- Thank you very much, chairman and ladies and gentlemen. The funding of this trial was from The Academy of Medical Sciences and The Royal College of Surgeons of England. AKI due to the influence EVAR is actually more common than we all think. This is being shown by prospective studies and registries.
Why is it important? Well, it's associated with a higher intra or inter hospital mortality, cardiovascular events and also long term cardiovascular events and longterm mortality. As even more common and complex, EVAR, and this can range from 22% up to 32%.
These are some of our cases, some of our first, including FEN astrate EVAR in 2010 Thoraco-Abdominal Branch repair 2016 and Fen astrated TEVAR 2018. These are longer procedures, usually with more contrast and direct ventilation after removing arteries.
What are the mechanisms for acute kidney injuries due to infer-renal EVAR? While this involves use of contrast, systemic inflammatory response syndrome, due to ischemic re-perfusion injury, manipulation of the thrombus, aorta and catheterizations which will ------ alpha
and also from high prophalinemia. There is no high-quality evidence for AKI prevention in EVAR. What about Sodium Bicarbonate? Well it's been well know to reduce what been used commonly to reduce CIN in high risk patients in perrifical and
corona graphy. There are two main mechanisms as to how this works. Firstly, from reducing renal tubular ischemia. Secondly, by reducing oxygen deprived free radical formation in the tubules. What is the evidence?
Well this is a met analysis, comparing Sodium Bicarbonate directly with hydration with normal saline, as shown in the orange box. There is no difference. We can look at the population ll
mostly CKD patients or diabetic patients, certainly Hartmann's patients but they are not EVAR patients. They are coronary patients or peripheral an-graphy patients. In addition, serum bicarbonate and the urine pH was not reported so we do not know how effective the Bicarbonate was in these RCT's.
The authors went on to look other outcomes including needful hemo dialysis, cardiac events, the mortality and they found no difference but they concluded the strength of this evidence was low and insufficient. A further Meta-analysis this time published in BMJ this time comes in favor of bicarbonate
but again this is comparing bicarbonate with saline no use of combination therapy. There are again no use of EVAR patients and these patients all have a low eGFR. The preserved trial, a large trial published earlier this year in the New England Journal again using various
treatments again comparing sodium bicarbonates and saline again no difference. But again this compares bicarbonate direct with saline with no combination therapies. In addition, there were no EVAR patients, and these are low eGFR patients.
The met-analysis also showed that by using bicarbonates as a bolus dose rather than a continuous infusion, which was actually the way they used bicarbonates in most of these patients might be better. And using a higher dose of bicarbonate may also be better as shown in this Japanese paper.
So we come to HYDRA trial. They're using a high dose bicarbonate in combination with hydration to protect renal function. We did a UK wide survey of anesthetists of day to day and they felt the best volume expander they would like to use was Hartmann's solution.
So we randomized patients between standard hydration with Hartmann's solution verses standard hydration Hartmann's plus high dose bicarbonate per operatively and low slow intravenous infusion bicarbonate during the surgery. Importantly, with these patients,
we kept the map within 80% of baseline, 90% of the time in contrary to all the RCT's coronary and angeo-porphyry. We're going to skip that slide. This is the inclusion criteria, any patient undergoing infra EVAR, with any renal disfunction,
the primary area you must look at is recruitment and the second area you must look at is AKI. We screened 109 patients of which, 58% were randomized and there were only 2 crossovers. There was a willingness for patients to participate and there was also a willingness for PET 4 Clinitions to
recruit as well. This is the demographics, which is typical of aortic patients they are all on by a few MRSA patients, have normal renal function. Most of the patients wear statins and anti pace agent, only 13% were diabetic.
The patients were matched in terms of hypertension and also fluid hydration pre-operatively measures of via impedance. Here are the results of the trial. The AKI instance in the standard hydration group was like 3% and 7.1% with standard hydration plus bicarbonate. And it was similar in terms of organotrophic support into
and postop and also contrast volume used. It's a safe regime with none of the patients suffering as a result of using bicarbonate. So to conclude, to answer professor Veith's question, about how was this trial different to all the other trials? Well, certainly the previous trials have compared
bicarbonate with saline, there's lack of combination studies that involve mostly coronary an peripheral procedures, not EVAR. And the the most only included patient with low eGFR. HYDRA is different, this is not a regime using high dose bolus of sodium bicarb combined with standard hydration.
It shows promise of reducing AKO. This is an EVAR specific pilot RCT. Again, Unlike previous trials using bicarbonate, 90% of the patients had normal or mild impaired renal function. And unlike previous trials, there's more aggressive management of hypertension intra and postoperatively.
Thank you for listening.
- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,
it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.
And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication
what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies
to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging
that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,
with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures
to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit
in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is
based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,
and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.
Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system
that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress
and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform
a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.
I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient
before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.
But we hope to present on that more solid data next year. Thank you very much.
- 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.
- Thank you, Larry, thank you, Tony. Nice to be known as a fixture. I have no relevant disclosures, except that I have a trophy. And that's important, but also that Prabir Roy-Chaudhury, who's in this picture, was the genesis of some of the thoughts that I'm going to deliver here about predicting renal failure,
so I do want to credit him with bringing that to the vascular access space. You know, following on Soren's talk about access guidelines, we're dealing with pretty old guidelines, but if you look at the 2006 version, you know, just the height--
The things that a surgeon might read in his office. CKD four, patients there, you want a timely referral, you want them evaluated for placement of permanent access. The term "if necessary" is included in those guidelines, that's sometimes forgotten about.
And, of course, veins should be protected. We already heard a little bit about that, and so out our hospital, with our new dialysis patients, we usually try to butcher both antecubital veins at the same time. And then, before we send them to surgery
after they've been vein-marked, we use that vein to put in their preoperative IV, so that's our vascular access management program at Christiana Care. - [Male Speaker] That's why we mark it for you, Teddy. (laughing)
- So, you know, the other guideline is patients should have a functional permanent access at the initiation of dialysis therapy, and that means we need a crystal ball. How do we know this? A fistula should be placed at least six months
before anticipated start of dialysis, or a graft three to six weeks. Anybody who tells you they actually know that is lying, you can't tell, there's no validated means of predicting this. You hear clinical judgment, you can look at
all sorts of things. You cannot really make that projection. Now there is one interesting study by Tangri, and this is what Premier brought to our attention last year at CIDA, where this Canadian researcher and his team developed a model for predicting
progression of chronic kidney disease, not specifically for access purposes, but for others. They looked at a large number of patients in Canada, followed them through chronic kidney disease to ESRD, and they came up with a model. If you look at a simple model that uses age, sex,
estimated GFR from MDRD equation and albuminuria to predict when that patient might develop end stage renal disease, and there's now nice calculators. This is a wonderful thing, I keep it on my phone, this Qx Calculate, I would recommend you do the same,
and you can put those answers to the questions, in this app, and it'll give you the answer you're looking for. So for instance, here's a case, a 75-year-old woman, CKD stage four, her creatinine's 2.7, not very impressive,
eGFR's 18. Her urine protein is 1200 milligrams per gram, that's important, this is kind of one of the major variables that impacts on this. So she's referred appropriately at that stage to a surgeon for arteriovenous access,
and he finds that she really has no veins that he feels are suitable for a fistula, so an appropriate referral was made. Now at that time, if you'd put her into this equation with those variables, 1200, female, 75-year-old, 18 GFR, at two years, her risk of ESRD is about 30%,
and at five years about 66%, 67%. So, you know, how do you use those numbers in deciding if she needs an access? Well, you might say... A rational person might say perhaps that patient should get a fistula,
or at least be put in line for it. Well, this well-intentioned surgeon providing customer service put in a graft, which then ended up with some steal requiring a DRIL, which then still had steal, required banding, and then a few months, a year later
was thrombosed and abandoned because she didn't need it. And I saw her for the first time in October 2018, at which time her creatinine is up to 3.6, her eGFR's down to 12, her protein is a little higher, 2600, so now she has a two-year risk of 62%, and a five-year risk of 95%,
considerably more than when this ill-advised craft was created. So what do you do with this patient now? I don't have the answer to that, but you can use this information at least to help flavor your thought process,
and what if you could bend the curve? What if you treated this patient appropriately with ACE inhibitors and other methods to get the protein down? Well, you can almost half her two-year risk of renal failure with medical management.
