- 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.
- 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.
- I'd like to thank Dr. Veith for this kind invitation and the committee as well. So these are my disclosures, there's none. So for a quick background regarding closure devices. Vascular closure devices have been around
for almost 20 years, various types. Manual compression in most studies have always been shown to be superior to vascular closure devices mainly because there's been no ideal device that's been innovated to be able
to handle all sorts of anatomies, which include calcified vessels, soft plaque, etc. So in this particular talk we wanted to look at to two particular devices. One is the Vascade vascular closure device
made by Cardiva and the other is the CELT arterial closure device made by Vasorum in Ireland. Both these devices are somewhat similar in that they both use a disc. The Vascade has a nitinol disc
as you can see here that's used out here to adhere to the interior common femoral artery wall. And then once tension is applied, a series of steps is involved to deploy the collagen plug
directly on to the artery which then allows it to expand over a period of time. The CELT is similar in that it also uses a stainless steel disc as you can see here. Requires tension up against the interior wall of the common femoral artery.
Nice and tight and then you screw on the top end of the device on to the interior wall of the artery creating a nice little cylinder that compresses both walls of artery. As far as comparability is concerned between the two devices you can see
here that they're both extravascular, one's nitinol, one's stainless steel. One uses a collagen material, the other uses an external clip in a spindle-type fashion. Both require about, anywhere between three to seven minutes of pressure
to essentially stop the tract ooze. But the key differences between the two devices, is the amount of time it takes for patients to ambulate. So the ambulation time is two hours roughly for Vascade, whereas for a CELT device
it's anywhere from being immediate off the table at the cath lab room to about 20 minutes. The data for Vascade was essentially showing the RESPECT trial which I'll summarize here, With 420 patients that was a randomized trial
to other manual compression or the device itself. The mean points of this is that the hemostasis time was about three minutes versus 21 minutes for manual compression. And time to ambulation was about 3.2 hours versus 5.7 hours.
No major complications were encountered. There were 1.1% of minor complications in the Vascade versus 7% in the manual compression arm. This was actually the first trial that showed that a actual closure devices
had better results than manual compression. The main limitations in the trial didn't involved complex femoral anatomy and renal insufficiency patients which were excluded. The CELT ACD trial involved 207 patients that were randomized to CELT or to manual
compression at five centers. Time to hemostasis was anywhere between zero minutes on average versus eight minutes in the manual compression arm. There was one complication assessed at 30 days and that was a distal embolization that occurred
early on after the deployment with a successfully retrieved percutaneously with a snare. So complication rate in this particular trial was 0.7% versus 0% for manual compression. So what are some pros and cons with the Vascade device?
Well you can see the list of pros there. The thing to keep in mind is that it is extravascular, it is absorbable, it's safe, low pain tolerance with this and the restick is definitely possible. As far as the cons are involved.
The conventional bedrest time is anywhere between two to three hours. It is a passive closure device and it can create some scarring when surgical exploration is necessary on surgical dissections.
The key thing also is you can not visualize the plug after deployment. The pros and cons of the CELT ACD device. You can see is the key is the instant definitive closure that's achieved with this particular device, especially in
calcified arteries as well. Very easy to visualize under fluoroscopy and ultrasound. It can be used in both antegrade and retrograde approaches. The key cons are that it's a permanent implant.
So it's like a star closed devised, little piece of stainless steel that sits behind. There's a small learning curve with the device. And of course there's a little bit of discomfort associated with the cinching under the (mumbles) tissue.
So we looked at our own experience with both devices at the Christie Clinic. We looked at Vascade with approximately 300 consecutive patients and we assessed their time to hemostasis, their time to ambulation,
and their time to discharge, as well as the device success and minor and major complications. And the key things to go over here is that the time to hemostasis was about 4.7 minutes for Vascade, at 2.1 hours for ambulation, and roughly an average
of 2.4 hours for discharge. The device success was 99.3% with a minor complication rate of .02% which we have four hematomas and two device failures requiring manual compression. The CELT ACD device we also similarly did
a non-randomized perspective single center trial assessing the same factors and assessing the patients at seven days. We had 400 consecutive patients enrolled. And you can see we did 232 retrograde. We did a little bit something different
with this one, we did we 168 antegrade but we also did direct punctures to the SFA both at the proximal and the mid-segments of the SFA. And the time to hemostasis in this particular situation was 3.8 minutes,
ambulation was 18.3 minutes, and discharge was at 38.4 minutes. We did have two minor complications. One of which was a mal-deployment of the device requiring manual compression. And the second one was a major complication
which was an embolization of the device immediately after deployment which was done successfully snared through an eighth front sheath. So in conclusion both devices are safe and effective and used for both
antegrade and retrograde access. They're definitely comparable when it comes, from the standpoint of both devices (mumbles) manual compression and they're definitely really cost effective in that they definitely do increase the
throughput in the cath lab allowing us to be able to move patients through our cath lab in a relatively quick fashion. Thank you for your attention.
- 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.
