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Tracheoinnominate Fistula|Angiography|45|Female
Tracheoinnominate Fistula|Angiography|45|Female
2016airwayanterioraortaarterialarteriesarterybenignbleedingbloodblowoutbronchialcarotidcommonlydiagnosisdifferentialembolizationendotrachealexternalfindingshemoptysisinflammatoryinternallaterallowermalignancymassivenecknoteoriginatepatientpatientspriorpseudoaneurysmradiationsinusSIRspinalstentsupplysyndromethoracictolerateultimatelyuppervessels
Update On The Advantages, Limitations And Midterm Results With The Terumo Aortic 3 Branch Arch Device: What Lesions Can It Treat
Update On The Advantages, Limitations And Midterm Results With The Terumo Aortic 3 Branch Arch Device: What Lesions Can It Treat
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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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Bailout Rescue Procedures When CEA Is Failing In A Critical Unstable Patient: ICA Stent Or Gore Hybrid Graft Or Standard PTFE Bypass: Indications For Each
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Octopus Technique To Treat Urgent Or Ruptured TAAAs With OTS Components: What Is It, Technical Tips And Results
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Below-The-Elbow Angioplasty For CLTI Of The Hand: Indications, Techniques Results
Below-The-Elbow Angioplasty For CLTI Of The Hand: Indications, Techniques Results
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Challenges And Solutions In Complex Dialysis Access Cases
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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
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Thrombo-Embolic Complications Of Inflammatory Bowel Disease: Nature, Etiology And Significance
Thrombo-Embolic Complications Of Inflammatory Bowel Disease: Nature, Etiology And Significance
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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
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Do Re-Interventions Cause EVAR Infections
Do Re-Interventions Cause EVAR Infections
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Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
adjunctsanatomicangioplastyarchballoonballoonsbrachiocephaliccephalicdeploymentfistulasfunctionalgoregraftgraftingInterventionspatencypredictorsprimaryradiocephalicrecurrentstenosesstenosisstentStent graftstentingsuperiorsurgicaltranspositionviabahn
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New Developments In The Management Of Blunt Aortic Injuries Using A Practical Grading System: Why It Matters
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Technical Tips For Open Conversion After Failed EVAR
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With Complex AAAs, How To Make Decisions Re Fenestrations vs. Branches: Which Bridging Branch Endografts Are Best
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Vacuum Assisted Thrombectomy With The Penumbra Indigo System For Visceral And Lower Limb Artery Occlusions
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Is Drug Neuroprotection After Thrombectomy For Acute Stroke Or Other Ischemic Cerebral Insults Feasible: Future Prospects
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Advantages Of Cook Zenith Spiral Z Limbs For EVARs Landing In The External Iliac Artery
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Non-Invasive 24/7 Flow Augmentation In Deep Venous Pathology
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Selective SMA Stenting With F/EVAR: When Indicated, Value, Best Bridging Stent, Technical Tips
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Update On The everlinQ Percutaneous Fistula Device
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Current Management Of Bleeding Hemodialysis Fistulas: Can The Fistula Be Salvaged
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Why Are Carotid Stenoses Under- And Over-Estimated By Duplex Ultrasonography: How To Prevent These Problems
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What Morphological Changes On CT After EVAR Predict The Need For Re-Interventions: From The DREAM Trial
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Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
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Italian National Registry Results With Inner Branch Devices For Aortic Arch Disease
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Value Of Statins In CAS Patients: What Drug, What Dose And When: How Do They Help
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Algorithms For Managing Steal Syndrome: When Is Banding Appropriate
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Transcript

This is a 45 year old female with a history of Locked-in Syndrome after a vertebral artery dissection in 2008. This is just this presented this year. Status post tracheostomy done

in May 2014, so not quite two years ago. Transferred from an outside hospital for massive hemoptysis, that's not quite the full story, she was at home and where her care takers take care of her and they were sunctioning out her tracheostomy and presented with massive hemoptysis immediately sent to the

hospital, they are locally multi several hours away unfortunately by vehicle and the bleeding was temporized with and endotracheal tube, the cuff on the endotracheal tube which was inflated and she was helicoptered actually to our institution, and at our institution a flexible bronchoscopy in the intensive care unit was then done by the NT specialist and team that were there ready to evaluate her on her arrival and again

noted massive bleeding from the trachea when they deflated endotracheal cuff, and then so she was sent emergently down to us, we were awaiting her as well for further evaluation. So we're getting into causes of airway bleeding and we broadely categorize these into upper and lower airway bleeding, we can get into some differential diagnosis for upper airways bleeding,

,malignant and benign causes are most frequently seen specifically sclerosis casanoma although there are etioologies, and then not only just from malignancy itself but it's secondary to the treatment of the malignancies particularly radiation can cause weakening of the blood vessels and ultimately bleeding from a variety of blood vessels

and we'll talk about some of this. Benign causes of upper airway bleeding include atrogenic tranchionnormal efficialla, inflammatory lesions, trauma, broncholithiasis, and we talk about lower airway bleeding there are a number of causes and this is just broad differential vasculitis and coagulapothy,

ABM's infection and again malignancy and all foreign body, so this is just broadly, we'll dive into a couple of these diagnosis such as teaching points or comparing cases embedded within this particular case. Carotid Blowout Syndrome is one that we see on occasion in our

institutions seems like we get to see this a handful of times a year as our ENT docs treat a number of patients, this is not common, but up to 4.3% of patients with head and neck cancers have been estimated to have this. Commonly seen with mesael casanoma prior to after a radical neck

surgery and concombinate radiation therapy, the risk factors include mucocutaneous fistuala and exposure of the artery to air and then their fore skin breakdown so in associated infection. Ultimately [INAUDIBLE] is thought to be a compromise to the vase of his arm that supplies the arterial wall and then ultimately the weakening and then blowout. Chaloupka and

colleagues sort to categorize Carotid Blowout Syndrome into three different distinct categories threatened, impending, and acute, and threatened was where radiologic imaging findings or endoscopy or some type of scope findings demonstrate the artery to be exposed to the oral cavity or the external environment. Impending where there was a sentinel bleed that occurred and then obviously Acute being

active bleeding, and scenarios. So this is a case example from our institution this past year, 32 year old gentleman with stage two squamous cell carcinoma of the left lateral tongue. We were called after a second episode of the hemoptysis / oropharyngeal bleeding.

