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Liver Cirrhosis, Chronic Pancreatitis | Splenic Embolization | Male
Liver Cirrhosis, Chronic Pancreatitis | Splenic Embolization | Male
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Is Drug Neuroprotection After Thrombectomy For Acute Stroke Or Other Ischemic Cerebral Insults Feasible: Future Prospects
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Challenges And Solutions In Complex Dialysis Access Cases
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How Should Lipids And Medical Therapy Be Managed In CTLI Patients And Those Undergoing Interventions For PAD
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Cloud Based System For Image Fusion Techniques With Mobile C-Arms (The Cydar System): How Does It Work And Advantages For All Vascular Interventions
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New Developments In Access Site Closure For Small Sheaths; For Large Sheaths
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Technical Issues And Experience With MIS2ACE In 50 Patients Undergoing Endo TAAA Repair
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How Accurate Is Ulcer Healing Assessment And What Happens When We Are Wrong
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Current Management Of Bleeding Hemodialysis Fistulas: Can The Fistula Be Salvaged
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Continued Tobacco Use Is Bad For PAD Patients But Does Not Negatively Affect Outcomes Of Endo Treatments For Intermittent Claudication
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Vacuum Assisted Thrombectomy With The Penumbra Indigo System For Visceral And Lower Limb Artery Occlusions
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Pitfalls Of Percutaneous EVAR (PEVAR) And How To Avoid Them
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The Impact Of Distal Drug Migration On Wound Healing After PTAs With DCBs: A Model To Measure Drug Levels In Tissues
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Below-The-Elbow Angioplasty For CLTI Of The Hand: Indications, Techniques Results
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Value Of Troponin Measurements Before All Vascular Procedures - Open Or Endo
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Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
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Value Of CO2 DSA For Abdominal And Pelvic Trauma: Why And How To Use CO2 Angiography With Massive Bleeding And When To Supplement It With Iodinated Contrast
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Status Of Dual Layer Stents For CAS: Is Acute Occlusion An Issue And How To Avoid It
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How To Use Hybrid Operating Rooms Optimally Beyond Vascular Procedures: How The Availability Of Mobile C-Arms Can Help
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Bailout Rescue Procedures When CEA Is Failing In A Critical Unstable Patient: ICA Stent Or Gore Hybrid Graft Or Standard PTFE Bypass: Indications For Each
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Overview Of Sclerotherapy Liquid Embolic Agents: A World In Endovascular Confusion And Chaos
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Thrombo-Embolic Complications Of Inflammatory Bowel Disease: Nature, Etiology And Significance
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Right Axillary Access For Complex EVARs And TEVARs: Advantages, Technical Tips And Preventing Strokes
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Imaging Tools To Increase The Safety/Accuracy Of Endovascular Procedures And Reduce Radiation And Contrast Media
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A New System For Treating Prosthetic Arterial And Aortic Graft Infections
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Transcript

and this is kind of a diagnostic dilemma if you will. This guy has the TIPS, he's a chronic pancreatitis patient

who developed cirrhosis, biliary cirrhosis as a result of it. Also an alcoholic who developed cirrhosis in this context, huge spleen has the TIPS, referred for encephalopathy. What are you going to do about that?

He has varices, he's at risk of bleeding, do you reduce the TIPS or what do you do? And so in this case we decided what we would do is actually reduce his spleen because by reducing the spleen you actually increase hepatic arterial inflow,

decrease portal vein inflow both of those things which make his risk of bleeding go down and make his encephalopathy go down. And actually in the studies that have looked at encephalopathy specifically it's durable in encephalopathy relief out to two years. So that's as far as any of them have follow up.

But it's actually durable to two years and this guy also had HIV, I forgot about that but pancreatitis was his initial presentation. And so anyway one of my partners actually embolized this patient this wasn't me and he does it a little different than I do he used gelfoam pledgets through a 4Fr catheter,

so we got a 4Fr cobra out there and then puts in some pledgets, does a real nice angiogram puts in some more pledgets, does a real nice angiogram. And then because he had liver disease this patient couldn't get my high dose steroids, I did

manage to talk him into two weeks of antibiotics and steroid taper and this is sort of what it looked like during the procedure. And then this gentleman comes back three days after discharge complaining of terrible pain, no eye count, no fever and they did a non con CT just to see where things looked at,

cuz we are just on a procedure and you see this on his non contrast CT. There's actually air in the spleen and the question is, is this a problem? Should I be worried about this?

And the answer is you can be it depends on if they have a white count, it depends on if they have any infection symptoms because actually in the vast majority cases this doesn't matter. This actually has also been studied in the Japaneses literature where they demonstrated that only 18% of the time when you see gas in the spleen after doing a splenic embo,

does it have any clinical significance at all. It's very much like a uterine artery embolization, where you can get nitrogen that actually comes out of the tissue as it neccrosis, and you end up seeing gas in the uterus and people freak out. When it really doesn't mean anything unless it's in the setting of actual

infectous symptoms. So, it's nice to know that because we talked our hepatologist and assured them that this was not a problem, and settle down, and he'd be fine. And he actually did do fine.

So, seven months later this is what he looked like. He's encephalopathy had improved, his platelets were up to 63 and pretty big spleen cell and his red blood cell count was up to 4.1. And it was 1 when he underwent the procedure, actually in his case

that probably is as important as anything else given his HIV.

- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old

but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,

and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.

- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,

and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was

revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.

In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat

was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.

Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone

returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.

Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy

with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,

the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.

Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.

So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really

how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017

in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.

Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at

five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery

to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional

independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.

So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,

but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could

help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.

