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Saddle PE (Submassive), Pregnant (33 Weeks)|Thrombolysis (Catheter-directed)|34|Female
Saddle PE (Submassive), Pregnant (33 Weeks)|Thrombolysis (Catheter-directed)|34|Female
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Transcript

Case two I think is more of a thought provoking case of, what do you do in this situation and how in your institution would you take care of this,

and who would be on your team to deal with this patient? So, it's a 34 year old female at 33 weeks of pregnancy. She presented with left Substernal chest pain, worsen with exertion. In the setting of a new onset right lower extremity edema and upper

thigh pain. So given that we're at a PE session I'm sure you can all guess she has a right lower extremity VVT and a PE. So here's her CT. Some selected images, and you can see she has this Saddle pulmonary

embolism drapped over the both pulmonary arteries and she has large thrombus burden extending into the low bar branches, in the coronal view you can see the same thing she has this large branches here. Here is the rest of her history, so her ultrasound showed Femoral

DVT. She has no history of in vitro fertilization and no other past medical history. Not a smoker, no recent travel, no family history of thrombosis. ECG shows sinus tachycardia and at this time,

her echo shows no right heart strain and you can see her vitals, she's a little bit tachycardic but other than that her vitals are pretty normal, she is requiring a good amount of O2. So at this point, I don't know,

what would you all do? Would anybody rush to doing catheter directed lysis at this point? I didn't think this would be a very responsive audience. So obviously we're not gonna treat this patient, this is a very much as stable submersive and higher situation but three days later her situation changed dramatically.

She started having increasing chest pain, dyspnea, increasing O2 requirement, she really couldn't lie flat, she was very, very uncomfortable. She couldn't even hold a conversation with us. Repeat transthoracic echo, showed mildly dilated RV and flattening

of the intraventricular septum. All this time she was in our medical ICU and we had OBGYN and very much involved and she was on getting routine non stress tests and there was fetal distress. Now what? So now you have a very challenging situation and what's the best method to treat this patients?

So as we always do, we have kinda four options so take each one by one. Take catheter directed thrombolysis as an option, overnight tpa infusion, we definitely have a high risk of the fetus cuz we're infusing tpa and she could have bleeding and she could potentially loose the fetus and we'll talk a little bit about what conversations you have to have with that.

Heparin and to quote one my colleagues in Cornell, Heparin and a little bit of hope, and here you really have a lot of risk to the mother, risk to the fetus and obviously deterioration of massive PE would lead to both of those. Surgical thrombectomy,

this is very challenging to consider in these patients obviously she's pregnant, there's a lot of risk here and to the fetus, major cardiac surgery. Where do we give Systemic lysis? And again, pretty high bleeding risk right there. And so

in our institution what we ended up doing is having a large meeting, we had myself, one of our cardiologists, whose part of our pro team, pulmonary critical care, we had our cardio thoracic surgeon, we also had our gynecologist on board,

we had our pediatricians from the [UNKNOWN] on board and we all had a very frank conversation as to what were the risks related to whichever one of this pathways we chose. And our gynecologist scared this woman to absolute death as far as what should she do if push came to shove who comes first,

her or the fetus and you know that her life really comes first in his mind and that needs to be a priority. So she ended up deciding on catheter directed thrombolysis and we did this in somewhat of a unique fashion. We did this in our hyper operating room,

we had everybody in the room at the same time so we had a surgical table open in the operating room, we had our cardiothoracic surgeon on standby in the room. We had the gynecologist available in case an emergency cesarean section

needed to be performed, and we had [UNKNOWN] staff for the baby in case we need to have them taken care of. So we get in, we do our pulmonary arteriogram and not really all that impressive on the DSA runs you can see just on this injection pretty good perfusion of both lungs don't really appreciate a lot of copper even though we know it's there.

This is a situation where I'd like to say doing those unsubtracting views you get to take a little better look sometimes at the clot and I don't know if it projects very well but you can see here kind of the outlining of this thrombus, it's just non-occlusive. So there's contrast flowing around it so it's not clearly visualized. Her pressure is not quite as bad as we expected but still mildly

elevated. So at this point we were kind of relieved, we said okay, maybe she's really not be sick as we think so we put in our perfusion catheters and we gave our usual dose of tpa 0.5 mg/hr on each side. We gave her a bolus of 6 mg to each pulmonary artery upon placement

of the infusion catheters, we brought her back the following day and this is the pulmonary arteriogram that we got, resolution of clot burden, her pressures are no different but not sure that really matters in this case. And I can tell you now she's doing very well

and had no sequel of this event at all.

- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal

and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks

after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.

So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.

That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied

to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience

there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,

or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.

In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted

for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.

This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,

and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak

and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.

Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.

You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,

so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.

And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR

is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program

with CT scan is of paramount importance after these procedures. I thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Speaker] Thank you. My disclosures. So upper extremity dvt occurs in 4-10% of all causes of venous thrombosis. And while a minority, dvt in the upper extremity can often be caused by thoracic outlet syndrome, effort thrombosis, occasionally

idiopathic venous thrombosis. The majority is more likely related to central venous catheters, pacemakers, cancer, etc. This is some of the presentation of someone with Paget Schroeder or venous thoracic outlet syndrome, we're all well aware of this.

Some features of this can be sudden onset of pain, discoloration and some of this subcutaneous collateral veins that we note. Initial treatment of this is traditionally with venous thrombolysis. Although the results are good, this thrombolysis can

be associated with bleeding complications, potential for renal insufficiency, prolonged dwell times, and increased cost. I think it's important that this is not just a talk about a technique but a technique in the context of an operation this is soon to come.

Whether you choose to take out the rib at the same setting or you choose to delay the operation by a week or two, by and large the complications associated with that venous thrombolysis are going to come back and haunt you in the next operations. I think that's the context of this talk.

One of the risks I just mentioned about some of these techniques is, that's sort of curious to me, is the acute kidney injury after AngioJet venous thrombolysis. You see here, this paper, of a hundred patients, 50 AngioJet, 50 catheter directed thrombolysis, shows a statistical significantly

increased risk of acute kidney failure in the AngioJet group. Eight fold odds ratio. The Indigo system enables operators to remove the thrombus in a single setting, while potentially reducing or eliminating the need for thrombolysis.

This has already been discussed by some of the prior speakers, you see the different iterations first introduced in 2014. The CAT8 is the largest device and you can see some of the features of this proprietary technology with the separator and the directional sheaths that

allow us to aspirate nicely. This continuous suction you see here, can be very nicely controlled with an on-off switch that minimizes blood loss. It's single operator design, very easy to set up, hands free aspiration, a very simple set up.

You also heard just recently about the volume that can be aspirated in 20 seconds you see, especially with the larger profile devices, quite impressive amount of thrombus can be removed. Again, with the careful control for blood loss. The directionality of the sheath is also important,

and you can see some of the different directionality sheaths. Here's a couple case examples of a Paget-Schroder patient comes in with an acute sudden onset of arm pain and swelling discoloration, and you can see the penumbra device being used to clean out that vein.

