- 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.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.
- Thank you, 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 Frank for the opportunity to speak on this important topic. 1987, I remember a cardiac surgeon colleague of mine mocking the cardiologist doing an angioplasty. He called it a scheduled heart attack. Back in an era when cardiac surgeons were the highest skilled in all of medicine,
why in the world should they be concerned about a clunky angioplasty catheter? How would they know that it would crush the career and the specialty of cardiac surgery? Such an entity where a powerhouse is attacked from below is called a creative disruption.
Let's look at it a little closer. On the vertical axis is performance. The horizontal is time, and the disruptor attacks from below, starts in an uncontested market, iterates by market pressures, and moves upstream. By the time the incumbent realizes it, it's too late.
Other examples are Borders books, Detroit auto, your stock broker, and even your travel agent. High achievers, such as vascular surgeons, are the most vulnerable because we tend to always focus on the highest ROI. I traveled to Harvard to talk with Clayton Christensen,
the architect of creative disruption. He's widely published and received many accolades. In fact, Forbes calls him the most influential business theorist of the last 50 years. But I must say, he's a warm and humble man, and we talked about how creative disruption applied
to our specialty vascular surgery. Turns out that vascular surgeon pioneers were disruptors. They took what cardiovascular surgeons didn't want to do and what general surgeons didn't do very well. More recently, Parodi and Veith disrupted the elegant world of open aortic surgery, and that took a page
right out of the playbook of the disruptor, starting out as clunky but rapidly iterating and moving upstream. Let's take a look. Initially for only high-risk poor surgical patients, then for easy anatomy, then for challenging anatomy,
then for thoracic locale and even side branches. Aortic stent grafting has been a ruthless and colossal success as it disrupted open aortic surgery. So, how can we be certain that our specialty won't be devoured by the next disruptor? Well if we fail, it's because we focus
only on what we do best, operate. It might look like this. Let podiatry admit the patient with the gangrenous toes. Let the hospital submit the DVT. They can call us if they need lysis. I don't pick scabs.
They can call me if they need a bypass. Let IR embolize that bleeding vessel. I'll get a good night's sleep and be ready to do my cases tomorrow. Have critical care admit that type B dissection. I'll stay and do the more lucrative cases.
And, that's all before cardiology decides they want to do our peripheral interventions. So now, we've lost our patient base, vascular surgery has collapsed. We've been reduced to being a subordinate proceduralist, a subordinate proceduralist.
So, what's the recipe for success? Professor Christensen said it relies on a job to be done. We need to focus on what our patient needs and not frame them by our attributes. What did they hire us for? To fix their broken blood vessels, and we need to do it
with whatever method possible, a scalpel, a stent, a statin, an eye of newt, a toe of frog. Gretzky succeeded by skating to where the puck was going, and we need to do the same by being able to scan, identify, and vet whatever methods are best for our patients. We need to resist the urge to just solo faster
and book another case, but rather discover new and emerging therapies. We need to refuse to be defined by an RVU generating commodity that handicaps us in our ability to champion our patients. We need to learn from our cardiac surgical colleagues
that just strengthen existing skills, but rather develop new skills and competencies. We definitely can't wait until we see a downturn in our business because at that point it's too late. I submit to you that there are disrupting clouds on the horizon for vascular surgery in the near future.
In this Darwinian world, it's not the strongest of species that survives nor the most intelligent but the ones that respond to change. So, it's absolutely critical that we form an independent American Board of Vascular Surgery, so we can be agile and responsive to change,
and we can leverage our asymmetric advantage of vascular surgeons that is perspective, motivation and skill. It will allow us to control our curriculum, to be disease process centered and outcomes driven. We can be agile, brand our specialty,
and champion our patients with the best therapy available. Victor Hugo says nothing is more powerful than an idea whose time has come, and I submit to you that an independent American Board of Vascular Surgery is an idea whose time has come, thank you.
- Thank you so much for the opportunity to present our experience. You are all familiar in this place with the SVS classification for blunt aortic injury, and you all know that it doesn't tell you what to do with each patient,
it doesn't guide treatment. A few years ago we presented a simple, practical grading system based on CAT scan findings for the management of these patients. When a patient has a minimal aortic injury, it's a patient with no aortic contour abnormality,
they have either an intimal flap or a small thrombus less than 10 mm. These patients we don't do any interventions. Patient's that present with an aortic contour abnormality or a large intimal flap or large thrombus have a moderate injury.
These patients get repair in a semi-elective manner once they have stabilized further injuries. One the other hand, persons that present with a severe injury, persons with active extravasation, this patient need to go to the OR because he's dying
and this takes precedence above any other injuries. So, since we implemented this system we took a three years look from 2014 to 2017 to see how are our results. We have 87 patients, 63 percent were moderate, 28 percent minimal, and nine percent severe.
None of the patients underwent open repair, and none of the patients with a minimal got fix. All but three of the patients with a moderate, and all but one of the patients with a severe have TEVAR as a repair method. These are very sick patients, high in the severity scores,
with high rates of intracranial hemorrhages and associated injuries. When we look at the anatomy, the patient with a severe injury are more likely to have a bovine arch anatomy. These are young patients with small aortas,
with a median aortic diameter of 23. The operative timing is the time since the patient hit the door of the emergency room to the patient getting to the OR, was 53 hours for a patient with a moderate injury, and three hours for a patient with a severe.
These are short procedures that can be done in less than 90 minutes with minimal contrast used, and around five minutes of fluoro time. We used intravascular ultrasound very widely. We have covered the subclavian artery
in around 40 percent of the patients. We do all this percutaneously. We are successful in around 86 percent of the cases. We have not had to revascularize any subclavian artery. We had one patient that required a plaque during the index case of the subclavian,
one patient that had a femoral pseudoaneurysm that we treated with thrombin, one patient that was already on a heparin drip for a PE. We took her to the OR more than 24 hours after the heparin drip was started, fixed the TEVAR.
After that the patient had a complete normal CAT scan. More than 12 hours after the heparin drip being restarted for the PE she had a worsening intracranial bleed. We don't know that was related to our procedure. We have no patient with new stroke
or worsening spinal cord injury for the procedure. 30-day followup CT scan had excellent remodeling in every single patient. We have not performed any delay interventions. Our 30-day mortality is very low. There is only one patient with an aortic-related mortality.
This is a patient that presented with a severe injury. She was more than 90 years old and the family elected to don't proceed with any treatment. So in conclusions, we consider the patients with minimal aortic injury do not require surgical treatment or followup imaging.
Patient with a moderate can be safely undergo TEVAR in a semi-elective manner once they are stable from other injuries, but the patient with a severe aortic injury require emergent repair. These procedures are very fast
and can be successfully performed percutaneously. Complications are rare, and the followup reveal excellent remodeling of the aorta that will likely result in longer interval surveillance requirements. Thank you.
- Great, thank you Tim and Dan, and thank you Dr. Veith, this is the first time actually we're presenting this. This is work that's been done between my fellow who's really the sophisticated one with this with his PhD, Luka Pocivavsek. Here's my disclosures, Luka doesn't have any.
Really three goals in mind when we looked at this methodology to try to assess the value and efficacy of long-term durability of necks. To identify patients that are high risk for device failure, potentially type one endoleak, device migration, failure of our proximal seal zone.
This is an example that this patient will come up through this entire presentation but someone that I treated with a rupture. Initially successful result, then developed a dilation of the neck and then needed an additional procedure
to treat a type one endoleak. Second goal is maybe to look at appropriate device selection and sizing so we can prevent these complications from happening. So as an example, I'll show you this case, which for many of us is challenging
to select the right size proximal aortic endograft. You have a reverse taper of this neck, the cone, trying to figure out whether a 36 device is best because of the 32 diameter, but you're 23 proximally and maybe this technology will be able to help us identify which devices
will do better in certain anatomy. And finally evaluate the mechanisms of the interface, the adhesion that we see between the device and aortic wall for the current technology and potentially evaluate new device development. So what is this?
What we did is extrapolate from what was known from finite element analysis and this patient, as I mentioned earlier, presented with a rupture. We were able to look at her pre-rupture CT scan and with our technique predict the area of rupture
which is what we saw on CT scan and you can see this high-stress area. So we were able to define the aortic wall that was in the danger zone for rupture, and then took that analysis and started to extrapolate that understanding to looking
at the interface between the device and the aortic neck. So what we see here is post-implant with slightly challenging anatomy. A short neck, a little bit of angulation, and with Luka's expertise, we were able to really start doing
what we call this cohesive zone method and look at doing a really statistical analysis of what happens with the device and I'll show you that a little bit more. So when you look at this equation, it tells you what is the available literature
that we know for device displacement looking at the displacement of the interface of the graft to the aortic wall, and then the contact zone. And we can alter that in the computer model to change the Newton force that exists
and get a lower adhesion and then a stricter tight adhesion between the device and the wall and see the impact that has. So this is just showing you from the CT scan looking at the vector of stress and strain that we're able to look at in this model.
And then specifically what we see when there's separation of the device and the wall, there's areas that are higher strain and stress and you can see the vector differences here versus this area where there's a stiff contact and we're able to create,
it's much less and the risk of separation of device and wall is much lower. So we're able to take certain understandings and look at different geometries, change our pressurization, have the boundary conditions appropriate
and then start to really look at the zone mechanics. So what this looks like is you have two different adhesion models here. One is with weak adhesions of the device to the wall and one is where we can specifically create stronger adhesion and how this would be done down the road
would be potentially something that you could look at with device design, development, and with the weak adhesion you can see how the device basically falls out of the this challenging anatomy and with strong adhesion it does a little bit better.
There is some migration but not to the same extent. So what we're trying to predict is who has loss of seal and can we prevent this? And one of the mechanisms that we've started to look at is whether or not when you add endoanchor technology to the proximal seal zone to prevent that migration
if we can prevent this loss of seal. This is way too complicated but you get it, this is what we're looking at computationally, and this is what we see clinically. This patient who a year and a half later, develops a type one endoleak,
it's systolic pressures that are elevated, it's more extreme, and we think that there's some loss of seal that happens just when patients' pressure goes up too high. So in conclusion, we think that this is a nice extrapolation
of what we know from finite element analysis. Can be applicable to not just understanding if we've successfully treated patients but to potentially even size appropriately and evaluate new devices. Thank you.
- Thanks Sam and obviously thank you Dr. Veith and the group for the invitation to participate. These are my disclosures. Aortic arch pathologies vary and are similar to many of the ones that we treat in the rest of the thoracic aortic including: aneurysms,
penetrating ulcers, and complex aortic dissections. As well as some thoracoabdominal aneurysms that may extent in the aortic arch, making the procedures more complicated. As we go farther into the aortic,
both open and in the vascular procedures tend to be more difficult, more complicated, and associated with a higher complication rate. But open repair up to now, has continued to be the gold standard for the management
of many of the patients that have aortic arch disease. Because of the high risk of many of the patients and the increase utilization in the vascular technique, hybrid procedures continue to be developed and continue to be used for the management of these patients in a variety of combinations.
