- [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 Lowell. - Good morning, and thanks Lowell and Jose, for the invitation to come back this year. I don't have any disclosures. Well, what we're going to talk is imaging the female pelvic veneous system. And the female pelvic venous system is a complex arrangement
of four interconnected venous systems, and really you have to understand the anatomy to understand the keys to imaging it and treating it, and that's the connections between the renal vein, both the left and the right ovarian veins, the tributaries of the internal iliac veins,
and the superficial veins of the lower extremity through the saphenofemeral junction. And central to all of this are the tributaries of the internal iliac vein. Which functions as a gateway between the pelvis and the leg, and really are exactly analogous to perforating veins,
connecting the deep veins of the pelvis to the superficial veins of the leg, and you have to have an intimate knowledge of this anatomy both to image it adequately, as well as to treat it. So classically, the internal iliac vein is thought as the confluence of three tributaries.
That is, the obturator vein anteriorly, tributaries of the internal pudendal vein, sort of in the middle of the pelvis, and the superior and inferior gluteal veins, and these communicate with the legs through four escape points
that the anatomists describe anteriorly as the obturator point or the "O" point, where the round ligament vein comes through the abdominal wall, the "I point. And medially in the thigh, pudendal or the "P" point, and posteriorly the gluteal point,
which communicates both with the posterior thigh as well as with the sciatic nerve and gives rise to sciatic varices. (coughs) From our standpoint today, I'm more interested in atypical, varices, that is, pelvic source lower extremity varices,
arising from the pelvis, anteriorly for the obturator vein, and from the round ligament vein, which communicate with the vulva, branches of the internal pudendal vein, which communicate with the perineum, and the medial thigh, and posteriorly, with branches of the superior and inferior gluteal vein.
So as far as imaging goes, we're interested primarily in two clinical scenarios which the imaging requirements are somewhat different. That is, atypical pelvic source varices without any pelvic symptoms, and atypical varices with pelvic pain, and the way that we study these with venography
are quite different. Although some people do pursue blind sclerotherapy from below, I do think imaging with venography adds substantially to both the control of the sclerosant, as well as how thoroughly you're able to embolize the pelvic tributaries.
And I personally like to do sclerotherapy of the varices with venography, and use direct puncture venography using either a 23 or a 25 gage butterfly needle, that's placed under ultrasound guidance. Contrast is then injected to calibrate both
the variceal bed as well as to track the tributaries, as I'll show a minute, up into the pelvis, and usually you can embolize about to the level of the broad ligament. Simultaneously, foam sclerotherapy is performed, using a combination of Sotradecol,
and Ethiodol as a contrast media, and then is followed both by Flouroscopy, using a reverse road mapping technique to subtract the bone and other things out, and follow the contrast through as well as with ultrasound as shown here.
And just as an example, here's some vulvar varicosities, that communicate both with the obturator vein up here, with the round ligament vein through the "I" point, as well as with the saphenofemoral junction here. And although you could do this blindly, I do think you get a much better understanding
of the anatomy and the volume of sclerosant required, doing it with venography. These are posterior thigh varicosities, that communicate through the "G" point here, and you can actually see the contrast refluxing into the inferior gluteal vein shown here,
and all of this can be treated with sclerosant. The second clinical scenario, is that of atypical varices with pelvic pain, in which case you do want to make sure you treat the pelvic variceal bed completely. And for this, the venography techniques are
balloon occlusion venography performed from above. My preference is right internal jugular vein approach, because it's easier to place the occlusion balloon into the right and left internal iliac veins, which a sequentially selected, and then I use a Berenstein occlusion balloon
and then place it just below the confluence of the internal iliac vein and the external iliac veins, inflate the balloon, inject contrast, which both blocks antegrade flow, and allows reflux into the varices. Most of the time you can't see these varices if you don't have an occlusion balloon,
and then as you see the varices, sequentially select more distal tributaries with a glide wire, put the balloon down, inflate it, and perform sclerotherapy and occasionally, depending on the size of the vein, use coils if you need to. Here is an example of the balloon
in the internal iliac vein, you see the "O" point. We've already sclerosed the contralateral obturator vein, and you see this classical obturator hook here, which is classical for the obturator vein. Here the occulsion balloon is in tributaries of the internal pudendal vein,
you see it communicating through the "P" point with varices in the medial thigh, and then with the great saphenous vein here, with a type two junction. Here the balloon is in the inferior gluteal vein. You see communication with the "G" point here,
as well as communication with sciatic varices, this classic horsetail look shown here. So in conclusion, understanding anatomy is critical to the treatment of pelvic venous disorders, you do clearly have to understand the anatomy of the internal iliac vein, as well as the escape points,
and vary your venographic technique, based on the patient's symptoms. Thank you very much.
- 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.
- 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.
- 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.
- Thank you, thank you Frank for inviting me, again. The ascending aorta, as you know, is still the holy grail of endovascular aortic therapy. Especially, when dealing with true aortic aneurysms. There are a lot of contraindications to ascending stenting as we have listed here. So, these are all good cases for aortic surgery.
On the other hand there isn't a reason to treat some of these patients as partially high-risk patients with Endo. What about the technique? Transvalvular manipulation is essential. You basically have to do what cardiologists
are doing when they perform a TAVI procedure. And you have to know how to get across the aortic valve. There are straight forward cases like pseudo aneurysms as you can see here, which you can treat with coronary angioplasty and subsequent stenting. But the problem
or the real challenge are true ascending aneurysms. So, there are two options, bending of the ascending aorta in order to create a proximal landing zone or bending of all the ascending aorta. What about the technical details? Of course, a mediastinotomy is required.
You can use a mediastinotomy and we prefer a polypropylene mesh, which you see here. Which is additionally covered with a PTFE wrap. Just in case a recent otomy is required to prevent adhesions between the posterior
surface of the sternum and the ascending aorta. This creates downsizing of the aorta and facilitates endo-grafting here. Here typical example, the usual configuration of the true ascending aortic aneurysm wrapping with polypropylene mesh is what you get.