A CT of the neck was done. You'll notice on that top image, there's a sinus tract in the left lateral hypopharynx developed as a complication we think to be from prior radiation. Which she's known to have, and then the pseudoaneurysm of the left

external carotid artery adjacent to that sinus which we thought was the source of this hero bleed, so this patient went on to agiography you can see that focal pseudoaneurysm near the vase of the external carotid artery, and that was treated with embolization and the patient went on to do well without hemoptysis.

Carotid blowout syndrome can be treated by a few different ways, basal sacrifice specifically embolization can be considered for an external carotid or potentially an internal carotid artery source, of course if an internal carotid artery

is going to be embolized you wanna be able to be sure the patient can tolerate this. This is obviously potentially significantly morbid, but in a patient who's issue is related to an internal carotid source unlike this case, you may wanna prior to embolization do a balloon test occlusion to see the patient's ability to tolerate such a treatment option

and be able to test the collateral supply via the circle. In other cases, and particularly in the internal carotid vessel preservation may be the means for these patients, and these cases we would employ a covered stent or a stent graft. However note that may just be kicking the can down the road a little

bit with long term complications with stent occlusions as we do really don't have long terms data on this. However, in some patients, these patients won't have a great long term prognosis so this may be the best option in those patients who cannot tolerate an embolization.

Lower airway bleeding it's important to note that there is a duo blood supply for the lung, pulmonary arteries provide the gas exchange with the alveolis we are aware of and provide 99% of the arterial supply, the lung, the bronchial arteries supply just a small remaining blood supply to the lungs.

However, generally the most common culprit for hemoptysis in the lower airway. The bronchial artery anatomy it's always important to note can be highly variable, but the majority arise in the proximal descending thoracic aorta between T5 and 6, but I have other sources

and it's important to note as well. And of course you can't talk about bronchial arteries or angiography without mention of the anterior spinal artery. And particularly of note if you have a right intercostal and common bronchial artery trunk, in up to 10% of those patients who can

see anterior spinal artery originate from that same spinal common trunk, and although that's often the artery itself is most commonly seen lower in the thoracic aorta can originate as high as T5 so just because you're approximately catheterized in the bronchial artery much higher, than what we typically anticipate

the spinal artery, we do have to look for that routinely with any angiogram. Again the vast majority of hemoptysis from lower airway bleeding is from the bronchial arteries, often with in the inflammatory setting potential TB, but we also see this in patients with chronic

bronchiectasis, particularly CF patients. Other causes as well can be seen.

- The only disclosure is the device I'm about to talk to you about this morning, is investigation in the United States. What we can say about Arch Branch Technology is it is not novel or particularly new. Hundreds of these procedures have been performed worldwide, most of the experiences have been dominated by a cook device

and the Terumo-Aortic formerly known as Bolton Medical devices. There is mattering of other experience through Medtronic and Gore devices. As of July of 2018 over 340 device implants have been performed,

and this series has been dominated by the dual branch device but actually three branch constructions have been performed in 25 cases. For the Terumo-Aortic Arch Branch device the experience is slightly less but still significant over 160 device implants have been performed as of November of this year.

A small number of single branch and large majority of 150 cases of the double branch repairs and only two cases of the three branch repairs both of them, I will discuss today and I performed. The Aortic 3-branch Arch Devices is based on the relay MBS platform with two antegrade branches and

a third retrograde branch which is not illustrated here, pointing downwards towards descending thoracic Aorta. The first case is a 59 year old intensivist who presented to me in 2009 with uncomplicated type B aortic dissection. This was being medically managed until 2014 when he sustained a second dissection at this time.

An acute ruptured type A dissection and sustaining emergent repair with an ascending graft. Serial imaging shortly thereafter demonstrated a very rapid growth of the Distal arch to 5.7 cm. This is side by side comparison of the pre type A dissection and the post type A repair dissection.

What you can see is the enlargement of the distal arch and especially the complex septal anatomy that has transformed as initial type B dissection after the type A repair. So, under FDA Compassion Use provision, as well as other other regulatory conditions

that had to be met. A Terumo or formerly Bolton, Aortic 3-branch Arch Branch device was constructed and in December 2014 this was performed. As you can see in this illustration, the two antegrade branches and a third branch

pointing this way for the for the left subclavian artery. And this is the images, the pre-deployment, post-deployment, and the three branches being inserted. At the one month follow up you can see the three arch branches widely patent and complete thrombosis of the

proximal dissection. Approximately a year later he presented with some symptoms of mild claudication and significant left and right arm gradient. What we noted on the CT Angiogram was there was a kink in the participially

supported segment of the mid portion of this 3-branch graft. There was also progressive enlargement of the distal thoracoabdominal segment. Our plan was to perform the, to repair the proximal segment with a custom made cuff as well as repair the thoracoabdominal segment

with this cook CMD thoracoabdominal device. As a 4 year follow up he's working full time. He's arm pressures are symmetric. Serum creatinine is normal. Complete false lumen thrombosis. All arch branches patent.

The second case I'll go over really quickly. 68 year old man, again with acute type A dissection. 6.1 cm aortic arch. Initial plan was a left carotid-subclavian bypass with a TEVAR using a chimney technique. We changed that plan to employ a 3-branch branch repair.

Can you advance this? And you can see this photo. In this particular case because the pre-operative left carotid-subclavian bypass and the extension of the dissection in to the innominate artery we elected to...

utilize the two antegrade branches for the bi-lateral carotid branches and actually utilize the downgoing branch through the- for the right subclavian artery for later access to the thoracoabdominal aorta. On post op day one once again he presented with

an affective co arctation secondary to a kink within the previous surgical graft, sustaining a secondary intervention and a placement of a balloon expandable stent. Current status. On Unfortunately the result is not as fortunate

as the first case. In 15 months he presented with recurrent fevers, multi-focal CVAs from septic emboli. Essentially bacteria endocarditis and he was deemed inoperable and he died. So in conclusion.