The use a branched devices for the management of patients that have arch disease, have been considered since the 1990's. But at the time some of the procedures that were attempted were associated with significant complications,
especially cerebral vascular complications. And then the concept of using a single branch device was developed, with additional extr atomic reconstructions, to try to limit some of those complications. Well in the United States currently,
there are multiple single branched devices that are undergoing evaluation and prospected trials. And some of the double branched devices, like the cook device, are being used in selective PSID's in the united states. Currently,
the Terumo double branch device, for the treatment of aortic arch disease, is the only multi branch device that is on their trials in the united states. This device is based on the the Relay NBS Plus platform. It's an off-the-shelf device that
in patients with a complex anatomy can be customized to be able to accommodate that anatomy. It has a large single window for ease of cannulation of the two internal tunnels that are usually used to cannulate and branch innominate of the left common carotid arteries.
And the devices intended for Zone 0 deployment combined with a variety of reconstructions, if necessary, depending on the patients anatomy. It leverages some of the patented proximal capture technology.
As well as improved our configuration and prevention of retroflex deployment of thoracic devices in these challenging anatomies. As a self-orienting pre-curved Nitinol guidewire lumen and additionally a dual sheath that is very helpful and designed to facilitate advancement into zone 0.
Currently, there's an early feasibility trial that is being conducted in the united state, for the management of thoracic aortic pahtologies requiring treatment proximal to the origin of the Innominate artery.
It's a prospective, multicenter, non-blinded, and non-randomized study. Which the goal of enrolling around 10 patients in this particular trial.
Six patients have been successfully treated with the first one being enrolled in January 2018. Two more patients are scheduled to be done in December, and hopefully we will finish this portion of the trial over the next few months.
There are for sites in the United States that are currently participating in this trial. When we look at some of the data that's currently available, this is all preliminary since the oldest patient in the trial has around nine months follow-up. Four patients were treated with Aneurysmal disease.
One patient with a dissection, and one patient an enlarging and symptomatic penetrating ulcer. At the time, 100 percent of the patients had technical success. And with a mean follow up with approximately four months,
very early follow-up in this group there have been no periprocedural or moralities, no major endoleaks, and no branch occlusions. There were a number of complications that happened
to this complex group of patients. The vast majority of them having resolved over the follow-up. And to note, the last two patients did have a neurological deficit that occurred, but most of these patients had atrial fibrillation,
chronic, and they were an anticoagulation. The first patient that had a neurological deficit occurred after patients discharge. It was minimally symptomatic, and the patient has completely resolved
within a day or two of the event. The second patient that had a neurological deficit this was noted around two to three days after the procedure was performed. The patient has partially recovered and has been discharged for the hospital
and is on close continued follow-up. This is the patient that was treated with a dissection with a complex aortic problem, and the device deployed very nicely in this complex anatomy, and the patient has continued to do well. So in conclusion,
This aortic arch multi branch device is the first on trials in the United states. The early feasibility experience has been highly encouraging. And the device tracks very well, self-aligns in the arch with minimal manipulation,
and deploys accurately. Based on the longer European experience and these early results, an international pivotal to study is under development. Thank you.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- Thank you, I've changed the title little bit, instead changes in AA neck morphology after standard EVAR and CHEVAS and they can be subtle and missed. And I'm a co-founder of endovascular diagnostics and my background of my slides is black because yesterday, Teo Fleugus passed away. Teo has served the endovascular fields
for more than two decades and Teo is an iconic and humorous Dutch giant and it's always been a pleasure and honor to work with him. The background of this presentation, slight changes in apposition and position of endograft in aortic neck can be missed
with standard imaging techniques like CT scans and duplex and the follow up imaging nowadays should prevent and should predict complications and not only show complications. That's why we, well we developed software, homemade software for precise determination
of the endograft position and apposition in the aortic neck post EVAR. And it serves, we transport the mesh of the aorta from a standard CT scan and use the 3D coordinates of a 3Mensio workstation and we definitely are able to calculate
and determine almost all the positional changes of the endograft in the neck post EVAR and also calculate the apposition of the endograft in the aortic neck. Well here, you can see some of the changes. The yellow bar is the apposition,
the circumferential apposition of the endograft in the aortic neck and during follow up, you can see that there is a loss of apposition, and of course, you want to avoid there is a complete loss in the patient coming with a type 1A endoleak and a rupture.
But to prove the concept of course, we had to prove that the software could really predict endografts' failure like migration and type 1A endoleak, so we had a co-ord of four groups of patients patients with type 1A endoleak,
patients with migration more than 1 centimeter, and those included 45 patients, then we had control patients without any endoleak or migration. We did a software analysis, so the determination of the apposition and position of the endograft in the aortic neck and we compared in the first
post-EVAR CTA scan and the late CTA scans, and here you can see what we mean with late CTA scan in the patients with type 1A endoleak and migration, it was the CT scan before the CT scan where the complication occurred.
Well, with the new software this is all on the CT scans before the complication in the patient with type 1A endoleak and migration, there is significantly loss of apposition, length, and also in the patient group with migration and the CTs
come before the complication really occurs the apposition is significantly lower. And also, there is more endograft expansion in the patients with migration, the endografts almost have expanded to 100%, and of course then
you will have a seal failure. What about EVAS? It is more challenging to calculate the apposition, so in the software we don't calculate the apposition but the non-apposition surface post
EVAS and post chimney EVAS. Here you can see one of the examples, the red area is the non-apposition, post-EVAS and also here you can see that sometimes it can be very subtle changes if you compare the one month and the
one year CT scan for these graft migrates because there is an increase in non-apposition. There are some different kind of migrations we call it displacement, post EVAS because it's not only a real migration but sometimes the endo backs and the stent frames bow,
and that causes also a kind of migration. And loss of apposition in inter-renal neck. And what is another important thing is you really have to determine the 3D position of the stent frames because here again we have the software usually in red
in the six months follow up, a slight displacement of the stent frames, and during one year, and 18 months here, you can see complete displaced stent frame, well of course again you want to have dealt complication before the complication
really occurs so you want to see it after 6 months. We have 20 patients with chimney EVAS. Five of them suffer a type 1A endoleak during follow up and again, we calculated the non apposition surface but also the other stent frames displacement and as you can see
here on this figure, there is a correlation between the displacement of the stent frames and the chimney grafts itself. Can we also predict (unclear), yes the five patients on the right is at a one-year CT scan, slight movement and displacement,
and here at more than one year, all those patients have type 1A endoleak and even one had a rupture. So to conclude, determination of the position and apposition of the stent grafts post-EVAR is, well it's necessary and we can
miss that with the standard CT scans so we advise to use them, the new software, which can really predict complications post-EVAR and EVAS, thank you very much.
- Good morning everyone. Right, I'm going to try and talk a little bit about really prediction in aortic dissection in TEVAR. These are my disclosures. If we're trying to predict poor outcome in acute aortic dissection there's a burgeoning list of factors
which we all recognize confer poor outcomes. Quite a few of these are easily seen on a CT scan, and (mumbles) looked at this for some time now. This is the latest and very good paper from Germany looking at number of factors which predict future aortic dilatation
after uncomplicated type B. So we know that there are images on static CT scans which imply to us that there's going to be a problem further down the line, and the key question is, which is still unanswered in my mind,
is do we actually treat the aorta properly with type B dissection by putting one or two stents into the thoracic aorta? Because we all know that whilst the TEVAR device will treat the immediately adjacent aorta very well and achieve false lumen thrombosis
it often does not do that with the abdomen, and you get continued false lumen perfusion and in some patients progressive abdominal aortic dilatation over time, and you can't really predict that from the beginning. I've got two pieces of data to show you really.
We've been looking at this with the engineers at Imperial College, and, first of all, I'm going to present a very quick volumetric analysis. We looked at 27 patients with four regions of interest, but we've only really got time
to focus on the 14 patients that underwent TEVAR, and divided aorta into the thoracic, visceral, infrarenal, and iliac segments and really looked at the baseline scans straight after TEVAR and a scan a year later and looked at changes in volume over time
and sorry, and at a number of these factors which anatomically you can see on CT scans to see if there was any correlations, and so what we found was that overall there was true lumen gain and false lumen loss once the patients had a TEVAR put in
which is what you hope for and expect, and that was really driven by the thoracic aortic segment because every single patient underwent true lumen positive remodeling and false lumen thrombosis in that part of the aorta. But if you look at the abdominal aorta
there was no such relationship, and many of these patients had false lumen perfusion and an increase in size over time, and that looked very much like the way that patients treated with beta medical therapy if you do a volumetric analysis of those.
And if we look at the factors that correlated with false lumen increase it was really the number of branches arising from the false lumen, the number of reentry tears in the thoracic aorta below the stent,
and there was an inverse relationship between the left subclavian and the first appreciable reentry tear in the thoracic aorta which I take to mean the greater the length of the stent you put in, the greater the chance of false lumen thrombosis,
and the same held true for the abdominal segment. The other thing we've been looking at is whether we can find a computational flow system which will accurately model false lumen thrombosis because if we could tell which patients from the very outset would have successful thrombosis,
then this could very much help with decision-making, and so we've been working on a system which basically relies on particles being accelerated through the entry tear, activating platelets that's disturbed in recirculating flow of the false lumen,
and you can start to see that some of these patients will thrombose their false lumen. And a year ago we published this which is really a model which the blue you see is thrombis forming in an aortic model. It's a real patient.
The CT scans at the end show that the actual prediction made by the model was quite accurate and show burgeoning thrombosis in this particular patient's false lumen. So we've now applied that to a more complex model which looks at a patient who's undergone a TEVAR,
and you can see that over about 20 or 25 cardiac cycles the false lumen, the prediction of whether or not flow is going to run in this is made by the algorithm, and this is the actual CT of the patient three years later. So there's quite a high degree of concordance, and this is another example of that.
So this model would appear to be quite successful in saying if you put a TEVAR we can tell from the outset of the 25, 26 cardiac cycles whether or not you are going to, the patient will thrombose the false lumen. So hopefully that will be a helpful tool.
I've run out of time but these are the conclusions. Thanks very much.
- BEVAR through the false lumen, it's rarely indicated. These are my disclosures. And usually, we proceed through the true lumen using BEVAR for post dissection aneurysm like in this case. From our experience, Regensburg and Nuremberg, at the moment the biggest surveys of 71 patient with post dissection aneurysm published
this year in European journal of Vascular and Endovascular Surgery. Sometimes it's necessary to go through the membrane from the true to the false lumen because of the urging of the arteries. And it was necessary in 14 out of 261
target vessels in this material. It makes about 5%. But sometimes, we have a very different cause of the chronic dissection. Like in this patient, where the true lumen shows a very big opening for the false lumen
and ends at the level of the renal arteries. And both legs are only perfused by the false lumen. So, what to do, and it was already some years ago, we decided to make a bypass from ascending to both femoral arteries and pseudoextenders use TEVAR for the aneurysm of the descending aorta.
Now, a case presentation, a 55 years old male patient with hypertension and nicotine consumption. He has had acute aortic dissection, 2014 with a true lumen collapse and dissection of superior mesenteric artery. He has had malperfusion of his intestine and right limb.
At that time, he was treated just by femoral-femoral bypass from left to the right and right hemicolectomy due to ischemic complication. Between 2014 to 2017, this dissection still started at the level of left subclavian artery. The aneurysm was progressive to 63 mm.
He has had the complete thrombosis of the thulomen at the level of the right renal artery with atrophic right kidney. He has had celiac trunk, left renal, and inferior mesenteric artery from the false lumen and dissected superior mesenteric artery.