- Yeah, thank you very much. We all know that DCBs are kind of a workhorse right now for SFA-PA disease but when it comes, this has been proven randomized controlled studies, but when it comes to real world patients this might not have been included in the randomized conduit study and therefore
these registries are very available. And I present on this BIOLUX P-III study [Unintelligible] the standard versus the non-standard sub-group. This is just a quick overlook about the Passeo-18 Lux DCB it's an O-18 platform, has three micrograms
[Unintelligible] Paclitaxel on the balloon The excipient is a BTHC and this is an hydrophobic excipient and the sizes available are from two to seven millimeter in diameter and four 80 and 100 millimeter in length. This is the overlooks about the Passeo-18 Lux
they are out there, we have from phase one to phase three studies, randomized controlled and global registries. 1,600 patients including in this clinical program. With regard to the full cohort at 12 month we have now 878 patients available, you see with regard to the clinical characteristics
heavy smokers... a high percentage of smokers, high percentage of diabetes, more than 40% of CLI, 76% calcified lesions, the lesion length was around 9 centimeter and one-third of the patients had TASC C or D lesions. This is a higher payload stenting rate
this is not surprising with this complex cohort about 20% and with that the primary patency of the full cohort at 12 months is 84.3% and the freedom from clinical driven TLR is 93.5%. So this is the overlook of the full cohort at 12 months. With regard to the different subgroups you see
you have a consistent freedom from clinical driven TLR primary patency and freedom from major target limb amputation throughout all the subgroups. And I just now want to highlight the bail-out stented versus the DCB only group because this follows the concept of the so-called leave, at least leave less behind
as possible, this so-called spot-stenting concept. Out of this 878 patients we had 715 treated with a DCB only and in the bail-out stent group we had 163 patients. The patients in the bail-out stented group had a longer lesion length... 11 compared to 8 centimeters
in the DCB only group. With regard to all the others correctors there was no difference besides TASC C and D lesions there had been a higher percentage of TASC C and D lesions in the bail-out stented group than in the DCB only group.
We did the same vessel prep for both arms and with that we had the freedom from clinical driven TLR in the bail-out stented group of 92.8 compared to 92.2% in DCB only group. Primary patency was a little bit lower but freedom from a major adverse event
at 12 months was the same. When we bring this into context to other randomized, other real-world data out there freedom from clinical driven TLR in comparison to the In.Pact global stented group is the same as well as in the Lutonix global stented group.
With regard to freedom from major adverse event we can only refer to the In.Pact global stented group which is the same. So just let me conclude the Passeo-18 Biolux P-III study continues to show consistent, clinical performance of the Passeo-18 Lux Drug Coated Balloon
throughout all subgroups. There is no difference in clinical performance between DCB only versus payload stented even for the bail-out stented group had more complex lesions and the results of the Biolux P-III payload stenting subgroups are in line with the results
of current Global registries stented subgroups. Thank you very much.
- 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.
- So thank you ladies and gentleman, thank you Doctor Veith for inviting me again this year. These are my disclosures. So more effective thrombolysis by microbubbles and ultrasound has been proven actually effective in earlier studies, treating a myocardial infarction or acute ischemic stroke.
But what are these microbubbles? These are 1 to 10 micrometers, gas-filled bubbles with a lipid shell. It oscillate when subjected to low intensity ultrasound, and can cavitate when subjected to high intensity ultrasound. Initially they were designed for diagnostic use
as intravascular contrast enhancers. However, they have many advantages, non-specifical mechanical effects, to induce thrombus breakdown due to mechanical force of microbubbles if they are subjected to ultrasound. So we conducted the first human trial
in peripheral arterial diseases in Microbubbles and UltraSound-accelerated Thrombolysis, the MUST study for peripheral arterial occlusions. Which is a single phase two trial for actually safety and feasibility study. The MUST-TRIAl consist out of 20 patients
for safety and feasibility, which in 10 patients will be treated with Urokinase, and 10 with Alteplase. And then added, for the first hour, microbubbles and we evaluated the VAS pain scores, duplex echography for circulation or revascularization, microcirculation and daily angiography as usual.
Included were men and women 18 to 85 years. A maximum of two weeks of symptoms of lower limb ischaemia due to thrombosed or occluded lower limb peripheral native arteries or venous or prosthetic bypass grafts. And Rutherford class 1 or 2A. They have to understand the nature of the procedure
and written informed consent. And excluded were all known factors that exclude standard thrombolysis therapy, hypersensitivity to contrast enhanced agents, a recent acute coronary syndrome. Endpoints, again, it's a safety
and then a technical feasibility trial. Also we looked at the organisation, and the treatment duration for technical, angiographic, and clinical success. We looked at the severe adverse event and mortality rates, VAS-pain scores and microcirculation.
If the patients came in, we inform them about the MUST trail, we performed an ECG analysis and informed consent. They fill out some questionnaires and when they come in to the angio-room, we started a thrombolysis with a catheter, the Mc Nemara.
And the first group, the Urokinase 10 patients, we treated with 500 units of bolus and then continued with a 50,000 units of Urokinase per hour. The Alteplase group had started with a 5 milligram bolus and then they continued with 1 milligram per hour
for the first 24 hours. And then, the ultrasound room, they got a bubble infusion for the first hour of treatment. Then we would continue with thrombolysis on a surgical ward, every sixth hour we'd look at if there was revascularization at the duplex ultrasound.
And if signs of revascularization are observed on the duplex ultrasound or on the next day, we routinely perform the angiography. Then we could cessate the thrombolytic therapy, and if necessary, acute or elective additional intervention to correct underlying lesions,
or to establish patencies. We check the wound and then we follow-up these patients every six weeks, three months, 6 months, and one year after thrombolytic therapy. So these are the patient characteristics, mostly of these were male, 70 years,
and five of them were native bypass, and five were a bypass occlusion, venous or prosthetic. And two of them had multiple occlusions, whether Rutherford class 1 or 2A. And these were the first 10 patients that were treated with Urokinase and I will present here
the results of these 10 patients first. So, very important, there were no deaths, no severe adverse events, and it was technical feasible. The flow at the duplex examination was there after 24 hours, but most of our patients actually had it already after 6 hours.
