- [Diego] Good morning, ladies and gentlemen. I'd like to thank you very much for the opportunity to present this topic: the complete endovascular aortic arch treatment using the transapical approach. These are my conflicts. As you may know, open surgery is still the gold standard for treatment of aortic arch disease.
But it requires a lot of steps, like deep hypothermia, circulatory arrest, and some kinds of brain cerebral protections. And even in a skew for hands, mortality can be as high as 12%, making it prohibitive in high-risk patients. Over the past few years, Tevar have become
the gold standard in treating descending lesions like true aneurysm, and dissections over the last few years. But the arch is still a frontier. In order to overcome these, a lot of alternatives have been proposed, like debranching, parallel prosthesis, single branch, in situ physician fenestrations,
and many others. Besides that alternatives other drawbacks is to persists like the endoleaks, migration, risk of retrograde type A dissections, femoral access problems, the need for open sternotomy, axial adjustments, and even aortic clamping sometimes is required
for that type of correction. In this scenario, a lot of companies have proposed some kind of branched prosthesis. But even then, a lot of limitations still persist, like stroke, coaxial adjustment, incomplete arch reconstructions, access problems, and the need of
cerebral blood flow maintenance during implant. So what could be the ideal solution for the arch? In our opinion, the ideal solution is a complete endovascular aortic arch three branch treatment using a transapical approach from Braile Biomedical. But why transapical?
Because transapical is in close proximity to the arch. The coaxial adjustment is easier, branch connection is easier, access to the branches is also easier, besides being more invasive when comparing to the transfemoral approach.
So what's the clinical scenario of this case? It's a 70-year old female deemed at risk for conventional surgery due to multiple risk factors, who have dissection lesions on the ascending and descending aorta as you can see here on the computer tomography and on 3D reconstruction.
The workflow for the case was that. Computer tomography was imported in the DICOM file inside OsiriX, and then exported to an STL file allowing us to print a 3D model of the aorta of the patient, and based on the 3D model we built a custom prosthesis with three branches
of the arch. A total of 40 days from the computer tomography to the final prosthesis model. The surgery was performed in a hybrid OR using a transapical and a transfemoral access with brachial and carotid punctures in order to aid
the navigation of the guide wires, and everything on TEE Echo monitoring, especially to monitor arch insufficience during the pass of the introducer sheath. These are deployment key steps. Here we can see the deployment of the main body
as low deployment without pacemaker. We can see that there are radio-opaque marks that define the branch for the left subclavian for the left carotid, and for the brachiocephalic trunk. Here we can see final deployment in this low fashion of the main body of the prosthesis.
Here we can see the transducer coming from the apex and a pigtail coming from the femoral artery. We can also see on the other video the catheterization of the left carotid artery. And then the deployment of VIABAHN to connect the left carotid to the main body of the prosthesis.
After that, a second VIABAHN was introduced through the apex as you can see here in this video connecting the brachiocephalic trunk to the main body again. On the next video you can see the deployment of the second VIABAHN with two thirds of the arch completely reconstructed now.
And on the next video you see the positioning of the last VIABAHN connecting the left subclavian artery to the main body of the prosthesis. The final angiography show the three branches connected to the main body with no endoleak, and a second main body treating the descending lesion
on the descending aorta. This is the final control computer tomography. We've no endoleak, the patient discharged after two days, and this computer tomography's for one year followup. As you can see here, no endoleak, and all the three branch splendid.
So transapical total endovascular aortic arch reconstruction's feasible, a faster recovery, decreased length of stay, and is really an alternative in high-risk patients. In the future we'll be now total endobental procedure that will be done on the next few weeks
in South America allowing us a new frontier in endovascular treatment of ascending aorta and the arch. Thank you very much.
This is basically kind of your anatomy in hemodynamics.
Celiac axis gives supply to the spleen, gives supply to the hepatic artery, and there's increased flow to the spleen for some reason. Then flow goes back from the gut and spleen back to the hepatic graft by the portal vein. This is kind of your general circulatory
kind of hemodynamics. What the Japanese for years have been talking about was a small for size graft, a completely different syndrome, called small for size graft. In other words the liver is actually too small
for the amount of portal flow that's coming to it. It's an undersized graft. So for example, a transplant in a kid put in an adult. The liver is too small for the amount of portal flow that's actually coming at it.
And what they found out was that there was slow flow in the hepatic artery as well, and they didn't know how that went about. So for years, the Germans were talking about splenic steal, and the spleen is stealing blood flow, the Japanese were talking about
there's a small size graft and there's increased portal flow, but as a coincidence we're looking at hepatic or slow arterial flow. Then, kind of the Americans came along and actually put it all together for them. This is probably a constellation of syndromes and problems
that are occurring at the same time. One can predominate, one can be the only sole problem, or it could be a group of problems. What happens when you increase flow to the liver by the portal vein, there is actually something
called the HABR, the hepatic artery buffer response. This is a partly-reciprocal, poorly understood relationship between the portal vein and the hepatic artery. If you increase portal flow to your liver right now when you eat, if you take a big meal,
portal flow will increase to your liver and your hepatic artery's gonna slow down, because 20% of flow to the liver is from the artery, and 80% goes from the portal vein. If you eat a lot, your portal vein flow increases, your hepatic artery compensates by dropping down to
maintain that flow to the liver. That's kind of a partly-reciprocal relationship. So when you put a small graft in a patient, with relatively high flow, too much flow for the portal vein, the hepatic artery slows down. Okay?