So, here you have your landing zone for the stent graft. When you dissect you have to circumferentially dissect the aorta. You have to make sure that you don't get into too close contact with the pulmonary artery. Here again, mediastinotomy in most cases,
is sufficient to do the procedure. Diameter reduction can be calculated according to this formula then I do know the length of my graft. You can combine this with supraoptic de-branching or bypass procedures whatever is
necessary in order to deal with this. In a lot of these cases get a landing zone for complete endo-treatment of the aortic arch with Sandwich grafts or similar techniques. We do know from these bio-mechanical studies that wrapping of the aorta reduces shear stress.
The whole concept only works in an ascending aorta up to a diameter of 6.5 cm, but no more. Here typical example, downsizing all the proximal landing zone. Subsequently, what you do get in some of these cases is in falling through here a stent graft makes sense
and then you can treat these patients with a stent graft. You would use a chimney in order to avoid compromising the origin of the innominate artery. Again, a typical example. The question is why do I have to use a stent graft at all after wrapping.
The answer is because you want to get a smooth inner surface and you don't want to have thrombus inflammation where the wrapping causes in-folding, but in all these cases you get very good results. Durable result, in term of the mediastinotomy. The mediastinotomy is very well tolerated
by these high risk patients. When you look at the age of these patients we have no neurological complications. No severe adverse events. This is a procedure, which can be offered to high risk patients
who have a lot of contraindications for open aortic surgery. Of course, this will be the future but not until maybe in ten years from now. Thank you very much.
- Thank you very much. The stuff Rubiole said about magic methods, but not concerning the large veins, as we heard, would be also about that or something. I don't have disclosures. We all like probably to treat such a pathology. It's quite common in our offices.
And most of us treat them without the problems. But probably we will be not much happy to having such a patients to treat, especially if we see such a pathologies, not this what you, really, I like, especially if patient is coming with the recurrence
in the same place for the third or fourth time. So of course, reflux identifications, we heard this based on ultrasounds. Small vessels, feeding vessels can be seen on the ultrasound and torso transillumination. In most cases, this will be probably sufficient,
but as we have no doubt about this case what to do. In many cases, or at least in some cases, we see the patient coming with sclerotherapy failure. And then probably the first thing that we should look for, it's a feeding vein. Persistence or persistent of a large vessel.
Reflux, what else, except physical examination, except transillumination we can use? Near Infrared light technology. And ultrasound especially. Ultrasound with high frequency that allows you to do exactly this what the static medicine doctors do.
So, to see the skin in a very good quality matches. So, concerning Vein Viveror of this transillumination, often of this wentetrotite methods that I think most of your are familiar with, this, we can use this in some cases, but as in this case it is quite easy and possible.
In this case, on the right side, I not sure what's really a problem in this patient because probably the feeding veins comes goes from, goes from the down in a perpendicular manner. So if you have such a lesion without any feeding veins visible in transillumination or in almentoteratity,
what can we do to close this? Then, I would like to encourage you to use high resolution ultrasound. This is the same lesion with 0.6 millimeter vessel just below, but this vessel goes perpendicular to one of the quite big perforators as you can see,
in a very perpendicular manner, probably none other methods can show us this kind of pathology. With this high resolution high frequency ultrasound, you can see reticular veins, but this is what is especially interesting,
you can see the connection with all vessels being below the lesion that can be not visible in any other technology. Perforators going oblique and going perpendicular are quite good visible. I can try to find the reflux in compressing the skin,
but quite often the reflux can be seen using the simple valsalva maneuvre, as the vessels are very small. Some examples what we can see the perforators, but also like on the right side, the novus scleroization coming from the
small vessels after this thing is removal. And we made some small study of 50 C1 lesions resistance to sclerotherapy failure, treated after the diagnosis made by augmented reality and 18 megahertz probe Venous ultrasound. All these lesions were previously treated,
as you can see some of them even three times, no major vessel reflux, no large branches, no axial reflux, and no vessel is visible in transillumination in the series. We found that in 50% there were the vertical or oblique course vessels feeding this lesions and
vertical plus horizontal additional 26, so we had the perpendicular going pathological reflux in 3/4ths of the patients, reflux sources in 62% were perforators or deep vein connectors. On this patient were treated with ultrasound guided sclerotherapy, or with augmented reality
guided sclerotherapy. And as you can see, 66% of the feeding veins were recognized by 18 megahertz ultrasound and we could probably not find this in any other way after six months follow-up. 90% of these lesions were obliterated.
However, 1/3 required the repeated treatments. In conclusion, the combined approach based on the augmented reality and the 18 megahertz ultrasound feeding vein identification improved the C1 sclerotherapy efficacy in the treatment of pathologies not applicable for the primary treatment
and is not for the standard approach. And we currently don't use this in standards approach, we use this for lesions that you saw. Thank you very much.
- Just going to do a little bit of a deeper dive into the types of nutcracker syndrome. I think most everyone knows this one. The anterior nutcracker syndrome in which the left renal vein is compressed as it passes between the aorta and the SMA, and this is definitely the most common
and certainly the most written about, but there's also posterior nutcracker syndrome in which there's a left renal vein which is retroaortic, and in this case it's compressed between the aorta and the spine, and then even more rare is the atypical nutcracker
in which there is a truncular vascular malformation trapping the left-sided IVC and renal vein between the SMA and aorta. Why do I mention these? I mention these because they inform the decision for open surgical repair when necessary.