This is another example, a 25-year old male with acute right arm swelling, sort of a body lifter type, and you can see here, this is the separator that's being moved forward and backwards, in and out to help break out the thrombus. This is the CAT8 device.

The pre-intervention picture seen here, we're crossing the lesion with a wire and and you can see the post-intervention on the right. You, of course, have the venous compression from the first rib, thoracic outlet, but the vein is widely open and now we can go ahead and see

the specimen that's retrieved as you've seen other videos in the prior presentations. This, of course, is what we're left with at the time of surgery. I only bring this up to remind us that there is a second stage to this treatment,

which is the rib resection. A combined experience that I just want to put together, very small numbers of course but, 16 patients with thoracic outlet who presented and were treated with the Penumbra system. You can see here, some of the demographic data.

I'll just point out the symptoms, of course, pain, swelling in these patients, imaging mostly venous duplex, occasionally CT or MR venogram. They all of course get venography at the time of procedure. The extent of the thrombus in all of them was complete occlusion and you can see some

of the extent in the subclavian axillary veins. Site of access can be the brachial or the basilic vein. The operative details as well, shown here, and I'll just point out the estimated blood loss, it can be very reasonable, especially with some experience you can sort of control that

on-off valve and minimize blood loss with this technique. Adjunctive therapies are shown here and of course, maybe because we're a little bit stuck on our ways, we did have a fair number of adjunctive lytic therapy. There were only three patients who had overnight lysis. A lot of venoplasty done at the time of the procedure.

All veins remained patent until the day of the rib resection but I will point out that one of these patients did develop a significant complication with hemothorax. This is one of those patients who had overnight lysis. And I point that out to stress that perhaps

this is what we're trying to move away from. So, in conclusion, mechanicothrombectomy using Indigo device shows promising initial results. Minimal blood loss, one complication of the hemothroax with the overnight lytics. No renal insufficiency or distal embolization.

The practice pattern, I think, need to adjust away from routing lytics to additionally minimize complications prior to surgery. Thank you.

- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.

Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen

and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol

at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.

If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.

But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,

We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.

You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.

That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month

we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with

Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,

One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,

the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,

straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,

according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy

If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy

and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.

Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.

So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.

(applause)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,

both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,

and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms

non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches

versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,

that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require

more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage

than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased

due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations

impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion

during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion

after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing

the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials

where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this

from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph

that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents

with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,

whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.

And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent

also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,

and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.

So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,

always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.

Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)

- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.

And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.

And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,

but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.

The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.

And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,

or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.

And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome

occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity

Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,

such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.

When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.

We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.

And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.

Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.

Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial

And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05

and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options

that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much. It's an hono ou to the committee for the invitation. So, I'll be discussing activity recommendations for our patients after cervical artery dissection. I have no relevant disclosures.

And extracranial cervical artery dissection is an imaging diagnosis as we know with a variety of presentations. You can see on the far left the intimal flap and double lumen in the left vertebral artery

on both coronal and axial imaging, a pseudoaneurysm of the internal carotid artery, aneurysmal degeneration in an older dissection, and an area of long, smooth narrowing followed by normal artery, and finally a flame-tipped occlusion.

Now, this affects our younger patients with really opposity of atherosclerotic risk factors. So, cervical artery dissection accounts for up to 25% of stroke in patients under the age of 45. And, other than hypertension, it's not associated with any cardiovascular risk factors.

There is a male predominance, although women with dissections seem to present about five years younger. And there is an indication that there may be a systemic ateriopathy contributing to this in our patients, and I'll show you some brief data regarding that.

So, in studies that have looked at vessel redundancy, including loops, coils, and in the video image, an S curve on carotid duplex. Patients with cervical artery dissection have a much higher proportion of these findings, up to three to four times more than

age and sex matched controls. They also have findings on histology of the temporal artery when biopsied. So one study did this and these patients had abnormal capillary formation as well as extravasation of blood cells between the median adventitia

of the superficial temporal artery. And there is an association with FMD and a shared genetic polymorphism indicating that there may be shared pathophysiology for these conditions. But in addition, a lot of patients report minor trauma around the time or event of cervical artery dissection.

So this data from CADISP, and up to 40% of cases had minor trauma related to their dissection, including chiropractic neck manipulation, extreme head movements, or stretching, weight lifting, and sports-related injuries. Thankfully, the majority of patients do very well after

they have a dissection event, but a big area of concern for the patient and their provider is their risk for recurrence. That's highest around the original event, about 2% within the first month, and thereafter, it's stable at 1% per year,

although recurrent pain can linger for many years. So what can we tell our patients in terms of reducing their risk for a recurrent event? Well, most of the methods are around reducing any sort of impulse, stress, or pressure on the arteries, both intrinsically and extrinsically,

including blood pressure control. I advise my patients to avoid heavy lifting, and by that I mean more than 30 pounds, and intense valsalva or isometric exercise. So shown here is a photo of the original World's Strongest Man lifting four

adult-sized males in addition to weights, but there's been studies in the physiology literature with healthy, younger males in their 20s, and they're asked to do a double-leg press, or even arm-curls, and with this exercise and repetitions, they can get mean systolic pressures,

or mean pressures up into the 300s, as well as heart rate into the 170s. I also tell my patients to avoid any chiropractic neck manipulation or deep tissue massage of the neck, as well as high G-force activities like a roller coaster.

There are some case reports of cervical artery dissection related to this. And then finally, what can they do about cardio? A lot of these patients are very anxious, they're concerned about re-incorporating exercise after they've been through something like this,

so I try to give them some kind of guidelines and parameters that they can follow when they re institute exercise, not unlike cardiac rehabilitation. So initially, I tell them "You can do light walking, but if you don't feel well,

or something's hurting, neck pain, headache, don't push it." Thereafter, they can intensify to a heart rate maximum of 70-75% of their maximum predicted heart rate, and that's somewhere between months zero and three, and then afterwards when they're feeling near normal,

I give them an absolute limit of 90% of their maximum predicted heart rate. And I advise all of my patients to avoid extreme exercise like Orange Theory, maybe even extreme cycling classes, marathons, et cetera. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much both. It was a great pleasure to see you. I continue to be grateful for the guidance you have given me over the years. Thank you to the organizers for advising me to speak. These are my disclosures. So really there are two questions posed by this topic.

One is, is the patent popliteal vein necessary? I would assume from this is it necessary for patency and symptom relief to be achieved in treating patients with both acute DVT and potentially chronic. And has the evolution formic mechanical therapy

led to over stenting. Which means we have to ask the question what is an appropriate rate for stenting. I am not sure we know the answer to that. So being able to answer over stenting requires us to know how many patients

actually need the stent in the first place in acute DVT treatments. The problem is essentially this. Is that when we form lithic therapies and this is a classic case of treatment formed with formic and mechanical device

but without a follow up using lithic in the patient for whom lithic was not feasible. You end up opening up a vessel but you can see from the image on the left hand side that there is a degree still of luminol contrast deficit suggesting some cult left behind

in the external iliac vein. Well there is obviously a May-Thurner legion at the top. The question of over stenting is one of do we just stent the May-Thruner and extend it down into the external iliac vein to trap that thrombus

or would a period of time of lithic have resulted in this clot resolving and not needed a stent at the end of it. To get to the question of how many people should be stented. The only way we can really do this

is try and exstipulate from the literature to some extent. This is the short and long term outcome from the Kevin study. Where there is ultrasound follow up of patients underwent standard treatment only.