- I 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 Dr. Sidawy and Dr. Marin. Good morning everyone. These are my disclosures. None of which is germane to this presentation. So the clinical imperative is quite obvious, in terms of the poor longterm survival of patients with symptomatic Peripheral Artery Disease,

particularly in patients with critical limb ischemia. And it is incumbent upon us to try and do something to modify our patients risk. The ACC/AHA guidelines for PAD recommend four specific therapies with a class I recommendation for aspirin, statin medications and smoking cessation,

and a IIa recommendation for ACE inhibitors. The question is does this really make a difference in terms of our patients outcomes, if we follow these guidelines? That's a question that Ehrin (mumbles) Armstrong and I addressed with our UC Davis PAD registry.

We published our result a few years ago. We looked at 739 patients with symptomatic PAD, 56% of which had critical limb ischemia. And we looked at outcomes for those patients that received all four guidelines recommended therapy, compared to those that did not.

And we saw in fact, that it did make a difference. There was a 36% reduction in MACE and a 45% reduction in MALE, in those patients who received all four of the specifically recommended therapies. Now I'm going to focus primarily on lipid lowering therapy

and it's role in patients with symptomatic PAD, particularly the CLI patient population. We've seen from the REACH registry, a very large registry of over 60,000 patients. Lookin' at specifically at patients with symptomatic PAD treated with statins over a four year time period.

There was a beneficial effect on limb vascular events, with a reduction in the need for peripheral revascularization procedures. And a reduction in the need for major amputation. But many of the trials that have looked

at statin use in PAD, have looked basically at patients with asymptomatic PAD or mildly symptomatic PAD. What about patients with severely symptomatic PAD or critical limb ischemia? Well, this is a publication from

the Prevent Three Cohort looking at patients with critical limb ischemia undergoing lower extremity bypass, 636 patients with CLI, 45% which were treated with statins, in only one year we saw a reduction in survival, or excuse me, a reduction in mortality,

with a survival advantage of 86% versus 81% in those patients treated with statin therapy. What about patients with critical ischemia, undergoing endovascular therapies? Well, this is from a group here in New York, looking a similar Cohort, 646 patients,

a little less than 50% of which were treated with statins, again, there was a significant benefit with regards to both limb outcomes, as well as overall survival at two years. We looked at our own patient population at UC Davis, again, patients with critical limb ischemia.

Now, 380 patients, 65% of which were prescribed a statin at baseline. There was some improvement over time, or some uptake in statin use over time but, the difference was not statistically significant. And, again, we showed a reduction

in major adverse cardiovascular events with the use of statins over a one year time period. And, very interestingly, the group that seemed to do the worse, in our experience, were patients with LDL levels of greater than 130. This is hot off the press.

These are the 2018 Guideline on the Management of Blood Cholesterol from ACC and HA and a variety of other societies. A hundred and twenty one pages for your reading pleasure. Very important to note that within these Guidelines patients

with symptomatic Peripheral Artery Disease were considered a very high risk group, on the same level as patients with recent ACS, history of MI, or of a history of ischemic stroke. And, it is recommended that these patients have aggressive lipid lowering therapy.

These are the recommendations with the class of recommendation and the level of evidence. You're used to seeing these types of documents. But, to summarize, in these new guidelines, if you see a patient with symptomatic PAD,

whose less than 75 years of age, you should initiate high intensity statin therapy. Atorva 40 milligrams or 80 milligrams, or Resuvastatin 20 milligrams or 40 milligrams. And if the LDL remains above 70 on that maximally tolerated therapy

then it's reasonable to add Ezetimibe 10 milligrams a day. And, if they're still above 70 milligrams per deciliter on maximally tolerated LDL lowering therapy then, it is reasonable to add a PCSK9 inhibitor, after a discussion about net benefits, safety and cost.

This is a recent publication of FOURIER Trial lookin' at a PCSK9 inhibitor in patients with Peripheral Artery Disease. In this study 3,642 patients were included. And, it was shown that the PCSK9 inhibitor reduced the primary end point

and reduced major adverse limb events, with a remarkable reduction in LDL cholesterol, with a background of statin therapy, with a median LDL level after the PCSK9 inhibitor of 31 milligrams per deciliter. There was a 3.5% absolute risk reduction

with regards to the primary endpoint, as well as the hard endpoints of stroke, death or MI. Almost double the benefit that was seen in non PAD patients. The obvious question though, is whether we can afford this?

This is from these recent 2018 Guidelines showing that at mid 2018 list prices PCSK9 inhibitors have a low cost value over $150,000.00 per quality of life adjusted years compared to a good cost value of less than $50,000.00. So, in some way good medical therapy

does make a difference. Adherence to guidelines does make a difference. And, I think if we're going to take care of our patients in the best way possible, we want to lower their LDL as much as possible.

Thank you very much 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

and improve clinical outcomes. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you, good morning everybody. Thank you for the kind invitation, Professor Veith, it's an honor for me to be here again this year in New York. I will concentrate my talk about the technical issues and the experience in the data we have already published about the MISACE in more than 50 patients.

So I have no disclosure regarded to this topic. As you already heard, the MISACE means the occlusion of the main stem of several segmental arteries to preserve the capability of the collateral network to build new arteries. And as a result, we developed

the ischemic preconditioning of the spinal cord. Why is this so useful? Because it's an entirely endovascular first stage of a staged approach to treat thoracoabdominal aortic aneurysm in order to reduce the ischemic spinal cord injury.

How do you perform the MISACE? Basically, we perform the procedure in local anesthesia, through a percutaneous trans-femoral access using a small-bore sheath. The patient is awake, that means has no cerebrospinal fluid damage

so we can monitor the patient's neurological for at least 48 hours after the procedure. So, after the puncture of the common femoral artery, using a technique of "tower of power" in order to cannulate the segmental arteries. As you can see here, we started with a guiding catheter,

then we place a diagnosis catheter and inside, a microcatheter that is placed inside the segmental artery. Then we started occlusion of the ostial segment of the segmental artery. We use coils or vascular plugs.