The amputation rate, right now, is zero. And also no bypasses were now needed. So we will continue this MUST trial right now and January we probably will have the inclusion of the group with the Alteplase, which I'll present next year.
And we think that microbubbles with Urokinase is a safe combination right now. We will further include the groups of adults placed and further optimalisation of the microbubbles technique with nanobubbles. Had a talk about that yesterday, so you can look it up.
And nanobubbles are nanoparticles of 5 to 500 nanometers, which are very small, they do not penetrate the endothelial barrier of the doubt and it damage. And it can carry the thrombolytics actually to the side the aorta catheter need it. You can also make the magnetic paste,
which means you can paste these patients on the MRI. Then you can have local treatment of thrombolytic therapy. So thank you for your attention.
- 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)
- [Speaker] Thank you. My disclosures. So upper extremity dvt occurs in 4-10% of all causes of venous thrombosis. And while a minority, dvt in the upper extremity can often be caused by thoracic outlet syndrome, effort thrombosis, occasionally
idiopathic venous thrombosis. The majority is more likely related to central venous catheters, pacemakers, cancer, etc. This is some of the presentation of someone with Paget Schroeder or venous thoracic outlet syndrome, we're all well aware of this.
Some features of this can be sudden onset of pain, discoloration and some of this subcutaneous collateral veins that we note. Initial treatment of this is traditionally with venous thrombolysis. Although the results are good, this thrombolysis can
be associated with bleeding complications, potential for renal insufficiency, prolonged dwell times, and increased cost. I think it's important that this is not just a talk about a technique but a technique in the context of an operation this is soon to come.
Whether you choose to take out the rib at the same setting or you choose to delay the operation by a week or two, by and large the complications associated with that venous thrombolysis are going to come back and haunt you in the next operations. I think that's the context of this talk.
One of the risks I just mentioned about some of these techniques is, that's sort of curious to me, is the acute kidney injury after AngioJet venous thrombolysis. You see here, this paper, of a hundred patients, 50 AngioJet, 50 catheter directed thrombolysis, shows a statistical significantly
increased risk of acute kidney failure in the AngioJet group. Eight fold odds ratio. The Indigo system enables operators to remove the thrombus in a single setting, while potentially reducing or eliminating the need for thrombolysis.
This has already been discussed by some of the prior speakers, you see the different iterations first introduced in 2014. The CAT8 is the largest device and you can see some of the features of this proprietary technology with the separator and the directional sheaths that
allow us to aspirate nicely. This continuous suction you see here, can be very nicely controlled with an on-off switch that minimizes blood loss. It's single operator design, very easy to set up, hands free aspiration, a very simple set up.
You also heard just recently about the volume that can be aspirated in 20 seconds you see, especially with the larger profile devices, quite impressive amount of thrombus can be removed. Again, with the careful control for blood loss. The directionality of the sheath is also important,
and you can see some of the different directionality sheaths. Here's a couple case examples of a Paget-Schroder patient comes in with an acute sudden onset of arm pain and swelling discoloration, and you can see the penumbra device being used to clean out that vein.
This is another example, a 25-year old male with acute right arm swelling, sort of a body lifter type, and you can see here, this is the separator that's being moved forward and backwards, in and out to help break out the thrombus. This is the CAT8 device.
The pre-intervention picture seen here, we're crossing the lesion with a wire and and you can see the post-intervention on the right. You, of course, have the venous compression from the first rib, thoracic outlet, but the vein is widely open and now we can go ahead and see
the specimen that's retrieved as you've seen other videos in the prior presentations. This, of course, is what we're left with at the time of surgery. I only bring this up to remind us that there is a second stage to this treatment,
which is the rib resection. A combined experience that I just want to put together, very small numbers of course but, 16 patients with thoracic outlet who presented and were treated with the Penumbra system. You can see here, some of the demographic data.
I'll just point out the symptoms, of course, pain, swelling in these patients, imaging mostly venous duplex, occasionally CT or MR venogram. They all of course get venography at the time of procedure. The extent of the thrombus in all of them was complete occlusion and you can see some
of the extent in the subclavian axillary veins. Site of access can be the brachial or the basilic vein. The operative details as well, shown here, and I'll just point out the estimated blood loss, it can be very reasonable, especially with some experience you can sort of control that
on-off valve and minimize blood loss with this technique. Adjunctive therapies are shown here and of course, maybe because we're a little bit stuck on our ways, we did have a fair number of adjunctive lytic therapy. There were only three patients who had overnight lysis. A lot of venoplasty done at the time of the procedure.
All veins remained patent until the day of the rib resection but I will point out that one of these patients did develop a significant complication with hemothorax. This is one of those patients who had overnight lysis. And I point that out to stress that perhaps
this is what we're trying to move away from. So, in conclusion, mechanicothrombectomy using Indigo device shows promising initial results. Minimal blood loss, one complication of the hemothroax with the overnight lytics. No renal insufficiency or distal embolization.
The practice pattern, I think, need to adjust away from routing lytics to additionally minimize complications prior to surgery. Thank you.
- 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.
- So I have the honor to provide you with the 12-month result of the TOBA II trial. I guess we all confirmed that this action is the primary mechanism of angioplasty. We all know that lesions of dissection have a TLR rate of 3.5 times higher than lesions without dissection.
