- After Dr. Mow-knee's excellent review I don't have much to add here, but just go by here. I have no conflict of interest. As he already said, Takayasu arteritis is a systemic disease, affecting entire wall. It's fundamentally different from atherosclerosis. I like to emphasize once again because same principle
to relieve ischemic symptom based on atherosclerosis should not be applied to Takaysu arteritis. That's what we learned for the last three decade. This is a primarily medical condition to need the medical treatment and not a surgical condition until it develops the complication,
hence the primary aim of treatment is to control active inflammation and induce remission just like Dr. Mow-knew gave a thorough review here. The inflammatory nature of TA waxes and wane with active or chronic system inflammation hence strict control of this condition is absolutely warranted before
any surgical or endovascular management is considered. After all, TA is a medical condition and not a surgical one from the outset. TA has a strong nature of the collateral development to provide excellent natural compensation sufficient to relieve the symptoms in general hence not all symptomatic
lesions actually require the intervention, that's what we also learned, for the intervention accompanied with significant morbidity, we already understand, restenosis, thrombosis, and stroke, etc. So intervention should be reserved for specific indication like uncontrolled hypertension, for example.
Open surgery with bypass has been able to relieve most of lesion to cause acute or chronic insufficiency and remain gold standard but it has excellent track record only for its end stage. It does not provide same good result in early stage. Therefore, bypass surgery should not be considered
as a panacea to relieve all the lesion and remains vulnerable through the rest of the life. So surgery should not be undertaken lightly and good only for those in advanced stage. Nevertheless, diffuse, proximal, multifocal involvement make surgical intervention with bypass often difficult
and such lesion would need some other way to try. That is endovascular approach with angioplastent has proven for safety and also effective alternative method. So main indication for the PTA and stent include clinically ischemia involving one or more vascular bed, we just heard.
Intervention gains popularity especially as interim management for the unsettled case, in particular with multiple lesions. Indeed the results of the endovascular intervention are less encouraging, we already heard, compared to open surgery.
The risk of restenosis in TA is significantly higher reaching over 50% at five years just like Mayo data, like ours data here. Our own results on 24 cases almost identical to what Mayo reported, and some other people as we published already.
So a diligent controlled disease activity prior to and following revascularization is crucial to prevent such complications. So as the conclusion, together with a bypass endovascular management with a PTA stent is now well accepted and symptomatic TA inactive chronic state can be managed
safely either by bypass or endovascular surgery. However, endovascular therapy accompanies higher rate of recurrence. Open surgery at present remains the preferred option delivering better long-term outcome and especially in the advanced stage.
Endovascular intervention fulfills its new role as an interim measure especially for the group open surgery carries too high risk like multivessel involvement. Thank you for attention.
- I have no disclosures that are relevant to this discussion. What I would start off with is, maybe you don't do it at all. Be careful what you ask for. This is very unforgiving work and know that going into it. The technical considerations a
absence of arteriosclerosis, it's a small vessel diameter and as we heard Dr. Eslami talk about, very high risk of vasospasm. The local clinical experience, I'm going to credit Dr. Jeff Friedman
who's one of our local reconstructive plastic surgeons, 10 patients underwent open surgery for repairs, eight arterial, two venous injuries. The age range 36 weeks of gestation to 12 months, Eight of the nine patients, 13 weeks of age or less. 90% of the injuries,
and we saw that again in Dr. Eslami's talk, are injuries that are iatrogenic as a result of invasive procedures performed on the effe cardiac catheterizations, arterial line placement,
direct arterial ligation, femoral vein injury, intra-arterial infusion or trauma. Most of these are like I menti femoral arterial lines, any sort of umbilical catheterizations,
femoral catheterizations and so on. One of the most important things is to do a real thorough evaluation, so in 70% of these cases they had a color flow doppler examination. Six patients had operative intervention. Doppler results verified intraoperative results
or ultrasound results in all cases and in one patient with preoperative arteriogram demonstrating accuracy of the diagnosis as well. No significant limb loss in these 10 patients, of course a small series despite prolonged ischemia times and I think that's probably one of the primary lessons
to take home is that kids tolerate ischemia fairly well and so to follow these would kind of be expectant treatment. Only one patient had toe amputations. Seven of the 10 patients survived, one early postop mortality, one late postop mortality and one nonoperative mortality.
Functional results were good, two with limb growth discrepancies. This is just to identify what you're looking at, make sure you're doing a good intraoperative ultrasound exam and know what you're getting into. This is just some examples of one child,
with obviously an ischemic limb there, this was from access from catheterization. You can see what the arm looks like, the hematoma down around the brachial artery and a microvascular repair there as you see. Going down and a little fasciotomy
all the way down into the hand, with a reasonable result. Of course, a nasty scar but a functional hand. The diagnosis am, doppler evaluation we place heavy weight on, the color doppler examination,
real time assessment of vessel patency, determine the level of occlusion. And then acutely the treatme acute intervention if obvious injury, discontinue the local catheter that's caused the injury,
anticoagulation with heparin, if possible, and really wait about six to eight hours before going unless the limb is totally threatened, warm packs, elevation, intervention if no improvement. And so, the operati
wide proximal and distal control, as you saw in that one case that I presented, complete division of the affected vessel, usually it's severely injured from the catheterization, proximal and distal thrombectomy using a #2 Fogarty, direct vascular repair if possible, vein grafts rarely.
I think Dr. Singh also mentioned that primary repair is better and we certainly believe the same way. And then fasciotomy is used liberally, postoperative anticoagulation again if possible.
suture usually with a microscope, interrupted sutures are a mainstay, papavarin and nitroglycerin generally work fairly well for vasospasm, again back to the ultrasound and then determine the appropriateness for operative intervention. You kind of need to know that going into it.
Operative intervention only in the case of no improvement and venous injuries are usually a little more difficult to treat and often surgical intervention gives poor results. If you just look at t am and doppler, suspected spasm or thrombosis,
conservative management first, if fails, six to eight hours eventually go to the operating room, if it resolves, obviously no care after that. In the future I think development of a team approach with plastic surgery, pediatric cardiology, pediatric surgery and neonatology is important,
establish early intervention program, and determine the possibility avoiding long term sequelae. Thank you very much.
- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.
They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression
if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.
Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.
This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,
and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients
who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,
and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,
symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.
There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,
again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,
six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,
it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse
if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective
in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.
This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent
because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common
in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.
So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,
those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,
like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.
And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,
get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.
If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners
over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,
it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,
look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.
That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,
then I would do something endovascular. Thank you.
- So I'll be talking about different bio-chemical profiles in both, inflammatory or non-healing and granulating wounds. Specifically venous leg ulcers. So, you've heard a lot about venous leg ulcers and there's a lot of treatments but, were going to look at some of the molecular differences that you can actually see in these wounds,
when we actually analyze some of the fluid. (clicking) Nothing to disclose. (clicking) Oop, I'm not going forward. Oh, there we go. So, actually, well go back to Bill Martson's work
with Stephanie Beidler and actually showed very early on that before compression there's a significant inflammatory component within these venous leg ulcers. This is by biopsies and then when these wounds are compressed, after four weeks
of compression, they actually reduce significantly a number of these cytokines and chemokines. As, well as increase the growth factor TGF-Beta. Indicating that, certainly, there's an inflammatory component but with compression, you actually change this to a healing component.
(clicking) We also evaluated work with Ferdinando Mannello in both inflammatory wounds and non-inflammatory wounds or non-healing wounds or granulating wounds in 32 patients and 16 granulating patients. These are all venous leg ulcers,
this is the demographics here. We analyze a number of factors cytokines, chemokines, growth factors and metalloproteinase. All by multiplex immunoassay. This is what the wounds look like before in the inflammatory phase.
I think you're very familiar with that. Then after debridement and after compression as well as interventions of the superficial system, this is what the wounds were looking afterwards. This is where we collected the wound fluid in these two different states.
We find the number of differences that were significant. And other individuals have also seen this. The red circles are actually the significant changes for inflammatory wounds, demonstrating the increase in interleukins. Interleukin-10,
which is actually an anti-inflammatory cytokine, but this is overly expressed in the inflammatory wounds over the granulating wounds. A chemokine IL-8, they're calling it Stimulating Factor Granulocyte Monocyte and also VEGF also consistent with what's
written in the literature, the VEGF's overexpressed in non healing wounds. What we did find actually in granulating wounds, that they expressed other things, specifically RANTES, which is very important in centralizing a number of these pathways
that's overexpressed in the granulating wounds as well as PDGEF factor BB, which is actually consistent again with the literature that PDGEF is actually a predictor of wounds that go on to heal. (clicking)
We then went on to also look at TGF-Beta, there's three different types of TGF-Beta. Three isoforms. And what we found that was significant is that TGF-Beta 3, which is not written too much about in the literature,
is significantly higher in inflammatory wounds. And why is this important? Because this is actually an antagonist to TGF-Beta 1. It actually causes significant inflammatory responses to take place, increases cytokines, increases metalloproteinase 9 and causes
the degradation of wounds leading to actually non healing. And we see that this was significantly elevated. Importantly, we found that endoglin is which is actually a co-factor for the TGF-Beta receptor was significantly elevated in granulating wounds. And that's significant because it has
significant anti-inflammatory properties by inhibiting the monocyte-endothelial activation. So, we found that this were significant changes. In looking at the proteases, we found that MMP-1, MMP-7 and MMP-13,
which are collagenases, and the stromelysin, were significantly elevated in the granulating wounds as opposed to seeing the degrading enzymes, such as, MMP-2 and MMP-9 and metalloelastase being higher in the inflammatory wounds.
Again, consistent with the literature, MMP-2 and '9,' which are the gelatinases, if you look at the literature, these are consistently higher in non-healing wounds. Oop, sorry, I think I went back there for a second. (clicking)
In looking at the TIMPs, TIMP-1 and '2,' are overly expressing in the inflammatory, which would be expected since they have a significant amount of protease activity. In TIMP-4 which is novel,
was overly expressed in the granulating wounds. Again, this could be a potential marker. Now, there's also the cytokines and the TAM/ligands, these are tyrosine kinase receptors and, the ligands for innate immunity. And just showing that there's actually difference,
both in inflammatory and non-healing wounds and granulating, or healing, wounds, both from the receptor standpoint as well as the ligands. Which again, shows that there's differences in innate immunity,
which could be a significant factor. Furthermore, like if you look at toll-like receptor 2, which again, also codes for innate immunity. In healing wounds all of these are decreased versus non-healing wounds. So, in conclusion,
there's significant expression of different cytokines and chemokines of growth factors in venous leg ulcers and wound fluid. The cytokines and proteinases have different signatures with in the healing state of a venous leg ulcer.
An innate immunity is also involved in a venous leg ulcer inflammation and healing. These could be specific, potential markers, but also pathways and possible targeted therapy for venous leg ulcers. Thank you.
- Thank you, Mr. Chairman. Good morning ladies and gentleman. I have nothing to disclose. Reportedly, up to 50 percent of TEVARs need a left subclavian artery coverage. It raises a question should revascularization cover the subclavian artery or not?
