- Good morning. Thank you very much. I realize the audience is a bit thin, but thank you very much Dr. Veith for the kind invitation to talk about this. As we all know, hyperbaric oxygen is a treatment that most of us
don't use in vascular surgery. However, we've been using it as a rescue treatment for spinal cord ischemia after all types of thoraco repair. These are my disclosures. So as we all know,
any type of thoracoabdominal aneurysm repair can result in interruption of the blood supply of the spinal cord. We know that some patients, about 10% will wake up with an immediate spinal cord injury, or often spinal cord injury can be delayed.
And the rates of spinal cord injury vary by both procedure and series. So open repairs, we all know the large experience published by Coselli, he had about a 9.6% total 30 day deficit rate, but ultimately only 2.9% had permanent paraplegia,
and 2.6 with permanent paraparesis. Now, fenestrated and branched cases, depending on which series you look at, and whether you look at meta-analysis, the rates of spinal cord injury rate between eight and 13%.
Now the spinal cord blood flow is a network of blood supply. We've got the anterior spinal artery which is the key collateral in the front of the spinal cord, which supplies the anterior two-thirds of the cord.
And that's where the important tracts that deliver motor and sensory signals to your legs exist. Now, segmental arteries play a key component of this, and we've all heard many years worth of talk about the Artery of Adamkiewicz,
but we know that's not the only artery that's important, and these small segmental vessels that are coming in to supply the spinal cord that you see in the cartoon on the bottom right, are critical in supplying the spinal cord blood flow. The etiology of cord injury is generally ischemic.
However, this can be potentiated by a systemic hypoperfusion. Some people believe that atheromatous embolic infarction is an important mechanism, and thrombosis of radicular arteries. We also have that mechanism of ischemia reperfusion
where there's ischemia during surgery and during clamp or after a deployment of an aortic graft, and that if you don't get reperfusion this proceeds to infarction. This cartoon on the left-hand side is from a recent article by Wynn and Archer
and it's really quite a good description of the mechanisms that lead to a spinal cord injury. Now, conventional therapy once spinal cord injury is discovered is really about maximizing perfusion to the cord by raising the mean blood pressure, optimizing hemoglobin delivery, CSF drainage,
but there are no proven drugs or adjuncts at the moment. Now why did we get interested in hyperbaric oxygen? Well there are many animal models and a lot of animal literature that suggests that hyperbaric oxygen has significant benefits. Now what are the mechanisms?
Well first of all, it's based on the fact that you can increase oxygen delivery to the cord by increasing the amount of dissolved oxygen. That's a fraction of the oxygen usually delivered by hemoglobin, but if you increase the amount of dissolved oxygen in the blood,
it can enhance diffusion into ischemic areas and that can have salutary effects on spinal cord function. The longer lasting effects have been documented in animal studies on anti-oxidant, oxidant mechanisms including nitric oxide, secretion of growth factors, modified inflammation and decreased
ischemia reperfusion injury. This is a recent article that we published based on our early experience, and basically what we do is patients who are identified as having spinal cord injury after thoracoabdominal aneurysm repair
get conventional therapy, with raising of the hemoglobin, raising of the blood pressure and enhanced spinal cord drainage. But if they don't respond and they're not improving, then we take them to the hyperbaric chamber
where they start out at 2.5 atmospheres and then are down to 2.4 for subsequent treatments. The main risk is oxygen toxicity and the patients are actually breathing 100% oxygen either through a hood or an endotracheal tube, and the other people that are monitoring them
in the chamber are at atmospheric pressure at, above atmospheric pressure, but having just regular 21% oxygen. The goal is to achieve supra physiologic concentrations of oxygen in the soluble in the plasma. And our initial therapy,
and this is described in seven patients, both a mixture of open and endovascular cases, and although not all patients recovered, we felt there was an important signal here. We've subsequently treated 18 patients, total of almost 90 therapies.
Average is five treatments per patient and we give it BID for the first two days. Six patients did not survive, but one of those completely recovered. We had nine patients who recovered from paraplegia and can ambulate, and three non, complete non-responders.
So in conclusion, hyperbaric oxygen is an experimental therapy. It raises the level of dissolved oxygen in the blood, potentially reperfusing the cord, and has about a 50% response rate after unresponsiveness to conventional therapy.
It's supported by limited animal data and it obviously requires larger studies and potentially randomized studies to determine its ultimate effectiveness. 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 very much for the very kind invitation, and I promise I'll do my best to stick to time. The answer is probably to this audience I don't really need to say very much about the ATTRACT trial, but I think it is quite important to note that the ATTRACT trials have now been out for some time, and it is constantly being
talked about in its various dimensions. So I'm going to just spend a few seconds really talking about the ATTRACT trial. A large number of patients screened. One in 41 patients were actually recruited into it and it was a trial that ran for a long time.
Wasn't really with respect to the primary endpoint any particularly good evidence, but for those people who had moderate or severe post-thrombotic syndrome, it probably was of benefit. And if you looked at the Villalta score
and the VCSS scores there was some evidence to support it. So overall, probably some positive take-home messages, but not as affirmative as people would have thought. Now the reason that I've dwelled a little bit on that is that actually, what do we mean when we talk about the post-thrombotic syndrome?
Because I would say in the upper limb, because I have never personally seen an ulcer in the upper limb. Has anybody seen an ulcer in the upper limb due to venous disease? No.
So in a way we are talking about a slightly different entity. We are talking about a limb that has undoubtedly much more finer movements. And there was depression by some people with the results of the ATTRACT trial.
But when you look at the five year results from the CaVenT trial, there was some evidence to suggest that actually, as you get further out, there may be some benefit. If you look at this summation analysis, and I completely accept this is related to the leg,
again, there may be some benefit from the CDT. Now, this is a case of mine. Now I wonder if any of you can tell me how many stages may have been involved from going from the right, to having a ballonplasty in the vein. Pick a number, anywhere between five and ten.
The answer is you have numerous checks of the thrombolysis, you may have a venoplasty, you might have a first rib excision. You may then have occlusion and then realize this before you go on and do the first rib. So all I'm suggesting to you that this is not
a cheap treatment to offer patients treatment to the upper limb. Then we looked forward to some help from the guidelines. Well we look at the American guidelines and give or take, I think the answer is we probably shouldn't be doing it and that we should be only offering anticoagulation.
So do the Brits help? Well actually if you look at the Brits, it sort of says well, you can think a bit about doing decompression, but really if I was standing up in a court of law, I really wouldn't want much support from this guideline
that I had done the right thing. And then the International Society of Thrombolysis and Hemostasis really says well, you can do a little bit of this that thoracic outlet syndrome may be a risk factor. But give or take, surgeries still are a little bit dubious.
So, really there's one good review out there, and this is the review of Vasquez that basically looked at 146 articles, and they found some data on just under 1300 patients. And they postulated and chose some evidence to suggest that there was some evidence
that first rib excision and thrombolysis reduce PTS, and that anticoagulation alone was not enough for the majority of the patients. Very difficult to work out how you selected which patients you should or should not intervene on. Now, I'm sure everybody is rather sick and tired
of me talking about money, and I accept it doesn't really apply here. But money is actually quite important. Five interventions to prevent something that may not happen and at worst may be just a few collateral veins across the chest.