The current tools for dissection repair, these are stents. They have limitations, really a large metal load left behind causing inflammation. This is leading to in-stent restenosis. So the Tack Endovascular System.
It's a delivery system over six French catheter. This is for above the knee with six implants pre-loaded on a single catheter. The Tack implant itself, it has an adaptive sizing, so it adapts to the diameter of the vessel from 2.6 up to 6.0 for SFA and PPA usage.
It's a nitinol implant with gold radiopaque markers for visibility. Has a unique anchoring system, which prevents migration, and a deck which is deployed in six millimeter in length. So with regard to the TOBA II study design,
this was a prospective multi-center single-arm non-blinded study at 33 sites in US and Europe. We enrolled 213 subjects. These were all subjects with post-PTA dissection. So only with a dissection visible on the angiogram, the patients could be enrolled into this study.
We had the usually primary safety end point, primary efficacy end points, which we are familiar from other trials and other studies so far. With regard to the inclusion criteria, I just want to look at this very briefly.
Mainly we had de novo or non-stented restenotic lesions in the SFA P1. If it was a stenosis, the lesion length could be up to 150 millimeter. If it was a total occlusion, the length was up to 10 centimeters.
They had to be the presence of at least one target run of vessel to the foot. They had to be a post residual, post-PTA residual stenosis of lower than 30%, and the presence of at least one dissection Grade A to F. With regard to the key lesion characteristics,
baseline for the different patients, there was not a big difference to other studies out there. The only difference was maybe we had slightly more patients with diabetes. The lesion, the target lesion length, the mean target lesion length was up to 74 millimeters.
We also had patients with calcification, mainly moderate but also some with severe calcification. There were two met the primary end points. The 30-day freedom from major adverse event, and also the primary efficacy end point at 12 months, which was a freedom from clinical driven TLR,
and freedom from core lab adjudicated duplex ultrasound derived binary restenosis. Now, with regard to patency in a patient cohort, where we really had 100% dissected vessel at 100% dissected vessel population, we had primary patency at 12-month of 79.3%
and a freedom clinical driven TLR of 86.5%. There was with regard to dissection severity, we had 369 total dissections we were treating. The number of dissections per subject was 1.8. The mean dissection length was two centimeters. So around 70% of subjects had a dissection of
Grade C or greater before using the Tack. In 92.1% of all dissections, this could be completely resolved with a Tack. With regard to the Tack stability and durability, in total, 871 Tacks have been deployed. So that was a number of 4.1 Tacks per subject.
The bailout stent rate was very low, just one. The freedom from Tack fracture at 12 months, 100%, and there was one minor Tack migration at 12 months with education by the core lab so the Tack was not seen at the same place as six months or 12 months before.
There was significant clinical improvement with Rutherford category improvement in 63%, which improved of up to two classes. There was also an improvement in ABI, walking impairment questionnaire. So just to conclude, TOBA II is a unique trial.
First to enroll 100% dissected vessels. Successfully met the primary efficacy and safety end points, and demonstrated the Tack is an efficient repair system for dissections after POBA or DCB with minimum metal left behind, low radial force, stable and durable design,
and preservation of future treatment options. There was only a very, very low bailout stent rate. This in combination with high patency rate and high freedom from clinical TLR. Thank you very much.
- [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.
- Thank you very much Mr. Chairman. Thank you Frank, for this kind invitation again to this symposium. This is my disclosure. With the drug coated balloons it is important to minimize the drug loss during the balloon transit during the inflation of the balloon.
Because Paclitaxel has a high degree of cytotoxicity that may induce necrosis and increase inflammation in the distal tissue, and we know that even with the best technique, we can loose 70 - 80% of the drop to the distal circulation,
the inference by different factors between them and the calcification of degree of these blood cells. There are adverse events secondary to drug coated balloons that have been reported recently. In animal molders it has shown that Downstream Vascular Changes are more frequent with
Drug Coated Balloons than with Drug-Eluting Stents. In animal molders it has been also shown that there is no evidence of significant downstream emboli or systemic toxicity with DCB's than with patients with controls. This was a study presented yesterday by (mumbles)
with a very nice and elegant study with a good methodology that shows in animals that there are different concentrations of the drug in distal tissue depending on the balloon that you are using. In this case, the range in balloon (mumbles)
those ones have the lowest concentration in the distal tissue. In clinical experience in this meta-analysis amputations and wound healing rate are lower with this series with controls. But there is controversy because
Complete Index Ulcer Healing is higher in this series than with control patients. But there are lower wound healing index in patients compared with drug-eluting stents. In the debate, (mumbles) and also in the dialux which are clinical trials in diuretic patients with CLI,
there we no issues of safety and no impair of the wounds healing. But, remember the negative result of the IN PACT DEEP trial in which there were more amputation at six months that could be influenced, but in all their factors, the lack of standardized
wound care protocols. (mumbles) has also reported recently good survival to 100% in patient treated with DCB's compared with plain balloons and with lutonic balloons. So in our institution, we did a study with the objective to examine
patient outcomes following the use of the drug-coated balloons in patients with CLI and diuretic patients with Complex Real World lesions undergoing endovascular intervention below-the-knee with the Ranger balloon coated with Paclitaxel.
This is a Two-Center Experience that is headed by the National University of Mexico in 30 patients with strict followup. With symptomatic Rutherford four to six. With the Stenosis and occlusion of infrapopliteal vessels and many degrees of calcification.
