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Rifampin Soaked Endografts For Treating Prosthetic Graft Infections: When Can They Work And What Associated Techniques Are Important
Rifampin Soaked Endografts For Treating Prosthetic Graft Infections: When Can They Work And What Associated Techniques Are Important
2 arch homograftsOpen Ilio-Celiac bypassSacular TAA ; Endograft AbscessTAAA repair with left heart bypassTEVARtherapeutic
2-Year Comparison Of F/B/EVAR And Ch/EVAR For Complex Aneurysms In A Single Institution: Both Are Effective And Have A Role In Their Treatment: Advantages And Limitations Of Each
2-Year Comparison Of F/B/EVAR And Ch/EVAR For Complex Aneurysms In A Single Institution: Both Are Effective And Have A Role In Their Treatment: Advantages And Limitations Of Each
able endografts (iCastard Cook Zfen endograft / Renal artery balloon expArtis ZeegoHybrid suiting (Viabahn) endograftsiemensStTherapeutic / DiagnosticVBX) / Self exp
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
Value Of Parallel Grafts To Treat Chronic TBADs With Extensive TAAAs: Technical Tips And Results
GORE MedicalGORE VIABAHNL EIA-IIA bypassleft carotid subclavian bypassstent graft systemTBAD with TAAAtherapeutic
Transcript

- This next topic I think, is about a different kind of future. It's an area that we've worked on now for four years. I want to give you a progress report and tell you where I think we're going. I'm bullish on telehealth and I think you'll see why. Telehealth will probably be as important

in vascular care follow-up in the future and probably have an impact similar to the financial impact of endovascular care. And I'll show you why that may be. Patients want access. They want access now, they don't want to wait

til you drive out to some clinic in a couple of weeks. Every time we drive out to some place, I used to have to drive two hours to and from a clinic that's really a waste of time if you think about it. And now the tele-technologies which you'll hear about in the next few talks

can monitor and remind patients to do what they need to do. Which about 50% of them do not do unless you remind them. So where are we now? The equipment now for these visits is highly sophisticated. We have actually added a Parks doppler to the system so a medical assistant at the other end can even

allow us to listen to fetal blood flow. About 70 to 80% of patients are willing to do this and the patient satisfaction's high. And now the G-codes, allow you under medicare and private payers to be reimbursed for this. And this is going to continue to improve.

So what do you need to start? You need some physicians that want to do it. Without physician champions it's not going to happen. And at the other end, you need a highly trained medical assistant to present the patient and be able to use a stethoscope

and help be part of the exam. That takes some training. It takes time. We worked on this for two years before we opened our first vascular telehealth center. And I would advise, if you're going to do this,

find someone young in the group. We have two of our young surgeons now who have taken this up and in the background you have to have some pretty experienced IT people. We've progressed to the point now that we are the first US telehealth center of excellence designated last year.

We have 40 people in our telehealth center, physicians, nurses, and IT people. And so now we do a clinic ever week with Murrells Inlet, it's a two hour drive away. We will soon be doing telehealth clinics around the state. We currently get 25% of our surgical and endovascular

volume from these endovascular telehealth clinics. And suddenly everyone likes it. The skeptics are enjoying it. We now have four surgeons doing this. The patients like it and the administrators like it because I'm not on the road, I'm not doing RVUs

nor are my partners. Let's see if we can hit okay here. So I think the future is near. Many of us have watches. Now this year there's an app, you can check to see what your heart rate is,

you can check blood pressure, blood sugars, all of these parameters for good care can be monitored. You can be reminded in the morning if you don't take your medication to take it. And I know there's certain days of the week that I forget. You can remind claudicants to exercise

and you can actually monitor whether they're doing it or not. Very soon there will be medicare reimbursement for a nurse to go to the home of a patient and with a system like this which is being developed in MEDiC university,

you can actually do a tele-visit at home. And you can remind patients to go to the doc. All this technology is here now, it's just simply not coordinated in most practices. So I think the tele-technologies will be more important going forward, they really make our life

and the patient's life easier. The technology and the reimbursement is here today and the adoption really takes a commitment of someone or someones in a group. It takes systems support cause this requires some money and it certainly takes a team

including the people at the other end of those clinics. So I would just say to you get going, take a swing. I think you'll find that you like it. Thank you.

- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.

Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates

an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.

You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't

or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.

CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,

we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.

She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.

So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.

Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.

It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign

and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there

but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?

Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy

and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.

So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,

a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,

gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection

it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible

before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains

in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low

or cut out the super renal fixations so you can take them out a little easier. Thank you.

- Dear chairman, dear colleagues and friends, it's my pleasure to be again with you. Nothing to declare. In our experience of CCSVI and angioplasty we have more than 1,300 patients with different neurological disorders. Not only MS, but also migraine,

lateral amyotrophic sclerosis, Parkinson's disease, left sided amaurosis. We published our data with an emphasis on the safety of the procedure. We had virtually zero percent of serious complication. What about the clinical improvement?

In fact, we noticed function improvement in more than 62.5% of these patients. And in fact, the group of Pierfrancesco Veroux showed similar between 50 and 60% of the patients restoring the normal blood venous flow. In fact, in their work was shown that the type

of anatomic disturbance, anatomic feature is very important predictor if the flow will be restored by the simple PTA. And the most important into the brave dream trial was also that, in fact, the restoration of the flow was achieved in around 70% of the patients.

And exactly in these 70% of the patients with restored flow like Paulo emphasized already, there were lesion, 91% of them were lesion-free on the MRI, and 77% of them were lesion-free on the six-month. We performed a substudy regarding the hypercapnia

and hypoxaemia of the jugular veins in the CCSVI-positive patients. And what we have described in this 178 patients with CCSVI and 50 healthy control group. In fact, we established that the patients CCSVI-positive the venous sample by the jugular veins was typical

with hypercapnia and hypoxaemia in desaturation, huge desaturation with improvement after the balloon angioplasty in all three parameters. What was the reason for that? In fact, in nine patients of our group we examined, the perfusion, the nuclear perfusion of the brain

before and after the treatment. I'm here presenting non-positive for MS young patient without MRI demyelization. And but on the brain perfusion he had deep hyperperfusion on the left side, and the patient was complaining with deep fatigue.

And we saw practically full occlusion of the enominate vein. And after the recanalization using first coronary and after it peripheral balloons, and in this particular case we had to stent finally. And you see still persistence of a huge crossover collateral even after ballooning.

But after stenting we saw practically full restoration of the flow. You see in less than three to four seconds it was very interesting to see on the perfusion imaging, nuclear perfusion, full restoration of the flow of this gentleman.

So this is very important to emphasize that there is direct relationship between the blood gas disturbances on the brain level, and demyelinization process. What about the PTA? It's probably not the optimal treatment.

We have to establish reliable clinical and anatomical predictors for vascular and clinical success in order to answer the important questions: who will be vascular responders, or MRI responders, and finally the clinical responders in this group of patients?

And concluding, ladies and gentlemen, the CCSVI is a real vascular pathologic entity and is probably a trigger for more than one neurologic degenerative disorder. Endovascular treatment, balloon, PTA, and stenting of CCSVI is feasible and safe.

Methods and strategies improving the early and late patency rate have to be elaborated because the good clinical result is strongly dependent on the vascular patency and flow restoration. And thank you very much for your attention.

- Ladies and gentlemen, I have nothing to disclose when regarding this topic. We know that TIAs are independent predictors of long-term mortality in the general population, however, they've been left underreported in almost all the randomized clinical trial. And we don't know the effect of TIAs on long-term survival

in patient with carotid disease. So what we have done, we have performed a study, looking at the effect of TIAs in populations submitted to carotid revascularization, either with endarterectomy, or stenting, and we achieved a pretty good long term result.

However, patient's with TIAs had a significantly lower survival compared with the patient without cerebral events. Similarly, patient with stroke, these reduce survival, and TIA behaves exactly like stroke in this population.

So, by multivariate analysis, TIA together with stroke, chronic renal failure, and age were independent predictors for late mortality. So, we have seen that TIAs have this effect in patient with carotid disease, but what about silent cerebral event?

The silent cerebral infarction has small, radiologically detected infarction without a history of acute dysfunction. And they're usually associated with a variety of condition. In the general population, these cerebral infarction are present in almost

one fifth of the population, 21%. And they are associated with significantly reduction in the stroke free survival in this population. For that reason, they are considered a high risk of stroke in patient with carotid disease.

So looking at the series of patient submitted carotid revascularization, we have seen that the presence of these silent brain infarction was significantly associated with either transient ischemic event and stroke. So, the important factors,

we wanted to further expand these experiences just looking at these phenomenon. In another series of 743 patients submitted to endarterectomy are looking at all the preoperative CT scan in this population. And again, we have found that significantly

association between silent cerebral infarcts and stroke. And by logistical regression analysis, this feature was independently associated with postoperative stroke. At long-term, this effect was also present in association with ipsilateral stroke.

And stroke combined stroke and death. Again, these effect was independent from all other feature. So what about their effect in stenting? Actually, there are no papers in the literature looking at this effect. So we perform a retrospective analysis on

420 patient submitted to a stenting procedure. And all patients were selected with preoperative evaluation of the brain. So, again, 30 day outcome, was not significantly affected by the presence of silent cerebral infarcts, however, when we look at the patient

with endarterectomy and stenting, we see that while in the endarterectomy group, there is a clear decrease of the stroke rate in patient without silent cerebral infarction. This effect is less pronounced

in the stenting group. So in conclusion, silent cerebral infarction increases the risk of postoperative events in carotid endarterectomy. This increased risk should be considered when in indication to revascularization is given.

In stenting, the effect is less pronounced, due to the higher overall risk of neurological event. Thank you.

- Well thank you and um, it's kind of a how to do it, how to tie your shoes type talk. And clearly now that these venous assessment tools have been present for more than two decades. It has created a common landscape for communication, for comparing outcomes.