Repair of complex arch pathologies is feasible with the 3-branch Relay arch branch device. Experience obviously is very limited. Proper patient selection important. And the third antegrade branch is useful for later thoracoabdominal access.

Thank you.

- 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 very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years

of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).

It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,

it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases

that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it

was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.

And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted

inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted

selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.

In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients

stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.

This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,

and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,

and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.

- This is from some work in collaboration with my good friend, Mike Dake. And, a couple of years of experience at Stanford now. First described by Kazy? years ago. This technical note of using multiple main-body endographs in a sandwich formation.

Up at the top but, then yielding multiple branches to get out to the visceral vessels and leaving one branch for a bifurcated graft. We've sort of modified it a little bit and generally either use multiple

grafts in order to create a branch the celiac and SMA. Left the celiac sometimes for a chimney, but the strategy really has been in one of the limbs to share both renals and the limb that goes down to the legs. We noticed early on that this really was not for

non-operative candidates, only for urgent cases and we recognize that the visceral branches were the most important to be in their own limb. I'll just walk you through a case. 6.8 centimeter stent for foraco above

the prior opened repair. The plan drawn out here with multiple main bodies and a second main body inside in order to create the multiple branches. The first piece goes in. It's balloon molded at the level of pulmonary

vein with enough length so that the ipsalateral limb is right next to the celiac. And we then, from above get into that limb and down into the celiac vessel and extend with either a limb or a viabahn. Next, we deploy a second main body inside

of the gate, thus creating now another two limbs to work through. And then through that, extend in its own branch a limb to the SMA. This was an eight by 79 vbx. Then we've got a third limb to go through.

We put a cuff that measures about 14. This is the math so that the double renal snorkle plus the main body fills up this hole. Now, double sheath access from above, looking for both renals. Sheaths out into both renals with viabahns

inside of that. Deployment of the bottom device and then a final angiogram with a little bit of a gutter that we often see when we have any kind of parallel graft configuration. Here's the post-op CT scan wherein

that limb is the two shared renals with the leg. This is the one year post-op with no endo leaks, successful exclusion of this. Here's another example of one of an eight and a half centimeter stent three thorico similar strategy, already with an occluded

celiac. Makes it a little bit easier. One limb goes down to the superior mesenteric artery and then the other limb then is shared again bilateral renals in the lower main body. Notice in this configuration you can get all the way up to the top then by putting a thoracic component

inside of the bifurcated subabdominal component. There's the final CT scan for that. We've spent some time looking at the different combinations of how these things will fill up to minimize the gutters through some more work. In collaboration with some friends in Kampala.

So we've treated 21 patients over the last couple of years. 73 years of age, 48 percent female usual comorbid factors. Oh, I thought I had more data there to show you. O.K. I thought this was a four minute talk.

Look at that. I'm on time. Octopus endovascular strategy is a feasible off the shelf solution for high risk patients that can't undergo open repair. You know obviously, sort of in this forum and coming to this meeting we see what's

available outside of the U.S. and I certainly am awaiting clinical trial devices that will have purpose specific teacher bi-graphs. The end hospital morbidity has still been high, at four percent. The one year survival of 71 percent in this select

group of 21 patients is acceptable. Paraplegia is still an issue even when we stage them and in this strategy you can stage them by just doing the top part plus the viscerals first and leaving the renals for another day. And branch patency thus far has been

in the short term similar to the purpose specific graft as well as with the parallel graft data. Thank you.

- Thank you, Dr. Ascher. Great to be part of this session this morning. These are my disclosures. The risk factors for chronic ischemia of the hand are similar to those for chronic ischemia of the lower extremity with the added risk factors of vasculitides, scleroderma,

other connective tissue disorders, Buerger's disease, and prior trauma. Also, hemodialysis access accounts for a exacerbating factor in approximately 80% of patients that we treat in our center with chronic hand ischemia. On the right is a algorithm from a recent meta-analysis

from the plastic surgery literature, and what's interesting to note is that, although sympathectomy, open surgical bypass, and venous arterialization were all recommended for patients who were refractory to best medical therapy, endovascular therapy is conspicuously absent

from this algorithm, so I just want to take you through this morning and submit that endovascular therapy does have a role in these patients with digit loss, intractable pain or delayed healing after digit resection. Physical examination is similar to that of lower extremity, with the added brachial finger pressures,

and then of course MRA and CTA can be particularly helpful. The goal of endovascular therapy is similar with the angiosome concept to establish in-line flow to the superficial and deep palmar arches. You can use an existing hemodialysis access to gain access transvenously to get into the artery for therapy,

or an antegrade brachial, distal brachial puncture, enabling you treat all three vessels. Additionally, you can use a retrograde radial approach, which allows you to treat both the radial artery, which is typically the main player in these patients, or go up the radial and then back over

and down the ulnar artery. These patients have to be very well heparinized. You're also giving antispasmodic agents with calcium channel blockers and nitroglycerin. A four French sheath is preferable. You're using typically 014, occasionally 018 wires

with balloon diameters 2.3 to three millimeters most common and long balloon lengths as these patients harbor long and tandem stenoses. Here's an example of a patient with intractable hand pain. Initial angiogram both radial and ulnar artery occlusions. We've gone down and wired the radial artery,

performed a long segment angioplasty, done the same to the ulnar artery, and then in doing so reestablished in-line flow with relief of this patient's hand pain. Here's a patient with a non-healing index finger ulcer that's already had

the distal phalanx resected and is going to lose the rest of the finger, so we've gone in via a brachial approach here and with long segment angioplasty to the radial ulnar arteries, we've obtained this flow to the hand

and preserved the digit. Another patient, a diabetic, middle finger ulcer. I think you're getting the theme here. Wiring the vessels distally, long segment radial and ulnar artery angioplasty, and reestablishing an in-line flow to the hand.

