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Outcome Assessment Of Venous Disease
Outcome Assessment Of Venous Disease
GSV refluxRt Leg VV with sx
DEBATE: CAS Is Justified Soon After Neurologic Symptoms If Certain Precautions Are Taken:  How Soon: What Precautions
DEBATE: CAS Is Justified Soon After Neurologic Symptoms If Certain Precautions Are Taken: How Soon: What Precautions
Carotid artery stent systemCarotid embolic prevention system)Cguard (InspireMDmesh carotid stent)RoadSaverScaffold (GOREterumo
What Is The Optimal Anticoagulant/Antithrombotic Regimen For Patients Undergoing Iliac Vein Stent
What Is The Optimal Anticoagulant/Antithrombotic Regimen For Patients Undergoing Iliac Vein Stent
Flow Augmentation Device (Covidine - Flow Aid)GekoNeuroestimation deviceSky Medical
Transcript

- Thank you very much, it's a great pleasure to be here. Thank you, both the organizers as well as Frank Veith for the opportunity. These are my disclosures. Now, for those of you use that use Ace bandages, when you're afraid to put something stronger on because a patient's pulses are a little weak,

or after a revascularization, stop it. The use of elastic bandages, kerlex, stockinette, TED hose, or tube gauze for leg swelling, venous stasis ulcers, or venous insufficiency-induced lymphedema is suboptimal at best. And this is what the elastic bandage versus the

short stretch bandage, the elastic bandage gives way, so you have to put it on tightly. And that's uncomfortable over the time and frankly dangerous for patients with arterial insufficiency. It has a low ambulatory pressure. When the patient gets up, the bandage gives way.

The edema increases, and there's no increase in the standing stiffness index, which is the difference between the lying and the standing pressure. This is what it looks like for ace bandages, TED stockings, stockinette, tube gauze, there's no change on the standing exercise or recovery.

Now, most people are unaware of the fact that the venous pressure in a giraffe is 250 millimeters. That is three times more than humans. Giraffes do not suffer from lymphedema or venous disorders. Physiologists have discovered the answer is in the skin. Giraffe skin is inelastic, so it doesn't stretch.

As their leg muscles contract, the veins in the leg are squeezed, forcing the blood toward the heart, thus giraffes are not susceptible to problems like lymphedema and venous disease, even though they may be on their feet 24 hours a day. Inelastic short-stretch compression is characterized

by a low resting pressure, comfortable at rest, a high walking pressure, which decreases edema, and the difference between the lying and standing and walking pressure is at least ten millimeters or more. There are many modalities, there's many roads to roam. Unna's boot, short stretch bandages, and velcro devices,

there's also the popular four layer bandage in which it is four elastic layers, when put over one another, create a somewhat inelastic environment. In addition to that, two very light stockings when put over one another, also become less elastic. Here's a typical elastic short stretch bandage

that we use, with a pressure of 60 millimeters, and a pressure of over 100, with a patient walking. You can't look at all the old literature on the comparison between four layer bandages and two layer short stretch because there was no dosing. There was no pressures measured.

And the hands, it's in the hands of the provider with short stretch compression. Velcro compression is ready to wear, and inelastic properties, it's adjustable, and this is the profile for this adjustable compression. And you can see as the patient stands and walks there's an

increase of pressure with the standing and walking. It has a low resting pressure, a high working pressure. This decreases the venous volume and edema. It's adjustable as edema decreases. People will come back and say well I put these things on but they're falling down, well you have to tighten them up.

And it's ideal for those unable to don or doff stockings. Many, many of my older patients have preferred this because they just couldn't wear, or couldn't don or doff the stockings. Stocking failures, postoperative leg swelling, lymphedema, but one of the most notable situations that

I've found, well first of all let's take a look at this. This is a typical venous insufficiency-induced lymphedema patient, who also had a prior DVT, and after weeks and months of good compression with the short stretch bandages first and then the velcro devices, was actually back to work and off of disability.

But anyways, a short stretch bandage slide. Anyway, one of the most notable uses in my experience is in patients who have fem pop bypasses and have post revascularization edema because of their ischemic limbs. Works beautifully for that. And it prevents that and sometimes if you ever do those

procedures and you're looking at the incisions, and they're swollen and they're bursting and somebody has an ace bandage on them, and I've done this a lot. Take them out of that, put them in short stretch compression, it's ideal, if there's any difficulty with a patient having any sort of symptoms,

they could loosen it, and adjust it. And it's very, very effective as time goes on, so remember that short stretch compression is the way to go. There's many different roads to roam, and I suggest that you also look into these devices. Thank you very much.

- Good morning, ladies and gentlemen. Thank you Dr. Kabnick for the kind introduction, and thank you to the Veith Symposium for the opportunity to be here. I have no disclosures. Superficial thrombophlebitis is uncommon, but certainly more common than DVT.

And it used to be thought of as quite a benign entity that could be treated with antibiotics and, oh sorry. Antibiotics and analgesia, apologies for that. However, it is been found to be a wolf in sheep's clothing. And actually, there is a significant risk of DVT,

and of asymptomatic and symptomatic pulmonary embolism. Particularly important for individuals with truncal involvement, and particularly if close to the junction. And actually anything that is less than three centimeters from the junction,

should be treated as a deep venous thrombosis, and requires anti-coagulation. Management sent us on to symptom, sort of addressment, prevention of SVT extension and recurrence, and prevention of venous thromboembolic complications. There've been a number of studies that have been produced

and summarized in different guidelines. The CHEST ACCP guidelines suggest that if you have a superficial vein thrombosis of at least five centimeters in length and more than three centimeters from the junction, you can treat it with prophylactic Fondaparinux

or low molecular weight Heparin for 45 days. And that is superior to no anticoagulation with a grade 2B recommendation. However, Fondaparinux is actually been found to be of higher level than low molecular weight heparin, and that should be used.

Importantly, patient choices also mentioned in these guidelines and the risk-benefit ratio as to whether to take anticoagulation or whether it's run the risk of getting a DVT, must be discussed with the patient. The Cochrane Review was published in February of this year,

and this is the latest summary of the evidence on this topic. They also suggest as per the CALISTO trial which was the largest randomized study on this topic, to give Fondaparinux, 2.5 milligrams for 45 days. And this was found, in this study it was found

that VT development, SVT extension and symptomatic recurrence were lower in the Fondaparinux group as opposed to placebo. Low molecular weight Heparin can also be used. There is some evidence for this, however as graded by the Cochrane library, this was found to be low evidence.

And most of the studies are actually of low quality as opposed to the ones with Fondaparinux. And again, patient choice and patient discussion and need to think about different risk factors for developing SVT. The SURPRISE trial looked at Rivaroxaban

versus Fondaparinux in prophylactic doses and found that Rivaroxaban was non-inferior. And actually this gives us an advantage to give an oral agent for individuals for the treatment of SVT. This is an algorithm that was published

by the British Journal of Hematology, again reminding us that anyone with a DVT or an SVT less than three centimeters away from the junction should be treated as a DVT. If it's more than three centimeters and more than five centimeters in length,

you can give Fondaparinux and I would suggest, also Rivaroxaban. And if the length of the SVT is less than five centimeters, or there's no SVT you don't need to treat. With regards to compression, it's mainly for symptomatic relief and there's very conflicting evidence

as to what the classes or what the length of time is. One study looked at compression versus no compression SVT and they found no additional benefit for compression. And the next pilot randomized study actually had to be halted due to poor recruitment and therefore was underpowered

and couldn't identify any difference between the groups. With regards to follow up, there's no clear guidance. It can be anywhere between eight weeks to six months. In the studies, it's really on a case by case basis based on the risk factors. But what we do know, is that even if we treat SVT,

there is a risk of developing a VT even with treatment dose low molecular weight Heparin. So if you identify thrombus extension, what do you do? Well some studies have looked at different treatment modalities. This randomized control trial by

a professor Nicolaides' team looked at different treatments including compression only, saphenous ligation, saphenous ligation and stripping, and anti-coagulation. And they found that in the stripping group you had less DVT instances or SVT extension. But with respect to newer ways of treating veins,

looking at endovenous saphenous vein ablation in individuals with SVT with refluxing vein this group looked at this and such and they didn't find any inferiority with, or any sort of particular side effects with using endovenous saphenous vein ablation,

however this was a retrospective study and was also underpowered and therefore there is a lack of evidence. So in conclusion, ladies and gentlemen, think SVT is not benign, there is a role for prophylactic Fondaparinux for 45 days,

Rivaroxaban should be considered. Compression is conflicting in evidence and the role of intervention is also unclear. Really we need to assess patients individually with their risk factors, and we need more data. Thank you very much.

- [Lecturer] I thank you, Mr. Chairman, and thank you Dr. Vieth. It is our great pleasure to open our primer endpoint result today in this meeting. I've nothing to disclose. There's been studies of

prospective multicenter registry in Japan, which started at 2012 by vascular surgeons and interventional cardiologists collaboratively. More than 550 CRTI patients were enrolled. More than 70% patients are diabetics and more than half of the patient

are dialysis dependent. So, very high risk patient are including in this observational study. Directing this patient background, so to study the patient while aiming infrapopliteal revascularization.

Taking a look at preoperative QOL, there are some difference between EVT group and surgery group, and the surgical intervention, while frequently selected in a more active or more motivated patient.

In terms of the foot lesion severity, there seemed not difference between two groups by Rutherford classification, but adapting a WIfI classification, so the feet underwent the surgical intervention was significantly similar

in terms of WIfI wound grade, ischemia grade, and foot infection grade. So, adjust this difference and to minimize the bias, we employed a propensity score matching result. Now, I would like to open our primer in the point,

amputation-free survival. As you can see, there are no difference between surgical group and endovascular group, and the AF risk at three years are around 50% for both groups.

There are no difference between the two groups in terms of freedom from MALE, but the freedom from major amputation or any reintervention rate was significantly lower in EVT group. These results came from a sum total of

highly heterogenic population, so it should include patients suitable for EVT and another patient group suitable for surgical intervention, so we have to find out the important factor for selecting intervention procedure.

So therefore, we performed the interaction analysis. This slide shows the impact of the foot lesion severity on selecting revascularization procedure. So, patient with high grade WIfI,

wound grade or infection grade are seemed suitable for bypass surgery, surgical intervention. In terms of general condition, patient who is diabetes, patient who is renal dysfunction

not seem suitable for bypass surgical intervention. So this analysis provides us five factors more favorable for surgical intervention. Each have a +1 point for each, and another five factors

less favorable for surgical reconstruction, which have a -1 point for each. Finally, we propose a favorability score model to select a proper revascularization procedure. If the total point is +2 or more, the patient is suitable

for surgical intervention. On the other hand, the point is -2 or less, the patient is suitable for endovascular treatment. So, the patient risk factor,

as well as foot lesion severity are very important to select the revascularization procedure. In conclusion, ladies and gentlemen, the SPINACH registry explores current clinical outcomes of CLI treatment

in real world setting in Japan, which provides the data recommending how to select adequate revascularization option, in respond to patient's general condition and foot lesion severity, and WIfI system is very useful,

not only assess foot status, but also selecting revascularization procedure. Now, our doctor, analyzing a secondary endpoint is now ongoing. I thank you for your kind attention.

- Thank you very much once again for invitation. I don't have any disclosures. Post-thrombotic syndrome rates ranges from 10 to 70% depends on the way of assessment of population treated in two major components where damage and vein obstruction are taken

into consideration. This surgery results of our study of 10 patients with proximal DVT with a main follow-up of 58 months, and we found the Postthrombotic Syndrome based on

Villalta score 74% with 6% of severe Postthrombotic Syndrome. One assert of this patient were the femoral. DVT patients and looking for the whole cohort.

Ultrasound result, persistent obstruction was present in 15%. Total vein system recanalisation 20. Residual thrombosis 65 but the major findings was pathological reflux in 72%. What about the risk factors?

We know that anticoagulat therapy does not dissolve probably the clot, but prevents the recurrence of DVT, which is the major factor for postthrombotic syndrome.