We don't recommend the use of fluids due to the possible distal embolization and the consequences. Since we have started this procedure, we have gained a lot of experience and we have started to ask,

what is a sufficient coilembolization? As you can see here, this artery, we can see densely packed coils inside, but you can see still blood flowing after the coil. So, was it always occluding, or is it spontaneous revascularization?

That, we do not know yet. The question, is it flow reduction enough to have a ischemic precondition of the spinal cord? Another example here, you can see a densely packed coil in the segmental artery at the thoracic level. There are some other published data

with some coils in the segm the question is, which technique should we use, the first one, the second one? Another question, is which kind of coil to use? For the moment, we can only use the standard coils

in our center, but I think if we have 3-D or volume coils or if you have microvascular plugs that are very compatible with the microcatheter, we have a superior packing density, we can achieve a better occlusion of the segmental artery, and we have less procedure time and radiation time,

but we have to think of the cost. We recommend to start embolization of the segmental artery, of course, at the origin of it, and not too far inside. Here, you can see a patient where we have coiled a segmental artery very shortly after the ostium,

but you can see here also the development of the collaterals just shortly before the coils, leading to the perfusion of segmental artery that was above it. As you can see, we still have a lot of open question. Is it every patent segmental artery

a necessary to coil? Should we coil only the large ones? I show you an example here, you can see this segmental artery with a high-grade stenotic twisted ostium due to aortic enlargement.

I can show you this segmental artery, six weeks after coiling of a segmental artery lower, and you can see that the ostium, it's no more stenotic and you can see also the connection between the segmental artery below to the initial segmental artery.

Another question that we have, at which level should we start the MISACE? Here, can see a patient with a post-dissection aneurysm after pedicle technique, so these are all uncovered dissection stent, and you can see very nicely the anterior spinal artery

feeded by the anterior radiculomedullary artery from the segmental artery. So, in this patient, in fact, we start the coiling exactly at the seat of this level, we start to coil the segmental artery that feeds the anterior spinal artery.

So, normally we find this artery of the Th 9 L1, and you can see here we go upwards and downwards. We have some challenges with aneurysm sac enlargement, in this case, we use this technique to open the angle of the catheter, we can use also deflectable steerable sheath

in order to reach the segmental artery. And you can see here our results, again, I just will go fast through those, we have treated 57 patients, most of them were Type II, Type III aortic aneurysms. We have found in median nine patent segmental artery

at the level of the aorta to be treated, between 2 and 26, and we have coiled in multiple sessions with a mean interval of 60 days between the sessions. No sooner than seven days we perform the complete exclusion of the aneurysm

in order to let the collateral to develop, and you can see our result: at 30 days we had no spinal cord ischemia. So I can conclude that our first experience suggest that MISACE is feasible, safe, and effective, but segmental artery coiling in thoracoabdominal aneurysm

can be challenging, it's a new field with many open questions, and I looking forward for the results with PAPA_ARTiS study. Thank you a lot.

- Yeah, I am not Mehdi Shishehbor. If you are here to listen to him talk, I'm sorry to disappoint you. He's stuck in Cleveland in the weather. So this is my disclosure. There are several companies, but it's uncompensated consulting.

So, when you look at all the guidelines that are out there, most of the guidelines do recommend ankle brachial index as the central point in terms of management of critical limb ischemia patients, this is the ACC/AHA guidelines from 2016. And the same thing PARC,

Peripheral Academic Research Consortium also talks about using ankle brachial indices in the management of critical limb ischemias. So Mehdi gives this example of a 82 yr old patient of his who came in with a Charcot joint and mid-foot ulceration. The ABI was in the .56 range,

so he takes her to the cath lab and finds SFA disease, PT is occluded. He gets the inflow improved, the anterior tibial also looks better, and the ankle brachial indices are now normalized to 1.12, and even the metatarsal and the digit PPGs are improved.

So he tells the patient to go home and rest, and the wound care is instituted. And the mid-foot ulceration heals, but when the patient comes back there is a heel ulceration, because the patient has been asked to take it easy, and with the non-vascular position,

which is above the level of the heart, or at the level of the heart rather than being down. Now she has sort of a pressure and ischemic ulceration on the heel, despite normal ABIs. So Mehdi goes in and do retro grade pedal axis and gets into the origin, revascularizes the arch,

and gets the PT opened up, and the DP opened up, and has a good arch, complete arch now, as you can see good result, and with good wound healing at 16 weeks it shows improvement and 21 weeks much more better looking, almost healed ulceration with some callous over that.

So the point of this is the clinical examination of the patient and continued follow up closely is very important and not just depend on ABIs. To further this thought, Mehdi looked at the Cleveland Clinic Data and 29% of patients with critical limb ischemia were noted to have, in fact,

ABIs that were almost normal. And then, the IN.PACT DEEP data, which you look at about 350 patients, all CLI patients, they looked at the hemodynamic parameters to diagnose critical limb ischemia. This was one of the trials that sort of lead to

removing ankle brachial index requirement in the critical limb ischemia below knee trials, as well. What they showed is, even though all these patients have critical limb ischemia, upwards of 28% actually had normal ABI and several had ABI greater than 1.4 And remember, all these are critical limb ischemia patients.

