goes. This is a project that I've been working on, Magnesium just to show you,

that if you compare Magnesium to ABSORB you see no thrombosis on the porcine model shunt. And this is even better than metallic DES stent. So I think we can able to solve the thrombosis rate. If we do that, then I think we see those technology coming back again.

What about the periphery? There's was one study at ESPRIT, very small one, with actually promising result. And again, it's up to the companies to see if they're going to encroach to the SFA program. So my final thoughts are that the unmet need

for Bioresorbable scaffolds remain despite improvement of second generation DES. The first generation BRS are inferior to the best in class DES and should not suitable for routine use. We always will have to show randomized trials

that at least we have known inferiority of Bioresorbable technique to metallic DES and then with second generation BRS we have the hope to make scaffolds great again. Thank you very much.

- Thank you Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try

to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.

And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,

secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group

is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted

by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.

And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use

those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,

but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.

For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions

for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,

and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.

But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,

so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at

the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions

at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR

predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive

of iliac limb reinterventions. Thank you very much.

- Thank you, Tim, and thank you, Frank, for giving me the opportunity to address this specific problem of the gutter endoleaks, which has been described up to 30% after ChEVAR and parallel grafting. But I have to say that in the most papers, not only gutter endoleaks were included,

but also new onset of type Ia endoleak. One paper coming from Stanford addressed specifically the question, how we should deal with the gutter-related type Ia endoleak, and they conclude that in the vast majority of the cases, these gutter endoleaks disappear

and the situation is benign. And based on my own experience, I can confirm this. This is one of the first cases treated with parallel grafts for symptomatic thoracoabdominal aneurysm. And I was a bit concerned as I saw this endoleak at the end of the angiography,

but the lady didn't have any pains and also no option for open or for other type of repair, so we waited. We waited and we saw that the endoleak disappeared after one month. And we saw also shrinkage of the aneurysm after one year.

So now, the next question was how to prevent this. And from the PERICLES registry, but also from the PROTAGORAS, we learned how to deal with this and how to prevent. And it's extremely important to oversize enough the aortic stent graft,

more than treating with the EVAR, normal EVAR. We should reach a sealing zone of at least 15, 20 millimeters. And we should avoid also to use more than two chimney grafts in such patients. The greater the number of the chimney used,

the higher is the risk of type Ia endoleak. And last but not least, we should use the right stent graft. And you see here the CT scan after using a flexible nitinol skeleton endograft on the left, and the gutters if you use a very stiff,

stainless steel skeleton in such situations. The last question was how to treat these patients. And based on the PERICLES, again, we should distinguish three different patterns. One is due to an excessive oversizing of the graft with infolding.

I have only one case, one professor of pathology, treated six years ago now without any endoleak due to this problem. The most are due to an undersized aortic endograft. And in the pattern C, we have an insufficient sealing zone and migration of the graft.

Now, we should consider the pattern B. And with an undersized aortic endograft and if the gutter is small, one possible solution would be to treat this patient with coiling, using coils or Onyx to occlude this gutter endoleaks,

like in this patient. And for the pattern C, if the sealing zone is insufficient, well, we should extend the sealing zone using the chimney parallel technique, as you can see in this case. So in conclusion, ladies and gentle,

gutters are usually benign and more than 95% disappeared in the follow-up. But in case of persistence, we should evaluate the CT scan exactly. And in case of oversizing and not enough oversizing and not enough length,

we should treat this patient accordingly. Thank you very much for your attention.

- 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.

- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.

And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.

Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,

it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized

due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage

of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,

which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal

in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak

which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.

And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success

is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent

Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,

an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,

retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered

balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.

At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed

if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.

The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR

combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,

and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.

- Thank you very much, I'm honored to be here. These are my disclosures. So first, just scope of the problem. One in four deaths worldwide is related to thrombosis. It's the leading cause of death throughout the world. And in the United States it's the third-leading cause of cardiovascular death,

accounting for $1.5 billion a year. More people die of a PE than breast cancer, car crashes, and AIDS combined. And you can see here from a study by John Heit that this problem is not going away. So how can we change these statistics?

Will looking for occult malignancy in patients who present with VTE, or testing for thrombophilia change these numbers? So I thought I'd start with a case. This is a 55-year-old avid tennis player, presented with sudden-onset shortness of breath.

And she had swelling in her right lower extremity. Her CT, as you can see here, showed bilateral stem emboli, and she clearly has an RV dilatation. Her vital signs, she's tachycardic, hypoxic, tachypneic. But fortunately her blood pressure is well-maintained.

Her troponin is minimally elevated, and her echo did show that she was demonstrating RV strain, and as Brian showed you, she has an elevated, her RV/LV ratio is clearly greater than one. So she was considered high-intermediate risk because of the strain, the troponin,

the tachycardia, the hypoxia, and the decision was to proceed with catheter-directed thrombectomy and lysis. There was no identifiable cause for her PE. So the question is, should she undergo extensive screening

for an occult malignancy? Well we know that about 5% to 10% of patients who present with an idiopathic VTE will be diagnosed with a cancer within the subsequent one to two years. We know that.

