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Vasospastic Syndrome, Reynaud's | Calcium-channel Blockers | 72 | Female
Vasospastic Syndrome, Reynaud's | Calcium-channel Blockers | 72 | Female
With Complex AAAs, How To Make Decisions Re Fenestrations vs. Branches: Which Bridging Branch Endografts Are Best
With Complex AAAs, How To Make Decisions Re Fenestrations vs. Branches: Which Bridging Branch Endografts Are Best
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NaHCO3 Plus Hydration Decreases Acute Kidney Failure After EVAR: Based On A Pilot RCT (The HYDRA Trial) Comparing It To Hydration Alone: Why Is It Different From Other Negative NaHCO3 RCTs
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How To Treat By EVAR Complex Aorto-Iliac AAAs In Patients With Renal Transplants, Horseshoe Or Pelvic Kidneys: Technical Tips
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Status Of Aortic Endografts For Occlusive Disease: Indications, Precautions, Technical Tips And Value
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Cloud Based System For Image Fusion Techniques With Mobile C-Arms (The Cydar System): How Does It Work And Advantages For All Vascular Interventions
Cloud Based System For Image Fusion Techniques With Mobile C-Arms (The Cydar System): How Does It Work And Advantages For All Vascular Interventions
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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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anastomosisangiogrambailbypasscarotidCarotid bypassCEACFAdurableembolicendarterectomygoregrafthybridHybrid vascular graftinsertedlesionnitinolpatencypatientperioperativeproximalPTAptferestenosisstenosistechniquetransmuralvascular graft
With Large Iliac Arteries, When Are Flared Limbs Acceptable And When Are IBDs Needed For Good Results
With Large Iliac Arteries, When Are Flared Limbs Acceptable And When Are IBDs Needed For Good Results
Anaconda / Cook / Gore / Medtronicanatomicalaneurysmarterycommoncommon iliaccomplicationcomplicationscontrastdevicesembolizationendograftendovascularevarFL DeviceflaredIBD (Gore-IBE) / IBD (Cook-ZBIS)iliaciliac arteryimplantedinterventionallatelimbsliteratureobservationaloutcomeperioperativesuboptimaltechnicallytherapeuticurokinase
Overview Of Sclerotherapy Liquid Embolic Agents: A World In Endovascular Confusion And Chaos
Overview Of Sclerotherapy Liquid Embolic Agents: A World In Endovascular Confusion And Chaos
How Best To Treat Pediatric Vascular Injuries
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DEBATE: Not So: Why Open Bypass First Is Best In Some CLTI Patients: Which Ones: What Percent Of CLTI Patients Will Require An Open Procedure At Some Point In Their Course
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Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
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cardiologistscarotidCASCEAcomplicationembolizationsendarterectomyincisioninterventioninterventionalinterventionalistmyocardialourielpatientsrangerevascularizationrobustsurgeonsurgeonsTCARTherapeutic / Diagnostictransfemoralvascular
Why A Reinvigoration Of CAS Is Justified By Better Embolic Protection And Newer Mesh Covered Stents; OCT Proves It
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carotidcarotid stentCASCEAcerebraldemonstratedembolicendovascularincidenceinteractionmicroembolicplaqueprotectionproximalRoadSaverstentstentingstrengthsTerumo interventional systemstherapeuticunprotected
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Right Axillary Access For Complex EVARs And TEVARs: Advantages, Technical Tips And Preventing Strokes
accessaorticarcharteryaxillaryCHEVARchimneydevicesendovascularextremityfenestratedFEVARFEVARChminimizemortalitypatientRt Axillary Artery ConduitsheathsheathsstrokesutureTEVARvisceralzone
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amputationarterycommoncommon femoralembolizationendarterectomyendovascularfemoralfemoral arteryhematomaInterventionsmehtamorbiditymortalitypatencypatientsperioperativeprimaryrestenosisrevascularizationrotationalstentstentingstentssuperficialsurgicalsurvivalTECCO
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abdominalangiogramarterialatrialbowelcolectomycoloniccomplicationsdiseasedyslipidemiaetiologyextremityfibrinolyticheparinincidenceincreaseinflammatoryinpatientinpatientsischemicIV HeparinmedicalocclusionoccurringpatientsprophylaxispulmonaryresectionrevascularizationriskRt PE / Rt Pulm Vein thrombosis / Lt Atrial thrombosissidedSMA thrombectomysubtotalsystemicthrombectomythrombosisthrombotictransverseulcerativeunderwentveinvenousvisceral
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accessAscending Aortic Repair - Suture line DehiscenceaugmentbasicallyDirect Percutaneous Puncture - Percutaneous EmbolizationembolizationembolizefusionguidancehybridimagingincisionlaserlocalizationlungmodalitypatientscannedscannerTherapeutic / Diagnostictraumavascular
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anesthesiaanterioranticoagulationarterybifurcationbladecarotidclopidogrelcranialendarterectomyincisionincisionsinternalinternal carotidinterventionalischemicmicenervepatientspediatricplaquepreoperativeproximalproximallystandardstentingtransversetypicallyVeith
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anastomosisarterialbasiliccomparablecomparedcumulativedatafavoredFistulafistulasgraftsjournalmaturationOne & Two Stage procedurespatenciespatencyprimaryrangeratesstagestagedstratifiedSuperficializationsuperiorTrans-positiontransectiontransposedtranspositiontunnelingvascularveinveinsversus
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ambulationantegradearteryassessingcalcifiedCardival Medicalcathcath labCelt ACD (Vasorum) - Vascular Closure DeviceclosurecollagencomplicationcomplicationscompressionconsconsecutivedeploymentdevicedevicesdiscembolizationfemoralhemostasismanualminorminutespatientsprosrandomizedrequiringretrogradestainlesssurgicaltherapeutictimetrialVascade VCDvascularVascular Closure Deviceversusvisualize
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How about the next example. Let me show you another example. This is a 72 year old lady. She's a licensed nurse with us, and she has a one week history of

bilateral lower extremity leg pain. I saw her and I saw these toes and I was like, wow, this is amazing. Initially when I was examining her, she had normal femoral pulses, normal popliteal, normal DP,

normal PT. She had on her physical exam, her cardiac exam was regular rate and rhythm. There were no murmurs and there was no evidence of an embolic source per say.

She was hypertensive and she was a very good historian and she tells me that this started about a week ago, we were in the middle of -40. Heaven forbid we had -40 I was waiting for ISET to start. >> Is that June?

>> This was right around ISET. I was like if Jim would move ISET a little bit closer to January we'd be better off. So what are your thoughts? What are you guys thinking? What do you wanna know?

Does anybody wanna pimp me? You wanna see noninvasive arterial studies? I will show you our noninvasive arterial studies, so that's part of our workup. And the ABIs are essentially normal if I would argue they're normal and she's got triphasic signals and I told you my exam.

[BLANK_AUDIO] One of my concerns was did she have an embolization, to me this looked like embolization. Now I'm lucky, in the sense that, when

I get stuck and trust me I get stuck a lot, I can walk down the hallway and ask people for help. And the Vassar/g medicine colleagues of mine are Tom Rook, Rob McMain and many others and so I can ask him. So initially I went through a did she embolize, and so my embolization

protocol is echo and a CTA to see if there's some kind of aortic ulcer or something. So that was all negative. So then I bring her back and talk to her, so I ordered that that in the morning, we get it all done and it's negative.

So when you talk to her you ask her when did this start, dooes she have symptoms or Raynaud's nodes. Turns out she's got symptoms of Raynaud's nodes and this is chronic perennial, which is basically vasospastic disease which occurs in frigid temperatures. And the way you treat this is with calcium blockers.