Risk increase concerning other factors that should Age, obesity, preexisting varicose veins as with us, considering DVT location, massive proximal DVT should be mentioned,

however, in this DVT patient, we also observed this kind of complication. There are also some factors related to the tre al thrombosis was thoroughly mentioned today.

Incomplete resolution of the symptoms or poor anticoagulation control. Concerning our group of 100 patient with the rate of postthrombotic symdrome 74%, pathological reflux was found in 65%. Obstructive lesions in the group of the

postthrombotic syndrome only in 16%. Residual thrombosis in 50% and looking for the main factors is possible for postthrombo occurrence we found the presence of the obstructed lesion in two segments with the

common femoral vein involvement especially as a major factor. And second the potential role of the reflux, especially in femoral popliteal segment. So can we avoid this, I will not go deeply into the ATTRACT study because

this will be discussed many times but still probably open for the discussion. I mean open vein concept. But what about other measures? Do we have something about the new drug in term of PTS prevention?

And we start to see the study concerning the subject this is an example. The study from Slovania from Professor Poredos group using the rivaroxaban. We can significantly- this was the randomized study.

We can significantly decrease the rate of postthrombotic syndrome in comparison with the group treated by warfarin therapy. What about the compression? After SOX trial complication,

we're a little bit confused. Despite all the (unidentifiable phrase) this is the level one of evidence, and in ACCP guidelines, we can find this addition that we should not use compression stocking routinely to prevent

postthrombotic syndrome, but we should probably be very careful with the final conclusion. If we look into All of this is from 2017,

a patient with DVT who wear elastic compression stocking are probably less likely to develop postthrombotic syndrome. However, from the same analysis, we see that the compression did not lead to reduction of

incidence of severe postthrombotic syndrome. So we try to look into this problem also in our study based on what our patient filed for for more than 50 months.

The percentage of the patient wearing compression within first three to six months was 75% for daily use of compression. And almost 70% wear this compression in the prolong phase of treatment including half of the patient more than two years.

And this are the results showing that there was no difference wearing, not wearing compression within first three to six months in term of preventing postthrombotic syndrome, so in both these groups, postthrombotic syndrome

occurred and to answer the question why there is such a difference. And this is probably the answer because the study was based not only on Villalta, but also on the Venus Clinical Severity- Venus Clinical Severity Score.

And as we can see, there was the higher score concerning Villalta and Venus Clinical Severity Score in patient wearing compression continuously. It means those patient that wear compression

had the higher rate of postthrombotic syndrome. It means that probably the patient with the lower rate of they should or they could not wear the compression stocking

as this treatment should be probably dedicate to the most symptomatic patient that we like to wear this in contrary to the group of patient without the symptoms. This comes from ultrasound observations from

the vitriture. And my last slide conclusion. We need to probably also more research in the fute. Precise PTS definition and validated assessment, and validated classification of

postthrombotic severity. And I would like once again to invite you to CRACOW's next year UIP meeting in CRACOW. Finally thank you very much.

- I'll be speaking about bridging anticoagulation. No disclosures. Given the increasing number of options available for long term oral anticoagulation, physicians need to be aware of how to manage these medications when these patients are undergoing surgery or invasive procedures.

The American College of Chest Physicians back in 2012 gave us some guidelines that help us stratify potentially which patients might need bridging and which patients might not need bridging. They break them down into those who are high risk,

moderate risk, and low risk for arterial or venous thromboembolism, classifying them according to common indications such as mechanical heart valves, atrial fibrillation, or venous thromboembolism. However, there are some additional factors which also come into play when deciding whether or not

to bridge these patients: what is the procedure-related bleeding risk, what are the pharmacokinetics of the oral anticoagulant medication in particular with regard to renal function, and what is the ability to re-administer these medications

and what is the absorptive capacity of the GI tract afterward in someone who may have had an abdominal surgery? With regard to the types of surgeries which might or might not be related to a high risk for bleeding or low risk for bleeding, several authors have tried

to compile lists that classify certain surgical procedures into minimal risk, low risk, or high risk procedures. Although vascular surgery is not shown on this list, most authors do classify vascular surgery as a high bleeding risk procedure, or field. So do we bridge these patients or do we not?

Older data from prior to 2010 were compiled into a meta-analysis with over 12 000 patients. And in this older study, the author's identify that whether you bridge or not there is no difference in perioperative thromboembolism but bridging was associated with a three

to five fold increase risk for perioperative bleeding. However those are usually single institution studies and many of you are familiar with the 2015 bridge study which took over 1800 patients with atrial fibrillation who required a procedure where they had been taking warfarin previously and had required interruption.

These patients were randomized to either low moleculoid heparin or placebo before the procedure, and after the procedure, at either 12 to 24 hours for low bleeding risk procedure, and 48 to 72 hours for high bleeding risk procedure. What the authors identified was that in patients

with fibrillation who had warfarin interrupted, forgoing bridging anticoagulation was not inferior to low moleculoid heparin bridging for prevention of arterial thromboembolism, but did decrease the risk of major bleeding and minor bleeding.

The limiting factors of this study included that only 3% of the patients were high CHAD score patients, and only 11% of patients had major surgery. That limiting factor may potentially be addressed with a study which is currently ongoing called the PERIOP 2 study which is actually looking

specifically at these highest risk individuals, such as those with prosthetic heart valves, or high risk a-fib or a-flutter who require a non-cardiac procedure. All these patients received low moleculoid heparin prior to the procedure, but then post operatively they were

randomized to either low moleculoid heparin or placebo until the INR achieved greater than 2.0. Recruitment was completed this month and hopefully we'll have some answers in the next year. How about with regard to the direct oral anticoagulants such as the Dabigatran, Rivaroxaban, and Apixaban?

There are no prospective trials involving these patients in bridging, but there is significant experience involving thousands of patients who underwent surgical procedures during these clinical trials. And what they identified was that there was no

significant difference in the perioperative thromboembolism or perioperative bleeding risk, but in the patients who did receive heparin bridging, it did not confer protection against arterial thromboembolism, but was associated, again, with a high risk of perioperative bleeding.

Shulman et al did review specifically a certain protocol with regard to perioperative bridging for Dabigatran specifically, looking in particular at the bridging protocol and basing it on the renal function. So if the renal function was significantly decreased,

those patients actually held the Dabigatran up to six days prior to the procedure.

- You've heard some of this earlier by Mark Passmin on Thursday. But the thing that I'm going to do different is I'm going to actually add a third dimension, he was only two dimensional. So let's talk about outcome assessment of chronic venous disease.

I have no disclosures for this topic. When we look at the 2011 guidelines, if you look at it we recommend classification, CEAP classification, VCSS score as an outcome assessment. We know that outcome assessments, treatment of varicose veins and more advanced chronic venous disease

includes standardized objective criteria that reflect patient symptoms, characteristics and objective measures of functional and disease-specific quality of life. If you look at what they do, they help determine the progress of a patient.

Specific questionnaires relevant to the patient's chief complaint. Given to the patient before treatment and again at various re-examination intervals. Considered to be indicators as to whether a patient is improving, staying the same, or getting worse.

That being said, the IAC which is the Intersocietal Accreditation Commission, has adopted the CEAP classification of VCSS as a standard here in the United States. So as a generic quality of life instruments, this allows comparison with population norms

and other disease states and provides a measure of any ill effects of treatment. Then there are a whole bunch of disease-specific quality of life instruments of which you see here and they've all be validated, as you can see, in terms of studies.

Now the one thing that I bring as a third dimension is the VVSymQ, which is a validated instrument that was used to gain access and approval of FDA for a drug in terms of foam sclerotherapy. It's a proprietary of drugs

and the registries now include this. The Vein Society and Lymphatic ... The American Vein and Lymphatic Society, as well as the AVF and the Society of Vascular Surgery registries all contain this instrument. So physician generated measurements

we again look at the CEAP and VCSS. We understand all of this in terms of what it looks like. Certain patient reported outcomes. And where I'm going to go, really, is to show you how we use these things rather than going in specifically to it.

The VVSymQ at NYU, we basically made it a patient fill out form that was on an iPad when they came in, so we didn't have to do anything with it. The VCSS score was done by our medical assistance and we graded the CEAP score because

I mean the CEAP classification because the reality was the MAs had trouble with that. So if you take this 48 year old female complaining of right leg varicose veins with symptoms and Great Saphenous reflux and you look at pre op and post ops,

you can see there are a lot of variations, good variations, in terms of the VCSS scores pre and post where the CEAP scores did not change very much. The VVSymQ did in terms of patient report. We take that same patient, I mean that same history different patient

and you look at the CEAP classification and that stayed the same because it's varicose veins. The VCSS scores stayed the same because it's a C2 patient. The VVSymQ stayed the same. Now when you look at this, if you have a patient and you've ablated a vein and

the patient doesn't feel any better, you're going to have a problem. So I think you need all three modalities to be able to figure out what's going on with a patient. I would submit to you that as I develop this stratification that I'll be able to figure

out how to partition C2 disease and get away from the cosmetic component of C2 disease. Thank you very much.

- I like this title because I do think this is probably the final study we're going to see on a large scale for pharmacomechanical thrombectomy and catheter-directed thrombolysis for acute DVT treatment. These are my disclosures. So, the CaVenT trial came on the heels

of a number of smaller single center series and sort of case studies on catheter-directed thrombolysis. And of course this was a randomized study in 24 different Norway hospitals that showed a patency advantage and a reduction in PTS on both early and late term, even out to five years

in patients treated with catheter-directed thrombolysis rather than anticoagulation alone. The ATTRACT trial of course is the follow up to this study in a sense, it was a large US trial, an NIH-funded multicenter trial that used a strategy of thrombus removal with

adjunctive catheter-directed thrombolysis for acute DVT and essentially this accrued over 50 or so hospitals throughout the US. Using either pharmacomechanical thrombectomy and/or catheter-directed thrombolysis versus standard treatment of anticoagulation.

Enrollment completed in 2014 was presented at SIR and has been published in a New England Journal article I show there. Inclusion criteria essentially involved acute DVT's defined as symptomatic DVT of less than 14, or less than or equal to 14 days duration

including the femoropopliteal and iliofemoral segment and I think that's kind of important, these two locations, so you could have isolated femoropopliteal disease. Randomization was a one to one between anticoagulation versus pharmacomechanical thrombectomy plus anticoagulation

and the analysis was stratified by plus or minus common femoral involvement. So you could have a group stratified to no iliac and no common femoral involvement. The PMT treatment was basically infusion first for IVC or popliteal vein thrombosis,

but everything else was treated with an attempt at single session pharmacomechanical thrombectomy followed by lytic therapy if needed to clear residual thrombus for up to 24 hours with adjunctive measures afterward including stunting, et cetera.

No IVIS imaging or any of that was prescribed. These are the primary efficacy and secondary efficacy endpoints, and these are important, I think, because it effects the outcome of our perception of the results of this trial. The primary efficacy endpoint was a binary presence of PTS

at any time point between six and 24 months. Defined as Villalta score of greater than five or a venous ulcer. Whereas secondary endpoints were not binary so much, but continuous, so severity of PTS, proportion of patients with moderate to severe, et cetera.

And then of course there are some quality of life measures, as well as symptoms: leg pain and leg size. These are the primary safety endpoints, primarily episodes of, issues of bleeding, recurrent thromboembolism, and death. So looking at the sort of meat of the study,

or the primary efficacy endpoint, this was considered a negative trial in the sense that this primary endpoint of reduction of the incidents of PTS did not occur in those patients undergoing pharmacomechanical thrombectomy or thrombolysis, and so there's no difference

between these two groups in this regard. On an other hand, there was an unfortunate increase in bleeding risk, both early on as well as any bleeding. So early major bleeding, and any bleeding within the first ten days.

So this was a finding that lead to, or, these two findings lead to the conclusion in the paper, that among patients with acute proximal deep-vein thrombosis, the additional pharmacomechanical catheter-directed thrombolysis to anticoagulation did not result in a lower risk of post-thrombotic syndrome.