Just by way of an extreme example, here's a patient with a vascular malformation with a chronically occluded radial artery at its origin, but a distal, just proximal to the palmar arch distal radial artery reconstitution, so that served as a target for us to come in

as we could not engage the proximal radial artery, so in this patient we're able to come in from a retrograde direction and use the dedicated reentry device to gain reentry and reestablish in-line flow to this patient with intractable hand pain and digit ulcer from the loss of in-line flow to the hand.

And this patient now, two years out, remains patent. Our outcomes at the University of Pennsylvania, typically these have been steal symptoms and/or ulceration and high rates of technical success. Clinical success, 70% with long rates of primary patency comparing very favorably

to the relatively sparse literature in this area. In summary, endovascular therapy can achieve high rates of technical, more importantly, clinical success with low rates of major complications, durable primary patency, and wound healing achieved in the majority of these patients.

Thank you.

- I think by definition this whole session today has been about challenging vascular access cases. Here's my disclosures. I went into vascular surgery, I think I made the decision when I was either a fourth year medical student or early on in internship because

what intrigued me the most was that it seemed like vascular surgeons were only limited by their imagination in what we could do to help our patients and I think these access challenges are perfect examples of this. There's going to be a couple talks coming up

about central vein occlusion so I won't be really touching on that. I just have a couple of examples of what I consider challenging cases. So where do the challenges exist? Well, first, in creating an access,

we may have a challenge in trying to figure out what's going to be the best new access for a patient who's not ever had one. Then we are frequently faced with challenges of re-establishing an AV fistula or an AV graft for a patient.

This may be for someone who's had a complication requiring removal of their access, or the patient who was fortunate to get a transplant but then ended up with a transplant rejection and now you need to re-establish access. There's definitely a lot of clinical challenges

maintaining access: Treating anastomotic lesions, cannulation zone lesions, and venous outflow pathology. And we just heard a nice presentation about some of the complications of bleeding, infection, and ischemia. So I'll just start with a case of a patient

who needed to establish access. So this is a 37-year-old African-American female. She's got oxygen-dependent COPD and she's still smoking. Her BMI is 37, she's left handed, she has diabetes, and she has lupus. Her access to date - now she's been on hemodialysis

for six months, all through multiple tunneled catheters that have been repeatedly having to be removed for infection and she was actually transferred from one of our more rural hospitals into town because she had a infected tunneled dialysis catheter in her femoral region.

She had been deemed a very poor candidate for an AV fistula or AV graft because of small veins. So the challenges - she is morbidly obese, she needs immediate access, and she has suboptimal anatomy. So our plan, again, she's left handed. We decided to do a right upper extremity graft

but the plan was to first explore her axillary vein and do a venogram. So in doing that, we explored her axillary vein, did a venogram, and you can see she's got fairly extensive central vein disease already. Now, she had had multiple catheters.

So this is a venogram through a 5-French sheath in the brachial vein in the axilla, showing a diffusely diseased central vein. So at this point, the decision was made to go ahead and angioplasty the vein with a 9-millimeter balloon through a 9-French sheath.

And we got a pretty reasonable result to create venous outflow for our planned graft. You can see in the image there, for my venous outflow I've placed a Gore Hybrid graft and extended that with a Viabahn to help support the central vein disease. And now to try and get rid of her catheters,

we went ahead and did a tapered 4-7 Acuseal graft connected to the brachial artery in the axilla. And we chose the taper mostly because, as you can see, she has a pretty small high brachial artery in her axilla. And then we connected the Acuseal graft to the other end of the Gore Hybrid graft,

so at least in the cannulation zone we have an immediate cannualation graft. And this is the venous limb of the graft connected into the Gore hybrid graft, which then communicates directly into the axillary vein and brachiocephalic vein.

So we were able to establish a graft for this patient that could be used immediately, get rid of her tunneled catheter. Again, the challenges were she's morbidly obese, she needs immediate access, and she has suboptimal anatomy, and the solution was a right upper arm loop AV graft

with an early cannulation segment to immediately get rid of her tunneled catheter. Then we used the Gore Hybrid graft with the 9-millimeter nitinol-reinforced segment to help deal with the preexisting venous outflow disease that she had, and we were able to keep this patient

free of a catheter with a functioning access for about 13 months. So here's another case. This is in a steal patient, so I think it's incredibly important that every patient that presents with access-induced ischemia to have a complete angiogram

of the extremity to make sure they don't have occult inflow disease, which we occasionally see. So this patient had a functioning upper arm graft and developed pretty severe ischemic pain in her hand. So you can see, here's the graft, venous outflow, and she actually has,

for the steal patients we see, she actually had pretty decent flow down her brachial artery and radial and ulnar artery even into the hand, even with the graft patent, which is usually not the case. In fact, we really challenged the diagnosis of ischemia for quite some time, but the pressures that she had,

her digital-brachial index was less than 0.5. So we went ahead and did a drill. We've tried to eliminate the morbidity of the drill bit - so we now do 100% of our drills when we're going to use saphenous vein with endoscopic vein harvest, which it's basically an outpatient procedure now,

and we've had very good success. And here you can see the completion angiogram and just the difference in her hand perfusion. And then the final case, this is a patient that got an AV graft created at the access center by an interventional nephrologist,

and in the ensuing seven months was treated seven different times for problems, showed up at my office with a cold blue hand. When we duplexed her, we couldn't see any flow beyond the AV graft anastomosis. So I chose to do a transfemoral arteriogram

and what you can see here, she's got a completely dissected subclavian axillary artery, and this goes all the way into her arterial anastomosis. So this is all completely dissected from one of her interventions at the access center. And this is the kind of case that reminded me

of one of my mentors, Roger Gregory. He used to say, "I don't wan "I just want out of the trap." So what we ended up doing was, I actually couldn't get into the true lumen from antegrade, so I retrograde accessed

her brachial artery and was able to just re-establish flow all the way down. I ended up intentionally covering the entry into her AV graft to get that out of the circuit and just recover her hand, and she's actually been catheter-dependent ever since

because she really didn't want to take any more chances. Thank you very much.