You tell them to wear warm shoes, warm gloves. You start them on a little bit of nifedipine, which I did. The problem with nifedipine in her is that she's very normotensive, almost 90 over 60.

You give her nifedipine and she bottoms out, she gets headaches and wakes up all groggy. And so what we ended up doing was starting on a low dose nifedipine and over time it allowed her to vasodilate and this all went away. So again highlighting the importance of not every person needs a intervention or even interventional radiologist,

some don't need us. So those are two examples of that. I'm gonna stop there and answer questions. I had more but I wanna be respectful if there's any questions. [BLANK_AUDIO]

From you guys, these guys always have questions for me but I can email them later.

- 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 very much, chairman and ladies and gentlemen. The funding of this trial was from The Academy of Medical Sciences and The Royal College of Surgeons of England. AKI due to the influence EVAR is actually more common than we all think. This is being shown by prospective studies and registries.

Why is it important? Well, it's associated with a higher intra or inter hospital mortality, cardiovascular events and also long term cardiovascular events and longterm mortality. As even more common and complex, EVAR, and this can range from 22% up to 32%.

These are some of our cases, some of our first, including FEN astrate EVAR in 2010 Thoraco-Abdominal Branch repair 2016 and Fen astrated TEVAR 2018. These are longer procedures, usually with more contrast and direct ventilation after removing arteries.

What are the mechanisms for acute kidney injuries due to infer-renal EVAR? While this involves use of contrast, systemic inflammatory response syndrome, due to ischemic re-perfusion injury, manipulation of the thrombus, aorta and catheterizations which will ------ alpha

and also from high prophalinemia. There is no high-quality evidence for AKI prevention in EVAR. What about Sodium Bicarbonate? Well it's been well know to reduce what been used commonly to reduce CIN in high risk patients in perrifical and

corona graphy. There are two main mechanisms as to how this works. Firstly, from reducing renal tubular ischemia. Secondly, by reducing oxygen deprived free radical formation in the tubules. What is the evidence?

Well this is a met analysis, comparing Sodium Bicarbonate directly with hydration with normal saline, as shown in the orange box. There is no difference. We can look at the population ll

mostly CKD patients or diabetic patients, certainly Hartmann's patients but they are not EVAR patients. They are coronary patients or peripheral an-graphy patients. In addition, serum bicarbonate and the urine pH was not reported so we do not know how effective the Bicarbonate was in these RCT's.

The authors went on to look other outcomes including needful hemo dialysis, cardiac events, the mortality and they found no difference but they concluded the strength of this evidence was low and insufficient. A further Meta-analysis this time published in BMJ this time comes in favor of bicarbonate

but again this is comparing bicarbonate with saline no use of combination therapy. There are again no use of EVAR patients and these patients all have a low eGFR. The preserved trial, a large trial published earlier this year in the New England Journal again using various

treatments again comparing sodium bicarbonates and saline again no difference. But again this compares bicarbonate direct with saline with no combination therapies. In addition, there were no EVAR patients, and these are low eGFR patients.

The met-analysis also showed that by using bicarbonates as a bolus dose rather than a continuous infusion, which was actually the way they used bicarbonates in most of these patients might be better. And using a higher dose of bicarbonate may also be better as shown in this Japanese paper.

So we come to HYDRA trial. They're using a high dose bicarbonate in combination with hydration to protect renal function. We did a UK wide survey of anesthetists of day to day and they felt the best volume expander they would like to use was Hartmann's solution.

So we randomized patients between standard hydration with Hartmann's solution verses standard hydration Hartmann's plus high dose bicarbonate per operatively and low slow intravenous infusion bicarbonate during the surgery. Importantly, with these patients,

we kept the map within 80% of baseline, 90% of the time in contrary to all the RCT's coronary and angeo-porphyry. We're going to skip that slide. This is the inclusion criteria, any patient undergoing infra EVAR, with any renal disfunction,

the primary area you must look at is recruitment and the second area you must look at is AKI. We screened 109 patients of which, 58% were randomized and there were only 2 crossovers. There was a willingness for patients to participate and there was also a willingness for PET 4 Clinitions to

recruit as well. This is the demographics, which is typical of aortic patients they are all on by a few MRSA patients, have normal renal function. Most of the patients wear statins and anti pace agent, only 13% were diabetic.

The patients were matched in terms of hypertension and also fluid hydration pre-operatively measures of via impedance. Here are the results of the trial. The AKI instance in the standard hydration group was like 3% and 7.1% with standard hydration plus bicarbonate. And it was similar in terms of organotrophic support into

and postop and also contrast volume used. It's a safe regime with none of the patients suffering as a result of using bicarbonate. So to conclude, to answer professor Veith's question, about how was this trial different to all the other trials? Well, certainly the previous trials have compared

bicarbonate with saline, there's lack of combination studies that involve mostly coronary an peripheral procedures, not EVAR. And the the most only included patient with low eGFR. HYDRA is different, this is not a regime using high dose bolus of sodium bicarb combined with standard hydration.

It shows promise of reducing AKO. This is an EVAR specific pilot RCT. Again, Unlike previous trials using bicarbonate, 90% of the patients had normal or mild impaired renal function. And unlike previous trials, there's more aggressive management of hypertension intra and postoperatively.

Thank you for listening.

- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.

And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,

as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,

presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,

as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.

So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.

Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,

and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.

Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there

in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,

but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,

but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,

but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion

that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer

and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.

And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.

And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,

treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.

And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.

We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat

with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,

and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.

So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.

Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen

and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.

(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.

Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.

And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily

arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,

it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this

florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.

We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation

in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,

which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen

of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.

- [Narrator] Okay, very interesting hypothesis.

- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing

renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is

near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital

pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency

and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,

except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward

endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac

endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.

The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open

conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small

accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited

incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,

but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis

and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

into the cost/benefit ratio. Thank you.

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

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

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

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

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

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

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

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

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

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

- Thank you so much. I have no disclosures. These guidelines were published a year ago and they are open access. You can download the PDF and you can also download the app and the app was launched two months ago

and four of the ESVS guidelines are in that app. As you see, we had three American co-authors of this document, so we have very high expertise that we managed to gather.

Now the ESVS Mesenteric Guidelines have all conditions in one document because it's not always obvious if it's acute, chronic, acute-on-chron if it's arteri

if there's an underlying aneurysm or a dissection. And we thought it a benefit for the clinician to have all in one single document. It's 51 pages, 64 recommendations, more than 300 references and we use the

ESC grading system. As you will understand, it's impossible to describe this document in four minutes but I will give you some highlights regarding one of the chapters, the Acute arterial mesenteric ischaemia chapter.

We have four recommendations on how to diagnose this condition. We found that D-dimer is highly sensitive so that a normal D-dimer value excludes the condition but it's also unfortunately unspecific. There's a common misconception that lactate is

useful in this situation. Lactate becomes elevated very late when the patient is dying. It's not a good test for diagnosing acute mesenteric ischaemia earlier. And this is a strong recommendation against that.

We also ask everyone uses the CTA angiography these days and that is of course the mainstay of diagnoses as you can see on this image. Regarding treatment, we found that in patients with acute mesenteric arterial ischaemia open or endovascular revascularisation

should preferably be done before bowel surgery. This is of course an important strategic recommendation when we work together with general surgeons. We also concluded that completion imaging is important. And this is maybe one of the reasons why endovascular repair tends to do better than

open repair in these patients. There was no other better way of judging the bowel viability than clinical judgment a no-brainer is that these patients need antibiotics and it's also a strong recommendation to do second look laparotomoy.

We found that endovascular treatment is first therapy if you suspect thrombotic occlusion. They had better survival than the open repair, where as in the embolic situation, we found no difference in outcome.