So should we? Well let's look at the data. This was a recent review and meta-analysis of 10 studies over 2,300 patients, most of them prospective, although there were three randomized controlled trials

looking at limited versus limited plus some kind of extension. Limited is like basic labs, chest x-ray, and then the extension one, one of them was limited plus an abdominal CT scan. This was based on a meta-analysis

that this author Carrier did, where they found that limited screening found about 50% of the cancers. But when an ab CT was performed, that increased it to about 67%. So that's what led to

this first randomized controlled trial, 845 patients, limited screening plus limited plus an ab CT. The second one was limited screening plus limited screening plus a CT scan of the chest, abdomen, and pelvis.

And the third randomized controlled trial was limited screening plus a PET scan. And you can see here, no difference in the number of cancers detected at baseline or at follow-up with adding an ab CT, at baseline or with follow-up

by adding a chest abdomen pelvis, or adding a PET scan. The only finding was that in the PET scan group, at two-year follow-up more cancers were identified in the limited screening group. Which means that the PET scan

found more cancers to begin with, but importantly, there was no difference in survival. So this meta-analysis did show that the cancer rate that they discovered was about 5% of these patients

that presented with idiopathic VTE. There was no significant difference in patients who got limited screening versus extensive screening. However, they did notice and remark on the fact that the cancer prevalence did increase linearly with age. So patients that were over 50

had a sevenfold increase in being discovered with cancer. And it was lowest in patients under 50 and in women who were on estrogen. So maybe we could define a population that would benefit from screening. And that's what the RIETE group did.

They found six factors that they looked at. Male, over the age of 70, if you were a tobacco smoker, high platelet count greater than 350, anemic, or a past history of VTE. And they found that if you had two or less of these factors, 3.8% of patients were diagnosed with cancer.

But if you had three or more, that number went to 11.8%. So I think this scoring system actually may justify having a new study where you could evaluate extensive screening in a particular population of patients that you know have high-risk features. At this point, however,

the available data based on a number of guidelines do not support an extensive search looking for occult malignancy. However, very important to do a thorough history and physical exam, do some basic labs, and make sure that patients don't have signs or symptoms

suggestive of an occult malignancy. For example, they come in and they say, "Oh, I've had six months of dysphasia." That person probably warrants a work-up. Make sure they're up-to-date with age-appropriate cancer-related screening as well.

So going back to our patient, she had no signs or symptoms of malignancy, labs were normal, and she was up-to-date with her age-appropriate cancer screening. So now the question is,

should we test her for a hypercoagulable condition, either inherited or acquired risk factors? And what is the data for this? Well we know that patients who are diagnosed with VTE, about 50% of them actually will be identified with an inherited thrombophilia.

Factor V Leiden being the most, about 20%. Prothrombin G mutation about 8%. Antithrombin three deficiency, protein C, and protein S are much less. So that's a pretty big number, 50% of the patients. So should we do thrombophilia testing on everybody?

Well, will it change our management? Knowing this information, is it going to affect how long we keep people on blood thinners? Will it predict their recurrence? Will it help us guide in thromboprophylaxis?

Can identify family members? So maybe if that person has a daughter, they shouldn't be on estrogen. And will the testing cause any harm? Well at this point, routine testing is not warranted for everybody.

And in fact, if you have a provoked blood clot, there's no indication to do any of this testing. And these are published guidelines from many different organizations, including American Society of Hematology and Society for Vascular Medicine.

All say that thrombophilic testing really does not change or assist in clinical decision making. So as Dr. Jash mentioned earlier, do people follow this? Well this is a published paper out of Stanford just recently where they had a best practice alert.

So if you tried to order thrombophilia testing, this alert went up, and on the screen came up the Choose Wisely ASH guidelines. Which said, do not test for these people, consider testing for these people. And they saw who went along and then ordered the test.

So non-hematology specialists and general medicine providers, 50% of the time and 44% of the time respectively, followed those guidelines. Hematologists followed it 10% of the time. Unbelievable, right?

So, what about first unprovoked blood clot? Well we know those people, about 42% of them will have an inherited disorder. But remember, the inherited disorder did not cause the blood clot. The unprovoked nature of that blood clot,

that is what's going to predict their future recurrence risk, and that's what is going to dictate their length of anticoagulation. And we know this, Dr. Merle just mentioned this. The VIENNA Prediction Model. If you look at patients with unprovoked blood clots,

and you take them off their blood thinner, their risk of having a recurrent clot is up to 25% at five years, and some up to 50% at 10 years. And the other two he showed, the DASH and the HERDOO2, none of them have thrombophilia status in their model

to predict who's going to get recurrent clots. So what about testing to prevent primary prevention in family members? Well the guidelines vary. And studies actually do show that if you have a first-degree relative

that had a blood clot with an inherited risk factor, you have a higher chance of having that inherited risk factor and a higher chance of getting a VTE. But, family history alone, even without a positive thrombophilia testing,

increases your risk of getting a blood clot. So if you have one family member that's had a blood clot, you're twofold higher increased risk of getting a blood clot compared to the general population. If you have more than one family member, that's increased fourfold,

regardless of what your thrombophilia testing shows. So a negative thrombophilia screening does not equate to a normal VTE risk. Now whom should we test? There's a number of guidelines out there, I'll just mention three that were published

in the last one to two years, one in the New England Journal, one that just came out in Vascular Medicine. And they're good, it kind of walks you through. Does the person have a provoked blood clot, unprovoked, weak risk factor, consider this, consider that.