So these considerations I think are important to the team, surgeon, nurses, nephrologists, etc., who are planning that vascular access with the patient. When to do and what to do. And then, you know, it's kind of old-fashioned to look at the trajectory.
We used to look at one over creatinine, we can look at eGFR now, and she's on a trajectory that looks suspicious for progression, so you can factor that into your thought process as well. And then I think this is the other very important concept, I think I've spoken about this here before,
is that there's no absolute need for dialysis unless you do bilateral nephrectomies. Patients can be managed medically for quite a while, and the manifestations of uremia dealt with quite safely and effectively, and you can see that over the years, the number of patients
in this top brown pattern that have been started on dialysis with a GFR of greater than 15 has fallen, or at least, stopped rising because we've recognized that there's no advantage, and there may be disadvantages to starting patients too early.
So if your nephrologist is telling I've got to start this patient now because he or she needs dialysis, unless they had bilateral nephrectomies that may or may not be true. Another case,
64-year-old male, CKD stage four, creatinine about four, eGFR 15, 800 milligrams of proteinuria, referred to a vascular access surgeon for AV access. Interesting note, previous central lines, or AICD, healthy guy otherwise.
So in April 2017 he had a left wrist fistula done, I think that was a very appropriate referral and a very appropriate operation by this surgeon. At that time his two-year risk was 49, 50%, his five-year risk 88%. It's a pretty good idea, I think, to get a wrist fistula
in that patient. Once again, this is not validated for that purpose. I can't point you to a study that says by using this you can make well-informed predictions about when to do vascular access, but I do think it helps to flavor the judgment on this.
Also, I saw him for the first time last month, and his left arm is like this. Amazing, that has never had a catheter or anything, so I did his central venogram, and this is his anatomy. I could find absolutely no evidence of a connection between the left subclavian and the superior vena cava,
I couldn't cross it. Incidentally, this was done with less than 20 CCs of dye of trying to open this occlusion or find a way through, which was unsuccessful. You can see all the edema in his arm. So what do you do with this guy now?
Well, up, go back. Here's his trajectory of CKD four from the time his fistula is done to the time I'm seeing him now, he's been pretty flat. And his proteinuria's actually dropped
with medical management. He's only got 103 milligrams per gram of proteinuria now, and his two-year risk is now 23%, his five-year risk is 56%, so I said back to the surgeon we ligate this damn thing, because we can't really do much to fix it,
and we're going to wait and see when it's closer to time to needing dialysis. I'm not going to subject this guy to a right-arm fistula with that trajectory of renal disease over the past two years. So combining that trajectory with these predictive numbers,
and improved medical care for proteinuria I think is a good strategy. So what do you do, you're weighing factors for timing too early, you've got a burden of fistula failure, interventions you need to use to maintain costs, morbidity, complications,
steal, neuropathy that you could avoid versus too late and disadvantages of initiating hemodialysis without a permanent access. And lastly, I'm going to just finish with some blasphemy. I think the risk of starting dialysis with a catheter is vastly overstated.
If you look at old data and patient selection issues, and catheter maintenance issues, I think... It's not such an unreasonable thing to start a patient with a catheter. We do it all the time and they usually live.
And even CMS gives us a 90-day grace period on our QIP penalties, so... If you establish a surgeon and access plan, I think you're good to go. So who monitors access maturation? I don't know, somebody who knows what they're doing.
If you look at all the people involved, I know some of these individuals who are absolute crackerjack experts, and some are clueless. It has nothing to do with their age, their gender, their training, their field. It's just a matter of whether they understand
what makes a good fistula. You don't have to be a genius, you just can't be clueless. This is not a mature usable fistula, I know that when I see it. Thank you.
- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery
and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely
at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer
or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.
Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.
There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking
at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?
And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,
this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients
with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.
I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,
and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients
who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually
living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,
you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data
over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,
more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.
These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?
I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.
I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at
the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,
such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time
camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.
If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.
Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.
There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series
where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,
limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.
But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.
So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.
So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.
If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.
- Good morning, thank you very much to Dr. Veith and Professor Veith and the organizers. So this is real holography. It's not augmented reality. It's not getting you separated from the environment that you're in. This is actually taking the 3D out of the screen
so the beating heart can be held in the palm of your hand without you having to wear any goggles or anything else and this is live imaging. It can be done intra-procedure. This is the Holoscope-i and the other one is the Holoscope-x
where in fact you can take that actually 3D hologram that you have and you can implant it in the patient and if you co-register it correctly then you can actually do the intervention in the patient
make a needle tract to the holographic needle and I'm going to limit this to just now what we're actually doing at the moment and not necessarily what the future can be. This is ultimate 3D visualization, true volumes floating in the air.
This is a CT scan. So it started working, So we get rid of the auto-segmented and you can just interact. It's floating 45 centimeters away from you and you can just hold the patient's anatomy here and you can slice into the anatomy.
This is for instance a real CT of an aorta with the aortic valve which they wanted to analyze for a core valve procedure. This is done by Phelps. If you take the information
and they've looked at the final element analysis and interaction between the stem and the tissue. So here you can make measurements in real time. So if you did the 3D rotation and geography and you had the aorta and you wanted to put in a stent graft EVAR TVAR, and you would see,
and you could put in a typical tuber that you would do, and you could see how it, and this is a dynamic hologram, so you can see how it would open up, you can mark where your fenestration's chimney is and all that type of stuff would be. And you can move it around, and you have
a complete intuitive understanding of a, can we go to the next slide please, I can't, it seems to be clicking, thank you. So how do we do all this? Well, to create a hologram, what you need to do is just conceptualize it as printing in light.
Like if you had plastic and you took the XYZ data and you just put it into a 3D printer, and it would print it for you in light, then you'd go, Okay, so I understand, if it was printed for you in plastic then you'd understand. But imagine it's printing in light.
So we have every single piece of light focused, each photon is focused so that you can see it with a naked eye, in a particular place, but the difference is that it's totally sterile, you don't have to take off your gloves, you don't have to use a mouse,
you can interact with it directly. And all the XYZ data is 100% in place, so we've just seen a beautiful demonstration of augmented reality, and in augmented reality, you have to wear something, it isolates you from the environment that you're in, and it's based on
stereoscopy, and stereoscopy is how you see 3D movies, and how you see augmented reality, is by taking two images and fusing them in one focal plane. But you can't touch that image, because if you look at me now, you can see me very well, but if you hold your finger up 45 centimeters
and you focus on your finger, I become blurred. And so, you can only focus in one plane, you can't touch that image, because that image is distant from you, and it's a fused image, so you have the focus plane and you have the convergence plane, and this is an illusion
of 3D, and it's very entertaining, and it can be very useful in medical imaging, but in intra-operative procedures it has to be 100% accurate. So you saw a very beautiful example in the previous talk of augmented reality, where you have gesturing, where you can actually gesture with the image,
you can make it bigger, you can make it smaller. But what RealView does by creating real holography, which is all the XYZ data, is having it in the palm of your hand, with having above 20 focal planes, here, very very close to your eye, and that in another way, of having all those focal planes not only actually lets you
do the procedure but prevents nausea and having a feeling of discomfort because the image is actually there as of having the illusion of the images there. So just to go back, all RealView imaging is doing, is it's not changing your 3D RA cone, BMCT, MRI,
we can do all those XYZ datas and we can use them and we can present them, all we're doing, so you use your acquisition, we're just taking that, and we're breaking open the 3D displays and seeing all that 3D data limited in the 2D screen, let's set it free and have it floating in the air.