So you can do both open or endo for embolus, like in this 85 year old man from Uppsala where we did a thrombus, or the embolus aspiration. Regarding follow up, we found that it was beneficial to do imaging follow-up after stenting, and also secondary prevention is important.

So in conclusion, ladies and gentlemen, the ESVS Guidelines can be downloaded freely. There are lots of recommendations regarding diagnosis, treatment, and follow-up. And they are most useful when the diagnosis is difficult and when indication for treatment is less obvious.

Please read the other chapters, too and please come to Hamburg next year for the ESVS meeting. Thank You

- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology

to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions

that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,

it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,

as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient

and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy

by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?

Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification

of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,

matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.

You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.

And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.

And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.

Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,

next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages

to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,

so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?

Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization

of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases

of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.

Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging

with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR

to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care

to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,

two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents

using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging

reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,

we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.

And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.

A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,

and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs

and improve clinical outcomes. 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.

- Mr Chairman, dear colleagues. I've nothing to disclose. We know that aneurysm or dilation of the common iliac artery is present in almost 20% of cases submitted to endovascular repair and we have a variety of endovascular solution available. The first one is the internal iliac artery

embolization and coverage which is very technically easy but it's a suboptimal choice due to the higher risk of thrombosis and internal iliac problems. So the flared limbs landing in the common iliac artery is technically easy,

however, the results in the literature are conflicting. Iliac branch devices is a more demanding procedure but has to abide to a specific anatomical conditions and is warranted by good results in the literature such as this work from the group in Perugia who showed a technical success of almost 100%

as you can see, and also good results in other registries. So there are unresolved question about this problem which is the best choice in this matter, flared limbs or iliac branch devices. In order to solve this problem, we have looked at our data,

published them in Journal Vascular Interventional Neurology and this is our retrospective observational study involving treatment with either flared limbs or IBD and these are the flared limbs devices we used in this study. Anaconda, Medtronic, Cook and Gore.

And these are the IFU of the two IBD which were used in this study which were Gore-IBE and Cook-ZBS. So we looked at the 602 EVAR with 105 flared limbs which were also fit for IBD. And on the other side, we looked at EVAR-IBD

implanted in the same period excluding those implanted outside the IFU. So we ended up with 57 cases of IBD inside the IFU. These are the characteristics of the two groups of patients. The main important finding was the year age which was a little younger in the IBD group

and the common iliac artery diameter which was greater, again in the IBD group. So this is the distribution of the four types of flared limbs devices and IBD in the two groups. And as you can see, the procedural time and volume of contrast medium was significantly

higher in the IBD group. Complications did not differ significantly however, overall there were four iliac complication and all occurred in the flared limbs group. When we went to late complications, putting together all the iliac complication, they were significantly

greater in the flared limbs group compared with the IBD with zero percent complication rate. Late complications were always addressed by endovascular relining or relining and urokinase in case of infusion, in case of thrombosis. And as you can see here, the late outcome

did not differ significantly in the two groups. However, when we put together all the iliac complication, the iliac complication free survival was significantly worse in the flared limbs group. So in conclusion, flared limbs and IBD have similar perioperative outcomes.

IBD is more technically demanding, needs more contrast medium and time obviously. The complications in flared limbs are all resolvable by endovascular means and IBD has a better outcome in the long term period. So the take-home message of my presentation

is that we prefer IBD in young patients with high life expectancy and in the presence of anatomical risk factors of flared limbs late complications. Thank you for your attention.

- I just like the title 'cuz I think we're in chaos anyway. Chaos management theory. Alright, unfortunately I have nothing to disclose, it really upsets me. I wish I had a laundry list to give you. Gettin' checks from everybody, it would be great. Let's start off with this chaos, what has been published.

Again "Ul Haq et al" is a paper from Hopkins. Bleomycin foam treatment of malformations, a promising agent. And they had 20 patients, 21 Bleomycin procedures. (mumbles) sclerosants in a few other patients, 40% complication rate, 30% minor, 10% major.

On a per procedure basis it was a 29% with about 7% major. All patients had decrease in symptoms. But to say "I use Bleomycin" or "I use X" because a complication (mumbles) is nonsense, you're mentally masturbating. It ain't going to be that way, you're going to have complications.

Alright, the use of Bleomycin should be reserved for locations where post-procedure swelling would be dangerous. Well they used it, and one patient required intubation for four days and another patient 15 days. So, it can happen with any agent.

So I don't know why that statement was made. "Hassan et al", noninvasive management of hemangiomas and vascular malformations using Bleomycin again, this handles the plastic surgery a few years ago. 71% effectiveness rate, 29% failure rate,

14% complication rate, 5 major ulcerations. Ulcerations happen with any agent. You're not going to escape that by saying, "Oh, well I'm not going to use alcohol because (mumbles)." No you're going to get it anyway. You all in the literature.

"Sainsbury", intra-lesional Bleomycin injection for vascular birthmarks five year experience again, 2011. 82% effectiveness, 17.3 for failure. Compli- severe blistering, ulcers, swelling, infections, recurrences. Okay, everybody's reporting it.

"Bai et al" sclerotherapy for lymphatic, oral and facial region, 2009. 43% effectiveness, but they found if they used it with surgery they had a higher effectiveness rate. Good. But again that's their effectiveness.

"Young et al", Bleomycin A5 cervico-facial vascular surgery, 2011. 81% effectiveness rate 19% failure for macrocystic. 37% failure from microcystic disease. Complications: ulcerations, hematoma, bleeding, fevers, soft tissue atrophy.

"Zhang et al." Now this is a study. They're goin' head-to-head alcohol versus Bleo. Oh, isn't that a nice thing to do. Huh, funny how that can happen sometimes. There's another paper out of Canada

that doesn't matter, there's 17 pages and there's no statistical significance for that. 138 patients, you got a lot of statistics. "Zhang et al", 138 children. 71 of 75 patients, which is 95% of that serie, were either cured,

markedly effective, or effective, with alcohol. In the Bleo group 41 of 63, that is 65% of the patients, had effective treatment. That means no cures, no markedly effective, just effective. That's their head-to-head comparison. Difference between Ethanol and

the Bleo group again was statistically significant. Ethanol at 75 patients of 14 cases skin necrosis. Bleo group at 63 patients of 5 cases skin necrosis. And in that group they stated it is statistically superior to Bleo. 95 versus 60, that's a big deal.

Again, cured, disappearance post-treatment without recurrence. Markedly effective, meant that greater than 80% was ablated. Effective means about less that 80% reduction but improved. Ineffective, no change. That was their criterion on that paper.

Again, 30 cases, superficial VMs effective rate was 95% in the Ethanol group and the deep group 94%. Okay. What was in the Bleo group? 68% superficial, 56% of deep group. So that's a statistical significance

of failure, between the two agents, comparing head-to-head in anatomic areas. Ethanol VM papers, let's go on to that, we're goin' to do other stuff. "Lee et al", advanced management, 2003, midterm results. 399 procedures in 87 patients,

95% significant or complete ablation, 12.4% complication. "Johnson et al", Kansas. University of Kansas med center, 2002. 100% success rate in tongues. One patient had a massive tongue and had breathing difficulties prior to treatment

remained intubated 5 days and then uneventfully discharged, that was their only complication. "Su et al", ethanol sclerotherapy, face and neck. Again, these are complex anatomies with complex issues of cranial nerves as well as airway control. 2010, 56 of 60 procedures, 90%, four minimal residual,

no skin necrosis, no nerve injuries. "Orlando", outpatient percutaneous treatment, low doses under local anesthesia. This is a very interesting paper out of Brazil. They did 'em under IV sedation, just a little bit by little bit.