So this is not just a steal phenomenon, this may also be a response or a reflex response to a high flow situation. The graft- and just to add a little bit more detail to this- the graft could be small, or the graft could be non-compliant and poor.
A poor graft, as well, can do the same thing. So it could be a big graft that's not functioning that well, and/or stiff, that would do the same thing as well. Okay? So increased portal flow, decreased hepatic arterial flow.
in that case. The next subject, which is splenic steal syndrome, which is a very complex subject.
Splenic steal syndrome, or NOHAH, that's non-exclusive hepatic artery hyperprofusion basically means that the hepatic artery's open, but there's slow flow in it, so it's not anatomical. This is a hemodynamic problem. It is not an anatomical defect.
It's not a thrombosis, it's not an aneurysm, it is not a stricture, it is not a kink. The artery is a wide open pump, but flow is going through it very slowly. The idea on this is to go as proximal as possible and is to impede flow, slow down the flow,
not necessarily shut it off, but slow down the flow significantly. Go proximal as possible to allow collaterals to keep the spleen alive. It is not a splenic artery embolization where you use particles.
Sometimes it is so tortuous that we can't even get a microcatheter across, and that's a problem. So what do we do there? In the old days, if you can't do that,
and you can't cross the aneurysm then the best way is to actually puncture the aneurysm self-percutaneously and put coils and thromen through the needle as well. We've been able to reduce the incidence of that by doing the Fong procedure, which is not, it's kind of like a cowboy way of doing it,
but it actually reduces the amount of times that we actually have actually gone to actually percutaneously puncture the aneurysm. What we do is we actually use glue. We actually use a very thick glue. And what we hope for is that we deploy this thick
glue plug and let it run in the aneurysm, go to the distal end and actually plug the distal splenic aneurysm-- splenic artery. And that is basically your distal coil equivalent. And then you put coils or glue to finish it off. And most of the time it works, sometimes it doesn't.
And when it doesn't, sometimes you kill the spleen. They key thing is to make thick, thick glue, okay? I know it's kind of like, 60% of the time, 100% of the time it works, or something like that. But it's pretty hairy, but we've been able to do that with minimal complications.
A thick glue, 1:1, fire it as a plug, it rotates through the aneurysm, goes distally, and then you actually coil it or glue proximally. This is an example of that. Large aneurysm. This is actually the inflow artery in the red arrow,
the outflow artery out of the aneurysm is the other red arrow, the smaller arrow at the top. And then there's another branch sneaking proximally around the aneurysm, not involving the aneurysm going to the spleen. That's good.
That's a good sign. There's a nice collateral that can grow, that actually can revive the spleen if you take out most of the spleen. That's the distal pancreatic tail. We were unable to cross this aneurysm. In fact we were barely into that aneurysm.
What we did was just deploy that thick glue. Sorry guys, it's not working for me here. This is what we have. This is actually that little piece of glue is actually in the distal outflow artery, okay? And the rest of it, this is actually in the inflow artery,
and we basically excluded this with just purely glue, without any coils. This is the kind of follow up imaging of the patient with an excluded aneurysm and a largely live spleen by actually excluding it this way.
- [Presenter] I will share with you some tricks, what do to when the complex stent grafts fail intraoperatively and this will be mainly about accidentally over-stented side branches of the aorta and about intraoperative leaks. When it comes to the over-stented side branches, this, I believe, is the very first chimney graft ever
in 1999, in Gothenburg, where we over-stented the renal, and that chimney stayed patent throughout the life of the patient, which was 14 years. We then used the technique on numerous occasions in the arch where we happened to over-stent the common carotid artery.
Because it is so simple to place a chimney on such occasions, it is definitely simpler than any of the open external carotid bypasses. Although, they are also seemingly simple in the neck. Much simpler in the abdomen. But still, I've seen all the various complications
from that type of procedure. When it comes to the renals, it happens when you place stent grafts very accurately that you over-stent the renals, and on most occasions, you will be able to use that same chimney technique from below
coming back into the renals, placing coverage stents, and opening up the renal arteries. But it's a different ballgame when it comes to the complex stent grafts, the fenestrated and branch stent grafts. Here's a quadruple fenestrated stent graft
where the renal arteries have been successfully cannulated through the fenestrations, and so has the celiac trunk, but the SMA seems gone, and we were unable to pass the wires through the SMA fenestration. On this occasion, it was, however, possible to go outside the stent graft, and park a long chimney
to re vascularize the SMA. That is the antegrade chimney. In this fenestrated stent graft, again, the renals are fine, but the SMAs are gone. And here it was impossible to go outside the stent graft from above,
so here we did a retrograde chimney by laparotomy where a branch of the SMA was isolated and then punctured with a micropuncture set, passing an 018 wire retrograde into the aorta prior to the aortic stent graft, snaring it form above. And then, over there to body-floss wire,
inserting a chimney with this type of end result. When it comes to the renals, again, the retrograde chimney technique can be used in a similar manner. Here is the Medtronic stent graft that was excellent to displaced cranially because it wouldn't detach
from the deployment mechanism. And both renals were over-stented. We were unable to get back into them from above, and instead, via laparotomy, renal artery was punctured, cannulated retrograde into the aorta, snared from above, and chimneys were inserted from above
with this type of end result. And this is one year follow-up of that particular patient. I think this offers less trauma than open various surgical solutions to that difficult problem. So when it comes to the over-stented branches,
I think you should avoid drastic bypasses, they are too much of a trauma. Chimneys and snorkels are an option in this difficult scenario. You can use retrograde puncture via laparotomy if you can't get back to the aortic side branch.