So we have the holoscope-i for structural cardiology and electrophysiology, and obviously the holoscope-x, which makes the patient x-rayed, completely visible. So its an over the head, this is now, obviously, free-standing when somebody buys us like Phillips or Siemens, it will be integrated into your lab,
come down from the ceiling, it's an independent system, and you just have a visor that you look through, which just goes up and down whenever you want to use it. You can interact with it the same as you do with your iPhone you can visualize, you can rotate, you can mark, you can slice, you can measure, as I showed you
some examples of it, and you can do this by voice as well, you just talk to it, you say slice and you slice it with your hand, it recognizes everybody's hand, there's no delay for whatever you're imaging. So structural cardiac procedures, this is what
a mitral valve will look like, floating in the air in front of you, you can see the anterior leaflet, the posterior leaflet. And once the catheter is inside and you're guiding the catheter inside the procedure, you can turn on your doppler, you'll be able to see that the catheter
movements, so for someone doing a mitral clip, or whatever, this would be very very useful. This is an electrophysiological procedure, and you can see how the catheter moves, when the catheter will move, and obviously, as my previous speaker was saying, you are appreciating 3D in a 2D screen,
so it's very difficult to appreciate, you'll have to take my word for it. But I think you can see dynamic colography at this quality, that you can interact with, that is something that is very special, we've presented at a number of conferences,
including at Veith, and we've already done a first in man, and the most exciting thing for now, is just this week, the first machine was installed at Toronto general, at the Peter Munk Cardiac Center, and they've done their first case, and so now we are launching and clinical trials in 2018, and hopefully,
I'll have something which is more vascular relevant, at the next time, Veith 2019, thank you very much.
- Good morning. Thank you for the opportunity to speak. So thirty day mortality following unselected non-cardiac surgery in patients 45 years and older has been reported to be as high as 1.9%. And in such patients we know that postoperative troponin elevation has
a very strong correlation with 30-day mortality. Considering that there are millions of major surgical procedures performed, it's clear that this equates to a significant health problem. And therefore, the accurate identification of patients at risk of complications
and morbidity offers many advantages. First, both the patient and the physician can perform an appropriate risk-benefit analysis based on the expected surgical benefit in relation to surgical risk. And surgery can then be declined,
deferred, or modified to maximize the patient's benefit. Secondly, pre-operative identification of high-risk patients allows physicians to direct their efforts towards those who might really benefit from additional interventions. And finally, postoperative management,
monitoring and potential therapies can be individualized according to predicted risk. So there's a lot of data on this and I'll try to go through the data on predictive biomarkers in different groups of vascular surgery patients. This study published in the "American Heart Journal"
in 2018 measured troponin levels in a prospective blinded fashion in 1000 patients undergoing non-cardiac surgery. Major cardiac complications occurred overall in 11% but in 24% of the patients who were having vascular surgery procedures.
You can see here that among vascular surgery patients there was a really high prevalence of elevated troponin levels preoperatively. And again, if you look here at the morbidity in vascular surgery patients 24% had major cardiac complications,
the majority of these were myocardial infarctions. Among patients undergoing vascular surgery, preoperative troponin elevation was an independent predictor of cardiac complications with an odds ratio of 1.5, and there was an increased accuracy of this parameter
in vascular surgery as opposed to non-vascular surgery patients. So what about patients undergoing open vascular surgery procedures? This is a prospective study of 455 patients and elevated preoperative troponin level
and a perioperative increase were both independently associated with MACE. You can see here these patients were undergoing a variety of open procedures including aortic, carotid, and peripheral arterial. And you can see here that in any way you look at this,
both the preoperative troponin, the postoperative troponin, the absolute change, and the relative change were all highly associated with MACE. You could add the troponin levels to the RCRI a clinical risk stratification tool and know that this increased the accuracy.
And this is additionally shown here in these receiver operator curves. So this study concluded that a combination of the RCRI with troponin levels can improve the predictive accuracy and therefore allow for better patient management.
This doesn't just happen in open-vascular surgery patients. This is a study that studied troponin levels in acute limb ischaemia patients undergoing endovascular therapy. 254 patients all treated with endovascular intervention
with a 3.9% mortality and a 5.1% amputation rate. Patients who died or required amputation more frequently presented with elevated troponin levels. And the relationship between troponin and worse in-hospital outcome remains significant even when controlling for other factors.
In-hospital death or amputation again and amputation free survival were highly correlated with preoperative troponin levels. You can see here 16.9% in patients with elevated troponins versus 6% in others. And the cardiac troponin level
had a high hazard ratio for predicting worse in-hospital outcomes. This is a study of troponins just in CLI patients with a similar design the measurement of troponin on admission again was a significant independent predictor
of survival with a hazard ratio of 4.2. You can see here that the majority of deaths that did occur were in fact cardiac, and troponin levels correlated highly with both cardiac specific and all-cause mortality. The value of the troponin test was maintained
even when controlling for other risk factors. And these authors felt that the realistic awareness of likely long term prognosis of vascular surgery patients is invaluable when planning suitability for either surgical or endovascular intervention.
And finally, we even have data on the value of preoperative troponin in patients undergoing major amputation. This was a study in which 10 of 44 patients had a non-fatal MI or died from a cardiac cause following amputation.
A rise in the preoperative troponin level was associated with a very poor outcome and was the only significant predictor of postoperative cardiac events. As you can see in this slide. This clearly may be a "Pandora's box".
We really don't know who should have preoperative troponins. What is the cost effectiveness in screening everybody? And in patients with elevated troponin levels, what exactly do we do? Do we cancel surgery, defer it, or change our plan?
However, certainly as vascular surgeons with our high-risk patient population we believe in risk stratification tools. And the RCRI is routinely used as a clinical risk stratification tool. Adding preoperative troponin levels to the RCRI
clearly increases its accuracy in the prediction of patients who will have perioperative cardiac morbidity or mortality. And you can see here that the preoperative troponin level had one of the highest independent hazard ratios at 5.4. Thank you very much for your attention.
- I'd like the thank Doctor Veith for inviting me back to speak. I have no disclosures, we will be discussing some slight off-label use of the anitcoagulants. As we all know, acute limb ischemia occurs as a result of acute thrombosis of a native artery or bypass graft or embolism from a proximal
source, dissection, or trauma. The incidence is not insignificant, 15 cases per 100 000 persons per year, or interestingly about 10 to 16% of our vascular workload. Despite the relative frequency of this condition, there are relatively few guidelines to
guide us for anticoagulation therapy. The last set of guidelines for the American College of Chest Physicians regarding PAD gives some very brief, generic recommendations from 2012. They state, suggest immediate systemic anticoagulation with unfractionated heparin.
We suggest reperfusion over no reperfusion, which seems pretty obvious to an audience of vascular specialists. One of the challenges with acute limb ischemia is that it is a fairly heterogenous group. It can be thrombosis or embolism to the aorticiliac segments to the infrainguinal segments, and
there's also the patients who develop ALI from trauma. So we actually looked at the various phases of anticoagulation for acute limb ischemia and then we do, as with many institutions, utilize intravenous heparin at the time of the diagnosis, as well as obviously at the time of surgery,
but we found that there was a significant variation with regard to the early, post-operative anticoagulation regimens. One option is to give therapeutic intravenous heparin on an adjusted dose, but what we found in a significant minority of patients across the country actually,
is that people are giving this fixed mini-dose 500 unit an hour of heparin without any standardization or efficacy analysis. Then, obviously you go the long-term anticoagulation. We reviewed 123 patients who had ALI at our institution, who underwent surgical revascularization.
And they had the typical set of comorbidities you might expect in someone who has PAD or atheroembolism. In these patients, the Rutherford Classification was viable or marginally threatened in the majority, with about 25% having immediately threatened limb.
Various procedures were performed for these patients, including thromboembolectomy in the majority, bypass operations, angioplasty and stenting was performed in the significant minority and then primary amputation in the various selects few. We divided these patients into
the first four days of anticoagulation. Therapeutic with unfractionated heparin early on versus subtherapeutic or this mini-dose unfractionated heparin and we found that 29% of our patients were receiving the mini-dose unfractionated heparin, again without much efficacy analysis.