They said they had trouble gettin' general so they had to figure another way. Smart, I like people thinkin' things out. Who here doesn't have a problem with anesthesia? Gettin' 'em not to quit before two o'clock? (laughs)

Alright, used local only 39 patients extremity VMs, main symptoms of pain. Cure or significant improvement in 94%. One ulcer, 3 transient paresthesias. "Lee et al", sclerotherapy craniofacial again, 2009. 87 patients, 75% were reductions.

71 of 87 excellent outcomes. One patient transient, tongue decreased sensation. One transient facial nerve palsy, no skin injuries. "Vogelzang" is a very important paper of a single center. Is that author- anybody here? Again, they did VMs and AVMs in this series

and then a per patient complication rate is 13.3, in AMVs 9.7 per patient, but I think what also is important is to do things with regards to procedures. And they listed both. So we'll just, it's about time to quit. This is our embolization series.

And neck, upper extremity, all the anatomies. And we're about a 10 to three ratio with regards to VM/LMs to AVMs in numbers. I think everybody's pretty much like that, a third of their practice. Again, our minor complications are that.

Major complications are these. Summary, what we found in the literature is that Ethanol publications state its efficacy rate routinely at 90 to 100%. And all other second tier sclerosants are 60 to 80%. So I think that's the take home message.

Thank you.

- Good afternoon, Dr. Veith, organizer. Thank you very much for the kind invitation. I have nothing to disclose. In the United States, the most common cause of mortality after one year of age is trauma. So, thankfully the pediatric vascular trauma

is only a very small minority, and it happens in less that 1% of all the pediatric traumas. But, when it happens it contributes significantly to the mortality. In most developed countries, the iatrogenic

arterial injuries are the most common type of vascular injuries that you have in non-iatrogenic arterial injuries, however are more common in war zone area. And it's very complex injuries that these children suffer from.

In a recent study that we published using the national trauma data bank, the mortality rate was about 7.9% of the children who suffer from vascular injuries. And the most common mechanism of injury were firearm and motor vehicle accidents. In the US, the most common type of injury is the blunt type

of injury. As far as the risk factors for mortality, you can see some of them that are significantly affecting mortality, but one of them is the mechanism of injury, blunt versus penetrating and the penetrating is the risk factor for

mortality. As far as the anatomical and physiological consideration for treatment, they are very similar to adults. Their injury can cause disruption all the way to a spasm, or obstruction of the vessel and for vasiospasm and minimal disruption, conservative therapy is usually adequate.

Sometimes you can use papevrin or nitroglycerin. Of significant concern in children is traumatic AV fissure that needs to be repaired as soon as possible. For hard signs, when you diagnose these things, of course when there is a bleeding, there is no question that you need to go repair.

When there are no hard signs, especially in the blunt type of injuries, we depend both on physical exams and diagnostic tools. AVI in children is actually not very useful, so instead of that investigators are just using what is called an Injured Extremity Index, which you measure one leg

versus the other, and if there is also less than 0.88 or less than 0.90, depending on the age of the children, is considered abnormal. Pulse Oximetry, the Duplex Ultrasound, CTA are all very helpful. Angiography is actually quite risky in these children,

and should be avoided. Surgical exploration, of course, when it's needed can give very good results. As far as the management, well they are very similar to adults, in the sense that you need to expose the artery, control the bleeding, an then restore circulation to the

end organ. And some of the adjuncts that are using in adult trauma can be useful, such as use of temporary shunts, that you can use a pediatric feeding tube, heparin, if there are no contraindications, liberal use of fasciotomy and in the vascular technique that my partner, Dr. Singh will be

talking about. Perhaps the most common cause of PVI in young children in developed countries are iatrogenic injuries and most of the time they are minimal injuries. But in ECMO cannulation, 20-50% are injuries due to

ECMO have been reported in both femoral or carotid injuries. So, in the centers are they are doing it because of the concern about limb ischemia, as well as cognitive issues. They routinely repair the ECMO cannulation site.

For non-iatrogenic types, if is very common in the children that are above six years of age. Again, you follow the same principal as adult, except that these arteries are severely spastic and interposition graft must accommodate both axial and radial growths of these arteries, as well as the limb that it's been

repaired in. Primary repair sometimes requires interrupted sutures and Dr. Bismuth is going to be talking about some of that. Contralateral greater saphenous vein is a reasonable option, but this patient needs to be followed very, very closely.

The most common type of injury is upper extremity and Dr. McCurdy is going to be talking about this. Blunt arterial injury to the brachial artery is very common. It can cause ischemic contracture and sometimes amputation.

In the children that they have no pulse, is if there are signs of neurosensory deficit and extremity is cold, exploration is indicated, but if the extremity is pulseless, pink hand expectant treatment is reasonable. As far as the injuries, the most common, the deadliest injuries are related to the truncal injuries and the

mechanism severity of this injury dictates the treatment. Blunt aortic injuries are actually quite uncommon and endovascular options are limited. This is an example of one that was done by Dr Veith and you can see the arrow when the stent was placed and then moved.

So these children, the long-term results of endovascular option is unknown. So in summary, you basically follow many tenets of adult vascular trauma. Special consideration for repair has to do with the fact that you need to accommodate longitudinal

and radial growth and also endovascular options are limited. Ultimately, you need a collaborative effort of many specialists in taking care of these children. Thank you.

- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery

and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely

at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer

or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.

Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.

There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking

at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?

And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,

this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients

with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.

I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,

and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients

who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually

living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,

you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data

over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,

more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.

These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?

I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.

I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at

the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,

such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time

camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.

If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.

Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.

There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series

where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,

limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.

But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.

So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.

So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.

If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.

- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.

So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift

could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.

For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.

Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting

that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.

Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.

So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.

Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.

Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient

and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people

that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug

by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.

And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.

So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,

but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.

Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite

and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents

of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.

Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.

Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.

4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,

that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.

I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.

If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,

if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.

So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.

Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.

- I congratulate Dr. Ken Ouriel for the great presentation, no? And I suppose the most important result of this presentation is the fact that after 15 years of turf battles many US vascular surgeons seems to accept CAS as an alternative to carotid endarterectomy

for the treatment of caro this is, for me, a great deal, a really great and nearly revolutionary news. But it's also unfair news, because using this technology, you try to exclude the interventionalist cardiologists

and radiologists from the CAS procedure without any scientific demonstration. The rationale for transcarotid revascularization is the fact that the main assertion is that advancing guide wires through the arch, you may provoke stroke.

Is this really the real situation? As interventional cardiologists, we have a fact that every day, many thousand of intervention passing the arch at least three times per intervention, and that terrible embolizations

are absolutely a rarity. Of course, if you have problem to manipulate the guide wire, and to navigate the balloons and catheter, guiding catheters, then of course you may have complication,

and you have to be very well-trained. I was asking some vascular surgeons in Germany and in other countries, and Professor Torsello said, if I expose the common carotid artery, then I expose also the internal carotid artery,

and I make a carotid endarterectomy, and Dr. Deloose in Belgium said, the incision is not so easy as described, and there is no evidence that using this technology, you reduce also the complication in comparison to the use of MOMA,

and his conclusion is endo is endo, and open is open. So, if you look through the published data of TCAR in 2018, are really not robust because you don't have only one article in press or a presentation, no more data.

And if you look at the fact that they are using only one stent, you cannot perform, as we are continuously trying to explain that you have to perform a tailored intervention and you have to use different stents, and not only one stent.