The first procedure was in October, 2017 with the branching and the Amplatzer to the left subclavian artery to prevent retrograde flow. Branch device and uni-iliac tube because of occluded right iliac artery. After the first operation, we have seen
thrombosis of the thoracic aorta and patent segmental arteries at the level of celiac trunk. The second operation was deployment of covered stentgrafts balloon-expandable covered stentgrafts to the superior mesenteric, left renal and inferior mesenteric artery, why?
If you remember, the patient has had mesenteric dissection and only the right hemicolectomy. So we try to preserve all the collaterals to the intestine. And the third procedure, after balloon occlusion of the celiac trunk and branch, drainage, MEPS, and intrasaccular pressure measurement
was a completion of the celiac trunk with two stent grafts. Preoperative CT, a staged procedure with open aorta at the level of renal and mesenteric arteries, and then completion postoperative with all arteries perfused. Now, what we learned after this.
We may have different methodology. This patient is stable, the reconstruction is well-functioning after 12 months of follow-up, but we should always remember to tailor the procedure to the morphology, it is one of the ways. Thank you very much.
- Good morning ladies and gentlemen. I would like to thank Dr. Veith for his invitation. My topic would be on Risk Factors for New Distal sign after TEVAR for TBA dissection. So clearly TEVAR is currently the first line therapy for complicated type B dissection, but after five years follow-up,
more than 1/3 of the patients without reintervention because of various complication. One of the complications that you may face during the followup of this patient is a distal SINE. You can have a distal untreat here caused by the stent grafts that we fill during the followup.
So what we have done, we have done a systematic review using the PRISMA guidelines and we have been able to include more than 1,400 patients, 1,300 patients with type b dissection and clearly these incidents are quite high. Almost 8% of patients without doing
the follow up the distal SINE. The mean time to discover is almost two years and it's a symptomatic disease in nearly all of the patients. That's why it's very important to have a followup of this patient after TEVAR dissection.
Treatment was successfully altercated. These are year-long plus additional stent-graft placement in 53% of the patients. Regarding the timing, the incidents of distal SINE is clearly higher, three times higher in patients with chronic sections.
It's probably related to the srping back force of the stent graft that could damage the intimial membrane. When you are treating a patient with an acute dissection, the aortic wall is more elastic
and can better adapt to the stent graft when compared to the fibrotic aortic membrane of chronic dissection. Regarding the stent-graft oversizing, patients with oversizing distal oversizing, over 20% have a significantly higher risk of distal SINE
and it's related to what we call the taper ratio of thoracic aorta because we land, proximal land in distal lumen and when compared to the diameter of the distal landing zone that will be compressed true lumen. Also factors such as angulation of the distal neck
and the stent-graft length was not, as was stated, was a risk of distal SINE. Association with SINE and Marfan was inconsistent among the studies. Only one found a higher risk of distal SINE for population treated with TEVAR in Marfan.
So how can we prevent this complication? There is a strong link between oversizing and it can be proximal with the aortic dissection or it can be distal, and as was stated, it's a risk factor for distal SINE during follow-up so it's important to advocate moderate
proximal and distal stent-graft oversizing in patients treated for dissection. So if you look at the diameter at the distal neck for this patient, if you take the outer diameter, it would be around 39, but in fact, we have to rely on the maximum diameter of the tube
which would only be 28 millimeter. So how can we achieve or moderate distal oversizing that should be around 5-10%? Use a tapered stent-graft and there's no way because most of the times, discrepancy is smaller than four millimeter in diameter.
It's to perform an ascending endovascular repair. You first deploy the distal, smaller compartment and after you discharge your proximal one, which would be larger. We should advocate and avoid any balloon dilatation that can injure the aortic membrane.
Other approaches being advocated to prevent this complication. So petticoat approach seems to reduce the risk of distal SINE and T Kolbel proposed to remove the distal Z-stent of the Cook device to lower distal radial force
of a thoracic stent-graft. So in conclusion, the incidence is not insignificant. About 8% of the patients would have a distal SINE without followup. It's something that we clearly see more commonly in patients with chronic dissection
because aortic membrane is stiff and can adapt to the stent-graft. It can be safely treated by medical therapy or additional TEVAR, but it's important to follow these patients because it would be a symptomatic in nearly almost all the patients.
It's a complication which is related to the fragility of the aortic wall in this section. So it's a specific disease condition. Oversizing is the most important factor because of the mismatch between proximal, neck and distal compressed true lumen.
And it's important to have an accurate sizing for this patient and tapered stent grafts and ascending endovascular repair for dissection. Thank you.
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
- Thank you, Captain, and I'd like to thank Doctor Veith for the opportunity today to further this discussion about vascular injury care, specifically endovascular options that have continued to emerge and become a bigger part of our practice. Vascular trauma remains a challenging entity
for anyone who takes care of trauma patients, on the battlefield it accounts for 12% of our trauma incidents and it's the second leading cause of death in both civilian and military trauma. And some of the most challenging
are those non-compressible sites which represent a majority of those that we really struggle with. There are a number of involving technologies and approaches that have been applied to trauma, we were going to talk in other talks about
REBOA and some of those options. But for the purpose of the talk here, I'm really going to talk about endovascular stent grafts as emergent and definitive tool managements. These make sense for a variety of reasons,
endovascular is becoming a bigger part of the trauma toolkit because we've had a significant shift in elective and emergency vascular work towards endovascular surgery. Every trauma center now, if they don't have one, is developing a hybrid OR environment
which is capable of providing high-end endovascular care. And we have an increase in familiarity both among surgeons, IR providers, and a variety of providers who take care of these trauma patients. Unfortunately, however, we as of yet do not have
any trials yet to prove the practice is better than open approaches. But we do have some success stories. A blunt thoracic aortic injury, if you have to pick one, is certainly a success story in trauma. Everyone in this audience is familiar
with the way that this has evolved. This is just one of a number of studies including the two AAST Center studies in 2008 and 2009 by the Aortic Trauma Foundation recently published in 2015 which showed that TEVAR was associated with lower transfusion requirements,
lower overall mortality, and lower aortic-correlated mortality compared to traditional open-repair modalities. And in the time that these technologies have been introduced, they have really changed practice. But what about other locations?
We have a variety of other anatomic locations that historically and traditionally have been challenging surgical exposures, the carotid at the base of the skull, the thoracic inlet, all these represent challenging options for open repair amongst trauma surgeons.
We do have some good evidence that needs to be expanded and further built upon that carotid capabilities from an endovascular stent graph repair perspective, particularly for those injuries at the base of the skull can be performed with a reasonable modicum of success. And with good followup to two weeks to two years,
patency rates are about 80% with low appreciable neurologic deficits after stent placement. Axillo-subclavian injuries represent another challenging open exposure for most trauma surgeons and an opportunity for vascular surgeons to introduce some more effective endovascular
stent graft technologies for application. Just one paper here from a myriad of trauma centers, a collaboration conducted by Doctor Branco, who showed that endovascular repair with injuries at these locations was associated with significantly lower mortality,
lower rates of surgical site infections, and a trend toward lower sepsis rates. And when you look overall at the invasion, if you will, of endovascular technologies this was a very nice review from a national trauma data bank of the American College of Surgeons,
which was conducted over nine years and over 40,000 vascular injuries. And you can see there, over time, we have seen a significant increase in use of endovascular procedures to deal with these injuries. I would say now that that is based upon data
from the PROOVIT Registry that is now roughly 20% of all vascular injuries have some endovascular technology applied. And these resulted in lowering hospital mortality following endovascular intervention and lower complication rate trends.
This is the most recent review, conducted by one of our visiting fellows when I was at David Grant, Major Robert Faulconer was a review of the AAST, or American Association for the Surgery of Trauma, perspective observational vascular injury treatment trial,
or called PROOVIT for short. And just very briefly, the punchline from this examination was that favorable outcomes were observed when arterial injury at non-compressible sites of truncal hemorrhage was managed with endovascular approaches.
The endovascular group, despite being more severely injured, had a lower mortality and a lower packed red blood cell requirement. And we're also learning that these technologies can be applied in hybrid techniques. This is just a simple example of a case
that was encountered at my own institution, this was a young man who had a gun shot wound through the right iliac artery and vein. He had an attempted interposition repair which blew out in the setting of small bowel contamination from associated bowel injury.
And we were really left with a very challenging situation in a patient who was physiologically depleted and would not tolerate a repeat definitive repair. And very little tissue to roll over the graft. So what we selected to do was what is known as a direct stent endo graft repair, or DSER.
And we basically bridged this gap with an endovascular stent graft utilizing the radial force to create a space for repair and not having a suture line now at risk in this contaminated field. This patient did quite well and
is now six months out with good results. This has been written about by several individuals and investigators to explain the use of stent grafts not only as a proxy or replacement for the typical plastic argyle shunt options, but these can actually potentially
become left in place when you come back for the repeat damage control surgery after initial repair. You can cover this with tissue graft and you now have a sutureless repair that is not prone to blow out as many of these injuries are in contaminated fields. Lots of unresolved issues with the investigation
and continued research in vascular traumas, particularly as it relates to endovascular graft repairs. Patient selection, we deal with young patients, small vessels, that natural history's not well established, anticoagulation and the definitive role of endovascular at a variety of locations is not well defined.
I mentioned the PROOVIT Registry, this has been going on for a number of years. It captures in-hospital outcomes and outpatient module questions. We do hope that this was able to answer some of the significant questions that we have in this area.
As of this month, we have over 4,000 patients in 27 centers, we still invite others to participate if anyone in the audience is interested. And we have a variety of issues we have already examined and will continue to examine in hopes that we can answer many of the questions
related to the optimal treatment of vascular injury. Thank you.
- Thank you. I'm going to skip on some of the things that have been covered today. These are my conflicts. This is, kind of what we think the basic is, the ideal imaging system. It's a Dicom Data set, it's portable.
We can acquire it basic in 3D and that allows us to move that electronically, import and fuse it. And that allows us to both, acquire a CT in the operating room but also to fuse CTs.
I believe this is the next surgical revolution. It's the presence of a 3D, imaging acquisition capability in the operating room and this is an example. Basically, what you can do with not just with a CT scan, basically with also with MR.
So, let me go on through this. There are a number of different ways of which you can basically create it. You can actually put a CAT scanner near the operating room or you can create it using Cone Beam CT. And Cone Beam CT is a standalone,
or it can be used at the cone beam format or biplanar imaging format to actually fuse a previously acquired dataset. That means you can take Mrs. Smith's CTA for an aneurysm that was done a month ago, fuse it on top of the patient,
give here minimal amount of dye and minimal amount of radiation. Whenever you see two different colors, it means two different datasets being fused. And a lot of this is done basically being bone, using bones but we don't operate on bones.
But the blood vessels that we operated on, have calcifications in the wall. We think these are the bones of the blood vessels. And we do actually image fusion using the fusion based upon wall calcifications. We believe that is a unique digital signature
for every individual patient. If they happen to have stent graft placed, you can actually use that. So there are a number of different ways which you can get highly accurate vascular fusion, not using the traditional fusion techniques.
And once you've got it fused, then you've got a dataset to again, use and dye and radiation given to the patient perhaps a month ago. But which you can segment out the things you're interested in, in this case the aorta.
You can acquire these center lines, which can be used for navigation and guidance. When we talk about robotics, think of this as a glide path for a robot. And we can define basically what these targets are. And I think you're probably going to hear more
about this in the next talk. So for example, here you can see we've marked the celiac, the SMA, the landing zone, the renals. And we come to actually implant this, you can see just how accurate some of those fusion techniques actually are.