We used the International Society for Thrombosis and Haemostasis Anticoagulation Outcome Guidelines to look at the ischemic complications, as well as major and minor bleeding for these patients, and we identified actually not a significant rate of difference between the
subtherapeutic category and the therapeutic category of patients, with regard to mortality, with regard to recurrent limb ischemia, MI, VTE, or stroke, major amputation, and we actually didn't find because it's a fairly small study, any significant difference in major or minor bleeding for these patients.
So, we do feel that this small study did justify some efficacy of mini-dose unfractionated heparin because we didn't find that it was causing recurrent lower extremity thromboembolsim in these patients. Now on to long-term anticoagulation, for these patients, after that first three or four days
after the surgery, the options are long-term vitamin K antagonists, the DOAC's or vitamin K antagonists if you have atrial arrhythmia, or in the patients who had no other comorbidities, there really is not much guidance until recently. The compass trial was recently published in 2018
in stable PAD and carotid disease patients, identifying that rivaroxaban plus aspirin had a significant benefit over aspirin alone in patients who had stable PAD. And then, an upcoming trial, which is still ongoing currently in patients who underwent recent
revascularization, whether open or endo, is hopefully going to demonstrate that rivaroxaban, again has a role in patients with lower extremity ischemia. So in conclusion, there is relatively a scarcity of clinical data to help guide anticoagulation after acute limb ischemia.
Unfractionated heparin pre and intraop are standardized, but postop anticoagulation is quite variable. The mini-dose, we consider to be a reasonable option in the first few days to balance bleeding versus rethrombrosis, and fortunately we are having larger randomized clinical trials to help demonstrate the benefit of the DOACs and
aspirin in patients who are stable or post-revascularization for PAD, thank you.
- Alright, thank you for asking me to speak. It's always worrisome when the interventional radiologist is talking about hematologic things, and I see some of the faces there that know probably a lot more about this me. There's not much literature written on this subject, with respect to vascular malformations.
Basically, the venous malformations particularly, originally thought to be a relatively benign phenomenon. But, Enjorlras and Mazoyer, I can't really see over there, did the first papers on this,
and they first noticed an association with purely venous malformations in a distinct hematologic syndrome that was different from Kasabach-Merritt syndrome. Now vascular malformations basically deal with Virchow's Triad,
and a venous malformation has a local environment that's very conducive to thrombosis. Basically you have altered blood flow with abnormal valveless vessels, relatively slow flow, and that leads to clotting. Similarly, I have endothelial injury,
which again leads to clotting. And this sets up a hypercoagulable viscous circle where you have increasing thrombosis and you can get localized intravascular coagulation. So in these original two papers back in '97 and 2002, they found that basically these patients had
episodes where they had a lot of bleeding during surgical procedures, and it led to lower levels of fibrinogen and increased degradation complex and they said a low platelet count, it was low-ish, but not abnormal.
And also leading to phlebolith formation and other bleeding complications peri-surgically. So what is LIC? Well we all know our coagulation pathway, the end of the cascade leading from fibrinogen to fibrin and what they've found is that with patients
who have LIC within a venous malformation, you can have elevated D-dimer levels. I won't get into the actual numbers. Suffice it to say, whatever your lab is, they're elevated. Fibrin degradation products are elevated. And then you can sometimes have low fibrinogen levels,
but it's important to realize that there's a normal PT, normal PTT, and normal platelet count in these patients. So how prevalent is this within this population? Well, in venous malformation in their original 1997 paper, it was very prevalent. 88% of patients had elevated D-dimers and
some had decreased fibrinogen and low-ish platelet counts. Again for the paper in 2002, you shouldn't expect to read that, but graphically I've got these, those little red lines increase how many more times normal the D-dimer levels were
and some of them were off the charts literally, and the other little set of little red dots over here are how many times less the fibrinogen levels were than what would be considered normal. So when it's present, it's really present. Now the thing is,
these are all the papers that actually talk about its prevalence that have ever been published. And each one of them, I'm just going to show you these sets of figures here, the important point to notice is that, sorry I'm going to go back, I apologize.
One second here. Is if you go through all of these, you'll see that incidence of localized intravascular coagulation is around 40 or 50 or even 60%, all things being considered equal. Now, what is the relationship between the incidence
of LIC and lesion characteristics? Well, this is a great paper from 2015 where they looked at 70 patients, and this is a great little diagram I like, is that if you look at just, they divvied up lesions from less than 250 CCs,
250 to 500, and then greater than 500, and looked at the incidence of LIC in their population. In the smaller lesion, there was hardly any, and if you look in the larger lesions, the patients who had LIC greatly outnumbered the ones that didn't.
So they also found that spongy lesions, and ones with phlebolith, as well as ones that were non-superficial, were the most likely to cause it. So why is LIC clinically relevant? Well, it causes pain, and over time, you can get lumps,
phleboliths within the lesion, and you can also have other thromboembolic complications as a result of it. But most important, it's relevant because LIC can proceed onto DIC, which is obviously a much more serious condition,
and the things that can stimulate that are trauma to the lesion, fracture, surgery, prolonged immobilization, menstruation, and pregnancy, and of course, sclerotherapy. So if you have a patient who suffers from LIC, messing with the lesion if they're vulnerable
can lead to DIC. So it's very important. And remember that DIC has all the components of LIC, but you have reduced platelet count and elevated PT and all other sorts of abnormalities, so it's the whole shebang.
Similarly too, when I was preparing for this talk, reading the hematologic literature, in addition to overt DIC, there's something between LIC and DIC, which they call non-overt DIC, so there's a spectrum. And there's all these different international criteria.
You don't want to get bogged down. But the meat and potatoes in the last three minutes of the talk here are when do we intervene clinically to address these hematologic issues, what parameters and what clinical setting are important,
and how do we stratify? Well, all patients with venous malformations, you're going to treat conservatively. Encourage activity, avoidance of activities that cause symptoms, and have compression garments. These can reduce the volume of the lesion
and make everybody feel better. They can decrease incidence of LIC symptoms and pain. We all know our heparin pathways, but the issue of heparin and anti-Xa therapy, looking at low molecular weight heparin, it's been found that when you give
low molecular weight heparin, in painful lesions the D-dimer levels drop precipitously. That's proven beyond a doubt. So what does that mean? Well, when should we use low molecular weight heparin? We assess risk.
All patients who have large sized, multi-focal lesions, venous ectasia or an overgrowth syndrome, or any kind of combined lesion should have a hematologic work up looking at the D-dimer, PT, PTT, fibrinogen, CBC. That's your first step.
If they don't have that, just conservative therapy, but if they do, and you're considering intervention, if you look at all of those risk factors, if they're negative for those risk factors, again conservative therapy, no low molecular weight heparin, compression garments.
But if they're positive, before you treat the venous malformation, either surgery or sclerotherapy, you give them half a milligram per kilogram of subcutaneous low molecular weight heparin, for one week before, look at the labs,
and give it another week. So basically, all literature says 10 to 14 days before you do something, give the goods. After therapy you give low molecular weight heparin too, and you pick the longest of two things. You either go for the same dose again
for two weeks after therapy, or until they're ambulatory, whatever is longest. So that's the most important slide. Chronic therapy, all venous malformations if you have these risk factors, if you have an elevated D-dimer
or if it's negative, go conservative. If it's positive, look at the fibrinogen level. If it's not elevated, go conservative. But if it is decreased, give low molecular weight heparin. Similarly, if your D-dimer level is elevated and you have pain,
give low molecular weight heparin. If not, conservative. A word on DOACs, direct oral anticoagulants. There's some early promise that if you look at this graph, this patient here received a DOAC instead of low molecular weight heparin,
and their fibrinogen levels bounced back up. We're radiologists here, pictures say everything. Here's a patient who was on low molecular weight heparin and their anti-Xa activity and all of their fibrinogen levels stayed the same. They were transitioned to dabigatran.