All treatment options for nutcracker are directed to reduce venous hypertension, and we have the generally armamentarium of vascular procedures as I've listed here. Today my task is to discuss the open surgical options and really the two most important ones
are the versions of left renal vein transposition that I've listed here and have been discussed by Dr. Gloviczki and then gonadal vein transposition which, in our institution, is preferred if the anatomy is suitable. So since I'm following Dr. Gloviczki
I had to list all the papers from his institution, but this is the one that's most (mumbles) to my talk. This is their experience with left renal vein transposition versus conservative management in 23 patients, about 50/50, and what they found, if you look at their results and the characteristics of the patients that they treated,
were that if they selected their patients well, and by that I mean patients with appropriate anatomy and appropriate symptoms, they had excellent results when using left renal vein transposition to treat nutcracker syndrome. This is the other manuscript that Dr. Gloviczki mentioned,
so this is a version of open repair that includes stenting plus left renal vein transposition with suturing the stent in place that I think they hope will deal with the issues of migration in renal vein stenosis. So far their early results are excellent.
And then this is a meta-analysis, also mentioned by Dr. Gloviczki, and one of the elements of this meta-analysis was a surgical arm, if you will, although it wasn't really an arm since it's not a study, but they describe those patients
that were treated surgically. So what did that look like? Well in this meta-analysis they found that open surgical approach was associated with resolution of symptoms in the majority of patients, there were very few complications,
no renal failure or mortality, few postoperative complications in this manuscript as well as in our experience. By far (mumbles) the most common postoperative complications are ileus and hematoma, and freedom from re-intervention was fairly good.
75% at a year and 70% at 12 months. So with regard to surgery, I think the selection of the surgical approach needs to based on the patient anatomy and the patient clinical characteristics. Ideally, master all techniques
so you can offer all of them to the patient. I'd like to highlight my favorite operation for this condition which is gonadal vein transposition. I'll go over how to do it in just a moment, but the idea is that you transect the gonadal vein. You mobilize it completely from
the pelvis to the left renal vein, and you transpose it onto the inferior vena cava, and this both achieves a decrease in pelvic hypertension and it decompresses the left renal vein beautifully but doesn't put the left renal vein itself at risk for thrombosis.
It also, which is important in young people, does not require a great saphenous vein harvest which sometimes may be necessary in certain versions of the left renal vein transposition. So here's the technique. You make a mini-laparotomy,
do standard retroperitoneal exposure, mobilize the gonadal vein, and implant it onto the IVC. Here is a case of posterior nutcracker syndrome. You can see that renal vein transposition would be really hard here. There's the gonadal vein.
This patient was successfully treated, and then another patient with atypical anatomy who was successfully treated with a right gonadal vein transposition, and we actually wrote this up in case reports. So lastly, I just wanted to quickly review our experience.
We've done 15 gonadal vein transpositions. We've had excellent success, 100% technical and 93% clinical. The caveat with that is we have a really short follow-up, so it's hard to say yet whether we'll have the problems with clinical recurrence and restenosis.
So in summary, I think we are waiting a good renal stent, but gonadal vein transposition currently, I think if it's a large gonadal vein, is the treatment of choice if you're going to go this surgical route. Thank you.
- Thank you so much. Seattle, like many other cities in the U.S. is facing a terrible, heroin epidemic crisis. We are the safety net for these patients. I was honored, when I was asked to came and share with you how we manage these patients at Harrow View Medical Center. Over the last few years, we have educated our ED doctors,
in order to avoid over-head page to vascular surgery. That they don't do any I&Ds at the bedside. If a patient with a history of IV drug use present with induration or pain on the groin. On those patients, they get triaged for sepsis, they get an IV access, can take some time.
They take labs, including blood cultures. If we can, we do ABIs, this is during the day, and we start the patient on broad-spectrum antibiotics. After that, the patient goes for a CAT Scan. The CAT Scan is really useful for us, it help us not only see the anatomy,
see if the cell is coming close to the external iliac or close to the bifurcation. But maybe even more important, it help us, and you can see the upper emissions, find a lot of needles that have broke and left over by the patients that --
It's a huge hassle for your team in the operating room. So once we have the CAT Scan. We go to the operating room, we get the patient under general anesthesia, we puncture the contralateral side, and this is our preferred method to
take care of this patient. We go up and over, we put the sheath at the end of the external iliac artery, we give some heparin, we do an angiogram that shows exactly where is the injury and we put an occlusion balloon,
usually like a 7 by 60 does the job. Once we have the ballon, we can then ride directly in the pseudoaneurysm. When you open, you take out all the clot and puss and all that tissue. And once you irrigate and debride,
you will see at the bottom, your wound. Usually you see the balloon inside the artery, with a rupture wall, and the proximal ends of the artery. So what we do with with arterial ligation, we resect to help the artery until we gain control, we paralyze vessel loops, remove the balloon
and we do the ligation both the stems and usually we try to preserve the bifurcation. It is a long puncture, it's not possible, we try to preserve our zincuflex, so the patient will have a collateral pathway to their leg. After that, we try to approximate the tissue on top,
or we do an sartorius flap. Now our patient that use black tar heroine, sometimes there's too much inflammation, too much puss, we just put the dressing and we come back in a couple of days for a wash out, to take care of the wound.
After that, the patient goes to intensive care unit, and you will notice that I didn't mention, we ever raise the foot. We don't put any pulse oximeters or do any studies. The foot is going to be okay. The patients usually have some kind of chronic compression
previously and they will tolerate ischemia pretty well. Patient goes to the ICU and the first thing that we do, we avoid hypotension, but we call ID and Pain Service. This patient's outcomes are going to be better if the pain is going to be well controlled, because they will be compliant with the treatment.
ID recommends that antibiotics treatment and helps with management other comorbidities. I know we're starting to have a lot of patients that have PE's during admission, so we try to rule out DVT study and we'll start the patients in treatment.
When we look at our cases, we have more than 50% patient that present with bacteremia, and of those, almost 40% was due to MRSA, so it's a very severe condition that the patient require several weeks of IV antibiotics. Post OP ABI, immediately,
we have a median of 0.41, so the leg is viable. And our amputation rate for these patients is very low. We have only lost 4 legs and of those 4 legs that we have to amputate, 2 patients we revascularized the immediate post-op period and both were infected.