- 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.

- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.

The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,

however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,

defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought

to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.

I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have

right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.

This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,

small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have

SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented

five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.

The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by

a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of

atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for

inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries

are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. 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.

- Good morning. I'd like to thank everybody who's in attendance for the 7 A.M. session. So let's talk about a case. 63 year old male, standard risk factors for aneurismal disease. November 2008, he had a 52 mm aneurism,

underwent Gore Excluder, endovascular pair. Follow up over the next five, relatively unremarkable. Sac regression 47 mm no leak. June 2017, he was lost for follow up, but came back to see us. Duplex imaging CTA was done to show the sac had increased

from 47 to 62 in a type 2 endoleak was present. In August of that year, he underwent right common iliac cuff placement for what appeared to be a type 1b endoleak. September, CT scan showed the sac was stable at 66 and no leak was present. In March, six months after that, scan once again

showed the sac was there but a little bit larger, and a type two endoleak was once again present. He underwent intervention. This side access on the left embolization of the internal iliac, and a left iliac limb extension. Shortly thereafter,

contacted his PCP at three weeks of weakness, fatigue, some lethargy. September, he had some gluteal inguinal pain, chills, weakness, and fatigue. And then October, came back to see us. Similar symptoms, white count of 12, and a CT scan

was done and here where you can appreciate is, clearly there's air within the sac and a large anterior cell with fluid collections, blood cultures are negative at that time. He shortly thereafter went a 2 stage procedure, Extra-anatomic bypass, explant of the EVAR,

there purulent fluid within the sac, not surprising. Gram positive rods, and the culture came out Cutibacterium Acnes. So what is it we know about this case? Well, EVAR clearly is preferred treatment for aneurism repair, indications for use h

however, mid-term reports still show a significant need for secondary interventions for leaks, migrations, and rupture. Giles looked at a Medicare beneficiaries and clearly noted, or at least evaluated the effect of re-interventions

and readmissions after EVAR and open and noted that survival was negatively impacted by readmissions and re-interventions, and I think this was one of those situations that we're dealing with today. EVAR infections and secondary interventions.

Fortunately infections relatively infrequent. Isolated case reports have been pooled into multi-institutional cohorts. We know about a third of these infections are related to aortoenteric fistula, Bacteremia and direct seeding are more often not the underlying source.

And what we can roughly appreciate is that at somewhere between 14 and 38% of these may be related to secondary catheter based interventions. There's some data out there, Matt Smeed's published 2016, 180 EVARs, multi-center study, the timing of the infection presumably or symptomatic onset

was 22 months and 14% or greater had secondary endointerventions with a relatively high mortality. Similarly, the study coming out of Italy, 26 cases, meantime of diagnosis of the infection is 20 months, and that 34.6% of these cases underwent secondary endovascular intervention.

Once again, a relatively high mortality at 38.4%. Study out of France, 11 institutions, 33 infective endographs, time of onset of symptoms 414 days, 30% of these individuals had undergone secondary interventions. In our own clinical experience of Pittsburgh,

we looked at our explants. There were 13 down for infection, and of those nine had multiple secondary interventions which was 69%, a little bit of an outlier compared to the other studies. Once again, a relatively high mortality at one year. There's now a plethora of information in the literature

stating that secondary interventions may be a source for Bacteremia in seeding of your endovascular graft. And I think beyond just a secondary interventions, we know there's a wide range of risk factors. Perioperative contamination, break down in your sterile technique,

working in the radiology suite as opposed to the operating room. Wound complications to the access site. Hematogenous seeding, whether it's from UTIs, catheter related, or secondary interventions are possible.

Graft erosion, and then impaired immunity as well. So what I can tell you today, I think there is an association without question from secondary interventions and aortic endograft infection. Certainly the case I presented appears to show causation but there's not enough evidence to fully correlate the two.

So in summary, endograft infections are rare fortunately. However, the incidence does appear to be subtly rising. Secondary interventions following EVAR appear to be a risk factor for graft infection. Graft infections are associated without question

a high morbidity and mortality. I think it's of the utmost importance to maintain sterile technique, administer prophylactic antibiotics for all secondary endovascular catheter based interventions. Thank you.

- 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 so much for the opportunity to present our experience. You are all familiar in this place with the SVS classification for blunt aortic injury, and you all know that it doesn't tell you what to do with each patient,

it doesn't guide treatment. A few years ago we presented a simple, practical grading system based on CAT scan findings for the management of these patients. When a patient has a minimal aortic injury, it's a patient with no aortic contour abnormality,

they have either an intimal flap or a small thrombus less than 10 mm. These patients we don't do any interventions. Patient's that present with an aortic contour abnormality or a large intimal flap or large thrombus have a moderate injury.

These patients get repair in a semi-elective manner once they have stabilized further injuries. One the other hand, persons that present with a severe injury, persons with active extravasation, this patient need to go to the OR because he's dying

and this takes precedence above any other injuries. So, since we implemented this system we took a three years look from 2014 to 2017 to see how are our results. We have 87 patients, 63 percent were moderate, 28 percent minimal, and nine percent severe.

None of the patients underwent open repair, and none of the patients with a minimal got fix. All but three of the patients with a moderate, and all but one of the patients with a severe have TEVAR as a repair method. These are very sick patients, high in the severity scores,

with high rates of intracranial hemorrhages and associated injuries. When we look at the anatomy, the patient with a severe injury are more likely to have a bovine arch anatomy. These are young patients with small aortas,

with a median aortic diameter of 23. The operative timing is the time since the patient hit the door of the emergency room to the patient getting to the OR, was 53 hours for a patient with a moderate injury, and three hours for a patient with a severe.

These are short procedures that can be done in less than 90 minutes with minimal contrast used, and around five minutes of fluoro time. We used intravascular ultrasound very widely. We have covered the subclavian artery

in around 40 percent of the patients. We do all this percutaneously. We are successful in around 86 percent of the cases. We have not had to revascularize any subclavian artery. We had one patient that required a plaque during the index case of the subclavian,

one patient that had a femoral pseudoaneurysm that we treated with thrombin, one patient that was already on a heparin drip for a PE. We took her to the OR more than 24 hours after the heparin drip was started, fixed the TEVAR.