Everything stayed the same. So it does work. Final slide. Aspirin therapy, anecdotal evidence only. Vitamin K therapy's only anecdotal as well. But you certainly don't want to give aspirin
in the pediatric population, and we don't know if there's more trouble and complications and again, vitamin K may be a good thing, may be not. That's sort of the tour of hematologic issues in venous malformations.
Not that much literature. Bottom line is follow the rules for low molecular weight heparin. I think these talks are online afterwards so you can get all of the little data on there. Thank you.
Any questions? - [Audience Member] (mumbling). I was finding after treatment, they started getting bruises and things (mumbling). A lot of these patients are positive D-dimers, low fibrinogens, and low platelets.
It's not unusual for us to treat (mumbling) foot malformation over several days. You can send them (mumbling). So anybody that's got a large malformation (mumbling) all these things to know ahead of time (mumbling) to improve the situation (mumbling).
They were there, did an angiogram (mumbling). Four inch hole. We almost lost this guy. 35 years old. This is a real event. How in the hell, killed by a four inch catheter.
He would have been DIC if we pulled (mumbling). - [Gerald] I think I've been whistling past the graveyard for years until recently, but you always hear these horror stories. (audience member mumbling) Yeah, exactly.
- [Audience Member] Gerald, what's the relationship between pain and the administration of low molecular weight heparin in some of these larger lesions? - [Gerald] It does decrease it. The literature shows they do get better.
It's the only thing proven in the several studies to make a difference. - [Audience Member] And in your experience, and that of others, has there been a dramatic decrease in pain, elimination of pain? Let's say you have a large painful lesion,
they haven't responded to conventional NSAIDs or conventional therapy, do you see any dramatic, or has anybody seem dramatic benefits in terms of pain reduction with low molecular weight heparin administration? (audience member mumbling)
Yeah, I understand. - [Gerald] But with oral (mumbling), the early literature coming up, but I bet you're going to see that's fertile ground to randomize between two groups and look at their visual analogs.
- [Audience Member] Because remember, the pain is the biggest issue. - [Gerald] Absolutely, it's not the lesion. - [Audience Member] But it depend of the cause of the pain. If the pain is really due to local thrombosis, it's very acute pain that will go away with
the low molecular weight heparin. If the pain is due to functional limitation, due to the extension of the VM, it will not help. - [Audience Member] Yeah but we also have patients who just have a painful lesion. It's not necessarily functional.
The thing hurts like hell and the question is, in those patients, obviously we treat them, but in those patients administration of low molecular weight heparin, can that reduce the pain? - [Audience Member] It depend on the biology. If they have very high D-dimer with
normal or normal low fibrinogen, I would think it would help, but if the coagulation is normal, it would not. - [Gerald] Yeah I think (mumbling) good for preventing acute episodes of pain and definitely better for painful episodes.
I agree with you, yes. - [Audience Member] Thank you. - [Audience Member] You've got to ask the patient is it a burning pain or is it a sharp pain? Burning pain is reflexive (mumbling). So you really have to ask (mumbling).
- [Audience Member] Maybe one last comment. We've been using at the beginning, 10 days before like you just said, but we realized that if the fibrinogen is normal, you can start just the day before. It's enough.
If the fibrinogen is low, then we usually send it at least one month before to the hematologist and usually give it until the fibrinogen is normalized before the sclerotherapy which take one to two months. - [Audience Member] Alright.
- [Audience Member] Thank you. Very important topic. - [Audience Member] Yes, very interesting topic and I think we learned a lot.
- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent
secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results
in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different
in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,
or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,
PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus
or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk
of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,
but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.
and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.
Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.
So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.
Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.
In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,
and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide
a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.
And an E-portal is being developed for dissemination. Thank you very much.
- So 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.
- 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.
- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing
renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is
near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital
pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency
and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,
except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward
endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac
endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.
The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open
conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small
accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited
incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,
but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis
and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.
- Great, thank-you very much, a pleasure to be here. My disclosures. So, we've talked a little bit about obviously percutaneous and thrombectomy techniques. Obviously we have catheter-directed thrombolysis with TPA, but what happens when we can't use TPA
mechanical techniques? We've discussed several of them already in this session, I'm going to try to kind of bring them together and note the differences and how they evolved. And really look at fragmentation, rheolytic therapy, vacuum assisted devices, and vacuum and suction devices.
So when do we need these? Patients that can't tolerate thrombolysis, can't get TPA, that have a high risk of TPA, or maybe there is a situation we need a rapid response. We're trying to create flow and establish flow as much as possible and a lot of times we use this
in combination therapy if we've already hurt. What's the ideal device? I think there are multiple different characteristic's that could define the ideal device. Obviously we want it simple to use, We want it to be reproducible,
we want it to remove a lot of thrombus, but minimize blood loss and trauma to the vessels and to the blood cell. These are just some of them. There's a lot of mechanical thrombectomy devices right now on the market continuing to grow,
both in the arterial and venous system so I think this is going to be an evolution. We started really using mechanical fragmentation with a pig tail and spinning a pig tail. We used that. A lot of times the patient with severe massive pulmonary embolism.
These we're really small antidotes, small case reports. Will Kuo, looked at these in the 2009 and basically saw over all clinical success, about 86% using these mechanical devices. Then we had some that were even more automated.
All these did was break up the clot. So you have the Trerotola Device , Cleaner Device, really almost in the dialysis space. Rheolytic Throbectomy, we've already heard about. Some of how it works and the advantages. Really I think this is the first time we've saw
a system which would try to aspirate and remove some of that thrombus as it got broken up. The PEARL registry really showed for the first time, maybe we can get this done within 24 hours, can we get this done in one session? Unfortunately in this registry only about three or
four percent of patients actually had just rheolytic therapy alone without any TPA. We've discussed a little bit about the use of Ango and this type of device in terms of bradyarrhythmia's and that may be a limitation. But I think we can still use it particularly
outside of the chest. So What about suction devices? You can have a catheter, I think a catheter suction device is very limited. We use that in the arterial tree when there is a small thrombus, a small embolus, I think
we're very limited, not only in the amount of thrombus we can remove but the amount of suction we can apply. Other types like almost mechanical, very simple to use systems is the aspire device. Well you can basically create and suction a
limited area and then help you aspirate the thrombus. And then to the other extreme. We're going to hear my next speaker talk about Angiovac, again a different system, a different system requires a patient on bypass large 26 french devices.
Where we can actually go in and deal with a large amount of thrombus, like this patient had a thrombus cave on both iliac veins. And to be able to basically come with this vacuum aspiration system over wires and kind of pulling them out and you get these little canisters,
seeing what you've actually removed. Very gratifying. But takes a lot of work to get it going. We've heard a little bit about vacuum assisted with the Indigo system. With a system of creating a constant continuous vacuum.
We now have eight french catheters with incredible aspiration volume, almost 20cc's, I'm sorry you can get up to 140cc's of thrombus in a minute can be aspirated quickly. Here is a patient, 80 years old, colorectal CA. You can see the thrombus in the right leg.
There was actually a mass invading this vein. That is where we wanted to use thrombolysis, really went a head and you can see the amount of thrombus. Cleared this out with some passage. You can see this here, the separator. You started seeing thrombus especially when
its acute it kind of looks like this. It's kind of gelatinous, things that we've already seen, and then went ahead and placed a stent, dilated that stent. Had to clean up some more with the device
on top of the stent, but with a good result without needing any TPA. Other types of extraction devices we've seen the Inari device, again this is like a stent Triever device, a nitinol ring we can use this in the pulmonary arteries.
And we've already seen previous and talked about the ClotTriever device Again remove that thrombus, put it into a bag and remove it. So again, capture and removal of thrombus. And this is a solution without the need of TPA. New kid in the block the JETi device
Again very similar to aspiration Indego device, but at the same time it has a jet to macerate the clot and kind of break up the clot a little to smaller areas so we can able to thromb and take more out. I think really here what I've seen and Dr. Razavi
showed me this case. Being able to treat a patient quickly, treat that patient very quickly you can see the amount of thrombus being able to, within about an hour and 15 minutes, get all that thrombus, then create patency in that vein and he showed
some early initial good data. Over the last year we did have a paper that was presented here and published this year in the Journal of Vascular Surgery, venous and lymphatic disorders and again pulled multiple patient's, again showing that
it affective and safe. We still need better data. We need to figure out which patients are best treated with which devices and which again will be affective. Thank-you very much.