So we actually avoid actively doing revascularizations in the accurate period. In conclusion, the vascular emergencies due to IV drug use are increasing and we as vascular surgeons should be prepared to deal with this and educate our colleagues
on how to treat them. Femoral artery ligation is well tolerated and we recommend not performing an immediate revascularization. The amputate rate is low and ID and Pain Service collaboration is essential for these procedures. Thank you so much.
- Thanks, Germano. Thanks, Gustavo. These are my disclosures as it pertains to this talk. I will be talking about the devices not yet FDA approved in the U.S. for use. We know that with endovascular repair, we need to consider all the aspects
and how we can potentially get this therapy into more people's hands. So, the Gore Company really talked to many of the key opinion leaders about the steps in doing these types of cases, how to make them simple,
they talked about anatomic screening and case planning needs to be thoughtful and careful. We emphasized with them the need to have minimized aortic coverage to limit spinal cord ischemic risk and also to talk about real world applicability
and make sure the device can be used in a wide variety of patients and not in a limited subset. If you look at the other device that has extensive use with off-the-shelf thoracoabdominal repairs, it really involves the t-Branch.
In this case, the device generally requires coverage up through 11 centimeters above the celiac artery. Marcella Ferrara has described ways to limit that with modification of the device but this is it in its current stage. With that, W.L. Gore really came up with a device
that shortened that length. It generally requires about six and a half centimeters of coverage above the celiac artery. It has been designed to work with their balloon-expandable VIABAHN device. You see on the right there,
the device has four preloaded hypo-tubes. That allows for passing four wires in to pre-catheterize each of the branches. That wire system is then brought out through a subclavian access, either right or left, through a DrySeal sheath
that then allows the implantation device in the deployment. The sequential deployment is done with the device being partially open. The portals are then catheterized from above, as you see on the far left,
and the wires placed in that. Once those have been successfully done, the branch stints are placed and then eventually the distal device is deployed and then the distal completion with the bifurcated and iliac components as necessary.
Now the technical aspects of this has been presented at this meeting and has recently been submitted and accepted for publication in JVS. Dr. Oderich is the lead author on this and really comprises the initial 13 implants with the 30-day outcomes.
Now those outcomes really focus on two things, you see the mean procedure time can vary quite a bit. That really depends upon some of the aspects about use of different axillary catheters and thoraco sheaths to get it done. But the other main thing was the blood loss
which can exceed, in a few cases, quite a bit. And that, in this trial, was mainly because they used the 12 French Flexible Cook Ansel Sheath and not the DrySeal. Once we moved to the DrySeal sheath, we see that the number of amount of blood loss
through the central port is a lot less and that's going to limit that in the future trial. Now, currently there have been 16 worldwide implants and this comprises the entire cohort that's been done. You see that early on, we only had access to the retrograde and about a third of the patients
had retrograde renal portals but since that time, mid Spring of 2016, we moved to an anterograde version alone. Most cases are type four thoracos that were done in this initial experience. What about the short-term outcomes?
Well the short-term outcomes are about 18 months. Overall survival 92 percent. One patient presented four months with multi-system failure from three vessels being occluded. The right renal had already been occluded at the time of the initial implant.
Serious adverse events. About 46 percent of patients, which is very typical, acute kidney injury and only 23 percent, and no type one or three endoleaks. There have been seven branch vessel occlusions, four in that one patient that presented acutely,
one patient a year and a half with renal artery occlusions from severe dehydration and one unilateral renal artery occulusion at approximately six months. That was managed with lysis and stenting. No difference in occlusion rates
between anterograde and retrograde. So in conclusion, the TAMBE device has completed its feasibility study with similar results for complete endovascular repair of thoracoabdominal aneurisms. Longer follow-up and a Pivotal study are planned
in pursuit of FDA approval. Thank you.
- Good morning. Happy to discuss with you some of the issues of the currently available stents. Nutcracker Syndrome patients most frequently present with left flank pain, pelvic pain, hematuria, usually due to a significant narrowing in front of the aorta between the aorta and the superior mesenteric artery.
Open surgical treatment has been kind of a gold standard. Left renal vein transposition done most frequently followed by gonadal vein procedures or even renal auto-transplantation. Renal vein stenting, in this country, has been done using Wallstents or SMART stents.
In our experience, where we reported 37 surgical patients. We used stents only for secondary procedures. Three of the six stents had problems of either migration or in-stent restenosis. There is a systematic review in the JVS-VL, recently published, 180 patients, 7 series.
Interestingly, 175 were treated in China with good clinical results in 6-126 months. Stent migration was observed from 0 to 6.7%, depending on the series. We have seen stent migration, sometimes it's immediately during t
and that's obviously the easiest to take care of. Or immediately after, before any healing, that is also a more favorable situation. The problem is when it travels to the heart. It is not frequent, but it happens.
This is the largest series, 75 patients, stented, 5 of them had migration. Two of them to the right atrium, one of them required a medium sternotomy to remove it. Stents not only migrate, although again it's rare,
but even one patient is too frequent in this series that usually involves young, female patients. Stents in this position unfortunately can also fracture. If they don't fracture, they can thrombos. If they don't thrombos, they can be compressed.
If they don't compress, that's a stiff stent, it practically always will perforate their renal vein because of the arching configuration of the renal vein and because the unavailability of less than four centimeter long stance. So it is a problem.
It can actually cause significant, severe migration, completely occluding the inferior vena cava together with perforation of the renal vein. Obviously these cases require open surgical repair,
and have a chance to remove a few of these stents. Percutaneous retrieval, fortunately, is possible in about 90% of the cases, and sometimes, if it doesn't cause significant cardiac injury even from the heart or the pulmonary artery and
we had several case reports, of stents, especially after the TIPS procedure, early on, that migrated into the central circulation that would be removed with different types of techniques, of snaring and pulling the lost stent into a large sheath,
whether you snare it at the end or you snare it in the middle. There are good case reports. This patient that we had, we could use a balloon, pull it down to the vena cava, and then from above and below, we could remove it
with a large sheath. Current stents, if you really don't want it to migrate, the only option we see is transposition patch and using hybrid procedure to fix the stents in the renal vein.