It will remain the question throughout the brachiograph available to all of us. SVS guidelines recommend routine revascularization in patients who need elective TEVAR with the left subclavian artery coverage. However, this recommendation
was published almost ten years ago based on the data probably even published earlier. So, we did nationwide in patient database analysis, including 7,773 TEVARs and 17% of them had a left subclavian artery revascularization.
As you can see from this slide, the SVS guideline did affect decision making since it was published in 2009, the left subclavian artery revascularization numbers have been significantly increased, however, it's still less than 20%.
As we mentioned, 50% of patient need coverage, but only less than 20% of patient had a revascularization. In the patient group with left subclavian artery revascularization, then we can see the perioperative mortality and morbidities are higher in the patient
who do not need a revascularization. We subgroup of these patient into Pre- and Post-TEVAR revascularization, as you can see. In a Post-TEVAR left subclavian revascularization group, perioperative mortality and major complications are higher than the patient who had a revascularization before TEVAR.
In terms of open versus endovascular revascularization, endovascular group has fewer mortality rate and major complications. It's safer, but open bypass is more effective, and durable in restoring original profusion. In summary, TEVAR with required left subclavian artery
revascularization is associated with higher rates of perioperative mortality and morbidities. Routine revascularization may not be necessary, however, the risks of left subclavian artery coverage must be carefully evaluated before surgery.
Those risk factors are CABG using LIMA. Left arm AV fistula, AV graft for hemodialysis. Dominant left vertebral artery. Occluded right vertebral artery. Significant bilateral carotid stenosis.
Greater than 20% of thoracic aorta is going to be or has been covered. And a history of open or endovascular aneurysm repair. And internal iliac artery occlusion or it's going to be embolized during the procedure. If a patient with those risk factors,
and then we recommend to have a left subclavian artery revascularization, and it should be performed before TEVAR with lower complications. Thank you very much.
- So thank you very much. I would like to acknowledge Suma Devata and Suma Sood, two hematologists who worked with me on this project, and the NIH for support, and the manuscript for this is under review at the moment. No disclosures. If you look at the current drugs that we have available
in yellow, and those in development in blue, they all target the coagulation system, and as such they're all going to have potential for bleeding. If you look for example, at the major bleeding with Enoxaparin, it's around 2%, for VTE prophylaxis and treatment, and even for,
(mouse clicking) it's not moving forward. Okay, I'm sorry, and even for the DOAC's, it's around 10%. And this is important because major bleeding can lead to a case fatality rate of around 10%. This is not moving forward.
There's a remote, okay, thank you, sorry. So if one could target the inflammatory system rather than the coagulation system, one could, theoretically, have a drug that's much safer. So how is inflammation and thrombosis related? When endothelium and platelets get up-regulated,
selectins become present on their surface. There are receptors for selectins on inflammatory cells. This leads to leukocyte endothelial, leukocyte platelet, leukocyte leukocyte interactions, the release of pro-coagulant microparticles, and thrombus amplification.
At the same time, other inflammatory cells come into play, such as activated neutrophils. They bind by other receptors, such as the Mac-1 receptor, leading to fibrin formation, platelet accretion, the release of nuclear material, and further thrombosis. So if you can inhibit that process, theoretically,
you could end up with a drug that is safer, that inhibits thrombosis, and also inhibits the fibrosis that can occur. Now we've been interested in E-selectin as an important regulator of thrombus formation and fibrin content.
We know that endotoxin induced tissue factor mediated coagulation is enhanced in humans carrying an E-selectin allele. And patients homozygous for this allele have an increased risk of VTE recurrence. And from our very early mouse studies we saw in fact that
E-Knockout mice had the least amount of thrombosis. So the compound they were interested in is called GMI-1271. It's an E-selectin antagonist from a company called GlycoMimetics. This drug was being looked at for treatment in sickle cell and cancer.
And we wanted to see if it would be possible to use it for VTE. So we did some initial studies, done by Dan Myers in our laboratory, this is the drug, where we showed that in fact, if you look at 10 and 20 milligrams per kilogram
of this drug, it's equivalent to six milligrams per kilogram of Lovenox in inhibiting thrombosis in our mouse model, without an increase in tail bleeding time. So this led to an application to the VITA Program, which is a program from the NIH to allow investigators to move drugs or other
products through the Valley of Death, so-called Valley of Death. We had three aims of this study. Aim one was to give the drug or Lovenox or saline one time, and then look for safety. Aim two was to give the drug daily for five days,
compared to Lovenox, and look for safety. And then aim three was to treat patients who had calf vein DVT. The reason we chose calf vein DVT is because it's frequent. Complications can occur, but there's clinical equipoise about whether or not you need to treat calf vein DVT.
In fact, the most recent study suggested that you don't need to treat. So the third aim was to give GMI-1271 or Lovenox daily for five days, and then follow the patients with duplex. We had a number of inflammatory coagulation, cell adhesion, and leukocyte and platelet activation biomarkers,
along with hematologic studies. In the first two aims, we found that there were no serious adverse events reported. Lovenox increased some of the TEG values, GMI-71 did not. E-selectin levels tended to be lower in the GMI-1271 treated volunteers,
and there was lower leukocyte and platelet activation in the volunteers. We had two patients before the contract ended that we were able to treat. This is the second patient, he was a 55 year old physician, who had thrombosis in one of his
paired posterior tibial veins. Here is his duplex imaging. You can see at baseline he was thrombosed. At day eight, the vein was still thrombosed. By day 19, the vein was open. And we happened to see him nine months, seven days later.
The non-compression on the left, the compression on the right. The veins were both still patent and open. So in conclusion, VTE is a very common problem. It's the third most common cardiovascular disease behind MI and stroke.
It's the most common cause of in-hospital death. Current drugs all carry significant bleeding complications, and they do not prevent the fibrosis of PTS. Targeting E-selectin is a new strategy to treat VTE, significantly lowering bleeding, and could decrease vein wall fibrosis.
Thank you very much.
- Thank you very much. Thank you, Frank, for inviting me again. No disclosures. We all know Onyx and the way it comes, in two formulas. We want to talk about presenter results when combining Onyx with chimney grafts. The role of liquid embolization or Onyx is listed here.
It can be used for type I endoleaks, type II endoleaks and more recently for treatment of prophylaxis of gutters. So what are we doing when we do have gutters? Which is not quite unusual. We can perform a watchful waiting policy, pro-active treatment in high flow gutters,
pro-active treatment low flow gutters, or we can try to have a maximum overlap, for instance with ViaBahn grafts 15 centimeters in length or we can use sandwich grafts in order to reduce these gutters in type I endoleaks. Here, a typical example of a type I leak treated with Onyx.
And here we have an example of a ruptured aneurysim treated with a chimney graft. And here is what everybody means when they're talking about gutters. Typical examples, this is what you get. You can try to coil these
or you can try to use liquid embolization. Here's the end result after putting a lot of coils into these spaces. What are these issues of the chimney-technique type I endoleak? Which are not quite infrequent as you see here.
Most of these resolve, but not all of them. So can we risk to wait until they resolve? And my bias opinion is probably not. Here, the incidents of these type endoleaks is still pretty high. And when you go up to the Arch
the results can even be different. And in our own series published here, type I endoleak at the Arch were as high as 28%. A lot of these don't resolve over time simply because it's a very high flow environment. Using a sandwich technique is one solution
which helps in a lot of cases but not all of these simply because you have a longer outlet compared to a straightforward chimney graft. You can't rely on it. So watchful waiting? There are some advocates who
prefer watchful waiting but in high flow gutters this is certainly not indicated. And the more chimneys you have, like in a thoracoabdominal aneurysm with four chimneys, the less you can wait. You have to treat these very actively,
like you see here, in these high flow areas. Here a typical example, again symptomatic aneurysm with sealing. Here Onyx was used but without any success. So what we did is we had to add another chimney and plus polymer sealing and then we had a good result.
Here some results, only small serious primary gutter sealing using Onyx with good results in a type I leak. But again, this is only a small series of patients. Sandwich technique already mentioned. When you use, like we did here for chimney grafts in the arteries, you do need Onyx otherwise you
always get problems with these gutters and they do not seal over time. Another example where liquid polymer was used. And here again, you see the polymer. The catheter in order to inject the polymer is very difficult to see but with a little bit of experience
you know where you are. And again, here it is, the Onyx, a typical example. Here another example of the Arch, bird beacon effect, extension, chimney graft. Again the aneurysm gets bigger. And so a combination of using proximal extensions
plus chimneys plus liquid embolization solves this problem after quite a long period of time. And here typically is what you see when you inject the Onyx. This does not work in all cases. Here we used Onyx in order to seal up the origin of the end tunnel.
This works very nicely but there is so ample space for improvement and in some cases it's probably better to use a fenestrated branch graft or even the opt two stabler instead of using liquid embolization. Thank you very much.
- Good morning, I want to thank Professor Vitta for the privilege of presenting on behalf of my chief, Professor Francesco Speziale, the result from the EXTREME Trial on the use of the Ovation stent graft. We know that available guidelines recommend to perform EVAR in patient presenting at least a suitable
aortic neck length of >10mm, but in our experience death can be a debatable indication because it may be too restrictive, because we believe that some challenging necks could be effectively managed by EVAR. This is why when we published our experience 2014,
on the use of, on EVAR, on the use of different commercially available device on-label and off-label indication, we found no significant difference in immediate results between patient treated in and out IFU, and those satisfactory outcomes were maintained
during two years of follow-up. So, we pose ourself this question, if conventional endografts guarantee satisfactory results, could new devices further expand EVAR indication? And we reported our experience, single-center experience, that suggests that EVAR by Ovation stent-graph can be
performed with satisfactory immediate and mid-term outcomes in patient presenting severe challenging anatomies. So, moving from those promising experiences, we started a new multi-center registry, aiming to demonstrate the feasibility of EVAR by Ovation implantation in challenging anatomies.
So, the EXTREME trial was born, the expanding indication for treatment with standard EVAR in patient with challenging anatomies. And this is, as I said, a multi-center prospective evaluation experience. The objective of the registry was to report the 30-day and
12 month technical and clinical success with EVAR, using the Ovation Stend-Graft in patient out of IFU for treatment by common endograft. This is a prospective, consecutively-enrolling, non-randomized, multi-center post market registry, and we plan to enroll at least 60 patients.
We evaluated as clinical endpoints, the freedom from aneurysm-related mortality, aneurysm enlargement and aneurysm rupture. And the technical endpoint evaluate were the access-related vascular complications, technical success, and freedom from Type I and III endoleaks, migration,
conversion to open repair, and re-interventions. Between March 17 and March 18, better than expected, we enrolled 122 patients across 16 center in Italy and Spain. Demographics of our patient were the common demographic for aneurysm patients.