- I congratulate Dr. Ken Ouriel for the great presentation, no? And I suppose the most important result of this presentation is the fact that after 15 years of turf battles many US vascular surgeons seems to accept CAS as an alternative to carotid endarterectomy
for the treatment of caro this is, for me, a great deal, a really great and nearly revolutionary news. But it's also unfair news, because using this technology, you try to exclude the interventionalist cardiologists
and radiologists from the CAS procedure without any scientific demonstration. The rationale for transcarotid revascularization is the fact that the main assertion is that advancing guide wires through the arch, you may provoke stroke.
Is this really the real situation? As interventional cardiologists, we have a fact that every day, many thousand of intervention passing the arch at least three times per intervention, and that terrible embolizations
are absolutely a rarity. Of course, if you have problem to manipulate the guide wire, and to navigate the balloons and catheter, guiding catheters, then of course you may have complication,
and you have to be very well-trained. I was asking some vascular surgeons in Germany and in other countries, and Professor Torsello said, if I expose the common carotid artery, then I expose also the internal carotid artery,
and I make a carotid endarterectomy, and Dr. Deloose in Belgium said, the incision is not so easy as described, and there is no evidence that using this technology, you reduce also the complication in comparison to the use of MOMA,
and his conclusion is endo is endo, and open is open. So, if you look through the published data of TCAR in 2018, are really not robust because you don't have only one article in press or a presentation, no more data.
And if you look at the fact that they are using only one stent, you cannot perform, as we are continuously trying to explain that you have to perform a tailored intervention and you have to use different stents, and not only one stent.
And if you look at this presentation of Peter Schneider, you see that you are in a range of complication of 2.7%, and if you look at this interesting slide, you see that the difference between endarterectomy and TCAR is practically minimal,
and to demonstrate a difference of .2%, you will need nearly 60 thousand patients per group, and if you want to make the same study with a transfemoral application of the MoMa system, probably you need 100 thousand patients per group. And we publish and redid in 2010,
in 1300 patients, and we had a complication rate of dissecting any type of arch, predominantly we had more than 50% Type II and III, we didn't have any myocardial infarction, although more than 50% of the patient had coronary artery disease,
and also in octogenarian, the complication rate is in a range of 2%, and all these data have been absolutely confirmed by the ARMOUR study, and you see that in the symptomatic patients, the complication rate was 0%,
and in the meta-analysis, you have a total incidence of 1.7% of complication, and if you look to the PROOF Silk, then you have a little more than 100 patients with a new lesion, 18%, however, only perfusion,
I'm sorry, has been performed only in 10 of 56%, for me it's very difficult to calculate 18% in 10 patients. If you look to our study with the MoMa, we are in a range of 26%, however, performing simultaneously
the diagnostic angiography. So, we do not have an important analysis, it's the fact that we don't have a consideration about the ability of the interventionalist or of the vascular surgeon regarding the reduction of complication,
and looking at the not robust literature, I have the impression that many vascular surgeon are at the moment looking for new application of a vascular knife, this is my final conclusion. Thank you.
- [Presenter] Thanks again, Laurel, for this kind invitation. We're going to discuss about how I do the treatment for varicose veins for the foot. And we're going to show you our experience for that. I have no disclosure. I came from Natal, Brazil.
There's our wonderful beach that we have there, but we don't have time to go there, unfortunately. This is our hospital, and these are the people that worked with us. To do this treatment we have to pay attention of the history and the physical examination.
It's very important to decide what you can do to these patients, because we have to associate some tools to do this kind of treatment. So phleboscopy, transillumination is very important to define the feeder veins,
so it's very important in this case to show us where is the veins that we feed these spider veins to treat that. And of course, the ultrasound associated with all the physical examinations of course and then the black scan. You can see in this case, a patient does not have any
varicose veins on the thigh, of the leg. They have only varicose veins by the foot. If you can see, the reflux of there, comes from the junction to the foot. If you don't have the good ultrasound
or duplex scan it can have a mistake and treat wrong way these patients. So, what are the tools we have to do to treat these patients? A lot of tools, you can see the liquid sclerotherapy with a low concentration of 75%.
Foam polidocanol for these two concentrations. Of course, transdermal laser, hooks that we can apply in the surgery and polidocanol laser. How about this procedure? This paper from the Netherlands, show us patient satisfaction after ambulatory phlebectomy
of varicose veins, what they conclude about that. The most important factors that influence the patient satisfaction is: discoloration, persistent pain, and the perception of varices after surgery. This last one is very important for us,
because the patient comes to us to be cleaning off veins of the foot, if we miss that everything we did, the patient will complain about after their surgery. We have two kinds of treatment, ambulatory treatment being the option
and the hospital we can do the procedures. We have separate patients with CO grade, CEAP classifications and C2 classifications. When we have a C1 grade classification we use transdermal laser and liquid sclerotherapy. You can see one case is a cosmetic
and one is a severe one. A C2 case we have ambulatory treatment, we have transdermal laser and we associate all this with foam sclerotherapy. But the concentrations are 0.5% and 0.25%, you can see its low concentrations.
At the hospital we have can do almost everything nearly in the same day. Transdermal laser, liquid sclerotherapy, foam sclerotherapy. Yes, we can associate liquid sclerotherapy, sometimes the people say that you cannot do that, but we do that.
In case like this, we also say transdermal laser in spider veins, phlebectomy and you can see in this case we have a use for sclerotherapy and is this is the result of 60 days. This other case that we use phlebectomy and we have to be careful because you
can take nerves, the patient will complain about after surgery. And these are the results. Polidocanol with laser tool, yes, but it's not our routine to use that. In conclusion:
Physical exam and a precise diagnosis of the feet varicose veins is essential to do a good surgery. With all these tools, that we have, the treatment of varicose veins of the foot is safe and effective. This is my fugu in Natal, Brazil.
- Good morning. I'd like to thank Dr. Veith and Symposium for my opportunity to speak. I have no disclosures. So the in Endovascular Surgery, there is decrease open surgical bypass. But, bypass is still required for many patients with PAD.
Autologous vein is preferred for increase patency lower infection rate. And, Traditional Open Vein Harvest does require lengthy incisions. In 1996 cardiac surgery reported Endoscopic Vein Harvest. So the early prospective randomized trial
in the cardiac literature, did report wound complications from Open Vein Harvest to be as high as 19-20%, and decreased down to 4% with Endoscopic Vein Harvest. Lopes et al, initially, reported increase risk of 12-18 month graft failure and increased three year mortality.
But, there were many small studies that show no effect on patency and decreased wound complications. So, in 2005, Endoscopic Vein Harvest was recommended as standard of care in cardiac surgical patients. So what about our field? The advantages of Open Vein Harvest,
we all know how to do it. There's no learning curve. It's performed under direct visualization. Side branches are ligated with suture and divided sharply. Long term patency of the bypass is established. Disadvantages of the Open Vein Harvest,
large wound or many skip wounds has an increased morbidity. PAD patients have an increased risk for wound complications compared to the cardiac patients as high as 22-44%. The poor healing can be due to ischemia, diabetes, renal failure, and other comorbid conditions.
These can include hematoma, dehiscense, infection, and increased length of stay. So the advantages of Endoscopic Vein Harvest, is that there's no long incisions, they can be performed via one or two small incisions. Limiting the size of an incision
decreases wound complications. It's the standard of care in cardiac surgery, and there's an overall lower morbidity. The disadvantages of is that there's a learning curve. Electro-cautery is used to divide the branches, you need longer vein compared to cardiac surgery.