In general, what these guidelines are saying, is provoked, no screening. Unprovoked, you can consider it in these situations. So if you have a young patient with a really strong family history, and that patient may have a lot of female relatives

that are considering about getting pregnant or being on the pill, you can think about that. Patients with recurrent or extensive thrombosis, you want to think about antiphospholipid. Thrombosis in multiple sites, you want to think about myeloproliferative disorder.

Maybe APS, antiphospholipid, and also something called PNH, or paroxysmal nocturnal hemoglobinuria. That's pretty rare. If someone presents with Warfarin-induced skin necrosis you think about protein C deficiency.

Arterial thrombosis you think about the myeloproliferative and antiphospholipid. And patients with an unprovoked VTE and a low bleeding risk despite having a high one of those models, so you may have a high score of getting a recurrent clot, if they're thinking about going off anticoagulation,

would testing change your mind? I would test only in these situations and only if it's going to change your management of the patient or the family member. So what do I do? Provoked, no role.

And what I do is a very specific shared decision making model with the patient to go through, okay what happens if we get a positive test, and what are we going to do about that? Unprovoked in a strong family history in a young patient I think about it.

The unusual sites, think about the ones I just mentioned, antiphospholipid, PNH, or myeloproliferative. Arterial events, and recurrent events. So going back to our patient, she did great. But one month later,

and this was a patient before the DOAC, so she was on Coumadin. And she was really good about being adherent, and her INRs were always therapeutic. She reappeared with a new blood clot, and her ultrasound showed a new DVT.

So this is actually one situation that I do think about cancer, and in fact she had an abdominal CT scan which showed she had ovarian cancer. So in recurrent clots being on therapeutic anticoagulation, I do worry about cancer and I do think about it.

So my closing reflections. Extensive screening for cancer in idiopathic blood clots is not indicated. However, please make sure that you are doing a thorough history, physical exam, basic labs, following up on any abnormal testing,

and making sure patients are appropriate age, appropriate cancer-related screening. Thrombophilia testing, it's not indicated in most situations. Definitely not in a provoked blood clot. But you can think about doing it in an unprovoked blood clot

if it is going to change your management of that patient or the family member. And remember to think about the risks and benefits and really be thoughtful about it. Thank you very much.

- Thank you very much Raul and our co-chair and also Frank Veith for inviting me again. I'm going to tell you a little bit about flow augmentation. And I have no disclosures related to this. Well, flow augmentation after venous stenting for venous obstruction potentially improves outcome. That's a statement that is

most of the people will support that. Important characteristic of noninvasive compression device after venous stenting is that they improve blood flow inside the newly stented patient,

they stimulate the calf pump muscle, and they're a synergistic tool along anticoagulation, and to decrease the risk for re-occlusion. Well, there are flow devices. Most of the people I think use intermittent pneumatic calf compression

for a few days after the procedure. That can be done but there are now neuromuscular stimulating devices like the FlowAid and the Geko device to stimulate nerves and then the calf won't contract. The physiologic effects of intermittent

pneumatic compression are there. They had been analyzed significantly. There's a decrease of venous stasis and venous pressure, increase flow, increase fibrinolysis, and the blood volume is better and the venous emptying is better.

There's an increased endothelial shear stress, increased the A-V pressure gradient, and there's a decrease in incidence of thrombosis. Those are already published in several papers. Well, what about the neurostimulation device? We have the FlowAid.

FlowAid is a battery powdered neuromuscular electro-stimulation device designed to increase blood flow in the veins. And again this also shows the sequential pattern of neuromuscular electrical stimulation at the calf and causes the calf muscle pump to expel blood

and increase venous, arterial, and microcirculatory blood flow. While these analyses have all been done with healthy volunteers and they show a better outcome then also in intermittent pneumatic compression.

The same is for the Geko device. It's a device which you put along and you stimulate the peroneal nerve, you get a calf contraction. And this also showed in several papers in healthy volunteers that it improves

venous flow, arterial flow, and microcirculatory flow. But it's all analyzed in healthy volunteers, so we said, well, let's do like a short pilot study and see if for even patient with PTS we get the same results, and we looked at that.

But we did a very short pilot in seven patients. We stopped it because we saw already that we need a bigger study, but I will just explain to you what we found in those seven patients. We measured the flow velocity and volume

before and after stenting in the iliac tract to see if we have the increased flow in the common femoral vein in those PTS patients. These are the seven patients, and as you can see it's important

that they don't have a VCSS of 6.4, and the diseased leg, and less than one in the healthy leg, and the Villalta scores will show above 11 on average. So those patients were analyzed and this is what you see. You see

the velocity in the femoral vein before stenting at baseline is, can I point it, yeah, okay, is here. That you see there's a very low velocity. You can increase the velocity with the neurostimulation but there's a higher velocity increase

with the intermittent pneumatic compression. After stenting you see luckily that the velocity has increased, and the stimulation of the neuromuscular is indeed also higher, but the intermittent

pneumatic compression does better. If you look at the volume flow, of course before the treatment, it's low, 32 cc a minute, and then you get an increase with the Geko and an increase with the intermittent

pneumatic compression which is much higher. And after stenting you see that it also improves, you see luckily the stent procedure was successful because we have a much higher flow rate than before the stent procedure. So in conclusion in the literature and the pilot studies

said that neurostimulatory devices have a proven good augmented blood flow in healthy subjects, even better than IPC devices, but there's no experience in PTS patients yet. So this small pilot study shows that the results obtained in healthy subjects

cannot be extrapolated to PTS patients or patients with post stent situations, therefore we are conducting now two randomized studies to compare FlowAid with IPC and the Geko device with IPC, and to see for if this has use, because why is this important?