And with that common language we really have a good guide of what to use. So. From a favorable standpoint you know the CEAP. And this is the revision from 2004. Really established good classification

across the clinical, etiologic, anatomic, pathophysiologic categories. And certainly with the clinical side of things, that really has taken off. Where the EAP has been more on the research side. But with this common language has come the ability

to communicate like versus like. And clearly if you look at the clinical classifications system. There's a clear line drawn really from C4 and greater, and some would include C3. Versus the C 1&2 in terms of disease severity.

And I think we're all familiar with classifications. But these are very categorical type classifications. And you know if you look at population based studies, certainly the c1 2 category counts for most. Where C3 is about 15% of population, and C4 grade are anywhere from 3-5% of the population.

You know the upsides of CEAP it's really proven to be effective in assisting in evaluation of various treatment modalities. Allows comparison of results from different institutions using universal language. It's really enhanced our understanding with these categories

of potential etiologic factors. And by doing so it's improved the scientific standards in the evidence. And allows for meaningful research and comparison of cohorts. Bu there's certainly some limitations to CEAP.

There's a degree of complexity that makes utilization difficult across all spectrums of clinical care. It's limited as a severity classification system, in that it's relatively static. And then even with improvement there's sometimes a little change that happens within the categories.

There's lack of reversibility. There's some problems with differentiation especially when you look at the clinical categories. Varicose veins, edema, and such. Clinical use of C category has been widely adapted. Where there's more limited use of EAP.

And really has raised the need and question to freshen up CEAP with reclassification. So over the last year or so, there's an American VF formed task force. Which has been tasked with revising CEAP. And I apologize I can't present the information just yet.

Because it's still under modification and maybe next year we'll have the revised CEAP classification to promote. With that in mind the Venous Clinical Severity Scoring came in behind CEAP. As a more sensitive scale to determine changes in treatment,

and it's really meant as a compliment to CEAP. And it has both clinical utility and research applications most recently revised in 2010. And again most of us are familiar with VCSS. In that it's several attributes that are rated across the spectrum of severity from 0-3.

From the standpoint of the revised system. It has been studied and it has been shown to have good inter and intra user reproducibility. Which is important in that it makes it consistent across users. And if you look at Michael Vasquez's publication here.

It shows a good practical use of both CEAP and VCSS. And that in this particular patient with some hemosiderin, a pigment change, a C4 category. When you plug in the VCSS it's a 15. And then after treatment there's still a C4,

but there VCSS fell to 11. And similarly the same patient here who starts with a CEAP of six and VCSS of 27. And then across the spectrum of treatment, still is a V6 about mid-treatment, but has improved to VCSS of 19.

And then after completion of treatment the best they can get is going from a C6 to a C5. But they're VCSS is now 5. And most of the benefit comes with pain, varicosity, and edema.

That's where you see most of the change in VCSS. And certainly the guidelines support the use of CEAP. This is varicose vein guidelines where the basic of more for clinical practice than the full CEAP for research. And same thing with the venous ulcer guidelines.

And I'll just leave you with this app which you can pull up on your phone. SVS iPG. Which actually has CEAP and VCSS embedded so you can have it at the bedside. Or you can embed it in your clinical templates.

So in conclusion yes they're helpful. There is no one universal tool but certainly both CEAP and VCSS used together, do achieve the needs of what they're intended to do. There's certainly some improvements that will be forthcoming with CEAP.

And I thank you.

- This is a controversial topic. Basically we have been following standard set-up on the arterial side to grade venous stenosis. But duplex, many people would look at the stenosis either by venogram or duplex and then compare it to the adjacent normal segment.

In arteries the stenosis is usually focal so this approach works well. But in iliac veins particularly, does not work well. On venogram this looks normal but actually on IVUS it's a severe stenosis, 67 square millimeters,

it should be somewhere around 200. So, you are looking at a 70% stenosis. So, just the standard does not work well in veins. You have, does not happen, that type of rokitaskis stenosis does not happen, all the time but is present in varying degrees in about 20% of patients.

Another standard that we have applied, without thinking too much, is so-called critical threshold. Most major arteries, as we know, is not hemodynamically significant until is is somewhere around 70% or so. If the region of resistance is low,

it maybe a little bit low, somewhere around 60%, 70%, 80% depending on local resistance. Why does that happen? It happens because of autoregulation. As increases stenosis there is pressure flow of arterial dilation.

At some point, usually somewhere around 70%, 80% the pressure flow of compensating vasodilation is maxed out. So as increases stenosis the flow goes down and the pressure goes up. I want to point out that the pressure going up is proximal, not downstream.

The pressure goes down downstream. And pressure does go up upstream but is so well compensated on the arterial side by off-load to other areas. Another way to look at it is consider peripheral assistance, as a stenosis in aggregate.

Now there's a fall of blood pressure from 100 mean to somewhere around 30 millimeters post arterial. So that represents a very high-grade stenosis. So any proximal stenosis, by the principle of tandem stenosis, has to exceed

this high value to become hemodynamically significant. So that's why the 70% critical threshold. On the venous side there's no autoregulation. And the only distal downstream stenosis is abdomen. Not very much, about five millimeters of mercury pressure. So, on the venous side, pressure rises

with incremental stenosis. There's no critical threshold, it's nonlinear but no sudden inflection point. So this theory of 70% should not hold on the venous side. As a practical matter, most stenosis are in that range. They are in the 60%, 70% range.

But every once in awhile, say about 10%-15% of cases, where you will come across a 20% or 30% stenosis, which is clinically significant, because the veins are post-thrombotic and they have poor compliance. So even a slight stenosis will increase the pressure.

This is a concept of inflow outflow. If the inflow matches outflow, then the pressure will be normal. So you can calculate from the size of the outflow, we know what is the optimal outflow, you can calculate from the outflow size

whether the stenosis is significant or not. Critics will say this is a morphologic method. Yes and no. It's morphologic but it is tightly connected to flow. So it is a quasi hemodynamic method to measure the outflow size.

And again, calculated by various, by flow femoral size. Thank you.

- Thank you, Mr. Chairman. Good morning ladies and gentleman. I have nothing to disclose. Reportedly, up to 50 percent of TEVARs need a left subclavian artery coverage. It raises a question should revascularization cover the subclavian artery or not?

It will remain the question throughout the brachiograph available to all of us. SVS guidelines recommend routine revascularization in patients who need elective TEVAR with the left subclavian artery coverage. However, this recommendation

was published almost ten years ago based on the data probably even published earlier. So, we did nationwide in patient database analysis, including 7,773 TEVARs and 17% of them had a left subclavian artery revascularization.

As you can see from this slide, the SVS guideline did affect decision making since it was published in 2009, the left subclavian artery revascularization numbers have been significantly increased, however, it's still less than 20%.

As we mentioned, 50% of patient need coverage, but only less than 20% of patient had a revascularization. In the patient group with left subclavian artery revascularization, then we can see the perioperative mortality and morbidities are higher in the patient

who do not need a revascularization. We subgroup of these patient into Pre- and Post-TEVAR revascularization, as you can see. In a Post-TEVAR left subclavian revascularization group, perioperative mortality and major complications are higher than the patient who had a revascularization before TEVAR.

In terms of open versus endovascular revascularization, endovascular group has fewer mortality rate and major complications. It's safer, but open bypass is more effective, and durable in restoring original profusion. In summary, TEVAR with required left subclavian artery

revascularization is associated with higher rates of perioperative mortality and morbidities. Routine revascularization may not be necessary, however, the risks of left subclavian artery coverage must be carefully evaluated before surgery.

Those risk factors are CABG using LIMA. Left arm AV fistula, AV graft for hemodialysis. Dominant left vertebral artery. Occluded right vertebral artery. Significant bilateral carotid stenosis.

Greater than 20% of thoracic aorta is going to be or has been covered. And a history of open or endovascular aneurysm repair. And internal iliac artery occlusion or it's going to be embolized during the procedure. If a patient with those risk factors,

and then we recommend to have a left subclavian artery revascularization, and it should be performed before TEVAR with lower complications. Thank you very much.

- Thank you, and thank you to Dr. Veith for his kind invitation. These are my disclosures. Basically, we took a single center two-year outcomes for the use of fenestrated grafts and compared to parallel grafts in treating patients with complex aortic aneurysms.

These included fenestrated grafts and parallel grafts for juxtarenal, suprarenal, and thoracoabominal aneurysms. And the usual risk factors, morbidity, mortality, patency, and re-intervention rates were evaluated. This is a retrospective review of a prospectively maintained database.

All consecutive patients were included with exception of those presenting with rupture. Symptomatic patients were included. The type of repair was the single surgeon decision based on urgency and the patient's anatomy. And the parameters, as we discussed, were measured.

The fenestrated technique is fairly well-described and as we found the standard the technique of using fenestrated grafts. We have a Zeego hybrid suit Siemens that we used for all our implants. Most of these patients were done are local anesthesia

with percutaneous access. iCast or VBX stents were used for the bridging stents. An SMA was selectively self-extended with a self expanding stent in the Zfen cases alone. We look at the parallel graft. We had some bias in that we put no more than

two parallel grafts at any one level such as you see here. We came in and put a stent and then cautherize the celiac and the SMA, deployed the stents here. Then put a bridging RA thoracic endograft and then came in with a second endograft down to the level of the renals and the second set.

This is to decrease the instance of gutter leaks and need for reintervention. This analysis was formed with Kaplan-Meier and with p value of 0.05 being considered significant. Results. Basically, we had a 117 complex aneurysms

that were performed with a 100% technical success rate. We didn't look to the patients with significant branch special involvement, not just an isolated vessel. And we see in the parallel grafts, we had good distribution between renal, SMA, and celiac.

Obviously with a fenestrated graft, we had a stronger bias to the celiac not being involved in the SMA and renals being more commonly involved. Demographics are similar between the two groups. And the comorbidities were similar with the highest is hypertension and tobacco use.