So probably ABI's not a good measure to assess critical limb ischemia. Similarly, the Michigan group, the Blue Cross Blue Shield group looked at 4,391 patients with CLI, and only 60% actually had mild to moderate disease,

and 14 had severe disease, and when you look at the number of patients that had normal ABIs, that was a quarter of them. So a quarter of CLI patients have normal ABIs. The other disturbing fact is that, when you look at noncompressible ABIs,

majority, up to 80% of these patients could potentially, especially the posterior tibial artery, could be upwards of 80% occlusion. So basically, if you get noncompressible vessels you could be looking at having a potential occlusion of the below knee vessel.

So in summary, about 30% of patients with CLI will have normal ABIs, or noncompressible ABIs. If they have noncompressible ABIs, upwards of 80% will have potential occlusion of severe stenosis. So at this time, in the absence of better profusion, tissue profusion imaging,

angiogram is probably the best way to assess. We need to consider TBI, pulse volume recordings, in the patients with Rutherford five and six. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- So PAD affects five million adults in the United States today, and we know the US population is aging. And 15 to 20% of folks 70 years and older have claudication, a minority of these progress to CLI, and the impact on lifestyle is often minimized, as demonstrated in decreased quality of life scores

in these patients. Now with active tobacco use, there is acceleration of disease towards claudication, and there are higher rates of amputation, MI, and death. But prior to open or endo intervention, the SVS Guidelines recommend supervised exercise,

medical therapy with statins, beta blockers, antiantiplatelets, and Cilostazol, and an aggressive multidisciplinary approach to smoking cessation, which should last no less than six months. But what if a patient can't stop smoking?

We've all had these patients. Should patients with lifestyle limiting claudication be denied open surgical or endo-revascularization? So let's look at the open literature. A meta-analysis performed in 2005 of 29 eligible studies. The results were that bypass graft failure

was three times that in smokers versus nonsmokers. There was a dose response relationship in smoking cessation prior to or after bypass, equalized patencies. A more recent study, published in JVS in September, queried the VSGNE, 1789 lower extremity bypasses, 971 were nonsmokers, 818 were smokers,

and what they found was that primary patency at two years was 48% in smokers, versus 61% in nonsmokers, and when they propensity matched these patients, there was even a greater difference. 10 year survival was also decreased. And in another article,

published in August of this year in JVS, again a VSGNE study, over 2,000 patients, almost 3,000 patients with lower extremity bypass for claudication. The results looked at MALE, amputation-free survival, limb loss, death, major limb events or death,

and they found that current smoking was a significant predictor of major adverse limb events, and major adverse limb events or death. But do active smokers have worse outcomes after endovascular interventions? So, let's look at the literature again.

And there is none. The only paper I could find was a Markov decision analysis, in which compared revascularization in active smokers to medical management, this was a retrospective study, and their results demonstrated better quality of life in smokers after revascularization versus medical therapy.

The quality of life was similar, after revascularization in nonsmokers and smokers, and there was no increase in amputation rates up to 36 months. Also, 26% of the folks that were revascularized, quit tobacco use after their quality of life was improved.

So we decided to do a small study at my hospital. The outcome of endovascular interventions in active smokers with lifestyle limiting claudication versus nonsmokers. This was retrospective. 138 total patients with endovascular intervention for claudication, 47 were current tobacco users,

91 were never or former smokers. The primary endpoints were reintervention, secondary endpoints, surgical bypass, limb loss, MI, stroke and death. And here you can see, as in most studies, the smokers were a younger population,

and anticoagulation, in our patient population, was more common. As far as comorbidities, they were more common, as in most studies, in the nonsmoking group. And in a mean followup of 3.6 years for both groups, there was no statistically significant difference

between the two groups for any of the outcome measures. So in conclusion, active smokers with lifestyle limiting claudication, we would advocate, of course, smoking cessation. Outcomes with respect to reintervention, surgical bypass and limb loss appear to be equivalent in these two groups.

We feel that these patients should not be denied endovascular intervention, and improved quality of life after intervention may result in an increase in smoking cessation in this patient population. Limitations are obvious, this was a very small study,

and retrospective, and we are actually extending this study to look at several hundred additional patients. So I thank you for your attention.

- I have nothing to disclose but what I will tell you is that the only way for me to learn the mechanics of treating low-flow malformations has been to learn from Wayne, follow what he's doing, and basically what I've done is I've filmed every single step he's taking,

dissect that, and then present you the way that he's doing it. The best way to do that is not listen to Wayne, but to film him, and just to check that afterwards. And he goes regularly to Cairo, this is the place of Dr. Rodovan sitting here

in front of us, and with Dr. Alaa Roshdy. I've learned a lot there from Wayne. This is Wayne's techniques, so normally if you look at puncture, the low flow malformations here then you get return or you aspirate so this is what happens, they inject contrast then they find volume

and inject whatever agent you prefer to inject. It happens to be alcohol but that is not essential. More often than not, there is no return. What to do then? There is a technique that Wayne has developed. Stab-Inject-Withdraw, just under high modification inject,

identify that you're not outside the vessel, get the vessel, start to fill slowly, and identify that and inject the alcohol. Of course you can do that under exposure just to see the effect of the alcohol thrombosing, et cetera.

Another example of no return is to subcutaneously certainly show that there is a low pressure system, and again, Stab-Inject-Withdrawal, and there is a cyst. Is it extravasation or is the malformation aspirate? And if it collapses, that's the malformation.

And then continue to fill in with contrast, define how big the malformation is, and then accordingly inject the amount of abrasive agent that you're using. Lymphatic malformation is very difficult to treat because the vessel's so small, would say microscopic,

and again, Stab-Inject-Withdraw, identify that it's not extravasating but it is the vessel, and start slowly, slowly to fill and any time in doubt that should there, just do a run, identify, and that is the vessel, or the network of the vessels and

start to fill that with the agent you're using. But there are certain zones that just don't inject anything, and these are the arteries. How often do arteries occur? When you puncture them. I just directly looked at all these 155 patients I've seen Wayne treat there a matter of,

I would say, 100 patients in three days. 30 patients per day, that's about six percent. And you see the artery by pulsating flow depending on the pressure that you apply. And we see again the artery pulsating and we have no doubt about that.