And a additional group in the patients had catheter-directed thrombolysis. We can see there that the patients did six months in catheter-directed thrombolysis group is around 60%. And the patency seen with the non treated group

is around 40%. If we kind of use these numbers as a guide we probably expect therefore that the stent rate would be somewhere between 40 and 60 percent. To account for treating the outflow structure that presumably patients see at six months.

But this is clearly not a very rebost method of being absolutely clear on who needs stents. Additional method is we don't really have and answer for who should be stented at the end of a procedure. So if you look at the massive variability

in the other studies. We see that attract stent rate is approximately 28% for the study. Which is obviously a operative discretion and has been criticized for that reason. But there is no comment on the Popliteal vein

or Popliteal vein patency. Cavent did an stent rate of 15% again with no real comment on whether the Popliteal vein was open and it wasn't a prerequisite for treatment in the study. This contrast with the Ansberg Aspirex Registry.

Which is a registry of a purely mechanical device to aspirex clot and the stent rate is 100%. Baekgaard Copenhagen used a catered-directed thrombolysis with a mandated open popliteal vein for purpose to be in the study. He has a stent rate of 60%.

My own personal experience of 160 odd patients is that were stenting around 80% of patients with outflow legion at the end of treatment. And were not really bothered by whether the popliteal vein is clear or not. But that doesn't necessarily answer the question

whether it makes a difference in the long run. So its very difficult even looking at the data we have because there is no standard definition of what a outflow stenosis is. There is no objective measure for an outflow stenosis. So stenting becomes and operative discretion decision.

But you would have to say that if your taking purely mechanical devices and the stent rates are going up to 100% that the inclination would be that there is potential for formic mechanical therapy to lead to overstenting and increase use

for stents for sure. In our experience then we had 81 patients who had CDT alone verse 70 patients who had AngioJet Thrombectomy. The basic characteristics of the group are pretty much identical.

With similar ages and no difference between whether the thrombus with left side or right side of body or so on. And these are the patency curves for the different groups with equivalent primary, primary assisted and secondary patency over two yeas.

We had no difference in stent rates with the median stenting of 80% in both groups with two stents used in average for each of those patients. However in our practice AngioJet is rarely used alone. So we had 70 patients for whom AngioJet was used. 24 of those where AngioJet was used up front

as the first line of treatment followed by some CDT. We have tended find that if we wanted full clock clearance. We have always had omit to some extent. And single stage therapy is quite difficult to achieve unless you spent a lot of time in it.

Patency in the popliteal vein is clearly affected by some extent. These are our follow up results if we don't have a patent popliteal vein at the end. It does drop off in stent patency. So the conclusions then I think.

Is that patent popliteal vein is necessary for long term results. But you can still treat patients that have acute popliteal vein for larsons that is not a contraindication. Pure mechanical therapies may well lead to higher stent rate.

But is this a bad thing or a good thing? We don't really know this at this stage as to what the long term outcomes will be. Thank you very much.

- I'd like the thank Doctor Veith for inviting me back to speak. I have no disclosures, we will be discussing some slight off-label use of the anitcoagulants. As we all know, acute limb ischemia occurs as a result of acute thrombosis of a native artery or bypass graft or embolism from a proximal

source, dissection, or trauma. The incidence is not insignificant, 15 cases per 100 000 persons per year, or interestingly about 10 to 16% of our vascular workload. Despite the relative frequency of this condition, there are relatively few guidelines to

guide us for anticoagulation therapy. The last set of guidelines for the American College of Chest Physicians regarding PAD gives some very brief, generic recommendations from 2012. They state, suggest immediate systemic anticoagulation with unfractionated heparin.

We suggest reperfusion over no reperfusion, which seems pretty obvious to an audience of vascular specialists. One of the challenges with acute limb ischemia is that it is a fairly heterogenous group. It can be thrombosis or embolism to the aorticiliac segments to the infrainguinal segments, and

there's also the patients who develop ALI from trauma. So we actually looked at the various phases of anticoagulation for acute limb ischemia and then we do, as with many institutions, utilize intravenous heparin at the time of the diagnosis, as well as obviously at the time of surgery,

but we found that there was a significant variation with regard to the early, post-operative anticoagulation regimens. One option is to give therapeutic intravenous heparin on an adjusted dose, but what we found in a significant minority of patients across the country actually,

is that people are giving this fixed mini-dose 500 unit an hour of heparin without any standardization or efficacy analysis. Then, obviously you go the long-term anticoagulation. We reviewed 123 patients who had ALI at our institution, who underwent surgical revascularization.

And they had the typical set of comorbidities you might expect in someone who has PAD or atheroembolism. In these patients, the Rutherford Classification was viable or marginally threatened in the majority, with about 25% having immediately threatened limb.

Various procedures were performed for these patients, including thromboembolectomy in the majority, bypass operations, angioplasty and stenting was performed in the significant minority and then primary amputation in the various selects few. We divided these patients into

the first four days of anticoagulation. Therapeutic with unfractionated heparin early on versus subtherapeutic or this mini-dose unfractionated heparin and we found that 29% of our patients were receiving the mini-dose unfractionated heparin, again without much efficacy analysis.

We used the International Society for Thrombosis and Haemostasis Anticoagulation Outcome Guidelines to look at the ischemic complications, as well as major and minor bleeding for these patients, and we identified actually not a significant rate of difference between the

subtherapeutic category and the therapeutic category of patients, with regard to mortality, with regard to recurrent limb ischemia, MI, VTE, or stroke, major amputation, and we actually didn't find because it's a fairly small study, any significant difference in major or minor bleeding for these patients.

So, we do feel that this small study did justify some efficacy of mini-dose unfractionated heparin because we didn't find that it was causing recurrent lower extremity thromboembolsim in these patients. Now on to long-term anticoagulation, for these patients, after that first three or four days

after the surgery, the options are long-term vitamin K antagonists, the DOAC's or vitamin K antagonists if you have atrial arrhythmia, or in the patients who had no other comorbidities, there really is not much guidance until recently. The compass trial was recently published in 2018

in stable PAD and carotid disease patients, identifying that rivaroxaban plus aspirin had a significant benefit over aspirin alone in patients who had stable PAD. And then, an upcoming trial, which is still ongoing currently in patients who underwent recent

revascularization, whether open or endo, is hopefully going to demonstrate that rivaroxaban, again has a role in patients with lower extremity ischemia. So in conclusion, there is relatively a scarcity of clinical data to help guide anticoagulation after acute limb ischemia.

Unfractionated heparin pre and intraop are standardized, but postop anticoagulation is quite variable. The mini-dose, we consider to be a reasonable option in the first few days to balance bleeding versus rethrombrosis, and fortunately we are having larger randomized clinical trials to help demonstrate the benefit of the DOACs and

aspirin in patients who are stable or post-revascularization for PAD, thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.