And did in fact lead to higher bleeding rates. So this is real and true, but looking deeper into the study, I would say that there are some other important secondary efficacy endpoints, and if you look at this, you see that along the continuous variables, and if you look at severity of PTS,

this was favored in the more aggressively treated arm across all time points. And so, if we're looking at degree of PTS, I think there's quite a difference. It's also true that there was a difference in leg pain severity, so subjective reporting of

pain as well as the actual index limb circumference. If you look at some other secondary endpoints, even though there was no difference in the binary metric of any PTS, across all-comers, if you looked at moderate to severe PTS, there was a significant difference, and this seemed to be more true in the patient

with the proximal iliofemoral DVT, rather than those patients with simply femoropopliteal DVT. So I think there are a lot of criticisms of the ATTRACT trial that we've probably heard and discussed. Large selection bias, large number of patients screened for those who were randomized, devices changed

over the course of time, no IVIS in the protocol, no patency assessment in majority of subjects, and probably the biggest issue is inclusion of femoropopliteal DVT, which is done largely to drive enrollment. And I would argue these issues are common to all

randomized trials, randomized trials do strike a balance between broad applicability to different patient populations while trying to still answer specific questions that are manageable. And so I think these are reasons why we have to look deeper into the trial results with some of the secondary endpoints,

rather than just focusing on that major headline. So I would say that in terms of lessons learned, the ATTRACT trial does confirm that this aggressive strategy of thrombus removal may not be appropriate for all patients with iliofemoral and femoropopliteal DVT

in part because of this increased risk of bleeding. I think this something that we know, and ATTRACT has confirmed that. Finally, this bleeding risk is extraordinarily low overall, so that makes me believe there are some patients who very much warrant it due to their symptoms

and their active status. And I do think it did show that the results in less severe PTS in those patients treated with aggressive strategies of thrombus removal. So this is what we want to avoid, a patient like this, who is very symptomatic,

very young, and very active, who has never had any discussion of thrombolytic therapy offered to him, and then referred only three months later or six months later, when there's really not as much we can do about that patient. So it's in conclusion the ATTRACT trial was well-designed

and rigorous with broad clinical scope. It confirms that decision to offer aggressive strategies of thrombus removal continue to require us to make artful clinical decisions in a patient specific manner. And I think it does illustrate that a certain subset of patients,

especially those younger active patients, probably do warrant thrombolytic therapy, thanks.

- We are to have a distinction between acute stroke at level of distal small vessels, in which we can see the core infarct in the penumbra around the infarct. And for the treatment of acute stroke, it's important to establish the eligible patient who will receive the

intravenous tissue plasminogen activator. It remains the only proven effective intervention for acute ischemic stroke. But what about the acute stroke for large vessel intra-arterial thrombolysis? What alternatives?

Mechanical revascularization strategies or stent-assisted revascularization. But, in the past, the earliest periods studied was anecdotal cases and no selection of the patients so bad results were recorded.

We have some exclusion criteria for the urgent treatment. Internal major stoke, cerebral ischemic lesion greater than 2.5 centimeter and CT scan, loss of consciousness,

signs of intracranial hemorrhage. But the real goal of early intervention is to stop the plaque embolization. So should we remove this plaque, or we can stent it. So, as what said Rothwell in 2004, time is brain.

And the benefit from CEA is maximal in symptomatic patients operated on within two weeks of the index event. But it's better after 48 hours. In 2010, I published Siena Carotid Artery Stenting Score

for elective patients. And in Italian registry, in order to evaluate that the field urgency of carotid emergency stenting of a symptomatic patient, we have noticed some clinicians had biomarkers spotted from a prospective registry.

And we have studied the Brain ischemia biomarkers such as PAPP-A, hs-CRP, and Interleukin six. But in the (mumbles) published only in European journal of Vascular and Endovascular Surgery said,

that the most effective management is the quickest one. So in this publication, I say that this closed cell stent design would be benefit for the treatment of urgent patients. In this same publication in the Annals of Vascular Surgery.

And in this year, we studied the early carotid artery stenting after onset of neurological symptoms. So we know very well that we are some cerebral protection devices in order to better protect the procedure,

and we had the necessity to obtain a better protection device with proximal absolute devices. So what about new carotid stent design? In order to better approach the symptomatic patients. This is an example at Terumo Roadsaver, with the control with optical cord and tomography.

This is an example of C-Guard with the control optical cord and tomography. We established some cases related to the study with OCT, and the slice-based analysis say that compared with conventional stents,

the incidence of plaque prolapse was lower. So how to choose in emergency. Carotid artery or carotid endarterectomy stenting, my personal opinion, carotid endarterectomy is still the gold standard. Or if we had the space for carotid stenting

in patients with severe comorbidities, in patients with anatomic complex situations, in case of tandem intracranial lesions, but requires correct expertise and plaque evaluation and correct stent and cerebral protection. So in conclusion,

the most effective management is the quickest one, according to a correct selection that allows recognition of those who can really take advantage for early treatment. And how to perform CAS safely in emergency with an appropriate knowledge of

anatomy, anomalies, and equipment. And with growing experience and the use of dedicated CAS technology, CAS can now be performed safely and efficiently by skilled operators even in urgent cases. Thank you for your attention.

- Thank you to the committee and Dr. Veith for inviting me to speak today. Here are my disclosures. Over the past several years there's been a large increase in the wave of opioid overdose deaths in both heroin and prescribed narcotics in the US. Infected pseudoaneurysms are a terrible problem

resulting from this that vascular surgeons are seeing more increasingly. With this increase in IVDA use, we want to evaluate the trends in the increase and treatment of groin pseudoaneurysms and we used the National Inpatient Sample.

This looked over ten years from 2004 to 2014. Patients with a primary diagnosis of aneurysm or pseudoaneurysm, as well as different ICD-9 codes which were related to drug abuse. Looking at these data from 2004 to 2014, there was a large increase in the diagnoses

of pseudoaneurysms in IV drug abusers. Looking at the demographics of these patients, around 75% of these were white males with the average age of 45. This data, the location was mostly the West, hospital type was usually at an urban teaching hospital. Only 15% of these patients had private insurance.

Most of them were Medicaid, self-pay or no charge. As far as operative approach, and again, this is from a large database using codes, the resection of vessel with replacement had the highest increase, but there was an increase in all the operative approaches, including vascular shunt or bypass or aneurysm repair.

Which leads us to the question of what's the optimal therapy for IV drug abuse mycotic pseudoaneurysms? There's several surgical options, including ligation debridement with non-selective revascularization, ligation debridement of the aneurysm with selective revascularization, just ligation and excision and the

possibility of stents has been brought to attention recently. This study from Iran looked at 41 patients who were IV drug abusers with infected pseudoaneurysms. Of these patients, 32 patients were primarily ligated and nine patients were ligated with revascularization.

Of those patients, the ligation and excision, there were nine of 32 patients had complications and there was one amputation in this study. With a ligation and early revascularization, six out of nine patients had complications and there were three early graph failures.

These patients were only followed up to nine months. Of note, in this population, studies are often poor as the follow-up, as you can imagine, at these institutions is not very good. This study from Dr. Padberg and Hobson's group from the early 90's looked at performing

selective revascularization and using external iliac clamping to assess distal flow with a hand-held doppler, although further studies have looked at use of pulse oximetry as well. If there was a dopplerable signal, they felt there was no need to reconstruct at the time of surgery.

Using these methods, six patients had just a ligation with no mortality, no re-operations. Twelve of the 18 patients had a revascularization as well, and there were three amputations, no mortality. There are other extra-anatomic ways to reconstruct. Dr. Caligaro will describe the lateral tunneling

in a further talk in this session. An obturator bypass is another good option. Axel popliteal bypasses have also been described by Dr. Veith and his group several years ago. A new method that I've used instead of external iliac artery clamping is getting

proximal control from the contralateral groin. I usually get a CTA on these patients and use a 8 to 12 millimeter ballon, which often saves a retroperitoneal incision. As far a stenting, there's some, few studies looking at the use of stent in this patient population.

This study from China, 29 patients with pseudoaneurysms in SFA were treated with a covered stent. There was only short-term follow-up, but there was no amputation, no pain in these patients. And five patients continued to inject at the site. Here's another small case series describing

a retrograde stenting after a cutdown on the SFA into the common femoral artery, and they had two patients in the series with no complications over two years. Conclusion, IV drug abuse is on the rise and we're seeing more of the pseudoaneurysms that we'll need to treat. The data is difficult, but ligation may be the

best outcomes if there is a dopplerable signal. And for an absolute emergency, stenting may be used, however, on these young, non-compliant patients it is unlikely to be a good long-term option. Thank you.

- Okay, is thermal ablation obsolete? No. My disclosures. Are nontumescent ablation procedures ready to take over? This is an article in 2014 by Michael Sadek and myself. No in 2014, no in 2019, and no in 2020, and I predict no in 2023. That's about as far as I can go.

So every time I hear this, I scratch my head, "oh my God." So, there's similar arguments regarding open surgery versus minimally invasive surgery. We know that they're both needed, in terms of different particular incidences of pathology. Risk/benefits, insurance coverage?

So if we look at everything, does size matter? And I would submit to you that right now, in terms of the non-thermals, size does matter. So if we look at 12mm or less, I think that's where the sweet spot for non-thermals are. If we look at trials, clinical correlation of success

in acute thrombotic of lower extremity endovenous thermal ablation, the subset showed that there was no real differences between RF and laser. If we look at this prospective study, looking at 1470 laser and radiofrequency, again, no difference.

If we look at this study, no difference, it all works. So in this particular paper by Professor Davies and his group, he looked at certain things and his summary for this article was thermal treatment with RFA and EVLA is the mainstay of varicose vein treatment at present.

Both RFA and laser appeared to have similar efficacies. If we look at this trial that was a pivotal trial in terms of cyanoacrylate and RFA, there's no inferior with regard to efficacy, etc. If we look at a multi-center randomized controlled trial comparing radiofrequency and mechanical occlusion

chemically assisted ablation of varicose veins, again, pain secondary to truncal ablation is less painful with MOCA than RFA with similar short-term technical and quality of life and safety outcomes. If we look at this trial we heard earlier today of partial exposing of this, mechanochemical ablation

versus cyanoacrylate adhesive for the treatment of varicose veins, study protocol for a randomized controlled trial, there is really no difference across the board. Just when you thought new RFA devices are now coming out. We know we talked earlier about

RFA continuous and segmental, and just understand that if it was obsolete, why would they come out? So Kabnick the fortune teller, better known as Carnac, is thermal ablation obsolete? I would submit to you in my crystal ball,

between the times of 2018 and 2023, the answer is no. And then I got my ouija board out, because I didn't understand what I was thinking about, and really the ouija board went "no." So ladies and gentlemen, in conclusion, as of now and 2023, there is not one perfect modality for

venous ablation, each has their sweet spot. Thermal long track records and larger veins, perforator approval, with thermal. Non-thermal, no tumescent, perhaps a shorter procedure and nerve sparing. Recommendation, most of us agree, if you can only

afford one device, I would do thermal. My recommendation would be to have thermal and non-thermal. Thank you very much.

- I'm going to talk about a vascular patient selection, vascular access patient selection app we've been working on for about six or seven years. Larry asked me to come back and talk about it, give an update. I have no disclosures, however, this app in the future may become commercialized.

The company that helped me develop it is looking into that, I'm not exactly sure whether it'd make any money or not, but if you look at the current status of vascular access, the outcome improvements have stalled. This is non-maturation of fistulas has increased,

catheter days have increased. The KDOQI is now beginning to de-emphasize the strong push for fistulas in the latest update. So it really poses the question of where we go from here. I think there's two approaches. First we can focus on surgical technique.

We've already heard this once in one of the talks, that surgeons probably don't know how to do the procedure. The solution to this might be training programs by experts, vascular access certification, or funneling those patients to surgeons who know how to do the operation. I think they're significant barriers to this.