And I want to report some anatomical features in this group. Please note, the infrarenal diameter mean was 21, and the mean diameter at 13mm was 24, with a mean aortic neck length of 7.75mm. And all grafts were released accorded to Ovation IFU. 74 patients out of 122
presented an iliac access vessel of <7mm in diameter. The technical success reported was 98% with two type I endoleak at the end of the procedure, and 15 Type II endoleaks. The Type I endoleak were treated in the same procedure
by colis embolization, successfully, and at one month, we are no new Type Ia endoleaks, nine persistent Type II endoleaks, and two limb occlusion, requiring no correction. I want to thank my chief for the opportunity of presenting and, of course, all collaborators of this registry,
and I want to thank you for your attention, and invite you, on behalf of my chief, to join us in Rome next May. Thank you.
- Thank you Michael and thank you Dr. Veith for the invite. These are my disclosures. The one really (mumbles) is that I'm the study PI for the ACCESS PTS trial. So when we talk about DVT and post-thrombotic sequelae. If you take one to two patient, patients per thousand
who develop acute DVT in the US. You look at the numbers of population in the US and globally. Extending out these data, you can estimate there's about 2.5 million patients in the US with PTS and about 61 million globally.
The pathophysiology of venous disease is whether you talk about obstructive or not obstructive issues. And they're not advancing. That everything around the pathophysiology of venous disease and the sequelae
is about venous hypertension. When we talk about fem-pop occlusions, femoral, the axialization that comes from femoral vein occlusion may not always be adequate to decompress the elevated venous pressures, and when we see popliteal complete occlusions
that can cause severe PTS below the knee into the calf. So the rationale of intervention was if you can reduce the luminal obstruction and restore flow you should be able to reduce the venous hypertension, reduce the severity of PTS sequelae, and improve quality of life.
And this is just a movie showing on the left what access into a tibial vein with an occlusion and chronic DVT, chronic thrombosis, shows with the hypertension compared to the second day when we had that catheter in still from the tibial vein
and the decrease in the pressure and flow. So changing the chronic DVT paradigm was about ACCESS PTS. This was a steering committee that I was very honored to work with. This was a multicenter prospective study of 29 sites that had lower extremity DVT for at least 6 months
documented by ultrasound who had a minimum of femoral DVT and who had failed three months of conservative therapy including therapeutic anticoagulation and compression with a Villalta score of at least eight. The protocol here was basically
crossing the obstruction with CTO techniques, balloon angioplasty, the size of the expected vessel, placing the ecosystem in overnight for 12 hours minimum, and then doing a follow-up the next day with additional therapy if needed. On discharge they were given activity instructions,
blood thinner, and compression. Enoxaparin was the drug of use for one month before they were transitioned to an oral anticoagulant. So here are the demographics. 78 patients, 82 limbs, four of which were bilateral.
Separated by at least a month. The DVT mean age was 13.2 months. Advancing is very bad. The patient enrollment you can see here. What's that? Okay, thank you.
The patient enrollment you can see here. Of the 73 patients that were evaluable by the protocol at 30 days was 77 limbs. If you look at the breakdown of the DVT, 2/3 of them were infrainguinal only disease. The primary endpoint was a goal of
greater than or equal to four point reduction in the Villalta at 30 days in more than 50%. The actual was we reached that goal by 66% of the patients had an at least four point reduction in Villalta for p-value as you see. When you look at the Villalta results
there was a mean improvement of 49% over one year from 15.5 to 7.8. Now notice the 15.5 indicates a severe PTS. When you look at VCSS results there was reduction, or excuse me, an improvement of 43% alt one year from enrollment and treatment.
When you look at the VEINES Quality of Life. Again, a 36% improvement from 61 to 80. When you look at doppler patency of the femoral segments including the popliteal you can see alt one year, 365 days. The percent of patency was seen
basically at the 90+ percentile rate. Washout was seen to be no different between baseline and post PTA. After EKOS there was a slight improvement, not statistically significant, but after the adjunctive therapy the second day
there was a significant improvement from baseline to the end of treatment in the washout phase. When you look at the venous scoring. Thrombus, which really was occlusion scores, all three venous scoring methods of Marder, AVR, and Ouriel were all improved
through the end of completion. The safety endpoint. There were 78 patients, one major bleed from epistaxis during intubation, and there was a recurrent DVT in three, one PE was out of the hospitalization.
Just an example of a two-year-old clot in the femoral popliteal segment, and this was after the follow-up. You can see that flow is restored. This was the two year follow-up doppler. That patient was a marathon runner, couldn't walk very well,
had venous claudication, was unable to run at all, and 6 months after treatment she went back to running a marathon, and this was her two year follow-up doppler showing patency. The conclusions are that ACCESS PTS was statistically significant,
the primary endpoint was reached, the Villalta VCSS, and VEINES Quality of Life improvements were all statistically significant, improvement in time-to-washout was significantly improved, and the persistent patency on doppler, you can see, was about 90+%.
So can ACCESS PTS change the paradigm of chronic DVT treatment? I think so. Removing luminal obstruction, restoring flow, seeing vein function as a conduit, improving on doppler ultrasounds,
with continuous and persistent reduction/resolution of venous hypertension, showing significant improvement in PTS sequelae after 365 days would suggest so. This is a safe and effective treatment for recanalizing chronic venous occlusions,
and hope is here for chronic DVT, post-thrombotic patients, that hopefully will lead to further studies and treat the, change the paradigm treatment. Thank you.
- These are my disclosures. So I'd like to just highlight first the Einstein PE DVT study. And just to tease out the cancer population, yeah, it this study. So as you can see, the cancer group, small in number with the rivaroxaban
versus the low molecular weight heparin and warfarin. And you can see the incidence of VTE in that population and the hazard ratio. And then bleeding, of course also once again, a small number of patients with a
you can see the incidence of bleeding in this patient population as well. Also like to take the AMPLIFY trial with apixaban and just tease out the cancer population. Little smaller in this group. As you can see, 81 patients in the apixaban group
and 78 in the enoxaparin warfarin group. And you can see the incidence of VTE in this cancer patient population. And I put side by side here the bleeding risk in each of the groups. As you can see, 2.3 and 5.0
in the patients getting enoxaparin and warfarin. The Hokusai study then was published, and this was in New England Journal and Medicine this past year. And this looked at low molecular weight heparin and then edoxaban, and then of course, dalteparin.
200 units per kilogram for the first month and then dalteparin. Clearly showing, looking at this population and looking at outcome. So let's look at recurrence rate in the edoxaban versus dalteparin.
And you can see it's 6.5 versus 10.3% direct comparison. And major bleeding was 6.3% in the edoxaban group and 3.2% in the patients getting dalteparin. The next study that came out looking at the DOACs, this was the SELECT-D trial. And in this trial they looked at rivaroxaban
versus dalteparin once again over a six month period. And what did they find in this study? They found that 11% recurred in the dalteparin group versus 4% in the patients receiving rivaroxaban. The major bleeding incidence was 6%
in the patients getting rivaroxaban and 4% in the patients getting dalteparin. So you can see that the DOACs maybe have a place in this patient population, so that they might be effective. And finally the ADAM study, which will be published soon,
just similar to the rivaroxaban study. Looking at apixaban versus dalteparin. Same model but we don't have any data on this study at this point in time. So the 2018
NCCN Guidelines and the ISTH guidelines of 2018, both show and list now that the DOACs can be part of the process of treating patients with cancer and DVT. So yes, I believe DOACs are ready for prime time. Selection is based on the cancer and cancer is important. Accepting the risk of bleeding as you saw.
We must consider concomitant chemo therapy and the ability to tolerate oral anticoagulants. Thank you very much.
- Thank you again for the opportunity to discuss this topic on acute or chronic vein. Acute or chronic ovarian vein thrombosis. No financial relationships for this particular topic. An etiology is generally obstetric, although even in the obstetric population, it's rare about one in 2000 deliveries.
It's tends to be associated with infectious etiologies including postpartum sepsis, group B strep, ruptured ectopic, hydatidiform mole. There are other potential non-obstetric causes as well. Inflammatory processes that tend to affect the pelvis or the retroperitoneum including pelvic surgery,
certain malignancies, pelvic inflammatory disease, appendicitis, diverticulitis and inflammatory bowel disease. So the pathophysiology in pregnancy and why it occurs is you get significant fluctuations in the ovarian vein itself. The diameter of the ovarian vein
increases up to three times. This corresponds to over 60 fold increase in ovarian blood volume which may lead to ovarian vein incompetence. This incompetence and stasis coupled with Virchow's Triad and pregnancy, particularly in the postpartum period
with stasis in volume contraction, endothelial injury from the delivery itself and just the overall, hypercoagulability of pregnancy, result in this pathology. The clinical features are that, unlike chronic reflux and pelvic congestion syndrome,
this tends to be more frequently right-sided 70 to 90% of the time in the majority of case series. It's bilateral in a small percentage of 11% and left-sided in two to three percent. The reason again being that this is typically a postpartum issue and there was a dextroposition
of the gravid uterus, this results in typical retrograde flow in the left ovarian vein. However, the right ovarian vein which may be compressed and have difficulty draining results and integrated flow stay stasis,
and then this postpartum ovarian vein thrombosis. When it does occur, tends to occur within a week or so within the first 10 days postpartum. And it has a classic triad of where the majority of patients will have fever because there was some infectious component
to what's going on, chills, right lower quadrant pain in more patients than left lower quadrant pain. Again, corresponding with the anatomic distribution of the disease. In certain dramatic instances, it's been described that you can palpate
a sausage shaped tender mass, although this may be challenging in a postpartum patient and in someone, who has an elevated BMI. And if it's asymptomatic, potentially it's not pregnancy related but malignancy related.
The differential diagnosis is all other causes of acute abdomen including appendicitis, adnexal torsion, tube ovarian abscess, pyelonephritis, etc. Imaging is critical. Complications from this include septic emboli,
IVC or renal vein thrombosis. Again, propagation of thrombus into the respective draining veins, pulmonary embolis, ureteral obstruction just from the adjacent inflammatory process and mass effect and chronic pelvic pain in the long run.
So the diagnosis, you have to have a high index of suspicion. A Diagnostic laparoscopy is frequently done by the gynecologist and it may determine the source of abdominal pain and identify this.
And then a duplex ultrasound will identify a hypoechoic, hydrogenous, and it's tube shaped mess with inner echos, again adjacent to the psoas muscle as shown on this diagram. The sensitivity is about 52% of duplex ultrasound. So really the diagnosis ends up getting made
by CT scan or MRI, as seen in the upper right hand corner. The CT scan will show this sausage shaped mass running along the paracolic gutter. MRI is nearly a 100% sensitive and it has the added benefit of determining the acute or subacute of the disease process.
So the treatment it's typically anticoagulation, for a full anticoagulation course for DVT as well as antibiotics. Interventional treatments are kept to a minimum and it can be an IVC filter which would have to be placed suprarenal in these instances,
partIcularly for the right gonadal vein. And then percutaneous thrombectomy and surgical techniques. Again, this is exceedingly rare but retroperitoneal or transparent neal exposures of the gonadal vein are relatively straightforward.
The treatment of chronic tends to be that for refluxing ovarian vein and pelvic congestion syndrome, and that's already been delineated. So to conclude, you have to have a high index of suspicion. MRI is the most sensitive study. It can tell you about acute and subacute.
