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anastomosisangiogrambailbypasscarotidCarotid bypassCEACFAdurableembolicendarterectomygoregrafthybridHybrid vascular graftinsertedlesionnitinolpatencypatientperioperativeproximalPTAptferestenosisstenosistechniquetransmuralvascular graft
Risk Assessment For Thrombosis Prophylaxis In Vascular Surgery - Necessary Or A Nuisance
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Percutaneous Pharmaco-Mechanical Intervention For PE: Is There A Rationale
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Angiodynamicsangiovaccannulacircuit for thrombiemboli removalFlowTriever (Infusion aspiration system - Inari) / Penumbra CAT8 (Thromboaspiration system - Penumbra) / AngioJet (Peripheral thrombectomy system - Boston Scientific)therapeutic
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arteryatheroscleroticbasilarclinicaldifficultECVAendovascularextracranialhemisphericincisionoutcomespatencyPathophysiologyrevascularizationtransversetypicallyvascularVeithvertebralvertebral artery
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accessarticlesCongenital Kidney DamageevidenceexternalfistulasguidelineshemointerventionalkdoqiLiving Donor for TransplantmortalitymultinephrologistpediatricradiologistrenalreviewtransplantvascularVascular access
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accessaneurysmalapproachArtegraftavoidbleedingbovineBovine Carotid Artery Graft (BCA)carotidcentersDialysisemergencyexperiencefatalFistulafistulasflapgraftgraftshemodialysishemorrhageinfectioninterpositionlesionLimberg skin flapnecrosispatencypatientpatientsptfeskinStent graftsubsequentsuturetourniquetulceratedulcerationsvascular

So here's the first case I'm gonna show really quick. I think that the general point that I wanna make here is that a lot of these cases happen from puncturing through the capsule. So this is kind of too far out and I actually don't have a biopsy

picture on this one cause it was back when we weren't as standardized in the way that pictures were taken. But looking at the CTA you can see that there's a blush there. I'm gonna go through these quickly but I will show you. This is the blush on the CTA there. So this was actually not read as a positive study. We had

night hawk/g people reading back when these were performed and that has since changed, but the hemoglobin drop is fairly precipitous and that definitely delayed intervention in this case.

- Thank you very much, I appreciate the invitation to this great meeting. So I'm going to talk a little more broadly about beta blockade, then Dr. Mollis, and let's review again some of the randomized control trial data. So, just like the first slide with prior speaker, this really kind of turned me on to beta blockade.

It did show a benefit to Atenolol over placebo, fairly far out with regards to when its effect really was manifest, but it started to change practice, and then really, the decrease one trial was a game changer based on, it was high risk vascular surgical patients all had a positive stress test, moderate dose of Bisoprolol,

and they found a significant reduction in death and MI out to 30 days, but as many of you are aware, many of these are discredited. They didn't really look back at decrease one to see if that was fraudulent of fictitious, but many of their further trials have since been discredited.

So then, the POISE Trial came, and again, this was previously mentioned, and it does include vascular, non-vascular patients, but 8300 patients, Troprolol, pretty high dose right around the time of surgery versus placebo, and you can see that the non-fatal MI was significantly reduced, as well as a composite endpoint,

but stroke and bradycardia were significantly increased, and in fact, if you look at this out to one year, you can see that it was a 16% increase in all cause mortality, no difference in CV mortality, and then again, non-CV mortality was increased 22% and caused 54 excess deaths

compared to placebo, so that's real. Put it another way, 1,000 patients treated with a beta blocker would benefit from reducing 12 MIs and six revascularization, but increase harm significantly with 13 deaths and six strokes. Some of these trials, again, were otherwise mentioned,

and this is in vascular surgical patients, howbeit, not just AAA patients, but about 50 in each group, relatively small, and with 30 day assessment, it again was 50 to 100 milligrams Metoprolol the day before or on the day of surgery, mortality was not significantly different at the time of their discharge.

Another, slightly larger trial in patients with diabetes and beta blockade, 100 milligrams of Metoprolol, at least two hours prior to the OR, and they did two tests dosing to make sure the patients tolerated this out to day eight, and then they did a control for those who had bradycardia

or hypotension weren't included, so about 460 patients in this trial, and again, early 30 day outcome, not significantly different, and out to 700 days, again, the composite of death and cardiovascular morbidities. Last trial in terms of this review, same dosing regimine, basically, with Metoprolol here, about 250 patients

in each group, and again, no significant difference at six months, but significantly increased intraoperative hypotension requiring treatment in intraoperative bradycardia. So, putting these together with meta-analyses, looking at the effect of beta blockade

and perioperative death, actually a significant increase based on this meta-analysis, and particularly more striking was the 73% increase in overall nonfatal strokes with beta blockade. Again, the thing it did reduce was nonfatal MIs out to 30 days, even if you did

discount the decreased trials. A database review was presented by Dr. Mallis, and this was a VA cohort study, slightly different one, 37,000 patients in the VA system propensity matched and had received beta blockade within one day of surgery and thereafter, and I'm pointing out that

the vascular surgical patients, whether they were low risk or high risk, all achieved no benefit from this. So again, it may be just as much an issue of two large a dose as too short of time for it to, the medication to be administered,

and if you don't totally disbelieve the decrease one trial, they found that when the heart rate was titrated less than 65 compared to over 65, the benefit was really striking there. So, what do the guidelines say about this? Well, the AHA and 2014 perioperative beta blockade

started with one day or less before non-cardiac surgery prevents non-fatal MI, but increases the risk of stroke, death, hypotension, and bradycardia. So, what do I recommend? Well, I think that you need to keep your patients on beta blockers, if they're on them for

any indication already, such as heart failure. If they're at high risk for perioperative MI, such as those with positive stress tests that aren't a candidate for revascularization, start low dose Metoprolol, and/or Atenolol, and at least 15 to 30 days in advance,

try to titrate that heart rate, avoid the dose on the morning of surgery, and really do need a randomized control trial of titrated low dose beta blockade in high risk patients, thank you.

- Thank you. Disclosure related to this talk. So the evidence on beta blocker use has been very controversial, and with the first randomized trial being discredited, this is one of the earliest trial that showed, actually, a benefit,

and this one was not discredited, and showed significant reduction in mortality in patient undergoing non-cardiovascular surgery, and this was persistent up to one and two years. This particular study that was published in Lancet

shows just the opposite, with larger number of patient to post trial, showing no benefit of beta blockers. In these two next slides I'm going to show you both of them were randomized trials, comparing metoprolol to a, basically a sham,

or placebo, and showed in vascular patient, no benefit. However, the problem with both of these randomized trial that they included apple and oranges in vascular surgery, so they included aneurism and peripheral vascular disease, axbifem, and even amputation. Very different procedures.

Despite this controversial evidence, both the European Society of Cardiology and American Heart Surgery revised their guideline and recommended to continue use of chronic beta blockers, but not to initiate beta blocker before surgery. And the problem that I have with a lot of this data is

that they did not really look at the specific type of beta blocker, the route of administration or dose, and also what I've showed you, the inclusion of apple and oranges, or even in the first 2 large randomized trial, not just vascular patient, they included colorectal patient,

plastic surgery and orthopedic. So what I wanted to do is to look at real world data and we used the Premier Health Data with a cut from the data from 2009 to 2015. And we included non-rupture aneurysms

in looking at all adverse events and mortality. And we did the usual statistical analysis. But you can see here, we had 6,500 patients, 1,000 of them were not on beta blocker, and the remainder receive a different kind of beta blockers. In table one, you see that the group that receive

beta blocker as expected were a little bit sicker, with the more urgent, non-rupture presentation, more statin use, and they had more coronary artery disease, as well as kidney disease. And the conclusion with the results was

that there was a lot more complication, actually, in the beta blocker user, but the mortality was significantly less, about 4 versus 8%, and there was significant rescue phenomenon, i.e., people who develop major adverse event,

but they survived the adverse event, was a lot higher in a group that received a beta blockers. And some of the predictor of mortality, the usual suspect being older, have more significant coronary artery disease, and other cardiovascular morbidity,

as well the urgency of the presentation, but the interesting thing that I'm showing you here, that when we tried to see if the coronary artery disease has an effect, and there was clearly an effect modification. Meaning, if you have coronary artery disease,

the benefit was a lot higher, as you can see, 80% reduction in mortality, versus 60%. And then when we further stratified this, having or not having adverse event, we saw the same thing in the group that have adverse event. The more benefit in coronary artery disease patient,

but the interesting finding, if you did not have coronary artery disease, and did not develop a complication, there is really no benefit for beta blocker. That is the only group that did not benefit. But the group that had no adverse event and

coronary artery disease, had the most benefit, 93% reduction in mortality. Another unique finding that I don't think any other the study looked at, we looked at different kind of beta blockers, and we found that if you give IV beta blockers,

you actually have higher mortality if you don't have beta blocker at all. And we found that metoprolol is the most beneficial, comparing to other kind. Another thing that we did, we showed that there is a dose response.