After that the patient had a complete normal CAT scan. More than 12 hours after the heparin drip being restarted for the PE she had a worsening intracranial bleed. We don't know that was related to our procedure. We have no patient with new stroke

or worsening spinal cord injury for the procedure. 30-day followup CT scan had excellent remodeling in every single patient. We have not performed any delay interventions. Our 30-day mortality is very low. There is only one patient with an aortic-related mortality.

This is a patient that presented with a severe injury. She was more than 90 years old and the family elected to don't proceed with any treatment. So in conclusions, we consider the patients with minimal aortic injury do not require surgical treatment or followup imaging.

Patient with a moderate can be safely undergo TEVAR in a semi-elective manner once they are stable from other injuries, but the patient with a severe aortic injury require emergent repair. These procedures are very fast

and can be successfully performed percutaneously. Complications are rare, and the followup reveal excellent remodeling of the aorta that will likely result in longer interval surveillance requirements. Thank you.

- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,

complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought

to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.

So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.

And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.

So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.

So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,

unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.

So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.

So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,

it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected

part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,

because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way

otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta

and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,

the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,

we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,

then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,

'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.

And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series

you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down

you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy

and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm

with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.

Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,

12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,

most of those were in the early experience. Thank you.

- Thank you 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 for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want

in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis

is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied

and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple

aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention

adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,

the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that

there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions

a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.

In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure

with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle

and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis

needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.

Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.

In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,

regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate

without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.

An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis

and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.

This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more

in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.

But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.

The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.

Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion

because I have a flight in a few hours. Thank you very much.

- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old

but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,

and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.

- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,

and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was

revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.

In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat

was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.

Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone

returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.

Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy

with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,

the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.

Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.

So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really

how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017

in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.

Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at

five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery

to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional

independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.

So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,

but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could

help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you 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.

- 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

- I'd like to thank Larry and John for the opportunity to speak today. This really is kind of an exciting time in Vascular Access 'cause you know this whole session's devoted to all the new tools and technologies, and they're really a lot of different options

that are available to us now to create functioning fistulas in patients. Those are my disclosures. I just want to mention one thing, when I was asked to give this talk, the name of the device was the Everlink device then,

and that was first developed by TBA Medical at Austin, Texas. Eventually the company was bought by Bard, and then Beckett Dickinson bought Bard, and then they changed the name of the device to the WaveLinq device,

just so that we're all on the same page here. The basic gyst of this system basically it's a two-catheter system, it involves punctures in the brachial artery and brachial vein above the elbow over wires, the catheters are then aligned

in the ulnar artery and ulnar vein. The venous catheter has an RF electrode on it, the arterial component has a ceramic foot plate, and there's rare earth magnets in the catheters that help them align in the artery and vein. They'll coapt, you deploy the foot plate,

and then you fire the RF energy from the RF generator, and the RF energy then creates a four millimeter hole between the artery and vein. This is just what it looks like under fluoroscopy, this is the arterial catheter going in here's the footplate here

this is the venous catheter then being directed and you can see the magnets on these they look like Lincoln Logs they'll kind of line up. You rotate the catheters 'til the foot plate aligns, you do some flyovers with the II make sure everything's lined up,

and then you create the fistula with the RF energy. Then this is just what Fistulagram looks like once the fistula's created. At the completion of that, for this device we then place coils, occluding coils, in the deep vein which was just beyond the sheath

where we accessed the brachial vein. And by putting those plugs in there, coils in there, It helps to direct the flow up to through the superficial veins which we cannulated for dialysis, and much like the other device

that Dr. Malia was talking before, this creates essentially a split vein fistula, it's going to mature both the cephalic and basilic if those veins are available through that from the perforator coming on out. This is just what it looks like you know,

this was in some early studies in the animal model, you can see that it creates exactly a four millimeter hole between the artery and vein. Eventually this will re-endothelialize they had endothelialization at 30 days. So really the nice thing about it is

it standardizes the size of the arteriotomy because it makes exactly a four millimeter fistula. Now, as I mention this is created at the level of the ulnar artery and ulnar vein, so the requirements basically to do this you need a adequate size obviously ulnar artery and vein,

but the big component is to have that adequate perforator vein that's going to help feed the superficial veins to mature that fistula. And then it's just creating a side to side fistula between the ulnar artery and vein.

This is just a composite of all the data that's been collected on the device so far so this is what the global registry looks like. The FLEX study was kind of the first studies in man. The NEAT trial was run in the Canada and the UK, that was one of the earlier trials.

Then there's a post-market registry, uh, in Europe that's being run now. The EASE trial is the trial with the Four French device and I'll share a little bit about that at one of the slides at the end. But basically pull all the data from this

there's almost 157 patients that they collected data on. And, you can see that with this the primary patency, or the primary patency's on at 75 percent, and the accumulative patency's almost 80 percent, and then the number of fistulas that were cannulated at six months successfully with two needles was 75 percent.