So, in general, open surgery remains the first line of intervention. Stents have a reported high mid-term success rate but migration, fracture, perforation, thrombosis, restenosis are problems and if you go to the FDA website, you see that there are much more cases than
those that are reported. So what do we need? We need dedicated renal vein stents that are short, flexible, resist fracture and migration, and we need them urgently. Thank you.
- Thank you for the opportunity again to discuss this topic on Angiovac Venous Thrombectomy. A large component of the talk was already completed and very eloquently. But, hopefully I can add a little bit extra. No financial relationships to disclose. This is just, briefly, to reinforce that
there are plenty of guidelines for dealing with medical management for deep veined thrombosis. For invasive treatment the attract trial has brought on additional insight into what's appropriate and certain considerations in terms of risks and benefits. But there's still questions, and so, ultimately, there's,
it's always a discussion about the risks versus the benefits, and the treatment is tailored to the patient. And what happens when you're, when you get to eliminate the risk of TPA, that certainly changes things. Some of the considerations are the severity of presentation,
certainly, like the picture, most of us would treat symptom duration. We would prefer to treat acute if we can. That's at least two weeks, at least for an acute component of an acute on chronic disease. But potentially longer.
Life expectancy, activity level, bleeding risk is what is in the back of our minds, even for patients who have to be heparinized, even if they don't have to be on TPA. And then it's a discussion. So, the patient has to be on-board. So, Angiovac when and where?
So, in general some of the patients whom we've trended towards treating, are those with contraindications. Either relative or a strict lytic therapy, acute thrombus, less than two weeks, but subacute thrombus can also potentially be dealt with, a thrombus that's been there for greater than two weeks.
In general, in terms of anatomic factors, it's really designed to take out intervascular foreign material from the venous system. And, it's generally starting to trend towards the right atrium. Whether it's PEs in-transit, pacemaker lead vegetations,
perhaps at the time of complex lead extraction. There have been additional case reports of tricuspid endocarditis and debulking that. And then large volume thrombus in the intravening cava, and in particular with filter thrombosis, and the cases, such as in the image here, where thrombus extends cephalad
to the filter. But again, all patients with ilio caval thrombus may be considered for this treatment. We had some combined data, that needs to be put forth. But, essentially 23 procedures, between two institutions. Most of them with strict contraindications to thrombolysis,
three of them with thrombus cephalad to filter. But as well, two aortic cases, and one right atrial case. And the results, were technically successful in 19 out of the 23 cases. In four cases, the thrombus was just too chronic, probably wasn't a patient who was, probably a patient
selection issue. And there were two mortalities on the three months follow up. And remember these are some of the most significant and advanced versions of disease. There is a registry data base still,
where data is still being accrued by Dr. Moriarty. But again, the tendency now is to move towards the cardiac, the right atrial, pathology. And most recently there is a series of case reports, on, that pertain to this approach for management of right-sided endocarditis and debulking
in addition to administration of antibiotics. So, how do you plan? A lot of it is just pre procedural imaging, knowing your inflow, outflow, and conduit with ultrasound, CAT scan and MR. A T, TE or a TEE maybe useful to determine if there is a
patent PFO microemboli that could potentially shower during these procedures. And so it's something to take into account. The reports are minimal, but something that be theoretically concerned about. IVC filters are sometimes utilized. Simultaneously,
with the filter placed in the super-renal location adjacent to the sheath. But, it's not necessarily because of the low risk for PE. And then, the crux of the procedure, is venovenous bypass. Typically with jugular, femoral, and, at least most individuals that I talk to who do this,
and myself included, get bilateral, jugular, and femoral vein access. Both for the circuit, as well as, for having additional access for utilizing your tools. Again, the goal is inflow, outflow and conduit. So, this is the proprietary portion of the procedure.
The Angiovac cannula is at 22 French cannula. It's the second generation, the third generation's coming out in a few months, most likely. It fits nicely through a 26 French dry seal sheath. It's got a ballon actuated angled funnel tip. Any reinfusion cannula is adequate, 18 French tends
to be appropriate. And you typically get a circuit with a bubble trap that gets your thrombus. You can run the venovenous bypass for up to six hours, recording into the IFU. And there's heavy utilization of adjunctive tools
to clear the thrombus. So, just some examples, with the a cannula in the right jugular and the reinfusion cannula in the left jugular bilateral, femoral vein access, and this is what the entire circuit might look like. And these are the kinds of results you get.
You get, you do one pass from the top and may do another pass from the bottom. Get your thrombus in the bubble trap and those are the results. So, who do we treat? It's a risk to benefit ratio discussion.
Ilio caval, right atrial thrombus, and mobile intravascular object pathologies. Less than two to four weeks ideally and venovenous bypass with extensive use of adjunctive tools. This was a patient with a super-renal filter
thrombused in renal failure and it all recovered, and the stent was plastered to the side. 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.
- 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.
- 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.
- 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.
- 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.
- 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
- Thank you, and thanks to Dr. Veith for the opportunity to share some of our data. These are my disclosures, some devices presented here are investigational and I want to acknowledge my friend Gustavo, who actually shared some of the slides that we'll show. And I want to reference some of his papers. So a spinal cord ischemia has been presented here
as a devastating complication, after both open and endovascular repair of thoracoabdominal aortic aneurysms. The spinal drains are routinely used to ameliorate the frequency and also the severity of spinal cord ischemia, the problem with this trains is that they may result inherent morbidity and mortality.