It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.

So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations

of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.

Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.

So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient

who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal

angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near

or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility

was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.

Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal

or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection

or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.

So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump

to prevent hip disarticulation. Thank you for much for your attention.

- So I'm going to be talking about allografts for peripheral graft infections. This is a femoral artery that's been replaced after a closure device infection and complication, and we've bypassed to the SFA and profunda femoris. These are my disclosures. So peripheral arterial infectious processes,

well the etiology either is primary or secondary. Primary can be from bacteremic states and seeding of ulcerated plaque or thrombus. Secondary reasons for infections can be the vast usage of percutaneous closure devices that really have flooded the market these days.

Prosthetic graft infections after either a bypass or patch in the femoral artery. So early onset infections usually are from break in sterility. Secondary infections can be from either wound breakdowns or late seeding of the prosthetic graft.

The presentation for these patients can be relatively minor such as cellulitis or draining sinus, or much more dramatic, such as sepsis or pseudoaneurysm or mycotic aneurysm. On the CT scan we can see infected mycotic aneurysm after infected closure device and bleeding complications.

The treatment is broad in range. Ligation is obviously one option, but it leads to a very high risk of major limb amputation. So ideally some form of reconstruction, either extra-anatomic through clean planes,

antibiotic graft as we heard from the previous speaker, the use of autologous replacement with deep vein, or we become big proponents of the use of cryopreserved arterial allografts for reconstruction. And much of this stems from our work from about 10 years ago, where we looked

at the use of aortic cryopreserved grafts for aortic graft infections. This was published about 10 years ago but we looked at a small series of patients with aortic infections. You can see the CT scan of an infected stent graft

and associated aneurysm. And then the intraoperative photo after we've resected the stent graft and replaced that segment of the aorta with a cryopreserved aortic segment. So using that as a springboard,

we then decided to look at the outcomes using these types of conduits, arterial conduits, for peripheral arterial reconstructions in contaminated or infected surgical fields. So retrospective review at our tertiary care center, we looked at roughly 60 patients over a 15-year period

and excluded any aortic-based reconstructions. So these are all peripheral reconstructions. Mean follow-up was 28 months. As you would expect, the distribution of treatment zones were primarily in the lower extremities, so 51 cases.

As you can see, there's a list of all the different types of cases that we treated. But then there were a few upper extremity visceral and then carotid. I've shown this slide before at this meeting in the past, with a carotid patch infection

that was treated after it had a blow-out, and it's obviously a infected aneurysm, and this was treated with resection and a cryopreserved arterial segment. Looking at our outcomes, the 30-day outcome showed a mortality rate of 9%.

The 30-day conduit-related complication rate was surprisingly low at 14%. We had four patients that had bleeding complications, four patients with recurrent infectious complications. All eight of those patients required a return back to the operating room for correction.

The late conduit-related complication rate was only 16%. As listed here, you can see there's only one case of reinfection, three cases of graft thrombosis, surprisingly only one major limb amputation, two pseudoaneurysms and one late bleeding complication.

And graphically depicted, you can see here, this area here is looking at the less than 30 days, this is primarily when the complications occur. When you get to six months, fewer complications, and then beyond six months, the primary complications that we would see are either thrombosis of the graft

or the development of late pseudoaneurysms, again relatively low. So in summary, I think peripheral arterial infectious complications can be treated with a cryopreserved arterial allografts. The advantage is it's a single stage operation,

maintains in-line flow, there's a low incidence of repeat infection. I think it's also important to mention that the majority of these patients had adjunctive muscle flap coverage to cover the large soft tissue defect

at the time of the operation. So I think that this is a valuable alternative conduit in a setting of peripheral arterial infections. Thank you.

[Speaker] - Thank you very much and I appreciate the ability to present some of our research. First off, some of this was supported by AHRQ we're going to go through. What's important is, I think, Hyperglycemia is underestimated and It's been shown in general surgery to be a marker of poor clinical outcomes

in a variety of surgical patients. When you look at post-operative Hyperglycemia, it's been studied in general surgery and cardiac surgery. It's been associated with mortality and the surgical site infection. But there really is a limited amount of data

within the vascular information. So, in general, you look at the general surgery, majority of literature shows it has increased risk of infection, it has increased risk of a reoperative surgery, as well as increased risk of death. So we decided we would look at patients

undergoing lower extremity bypasses, open and Endo. And we found that in this study, one in five patients undergoing vascular procedures have hyperglycemia in their postoperative period. And, what was interesting is that diabetes was not an indicator for poor outcomes.

To do this we used the American Association of Endocrinology guidelines, which suggested optimal glucose would be between 80 and 180. Greater than 180 would be considered suboptimal. We then used Cerner information, which is EMR data. We divided the patients between open and endovascular

surgeries. We looked at our glucose targets and we looked at our outcomes. So I think what's most important is we looked at 4,000 patients. Mean years were 67 years in age. But what's more important to actually notice is that hyperglycemia was common,

more common in younger than old. It had an ethnic variability where African-Americans were likely to have hyperglycemia. But still, one in five patients after a lower extremity intervention, open or Endo, had hyperglycemia. So we're really not paying attention to it.

You can see that it occurred in equal percentages within open and endovascular surgery. And when you do a multi-vari logistic regression, we found that hyperglycemia, you had 1.3 times more likely risk of infection during your stay. You have a higher risk length of stay.

You had almost eight times greater risk of death. So, actually what's interesting is that diabetes was found to be productive, which suggests that it's really not diabetes, it's actually hyperglycemia is the main driver. As well, we found that certain medications will increase your hyperglycemia,as well as your disease severity.

We then move through this, we say that one in five patients have hyperglycemia. It's associated with increased lower extremity complications ,increased length of stay, as well as increased mortality. It was actually also unexpected that diabetes was not associated with inferior outcomes

and it's suggested it actually may be a marker with or without diabetic patients. We then looked at hyperglycemia in general surgery patients. We wanted to find out there was a risk in infection, as it's been shown. The general surgery population has thought

that maybe hyperglycemia is the most important risk factor for surgical site infection. We then looked at readmission of patients that underwent lower extremity bypass, to see why they were coming back. We found and infection at the index diagnosis was most significant for having a chance of readmission.

As well as anemia was highly also correlated with readmission. So, infection certainly is an important component to readmission. As well as Hyperglycemia is associated with readmission. It's important to remember that of the patients that come back for readmission after lower extremity procedures, almost half

of the lower extremity bypass procedures were associated with and infectious complication. And finally predictors of readmission, would include Hyperglycemia as it was associated with increased risk of infection at the index study. We then also wanted to see, other patients other studies

have looked to see if it can be controlled. This actually was a nice study, which is a perspective or analyzed study looking at insulin infusion protocol to improve outcomes. They show that surgical site infection was not reduced, they did well to look and see if they could control Hyperglycemia events

with an infrarenal bypass and open surgical repairs. And they used similar metrics for their Optimal Glycemic Control values. This study actually shows which is most interesting, that the most difficult patients to control were the patients with diabetes and the patients undergoing lower extremity bypass.