And if you look at this presentation of Peter Schneider, you see that you are in a range of complication of 2.7%, and if you look at this interesting slide, you see that the difference between endarterectomy and TCAR is practically minimal,

and to demonstrate a difference of .2%, you will need nearly 60 thousand patients per group, and if you want to make the same study with a transfemoral application of the MoMa system, probably you need 100 thousand patients per group. And we publish and redid in 2010,

in 1300 patients, and we had a complication rate of dissecting any type of arch, predominantly we had more than 50% Type II and III, we didn't have any myocardial infarction, although more than 50% of the patient had coronary artery disease,

and also in octogenarian, the complication rate is in a range of 2%, and all these data have been absolutely confirmed by the ARMOUR study, and you see that in the symptomatic patients, the complication rate was 0%,

and in the meta-analysis, you have a total incidence of 1.7% of complication, and if you look to the PROOF Silk, then you have a little more than 100 patients with a new lesion, 18%, however, only perfusion,

I'm sorry, has been performed only in 10 of 56%, for me it's very difficult to calculate 18% in 10 patients. If you look to our study with the MoMa, we are in a range of 26%, however, performing simultaneously

the diagnostic angiography. So, we do not have an important analysis, it's the fact that we don't have a consideration about the ability of the interventionalist or of the vascular surgeon regarding the reduction of complication,

and looking at the not robust literature, I have the impression that many vascular surgeon are at the moment looking for new application of a vascular knife, this is my final conclusion. Thank you.

- Thanks Frank, for inviting me again. We know very well that CAS and CEA are, and will remain, emboli-generating. This is an algorithm in which we can see the microembolic profile during unprotected carotid stenting. But I am a vascular surgeon, oriented to an endovascular approach, and I believe strongly

in carotid artery stenting renaissance, when we use tips, tricks and new devices. So the real difference between the two procedures are between 0 and 30 days, and this is demonstrated by the result of 10 year by CREST and by ACT 1. So, but the procedure must be protected.

Because as the Kastrup metanalisys said, the unprotected procedure are three, four-fold increase for cerebral protection embolic. And these are the recommendations from European Society of Cardiology and American Heart Association, regarding

the use of embolic protection devices. But what kind of embolic protection device? We know very well that the cerebral distal protection have some strengths and some weaknesses. And the same is for the cerebral proximal protection with the strengths and weaknesses.

So, but this is rarely used, both in the rest of Europe and in Italy. But what about dissent? We are four studies with only prospective, including a population cohort larger than 100 patients. From Italy, from Germany, from Piotr Michalik,

from Poland, again from Italy. As these are the results that are near with the rod centered stent, with very satisfactory results. With very low rate of... This is the CLEAR-ROAD study, with very low rate of complication.

This is a total of 556 patients who underwent stenting with the new generation of stent. This is the incidence of adverse events at 30 days. So, how we can apply the benefit to our procedures with OCT? And OCT demonstrated the safety of new stent design. And why I use OCT in carotids?

With two main issues. A high definition of carotid plaque, and the correct interaction between plaque and stent. With the high definition of carotid dark in order to identify the plaque type. The degree and area of stenosis,

the presence of ulceration, and the thrombus. I study the interaction between plaque and stent. In order to study the stent apposition, the stent malapposition, the fibrous cap rupture, and the plaque micro-prolaps. So this data I published last year on

EuroIntervention, with the conclusion that in relation to the slice-based analysis, we have the correct comparison with conventional stents, and the incidence of plaque prolapse was absolutely lower. So in conclusion, why I strongly believe in a reinvigoration of carotid stenting?

For the use of better embolic protection device. For the use of newer mesh covered stents, and definitively, OCT proves it as shown. Thank you for your attention.

- Good morning everybody. Here are my disclosures. So, upper extremity access is an important adjunct for some of the complex endovascular work that we do. It's necessary for chimney approaches, it's necessary for fenestrated at times. Intermittently for TEVAR, and for

what I like to call FEVARCh which is when you combine fenestrated repair with a chimney apporach for thoracoabdominals here in the U.S. Where we're more limited with the devices that we have available in our institutions for most of us. This shows you for a TEVAR with a patient

with an aortic occlusion through a right infracrevicular approach, we're able to place a conduit and then a 22-french dryseal sheath in order to place a TEVAR in a patient with a penetrating ulcer that had ruptured, and had an occluded aorta.

In addition, you can use this for complex techniques in the ascending aorta. Here you see a patient who had a prior heart transplant, developed a pseudoaneurysm in his suture line. We come in through a left axillary approach with our stiff wire.

We have a diagnostic catheter through the femoral. We're able to place a couple cuffs in an off-label fashion to treat this with a technically good result. For FEVARCh, as I mentioned, it's a good combination for a fenestrated repair.

Here you have a type IV thoraco fenestrated in place with a chimney in the left renal, we get additional seal zone up above the celiac this way. Here you see the vessels cannulated. And then with a nice type IV repaired in endovascular fashion, using a combination of techniques.

But the questions always arise. Which side? Which vessel? What's the stroke risk? How can we try to be as conscientious as possible to minimize those risks? Excuse me. So, anecdotally the right side has been less safe,

or concerned that it causes more troubles, but we feel like it's easier to work from the right side. Sorry. When you look at the image intensifier as it's coming in from the patient's left, we can all be together on the patient's right. We don't have to work underneath the image intensifier,

and felt like right was a better approach. So, can we minimize stroke risk for either side, but can we minimize stroke risk in general? So, what we typically do is tuck both arms, makes lateral imaging a lot easier to do rather than having an arm out.

Our anesthesiologist, although we try not to help them too much, but it actually makes it easier for them to have both arms available. When we look at which vessel is the best to use to try to do these techniques, we felt that the subclavian artery is a big challenge,

just the way it is above the clavicle, to be able to get multiple devices through there. We usually feel that the brachial artery's too small. Especially if you're going to place more than one sheath. So we like to call, at our institution, the Goldilocks phenomenon for those of you

who know that story, and the axillary artery is just right. And that's the one that we use. When we use only one or two sheaths we just do a direct puncture. Usually through a previously placed pledgeted stitch. It's a fairly easy exposure just through the pec major.

Split that muscle then divide the pec minor, and can get there relatively easily. This is what that looks like. You can see after a sheath's been removed, a pledgeted suture has been tied down and we get good hemostasis this way.

If we're going to use more than two sheaths, we prefer an axillary conduit, and here you see that approach. We use the self-sealing graft. Whenever I have more than two sheaths in, I always label the sheaths because

I can't remember what's in what vessel. So, you can see yes, I made there, I have another one labeled right renal, just so I can remember which sheath is in which vessel. We always navigate the arch first now. So we get all of our sheaths across the arch

before we selective catheterize the visceral vessels. We think this partly helps minimize that risk. Obviously, any arch manipulation is a concern, but if we can get everything done at once and then we can focus on the visceral segment. We feel like that's a better approach and seems

to be better for what we've done in our experience. So here's our results over the past five-ish years or so. Almost 400 aortic interventions total, with 72 of them requiring some sort of upper extremity access for different procedures. One for placement of zone zero device, which I showed you,

sac embolization, and two for imaging. We have these number of patients, and then all these chimney grafts that have been placed in different vessels. Here's the patients with different number of branches. Our access you can see here, with the majority

being done through right axillary approach. The technical success was high, mortality rate was reasonable in this group of patients. With the strokes being listed there. One rupture, which is treated with a covered stent. The strokes, two were ischemic,

one hemorrhagic, and one mixed. When you compare the group to our initial group, more women, longer hospital stay, more of the patients had prior aortic interventions, and the mortality rate was higher. So in conclusion, we think that

this is technically feasible to do. That right side is just as safe as left side, and that potentially the right side is better for type III arches. Thank you very much.

- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.

Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.

Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care

over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.

Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.

And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed

with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better

treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?

That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents

shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,

deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.

Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.

Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.

Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same

that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?

More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article

a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.

Thank you.

- 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 to the moderators, thank you to Dr. Veith for having me. Let's go! So my topic is to kind of introduce the ATTRACT trial, and to talk a little bit about how it affected, at least my practice, when it comes to patients with acute DVT.