However, it could be difficult to see. Depending on how much you push in the contrast and you see these being ornery so there's a No-Go-Zone, no injection of any agent and again, a tiny bit of lottery there in the foot could be disastrous.

You inject any agent, any, you will have ended up with necrosis of course if you don't inject inhibitors, but not yet. The humorous may not end up with necrosis when all the mysticism with puncture will be gone. So we have extravasation, when you say extravasation

like starting injecting, still good, looking good, but you see how the extravasation even blows up and at the end it bursts, again under pressure they should apply, so pressure is really important to control and then you stop and don't inject any more.

Extravasation, you see how its' leaking in the back there, but you correct the position of the needle, identify all the vessels, the tiny little vessels, just have to be used to identify the pattern and then you start to inject the agent again.

Control is very essential. Here is the emphatic malformation labia and though there is this tiny little bity extravasation you continue because there is you know, run-off, it is filling the system and you can safely inject the alcohol.

Intraarticular could be malformation there and this is definitely safe pla however, if it is in the free space in the the joint, that's again, it's No-Go-Zone. How you see that is just be used to

the pattern recognition and you find that this is free. It's around the condyle there so there is no injection. Compression is again good to note to control by compression where the agents go. This is a normal vein, certainly at risk of getting with alcohol, whatever agent

you're using deep in the system, avoid that by compression. Compression can be applied manually and then that gives you a chance to fill the malformation itself and not strike connection too deep in the system. Intraosseous venous malformation,

low-flow malformations can occur anywhere, here in the spine and the axis is transpedicular patient prone because it's soft. The malformation has softened up the bone. You can just use a 21-gauge needle and identify the malformation and follow

by the agent you're using. Peculiar type of venous malformation called capillary venous malformation. Basically it's a low-flow malformation without any shunt here in the sciatic notch of the patient and geography shows that there is no shunt

there is just big veins and intense pacification. And identify the veins by indirect puncture again, see the pattern of that and inject alcohol and following geography we can see that there has decreased the density but it is a lot more left to be done.

In conclusion, direct puncture is the technique in this low-flow malformation but Stab-Inject-Withdraw is the really helpful technique for successful treatment of microvascular, microcystic lesion. No-Go-Zones for certain when you see arteries

and anytime in doubt you just have to do a run to identify if they're arteries or not. Intraarticular free space and extravasation and normal veins, similarly, No-Go-Zone. Capillary venous, intraosseous malformations can be treated successfully. Thank you.

(audience applause) - [Facilitator] Thank you, Crossey. Excellent talk, very practical and pragmatic. Any comments or questions? Dr. Yakes. - [Dr. Yakes] We have been to many meetings and people have talked about doing

other ultrasound guides, accessing the malformations. You'll never see those arteries by ultrasound. - [Facilitator] That's absolutely correct. I concur. I concur and I think some of the disasters we've seen where suddenly something falls off

have been in these situations because they don't understand or in expansile foam-based therapies, I've seen that. I've seen plenty of these, so it's always present, potentially.

- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want

in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis

is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied

and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple

aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention

adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,

the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that

there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions

a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.

In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure

with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle

and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis

needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.

Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.

In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,

regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate

without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.

An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis

and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.

This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more

in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.

But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.

The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.

Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion

because I have a flight in a few hours. Thank you very much.

- Thank you very much and I would like to thank Dr. Veit for the kind invitation, this is really great meeting. Those are my disclosures. Percutaneous EVAR has been first reported in the late 1990's. However, for many reasons it has not been embraced

by the vascular community, despite the fact that it has been shown that the procedure can be done under local anesthesia and it decreases OR time, time to ambulation, wound complication and length of stay. There are three landmark papers which actually change this trend and make PEVAR more popular.

All of these three papers concluded that failure or observed failure of PEVAR are observed and addressed in the OR which is a key issue. And there was no late failures. Another paper which is really very prominent

is a prospective randomize study that's reported by Endologix and published in 2014. Which revealed that PEVAR closure of the arteriotomy is not inferior to open cut down. Basically, this paper also made it possible for the FDA to approve the device, the ProGlide device,

for closure of large bore arteriotomies, up to 26 in the arterial system and 29 in the venous system. We introduced percutaneous access first policy in our institution 2012. And recently we analyzed our results of 272 elective EVAR performed during the 2012 to 2016.

And we attempted PEVAR in 206 cases. And were successful in 92% of cases. But the question was what happened with the patient that failed PEVAR? And what we found that was significantly higher thrombosis, vessel thrombosis,

as well as blood loss, more than 500 cc in the failed PEVAR group. Similarly, there was longer operative time and post-operative length of stay was significantly longer. However, in this relatively small group of patients who we scheduled for cut-down due to different reasons,

we found that actually there was no difference between the PEVAR and the cut-down, failed PEVAR and cut-down in the terms of blood loss, thrombosis of the vessel, operative time and post-operative length of stay. So what are the predictors of ProGlide failure?

Small vessel calcification, particularly anterior wall calcification, prior cut-down and scarring of the groin, high femoral bifurcation and use of large bore sheaths, as well as morbid obesity. So how can we avoid failures?

I think that the key issue is access. So we recommend that all access now or we demand from our fellow that when we're going to do the operation with them, cut-down during fluoroscopy on the ultra-sound guidance, using micropuncture kits and access angiogram is actually mandatory.