But they did show that by increasing glucose control, patients had lower rates of, lower lengths of stay. As well as had lower overall costs. So moving along we then looked at AAA. One in six patients who had undergone endovascular repair and open repair of AAA had hyperglycemia.

And we also did not find diabetes reported or predicted for outcome. We found that infections complications were significantly higher if you had postoperative hyperglycemia. Even in endovascular surgery 1.8 times is more likely. We also found diabetes not to be a factor.

So it's obviously more complex than diabetes. Once again mortality was also associated with hyperglycemia after open AAA and endovascular AAA. And we can see again that diabetes was not really playing a role. So AAA, increased mortality is associated with postoperative hyperglycemia.

If you have an EVAR it's 8 times more likely to have mortality. The diabetes was actually somewhat protective. And postoperative hyperglycemia is associated with infectious complications and increased length of stay. There's been suggestion hyperglycemia may be associated with stroke. We looked at this information,

we basically found that the crude rates of stroke were significantly greater for patients with hyperglycemia. We then did a regression analysis to evaluate. We found that stenting actually had a risk of stroke, but hyperglycemia as well also had a higher risk of stroke on this study. And once again diabetes

was not associated. So you can see after hyperglycemia with carotid studies, actually 1 in 7 after elective carotid procedures had hyperglycemia. And they were 8 times more likely to have mortality. 1 point times 7 more likely to have a stroke. So in conclusion, this study actually showed

that you can by involving glycemic control can be managed by using a management service. So you can be improved. This is by Goodney. In conclusion, hyperglycemia is a modifiable event. Postoperative hyperglycemia is very common in vascular surgery population. Between 1 in 5 after lower extremity to 1 in 7 after

elective carotid repair. That actually diabetes was not really the main associated or driver for hyperglycemia. We associate it with infection, length of stay and mortality. And regardless of etiology it can associate with mortality and inferior outcomes. Patients undergoing vascular surgery need

to have hyperglycemic management. And this evidence suggests this may decrease infections as well as complications and mortality. Thank you very much.

- Good morning. I'd like to thank Dr. Veith and Symposium for my opportunity to speak. I have no disclosures. So the in Endovascular Surgery, there is decrease open surgical bypass. But, bypass is still required for many patients with PAD.

Autologous vein is preferred for increase patency lower infection rate. And, Traditional Open Vein Harvest does require lengthy incisions. In 1996 cardiac surgery reported Endoscopic Vein Harvest. So the early prospective randomized trial

in the cardiac literature, did report wound complications from Open Vein Harvest to be as high as 19-20%, and decreased down to 4% with Endoscopic Vein Harvest. Lopes et al, initially, reported increase risk of 12-18 month graft failure and increased three year mortality.

But, there were many small studies that show no effect on patency and decreased wound complications. So, in 2005, Endoscopic Vein Harvest was recommended as standard of care in cardiac surgical patients. So what about our field? The advantages of Open Vein Harvest,

we all know how to do it. There's no learning curve. It's performed under direct visualization. Side branches are ligated with suture and divided sharply. Long term patency of the bypass is established. Disadvantages of the Open Vein Harvest,

large wound or many skip wounds has an increased morbidity. PAD patients have an increased risk for wound complications compared to the cardiac patients as high as 22-44%. The poor healing can be due to ischemia, diabetes, renal failure, and other comorbid conditions.

These can include hematoma, dehiscense, infection, and increased length of stay. So the advantages of Endoscopic Vein Harvest, is that there's no long incisions, they can be performed via one or two small incisions. Limiting the size of an incision

decreases wound complications. It's the standard of care in cardiac surgery, and there's an overall lower morbidity. The disadvantages of is that there's a learning curve. Electro-cautery is used to divide the branches, you need longer vein compared to cardiac surgery.

There's concern about inferior primary patency, and there are variable wound complications reported. So recent PAD data, there, in 2014, a review of the Society of Vascular Surgery registry, of 5000 patients, showed that continuous Open Vein Harvest

was performed 49% of the time and a Endo Vein Harvest about 13% of the time. The primary patency was 70%, for Continuous versus just under 59% for Endoscopic, and that was significant. Endoscopic Vein Harvest was found to be an independent risk factor for a lower one year

primary patency, in the study. And, the length of stay due to wounds was not significantly different. So, systematic review of Endoscopic Vein Harvest data in the lower extremity bypass from '96 to 2013 did show that this technique may reduce

primary patency with no change in wound complications. Reasons for decreased primary patency, inexperienced operator, increased electrocautery injury to the vein. Increase in vein manipulation, you can't do the no touch technique,

like you could do with an Open Harvest. You need a longer conduit. So, I do believe there's a roll for this, in the vascular surgeon's armamentarium. I would recommend, how I use it in my practices is, I'm fairly inexperienced with Endoscopic Vein Harvest,

so I do work with the cardiac PA's. With increased percutaneous procedures, my practice has seen decreased Saphenous Vein Bypasses, so, I've less volume to master the technique. If the PA is not available, or the conduit is small, I recommend an Open Vein Harvest.

The PA can decrease the labor required during these cases. So, it's sometimes nice to have help with these long cases. Close surveillance follow up with Non-Invasive Arterial Imaging is mandatory every three months for the first year at least. Thank you.

- Thank you very much for the very kind invitation, and I promise I'll do my best to stick to time. The answer is probably to this audience I don't really need to say very much about the ATTRACT trial, but I think it is quite important to note that the ATTRACT trials have now been out for some time, and it is constantly being

talked about in its various dimensions. So I'm going to just spend a few seconds really talking about the ATTRACT trial. A large number of patients screened. One in 41 patients were actually recruited into it and it was a trial that ran for a long time.

Wasn't really with respect to the primary endpoint any particularly good evidence, but for those people who had moderate or severe post-thrombotic syndrome, it probably was of benefit. And if you looked at the Villalta score

and the VCSS scores there was some evidence to support it. So overall, probably some positive take-home messages, but not as affirmative as people would have thought. Now the reason that I've dwelled a little bit on that is that actually, what do we mean when we talk about the post-thrombotic syndrome?

Because I would say in the upper limb, because I have never personally seen an ulcer in the upper limb. Has anybody seen an ulcer in the upper limb due to venous disease? No.

So in a way we are talking about a slightly different entity. We are talking about a limb that has undoubtedly much more finer movements. And there was depression by some people with the results of the ATTRACT trial.

But when you look at the five year results from the CaVenT trial, there was some evidence to suggest that actually, as you get further out, there may be some benefit. If you look at this summation analysis, and I completely accept this is related to the leg,

again, there may be some benefit from the CDT. Now, this is a case of mine. Now I wonder if any of you can tell me how many stages may have been involved from going from the right, to having a ballonplasty in the vein. Pick a number, anywhere between five and ten.

The answer is you have numerous checks of the thrombolysis, you may have a venoplasty, you might have a first rib excision. You may then have occlusion and then realize this before you go on and do the first rib. So all I'm suggesting to you that this is not

a cheap treatment to offer patients treatment to the upper limb. Then we looked forward to some help from the guidelines. Well we look at the American guidelines and give or take, I think the answer is we probably shouldn't be doing it and that we should be only offering anticoagulation.