There's going to be resistance from organizations and from surgeons themselves. I don't think there are enough master vascular access surgeons in the country to be able to do all the access out there, and it would result in significant cost.

Another approach is to improve our patient selection. The hypothesis behind this is patient factors drive outcomes and we need to identify some baseline patient selection or patient selection should kind of have a baseline that is based on those factors. To start, it would be great if we could

standardize procedure selection. That's easier said than done. There's a significant problem now that fistula, the KDOQI is kind of backing away from Fistula First a little bit. Now, you've basically pulled the rug out

from all those surgeons in the United States that really simplified their approach to patient selection by pushing fistula in every single case and thinking that they're creating value or they're doing quality surgery the higher their fistula rate is.

So how do we improve or standardize patient to selection for vascular access? About three years ago, I partnered with Karen Woo, Associate Professor of Surgery out at UCLA, and we ran a consensus process called, using the RAND Appropriateness Method.

It's a consensus process like KDOQI. It combines best evidence with expert opinion. It's done when randomized control trials are not feasible, but it's different in that rather than creating general recommendations, it creates patient-specific recommendations,

and to set the stage for this consensus process, we developed 3,700 clinical scenarios. It's a standardized technique, and it's been done many times and for many other areas of surgery,

but it hadn't been done for vascular access. These are the expert panelists, nephrologists, surgeons from transplant surgeon, from U.S., Canada, and Europe. It resulted in two publications in the Journal of Vascular Surgery.

This was the later study, which identified the factors that were deemed important that influence outcome. But this paper was not user-friendly. Nobody could look at this manuscript and say, oh this is how I need to take care of this particular patient.

But the database that was created to develop this paper had about 400,000 data points. It did have the basis on which to develop a mobile app. So from that database, I developed this mobile app where you just input patient characteristics into the app and from that, it would generate panelists' ratings

as either, a particular procedure was either appropriate, it was inappropriate, or there was controversy among the experts or inadequate information to determine whether it was appropriate or inappropriate. This is the mobile app. You enter the patient's age,

the quality of the cephalic and the basilic vein, are they on dialysis or is this done well in the future. It might ask other information regarding whether are they fully functional, are they in a facility, their BMI, artery size, and then based on that, it will print out the options and rank them.

We also have included resource areas in this app and hopefully we would have expert surgeons across the country contributing videos. It would have a list of key manuscripts describing the latest key literature on vascular access. We did a validation study at our institution,

a retrospective study of 201 consecutive patients. It's interesting and I want to emphasize this, this builds on the Fistula First program. In that series that we looked at, it had an AV fistula recognized as most appropriate in 85% of patients.

Now they may have been also, AV graft might also, have been deemed appropriate, but this really does push fistulas in those case where it's deemed appropriate, and in those that we actually did an AV fistula as it was recommended,

the maturation rate of those fistulas was 78%. So where are we now? This app is fully functional. It's launch date will coincide with the KDOQI update. It is included in the latest KDOQI algorithm. I've been asked to serve on the implementation team

to get this launched. I see this as an iterative tool that will improve with use and research. The changes in this app will be approved by the KDOQI team, thank you.

- Thank you and good morning. I have no relevant financial disclosures. At Mayo, we have long been proponents of in-situ replacement of infected, both open and endografts with good results, both in terms of mortality and limb salvage. Our approach to graft infection involves

draining abscesses prior to the operation. Completely removing the infected graft and debriding the periaortic tissues, and replacement in-situ with a new graft sewn to help the aorta. Covering the graft 360 degrees

with omentum and long term suppressive antibiotic therapy. Rifampin-soaked conduits work well for low grade infections and aortaonteric fistula, but for patients with large abscesses we prefer cryopreserved allografts. Naturally para and suprarenal aortic graft infections

add another measure of challenge in the form of need for preservation of renal and visceral blood flow and sometimes presence of large abscesses around the grafts create further challenges to in-situ repair requiring creative

positioning and tunneling of the grafts. Dr.Milina mentioned the Swedish registry and yes, there are encouraging early results of EVAR for infected aortas, but mind you, these were all primary mycotic aortic aneurysms

and not infected grafts which are a different level of infection as he pointed out as well. So, we still prefer in this situation as well, in-situ reconstruction for most patients, but periaortic abscess may dictate the need for remote reconstruction,

and treatment needs to be customized to each patient's different anatomy. And it's important to have a multidisciplinary team. Our treatment strategy includes a single stage procedure with sequential visceral and aorto-iliac reconstruction. We like to have several plans for reconstruction ready

as CT often underestimates the amount of periaortic inflammation. And we like to perform separate bypasses for the renal or visceral arteries prior to the aortic reconstruction to reduce the physiologic stress.

This is one example of antegrade debranching of the viscerals and renals, and a synthetic graft replacement. And here, one for an infected endograph with cryopreserved aorta. This is a gentleman who presented

with an infected infrarenal opening aortic graft and a suprarenal mycotic aneurysm. Osteomyelitis extensively in the spine. He was status post lumber decompression and suffered a post operative myocardial infection as well. PCR demonstrated Q fever and he

had a large paraspinal abscess that had been drained preoperatively. He underwent a decompressing axillofemoral graft temporarily to offload the heart. And then an intra-abdominal exposure of the supraceliac aorta,

And debranching of the viscerals and the right renal artery. Tunneling these grafts to the foramen of Winslow, to the right side of the abdomen. And then tunneling similarly, an aortic replacement graft

in the right paracolic gutter and down into the pelvis, followed finally by a left medial visceral rotation and dealing with the left-sided paraspinal abscess debridement of the periaortic tissues as well as the vertebral bodies. And this is the final result with a post operative CT.

Another patient with an infected endograft and a aortoenteric fistula, who underwent a similar reconstruction tunneled on to the left side of the abdomen in the paracolic gutter, and appropriate pre-debranching of the visceral and renal arteries

to reduce that physiologic stress. In this patient we used saphenous vein grafts to perform the renal artery bypasses in a similar fashion. Sometimes you do have to go to the thoracic aorta to do the debranching to the viscerals and renals,

to stay away from the infected tissue. And lastly, this is a patient with an infected Carrel patch aneurism after the thorocoabdominal repair previously debranched in this fashion, preserving part of the patch and then wrapping the whole graft with omentum.

So, thus far we have experience with 16 such patients with paravisceral graft infection. Just over half were dealt with in a trans-abdominal manner, about two-thirds with in-situ reconstruction using Dacron and majority underwent Omentoplasty. About half of them underwent only renal,

and the other half renal and visceral reconstruction concomitantly. Majority with rifampin-soaked polyester. 30 day mortality was zero, however these are very sick patients, and three patients did succumb within the next 90 days, from multisystem organ failure

and just overall debility. Major renal and respiratory complications were of the order of about 15% but there was no further mortality over a median clinical follow-up of six years. And no graft thrombosis or reinfections.

So, although challenging single stage infected aortic graft excision with visceral and aortic reconstruction can be safely performed. Sequentially to decrease the physiologic stress. The new grafts can be successfully routed away from areas of major sepsis.

Early mortality and morbidity are significant but complete graft excision results in low risk of reinfection in survivors. I thank Dr.Veith for the kind invitation.

- Thank you for the introduction. Good afternoon, ladies and gentlemen. I have no disclosures. We fly a lot and we're going to continue flying a lot, particularly in specific markets such as India and China.

Now the association between VTE and travel was first mentioned by John Hermans in 1953 or four when he described a VTE event in one of his colleagues who flew from Boston to Caracas, which is an eight hour flight. And this is often associated with the economy class

where you're sat at the back of the plane in cramped consitions with people invading your personal space. And different airlines have provided information for patients that you need to actively look for on the website with respect to how you prevent VTE.

However, it has been postulated that more should be done to make patients aware of the risk of travel-related thrombosis and this phlebology article from 2010 provided some advice with respect to the measures that patients can take.

In highlight of the fact that these conversations need to be had, I would slightly disagree with that. Now I think patients are well aware of the risk of DVT and flying and that is certainly one of the question that often, as Dr. Papis mentioned, comes up when you consult patients.

There is difficult evidence out there with respect to the increased risk of DVT and flying, but certainly there appears to be an increased risk. This was a study that assessed patients on an eight hour flight, eight hour movie marathon, and patients going on with their daily lives.

And what they found was that one huge difference is between individuals who had sat for eight hours as apposed to flying for eight hours, but certainly a throm and antithrombin complex appear to be of higher intensities as such after flying.

And there are a number of different reasons why this might happen. Some of which have been shown to be of relevance such as Hypoxia, but things such as stress, dehydration, air pollution and infection have had

absolutely no evidence, but hypoxia and immobilization appear to be two factors that may be of relevance. The CHEST guidelines have confirmed that there is, looking at the evidence, an increased risk of VTE. Particularly if you fly for over eight hours,

but if you fly for more than four hours and happen to be sat or difficult mobility, sat in a window seat, obese and have had recent surgery, you're at a particularly high risk. I've put on this busy slide, on the top left hand corner the different risk factors,

but what they've suggested is that you should frequently ambulate the firm calf muscle exercises and sit in an isle seat if you can, because that makes you more likely to get up and move. Below knee compression stocking can be given with a grade 2 C recommendation,

however, this only applies to high-risk patients and if you're very low risk, there is no reason to give you anything. And certainly Aspirin or anticoagulants are not warranted for low risk patients. What they have also said is that dehydration

travel and economy class drinking alcoholic beverages do not increase your risk. What do doctors do? So, this was a survey in individuals who went to the international Society of Thrumbosis and Haemostasis.

And whether you were a medic or an clinical scientist or a research fellow, the vast majority took conservative measures such as walking. 20% wore stockings and 20% took Aspirin, and very few took low molecular weight heparin or vitamin K antagonists.

Aspirin is easily available. You can buy it over the counter and patients often think that will decrease your risk of VTE. The LONFLIT studies looked into this. These were performed a while ago

and basically they confirmed that you had and increased risk of VTE in high risk patients. Wearing compression stockings decreased your risk. But if you took Aspirin or took low molecular weight heparin you might as take the low molecular weight heparin, because the Aspirin did not significantly

decrease your VTE risk. And Aspirin is not advised as a preventive or prophylactic measures in long haul flights. What happens if you've just had intervention though? Are you more likely to have a blood clot? Well, you are according to the evidence.

A recent surgery increases your odds ratio of getting a DVT. Particularly over the last 28 days and particularly if it's orthopedic or pelvic surgery or cancer related surgery, which is to be expected really.

But what about if you're flying before intervention? You might have patients that fly to see you. You might be very good and they might want ten hours to come and see you. Well there is evidence that you're more coagulopathic for the next two weeks

or up to six weeks, but really the first two weeks are key and then the rates of DVT decrease following that. So that might be something that needs to be discussed with a patient or lead you to take further measures to reduce the risk of VTE.

When we're talking about superficial venous interventions, we're talking about minimally invasive surgery now a days. And there's very little evidence to say whether this has any effect on your VTE rates or not. We know that varicose veins are an increased risk of VTE as per the Caprini Risk Assessment Score.

And one can say that having had an ambulatory procedure might increase your risk somewhat. So in conclusion ladies and gentleman, when you patients come and see you there's no evidence to delay flights if you're having minimally invasive

superficial venous surgery. You may consider avoiding intervention. We certainly ask our patients who come in on the NHS whether they've flown in the previous two weeks and we might consider delaying their treatment for that. It is of course individual risk assessment.

And if you can, I would suggest sitting in an isle seat and mobilizing. Thank you very much.