It was mandatory for all patients to have Pre-dilation before the use of DCB. We studied some endpoints like efficacy. (mumbles) Limb salvage, sustained clinical improvement, wound healing rate
and technical success and some other endpoints of safety. This is an example of multi level disease in a patient that has to be approached by (mumbles) access with a balloon preparation of the artery before the use of the DCB, and after this, we treated the anterior artery
and even to the arch of the foot. This is the way we follow our patient with ultra sound duplex with an index fibular of no more that 2.4. All patients were diabetic with Rutherford 5-6. 77% have a (mumbles) at the initial of the study.
And as you can see there were longer lesions and with higher degree of calcification and stenosis only in two of them we produced (mumbles). There were bailout stent placements in five patients and we did retrograde access in 43 patients.
Subintimal angioplasty was done in 32 patients, and Complete Index Wound Healing was in 93 of our patients. This is our Limb Salvage 94%. The Patency rate was 96% with this Kaplan Meir analysis. And in some patients we did a determination of Paclitaxel concentration in distal tissue
with the High Pressure Liquid Chromatography method. We only did this in five patients because of the lack of financial support, and technical problems. As you can see in three of them we had Complete Wound Healing.
Only one we had major amputation. This was the patient with the higher concentration of Paclitaxel in the distal tissue, and in one patient, we could not determine the concentration of Paclitaxel. This is the way we do this.
They take the sample of the patient at the moment we do the minor amputation. During day 10 after the angioplasty, we also do a (mumbles) analysis of the patient we have a limb salvage we can see arterial and capillar vessel proliferation and hyperplasia of the
arteriole media layer. But, in those patients that have major amputation even when they have a good sterio-graphic result like in this case, we see more fibrinoid necrosis which is a bad determination. So in conclusion,
angioplasty with the (mumbles) balloon maintain clinical efficacy over time is possible. We didn't see No Downstream clinical important or significant effects and high rates of Limb Salvage in complex CLI patients is possible.
Local toxic effects of paclitaxel and significant drug loss on the way to the lesion are theoretical considerations up to now because there is no biological study that can confirm this. Thank you very much.
- 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.
- 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
- [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.
- Pleasure to be here again this year, discussing now something very exciting that we're going to be a part of at Baylor. Some disclosures, of which probably the fact that I educate and train for Boston may be relevant to this topic. Quick picture showing some of my own patients
that had chronic limb threatening ischemia over a year ago and just recently we had to do an angio again for some more proximal disease. And obviously not a surprise but at one year after drug alluding stenting, obviously balloon expandable stenting, the patency, actually it was more than that,
13, 14 months, it was fantastically open. On another terrible case, I had a patient that had a failed distal bypass and that one area of occlusion was the area where the bypass was amassed the most. Unfortunately after atherectomy, after balloon angioplasty
there was still acute recoil and I had to stent that area. I had to take the patient back a few months later for assisted primary patency and that stent had just become a mesh of useless metal and that's because that mobility at that proportion of the tibials is a lot.
So there's a lot to be said about the utilization of a non crushable scaffold in this segment. Tibial disease as is no secret to any of us is very diffuse, specifically in diabetics. And can be seen in a multitude of studies that there is an advantage of a scaffold
that has biological effect. Now granted most of these lesions have been very small and very short because of the availability of the structures and also because of what we've learned about the anatomy of the tibial and the areas of the tibials we've learned that not every single
part of the tibial vessels are actually amenable to a balloon expandable scaffold. Drug coated balloons have tried to expand the indication with some variable results as you look at the entirety of the studies out there. Now looking at what the patency has shown,
restenosis and freedom from TLR, it's been very obvious that those cases that have been scaffolded at 12 months have actually done very good, obviously the criticism and the constraint has always been lesion length. Smaller lesions have responded really well.
Now what would happen after that first year, we know from the PADI stud at 5 years is that when compared to PTA and bare meta stenting there is a very clear advantage that is maintained up to five years by using biological affects. So the SAVAL pivotal trial is a global pivotal trial
of a drug eluting system called the SAVAL stent. It's the first time that the differentiated technology selected for expedited access pathway has been awarded by the FDA and the anticipated enrollment us going to be Q3 2018, the idea of this flexible Nitinol self expanding stent is that it's going to be
compliant to most of the anatomy of the tibials. This is a polymer drug coating based scaffold. Somewhat in accordance or at least the same one that has been used previously for the Aluvia, that has been recently approved. This study is randomized, comparing DES below the knee
to percutaneous angioplasty alone below the knee. Doctor Mustapha is the global PI and Patrick Geraghty, Hans Overhagen and Masato Nakamura are going to be the co PIs for the global perspective as it will be conducted in Japan, in EU and in the United States.
There will be a perspective phase for this, so a two to one study with a limited size of 80 millimeter in length scaffold and then a phase B where they will allow us to put more than one scaffold, allowing longer lesions to be treated.
The objective is to get 200 patients, randomize again to two to one in 50 centers and we're looking for obviously CLTI patients Rutherford's class four and five, greater than 70 percent stenosis. Reference vessel diameter is going to be two five to
three 75 and total target lesion length is going to be initially less than 70 for coverage with one scaffold and then after that it's going to be freed up to hopefully less than 140 lesions. Primary patency at six months, it's going to be a superiority versus the PTA branch.
Certainly a major adverse events are going to be defined by above the ankle amputation, major reintervention and mortality. So the key features, primary patency measured at one, six, 12, 24 and 36 months. TLRs are going to be also seen.