So do the Brits help? Well actually if you look at the Brits, it sort of says well, you can think a bit about doing decompression, but really if I was standing up in a court of law, I really wouldn't want much support from this guideline

that I had done the right thing. And then the International Society of Thrombolysis and Hemostasis really says well, you can do a little bit of this that thoracic outlet syndrome may be a risk factor. But give or take, surgeries still are a little bit dubious.

So, really there's one good review out there, and this is the review of Vasquez that basically looked at 146 articles, and they found some data on just under 1300 patients. And they postulated and chose some evidence to suggest that there was some evidence

that first rib excision and thrombolysis reduce PTS, and that anticoagulation alone was not enough for the majority of the patients. Very difficult to work out how you selected which patients you should or should not intervene on. Now, I'm sure everybody is rather sick and tired

of me talking about money, and I accept it doesn't really apply here. But money is actually quite important. Five interventions to prevent something that may not happen and at worst may be just a few collateral veins across the chest.

So ladies and gentlemen, I would want you to think very hard, is it actually cost-effective to be offering all patients presenting with an early auxiliary vein thrombosis thrombolysis, and then subsequently first rib excision? These are some of the truths, I think the answer is

it does seem to work. You do need to recognize and make the diagnosis. Usually delayed thrombolysis doesn't work, but there are lots of questions that are unanswered. And how would you defend what you have done in a court of law?

Somebody has a stroke, you then do the first rib, they get a large hemothorax, and they then die because there had been too much TPA on board. Yes, give it some thought. So ladies and gentlemen, I'm afraid I haven't actually answered the question,

but I think you need to give it careful consideration, what are the indications and merits? Thank you very much.

- Afternoon. It's a privilege to be presenting this today. I have no disclosures. If you look at this, this is a picture of the last 10 IVC filters approved by the FDA. You'll notice that they all have some mechanism of removal most commonly hooks.

You may ask yourself, why is that? And the reason for this is basically one or two studies. Basically the PREPIC study which was originally published in 1998 with two-year data, followed by a publication in Circulation with eight-year data.

Now the PREPIC itself, the study itself was the first prospective, randomized trial comparing anticoagulation to IVC filters. It was performed from 1991 to 1995 in France. 400 patients with DVT that were considered at risk for PE were enrolled.

And they were randomized at first either unfractionated versus fractionated heparins, and then IVC filter versus no IVC filter. And the filters used are demonstrated here, the Greenfield, the Cardinal, LGM, and Bird's Nest. And all patients were anticoagulated with warfarin

at the time of discharge whenever possible. Primary outcome was pulmonary embolism. The secondary outcomes were DVT, death, major filter complications, and major bleeding. And again, the data was published at two and eight years. So the two-year results, the PREPIC study,

they presented first some data on unfractionated versus fractionated heparin, but then this table. And this table shows basically that there was no difference in symptomatic PE between groups. But there was a difference in recurrent DVT

with patients having a filter in place having a higher incidence of DVT than those that did not. And the thought was that this presence of the filter increased the risk of DVT. Now the data at eight years, published in Circulation, did show a difference between symptomatic pulmonary embolism

with patients having a filter having a lower incidence of recurrent PE. However, the symptomatic DVT remained elevated in patients that had filters in place. And this was statistically significant. Of note, there was a fairly significant number of patients

that had cable thrombosis in the group that had filters that may have contributed to this number. So if you want to be critical about the study, there are a few things that are a little bit unperfect I guess you could say. It's now thought as a study of filter randomization

in patients with DVT, but it was actually also a study looking at unfractionated and low molecular weight heparins. And this lends itself to be a fairly weak study designed to make conclusions on IVC filters, the performance of IVC filters, and it's underpowered really to make a definitive conclusion.

The other problem with this study is that there's a wide variety of filters, I mean a Bird's Nest and the Greenfield, they're very different filters. And that lack of standardization I think is problematic. These filters both can have different rates

of IVC thrombosis, which can affect the data. So the statistical analysis was less than perfect. They should have corrected for multiple comparisons which they did not. And it also showed that PE can occur remotely, and if you don't have a filter in place,

it's probably not protective, obviously. So a PREPIC study was recently published, the PREPIC 2 in 2015. And this asks the question, do patients with acute PE at high risk of recurrence benefit from IVC filter in addition to anticoagulation?

So it was a multicenter trial in France. They had about 400 patients that were randomized, half into filters, half into no filters. Their risk factors are listed, and they're quite broad. And all filters were removed at three months. And they had follow up at three and six months.

And this is the data. The data at three months shows that there was no difference in recurrent PE between the patients with filters and the patient without filters. And at six months this remained the same. And there was no difference in DVT

between groups at six months. So fact or fiction? Well I think the PREPIC studies are mostly fact with maybe a little bit of fiction thrown in. The data from PREPIC suggests that patients with IVC filters have an increased risk of DVT long term,

but a decreased risk of PE long term. PREPIC 2 suggests that IVC filters may not decrease the risk of PE in high-risk patients, and did not show an association between filters and recurrent DVT at six and three months. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Good morning. Thank you for the opportunity to speak. So thirty day mortality following unselected non-cardiac surgery in patients 45 years and older has been reported to be as high as 1.9%. And in such patients we know that postoperative troponin elevation has

a very strong correlation with 30-day mortality. Considering that there are millions of major surgical procedures performed, it's clear that this equates to a significant health problem. And therefore, the accurate identification of patients at risk of complications

and morbidity offers many advantages. First, both the patient and the physician can perform an appropriate risk-benefit analysis based on the expected surgical benefit in relation to surgical risk. And surgery can then be declined,

deferred, or modified to maximize the patient's benefit. Secondly, pre-operative identification of high-risk patients allows physicians to direct their efforts towards those who might really benefit from additional interventions. And finally, postoperative management,

monitoring and potential therapies can be individualized according to predicted risk. So there's a lot of data on this and I'll try to go through the data on predictive biomarkers in different groups of vascular surgery patients. This study published in the "American Heart Journal"

in 2018 measured troponin levels in a prospective blinded fashion in 1000 patients undergoing non-cardiac surgery. Major cardiac complications occurred overall in 11% but in 24% of the patients who were having vascular surgery procedures.

You can see here that among vascular surgery patients there was a really high prevalence of elevated troponin levels preoperatively. And again, if you look here at the morbidity in vascular surgery patients 24% had major cardiac complications,

the majority of these were myocardial infarctions. Among patients undergoing vascular surgery, preoperative troponin elevation was an independent predictor of cardiac complications with an odds ratio of 1.5, and there was an increased accuracy of this parameter

in vascular surgery as opposed to non-vascular surgery patients. So what about patients undergoing open vascular surgery procedures? This is a prospective study of 455 patients and elevated preoperative troponin level

and a perioperative increase were both independently associated with MACE. You can see here these patients were undergoing a variety of open procedures including aortic, carotid, and peripheral arterial. And you can see here that in any way you look at this,

both the preoperative troponin, the postoperative troponin, the absolute change, and the relative change were all highly associated with MACE. You could add the troponin levels to the RCRI a clinical risk stratification tool and know that this increased the accuracy.