And this is a durable technique with less trauma than open surgical repair. The other thing I want to discuss was leaks. Even after the complex stent grafts, you do see leaks. You then may need to extend the stent graft. The problem here is you have the fenestrated branches
protruding into the aortic lumen. It's not just renals, it's also the SMA branches, etc. It's not so easy to place a fenestrated stent graft into this type of device. And here again, the snorkle technique, the chimney reversed technique,
is an option, which you then can over-stent to extend your device. Another option that we have heard about when it comes to the dislodged branches that simply fall out, I think Tim Chuter mentioned this,
in this type of scenario, usually you are able to pass a wire back in and then extend the branch into that target vessel. The problem now is that the renal arteries are short, and you tend to get relatively deep into the renal artery. Then you create that type of kink
that Tim discussed beautifully, and the routine treatment for that today is that you extend with a soft bare stent. The problem with that, again, then, is that in this scenario, you get pretty close to the hilus of the kidney,
and I believe that this, probably, is risk for late thrombosis as is mentioned by other speakers. So, in conclusion, ladies and gentlemen, when it comes to bailout of the complex stent grafts, I don't think you should primarily do massive open surgery. When it comes to over-stented branches,
they can usually be fixed with chimneys or snorkels, antegrade or retrograde. And when it comes to the leaks, you need to re-line or extend the stent graft, which then again can be facilitated by the chimneys. Thank you for your attention.
- [Henrik] First of all, thank you very much to the organizers, Frank for bringing me back to this lovely city. So whereas the Doppler velocity measurements for assessment of stenosis is very reproducible, imaging of carotid plaques is actually not. So what's the value of plaque morphology? Interestingly, the signal in plaque morphology is so
strong that when we test at first assessments, it's actually quite good and we see there is some evidence behind it. But if you look at morphology over time, it's not so good. And the reason is the impact of what's called the fixed elevation focus just like when you focus your camera
to make a certain image sharp, the same thing we do with ultrasound. Meaning that we only see a thin slice of the carotid artery as illustrated here. And for instance if you're going to scan this patient, what you see with this angle is nothing, and then with
the patient turns his neck a little bit, you're going to see this plaque. So this is the caveat of reproducibility of 2D, that's why we need 3D. And actually 3D is not new, David Spence's group has been pioneers in this and used it for 10 years, however,
their equipment has been research equipment. You can see handheld 3D on the top left, which is not really good for daily practice. And that equipment is actually getting out there now. The transducer seen in the middle is a so-called matrix transducer where you can do volume imaging
in real time. And what you get is, for instance, two planes, simultaneously that you see here. So when you want to do volumes, you simply do tomography like you do with a CT and you can calculate the area of the plaque in each cross section, and if you know the
distance in between, you can calculate the volume. The problem is, where does the plaque begin and where does it end? And if you look at this image, you can see it's not that easy to define where it begins and ends. So we did some work on this and I'm going to give you
the short story. This is what we ended up with, defining a patch of plaque volume centered around the thickest part, calculated from the true center line derived from the 3D image. And this work is being published in the Ultrasound in
Medicine and Biology, where we looked at the volume defined one centimeter around the thickest part of the plaque, we had two investigators scanning 37 plaques. They were blinded from each other's findings. Patients were standing in between exams. And the ultrasound machines were reset.
And you can see this very very nice correlation in these 37 cases. I will admit that there was some selection because cases with calcification were omitted from this analysis. So, looking at the declining stroke risk in asymptomatic stenosis, it is down to below 1%, and in a recent study
from Kansas where they looked at 860 patients followed over six years, all with carotid stenosis, they found that patients who were optimally treated for risk factors and preventive medications had a combined stroke TIA and revasc rate of 0.6%. It's almost gone guys.
And we in the BioImage Study for scans 6,000 Americans and followed them for three years, and among those 6,000, there were 349 with carotid stenosis, and over four years, sorry, three years, four people develop a stroke, only two of them being ipsilateral. But a lot of them had cardiovascular events.
So asymptomatic carotid stenosis has very very very low risk of stroke, but a high risk of cardiovascular events, so therefore it's very important with the aggressive medical management. It is difficult to see where carotid endarterectomy and stenting has its place there today, unless of course,
high risk plaque can be identified. So 3D is a game changer because plaque volume can be reliably measured. Plaque volume may be the new surrogate to observe and follow. It allows for accurate repeated measurements,
plaque morphology can probably be assessed accurately and followed over time. Thank you for your attention.