So you really are just doing all the catheterization based upon that alone. Let me give you a couple of examples, from using image guided techniques and needle tracking techniques. There's a case from a partner of mine,
who'd done a ascending repair of a patient, about two weeks post surgery we got chest pain and was phoned to have sutured line dehiscence. And that suture line dehiscence had a little pin point entry point which we opted to try and catheterize endovascularly.
Couldn't do it. So, we decided to watch this while it got bigger, so we really felt that the pseudoaneurysm needed to be treated. He wasn't too enthused about going back and through a relatively fresh sternotomy.
So we opted to try and do the percutaneous lane. Again, you can see the marks, you know, we had already used related target there so here we're actually using the sternum wire to actually do the image fusion. And then we used this laser guidance technique
which tells us 'stick needle here' and we can track that along this needle guidance pathway and we can stick it using techniques that were developed, well some of them by us, for long nodule localization translumbar embolization. And that allows us to stick that needle straight,
percutaneously, part of the sternal end of the pseudoaneurysm. And we inject it, you see you've got nice aortogram when you fill the mediastinum. That then allowed us some place to deliver those coils, parasternal, through the skin,
straight into that pseudoaneurysm. And then on completion angiogram you can see that it is completely excluded and she is now actually out for about three or four months, and it continues to be excluded. And this is simply a way
of actually using these kind of techniques to actually address the patient. Here's another example of fusion. You don't have to just fuse patient data, we actually scanned an LVAD because the surgeons wanted help
and planning the implantation of this. The inlet nozzle has to project directly towards the mitral valve. So here we scan the device, what you see is what you get with these devices. And fused that and the patient
and completely designed the operation and a workstation and then executed this basically on the approach to the order and to the apex basically of the left ventricle, in this case. And then you can see,
you can actually test this post operatively. You can also fuse MR images as a patient that was treated using a Feraheme MR with fusion. And then use basically to navigate. Now touch briefly on aortic, on the robotics basically for a finished,
of one other example as an interrupted aorta. Of which we used this, kind of needle guidance tracking system to actually perforate from one side to another. And then go ahead and actually deploy the stent. So, my time is running out,
I wanted to actually talk a little bit about robotics, really from Celia and Hansen have of course taken over and this is not actually available. What is available at the moment, let me just finish with this, is the Corindus robot,
this is actually approved for coronary intervention, peripheral interventions and now it's approved for neuro interventions. And in light of some of the discussions, from the previous discussions we believe that this is the way about which remote stroke intervention
is going to be able to be performed. And this is something just accepted in neurosurgery, in which the first robotic interventions were performed with embolization vision clot removal basically inside the brain, of an animal. So we think that bright hopes for the future.
Thank you very much for your attention.
- First of all, I will like to thanks to Frank Veith for his kind invitation. This is my disclosure. Three years ago we all (mumbling) attention to association between AAA and cancer detected by PET CT during follow up AAA by PET CT. And last year, we had opportunity to present
the preliminary results of our study on the relationship between AAA and cancer, and discuss on the, we discuss on the potential mechanisms. During this study, the 96 months incidence of neoplasia was significantly higher in the group of the AAA patients, compared to control group with coronary artery disease.
And then we look after the neoplasia free survival in coronary artery disease and AAA patients. The difference is significantly lower in the patients compared to general population. We observed that the incidence of the death, it was very high (mumbling) in AAA patients,
so the patients don't have enough time to present to the cancer. And reason why we recalculate it and we look after the cumulative risk of developing neoplasia after adjusting for that, and once again, the incidence of the neoplasia
in AAA patients significantly higher compared to Belgian populations. Currently, we are looking the incidence of the neoplasia in the patient with thoracic aortic dissection. It concern 240 consecutive patients. 145 Type A, and 95 Type B,
with mean follow up of 44 months for Type A, and 57 months for Type B dissections. At the beginning of this study, 25 patients had a recent history of cancer within five years, and in admission in all patients we are perform PET CT and we found three new cancer
in the patient with Type B and Type A dissections. And during the follow up period, 15 patients developed cancer and diagnosed by PET CT. Then we look after the incidence of the cancer in both group as AAA patients more than 65 years. You can see here easily the incidence of the cancer
in both group Type A and Type B dissections is significantly higher. The five years Belgian general population incidence rate of neoplasia is about only 9.5%. We look also, the incidence of the AAA in the male patient with cancer who admitted to our hospital
for PET CT for their staging of cancer, and you can see here the incidence of the cancer, AAA in this population is very high. Recently in circulation, one special issue published on the relationship between cardiovascular disease and oncology.
Different authors developed several hypotheses, but everybody's agreed that some common risk factors exist for both cancer and cardiovascular disease, especially chronic inflammation and oxidative stress. And another group from Italy, they show clearly that the inflammation and oxidative stress
play a major role during the development of the cancer in the patient with heart failure. In the past, we're interested also with the oxidative stress in AAA patients, and we observed increased oxidative stress status in the patients with abdominal aortic aneurysms.
And we performed similar study in our patient in our ongoing study, and we found similar results that they have an increased antioxidant status. And we know also the inflammation involved in the physiopathology of the aortic dissection as a AAA, so one of the cause of the dissection is inflammation.
So, my conclusion, ladies and gentlemen, there are significant association between AAA, TAD and cancer. Recent publications reinforced our hypothesis that our finding is not only occasional or related to age of both patients group,
but may be due to the presence of chronic inflammatory cells and cytokines in AAA and TAD patients, as well as their angiogenesis and antioxidant status. Thank you very much for your attention.
- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- Thank you Tim, Manny, Dr. Veith. Again thank you for the kind invitation. Um, here are my disclosures. The Chimney Snorkel Sandwich technique is really one that's been used and discussed many times throughout this great meeting in years past.
I've been asked to kind of see how we expand the use for thoracoabdominal aneurysms. Um, basically it's a matter of putting a parallel graft and then having an inner graft that will help seal the aneurysm sac itself by maintaining
perfusion to the visceral vessels. Um, the number of parallel grafts has been shown to be of note, and generally if you get beyond two parallel grafts at any one location, that tends to dramatically increase the incidence of
gutter leaks and potential for continued perfusion of the aneurysm sac. Here again showing at two, they still keep a reasonable aortic diameter, but once you start going three and four parallel grafts you tend to have significant compression
of the main aortic graft itself, as well as the potential for gutter leaks. Um, the PERICLES Registry certainly looked as I know has been discussed earlier in this meeting, and basically what it showed was that this was a reasonable way of treating
some of these complex aneurysms with a durable outcome going out to two to three years, uh, at a survival rate of over 70 percent. So, to show how we use this for patients with thoracoabdominal aneurysms, this was a 67 year, I use the term is,
a 67-year-old gentleman presented urgently with a sudden onset of back and abdominal pain. Apparently he was, uh, had a new wife and was trying some sexually enhancing medications from the DR. Had a history of coronary artery disease,
erectile dysfunction, and congestive heart failure, and CT scan revealed a type four thoracoabdominal dissection with a eight centimeter juxtarenal aneurysm, and he was in acute pain. Uh, here is the CT scan as we go through,
and you can see obviously the very complex dissection. You had a small segment of perfusion still around the level of the celiac going down into the SMA, uh, and then this rather, again the renals were
also with a small luminal area, and then a large aneurysm going up to eight centimeters going down into the abdominal component, and then reasonable access vessels from below. This shows the dissection extending down
through the thoracoabdominal segment, and again, he was in acute pain. Uh, so we came in and did an angiogram and IVUS, uh, and here we show the area of the dissection going down as well as the take-off of the subclavian artery.
Again, the true lumen being here. This was confirmed with IVUS. The IVUS sash, and this is the true lumen here, the false lumen being around the periphery, and as you go through you can see there's almost complete collapse of that
true lumen throughout the cardiac cycle. Uh, we performed a left carotid subclavian bypass, and embolized the left subclavian artery and put a thoracic endograft in, covering that lead point as you go in and taking it really almost up to the level of the left carotid artery.
There you can see the occluded subclavian. Uh, with that in place we then prepared to do a four vessel sandwich, or double sandwich, technique. Here we came down, we brought the grafts down to about the level of the takeoff of the celiac access with thoracic endografts.
Lateral shows the takeoff of the celiac and the SMA. Uh, we were able to catheterize both those vessels from the axillary region and put stents going out in this two sandwich technique, uh, and then actually put our stents going out from both the celiac and SMA.
We then were able to do that once we had those stents in place with adequate overlap and no real gutter leak, we then came down and similarly put another graft down to the takeoff of the renal vessels and then selectively catheterized
the right and left renal. Here you can see the stenosis near the origin of the right renal artery. With that we then performed balloon angioplasty with covered stents, I believe these were VBX stents going out,
and then covered that further down as we went down into the area of the eight centimeter aneurysm. And here we come in building down from that area and the perivisceral segment down and then to the iliacs showing good perfusion down to the takeoff of the
hypogastric, and then finally angiogram showed we had good perfusion to celiac, SMA, both renal vessels, and then down through the aneurysm sac itself. This is, uh, he remains stable. His postoperative course actually was uneventful.
He was discharged from the hospital at day four. He's been seen back now at one year follow up at six and 12 month follow up and he's remained stable with no evidence of endo-leak. So I appreciate the opportunity to try and present a more novel way of managing
these patients in the acute setting. Thank you very much.
- Thank you, I've been asked to speak about the next frontier for endovascular therapy, that is the proximal aorta. When we address this, I think there's two important questions we always have to ask is first of all, should we, before we ask can we.
We do proximal aortic surgery incredibly well, especially at high-volume institutions where the observed to expected ratio is significantly low. But there are some unmet needs, like the patients with type A dissection who are turned down for surgical repair.
When we looked at these patients in our experience, we found that nearly 80% of them would be treatable if we had an ideal device and 2/3 of these patients, the reason they were turned down, were for high-risk reasons not totally prohibitive reasons. So there is a population that could be treated.
When it comes to Arch disease, similarly we saw about 20% of these patients required emergency surgery, and although our outcomes are good, I'm certain that we're not treating all of the patients. Each patient we make a decision
about how to tailor their therapy around our own expertise, the patient's anatomy and comorbidities, but there's definitely a new group of patients that patients require new therapies that fall outside of this decision-making process. New devices have made us think about
these diseases differently. Arch branch devices have certainly arrived. We know that there are two arch single branch devices currently investigation, the Mona LSA and the TBE from Medtronic and Gore, and these devices can be used in various configurations
not just for the left subclavian artery but with additional debranching that can be used to treat much of the aortic arch. The arch double branch devices are also in development and investigation from at least three different companies, and there's probably more in research and development,
and we know that three-branch or triple branch arch devices are also currently in research and development phases. But we've learned quickly that there are limitations, certainly anatomic limitations, when it comes to landing in the proximal aorta even in patients who've had previous grafts.
You can see a specimen in the upper right of one such patient that I've treated. We've got a particularly short graft and this is not uncommon to see. Plus we have to ask these devices to sit, sometimes through very angulated tortuous aortas
and sometimes even an old graft is kinked in a way that doesn't combine well with the device, so we also have to think about new technology to treat the ascending aorta as we've heard from our last couple of speakers. There have been many reports that demonstrate it can be done
but as Mike Dake tells us, "Even though it can be done "is that current technology ready?" Well, in our experience we've done nearly 50 of these kinds of operations over the last decade or more,
and we've learned many lessons about this technology. One thing that's become obviously apparent is that we have to respect the fact that the ascending aorta is very much a curved structure, different anatomically than the other portions of the aorta that we've been treating endovascularly
and the current devices, some of the devices, that are not curved are not going to fit well in this space. Another thing that we learned is crucial for success is that the devices need to be placed coaxially at the sinotubular junction. It is absolutely critical for technical success.