It's the standard of care anticoagulation with antibiotics and for refractory patients, endovascular versus surgery, and then for chronic, the treatment for pelvic congestion syndrome. Thank you.
- Okay, thank you. We know that inflammatory AAA have quite low incidence. The main problem is related to the thickness of the aortic wall and to the retroperitoneal fibrosis that involves the organs that are close to the aorta. Open surgery is quite difficult for these reasons. And these imply a higher mortality rate
that is threefold the one for standard AAA. And the higher morbidity related to the surgical dissection in fibrosis with risk of iatrogenic injury of the involved organs. So that some authors suggest the supraceliac clamping. That of course have some other issues.
A recent paper suggests that a pre-op treatment with a cortical steroid therapy can be useful to reduce inflammatory signs and so minimize the operative risk for these patients. On the other hand, endovascular treatment has been proposed since 1997 with different outcomes.
Certainly mortality rate is lower when compared to open surgery, and even the one year mortality is lower. But we have a problem with periaortic fibrosis that does not decrease as well as with open surgery. And there is some progression, in some cases, with higher nephrosis that leads
to other types of complication. This is not a standard. You see in this paper that there is no problem with periaortic fibrosis after endovascular treatment. But in other papers, the situation is different. There is a worsening fibrosis and even the development
of fibrosis after standard EVAR in patients with no history of inflammatory AAA. And certainly the phenotype eg4 seems to be related to a worse outcome after EVAR. So, based on this situation, what we have done in the last year is to use a systemic steroid protocol
for our patients with inflammatory AAA that is the same that is used for arteritis and retroperitoneal fibrosis. And you see how impressive is the situation in this case. We had only four days of therapy, and we have a decrease in periaortic fibrosis of 28%.
We studied all our patients with PET/CT. We made a comparison with the patient with standard AAA, and we observed an increased level of captation that was really significant. This is our population. All of the patients had immunological screening,
and the evaluation of the inflammatory level. This is the operative situation. All the patients had a good result with no mortality at 30 days. Only one patient died three months later for other reasons. And what we observed is that in almost all cases,
the periaortic fibrosis reduced significantly with the, even with PET/CT. All the patients were asymptomatic. And all the patients with hydronephrosis have a release of the situation. You see that the diameter of the aorta decreased
of 9.76 millimeters, and there was a decrease in periaortic fibrosis of more or less one centimeters. So this is really significant, as you can see. And there was a reduce in the uptake for all the patients but one. We don't know exactly, he had a type two endoleak.
Don't know if this can be a correlation because it's a single patient. And another patient stopped corticosteroid therapy, and so there was a recurrence of this problem. The CRP reduced globally, but of course, it's not specific. So in some patients we had an increase for other reasons.
But our policy now is that we do EVAR, when feasible, associated to steroid therapy. That, in our practice, is effective. We use open surgery in patients unfit for standard EVAR, and probably, even for these patients, steroid therapy can be a choice.
- Thank you for the opportunity to present this arch device. This is a two module arch device. The main model comes from the innominated to the descending thoracic aorta and has a large fenestration for the ascending model that is fixed with hooks and three centimeters overlapping with the main one.
The beginning fenestration for the left carotid artery was projected but was abandoned for technical issue. The delivery system is precurved, preshaped and this allows an easy positioning of the graft that runs on a through-and-through wire from the
brachial to the femoral axis and you see here how the graft, the main model is deployed with the blood that supported the supraortic vessels. The ascending model is deployed after under rapid pacing.
And this is the compilation angiogram. This is a case from our experience is 6.6 centimeters arch and descending aneurysm. This is the planning we had with the Gore Tag. at the bottom of the implantation and these are the measures.
The plan was a two-stage procedure. First the hemiarch the branching, and then the endovascular procedure. Here the main measure for the graph, the BCT origin, 21 millimeters, the BCT bifurcation, 20 millimeters,
length, 30 millimeters, and the distal landing zone was 35 millimeters. And these are the measures that we choose, because this is supposed to be an off-the-shelf device. Then the measure for the ascending, distal ascending, 35 millimeters,
proximal ascending, 36, length of the outer curve of 9 centimeters, on the inner curve of 5 centimeters, and the ascending model is precurved and we choose a length between the two I cited before. This is the implantation of the graft you see,
the graft in the BCT. Here, the angiography to visualize the bifurcation of the BCT, and the release of the first part of the graft in the BCT. Then the angiography to check the position. And the release of the graft by pushing the graft
to well open the fenestration for the ascending and the ascending model that is released under cardiac pacing. After the orientation of the beat marker. And finally, a kissing angioplasty and this is the completion and geography.
Generally we perform a percutaneous access at auxiliary level and we close it with a progolide checking the closure with sheet that comes from the groin to verify the good occlusion of the auxiliary artery. And this is the completion, the CT post-operative.
Okay. Seven arch aneurysm patients. These are the co-morbidities. We had only one minor stroke in the only patient we treated with the fenestration for the left carotid and symptomology regressed completely.
In the global study, we had 46 implantations, 37 single branch device in the BCT, 18 in the first in men, 19 compassionate. These are the co-morbidities and indications for treatment. All the procedures were successful.
All the patients survived the procedure. 10 patients had a periscope performed to perfuse the left auxiliary artery after a carotid to subclavian bypass instead of a hemiarch, the branching. The mean follow up for 25 patients is now 12 months.
Good technical success and patency. We had two cases of aneurysmal growth and nine re-interventions, mainly for type II and the leak for the LSA and from gutters. The capilomiar shows a survival of 88% at three years.
There were three non-disabling stroke and one major stroke during follow up, and three patients died for unrelated reasons. The re-intervention were mainly due to endo leak, so the first experience was quite good in our experience and thanks a lot.
- So, when we're looking at the pattern of refluxes, as Mark talked to us about it, and you can have all these patterns that we see in here, with or without pelvic lower limb reflux. Now, you can have also a reflux in the internal iliac veins alone,
or the pelvic floor, but we do not see a reflux in ovarian vein without pelvic varices. Now, for the patterns, only some publications exist, but there is no standardized technique, not all areas are reported,
there are no clearly defined patients, and there is no correlation with the pattern and symptoms. What we did, we did a standardized ultrasound approach to labropoulos phlebology a year ago. And actually, we took a patient and make a drawing on the patients' belly,
exactly what you see in marks on your venogram. You can, I'm going to go over the details of this technique, but you can read the paper, but it's fairly easy. So easy, actually, even (inaudible name) can do it. He proved that in a meeting, he actually did it. The advantage of this technique is you can use
the resperanerial lido using the linear probe, like how the examiner deciphers when with a linear probe, they're exactly the same. And you see the different points that Mark talked earlier like you see in here. You see the perineal point, the gluteal,
the obturator, and the inguinal. And, actually, it's very easy to see it. In this technique, if you know what you're looking at, it basically takes you a couple of minutes to know if there is a reflux or not where it is for this (inaudible) But, to see the ovarian vein, of course, go higher up
and use, again, a linear probe, because most of these people are thin. Their BMI of less than 25. Use as a landmark their iliopsoas muscle. You see the vein is dilated, here it has a reflux. This is a reflux on the left ovarian vein,
is one of the most common patterns of reflux. Then, you can see the right ovarian vein, it's a bit harder, but it's actually the same technique, except the entry of the right ovarian vein to the inferior vena cava. You see a normal flow, but here, especially,
the reflux in the (inaudible) is the exact same flow like the ovarian vein. Often what we notice, and what we publish, that the right ovarian vein is dilated in a compensatory manner because there is the reflux from the left ovarian, right, and the blood goes back to the cava.
You see how the vein is 8 millimeters here, but the flow still goes to the vena cava. Unfortunately, in this climate right now, many people treat this vein for the wrong reasons, based on diameter, not on function. We also have noticed that the ovarian vein,
like in this case, both on the left and the right, can be absolutely normal, but have tremendous reflux in the peri-uterine veins or the pelvic floor. So, you don't have to have ovarian vein reflux all the time. Here, you see a female, 35 years old with 3 children, with bilateral lower extremity varicose veins
and perineal space symptoms. If you see here, with the technique we're doing, pressing the ovarian complex, right, you push blood up like you do with the saphenos, and then the valve holds, because the ovarian vein has two to three valves, then there's no reflux.
And you see, both the left and the right ovaries are normal, but there is huge reflux on the peri-uterine veins, the deep internal pudendal veins, and down to the pelvic floor. Here, you see, just simply with the B mode, the bunch of grapes on the left peri-uterine space
with all these varicose left marks on the venogram, and you see reflux in spiked position. But when you stand the patient, just with the linear probe, everything is so obvious. Here you see a reflux in the peri-uterine veins, you look at the exam that says
well, it's like 1 second, 2 seconds. Usually, when you see reflux here, its like you see in this picture, nonstop. It's like 14, 15 seconds and still goes. And here is an example of like Mark told us, the deep internal pudendal vein,
you find like from the P point, and you see very nice reflux going down to the space and you see the vein is 9 millimeters. Here is the reflux of the inferior gluteal veins, actually on both sides, and you see a significant amount of reflux.
In this particular patient, there is bilateral Sciatic nerve vein reflux. So, from the video earlier from Mark, the connection between inferior gluteal and Sciatic veins. Here, the little hook, if you're a little bit experienced, you can see very nicely, the hook on the opturator vein
on both sides, and the reflux on both obturator veins of this patient. And here you see tributaries of the saphenos connecting with the pelvis you see very nicely near the junction and this (inaudible) is dived down, right, on the pelvis. And here you see tributaries medial saphenofemoral junction
that do not touch or connect to saphenos and they give no saphenos varicoses down the leg. And here you see perineal varicoses extending posterior, postero-medial thigh, very big, You can see actually with your physical exam. For the Nutcracker, if you can see high flow like this one,
which you don't need to induce it. You make, indirectly, the diagnosis of Nutcracker phenomenon which can go directly with the ultrasound, if you want to and do, using this criteria, your diagnosis. Mark talked about these things on time. Thank you very much.
- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --
- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.
But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,
is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy
in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.
The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation
so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later
that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low
and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse
even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean
as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques
different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between
pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients
are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system
you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because
this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out
now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference
between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing
a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is
the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories
and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here
again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result
and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not
fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again
look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as
the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here
This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you
- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.
Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates
an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.
You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't
or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.
CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,
we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.
She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.
So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.
Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.
It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign
and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there
but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?
Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy
and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.
So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,
a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,
gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection
it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible
before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains
in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low
or cut out the super renal fixations so you can take them out a little easier. Thank you.