- Thanks very much, and thanks Frank for the invitation to join us once again at this excellent meeting. These are my disclosures. Now, it's well documented and all of you are fully aware that the periprocedural risk of stroke and death following transfemoral CAS

has been shown to be twice that of when compared with CEA in the important non-industry supported trials of EVA3s, ICSS, and CREST. The increase in the rate of events with CAS however,

is front loaded and occurs, certainly within the first 30 days, and more often than not within the first day or two, after that the subsequent event rates and durability parallel that of CEA. And this is nicely shown in the four-year data from EVA 3S, where we can see that the big jump in event rates

between CAS and CEA occurs upfront, after which, these two curves become entirely parallel. The 10-year data from CREST has been published, and the same phenomenon occurs here, and that is that the higher event rate with stenting compared with carotid endarterectomy occurs right here,

after which the two curves become entirely parallel. So, one has to ask what are the potential causes for periprocedural events with transfemoral CAS and it's already been discussed, a diseased aortic arch, a Type 3 aortic arch making catheterization of the right carotid artery more challenging,

and finally the need to traverse the lesion in order to place a distal embolic protection device. Obviously the embolic protection device doesn't work until it's in place, and when you pass it over the lesion the possibility of knocking free embolic debris is quite high.

I don't expect anybody to read this from the back of the room, but in 2004 there were two seminal papers that were published looking at the possibility of a direct approach to carotid artery stenting, thus avoiding the aortic arch and using flow reversal

by clamping the common carotid artery and diverting blood flow in a reverse direction back to the venous system and were showed excellent results. Along comes industry to provide us with the hardware with which to do this,

these are the components from Silk Road, and basically a small cutdown over the common carotid artery, the placement of the sheath clamping the carotid artery with reversal of flow, thus carrying any embolic material before the placement of a stent is neuroprotective.

One other thing that wasn't mentioned this morning and one of the advantages of flow reversal and the possibility of encouraging all of the release of the embolic material initially is to carry out predilatation of the lesion before placing the stent and not postdilate.

The first-in-man data on the use of this technique was published in Germany and in the proof study, in the proof study there were 44 patients undergoing TCAR, no deaths, no strokes, silent brain infarction rate of 16%, which was entirely comparable to that of carotid endarterectomy.

Along comes the ROADSTER trial at ROADSTER 141 pivotal patients deemed to be high risk by either anatomic or medical criteria, carried out in 20 US sites, there was no major strokes, there were two minor strokes, two deaths, no permanent cranial nerve injuries. And if we compare the TCAR data with CREST data,

here's the transfemoral CAS data out of CREST, 4.1%, 2.3% with carotid endarterectomy, 1.4% with TCAR. And here are the ROADSTER 2 data, if we look at stroke and death in asymptomatic patients in ROADSTER 1, 1.3% dropping to .9%,

stroke and death, ROADSTER 1 in symptomatic patients 2.2% dropping to an astonishing 0.8%. So, from my personal perspective I can offer patients either TCAR or CEA based upon selection criteria with a high degree of comfort that

both of these are going to result in excellent results. How about CREST-2, as you know this is two studies in one, comparing CAS with intensive medical therapy alone and CEA with intensive medical therapy versus intensive medical therapy alone. The future of invasive intervention

to treat asymptomatic carotid stenosis will really depend upon the results of this trial. What are the possible outcomes? Intensive medical management may be equal to or better than either, carotid endarterectomy and CAS may be better than intensive medical management,

or CEA but not CAS may be better than intensive medical management alone, those are the possible possibilities To date, half of the patients have been enrolled, so stay tuned, and thanks very much for your attention.

- I have no disclosures related to this presentation. Foam sclerotherapy, as we've heard a lot about this morning already, was made popular in 1993 by Cabrera. The Tessari method is commonly used to create this with polidocanol and STS being the most widely used detergent sclerosants to make physician compounded foam.

I just want to emphasize that this is different than the commercial preparation of Varithena, which is a polidocanol microfoam. Varithena's for the great saphenous anterior accessory and large varicosities, not reticulars, so we won't be discussing that.

So physician compounded foam is widely used to treat varicosities and perforators in the US. It's used to treat saphenous reflux in Europe and with or without ultrasound guidance. There's little doubt that polidocanol and STS is more potent than liquid sclero.

Well what should we do about the little guys? What should we do about reticular veins? These are one to three millimeter veins visible below the surface of the skin. They're generally asymptomatic and can be injected with liquid, although this may require

many injections and/or treatments. Foam, either using polidocanol or STS, works well. Telangectasias, that we just heard about, are dilated intradermal venules and these may cause itching or point tenderness, but are usually treated for cosmetic reasons.

They can be treated with liquid polidocanol, STS, hypertonic saline, or glycerin. Here's a patient of mine who has visible lateral thigh reticular veins. This is a good example of what Dr. Mackay was talking about with the injection

into the feeding vein and you can see the foam going up into the venules that emanate from this. And this was her result six weeks later. Which one is the best agent? Using liquid sclerotherapy, a Cochrane Review found no difference in efficacy comparing

hypertonic saline, polidocanol, or STS. They found that more complications occurred at higher concentrations and that polidocanol may be best tolerated, but there was no superior agent. Foam or liquid? Foam uses smaller amounts of sclerosant

and has a more homogenous coating effect in the vein. It's more potent and it's able to be seen with the naked eye. It may cause more phlebitis and hyperpigmentation of the skin, but this has not been proven in the literature.

There's no evidence that ulceration is more common or that foam is better than liquid. What about the complications? There a couple large multicenter registries that reported immediate and midterm results. I should emphasize that in less than 1%

of the injections, they observed complications. So overall, these are very safe procedures. But when they did see complications, it was more often with foam. And this was especially common in visual disturbances and other neurologic complaints.

They found that foam was the agent used most often and it was more common in surface injections rather than in large veins that were injected under ultrasound guidance. Migraine history and right to left cardiac shunting seemed to be more common in women

who reported neurologic symptoms. What about using CO2? Nick Morrison reported that CO2, in comparing CO2 versus air, where he injected quite large volumes of foam, he saw side effects in almost 40% of his air patients

and 11% of his CO2 patients. And this was a statistically significant difference. All the effects were transient, but he concluded that side effects decrease significantly with CO2. So should we all be using physiologic gases?

CO2 costs extra. It requires additional storage and disposal. The foam is less stable and there's no difference that there's any decrease in efficacy. A recent review showed that patients who had migraine with aura or a known PFO

may benefit from physiologic gases. In conclusion, polidocanol or STS foam for reticular and spider veins is easy, fast, and effective. There's no hard evidence that there are increased skin complications, but I think

we have pretty good evidence that air-based foam leads to more neurologic complications. There's good evidence that reticular and spider injections have more neurologic complications than larger ultrasound guided vein injections. So therefore, there's little support for

foam versus liquid for reticular and spider veins. If it's used for large clusters or in high risk patients, probably CO2 should be the agent of foam generation and we should stick to less than 10 ccs of foam per treatment and consider moving to physiologic gases for all of our patients for safety reasons.

Thank you.

- In preparation for tonight's debate I thought I would take us back and look at something a little bit interesting, maybe not all that relevant, but uh but maybe, and that's the open vessel hypothesis, and the applicability to DVT. So here are my disclosures. What is the open vessel hypothesis? And of course I thought I'd be the first person to talk

about this related to veins but certainly I'm not, but maybe I'll be able to bring it to your attention. It really goes back to 1941, and um and it goes back to uh acute MI um experimentally in dogs was related to the duration of coronary artery occlusion. And the hypothesis back in 1941 was termed the

time-dependent open artery hypothesis, because it was postulated that the extent of myocardial damage was related to the time that was required to reopen the lesion at least experimentally. And it wasn't until about 1990, where the um M-I-T-I MITI trial demonstrated that patients who were given

t-PA, within 70 minutes of coronary symptoms had a 1% mortality compared to 10 times that, if in this case, thrombolytic agent was given after 70 minutes of symptom onset and of course, this is the whole reason there's so much emphasis on getting people to the cath lab quickly.

Well what does this have to do with DVT? Well I think if we look at the findings of the ATTRACT trial at least the findings that we know from presentations so far I think it can be explained in part by the open vessel hypothesis applied to veins, so ATTRACT, I won't go into this, we've already uh seen uh the results

but I will um give Tim Yates credit for talking about the open vein hypothesis, oh about six months ago, at New Cardiovascular Horizons. The um primary endpoint of ATTRACT, we saw that not different secondary findings though, again we saw some benefit and the benefit seem to be related

primarily to those patients with iliofemoral DVT. So now I'm going to take you back to the National Venous Registry. Mark Mewissen presented this and let's look at the extent of thrombolysis in the iliofemoral and femoropopliteal segments and more lysis is to our right.

And uh grade three is more lysis than grade two. Um, the bottom line of this was the acute resolution of the thrombus was almost identical for iliofemoral or femoropopliteal DVT. A little bit surprising to me, but something that was demonstrated uh almost 20 years ago.

And here is the patency, iliofemoral DVT uh after treatment uh 64% uh vs. 47% in the femoropopliteal segment that's at 12 months. Again, not all that surprising. So here's the open vessel hypothesis applied to veins. Symptoms will improve when the large vessels can be reopened

and when they remain open over the long term. And we're more successful in preserving, I won't say I won't emphasize restoring or preserving long term patency for the iliofemoral vs. the femoropopliteal segments and for this um uh reason, venous stents work quite well in the pr

work so well in the femoropopliteal system but for this reason the ATTRACT results may be a reflection of not so much what happens with thrombolysis um mechanical uh uh pharmacologic thrombectomy but what happens over the longer term with stents. And the speculation is the veins with acute DVT

can be recanalized equally well. Uh the availability of devices however for the iliofemoral reason to preserve iliofemoral region to preserve patency uh contrasts with no such devices at least right now for the more (inaudible) venous system. So the open vessel hypothesis is applied to veins over

two year follow-up, might explain the primary endpoint failure of ATTRACT and had the trial been conducted on the iliofemoral DVT population alone, I think it is uh evident

- Thanks, so we've talked about open techniques, and as Marsham mentioned, wouldn't it be nice if we could develop some type of endovascular valve replacement or any reflux procedure. There are a subset of patients that require this, as we get out in these more severe disease severity, is when start seeing more

of a higher prevalence of deep venous incompetence. This tends to be a mix of primary deep venous incompetence and post-thrombotic, which also gives you a mix of the pathology of reflux and obstruction along the axial vein tree. And really, it's to find the most critical

site of disease for repair. As you've heard, the open surgical techniques have been the mainstay now, conservative would be compression, and we're now going to talk about implantable valves. Kistner, as we know, has been the father of this,

and really, his concept has been that in the deep axial system, that we have the, really, the external iliac, 25% percent of the time, has one valve. But, in general, the iliac system is valveless. But, we're choosing the common femoral vein,

the femoral vein profunda, or popliteal, that we need one competent valve somewhere along those axial segments to get the control of venous hypertension. That's really the goal. We've heard about external repair, or reefing,

that's available if the valve is intact. However, if the valve is not intact, and destroyed, then you need to bring in a new valve, either transplanted from the axillary, or transposing from good valve, to an axial segment. And really, this has been the data with open repair.

Yes, you can get ulcer healing, but there's a pretty rapid fall off at about three to five years with all these open techniques, with valve fatigue, or scarring, or enamel hyperplasia, or thrombosis. This is really, so Dusan Pavcnik at Dotter Institute

in Oregon, has been working on this for a while, the bioprosthetic valve. The first-generation, he was using sub intestinal submucosa, which basically gave you a collagen skeleton, with growth factors sewn onto a metal frame.

And then that gets implanted, and the idea was that hopefully, it'll repopulate with endothelial cells and mimic a human valve. The problem with this one was mostly tilting of the frame in vivo.

And this is kind of what it looks like, developed, delivered through its delivery system. The second-generation valve, they worked more on the frame, and still, you know, with a prosthetic in here, you do see good incorporation of the bioprosthetic valve in a vein wall with population of endothelial cells.

They've also looked at transplanting native valve to native valve on a frame, so using jugular of one side, taking it out, sewing it onto a frame, and placing it on the other side in sheep.