Additional unanswered questions relate to the boundary conditions of this space. As with any new technology, we start to look at the disease in different perspectives. We need to understand the disease processes that are occurring.
We just learned from Rachel, of course, that this aorta stretches 20% in this systolic phase. There are new devices though that respect some of these ideas. This new ascending stent graft device, we used in this patient.
We were able to identify her entry tear. It was two centimeters above the coronary arteries. She had a decent landing zone at the sinotubular junction. We've learned that we have to measure along the greater curve of the aortic arch and this device worked very well in this patient
with a partial expansion in the first portion of the delivery, which we see in this video, followed by angulation along the coaxial area of the sinotubular junction. And then final deployment of the device as shown here.
We had an excellent result not perfect. There's still a little flow on the false lumen but you can see we got this device aligned just how we expected it to be, and these devices can be used with some of the branch technology we've talked about
but we still have a lot to learn when we use these in the patients with dissections who will have flow from other locations, and the most common proximal disease is fusiform where we also have to think about the valve and the coronary arteries.
We'll hear a little later about this idea of combining TEVAR with ascending devices, not only do we need to treat the coronaries, which can be done, but we need to respect the fact that paravalvular leak is not only sometimes seen but commonly seen in a mild intensity,
and so we've learned in this experience that as the technology develops, we need to think about the disease differently and what we learned in our experience is each segment of that proximal aorta acts a little bit differently, and we will continue to learn more
and advance this technology going forward. Thank you.
- 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.
- Relevant disclosures are shown in this slide. So when we treat patients with Multi-Segment Disease, the more segments that are involved, the more complex the outcomes that we should expect, with regards to the patient comorbidities and the complexity of the operation. And this is made even more complex
when we add aortic dissection to the patient population. We know that a large proportion of patients who undergo Thoracic Endovascular Aortic Repair, require planned coverage of the left subclavian artery. And this also been demonstrated that it's an increase risk for stroke, spinal cord ischemia and other complications.
What are the options when we have to cover the left subclavian artery? Well we can just cover the artery, we no that. That's commonly performed in emergency situations. The current standard is to bypass or transpose the artery. Or provide a totally endovascular revascularization option
with some off-label use , such as In Situ or In Vitro Fenestration, Parallel Grafting or hopefully soon we will see and will have available branched graft devices. These devices are currently investigational and the focus today's talk will be this one,
the Valiant Mona Lisa Stent Graft System. Currently the main body device is available in diameters between thirty and forty-six millimeters and they are all fifteen centimeters long. The device is designed with flexible cuff, which mimics what we call the "volcano" on the main body.
It's a pivotal connection. And it's a two wire pre-loaded system with a main system wire and a wire through the left subclavian artery branch. And this has predominately been delivered with a through and through wire of
that left subclavian branch. The system is based on the valiant device with tip capture. The left subclavian artery branch is also unique to this system. It's a nitinol helical stent, with polyester fabric. It has a proximal flare,
which allows fixation in that volcano cone. Comes in three diameters and they're all the same length, forty millimeters, with a fifteen french profile. The delivery system, which is delivered from the groin, same access point as the main body device. We did complete the early feasibility study
with nine subjects at three sites. The goals were to validate the procedure, assess safety, and collect imaging data. We did publish that a couple of years ago. Here's a case demonstration. This was a sixty-nine year old female
with a descending thoracic aneurysm at five and a half centimeters. The patient's anatomy met the criteria. We selected a thirty-four millimeter diameter device, with a twelve millimeter branch. And we chose to extend this repair down to the celiac artery
in this patient. The pre-operative CT scan looks like this. The aneurysm looks bigger with thrombus in it of course, but that was the device we got around the corner of that arch to get our seal. Access is obtained both from the groin
and from the arm as is common with many TEVAR procedures. Here we have the device up in the aorta. There's our access from the arm. We had a separate puncture for a "pigtail". Once the device is in position, we "snare" the wire, we confirm that we don't have
any "wire wrap". You can see we went into a areal position to doubly confirm that. And then the device is expanded, and as it's on sheath, it does creep forward a bit. And we have capture with that through and through wire
and tension on that through and through wire, while we expand the rest of the device. And you can see that the volcano is aligned right underneath the left subclavian artery. There's markers there where there's two rings, the outer and the inner ring of that volcano.
Once the device is deployed with that through and through wire access, we deliver the branch into the left subclavian artery. This is a slow deployment, so that we align the flair within the volcano and that volcano is flexible. In some patients, it sort of sits right at the level of
the aorta, like you see in this patient. Sometimes it protrudes. It doesn't really matter, as long as the two things are mated together. There is some flexibility built in the system. In this particular patient,
we had a little leak, so we were able to balloon this as we would any others. For a TEVAR, we just balloon both devices at the same time. Completion Angiogram shown here and we had an excellent result with this patient at six months and at a year the aneurysm continued
to re-sorb. In that series, we had successful delivery and deployment of all the devices. The duration of the procedure has improved with time. Several of these patients required an extension. We are in the feasibility phase.
We've added additional centers and we continue to enroll patients. And one of the things that we've learned is that details about the association between branches and the disease are critical. And patient selection is critical.
And we will continue to complete enrollment for the feasibility and hopefully we will see the pivotal studies start soon. Thank you very much
- Good afternoon. I'm going to try to answer those two questions of what is the proof to use EndoAnchors to actually improve difficult TEVAR. And to be able to do that, obviously the first thing is we have to understand what are the modes of failure of TEVARs?
And you can see that the endoleak rate and reintervention rates are quite high as reported in the literature. But also the question that we really don't know is what are truly difficult TEVARS? We know that when you have to work harder at it,
it feels like it's difficult when it doesn't work at all or when it doesn't last. But there is really no good way until recently to really try to quantify the difficulty of a TEVAR, so we created an anatomic severity grading score the same way that's what's been used for EVAR in the past.
We created that for thoracic aneurism. And really it shows here two cases of ASG score, one of the ASG score of 24 and then one of 43. And it really correlates very well with the difficulty of doing a TEVAR. It also correlates very well with the ability
to predict which TEVAR will fail. And in this series, we had a freedom from aortic related reintervention of 100% in the low score patients, but it dropped all the down to 68% at two years in patients with high score.
And that high score was a score of 24. So what is the proof? How can you prove the utility of using EndoAnchors in difficult TEVAR? Well you have to answer those two questions. Can EndoAnchors treat an endoleak in a thoracic aorta?
And can EndoAnchors prevent an endoleak? So to answer the first question, I think that anecdotal evidence is probably sufficient to answer yes. Obviously case series or more longitudinal analyses are needed to know exactly what types of anatomy
and in which patient it will work and how durable it will be. But to prevent an endoleak, anecdotal evidence is actually not useful at all. And the current answer is that we truly don't know right now.
Obviously, more analyses or other comparative cohort, like comparing a cohort of patients with and without EndoAnchors and the same kind of anatomy would be very useful. And an RCT would be even better because it would give us some level one evidence,
which we do not have. Here's an example of anecdotal evidence for redo TEVAR, a patient with a proximal type one endoleak. This is the arch study before the redo TEVAR. We did a redo TEVAR zone one. There was a persistent endoleak.
And after it was rescued by placing EndoAnchors on level of the inner arch. This is a series we just published recently of a difficult TEVAR. This was a 27. Half of those patients were actually redo cases
in whom we use EndoAnchors. Two third of those patients we landed in the arch. And it led that when we use prophylactic EndoAnchors in that series, we actually had no EndoAnchor related reintervention. No type one endoleak at all at up to two year follow up.
So we decided to do a cohort comparison, but to focus only on patients that actually have high ASG score, score of 24 and greater. So we had 63 patients and two who measured that score. 43 patients had the simple TEVAR
and 20 patients had a TEVAR with prophylactic EndoAnchors. And you can see here, we basically were able to reduce the reintervention rate and the type one endoleak rate extremely low by using those prophylactic EndoAnchors in patients with high ASG score.
When we look at the freedom from aortic related reintervention and the freedom from type one endoleak, we obtain 95% and 100% at up to two to three year follow up. But in the patient in whom no prophylactic EndoAnchors were used in those high ASG scores,
we ended up with much much worse results and a much higher need for reintervention because of Type 1A or Type 1B endoleaks. Can you advance the next slide? Thank you. So how to use them?
It's, the reason why it's so important to really select the guide very properly, because the deployment of EndoAnchors and the thoracic aorta, it's all about the angle of attack. You need to really have a 90 degree angle
to be able to have the anchor penetrate the aortic wall safely and properly. And these two videos I think illustrate that very nicely. That table shows the anchors that we placed in those patients. And you can see that there are really two zones
that the EndoAnchors are placed. One is in the zone, zone zero, one and two. So basically at the level of the arch, this is really an area where EndoAnchors are beneficial at the level of the inner curvature of the arch. And the second zone,
that's the most frequently where we placed EndoAnchor zone five, which is right above the celiac artery to be able to prevent that cephalad migration. So in summary, EndoAnchors can improve TEVAR outcomes by treating endoleaks and graft malapposition
and by preventing endoleaks and graft migration. I think to prove that EndoAnchors can improve the outcomes of difficults TEVARs have been substantiated by anecdotal evidence, case series, and a comparative cohort analysis. To decrease the need for aortic reintervention after TEVAR,
EndoAnchors are best used at the inner curve of the arch to treat or prevent type 1A endoleaks and at the distal end of the graft to prevent cephalad graft migration and type 1B endoleaks. Thank you.
- [Stephan Haulon] I'm going to present a case that was quite a challenging case. Those are my usual disclosures. And this patient I'm quoting is a patient that had dissecting thoracoabdominal aneurysm that was more than 18 centimeter long. You can see that there's major issues with the kinks
in the mid-descending thoracic aorta, two over 90 degree kinks, and you can also see that we're working in the narrow true lumen here, and what I want to show you here is that the SMA looks kind of occluded or with a mild perfusion, and you can see that above the celiac trunk,
it is nicely perfused, whereas you can see here that the true lumen is completely collapsed at the level of the visceral vessels. So there was a couple of issues associated with this case. This is a lateral mid-view showing you that the true lumen is completely collapsed here.
I'm not exactly sure what's happening with the SMA here. Sorry, and this is the IMA, lower, and you can see that there's a very large IMA that was patent and perfused by the true lumen. So we decided to treat this patient with a free thoracic endograft done proximal, then a TEVA,
and then the distal tubular graft that was landed just above the origin of this IMA. I designed the graft with a branch for the SMA not knowing exactly what I would look for, and the previous surgeon that referred the case to me
didn't manage to get a thoracic device up in this patient so there was a real concern that we would struggle during the case. The patient is contraindicated in the age, not far from his 80s, and had severe COPD, that's why he was not a candidate for an open approach.