The mortality was not statistically different with about a 3% to 2.6% perioperative mortality. Again that's one patient in each group. We had reinterventions. It was higher in the parallel graft group and that was later in the series at 7% compared to 5.3%.

Again not statistically significant. The reinterventions were similar for the fenestrated group. We had two renal stent occlusions, one colonic ischemia, one iliac limb occlusion, requiring reintervention, and one perinephric hematoma from a wire perforation.

And then in the parallel group, we had three endoleaks, two renal graft thrombosis, one celiac thrombosis, one renal stent kink, and one gutter leak. So again, using those two parallel grafts only at one level tended dramatically decreased our instance of gutter leak

compared to the reported literature. Freedom from aortic mortality. They were not different. We had 97% freedom from aortic mortality in those patients with fenestrated, 94% in those patients with parallel grafts.

Overall survival again was the same at 78% going out to two and a half years in both groups. Reintervention we saw again as we mentioned in the fenestrated graft once they plateaued around 12 months they seemed to fairly stable. But those going with the parallel graft,

we did see further late need for reintervention. So in conclusion, I think certainly in this retrospective review of parallel and fenestrated grafts, they have an acceptable perioperative mortality noted for juxtarenal, suprarenal, and thoracoabdominal aneurysms.

Parallel graft and technology has acceptable patencies with a low rate of reintervention and very low rate of gutter leaks in this series. The snorkel-sandwich technique is a very viable option especially when four vessels are involved or a sense of urgency when you don't have time

to get a fenestrated graft if it's available in your institution. And we certainly if we have a type two or three thoracoabdominal in parallel grafts we tended to stage those to decrease the paraplegia rate. Thank you very much for your attention.

- Well, thank you Dr. Veith, and thank you very much for allowing me to speak on the topic. I have no disclosures. This is a nice summary that Dr. Veith is actually second author, that summarize what we know about predicting who will benefit from intervention among the patients with asymptomatic aortic disease.

You look at this eight means that we have, you realize that only one of those related to the fluid deprivation. The rest of them are related to embolic events. And that's very interesting because we know that antiplatelets have very little effect

on prevention of this. That's summarizing that review. Partially because what we focused on is that mechanism of thrombosis which requires platelet activation and attachment to the wall.

And that's where those antiplatelets that we use, act upon. However, you realize if you just look at the any ultrasound, that because of the velocities that we have and the lengths of the stenosis in carotid disease there is no way how the platelets can be attached to that

due to that mechanism. They just fly away too fast and don't have any time to do this. And it's even more because all the studies, basic science, show that at those shear rates that we have in carotid disease

that is more that 70%. There is very little probability of either platelet attachment or Von Willebrand factor attachment, or as a matter of fact even fibrinogen attachment in that particular area. So on the other hand we also know

that at those shear rates that we have, the Von Willebrand factor molecules unfold revealing tens of thousands more adhesive sites that allow them, not only to the platelets but also to the wall at that particular spot. And then the most likely mechanism

of what we dealing with in the carotid disease is this that the Von Willebrand factor attach and this unactivated platelets form conglomerates which can easily, because they don't attach to each other, easily fly. And that is probably one of

the most likely causes of the TIA. So if you look at the antiplatelet that we use on this particular mechanism, is right here. And those aspirin and clopidogrel, and combination of those we usually use, have very little, if any, effect on this particular mechanism.

So if, on the other hand, you can see that, if you specifically address that particular site you may have a much substantial effect. Now, how can we identify it? Well actually, the calculation of near-wall shear rate is quite simple.

All you need is just highest velocity and smallest diameter of the vessel. Of course, it is an estimate and actual shear rate is much higher but that's even more, because you, better than you prevent, more higher rate. Just to demonstrate, you can have the same velocity,

similar velocity, but different diameters. This stenosis technique will give different shear rate, and vice versa. So it's not really duplicating neither one of them. So we decided to look at this. We did a case control study that was published,

still online in the Journal of Vascular Surgery. And what you can see on the ROC curve, that in fact shear rate predicts symptomatic events much better than either velocity or the degree of the stenosis. And we look specifically at this group

with this thresh point of 8,000 per second and you can see that those patients who have those shear rates and the stenosis are 12 times more likely to have ischemic events. We look at the other means like microembolism. It's ongoing study, it's unpublished data that I show you.

And it's a very, very small sample but so far we have the impression that those microemboli that we can decide for, make a decision for intervention, actually happen only in this category of patient that have high shear rate. Based on this, this is our proposed algorithm,

how we deal with this. If you have asymptomatic patients with more than 70% degree of their stenosis and shear rate that exceeds certain level, we think it's about 8,000 per second, that may be an indication for intervention.

On the other hand if you a have lower shear rate then you can use other means. And what we use is microembolis per hour. Then you can duplicate their areas. If TCD on the other hand is normal you can continue best medical therapy and repeat the ultrasound in a year.

It's arbitrary. This is proposal agreed and based on our studies and that's, I'm thankful for the opportunity to share it with you. Thank you very much.

- Thank you so much for having me here. I must confess it's not my talk. It's Professor Veroux's talk. Veroux couldn't join us, so I hope you will forgive me if I cannot read it properly as he would have done. It's just a friendship act of being here.

Talking with you about the potential of these treatment of ventricular veins for relief symptoms, headache like. Professor Veroux published on PlosOne Single-center open label observational study was conducted from January 2011 to December 2015.

Basically focused on 113 headache positive patients. As you see there were different kinds of MS patients involved. 82 were relapsing emitting. 22 were secondary progressive. Nine were primary progressive.

Basically the including criteria included headache resistant to the best medical therapy. There was a bilateral internal jugular vein with a stenosis bigger than 50% of moderate to severe insufficiency of the flow. The stenosis of course were suitable for treatment

and they were followed up at least for 12 months. Basically the followup included a variation of the MIDAS, Migraine Disability Assessment Score. It was preformed the day before angioplasty. Then three months after angioplasty and then at the end of the follow-up.

As it was appears,. Of curse we can add the different kinds of lesions of the juvenile level. As it was previously reported, the Professor Veroux ended selection. It is mandatory in these kinds of procedures.

Adding the transversal defect the single most important criteria for determining if the PTA would be successful or not. Of course, again, transversal rather than longitudinal defects are preferred in the treatment of

this kind of patients. The exclusion criteria were the possibility of hypoplasia or extreme muscle compression. In particular, as you know there is the omohyoid possibility of compression.

Looking at a followup that is significantly of three years or more. The clinical results in these patients affected by headaches lead to significant reduction. And 86% of them with an improvement of the MIDAS scores in the three months following up.

At the same time, the improvement was maintained throughout the followup period up to three years. Mainly in the relapse remitting and the secondary progressive patients. So the conclusion of the investigation you can again (mumbles)

is that patient selection is mandatory, of course, again, on the transverse lesion mainly. Balloon valvuloplasty is feasible in these patients and has succeeded with a good result at three years followup in the MIDAS score. Of course, these findings are suggesting

that it could be a useful intervention for selected MS patients with persistent headaches and of course, non-thrombosis stenosis of the IJVs. Thank you so much.

- So thank you to the organizers and to Dr. Veith, and thank you to Dr. Ouriel for giving me the introduction of the expense of an unsuitable procedure for pain patients. We have no disclosures.

I think when you look at MRV or Venous interventions, you can look at it as providing you a primary diagnosis, confirming a diagnosis if there's confusion. Procedural planning, you can use it as a procedural adjunct,

or you can use it as a primary procedural modality. In general, flow-dependent MRI has a low sensitivity and a slow acquisition time, making it practically impractical. Flow-independent MRI has become more popular, with sensitivity and specificities

rounding at 95 to 100%. There's a great deal of data on contrast-enhanced MRI, avoiding adanalenum using the iron compounds, and you'll hear later from Dr. Black about Direct Thrombus Imaging. There has been significant work on Thrombus Imaging,

but I will leave it up to him to talk about it. MR you can diagnose a DVT, either in both modalities, and you can see here with the arrows. It will also provide you data on the least inaccessible areas for duplex and other modalities,

such as the iliac veins and the IVC, as can be seen here. It is also perhaps easier to use than CTV, because at least in my institution CTV always comes out as a CTA, and I can't help that no matter what happens.

MR can also show you collaterals, which may be very important as you are trying to diagnose a patient. And in essence it may show you the smaller vein that you're more interested in, particularly in pelvic congestion syndrome,

such as this patient with an occluded internal iliac vein. It can also demonstrate, for those of you who deal with dialysis access, or it's central line problems, central venous stenosis and Thrombus. But equally importantly

it may show you that a stenosis is not intrinsic to the wall, but it's actually intrinsic to extravascular inflammation, as in this patient with mediastinal fibrosis, and which will give you a different way of what you wish to do and treat.

The European guidelines have addressed MR in it's future with chronic venous disease and they give it a 1C rating, and they recommend that if doesn't work you should proceed to Ibes. It can be used for the diagnoses of pulmonary embolism,

it can eliminate the use of ECHO, one can diagnose both the presence of the Thrombus, the dilatation of the ventricul, and if one is using Dynamic MR Imaging one can also see mcconnell sign or the equivalent on the septum between the two ventricles.