So ladies and gentlemen, I would want you to think very hard, is it actually cost-effective to be offering all patients presenting with an early auxiliary vein thrombosis thrombolysis, and then subsequently first rib excision? These are some of the truths, I think the answer is
it does seem to work. You do need to recognize and make the diagnosis. Usually delayed thrombolysis doesn't work, but there are lots of questions that are unanswered. And how would you defend what you have done in a court of law?
Somebody has a stroke, you then do the first rib, they get a large hemothorax, and they then die because there had been too much TPA on board. Yes, give it some thought. So ladies and gentlemen, I'm afraid I haven't actually answered the question,
but I think you need to give it careful consideration, what are the indications and merits? Thank you very much.
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- Thank you very much. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,
12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end
or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three
now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing
that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,
they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.
The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal
and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients
were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.
That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.
Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known
that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage
for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available
in about a month, thank you.
- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,
it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.
And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication
what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies
to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging
that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,
with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures
to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit
in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is
based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,
and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.
Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system
that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress
and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform
a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.
I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient
before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.
But we hope to present on that more solid data next year. Thank you very much.
- Here are my disclosures, none are relevant to today's talks. So what is the role of compressions stockings to prevent Postthrombotic Syndrome for patients with acute DVT? Well it's become rather complicated because as shown by recent studies,
it depends on what question is being asked. Question one is do compression stockings started at the time of DVT diagnosis prevent PTS, such as the Socks trial and other similar trials? Or question two, if you're already worn compression stockings for a period of time after DVT
and have not developed PTS, does stopping them increase the risk of developing PTS, such as the recent OCTAVIA and IDEAL trials? This is a meta-analysis that was done to address question one, namely the role of compression stockings started at the time of DVT diagnosis,
and this meta-analysis considered unblinded studies. The one blinded study, which was the Socks trial, and then attempted to combine that data, and you can see that if one looks at the unblinded studies there's suggestion of a 30% protective effect, or, excuse me, 40% protective effect.
The blinded study showed no effect of compression stockings. And combining all the studies together seemed to show about a 30% protective effect, however the confidence interval crossed one. There's very low confidence in this total estimate because of the substantial heterogeneity across studies.
And indeed, in their discussion, the authors point out the following: "We have very serious concerns about the unblinded studies because such designs may inflate treatment effects". And also, "differing results across studies suggest that the decision to use compression stockings
may be value and preference dependent for our patients". And we'll come back to that shortly. What about question two, if you've already worn compression stockings for a period of time after DVT, and you haven't developed PTS, does stopping them increase the risk of getting PTS?
There've been two new trials. One is the OCTAVIA study, of 518 proximal DVT patients. All wore compression stockings for one year after their DVT. If they were free of PTS at one year, they were randomized to continue for an additional year, or to stop.
And the results of this trial showed that stopping after one year was inferior to continuing for two years for the PTS outcome. On the other hand, we have the IDEAL study, of 865 proximal DVT patients. In this study, all patients wore compression stockings
for six months after proximal DVT, and if they were free of PTS at six months, they were randomized to continue for an additional 18 months, or to tailor continued use of stockings according to the Villalta score that was assessed every three months
at study follow-up visits. And the results of this trial showed that tailoring use after six months, which was the experimental arm, was actually non-inferior to continuing for 18 more months. So these results are interesting but somewhat conflicting. So how do I use compression stockings in 2018?
I don't routinely prescribe stockings to all of my proximal DVT patients. They can be difficult to apply, uncomfortable, expensive, and they need to be replaced every few months. And we all know that many patients won't wear them
in real life, especially if they have no symptoms whatsoever. And also, it's really not clear to me whether stockings prevent Postthrombotic Syndrome versus merely palliate symptoms of Postthrombotic Syndrome that has already developed.
And it may simply be as effective and more convenient and we may achieve better compliance if we ask our patients to start compression stockings at the time they develop symptoms of Postthrombotic Syndrome. I do however prescribe a trial of stockings
to any DVT patient, whether they have proximal or distal DVT who has residual symptoms after their DVT, and I'd continue them for as long as the patient derives symptomatic benefit or is able to tolerate them, and I certainly take patients' values and preferences into account
in making this decision. Moving on to the role of interventional treatment for patients with acute DVT. We have all heard and seen the results of the ATTRACT trial. Just very briefly, we know that the primary study outcome, any Postthrombotic Syndrome was not different
in the PCDT arm versus the No-PCDT arm. However, it did appear that PCDT reduced the risk of developing moderate or severe Postthrombotic Syndrome, and this was driven primarily by the subgroup with Iliofemoral DVT. In terms of short-term results, PCDT caused more
bleeding, major and any bleeding, and it caused statistically significant but clinically modest improvements in leg pain and leg swelling. Based on these results, what's the role of interventional treatment for patients with acute DVT? I would say that it's not indicated for routine use
in proximal DVT, it doesn't prevent Postthrombotic Syndrome, it does increase bleeding, and older patients above the age of 60 to 65 or more appear to be particularly poor candidates because of more bleeding and less efficacy. And further study in clinical use of these modalities
should be targeted. One would still consider PCDT in patients with severe symptoms, Iliofemoral DVT, and the other factors shown here on the slide. And finally, always remember that it's always an option to anticoagulate first for the initial
five to seven days if the limb is not acutely threatened. Thank you very much.
- 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
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
Thanks very much, Tom. I'll be talking about thermal ablation on anticoagula is it safe and effective? I have no disclosures. As we know, extensive review of both RF and laser
ablation procedures have demonstrated excellent treatment effectiveness and durability in each modality, but there is less data regarding treatment effectiveness and durability for those procedures in patients who are also on systemic anticoagulation. As we know, there's multiple studies have been done
over the past 10 years, with which we're all most familiar showing a percent of the durable ablation, both modalities from 87% to 95% at two to five years. There's less data on those on the anticoagulation undergoing thermal ablation.
The largest study with any long-term follow up was by Sharifi in 2011, and that was 88 patients and follow-up at one year. Both RF and the EVLA had 100% durable ablation with minimal bleeding complications. The other studies were all smaller groups
or for very much shorter follow-up. In 2017, a very large study came out, looking at the EVLA and RF using 375 subjects undergoing with anticoagulation. But it was only a 30-day follow-up, but it did show a 30% durable ablation
at that short time interval. Our objective was to evaluate efficacy, durability, and safety of RF and EVLA, the GSV and the SSV to treat symptomatic reflux in patients on therapeutic anticoagulation, and this group is with warfarin.
The data was collected from NYU, single-center. Patients who had undergone RF or laser ablation between 2011 and 2013. Ninety-two vessels of patients on warfarin at the time of endothermal ablation were selected for study. That's the largest to date with some long-term follow-up.
And this group was compared to a matched group of 124 control patients. Devices used were the ClosureFast catheter and the NeverTouch kits by Angiodynamics. Technical details, standard IFU for the catheters. Tumescent anesthetic.
And fiber tips were kept about 2.5 centimeters from the SFJ or the SPJ. Vein occlusion was defined as the absence of blood flow by duplex scan along the length of the treated vein. You're all familiar with the devices, so the methods included follow-up, duplex ultrasound
at one week post-procedure, and then six months, and then also at a year. And then annually. Outcomes were analyzed with Kaplan-Meier plots and log rank tests. The results of the anticoagulation patients, 92,
control, 124, the mean follow-up was 470 days. And you can see that the demographics were rather similar between the two groups. There was some more coronary disease and hypertension in the anticoagulated groups, and that's really not much of a surprise
and some more male patients. Vessels treated, primarily GSV. A smaller amount of SSV in both the anticoagulated and the control groups. Indications for anticoagulation.