- [Robyn] Good, morning, thank you, Dr. Veith, for asking me to speak. I have no disclosures over 40,000 people in the United States annually are diagnosed with head and neck cancer, 75% of these patients undergo radiation therapy. Almost 80,000 patients in the US population annually
are diagnosed with lymphoma and about 20 to 30% of these patients undergo radiation therapy to the head and neck. This gives us about 50,000 patients annually undergoing head and neck radiation. With a 25% incidence of carotid stenosis
we are diagnosing about 12,500 patients with radiation arteritis annually. This occurs due to direct endothelial cell damage from the radiation beam, which then causes platelet aggregation, fibrin deposition, obstructed capillary lumens,
and vaso vasorum, focal necrosis, and finally extrinsic compression and luminal narrowing. Patients present similar to atherosclerosis with asymptomatic disease or TIAs and strokes. Recommendation is to screen these patients with ca
there is currently no consensus on when this screening should begin after completion of the radiation therapy. Most physicians recommend five to 10 year later. Once a patient is diagnosed and if surgery is considered,
due to the uncommon location and diffuse lesions of these radiation arteritis patients, patients should undergo either MRA, CTA, or catheter-based arteriogram for preoperative planning. Management options include medical management with traditional risk factor modification
and surgical management should be considered in patients with a symptomatic lesion greater than 50%, an asymptomatic lesion greater than 60%, or deemed to be a low peri-procedural risk. However, due to the more stable morphology of radiation arteritis, most asymptomatic patients
should wait until about 80% stenosis. Looking at the Society for Vascular Surgery guidelines pertaining to carotid disease, they find that a history of neck radiotherapy, the resultant local fibrotic changes of the skin and soft tissues, to be an anatomic criteria
to consider carotid stenting. However, they do feel that carotid endarterectomy remains a safe option. When deciding between carotid endarterectomy and carotid stenting there are many anatomic and physiologic factors to help make that decision.
Carotid endarterectomy should be favored in patients aged greater than 70, those with a type III arch or severe arch calcification, those with carotid artery tortuosity, severe plaque calcification, ulcerated plaque, near-occlusive lesions or extensive lesions.
Carotid stenting should be favored in patients with a history of prior neck radiation or radical neck dissection, those with a tracheostomy, those with prior carotid endarterectomy or cranial nerve injury,
those with a common carotid artery stenosis proximal to the clavicle, or distal internal carotid artery stenosis distal to C2 and those with a large amount of cardiac comorbidities. If carotid endarterectomy is decided upon there are several technical tips we can recommend.
First, given the difficulty of dissection, general anesthesia is preferred. The groin should always be prepped for potential greater saphenous vein harvest, particularly if the patient has a tracheostomy or previous extensive neck dissection.
A longitudinal neck incision is preferred for the ability to extend either proximally or distally. The surgeon should anticipate a more tedious dissection and take careful time to identify the cranial nerves. Once starting the operation the surgeon should anticipate that possibly the endarterectomy plane could be obliterated
and they may require a common to internal carotid artery bypass with greater saphenous vein. If there is significant involvement of the common carotid artery a subclavian to internal carotid artery bypass maybe done with PTFE,
and the patient may need a myocutaneous flap for coverage at the end of surgery. If carotid stenting is considered, the procedural steps are identical to that used for atherosclerosis. However, the surgeon should anticipate,
due to the extensive nature of the plaque, that multiple stents may be required and there's a higher occurrence of filter clotting. Looking at results for carotid endarterectomy, most reports are single institution case reports or case series.
All of them have similar results showing 30-day stroke and death rates ranging between zero to 3%, which is similar to that what we see for atherosclerosis. However, cranial nerve injury rates up to 22% and wound complication rates up to 8% are higher. Of note, in patients that do have cranial nerve injuries,
similar to atherosclerosis, they do resolve in about six weeks. Looking at results for carotid stenting, again, these are single institution case reports and case series and show similar results for death
and stroke rates at 30 days of zero to 9%, which is similar to what we see for atherosclerosis. Here we don't have to worry about cranial nerve injuries, and we do have some groin complications, about 6% of the time. A meta-analysis was done by Davies
that showed similar results with asymptomatic and symptomatic carotid stenting and carotid endarterectomy having similar stroke and death rates at 30 days. However, there is a higher rate of re-stenosis and re-intervention, and most deaths were related to the original cancer.
In conclusion, both carotid endarterectomy and carotid stenting are technically feasible in patients with radiation arteritis. Both carotid endarterectomy and carotid stenting are just as safe as in patients with atherosclerotic disease,
and while considering carotid intervention the patient's oncological prognosis should also be considered. Thank you.