And that was mixed with a variety of problems, as always enamel hypoplasia and thrombosis are the main two actors that cause these to fail. Then the last thing that I've seen, that I haven't seen any results on, was this idea of the autologous endothelial monolayer

on a valve, which, when you then put it in the circulation, then you've got flow conditions, and then you worry about the sheer and the flow disrupting the populated cells from the valve. So, I asked Tim Liem, who's,

whom you've met earlier, he's out there in Oregon, and knows the Dotter institute, and I wanted to see the fate of these valves that we just talked about, with autologous, and they've implanted some in Korea and Europe. They lasted for about three months

and they all go on to fibrose or thrombose. So, it's been a challenge with the autologous valves. We've heard about neovalves already, which again is open monocusp, and now there's an endovascular system under development, where they use

intra-vasc or ultrasound mounted on a catheter, a blade, and a balloon, to create an endovascular monocusp valve. So, that's been under development for a while. But, in conclusion, a percutaneous valve is an unmet need in a small subset of patients

who come to us with wide open deep venous incompetence, ulceration, and a miserable quality of life, and currently there's not a great option, except for open surgery, which doesn't last more than five years or so. Thank you.

- So, I have no disclosures. So, my talk is based upon things that happened last year when Novitas, which is one of the local Medicare carriers, decided that they were going to try to not cover our venous related diseases, and this was what stimulated it. Over the past decade or so, Medicare has noticed

an enormous increase in endovenous procedures. And most of this increase happened, not from traditional vascular surgeons, but it was mostly noted in cardiologists, radiologists, and general surgeons and other specialties that got into the endovenous world. So, this prompted the Medicare Carrier Advisory Group

to meet to evaluate the level of information. They contracted with the AHRQ, which did a really bad job on the study, but they came out with some suggestions saying that there was a lack of data on Medicare beneficiaries on the effectiveness and the outcomes of the current therapies that are being done.

So, this prompted our group at the Center for Vein Restoration to look at our database. And we looked at 38,750 patients of CVI related treatments over a two-year period. We then subdivided those patients into Medicare and Non-Medicare beneficiaries.

And we looked at our experience in 69 centers over 10 states. So, this was a pretty broad group of patients that was indicative of an American population. So, in terms of symptoms, what we found was that pain, heaviness, fatigue and aching were more commonly

complained of in the Non-Medicare beneficiaries. And what we saw was swelling, skin changes and venous ulcers were common in the Medicare beneficiaries. So, much more severe disease in the Medicare beneficiaries. When we did a regression analysis, we saw that there was a very high odds ratio of these symptoms being

associated with the presence of venous disease, which was another complaint of the MEDCAC was that the symptoms were too vague and that they weren't specific to Medicare beneficiaries. So then what we did, was we looked at the percentage of patients that presented

with the disease according to CEAP classification. So, as you can see, the largest number of patients had C3 disease. Of these patients, there was about a 15% recommendation rate for therapy. And of those, between 11 and 12%

actually agreed to have therapy. So, even though the percentage of patients with the disease was higher, the number of patients that actually went on to get the disease was less than a third. Then, of those patients that went on to get something done, what we found was that the Non-Medicare beneficiaries

were more likely to have C2 disease. In other words, working class people had a higher likelihood of wanting to get their veins treated because it was bothering them. C3 disease was almost identical between the two groups. But then when you look at the more severe disease

four, five and six, much higher prevalence in the Medicare beneficiaries. So, then we said, "Well, okay. "Let's look at outcomes based on rVCSS." So, we did it across CEAP categories. And what we found was, regardless of whether you are a

Medicare and Non-Medicare beneficiary, you had an improvement after a series of interventions. So, the next question is, "Well, what were those interventions?" So, then we looked at various combinations of interventions. Whether you had an ablation alone,

ablation with a phlebectomy, whatever. And you can see, for the most part, they're all identical. So, whatever your treatment paradigm was to treat your CVI, you basically saw a benefit from it. And the other thing that I didn't show in this slide was that the average number of procedures per patient.

So, in the Medicare beneficiaries, they ended up getting an average number of seven, so that relates to about two ablations, two phlebectomies, plus minus an ultrasound-guided foam sclerotherapy. Whereas, the Non-Medicare beneficiaries had an average of around five procedures.

So, this data is based upon a complete treatment algorithm starting to when we first saw them to when we were done with them. And then we reevaluated them at one month to get a one-month evaluation. And that's what the post RVSS scores were.

So, in conclusion, all definitive therapies for CVI must address the underlying cause, which is the venous hypertension. The history and physical exam of venous duplex scan must correlate and establish the diagnosis of symptomatic venous insufficiency.

Physician and patient reported outcomes measurements must be utilized to assess the degree of impairment and post intervention. We've, over the past two years, now also added the CIVIQ score. So, in our future studies,

we're going to be adding quality of life measurements as well, which is a patient reported outcome. And we also believe that arbitrary vein diameter should not be utilized in part of the carrier group's decision. Compression therapy is not definitive therapy.

All it does is treat symptoms. But as you know, most insurance companies use this to delay therapy. And CVI disease progression increases with age. Early intervention decreases this development. And CVI is not curable.

What we do is palliative. And, in addition, we also just recently reported some data on BMI. And we also think that, based upon our BMI data, we should go back and look at RVSS and add BMI as one of the indicators of outcome.

Thank you.

- Thank you Mr. Chairman. Good morning ladies and gentlemen, and thank you for Frank, for inviting me to be here. I have no disclosure. For the diagnoses of the infected aneurysm we rely on the positive culture specimen, blood test. We didn't rely on the negative culture

with the eccentric aneurysm sign of infection of preoperative treatment of antibiotics. For the principle of operative treatment of the infected aneurysm, initially antibiotics and surgical treatment to excise the infected artery and surrounding tissue.

Arterial reconstruction in-situ or extra-anatomical and followed by appropriate postoperative antibiotics. Diagnosis of the infected, okay, oh, back again. Endografts for the treatment of the infected aneurysms started at 1992,

two years after EVAR. It's a less invasive method and alternative to open surgery and a better choice for the critically ill patient. The earlier report, very successful because of using of the broad spectrum antibiotic

and most of the surgery, they have negative result for the culture. Some of them used the antibiotic coat graft and adjunct procedures such as drainage or debridement. Followed by prolonged postoperative antibiotic therapy. We have a role for the EVAR

in the treatment of the infected aneurysm in the well controlled patient with the active infection by broad-spectrum antibiotic and with the patient without fever and stable hemodynamic. In acute presentation with fever

and active bleeding or aneurysm rupture. We have experience with both, EVAR and also open surgery at the same time on the three year period. For all of the five cases that elective open repair we have no mortality in 30 days

with a significant operative complication in 40% and surgical complication 21%. All patients survived. But for the patient with the EVAR all survived but we have a problem with the infected stent graft in two

and we need a CT guideline drainage and end it by explanation in two. In emergency EVAR we have one infected stent graft that need CT guideline and the patient don't want to have an operation by experimentation and after that, she died.

All of the bicasted operative treatment we have 60% for the mortality rate. We then certify with the endovascular stenting for infected graft because of the precedent of graft in the infected area.

It doesn't resolve the infection. Okay. Okay. And in conclusion, good immediate results for the infected graft with the EVAR. Good immediate result, no poor mortality there.

But a problem with the persistent infection. For the infected stent graft, after how do we treat. Okay. For the conventional open repair of the infected, in about two percent, EVAR for less than one percent,

and EVAR for the infected graft, one third. Mechanism of the graft infections is contamination and re-intervention. Here's now four cases with the infected stent graft. Four for the infected aneurysm and one for the patient disease that have a

explanation and eto-entric fistula. A primary goal of the treatment is the removal of the infected graft. When is non-excision of the infected graft acceptable for the treatment? We have to consider this.

For the patient with the major criteria we should go over what stent graft explantation. It maybe have a role in the minor criteria. Conservative management have a high mortality rate, nearly 100%. It depends on bacterial virulence,

onset of the graft infection, and localization. To consider that we should treat them conservatively or not. In conclusion, conservative treatment should be used in the moribund patient, high risk to operation and minimal graft contamination. Thank you for attending.

- Well that you very much and thanks for people showing up this morning. I have no disclosures. Popliteal entrapment syndrome is an uncommon disorder. It involves compression of the popliteal artery leading to symptoms of lower extremity ischemia. It's often seen in younger patients

and those that are athletes or soldiers, if you don't see these patients you may never see popliteal entrapment in your practice. As such it's often misdiagnosed and these patients would have seen numerous physicians prior to seeing you.

And there is no standard protocol for the diagnosis and treatment to assist some of the primary care providers in referring these patients. We think about the presentation of these patients, the systemic review of over 30 studies looking at popliteal entrapment

intermittent claudication was the most common presenting symptom. Acute ischemia occurred in 11% of the patients, and 15 of the 30 studies revealed a median of 13.5% of post-stenotic dilatation. And the median duration of the symptoms

was noted to be 12 months. So how do you optimize the diagnosis? It starts with the history, you need to have a high index of suspicion particularly in a young patient presenting with claudication and those that have acute ischemia as well.

The pulse evaluation with provocative maneuvers is another modality but that could be misleading. And then non-inva treadmill ABIs and duplex with provocative maneuvers. And on a duplex you could see the patient at rest

and a patient who you suspect has popliteal entrapment syndrome you will have compression of the popliteal artery that could be easily visualized. Axial imaging is another modality, MRI, MRA has been used. The majority of people will get that

to look for abnormal positioning of the popliteal artery as well as compression. And CTA which is readily available too but these are both reproducible, I think with the CTA in particular but they're both static imaging

and you can miss popliteal entrapment on this. Now provocative imaging is now being commonly employed with the MRI and CTA and Dr. Lee will talk about that, they have a very nice protocol at Stanford for the CT provocation. I still believe in arteriography for these patients,

I think you can obtain detailed vascular findings in the dynamic component, it is much easier to visualize versus static imaging. In addition we've been using IVUS for the last six to seven years to evaluate for interval changes

and to confirm the area of compression of the popliteal artery. And again these are your classic popliteal entrapment angios, the initial image you could see and the initial plantarflexion with prolonged plantarflexion

you can see complete effacement of the popliteal artery with outflow distally. Again, IVUS is another modality that we use, we believe in and I think the one thing is that sometimes these patients have had repetitive trauma,

the vessel may be injured and it'll allow you to understand whether a patient needs an interposition graft or to be cognizant of that after release. So the treatment options for popliteal entrapment, non-operative management's not common

and these are young active patients repetitive trauma to the artery can lead to limb threatening events but it mandates surveillance and those patients that don't want to have an operation they need to be surveyed

because they can have occlusion to the popliteal artery later on. Those that present later in life can be observed and told to curtail their activities but they need to be monitored again. Cause this is what you'll see,

patients who've had repetitive trauma will have an occluded popliteal artery that leads to an interposition graft later in life. The surgical approach, there's a medial approach and a posterior approach. The medial approach is advantageous

because most surgeons are comfortable with it. The disadvantage is you can't really visualize the popliteal artery as well. For the posterior approach the advantage is its excellent visualization of the popliteal fossa, the disadvantage is most people aren't

that comfortable with that but if you get used to the posterior approach you get to see these kinds of images and the detailed anatomy that you see as you're exposing the popliteal vein and the tibial nerve, and being able to dissect the popliteal artery

completely free that area. And really I think this is the way to go for popliteal entrapment. Optimizing treatment, we believe in intraoperative duplex in regards to functional popliteal entrapment which Dr. Lee will talk

more about, and their methods, but we use intraoperative duplex to confirm that we have adequate decompression. So we'll place the ultrasound probe over the popliteal artery and get a base line and neutral position duplex.

We'll then perform our clinical resection and after performing the clinical resection we'll repeat the intraoperative duplex. If there's still compression we will resect more muscle at that point until our duplex looks like there is no compression

and the velocities are stable. If you look at the operative results of a large series a lot of these report 100% return to prior level activity. You know the caveat to this is that they're young patients and the long term follow up is somewhat suspect. But there is 15% complication rate

and the majority are wound related. So new modalities, there are case reports of successful treatment with endovascular treatment but I wouldn't advocate for this cause it is a mechanical compression. Botulinum toxin has been reported

as well in a case series, you know again, there's not a lot of non-operative treatment for popliteal entrapment. So I think in conclusion, you need to optimize the diagnosis. Strong index of suspicion, dynamic imaging is important,

arteriography with IVUS is important, axial imaging based on your institution. To optimize the treatment a posterior approach allows for excellent exposure, and intraoperative duplex confirms adequate resection particularly for functional popliteal entrapment. Thank you.