And this is additionally shown here in these receiver operator curves. So this study concluded that a combination of the RCRI with troponin levels can improve the predictive accuracy and therefore allow for better patient management.

This doesn't just happen in open-vascular surgery patients. This is a study that studied troponin levels in acute limb ischaemia patients undergoing endovascular therapy. 254 patients all treated with endovascular intervention

with a 3.9% mortality and a 5.1% amputation rate. Patients who died or required amputation more frequently presented with elevated troponin levels. And the relationship between troponin and worse in-hospital outcome remains significant even when controlling for other factors.

In-hospital death or amputation again and amputation free survival were highly correlated with preoperative troponin levels. You can see here 16.9% in patients with elevated troponins versus 6% in others. And the cardiac troponin level

had a high hazard ratio for predicting worse in-hospital outcomes. This is a study of troponins just in CLI patients with a similar design the measurement of troponin on admission again was a significant independent predictor

of survival with a hazard ratio of 4.2. You can see here that the majority of deaths that did occur were in fact cardiac, and troponin levels correlated highly with both cardiac specific and all-cause mortality. The value of the troponin test was maintained

even when controlling for other risk factors. And these authors felt that the realistic awareness of likely long term prognosis of vascular surgery patients is invaluable when planning suitability for either surgical or endovascular intervention.

And finally, we even have data on the value of preoperative troponin in patients undergoing major amputation. This was a study in which 10 of 44 patients had a non-fatal MI or died from a cardiac cause following amputation.

A rise in the preoperative troponin level was associated with a very poor outcome and was the only significant predictor of postoperative cardiac events. As you can see in this slide. This clearly may be a "Pandora's box".

We really don't know who should have preoperative troponins. What is the cost effectiveness in screening everybody? And in patients with elevated troponin levels, what exactly do we do? Do we cancel surgery, defer it, or change our plan?

However, certainly as vascular surgeons with our high-risk patient population we believe in risk stratification tools. And the RCRI is routinely used as a clinical risk stratification tool. Adding preoperative troponin levels to the RCRI

clearly increases its accuracy in the prediction of patients who will have perioperative cardiac morbidity or mortality. And you can see here that the preoperative troponin level had one of the highest independent hazard ratios at 5.4. Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Narrator] Okay, very interesting hypothesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you, Larry, thank you, Tony. Nice to be known as a fixture. I have no relevant disclosures, except that I have a trophy. And that's important, but also that Prabir Roy-Chaudhury, who's in this picture, was the genesis of some of the thoughts that I'm going to deliver here about predicting renal failure,

so I do want to credit him with bringing that to the vascular access space. You know, following on Soren's talk about access guidelines, we're dealing with pretty old guidelines, but if you look at the 2006 version, you know, just the height--

The things that a surgeon might read in his office. CKD four, patients there, you want a timely referral, you want them evaluated for placement of permanent access. The term "if necessary" is included in those guidelines, that's sometimes forgotten about.

And, of course, veins should be protected. We already heard a little bit about that, and so out our hospital, with our new dialysis patients, we usually try to butcher both antecubital veins at the same time. And then, before we send them to surgery

after they've been vein-marked, we use that vein to put in their preoperative IV, so that's our vascular access management program at Christiana Care. - [Male Speaker] That's why we mark it for you, Teddy. (laughing)

- So, you know, the other guideline is patients should have a functional permanent access at the initiation of dialysis therapy, and that means we need a crystal ball. How do we know this? A fistula should be placed at least six months

before anticipated start of dialysis, or a graft three to six weeks. Anybody who tells you they actually know that is lying, you can't tell, there's no validated means of predicting this. You hear clinical judgment, you can look at

all sorts of things. You cannot really make that projection. Now there is one interesting study by Tangri, and this is what Premier brought to our attention last year at CIDA, where this Canadian researcher and his team developed a model for predicting

progression of chronic kidney disease, not specifically for access purposes, but for others. They looked at a large number of patients in Canada, followed them through chronic kidney disease to ESRD, and they came up with a model. If you look at a simple model that uses age, sex,

estimated GFR from MDRD equation and albuminuria to predict when that patient might develop end stage renal disease, and there's now nice calculators. This is a wonderful thing, I keep it on my phone, this Qx Calculate, I would recommend you do the same,

and you can put those answers to the questions, in this app, and it'll give you the answer you're looking for. So for instance, here's a case, a 75-year-old woman, CKD stage four, her creatinine's 2.7, not very impressive,

eGFR's 18. Her urine protein is 1200 milligrams per gram, that's important, this is kind of one of the major variables that impacts on this. So she's referred appropriately at that stage to a surgeon for arteriovenous access,

and he finds that she really has no veins that he feels are suitable for a fistula, so an appropriate referral was made. Now at that time, if you'd put her into this equation with those variables, 1200, female, 75-year-old, 18 GFR, at two years, her risk of ESRD is about 30%,

and at five years about 66%, 67%. So, you know, how do you use those numbers in deciding if she needs an access? Well, you might say... A rational person might say perhaps that patient should get a fistula,

or at least be put in line for it. Well, this well-intentioned surgeon providing customer service put in a graft, which then ended up with some steal requiring a DRIL, which then still had steal, required banding, and then a few months, a year later

was thrombosed and abandoned because she didn't need it. And I saw her for the first time in October 2018, at which time her creatinine is up to 3.6, her eGFR's down to 12, her protein is a little higher, 2600, so now she has a two-year risk of 62%, and a five-year risk of 95%,

considerably more than when this ill-advised craft was created. So what do you do with this patient now? I don't have the answer to that, but you can use this information at least to help flavor your thought process,

and what if you could bend the curve? What if you treated this patient appropriately with ACE inhibitors and other methods to get the protein down? Well, you can almost half her two-year risk of renal failure with medical management.

So these considerations I think are important to the team, surgeon, nurses, nephrologists, etc., who are planning that vascular access with the patient. When to do and what to do. And then, you know, it's kind of old-fashioned to look at the trajectory.

We used to look at one over creatinine, we can look at eGFR now, and she's on a trajectory that looks suspicious for progression, so you can factor that into your thought process as well. And then I think this is the other very important concept, I think I've spoken about this here before,

is that there's no absolute need for dialysis unless you do bilateral nephrectomies. Patients can be managed medically for quite a while, and the manifestations of uremia dealt with quite safely and effectively, and you can see that over the years, the number of patients

in this top brown pattern that have been started on dialysis with a GFR of greater than 15 has fallen, or at least, stopped rising because we've recognized that there's no advantage, and there may be disadvantages to starting patients too early.

So if your nephrologist is telling I've got to start this patient now because he or she needs dialysis, unless they had bilateral nephrectomies that may or may not be true. Another case,

64-year-old male, CKD stage four, creatinine about four, eGFR 15, 800 milligrams of proteinuria, referred to a vascular access surgeon for AV access. Interesting note, previous central lines, or AICD, healthy guy otherwise.