A potential benefit of the neurostimulation is that you can use it mobile and 24/7 instead of with the IPC procedure which you can only use in a bedridden patient. So if it is as good as or close to, you can use it for a few weeks after stenting

to get the flow up and running and that you have less early stent occlusions. We are also analyzing for if it can replace AV fistula which we do after end of phlebectomies and to prevent really early re-occlusion. And as I said we need those studies to be done

but that the important message is that we don't go home with the fact that those devices, although in healthy volunteers show a very good outcome, they have to be tested in patients with PTS. Thank you very much.

- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,

both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,

and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms

non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches

versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,

that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require

more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage

than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased

due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations

impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion

during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion

after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing

the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials

where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this

from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph

that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents

with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,

whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.

And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent

also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,

and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.

So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,

always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.

Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)

- Thank you, I have no conflict of interest. Although less represented in studies, it has been clearly shown that women are less likely to benefit and more likely to suffer carotid procedural stroke or death compared to men. So let's look at procedural benefit for women in particular first, carotid endarterectomy first.

The only women with carotid stenosis who have been shown to receive a statistically significant overall benefit from carotid endarterectomy have been symptomatic women with 70 to 99% NASCET stenosis without near occlusion who had carotid endarterectomy performed within two

to three weeks of their last cerebral event. They also had to satisfy all the trial inclusion and exclusion criteria. So, symptomatic women in the randomized trials did not receive a benefit from endarterectomy compared to medical treatment on its own

if they had 70 to 99% NASCET stenosis, and endarterectomy was performed more than two to three weeks from the last cerebral event. Or if they had 50 to 69% NASCET stenosis no matter the timing of the endarterectomy. Now, symptomatic men in the

randomized trials had more benefit. Symptomatic men with 70 to 99% NASCET stenosis actually had an overall statistically significant benefit from endarterectomy up to at least three months after their last cerebral event. And I haven't seen it published exactly

when that benefit period finished. Also, men with 50 to 69% NASCET stenosis had overall benefit from endarterectomy, but only if the surgery was performed within two to three weeks of their last cerebral ischemic event. With respect to asymptomatic women,

there's been no clear benefit from endarterectomy in randomized trials. So they did not benefit in ACAS, and the closest to benefit ACST were aged less than 75 years of age. But this was only borderline statistically significant. Asymptomatic men also had more benefit in the randomized

trials of endarterectomy versus medical treatment. So, overall, they had a benefit if they had at least 60% NASCET stenosis, and they were aged less than 75 to 80. What about transfemoral, transaortic stenting? Women and men have not been shown to benefit from stenting

compared to medical intervention alone or endarterectomy. Now, I've head some rumors that women in ACT-1 trial had less harm from stenting compared to endarterectomy. But I haven't seen that result published yet. And when it is published they need to include the peri-procedural risk of stroke and death.

Of course, women and men are much less likely to benefit from any carotid procedure now due to advances in medical intervention. What about procedural harm, endarterectomy? Well, in the randomized trials of endarterectomy versus medical treatment and other studies women

are more likely to have peri-operative stroke and death compared to men. That's seen in randomized trials, but also in non-randomized trials. What about trans-femoral/aortic stenting? Randomized trials and other studies

have been underpowered to compare outcomes with stenting in symptomatic women versus men, but across both sexes stenting has significantly more harm associated with it. In a meta-analysis of randomized trials symptomatic women had one and a half times more peri-procedural stroke

and death with stenting compared to endarterectomy. Again, for asymptomatic patients the trials have been underpowered, but a trend to more harm with stenting. And, also, seen in CREST with combined symptomatic and asymptomatic women.

As Cosmas mentioned, more harm with stenting. TCAR, doesn't look like we're planning to do adequate comparisons with current medical treatment, so no current indication. In summary, overall, the only women shown to benefit from endarterectomy were symptomatic

with 70 to 99% stenosis with endarterectomy within two to three weeks of the last event. Overall, all women are more likely to be harmed by endarterectomy compared to men, and to be harmed by stenting compared to endarterectomy. Everyone is less likely to benefit

from these procedures now. So given all this information, why are we doing so many procedures in women? Thank you.

- Thank you for asking me to speak. Thank you Dr Veith. I have no disclosures. I'm going to start with a quick case again of a 70 year old female presented with right lower extremity rest pain and non-healing wound at the right first toe

and left lower extremity claudication. She had non-palpable femoral and distal pulses, her ABIs were calcified but she had decreased wave forms. Prior anterior gram showed the following extensive aortoiliac occlusive disease due to the small size we went ahead and did a CT scan and confirmed.

She had a very small aorta measuring 14 millimeters in outer diameter and circumferential calcium of her aorta as well as proximal common iliac arteries. Due to this we treated her with a right common femoral artery cutdown and an antegrade approach to her SFA occlusion with a stent.