Now, intraoperative neuromonitoring has been used to not only monitor, but also to manage potential cases of spinal cord ischemia, this is a study by the group at the Mayo Clinic, led by Gustavo. 49 patients, of which 90% had thoracoabdominal aortic aneurysms, all these patients have spinal drain splice,
spinal cord ischemia was seen in six patients. But interestingly, 63% of the patients had significant decrease in the amplitude of both motor and somatosensory evoked potentials. And interestingly all of these changes came back to baseline except in one patient once
their lower legs were reperfused. However, and despite all of these papers that have, you know, talk about the use of spinal drains for endovascular reparative thoracoabdominal aortic aneurysms against the effectiveness of the spinal drains has not been shown.
And the aim of our study was to assess the outcomes of spinal cord protection without the routine use of spinal drains. We actually has some complications in this report, we decided that we were going to use only selectively in our series, the device is used for this in patients
were all part of a physician-sponsored investigational device exemption, demonstrating branch devices were used including the drainage device. We use a similar protocol as the one described by the Mayo Clinic group, which rely on permissive hypertension maintaining the maps above 90 or 100,
and the systolic pressures above 140. However, as mentioned, we did not place spinal drains routinely, the spinal drains were only considered in those patients that had persistent motor evoked potential deficits, at the end of the procedure. Once the legs have been reperfused, we did not use
conduits, we did percutaneous access in all patients. But of note, we did use endo conduits in all patients that have significant iliocclusive disease, not only to be able to deliver the device, but also to maintain flow to the lower extremities, to avoid distal ischemia. So 34 patients were enrolled in this study,
all patients had intraoperative neuromonitoring, and select spinal drains were placed. 10 patients, 29%, were extent 4 thoracoabdominal repairs, and 24 were extent type one to three. Important all patients with type one and three thoracoabdominal aneurysms underwent a staged repair.
We use in 20% of the cases off-the-shelf device is specifically the debranch, and 80% underwent custom made devices, all these devices were pre-loaded with wires. So, of these patients, 73 were male, 9% Type I, 38% Type II, 24% were Type III,
and 29% were Type IV. We saw significant changes in the evoked potentials in 80% of the patients. In all of them those changes came back to baseline except in one patient, who actually had a spinal drain at the end of the procedure.
30-day mortality in two patients, spinal drain was required eventually in only four patients, that's 12%. One because of sustained changes in the motor evoked potentials, spinal cord ischemia occurred in four patients, in all cases secondary to hypertension. After a procedure, in these cases two were permanent,
the cases had spinal drain splice, however, the deficit persisted, two had transient paraplegia, one resolved with permissive hypertension, and one resolved with a spinal drainage, I mean, the spinal drain was only effective in half of those patients. We did have two cases of intracranial bleeding,
associated with hypertension. So in conclusions, we don't believe that the spinal drains are necessary in all patients. A standard protocol that relies on perioperative maintenance of adequate blood pressure in intraoperative neuralmonitoring is however required.
And we believe that tight blood pressure control is mandatory to avoid possible complications related to uncontrolled hypertension, thank you.
- 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.
- 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.
- [Presenter] Dear colleagues, good afternoon. I present an update on the double-blinded trial on CCSVI Brave Dreams. This is my disclosure. The first data coming out from the Brave Dreams trial were affected by the (mumbles). Where venous PTA did not demonstrate additional effect
on the measure of disability and the new MRI lesion in relapsing remitting (RR) Multiple Sclerosis group at 12 month follow up. The major limitation of the trial is the inefficiency of balloon angioplasty in restoring flow in all the presentation of CCSVI
because in the prime, the flow was restored just in 79% of people. It means in favor of gravity and CCSVI criteria were solved in only 54% of the PTA arm. However, the technique demonstrated to be safe. Pre-operatory morphology affects the effectiveness
of PTA in jugulars, and Giaquinta demonstrated that patients who exhibit hypoplasia, external compression, or longitudinal endoluminal defects did not respond very well to the treatment. And commenting on this, Moneta proposed an additional post hoc analysis focusing
on the PTA responder group identified by Giaquinta in the materials of Brave Dreams trial. So Ladies and Gentlemen, is the hypothesis to be rejected? The CCSVI hypothesis could be considered valid if the subgroup with restored flow
following balloon angioplasty shows benefits compared to the subgroup in which the PTA did not work. So we performed a sub-analysis by comparing the patients with jugular flow not Doppler detectable in upright at 12 months, respect to those
who presented a mono-directional phasic jugular flow. The flow data of the balloon angioplasty arm was matched with a caffeine point, which have accumulation of new lesion on MRI. And the result was extraordinary because 91% of people with restored flow in upright
showed no lesion accumulation. This time the analysis was significant also at 0-12 months where we found 77% of people with restored flow, lesion free. And more than 20% of people protected by PTA were near follow up.
So Ladies and Gentlemen, in conclusion, PTA is safe but restored the flow in favor of gravity in the jugulars in just 79% of patients. However, a post-hoc analysis demonstrates a significant decreased risk of new lesion development at MRI in patients with restored jugular flow
following balloon angioplasty, as compared to those with absent flow and/or to sham. Further analysis and investigation may provide the pre-operatory ID of such a subgroup of responders. Thank you very much.
- Thank you, honored to present this work on behalf of our group at the VA, the Michael E. DeBakey VA in Houston, led by Dr. Kougias. Disclosures are here, Dr. Kougias does consultation for Cook Medical. So compared to EVAR, FEVAR has greater lower extremity ischemic times due to larger sheaths,
visceral cannulation, complexity of procedures. And lower extremity complications have been reported as high as 15%, but there's not been a careful analysis of this. So we decided to look at the incidence of lower extremity sensory or motor deficit
after FEVAR, and to look specifically at lower extremity ischemic time, iliac artery occlusive disease, and lower extremity neurologic impairment after FEVAR. So this is a retrospective study over a four-year period. Early experience with our FEVAR cases was included,
and we generally used bilateral femoral access. Iliac stenotic lesions were dilated when required to allow an 18 or 20 French sheath to be placed. Graft alignment was achieved by centering the graft over at least two sheaths in the visceral arteries
before releasing the diameter-reducing wire. Visceral stents were used for all fenestrations and selectively for some scallops. We used perfusion adjunct techniques selectively, such as antegrade 7 French sheath placement into the FSA or sometimes a Dacron conduit into the common
femoral artery, which allows you to retract the sheath. A primary outcome was neurologic impairment. Secondary outcomes were major amputations and ability to ambulate at 30 days after surgery. We measured continuous lower extremity ischemic time from the time of the large sheath insertion into
the femoral artery until it was removed. If we used perfusion adjuncts, we measured the time from the sheath insertion to the perfusion initiation via the adjunctive modality, and the longest ischemic time for each extremity was recorded. We measured common iliac artery lumen diameters.