But what happened when there is a lack of hemostasis once we've deployed two PEVARs? Number one, we try not to use more than three ProGlide on each side. Once the three ProGlide failed we use the angioseal. There's a new technique that we can have body wire

and deployed angioseal and still have an access. We also developed a technique that we pack the access site routinely with gelfoam and thrombin. And also we use so-called pull and clamp technique, shown here. Basically what it is, we pull the string of the ProGlide

and clamp it on the skin level. This is actually a very very very good technique. So in conclusion, PEVAR first approach strategy successful in more than 90% of cases, reduced operative time and postoperative length of stay, the failure occurred more commonly when the PEVAR

was completed outside of IFU, and there was no differences in outcome between failed PEVAR and planned femoral cut-down. Thank you.

- Thank you very much Mr. Chairman. Thank you Frank, for this kind invitation again to this symposium. This is my disclosure. With the drug coated balloons it is important to minimize the drug loss during the balloon transit during the inflation of the balloon.

Because Paclitaxel has a high degree of cytotoxicity that may induce necrosis and increase inflammation in the distal tissue, and we know that even with the best technique, we can loose 70 - 80% of the drop to the distal circulation,

the inference by different factors between them and the calcification of degree of these blood cells. There are adverse events secondary to drug coated balloons that have been reported recently. In animal molders it has shown that Downstream Vascular Changes are more frequent with

Drug Coated Balloons than with Drug-Eluting Stents. In animal molders it has been also shown that there is no evidence of significant downstream emboli or systemic toxicity with DCB's than with patients with controls. This was a study presented yesterday by (mumbles)

with a very nice and elegant study with a good methodology that shows in animals that there are different concentrations of the drug in distal tissue depending on the balloon that you are using. In this case, the range in balloon (mumbles)

those ones have the lowest concentration in the distal tissue. In clinical experience in this meta-analysis amputations and wound healing rate are lower with this series with controls. But there is controversy because

Complete Index Ulcer Healing is higher in this series than with control patients. But there are lower wound healing index in patients compared with drug-eluting stents. In the debate, (mumbles) and also in the dialux which are clinical trials in diuretic patients with CLI,

there we no issues of safety and no impair of the wounds healing. But, remember the negative result of the IN PACT DEEP trial in which there were more amputation at six months that could be influenced, but in all their factors, the lack of standardized

wound care protocols. (mumbles) has also reported recently good survival to 100% in patient treated with DCB's compared with plain balloons and with lutonic balloons. So in our institution, we did a study with the objective to examine

patient outcomes following the use of the drug-coated balloons in patients with CLI and diuretic patients with Complex Real World lesions undergoing endovascular intervention below-the-knee with the Ranger balloon coated with Paclitaxel.

This is a Two-Center Experience that is headed by the National University of Mexico in 30 patients with strict followup. With symptomatic Rutherford four to six. With the Stenosis and occlusion of infrapopliteal vessels and many degrees of calcification.

It was mandatory for all patients to have Pre-dilation before the use of DCB. We studied some endpoints like efficacy. (mumbles) Limb salvage, sustained clinical improvement, wound healing rate

and technical success and some other endpoints of safety. This is an example of multi level disease in a patient that has to be approached by (mumbles) access with a balloon preparation of the artery before the use of the DCB, and after this, we treated the anterior artery

and even to the arch of the foot. This is the way we follow our patient with ultra sound duplex with an index fibular of no more that 2.4. All patients were diabetic with Rutherford 5-6. 77% have a (mumbles) at the initial of the study.

And as you can see there were longer lesions and with higher degree of calcification and stenosis only in two of them we produced (mumbles). There were bailout stent placements in five patients and we did retrograde access in 43 patients.

Subintimal angioplasty was done in 32 patients, and Complete Index Wound Healing was in 93 of our patients. This is our Limb Salvage 94%. The Patency rate was 96% with this Kaplan Meir analysis. And in some patients we did a determination of Paclitaxel concentration in distal tissue

with the High Pressure Liquid Chromatography method. We only did this in five patients because of the lack of financial support, and technical problems. As you can see in three of them we had Complete Wound Healing.

Only one we had major amputation. This was the patient with the higher concentration of Paclitaxel in the distal tissue, and in one patient, we could not determine the concentration of Paclitaxel. This is the way we do this.

They take the sample of the patient at the moment we do the minor amputation. During day 10 after the angioplasty, we also do a (mumbles) analysis of the patient we have a limb salvage we can see arterial and capillar vessel proliferation and hyperplasia of the

arteriole media layer. But, in those patients that have major amputation even when they have a good sterio-graphic result like in this case, we see more fibrinoid necrosis which is a bad determination. So in conclusion,

angioplasty with the (mumbles) balloon maintain clinical efficacy over time is possible. We didn't see No Downstream clinical important or significant effects and high rates of Limb Salvage in complex CLI patients is possible.

Local toxic effects of paclitaxel and significant drug loss on the way to the lesion are theoretical considerations up to now because there is no biological study that can confirm this. Thank you very much.