We then converted the sheath to a retrograde approach, place a percutaneous left common femoral artery access and then placed an Endologix AFX device with a 23 millimeter main body at the aortic bifurcation. We then ballooned both the aorta and iliac arteries and then placed bilateral balloon expandable

kissing iliac stents to stent the outflow. Here is our pre, intra, and post operative films. She did well. Her rest pain resolved, her first toe amputation healed, we followed her for about 10 months. She also has an AV access and had a left arterial steel

on a left upper extremity so last week I was able to undergo repeat arteriogram and this is at 10 months out. We can see that he stent remains open with good flow and no evidence of in stent stenosis. There's very little literature about using endografts for occlusive disease.

Van Haren looked at 10 patients with TASC-D lesions that were felt to be high risk for aorta bifem using the Endologix AFX device. And noted 100% technical success rate. Eight patients did require additional stent placements. There was 100% resolution of the symptoms

with improved ABIs bilaterally. At 40 months follow up there's a primary patency rate of 80% and secondary of 100% with one acute limb occlusion. Zander et all, using the Excluder prothesis, looked at 14 high risk patients for aorta bifem with TASC-C and D lesions of the aorta.

Similarly they noted 100% technical success. Nine patients required additional stenting, all patients had resolution of their symptoms and improvement of their ABIs. At 62 months follow up they noted a primary patency rate of 85% and secondary of 100

with two acute limb occlusions. The indications for this procedure in general are symptomatic patient with a TASC C or D lesion that's felt to either be a high operative risk for aorta bifem or have a significantly calcified aorta where clamping would be difficult as we saw in our patient.

These patients are usually being considered for axillary bifemoral bypass. Some technical tips. Access can be done percutaneously through a cutdown. I do recommend a cutdown if there's femoral disease so you can preform a femoral endarterectomy and

profundaplasty at the same time. Brachial access is also an alternative option. Due to the small size and disease vessels, graft placement may be difficult and may require predilation with either the endograft sheath dilator or high-pressure balloon.

In calcified vessels you may need to place covered stents in order to pass the graft to avoid rupture. Due to the poor radial force of endografts, the graft must be ballooned after placement with either an aortic occlusion balloon but usually high-pressure balloons are needed.

It usually also needs to be reinforced the outflow with either self-expanding or balloon expandable stents to prevent limb occlusion. Some precautions. If the vessels are calcified and tortuous again there may be difficult graft delivery.

In patients with occluded vessels standard techniques for crossing can be used, however will require pre-dilation before endograft positioning. If you have a sub intimal cannulation this does put the vessel at risk for rupture during

balloon dilation. Small aortic diameters may occlude limbs particularly using modular devices. And most importantly, the outflow must be optimized using stents distally if needed in the iliac arteries, but even more importantly, assuring that you've

treated the femoral artery and outflow to the profunda. Despite these good results, endograft use for occlusive disease is off label use and therefor not reimbursed. In comparison to open stents, endograft use is expensive and may not be cost effective. There's no current studies looking

into the cost/benefit ratio. Thank you.

- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%

in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.

They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.

If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.

And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.

If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.

The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis

greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,

including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,

the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,

at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft

rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.

We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.

And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.

And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.

Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,

cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered

earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.

- Thank you Professor Veith. Thank you for giving me the opportunity to present on behalf of my chief the results of the IRONGUARD 2 study. A study on the use of the C-Guard mesh covered stent in carotid artery stenting. The IRONGUARD 1 study performed in Italy,

enrolled 200 patients to the technical success of 100%. No major cardiovascular event. Those good results were maintained at one year followup, because we had no major neurologic adverse event, no stent thrombosis, and no external carotid occlusion. This is why we decided to continue to collect data

on this experience on the use of C-Guard stent in a new registry called the IRONGUARD 2. And up to August 2018, we recruited 342 patients in 15 Italian centers. Demographic of patients were a common demographic of at-risk carotid patients.

And 50 out of 342 patients were symptomatic, with 36 carotid with TIA and 14 with minor stroke. Stenosis percentage mean was 84%, and the high-risk carotid plaque composition was observed in 28% of patients, and respectively, the majority of patients presented

this homogenous composition. All aortic arch morphologies were enrolled into the study, as you can see here. And one third of enrolled patients presented significant supra-aortic vessel tortuosity. So this was no commerce registry.

Almost in all cases a transfemoral approach was chosen, while also brachial and transcervical approach were reported. And the Embolic Protection Device was used in 99.7% of patients, with a proximal occlusion device in 50 patients.

Pre-dilatation was used in 89 patients, and looking at results at 24 hours we reported five TIAs and one minor stroke, with a combined incidence rate of 1.75%. We had no myocardial infection, and no death. But we had two external carotid occlusion.

At one month, we had data available on 255 patients, with two additional neurological events, one more TIA and one more minor stroke, but we had no stent thrombosis. At one month, the cumulative results rate were a minor stroke rate of 0.58%,

and the TIA rate of 1.72%, with a cumulative neurological event rate of 2.33%. At one year, results were available on 57 patients, with one new major event, it was a myocardial infarction. And unfortunately, we had two deaths, one from suicide. To conclude, this is an ongoing trial with ongoing analysis,

and so we are still recruiting patients. I want to thank on behalf of my chief all the collaborators of this registry. I want to invite you to join us next May in Rome, thank you.