- [Henrik] Thank you very much, thank you Frank. I don't know what I did to get that title, for it's certainly long. If some of you were here 6:40 this morning you may recognize some of the slides, because I had a similar title at that time. The risk of stroke in asymptomatic patients
is low, and you can see from this publication that shows the annual risk declining, with the year of the publication. Just a few months ago there was this publication from Kansas where a group looked at 864 with 1400 Stenotic Carotid arteries,
followed them for seven years, and they looked at how many goals of risk reduction were accomplished, and you can see that the step-wise reduction in the black bar, which is the combined end point of Stroke TIA or Carotid Revasc, how that is lowered
from 3.5 to .6% annually if you reach all the goals of healthy lifestyle and take the right drugs. Interestingly also looked at how the risk of stenosis progression similarly was reduced step-wise. They concluded that the risk of TIA, Stroke and Revasc becomes extremely low if risk factors are treated
appropriately, and I would say progression of carotid stenosis is a sign of insufficient risk factor control, and preventive treatment rather than sign of increased risk of stroke. And similarly, we looked at 7,000 patients in the bio image study, where we scanned the carotids,
and we found that 6% had a carotid stenosis, they were followed for three years, and four had a stroke, of which two were ipsilateral. However, a lot had cardiovascular events, which we know. For Asymptomatic Carotid Stenosis, very, very low risk of stroke, maybe .3 to .4%.
It's a high risk of cardiovascular events instead, so therefore, it's very important with preventive treatment and the lifestyle adjustment. And Carotid endarterectomy, or CAS, in general is not warranted, unless a high risk plaque can be identified, of course.
And together, with one of the Chairman, we looked at that a couple of years ago, and published in European journal, and notice how stenosis progression is actually the least important of those listed here. However, these data are also ancient since most of these studies included patients that were gathered
or investigated 10 - 20 years ago, so the risk today is probably less than half of what is shown there or maybe even less. Presence of Carotid Stenosis does not tell it all. We need 3D Ultrasound. And the previous speaker
is a pioneer of this and up in the zeros, published a number of papers, and this is just one of them, using a research tool as you can see in the top left, is handheld, but demonstrated to be very reproducible, but now we can get these as what's called Matrix Transducers where we instead of having just
one array as you see here, we have multiple arrays in both dimensions, and therefore we can do volume imaging, or we can have two plain simultaneously as you see in this slide. We recently looked at how accurate can you measure plaque volume using an instrument like this, and it's simply
tomography as you're used to with CT, you take slices and you look at the area in each slice, you know the difference, sorry the distance in between you can calculate the volume. We did that, and this is what came out when we had two blinded investigators scan the same 37 PAD patients.
The patient was up standing in between exams, the ultrasound machines was reset, so this is fully blinded two independent acquisitions. This is actually much more accurate than if you do two LDL blood tests, what you see here. I shall admit that these patients were a little bit
selected because patients with calcified plaques were excluded. 3D will improve plaque qualification, both volume and morphology. Assessment of degree of stenosis, will be better because the angle-compensation can be done
more accurately in 3D. Speed of examination will increase, and will be more easy to perform a good scan. What can we use it for? For risk assessment in carotid disease , who to operate will be more accurate, we can do better morphology
using this technique, and we can also monitor if we treat the patients appropriate with general prevention. Is the plaque stabilized? And maybe more important, has the atherosclerotic burden stopped growing, and I would suspect or expect
that this method may replace LDL measurement in the future when you want to see if the preventive treatment works. Thank you for attention. (clapping)
The treatment of this is the same. It's to break the cycle.
And the best way to break the cycle is a splenic artery embolization. You embolize the spleen, whether it's gonna be steal, you're emnbolizing the splenic artery. Whether it's portal flow, increased flow, or a liver that can't handle portal flow,
you still embolize the spleen to actually close the circuit and reduce that portal flow coming back to the liver, and both work. So all what I told you as far as the complexity and the reasons is actually academic. The treatment is the same.
It's splenic artery embolization. As proximal as possible, to allow as much collateral. This is what we've done here, where we've embolized the spleen proximally. I'll show you this. This is just after an embolization.
You see numerous collateral left gastric hiploic arcade reviving the spleen. The spleen is alive and well. We've embolized it. This is before and after. This is a true splenic steal procedure,
before and after embolization, frame for frame. Same injection rates, same catheter, same catheter position, same frame rates, no cheating, okay? Frame for frame. You inject, and you actually see initially there's
absolutely no flow in the hepatic artery, now you've got more flow in the hepatic artery, running almost parallel with the splenic bed. You've basically tilted that back towards flow in the hepatic artery, regardless of what the cause is.
Is it a big spleen that's stealing blood? Or is it a graft portal, you know, scale problem? These are just some pretty kind of hemodynamics analysis of what gestalt I just showed you on different slides of increased flow to the liver and decreased flow to the spleen.
Next approach, which is the most common approach and the most technically feasible approach usually is to actually cross the splenic artery,
go distal, coil embolize the spleen, splenic artery distal to the aneurysm and then pull back and coil embolize proximal to the aneurysm itself and that's the most common one and that's the most technically feasible because you can do that with more flexible, lower platforms with microcatheters and catheters.
With younger physicians, I'm gonna show you a procedure. You will find that they're actually coiling in the aneurysm itself and putting a lot more coils in the aneurysm itself, which there's nothing wrong with that, you're just putting a lot-- too much coils in procedure. But ideally, this is what you need to do.