- Alright, that's our beautiful city by our inland freshwater ocean. I'm against the proposal because, in my opinion, ONYX and the polymerizing agents don't do what they're supposed to do, which is cure. You know, we could talk about this, but in preparation for this, I looked at the

relatively sparse, but available, literature on ONYX, and the fact of the matter is, repeatedly when one looks at what is in the literature, ONYX does not cure with a few exceptions. For example, this is the curative exception. This is a mandibular AVMs, three of them cured

at one year angiographic followup. Now, I consider cure a very simple metric: is it gone at one year followup angiography or imaging? And this meets that criteria, but again, we know that mandibular AVMs, as Dr. Fannis has so nicely shown, this is a bone cyst, essentially,

fill it with anything, it'll get cured. All venous predominant legions, three A. So, yes, cure is possible in isolated circumstances. I think Walter has acknowledged that. But, all the other data, including Dr. Loglos' own data, is that there is no angiographic

followup, short clinical followup. Other papers, Embolization of peripheral high-flow AVMs by Kilani et. al, surgical excision in nine out of 19. Right, that's not the same thing, but it is one aspect of doing it, and there's no angiographic followup. And we see this again and again and again.

Very short clinical followup. So paper after paper refused to tell us that we don't really know what the behavior of ONYX is, as defined by the very simple metric of cure. Although complete, in this paper for example, although complete angiographic exclusion of the nidus

is obtained in a minority, 36 percent, of cases, there's no angiographic followup, so the exclusion is presumably based on immediate post-embolization angiography. In other words, ONYX looks good, acts bad. Other embolization agents in this paper also used,

probably some of them ethanol, which actually got the job done. And then finally, another paper with zero clinical or angiographic followup. So the answer is obvious: ONYX, while it is used copiously by some of the participants in this debate, does not cure,

and I, as my Chinese friends said, think ONYX is garbage. I don't think it works. Few examples of that, here's a young woman, a patient of Dr. Yakes, who, 12 years old, extensive facial maxillary scalp AVM, nine ONYX embolizations, left blind in the right eye

with persistent massive oral and nasal hemorrhage, and after appropriate embolizations, patient was stabilized clinically, and the ONYX was resected. She's stable now, not cured, but she's actually had an excellent clinical result. And you can see that's what it looks like.

Now that's hideous, that's not going to work. And it also, I think, points out what Dr. Walgramuth has actually admitted to, which is it's very difficult to see through this stuff. Radiation dose is increased, and identifying what to do and where to go is a real challenge.

Another such example, I think, suffice it to say a picture is worth a thousand words is this illustrative case of an extensive pelvic AVM, treated with what appeared to be gallons of ONYX, with very little benefit, and an enlarging ulcer. This was later treated by direct alcohol injection

with cure and improvement resolution of that ulcer. So, in summary, it's real simple, folks. There's no evidence in the literature that polymerizing agents have cured AVMs with an exception of a few venous predominant legions. And as I said, you could probably put Jello

in the outflow of those things and it'd work. My own personal experience is repeatedly had ONYX failures, and importantly, many patients are worsened by this treatment, and actually, their subsequent curative treatments are hampered. Thanks very much.

- Thank you, Mr. Chairman. The same institution I guess means the West Coast. So I was asked to talk about surgical management of functional popliteal entrapment in athletes. This comes from a paper we just submitted to the journal in collaboration with

our sports medicine colleagues at Stanford. These are my disclosures. I think we've heard a nice summary of some of the overview. I think I wanted to highlight more from the functional standpoint particularly in the athletes that develop this.

So this is just a reminder of the normal anatomy of the popliteal space. For the younger people in the audience that still have to take some tests the classic is where the popliteal artery is medial to the medial head of the gastrocnemius.

Type V includes any venous kind of impingement and functional has been described as Type VI where there's normal anatomy but you still have the similar symptoms that Dr. Sing had brought up. Purpose of this talk is to describe

our surgical technique for the management of functional popliteal entrapment particularly in athletes using an imaging protocol to help find the portion of the medial head of the gastroc that is compressing on the popliteal artery

and to look at outcomes based on this procedure. Our work up is similar to what the University of Washington does. We start with digit plethysmography in plantar and dorsiflexion. We actually have a pressure meter

to gauge and sort of use so that we can somewhat consistently see what their effort is on this and you see that with plantar flexion on this gentleman the left toe obliterates.

We then do the CTA in plantar flexion. We have a protocol with either a blanket or rope. You go into the CT scanner, get a scan at rest, and then with plantar flexion.

These are what the images look like. Play, so in the relaxed state in the scanner you see a normal nice anatomy with flow throughout the thing. In plantar flexion much like the angiograms Dr. Sing showed

complete obliteration then of the popliteal region. When you look on cross-sectional imaging it helps you identify which part of the gastroc. We found that it often when you draw out the medial head of the gastroc the portion that's compressing

is the anterolateral quadrant compressing it against the lateral femoral condyle. We've treated 36 patients in this series that were all athletes. Half were female. They were all young

with normal resting ABIs and interestingly not a drop in their exercise ABIs indicating, really, that it's a drop of performance that was noted. Mainly track and field folks, soccer players, some water sports,

lacrosse, basketball, skiing, gymnastics and climbing, many of them high school athletes. Many of them are our own local college athletes and a handful of semi-pro athletes. This is the operative technique.

We actually prefer the posterior approach. We take down many side branches of the geniculates, free up the popliteal artery. Here's a video then. Intra-operatively we plantar dorsiflex at the foot level

to see which portion of the artery is being compressed by the bulky gastrocnemius muscle. We choose this section. We use this Liga-sure to then resect the portion of the muscle.

We then continue those prerogative maneuvers until we think that we don't visualize compression anymore. I think using ultrasound like Dr. Sing showed is also a nice way to do that. We've done 56 operations on these 36 patients.

The mean volume of tissue removed as listed. Takes about two hours. Post-operative ABIs are stable. Usually wound issues post-operatively and then the regimen is six to 12 weeks of physical therapy

and then allowed to return to full sport and or the team in four to six weeks. Many of the college athletes wind up having to red shirt that year. The average follow up time for our series has been over four years.

The resolution of symptoms meaning the improvement that allows them to at least return partially to their sport at six months is 87% at a year is nearly all of the patients at at long-term follow up

100% of the patients were back to that type of activity. The more important question particularly for the high school or collegiate or pro athlete is what's the likelihood to get back

to their prior best level of competitive sports and it's about three quarters of patients. Again, all of them, because of functional resolution have been able to get back to casual sport for that. That's in graphical format.

These are what the pictures look like. This is a preop and a postop, the postop now in the same flex position with no longer compression there on the right leg. So in summary about three quarters of the athletes limited

by functional popliteal entrapment demonstrate full return to prior competitive levels. 100% are able to get back to recreational sports. We think the CTA protocols help find the region of the gastroc muscle to reset and we think that this is a good option

in athletes with wanting to get back to their sport, thanks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

- Symptomatic post-thrombotic disease affect at least 30-50% of patients with deep vein thrombosis. Regular wearing of individually selected compression garments with regular follow-up alleviate symptom in many patients. However, compression therapy doesn't eliminate chronic structural post-thrombotic changes,

implies lifelong treatment, ineffective of many cases, and low overall patient compliance remain a serious challenge. Raju S. Et., alia Asia. Percutaneous balloon angioplasty and stenting of iliofemoral venous segment have recently improved

the outcomes for patients with severe PTS, related to venous outflow obstruction. Postinflammatory vein wall remodeling and destruction of the venous value is considered to be the morphological substrate for PTS. Auto transplantation of valve-containing venous segment

demonstrated good five year results of half of patients, 50%. Maletti., Perrin., 10 years ago. However, there is currently low correlation between hemodynamic effect and clinical success of deep vein surgery in published literature.

The main goal of this study is to develop a novel surgical technique on venous neo-valve formation to correct deep axial reflux and improve venous outflow in post-thrombotic disease We perform the first series of in vitro experiments

using methods of mathematical modeling to develop a novel surgical technique on venous neo-valve formation. Five macroscopically intact common femoral veins were taken out autopsies from individuals without history of venous thrombosis.

And five common femoral veins were taken off autopsies from individuals with PTS. It was very difficult. The surgical technique involves complete transection of the common femoral vein, eversion of the proximal end of the vessel

with simultaneous endo-phlebectomy and creation of neo-leaflets from the inverted vein wall by interrupted sutures. Transection of the femoral vein and eversion of the approximal end of the vessel. During mathematical modeling appropriate dimensions

of the neo-valve were determined to resemble morphology of a native valve. An optimal vein wall thickness for neo-leaflets was determined to enable appropriate elasticity and coaptation. The hydraulic probe demonstrated good competency

of the neo-valve at 1.5 atmospheric in vitro. The absence of outflow obstruction was predicted as less than 20% stenosis during the maximal valve leaflets separation. In conclusion: A novel experiment model was autologous deep

venous neo-valve was created and evaluated in vitro. In vivo experiments to evaluate hemodynamic effect, thrombosis risk, and long term hemodynamic effect. Thank you very much.

- Alright-ey, hands put up. Who is for Onyx? Put your arms up. - [Male Audience Member] Who supports the Onyx Motion? - Onyx Motion, that's correct. He should've gone to law school. Who supports the alcohol motion?

Who supports the motion in the ocean? Alright, thank you I think we covered a lot of territory today. We want to have theses things and we are so glad that everybody came. I think this is Tony's first time,

Walter's first time here, Loronze and we really learned a lot today. I'm really glad Pletio Rossi was here because without him and his development of selective catheterization, I mean where would we be

sticking needles in every artery like that, trying to do angiograms, much less advanced sheaths or anything else. Pletio was wonderful having him here, one of my hero's. Anybody like to say anything?

Anybody got any questions or anything? - [Female Audience Member] The HHT scientific meeting's in June in Puerto Rico if you want some more good-- - Do they have electricity there yet? - [Female Audience Member] I hope so, I knew it looked nice before.

- Oh, okay, okay. Alright, well thank ya'll so much and we'll see you next year. (Clapping)

- 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.

- Thank you very much. Presentation's about drugs for venous symptoms. The goal of the medical treatment is to improve symptoms of chronic venous insufficiency like leg pain, cramps, heaviness, edema, pruritus and so forth. Medications are available but the results are not clear.

We have no disclosures for this presentation. The main drugs for treatment of the venous the Alfa Benzopirones, which has this subgroup here, with this big name and the brand name in Brazil is Venalot. The Gama Benzopirones are another group

with more subgroups like the Calcium Dobesilate and the Flavonoids. Flavonoids we have subgroups like flavonas and diosmin and flavanas, which are flavononas and hesperidine. These are subgroups of these Benzopirones. This drug comes from, a natural drug called Indian Chestnut

or Castanha Da India and you have this pure medication here or to its subgroups like Escina and other subgroups like the Saposidios and the naftazone. The name, Castanha Da India comes from 16th century. The Portuguese, as you know went to Africa and then to India looking for spices

and they had to fight for these spices and they noticed that the horses of the Portuguese on the next day of the battle were not as good as the Indian and Chinese horses. So, they thought something's wrong with our horses or better with their horses and they bribed a guy

who was taking care of the Indian horses and found out they were given a nut, a chestnut from a tree. So they managed to get a tree, took it back to Portugal and then sent it back to Brazil, which was a colony of Portugal at that time. But this was a war secret, they kept it as a war secret.