It was the distance of inner wall to inner wall, the narrowest segment of each common iliac artery. And we entered this as a binary variable based on eight millimeters. Statistics, we did both uni- and multivariate analysis, and I'll just run through that here quickly.
And we did an interaction model looking at the association between lower extremity ischemic time, size of the residual patent common iliac artery lumen versus neurologic impairment in the lower extremities. So there was 101 FEVAR patients with 202 limbs.
Percutaneously done in 16% of cases, we used perfusion adjuncts based on understanding of the case and how long it was going to take. Conduit in eight cases, and antegrade SFA sheath placement in three cases. The configurations are shown here.
Majority were one scallop and two fens, and the ischemic times are shown there. Operative time was about three hours was the average, but the standard deviation was 122 minutes. You can see the fluid requirements there. We looked at intra- and postoperative transfusions.
Then we looked at patients with neurologic impairment. So there were 18 patients who had some neurologic impairment postoperatively. 12 of these patients has mild sensory loss, eight has complete sensory loss, and only two had motor dysfunction.
The deficits tended to resolve within four days, almost all within 14 days. But we had four limbs with persistent sensory deficits, and only one with a persistent motor deficit. Two patients could not ambulate normally at 30 days. No patient underwent an amputation.
If you look at the univariate analysis, limb ischemic time, common iliac lumen less than eight millimeters, intraoperative blood loss, change in hemoglobin, and total transfusion all seem to indicate lower extremity motor dysfunction or sensory dysfunction.
But on multivariate analysis, there are only two factors: limb ischemic time and common iliac artery diameter less than eight millimeters. If you looked at the interaction model we prepared, if the common iliac artery diameter was less than eight millimeters after about two and
a half hours of continuous ischemia, the incidence of neurologic impairment went up. This went up more slowly if it was more than three hours if the iliac artery diameter is greater than eight millimeters. So, in conclusion, lower extremity permanent
neurologic impairment is very low after FEVAR, but there is a relatively high instance of reversible neurologic impairment associated with two things: extremity ischemic time and the presence of pre-existing occlusive disease in the common iliac artery.
We acknowledge this was a single center study. We weren't able to look at extent of aortic coverage or associated spinal cord ischemia, but we conclude that when you anticipate long ischemic times based on the iliac artery diameter, you should consider adjunctive perfusion techniques.
- 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.
- 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.
- Thank you, thanks to Dr. Veith and the program committee for allowing me to present this morning. My disclosure. So, uh, I think that there's been an abundance of literature over the years that is suggested that venography may have poured diagnostic sensitivity for identifying iliac and, and
common femoral vein obstruction. Uh, in uh published literature, 34% of patients who have chronic venous symptoms of a severe degree had iliac vein obstruction on imagining techniques other than venography such as IVUS with normal venograms and often times
patients have significant outflow obstruction and there are no pelvic collaterals present so this is not a reliable though maybe specific indicator of outflow obstruction. The video study was designed to prospectively compare multiplanar venography vs. IVUS
to address the question if you do enough views on venogram do you find the same lesions that you might detect with IVUS. And we also wanted to look, does the imaging that you do to look for iliac and common femoral vein outflow track obstruction
effect your clinical decision about intervention. These are the patients in the video trial CEAP 4 through CEAP 6. And so 100 patients were randomized in this or not randomized, but rather entered entered this prospective multi-center single-arm study
at 14 sites in the US and Europe. This was half CEAP 6 patients and the remainder were CEAP 4 and 5. The patients underwent multiplanar venography. The site investigator was asked to make a decision about whether there was a significant lesion
and how they would treat that lesion and then once that was recorded IVUS was preformed and then again after the pull back the investigator was asked to make a decision about whether there was a significant lesion and how they would treat it.
We standardized venography with a hand injection in 3 views as noted. A 30 degree RAO and LAO and an AP view and the catheter was placed at the cranial portion of the femoral vein we adopted the standards and the literature
of a 50% diameter stenosis. And venography in a 50% CSA reduction on IVUS as a significant lesions. The uh, study cohort was approximately 43 women. The left leg was the index limb and 2 to 1 ratio to uh, to the right.
The age average 62 and you can see the majority of the patients were CEAP 4 and CEAP 6. What we identified with IVUS is a 21% greater (mumbling) identification of outflow obstruction. Venography was a lot less sensitive
at identifying these lesions and therefor suggesting that IVUS is a more sensitive imaging modality for identifying outflow obstruction vs. multiplanar venography. And when you looked at the core lab over read
this was for both the IVUS imaging and for the venography. And we at first calculated the diameter stenosis for both modalities we saw that with the multiplanar venography you tended to underestimate
the degree of diameter stenosis compared to IVUS and this resulted in missing about a quarter of the lesions that were greater than 50% diameter stenosis. And in part IVUS intended to score the lesions more severe for the same lesions compared to venography and this was statistically significant.
When we looked at CSA measurements from the IVUS system and also calculated off the venography in the core lab we saw again that venography missed about 18% of the significant greater than 50% CSA lesions even with reviews.
And this resulted in a change of procedure in about 60% of the patients there was a change in the decision about whether to treat of not and in 50 of the patients the number of stents changed from either no stent to 1 stent or 1 stent to 2 stents.