And the reason for that is you need to go as distal as possible in the splenic artery, but just proximal to the aneurysm to provide collateral flow to actually circumvent or bypass the aneurysm and actually continue to revive and keep the spleen alive.
That's basically the whole idea of doing this. The distal embolization is for prevention of back bleeding from these collaterals. So whenever you're embolizing in any celiac axis branch, it's not only the splenic, it's the splenic, the hepatic, the GDA, pancreatic audidenal,
you always have to embolize, whether it's a bleed or an aneurysm, distal and proximal because of all those collaterals and that back bleeding that you actually will pre-fill or re-bleed from the bleed, so this is a typical example where you don't have to go distal to prevent that back bleeding from
filling up that aneurysm. This is an example of a very tortuous splenic artery, with a large splenic artery aneurysm, with an eggshell calcification. So this is the aneurysm here, and what they did was embolize right across the splenic aneurysm from distal
in the aneurysm as well as proximal. And that's the aneurysm kind of excluded.
- [Hosam] Thank you Dr. Ouriel, thank you Dr. Veith for inviting me to present on this subject this year. No disclosures. This is a very big problem that is growing in our population. We have over nine million Americans who are above 80 years old.
And if we do the math, we should have in between 100,000 and 200,000 patients with critical limb ischemia that we have to deal with in this age group. This patient group is different compared to the younger population,
where there are multiple comorbidities, high morbidity, and mortality whatever intervention we do to them. They have a short life expectancy and other, that's why other parameters like pain control, maintenance of independence and maintenance of ambulation
might be as important, if not more important, than just limb salvage and patency. Questions we're trying to answer today is: Is it worthwhile trying to vascularize those? Is it different revascularizing infrainguinal from infrapopliteal disease?
And is it bypass is better or endovascular is better? To answer the first question, multiple series have shown that revascularization is effective improving symptoms, quality of life, and limb salvage when compared to conservative therapy in this age group,
and actually, this might be comparable to non-octogenerian, and sometimes and even better. This is a study that was done back in 2007 following over 400 critical limb ischemia patients, some of them were octongenerians, some of them were not.
And they found that regarding functional status and limb salvage, conservative therapy was worse compared to revascularization, but the benefit that the octagenarians got was actually better than non-octogenarians.
When it comes to primary amputation, definitely primary amputation is associated with loss of independence and ambulation. But when it comes to survival, the picture is not as clear. Some of the studies
showed poorer survival following amputation compared to revascularization. Other studies showed no difference, but some other studies actually showed there is a survival advantage for patients who get an amputation.
My answer to that is maybe these patients are not created equal. Some of them are so sick that they should not get a revascularization procedure. Infrainguinal compared to infrapopliteal disease, it was found that infrapopliteal revascularization
is as good as infrainguinal revascularization in that age group. And some studies actually showed that infrapopliteal revascularization in that age group are better compared to non-octogenarians
when they have the same intervention. It appears that the level of disease does not alter the amputation-free survival or a patient's survival. Now, the big question is open versus endo. We do not have an answer to that yet.
Like any other patient, we have no available level one evidence. Most of the studies that are bias prone studies and that's because the question is very complex. Many factors are involved. Perioperative morbidity and mortality,
limb salvage, patient survival, and quality of life and functional status. When it comes to preoperative morbidity and mortality across the board they are kind of similar, they are much higher than non-octogenarians. Most of the series will show that
morbidity and mortality are higher in the bypass group compared to endovascular. Some studies showed no difference, but actually there is a study, it's a population study, that shows that endovascular in this particular age group
have actually a higher risk of life threatening complications compared to bypass. When it comes to long term survival, again, long term survival is dismal in that patient, and some studies show
that the survival is better in the bypass group but this might be because of the bias selecting more fit patients to get that kind of therapy. And it appears that the mere age and other comorbidities are more important than the type of intervention
for long term survival. When it comes to limb salvage, due to the short life expectancy, death is actually more common than amputation in that age group. So there is no real effect
of the type of therapy on limb salvage. Some studies show the bypass have less limb salvage in those patients but this might be, again, due to bias, selecting more patients who have gangrene and doing that. Meta-analysis shows no difference
between the two interventions. For the functional status, any intervention we do will lead to reduction of the functional status and gradual recovery from that. The reduction is more in the bypass group
and the recovery is actually also more in the bypass group. That makes it complicated. So in conclusion, ladies and gentlemen, the critical limb ischemia in octogenerians is a growing problem.
Revascularization is recommended whenever possible. Primary amputation is the way to go for selected non-ambulatory patients. Level of the disease should not change the treatment decision. Open versus endo,
we do not have an answer for that yet. Meanwhile, common sense and sound clinical judgment should be the tools to be followed until we have the results of the basal two trial and the best CLI trail. Thank you very much.