About half of the patients were in atrial fibrillation. Another 30% had a remote DVT in the contralateral limb. About 8% had mechanical valves, and 11% were for other reasons. And the results. The persistent vein ablation at 12 months,
the anticoagulation patients was 97%, and the controls was 99%. Persistent vein ablation by treated vessel, on anticoagulation. Didn't matter if it was GSV or SSV. Both had persistent ablation,
and by treatment modality, also did not matter whether it was laser or RF. Both equivalent. If there was antiplatelet therapy in addition to the anticoagulation, again if you added aspirin or Clopidogrel,
also no change. And that was at 12 months. We looked then at persistent vein ablation out at 18 months. It was still at 95% for the controls, and 91% for the anticoagulated patients. Still not statistically significantly different.
At 24 months, 89% in both groups. Although the numbers were smaller at 36 months, there was actually still no statistically significant difference. Interestingly, the anticoagulated group actually had a better persistent closure rate
than the control group. That may just be because the patients that come back at 36 months who didn't have anticoagulation may have been skewed. The ones we actually saw were ones that had a problem. It gets harder to have patients
come back at three months who haven't had an uneventful venous ablation procedure. Complication, no significant hematomas. Three patients had DVTs within 30 days. One anticoagulation patient had a popliteal DVT, and one control patient.
And one control patient had a calf vein DVT. Two EHITs. One GSV treated with laser on anticoagulation noted at six days, and one not on anticoagulation at seven days. Endovenous RF and EVLA can be safely performed
in patients undergoing long-term warfarin therapy. Our experience has demonstrated a similar short- and mid-term durability for RF ablation and laser, and platelet therapy does not appear to impact the closer rates,
which is consistent with the prior studies. And the frequency of vein recanalization following venous ablation procedures while on ACs is not worse compared to controls, and to the expected incidence as described in the literature.
This is the largest study to date with follow-up beyond 30 days with thermal ablation procedures on anticoagulation patients. We continue to look at these patients for even longer term durability. Thanks very much for your attention.
- 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 very much. It's an hono ou to the committee for the invitation. So, I'll be discussing activity recommendations for our patients after cervical artery dissection. I have no relevant disclosures.
And extracranial cervical artery dissection is an imaging diagnosis as we know with a variety of presentations. You can see on the far left the intimal flap and double lumen in the left vertebral artery
on both coronal and axial imaging, a pseudoaneurysm of the internal carotid artery, aneurysmal degeneration in an older dissection, and an area of long, smooth narrowing followed by normal artery, and finally a flame-tipped occlusion.
Now, this affects our younger patients with really opposity of atherosclerotic risk factors. So, cervical artery dissection accounts for up to 25% of stroke in patients under the age of 45. And, other than hypertension, it's not associated with any cardiovascular risk factors.
There is a male predominance, although women with dissections seem to present about five years younger. And there is an indication that there may be a systemic ateriopathy contributing to this in our patients, and I'll show you some brief data regarding that.
So, in studies that have looked at vessel redundancy, including loops, coils, and in the video image, an S curve on carotid duplex. Patients with cervical artery dissection have a much higher proportion of these findings, up to three to four times more than
age and sex matched controls. They also have findings on histology of the temporal artery when biopsied. So one study did this and these patients had abnormal capillary formation as well as extravasation of blood cells between the median adventitia
of the superficial temporal artery. And there is an association with FMD and a shared genetic polymorphism indicating that there may be shared pathophysiology for these conditions. But in addition, a lot of patients report minor trauma around the time or event of cervical artery dissection.
So this data from CADISP, and up to 40% of cases had minor trauma related to their dissection, including chiropractic neck manipulation, extreme head movements, or stretching, weight lifting, and sports-related injuries. Thankfully, the majority of patients do very well after
they have a dissection event, but a big area of concern for the patient and their provider is their risk for recurrence. That's highest around the original event, about 2% within the first month, and thereafter, it's stable at 1% per year,
although recurrent pain can linger for many years. So what can we tell our patients in terms of reducing their risk for a recurrent event? Well, most of the methods are around reducing any sort of impulse, stress, or pressure on the arteries, both intrinsically and extrinsically,
including blood pressure control. I advise my patients to avoid heavy lifting, and by that I mean more than 30 pounds, and intense valsalva or isometric exercise. So shown here is a photo of the original World's Strongest Man lifting four
adult-sized males in addition to weights, but there's been studies in the physiology literature with healthy, younger males in their 20s, and they're asked to do a double-leg press, or even arm-curls, and with this exercise and repetitions, they can get mean systolic pressures,
or mean pressures up into the 300s, as well as heart rate into the 170s. I also tell my patients to avoid any chiropractic neck manipulation or deep tissue massage of the neck, as well as high G-force activities like a roller coaster.
There are some case reports of cervical artery dissection related to this. And then finally, what can they do about cardio? A lot of these patients are very anxious, they're concerned about re-incorporating exercise after they've been through something like this,
so I try to give them some kind of guidelines and parameters that they can follow when they re institute exercise, not unlike cardiac rehabilitation. So initially, I tell them "You can do light walking, but if you don't feel well,
or something's hurting, neck pain, headache, don't push it." Thereafter, they can intensify to a heart rate maximum of 70-75% of their maximum predicted heart rate, and that's somewhere between months zero and three, and then afterwards when they're feeling near normal,
I give them an absolute limit of 90% of their maximum predicted heart rate. And I advise all of my patients to avoid extreme exercise like Orange Theory, maybe even extreme cycling classes, marathons, et cetera. Thank you.
- Yeah now, I'm talking about another kind of vessel preparation device, which is dedicated to prevent the occurrence of embolic events and with these complications. That's a very typical appearance of an occluded stent with appositional stent thrombosis up to the femur bifurcation.
If you treat such a lesion simply with balloon angioplasty, you will frequently see some embolic debris going downstream, residing in this total occlusion of the distal pocket heel artery as a result of an embolus, which is fixed at the bifurcation of
the anterior tibial and the tibial planar trunk, what you can see over here. So rates of macro embolization have been described as high as 38% after femoral popliteal angioplasty. It can be associated with limb loss.
There is a risk of limb loss may be higher in patients suffering from poor run-off and critical limb ischemia. There is a higher rate of embolization for in-stent restenosis, in particular, in occluded stents and chronic total occlusions.
There is a higher rate of cause and longer lesions. This is the Vanguard IEP system. It's an integrated balloon angioplasty and embolic protection device. You can see over here, the handle. There is a rotational knob, where you can,
a top knob where you can deploy, and recapture the filter. This is the balloon, which is coming into diameters and three different lengths. This is the filter, 60 millimeter in length. The pore size is 150 micron,
which is sufficient enough to capture relevant debris going downstream. The device is running over an 80,000 or 14,000 guide-wire. This is a short animation about how the device does work. It's basically like a traditional balloon.
So first of all, we have to cross the lesion with a guide-wire. After that, the device can be inserted. It's not necessary to pre-dilate the lesion due to the lower profile of the capture balloon. So first of all, the capture filter,
the filter is exposed to the vessel wall. Then you perform your pre-dilatation or your dilatation. You have to wait a couple of second until the full deflation of the balloon, and then you recapture the filter, and remove the embolic debris.