There's concern about inferior primary patency, and there are variable wound complications reported. So recent PAD data, there, in 2014, a review of the Society of Vascular Surgery registry, of 5000 patients, showed that continuous Open Vein Harvest
was performed 49% of the time and a Endo Vein Harvest about 13% of the time. The primary patency was 70%, for Continuous versus just under 59% for Endoscopic, and that was significant. Endoscopic Vein Harvest was found to be an independent risk factor for a lower one year
primary patency, in the study. And, the length of stay due to wounds was not significantly different. So, systematic review of Endoscopic Vein Harvest data in the lower extremity bypass from '96 to 2013 did show that this technique may reduce
primary patency with no change in wound complications. Reasons for decreased primary patency, inexperienced operator, increased electrocautery injury to the vein. Increase in vein manipulation, you can't do the no touch technique,
like you could do with an Open Harvest. You need a longer conduit. So, I do believe there's a roll for this, in the vascular surgeon's armamentarium. I would recommend, how I use it in my practices is, I'm fairly inexperienced with Endoscopic Vein Harvest,
so I do work with the cardiac PA's. With increased percutaneous procedures, my practice has seen decreased Saphenous Vein Bypasses, so, I've less volume to master the technique. If the PA is not available, or the conduit is small, I recommend an Open Vein Harvest.
The PA can decrease the labor required during these cases. So, it's sometimes nice to have help with these long cases. Close surveillance follow up with Non-Invasive Arterial Imaging is mandatory every three months for the first year at least. Thank you.
- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide
and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter
is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues
that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement
of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side
and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,
then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,
coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,
and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques
with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation
of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.
We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go
so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side
or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.
Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.
On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded
and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.
Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.
Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,
despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients
to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,
and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,
and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.
- Thank you very much. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,
12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end
or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three
now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing
that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,
they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.
The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal
and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients
were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.
That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.
Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known
that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage
for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available
in about a month, thank you.
- Thank you very much, so my disclosures, I'm one of the co-PIs for national registry for ANARI. And clearly venous clot is different, requires different solutions for the arterial system. So this is a device that was built ground up to work in the venous system. And here's a case presentation of a 53 year old male,
with a history of spondylolisthesis had a lumbar inner body fusion, he had an anterior approach and corpectomy with application of an inner body cage. And you can see these devices here. And notably he had application of local bone graft and bone powder
and this is part of what happened to this patient. About seven days later he came in with significant left leg swelling and venous duplex showed clot right here, and this extended all the way down to the tibial vessels. And if you look at the CT
you can see extravasation of that bone powder and material obstructing the left iliac vein. And had severe leg swelling so the orthopedic people didn't want us to use TPA in this patient so we considered a mechanical solution. And so at this day and age I think goals of intervention
should be to maximize clot removal of course and minimize bleeding risk and reduce the treatment or infusion time and go to single session therapy whenever possible. Our ICUs are full all the time and so putting a lytic patient in there
reduces our ability to get other patients in. (mouse clicks So this is the ClotTriever thrombectomy device. It has a sheath that is a 13 French sheath and they're developing a 16 French, that opens up with a funnel
after it's inserted into the poplitiel. So the funnel is in the lower femoral vein and this helps funnel clot in when it's pulled down. The catheter has this coring element that abuts the vein wall and carves the thrombus off in a collecting bag
that extends up above to allow the thrombus to go into the bag as you pull it down. So you access the popliteal vein, cross the thrombosed segments with standard techniques and you need to then put an exchange length wire up into the SVC
or even out into the subclavian vein for stability. And then the catheter's inserted above the clot and is gradually pulled down, sort of milking that stuff off of the wall and into the bag that is then taken down to the funnel and out of the leg.
So this is the patient we had, we had thrombus in the femoral and up into the IVC. Extensive, you can see the hardware here. And it was very obstructed right at that segment where it was, had the bone material pushing on the vein it was quite difficult to get through there
but finally we did and we ballooned that to open a channel up large enough to accommodate ClotTriever catheter. We then did multiple passes and we extracted a large amount of thrombus. Some looking like typically acute stuff
and then some more dense material that may have been a few days worth of build up on the wall there. We then stinted with an 18 by 90 across the obstructed segment and this was our completion run.
It's not perfect but it looks like a pretty good channel going through. This is the hardware not obstruction at that level. Hospital course, the patient had significant improvement in their swelling by post-op day one. Was discharged on compression and anti-coagulation.
He returned about two months ago for his three month follow-up and really had very minimal symptoms in the left leg. Venous duplex showed that the left common femoral was partially compressible but did have phasic flow and the stent appeared to be open through it's course.
So of course this is an anecdote, this is early in the experience with this catheter. There have been numerous improvements made to ease the use of it and do it in fewer steps. And so we're starting a ClotTriever outcomes registry
to enroll up to 500 patients to begin to define outcomes with this device. It does offer the promise of single session therapy without lytic administration and we'll see how it performs and which patients it works best in through the registry.
Thank you very much.
- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.
It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.
So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations
of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.
Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.
So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient
who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal
angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near
or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility
was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.
Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal
or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection
or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.
So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump
to prevent hip disarticulation. Thank you for much for your attention.
- 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. Once again, thank you for the invitation. Last large chronic venous disease epidemiological study in Poland was done years ago, 2003, published by Arkadiusz Jawien and this was based on the 40,000 population of the patients visiting GPs.
This was the prevalence of the disease. 48% for female and 37% for male population. So this was the study concept background. The population changes, lifestyle changes also observed and we probably can also have some changes in the prevalence and the character
of the risk factors like obesity, physical activities. So it's perhaps time to update the knowledge concerning the emergence of the chronic venous disease. And that's why we presented ZEUS study. Zbroslawice, Epiedmiological Ultrasound Supported Study on the prevalence and risk factors
for the chronic venous disease and done in Poland. There is Poland, there is Zbroslawice. Small commune in the Silesia region with 1,500 people, the population. We randomly selected from the database of the commune of Zbroslawice 1,314 patients
and took these patients for exam between risk factor assessment, symptom assessment, sign evaluation on both extremities and also the clinical severity for classification CIVIQ. We know the patients and their ultrasounds were performed. The results is of the first 800 patients.
They're aged from 18 to 80 years. Similarly amount of female patients, median age of 53. And this is the year 2018 and the prevalence of chronic venous disease in Poland seems to be 68% of female population and 39% for male population concerning symptoms and/or signs of chronic venous disease.
This is also age-dependent but also in the population below 30, we can see that more than 40% of female population and 20% of male population suffer from this kind of disease. This is the highest c class reported in the group. So far it remains the highest class in 16% of females and 11% of males and C0s prevalence 4% in the study group.
This is the rate of the signs of chronic venous disease in general population with the prevalence of C1 lesions 62% in female population and 35 in male population. Concerning the general population, 32%, women 22%. Men is also dependent on the age of the patients growing up with the patient age together considering
both male and female population. Concerning the ultrasound studies, all the patients were studied. C1 presence in the patients with truncal/saphenous reflux was 41% and C1 presence in case of any reflux detected was almost 60%.
C2 presence and truncal/saphenous vein reflux, 69% and 11% of cases we found truncal/saphenous vein but without ostial incompetence. And concerning C3 pathology, more than half of these patients positive in terms of reflux present. Symptoms, as the symptoms were also evaluated,
in general population, symptomatic patients is more than half of female population and 30% of male population. In the group of patients with C1-C4, the classification a much higher rate was reported. More than 50% concerning all these symptoms investigated
and as you can see, the severity grows with the class C reported. Concerning venous clinical severity score, it's changing together with C class but also the age of the patient as reported on this slide. Looking for the risk factors,
we identified genetic predisposition and also one of the major and confirmed factors for the disease presence and also BMI especially in the patients in their 40s appears to be a a risk factor for varicose vein occurrence. Considering pregnancy importance in terms of C1 lesion, occurrence and also concerning varicose vein ratio
for pregnancy is 2.6. No relationship between working in sitting position and standing position and performance of sport activities. So conclusion, the prevalence is high and the number of symptomatic patients growing up in accordance to the age of the patient
and also the clinical severity. BMI presence and the number of pregnancies as well as genetic predispositions remains the major risk factors influencing on the disease occurrence. I would like to especially thank
the Zbroslawice Commune Council and this is my slide. If possible, and if you have time next year, I would like to invite you to CRACOW UIP meeting. Thank you very much.