So we used this four branch device, and what is specific about this device is that it has a TPDS delivery system, so what is that? This is something that I learned from Piotr Karpzak's research, it's a system where you have four pre-loaded wires that are already through the branches
so they're outside the graft, through the branch, inside the internal lumen, and you will see on the next video, this is the delivery system, and you can see that the pre-loaded wires are actually in a sheath above the delviery system. So you work over a through and through wire,
and this is Piotr's hand that you can see, you have a four meter through and through wire coming from the left axillary to the groin. Over this through and through wire, you advance a catheter from the top, and on the other side you will get the delivery system of the endograft,
you will see that very soon. You can see here is the sheath that is on top of the delivery system of the endograft, where you have the pre-loaded wires. So you're going to get the whole system up and get this proximal sheath from the axillary approach,
and then you have those wires that will direct you directly to the branches. So this is the case, you can see we have through and through access, and as I told you, the beginning of the case was trying to get access to the SMA to understand if the SMA was perfused by the true
lumen, or the false lumen. So here I'm looking from the false lumen, now I'm in the true lumen, trying from above, from below, and actually I never find access to the origin of the SMA, so I did this selective angio 3D image, and you
can see that the SMA is actually perfused from the IMA, so I was wrong to design a branch for the SMA, and I decided to occlude the branch. So to handle those huge kinks, I used the push and pull technique, you know, and you can see how I'm getting this graft up over all those kinks,
this is the first thoracic endograft. You will see on the next picture that once the graft is in position, I push on both ends of the wire so that it loops in the ascending. I position it just distal here to the left subclavian artery, and we're going to release this
first thoracic endograft, then get the second component up, and you can see it's still quite a challenge. And then we get it up, we need to have at least three or four stents overlap to release it, and remember this major kink that we had in the
mid-descending thoracic aorta. You will see that there's going to be sort of eructation. The patient, his blood pressure raised very significantly once I released the second graft so I had to use this scleroballoon right away to reopen the endograft lumen.
This is the third thoracic endograft that is positioned just above the celiac trunk, and now we're advancing the delivery system. You can see this is the sheath at the top of the delivery system where you have the pre-loaded wires, it goes inside the sheath, and I'm
getting the T-branch or the full branch endograft up here and we will position it like the other ones using this through and through technique, pushing from below and pulling from above. This is an angio to check that my fusion markers
are in a good position, and then we're going to open the endograft, making sure that the celiac trunk is above the celiac trunk marker, SMA above, and those are the two renal fenestrations above the origin of the two renal arteries. And then, using this pre-loaded wire, I push the catheter
directly through the fenestration from the top, getting access to the left renal artery. Once I have positioned a rosin wire into this left renal artery, I advance a Covera stent here, in this case I use Covera stents for the renals and BeGraft Plus for the visceral.
What you can see here is I'm actually releasing this Covera stent with quite a significant amount of the stent within the renal artery to have a very stable platform. At the top, you need to make sure that you have a full overlap with the branch.
I'm obviously not going to show you the four branches, I'm going to skip directly to the completion angiogram, and you can see the completion angiogram with the celiac trunk, both renals, and then the IMA feeding retrogradely the IMA, the SMA. So I was quite happy with this result.
Oops, now I need to go to the next slide please. There you are, thank you. So this was the post-op CT, and everything looked good at a first glance, but when looking more carefully on this CT scan, what I found is actually I had a very
large type 2 endoleak from this SMA that I never managed to access from the aortic lumen. And you can see the SMA is filled retrogradely and then is feeding the aneurysm sac, so now I have a big type 2 endoleak, which I think we'll never seal spontaneously because it's perfused by the SMA.
So I had to take this patient a couple of weeks later back to the OR under local anesthesia again using fusion guidance, and you can see here that I'm getting access to the IMA, injecting contrast to check that I'm in the right position, and then I'm
going to push a micro-catheter inside. You can see the microcatheter going up here, I'm going to inject again to check that I'm going the right direction. So this is the tip of the micro-catheter here, I have a lot of markers showing me the way to go,
the micro-catheter is now advancing, and I'm now almost where I need to be, and I'm going to check on the lateral view now. You can see, this is where is the tip of the micro-catheter, and I'm checking with the diffusion that I'm actually now at the origin of the SMA, this is an outline
of my fusion mask, and this is with the 3DVR. You see that I'm really where I need to be, and now I'm just advancing a couple of micro-coils at the origin of the SMA and just looking. This is the first branch of the SMA so I know that I'm not blocking anything special here.
A couple of coils, and then I'm going to check what's going on with my micro-catheter. And you can see that there's still flow going through those coils, so I added a couple of coils, smaller coils to get a nicely packed embolization. You can see a couple of coils that are advanced again.
And then this is the completion angio. You can see we're actually feeding the SMA, but not anymore the aneurysm sac. Can we move to the next one please? Thank you very much. So this is now the CT scan after this embolization.
You see the coils are just at the origin of the SMA. I don't have any more endoleak inside, those are artifacts from the coils, and we finally have completely excluded this complex thoracoabdominal aneurysm. So I think that the trick here was to use those
pre-loaded delivery, sorry, branches to the visceral and renal arteries, to use a through and through wire to get the device up, to use fusion imaging to know if we were in the true/false lumen, to know where the origin of the target vessel was, and as usual for
those complex dissection, you have to expect staged procedures to completely exclude the false lumen from aortic flow. Thank you very much for your attention. - [Speaker 1] Thanks Stephan, for a wonderful case. Any questions or comments, maybe just while you're
thinking about it? So I just missed a little bit in terms of the pre-loaded SMA wire, you can obviously use that to get through, and I presume you used an Amplatzer plug, or how did you embolize? - [Stephan Haulon] So, how did I block the SMA branch?
So usually the way I do it, I put a balloon expandable covered stent that is quite long, 47 or 57, and then I put an Amplatzer inside. - [Speaker 1] So that's a good tip, yeah. Obviously the trunk itself is too short to be confident with that.
- [Stephan Haulon] Yeah, at the beginning of the experience, I was just putting an Amplatzer in the trunk, and we had a couple of failures, and now I feel more secure positioning a nice landing zone. I mean, having a longer branch with this being expandable. - [Speaker 1] So that's a very good tip, thanks for that.
- [Speaker 2] I have a question, I mean, we know how important is the SMA, especially in these patients, but if you have to do another case like this one, do you think this could be more useful to do a first stage total to reopen the SMA to the celiac or to the IMA?
- [Stephen Haulon] The problem here was that the true lumen was completely collapsed, and I didn't know if it was just a dynamic malperfusion, or if there was some kind of stenosis. I still don't understand exactly. The idea when I started the case was that if I could
actually access the SMA, was to do exactly what you're saying, I was going to probably stent it to reopen it at the beginning. But I never managed to access the SMA from the true, the false lumen, from above, from below. Probably this was
because, maybe because the IMA was perfusing with a very nice flow this SMA. So I think there was some kind of retraction of the origin of the SMA. - [Speaker 2] Okay. - [Speaker 1] Stephan that thoracic component that's
got a tortuosity of 270 degrees, or worse, you know, in your experience you did a great job delivering the graft, but how's that going to perform, do you think, in terms of, you know, when we see remodeling, and do you think there's a risk of significant kinking and stenosis of the lumen?
- [Stephan Haulon] So I mean, the second graft when it went through that specific curve, occluded the true lumen right away. The blood pressure went up like an acute coarctation, and I think that with my coated balloon I actually burst the dissection flap, and that's why it's now
open, and I checked on the CPR that I have a nice lumen. But it's a concern, I think very importantly when you have such angulation, you need to be very aggressive with the overlap between the various components because you don't know what's going to happen, and you see we have I think almost four or five stents overlap between the
various components. - [Speaker 1] Okay, well thank you very much.
- Good afternoon to everybody, this is my disclosure. Now our center we have some experience on critical hand ischemia in the last 20 years. We have published some papers, but despite the treatment of everyday, of food ischemia including hand ischemia is not so common. We had a maximum of 200 critical ischemic patients
the majority of them were patient with hemodialysis, then other patients with Buerger's, thoracic outlet syndrome, etcetera. And especially on hemodialysis patients, we concentrate on forearms because we have collected 132 critical ischemic hands.
And essentially, we can divide the pathophysiology of this ischemic. Three causes, first is that the big artery disease of the humeral and below the elbow arteries. The second cause is the small artery disease
of the hand and finger artery. And the third cause is the presence of an arterial fistula. But you can see, that in active ipsillateral arteriovenous fistula was present only 42% of these patients. And the vast majority of the patients
who had critical hand ischemia, there were more concomitant causes to obtain critical hand ischemia. What can we do in these types of patients? First, angioplasty. I want to present you this 50 years old male
with diabetes type 1 on hemodialysis, with previous history of two failed arteriovenous fistula for hemodialysis. The first one was in occluded proximal termino-lateral radiocephalic arteriovenous fistula. So, the radial artery is occluded.
The second one was in the distal latero-terminal arteriovenous fistula, still open but not functioning for hemodialysis. Then, we have a cause of critical hand ischemia, which is the occlusion of the ulnar artery. What to do in a patient like this?
First of all, we have treated this long occlusion of the ulnar artery with drug-coated ballooning. The second was treatment of this field, but still open arteriovenous fistula, embolized with coils. And this is the final result,
you can see how blood flow is going in this huge superficial palmar arch with complete resolution of the ischemia. And the patient obviously healed. The second thing we can do, but on very rarely is a bypass. So, this a patient with multiple gangrene amputations.
So, he came to our cath lab with an indication to the amputation of the hand. The radial artery is totally occluded, it's occluded here, the ulnar artery is totally occluded. I tried to open the radial artery, but I understood that in the past someone has done
a termino-terminal radio-cephalic arteriovenous fistula. So after cutting, the two ends of the radial artery was separated. So, we decided to do a bypass, I think that is one of the shortest bypass in the world. Generally, I'm not a vascular surgeon
but generally vascular surgeons fight for the longest bypass and not for the shortest one. I don't know if there is some race somewhere. The patient was obviously able to heal completely. Thoracic sympathectomy. I have not considered this option in the past,
but this was a patient that was very important for me. 47 years old female, multiple myeloma with amyloidosis. Everything was occluded, I was never able to see a vessel in the fingers. The first time I made this angioplasty,
I was very happy because the patient was happy, no more pain. We were able to amputate this finger. Everything was open after three months. But in the subsequent year, the situation was traumatic. Every four or five months,
every artery was totally occluded. So, I repeated a lot of angioplasty, lot of amputations. At the end it was impossible to continue. After four years, I decided to do something, or an amputation at the end. We tried to do endoscopic thoracic sympathectomy.
There is a very few number of this, or little to regard in this type of approach. But infected, no more pain, healing. And after six years, the patient is still completely asymptomatic. Unbelievable.
And finally, the renal transplant. 36 years old female, type one diabetes, hemodialysis. It was in 2009, I was absolutely embarrassed that I tried to do something in the limbs, inferior limbs in the hand.
Everything was calcified. At the end, we continued with fingers amputation, a Chopart amputation on one side and below the knee major amputation. Despite this dramatic clinical stage, she got a double kidney and pancreas transplant on 2010.
And then, she healed completely. Today she is 45 years old, this summer walking in the mountain. She sent to me a message, "the new leg prostheses are formidable". She's driving a car, totally independent,
active life, working. So, the transplant was able to stop this calcification, this small artery disease which was devastating. So, patients with critical high ischemia have different pathophysiology and different underlying diseases.
Don't give up and try to find for everyone the proper solution. Thank you very much for your attention.