So if you go from no dose to intermediate, to low dose to intermediate, you see the mortality dramatically dropping, specifically from 5 to 2% within the dose, so the dose has an effect, and if you go supertherapeutic dose,

you actually have no benefit. Limitation, of course, the usual retrospective study. And the conclusion is that in hospital mortality was reduced by 55%, there was failure to rescue, with 60% lower in the group that received beta blockers. There was a dose response,

and metoprolol is the most beneficial. And based on that, I think recommendations should be revised, specifically for triple A. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.

And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.

Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.

Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.

It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,

if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?

You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you

about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,

and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may

be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.

A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased

the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,

and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.

But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history

or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?

Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because

more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.

Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.

They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.

To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history

in various degrees of relatives. So with that, thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. So, this audience certainly knows that the higher the triglyceride, the greater the cardiovascular morbidity mortality, similarly if you have a low HDL that same relation holds, and certainly for the non-HDL-C or LDL-C calculated the higher the worse outcome and there's

multiple drugs related to this. Similarly with stroke, triglyceride the same relationship. Ischemic stroke increased with low HDL and again LDL-C correlates. So the historical precedent has been that you should get a fasting lipid level

when you first encounter the patient, but to make this simple that's really probably not true. So there's various things that are measured and that are calculated, but LDL is generally calculated, HDL is measured and then the triglycerides are calculated as remnant cholesterol.

So if you compare just the measured LDL compared to calculated LDL in a non-fasting state, it's a little bit of a wider linear relationship here as compared with the fasting, it's a little bit tighter. But when you look at this in more depth, and this reference here really nicely puts it all together

but the total cholesterol really doesn't vary if you've fasted one hour or 16 hours, similarly between men and women. The only thing that varies a little bit is triglycerides and we'll go on to that in just a little bit of depth.

But again that's variable, triglycerides go up if you eat really not much difference with the other lipid levels. And if you look just in terms of triglycerides, they overlap between non-fasting and fasting, really at almost all levels

so there's not really discrepancy. Similarly with LDL, same amount of overlap here whether or not you have diabetes it doesn't seem to make a difference. So for lipid panels, profile testing, in most patients you can get a non-fasting

initial lipid profile in any patient for cardiovascular risk assessment, I'd say that's where it's most commonly done in most of our practices. Similarly with acute coronary syndrome, if preferred by the patients et cetera.

But really it's where the non-fasting triglycerides are highly elevated that you want to get a fasting lipid panel. So what causes secondary hyperlipidemia related particularly to hypertriglyceridemia? Certainly certain diet factors, certain drugs,

cyclosporins for example, biliary obstruction and hypothyroidism. And so, one algorithm is that in terms of screening with non-fasting, and if it's less than 200 you're good to go, you really don't need to do anything further,

and if it's greater than 200 then probably a fasting lipid profile, lipoprotein panel is indicated. So reasons that non-fasting lipid measurement is fine most of the time is that again most trials have used non-fasting levels for determination of effectiveness of various medications.

This Friedewald formula actually uses total cholesterol, HDL, and triglycerides to calculate LDL-C, and LDL really is not directly measured, it's not standardized by the CDC such as these other cholesterol moieties are. And again most CV risk factor calculators don't use LDL-C.

So again, non-fasting is acceptable for the initial risk estimation in untreated and primary prevention screening. For patients with genetic hyperlipidemia probably fasting is required. Diagnosis of metabolic syndrome, non-fasting is fine.

And again some other more highly specialized scenarios you may want a fasting profile. Thank you.

- Alright, good morning, I'd like to thank Dr. Veith for having me here. Before I begin, I would just like to ask for a recount in the spirit of the times. So I'm going to try and bring us back on time and talk about the optimal medical therapy

for critical limb ischemia. These are my disclosures, non-relevant to this topic. So PAD patients, the mortality is high, as you all know. And in critical limb ischemia, the numbers are even worse as you can see here. The older the patients,

the more risk factors they have, the worse the mortality. And it is quite dismal over years. So treatment should definitely follow causes of mortality. So why do these patients die? So actually most of the reasons for these patients to die are actually nonvascular, as you can see here.

And it's obviously beyond the scope of this talk to explain what to do with these conditions, and obviously they're variable. But for cardiac and vascular causes of death, the treatment is medical and obviously not opening up the flow channel to be to the foot.

So just to answer the topic of the talk, my interim first conclusion is that even today, intervention is insufficient for CLI patients. And obviously medical therapy is key. But the goals of therapy should not only focus on the mortality,

but also obviously on morbidity. So my second interim conclusion is that for morbidity and complications, even in 2028, you know even in 10 years, medical therapy will not be sufficient to replace intervention.

And because I have very little time, instead of going into the data about each and every potential medical therapy that could be offered to these patients, I'd like to give sort of a focused bottom line and a few chosen medical therapies

that are relevant to this population. Anti-platelet therapies in peripheral artery disease, and obviously in CLI also, reduce mortality in a significant manner. And obviously patients with CLI should and will be, I think, still on an anti-platelet agent in the future.

Adverse events including mortality and vascular amputations are very much increased when patients have a major adverse limb event. And so for that reason, affecting these limb events is crucial. And identifying anti-platelet agents

that are safe but also reduce adverse limb events is key. So Vorapaxar did reduce acute limb ischemia. However, the price of excess bleeding, and for that reason is not being used routinely in these patients. However, I hope that in the future

we will have other options that targets not only mortality but also acute limb events. Ticagralor reduced both MACE and MALE, so both adverse cardiovascular events and also limb events. And so this is the cardiovascular events and this is the limb events.

And so it was very impressive in patients with PAD. What about a completely different mechanism? So plaque rupture may induce atherothrombosis, so there could be atherosclerosis as a result of plaque rupture with a thrombotic component, locally resulting in critical limb ischemia.

And indeed in this pathological study of 75 patients with CLI, post-amputation thrombosis in the lumen was seen in many of these patients. So is there a role for anticoagulation? Well you've heard of the COMPASS trial

in the previous session from two speakers, and indeed low-dose Rivaroxaban resulted in fewer events. And although there were more bleeds, there was net benefit for this therapy, which was recently approved by the FDA. Statins, as you've heard from most previous speakers,

reduce major adverse cardiovascular events, but also reduce adverse limb outcomes, specifically high-intensity statins. And what about PCSK9 inhibitors? Well the reason I put them here and not at the sort of cardiovascular events

is just because their use is still very limited. But still they were very impressive, specifically in the PAD sub-analysis of Fourier. And what you can see here, that there's a very low number needed to treat in order to reduce adverse cardiovascular events

with these medications, even if many of them were on high-intensity statins. So my third interim conclusion is that in my opinion, by 2028 every CLI patient will be on an anti-platelet agent, on a statin and perhaps another anti-lipid medication. And likely on an anticoagulant of some sort.

However, in 2028 I still think that CLI will remain a team sport. Medical therapy and intervention I think will still go hand in hand, and I don't think one will replace the other. Thank you very much.

- Thank you for the opportunity to speak today. I have no disclosures. We've heard a lot about this, this morning, but, I'll just reiterate, for those of you who may or may not be familiar, The Fourier trial was a randomized trial of Evolocumab versus placebo in nearly 30,000 patients with atherosclerotic disease, and that the primary end point

was a composite of cardiovascular death, MI, stroke and hospital admission as well as some secondary end points as well. So what about these inhibitors in Peripheral Arterial Disease? Well, a sub analysis investigated the efficacy and safety of

Evolocumab in patients with PAD. And patients were defined as having PAD at baseline, if they had either intermittent claudication and an ankle brachial index of <0.85 or if they had a prior peripheral vascular procedure. So of the total cohort, 3,600 and some patients where 13%

had PAD based upon this definition, Evolocumab significantly reduced the primary end point consistently in patients with PAD with a hazard ratio of 0.79. What about Cardiovascular efficacy in the PAD population? Evolocumab significantly reduced both the primary end point

and the composite end point of cardiovascular death, MI or stroke very significantly and you can see in looking at this slides that the relative risk reduction was of higher magnitude in the patients with PAD than without PAD. Major advers limb events were significantly reduced in the overall population

as well as the patients with PAD and the results with regards to major amputation, I think are quiet compelling here. Again if you look at major advers limb event reduction you can see here in all patients and in patients with PAD there was a market reduction in events.

And then if we finally look at a composite outcome of MACE, and Male in patients with PAD, overall Evolocumab again reduced this composite outcome by nearly 21%, and if you look at the slide again, you can see that the magnitude of reduction, was of higher magnitude in the PAD group.