- Thank you, Dr. Ascher. Great to be part of this session this morning. These are my disclosures. The risk factors for chronic ischemia of the hand are similar to those for chronic ischemia of the lower extremity with the added risk factors of vasculitides, scleroderma,

other connective tissue disorders, Buerger's disease, and prior trauma. Also, hemodialysis access accounts for a exacerbating factor in approximately 80% of patients that we treat in our center with chronic hand ischemia. On the right is a algorithm from a recent meta-analysis

from the plastic surgery literature, and what's interesting to note is that, although sympathectomy, open surgical bypass, and venous arterialization were all recommended for patients who were refractory to best medical therapy, endovascular therapy is conspicuously absent

from this algorithm, so I just want to take you through this morning and submit that endovascular therapy does have a role in these patients with digit loss, intractable pain or delayed healing after digit resection. Physical examination is similar to that of lower extremity, with the added brachial finger pressures,

and then of course MRA and CTA can be particularly helpful. The goal of endovascular therapy is similar with the angiosome concept to establish in-line flow to the superficial and deep palmar arches. You can use an existing hemodialysis access to gain access transvenously to get into the artery for therapy,

or an antegrade brachial, distal brachial puncture, enabling you treat all three vessels. Additionally, you can use a retrograde radial approach, which allows you to treat both the radial artery, which is typically the main player in these patients, or go up the radial and then back over

and down the ulnar artery. These patients have to be very well heparinized. You're also giving antispasmodic agents with calcium channel blockers and nitroglycerin. A four French sheath is preferable. You're using typically 014, occasionally 018 wires

with balloon diameters 2.3 to three millimeters most common and long balloon lengths as these patients harbor long and tandem stenoses. Here's an example of a patient with intractable hand pain. Initial angiogram both radial and ulnar artery occlusions. We've gone down and wired the radial artery,

performed a long segment angioplasty, done the same to the ulnar artery, and then in doing so reestablished in-line flow with relief of this patient's hand pain. Here's a patient with a non-healing index finger ulcer that's already had

the distal phalanx resected and is going to lose the rest of the finger, so we've gone in via a brachial approach here and with long segment angioplasty to the radial ulnar arteries, we've obtained this flow to the hand

and preserved the digit. Another patient, a diabetic, middle finger ulcer. I think you're getting the theme here. Wiring the vessels distally, long segment radial and ulnar artery angioplasty, and reestablishing an in-line flow to the hand.

Just by way of an extreme example, here's a patient with a vascular malformation with a chronically occluded radial artery at its origin, but a distal, just proximal to the palmar arch distal radial artery reconstitution, so that served as a target for us to come in

as we could not engage the proximal radial artery, so in this patient we're able to come in from a retrograde direction and use the dedicated reentry device to gain reentry and reestablish in-line flow to this patient with intractable hand pain and digit ulcer from the loss of in-line flow to the hand.

And this patient now, two years out, remains patent. Our outcomes at the University of Pennsylvania, typically these have been steal symptoms and/or ulceration and high rates of technical success. Clinical success, 70% with long rates of primary patency comparing very favorably

to the relatively sparse literature in this area. In summary, endovascular therapy can achieve high rates of technical, more importantly, clinical success with low rates of major complications, durable primary patency, and wound healing achieved in the majority of these patients.

Thank you.

- 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.

Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.

Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.

Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.

It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,

you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations

so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times

and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.

It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.

If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2

travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail

for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,

with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.

So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast

before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.

CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries

and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see

actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.

There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.

You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.

This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver

with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss

with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.

We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.

- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.

CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo

t air contamination during the CO2 angiograms. Thank you.

- Thank you very much for the kind introduction, and I'd like to thank the organizers, especially Frank Veith for getting back to this outstanding and very important conference. My duty is now to talk about the acute status of carotid artery stenting is acute occlusion an issue? Here are my disclosures.

Probably you might be aware, for sure you're aware about pore size and probably smaller pore size, the small material load might be a predisposing factor for enhanced thrombogenicity in these dual layer stents, as you're probably quite familiar with the CGUARD, Roadsaver and GORE, I will focus my talk a little bit

on the Roadsaver stent, since I have the most experience with the Roadsaver stent from the early beginning when this device was on the market in Europe. If you go back a little bit and look at the early publications of CGUARD, Roadsaver and GORE stent, then acute occlusion the early reports show that

very clearly safety, especially at 30 days in terms of major cardiac and cerebrovascular events. They are very, very safe, 0% in all these early publications deal with these stents. But you're probably aware of this publication, released end of last year, where a German group in Hamburg

deals with carotid artery stenosis during acute stroke treatment. They used the dual layer stent, the Roadsaver stent or the Casper stent in 20 cases, in the same time period from 2011 to 2016, they used also the Wallstent and the VIVEXX stent,

in 27 cases in total and there was a major difference, in terms of acute stent occlusion, and for the Roadsaver or Casper stent, it was 45%, they also had an explanation for that, potential explanations probably due to the increase of thrombogenic material due to the dual layer

insufficient preparation with antiplatelet medication, higher patient counts in the patients who occluded, smaller stent diameters, and the patients were not administered PTA, meaning Bridging during acute stroke patient treatment, but it was highlighted that all patients received ASA of 500mg intravenously

during the procedure. But there are some questions coming up. What is a small stent diameter? Post-dilatation at what diameter, once the stent was implanted? What about wall apposition of the stent?

Correct stent deployment with the Vicis maneuver performed or not and was the ACT adjusted during the procedure, meaning did they perform an adequate heparinization? These are open questions and I would like to share our experience from Flensburg,

so we have treated nearly 200 patients with the Roadsaver stent from 2015 until now. In 42 patients, we used this stent exclusively for acute stroke treatment and never, ever observed in both groups, in the symptomatic and asymptomatic group and in the group of acute stroke treatment,

we never observed an acute occlusion. How can we explain this kind of difference that neither acute occlusion occurred in our patient group? Probably there are some options how we can avoid stent thrombosis, how we can minimize this. For emergency treatment, probably this might be related

to bridging therapies, though in Germany a lot of patients who received acute stroke treatment are on bridging therapy since the way to the hospital is sometimes rather long, there probably might be a predisposing factor to re-avoid stent thrombosis and so-called tandem lesions if the stent placement is needed.