I'm on the scientific advisory board for a company that makes IVC filters, and I also advise to BTG, so you guys can ask me about it later if you want. So let's talk about a case. A 50-year-old man presents

from an outside hospital to our center with left lower extremity swelling. And this is what somebody looks like upon presentation. And pulses, motor function, and sensation are actually normal at this point.

And he says to us, "Well, symptoms started "three days ago. "They're about the same since they started," despite being on anticoagulation. And he said, "Listen guys, in the other hospital, "they wouldn't do anything.

"And I want a procedure because I want the clot "out of me." so he's found to have this common femoral vein DVT. And the question is should endovascular clot removal be performed for this patient?

Well the ATTRACT trial set off to try and prevent a complication you obviously all know about, called the post-thrombotic syndrome, which is a spectrum from sort of mild discomfort and a little bit of dyspigmentation and up

to venous ulcerations and quite a lot of morbidity. And in ATTRACT, patients with proximal DVT were randomized to anticoagulation alone or in combination with pharma mechanical catheter-directed thrombolysis.

And the reason I put proximal in quotes is because it wasn't only common sort of femoral vein clots, but also femoral vein clots including the distal femoral vein were included eventually. And so patients with clots were recruited,

and as I said, they were randomized to those two treatments. And what this here shows you is the division into the two groups. Now I know this is a little small, but I'll try and kind of highlight a few things

that are relevant to this talk. So if you just read the abstract of the ATTRACT trial published last year in the New England Journal of Medicine, it'll seem to you that the study was a negative study.

The conclusion and the abstract is basically that post-thrombotic syndrome was not prevented by performing these procedures. Definitely post-thrombotic syndrome is still frequent despite treatment. But there was a signal for less severe

post-thrombotic syndrome and for more bleeding. And I was hoping to bring you all, there's an upcoming publication in circulation, hopefully it'll be online, I guess, over the weekend or early next week, talking specifically about patients

with proximal DVT. But you know, I'm speaking now without those slides. So what I can basically show you here, that at 24 months, unfortunately, there was no, well not unfortunately,

but the fact is, it did cross the significance and it was not significant from that standpoint. And what you can see here, is sort of a continuous metric of post-thrombotic syndrome. And here there was a little bit of an advantage

towards reduction of severe post-thrombotic syndrome with the procedure. What it also shows you here in this rectangle, is that were more bleeds, obviously, in the patients who received the more aggressive therapy.

One thing that people don't always talk about is that we treat our patients for two reasons, right? We want to prevent post-thrombotic syndrome but obviously, we want to help them acutely. And so what the study also showed,

was that acute symptoms resolved more quickly in patients who received the more aggressive therapy as opposed to those who did not. Again, at the price of more bleeding. So what happened to this patient? Well you know,

he presented on a Friday, obviously. So we kind of said, "Yeah, we probably are able "to try and do something for you, "but let's wait until Monday." And by Monday, his leg looked like this, with sort of a little bit of bedrest

and continued anticoagulation. So at the end of the day, no procedure was done for this particular patient. What are my take home messages, for whatever that's worth? Well I think intervention for DVT

has several acute indications. Restore arterial flow when phlegmasia is the problem, and reduce acute symptoms. I think intervention for common femoral and more proximal DVT likely does have long-term benefit, and again, just be

on the lookout for that circ paper that's coming out. Intervention for femoral DVT, so more distal DVT, in my opinion, is rarely indicated. And in the absence of phlegmasia, for me, thigh swelling is a good marker for a need

for a procedure, and I owe Dr. Bob Schainfeld that little tidbit. So thank you very much for listening.

- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,

It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources

if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,

you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.

We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that

you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,

otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are

being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op

in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do

with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite

down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,

and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing

translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a

sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,

and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's

respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,

you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules

and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,

we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about

the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.

This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,

he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be

oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,

still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system

I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively

and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons

so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.

- Good afternoon. On behalf of my co-author Danielle Lyon I'd like to thank Dr. Veith for allowing us to present our data. No disclosures are relevant to this talk. So, why a small incision carotid endarterectomy? I actually came on to it maybe a decade ago when in debates for carotid stenting versus

carotid endarterectomy my interventional colleagues would show pictures like this. And pictures like this, with big incisions which is how I was trained from sternal notch to the angle of the mandible and above. Then I started thinking you know, maybe this could be done

through a smaller incision safely. So it's a smaller incision, it's cosmetically much more acceptable especially in ladies. Endarterectomy typically only involves about three centimeters of artery anyways. And, there's decreased tissue trauma

with a smaller incision. All of my patients are operated on clopidogrel and aspirin and we also operate on patients on full warfarin anticoagulation without reversal which we published in the annals a few years ago. So first, rely on the preoperative imaging.

So I always get a CTA to confirm the duplex ultrasound. Here you can see a very focal plaque in the proximal internal carotid artery. Here's a more heterogeneous plaque and opposite a carotid stint. I typically do these with,

under general anesthesia with EEG monitoring. The self-retaining retractor I use to stretch the incision would be, I think, a challenge in an awake patient. I image the carotid bifurcation, just like our previous speaker, with ultrasound ahead of time. Just a regular Site-Rite ultrasound,

you don't need a duplex. I typically call my friend Russell who comes with the ultrasound, and doing both longitudinal and transverse views to identify the carotid bifurcation and confirm the extent of the plaque. The incision is typically around three centimeters,

but clearly less than four centimeters, and it's centered over the previously marked carotid bifurcation. I use a standard incision along the anterior border of the sternomastoid muscle. And then use a self-retaining retractor to stretch the incision a bit.

This is a pediatric omni retractor which works really well for this purpose. It's very important, especially for the more-sef-full-ab blade to make sure that you identify the hypoglossal nerve as you can put a fair bit of traction on that upper blade and sometimes the incision is small enough that I actually

make a little counter incision for the proximal clamp. I've found that the use of a shunt can be challenging with this technique. There's one case out of 124 that I had to extend more proximally in order to safely put a shunt. I do, though, use acute ischemic preconditioning.

So typically the mean blood pressure is 90 or above, the patient's fully anticoagulated. I'll clamp the distal internal carotid artery and if there are EEG changes I'll unclamp it, raise the pressure just a little bit more and in most occasions the second or sometimes third time the internal

carotid artery is clamped the EEG does not change. And again, you can extend the incision if necessary as patient safety is absolutely paramount. So the technique is safe. In 124 consecutive patients there were no strokes or deaths.

There was one temporary cranial nerve injury which was the marginal mandibular. A complete endarterectomy can be achieved. Again, no increase in cranial nerve injury compared with a standard incision. And it really is a superior cosmetic result.

So here's a photo that I received from silk road, you probably did too. So here's the TCAR incision compared with a standard carotid endarterectomy incision on the other side. Here's a couple of my recent patients, so you can do this operation with an incision

that is about the same size as that utilized for TCAR. Thank you.

- This is a little bit more detailed explanation of the pathophysiology behind Type IV AVM's. Medical disclosures are none. And this is the Yakes classification and this is Type IV lesion we are going to talk about now. So, this angioarchitecture has not been described before, and was first described in the Yakes classification.