So when to use it? Well, at higher risk for embolization, I already mentioned, which kind of lesions are at risk and at higher risk of clinical consequences that should come if embolization will occur. Here visible thrombus, acute limb ischemia,
chronic total occlusion, ulceration and calcification, large plaque volume and in-stent reocclusion of course. The ENTRAP Study was just recently finished. Regarding enrollment, more than 100 patients had been enrolled. I will share with you now the results
of an interim analysis of the first 50 patients. It's a prospective multi-center, non-randomized single-arm study with 30-day safety, and acute performance follow-up. The objective was to provide post-market data in the European Union to provide support for FDA clearance.
This is the balloon as you have seen already. It's coming in five and six millimeter diameter, and in lengths of 80, 120 and 200 millimeters. This is now the primary safety end point at 30 days. 53 subjects had been enrolled. There was no event.
So the safety composite end point was reached in 100%. The device success was also 100%. So all those lesions that had been intended to be treated could be approached with the device. The device could be removed successfully. This is a case example with short lesion
of the distal SFA. This is the device in place. That's the result after intervention. That's the debris which was captured inside the filter. Some more case examples of more massive debris captured in the tip of the filter,
in particular, in longer distance total occlusions. Even if this is not a total occlusion, you may see later on that in this diffused long distance SFA lesion, significant debris was captured. Considering the size of this embolus,
if this would have been a patient under CLI conditions with a single runoff vessel, this would have potentially harmed the patient. Thank you very much.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- [Narrator] So my assignment is, CMS policy update on non-thermal ablation techniques, and as most of you know, there is not one National CMS policy, so there are a variety of local cover determinations or policies that we're going to look at. I may bore you for a couple minutes
but I found a surprise at the end. So I went to the website, CMS website, and looked up varicose vein LCDs and these seven came up, interestingly Novitas, everybody's favorite, didn't come. So I looked at separately, we're going to look at all these as well.
And here is Novitas, Novitas and their previous LCD had no mention of non-thermal techniques, but in this proposed LCD, which has a lot of people up in arms, they say that the non-thermal techniques are experimental, investigational, and unproven,
and therefore will not be covered. This is next LCDs, this is two from Medicare contractor Noridian, they go on to talk about sclerotherapy and foam sclerotherapy, but they are not going to cover it. And somewhat bizarrely these codes in red here,
which are for Venaseal and Verithena, are listed as indications for RF or laser ablation, which kind of shows you they don't know what they're talking about. And there is no mention of MOCA or Claravein. Wisconsin Physicians Services and other MAC contractor,
and I looked at their LCD, there is no mention of non-thermal techniques. Next up is First Coast Service Options, with these jurisdictions over here on the right. And they get down to the C-classification, VCSS score, and talk about compressive therapy and conservative therapy.
They do mention Clarivein or MOCA. However, they state that it does not meet the Medicare necessity for coverage, and so they won't. And there's absolutely no mention of Verithena or Venaseal in their LCD. Palmetto GBA is another contractor,
with these jurisdictions on the right, and they actually discuss and approve Varithena, microfoam sclerotherapy. They discuss it here in their LCD, they have some restrictions that the physician needs to be competent and experienced with Varithena,
and ultrasound, there is no mention of Clarivein or Venaseal in their LCD. And these are also the folks that tell us how to do stab phlebectomy with 2 mm incisions and a crochet hook. So don't use a 3 mm incision and a hemostat,
it'd probably get denied. Next is CGS Administrators, and this busy slide, they go on to talk about sclerotherapy quite a bit, and all these in the main body, what they are not going to cover for sclerotherapy. They mention that foam sclerotherapy
is basically the same as liquid sclerotherapy, and therefore will not cover it, and again no mention of other treatments of non-thermal techniques. Which brings us to the last LCD, which is National Government Services,
and amazingly they state that the accepted treatments for eliminating reflux and the great saphenous anterior accessory, and small saphenous vein, include RFA, laser, polidocanol, Venaseal, and Verithena. And even more interestingly, they use their Rationale for Determination for MOCA.
The amount and consistency of the data, in addition to the two recent systematic reviews and the strong recommendation of the American Venous Forum, have convinced NGS that Medicare coverage is met. And for PEM, Varithena, the combination of RCTs, meta-analyses, systematic reviews,
the strong recommendation of the AVF, and endorsements from the SVS, ACP, SCAI, and SIR, have convinced them that coverage is appropriate. And the same for Venaseal, same thing. This is craziness. On one Medicare hand,
you have Novitas saying that, treatment is experimental and unproven, and they won't cover it. And on the other Medicare hand, you have this contractor that says, based on the recommendations of the experts,
that it's appropriate, and will be covered. And this is the reason why we need a National Coverage Determination. So, to find out what your policy is, you have to go to the website, you have to find out who your provider is,
or contractor, and see what the policy cause it differs depending upon where you are. Thank you for your attention.
- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide
and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter
is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues
that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement
of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side
and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,
then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,
coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,
and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques
with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation
of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.
We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go
so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side
or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.
Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.
On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded
and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.
Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.
Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,
despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients
to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,
and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,
and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.
- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent
flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue
but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using
a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient
and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta
and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once
the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide
and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug
over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect
of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve
and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.
This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft
to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing
in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment
of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)
- Thank you, good morning everybody. Thank you for the kind invitation, Professor Veith, it's an honor for me to be here again this year in New York. I will concentrate my talk about the technical issues and the experience in the data we have already published about the MISACE in more than 50 patients.
So I have no disclosure regarded to this topic. As you already heard, the MISACE means the occlusion of the main stem of several segmental arteries to preserve the capability of the collateral network to build new arteries. And as a result, we developed
the ischemic preconditioning of the spinal cord. Why is this so useful? Because it's an entirely endovascular first stage of a staged approach to treat thoracoabdominal aortic aneurysm in order to reduce the ischemic spinal cord injury.
How do you perform the MISACE? Basically, we perform the procedure in local anesthesia, through a percutaneous trans-femoral access using a small-bore sheath. The patient is awake, that means has no cerebrospinal fluid damage
so we can monitor the patient's neurological for at least 48 hours after the procedure. So, after the puncture of the common femoral artery, using a technique of "tower of power" in order to cannulate the segmental arteries. As you can see here, we started with a guiding catheter,
then we place a diagnosis catheter and inside, a microcatheter that is placed inside the segmental artery. Then we started occlusion of the ostial segment of the segmental artery. We use coils or vascular plugs.
We don't recommend the use of fluids due to the possible distal embolization and the consequences. Since we have started this procedure, we have gained a lot of experience and we have started to ask,
what is a sufficient coilembolization? As you can see here, this artery, we can see densely packed coils inside, but you can see still blood flowing after the coil. So, was it always occluding, or is it spontaneous revascularization?
That, we do not know yet. The question, is it flow reduction enough to have a ischemic precondition of the spinal cord? Another example here, you can see a densely packed coil in the segmental artery at the thoracic level. There are some other published data
with some coils in the segm the question is, which technique should we use, the first one, the second one? Another question, is which kind of coil to use? For the moment, we can only use the standard coils
in our center, but I think if we have 3-D or volume coils or if you have microvascular plugs that are very compatible with the microcatheter, we have a superior packing density, we can achieve a better occlusion of the segmental artery, and we have less procedure time and radiation time,
but we have to think of the cost. We recommend to start embolization of the segmental artery, of course, at the origin of it, and not too far inside. Here, you can see a patient where we have coiled a segmental artery very shortly after the ostium,
but you can see here also the development of the collaterals just shortly before the coils, leading to the perfusion of segmental artery that was above it. As you can see, we still have a lot of open question. Is it every patent segmental artery
a necessary to coil? Should we coil only the large ones? I show you an example here, you can see this segmental artery with a high-grade stenotic twisted ostium due to aortic enlargement.