More interestingly it can also be used now in the chronic thrombuc, pulmonary hypertension, where it can show both the legions that are treatable and untreatable, as some of you may have heard from Dr. Roosevelt

earlier in the day, where they're now treating the outlying lesions with balloon angioplasty serial sessions. It can also look at the ventricul and give you some idea of where the ventricul stands with regard to it's performance,

we're looking at and linking this to the lungs. It can also show you the unusual, such as atresia of the IVC or it can help with you the diagnosis of Pelvic Congestion Syndrome. And it is extremely valuable

in dealing with AVM's, although it may take one, two, or three sessions with differing contrast bulosus to identify both the arterial, the intrinsic lesion, and the outflow lesions,

but a very valuable adjunct. In renal carcinoma it has two values, one is that it can may diagnosis venous invasion, and it may also let you understand whether or not you are dealing with bland thrombus or tumor thrombus,

which can change the staging for the patient and also change the actual intervention that you may perform. If you use flash imaging one will get at least an 89% sensitivity of the nature of thrombus,

whether it's bland or tumor thrombus, which may change what you need to do during the procedure. It could also tell you whether there's actual true wall invasion, which will require excision of the IVC

as opposed to the simple thromboendarterectomy. And this can run up to a specificity of 88% to exclude it. In the brain it's commonly used to diagnose the intra tumor vasculature. Diagnosing between veins and arterial systems, which can be helpful

particularly if one is considering percutaneous or other interventions. With regard to central venous stenosis there is some data and most people are now using an onlay technique where they take the MRI,

they develop the lines for the vessels and then use that as guide in one or two dimensions with fusion imaging to achieve access with a wire, catheter and balloon, as opposed to a blind stick technique.

There is data to show that you can image with the correct catheter balloons within the vessels and do serial MR's to show that it works. And finally with guidance catheters EP is now able to guide the catheter further and further in to achieve from the,

either the jugular or the venous access across the septum and to burn the entrium as appropriate. And finally, one can use MR to actually gain access, burn, and then actually use the MR to look at the specific tissue,

to show that you've achieved a burn at the appropriate area within the cardiac system and thus prove that your modality has achieved it. So in summary, we can use it for primary diagnosis, confirmatory diagnosis,

procedural planning, and procedural adjunct, but we're only still learning how to use it as a primary procedural modality. Thank you so much.

- Sam, Louis, thank you very much. I also kind of reduced the title to make it fit in a slide. Those are my disclosures. We've switched to using a hybrid room routinely a couple of years ago and what happened then is that we started using 3D imaging

to guide us during the procedure using a fusion overlay. Obviously this was a huge benefit but the biggest benefit was actually 3D imaging at the end of the procedure so rather than doing an AP fluoro run, we would do a 3D acquisition in a cone beam CT

and have those reconstructions available to check technical success and to fix any issues. We've been using this technique to perform translumbar type 2 endoleak treatment and what we do is we do a cone beam CT non contrast and we fuse the pre-op CT on top of this cone beam CT

and it's actually quite easy to do because you can do it with the spine but also obviously with the endograft so it's a registration on the graft on top of the endograft and then the software is really straightforward. You just need to define a target in the middle

of the endoleak. You need to define where you want to puncture the skin and then the system will automatically generate to you a bull-eye view which is a view where you puncture the back of the patient and the progression view you obviously see the needle

go all the way to your target. And what is interesting is that if you reach the target and if you don't have a backflow so you're not in the endoleak, you have this stereo 3D software which is interesting because you do two lateral fluoro runs

and then you check the position of the needle and then it shows you on the pre-op CT where you are. So here in this specific patient, I didn't advance the needle far enough. I was still in the aortic wall,

that's why I didn't get backflow so I just slightly advanced the needle and I got backflow and I could finish the embolization by injecting contrast, close and then ONYX to completely exclude this type 2 endoleak. So now let's go to our focus today is fenestrated endograft.

You see this patient that were treated with a fenestration and branches. You can see that the selective angio in the left renal looks really good but if on the cone beam CT at the end of the procedure we actually had a kink on the left renal stent

so because I had depicted it right away at the end of the procedure I could fix it right away so this is not a secondary procedure. This is done during the index procedure so I'll go directly to what we did is we reinflated a ballon,

we re-fed the balloon and then had a nice result but what happen if you actually fail to catheterize? This was the case in this patient. You see the left renal stent is completely collapsed. I never managed to get a wire from the aortic lumen and back into the renal artery

so we position the patient in the lateral position, did a cone beam CT and used the same software so the target is now the renal artery just distal to this crushed renal stent and we punctured this patient back in the target and so you can see is right here

and you can see that the puncturing the back. We've reached the renal artery, pushed a wire through the stent now in the artery lumen and snared the wire and over this through and through wire coming out from the back we managed

to reopen this kinked left renal stent. You can see here the result from this procedure and this was published a couple of years, two years ago. Now another example, you can see here the workflow. I'm actually advancing the needle in the back

of the patient, looking at the screen and you can see in this patient that had a longer renal stent I actually punctured the renal stent right away because at the end of the procedure I positioned another covered stent inside

to exclude this puncture site and then, oops sorry, and then, can we go to the, yeah great thank you. And then I advance the wire again through this kinked renal stent into the endograft lumen and this is a snare from the groin

and I got the wire out from the groin. So you see the wire is coming from the back of the patient here, white arrow, to the groin, red arrow and this is the same patient another view and over this through and through wire

we manged to re advance and reopen this stent and we actually kinked the stent by getting the system of branched endograft through a previous fenestrated repair and fortunately my fellow told me at the end of the procedure we should check the FEVAR

with a cone beam CT and this is how we depicted this kink. So take home message, it's a very easy, straightforward workflow. It's a dedicated workflow that we use for type 2 endoleak embolization. We have this intermediate assessment with Stereo 3D

that helps us to check where we are so with 3D imaging after the learning curve it's become routine and we have new workflows like this way of salvaging a kinked renal stent. Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. The stuff Rubiole said about magic methods, but not concerning the large veins, as we heard, would be also about that or something. I don't have disclosures. We all like probably to treat such a pathology. It's quite common in our offices.

And most of us treat them without the problems. But probably we will be not much happy to having such a patients to treat, especially if we see such a pathologies, not this what you, really, I like, especially if patient is coming with the recurrence

in the same place for the third or fourth time. So of course, reflux identifications, we heard this based on ultrasounds. Small vessels, feeding vessels can be seen on the ultrasound and torso transillumination. In most cases, this will be probably sufficient,

but as we have no doubt about this case what to do. In many cases, or at least in some cases, we see the patient coming with sclerotherapy failure. And then probably the first thing that we should look for, it's a feeding vein. Persistence or persistent of a large vessel.

Reflux, what else, except physical examination, except transillumination we can use? Near Infrared light technology. And ultrasound especially. Ultrasound with high frequency that allows you to do exactly this what the static medicine doctors do.

So, to see the skin in a very good quality matches. So, concerning Vein Viveror of this transillumination, often of this wentetrotite methods that I think most of your are familiar with, this, we can use this in some cases, but as in this case it is quite easy and possible.

In this case, on the right side, I not sure what's really a problem in this patient because probably the feeding veins comes goes from, goes from the down in a perpendicular manner. So if you have such a lesion without any feeding veins visible in transillumination or in almentoteratity,

what can we do to close this? Then, I would like to encourage you to use high resolution ultrasound. This is the same lesion with 0.6 millimeter vessel just below, but this vessel goes perpendicular to one of the quite big perforators as you can see,

in a very perpendicular manner, probably none other methods can show us this kind of pathology. With this high resolution high frequency ultrasound, you can see reticular veins, but this is what is especially interesting,

you can see the connection with all vessels being below the lesion that can be not visible in any other technology. Perforators going oblique and going perpendicular are quite good visible. I can try to find the reflux in compressing the skin,

but quite often the reflux can be seen using the simple valsalva maneuvre, as the vessels are very small. Some examples what we can see the perforators, but also like on the right side, the novus scleroization coming from the

small vessels after this thing is removal. And we made some small study of 50 C1 lesions resistance to sclerotherapy failure, treated after the diagnosis made by augmented reality and 18 megahertz probe Venous ultrasound. All these lesions were previously treated,

as you can see some of them even three times, no major vessel reflux, no large branches, no axial reflux, and no vessel is visible in transillumination in the series. We found that in 50% there were the vertical or oblique course vessels feeding this lesions and

vertical plus horizontal additional 26, so we had the perpendicular going pathological reflux in 3/4ths of the patients, reflux sources in 62% were perforators or deep vein connectors. On this patient were treated with ultrasound guided sclerotherapy, or with augmented reality

guided sclerotherapy. And as you can see, 66% of the feeding veins were recognized by 18 megahertz ultrasound and we could probably not find this in any other way after six months follow-up. 90% of these lesions were obliterated.

However, 1/3 required the repeated treatments. In conclusion, the combined approach based on the augmented reality and the 18 megahertz ultrasound feeding vein identification improved the C1 sclerotherapy efficacy in the treatment of pathologies not applicable for the primary treatment

and is not for the standard approach. And we currently don't use this in standards approach, we use this for lesions that you saw. Thank you very much.

- Thank you, my disclosure says it pertains to this Centerline Biomedical specifically. As many of you know, real-time Dose Monitoring has shown that the EVAR procedures really exposes to the most amount of radiation, Of all the endovascular procedures that we do. Obviously the complexity of those

has something to do with that. But even a straight forward EVAR shows that. And most studies show that vascular surgeons are probably the least educated and knowledgeable about ways to reduce your exposure to radiation. Now Gustavo talked about this,

when you look at the radiation scatter when you're in a hybrid room you see that once the imaging intensifier moves to anything other than AP position the amount of scatter starts to increase. And it's that scatter which exposes most of us

that are near the patient to this. In addition, I will tell you that most of your patients that we operate on were right near the imaging beam, where as most peripheral interventions we do step out of the room,

during any of the major flouroscopic treatment time in DSA angiograms, as Gustavo said. So what can you do from protection strategy standpoint? Well you can use protective equipment, which includes drapes and shielding which I go over.

But the majority of it is what procedural details much of which Gustavo has gone over. Now in our institution I highlighted two things there, for many years I've used the zero gravity suit this has two advantages, number one it covers your head from exposure,

but it does not extend down to below the legs and I'll talk about that. I know that Bijan is on the podium and he probably has better education, and can talk more about his study than I know. But we have added leggings to that aspect.