If you look at some of the interventions that've had to be done it really seems to be a lower number of interventions that have to be done to get a mature functioning fistula, uh, using this device. I just want to point out a couple things on this slide,

there was never any requirement for angioplasty at the uh, the ulnar artery the ulnar vein anastomosis, and there was, you know, with these embolizations that were performed, 12 of these were performed on patients prior to incorporating that into the procedure itself,

so right now in the IFU it says that the deep veins should be coiled to help direct that flow up into the superficial veins. Now as, uh, was alluded to earlier with the Ellipsys device this kind of falls somewhere between, uh, the radiocephalic fistula and a brachiocephalic fistula,

and again comparing these two devices basically you're creating, this is the Ellipsys device is radial-radial, and this device is really ulnar-ulnar, but again you're creating that split-flow fistula it's going to allow flow both up

into the basilic and cephalic veins. So, where can this be used? It can be used for primary access creation so that's the first option to provide a patient with a functioning fistula. It can be a secondary option to radiocephalic fistula,

or those that have failed the radiocephalic fistula, and it also is an alternative to surgery so there are patients that may not want to have open surgery to have a fistula created, and this obviously provides an option for those patients. In the UK now they're using it to condition veins,

so they'll create the fistula hoping to condition the cephalic and basilic veins to allow them to become usable for dialysis, and they're also using it in patients that have no superficial veins actually using it to mature the brachial vein

or the deeper veins, uh, and then superficializing the brachial vein to create a native fistula for patients who don't have adequate superficial veins. Now I mentioned the Four French device and what the Four French device allows is basically access

from a lot of different points. So now because it's a smaller device, we can place it, if the vein and artery are large enough, it can be placed at the wrists, so radial-radial fistula, so you come in from the wrist, put both catheters up, create the fistula at the radial-radial,

you can do it from the ulnar-ulnar, so it's just two catheters up from the wrist. And these cases are nice, the other option is you can come arterial from the wrist and you can come from the vein at the top, match up the catheters in a parallel

and create that fistula at the ulnar-ulnar level. And the nice thing about this is it really makes managing the puncture very easy you just put a TR band on 'em, and then you're good to go. So it really kind of opens up a lot of different options for creating fistulas.

So in summary this device seems to create a functional fistula without the need for open surgery. It has very good primary and cumulative patencies and seems to take fewer interventions to maintain and mature the functioning fistula, and this may add another tool that we have to create

functioning fistulas in patients who are on dialysis. So 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.

- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop

and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about

the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,

the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience

in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come

from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which

they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.

So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.

Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.

Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.

But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap

and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.

When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.

If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis

of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft

or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at

how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure

they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE

as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition

a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use

the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with

a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.

Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned

even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,

well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.

If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula

but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.

Prevention is vital and educating our patients and dialysis centers is key. Thank you.

- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.

Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance

between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.

Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.

Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100

consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any

stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria

having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this

on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher

than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of

the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,

you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because

the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity

because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish

this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,

regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. Thank you very much.

- 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.

- Thanks (mumbles) I have no disclosures. So when were talking about treating thoracoabdominal aortic aneurysms in patients with chronic aortic dissections, these are some of the most difficult patients to treat. I thought it would be interesting

to just show you a case that we did. This is a patient, you can see the CT scrolling through, Type B dissection starts pretty much at the left subclavian, aneurysmal. It's extensive dissection that involves the thoracic aorta, abdominal aorta,

basically goes down to the iliac arteries. You can see the celiac, SMA, renals at least partially coming off the true and continues all the way down. It's just an M2S reconstruction. You can see again the extent of this disease and what makes this so difficult in that it extends

from the entire aorta, up proximally and distally. So what we do for this patient, we did a left carotid subclavian bypass, a left external to internal iliac artery bypass. We use a bunch of thoracic stent grafts and extended that distally.

You can see we tapered down more distally. We used an EVAR device to come from below. And then a bunch of parallel grafts to perfuse our renals and SMA. I think a couple take-home messages from this is that clearly you want to preserve the branches

up in the arch. The internal iliac arteries are, I think, very critical for perfusing the spinal cord, especially when you are going to cover this much. And when you are dealing with these dissections, you have to realize that the true lumens

can become quite small and sometimes you have to accommodate for that by using smaller thoracic endografts. So this is just what it looks like in completion. You can see how much metal we have in here. It's a full metal jacket of the aorta, oops.

We, uh, it's not advancing. Oops, is it 'cause I'm pressing in it or? All right, here we go. And then two years post-op, two years post-op, you can see what this looks like. The false lumen is completely thrombosed and excluded.

You can see the parallel grafts are all open. The aneurysm sac is regressing and this patient was successfully treated. So what are some of the tips and tricks of doing these types of procedures. Well we like to come in from the axillary artery.

We don't perform any conduits. We just stick the axillary artery separately in an offset manner and place purse-string sutures. You have to be weary of manipulating around the aortic arch, especially if its a more difficult arch, as well as any thoracic aortic tortuosity.

Cannulating of vessels, SMA is usually pretty easy, as you heard earlier. The renals and celiac can be more difficult, depending upon the angles, how they come off, and the projection. You want to make sure you maintain a stiff wire,

when you do get into these vessels. Using a Coda balloon can be helpful, as sometimes when you're coming from above, the wires and catheters will want to reflux into that infrarenal aorta. And the Coda balloon can help bounce that up.

What we do in situations where the Coda doesn't work is we will come in from below and a place a small balloon in the distal renal artery to pin the catheters, wires and then be able to get the stents in subsequently. In terms of the celiac artery,

if you're going to stent it, you want to make sure, your wire is in the common hepatic artery, so you don't exclude that by accident. I find that it is just simpler to cover, if the collaterals are intact. If there is a patent GDA on CT scan,

we will almost always cover it. You can see here that robust collateral pathway through the GDA. One thing to be aware of is that you are going to, if you're not going to revascularize the celiac artery you may need to embolize it.

If its, if the endograft is not going to oppose the origin of the celiac artery in the aorta because its aneurysmal in that segment. In terms of the snorkel extent, you want to make sure, you get enough distal purchase. This is a patient intra-procedurally.

We didn't get far enough and it pulled out and you can see we're perfusing the sac. It's critical that the snorkel or parallel grafts extend above the most proximal extent of your aortic endograft or going to go down. And so we take a lot of care looking at high resolution

pictures to make sure that our snorkel and parallel grafts are above the aortic endograft. This is just a patient just about a year or two out. You can see that the SMA stent is pulling out into the sac. She developed a endoleak from the SMA,

so we had to come in and re-extend it more distally. Just some other things I mentioned a little earlier, you want to consider true lumen space preserve the internals, and then need to sandwich technique to shorten the parallel grafts. Looking at a little bit of literature,

you can see this is the PERCLES Registry. There is a number of type four thoracos that are performed here with good results. This is a paper looking at parallel grafting and 31 thoracoabdominal repairs. And you can see freedom from endoleaks,

chimney graft patency, as well as survival is excellent. This was one looking purely at thoracoabdominal aneurysm repairs. There are 32 altogether and the success rates and results were good as well. And this was one looking at ruptures,

where they found that there was a mean 20% sac shrinkage rate and all endografts remained patent. So conclusion I think that these are quite difficult to do, but with good techniques, they can be done successfully. Thank you.