- Bill outlined why some of these trials fail. And there's so many pathways that are involved in the pathophysiology of venous leg ulcers. And I'm going to just talk about the proteins and the degradomes involved. And certainly you can talk about free radicals, you can talk about map kinases,
you can talk about TGF beta pathways, there's a lot. First some definitions. Proteomics, large scale study of proteins particularly their structure and function. The proteome is the entire set of proteins produced
or modified by an organism. In humans, just to give you an example, there's 27,000 proteins, that does not even include the ones that are actually post-translationally modified by glycosylation and phosphorylation and other mechanisms. The degradome, degradomics, aims to identify proteases
and protease substrates, the repertoires or degradomes of an organism wide-scale, identifying new roles for proteases in vivo. The study of degradome is directly related to measurement of enzymatic activities and will facilitate the identification of new
pharmaceutical targets to treat disease. So we actually did a review of analysis back in 2016, just to see what has been found in the venous leg ulcer, whether it was biopsied or whether it was wound fluid. And these are all the different types of
cytokines and proteins. There's ferritin, there's transferrin, there's hyaluronic acid, lactate, lactotransferrin, monoperoxidase, you go on and on and on. And of course, as I've mentioned, there's a number of cytokines and growth factors
that have been identified. And these are, whether they're cause and effect we don't know. But certainly we know they're present, they definitely have an influence, they've been measured,
and they've been associated with healing and non healing wounds. To go on, you can actually see some of these other proteins and proteases both serine proteases and metalloproteinase, and some of these things we don't even know what their function is, or what they're
doing in the venous leg ulcers, and that's really important. And again, here's further showing cathepsins and caspases and kallikrein, and different TIMPs. So all of these things have actually be found in venous leg ulcer wound, whether fluid or biopsy. This actually, probably a seminal article
that looked at, for the first time, the proteomics in patients with both healing and non healing venous leg ulcers. This was collected by wound fluid, it was analyzed by liquid chromatography and mass spectroscopy.
And what they identified was 149 proteins that had differential detection. In the healing there was 23 that were identified, in non healing 26. And actually they then looked at three proteins and analyzed a series of patients,
and these are the number of patients that they've analyzed, to evaluate. And this is what they found, a lactotransferrin S100A9 and the annexins have different expression whether you're healing or non healing. And that's important because these proteins
have some significance, and this is what their significance. Lactotransferrin is important in iron scavenging. And we know that free iron, if it's in the wounds, it's actually very toxic leading to different types of peroxides that are developed, and also cellular pathways that can be disrupted.
So annexins are also important in inflammatory response, and they play a significant role not in just wound healing, but also in the detriments of venous leg ulcers. And S100A9 is actually a calcium binding protein that has significance in wound healing also. So in conclusion it's actually very complex,
the proteomics and degradomics. But they provide an opportunity to study novel proteins, function, and activity in venous leg ulcer. They do provide some proof of concept and possible mechanisms of venous leg ulcer pathology. They identify possible biomarkers, both for
identification of wounds that go on to heal versus the ones that don't go on to heal, as well as treatment and prognosis. And obviously possible targets for therapy. Thank you very much.
- Thank you Mr. Chairman. Thank you, Dr. Veith for you kind invitation. Okay, there we go. Excuse me. DEVASS stands for Dutch EVAS study Group. We all know that women have a twofold, increased risk frequency of rupture.
The average aortic size at rupture is five millimeters smaller. They have a higher rate of undiagnosed cardiovascular diseases. They have smaller ileofemo
more concomitant iliac aneurysms They have a more challenging aortic neck. Smaller proportion is eligible for EVAR and, therefore less likely to meet EVAR IFU. They have a longer length of hospital stay after EVAR, a higher re-admission rate, more major complications,
a higher mortality rate. So, women and AAA is a challenging combination. The rationale behind EVAS is known to you all, I think. The DEVASS cohort is from three high volume centers in The Netherlands. It's a retrospective cohort of 355 patients,
included from April, 2013 to December 2015. So I have two years of result data. If you look at the baseline characteristics, 45 females were in this cohort, with the age of 76 and with some known comorbidities. They were within the instructions for use of 2013, at 28.9%
and even less in the IFU of 2016. These are some more anatomical characteristics with the AAA outer diameter 5.6 centimeters. This is the procedure, most of the patients were under general anesthesia, with the cutdown and the procedure time
was about 100 minute. Straight forward procedure 33 cases out of these 45. Let's have a quick look at the clinical outcomes. The re-intervention's done in the first 12 month. One patient had to conversion to open repair at month 11 due to type 1A Endoleak, and the others were not directly
related to the procedure itself. Although, there was thrombus in approximate stand. In the second month we saw, in the second year we saw some more type 1A migrations and a Stenosis that needed relining, and two out of these patients were within IFU.
If you look at the total cohort of type 1A Endoleak, one patient was not operated on and the other were, either open conversion or relining, and one patient was within IFU. A quick look at the death characteristics. Only one patient was within IFU,
and died after open procedure. So the re-interventions, once again, the first year four patients, in the second year five patients. Conversion to open repair, in total three patients. Endovascular re-intervention was performed
in the first year in two patients and in the second year there were three relinings performed. Endoleak 1A, in total six as stated before. No type two Endoleak reported, and in the first year five patients died, which one was aneurisym related, as in the second year, two patients died,
which one was aneurysm related. If we compare this data with the EVAS Global data, of two years not the three year data, this is the freedom from all persistent Endoleak, close to 98% which is good. Freedom from type 1A Endoleak is within IFU, 97% in the global and outside IFU 85%,
and remind these patients 71% were outside IFU. Freedom from secondary interventions, we had to re-intervene in nine patients and its comparable with outside IFU. Freedom from mortality at two years, a bit higher, aneurism related mortality is 95% which is higher, and also the all cost mortality is higher in women.
So to conclude, this is the first cohort that focuses on women after EVAS. The majority of the patients was outside IFU, and as in EVAR women do not that very good in result, appear to be very much like an EVAR. Thank you.
- I'd like to thank Dr. Veith, program committee, and the moderators for the honor of presenting on this topic. Here's my disclosures, not relevant to this topic. One fairly large randomized trial, and a handful of retrospective studies have shown benefit to anticoagulation
and the patency of either prosthetic or high risk vein bypasses. And this data's formed the primary basis for what is common, but not universal surgical practice which is aspirin for standard vein bypasses or prosthetic to the above knee popliteal artery.
And then the addition of warfarin for prosthetic bypass below the knee or high risk conduits or poor outflow. But really, guidelines for medical therapy after low extremity bypass are weak and high variable. SVS guidelines recommend only antiplatelet therapy
and specifically say that evidence is inadequate to comment on anticoagulation. And guidelines from other important societies are largely silent on this topic as well. Of course we know that our bypass patients have other indications for anticoagulation.
Their coronary disease, there's cerebrovascular disease, and so ultimately, about 25 or 30% of bypass patients are discharged on anticoagulation. Enter the NOACs or the Novel Oral Anticoagulants. Instead of working on Vitamin K dependent factors, they either directly inhibit factor 10A or thrombin itself.
And many of the advantages are well known. These are approved for non-valvular AFib, DVT and PE, and I highlight a few of the approval dates here. I highlight dabigatran and rivaroxaban because these are two captured in the VQI data registry
that I'm going to highlight and show some data on. We hypothesize in this analysis that my colleagues and I performed that these are increasingly utilized as off-label anti-thrombotic therapy in PAD, and specifically in bypass patients.
And we wanted to do an analysis to look at the contemporary utilization of NOACs and their impact on graft outcomes and limb outcomes. WE looked at 19,000 bypasses in the VQI over three years. Now, we stared in 2014 because that's when NOACs were first captured in this data.
When you exclude patients who had less than one year follow up, and some other patients, we're left with about 7,100 bypasses, of whom about 3.5% were discharged after bypass on a NOAC, 21% on warfarin, 76% with none.
This graph plots the utilization over time of NOACs and warfarin. We see that warfarin utilization went from 24% on discharge in the beginning, to 15% over the time period and then correspondingly, NOACs increased from 0.6% of discharges to 6%.
We naturally looked at a lot of bypass patient characteristics to figure out which patients had been selected for either warfarin or NOAC, and they were actually similar. Tibial bypasses, prosthetic bypasses, and long operative times, that should be 300 minutes,
were all chosen for, at some form of anticoagulation. When we look at patency of bypasses on warfarin and NOACs, we see that those bypasses that are not placed on anticoagulation have superior primary patency and that bypasses on warfarin and NOACs have inferior and not different between the two.
The same holds true for assisted patency. And the same holds true for secondary patency where bypasses on anticoagulation inferior to those not on anticoagulation and no significant difference between warfarin and NOACs. When we look at freedom from major adverse limb events,
we see that again, a similar trend. Patients on warfarin and NOAC have inferior freedom from major adverse limb events compared to patients on no anticoagulation after their bypass. Naturally, we did multi varied analysis to look and see
if these were independent predictors of failure. And in fact, they were. Both warfarin and NOAC, even when you control for a variety of patient anatomic characteristics, both were independently associated with failed patency at the hazard ratios you see.
Other predictors of patency were things that are commonly described to date. Same thing is true with major amputation and major adverse limb events. Both warfarin and NOAC were independently associated with major adverse limb events after bypass.
Other factors associated with MALE have been described in the literature as well. So certainly, there are a lot of limitations to this sort of analysis. The registry might not capture important factors that influence the selection of patients
who receive NOACs or their outcomes. This is also limited by the fact that the only NOACs captured in this analysis are dabigatran and rivaroxaban, not the more newly approved NOACs. And this follow-ups naturally limited to one year.
But based on this retrospective data, we see that NOACs and warfarin are utilized after infrainguinal bypass in high-risk patients with high-risk graph characteristics. NOAC utilization is definitely increasing while warfarin is decreasing.
At one year, NOACs and warfarin were associated with worse mid-term graft outcomes and limb related outcomes even after controlling for other factors. And there was really no difference in the outcomes between NOACs and Coumadin. There's a lot of ongoing work in this area.
The COMPASS trial does include some patients of small minority who had previous low extremity revascularization, though they certainly were not all bypasses. Upcoming data from the Voyager-PAD trial where low dose rivaroxaban is tested against aspirin alone
may shed some light on optimal management of anticoagulation. But certainly, based on this data, ongoing study of the impact of NOACs on graft-related and limb-related outcomes is warranted. Thank you very much.
- I'd like to thank Dr. Veith for allowing me to come back to present here. I have no disclosures. A recent large study, retrospective study from Canada looked at the bleeding complications associated with oral anticoagulants, and they identified that there were
significant differences in the patterns of bleeding when compared to the DOACs with Warfarin. Patients receiving Warfarin had a slightly higher rate in intercranial hemorrhage and hematuria, whereas patients receiving DOACs had a significantly higher rate
of gastrointestinal bleeding. In their review of the treatment patterns for these bleeding complications, the patients receiving Warfarin had a significantly higher rate of a Vitamin K administration as would be assumed
and prothrombin complex concentrate administration significantly higher than in the DOAC group. The DOAC group did because they had a higher rate of GI bleeding. Probably had higher rate of packed red blood cells transfusion as well.