The other thing about the Zero Gravity Suit is from a longevity for you as a physician you do not have the weight of the lead on your shoulders so over time the amount of neck and injuries from that aspect is probably going to be decreased. Now this is taken from Bijan's paper

it's about the Radiation Induced DNA Damage and you can see that patients that are people that did EVAR procedures had an increase in the amount of radiation damage, compared to if they did an open repair. And you can see the difference there

in purple between EVAR and branched and fenestrated repairs but the most important thing, I think that many of us took away from his paper, was that when you added leggings to it you can see in the bottom left, the amount

of radiation and DNA damage was the same. But the amount of DNA damage went way down on the black bars there, compared to the red bars pre-imposed. So why that was, is probably the subject of many more papers

and a lot of grant money for Bijan to do. I think this is going to be a very important topic in the next several years. Now Gustavo had eight things, I have a list of ten things that you can do, to help during procedure. But the biggest as he mentioned, was the

obliquity of the orientation of the tube. Eye protection is a very important approximately about 30% of the radiation comes around your eye protection wear. So either using the shield like I showed you from zero gravity, or side shields are very important.

You need to save images, optimize images use non DSA or exit the room for DSA things. Varying the technique, adding barriers, slow your frame rate down. Now Gustavo says, he said seven and a half or typically a two.

If I wanted to get a better image I will go to three or to a seven. But generally we are at two frames per second for most of our work. I unfortunately do not have yet digital zoom that's probably coming in the next version

of the models that we use. Increasing the table height, getting the table high and the imaging intensifier down is very important. What about other things? Well we have to change our habits,

most of this is getting in the right habit. And most of our radiation badges tell us a month later what happened. But we don't know what case and what we did during the case to change it. That's more modern day badges,

this is an early detection system. Basically you see your dose on the screen, as the case is going along. And it gives you direct feedback that you might need to change what you're doing. Add barriers to between you and the source

so when your dose is going higher than other people in the room. It's kind of like the concept of the canary in the coal mine. When the canary is starting to have problems and went to the bottom of the cage

the coal miners new that they needed to get ut of the coal mine because they were being exposed to lethal gasses. So what does this do? If you look at the dose aware data, it shows you here in purple

that the level of radiation exposure, once they started to use the Dose Aware, went down compared to the number of incidents of over-exposure, in the system. Gustavo talked a little bit about Intra-Operative Guidance,

vessel deformation, and customized options. Are coming down the guidelines. And you can see this is a paper with Stephan Haulon and Rob Rhee about how they reduced their dose. Lastly we need to think about moving

away from fluoroscopy and this is what's coming down the future, with Centerline Biomedical. Using electro-magnetic navigation to track devices, cathers, and wires through the system, Without ionizing radiation. And this will be the future.

So in conclusion, current advancements in vascular therapy significantly increase the exposure of vascular specialists, to the harmful effects of ionizing radiation. Maximal efforts should be employed by proceduralists to protect themselves.

Including the legs, and the neck, and the head. An immediate intra-procedural feedback is important for developing proper techniques and prevention. Future research should be focused at identifying non-ionizing methods for navigation and device implantation.

Thank you.

- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company

for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.

The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the

middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,

which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up

in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.

Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,

embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,

we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,

which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.

We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,

excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success

just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and

no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.

We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,

and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.

We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,

post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch

blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it

through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,

we actually have several publications out, demonstrating safety and ethicacy. Thank you.

- [Presenter] Thanks Bill. And again I have no disclosures to make on this particular presentation. So, in terms of variance, the anterior accessory GSV is not a variant. It's present in most of us, but it's an unusual cause of primary varicose veins,

although a very common cause of secondary varicose veins after primary treatment. It runs parallel to the great saphenous vein, in the saphenous space, and courses a bit more anteriorly in the thighs, so that on ultrasound, you'll see a lining here,

in this case inside the saphenous space, aligning with the superficial femoral artery and the femoral vein. In some cases, it can be the primary saphenous vein along the medial aspect of the thigh, in association with hypoplasia of the great saphenous vein

as listed on the left, and the right picture with aplasia of the great saphenous vein. And many times physicians are treating what they think is the great saphenous vein, and really it's this embryologic variant,

the anterior accessory vein, with a different takeoff. A different vein to talk about in terms of variance is the superficial accessory saphenous vein. It's present in many patients. It's really a tributary of the great saphenous vein,

running in the subcutaneous fat outside the superficial fascia that eventually joins into the great saphenous vein. So on this longitudinal view, it creates this sort of appearance with the great saphenous vein below its entry

as a smaller caliber vein. Consequently, it has the name of the H-vein, and on ultrasound, below the level of its joining with the great saphenous vein, the great saphenous vein is small,

and in this particular case with varicose veins, associated with reflux in the superficial accessory saphenous vein. It's a larger caliber, and then up higher, you can see that it drains into the great saphenous vein, and it's no longer visible.

The small saphenous vein has a lot of variability related to the differences in its termination on the posterior aspect of the calf and the thigh. Many patients have what we can call saphenopopliteal junction dominant drainage, and other patients have what we might consider

thigh extension dominant drainage. It's a spectrum, most patients have these connections, and if you look carefully, you'll find the thigh extension connection even in the majority of patients that have primarily saphenopopliteal junction termination.

The termination higher on the thigh can be into a perforator on the back of the thigh, it can be into the gluteal venous system in the pelvis, and it can travel up through an intersaphenous or Giacomini vein toward the inner thigh,

and sometimes to the great saphenous vein. Duplications of the deep system are very common, particularly in the femoral vein in up to 20% of the patients. Isolated popliteal vein duplications are uncommon, but in association with femoral duplications

occur in up to 6% of the variations. These duplications all travel through the adductor canal and follow the normal course of the vein. In contrast, remnants of the sciatic vein can introduce different variants. The sciatic vein is an embryonic vein

that was the primary drainage of the lower limb in a very small fetal stage. At some point, most of it regresses, and so the popliteal vein, which is the sciatic vein remnant, eventually connects up with the pelvic circulation

through the common femoral vein and the external iliac vein which develop later. The saphenous remnants regress, with the exception of the popliteal vein, and portions of the internal iliac vein. A true sciatic vein variant is a less common variant,

where the popliteal vein is in continuity with a large caliber vein that follows the sciatic nerve up into the pelvis, draining into the internal iliac vein. But in contrast, sciatic vein remnants are not uncommon,

and it's not unusual for one to find the primary drainage of the popliteal vein not going through the adductor canal, but to ascend upward variable lengths along the course of the sciatic vein, to eventually terminate either in the femoral vein directly

or into the deep femoral vein up higher, with or without hypoplasia, or in rare cases, aplasia of the femoral vein. And so it's important to recognize these variants in distinction to post-thrombotic changes

in the femoral vein. When you have a small vein, that small vein can be normal anatomically by all other features, and may represent a variant rather than a post-thrombotic complication.

And this was recognized by Dr. Raju in 1991 in a publication where he demonstrated venograms in a patient with a post-thrombotic femoral vein, and well-formed collaterals between the popliteal vein and the profunda, in contrast to this patient,

which had no post-thrombotic changes in the femoral vein, but well-defined congenital variation connections between the popliteal vein and the deep femoral vein. So in summary, superficial venous variability is related to the variable terminations

of the small saphenous vein, the anterior accessory saphenous vein, which is inside the saphenous sheath, superficial accessory saphenous veins, which are outside the saphenous space. It's important to recognize deep vein variablity,

'cause you want to avoid false negative diagnoses of acute deep vein thrombosis by not recognizing thrombosis in a duplication, and you want to avoid false positive diagnoses of post-thrombotic syndrome

- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.

They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression

if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.

Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.

This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,

and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients

who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,

and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,

symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.

There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,

again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,

six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,

it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse

if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective

in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.

This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent

because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common

in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.

So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,

those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,

like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.

And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,

get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.

If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners

over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,

it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,

look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.

That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,

then I would do something endovascular. Thank you.

- I find it very difficult to get into an argument with one of my mentors, Dr. Raju, and I apologize for going off on a little tangent. And I will submit to you that when we look at this, this may be a better way of looking at it because we're taking an instance of non-flow dynamics as well as collapsible tubes

and everything's not perfect. So I have no real disclosures with this. And with the emergence of dedicated venous stents and understanding the role of individual design elements, cell architecture, radial strength, flexibility, and the performance of stents,

and more importantly how this therapy improves patients outcomes is critical in continuing the treatment pathway and continued improvement in stents. My take home message are very clear. For a given perimeter, lumen shape impacts area,

lumen shape impacts pressure, aspect ratio is a better predictor of flow and patient outcomes versus area. So, what is aspect ratio? It's the Degree of Roundness. And if you look at aspect ratio is equal to

the maximum diameter to the minimal diameter and if keep the change the keep the perimeters the same, you see what happens to the area, it actually decreases.

And you can see what happens to the aspect ratio. So the perfect aspect ratio is one. As we get to a more elliptical area, or an oval, it changes to four. So, if we look at this again, when we look at the whole area here,

even keeping the perimeters the same, you can see what happens to the area. The area shrinks. As the aspect ratio also changes. But more importantly, as we look at a mathematical calculation of shape and area,

round equals more area and less drag and thus better flow. Remember we're dealing not with arteries, we're dealing with veins and collapsible tubes. And increasing the flatness as you go across the X axis equals less area and more drag and thus less flow. And we always look at Poiseuille's Law,

but Poiseuille's Law's only important for perfect circles. And what I'm trying to submit to you, is that vein's are certainly not perfect circles, but as we get to figuring out what a perfect circle is and using a stent then this does apply.

And so, shape impacts on flow and pressure for a given perimeter summary. Shape directly impacts area. Area has an indirect impact on flow and pressure. The greater the aspect ratio the smaller the area. And shape becomes flatter

flow decreases and pressure increases. So, if we look at this publication by Dr. Cho, he looked at a better accuracy, patency associated with a rounder lumen. And he took 48 patients with iliac compression and acute DVT followed for an average of 20 months.