I can show you this segmental artery, six weeks after coiling of a segmental artery lower, and you can see that the ostium, it's no more stenotic and you can see also the connection between the segmental artery below to the initial segmental artery.
Another question that we have, at which level should we start the MISACE? Here, can see a patient with a post-dissection aneurysm after pedicle technique, so these are all uncovered dissection stent, and you can see very nicely the anterior spinal artery
feeded by the anterior radiculomedullary artery from the segmental artery. So, in this patient, in fact, we start the coiling exactly at the seat of this level, we start to coil the segmental artery that feeds the anterior spinal artery.
So, normally we find this artery of the Th 9 L1, and you can see here we go upwards and downwards. We have some challenges with aneurysm sac enlargement, in this case, we use this technique to open the angle of the catheter, we can use also deflectable steerable sheath
in order to reach the segmental artery. And you can see here our results, again, I just will go fast through those, we have treated 57 patients, most of them were Type II, Type III aortic aneurysms. We have found in median nine patent segmental artery
at the level of the aorta to be treated, between 2 and 26, and we have coiled in multiple sessions with a mean interval of 60 days between the sessions. No sooner than seven days we perform the complete exclusion of the aneurysm
in order to let the collateral to develop, and you can see our result: at 30 days we had no spinal cord ischemia. So I can conclude that our first experience suggest that MISACE is feasible, safe, and effective, but segmental artery coiling in thoracoabdominal aneurysm
can be challenging, it's a new field with many open questions, and I looking forward for the results with PAPA_ARTiS study. Thank you a lot.
- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.
And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.
And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,
but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.
The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.
And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,
or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.
And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome
occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity
Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,
such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.
When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.
We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.
And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.
Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.
Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial
And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05
and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options
that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.
- [Bill] Thank you Vikay. I think this is an interesting topic for many reasons but one of the key ones is that if you look at our health care policies by insurers, this tends to define our practice. So I looked at BlueCross BlueShield's policy and they say that treatment of the GSV or SSV
is medically necessary when there is demonstrated saphenous reflux and I looked for more and there was no more. That's all they said so they must think that reflux a time correlates with venous severity. So is this true?
I think, personally, that there are other things that are involved and that volume is really the key. Time, velocity and the diameter of the vein are likely all part of the process and we all know that obstruction
is also critically important as well and probably the worse patients are those that have both reflux and obstruction. Probably reflux is worse in the deep system but we know that large GSV and SSV patients can develop CEAP four to six symptoms
and do very well with saphenous ablations. And I think this is a nice analogy. I love this guy, it looks like he came off of his lawn chair to help the firefighters out but he's probably not going to do so much with his little garden hose now, is he?
So I think size and velocity do matter. What does the literature tell us? Chris Lattimer and his group have done an elegant set of studies looking at how various parameters correlate to air plethysmography and venous filling times. They did show that there is a correlation
between venous filling time and reflux time. However, other things were probably more correlated such as GSV diameter and reflux velocity. And in this nice study of 300 patients they found that there was a relatively weak correlation between reflux time and clinical severity
and their conclusion was that it was a good parameter to identify reflux but not for quantifying the severity. So here's how we use this clinically in my practice. So you see many patients such as this that have mixed venous disease.
53-year-old female, severe edema. You do her studies and she's got reflux in the deep and the superficial system. So how to we decide if saphenous ablation is going to help this patient or not and correct these symptoms, prevent further ulcerations?
So all reflux is not created equal. The top is a popliteal tracing where the maximum reflux velocity is about five centimeters per second versus the bottom one that's about thirty to forty centimeters per second
so these probably aren't going to behave similarly in when we look at them. So we studied this in 75 patients and reported this back in 2008. We look at the maximum reflux velocity in the popliteal vein to tell if these patients
would improve after we ablated their saphenous or not. We found that this was a significant predictor of both improvement in venous filling index and the venous clinical severity score so we think velocity really does matter. And this is where we're seeing this clinically.
This is a patient that was referred to me for a second opinion concerning whether she would need ablation of her great saphenous vein. And this is the reflux tracing and you can see the scale here is turned up so that this is a measurement of reflux at about two centimeters per second.
This was used to document abnormal reflux and to justify ablation of the saphenous. So I checked one of our tracings. This is what it looks like.
- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.
And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,
as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,
presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,
as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.
So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.
Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,
and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.
Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there
in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,
but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,
but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,
but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion
that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer
and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.
And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.
And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,
treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.
And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.
We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat
with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,
and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.
So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.
Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen
and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.
(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.
Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.
And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily
arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,
it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this
florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.
We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation
in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,
which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen
of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.
- [Narrator] Okay, very interesting hypothesis.
- Talk to you a little bit about again a major paradigm shift in AVMs which is the retrograde vein approach. I mean I think the biggest benefit and the biggest change that we've seen has been in the Yakes classification the acknowledgment
and understanding that the safety, efficacy and cure rate for AVMs is essentially 100% in certain types of lesions where the transvenous approach is not only safer, but easier and far more effective. So, it's the Yakes classification
and we're talking about a variety of lesions including Yakes one, coils and plugs. Two A the classic nidus. Three B single outflow vein. And we're talking now about these type of lesions. Three A aneurysmal vein single outflow.
Three B multiple outflows and diffuse. This is what I personally refer to as venous predominant lesions. And it's these lesions which I think have yielded the most gratifying and most dramatic results. Close to 100% cure if done properly
and that's the Yakes classification and that's really what it's given us to a great degree. So, Yakes one has been talked about, not a problem put a plus in it it's just an artery to vein.
We all know how to do that. That's pulmonary AVM or other things. Yakes two B however, is a nidus is still present but there is a single outflow aneurysmal vein. And there are two endovascular approaches. Direct puncture, transarterial,
but transvenous retrograde or direct puncture of the vein aneurism with the coil, right. You got to get to the vein, and the way to get to the vein is either by directly puncturing which is increasingly used, but occasionally transvenous. So, here's an example I showed a similar one before,
as I said I think some of these are post phlebitic but they represent the archetype of this type of lesion a two B where coil embolization results in cure, durable usually one step sometimes a little more. In the old days we used to do multiple
arterial injections, we now know that that's not necessary. This is this case I showed earlier. I think the thing I want to show here is the nature of the arteriovenous connection. Notice the nidus there just on this side of the
vein wall with a single venous outflow, and this can of course be cured by puncture, there's the needle coming in. And interestingly these needles can be placed in any way. Wayne and I have talked about this.
I've gone through the bladder under ultrasound guidance, I've gone from behind and whatever access you can get that's safe, as long as you can get a needle into it an 18 gauge needle, blow coils in you get a little tired, and you're there a long time putting in
coils and guide wires and so on. But the cures are miraculous, nothing short of miraculous. And many of these patients are patients who have been treated inappropriately in the past and have had very poor outcomes,
and they can be cured. And that a three year follow-up. The transcatheter retrograde vein is occasionally available. Here's an example of an acquired but still an AVM an acquired AVM
of the uterus where you see the venous filling on the left, lots of arteries. This cannot be treated with the arterial approach folks. So, this one happened to be available
and I was having fun with it as well, which is through the contralateral vein in and I was able to catheterize that coil embolization, cured so. Three A is a slightly different variant but it's important it is different.