- Thank you Dr Veith, and thank you for inviting me, once again, to this excellent meeting. So, I'll talk about the differences in randomized clinical trials and registry results for stenting, and how they are important. Now as you probably all know, in July 2010

a landmark randomized controlled trial CREST reported that among patients with symptomatic or asymptomatic carotid stenosis, the risk of the composite primary outcome of stroke, MI, or death did not differ significantly

in the group undergoing carotid-artery stenting and the group undergoing carotid endarterectomy. Based largely on these CREST results, the American Stroke Association, a Division of American Heart Association, five months later published their guidelines

where stenting was indicated as an alternative to CEA for symptomatic patients. We did not agree with this recommendation, and Dr Veith kindly invited the SVS representatives, Dr Riles and Dr Moore, and together we published this commentary

saying that it's easy for the term "alternative" to be misinterpreted as "equivalent", which is clearly not true. Following this, we looked at stroke and death rates following carotid artery stenting and carotid endarterectomy

in real life dataset registries, to see if the results from registries actually agree with CREST, and this is a graph that shows the stroke and death rates in asymptoma

the blue dots are for endarterectomy, the red dots are for stenting. There's a line across the 3%, which is the recommended thresholds in asymptomatic patients, as you will see,

there is only one registry for CA above the 3%, whereas there are several stenting registries above the 3%. The size of the dots represents the size of the registries. This registry included more than 1.5 million patients, so these were real strokes, and real deaths. For symptomatic patients the situation was even worse.

Again, you see the blue dots are the endarterectomy and the red dots are the stenting ones, and the 6% is the recommended threshold, by the American Heart Association. You will see that many CAS registries had higher than 6% stroke and death rates.

So, why is this difference and why is it important? First of all, there was a difference in experience and expertise between CAS practitioners participating in randomized controlled trials, and in real life. There were several CAS practitioners

which were performing less than 10 CAS procedures a year. So that was one of the reasons for the results. Also, registries don't have any inclusion/exclusion criteria, there is no cherry-picking, and they include all-comers, so they report results as they occur.

In fact, the Society for Vascular Surgery guidelines show clearly which patients are preferred for stenting instead of CEA, and these include those with tracheal stoma, those with scarred necks, with fibrotic necks, or those after external beam radiotherapy.

Carotid endarterectomy is preferable to CAS for patients older than 70 years, or symptomatic patients, and for females. And in fact, the CREST subgroup analysis showed exactly that. This is the first subgroup analysis

for bisymptomatic status, and you can see here that the perpirocedural stroke and death rates were almost double for stenting compared with endarterectomy. And here's the second subgroup analysis by gender,

which showed that men had similar outcomes whether undergoing stenting or endarterectomy, but women, they had more than 2.5-fold higher stroke and death rates, and this is very significant differences. That's the third subgroup analysis, by age,

which showed that actually the age of 70 years was the time when the outcomes of the stenting were similar with endarterectomy, after that, stenting was considerably worse. By this I would like to thank you all for your attention.

- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.

You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience

the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,

as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.

If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.

We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.

Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.

No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time

of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities

and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice

In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases

due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.

We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.

So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed

with multi-institution trial and longer follow-up

- Thank you and maybe we trying to get rid of women's, I don't know, we'll see. Thank you Dr. Veith. No relevant disclosures to this talk. But we know statin is very beneficial in carotid endarterectomy. Several published data already,

one of them is threefold reduction in the risk of stroke and fivefold reduction in the risk of death done by Dr. Perler over 1,500 patients. Another study by Kennedy, showing 75% reduction in the risk of stroke as well and this is one larger cohort, about 3,300 patients.

So what about carotid stenting? If you look at the data, there's not a lot of data out there so we did a lot of work looking at medication in general in carotid stenting. For instance, we know that dual antiplatelet therapy is very beneficial.

We don't have one, we actually have two randomized trials comparing clopidogrel or ticlopidine with asprin versus Heparin and asprin. Both studies showed significant reduction in the risk of neurological event. In the first study, reduction from 25% to 0%.

In the second one, from 16% to 2%. So beta-blockers, not a lot of people believe this data but this is very powerful study, a large cohort of patients that received beta-blockers. There was a 65% reduction in the risk of stroke and death in carotid artery stentings

and mainly in the group who developed hypertension after the procedure. So how about statin? Statin and carotid artery stenting, if you look in the literature, very poor data. This is one of the largest studies out there,

it has about a thousand patients, a little over a thousand patients, about 40% of them are on statin and in this particular study there was 70% reduction in the risk of stroke and death if you're on a statin versus not.

And that persisted at long term followup. So if you're on statin at five years, your risk of mortality overall was reduced by 50% and your risk of stroke also was reduced by about 60%. We went out to see what happened in real world data so we used the Premier dataset

to represent 20% of all discharges in the United States. And it has more than 700 hospitals. So we have from 2009 to 2015, 17,800 carotid stent, making this the largest retrospective study done to date. 70% of these patients were on statin and as you can expect they're slightly older, more male,

more history of hypertension, diabetes and prior stroke, prior MI and coronary artery disease, there was significantly more CHF, COPD. Bottom line, they were a lot more sicker and that's why they were on statins. But the group that did not receive statin,

were more likely to receive an urgent or emergent carotid artery stenting. Surprising was that actually the risk of stroke and MI was larger in the group who are on statin but the death was half. So that making a case for a rescue phenomenon

and as you can see here, chances of dying, if you're on statin and develop major stroke or MI after carotid stenting was reduced from 26% to 11%. When we did the adjusted analysis, the difference in stroke went away but the difference in MI persisted.