Stent compression considered significant if lumen compression was greater than 50 percent. And significant stent compression was inversely correlated with stent patency. And so, healthy veins are not round. What shape results in better outcomes?

So, if look at the VIRTUS trial, and looking at the feasibility trial, we looked at aspect ratios, and I would submit to you that if you look at the pre-stent aspect ratio, you can see it starting at 2.51

and then as over the 12 months, it was figured at 1.23. So as we get closer to one, it becomes more oval. And the same thing, the areas improved as well. But if you look at this scattergram, the relationship between post-stent vessel change

and 12-month patient outcome, this being a change in VCSS scores, so anything greater than a VCSS score of change of 2, there was no correlation in terms of Pearson coefficient here, but there was a mild correlation here,

with looking at aspect ratio. One would expect a positive correlation with area if we went with Dr. Raju, however just for this limited trial, there was none. And if we're looking at the graphs, there was no clear pattern for area change,

well the change in aspect ratio is clear. Moderately positive relationship between decreased ellipticity and clinical improvement. And patients with greatest luminal change oval to round most likely to exhibit clinical improvement. And I submit to you that aspect ratio is something

that we should consider as we go forward. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. Thank you, Frank, for inviting me again. No disclosures. We all know Onyx and the way it comes, in two formulas. We want to talk about presenter results when combining Onyx with chimney grafts. The role of liquid embolization or Onyx is listed here.

It can be used for type I endoleaks, type II endoleaks and more recently for treatment of prophylaxis of gutters. So what are we doing when we do have gutters? Which is not quite unusual. We can perform a watchful waiting policy, pro-active treatment in high flow gutters,

pro-active treatment low flow gutters, or we can try to have a maximum overlap, for instance with ViaBahn grafts 15 centimeters in length or we can use sandwich grafts in order to reduce these gutters in type I endoleaks. Here, a typical example of a type I leak treated with Onyx.

And here we have an example of a ruptured aneurysim treated with a chimney graft. And here is what everybody means when they're talking about gutters. Typical examples, this is what you get. You can try to coil these

or you can try to use liquid embolization. Here's the end result after putting a lot of coils into these spaces. What are these issues of the chimney-technique type I endoleak? Which are not quite infrequent as you see here.

Most of these resolve, but not all of them. So can we risk to wait until they resolve? And my bias opinion is probably not. Here, the incidents of these type endoleaks is still pretty high. And when you go up to the Arch

the results can even be different. And in our own series published here, type I endoleak at the Arch were as high as 28%. A lot of these don't resolve over time simply because it's a very high flow environment. Using a sandwich technique is one solution

which helps in a lot of cases but not all of these simply because you have a longer outlet compared to a straightforward chimney graft. You can't rely on it. So watchful waiting? There are some advocates who

prefer watchful waiting but in high flow gutters this is certainly not indicated. And the more chimneys you have, like in a thoracoabdominal aneurysm with four chimneys, the less you can wait. You have to treat these very actively,

like you see here, in these high flow areas. Here a typical example, again symptomatic aneurysm with sealing. Here Onyx was used but without any success. So what we did is we had to add another chimney and plus polymer sealing and then we had a good result.

Here some results, only small serious primary gutter sealing using Onyx with good results in a type I leak. But again, this is only a small series of patients. Sandwich technique already mentioned. When you use, like we did here for chimney grafts in the arteries, you do need Onyx otherwise you

always get problems with these gutters and they do not seal over time. Another example where liquid polymer was used. And here again, you see the polymer. The catheter in order to inject the polymer is very difficult to see but with a little bit of experience

you know where you are. And again, here it is, the Onyx, a typical example. Here another example of the Arch, bird beacon effect, extension, chimney graft. Again the aneurysm gets bigger. And so a combination of using proximal extensions

plus chimneys plus liquid embolization solves this problem after quite a long period of time. And here typically is what you see when you inject the Onyx. This does not work in all cases. Here we used Onyx in order to seal up the origin of the end tunnel.

This works very nicely but there is so ample space for improvement and in some cases it's probably better to use a fenestrated branch graft or even the opt two stabler instead of using liquid embolization. Thank you very much.

- Thank you, thanks to Dr. Veith and the program committee for allowing me to present this morning. My disclosure. So, uh, I think that there's been an abundance of literature over the years that is suggested that venography may have poured diagnostic sensitivity for identifying iliac and, and

common femoral vein obstruction. Uh, in uh published literature, 34% of patients who have chronic venous symptoms of a severe degree had iliac vein obstruction on imagining techniques other than venography such as IVUS with normal venograms and often times

patients have significant outflow obstruction and there are no pelvic collaterals present so this is not a reliable though maybe specific indicator of outflow obstruction. The video study was designed to prospectively compare multiplanar venography vs. IVUS

to address the question if you do enough views on venogram do you find the same lesions that you might detect with IVUS. And we also wanted to look, does the imaging that you do to look for iliac and common femoral vein outflow track obstruction

effect your clinical decision about intervention. These are the patients in the video trial CEAP 4 through CEAP 6. And so 100 patients were randomized in this or not randomized, but rather entered entered this prospective multi-center single-arm study

at 14 sites in the US and Europe. This was half CEAP 6 patients and the remainder were CEAP 4 and 5. The patients underwent multiplanar venography. The site investigator was asked to make a decision about whether there was a significant lesion

and how they would treat that lesion and then once that was recorded IVUS was preformed and then again after the pull back the investigator was asked to make a decision about whether there was a significant lesion and how they would treat it.

We standardized venography with a hand injection in 3 views as noted. A 30 degree RAO and LAO and an AP view and the catheter was placed at the cranial portion of the femoral vein we adopted the standards and the literature

of a 50% diameter stenosis. And venography in a 50% CSA reduction on IVUS as a significant lesions. The uh, study cohort was approximately 43 women. The left leg was the index limb and 2 to 1 ratio to uh, to the right.

The age average 62 and you can see the majority of the patients were CEAP 4 and CEAP 6. What we identified with IVUS is a 21% greater (mumbling) identification of outflow obstruction. Venography was a lot less sensitive

at identifying these lesions and therefor suggesting that IVUS is a more sensitive imaging modality for identifying outflow obstruction vs. multiplanar venography. And when you looked at the core lab over read

this was for both the IVUS imaging and for the venography. And we at first calculated the diameter stenosis for both modalities we saw that with the multiplanar venography you tended to underestimate

the degree of diameter stenosis compared to IVUS and this resulted in missing about a quarter of the lesions that were greater than 50% diameter stenosis. And in part IVUS intended to score the lesions more severe for the same lesions compared to venography and this was statistically significant.

When we looked at CSA measurements from the IVUS system and also calculated off the venography in the core lab we saw again that venography missed about 18% of the significant greater than 50% CSA lesions even with reviews.

And this resulted in a change of procedure in about 60% of the patients there was a change in the decision about whether to treat of not and in 50 of the patients the number of stents changed from either no stent to 1 stent or 1 stent to 2 stents.

So without IVUS your likely under treating iliac and common femoral vein obstruction. This was the uh, rVCSS scores after treatment in this group. On the right here in green is the improvement on the left worsening.

And you can see in large part these patients all improved uh, expect for this outlier here and then some patients there was no improvement and when you looked at a score a VCSS score greater than 4 as being significant at 1 and 6 months there was a significant improvement post intervention.

And we see here in this receiver operating curve that IVUS best predicted clinical improvement at 6 months. And so we see that IVUS was more sensitive accurate for identifying significant lesions and the iliac and common femoral vein segments. It was the best guide for stent intervention

and it appears that if use a 50% cut off either diameter or CSA reduction it best predicts that intervention will lead to an improved clinical outcome at 6 months. Thank you.

- [Presenter] Dear colleagues, good afternoon. I present an update on the double-blinded trial on CCSVI Brave Dreams. This is my disclosure. The first data coming out from the Brave Dreams trial were affected by the (mumbles). Where venous PTA did not demonstrate additional effect

on the measure of disability and the new MRI lesion in relapsing remitting (RR) Multiple Sclerosis group at 12 month follow up. The major limitation of the trial is the inefficiency of balloon angioplasty in restoring flow in all the presentation of CCSVI

because in the prime, the flow was restored just in 79% of people. It means in favor of gravity and CCSVI criteria were solved in only 54% of the PTA arm. However, the technique demonstrated to be safe. Pre-operatory morphology affects the effectiveness

of PTA in jugulars, and Giaquinta demonstrated that patients who exhibit hypoplasia, external compression, or longitudinal endoluminal defects did not respond very well to the treatment. And commenting on this, Moneta proposed an additional post hoc analysis focusing

on the PTA responder group identified by Giaquinta in the materials of Brave Dreams trial. So Ladies and Gentlemen, is the hypothesis to be rejected? The CCSVI hypothesis could be considered valid if the subgroup with restored flow

following balloon angioplasty shows benefits compared to the subgroup in which the PTA did not work. So we performed a sub-analysis by comparing the patients with jugular flow not Doppler detectable in upright at 12 months, respect to those

who presented a mono-directional phasic jugular flow. The flow data of the balloon angioplasty arm was matched with a caffeine point, which have accumulation of new lesion on MRI. And the result was extraordinary because 91% of people with restored flow in upright

showed no lesion accumulation. This time the analysis was significant also at 0-12 months where we found 77% of people with restored flow, lesion free. And more than 20% of people protected by PTA were near follow up.

So Ladies and Gentlemen, in conclusion, PTA is safe but restored the flow in favor of gravity in the jugulars in just 79% of patients. However, a post-hoc analysis demonstrates a significant decreased risk of new lesion development at MRI in patients with restored jugular flow

following balloon angioplasty, as compared to those with absent flow and/or to sham. Further analysis and investigation may provide the pre-operatory ID of such a subgroup of responders. Thank you very much.