What about the safety? There were no differences in the incidents of adverse or serious events with the medication in patients with PAD. And importantly there was a consistent relationship between lower achieved LDL levels and lower risk of limb events that extended down to

very low levels of LDL cholesterol. So in summary Evolocumab significantly reduced the primary end point with patients with PAD because of their overall higher risk, patients with PAD actually had a larger absolute risk reduction for many of this end points than many patients without PAD and Evolocumab

significantly reduced major adverse limb events in all patients and in patients with PAD. What about Coronary disease as doctor Veith asked me to address? With in the of patients with prior MI, it was hypothesized that may be we could identify some that would

benefit more from this medication. So, 22,000 patients had a prior MI, and they were classified in several areas, one of them being, that based on the time of their most recent MI, 8,400 patients or 38 percent were with in two years of their most recent MI,

and this recent MI as well as other factors were independent predictors of a future cardiovascular outcome. So, if you see her in the placebo arm compared with patients with a remote MI , those with a recent MI were significantly higher risk in the placebo arm for the primary end point.

The relative risk reductions for the primary end point was greater in these high sub groups including recent MI, than for those with remote MI, and you can see this here in this slide as well. And patients with a recent MI and with remote MI and the magnitude of the reduction being much greater in the higher risk group.

So in conclusion recent MI, was felt to be a high risk condition and that these patients significantly benefit from cholesterol lowering with Evolocumab. So it's being reiterated here this morning, how low should we go, the targets are constantly changing and again changed just as recently as last week, and there

are a lot of good arguments for extensive lowering of LDL cholesterol, it's important to realize that because of the anticipated extreme reductions in LDL cholesterol regulatory agency require enhanced monitoring of adverse events. Particularly neuro-cognitive events, and in a sub study of FOURIER, there were no group differences in many of these

parameters between the placebo and medicated groups. in FOURIER the reduction in the primary and secondary composite end points was in fact linearly relate to the achieved LDL cholesterol. And in a post hoc analysis five percent of these patients achieved extraordinarely low levels.

In this group importantly, there were no associations between this achieved levels and predetermined safety event. So I tried very hard to find a slide that said when they go high we go low but unfortunately no one wanted to make that so I'll just say go low or go home.

- Thank you Dr. Asher. What an honor it is to be up here with Dr. Veith and Dr. Asher towards the end. You guys are leading by example being at the end of the meetings. So, thank you for allowing me to be up and talking about something

that not a lot of vascular surgeons have experience with, including me. I have no disclosures. On your left, I have listed some of the types of diseases that we most commonly see in the vertebral artery, and there are quite a lot.

And on the right, the standard types of treatment that we pursue in vascular surgery or as a vascular specialist. And often, in the vertebral artery, if we are going to pursue treatment, it's the endovascular route.

But I'll talk a little bit about open surgery. The clinical presentation is often vague. And the things I wanted to point out here in this long list are things like alternating paresthesias, dysphagia, or perioral numbness may be something in the history to look for

that you may not be thinking about when you're thinking about vertebral basilar disease. The anatomy looks straightforward in this picture, with the four segments, as you can see. It gets a little more complicated with just the arterial system,

but then when you start looking at all these structures, that you have to get out of of the way to get to the vertebral artery, it actually can be a difficult operation, particularly even in the V1 segment. The V1 typically is atherosclerotic disease.

V2 is often compression, via osteophyte or musculo-tendon structures. And V3 and V4, at the top, are typically from a dissection injury from sort of stretch or trauma injury. The pathophysiology isn't that well understood.

You have varying anatomy. It's very difficult to access this artery. Symptoms can be difficult to read, and treatment outcomes are not as reliable. But I'm going to take you through a very quick path through history here in the description

of the V1 segment exposure by Dr. Rentschler from 1958. And I love these pictures. Here is a transverse incision over the sternocleidomastoid, just above the clavicular head on the right side. And once you get the sternoclavicular head divided, you can see the longus colli muscle there.

Anteromedial is the carotid. Of course, you surround that with a Penrose drain. And then once you do that, you can separate your longus colli, and deep to that, the vertebral artery just easily slips right up, so you can do your transposition.

It's not quite that easy. I've done one of these operations, and it was difficult finding t e. And, again, here is on the opposite side, you can see the transposition in this cartoon.

Dr. Berguer is the world's expert, and a lot of this open surgical work comes out of the University of Michigan. Here is a study looking at 369 consecutive extracranial vertebral artery reconstructions. You can see the demographics of clinical presentation.

And note that about 34% of patients are presenting with hemispheric symptoms, with 60% in the vertebral basilar distribution. 300 of these reconstructions were for atherosclerosis. And the outcomes were pretty good. Before 1991, there wasn't really a protocol in place

in assessing and doing these procedures. And you can see the stroke and death rates of 4.1 and 3.2% respectively. And then the outcomes after 1991 are considerably better with a five year patency rate of 80%. So, in summary, vertebral artery disease is,

I think if you review this, is somewhat under diagnosed. Revascularization is a viable option. Most often, it's endovascular. But if you have endo-hostility, then an open, particularly for the V1 segment, may be a better option.

And this requires people with good operative experience. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thanks very much, Tom. I'll be talking about thermal ablation on anticoagula is it safe and effective? I have no disclosures. As we know, extensive review of both RF and laser

ablation procedures have demonstrated excellent treatment effectiveness and durability in each modality, but there is less data regarding treatment effectiveness and durability for those procedures in patients who are also on systemic anticoagulation. As we know, there's multiple studies have been done

over the past 10 years, with which we're all most familiar showing a percent of the durable ablation, both modalities from 87% to 95% at two to five years. There's less data on those on the anticoagulation undergoing thermal ablation.

The largest study with any long-term follow up was by Sharifi in 2011, and that was 88 patients and follow-up at one year. Both RF and the EVLA had 100% durable ablation with minimal bleeding complications. The other studies were all smaller groups

or for very much shorter follow-up. In 2017, a very large study came out, looking at the EVLA and RF using 375 subjects undergoing with anticoagulation. But it was only a 30-day follow-up, but it did show a 30% durable ablation

at that short time interval. Our objective was to evaluate efficacy, durability, and safety of RF and EVLA, the GSV and the SSV to treat symptomatic reflux in patients on therapeutic anticoagulation, and this group is with warfarin.

The data was collected from NYU, single-center. Patients who had undergone RF or laser ablation between 2011 and 2013. Ninety-two vessels of patients on warfarin at the time of endothermal ablation were selected for study. That's the largest to date with some long-term follow-up.

And this group was compared to a matched group of 124 control patients. Devices used were the ClosureFast catheter and the NeverTouch kits by Angiodynamics. Technical details, standard IFU for the catheters. Tumescent anesthetic.

And fiber tips were kept about 2.5 centimeters from the SFJ or the SPJ. Vein occlusion was defined as the absence of blood flow by duplex scan along the length of the treated vein. You're all familiar with the devices, so the methods included follow-up, duplex ultrasound

at one week post-procedure, and then six months, and then also at a year. And then annually. Outcomes were analyzed with Kaplan-Meier plots and log rank tests. The results of the anticoagulation patients, 92,

control, 124, the mean follow-up was 470 days. And you can see that the demographics were rather similar between the two groups. There was some more coronary disease and hypertension in the anticoagulated groups, and that's really not much of a surprise

and some more male patients. Vessels treated, primarily GSV. A smaller amount of SSV in both the anticoagulated and the control groups. Indications for anticoagulation.

About half of the patients were in atrial fibrillation. Another 30% had a remote DVT in the contralateral limb. About 8% had mechanical valves, and 11% were for other reasons. And the results. The persistent vein ablation at 12 months,

the anticoagulation patients was 97%, and the controls was 99%. Persistent vein ablation by treated vessel, on anticoagulation. Didn't matter if it was GSV or SSV. Both had persistent ablation,

and by treatment modality, also did not matter whether it was laser or RF. Both equivalent. If there was antiplatelet therapy in addition to the anticoagulation, again if you added aspirin or Clopidogrel,

also no change. And that was at 12 months. We looked then at persistent vein ablation out at 18 months. It was still at 95% for the controls, and 91% for the anticoagulated patients. Still not statistically significantly different.

At 24 months, 89% in both groups. Although the numbers were smaller at 36 months, there was actually still no statistically significant difference. Interestingly, the anticoagulated group actually had a better persistent closure rate

than the control group. That may just be because the patients that come back at 36 months who didn't have anticoagulation may have been skewed. The ones we actually saw were ones that had a problem. It gets harder to have patients

come back at three months who haven't had an uneventful venous ablation procedure. Complication, no significant hematomas. Three patients had DVTs within 30 days. One anticoagulation patient had a popliteal DVT, and one control patient.

And one control patient had a calf vein DVT. Two EHITs. One GSV treated with laser on anticoagulation noted at six days, and one not on anticoagulation at seven days. Endovenous RF and EVLA can be safely performed

in patients undergoing long-term warfarin therapy. Our experience has demonstrated a similar short- and mid-term durability for RF ablation and laser, and platelet therapy does not appear to impact the closer rates,

which is consistent with the prior studies. And the frequency of vein recanalization following venous ablation procedures while on ACs is not worse compared to controls, and to the expected incidence as described in the literature.