- Okay, so I never knew that there was so much controversy about statins this weekend, but I love this cartoon. "We found a bunch of these clogging your arteries. They're cholesterol pills." So statins in CLI. There's extensive evidence of statins lowering
cardiovascular events and mortality, however many studies do not necessarily differentiate between symptomatic PAD and CLI. The use of statins in patients undergoing revascularization is clearly recommended. They may reduce the need for revascularization
and my improve the outcomes. Reduction in amputation rates has not been consistently shown. So what about statins and mortality in PAD patients? Well, here's a randomized study from 2004, clearly showing that short-term treatment
with atorvastatin reduced the incidence of major adverse cardiovascular events. Another study from Dr. Schanzer in 2008, this one really concentrating on critical limb ischemia patients, showing that statin use was associated with improved
survival after revascularization. The DECREASE study in 2009, another randomized study again showing markedly improved perioperative outcome in vascular surgery patients. A study from the JVS in Vascular Medicine in 2014
noted significant difference in amputation-free survival survival in patients who presented with CLI in their study. And finally, in 2015 in the JVS, the study's showing that statin therapy after infrainguinal bypass surgery specifically for critical limb ischemia was associated and proved that five-year survival.
And here are the Kaplan-Meier curves from that study. What about limb and revascularization related outcomes? Well here again, there is an enormous amount of data to talk about. This study in 2004 showed that statin therapy was associated with improved patency of
autogenous inguinal bypass grafts, the risk of graft failure was 3.2-fold higher in the control group. And you can see here the Kaplin Kaplan-Meier curves from that study. Another study again, concentrating on specifically
critical limb ischemia, a retrospective review of 646 patients, and at 24 months, the statin-treated group had higher rates of primary patency, secondary patency, limb salvage and overall survival. You can see her the curves for primary patency, secondary patency and limb salvage
which were all significant. Over here, using multivariate regression, the odds ratio for statin use with the limb salvage was quite high. Dr. Voglin, circulation in 2013, studied the Medicare database as we've previously seen
and this included all patients with different types of PVD. And the conclusion here was that preoperative statins were again associated with improved one year limb salvage after revascularization. This was better for the diagnosis of claudication and rest pain or ulceration or gangrene.
The REACH Registry Symptomatic PAD in 58 hundred patients, noted 18% lower rates of adverse limb outcomes. And they suggested that statins clearly favorably affect limb prognosis. I may skip to the most current studies. There have been several large studies on this,
just published this last year. The study in Germany on patients with critical limb ischemia, showed that statins were clearly associated with improved amputation-free survival after both endovascular therapy and bypass for critical limb ischemia. But, they were not associated with raw amputation rates.
So again, amputation-free survival, but not limb salvage rates. A large study from Japan in patients with diabetes and peripheral artery disease, perhaps our most difficult group of patients did show that statins
were associated with decreased primary lower-extremity amputation. And finally, this large study from the Journal of the American Heart Association this year, showed that high intensity statin therapy was associated with both improved survival and decreased major adverse
cardiovascular event rates. So, many of you have seen this slide this week. This is hot off the press from the American Heart last week from the FOURIER Trial with PCSK9 inhibitors. This is obviously not statins, but I think this drums home the point with LDL lowering therapies.
And this is really the key slide. This study clearly showed that major adverse limb events in patients with known and without known PAD, were markedly reduced in patients with PCSK9 inhibitors. So in conclusion, statins or I will say lowering of the LDL, clearly reduces cardiovascular event rates and mortality
in patients with PAD. Statins and lowering of the LDL will very likely reduce the rates of major adverse limb events. Our patients with PAD and CLI should be treated as the highest risk patients and placed on maximum anti-lipid therapy and these medications should be continued
throughout the perioperative or periprocedural period. Thank you for your attention.
- [W. Anthony] On behalf of the Preserve II investigators, I'd like to give an update on the Preserve II clinical trial conducted in the United States. To this day, Preserve II clinical trial and the Zenith IBD devices and investigational device. As we all know, aortoiliac aneurysms, as well as a more less commonly isolated
common iliac aneurysms, lack a suitable distal landing zone for endovascular procedures. Adjunctive techniques, such as parallel grafts or hypogastric surgical revascularizations can add significant morbidity to the procedure as well as complexity.
And acute hypogastric artery occlusion can be associated with up to 30 to 40% of pelvic ischemic systems, such as buttock claudication or impotence. The Cook Zenith IBD device is a bifurcated endograft that's off the shelf. It has several configurations, both in the common iliac,
external iliac, and hypogastric artery branch segments that yield eight discrete configurations in total. It is comprised of both stainless steel, nitinol, and dacron elements. The Preserve II clinical trial, which is the subject of this presentation,
follows in the footsteps of the Preserve I clinical trial, which was prematurely halted secondary to type three endoleaks that occurred in the bridging stent connecting the hypogastric artery branch to the native hypogastric artery itself.
The Preserve II clinical trial design is almost identical to the Preserve I trial with the substitution of the Connect SX stent with the more widely available and familiar Atrium iCAST stent. The 40 patients that were required in the pivotal study has completed enrollment.
The average age of the patient 68 years, and overwhelming majority of the patients were white males. Approximately 2/3 of the patients had bilateral iliac aneurysm involvement, and the maximum common iliac artery aneurysm treated was 3.7 centimeters.