- Thank you, good afternoon. I have no disclosures. Well, obesity really is a worldwide epidemic, but among all of the industrialized nations the United States seems to lead the league in terms of the percentage of our population overweight and/or obese.

We're all aware of the adverse health effects of obesity including predisposing to diabetes, itself an epidemic problem, at least in this country. In fact the AMA has suggested obesity should now be declared a disease state with its own ICD-10 code. If that's true as this article in time magazine said

if obesity is a disease why are so many obese patients seemingly healthy? We do know that obese patients tend to have smaller myocardial infarct size, they have improved survival after episodes of heart failure, there's improved survival

after CABG and coronary angioplasty procedures, and there's reduced early and late mortality after acute stroke. In fact we're seeing this so-called obesity paradox play out in vascular surgery. This was an early review of 7500 patient undergoing

a variety of vascular surgical procedures and what you see is this U-shaped curve where is overweight, mildly and moderately obese patients have significantly lower operative mortality. This was a similar NSQIP analysis of over 5000 patients undergoing AAA repair and among all procedures

again you see that same U-shaped curve largely reflected the reduced mortality for open surgery for overweight, mildly and moderately obese patients. We became interested in whether this would play out on a low risk procedure, relatively speaking, carotid endarterectomy.

We investigated 23000 patients undergoing carotid endarterectomy in the NSQIP database. Only a quarter of our patients were normal weight, about 40% over weight, and then nearly 30% were obese. And we found the very same thing, although mortality is exceedingly low, 0.6%,

it was significantly lower in overweight, mildly and moderately obese patients. The overall stroke rate was 1.4% and again that very same U-shaped curve. Stroke rate lower in overweight, mildly and moderately obese patients.

In the most recent and the largest data set ever analyzed, 92000 patients undergoing the spectrum of vascular surgical procedures. A third of the patients only normal weight, about a third overweight, and more than a quarter severely overweight.

We found that mortality was actually higher in underweight compared to normal weight individuals. So it's not good to be thin, many of us take comfort in that. We found that, they found that mortality was lower in overweight compared to normal weight individuals.

Mortality was lower in obese compared to normal rate individuals and this reflected the fact that cardiac complications occurred significantly less often in obese compared to normal weight individuals. And respiratory complications occurred less often

in obese compared to normal weight individuals. How do you explain this? Well this was a fascinating report from the Health Professionals Follow-Up Study. 38000 individuals, men middle-aged who have been followed for up to 25 years, and if you look at overall

mortality, again that very same U-shaped curve. But what they did in this study was they divided BMI into lean body mass and fat body mass and as you can see there is that U-shaped relationship with respect to lean body mass, but when they ferreted out statistically fat body mass

there was a direct proportional correlation with mortality. How do we explain this? Well we're learning that adipose tissue is more than just a storage depot for energy, it is also an endocrine organ. Adipose tissue produces molecules called adipokines

the most important of which is adiponectin. An elevated BMI is associated with reduced levels of adiponectin which has a positive impact on cardiovascular complications. So in summary, the impact of weight on vascular outcomes is complex.

Modest excess weight appears to be protective for perioperative mortality and cardiorespiratory morbidity. Excess weight is a risk factor for wound complications but the obesity paradox may be related to the endocrine function of adipose tissue. Thank you.

- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans

can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.

But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.

What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?

Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for

all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',

and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.

He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.

So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.

It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,

and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after

you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,

and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.

That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.

How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.

But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.

In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,

the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors

such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants

to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study

because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.

So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist

on maximal protection and assume that all radiation is dangerous. Thank you very much.

- After Dr. Mow-knee's excellent review I don't have much to add here, but just go by here. I have no conflict of interest. As he already said, Takayasu arteritis is a systemic disease, affecting entire wall. It's fundamentally different from atherosclerosis. I like to emphasize once again because same principle

to relieve ischemic symptom based on atherosclerosis should not be applied to Takaysu arteritis. That's what we learned for the last three decade. This is a primarily medical condition to need the medical treatment and not a surgical condition until it develops the complication,

hence the primary aim of treatment is to control active inflammation and induce remission just like Dr. Mow-knew gave a thorough review here. The inflammatory nature of TA waxes and wane with active or chronic system inflammation hence strict control of this condition is absolutely warranted before

any surgical or endovascular management is considered. After all, TA is a medical condition and not a surgical one from the outset. TA has a strong nature of the collateral development to provide excellent natural compensation sufficient to relieve the symptoms in general hence not all symptomatic

lesions actually require the intervention, that's what we also learned, for the intervention accompanied with significant morbidity, we already understand, restenosis, thrombosis, and stroke, etc. So intervention should be reserved for specific indication like uncontrolled hypertension, for example.

Open surgery with bypass has been able to relieve most of lesion to cause acute or chronic insufficiency and remain gold standard but it has excellent track record only for its end stage. It does not provide same good result in early stage. Therefore, bypass surgery should not be considered

as a panacea to relieve all the lesion and remains vulnerable through the rest of the life. So surgery should not be undertaken lightly and good only for those in advanced stage. Nevertheless, diffuse, proximal, multifocal involvement make surgical intervention with bypass often difficult

and such lesion would need some other way to try. That is endovascular approach with angioplastent has proven for safety and also effective alternative method. So main indication for the PTA and stent include clinically ischemia involving one or more vascular bed, we just heard.

Intervention gains popularity especially as interim management for the unsettled case, in particular with multiple lesions. Indeed the results of the endovascular intervention are less encouraging, we already heard, compared to open surgery.

The risk of restenosis in TA is significantly higher reaching over 50% at five years just like Mayo data, like ours data here. Our own results on 24 cases almost identical to what Mayo reported, and some other people as we published already.

So a diligent controlled disease activity prior to and following revascularization is crucial to prevent such complications. So as the conclusion, together with a bypass endovascular management with a PTA stent is now well accepted and symptomatic TA inactive chronic state can be managed

safely either by bypass or endovascular surgery. However, endovascular therapy accompanies higher rate of recurrence. Open surgery at present remains the preferred option delivering better long-term outcome and especially in the advanced stage.

Endovascular intervention fulfills its new role as an interim measure especially for the group open surgery carries too high risk like multivessel involvement. Thank you for attention.

- Yeah, thank you very much. Unfortunately Dierk Scheinert couldn't come, so thankfully he's allowed me here to take this presentation over so thanks a lot for this. So these are the latest 5-year results of the INCRAFT device from Cordis Devices currently under FDA review not yet approved

in the US, but in Europe. These are the conflict of interests, this is (mumbles). So this device is a three-piece modular system, low porosity polyester. You can bilaterally in-situ length adjust it up to 3cm. And the main feature I think with this device

is it's a low-profile device, 13 Fr inside 14 Fr outside except the biggest body which has an outer diameter of 16 Fr. The innovation study that was 60 patients, you can see here some objectives. So the question was whether you could deploy it

accurately where you wanted to have it without any type I, III, and IV endoleaks and of course there were also some other primary and secondary endpoints and again follow-up had to be done up to five years. This is a busy slide just showing you,

please look to the right side, to show you that there were quite some violations of the recommendations in which kinds of anatomies to implant this craft. Here for example neck lengths less than 10mm, here were some patients implanted.

Also angulations over 60 degrees, three patients, there were some thrombus in the neck, and here you can see aortic bifurcation smaller than 18mm, there were quite some patients and especially the iliac sealing length was shorter than 10mm in nearly 50% of the patients

and also the diameter of the external iliac arteries were nearly 50% lower than 7mm. Here the freedom from endoleaks type I was one at 30 days which has been resolved and another one developed after 30 days which also has been involved. No type III.

Stent graft patency after 30 days also 100% and otherwise also no other adverse events with this device at thirty days. So to answer the question with this device to the first question of (mumbles) will lighter fabrics and stent material decrease EVAR durability?

Will there be more endoleaks I, III, or IV? You can see here the long-term data so no Ia endoleak developed over four and five years, there was one Ib endoleak which developed at four years which also was apparent at five years. No type III endoleak.

One graft patency failure with a (mumbles) occlusion here at four years which also was here at five years. No migration, one fraction of the (mumbles) proximal third graft, otherwise it was very safe. You can see here once again the Kaplan-Meier curve for type I endoleaks through five years here

with type Ib here later on, and this is the patency Kaplan-Meier curve also showing here the good patency at five years, and this is freedom from second large vent. Here I don't have any data whether this is type II endoleak or not so this still has to be reported and clarified.

So to conclude the INCRAFT performed well on long-term while overcoming more difficult access morphologies. The endograft can be utilized in patients with demanding access and vessel morphology, and there are more studies ongoing.

There is one in the US and Japan where we wait for long-term data, 190 patients and also from Europe's 180 patients also there we still wait for long-term data. Thank you.

- Yeah, thank you Mr. Chairman. These are my disclosures. Well, we know that the Heli-FX EndoAnchor System provide fixation and seal in aortic necks, and it can prevent or resolve migration or endoleaks. It's important to have an even spacing around aortic circumference and

to resolve type 1A endoleaks, you need successful, of course, deployment of EndoAnchors and adequate penetration into the aortic wall. The objectives for this study was to quantify the EndoAnchor penetration into the aortic wall in patients undergoing EVAR

and to assess the predictors of successful penetration and to associate that with postprocedural type 1A endoleaks. We searched in the ANCHOR database, and we included patients that has been treated for a type 1A endoleak, and we had to have a good quality

first postprocedure contrast-enhanced CT scan without any artifacts due to metal or glue, and without implantation of adjuvant aortic extension cuffs or stents. And then we selected two patient cohorts, patients with successful treatment

after the implantation of EndoAnchors for a type 1A endoleak, and patients with a persistent type 1A endoleak after the EndoAnchor implantation. Well, this is to show how we determined the position of the EndoAnchors, this is a good penetrating EndoAnchor

more than two millimeters in the aortic wall. This is borderline, and this means there is still a gap between the endograft and the aortic wall or the EndoAnchor itself is penetrating less than two millimeters. And this of course, a non-penetrating EndoAnchor.