This is the largest study to date with follow-up beyond 30 days with thermal ablation procedures on anticoagulation patients. We continue to look at these patients for even longer term durability. Thanks very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you Michael for the invitation. We're going to look at this, these are m disclosures. And I wanted to focus on, so, we heard about Raghu presented the patient with this acute event big pulmonary embolism then we saw the imaging, we just saw which I think was very helpful and now we have to decide like,

what therapies are we going to use and we're not talking about thrombolytic therapy but what are the other alternative therapies and we're focusing really, mainly on this intermediate and this low-risk group since the massive PE group is going to have a more aggressive intervention for management.

So, if we look at these four trials that have been done out there, I just want to highlight for this audience the fact that, these patients were randomized to the standard treatment which was low molecular weight heparin then bridge to warfarin

and they were compared head-to-head. In Amplify and Einstein, the patients received the Rivaroxaban and Apixaban initially for the treatment of pulmonary embolism. So, it didn't have any kind of lead in therapy. I just want to show you that they excluded people

who actually got low molecular weight heparin or unfractionated heparin. So, they really had a good head-to-head comparison to the standard of care we know. The other two trials of course, had lead in therapy for their management.

That being said, everyone in the audience wants to know how bad were the PEs in these trials so, I put the two trials there, the Amplify study and the Einstein PE study showing that the patients did have substantial pulmonary embolism thrombus load in this patient population.

They were treating people that were involved extensively with pulmonary, not massive PE. So, it's good head-to-head comparison sort of challenging the standard of care that we know. Rachel and I wrote this paper to really look at, remember dosing correctly for this patient population

for in the trials, it's clear to remember that it's 21 days for Rivaroxaban at 15 milligrams twice a day and it's Apixaban is 10 milligrams twice a day. Often forgot because people start the patient immediately on the lower doses of these medication.

I highlighted all the trials together in one slide so you can see when you actually compare them to the standard of care, there's non-inferiority for each of the trials compared to low molecular weight heparin bridge to warfarin therapy in management.

So, I wanted you to see a composite of all the trials. The next thing all of us want to know, is what about bleeding and I put all the trials together and looking at the DOACs compared to the standard of care and many of you are looking at this and saying, "Gee, "it looks like the DOACs have a lower incidence

"of major bleeding compared to the standard of care," which was warfarin, remember now 'cause it's low molecular weight heparin bridge to warfarin. So, just keep that in mind that, when you look at this, the DOACs do have a lower incidence of major bleeding when you compare it to the standard of care

which is warfarin. They're not compared against each other but against the standard of care. So, if we have a PE, are we going to select a DOAC after that first initial assessment like we saw in Raghu's case, are we going to select a DOAC

at that point in time for management? Remember, what did Raghu select? They selected low molecular weight heparin bridge to warfarin standard of care? Could we have started that patient on a DOAC instead of the standard of care, because

according to the data I just show you, they're non-inferiority for the DOACs? We always like to go to a guideline. If you go to the ACCP Guideline 2016, I know there's a newer guideline coming out relatively soon, if a patient has no cancer, the recommendation

is to treat those patients for three months, that's the recommendation. If they have cancer, of course, they recommend low molecular weight heparin as part of that management over vitamin K antagonists or the DOACs.

And unprovoked PE which is another group that we're going to talk about here, the key here for us is to keep in mind is that, in that group, if there's a low risk for bleeding in the population, you want to do extended management with no date for stop. But if there's a high risk for bleeding,

you'll go with the lower time period of three months for the management and then follow those patients. Some new guidelines just came out on cancer, I just want to highlight them from, they're hot off the press 2018, both ISTH and NCCN, both now recommending that the DOACs and in this case,

they picked Rivaroxaban and Edoxaban based upon trials that these be part of the management now, considered part of the management of a patient who has malignancy and pulmonary embolism for their management. Some of you have not adopted that,

we have not gone whole hog on that at this point in time but I just wanted to highlight this for the group. Let's look at the unprovoked group. We saw in the case, Raghu looked at the patient for management, sent the gentleman out on low molecular weight heparin

and then switched that patient to warfarin therapy, bridged them over. We could have selected Apixaban or Rivaroxaban as the management for that gentleman but Raghu selected the standard management. Maybe he felt uncomfortable, I don't know.

But the data says, we could have used one of the DOACs. Now, you're out of the hospital and you're on a DOAC and you have to decide what you're going to do in terms of management. All of us are going to be treating the patients by standard management i.e. look at this this chart here

going through all the agents. And this is looking at preventing recurrence during that period of time in terms of management. This is preventing patients for longer term management looking at this group. Everyone, if you look at the trials here,

different dosing. Everyone gets treated with five milligrams of Apixaban twice a day, for three months and then if you're going to decide to extend management you can go to the lower dosing schedule of 2.5, twice a day and this was the comparison.

What can you glean from this? When you look at this, they looked at unprovoked VTE and what you can glean from this, if you look at the placebo groups here, look at the placebo group, patients who had placebo after being treated three or six months,

look the recurrence rate in the placebo group, 5.6, 8.8, 7.1 and of course, in the last study, there was no placebo group. What it shows us is the recurrence rate which all of us think about especially for the unprovoked PE.

Some of you in the room say, can you give us a risk index that can predict the patient who would get recurrent PE? I'm going to show you three risk tools that we would consider to use to define who would have recurrent events for PE.

I want to show you the Vienna Prediction Model which we use. You go online there to the, to the website, you do the calculation and it gives the patient something that you can discuss with them your risk of recurrence for an unprovoked PE

as your risk for recurrence of that event again. You can use the DASH Score, that's another score that's been used. Or you can use the MEN Continue and HER DOO2 Score, which I thought was very interesting, look at the parameters for this.

People have tried to give us, clinicians, a risk index to predict recurrence for unprovoked PE. Going back to this, I just want you to keep this in mind, the duration and look at the Riva study at the bottom where Aspirin was used. Some of us in the room,

I don't know how Jeff Olin feels about this or Rachel Rosovsky. You treated a patient for three months unprovoked VTE, the patient doesn't want to be on one of the agents, can aspirin be used as a prevention for recurrence? We all know there's two big Aspirin studies,

well, this is another addition to that Aspirin data looking at that as a prevention for recurrence. How do I look at this? I look at it as the first few days of the PE, the first day, one or two, remember, we want to get the patient out of the hospital

as quickly as possible 'cause Dr. Jeff will be very upset at your length of stay with respect to the management of PE. So, he's going to want to know, can you get them out quickly. I like to look at what's happening in that first day or so. Raghu did it in, I don't know, less than 24 hours,

he made the decision, got the patient out 'cause he wanted to leave. The point is, you need to decide what you're going to do in that first 24 hours, that's your decision point. In that decision point, will come up,

does the patient have resources for medication, where do they live, what's their family structure? And by the way, you're all doing that in light of the patient's pulmonary status with respect to how they are. Then you make that decision on what agent you're going to use,

pretty straightforward. Either you're going to use low molecular weight heparin during that phase of three to five days and then you're going to consider switching them over to the DOAC and then looking at the three to six month period where you select the DOAC for management

and finally, you'll decide if it's unprovoked or it's cancer or it's antiphospholipid antibody syndrome triple positive, you're going to decide then, one management is going to be for long term. So you can see, this truly is a team sport, it's not just the team getting together to discuss

if we're going to use catheter directed lytic therapy or not, it's really, that then plus all the management that comes with pulmonary embolism in the back end of the process. So, DOACs are here to stay, DOACs, I believe, can be used in the acute event

in that intermediate group. They've definitely shown to be non-inferior, lower risk of bleeding and I think they would be a successful long-term management in patients should you decide to do that. So, thank you very much.

- [Michael] A couple of questions on this Geno. First of all, not all acute PEs in the first, one to two days would you hospitalize on heparin-- - That's correct. That low-risk group. - [Michael] So, incidentally found

peripheral pulmonary embolus that the scan probably shouldn't have been done in the first place. You might even consider not treating those, I presume. - No, I would consider treating depending upon the circumstances Mike. If they're a cancer-based as part of staging,

I would treat those patients. It's that other group that's non-cancer incidental sub-segmental PE, I would not treat that. - [Michael] What data, just in general, changed those guidelines to include DOACs as a primary therapy for cancer associated VTE?

- I think the two trials, the Edoxaban study that was done, looking at Edoxaban in this population and the SELECT-D study which was done looking at Rivaroxaban versus Dalteparin for the treatment. Dalteparin was also the comparator in the Edoxaban study. Those two trials clearly showed that these agents do work

except, we must keep in mind, there was an increased incidence in major bleeding in those studies. You have to measure that. - [Michael] And what about in patients who have failed anticoagulation in cancer-associated VTE?