So in April 2017 he had a left wrist fistula done, I think that was a very appropriate referral and a very appropriate operation by this surgeon. At that time his two-year risk was 49, 50%, his five-year risk 88%. It's a pretty good idea, I think, to get a wrist fistula

in that patient. Once again, this is not validated for that purpose. I can't point you to a study that says by using this you can make well-informed predictions about when to do vascular access, but I do think it helps to flavor the judgment on this.

Also, I saw him for the first time last month, and his left arm is like this. Amazing, that has never had a catheter or anything, so I did his central venogram, and this is his anatomy. I could find absolutely no evidence of a connection between the left subclavian and the superior vena cava,

I couldn't cross it. Incidentally, this was done with less than 20 CCs of dye of trying to open this occlusion or find a way through, which was unsuccessful. You can see all the edema in his arm. So what do you do with this guy now?

Well, up, go back. Here's his trajectory of CKD four from the time his fistula is done to the time I'm seeing him now, he's been pretty flat. And his proteinuria's actually dropped

with medical management. He's only got 103 milligrams per gram of proteinuria now, and his two-year risk is now 23%, his five-year risk is 56%, so I said back to the surgeon we ligate this damn thing, because we can't really do much to fix it,

and we're going to wait and see when it's closer to time to needing dialysis. I'm not going to subject this guy to a right-arm fistula with that trajectory of renal disease over the past two years. So combining that trajectory with these predictive numbers,

and improved medical care for proteinuria I think is a good strategy. So what do you do, you're weighing factors for timing too early, you've got a burden of fistula failure, interventions you need to use to maintain costs, morbidity, complications,

steal, neuropathy that you could avoid versus too late and disadvantages of initiating hemodialysis without a permanent access. And lastly, I'm going to just finish with some blasphemy. I think the risk of starting dialysis with a catheter is vastly overstated.

If you look at old data and patient selection issues, and catheter maintenance issues, I think... It's not such an unreasonable thing to start a patient with a catheter. We do it all the time and they usually live.

And even CMS gives us a 90-day grace period on our QIP penalties, so... If you establish a surgeon and access plan, I think you're good to go. So who monitors access maturation? I don't know, somebody who knows what they're doing.

If you look at all the people involved, I know some of these individuals who are absolute crackerjack experts, and some are clueless. It has nothing to do with their age, their gender, their training, their field. It's just a matter of whether they understand

what makes a good fistula. You don't have to be a genius, you just can't be clueless. This is not a mature usable fistula, I know that when I see it. Thank you.

- Great, thank-you very much, a pleasure to be here. My disclosures. So, we've talked a little bit about obviously percutaneous and thrombectomy techniques. Obviously we have catheter-directed thrombolysis with TPA, but what happens when we can't use TPA

mechanical techniques? We've discussed several of them already in this session, I'm going to try to kind of bring them together and note the differences and how they evolved. And really look at fragmentation, rheolytic therapy, vacuum assisted devices, and vacuum and suction devices.

So when do we need these? Patients that can't tolerate thrombolysis, can't get TPA, that have a high risk of TPA, or maybe there is a situation we need a rapid response. We're trying to create flow and establish flow as much as possible and a lot of times we use this

in combination therapy if we've already hurt. What's the ideal device? I think there are multiple different characteristic's that could define the ideal device. Obviously we want it simple to use, We want it to be reproducible,

we want it to remove a lot of thrombus, but minimize blood loss and trauma to the vessels and to the blood cell. These are just some of them. There's a lot of mechanical thrombectomy devices right now on the market continuing to grow,

both in the arterial and venous system so I think this is going to be an evolution. We started really using mechanical fragmentation with a pig tail and spinning a pig tail. We used that. A lot of times the patient with severe massive pulmonary embolism.

These we're really small antidotes, small case reports. Will Kuo, looked at these in the 2009 and basically saw over all clinical success, about 86% using these mechanical devices. Then we had some that were even more automated.

All these did was break up the clot. So you have the Trerotola Device , Cleaner Device, really almost in the dialysis space. Rheolytic Throbectomy, we've already heard about. Some of how it works and the advantages. Really I think this is the first time we've saw

a system which would try to aspirate and remove some of that thrombus as it got broken up. The PEARL registry really showed for the first time, maybe we can get this done within 24 hours, can we get this done in one session? Unfortunately in this registry only about three or

four percent of patients actually had just rheolytic therapy alone without any TPA. We've discussed a little bit about the use of Ango and this type of device in terms of bradyarrhythmia's and that may be a limitation. But I think we can still use it particularly

outside of the chest. So What about suction devices? You can have a catheter, I think a catheter suction device is very limited. We use that in the arterial tree when there is a small thrombus, a small embolus, I think

we're very limited, not only in the amount of thrombus we can remove but the amount of suction we can apply. Other types like almost mechanical, very simple to use systems is the aspire device. Well you can basically create and suction a

limited area and then help you aspirate the thrombus. And then to the other extreme. We're going to hear my next speaker talk about Angiovac, again a different system, a different system requires a patient on bypass large 26 french devices.

Where we can actually go in and deal with a large amount of thrombus, like this patient had a thrombus cave on both iliac veins. And to be able to basically come with this vacuum aspiration system over wires and kind of pulling them out and you get these little canisters,

seeing what you've actually removed. Very gratifying. But takes a lot of work to get it going. We've heard a little bit about vacuum assisted with the Indigo system. With a system of creating a constant continuous vacuum.

We now have eight french catheters with incredible aspiration volume, almost 20cc's, I'm sorry you can get up to 140cc's of thrombus in a minute can be aspirated quickly. Here is a patient, 80 years old, colorectal CA. You can see the thrombus in the right leg.

There was actually a mass invading this vein. That is where we wanted to use thrombolysis, really went a head and you can see the amount of thrombus. Cleared this out with some passage. You can see this here, the separator. You started seeing thrombus especially when

its acute it kind of looks like this. It's kind of gelatinous, things that we've already seen, and then went ahead and placed a stent, dilated that stent. Had to clean up some more with the device

on top of the stent, but with a good result without needing any TPA. Other types of extraction devices we've seen the Inari device, again this is like a stent Triever device, a nitinol ring we can use this in the pulmonary arteries.

And we've already seen previous and talked about the ClotTriever device Again remove that thrombus, put it into a bag and remove it. So again, capture and removal of thrombus. And this is a solution without the need of TPA. New kid in the block the JETi device

Again very similar to aspiration Indego device, but at the same time it has a jet to macerate the clot and kind of break up the clot a little to smaller areas so we can able to thromb and take more out. I think really here what I've seen and Dr. Razavi

showed me this case. Being able to treat a patient quickly, treat that patient very quickly you can see the amount of thrombus being able to, within about an hour and 15 minutes, get all that thrombus, then create patency in that vein and he showed

some early initial good data. Over the last year we did have a paper that was presented here and published this year in the Journal of Vascular Surgery, venous and lymphatic disorders and again pulled multiple patient's, again showing that

it affective and safe. We still need better data. We need to figure out which patients are best treated with which devices and which again will be affective. Thank-you very much.

- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update

about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures

and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.

So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy

and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.

As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura

off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image

of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures

including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut

because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein

are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,

I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.

23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,

first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious

about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,

and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases

of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged

on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required

in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.

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