Hemodynamic outcomes will be managed and assessed. Wound assessment will be also closely followed. Major amputation rate, Rutherford classification, quality of life and hospital readmissions. So in conclusions CLTIs associated with high amputation rates and poor clinical outcomes.
CLTI is commonly associated with below the knee lesions and challenging anatomy. Endovascular treatment has potential to increase wound healing and reduce amputation rates and the SAVAL clinical study will investigate safety and efficacy of a self expanding
drug eluting stent design particularly for the below the knee vessels, 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.
- 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.
- 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 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.
- So this was born out of the idea that there were some patients who come to us with a positive physical exam or problems on dialysis, bleeding after dialysis, high pressures, low flows, that still have normal fistulograms. And as our nephrology colleagues teach us, each time you give a patient some contrast,
you lose some renal function that they maintain, even those patients who are on dialysis have some renal function. And constantly giving them contrasts is generally not a good thing. So we all know that intimal hyperplasia
is the Achilles Heel of dialysis access. We try to do surveillance. Debbie talked about the one minute check and how effective dialysis is. Has good sensitivity on good specificity, but poor sensitivity in determining
dialysis access problems. There are other measured parameters that we can use which have good specificity and a little better sensitivity. But what about ultrasound? What about using ultrasound as a surveillance tool and how do you use it?
Well the DOQI guidelines, the first ones, not the ones that are coming out, I guess, talked about different ways to assess dialysis access. And one of the ways, obviously, was using duplex ultrasound. Access flows that are less than 600
or if they're high flows with greater than 20% decrease, those are things that should stimulate a further look for clinical stenosis. Even the IACAVAL recommendations do, indeed, talk about volume flow and looking at volume flow. So is it volume flow?
Or is it velocity that we want to look at? And in our hands, it's been a very, very challenging subject and those of you who are involved with Vasculef probably have the same thing. Medicare has determined that dialysis shouldn't, dialysis access should not be surveilled with ultrasound.
It's not medically necessary unless you have a specific reason for looking at the dialysis access, you can't simply surveil as much as you do a bypass graft despite the work that's been done with bypass graft showing how intervening on a failing graft
is better than a failed graft. There was a good meta-analysis done a few years ago looking at all these different studies that have come out, looking at velocity versus volume. And in that study, their conclusion, unfortunately, is that it's really difficult to tell you
what you should use as volume versus velocity. The problem with it is this. And it becomes, and I'll show you towards the end, is a simple math problem that calculating volume flows is simply a product of area and velocity. In terms of area, you have to measure the luminal diameter,
and then you take the luminal diameter, and you calculate the area. Well area, we all remember, is pi r squared. So you now divide the diameter in half and then you square it. So I don't know about you,
but whenever I measure something on the ultrasound machine, you know, I could be off by half a millimeter, or even a millimeter. Well when you're talking about a four, five millimeter vessel, that's 10, 20% difference.
Now you square that and you've got a big difference. So it's important to use the longitudinal view when you're measuring diameter. Always measure it if you can. It peaks distally, and obviously try to measure it in an non-aneurysmal area.
Well, you know, I'm sure your patients are the same as mine. This is what some of our patients look like. Not many, but this is kind of an exaggerated point to make the point. There's tortuosity, there's aneurysms,
and the vein diameter varies along the length of the access that presents challenges. Well what about velocity? Well, I think most of us realize that a velocity between 100 to 300 is probably normal. A velocity that's over 500, in this case is about 600,
is probably abnormal, and probably represents a stenosis, right? Well, wait a minute, not necessarily. You have to look at the fluid dynamic model of this, and look at what we're actually looking at. This flow is very different.
This is not like any, not like a bypass graft. You've got flow taking a 180 degree turn at the anastomosis. Isn't that going to give you increased turbulence? Isn't that going to change your velocity? Some of the flow dynamic principles that are important
to understand when looking at this is that the difference between plug and laminar flow. Plug flow is where every bit is moving at the same velocity, the same point from top to bottom. But we know that's not true. We know that within vessels, for the most part,
we have laminar flow. So flow along the walls tends to be a little bit less than flow in the middle. That presents a problem for us. And then when you get into the aneurysmal section, and you've got turbulent flow,
then all bets are off there. So it's important, when you take your sample volume, you take it across the whole vessel. And then you get into something called the Time-Averaged mean velocity which is a term that's used in the ultrasound literature.
But it basically talks about making sure that your sample volume is as wide as it can be. You have to make sure that your angle is as normal in 60 degrees because once you get above 60 degrees, you start to throw it off.
So again, you've now got angulation of the anastomosis and then the compliance of a vein and a graft differs from the artery. So we use the two, we multiply it, and we come up with the volume flow. Well, people have said you should use a straight segment
of the graft to measure that. Five centimeters away from the anastomosis, or any major branches. Some people have actually suggested just using a brachial artery to assess that. Well the problems in dialysis access
is there are branches and bifurcations, pseudoaneurysms, occlusions, et cetera. I don't know about you, but if I have a AV graft, I can measure the volume flow at different points in the graft to get different numbers. How is that possible?
Absolutely not possible. You've got a tube with no branches that should be the same at the beginning and the end of the graft. But again, it becomes a simple math problem. The area that you're calculating is half the diameter squared.
So there's definitely measurement area with the electronic calipers. The velocity, you've got sampling error, you've got the anatomy, which distorts velocity, and then you've got the angle with which it is taken. So when you start multiplying all this,
you've got a big reason for variations in flow. We looked at 82 patients in our study. We double blinded it. We used a fistulagram as the gold standard. The duplex flow was calculated at three different spots. Duplex velocity at five different spots.