- 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.

- Thank you. Thank you again for the invitation, and also my talk concerns the use of new Terumo Aortic stent graft for the arch. And it's the experience of three different countries in Europe. There's no disclosure for this topic.

Just to remind what we have seen, that there is some complication after surgery, with mortality and the stroke rate relatively high. So we try to find some solution. We have seen that we have different options, it could be debranching, but also

we know that there are some complications with this technique, with the type A aortic dissection by retrograde way. And also there's a way popular now, frozen elephant trunk. And you can see on the slide the principle.

But all the patients are not fit for this type of surgery. So different techniques have been developed for endovascular options. And we have seen before the principle of Terumo arch branch endograft.

One of the main advantages is a large window to put the branches in the different carotid and brachiocephalic trunk. And one of the benefit is small, so off-the-shelf technique, with one size for the branch and different size

for the different carotids. This is a more recent experience, it's concerning 15 patients. And you can see the right column that it is. All the patients was considered unfit for conventional surgery.

If we look about more into these for indication, we can see four cases was for zone one, seven cases for zone two, and also four cases for zone three. You can see that the diameter of the ascending aorta, the min is 38,

and for the innominate artery was 15, and then for left carotid was eight. This is one example of what we can obtain with this type of handling of the arch with a complete exclusion of the lesion, and we exclude the left sonography by plyf.

This is another, more complex lesion. It's actually a dissection and the placement of a stent graft in this area. So what are the outcomes of patients? We don't have mortality, one case of hospital mortality.

We don't have any, sorry, we have one stroke, and we can see the different deaths during the follow-up. If we look about the endoleaks, we have one case of type three endoleak started by endovascular technique,

and we have late endoleaks with type one endoleaks. In this situation, it could be very difficult to treat the patient. This is the example of what we can observe at six months with no endoleak and with complete exclusion of the lesion.

But we have seen at one year with some proximal type one endoleak. In this situation, it could be very difficult to exclude this lesion. We cannot propose this for this patient for conventional surgery, so we tried

to find some option. First of all, we tried to fix the other prosthesis to the aortic wall by adjusted technique with a screw, and we can see the fixation of the graft. And later, we go through the,

an arrangement inside the sac, and we put a lot of colors inside so we can see the final results with complete exclusion. So to conclude, I think that this technique is very useful and we can have good success with this option, and there's a very low

rate of disabling stroke and endoleaks. But, of course, we need more information, more data. Thank you very much for your attention.

- 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.

- Thank you for the opportunity to present this arch device. This is a two module arch device. The main model comes from the innominated to the descending thoracic aorta and has a large fenestration for the ascending model that is fixed with hooks and three centimeters overlapping with the main one.

The beginning fenestration for the left carotid artery was projected but was abandoned for technical issue. The delivery system is precurved, preshaped and this allows an easy positioning of the graft that runs on a through-and-through wire from the

brachial to the femoral axis and you see here how the graft, the main model is deployed with the blood that supported the supraortic vessels. The ascending model is deployed after under rapid pacing.

And this is the compilation angiogram. This is a case from our experience is 6.6 centimeters arch and descending aneurysm. This is the planning we had with the Gore Tag. at the bottom of the implantation and these are the measures.

The plan was a two-stage procedure. First the hemiarch the branching, and then the endovascular procedure. Here the main measure for the graph, the BCT origin, 21 millimeters, the BCT bifurcation, 20 millimeters,

length, 30 millimeters, and the distal landing zone was 35 millimeters. And these are the measures that we choose, because this is supposed to be an off-the-shelf device. Then the measure for the ascending, distal ascending, 35 millimeters,

proximal ascending, 36, length of the outer curve of 9 centimeters, on the inner curve of 5 centimeters, and the ascending model is precurved and we choose a length between the two I cited before. This is the implantation of the graft you see,

the graft in the BCT. Here, the angiography to visualize the bifurcation of the BCT, and the release of the first part of the graft in the BCT. Then the angiography to check the position. And the release of the graft by pushing the graft

to well open the fenestration for the ascending and the ascending model that is released under cardiac pacing. After the orientation of the beat marker. And finally, a kissing angioplasty and this is the completion and geography.

Generally we perform a percutaneous access at auxiliary level and we close it with a progolide checking the closure with sheet that comes from the groin to verify the good occlusion of the auxiliary artery. And this is the completion, the CT post-operative.

Okay. Seven arch aneurysm patients. These are the co-morbidities. We had only one minor stroke in the only patient we treated with the fenestration for the left carotid and symptomology regressed completely.

In the global study, we had 46 implantations, 37 single branch device in the BCT, 18 in the first in men, 19 compassionate. These are the co-morbidities and indications for treatment. All the procedures were successful.

All the patients survived the procedure. 10 patients had a periscope performed to perfuse the left auxiliary artery after a carotid to subclavian bypass instead of a hemiarch, the branching. The mean follow up for 25 patients is now 12 months.

Good technical success and patency. We had two cases of aneurysmal growth and nine re-interventions, mainly for type II and the leak for the LSA and from gutters. The capilomiar shows a survival of 88% at three years.

There were three non-disabling stroke and one major stroke during follow up, and three patients died for unrelated reasons. The re-intervention were mainly due to endo leak, so the first experience was quite good in our experience and thanks a lot.

- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed

is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome

is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement

and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.

So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.

We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy

which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures

that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.

As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.

So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,

and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.

So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.

It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,

'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula

and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.

It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically

a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.

Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal

vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.

Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding

the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody

who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test

confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,

so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,

although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.

It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get

a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.

And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,

immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.

We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.

So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,

and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.

DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,

when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.

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