Multiple in-flow arteries into an aneurysmal vein wall. And the important identification Wayne has given us is that the vein wall itself is the nidus and there's a single out-flow vein. So, once again, attacking the vein wall by destroying the vein, packing
and thrombosing that nidus. I think it's a combination of compression and thrombosis can often be curative. A few examples of that this was shown earlier, this is from Dr. Yake's experience but it's a beautiful example
and we try to give you the best examples of a singular type of lesion so you understand the anatomy. That's the sequential and now you see single out-flow vein. How do you treat this?
Coil embolization, direct puncture and ultimately a cure. And that's the arteriogram. Cured. And I think it's a several year follow-up two or three year follow-up on this one.
So a simple lesion, but illustrative of what we're trying to do here. A foot AVM with a single out-flow vein, this is cured by a combination of direct puncture right at the vein. And you know I would say that the beauty of
venous approach is actually something which it isn't widely acknowledged, which is the safety element. Let's say you're wrong, let's say you're treating an AVM and you think okay I'm going to attack
from the vein side, well, if you're not successful from the vein side, you've lost nothing. The risk in all of these folks is, if you're in the artery and you don't understand that the artery is feeding significant tissue,
these are where all the catastrophic, disastrous complications you've heard so much about have occurred. It's because the individuals do not understand that they're in a nutrient artery. So, when in doubt direct puncture
and stay on the venous side. You can't hurt yourself with ethanol and that's why ethanol is as safe as it is when it's used properly. So, three B finally is multiple in-flow arteries/arterioles shunting into an aneurysmal vein
this is multiple out-flow veins. So direct puncture, coils into multiple veins multiple sessions. So, here's an example of that. This is with alcohol this is a gentleman I saw with a bad ulcer,
and this looks impossible correct? But look at the left hand arteriogram, you can see the filling of veins. Look at the right hand in a slight oblique. The answer here is to puncture that vein. Where do we have our coil.
The answer is to puncture here, and this is thin tissue, but we're injecting there. See we're right at the vein, right here and this is a combination arteriogram. Artery first, injection into the vein.
Now we're at the (mumbles), alcohol is repeatedly placed into this, and you can see that we're actually filling the nidus here. See here. There's sclerosis beginning destruction of the vein
with allowing the alcohol to go into the nidus and we see progressive healing and ultimately resolution of the ulcer. So, a very complex lesion which seemingly looks impossible is cured by alcohol in an out-flow vein.
So the Yakes classification of AVMs is the only one in which architecture inform treatment and produces consistent cures. And venous predominant lesions, as I've shown you here, are now curable in a high percentage of cases
when the underlying anatomy is understood and the proper techniques are chosen. Thanks very much.
- So I'm going to be talking about allografts for peripheral graft infections. This is a femoral artery that's been replaced after a closure device infection and complication, and we've bypassed to the SFA and profunda femoris. These are my disclosures. So peripheral arterial infectious processes,
well the etiology either is primary or secondary. Primary can be from bacteremic states and seeding of ulcerated plaque or thrombus. Secondary reasons for infections can be the vast usage of percutaneous closure devices that really have flooded the market these days.
Prosthetic graft infections after either a bypass or patch in the femoral artery. So early onset infections usually are from break in sterility. Secondary infections can be from either wound breakdowns or late seeding of the prosthetic graft.
The presentation for these patients can be relatively minor such as cellulitis or draining sinus, or much more dramatic, such as sepsis or pseudoaneurysm or mycotic aneurysm. On the CT scan we can see infected mycotic aneurysm after infected closure device and bleeding complications.
The treatment is broad in range. Ligation is obviously one option, but it leads to a very high risk of major limb amputation. So ideally some form of reconstruction, either extra-anatomic through clean planes,
antibiotic graft as we heard from the previous speaker, the use of autologous replacement with deep vein, or we become big proponents of the use of cryopreserved arterial allografts for reconstruction. And much of this stems from our work from about 10 years ago, where we looked
at the use of aortic cryopreserved grafts for aortic graft infections. This was published about 10 years ago but we looked at a small series of patients with aortic infections. You can see the CT scan of an infected stent graft
and associated aneurysm. And then the intraoperative photo after we've resected the stent graft and replaced that segment of the aorta with a cryopreserved aortic segment. So using that as a springboard,
we then decided to look at the outcomes using these types of conduits, arterial conduits, for peripheral arterial reconstructions in contaminated or infected surgical fields. So retrospective review at our tertiary care center, we looked at roughly 60 patients over a 15-year period
and excluded any aortic-based reconstructions. So these are all peripheral reconstructions. Mean follow-up was 28 months. As you would expect, the distribution of treatment zones were primarily in the lower extremities, so 51 cases.
As you can see, there's a list of all the different types of cases that we treated. But then there were a few upper extremity visceral and then carotid. I've shown this slide before at this meeting in the past, with a carotid patch infection
that was treated after it had a blow-out, and it's obviously a infected aneurysm, and this was treated with resection and a cryopreserved arterial segment. Looking at our outcomes, the 30-day outcome showed a mortality rate of 9%.
The 30-day conduit-related complication rate was surprisingly low at 14%. We had four patients that had bleeding complications, four patients with recurrent infectious complications. All eight of those patients required a return back to the operating room for correction.
The late conduit-related complication rate was only 16%. As listed here, you can see there's only one case of reinfection, three cases of graft thrombosis, surprisingly only one major limb amputation, two pseudoaneurysms and one late bleeding complication.
And graphically depicted, you can see here, this area here is looking at the less than 30 days, this is primarily when the complications occur. When you get to six months, fewer complications, and then beyond six months, the primary complications that we would see are either thrombosis of the graft
or the development of late pseudoaneurysms, again relatively low. So in summary, I think peripheral arterial infectious complications can be treated with a cryopreserved arterial allografts. The advantage is it's a single stage operation,
maintains in-line flow, there's a low incidence of repeat infection. I think it's also important to mention that the majority of these patients had adjunctive muscle flap coverage to cover the large soft tissue defect
at the time of the operation. So I think that this is a valuable alternative conduit in a setting of peripheral arterial infections. Thank you.
- The main results of the mid-term, I would call it rather than long-term, there were three years of the improved trial, were published almost immediately after the Veith Symposium last year. I have no disclosures other than to say this was a great team effort, and it wasn't just me,
it was all the many contributors to this project. I think the important thing to start with is to understand the design. This was a randomized trial of unselected patients with a clinical diagnosis of ruptured abdominal aortic aneurysm.
The trial was to investigate whether EVAR as a first option, or an endovascular strategy, would save lives compared with open repair. We randomized 613 patients quite quickly across 30 centers, and this comprised 67 percent of those who would have been eligible for this trial, so good external validity.