- Mister Chairman, ladies and gentlemen it's a pleasure to be here. I have no disclosure. Although Eagle syndrome is a well known condition to ENT and maxfax surgeons, vascular surgeons are less familiar with this entity and it presents with multiple symptoms
and the symptoms are associated with an abnormal styloid process. Doctor Eagle in 1937 described two clinical presentation, the classical and the stylocarotid syndrome. Anatomically the stylohyoid complex include hyoid bone, the styloid ligament and the styloid process
and both evolves from the Reichert's cartilage of the second branchial arch. The styloid process provide anchor to important muscles, the styloglossus, the stylopharyngeal and the stylohyoid. It is a rare condition and only four to 10%
of patient became symptomatic. Anatomically usually it's bilateral but the symptoms are mainly unilateral and the main aetiological factor is trauma leading to hyperplasia and metaplasia. The classical Eagle syndrome presented
with a triad with neck pain, otalgia and foreign body sensation in the pharynx while the stylocarotid syndrome is mainly caused carotid artery dissection. In this paper it seems to be an elongated styloid process give a four times risk to develop carotid artery dissection.
Also cartoidstyloid syndrome is we now associate it with the standard TIA and stroke and the carotid stent fracture as well. CT angiogram is paramount to making the diagnosis but duplex scan and TCD are very important in the technique and multi dynamic significant stenosis due
to the compression. I was lucky enough two years ago to be referred for a third opinion. A young patient who had been experiencing for the past three years left arm weakness after keeping the neck rotated to the right
for a few minutes so while I was trying to figure out if these symptoms were genuine I went with him to the vascular lab department and scanning the patient in the neutral position showed a normal common carotid artery,
a double kinking of the internal carotid artery and normal flow in the MCA but when we asked the patient to rotate the neck to the right the patient after two minutes genuinely experienced weakness in the left arm.
You can see the dramatic decrease in the flow in the MCA so I requested a CT angiogram. You can see the massive elongated styloid process with a double kinking of the internal carotid artery. This picture is very nice, only a picture
but you can see that this is bilateral. So I decide to take him to theater and I prefer the anterior approach. You can see the internal carotid artery kinking is quite well evident. While I was dissecting the elongated styloid process
I was very aware to see where the intersection of the three mass were where and also before resecting the bone I wanted to leave one centimeter behind to not to be very close to the facial nerve. This one is the bone resected
and while double kinking I thought at the time the resected internal carotid and perform an endo anastomosis was the right thing to do. This CT angiogram shows the bone resected and the carotid straightened.
So in conclusion ladies and gentlemen, it is a very uncommon entity but vascular surgeons should be aware of this because it can cause carotid dissection which is one of the most important cause of stroke and TIA in young adult
and also we should think probably while in one case was reported, identifying this condition prior occluded artery stenting. There are no treatment guidelines so surgery should be decided on individual basis with all the symptomatic patient
and also the patient with the CT scan you see evident compression of the styloid process on the carotid artery. Anterior approach for us, as a vascular surgeon, is the most common approach rather than transoral and what I recommended as well.
Thank you very much for your attention.
- I'd like to thank Dr. Veith and the committee for the privilege of presenting this. I have no disclosures. Vascular problems and the type of injuries could be varied. We all need to have an awareness of acute and chronic injuries,
whether they're traumatic, resulting with compression, occlusion, tumoral and malformation results, or vasospastic. I'd like to present a thoracoscopic manipulation of fractured ribs to prevent descending aortic injury
in a patient with chest trauma. You know, we don't think about this but they can have acute or delayed onset of symptoms and the patient can change and suddenly deteriorate with position changes or with mechanical ventilation,
and this is a rather interesting paper. Here you can see the posterior rib fracture sitting directly adjacent to the aorta like a knife. You can imagine the catastrophic consequences if that wasn't recognized and treated appropriately.
We heard this morning in the venous session that the veins change positions based on the arteries. Well, we need to remember that the arteries and the whole vascular bundle changes position based on the spine
and the bony pieces around them. This is especially too when you're dealing with scoliosis and scoliotic operations and the body positioning whether it's supine or prone the degree of hypo or hyperkyphosis
and the vertebral angles and the methods of instrumentation all need to be considered and remembered as the aorta will migrate based on the body habits of the patient. Screws can cause all kinds of trouble.
Screws are considered risky if they're within one to three millimeters of the aorta or adjacent tissues, and if you just do a random review up to 15% of screws that are placed fall into this category.
Vertebral loops and tortuosity is either a congenital or acquired anomaly and the V2 segment of the vertebral is particularly at risk, most commonly in women in their fifth and sixth decades,
and here you can see instrumentation of the upper cervical spine, anterior corpectomy and the posterior exposures are all associated with a significant and lethal, at times, vertebral artery injuries.
Left subclavian artery injury from excessively long thoracic pedicle screws placed for proximal thoracic scoliosis have been reported. Clavicular osteosynthesis with high neurovascular injury especially when the plunge depth isn't kept in mind
in the medial clavicle have been reported and an awareness and an ability to anticipate injury by looking at the safe zone and finding this on the femur
with your preoperative imaging is a way to help prevent those kinds of problems. Injuries can be from stretch or retraction. Leave it to the French. There's a paper from 2011 that describes midline anterior approach
from the right side to the lumbar spine, interbody fusion and total disc replacement as safer. The cava is more resistant to injury than the left iliac vein and there's less erectile dysfunction reported. We had a patient present recently
with the blue bumps across her abdomen many years after hip complicated course. She'd had what was thought to be an infected hip that was replaced, worsening lower extremity edema, asymmetry of her femoral vein on duplex
and her heterogeneous mask that you can see here on imaging. The iliac veins were occluded and compressed and you could see in the bottom right the varicosities that she was concerned about. Another case is a 71-year-old male who had a post-thrombotic syndrome.
It was worsened after his left hip replacement and his wife said he's just not been the same since. Initially imaging suggests that this was a mass and a tumor. He underwent biopsy
and it showed ghost cells. Here you can see the venogram where we tried to recanalize this and we were unsuccessful because this was actually a combination of bone cement and inflammatory reaction.
Second patient in this category, bless you, is a 67-year-old female who had left leg swelling again after a total hip replacement 20 plus years ago. No DVTs but here you can see the cement compressing the iliac vein.
She had about a 40% patency when you put her through positioning and elected not to have anything done with that. Here you could see on MR how truly compressed this is. IVA suggested it was a little less tight than that.
So a vascular injury occurs across all surgical specialties. All procedures carry risk of bleeding and inadvertent damage to vessels. The mechanisms include tearing, stretching, fracture of calcific plaques,
direct penetration and thermal injury. The types of injuries you hear are most common after hip injuries, they need to be recognized in the acute phase as looking for signs of bleeding or ischemia. Arterial lesions are commonly prone then.
Bone cement can cause thermal injury, erosion, compression and post-implant syndrome. So again, no surgery is immune. You need to be aware and especially when you look at patients in the delayed time period
to consider something called particle disease. This has actually been described in the orthopedic literature starting in the 70s and it's a complex interaction of inflammatory pathways directed at microparticles that come about
through prosthetic wear. So not only acute injury but acute and chronic symptoms. Thank you for the privilege of the floor.
- Thank you Tal. It's a privilege again to take the podium here. No disclosures. Everyone in here in this audience understands how important Traumatic Aortic Injury is, the second leading cause of death, primarily due to blunt mechanisms,
that are well known to the trauma and vascular community. And, we've learned a lot about how to care for these patient's in the transition in the vascular age. And, that began with the American Association for the Surgery of Trauma Studies in 2008 and 2009, which showed that TEVAR was associated
with an improved mortality and decreased paraplegia compared to older modalities. And, these are the graphs at my old training grounds at UT Houston, which, I'm sure would be the same at most other centers. A gradual transition to almost completely TEVAR
for every patient who has appropriate anatomy. And, we now have over a decade worth of survival data to show the outcome comparisons are the same as the older modalities. But the question has become now, are we over treating some of these injuries?
We need an optimal algorithm and an optimal algorithm requires an optimal grading system. And, that grading system should determine the treatment we utilize, it should guide the timing of the treatment. And, should provide some prediction of the natural history
in those patient's that we do not immediately treat. The SVS in 2011 developed a very nice anatomical based grading system, however, this is a lesionology type algorithm if you will, and not incorporating any of the valuable information that the patient also may possess
in terms of associated injuries. There have been alternative proposals: Vancouver, the Harborview "Minimal Aortic Injuries" is one that is very familiar and commonly utilized in the literature. And, even the Baltimore Classification which includes some physiology elements.
And the reality is, there are also other elements of ongoing issues Blunt Thoracic Aortic Injury, including not only how to manage those Grade 1/Grade 2 injuries but the timing of repair. How do we prioritize repair in the context of other sev
rain Injury and other bleeding solid organs and what's the optimal follow up regimen for these patients? It was with those questions in mind that 3 years ago we developed the Aortic Trauma Foundation. This is a non-profit organization with a Multispecialty
International Medical Advisory Board and a Board of Directors. We really wanted to improve outcomes of patient's with Traumatic Aortic Injury through education and research. We started with several initial, kind of low hanging fruit exercises, the first of which was a practice pattern survey
from members of the SVS, trauma organization, thoracic surgery organizations in interventional radiology and we found that there were some contingents here, and some very interesting findings in this survey. In fact, a majority of providers who care for these injuries don't rely on any guidelines at all.
Just their own personal knowledge of literature and their experience over their practice lifespan. Likewise, these mid-grade injuries represent some significant controversy with almost half the providers thinking that these just need medical therapy and observation as an outpatient.
And the remainder treating them emergently with TEVAR. Or, urgently with TEVAR. And we also conducted a large Retrospective Multicenter Study, 382 patient's from US Level 1 Trauma Centers and we found the at TEVAR compared to Open Repair
was associated with lower transfusion, lower overall mortality, lower aortic related mortality. None of these were surprising findings. But again, this study identified some controversy here, particularly with the, there's no difference in outcomes with those Minimal BTAI patient's if they're treated
with TEVAR or undergo medical non-operative management. Which suggests at least that in some of these patient's we are actually over-treating them. We have, as ongoing effort, our Aortic Trauma Foundation International, Multicenter PROSPECTIVE Blunt Thoracic Aortic Injury Registry
designed to identify predictors of early rupture, develop some multi-specialty consensus guidelines on treatment and management and establish long term outcomes. Anyone in this audience can join this effort, we have always gotten good contribution from VEITH.
We have a region based involvement, mechanism to promote the not only ATF involvement but the prospective registry in the US and abroad. And, we've had some good results. This initial registry went live in 2016, as of 2018, we have 381 patient's
in 23 centers internationally. And we plan to do a feasibility report when we cross the 500 patient threshold. And we invite anyone who seeks to become a member of the Aortic Trauma Foundation and actively contributes to utilize this data.
We all want to as a community, identify and define optimal care practices. We are going to actively solicit and review proposals for use and we hope that this data will produce a foundational platform upon which we can develop some really meaningful multi-specialty guidelines
that are evidence and practice based. Thank you.