The good ones are green, the borderlines are orange, and the non-penetrating are flagged red. Here are results, the anatomical criteria to predict type 1A endoleaks, as you can see here, at the left, in the type 1A endoleak patients, there is a larger aortic diameter

with a median of 30 millimeters, and neck length is shorter, less than one centimeter, compared to the patients with no endoleak. Then about the EndoAnchor penetration, in the patients with a persistent type 1A endoleak, there are significantly more EndoAnchors

which are borderline or non-penetrating. What are the predictors for a successful EndoAnchor penetration. Well, protective factors, oversizing of the endograft compared to the diameter of the infrarenal aortic neck, and the use of the endurant stents.

Independent risk factors are the aortic diameter at the lowest renal artery, and five and 10 millimeters below more than 30 millimeters, a significantly neck thrombus and calcium around the circumference and also a more than two millimeter thickness.

Predictors for a type 1A endoleak, protective factors is the neck length more than one centimeter, and good penetrating EndoAnchors and risk factors for a type 1A endoleak is, again, the aortic diameter five millimeters

below the lowest renal artery more than 30 millimeters, and also boerderline and non-penetrating EndoAnchors and in this logistic regression model, a non-penetrating EndoAnchor is really predictive for a type 1A endoleak, or a persistent type 1A endoleak. A few cases, this is an excellent job,

there are four EndoAnchors placed, and they all penetrate well, although they are not circumferentially divided around the circumference. The majority of the problems in the patients in the ANCHOR database, if a persistent type 1A endoleak

is mainly due to an incorrect indication, these are EndoAnchors red and orange, non-penetrating and borderline. That is because they are above the fabric, or they are in a no-neck aneurysm, so the indication is not correct.

This is again, a patient with an undersized endograft, of course, the EndoAnchors will never penetrate the aortic wall at a post-serial part of the aorta. This is another example of misdeployment, a huge load of calcium and thrombus, and again, to defined a no-neck aneurysm,

and again, well it's obvious that the EndoAnchors will not do their job. These are then the EndoAnchor distribution in successfully treated type 1A endoleaks at the left, 332 EndoAnchors, but if you select only the patients

with an EndoAnchor which are inside recommended use at the right, you can see that more than 90% of those EndoAnchors are good penetrating. Here are the patients at the left with a persistent type 1A endoleak, 248, and you can see the majority is red or orange,

and that means that majority of those patients had an EndoAnchor deployment beyond the recommended use. So to conclude, good EndoAnchor penetration is less likely when there is large aortic diameter, the EndoAnchor is not perpendicular to the stentgraft during deployment,

and it's beyond the recommended use, more than two millimeters of thrombus, not in the infrarenal neck, or a gap more than two millimeters. And in borderline or non-penetrating EndoAnchor, it's predictive for a type 1A endoleak.

Thank you very much.

- [Neil] Thanks Tom and thanks Jose and Lowell for inviting me to participate in this great symposium. And I have no relevant disclosures to this talk. Clinical decision making, communication amongst ourselves, in the literature, and to some extent prognosis of patients is dependent a bit on the pattern of reflux in a given patient.

So that's the topic of today's talk for me. Those can be categorized into three rough bins, great saphenous vein reflux, small saphenous vein reflux, and non-saphenous vein or non-truncal reflux. More than one pattern can exist in a given patient, and that obviously has implications

in terms of what needs to be done in recurrence. Even great saphenous vein reflux can be divided into different components based on a variety of elements such as the source of the reflux, which we typically think of

as saphenofemoral junction derived. But the source can be below the junction, either from perforating veins or tributary veins. Sometimes those tributary veins are pelvic derived as in the image on the right. The extent of reflux is obviously very variable.

Sometimes it ends in varicose veins in the thigh and calf and obviously those patients are different than those that have reflux going all the way down to the malleolus or reflux that would be segmental, where it involves the trunk, leaves the trunk into tributaries,

and then comes back into the trunk. The anterior accessory great saphenous vein and saphenofemoral junction can be a cause of great saphenous vein reflux as well as depicted in this diagram where varicose veins shunt the flow from the anterior accessory great saphenous vein

to the great saphenous vein, leading the saphenous vein reflux. Some of the co-panelists for today's session, Dr. Chastanet and Dr. Pitaluga have looked at 1800 patients and categorized their ultrasounds to look at the patterns that exist

in great saphenous vein reflux and identified five different types. The most common type was great saphenous vein reflux with saphenofemoral junction incompetence leading to varicose veins. The second most common type was great saphenous vein

tributary reflux alone. And the third most common type was great saphenous vein reflux with varicose veins without saphenofemoral junction incompetence. This is more than just an academic exercise because if we look at these two types,

type three and type four we'll see that there's a difference in these patients in terms of the phenotypes that they present with their venous disease, specifically in the absence of saphenofemoral junction incompetence,

although, the great saphenous vein and varicose veins are both reflux in the incidence of advanced C4 through C6 venous disease is only 1%. But if you add the saphenofemoral junction component to that patient, the incidence of C4 through C6 disease is 10%.

So that's where the prognosis comes in. Small saphenous vein reflux can be categorized as well. The typical form is derived from the saphenofemoral, sorry, saphenopopliteal junction and leads to sapheno, sorry small saphenous vein reflux and varicose veins.

But that reflux can begin at a higher level, in this case in a perforating vein on the posterior thigh involving the thigh extension and then the small saphenous vein with downward reflux. And it could also begin even in the pelvis with varicose veins leading

to thigh extension reflux downward into the small saphenous vein. Or even at the saphenofemoral junction with reflux through the posterior circumflex vein into the thigh extension and down into the small saphenous vein.

A unique form of what we might call paradoxical reflux that involves the posterior circulation of the venous system superficially would be saphenopopliteal junction where that reflux, in essence, decompresses upward and leads to great saphenous vein reflux and varicose veins.

So all of these different patterns likely have different means to treat, but certainly also may have different long-term prognoses. And then finally varicose veins can be coming from non-saphenous veins. Up to 30% of patients have

non-saphenous related varicose veins. The majority of these patients are female and a lot of these are pelvic-derived varicose veins as you see in the diagram on the right. And many of these are also related to incompetent perforating veins in a number of locations,

particularly the mid thigh, lateral thigh, and popliteal fossa. So in conclusion categorizing reflux in patterns

- Thank you, and thanks to Dr. Veith for the opportunity to share some of our data. These are my disclosures, some devices presented here are investigational and I want to acknowledge my friend Gustavo, who actually shared some of the slides that we'll show. And I want to reference some of his papers. So a spinal cord ischemia has been presented here

as a devastating complication, after both open and endovascular repair of thoracoabdominal aortic aneurysms. The spinal drains are routinely used to ameliorate the frequency and also the severity of spinal cord ischemia, the problem with this trains is that they may result inherent morbidity and mortality.

Now, intraoperative neuromonitoring has been used to not only monitor, but also to manage potential cases of spinal cord ischemia, this is a study by the group at the Mayo Clinic, led by Gustavo. 49 patients, of which 90% had thoracoabdominal aortic aneurysms, all these patients have spinal drain splice,

spinal cord ischemia was seen in six patients. But interestingly, 63% of the patients had significant decrease in the amplitude of both motor and somatosensory evoked potentials. And interestingly all of these changes came back to baseline except in one patient once

their lower legs were reperfused. However, and despite all of these papers that have, you know, talk about the use of spinal drains for endovascular reparative thoracoabdominal aortic aneurysms against the effectiveness of the spinal drains has not been shown.

And the aim of our study was to assess the outcomes of spinal cord protection without the routine use of spinal drains. We actually has some complications in this report, we decided that we were going to use only selectively in our series, the device is used for this in patients

were all part of a physician-sponsored investigational device exemption, demonstrating branch devices were used including the drainage device. We use a similar protocol as the one described by the Mayo Clinic group, which rely on permissive hypertension maintaining the maps above 90 or 100,

and the systolic pressures above 140. However, as mentioned, we did not place spinal drains routinely, the spinal drains were only considered in those patients that had persistent motor evoked potential deficits, at the end of the procedure. Once the legs have been reperfused, we did not use

conduits, we did percutaneous access in all patients. But of note, we did use endo conduits in all patients that have significant iliocclusive disease, not only to be able to deliver the device, but also to maintain flow to the lower extremities, to avoid distal ischemia. So 34 patients were enrolled in this study,

all patients had intraoperative neuromonitoring, and select spinal drains were placed. 10 patients, 29%, were extent 4 thoracoabdominal repairs, and 24 were extent type one to three. Important all patients with type one and three thoracoabdominal aneurysms underwent a staged repair.

We use in 20% of the cases off-the-shelf device is specifically the debranch, and 80% underwent custom made devices, all these devices were pre-loaded with wires. So, of these patients, 73 were male, 9% Type I, 38% Type II, 24% were Type III,

and 29% were Type IV. We saw significant changes in the evoked potentials in 80% of the patients. In all of them those changes came back to baseline except in one patient, who actually had a spinal drain at the end of the procedure.

30-day mortality in two patients, spinal drain was required eventually in only four patients, that's 12%. One because of sustained changes in the motor evoked potentials, spinal cord ischemia occurred in four patients, in all cases secondary to hypertension. After a procedure, in these cases two were permanent,

the cases had spinal drain splice, however, the deficit persisted, two had transient paraplegia, one resolved with permissive hypertension, and one resolved with a spinal drainage, I mean, the spinal drain was only effective in half of those patients. We did have two cases of intracranial bleeding,

associated with hypertension. So in conclusions, we don't believe that the spinal drains are necessary in all patients. A standard protocol that relies on perioperative maintenance of adequate blood pressure in intraoperative neuralmonitoring is however required.

And we believe that tight blood pressure control is mandatory to avoid possible complications related to uncontrolled hypertension, thank you.

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