Survival was the primary outcome for this trial. This was assessed at 30 days, one, and three years. At 30 days as you can see there was no difference between the endovascular strategy group in blue, and the open repair group in red. However, already at 30 days we noticed
that of the discharges in the endovascular strategy group, 97 percent of these went home, versus only 77 percent in the open repair group. No significant difference in survival at one year, but now out at three years, the survival is 56 percent in the endovascular strategy
group versus 48 percent in the open repair group. This is not quite significant. If we look only at the 502 patients who actually had a repair of a rupture, the benefits of the endovascular strategy are much stronger. And a compliance analysis,
because there were some crossovers in this pragmatic trial, shows very similar results. And for the 133 women, these were the real beneficiaries of an endovascular strategy. The cumulative incidence of re-interventions to three years are shown here, and no difference between open
and endovascular strategy. And I'll dwell on these in more detail in a later presentation. But this did mean that there was no additional cost to the endovascular strategy over the three year period. I'd also like to point out to you that
apart from the re-interventions, the need for renal support in the early days was 50 percent more common after open repair. Patients had rather different concerns about their complications to clinicians. And when we discussed this with patients they were most
concerned about limb amputation and possibly unclosed stomas. All of these were relatively uncommon, but we had a great collaboration with the other two ruptured aneurysm trials in Europe, AJAX and ECAR. And we put our data together.
Took 12 months, and here you can see the very consistent results. That amputations are considerably less common after endovascular repair for rupture than open repair. We've just heard about quality of life. In Improve Trial there were real gains in quality of life.
Up to three years in the endovascular strategy group. And since costs were lower, this meant that this strategy was highly cost-effective. So in summary, at three years an endovascular strategy proves to be better than open repair. With better survival, higher qualities for the patients
in the endovascular strategy group, marginally lower costs, and it's cost-effective. And we've heard quite a lot even at this meeting about our new NICE guidelines in the UK. But an endovascular strategy is actually being recommended by them for the repair of ruptures.
And I think the most cogent reasons to recommend endovascular repair are the fact that it has benefits for patients at all time points. It gives them what they want: Getting home quickly, better quality of life, lower rates of amputation and open stoma,
and better midterm survival. Thank you very much.
- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years
of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).
It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,
it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases
that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it
was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.
And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted
inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted
selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.
In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients
stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.
This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,
and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,
and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.
- Thank you very much for inviting me here again and I'll be talking about thermal ablation RCTs. My coauthor, Michel Perrin from Lyon, in France, the gourmet capital in the world has collected RCTs on operative treatment of CVD since 1990. Today he has 186 collected RCTs
of the which 84 involve thermal ablation. You can find all this data for free in Phlebolymphology.org. Do we need further RCTs? Well systematic reviews and meta-analyses increasingly important in evidence-based medicine. And this development is well-described
by Gurevitch in Nature this year and criticized by Ioannidis two years earlier. Common sense is a good principle when you try to understand meta-analyses. Do most studies point in the same direction?
Is the effect significant? Are the patient-related outcome measures relevant and what happens if you exclude one study? Since 2008, 10 years back, these are the available meta-analyses and the last came from Ireland earlier this year.
It was published in the JVS, endovenous and in fact this is in March. And they found nine RCTs comparing conventional surgery and endovenous therapy with five years or more follow-up that were selected. Primary outcome was recurrence rate.
There is some sole recurrence rate was that there is no significant difference in laser versus surgery, same for radioactive frequency versus surgery and radioactive frequency versus laser. They found an inferiority
of ultrasound guided foam sclerotherapy versus laser and surgery. Their conclusions were that the quality of evidence is poor therefore more trials that are well-powered to examine long-term outcomes are warranted. The new kids on the block,
steam, MOCA, and Venaseal, are not included in the meta-analyses due to lack of more than five years follow-up in their paper. Obsolete RCTs. Endovenous laser in the presented long-term RCTs
were performed by 810-980 nanometer wavelength using a bare fiber. There is a paucity of RCTs comparing open surgery with novel endovenous laser and new RF techniques. Recent criticism against endovenous ablation, is the pendulum swinging towards high ligation
and stripping again? Olle Nelzen from Sweden in an editorial in British Journal of Surgery reconsidering the endovenous revolution, wrote that neovascularization is a dominant finding following high ligation and stripping
but proximal venous stumps and incompetent anterior accessory saphenous veins are the main factor after endovenous ablation. So long-term follow-up suggests that the recurrence rate after endovenous ablation seem to increase over time. A substantial number of patients who have undergone
endovenous ablation will eventually develop symptomatic recurrence requiring repeat therapy. And such scenario would change the equation regarding patient benefit and costs making endovenous ablation less competitive and challenging current guidelines.
So summary of needs for further RCTs. Quality of present RCTs poor in several meta-analyses, no thermal endovenous technique is superior to open surgery, RCTs rapidly obsolete due to change in technology, and more trials that are well-powered to examine long-term outcomes are warranted.
So final point, apparently we need more RCTs to satisfy the quality requirements for clinically important systematic reviews and meta-analyses. And what about the clinical guidelines? Thank you very much.
- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- (speaks French) liver surgeon I perform hepatobiliary surgery and liver transplantation. Maybe I don't belong here, I so probably more rested than anybody in the room here. But today I will present about liver surgery and hepatectomy. I work at The Royal Free where I have the honor and pleasure to have seen Krassi. We are in the
little island in the North Sea. There is many things going wrong there including Brexit but, the guys uh, we have a major advantage. The NHS favors centralization. Centralization look there: London is bigger than New York Uh, eight million, 50 million greater London
and we drain about six millions of people with our HPB center. In the center we perform about 2,000 operations, of major surgery. In five years, half of them are liver surgery. And most of them have uh, benign, malignant tumor. A very small percentage have benign tumor.
I count here for complications uh, and mortality look there, 3.1% of only the malignant because the benign are young people and we perform a different strategy, they have no mortality. Today Hepatic Hemangioma, look there it is uh, 1898 is a key year. Not only the first description
of the lady that died after bleeding out in an autopsy but also, Hermann Pfannenstiel uh, Professor Pfannenstiel. I will introduce you to him. He described the first operation. Now, we're talking of congenital malformations, they uh, lesions occur in the liver and they may grow,
but only 20% they grow. They have a chaotic network of vessels and they have fibrotic, fibrotic development within it. I introduce you Hermann Pfannenstiel, he was a gynecologist, famous, famous, important incision that we still use today.
Remember him, we'll talk to him later. Microscopically, the microscopic is our well-circumscribed lesion, they're compressible. Important you see down there that they compress the liver that is normal close to it. This has an implication because if you operate,
you fill find a blood duct or a vessel and it will bleed or leak by. Microscopically, they are ectatic blood vessels and they are fed by arteries. This is also an important point, for therapy. Separated by fibrous septa, this is also important
because they become harder and they become bigger. And they have distorted blood vessels. They're more frequent uh, benign tumor. Prevalence up to 7%, they have non-neoplastic this must be clear, they are non-cancer. The proliferation of endothelial cells, women
have more and particularly pregnant women, more pregnancy or contraceptive. We divide them in cavernous and capillary and we'll have a word on that. Symptomatic being half of the cases, multiple in 10%, they rarely bleed and they rarely rupture.
Capillary Hemangiomas cells small, I show you an MRI here. The differential with HCC liver cancer is most important. They both are theorized but they continue to appear on late face. They are asymptomatic please, do not touch them, they do no harm.
And so we will not speak of them. We speak only of the cavernous hemangioma. And here, the cavernous hemangioma bleeds Oh my God, no, it's not true. There are 83 reports of bleeding since the report of Hermann Pfannenstiel. Uh, 97 cases, adenomas bleed more frequently.
Frequently, in the past they were confused. Hemangioma and adenoma, adenoma does bleed. There are only true cases, 46 in the literature. Size is not important and they are very rare in elderly people.