They have a diagnosis of a cancer-associated VTE, they're being treated for their cancer, they get whatever you want to use, low molecular weight heparin full dose, they have another event, do we have any data on the optimal therapy

for those patients? - Answer Mike's question, so you have a recurrence on management. The CHEST Guidelines actually recommend, increasing the dose of low molecular weight heparin as your approach to managing this patient population.

The DOACs, I don't have anywhere to go with them 'cause there's no increasing the dose to see more efficacy at this point in time, so, in low molecular weight heparin, my choice, increasing the dose, 20%. - [Michael] And how about antiphospholipid syndrome, that's a different marker, right?

- Yes, antiphospholipid antibody syndrome either triple positive or one positive, those patients the recommendations are, not to use DOACs and to stay with low molecular weight heparin bridge to warfarin therapy, that's what I would do. - [Michael] Do you ever try and monitor any lab tests

in patients on DOACs? - I don't but I can tell you, we just completed a study called ADIOS in which we measured plasma levels of Apixaban. And we showed, discontinuing the drug then looking at it while the patients were on the agent

and then after discontinuing for surgery. I got to tell you, I think plasma levels may be a way of telling us the anticoagulation status of a patient, by the way, there was no correlation with the 10A levels, that was sort of surprising.

We had positive 10A levels but the plasma level was less than 30 nanograms per deciliter. So, we were actually picking up positivity of factor 10A levels but yet, there was not a significant plasma level of the drug. So, I think the 10A levels are little too sensitive

to tell us the anticoagulation. And hopefully, that study will be published fairly soon. - Great Geno, thanks. - Thanks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- So this is what I've been assigned to do, I think this is a rich topic so I'll just get into it. Here are my disclosures. So I hope to convince you at the end of this talk that what we need for massive PE when we're talking about catheter based therapy is a prospective registry. And what we need for catheter based therapy for

submassive PE is a randomized controlled trial. So we'll start with massive PE and my rational for this. So you know, really as you've heard, the goal of massive PE treatment is to rescue these patients from death. They have a 25 to 65% chance of dying

so our role, whatever type of physician we are, is to rescue that patient. So what are our tools to rescue that patient? You've heard about some of them already, intravenous thrombolysis, surgical embolectomy, and catheter directed therapy.

The focus of my talk will be catheter directed therapy but let's remember that the fastest and easiest thing to do for these patients is to give them intravenous thrombolysis. And I think we under utilize this therapy and we need to think about this as a first line therapy for massive PE.

However, there's some patients in whom thrombolytics are contraindicated or in whom they fail and then we have to look at some other options. And that's where catheter directed therapy may play a role. So I want to show you a pretty dramatic case and this was an eye-opening case for me

and sort of what launched our PERT when I was at Cornell. It's a 30 year old man, transcranial resection of a pituitary tumor post-op seizures and of course he had a frontal lobe hemorrhage at that time. Sure enough, four or five days after this discovery

he developed hypertension and hypoxia. And then is he CT of the chest, which I still remember to this day because it was so dramatic. You see this caval thrombosis right, basically a clot in transit

and this enormous clot in the right main pulmonary artery. And of course he was starting to get altered, tachycardiac and a little bit hypotensive. So the question is, what to do with this patient with an intracranial hemorrhage? Obviously, systemic thrombolytics are

contraindicated in him. His systolics were in the 90 millimeter of mercury ranged, getting more altered and tachycardiac. He was referred for a CDT and he was brought to the IR suite. And really, at this point,

you could see the multidisciplinary nature of PE. The ICU attending was actively managing him while I was getting access and trying to do my work. So this was the initial pulmonary angiogram you can see there's absolutely no flow to the right lung even with a directed injection

you see this cast of thrombus there. Tried a little bit of aspiration, did a little bit of maceration, even injected a little TPA, wasn't getting anywhere. I was getting a little bit more panicked as he was getting more panicked

and I remembered this device that I had used in AV fistula work called the Cleaner. Totally off label use here, I should disclose that and I have no interest in the company, no financial interest in the company. And so we deployed this thing, activate it a few times,

it spins at 3,000 rpm's, he coughed a little bit, and that freaked us all out also. But low and behold we actually started seeing some profusion. And you can see it in the aortogram actually in this and that's the whole point of massive PE treatment with CDT,

is try to get forward flow into the left ventricle so that you have a systemic blood pressure. Now, you know, when we talk about catheter based therapies we have all sorts of things at our disposal. And my point to you is that you know really, thank you...

You guys can see that, great. So really, the point of these catheter therapies is that you can throw the kitchen sink at massive PE because basically your role is to try to help this patient live. So, if I can get this thing to show up again.

There we go. It's not working very well, sorry. So, from clockwise we have the AngioVac circuit, you have, let's see if this will work again, okay. Nope, it's got a delay. So then you have your infusion catheter,

then you have the Inari FlowTriever, you saw the Cleaner in the previous cast, and you have the Penumbra aspiration device the CAT 8. And some of these will be spoken about in more detail in subsequent talks. But really, you can throw the kitchen sink at massive PE

just to do whatever it takes to get profusion to the left side. So, the best analysis that has been done so far was Will Kuo in 2009. He conducted a meta-analysis of about 594 patients and he found this clinical success rate of 86.5%.

This basically meant these patients survived to 30 days. Well, if that we're the case, that's a much lower mortality than we've seen historically we should basically be doing catheter directed therapy for every single massive PE that comes into the hospital. But I think we have to remember with this meta-analysis

that only 94 of these patients came from prospective studies, 500 came from retrospective, single center studies. So even though it was a very well conducted meta-analysis, the substrate for this meta-analysis wasn't great. And I think my point to you is that

we really are going to have a hard time studying this in a prospective fashion. So what is the data, as far as massive PE tell us and not tell us? Techniques are available to remove thrombus, it can be used if systemic lysis is contraindicated,

but it doesn't tell us whether catheter based therapies are better than the other therapies. Whether they should be used in combination with them and which patients should get catheter based therapy, which should get surgery and which techniques are most effective and safe.

Now, I think something we have to remember is that massive PE has a 5% incidence which is probably a good thing, if this was even higher than that we would have even more of an epidemic on our hand. But this is what makes massive PE very difficult to study.

So, if you looked at a back of the envelope calculation an RCT is just not feasible. So in an 800 bed hospital, you have 200 PE's per year, 5% are massive which means you get 10 per year in that hospital, assume 40% enroll which is actually generous,

that means that 4 massive PE's per year per institution. And then what are you going to do? Are you going to randomize them to IV lytics versus surgery versus interventional therapy, a three arm study, what is the effect size, what difference do you expect between these therapies

and how would you power it? It's really an impossible question. So I do want to make the plug for a Massive PE Prospective Registry. I think something like the PERT consortium is very well-suited to run something like this

especially with this registry endeavors. Detailed baseline characteristics including all these patients, detailing the intervention and looking at both short and long-term outcomes. Moving on to submassive PE. As you've heard much more controversial,

a much more difficult question. ICOPER as you already heard from the previous talk, alerted the world to RV dysfunction which this right ventricular hypokinesis conferring a higher mortality at 90 days than no RV dysfunction. And that's where PEITHO came in as you heard.

This showed that the placebo group met the primary endpoint of hemodynamic decompensation more commonly than the Tenecteplase group. Of course, coming at the risk of higher rate of major bleeding and intracranial hemorrhage. So I just want to reiterate what was just said

which is that systemic thrombolysis has a questionable risk benefit profile and most patients with submassive PE, as seen in the guideline documents as well. So that sort of opens a sort of door for catheter directed therapy.

Is this the next therapy to overcome some of the shortcomings of systemic thrombolysis? Well what we have in terms of CDT is these four trials, Ultima, Seattle II, Optalyse, and Perfect. Three of these trails were the ultrasound assisted catheter, the Ekos catheter.

And only one of them is randomized and that's the Ultima trial. I'm going to show you just one slide from each one of them. The Ultima trial is basically the only randomized trial and it showed that if you put catheters in these patients 24 hours later their RV to LV ratio will be lower

than if you just treat them with Heparin. Seattle II is a single arm study and there was an association with the reduction in the RV to LV ratio at 48 hours by CTA. PERFECT, I found this to be the most interesting figure from PERFECT which is that you're going to start it at

systolic pulmonary artery pressure of 51 and you're going to come down to about 37. Optalyse, a brand new study that was just published, four arms each arm has increasing dose associated with it and at 48 hours it didn't matter, all of these groups had a reduction in the RV to LV ratio.