Their treatment patterns were in general agreement with generally accepted practice guidelines for Vitamin K antagonist-associated bleeding and that includes for non-major bleeding Vitamin K administration, transfusion of blood components as necessary
for red cells and platelets as necessary but for major bleeding a slightly higher rate of Vitamin K administration, and then the Kcentra, or the 4-factor prothrombin complex concentrates which are administered on a dosing
which depends on the patient's initial presenting INR. The cost of a 4-factor prothrombin complex concentrate's average wholesale price is about $1.20 to $1.60 per unit which equates to about $2200 to over $5000 per treatment for patients receiving Kcentra. This is in contrast to patients receiving FFP
with a cost of about $1600 per patient. We, in our institution, tend to underutilize the 4-factor prothrombin complex concentrates despite their advantages. The advantages of the 4-factor PCCs for reversing Vitamin K antagonist-associated bleeding
include much more effective hemostasis, much more rapid INR correction, 62% versus 9% for plasma, and then median total volume which was significantly lower with the 4-factor PCCs compared to a much higher volume needed to resuscitate and to reverse the INR, fairly ineffectively, in the patients receiving plasma.
Now moving a little bit on to the direct thrombin inhibitors and the factor Xa inhibitors. They are ubiquitous in our practices in vascular surgery and cardiology. That's just going to increase even more with the recent FDA approved indication
for major cardiovascular event reduction in the patients with PAD. Fortunately, the patients receiving DOACs have a somewhat lower rate of bleeding complications compared to the Vitamin K antagonists, although that's not zero.
I'll go a little bit into the specific reversal agents for the DOACs. The first of these being Idarucizumab which is an antibody fragment directed against Dabigatran. It has a dosing, which is fairly simply, of five grams of intravenous bolus
with an additional five gram intravenous bolus which can be administered if there's ongoing bleeding. It's a fairly short half-life, 47 minutes. The cost of this medication is fairly similar. $3600 to $3800 dollars per dose for these patients. The benefit of this is that it actually
irreversibly binds to the Dabigatran and increases the illumination of that medication. I will just very briefly go into the clinical studies that led to the approval of Andexanet. Patients, basically 67 patients, who had major bleeding, gastrointestinal bleeding, intracranial hemorrhage,
and there was, in brief, just a very significant robust reduction in the factor Anti-Xa activity approved in May of 2018. It is used to treat Rivaroxiban and Apixaban. It has a fairly complex dosing protocol which is dependent on the type of
DOAC which is being administered. The last dose and the last timing for the last dose. The cost of this medication is way out of the ball park compared to the other medications. $3300 per 100 milligram vial equating to a low dose infusion of $26000
and a high dose infusion of $59000. CMS does allow for additional payment of $14 to $15000 per patient, but that still does not counteract that significant cost. There is also the problem with regard to the rebound activity which occurs at
four to six hours later. So I'll briefly go into the CHEST guidelines which just came out in August of this year saying that for minor bleeding, NOAC, and Vitamin K bleeding you just reduce the dose or decrease it. For moderate bleeding, transfusion as necessary
and consider charcoal for Dabigatran, and for severe, life-threatening bleeding consider the specific anticoagulant reversal agents. However, I predict that our hospitals over the next year are going to be grappling with who will be doing the approval for these medications
and how many will be administered at any one time point. Thank you.
- [Narrator] Thank you, thank you Dr. Veith and the committee for the kind invitation. No related disclosures. Carotid webs are rare, noninflammatory arteriopathy that are also known as pseudovalvular folds, as well as other pseudonyms for this. They are small, shelf-like linear filling defects,
arising posteriorly from the posterior proximal-most ICA and project superiorly into the lumen. They're generally regarded as a developmental anomaly of the brachiocephalic system, and histopathology lacks atheromatous changes and inflammation of the tunica intima.
They may be associated with FMD, or be considered an atypical form of intimal fibroplasia, and generally arise from dysplasia within the media. They will as we will see, carry a considerable stroke risk based on laminar flow disruption and irregular shear profile.
This is the mechanism by which they produce strokes, seen clockwise from the top upper-left. There are areas of stasis in which thrombus can develop behind the web. The thrombus can enlarge and eventually embolize. Operative findings and pathologic findings include
these webs seen here behind this nerve hook, and generally smooth muscle with extensive myxoid degenerative changes. Over the last several years we have treated 10 patients with carotid endarterectomy for symptomatic webs. The mean age of these patients
is generally quite young, in the 40s. The majority are female, one patient had a bilateral web and 70% of these patients had no atherosclerotic risk factors whatsoever. The mean maximum peak systolic velocity on duplex was 77 centimeters,
and five of the cases were closed primarily without a patch. There were no strokes perioperatively in this group, no mortalities, and there have been no new neurological events nor restenosis. Several other groups have looked at this phenomenon as well,
this is a case series of which 7 patients were identified prospectively having had an ischemic stroke. Again, the mean age was young. Of note, five of these patients had a recurrent ipsilateral stroke to the web. No FMD was seen throughout the other vascular beds
and four out of five of these patients, the recurrent patients had CEAs with no recurrence at approximately a year. Another review identified 33 patients who had excellent CAT scan imaging. These were younger patients over a six year period,
with cryptogenic stroke. The prevalence of webs within that group was 21%. Symptomatic patients within that group with webs were 7 patients out of 33 and again you see a young age, predominance of women,
in this study of predominance of African American patients 3 bilateral webs, all patients had MCA infarcts. And oh, 1.6% of the webs in the control group were without a stroke. Another case-control study looked at 62 cases over four years.
They were able to match 53 of these patients with other cerebrovascular pathology, webs were found in 9% of the cases, but only 1% of the controls. And again of the webs, predominance of young patients
and women with two bilateral strokes. So what about diagnosis? Even large webs generally do not meet the velocity criteria for significant stenosis, and while you may see a filling defect, you're generally dependent on B mode imaging,
and having a high level of suspicion, for identifying this process. CTA is the gold standard, it's got rapid, high-resolution imaging, reformatting across planes, makes this an excellent modality
in associated findings of thrombus, and atherosclerosis can also be detected. Angiogram again, as always, gives you a good view of flow dynamics, intra and extra cranial pathology, and in general the finding is of contrast pooling,
which you have to look for behind the web. MRA is one method that's been used to characterize this, in this modality you can see slowed blood flow distal to the web, blood pooling distal to the web, and generally this all leads to an atypical pulsatility, of the carotid wall near the area of the web,
suggesting impaired hemodynamics in this condition. Management is with a carotid endarderectomy which has been the preferred treatment, although some have advocated medical management with formal anticoagulation, patients have had strokes
while on anti platelet therapy, and there are several case series now appearing of acute stroke treated with stents, these are generally delayed following thrombectomy. There's one latrogenic dissection in these groups. These patients have few atherosclerotic risk factors,
in the same demographics as noted above. So in conclusion, these are associated with FMD and intimal fibroplasia. The prevalence is low. The prevalence may be increasing but it's not clear whether this is a true prevalence increase,
or simply increased detection. They're associated with recurrent symptoms even in the setting of adequate medical therapy and is an underappreciated cause of stroke, and are now becoming a recognized, and rather than a cryptogenic cause of stroke.
They are generally not identified by current duplex criteria in asymptomatic patients, and duplex may miss them entirely. Axial imaging is essential and currently we don't stratify these based on either legion characteristics or demographics.
So while the optimal management is not completely defined given the recurrent stroke risk CEA seems prudent especially in young, medically fit patients with or without patch angioplasty, which may have some impact on quality metrics
at least in the United States. We've treated patients with three months of antiplatelet therapy, aspirin indefinitely. Right now the role of statins is undefined, and the durability and role for endovascular approaches remains also undefined.
- Thank you Rod and Frank, and thanks Doctor Veeth for the opportunity to share with you our results. I have no disclosures. As we all know, and we've learned in this session, the stakes are high with TEVAR. If you don't have the appropriate device, you can certainly end up in a catastrophe
with a graph collapse. The formerly Bolton, now Terumo, the RelayPlus system is very unique in that it has a dual sheath, for good ability to navigate through the aortic arch. The outer sheath provides for stability,
however, the inner sheath allows for an atraumatic advancement across the arch. There's multiple performance zones that enhance this graph, but really the "S" shape longitudinal spine is very good in that it allows for longitudinal support.
However, it's not super stiff, and it's very flexible. This device has been well studied throughout the world as you can see here, through the various studies in the US, Europe, and global. It's been rigorously studied,
and the results are excellent. The RelayPlus Type I endoleak rate, as you can see here, is zero. And, in one of the studies, as you can see here, relative to the other devices, not only is it efficacious, but it's safe as well,
as you can see here, as a low stroke rate with this device. And that's probably due to the flexible inner sheath. Here again is a highlight in the Relay Phase II trial, showing that, at 27 sites it was very effective, with zero endoleak, minimal stent migration, and zero reported graph collapses.
Here again you can see this, relative to the other devices, it's a very efficacious device, with no aneurism ruptures, no endoleaks, no migration, and no fractures. What I want to take the next couple minutes to highlight, is not only how well this graph works,
but how well it works in tight angles, greater than 90 degrees. Here you can see, compliments and courtesy of Neal Cayne, from NYU, this patient had a prior debranching, with a ascending bypass, as you can see here.
And with this extreme angulation, you can see that proximally the graph performs quite well. Here's another case from Venke at Arizona Heart, showing how well with this inner sheath, this device can cross through, not only a tortuous aorta, but prior graphs as well.
As you can see, screen right, you can see the final angiogram with a successful result. Again, another case from our colleagues in University of Florida, highlighting how this graph can perform proximally with severe angulation
greater than 90 degrees. And finally, one other case here, highlighting somebody who had a prior repair. As you can see there's a pseudoaneurysm, again, a tight proximal, really mid aortic angle, and the graph worked quite well as you can see here.
What I also want to kind of remind everybody, is what about the distal aorta? Sometimes referred to as the thoracic aorta, or the ox bow, as you can see here from the ox bow pin. Oftentimes, distally, the aorta is extremely tortuous like this.
Here's one of our patients, Diana, that we treated about a year and a half ago. As you can see here, not only you're going to see the graph performs quite well proximally, but also distally, as well. Here Diana had a hell of an angle, over 112 degrees,
which one would think could lead to a graph collapse. Again, highlighting this ox bow kind of feature, we went ahead and placed our RelayPlus graph, and you can see here, it not only performs awesome proximally, but distally as well. And again, that's related to that
"S" shaped spine that this device has. So again, A, it's got excellent proximal and distal seal, but not only that, patency as well, and as I mentioned, she's over a year and a half out. And quite an excellent result with this graph. So in summary, the Terumo Aortic Relay stent graph is safe,
effective, it doesn't collapse, and it performs well, especially in proximal and distal severe angulations. Thank you so much.
- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans
can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.
But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.
What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?
Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for
all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',
and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.
He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.
So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.
It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,
and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after
you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,
and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.
That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.
How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.
But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.
In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,
the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors
such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants
to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study
because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.
So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist
on maximal protection and assume that all radiation is dangerous. Thank you very much.
- So thank you to the organizers and to Dr. Veith, and thank you to Dr. Ouriel for giving me the introduction of the expense of an unsuitable procedure for pain patients. We have no disclosures.