So if you're on statin, twice as much MI. Obviously, this is why you're on statin in the first place because you have a lot of coronary artery disease so it is not surprising why there is more MI. But again, the risk of death was reduced by more than 60% and the risk of death following a major stroke

or major MI was reduced by 63%. Limitation, of course, is a retrospective analysis. We only looking at post-operative outcomes, we don't know really the exact, we do but we didn't analyze the dosage and the type of statin, that's another study.

But this study is published recently in the Journal of Vascular Surgery. And in conclusion, 64% reduction in odd of death, 18% reduction in odd of stroke and death if you're in statin verus not and undergo a carotid artery stenting.

And most interesting finding, 63% reduction in failure to rescue. And I urge you to have all your patients on statin, if you're performing carotid artery stenting based on this and other data but we need further study to look at the dose effect

and the type of statin that need to be used. Thank you so much.

- Here are my disclosures. Okay, so I'm going to start things as well with an unknown case. This is a 29 year old Caucasian male with severe shortness of breath, diaphoresis, low blood pressure, worsening fatigue and was recently seen to be subtherapeutic on his warfarin dosing.

His history included antiphospholipid antibody syndrome, lupus anticoagulant positive and what test do we start with? A CT, a VQ scan, ultrasound, MRI, what additional tests might we get? So, you know, I'm going to quote the man sitting next to me here and it's important to remember

and this will come up throughout our discussion here. Is the yield of a CT pulmonary angiogram is actually relatively low, that's because of, as Dr. Calori just mentioned, if you suspect it, you should get it off the table. And it's Gestalt really does matter, especially, expertise,

I think doesn't always factor into these published studies, but if you're Gestalt tells you, you should look, you should look, we should really lower the burden, the bar to looking. If you look, when there's no thromboembolic risk factors, that's exceedingly low, so something like two percent.

If you look at, so let's take that six, that low yield and then let's look at those patients and what happens to them. If you look at the positive PE studies, out of the broad number of scans we do, only a very small fraction will have mortality.

So you're talking about, in this highest risk, the massive pulmonary embolism, only five percent of patient qualify as massive PE and just over half of those will actually have a mortal PE. Whereas the submassives, a large number of 40%,

22% morality and then the low risk ones, they do pretty well, it's over less than one percent and that's more than half. You know, when we do a CT scan, just to say we're going to make the diagnosis in the first place, you're going to look for filling defects.

So the whole basis of the exam is just, is there absence of filling of a pulmonary artery with contrast, if it's timed appropriately, we should have no problem doing this. So you can see, in the middle, you've got a central pulmonary embolism, on the right and left branches here,

you can see these are low bar PEs, but they're also peripheral. So they're not central, you can actually see the calcification on the left here. So it's not quite the simple story of just this is a PE, you can see, that the calcification is a mark

of chronic thrombus and the peripheral location chronicity. The appropriate criteria and you can read any one you like, I just picked the ACR from 2016 shows, that short of X ray CTA is the first test you should do. And part of the reason, I think CT and X ray trump the VQ scan is, that you can see alternative diagnosis

and when the yield is low, you can look for other causes. The other thing is, that the VQ scan is a little more cumbersome and a CT scan is much more available in most locations. So we're going to look at the CT scan, we're going to look for filling defects,

the character of the defect, location, the shape of it. The calcification, chronicity, positioning within the pulmonary radially. The burden of the thrombus overall, we have seen, that it's really not going to predict outcomes. And then there's other findings, that are ancillary

regarding pulmonary embolisms, such as bronchial artery hypertrophy and cardiac chamber enlargement, especially the right ventricle. You can see here, when you look at the, on the bottom right image here, that's an invasive angiogram and you can imagine why there's difficulty seeing

what's not there. It's not, that we don't see the filling defect in this large left lower lobe pulmonary embolism, it's that you don't know where the vessel should be and then the CT, it shows the location of the vessel and then the lack of filling within it.

When we're going to look at the chamber enlargement, the first thing you should do is look for right heart enlargement, it's for free. You're probably making this as your initial test, although, if you're highly efficient, like Roger, then you're actually doing the echo in your clinic

and then sending the patient, but the CT scan images the heart anyway, so why not take a look. You know, there's been a bunch of publications, some looking at doing cardiac reformatting to look at the heart the way we would look with an echo. And that's nice, that cost time and energy

and not always available, not already all of us have the skill, not all departments have the workstations. It turns out you don't need to, you can look for RV to LV enlargement. For the purpose of this slide, I just picked on a single image, but you're actually allowed

to look at different slices. And you're looking for ratio to keep it simple, greater than one. So if the intraluminal diameter of the right ventricle is greater than the left ventricle, which, even though, we don't have a great left sided contrast on this image,

you can still see it. That's a ratio greater than one and you can train most radiologists to do that, even if they're not comfortable with doing special processing and reformatting. Now, if you want to get fancy and do a cardiac gated CT

or even an MRI, you can and just starting with CT, since you're already using that as your gold standard diagnostic test, you can do ECG gating in the temporal resolution of CT scans, it's as low as 66 milliseconds. Just a few years ago, it was as high as 200 milliseconds,

so that's the time, the number of projections to acquire enough data to make one image. So when you look at that, you can really see the heart, even when you don't intend to and if you do it with an ECG mapping, you can actually get multiple frames in time and with a price of a little bit

of increased radiation, you can get moving, beating images, like this. But now you've got a lot more data, that's more time to cross over to your data archive, more time to interpretation. And you need to think about the yield.