This is what we see when they are giant cavernous hemangiomas, they're serious, they are rather easy to diagnose. Diagnostic criteria, uh, look up typical for uh, cavernous hemangioma. How do you point here? Yep, you stop. If you then see that you have
an atypical hemangioma, you jump over to an MRI. MRI is too nowadays, diagnostic and uh, the important thing is you stop. Once you have the diagnosis with MRI, you stop, do nothing yet, do not follow, bye-bye. Treatment modalities surgery: Selective TAE, Radiotherapy, Medication: two classes,
Propranolol, to decrease the hyper circulation. Bevacizumab as a class of drugs of inhibitors of inferior growths and endories, eventually are cold. This is seminal paper, about 35 years ago "Do not treat asymptomatic patients." This is a key: do not bother with hemangioma.
If you do have the algorithm, you look at complaints that can present incidentally when they have complained, not complained, no treatment of abdominal pain. Unrelated to no treatment, we have to eventually make sure that the pain is not related to the cavernous hemangioma. If there is other futures
like compression giant, you can do surgery. If you have a doubt in diagnosis, today rare with MRI, then you can perform a biopsy. The surgical indication then remain progress, severe, disabling symptoms. Diagnostic uncertainty nowadays not the case, with MRI.
Consumptive coagulopathy or Kasabach-Merritt syndrome is a serious, we will see when you perform human transplants. Spontaneous rupture with bleeding as an emergency. Rapid growth in 25%. This is a paper that shows that the size of the cavernous hemangioma is here,
and you can see that operation has been performed for larger size, however, look that even in non-symptomatic or partially asymptomatic patients, you can reach sizes up to 15 centimeters. And this a review of the literature from a Chinese group where they revised a thousand to a hundred cases,
no mortality in the series and enucleation versus the anatomic resection is better. Less complications, less blood less, less time of surgery, and less hospital stay. So please, in this case of surgery, we do enucleation. I was asked by my society the HPBA to speak
about transplantation for liver tumor. You can that an indication is unresectable disease, severe symptoms and mass occupying effects. Pre-cancerous behavior is not for hemangioma only for adenoma differential diagnosis with HCC. And you have to be attentive that you avoid
liver insufficiency during your resection. So, in conclusion, for benign lesions, hemangioma technically is the only indication. And now the systematic review that shows around several emothing United States UNOS and the ELTR Several, several benign tumors but if you break down
for type of tumors you see that most of them are Polycystic disease or partly cavernous hemangioma are very low. 77 in Europe, out of 97,000 operation of transplantation. So, let's get an old paper. The pioneer of transplantation again, extremely low,
one out of 3,200. An extremely low percentage. It's my personal experience I was working at Essen, Germany. Almost a thousand transplants we performed. Unfortunately most of them I did and we never transplanted one hemangioma, my experience for transplantation is zero because it should not be done.
So, my advice for hemangioma. Biopsy not advised, see a liver surgeon in a serious center, diagnosis is done my MRI, observe doubt symptoms and observe. Let the patient beg you for surgery, if significant increase in size and symptoms, we can do surgery. Embolization is possible.
Sometimes it's harmful. The role of the surgeon is to confirm the diagnosis, differentiate it from cancer, exclude causes of other symptoms and avoid unnecessary surgery that's the main thing. Surgery for severe symptoms of Kasabach-Merritt. Only for complicated symptomatic lesions, or where the
diagnosis is uncertain. Ladies and gentleman, I will conclude with a couple of questions. If you have a daughter or son with a liver tumor, would you go to a center or a competent surgeon or to a gynecologist. Professor Pfannenstiel for instance or another doctor. If your car has a problem,
would you go to a good mechanic once for all, or to a small shop for 20-40 times. It is a matter of experience and a matter of costs. And with this, I am ready for your questions. - [Audience Member #1] When have you personally operated on these lesions?
- [Speaker] I am. And the experience that I have in the past I seemed young but I practiced for many years. When I started 25-30 years ago, we were operating many of these because we were not so certain. Then MRI came, and MRI basically made the diagnosis so easy and straight-forward and we started observing
patients. We still do operate today, but they are very large tumors and when I do personally, I avoid the androbolization before because you have more skylotec reaction, just (grainy sound effect) to peel it away from the normal parenchymal.
This is our experience. - [Audience] Thank you. - [Speaker] Thank you very much, yes? - [Audience Member #2] Yes, one question. When you operate, and with all of the experience you have, what are the complications of
(mumbles) - [Speaker] The main, so first of all, there has been also an evolution in the type of operation we don't do anymore the resections where you have some bi-leaks. If you operate correctly, it's bleeding and one infection not one born. If you have to watch bi-leak is the one
that you have to watch and that's because the tissue is pushed away and you may miss something during the enucleation.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- So thank you for the kind introduction and thanks for professor Viet for the invitation again this year. So, if we talk about applicability, of course you have to check the eye views from this device and you're limited by few instructions for users. They changed the lengths between the target vessel
and the orifice and the branch, with less than 50 mm , they used to be less than 25 mm. Also keep in mind, that you need to have a distance of more than 67 mm between your renal artery cuff and your iliac bifurcation. The good thing about branch endografts
is that if you have renal artery which comes ... or its orifice at the same level of the SME, you can just advance and put your endorafts a bit more proximally, of course risking more coverage of your aorta and eventually risking high rate
of paraplegia or spinal cord ischemia. Also if your renal artery on one side or if your target vessel is much lower with longer bridging stent grafts which are now available like the VBX: 79 mm or combination of bridging stem grafts, this can be treated as well.
Proximally, we have short extensions like the TBE which only allows 77 or 81 mm. This can also expand its applicability of this device. The suitability has already been proven in.. or assessed by Gaspar and vistas and it came around plus 60%
of all patients with aortic aneurysms. Majority of them are limitations where the previous EVAR or open AAA repair or the narrow diameter reno visceral segment in case of diabetes sections. So, what about the safety of the T-branch device?
We performed an observational study Mister, Hamburg and Milner group and I can present you here the short term results. We looked at 80 patients in prospective or retro prospective manner with the t-branch as instructed for use.
Majority were aneurysms with the type two or type four Crawford tracheal aneurysms, also a few with symptomatic or ruptured cases. Patient characteristics of course, we have the same of the usual high risk cardiovascular profiling,
this group of patients that has been treated. Majority was performed percutaneously in 55%. The procedure time shows us that there is still a learning curve. I think nowadays we can perform this under 200 minutes. What is the outcome?
We have one patient who died post operative day 30, after experiencing multiorgan failure. These are 30 day results. No rupture or conversion to open surgery. We had one patient with cardiac ischemia, seven patients with spinal cord ischemia
and one patient has early branch occlusion. There was both renal arteries were occluded, he had an unknown heparin induced thrombocytopenia and was treated with endovascular thrombectomy and successfully treated as well. Secondary interventions within 30 days were in one patient
stent placement due to an uncovered celiac stent stenosis In one patient there was a proximal type one endoleak with a proximal extension. One patient who had paraplegia or paraparesis, he had a stenosis of his internal iliac artery which stem was stented successfully,
and the paraparesis resolved later on in this patient. And of course the patient I just mentioned before, with his left and right renal artery occlusion. So to conclude, the T-branch has wide applicability as we've seen also before, up to 80% especially with adjuvant procedures.
Longer, more flexible bridging stent grafts will expand the use of this device. Also the TBE proximal extensions allows aortic treatment of diameters for more than 30 mm and I think the limitations are still the diameter at reno visceral segment,
previous EVAR or open AAA repair and having of course multiple visceral arteries. Thank you.
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