I think when you look at MRV or Venous interventions, you can look at it as providing you a primary diagnosis, confirming a diagnosis if there's confusion. Procedural planning, you can use it as a procedural adjunct,
or you can use it as a primary procedural modality. In general, flow-dependent MRI has a low sensitivity and a slow acquisition time, making it practically impractical. Flow-independent MRI has become more popular, with sensitivity and specificities
rounding at 95 to 100%. There's a great deal of data on contrast-enhanced MRI, avoiding adanalenum using the iron compounds, and you'll hear later from Dr. Black about Direct Thrombus Imaging. There has been significant work on Thrombus Imaging,
but I will leave it up to him to talk about it. MR you can diagnose a DVT, either in both modalities, and you can see here with the arrows. It will also provide you data on the least inaccessible areas for duplex and other modalities,
such as the iliac veins and the IVC, as can be seen here. It is also perhaps easier to use than CTV, because at least in my institution CTV always comes out as a CTA, and I can't help that no matter what happens.
MR can also show you collaterals, which may be very important as you are trying to diagnose a patient. And in essence it may show you the smaller vein that you're more interested in, particularly in pelvic congestion syndrome,
such as this patient with an occluded internal iliac vein. It can also demonstrate, for those of you who deal with dialysis access, or it's central line problems, central venous stenosis and Thrombus. But equally importantly
it may show you that a stenosis is not intrinsic to the wall, but it's actually intrinsic to extravascular inflammation, as in this patient with mediastinal fibrosis, and which will give you a different way of what you wish to do and treat.
The European guidelines have addressed MR in it's future with chronic venous disease and they give it a 1C rating, and they recommend that if doesn't work you should proceed to Ibes. It can be used for the diagnoses of pulmonary embolism,
it can eliminate the use of ECHO, one can diagnose both the presence of the Thrombus, the dilatation of the ventricul, and if one is using Dynamic MR Imaging one can also see mcconnell sign or the equivalent on the septum between the two ventricles.
More interestingly it can also be used now in the chronic thrombuc, pulmonary hypertension, where it can show both the legions that are treatable and untreatable, as some of you may have heard from Dr. Roosevelt
earlier in the day, where they're now treating the outlying lesions with balloon angioplasty serial sessions. It can also look at the ventricul and give you some idea of where the ventricul stands with regard to it's performance,
we're looking at and linking this to the lungs. It can also show you the unusual, such as atresia of the IVC or it can help with you the diagnosis of Pelvic Congestion Syndrome. And it is extremely valuable
in dealing with AVM's, although it may take one, two, or three sessions with differing contrast bulosus to identify both the arterial, the intrinsic lesion, and the outflow lesions,
but a very valuable adjunct. In renal carcinoma it has two values, one is that it can may diagnosis venous invasion, and it may also let you understand whether or not you are dealing with bland thrombus or tumor thrombus,
which can change the staging for the patient and also change the actual intervention that you may perform. If you use flash imaging one will get at least an 89% sensitivity of the nature of thrombus,
whether it's bland or tumor thrombus, which may change what you need to do during the procedure. It could also tell you whether there's actual true wall invasion, which will require excision of the IVC
as opposed to the simple thromboendarterectomy. And this can run up to a specificity of 88% to exclude it. In the brain it's commonly used to diagnose the intra tumor vasculature. Diagnosing between veins and arterial systems, which can be helpful
particularly if one is considering percutaneous or other interventions. With regard to central venous stenosis there is some data and most people are now using an onlay technique where they take the MRI,
they develop the lines for the vessels and then use that as guide in one or two dimensions with fusion imaging to achieve access with a wire, catheter and balloon, as opposed to a blind stick technique.
There is data to show that you can image with the correct catheter balloons within the vessels and do serial MR's to show that it works. And finally with guidance catheters EP is now able to guide the catheter further and further in to achieve from the,
either the jugular or the venous access across the septum and to burn the entrium as appropriate. And finally, one can use MR to actually gain access, burn, and then actually use the MR to look at the specific tissue,
to show that you've achieved a burn at the appropriate area within the cardiac system and thus prove that your modality has achieved it. So in summary, we can use it for primary diagnosis, confirmatory diagnosis,
procedural planning, and procedural adjunct, but we're only still learning how to use it as a primary procedural modality. Thank you so much.
- Ladies and gentlemen, I have nothing to disclose when regarding this topic. We know that TIAs are independent predictors of long-term mortality in the general population, however, they've been left underreported in almost all the randomized clinical trial. And we don't know the effect of TIAs on long-term survival
in patient with carotid disease. So what we have done, we have performed a study, looking at the effect of TIAs in populations submitted to carotid revascularization, either with endarterectomy, or stenting, and we achieved a pretty good long term result.
However, patient's with TIAs had a significantly lower survival compared with the patient without cerebral events. Similarly, patient with stroke, these reduce survival, and TIA behaves exactly like stroke in this population.
So, by multivariate analysis, TIA together with stroke, chronic renal failure, and age were independent predictors for late mortality. So, we have seen that TIAs have this effect in patient with carotid disease, but what about silent cerebral event?
The silent cerebral infarction has small, radiologically detected infarction without a history of acute dysfunction. And they're usually associated with a variety of condition. In the general population, these cerebral infarction are present in almost
one fifth of the population, 21%. And they are associated with significantly reduction in the stroke free survival in this population. For that reason, they are considered a high risk of stroke in patient with carotid disease.
So looking at the series of patient submitted carotid revascularization, we have seen that the presence of these silent brain infarction was significantly associated with either transient ischemic event and stroke. So, the important factors,
we wanted to further expand these experiences just looking at these phenomenon. In another series of 743 patients submitted to endarterectomy are looking at all the preoperative CT scan in this population. And again, we have found that significantly
association between silent cerebral infarcts and stroke. And by logistical regression analysis, this feature was independently associated with postoperative stroke. At long-term, this effect was also present in association with ipsilateral stroke.
And stroke combined stroke and death. Again, these effect was independent from all other feature. So what about their effect in stenting? Actually, there are no papers in the literature looking at this effect. So we perform a retrospective analysis on
420 patient submitted to a stenting procedure. And all patients were selected with preoperative evaluation of the brain. So, again, 30 day outcome, was not significantly affected by the presence of silent cerebral infarcts, however, when we look at the patient
with endarterectomy and stenting, we see that while in the endarterectomy group, there is a clear decrease of the stroke rate in patient without silent cerebral infarction. This effect is less pronounced
in the stenting group. So in conclusion, silent cerebral infarction increases the risk of postoperative events in carotid endarterectomy. This increased risk should be considered when in indication to revascularization is given.
In stenting, the effect is less pronounced, due to the higher overall risk of neurological event. Thank you.
- I wanted to discuss this topic because some of us are more sensitive to DNA damage than others. And it's a complicated ethical issue. I have a disclosure in that I developed a formulation to premedicate patients prior to CT and x-ray. We all know that we stand in fields of radiation for most of our careers,
and we also know that many of us have no hair for example on the outside of our left leg. This is a picture that a bunch of us took for fun demonstrating this. But this is in fact radiation dermatitis. We know that the founders of our field
suffered consequences from the chronic high doses that they received in the 1920's. And they lost digits, they lost ears, they lost noses any many of them died of cancers or cardiovascular disease. The mechanism of injury is the x-rays
impinge upon water molecules in our cells. They create free radicals. These free radicals bind with our DNA and then Oxygen binds with that site resulting in an oxidative injury which can be reduced by the use of anti-oxidants.
I studied this over the last eight or nine years and I looked at the issue of chronic low dose radiation. Now this is different from the data that we collect from Nagasaki and Hiroshima and from Chernobyl and elsewhere. There are cancer risks but there
are also cardiovascular risks. And there are risks from chronic inflammation from increased reactive Oxygen species circulating with our system. I've been in touch with the IAEA recently about this and they didn't actually
realize that we don't wear our badges. So they thought the data they were getting on the doses that we were receiving were accurate. So that was a very interesting conversation with them. So cardiologists have been known
to get lifetime doses of of over one Gray. There's a lot of literature on this in public health literature. For example for every 10 milliSieverts of low dose ionizing radiation and received by patients with acute MI's,
there's a 3% increase in age and sex adjusted cancer risk in the follow-up five years. There's an excellent paper from Kings College London demonstrating that when endovascular surgeons were studied with two specific immunofluorescence tests, P53 and H2 alpha,
they were able to demonstrate that some endovascular surgeons are more sensitive to radiation dose than others. So why would that be? Well it's interesting if you look at this genetically and you look at the repair mechanisms
and in this whole thing I think in fact the lens is kind of the canary in the coal mine. When you get radiation induced cataracts, it's in the posterior chamber of the lens not the middle or anterior, which is where age-related injury occurs.
And this is the germinal layer or reproductive layer. The growth layer in the lens itself. And this is where cataracts develop. And this is really kind of a harbinger I think of injury that occurs elsewhere in our system. We know that when we wear DLDs on our chest,
on our bodies, on our arms, that the dose to the left side of our head is six times higher than to the right. In fact they dosed the left lens as higher than the right. And most of us who have lens replacements have it of the left eye.
This literature from adjacent fields that we may no be aware of. In the flight safety literature for pilots and stewardesses. There's extensive literature on cosmic radiation to flight crews who's doses annually are in the same range as ours.
So when you look at medical staff, you have to look at the overall context of the human in the Angio suite. Many of our medical staff will not be well. They may have chronic cardiac disease. They may be on say drugs for auto
immune disease or Methotrexate. They may have other illnesses such as Multiple Myeloma. They may have antibiotics on board that alter the DNA repair ability like Tetracycline. And they have chronic stress and sleep dysfunction. Cigarettes and alcohol use.
All of these things decrease their ability to repair DNA damage. If you look at DNA repair mechanisms, there are constantly the terms BRCA1 and two, PARP, P53, and ATM that show up. And deficiencies in these,
I'm going to skip all this to show you, can result in increased injury from a same dose being received by two different individuals. Now who is at risk from this is well understood in adjacent fields.
Here are 37 references from the public health literature related to mutations and SNPs or polymorphisms in DNA structure known to cause increased sensitivity to radiation. So I would propose that in, and here are papers on that topic
in adjacent fields that we don't read. So when we talk about personalized medicine for our patients, we need to also think about personalized career choices based on our DNA repair ability when we decide what we do. This has to be done in the context
of empathetic compassionate approach. It may begin with screening based on family history and personal history, and then advance in the right context to genetic screening through mutations and SNPs that can decrease their ability
to repair DNA damage from our occupational exposure. I'll skip all this because I'm out of time. But one other issue to think about, mitochondrial DNA is inherited purely maternally. So maternal DNA damage, mitochondrial DNA damage could be transmitted across generations
in female interventionalists. Also screening is important. It's emotionally complex. It's ethically complex. But it's an important conversation to begin to have. Thank you.
- Well, thank you Dr. Veith, and thank you very much for allowing me to speak on the topic. I have no disclosures. This is a nice summary that Dr. Veith is actually second author, that summarize what we know about predicting who will benefit from intervention among the patients with asymptomatic aortic disease.
You look at this eight means that we have, you realize that only one of those related to the fluid deprivation. The rest of them are related to embolic events. And that's very interesting because we know that antiplatelets have very little effect
on prevention of this. That's summarizing that review. Partially because what we focused on is that mechanism of thrombosis which requires platelet activation and attachment to the wall.