And there was no control group here as well. What is interesting is that the more thrombolytics you used the more thrombus you cleared at 48 hours. What that means clinically is uncertain at this point. There is bleeding with CDT. 11% major bleeding rate in Seattle II,

no intracranial hemorrhages. Optalyse did have five major bleeds, most of the major bleeds happened in the highest dosed arms. So we know that thrombolytics cause bleeding that's still an issue. Now, clot extraction minus fibrinolytic,

this is an interesting question. We do have devices, you're going to hear about the FLARE trial later in this session. EXTRACT-PE is ongoing which we have enrolled about 75 patients into. What the data does and does not tell us

when it comes to CDT for submassive PE it probably reduces the RV to LV ratio at 24 hours, it's associated with a reduction at 48 hours, major bleeding is seen, we do not know what the short and long-term clinical outcomes are

following CDT for submassive PE. Whether it should be routinely used in submassive PE and in spite of the results of Optalyse this is a preliminary trial, we don't know the optimal dose and duration of thrombolytic drug. And even is spite of these early trials

on these non-lytic techniques, we don't know their true role yet. I'd liked to point out that greater than 1,600 patients have been randomized in systemic lytic trails yet only 59 have been randomized in a single, non-U.S. CDT trial.

So this means that you can randomize patients with submassive PE to one treatment or the other. And we want to get away from this PERT CDT roller coaster where you get enthusiasm, you do more cases, then you have a complication, then the number of cases drops.

You want that to be consistent because you're basing it on data. And that's where we're trying to come up with a way of answering that with this PE-TRACT trial. Which is a RCT of CDT versus no-CDT. We're looking at clinical endpoints

rather than radiographic ones greater than 400 patients, 30 to 50 sites across the country. So in summary I hope I've convinced you that we need a Prospective Registry for massive PE and a Randomized Controlled Trail for submassive PE. Thank you.

- Ladies and gentlemen, I thank Frank Veith and the organizing committee for the invitation. I have no disclosures for this presentation. Dialysis is the life line of patients with end-stage renal failure. Hemodialysis can be done by constructing an A-V fistula, utilizing a graft or through a central venous catheter.

Controversy as to the location of A-V fistula, size of adequate vein and priority of A-V fistula versus A-V graft exists among different societies. Our aims were to present our single center experience with A-V fistulas and grafts. Compare their patency rates,

compare different surgical sites, and come up with preferences to allow better and longer utilization. We collected all patients who underwent A-V fistula or A-V graft between the years 2008 through 2014. We included all patients who had preoperative

duplex scanning or those deemed to have good vessels on clinical examination. Arteries larger than two point five millimeter and veins larger than three millimeter were considered fit. Dialysis was performed three times per week. Follow up included check for a thrill,

distal pulse in the arter non-increased venous pressure or visible effective dialysis and no prolonged bleeding. Any change of one of the above would led to obtaining

fistulogram resulting in either endovascular or open repair of the fistula. We started with 503 patients, 32 of which were excluded due to primary failure within 24 hours. We considered this, of course, the surgeon's blame. So we left with 471 patients with a mean age of 58 years,

51 were older than 60, there was a male predominance of 63%, and over half were diabetics. The type of fistula was 41% brachio-cephalic fistula, 30% radio-cephalic fistula, 16% A-V Graft, and 13% brachio-basilic fistula.

Overall, we had 84% fistulas and 16% grafts. The time to first dialysis and maturation of fistula was approximately six weeks. First use of grafts was after two weeks. 11 patients with A-V fistula needed early intervention prior to or after the first dialysis session.

In sharp contrast, none of the A-V grafts needed early intervention. 68 patients were operated for their first ever fistula without duplex scanning due to clinically good vessels. Their patency was comparable to those who underwent a preoperative scanning.

Looking at complications, A-V grafts needed more reintervention than fistulas. All of them were late. Infection was more prominent in the graft group and pseudoaneurysms were more prominent in the A-V fistula group, some of them occluded

or invaded the skin and resulted in bleeding. Here's a central vein occlusion and you can see this lady is after a brachio-basilic A-V shunt. You can see the swollen arm, the collaterals. Here are multiple venous aneurysms. Here's an ulcer.

When we looked at primary patency of A-V fistulas versus graft, A-V fistulas fared better than grafts for as long as five years. When you looked at 50% patency in grafts, it was approximately 18 months, in Fistula, 13. Here's an assisted primary patency by endovascular technique

and when we looked at the secondary patency for the first 24, two years, months, there was no difference between A-V fistulas and A-V grafts, but there's a large difference afterwards. Comparing radio-cephalic fistula to brachio-cephalic fistula there was really no big difference in maturation.

The time was approximately six weeks. As for primary patency there is a trend towards better patency with brachio-cephalic fistula after six months, one year, and two years, but it didn't reach statistical significance. For patients with diabetes,

differences were statistically significant. Brachio-cephalic fistula showed a trend toward shorter maturation time, needed less reintervention, and had a longer patency rate. In conclusions then, ladies and gentlemen, A-V fistula require a longer maturation time

and have higher pseudoaneurysm formation rate, but better patency rates compared to A-V grafts. A-V grafts have a faster maturation time, but more late interventions are required and infection is more common. Finally, diabetic patients have a better result

with proximal A-V fistulas. Thank you for the opportunity to present our data.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Good morning everybody, and thank you for inviting me again for the same topic since five years now. Every time I have to rebuild my slides, and you will see why. So, you all know this story, renal denervation was almost destroyed by The Earthquake on January 9, 2014, and that was when Medtronic announced that HTN-3

did not make it to primary endpoint. What has been achieved since the earthquake? Better techniques with old devices, positive trials with old devices, new devices, and some positive trials with new devices. So, what about better technique?

More is better, that's what we learned, total number of ablation is important, circumferential ablation is important. Go distal is important in distal vessel segments, the nerves are closer to the vessel wall. We have the DENER-HTN heart trial with the old system

which was positive, and we have new devices, like the Symplicity Catheter, Spyral Catheter, the Vessix, Paradise, and Peregrine. So, what about new trials with new devices? Spyral HTN-OFF MED, HTN-ON MED, REDUCE HTN, RADIANCE HTN SOLO, RADOSOUND-HTN,

and Peregrine PMS - TARGET BP OFF-MED trial. SPYRAL HTN - OFF MED was a trial with patients without medications, or permitting discontinuing the oral drug therapy at that time, and they had to make certain values of blood pressure office and 24 hours, and you can see the results.

There was a significant effect in all parameters in systolic blood pressure ties to the blood pressure. 24-hour blood pressure and all these differences have been significant in favor of innovative denervation, so renal denervation certainly works. What about in those patients who are on meds,

and this has also been reported now. You see the patients had to have one to three anti-hypertensive medications. Again, they had to fulfill certain criteria regarding their blood pressure, and when you look at the result safety, it's very safe procedure,

no adverse events occurred, and office blood pressure changed from baseline to six months, it was a significant decrease systolic and diastolic blood pressure as well as 24-hour blood pressure, so renal denervation also works in patients

who are on anti-hypertensive medication. Reduce HTN was a trial with the Vessix system, which is not really a new system, but this is a new trial, and they used a balloon-based radiofrequency technique. They did an off-med study, the primary endpoint was reduction in 24-hour ambulatory blood pressure,

at eight weeks, which probably was too early, and the trial was stopped early due to slow enrollment and because it was determined that the trial could not achieve its primary endpoint at eight weeks, but when you look at the long-term results with this trial, there was actually a significant rate

of proportion of Vessix patients with office blood pressure below 140 versus control after six months, and this was significant and there was also over six months, systolic blood pressure continued to decrease in the Vassix group with a lesser decrease in the control group, and these differences

also have been significant to the match major part. RADIANCE HTN-SOLO trial is using the Ultrasound Based Renal Denervation using a balloon technology. You can see that these patients responded. There was a clear benefit in favor of the technique compared to a placebo group, significant difference 0.001.

Radiosound HTN was a trial, a randomized blinded trial comparing the different techniques, like ablation of the center part of the renal artery, distal part of renal artery, and ultrasound, and there was a significant benefit of ultrasound compared to the ablation of the proximal renal artery only.

Peregrine is using alcohol injected into the adventitial space, also significant effect of this technique, so now we have multiple randomized blinded renal denervation trials, OFF and ON meds, which are clearly positive. The decrease of blood pressure is, without any question,

clinically relevant, but it is smaller than expected and hoped. Everybody is asking, "Does it justify an invasive procedure? "So better not to do it?" At the same time, no major adverse events occurred, so why not to do it?

Everybody agrees that more research is needed. There are other device based approaches which are either stopped or covered by other talks in this, so I'm going to skip this. Thank you much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,

valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction

but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique

to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the

sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness

but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have

smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.

Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse

and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap

we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid

valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility

to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put

in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction

disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.

Thank you.

- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper

that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.

Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.

So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.

The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.

And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome

certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups

and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written

and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?

If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.

If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk

of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.

We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,

quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,

but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.

So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.

It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.

And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.