But we also take care of antiplatelet medication peri-procedurally, and we do this with ASA, as the Hamburg group did and at one day, we always start, in all emergency patients with clopidogrel loading dose after positive CT where we could exclude any bleeding and post-procedurally we go

for dual anti-platelet therapy for at least six months, meaning clopidogrel and ASA, and this is something probably of utmost importance. It's quite the same for elective patients, I think you're quite familiar with this, and I want to highlight the post-procedural clopidogrel

might be the key of success for six months combined with ASA life-long. Stent preparation is also an issue, at least 7 or 8 diameters we have to choose for the correct lengths we have to perform adequate stent deployment and adequate post-dilatation

for at least 5mm. In a lot of trials the Roadsaver concept has been proven, and this is due to the adequate preparation of the stent and ongoing platelet preparation, and this was also highlight in the meta-analysis with the death and stroke rate of .02% in all cases.

Roadsaver study is performed now planned, I am a member of the steering committee. In 2000 patients, so far 132 patients have been included and I want to rise up once again the question, is acute occlusion and issue? No, I don't think so, since you keep antiplatelet medication

in mind and be aware of adequate stent sizing. I highly appreciated your attention, 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you.

- Good 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 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.

- 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.

- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro

or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire

because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,

or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,

very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D

in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--

radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about

to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.

So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where

the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist

to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here

to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric

reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I

mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic

close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to

understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.

Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use

Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.

We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.

You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.

Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial

phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,

the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,

very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone

and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.

In other words can offer higher value in patient care. Thank you.

- Thanks Fieres. Thank you very much for attending this session and Frank for the invitation. These are my disclosures. We have recently presented the outcomes of the first 250 patients included in this prospective IDE at the AATS meeting in this hotel a few months ago.

In this study, there was no in-hospital mortality, there was one 30-day death. This was a death from a patient that had intracranial hemorrhage from the spinal drain placement that eventually was dismissed to palliative care

and died on postoperative day 22. You also note that there are three patients with paraplegia in this study, one of which actually had a epidural hematoma that was led to various significant and flacid paralysis. That prompted us to review the literature

and alter our outcomes with spinal drainage. This review, which includes over 4700 patients shows that the average rate of complications is 10%, some of those are relatively moderate or minor, but you can see a rate of intracranial hemorrhage of 1.5% and spinal hematoma of 1% in this large review,

which is essentially a retrospective review. We have then audited our IDE patients, 293 consecutive patients treated since 2013. We looked at all their spinal drains, so there were 240 placement of drains in 187 patients. You can see that some of these were first stage procedures

and then the majority of them were the index fenestrated branch procedure and some, a minority were Temporary Aneurysm Sac Perfusions. Our rate of complication was identical to the review, 10% and I want to point out some of the more important complications.

You can see here that intracranial hypotension occurred in 6% of the patients, that included three patients, or 2%, with intracranial hemorrhage and nine patients, or 5%, with severe headache that prolonged hospital stay and required blood patch for management.

There were also six patients with spinal hematomas for a overall rate of 3%, including the patient that I'll further discuss later. And one death, which was attributed to the spinal drain. When we looked at the intracranial hypotension in these 12 patients, you can see

the median duration of headache was four days, it required narcotics in seven patients, blood patch in five patients. All these patients had prolonged hospital stay, in one case, the prolongation of hospital stay was of 10 days.

Intracranial hemorrhage in three patients, including the patient that I already discussed. This patient had a severe intracranial hemorrhage which led to a deep coma. The patient was basically elected by the family to be managed with palliative care.

This patient end up expiring on postoperative day 21. There were other two patients with intracranial hemorrhage, one remote, I don't think that that was necessarily related to the spinal drain, nonetheless we had it on this review. These are some of the CT heads of the patients that had intracranial hemorrhage,

including the patient that passed away, which is outlined in the far left of your slide. Six patients had spinal hematoma, one of these patients was a patient, a young patient treated for chronic dissection. Patient evolved exceptionally well, moving the legs,

drain was removed on postoperative day two. As the patient is standed out of the bed, felt weakness in the legs, we then imaged the spine. You can see here, very severe spinal hematoma. Neurosurgery was consulted, decided to evacuate, the patient woke up with flacid paralysis

which has not recovered. There were two other patients with, another patient with paraplegia which was treated conservatively and improved to paraparesis and continues to improve and two other patients with paraparesis.

That prompted changes in our protocol. We eliminated spinal drains for Extent IVs, we eliminated for chronic dissection, in first stages, on any first stage, and most of the Extent IIIs, we also changed our protocol of drainage

from the routine drainage of a 10 centimeters of water for 15 minutes of the hours to a maximum of 20 mL to a drainage that's now guided by Near Infrared Spectroscopy, changes or symptoms. This is our protocol and I'll illustrate how we used this in one patient.

This is a patient that actually had this actual, exact anatomy. You can see the arch was very difficult, the celiac axis was patent and provided collateral flow an occluded SMA. The right renal artery was chronically occluded.

As we were doing this case the patient experienced severe changes in MEP despite the fact we had flow to the legs, we immediately stopped the procedure with still flow to the aneurysm sac. The patient develops pancreatitis, requires dialysis

and recovers after a few days in the ICU with no neurological change. Then I completed the repair doing a subcostal incision elongating the celiac axis and retrograde axis to this graft to complete the branch was very difficult to from the arm

and the patient recovered with no injury. So, in conclusion, spinal drainage is potentially dangerous even lethal and should be carefully weighted against the potential benefits. I think that our protocol now uses routine drainage for Extent I and IIs,

although I still think there is room for a prospective randomized trial even on this group and selective drainage for Extent IIIs and no drainage for Extent IVs. We use NIRS liberally to guide drainage and we use temporary sac perfusion

in those that have changes in neuromonitoring. Thank you very much.

- 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)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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