So without IVUS your likely under treating iliac and common femoral vein obstruction. This was the uh, rVCSS scores after treatment in this group. On the right here in green is the improvement on the left worsening.
And you can see in large part these patients all improved uh, expect for this outlier here and then some patients there was no improvement and when you looked at a score a VCSS score greater than 4 as being significant at 1 and 6 months there was a significant improvement post intervention.
And we see here in this receiver operating curve that IVUS best predicted clinical improvement at 6 months. And so we see that IVUS was more sensitive accurate for identifying significant lesions and the iliac and common femoral vein segments. It was the best guide for stent intervention
and it appears that if use a 50% cut off either diameter or CSA reduction it best predicts that intervention will lead to an improved clinical outcome at 6 months. Thank you.
- Dear chairman, dear colleagues and friends, it's my pleasure to be again with you. Nothing to declare. In our experience of CCSVI and angioplasty we have more than 1,300 patients with different neurological disorders. Not only MS, but also migraine,
lateral amyotrophic sclerosis, Parkinson's disease, left sided amaurosis. We published our data with an emphasis on the safety of the procedure. We had virtually zero percent of serious complication. What about the clinical improvement?
In fact, we noticed function improvement in more than 62.5% of these patients. And in fact, the group of Pierfrancesco Veroux showed similar between 50 and 60% of the patients restoring the normal blood venous flow. In fact, in their work was shown that the type
of anatomic disturbance, anatomic feature is very important predictor if the flow will be restored by the simple PTA. And the most important into the brave dream trial was also that, in fact, the restoration of the flow was achieved in around 70% of the patients.
And exactly in these 70% of the patients with restored flow like Paulo emphasized already, there were lesion, 91% of them were lesion-free on the MRI, and 77% of them were lesion-free on the six-month. We performed a substudy regarding the hypercapnia
and hypoxaemia of the jugular veins in the CCSVI-positive patients. And what we have described in this 178 patients with CCSVI and 50 healthy control group. In fact, we established that the patients CCSVI-positive the venous sample by the jugular veins was typical
with hypercapnia and hypoxaemia in desaturation, huge desaturation with improvement after the balloon angioplasty in all three parameters. What was the reason for that? In fact, in nine patients of our group we examined, the perfusion, the nuclear perfusion of the brain
before and after the treatment. I'm here presenting non-positive for MS young patient without MRI demyelization. And but on the brain perfusion he had deep hyperperfusion on the left side, and the patient was complaining with deep fatigue.
And we saw practically full occlusion of the enominate vein. And after the recanalization using first coronary and after it peripheral balloons, and in this particular case we had to stent finally. And you see still persistence of a huge crossover collateral even after ballooning.
But after stenting we saw practically full restoration of the flow. You see in less than three to four seconds it was very interesting to see on the perfusion imaging, nuclear perfusion, full restoration of the flow of this gentleman.
So this is very important to emphasize that there is direct relationship between the blood gas disturbances on the brain level, and demyelinization process. What about the PTA? It's probably not the optimal treatment.
We have to establish reliable clinical and anatomical predictors for vascular and clinical success in order to answer the important questions: who will be vascular responders, or MRI responders, and finally the clinical responders in this group of patients?
And concluding, ladies and gentlemen, the CCSVI is a real vascular pathologic entity and is probably a trigger for more than one neurologic degenerative disorder. Endovascular treatment, balloon, PTA, and stenting of CCSVI is feasible and safe.
Methods and strategies improving the early and late patency rate have to be elaborated because the good clinical result is strongly dependent on the vascular patency and flow restoration. And thank you very much for your attention.
- Thank you, Dr. Veith. Mr. Chairman, ladies, and gentlemen. I've no disclosure for this talk. However, one of the co-author is a consultant for Cook Medical. We know that the endovascular treatment for rapture thoracoabdominal aneurysms is increasing lately.
And with the great advantages, in term of, mortality and morbidity, particularly, if we consider pulmonary morbidity. Given these results, endovascular treatment has been employed these several centers and as you can see, some of these centers
used technique with a t-Branch endograft device. As you have seen this morning in different presentation, the Zenith t-Branch device is a four-branches device with branches for the visceral vessels is a 22 French delivery system. And as you can see here, there are branches
for all the visceral vessels, specifically SMA, celiac trunk, and the two renals. This kind of configuration allows you to treat cases like the one you can see now. The other case of rapture which is shown in this slide here. So what we have to see if there is an anatomical suitability
of t-Branch stent-graft and the results, we can obtain in this setting. Obviously, we have to perform a plan according to the characteristic of our t-Branch device. And according with these characteristics the eligibility criteria
in the normal TA thoracoabdominal aneurysm is up to 88%. However, if we consider rupture cases, these eligibility can be as low as 22% with some papers describing 33% anatomical suitability. In our series, we have a 40% possibility of accommodating these endograft.
So the results we can obtain are shown in these next slides. As you can see, we have 17 cases treated urgently. Of those, four had a contained rupture. Other four were symptomatic and nine cases had a diameter greater than eight centimeters. These cases has been described in this study
published last year in Journal of Vascular Surgery. And we had a technical success of 75% only in the ruptured cases. One case was not accomplished due to inability to cannulate the renal artery. I show you that the this inability
was caused by different orientation of the renal artery. We described different kind of orientation with possibility of cannulating them in a paper published this year in a European Journal of Vascular and Endovascular Surgery. There were three cases of reintervention at 30 days as you can see here.
And again by putting together all the cases treated in a multicenter study performed in Italy, the there is a quite good survival overall in thoracoabdominal aneurysm treated by endovascular means. However, the survival in patient with ruptured aneurysm is significantly lower as everyone can expect.
So in conclusion, we see that the emergency treatment with t-Branch is technical feasible in many instances and in ruptured cases there are a number of anatomical obstacles, which can violate the suitability of the t-Branch device. However, with the adjunctive devices and team experience,
we can overcome these obstacles and get good overall result in this difficult setting. Thank you for your attention.
- 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.
- 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.
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