- Thank you for the opportunity to share with you the experience with the new nano coated DCB and to present the 12 months results from the EffPac RCT. Please let me first introduce the unique nanotechnology coating for this balloon, special, organic, biocompatible, lipophilic is used and together with the paclitaxel, this mixture is applied
to the balloon by a special ultrasound technology as nano drops. And so we have a uniform coating sort of balloon, and homogenous structures. Another point is the multi-layer technology, which allowed coating durability
during the procedure, and one important precondition for the function of this balloon is the dry-off technique because we need microcrystalline structure of the coating. As you know, we can have the paclitaxel in tw
an amorphous structure or in crystalline, but the crystalline has more surface and more capacity to be attached to the surface of the vessel. So we have minimum loss during the navigation and
inflation, fast absorption, and an excellent drug transfer to the arterial wall. Also, in the Preclinical porcine model, we found 50% less restenosis than in
this is not really a surprise. But also a 23% less restenosis than in other commercial a could be demonstrate.
So now I would like to switch to the Eff-Pac trial. This is the study which investigated this balloon as a Multicenter Randomized Controlled Trial to access the effectiveness of the Paclitaxel-Coated balloon catheter versus uncoated balloon catheter in the SF and popliteal arteries.
This is an intention-to-treat trial and two arms- randomized study, and the sponsor is the University of Jena. We had 11 study sites from Germany, and there are all trial design and endpoints. The primary efficacy endpoint
is the Late Lumen Loss after six months, and of course we have some secondary efficacy endpoints, like the Freedom from TLR, the patency, change of ABI, and the Rutherford stage. The recruitment of the study was completed in
December two thousand and sixteen with one hundred and seventy-one patients. There was a 1-to-1 randomization between the both groups. The Baseline Patient Cha
a lot of different between the DCB and the POBA group, and the most of the included patients had a severe claudication- (incoherent phrase)
The mean lesion lengths was 59 there was about 22, 25% of total occlusions, and more than 90% of calcifications, or calcified vessels. This slide is important because
we had a, I think, very good vessel there was a 100% pre-dilatation in the Luminor group and the DCB group,
but also in the POBA group, a near 100% vessel preparation, and maybe this is one of the preconditions for the good results. This is the prim Late Lumen Loss afte
and as you can see, there was a high significant difference between the DCB and the POBA group, 0.14 versus more than 1 millimeter, and this is the comparison between the EFFPac trial
and other today published trials, and you can see we have good results, not on the- in the DCB group but also in the control group. Now, in more, in our clinical point of view because for the patient,
it's not so interesting to know the personal letliment laws or it's more important to know the working capacity and you can see, after 12 months, we have an about 75% improvement
of the Rutherford stage, of two or more stages compared to about 50% of the POBA group. Another secondary endpo dpoint, TLR rate after
six and twelve months, and you can see this TLR rate was very low in the DCB group, only one patient needed a TLR after six and also after twelve months compared to
13 and 14 patients. That means the number needed to treat, to prevent one TLR is six or seven respectively. Again, in comparison to other
and this is the patency to- (incoherent words) of the patency, and finally the ad we didn't see any adverse events
after twelve months, any unexpected adverse events. So I would like to conclude my the Luminor DCB demonstrates to be clinical highly effective and safe in inhibiting restenosis,
the innovative coating technique matters and is shown not only in the patency, Late Lumen Loss, and TLR data, but also in an improvement of the Ruth
and the results of the study allow direct comparison to other already completed RCTs applying Paclitaxel. Thank you for your attention. (Audience applause) - Yeah, thank you very much for this nice
overview of this new drug-coated balloon. Here's so - Is this nano technique improving, also the
push ability of the stent or you'll have the problems in all drug-coated balloon that push ability is not solute? - [Marcus] I think the push ability is not
but we have seen that the loss of the drug is very low during the proceed of the balloons to the segment of the vessel. And so, it could be better to have this nano
technology coating. - Steven, just a gene Not to you, Marcus, but to maybe Professor Biemene and Andrea and everybody else that
whenever I look at a DCB trial, it's a drug on a balloon, and one of the problems with putting the drug on the balloon is we are evaluating the effect of the drug, but maybe we are not really standardizing
the effect of the balloon. So whenever I look at all the DCB trials, I always wonder, what is the residual recoi and what pressures do t
what is the sizing of the balloon. And I'm just wondering, with all the DCB trials, and the negative and positive results in a mixed environment,
should we really be looking at either vessel preparation or standardizing the balloon in order to evaluate the effect of the drug, and what is your opinion? - [Marcus] Yes, I'm fully agree
of course the vessel preparation is one important point, and you have seen we had a good preparation, and another point the size of the balloon must be one or more than one
in comparison t and as for the inflation time, it was 120 seconds and truly necessary.
One hundred and twenty seconds- - And two minutes. - [Marcus] And two minutes, yeah. Of course we have only 170 patients in this study, and we need a bigger database of course in the future. - Doctor Perion, what is your opinion?
Do we need to standardize to evaluate one drug versus another drug versus another combination of nano and do we need to standardize the way that we're inflating the balloon between the studies or how do we evaluate that?
- I suppose in the meantime it's extraneous that we acc how to perform such type of intervention and how long you'll at least hav
that nobody take care and everybody's doing a different technique so that you can't compare any of the results, and I am still waiting. I will probably,
I will not survive the time when I will have a definition of vessel preparation, and everybody is speaking about vessel preparation, but nobody is saying to me what is vessel
and this is a big problem. You cannot compare every study because if you have a pre-dilatation of one minute, and the next patient five minutes, and the next is two, no pre-dilatation at all,
but a direct balloon, a drug-coated balloon's application, you cannot compare the data. - And if I use three balloons with the four centimeter length, one balloon with fifteen centimeter length,
it's also totally different because the distribution of the pressure is total and the only way to go is to define, (incoherent phrase)
cr you know exactly what he is doing, is destroying the vessel and reconstructing the vessel with a stent, and a real one.
But this is the only definition that I know. First, destroy everything, then use some technology to have an endovascular micros.
But this is the big problem, and nobody can give an answer. I don't know if in sync, if you are preparing an answer. - No, no, no, not really. We're looking towards everybody else.
- The last question, is there also a balloon for below-the-knee available, or- - Yes, we have. - Okay.
- Thank you again to Dr. Veith for the kind invitation. This is my disclosures. Open thoracic conversion is an increasing problem. Jose Jucadel speak two years ago in my congress in Milano showing the number of obstruction increase. The my experience in Milano in 25 years, we did global number of 2400 operation for
arch, descending thoracic artery, and thoracoabdominal and particularly more than 1000 open thoracoabdominal. And you have on this number, a total of 206 reintervention after TEVAR in particular for our center 84 patients and 9.8% after treatment.
There are different type of reintervention Endo Relining, Open conversion, and hybrid approach. Today we speak about open conversion. Why open conversion? Open conversion because sometimes the patients are young or fit, for an unstable condition and emergency,
infection of fistula, no proximal neck, and some anatomical barrier like MFM and PETTICOAT. And this is the first case, it's a patient with a dissection with multitreatment a young patient you see acute type B dissection treated in emergency for impending rupture
with three Gore TAG and from left subclavian artery to the super mesenteric artery covering the celiac trunk. Five month later you see "home-made" occluder for false lumen perfusion, but one month later, still perfusion you see a large perfusion of the false lumen with the sac expansion and pain.
So you decide to open the patient with the thoracofemoral approach with a thoracoabdominal operation, you see the proximal clamping opening on the aorta and you see the removing of the prosthesis and partial graft excision near to the neck
of the aneurysm for preparing the anastamosis The anastamosis with a triple-layer technique with a strip of felt and false lumen thrombus removal you see the normal distal and the occlusal false lumen device removal. You start with re-implantation of the single vessel
with complete left renal artery re-implantation of the true vessel. And you see the final result. This is another case, conversion of the patient after PETTICOAT. This is a patient with Marfan syndrome
in 2015 TVAR and PETTICOAT for acute type B dissection and enlargement in the next two years of thoracic and abdominal aorta. So decide for open conversion. You can see here through thoracofemoral operotomy the petticoat on the serosa of the aorta
and you see the stent complete removal after acute declamping and you see visceral renal perfusion and endartherectomy of the petticoat. Perfusion through the PETTICOAT and you see a large endartherectomy of the old PETTICOAT
and this intima-media of the aorta. And here the final result. Our definitive result, we performed a total of 81 open conversions with a mortality of 13%. Major morbidity with respiratory, renal, and parapalegia 7%. And the result is strictly dependent
from the kind of conversion. You see an indication to conversion, in endoleak, you have 6% mortality at one month, for endograft migration and failure 12% mortality, for retrograde dissection 33% mortality, for infection and fistula 30% mortality.
So in conclusion, Mr. Chairman, ladies and gentlemen, I think that close follow up after TEVAR is more and more necessary. Open conversion is always a technical challenge, acceptable in high volume centers, and increased mortality, my experience is due mainly
to retrograde dissection and infection. Thanks for attention.
- And this is my disclosure. Last month had been published European Guidelines on Aortic Arch Surgery, produced by Martin Czerny. I was honored to be in the group that made this. (stammers) There are published on it and on ESVS. And now I present another review
of aortic arch repair technique. Open surgery today, in a Center of Excellence, like the center of Joe Coselli. You see the mortality is below five percent. But the literature said the open surgery there is a median mortality 11%, stroke 10%.
So the recommendation for open surgery said that repair should be considered when concomitant aortic valve pathology of patient at high risk for retrograde type A dissection. In the symptomatic patient with floating aortic arch thrombi it might be used when a patient are symptomatic
with extensive mural aortic arch and thrombus. Frozen elephant trunk. Frozen elephant trunk is a normal evolution of open surgery when we need to treat the downstream aortic pathology. And this is our experience with a
custom-made E-vita from Jotec. He designed this with a supraaortic branch for reimplantation and the reperfusion branch. We see the technique. He performed this in 32 cases, no mortality, 3% of stroke. You see supraaortic reimplantation
before stent graft deployment in descending aorta, proximal anastomosis with reperfusion with insertion of the cannula for reperfusion, and finally the supraaortic trunk reimplantation. The guidelines say about FET that it should be considered this technique when to
close the primary entry tear in type A dissection in the distal aortic arch, type A dissection in distal aortic arch, in type B dissection where TEVAR is contraindicated, and in patient with concomitant distal thoracic or thoracoabdominal aneurysm.
Hybrid surgery, this is the last technique that's used. Maquet four branches with supraaortic branching and Prolene around the proximal anastamosis. Our experience in 20 years, 242 cases for Zone Zero, Zone One, and Zone Two. (clears throat)
Our focus is the stroke prevention. To do this you use a plug to clog an artery to reduce the stroke and it statistically reduce it with this technique, and use a cerebral filter like for TAVR. Hybrid surgery recommendations,
when it's considered in unfit patient but with suitable anatomy, not recommended if the landing zone is lower than 25 millimeter and maximum diameter over 38 millimeter. Not recommended in connective disease. Chimney and periscopes, the big problem is gutters.
But the parallel graft technique should be considered with very good result in urgent TEVAR. Not really first option in cases if other strategy are available. And multilayer technique not recommended for the pathology of the aortic arch.
(clears throat) Double branched arch custom-made devices. This is the experience of the two most important authors that we show in this section, presentation, Tilo Kobel and Stephan Haulon. And my experience is limited to six cases
with Cook A branch and you have no mortality and 3% of stroke. And the guidelines said for total endovacular aortic arch repair should be considered in poor surgical patients but with suitable anatomy. In conclusion, Mr. Chairman, ladies and gentlemen,
I think that today the guideline produced from European guidelines, open surgery, show acceptable result in patient with frozen elephant. Hybrid, currently the best choice in high, moderate risk patients. Total endo, future perspective.
Thank you for attention.
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