And then the diameters and aneurysmal areas were noted. This is the data. And basically, what it showed, was something totally non-significant. We really couldn't say anything about it. It was a trend toward lower flows,
how the gradients (mumbles) anastomosis, but nothing we could say. So as you all know, you can't really prove the null hypothesis. I'm not here to tell you to use one or use the other, I don't think that volume flow is something that
we can use as a predictor of success or failure, really. So in conclusion, what we found, is that Debbie Brow is right. Clinical examinations probably still the best technique. Look for abnormalities on dialysis. What's the use of duplex ultrasound in dialysis or patients?
And I think we're going to hear that in the next speaker. But probably good for vein mapping. Definitely good for vein mapping, arterial inflow, and maybe predicting maturation. Thank you very much.
- 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.
- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.
Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance
between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.
Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.
Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100
consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any
stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria
having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this
on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher
than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of
the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,
you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because
the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity
because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish
this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,
regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. Thank you very much.
- [Speaker] Good morning everybody thanks for attending the session and again thanks for the invitation. These are my disclosures. I will start by illustrating one of the cases where we did not use cone beam CT and evidently there were numerous mistakes on this
from planning to conducting the case. But we didn't notice on the completion of geography in folding of the stent which was very clearly apparent on the first CT scan. Fortunately we were able to revise this and have a good outcome.
That certainly led to unnecessary re intervention. We have looked at over the years our usage of fusion and cone beam and as you can see for fenestrated cases, pretty much this was incorporated routinely in our practice in the later part of the experience.
When we looked at the study of the patients that didn't have the cone beam CT, eight percent had re intervention from a technical problem that was potentially avoidable and on the group that had cone beam CT, eight percent had findings that were immediately revised with no
re interventions that were potentially avoidable. This is the concept of our GE Discovery System with fusion and the ability to do cone beam CT. Our protocol includes two spins. First we do one without contrast to evaluate calcification and other artifacts and also to generate a rotational DSA.
That can be also analyzed on axial coronal with a 3D reconstruction. Which essentially evaluates the segment that was treated, whether it was the arch on the arch branch on a thoracoabdominal or aortoiliac segment.
We have recently conducted a prospective non-randomized study that was presented at the Vascular Annual Meeting by Dr. Tenario. On this study, we looked at findings that were to prompt an immediate re intervention that is either a type one
or a type 3 endoleak or a severe stent compression. This was a prospective study so we could be judged for being over cautious but 25% of the procedures had 52 positive findings. That included most often a stent compression or kink in 17% a type one or three endoleak
in 9% or a minority with dissection and thrombus. Evidently not all this triggered an immediate revision, but 16% we elected to treat because we thought it was potentially going to lead to a bad complication. Here is a case where on the completion selective angiography
of the SMA this apparently looks very good without any lesions. However on the cone beam CT, you can see on the axial view a dissection flap. We immediately re catheterized the SMA. You note here there is abrupt stop of the SMA.
We were unable to catheterize this with a blood wire. That led to a conversion where after proximal control we opened the SMA. There was a dissection flap which was excised using balloon control in the stent as proximal control.
We placed a patch and we got a good result with no complications. But considerably, if this patient was missed in the OR and found hours after the procedure he would have major mesenteric ischemia. On this study, DSA alone would have missed
positive findings in 34 of the 43 procedures, or 79% of the procedures that had positive findings including 21 of the 28 that triggered immediate revision. There were only four procedures. 2% had additional findings on the CT
that were not detectable by either the DSA or cone beam CT. And those were usually in the femoro puncture. For example one of the patients had a femoro puncture occlusion that was noted immediately by the femoro pulse.
The DSA accounts for approximately 20% of our total radiation dose. However, it allows us to eliminate CT post operatively which was done as part of this protocol, and therefore the amount of radiation exposed for the patient
was decreased by 55-65% in addition to the cost containment of avoiding this first CT scan in our prospective protocol. In conclusion cone beam CT has allowed immediate assessment to identify technical problems that are not easily detectable by DSA.
These immediate revisions may avoid unnecessary re interventions. What to do if you don't have it? You have to be aware that this procedure that are complex, they are bound to have some technical mistakes. You have to have incredible attention to detail.
Evidently the procedures can be done, but you would have to have a low threshold to revise. For example a flared stent if the dilator of the relic gleam or the dilator of you bifurcated devise encroach the stent during parts of the procedure. Thank you very much.
- Lymphatic, so it's fun, actually, not to talk on venous interventions for once. And, naturally, the two systems are very different. But, on the other hand, they're also related in several ways and I will come back to that later. I have no disclosures, maybe only my gratitude to this man, Dr. Maxim Itkin,
who actually got me started in the field, and was gracious enough to supply me some of his material. And who is also responsible for making our lives way easier over the last years. Because in former times, we needed to do, to visualize the lymphatic system,
we needed to do pedal lymphangiography and that was very, very cumbersome. It took a long time and was very painful for the patient. And he introduced the ultrasound guided intranodal lymphangiography,
and that's fairly easy for most of us. With ultrasound you find a lymph node in the groin, you puncture that and you can control the needle position with contrast enhanced ultrasound and once you establish that position, you might do a MR lymphangiography.
Thereby showing, in this case, a beautiful, normal anatomy of the thoracic duct. I need to say, the variations in lymphatics are extreme. So, you can also visualize, naturally, the pathology, like for example, pulmonary lymphatic perfusion syndrome.