- I want to talk to you today about the MobiusHD device. And the question is can we modulate hypertension through the carotid bulb? My only disclosure is that I'm the site principle investigator for the CALM-2 trial at our site at SIU. Well cardiovascular death risk doubles with each

10/20 increase in blood pressure. And we know that hypertension causes or contributes to 60% of cerebrovascular disease, ischemic heart disease, as well as renal disease. And pharma has not really solved this problem for us. First off lifestyle modifications are usually inadequate,

patients often aren't compliant with their drugs. Drugs only work for as long as they're taken. And we know from our own clinical practice only about a third of patients actually have their hypertension adequately controlled. As well, 15 to 20 percent are resistant

to maximal medical therapy in the first place. And say, average effect of any single drug is a reduction only of only about 10/5. So, the question is what if there was a one time treatment with a durable effect? So, we're all familiar with

the carotid sinus baroreceptors. That may be a little bit of a misnomer because they don't actually sense pressure, they're responsive to stretch rather than pressure itself. But that's a surrogate for pressure.

And we know, or have learned that sustained activation only occurs if you have pulsatile stretch. Hence the concept of the MobiusHD device. This is a Nitinol self expanding internal carotid implant that goes into the carotid bulb. And the concept is that it changes the shape

of the carotid sinus in the diastolic phase. So, several different sizes of this. Its sized specifically to exert just enough radial force on the vessel to reshape it in diastolically, but prevent migration in systolically. And reshaping this vessel increases

mathematically the differential strain and therefore stretch. Which is what's measured by the baroreceptors. The device is similar to many of the implants we use. It has delivery system. Here you can see it prior to deployment.

It can be partially deployed and then recaptured and repositioned if necessary to get it in exactly the proper position where you want it. So, the first-in-man trials. So, the first-in-man trials.

So, these were performed in Europe. The feasibilies if you wish. 30 patients with multidrug resistant hypertension with an average of 4.4 antihypertensive drugs, all had successful insertion of the device. And there were five SAE's in four patients.

Interestingly, two of those SAE's were actually hypotension. Symptomatic hypotension, which may in fact speak to the efficacy of the implant. So, heres some of the data from that if you look at office blood pressures. The mean office blood pressure at the beginning

was 184/109 in these groups. And you can say statistically significant reductions in both systolic and diastolic office blood pressures out at to six months here. What about ambulatory blood pressure? Same thing here you can see significant reductions

at three and six months in ambulatory blood pressure in these patients reduced by an average of 21/12 millimeters of mercury in these populations. But does it have any kind of a long term effect? Well, as you can see the numbers get pretty low, the further out you get on this.

But nonetheless, it does appear to have a sustained, durable effect on reduction of blood pressure and this. And the other interesting thing is the concept of the DDD, which is the daily defined dose. So, not only are the blood pressures being lower,

but the amount of medications that these patients are having to take is also being reduced somewhat as well. So, hence after the feasibility trial on these results, the company has decided to launch what is being named the CALM-2 trial. I'm proud to report that SIU randomized the first patient

in this trial on July fifth 2018. So, the trials still very much in the early phases. The trial will enroll 300 patients at up to 75 European and US centers, with a 1:1 randomization to a sham procedure. The sham patients actually get a sixth French sheath

in the carotid artery. Get their full angiographic evaluation and then they are randomized on the table. And there's a script we go through if they randomize to nothing. And if they randomize to the device

obviously we proceed and implant the device. There's a primary effectiveness endpoint at six months. And that will be assessed by the ambulatory blood pressure and a safety endpoint at three months of the composite cardiac and neuro events. So, in conclusion then, mechanical stimulation

of the carotid sinuses been demonstrated to effectively lower blood pressure. At least in the short term. And the clinical applicability of this we hope to get more information from in this trial. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thanks again for the invitation to talk about, I think a lot of excitement on these new medications, and you've heard a lot from our prior speakers. So, first focusing on antiplatelet, antithrombotic therapy, this very simple cartoon. Certainly, we've known about aspirin forever. Xa inhibitors, thrombin inhibitors,

the PAR inhibitors now are coming about to to prevent this atherothrombosis. And this, I think pretty well done analysis, looking at peripheral arterial disease patients, looked at which agents perhaps are the most efficacious. And what was shown here is ticagrelor and aspirin

or clopidogrel. Put another way that looks at both safety and efficacy, really, clopidogrel and ticagrelor and aspirin stand out more than aspirin alone. So you've already heard about the COMPASS Trial in a fair bit of detail, but again,

this was rivaroxaban plus aspirin versus aspirin alone. And this substudy in patients with a PAD specifically looked at MALE, AMP, et cetera. 6300 patients, and you can see a significant reduction with, again, rivaroxaban plus aspirin versus aspirin alone. 43% reduction MALE, 67% reduction to amputation,

decreased vascular interventions, but at the cost of increased bleeding. Vorapaxar is a PAR inhibitor. It's gotten a little less use because of the bleeding events, but of interest in patients, a substudy of patients with PAD, 3700 patients,

again, there was no difference in the composite CV outcome, but acute limb ischemia was significantly reduced, incident acute limb ischemia, and the need for revascularization. So there's a lot of these agents, and Dr. Hiatt, I think in this nice review in JAMA Insights,

helped clarify this with this table. So if you have asymptomatic patients with PAD, probably antithrombotic therapy aspirin may not be of benefit, but for patients with PAD-associated limb symptoms, probably clopidogrel or ticagrelor monotherapy

is most efficacious to prevent long-term cardiovascular events. Still, with patients with revascularization, a bypass aspirin should be maintained. For patients with polyvascular disease, PAD plus manifest CAD, again,

antithrombotic therapy for stable cardiovascular disease, either adapt or clopidogrel alone. For patients who are at risk of cardiac and ischemic limb events, either ticagrelor plus aspirin is probably better than Plavix, or low-dose rivaroxaban.

Again, you heard about the COMPASS Trial. And probably vorapaxar, less likely to recommend that. From Dr. Rockman, you just heard a nice overview in terms of LDL, but again, the greater the reduction, the greater the decrease in events. This meta-regression just shows

that it does matter where you start. So if you start at a pretty high LDL level, and you get one of these agents, you have a greater relative risk reduction as comparative if you're already starting fairly low. Again, from this same summary,

for patients that were already at a low level LDL, you still gained a benefit from the addition of the PCSK9 inhibitors without any increase adverse events. So, just again, you heard about this from the last speaker, but this, again, focusing on patients with PAD. Here, overall it was 27,000 patients in this large trial,

follow up, 2.2 years, and again, as was highlighted previously, those with PAD gained a greater benefit than those without PAD. And again, major adverse limb events significantly reduced, 37% over time.

How about ezetimibe that blocks cholesterol at the GI tract level. Safe drug, this was a randomized controlled trial of ezetimibe versus simvastatin, plus simvastatin. 18,000 patients, these weren't PAD-specific. Acute coronary syndrome was the inclusion.

And here, they really decrease the LDL from 70 to 54, with about a 7% decrease overall cardiovascular morbidity and mortality. Raising HDL, you heard from one of the very early speakers, this is off the market now, really not worthwhile to do. And Dr. Berger noted that this agent just was presented

the American Heart Association, I think it's very interesting, patients with hypertriglyceridemia in this derivative of Omega 3, iscosapent ethyl, five year out follow-up, and everything they looked at was significantly reduced,

which I think is quite exciting. So what should we do about our high-risk PAD patients? Aspirin, but really probably lean more toward Plavix should be the first line therapy for symptomatic PAD patients. Consider rivaroxaban in those with coronary artery disease

would be my first line, and again, reducing both cholesterol and inflammation with statins should be standard. If you can't get that LDL less than around 70, maybe add ezetimibe, that seems to be safe and efficacious. PCSK9 inhibitors in refractory patients,

particularly those that are still above 200, there seems to be no lower limit of LDL, and again, keep your eye on this new triglyceride-lowering drug. Thank you!

- Okay, it's great to be back. Thank you. So, moving on. So we know that inflammation is very important in the pathogenesis of cardiovascular disease. In this figure on the left, do you see how macrophages, mast cells, T-cells, all contribute to endothelial cell activation, eventually contributing to thrombus formation.

There is a large literature out there that when you measure biomarkers of inflammation in. In this figure on the right, when you measure levels of high sensitivity C-reactive protein, the higher the level whether you're on placebo, whether you're on aspirin, the higher your risk of cardiovascular events.

So, I think most people now believe strongly that you can discriminate cardiovascular risk by levels of inflammation in your blood. As low level, average, or high, depending on your level of high sensitivity CRP. Further to this, is this idea that when you look

at some of the statin therapy trials, like on the left, prove it, or even the ezetimibe trial on the right. When you lower both inflammation and LDL cholesterol, in the red bar, patients do better. If you don't lower LDL cholesterol or inflammation,

as seen in the blue bar, patients did really bad. If you lower one, regardless of which one it was, patients had this intermediate phenotype. So the lower your inflammation, the lower your cholesterol, patients do better. There is this idea that we have

this residual risk paradigm. Right? If you have an elevated cholesterol, as seen on the right side of this figure, then you have this residual cholesterol risk. Sorry, on the left side. If you have low cholesterol but you still have high levels of inflammation, you're believed to have

this residual inflammatory risk. So with this idea, the Cantos trial was performed. This was looking at canakinumab, which is an interleukin-1 beta receptor antagonist for the prevention of cardiovascular disease. Now, what's really interesting, is this figure on the left.