And that's where those antiplatelets that we use, act upon. However, you realize if you just look at the any ultrasound, that because of the velocities that we have and the lengths of the stenosis in carotid disease there is no way how the platelets can be attached to that
due to that mechanism. They just fly away too fast and don't have any time to do this. And it's even more because all the studies, basic science, show that at those shear rates that we have in carotid disease
that is more that 70%. There is very little probability of either platelet attachment or Von Willebrand factor attachment, or as a matter of fact even fibrinogen attachment in that particular area. So on the other hand we also know
that at those shear rates that we have, the Von Willebrand factor molecules unfold revealing tens of thousands more adhesive sites that allow them, not only to the platelets but also to the wall at that particular spot. And then the most likely mechanism
of what we dealing with in the carotid disease is this that the Von Willebrand factor attach and this unactivated platelets form conglomerates which can easily, because they don't attach to each other, easily fly. And that is probably one of
the most likely causes of the TIA. So if you look at the antiplatelet that we use on this particular mechanism, is right here. And those aspirin and clopidogrel, and combination of those we usually use, have very little, if any, effect on this particular mechanism.
So if, on the other hand, you can see that, if you specifically address that particular site you may have a much substantial effect. Now, how can we identify it? Well actually, the calculation of near-wall shear rate is quite simple.
All you need is just highest velocity and smallest diameter of the vessel. Of course, it is an estimate and actual shear rate is much higher but that's even more, because you, better than you prevent, more higher rate. Just to demonstrate, you can have the same velocity,
similar velocity, but different diameters. This stenosis technique will give different shear rate, and vice versa. So it's not really duplicating neither one of them. So we decided to look at this. We did a case control study that was published,
still online in the Journal of Vascular Surgery. And what you can see on the ROC curve, that in fact shear rate predicts symptomatic events much better than either velocity or the degree of the stenosis. And we look specifically at this group
with this thresh point of 8,000 per second and you can see that those patients who have those shear rates and the stenosis are 12 times more likely to have ischemic events. We look at the other means like microembolism. It's ongoing study, it's unpublished data that I show you.
And it's a very, very small sample but so far we have the impression that those microemboli that we can decide for, make a decision for intervention, actually happen only in this category of patient that have high shear rate. Based on this, this is our proposed algorithm,
how we deal with this. If you have asymptomatic patients with more than 70% degree of their stenosis and shear rate that exceeds certain level, we think it's about 8,000 per second, that may be an indication for intervention.
On the other hand if you a have lower shear rate then you can use other means. And what we use is microembolis per hour. Then you can duplicate their areas. If TCD on the other hand is normal you can continue best medical therapy and repeat the ultrasound in a year.
It's arbitrary. This is proposal agreed and based on our studies and that's, I'm thankful for the opportunity to share it with you. Thank you very much.
- Thanks again. So I've been charged with talking about drug drug interactions with statins and I have no disclosures. (reads on screen definition) Using that definition, statins have very little, if any,
chemical interactions with other drugs However, what the intent I think of the title is looking at statin levels. How statin levels are affected by drugs which alter the enzmyatic pathways of statin metabolism.
And we know that statins are HMG CoA reducatase is responsible for the rate limiting step of cholesterol synthesis and drugs that inhibit HMG CoA reduce cholesterol.
(reads slide) P-glycoprotein is a transporter protein that moves substances across cell membranes. And this is a list of the common statins and how they interact with P450 substrates. We have the CYP3A4 substrate
and atorvastatin is a major example there and the CYP2C9 substrates and Rosuvastatin. And I'll call you attention to the fact that the most commonly used and most effective statins, Atorvastatin and Rosuvastatin,
are both long half lives compared to the other statins. Now another thing I want to call your attention to 'cause it has clinical implications is the variation in breast cancer resistant protein (BCPR) gene but it alters the absorption
and it significantly increases the absorption of statins from the GI tract. And you can see that Asians are particularly affective and that's why recommendations for beginning statins in Asians are to start at a lower dose and then ramp up rather than start
at the typically maximal dose for most of our arthoscopic patients. Now risk factors thought to be due to interactions are advanced age, frailty, hepatic dysfunction, those with alcohol abuse, renal dysfunction, hyperthyroidism, woman and Asians.
And if they have any of these, we want to dose adjust but that's for risk factors. (reads on screen definition) Now grapefruit juice is often talked about and its due to its interactions with furocoumarins
and Atorvastatin has a large effect and Rosuvastatin very little effect when grapefruit juice is taken. If a patient want to drink six or seven ounces of grapefruit juice a day or every other day, that's fine, we don't want them
drinking a quart of grapefruit juice a day. Simvastatin is particularly a risky statin. It's at higher risk for drug interactions. It's at high risk for being involved with genetic polymorphisms. It has a dose related toxicity
unlike Rosuvastatin and Atorvastatin. And I told you about the FDA warnings. So lets make it easy on how to manage the patients. If a patient has liver disfunction or they're on Niacin, and if they're on Niacin,
I'd rather discontinue the Niacin and keep the statin, treat them with caution. If a patient has renal dysfunction for all statins except for Atorvastatin, adjust the dose.
If a patient is on Digoxin, monitor the dige-level in these patients if they are on a statin because the dige-level can increase. And then we want to avoid statins in patients that need
any of the azol antifungal such as ketoconazole or the mycin antibiotics or cyclosporine. Avoid fibrates and especially genfibrozil and the protease inhibitors if your patient is on an HIV protease inhibitors. (reads on screen information)
Thank you very much.
- Thank you so much for having me here. I must confess it's not my talk. It's Professor Veroux's talk. Veroux couldn't join us, so I hope you will forgive me if I cannot read it properly as he would have done. It's just a friendship act of being here.
Talking with you about the potential of these treatment of ventricular veins for relief symptoms, headache like. Professor Veroux published on PlosOne Single-center open label observational study was conducted from January 2011 to December 2015.
Basically focused on 113 headache positive patients. As you see there were different kinds of MS patients involved. 82 were relapsing emitting. 22 were secondary progressive. Nine were primary progressive.
Basically the including criteria included headache resistant to the best medical therapy. There was a bilateral internal jugular vein with a stenosis bigger than 50% of moderate to severe insufficiency of the flow. The stenosis of course were suitable for treatment
and they were followed up at least for 12 months. Basically the followup included a variation of the MIDAS, Migraine Disability Assessment Score. It was preformed the day before angioplasty. Then three months after angioplasty and then at the end of the follow-up.
As it was appears,. Of curse we can add the different kinds of lesions of the juvenile level. As it was previously reported, the Professor Veroux ended selection. It is mandatory in these kinds of procedures.
Adding the transversal defect the single most important criteria for determining if the PTA would be successful or not. Of course, again, transversal rather than longitudinal defects are preferred in the treatment of
this kind of patients. The exclusion criteria were the possibility of hypoplasia or extreme muscle compression. In particular, as you know there is the omohyoid possibility of compression.
Looking at a followup that is significantly of three years or more. The clinical results in these patients affected by headaches lead to significant reduction. And 86% of them with an improvement of the MIDAS scores in the three months following up.
At the same time, the improvement was maintained throughout the followup period up to three years. Mainly in the relapse remitting and the secondary progressive patients. So the conclusion of the investigation you can again (mumbles)
is that patient selection is mandatory, of course, again, on the transverse lesion mainly. Balloon valvuloplasty is feasible in these patients and has succeeded with a good result at three years followup in the MIDAS score. Of course, these findings are suggesting
that it could be a useful intervention for selected MS patients with persistent headaches and of course, non-thrombosis stenosis of the IJVs. Thank you so much.
- Thank you Louie, that title was a little too long for me, so I just shortened it. I have nothing to disclose. So Takayasu's arteritis is an inflammatory large vessel vasculitis of unknown origin. Originally described by Dr. Takayasu in young Japanese females.
The in-di-gence in North America is fairly rare. And its inflammation of the vessel wall that leads to stenosis, occlusion or aneurysmal formation. Just to review, the Mayo Clinic Bypass Series for Takayasu's, which was presented last year, basically it's 51 patients, and you can see
the mean age was 38. And you can see the breakdown based on race. If you look at the early complication rate and we look at specific graft complications, you had two patients who passed away, you had two occlusions, one stenosis, one graft infection.
And one patient ruptured from an aneurysm at a distant site than where the bypass was performed. If you look at the late complications, specifically graft complications, it's approximately 40%. Now this is a long mean follow up: this is 74 months, a little over six years.
But again, these patients recur and their symptoms can occur and the grafts are not perfect. No matter what we do we do not get superb results. So, look at the graft outcomes by disease activity. We had 50 grafts we followed long-term. And if you look at the patency, primary patency
right here of active disease versus non-ac it's significantly different. If you look at the number of re-interventions it's also significantly different. So basically, active disease does a lot worse
than non-active disease. And by the way, one of our findings was that ESR is not a great indicator of active disease. So we're really at a loss as to what to follow for active or non-active disease. And that's a whole 'nother talk maybe for another year.
So should endovascular therapy be used for Takayasu's? I'd say yes. But where and when? And let's look at the data. And I have to say, this is almost blasphemy for me
to say this, but yes it should be used. So let's look at some of the larger series in literature and just share them. 48 patients with aortic stenosis fro all were treated with PTA stenting.
All were pre-dilated in a graded fashion. So they started with smaller balloons and worked up to larger balloons and they used self expanding stents in all of them. The results show one dissection, which was treated by multiple stents and the patient went home.
And one retro-paret-tin bleed, which was self limiting, requiring transfusion. Look at the mean stenosis with 81% before the intervention. Following the intervention it was 15%. Systolic gradient: 71 milligrams of mercury versus 14. Kind of very good early results.
Looking at the long term results, ABI pre was .75, increased to .92. Systolic blood pressure dropped significantly. And the number of anti-hypertensive meds went from three to 1.1. Let's look at renal arteries stenosis.
All had a renal artery stenosis greater than 70%. All had uncontrolled hypertension. They were followed with MRI or Doppler follow up of the renal arteries. So, stents were used in 84% of the patients. Restenosis occurred in 50% of them.
They were, all eight were treated again, two more developed restenosis, they ended up losing one renal artery. So at eight years follow up, there's a 94% patency rate. What about supra-aortic lesions? And these are lesions that scare me the most for endovascular interventions.
Carotids, five had PTA, two had PTA plus stent. Subclavian, three PTA, two PTA. One Innominate, one PTA plus stent. One early minor stroke. I always challenge what a minor stroke is? I guess that's one that happens to your ex mother-in-law
rather than your mother, but we'll leave it that way. Long term patency at three years, 86%. Secondary patency at three years, 76%. Fairly good patency. So when Endo for Takayasu's, non-active disease is best. The patient is unfit for open surgery.
I believe short, concentric lesions do better. In active disease, if you have to an urgent or emergent, accept the short term success as a bridge to open repair. If you're going to do endovascular, use graded balloons or PTAs, start small. Supra-aortic location, short inflation times
I think are safer. And these three, for questions for the future. I guess for the VEITHsymposium in three years. Thank you.
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