What's going on there. Normally, lymph courses up through thoracic duct, but in this case, you kind of have a reflux in the bronchial tree and lymph leakage. And you can image that again, beautifully with MR, which you can show extensive leakage
of lymph in the lung parenchyma. So you can treat that. How can you treat that? By embolization of the thoracic duct. But first we need to get into there, and that's not a very easy thing to do.
But now, again, with access to a lymph node in the groin, you can push lipiodol, and then visualize the cisterna chyli and access that transcutaneously with a 21/22 gauge needle and then push up a O-18 wire high up in the thoracic duct.
First you deploy some coils to prevent any leakage of glue inside the venous system, and then by microcatheter, you infuse glue all the way down, embolizing the thoracic duct. So, complete different group of lymphatic disorders is oriented in the liver and hepatic lymphatic disorders.
And maybe not everybody knows that, but 80% of the flow in the thoracic duct is caused by the liver and by the intestine. And many times in lymphatic disorders, there needs to be a combination of two factors. One factor is a venous variation of a,
sorry, an anatomical variation in lymph vessels and the other one is that we have an increase in lymph flow. And in the liver, that can be caused by a congestion of the liver, for example, cirrhosis, or a right side, that's congested heart failure.
What happens then is you increase the flow, the lymph flow, tremendously and if you also have a variation like in this case, when the vessels do not directly course towards the cisterna chyli, but in very close contact to the abdomen,
then you can have leakage of the lymph and leakage of proteins, which is a serious problem. So, what is then, to do next? You can access the lymph vessels in the liver by percutaneous access in the periportal space,
and induce some contrast and then later, visualize that one back, visualize that with dye that you can see with an endoscopy, thereby proving your diagnosis, and then, in a similar way,
you can induce lipiodol again with glue, embolizing the lymph vessels in the liver, treating the problem. In summary, popularity of lymphatic interventions really increased over the last years mainly because novel imaging,
novel interventional techniques, new approaches, and we all gained more experience. If you would like, I would guess that, we are at a phase where we were at venous, like 10, 15 years ago. If we are a little bit positive,
then the future is very bright. And within 10, 15 years, we find new indications and probably have much more to tell you. Thank you for your attention.
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- (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.
- 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, chairman. Good afternoon, ladies and gentlemen. I've not this conflict of interest on this topic. So, discussion about double-layer stent has been mainly focused about the incidence of new lesions, chemical lesions after the stenting, and because there are still some issue
about the plaque prolapse, this has still has been reduced in a comparison to conventional stent that's still present. We started our study two years ago to evaluate on two different set of population of a patient who underwent stent, stenting,
to see if there is any different between the result of two stents, Cguard from Inspire, and Roadsaver from Terumo in term of ischemic lesion and if there is a relationship between the activity of the plaque evaluated with the MRI
and new ischemic lesion after the procedure. So, the population was aware of similar what we found, and that there's no difference between the two stent we have had, and new ischemic lesions is, there's a 38%, for a total amount of 34 lesions,
and ipsilateral in 82% of cases. The most part of the lesion appeared at the 24 hours, for the 88.2% of cases, while only the 12% of cases, we have a control at our lesion. According to the DWI, we have seen that
the DWI of the plaque is positive, or there is an activity of the plaque. There's a higher risk of embolization with a high likelihood or a risk of 6.25%. But, in the end, what we learned in the beginning, what there have known,
there's no difference in the treatment of the carotid stenosis with this device, and the plaque activity, when positive at the DWI MR, is a predictive for a higher risk of new ischemic lesions at 24 hours. But, what we are still missing in terms of information,
where something about the patency of the stents at mid-term follow-up, and the destiny of external carotid artery at mid-term follow-up. Alright, we have to say we have an occlusion transitory, occlusion of the semi-carotid artery
immediately after the deployment of the Terumo stent. The ECA recovery completely. But in, what we want to check, what could happen, following the patient in the next year. So, we perform a duplicate ultrasound, at six, at 12, and 24 months after the procedure,
in order to re-evaluate the in-stent restenosis and then, if there was a new external carotid artery stenosis or occlusion. We have made this evaluation according to the criteria of grading of carotid in-stent restenosis proposed on Stroke by professors attache group.
And what we found that we are an incidence of in-stent restenosis of 10%, of five on 50 patient, one at six month and four at one year. And we are 4% of external carotid artery new stenosis. All in two patient, only in the Roadsaver group.
We are three in-stent restenosis for Roadsaver, two in-stent restenosis for Cguard, and external new stenosis only in the Roadsaver group. And this is a case of Roadsaver stent in-stent restenosis of 60% at one year. Two year follow-up,
so we compare what's happening for Cguard and Roadsaver. We see that no relation have been found with the plaque activity or the device. If we check our result, even if this is a small series, we both reported in the literature for the conventional stent,
we've seen that in our personal series, with the 10% of in-stent restenosis, that it's consistent with what's reported for conventional CAS. And the same we found when we compared our result with the result reported for CAS with conventional stent.
So in our personal series, we had not external carotid artery occlusion. We have 4% instance, and for stenosis while with conventional CAS, occlusion of external carotid artery appear in 3.8% of cases.
So, what can we add to our experience now in the incidence, if, I'm sorry, if confirmed by larger count of patient and longer study? We can say that the incidence of in-stent restenosis for this new double-layer stent and the stenosis on the external carotid artery,
if not the different for all, with what reported for conventional stent. Thank you.
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