You see on the top, when you're looking at high sensitivity CRP, there was a dramatic reduction in CRP levels with this therapy. No difference in LDL cholesterol. No difference in HDL cholesterol, and no difference in triglycerides.

So finally we were going to be able to answer the inflammatory hypothesis. When you look at major adverse cardiac events, when you combine two of the doses of canakinumab, there was a significant 15% reduction in the incidence of cardiovascular events.

Now, the authors really nicely went back and saw, "What about the people who had "the greatest inflammatory reduction?" so those with the lowest levels of CRP, that's the red group right here. Showing that in that group that had

the lowest levels of inflammation, once again, had the lowest risk of cardiovascular events. So this was very exciting. But, there was some very significant adverse events. Adverse and actually pro. So in the green, you actually see that fatal cancer

was actually lower in the group that received canakinumab. But there was significant leukopenia, there was was significant thrombocytopenia in the group. So, this was sort of a mixed picture. I think because of this, and because of the less than compelling primary outcome,

the FDA as of a few weeks ago, did not approve this drug, for the reduction of cardiovascular events. So, I think it raises this hypothesis, but clearly it did not definitively stated, and we're not going to be giving it to patients

also because of this significant cost. So, what about other inflammatory drugs? As of three days ago, the New England Journal published this cert trial as an NIH funded trial. Looking at low dose methotrexate for the same purpose. Done by the same group of investigators.

As you can see, the hazard ratio was 0.96. There was no significant reduction in the endpoint of cardiovascular events. So, inflammation and cardiovascular disease. Is the inflammation hypothesis viable? I personally think the answer is yes,

but I believe that we need future trials that focus on specific pathways that will not have untoward side effects, that will be able to sort of target specifically what the issue is. I think future trials are being considered as we speak.

I think it's a very exciting time, but I think for once we can say that when you target inflammation, at least using the IL-1 receptor antagonist, you can lower the risk of cardiovascular events. Thank you very much.

- [Lecturer] Here we go. These are my disclosures. In 2013 the ACC and AHA wrote updated lipid management guidelines, which for the first time included specific recommendations for patients with peripheral arterial disease.

They also shifted the focus away from specific LDL targets, but instead they targeted statin intensity. This is the overview of the guidelines,

but in terms of the specific recommendations for PAD patients it's a fairly focused section. After excluding recommendations about dialysis patients because of a lack of data,

they basically broke it down that anyone with PAD who's less than 75 should be on a high intensity statin. Anyone above 75 should be on a moderate intensity statin.

What are the high intensity statins? These are the ones that you need to remember. It's Atorvastatin 40 or 80, or Rosuvastatin 20 or 40. This table is available in their paper

and in ours. We wanted to look at the impact of statins, and in particular the statin dosing. According to these guidelines, our patients undergoing revascularization

either endovascular or open surgery, for CLTI at our institution from 2005 through 2014 we used propensity scoring to account for baseline differences in patients. We had 11 hundred limbs

and 930 patients after excluding the dialysis cohort. Our follow up was 380 days. Our primary outcome was overall survival, but we also looked at major

adverse limb events, which has noted our amputation and major re-interventions. Our statin use over time did increase as of 2014. 90% of our patients

were discharged on a statin, but in terms of whether they were on the guideline appropriate dose, that was pretty dismal albeit the guidelines didn't come out until the end of this period.

When we looked at it based on age, you can see that in patients under 75, they're suppose to be on high intensity here in red and we're not very good at that although we were increasing over time.

Most were on moderate dose. In the patients over 75 who were suppose to be on moderate intensity we see that that's actually decreasing and largely being replaced

by high intensity statins. In terms of what's the benefit of statin versus no statin, there is a significant reduction in mortality and this is long term survival

in patients discharged on a statin compared to no statin. For limb events, there was a benefit in the sub group of patients over age 75 only.

When we looked to see if there was additional benefit to being on the guideline directed dose, we did find a significant benefit in overall survival

and in limb events in being on the appropriate intensity statin. Since there was a suggestion that in the older age group they should perhaps be on the moderate rather

than the high intensity statin, we looked specifically at this subject group and we actually did not find a significant difference between moderate or high intensity

dosing in that group. We also noted that adherence is poor so we wanted to look at what happened one year, how many patients stopped their statins or dropped the dose

and then how does that impact survival after a year. What we found is that it wasn't so much the guideline directed dose so much as just being on either a high

or a moderate intensity statin was associated with significantly improved survival compared to no statin or low dose statin after one year. We also found that 12%

of our patients stopped taking their statin or decreased the dose. The best survival was in those who remained on their statins and a close second was those who started statin

or increased their dose, but the patients who stopped taking their statin or dropped the dose had no survival benefit compared to patients who were never on a statin.

Statins are associated with an improved survival and a decreased limb events after revascularization for CLTI and the correct dose based on the 2013 ACC guidelines

does provide incremental benefit. 2/3 of our patients are not on the recommended doses. Moderate and high intensity statin after a year is associated with improved long term survival

and discontinuation or decreasing the dose is common and results in a loss of this benefit. It's not enough to just discharge patients on a statin,

we have to make sure that it's the right dose and we have to make sure that they stay on that during follow up. Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- This is what we're going to talk about today. It's a vascular approach to hypertension and AV fistula. This implant was first designed in the early 2000s and directed, actually, at COPD, but then redirected to hypertension. Disclosures. Hypertension, as we age, is largely a result

of the loss of compliance in our arteries. Approximately 85% of uncontrolled hypertension patients are those over 50 with predominantly mechanical hypertension. This is the implant and the procedure. It's simply an AV fistula created

in the external iliac artery with an endovascular procedure done under local. Takes about an hour to do, and it creates a very precise AV fistula that doesn't grow over time, about four millimeters, mediated by the implant.

This is a just sort of appetizer before we get into the data. This is a patient done recently and presented in June of 2018. Patient in Toulouse, France. The difference from renal denervation, of course,

is that it get an immediate effect on the table, a very large drop in blood pressure. And you can see ambulatory blood pressure is roughly 30 points lower systolic, 20 diastolic. And as we'll see that's backed up by long-term data. This is the main body of data that's been generated

to date, a randomized trial in Europe, has six and 12 month data now, and we'll review that. So the Prospective Trial, 83 patients, 44 treatment, 39 control. All of these patients had to be on maximal medical therapy. And the exclusion criteria

were generally cardiovascular morbidities. You can see the groups are very similar. And actually, these results are for the prior renal denervation group. So of note, patients who have had prior renal denervation also respond to this therapy quite well.

Here you can see a very significant drop in both office and ambulatory blood pressure at six months. Here's the broader study. Both six and 12 month data with the right panel being a consistent cohort, just the patients that were not lost to followup.

But you see very consistent results. Again, significant drops, 26 points and 20 points for systolic and diastolic respectively. And if we look at 24-hour ambulatory blood pressure changes at six and 12 months, not quite as much, but still very significant, 13 drop

in both systolic and diastolic. There was a crossover group after six months. Those randomized to no therapy can be crossed over to the therapy, and we see that those respond as well, much smaller group. The primary complication in this procedure

is not congestive heart failure or anything like that, it's iliac vein stenosis. We see this with our other work in arteriovenous fistulas for dialysis. As we know, stent therapy for iliac vein stenosis is very successful in non-thrombotic patients,

and so all of these patients were treated with an iliac vein stent and all resolved without incident or recurrence. Some of these patients in the European study were done from the left and it's always done from the right to avoid the May-Thurner physiology.

Two patients didn't respond. And now the therapy is going into a much larger trial, a 500-patient randomized trial. This is an adaptive study, double blind, sham-controlled, and of course multicenter. These patients have to have, as a primary endpoint,

of 24-hour ambulatory blood pressure and then secondary endpoint of office blood pressure. The inclusion criteria are very rigorous. These patients have to be on maximal drug therapy. They have to be on that same drug therapy and have the same blood pressures on multiple checks

over a three-month period before they're randomized and stay on that same drug therapy, if possible, for six months after randomization. The exclusions are similar to the European study. So in summary we look at this technique of using an AV fistula to reduce blood pressure.

With denervation we don't have a procedural endpoint on the table. Often it's a smaller and less consistent blood pressure effect. What we don't talk about is the fact that autonomic nerves do regenerate,

it's dependent on renal artery anatomy, and there's some risk of renal artery injury, albeit small. But with an AV fistula there's a very immediate and significant effect. It's scalable and reversible with covered stent. It's independent of the renal artery anatomy,

and it's effective in patients with prior renal denervation and durable. Thank you very much.

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