So basically, for about, you know, a three milli sec at the right and left heart function, the amount of time to analyze that accurately takes time. You can see here, we can also look at the coronary arteries. You'd probably want to give nitro glycerin, if you were doing a full coronary rollout, if possible.

We can look at coronary plaque. You can reformat the images, you can even see there's a volume rendered on the bottom right here. Volume's over the RV at endo diastolic and then endo systolic. So you can actually get the true RV ejection fraction.

Which does have some prognostic significance. Dual energy CT is another way to use modern technology and this is kind of becoming our standard of care at our hospital. One of the reasons is patients like this. This is a very large patient, BMI was 44,

a lot of risk factors and high clinical suspicion and you can see on the single energy reformat is the way of strolling actually here. It's a little difficult to see those filling defects, but what you can do is take that source image and then you can deconstruct it into different energies,

so it's sort of like playing with a bass and a tremble on your stereo and you can bring out the contrast, and so that's what we've done here with a low KEV image. And you can see, on the arrows there, it improves the conspicuity of the contrast filing defects.

Or you can make really fancy pictures, which is great for talks and good for diagnosis. As you can see here, this is a ventilation perfusion map made purely from the CT scan, so we're mapping iodine to be orange, so when you see all the bronchial tree in white, you can see the absence of iodine getting

to the lung in this personal bilateral lower lobe PEs. Excuse me, so back to our case at hand. The 29 year old with a lot of risk factors, and APLS and lupus anticoagulant, and he's subtherapeutic on this meds. We looked at the source images.

Not a dual energy scan, but it's a decent exam. You can see he's a larger individual, we didn't see any filling defects, the right heart doesn't look enlarged, is there anything else we can do, while we have him at making this initial diagnosis. What's the incremental value of a Venus evaluation?

Well, we can do doppler and you can see here, that doppler, you know, has a lot of subtle findings as well as obvious findings, like the presence of a non compressible thrombus. We can also do that with a CT scan, we can just chase the contrast two minutes later

and look at the lower extremities and it basically has a very similar sensitivity. We can look for a filling defect. In our case here, we didn't have that. This is an example of somebody else, that did have a DVT and an abstracting pelvic cancer

creating abdominal waveforms. But this comes out in the guidelines as, you know, sometimes appropriate to look at the lower extremities with the contrast and it's really just the same exam, so it doesn't involve another test. Although, if you have doppler widely available,

it seems, like the obvious thing to do, there's no radiation, that's reproducible, just costs a little bit of time and money. Also important to remember, when we're looking at the CT scan, that the mimics of the pulmonary embolism can actually be more common than actually diagnosis,

when you have a low yield. So all four of these cases were initially called as pulmonary embolism, but they were actually going clockwise on the top left. That's a pulmonary sarcoma, you can see enhancement, it's a very large defect

and presented much more inconspicuously. The top right is a mixing artifact, that's very common, especially, when you have heart failure, as this patient does. The bottom left, that's endocarditis and a patent ductus arteriosus and the tissue

can develop infection. And then the bottom right is probably the most common one you'll see, which is mucus in the bronchi, so this is something, that looks like a filling defect, but you can see it's in the bronchi, if you scroll up and down.

They're next to the pulmonary arteries, not in the pulmonary arteries. Lung cancer patient with pulmonary embolism. Important to remember, that not all filling defects are actually thrombi, this is a patient of Rachel's and she'll probably comment on it more later,

but this is somebody, who kept coming back with on and off PEs and what it actually was was lack of filling, because there's lack of lung. What you'll see here is the patient has a couple of CCs left of normal lung and so you don't have filling and the perfusion with normal lung.

So when we brought the patient back with delayed images, that filled right in, so this is just slow flow in an area, that should have slow flow, because it's not normally perfused. VQ scans have become a coin flip and I think that's probably because it's a lost art, but also, when you're looking at,

you know, a lack of perfusion in a new area and you're not sure what the anatomy is, it's difficult and we never had much more than probability. MRI is not ready for primetime, I don't think it ever will be. This is an image from the PIOPED three study,

you can see, that the exam is really good and you can see the filling defects, when you can see them, but about a quarter of the scans were actually technically inadequate. Also requires getting contrast, which is nobodies favorite. So back to our patient, this is a patient,

who actually did not have a PE, but actually had his hemodynamic collapse due to bilateral, bilateral adrenal hemorrhage. So he had, actually, a scan about a week earlier and you can see the adrenals, that actually hemorrhaged due to the massive hemorrhage causing his hemodynamic

instability and a very scary scenario, that looked a lot like pulmonary embolism and a high risk patient. So anyway, in summary, the CTA is your first line and your second line, VQ scan can be useful, but is really a lost art, MRI is not quite ready

for primetime, MRI can be done for any of these functional tests as well as instead of CT. So it might be a selected test. Don't forget the mimics of pulmonary embolism and remember, the overall low yield of a CTPA and think about the risk factors, and put it in context.

And I would also recommend all outside calls of PE get a local over-read by your radiologist. And you're part of a PERT team, I'm sure we'll hear more about that later, thank you.

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