In the 18th century, the English went to fight with some tribes in north of Europe, which we call now Russia, and they noticed the same thing. The next day of the battle the English horses were tired, where the tribes' horses were great. So they did the same thing as the Portuguese,

they bribed a guy, got the plant, sent it to England and later to America which was a colony of Portugal at that time. This was kept as a horse nut in England and in America because they use it only for horses. Like in Brazil with time,

they started using the same thing to people and they noticed that it improved symptoms of leg pains of people too. But if you see it's the same drug as Aesculus hippocastanum which is called here, Horse Chestnut and in Brazil, Indian Chestnut.

This is the tree. You can see it's a beautiful tree with a shadow here so India, not the Indians from United States, Indians from India is very hot so what the horse do is stay here nicely and eat this thing here which is the chestnut.

There are other drugs also, some are natural like this one here, others are made by industry like rutina, tribenodium, aminoftona and the Picnogenol. Pycnogenol is also a tree, actually it's the bark of this tree,

which is common in the coastal area of France and they take this bark and make a drug. It's Pycnogenol, a pill you can take it and also a liquid you can use on skin. This thing here, has a lot of studies made by the industry that's producing Pycnogenol.

When you go to give these medications to your patient you have to give one because they are almost like the same. So you select one of these and that's enough. What do they do? They decrease venous inflammatory response, increase lymph cathecol-O-methyltransferase

leading to venous constriction, increase lymph flow, increase permeability of the veins and lymphatic and this reduces edema and its symptoms. These are one of the studies about this, the Cochrane Review which says that they improve quality of life, reduce edema and basically they have few side effects.

The other studies 2018 and same thing, quality of life is improved, no difference compared to placebo in ulcer healing, so they do not heal ulcers and few side effects. So, does it work? Yes, for the patient, it reduces symptoms edema and itching.

No, for the healing ulcers and no for some doctors because they are not giving Horse-Nuts to their patients because the name here is horse nut. But maybe they are good. So, that's it. Thank you so much.

- Great thank you for, thank you to the committee for having me, and it's a pleasure to present the information. No relevant disclosures. I submit to you that Endovenous Ablation is a minimally invasive technique. It works well, it's widely accepted,

most of us perform that. And I will also submit to you that laser is about equally efficacious when compared to radiofrequency. We can get into the nuances of different wavelengths but I submit to you that they both work.

They're good techniques, they're safe and they're well accepted. Compression has traditionally been prescribed after ablation with no good evidence showing that it works. Some patients are uncomfortable, some patients say it causes irritation, blistering.

Some patients, the worst part of the whole experience is actually wearing the compression stocking. They did well with the procedure but in follow up they're just, hey doc the only thing that bothers me is the compression stocking, or do I have to still wear this thing.

That's the question or comment that we all get when we see these patients in follow up. So the literature is right decades ago with compression stockings in regards to vein stripping. Studies out the U.K. looked at strength, low compression versus high grade compression,

as far as bruising, pain, phlebitis and really no differencea were seen. When it comes to duration 1 week versus 3 weeks, again vein stripping patients not the thermal ablation patients, we saw the pain complications, time to work

and patient satisfaction all very similar in the groups. And then lastly when you look at compression versus no compression, in vein stripping patients, again no significant difference with limb edema, pain, complications. But in this last study there was a decreased

time to work in the compression group, So the optimal duration. There's been meta analyses done looking at short term 3-10 days versus 3-6 weeks. No benefit of long term compression therapy in regards to any of the factors that you see listed there.

So what about endovenous ablation? There's a prospective, randomized trial for looking at laser patients, where patients were randomized into two different groups, Group A and B. Group A for two days Group B for seven days

they looked at pain scores, quality of life both at 48 hours one week and six weeks. All patience received a duplex at three months. And there was really, at one week there was improvement in physical function and vitality in Group B. So the seven day compression group did

generate a better benefit in these two categories. GSV rates of occlusion were 100% at the three month mark in both groups. Another randomized trial published in 2015 looked a four hours of compression versus three days of compression

and found no difference in leg pain or edema. They found that the shorter duration had less complications as far as blistering and skin irritation, again this is published, but you know in our practice I think that we don't really see a lot of these problems just after such a short duration of compression stockings.

But nonetheless, the data is out there. Another study published in 2014 looked at 111 patients randomized to one day of bandages versus two weeks of high grade compression, looking at pain scores. They also looked at the Aberdeen Varicose Vein Questionnaire RAND scores, patient satisfaction,

time before returning to work and adverse events and really did not find a significant difference in these patients. With the exception of pain, that's a pain score that you see there, you could see perhaps a slightly better result with pain

in the compression group. And more apropos to that, less anogesics in the compression group. Well, we published a study last year, our prospective, randomized controlled trial investigating the therapeutic role

of compression after ablation. We randomized patients to wearing thigh high compression stockings for one week versus no compression stockings at all. An no compression at all actually received an ACE Bandage for 24 hours.

hey went home the next day took the bandage down and then wore nothing. We have the inclusion and exclusion criteria there. Of note we did exclude concomitant phlebectomys. We thought that would muddy the water, so these were just pure ablation patients.

We looked at the efficacy of ablation based on duplex at one week, three to six months, one years. And we then reexamined it at two years as well. We looked at the CIVIQ-2 scores VCSS scores, pain scores, bruising scores. 85 limbs were randomized,

46 into the compression group 39 into the no compression group. 3/4 of them were women. You can see the CEAP scores there. We found with the CIVIQ-2 questionnaire that there was no significant difference.

Both groups enjoyed a benefit and decreasing CIVIQ-2 scores that did not reach statistical significance but both groups enjoyed derived benefit, there was no significant difference. VCSS scores similarly not statistically significant. Both groups decreased VCSS scores.

Bruising scores also similar in both groups. We grade on 1-5, no significant difference in bruising. When it comes to pain, this was the the only thing that reached statistical significance. There was better pain control in the compression group over no compression.

The closure rates were 100% in both groups. Small patient size but 100% closure even up to two years. So in conclusion we think that patients with compression may derive a small benefit with regards to pain control but there's really not much other advantage to compression. I'm wearing them now.

Hopefully you guys are wearing compression stockings now. A properly fitter compression stocking feels good and they do work but we do not routinely recommend them after ablation. Thank you.

- I'm humbled to be introduced by a man with your integrity, so thank you for sharing that case. I don't perform procedures and now I know why. - [Man] Maybe you should, having seen that? - (laughs) I don't have the heart for it, I think. So, okay, so you met me before but if you haven't, these are still my disclosures.

The first is an IVC filter company and the second is a company that makes, has all sorts of assets in the venous space. You're more than welcome to ask me about these if you feel the need to. So, a 50 year old man presents from an outside hospital

with left lower extremity swelling. His left lower extremity looks like this. And pulses, motor function and sensation are normal and symptoms started three days ago and are about the same despite anticoagulation. For those of you who were here in the previous session,

you've heard that he wants a procedure done and he wants this clot out. He has a common femoral vein clot and so, he underwent pharmacomechanical catheter-direct thrombolysis and a stent was deployed like you can see here.

So, the topic of my few minutes is how do we avoid stent thrombosis basically? What is the right thing to do now from a medical standpoint so we don't experience stent thrombosis or even thrombosis within a stent.

You know, even reduction in the luminal diameter within a stent. How do we make sure that these stents remain patent as best as they can be patent? Well, you know, whatever it is we're doing and I can tell you

that there isn't any surprise in this talk, there is no standardization to what we're doing but whatever it is we're doing is probably working because overall stent patency rates are quite high for the venous system. And there is much variability in care.

What you can see here is that people treat, by the way, obviously stenting can be done for various reasons and I'm talking about post-DVT, right? So, sometimes people treat with low molecular weight heparin to Coumadin. DOACs are being used more for varying durations.

Sometimes with and sometimes without a combination of an antiplatelet agent. So you know, all the options you can think of are basically being done and the outcomes are like I showed you before, pretty good overall.

Now despite variability, some consensus exists and to be honest with you, I'm not going to show you all these points of consensus. What this is, this graph shows is a result of a, sort of a, questionnaire that was sent to peers in no standardized fashion

and what these people, in some of these statements that there's consensus about, I didn't agree with, so I decided not to bring forward for this discussion. But basically, people say that anticoagulation is preferable to antiplatelet therapy and most people treat for six to 12 months

after such a procedure. Lifelong antiplatelet therapy is recommended if anticoagulation is stopped, people said. And following lysis and stenting, anticoagulation can be discontinued after six to 12 months and people said that it depended

on whether or not the patient has a known thrombophilia or a known reason for the thrombosis. So, you know, as I said, there's variability and despite that variability, things are going okay. What about whether or not we should use vitamin K antagonist or a DOAC such as Rivaroxaban?

Well this small series of 111 patients basically showed the p value was not significant and over two years, the patency rates were very similar. So, you know, given all that, and I'm not showing you data because there are no data to show you,

then what is my practice and what are the limitations of that? Well, what we do after these procedures is that we give a dual antiplatelet agent for one month after the procedure. We treat with one antiplatelet agent

typically aspirin lifelong afterwards. Anticoagulation is only if the indication was of a DVT and basically, we don't do the same thing for every patient. So if there was iliac vein compression that we are sure of as the reason for the thrombosis,

we treat for only three months post-procedure as if this was provoked event, but if the etiology is unclear, we do treat long-term per guidelines for DVT as the same way you would do for any other unprovoked DVT. So thank you again for the opportunity

and thank you for listening.

- Thank you Jose and Marcia. No disclosures. So the primary valve incompetence treatment techniques was started by Bob Kistner and the techinique involved a longitudinal internal valvuloplasty by longitudinal incision and tacking of the redundant valve edges.

And the next treatment available was a transverse valvuloplasty which was again under vision and the valves were tacked at the at the commissures but the incision was transverse. And a combination of the two techniques resulted in the technique of Sottiurai, the T internal valvuloplasty

which was later modified by Michel Perrin to be able to evaluate all aspects of the valve. Further to that, we developed the trapdoor internal valvuloplasty in which a trapdoor was created. All these techniques, the mainstay was reefing of the valve commissures.

On the left hand side, you can see a redundant valve, prolapsing cusps, and on the right hand side, a repaired valve after the reefing. But you can see that the commissure is quite heavily placated. So the possible disadvantage of reefing technique

is the resultant heaped up commissural junctions. This creates valvular rugal folds and obviously when healing occurs it will have increased cicatrization, it will occupy the space, and reduction of functional valve area. When we evaluated the various thrombosis results of

supra-valvular technique, modified T technique, and the trapdoor technique, we found that on an average, there was about a 4.5 to 9% incidence of valve thrombosis. And we also found that in another 6.1% patients there, the valve stations resolved. Cumulatively, these two complicates accounted

for almost 13% of all valvuloplasties. We published a new technique of reduction internal valvuloplasty on the lessons that we leared from Dr. Lugli's experience. And we wanted to quantify the repairs that we do by measuring intra valvular distances and

trans-commissural diameters preoperative as well as intra-operative by ultrasound. We used various techniques, we devised measuring forceps and this is how it's done, whereby we are able to excise the redundant valve and stitch it back onto the valve

and have no rugal folds at the end. And this can induce, this can reduce incision in high shear areas as well. And therefore, give you a good result. This is intra-operative result of competence where you can see the patient is doing valsalva

and you can see the two valve leaflets and this is the stripping technique. And a post-operative descending angiogram or venogram shows a competent valve. So when we looked at the relationship of reflux, valve repair, and ulcer healing,

we found that when we did single level repairs, we only found 50% ulcer healing. But when we did multiple level repairs, the healing was 100% in a short period of time. And the valve competency always did not correlate with ulcer healing.

In our case the valve competency levels were 87.5% and ulcer healing was 88.9% but mainly due to the single level repairs, that did not really work. So the Rival Technique in conclusion ladies and gentlemen is a complete departure from the reefing technique which has been the mainstay of valvuloplasties.

At two years, we've had 100% patency and about 87% competency of repaired valves, with a freedom from C6 ulcers at two years about 89%. Rival Technique has now replaced our technique, earlier techniques, and is the preferred technique in our center.

Thank you for your attention.

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