What is so unique? It has multiple arteries, arterioles, but these arterioles form innumerable fistulas that are of a microsize, and they infiltrate the affected tissue. So, this is, this can affect every kind of tissue,

skin involvement and muscle involvement, and other than brain AVM, bleeding occurs if mucosa involvement is present or if an ulcer is present. So, we have to think about the definition of an AVM, which is an artery to vein connection

without an intervening capillary bed. But, what applies in Type IV? As you can see here, very nice example of this infiltrating type is that the tissue where the AVM is located is also viable, so the assumption is that

normal capillary beds are interspersed into these innumerable AVMs existing next to the malformed AVM fistulas, and this is a new definition of AVM. So, how to access this lesion? Of course, transarterial is possible

with a catheter or micro catheter. If anatomy doesn't allow transarterial approach, direct puncture is an option. Also, as you can see, in the direct puncture in the lower video, you can see the venus drainage of these fistulas,

and direct puncture of the vein compressed to reflux ethanol into the fistulas is also an approach. But, what is the challenge here? If you want to treat this lesion, you have to keep in mind

that you don't want to occlude the capillaries that are supplying the tissue. So, to find the right treatment approach, the physiologic concept is often important to understand that the arteriovenous fistulas drain into multiple veins and arterialize these veins

so we have a high pressure on this venus outflow site. The normal capillaries have a normal outflow too but this is of lower pressure, and this comes to competition between the arterialized veins and the normal venus outflow, which is, which is inferior to the normal capillary outflow.

So, what follows is a restriction of normal tissue flow with back-up to the capillaries, and backing up into the arterial inflow. So, we have the situation that the arterial venus fistulas have a lower pressure, lower resistance, and an increased arterial flow

compared to the normal capillaries, and this has to be taken into advantage for treatment. How can this be achieved? Thicken the fluid and dilute the ethanol by creating a mixture of 50/50 contrast and ethanol. So, this mixture will follow the preferential flow

into the arteriovenous fistulas in transarterial injections bearing the normal capillaries. So, if it's possible to puncture into the fistulas, pure ethanol can be used, but especially in transarterial access where normal nutrient vessels can be filled,

50:50 mixture contrast is the key to treat a Type IV AVM, Type IV Yates AVM, and here, you can see, using this approach, how this AVM can partly be treated in many several treatment sessions. And here you can see the clinical result. So, this huge ulcer, after seven treatments, healed

because of the less venus hypertension in the lesion. So the additional benefit of 50/50% ethanol contrast mixture is that your injection is visible on flouroscopy so you can see if which vessels you are including. You can react and adjust the pressure you're injecting. So, it also has to be considered

that the more you give diluted, the more total ethanol can be needed, but it's not efficient in larger vessels. This is also the advantage that you just treat the microfistulas. It's of importance that you use non-ionic contrast

as ionic contrast precipitates in the mixture. So here, you can see again, see the Type IV AVM of the arm and hand, which I already showed in my first talk, and here, you see the cured result after multiple sessions showing good arterial drum without fistulas remaining.

So, the conclusion is that Yakes Type IV is a new entity. It's crucial to understand the hemodynamics and the concept of 50/50 contrast ethanol mixture to treat this lesion with also a curative approach. Thank you very much.

- I will be talking about new KDOQI guidelines. I know many of you have heard about KDOQI guidelines being revised for the past maybe over a year or maybe two. Yes, it is being done, and it is going slow only because it's being done in a very different way. It's more than an update.

It's going to be more of an overhaul for the entire KDOQI guidelines. We in KDOQI have looked at access as a solitary problem like we talked about grafts, catheters, fistulas for access, but actually it sort of turns out

that access is part of a bigger problem. Fits into a big ESKD lifeline of a patient. Instated distal patients come in many varieties. It can affect any age, and they have a lot of other problems so once you have chronic renal failure, renal replacement mortality fits in

only when it becomes Stage IV or Stage V. And renal replacement mortality is not just access, it is PD access, it's hemo access, it is transplant. So these things, we need to see how they fit in in a given person. So the new KDOQI guidelines concentrates more

on individualizing care. For example, here the young Darien was an 11 year old with a prune belly syndrome. Now he has failed PD. Then there's another person here who is Lydia who is about 36 or 40 year old lady

with a insulin dependent diabetes. Already has bad vascular pedicle. Lost both legs. Needs access. Now both these patient though they need access, it's not the same.

It's different. For example, if you think of Darien, he was in PD but he has failed PD. We would love to get him transplanted. Unfortunately he's got terrible social situation so we can't get him transplanted.

So he needs hemo. Now if he needs hemo, we need to find an access that lasts for a long time because he's got many years ahead of him. On the other hand we have Lydia, who has got significant vascular disease.

With her obesity and existing infectious status, probably PD won't be a good option for her. So she needs hemo, and she's obviously not a transplant candidate. So how are we going to plan for hemo? So these are things which we are to more concentrate

and individualize when we look at patients, and the new guidelines concentrate more on these sort of aspects. Doing right access for right patient, right time, and for right reasons. And we go about planning this keeping the patient first

then a life plan ESKD lifeline for the patient, and what access we are looking at, and what are the needs of the patient? Now this is also different because it has been done more scientifically. We actually have a evidence review team.

We just poured over pretty much 1500 individual articles. Recent articles. And we have looked through about 4000 abstracts and other articles. And this data is correlated through a workgroup. There a lot of new chapters.

Chapter specific surgery like peri-operative, intra-operative, post-operative, cat issues, managing complication issues. And we started off with the coming up with the Scope of Work. The evidence review team took the Scope of Work

and tried to get all the articles and sift through the articles and came up and rated the evidence using a certain rating system which is very scientific. The workgroup then kind of evaluated the whole system, and then came up with what is clinically relevant.

It's one thing for statisticians to say how strong evidence this is, but it's another thing how it is looked upon by the clinicians. So then we kind of put this into a document. Document went through internal and external review process.

This is the process we have tried to do it. Dr. Lok has been the Chair of the group. Myself and Dr. Yevzlin are the Vice-Chairs. We have incredible workgroup which has done most of the work. And here are the workgroup members.

We comprised of nephrologist, transplant surgeons, vascular surgeons, Allied Health personnel, pediatric nephrologist so it's a multi interventional radiologist and interventional nephrologist. This is a multi disciplinary group which has gone through this process.

Timothy Wilt from Minnesota was the head of the Evidence Review Team, who has worked on the evidence building. And now for the editorial sections we have Dr. Huber, Lee, and Dr. Lok taking care of it. So where are we today?

We have pretty much gone through the first part of it. We are at the place where we are ready for the Internal Review and External Review. So many of you probably will get a chance to look through it when it comes for the External Review and would love

to have your comments on this document. Essentially, we are looking at access in the context of end stage renal disease, and that is new. And obviously we have gone through and done a very scientific review, a very scientific methodology to try

to evaluate the evidence and try to come up with guidelines. Thank you.

- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations

related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,

and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be

a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation

of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest

as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher

patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.

The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence

that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization

versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,

in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,

one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients

who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored

superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months

for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.

But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear

to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.

Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.

- Thank you, ladies and gentlemen. And our faculty here. Thank you so much for having me, and I'm thrilled to be here as I think some of the few interventionalists who are here. So, the idea was, what is the, is the stance

being overused after the Orbita Trial? And I bring it up because what is the Orbita Trial? This was a trial that really got a lot of, a lot of attention and I think it's important for you to kind of think about it.

It was actually the very first sham-controlled study of 230 patients who were enrolled, 200 who were randomized. Comparing actually PCI to placebo in patients with severe single vessel disease who were medically optimized but were stable.

Very, very interesting. They followed up these patients and the, based, looked at the change in exercise time in these patients and found absolutely no benefit for PCI in changing the exercise time.

So they said, in medically, in patients with medically-treated angina and severe coronary artery stenosis, PCI did not increase exercise time by by, in any difference from placebos. So, this really, really brought up so much attention

and that we were really, really doing unnecessary procedures and the last thing we heard is the last nail in the coffin of PCI. And so, I think it's important to think about what were the issues with that important disease and where we are with the scope of coronary disease.