- 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.
- 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.
- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.
Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.
Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care
over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.
Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.
And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed
with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better
treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?
That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents
shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,
deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.
Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.
Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.
Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same
that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?
More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article
a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.
- Like to thank Dr. Veith and the committee for asking me to speak. I have no conflicts related to this presentation. Labial and vulvar varicosities occur in up to 10% of pregnant women, with the worst symptoms being manifested in the second half of the pregnancy.
Symptoms include genital pressure and fullness, pruritus, and a sensation of prolapse. These generally worsen with standing. Management is usually conservative. Between compression hose, cooling packs, and exercise, most women can make it through to the end of the pregnancy.
When should we do more than just reassure these women? An ultrasound should be performed when there's an early presentation, meaning in the first trimester, as this can be an unmasking of a venous malformation. If there are unilateral varicosities,
an ultrasound should be performed to make sure that these aren't due to iliac vein thrombosis. If there's superficial thrombosis or phlebitis, you may need to rule out deep venous extension with an ultrasound. When should we intervene?
You may need to intervene to release trapped blood in phlebitis, or to give low molecular weight heparin for comfort. When should a local phlebectomy or sclerotherapy be performed? Should sclerotherapy be performed during pregnancy?
We know very little. Occasionally, this is performed in a patient who is unknowingly pregnant, and there have been no clear complications from this in the literature. The effectiveness of sclero may also
be diminished in pregnancy, due to hormones and increased venous volume. Both polidocanol and sodium tetradecyl sulfate say that there is no support for use during pregnancies, and they advise against it. So what should you do?
This following case is a 24 year old G2P1, who was referred to me at 24 weeks for disabling vaginal and pelvic discomfort. She couldn't go to work, she couldn't take care of her toddler, she had some left leg complaints, but it was mostly genital discomfort and fullness,
and her OB said that he was going to do a pre-term C-section because he was worried about the risk of hemorrhage with the delivery. So this is her laying supine pre-op, and this is her left leg with varicosities visible in the anterior and posterior aspects.
Her ultrasound showed open iliac veins and large refluxing varicosities in the left vulvar area. She had no venous malformation or clot, and she had reflux in the saphenofemoral junction and down the GSV. I performed a phlebectomy on her,
and started with an ultrasound mapping of her superficial veins and perforators in the labial region. I made small incision with dissection and tie ligation of all the varicosities and perforators, and this was done under local anesthesia
with minimal sedation in the operating room. This resulted in vastly improved comfort, and her anxiety, and her OB's anxiety were both decreased, and she went on to a successful delivery. So this diagram shows the usual location of the labial perforators.
Here she is pre-op, and then here she is a week post-op. Well, what about postpartum varicosities? These can be associated with pelvic congestion, and the complaints can often be split into local, meaning surface complaints, versus pelvic complaints.
And this leads into a debate between a top down treatment approach, where you go in and do a venogram and internal coiling, versus a bottom up approach, where you start with local therapy, such as phlebectomy or sclero.
Pelvic symptoms include aching and pressure in the pelvis. These are usually worse with menstruation, and dyspareunia is most pronounced after intercourse, approximately an hour to several hours later. Surface complaints include vulvar itching, tenderness, recurrent thrombophlebitis, or bleeding.
Dyspareunia is present during or at initiation of sexual intercourse. I refer to this as the Gibson Algorithm, as Kathy Gibson and I have talked about this problem a lot, and this is how we both feel that these problems should be addressed.
If you have an asymptomatic or minimally symptomatic patient who's referred for varicosities that are seen incidentally, such as during a laparoscopy, those I don't treat. If you have a symptomatic patient who has pelvic symptoms, then these people get a venogram with coils and sclerotherapy as appropriate.
If they are not pregnant, and have no pelvic symptoms, these patients get sclero. If they are pregnant, and have no pelvic symptoms, they get a phlebectomy. In conclusion, vulvar varicosities are a common problem, and usually conservative management is adequate.
With extreme symptoms, phlebectomy has been successful. Pregnancy-related varicosities typically resolve post-delivery, and these can then be treated with local sclerotherapy if they persist. Central imaging and treatment is successful for primarily pelvic complaints or persistent symptoms.
- 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.
- Now we are delighted that there's apparently two things that we came up with years ago proved useful. This is the Near-Infrared Spectroscopy slide by Joe Bavaria from UPENN providing patient data on delayed paraplegia. That's a problem that we see in open NN (mumbles) very frequently.
How does the NIRS work? And again to this illustrative picture and now imagine the spinal cord sitting here in the spine canal and there's no more blood flow and this is the end result. When you know the oxygenation in the collateral network
and there was the problem with this technology that had been attempted 12 years back already, in Houston, I bet they put the NIRS optodes in the midline and the light cannot penetrate bone so it didn't work. But if you put it on the collateral network
and you measure the oxygen in this area, you obviously know it in the spinal canal. Dorsal view, again, so this is position of the optodes and this is oxygen content way interested in it. This is another cast just to illustrate
how these segmentals are regionally connected into the spinal canal, obviously. Experimental validation and pilot series in the next two minutes. Experimental cross clamping, this is the setup so years mentoring Laser Doppler Flow
to a real time evaluation of what you measure with your infrared setup in the animal lab and we see here, correlation is very nice between the lumbar NIRS, optodes, and the actual lumbar spinal cord oxygenation measured by Laser Doppler which is evaluated
with other techniques. Very nice to see the corelation between the two. So lumbar collateral network NIRS directly reflects spinal cord tissue oxygenation. After we have proven that step, next step was serial segmental artery occlusion.
As this is a technology that we or the strategy that we using, obviously want to know with our monitoring works for that. You see here, experimental setup basically the same. Starts with anesthesia, exposure of the segmentals. Now an open approach
and then you get 120 minutes surveillance period. You got a drop or dip in the NIRS measurements. Interestingly in the experimental setup in the recovery group, you see here that the new logical function comes back after the procedure and the NIRS comes back after the procedure.
Paraplegic group, all segmentals sacrificed NIRS, drops after the procedure in the first couple days, and the neurologic function does not recover. So experimental evidence that actually works. Nice corelation, again, so the experimental validation proves that lumbar NIRS
reflects lumbar spinal cord oxygenation and reacts to occlusion, of segmental arteries in real-time, but careful it's only regional so where ever you put your optodes, this is the area where you can monitor
your collateral network associated dip when you coil or include the segmental arteries. First clinical results published a couple years ago, I think you have all seen this video. Optodes are putting in the back of the patient, same setup for endo and open
and then we take the monitors theory and we have real-time monitoring on oversights midline here, this is (mumbles). Concept validation from 2016 with the first clinical data and now we're working on the clinical evaluation
of the use of this technology in EVAR and in clinical coil-embolization. 11 patients have been included so far for the EVAR group and you see here, it is very sensitive when you put stent in, stent deployment, but we have to still work so to speak
on the area that we have to monitor. There's a lot of work to do and probably also device modifications are necessary. MISACE, last couple words, on this you see pretty stable, NIRS all over the time course and actually this is nothing we wouldn't have expected
because the patient obviously were protected from spine cord anesthesia. So also here but sometimes we see a significant drop and this is when you should be careful and that's when you usually stop the procedure. So in conclusion, minor changes
in Collateral Network oxygenation have been seen in EVAR in this preliminary results using the nearest technology and to establish one very nice ... Nicely how clinical practice is already guided at his institution.
There's no immediate complete occlusion of covered segmental arteries and there's ongoing study in very heterogeneous patient group. There's no relevant changes with the chlorine technology so far,
but that, just to remind you, is the purpose of this technology, that we do not harm the patient during the preparation period. Thank you very much for your attention.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
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