Which is not insignificant. At the moment, with 326 million patients in the United States, and prevalence of CAD at 16.5, PCI is being performed in 667,000 patients per year. And I think it is important to note

that for the most part, about 50% of this is for acute coronary syndromes, which is not all the Orbita Trial. It's supportive evidence for routine revascularization with guideline-based therapy, directive therapy.

Very, very important that observational data does show a very important relationship between ischemia and death and MI. Revascularization relieves ischemia and that is what it's supposed to do. Large scale studies have shown

a reduction in spontaneous MI, following revascularization versus guideline-directed therapy. And importantly, continued improvement in both PCI and CABG techniques have really shown excellent relief of symptoms

and that we are not here to really, really think about death and MI in the big, big picture. But more immediate reductions as preferred by patients and importantly, we have to note that ischemia directed therapy with revascularization can have important issues.

Regarding whether or not there is an overuse of PCI's, let me just take a, show you the map of the United States. The heat map. The hotter, the more PCI's. And you can see, it really is very much variable and that there is important appropriate use criteria

for coronary revascularization that continues to be updated on a very, very important issue. And there's no question that the media loves the hysteria about overuse of PCI. But I wanted to put that into the context

of what we were doing. In PCI, we are using FFR guidance and physiology guided PCI to show an enhanced outcome. And more and more, we're incorporating that into the armamentarium of both AUC, Appropriate-Use Criteria, as well as evaluating

the valuable patients. And it is important for you to take a look at what have we shown. So far, based on revascularization versus optimal medical therapy in relieving angina and has been a very, very important

improvement in exercise capacity. Albeit, that the one and only trial of the sham procedure didn't show a change in exercise, but there are a lot of issues in this underpowered study that shouldn't really, really turn you away.

For the fact that PCI does relive symptoms. Because there's a tremendous amount of evidence in, in view of reducing angina with a really, really good p value of 12 randomized clinical trials in this area. It is also important that the freedom of angina is shown.

Not just within the Orbita Trial that actually did show a reduction in angina, but very similar to previous studies. And the guidelines are telling us a very, very important Class 1A indication for patients with CID for both

prognosis and treatment. There is an upcoming ischemia trial in ischemic heart disease that will show in 8,000 patients on their NHLBI, with evidence of ischemia hopefully that we could show

that there is benefits. So to conclude, the current guidelines recommend use of revascularization for relief of symptoms with patients with ischemic, a stable ischemic disease. And while placebo remains an important aspect of this medical management up front,

and making sure that there is an important management, we should really, really understand that there's no question that optimal medical therapy has to stay in the background. And the use of PCI is, continues to be of important value.

Thank you for your attention.

- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first

before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.

We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column

from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.

Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,

which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied

and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal

amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,

but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced

from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,

organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC

seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.

You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.

So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these

biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...

Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be

most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.

We have to work that out, I hope. Calcification is generally a very late feature in this process. 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.

- I'd like to thank Dr. Veith for this kind invitation and the committee as well. So these are my disclosures, there's none. So for a quick background regarding closure devices. Vascular closure devices have been around

for almost 20 years, various types. Manual compression in most studies have always been shown to be superior to vascular closure devices mainly because there's been no ideal device that's been innovated to be able

to handle all sorts of anatomies, which include calcified vessels, soft plaque, etc. So in this particular talk we wanted to look at to two particular devices. One is the Vascade vascular closure device

made by Cardiva and the other is the CELT arterial closure device made by Vasorum in Ireland. Both these devices are somewhat similar in that they both use a disc. The Vascade has a nitinol disc

as you can see here that's used out here to adhere to the interior common femoral artery wall. And then once tension is applied, a series of steps is involved to deploy the collagen plug

directly on to the artery which then allows it to expand over a period of time. The CELT is similar in that it also uses a stainless steel disc as you can see here. Requires tension up against the interior wall of the common femoral artery.

Nice and tight and then you screw on the top end of the device on to the interior wall of the artery creating a nice little cylinder that compresses both walls of artery. As far as comparability is concerned between the two devices you can see

here that they're both extravascular, one's nitinol, one's stainless steel. One uses a collagen material, the other uses an external clip in a spindle-type fashion. Both require about, anywhere between three to seven minutes of pressure

to essentially stop the tract ooze. But the key differences between the two devices, is the amount of time it takes for patients to ambulate. So the ambulation time is two hours roughly for Vascade, whereas for a CELT device

it's anywhere from being immediate off the table at the cath lab room to about 20 minutes. The data for Vascade was essentially showing the RESPECT trial which I'll summarize here, With 420 patients that was a randomized trial

to other manual compression or the device itself. The mean points of this is that the hemostasis time was about three minutes versus 21 minutes for manual compression. And time to ambulation was about 3.2 hours versus 5.7 hours.

No major complications were encountered. There were 1.1% of minor complications in the Vascade versus 7% in the manual compression arm. This was actually the first trial that showed that a actual closure devices

had better results than manual compression. The main limitations in the trial didn't involved complex femoral anatomy and renal insufficiency patients which were excluded. The CELT ACD trial involved 207 patients that were randomized to CELT or to manual

compression at five centers. Time to hemostasis was anywhere between zero minutes on average versus eight minutes in the manual compression arm. There was one complication assessed at 30 days and that was a distal embolization that occurred

early on after the deployment with a successfully retrieved percutaneously with a snare. So complication rate in this particular trial was 0.7% versus 0% for manual compression. So what are some pros and cons with the Vascade device?

Well you can see the list of pros there. The thing to keep in mind is that it is extravascular, it is absorbable, it's safe, low pain tolerance with this and the restick is definitely possible. As far as the cons are involved.

The conventional bedrest time is anywhere between two to three hours. It is a passive closure device and it can create some scarring when surgical exploration is necessary on surgical dissections.

The key thing also is you can not visualize the plug after deployment. The pros and cons of the CELT ACD device. You can see is the key is the instant definitive closure that's achieved with this particular device, especially in

calcified arteries as well. Very easy to visualize under fluoroscopy and ultrasound. It can be used in both antegrade and retrograde approaches. The key cons are that it's a permanent implant.

So it's like a star closed devised, little piece of stainless steel that sits behind. There's a small learning curve with the device. And of course there's a little bit of discomfort associated with the cinching under the (mumbles) tissue.

So we looked at our own experience with both devices at the Christie Clinic. We looked at Vascade with approximately 300 consecutive patients and we assessed their time to hemostasis, their time to ambulation,

and their time to discharge, as well as the device success and minor and major complications. And the key things to go over here is that the time to hemostasis was about 4.7 minutes for Vascade, at 2.1 hours for ambulation, and roughly an average

of 2.4 hours for discharge. The device success was 99.3% with a minor complication rate of .02% which we have four hematomas and two device failures requiring manual compression. The CELT ACD device we also similarly did

a non-randomized perspective single center trial assessing the same factors and assessing the patients at seven days. We had 400 consecutive patients enrolled. And you can see we did 232 retrograde. We did a little bit something different

with this one, we did we 168 antegrade but we also did direct punctures to the SFA both at the proximal and the mid-segments of the SFA. And the time to hemostasis in this particular situation was 3.8 minutes,

ambulation was 18.3 minutes, and discharge was at 38.4 minutes. We did have two minor complications. One of which was a mal-deployment of the device requiring manual compression. And the second one was a major complication

which was an embolization of the device immediately after deployment which was done successfully snared through an eighth front sheath. So in conclusion both devices are safe and effective and used for both

antegrade and retrograde access. They're definitely comparable when it comes, from the standpoint of both devices (mumbles) manual compression and they're definitely really cost effective in that they definitely do increase the

throughput in the cath lab allowing us to be able to move patients through our cath lab in a relatively quick fashion. Thank you for your attention.

- 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.

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