Technical success, defined as deployment of the endograft in the intended location, occurred in a hundred percent of the subjects with over half the patients being procedures being performed percutaneously using the pre-close technique. The average procedure time was 167 minutes
with the fluoroscopy time of 38 minutes. Of the eight device configurations that were available for the clinical trial, two of the device configurations comprised over 50% of the devices implanted. In the clinical trial, two, only two iCAST stents
were available, and of those, the shorter of the two 38 millimeter lengths were used in majority of the cases, and in only 15% of the cases were more than one iCAST stent required to complete the repair.
For the purposes of this presentation, data were analyzed up to June 2017, and at that time, mean followup was 29 months ranging from two to 39 months. There were no aneurysm related mortality, conversion, or ruptures. There was one late death due to a preexisting heart failure.
There were no stent fractures, device migrations, or aneurysm growth. There was one type 1c endoleak that occurred at the distal end of the iCAST stent that was seen by the core lab at 12 months. This underwent re-intervention, and it initially resolved,
and at two years, it recurred again, and no further intervention was performed. There was one case of buttock claudication that was bilateral that occurred quite late in the followup period. No treatment was performed,
and the hypogastric branch was patent. And there were four cases of either new or worsening impotence, all with patent branch stents. The primary endpoint, which was six months freedom from patency related intervention on the branch graft itself,
was met in hundred percent of subjects followed. There were four patients who underwent six re-interventions on the same side of the branch graft, and most of the interventions were either due to occlusive or thrombotic disease that occurred more specifically in the either the common iliac or external iliac artery segments.
And I'd like to emphasize that none of them occurred in the actual branch segment itself. Additionally, one patient underwent four re-interventions on the opposite side of the IBD implantation secondary to events that occurred that was likely embolization during the original index procedure.
Therefore in conclusion, the mid-term results from the US Preserve II multicenter clinical trial appear quite favorable for the IBD stent used in combination with the Atrium iCAST stent. There were no patency related re-interventions within the six months on the hypogastric artery treated
by the the branch graft along with no aneurysm related mortality, rupture, or conversion. At the present time, the clinical trial is in the continuing access phase with 23 patients enrolled. Thank you very much.
To conclude, interventional radiology provides percutaneous therapeutic techniques for the treatment of symptomatic disc herniations and these techniques are efficacious with a success rate approximately 80 to 85%,
save with a complication rate below 0.5% and they can be attractive alternatives to endoscopic surgical techniques with a longer lasting effect than conservative therapy. Thank you very much. (applause)
[BLANK_AUDIO] Mark, thank you very much, thank you very much, Joseph. Thank you very much. I'd like to sort of to spend the next five minutes telling you why size may not be important. One of the big questions is should we treat everybody?
Should we treat no one? And how should we think about rationing care? One of the easiest measurements be it, if you're not looking at symptoms, is to actually take a duplex measurement of diameter. If you look at the two major guidelines that have come out of from
the UK, or from the United States when you are looking at treatment options for patients, there really is no mention of diameter in any of the treatments strategies or for rationing. However, certainly in the UK, and I gather in the United States,
there's been various attempts to decide that if a patient's veins are of a certain size, they should not be offered an interventional treatment. One of the typical things found in the United Kingdom is a audit commission report that may make some suggestions,
and we all know that veins are common but here you can see that they suggest that of the veins are less that 3 millimeters, this is an important cut-off for looking at treatment. However, we know that of we look at many of the studies out there,
there's a lot of heterogeneity as to what is actually reported and often people don't report their outcomes with respect to diameter. And we also know that looking at quality of life measures or physician reported outcomes, none of them are good enough for rationing patient care. So what about size.
I'd like to present some data that we have conducted. When we previously presented, we took 461 patients and you can see overall they were relatively typical of a group of patients being treated for varicose veins. If we then compared the preoperative vein diameter with a CEAP classification, yes you can see that there is a correlation.
But I think the graph in a way speaks for itself. If you then look at a comparison, looking at the vein clinical severity score and the vein diameter, again you can see that while there is a correlation, there is a very widespread with respect to the
results. If you look at the Aberdeen Varicose Vein Questionnaire, similarly a good coefficient but again an overall spread. If we then look at the EQ5D and the EQ5D vasc again, a very similar fact that you really, there's not much discrimination between vein
diameter and quality of life. There is again small relationship with respect to BMI which is statistically significant but again you can see that the dots are very well spread. Now unfortunately working in a NHS system is unless we are entering people into clinical trials we don't actually follow everybody
up and therefore do not have duplex evaluation of of all these patients, but you can see that of those patients that we were able to follow up which probably represent about 45% of the patients, these are going to just present you some of the post-operative results.
So this is looking at the preoperative Vein Diameter to compared to the postoperative Aberdeen Varicose Vein Questionnaire. Again, you can see that there are some correlation but, overall a very wide spread of the dots. So while you can say that there's some statistical significance
with respect to the correlations being preoperative diameter and the postoperative Aberdeen Varicose Vein Questionnaire, and the generic quality of life to EQ-5D, there was no correlation found between CEAP and the physician reported VCSS score. So the conclusion are,
while there is some statistical association but not really with respect to clinical severity of patient symptomatology, this association is not clinically significant.
Any questions? Yes go ahead.
- [Woman] What was the timeframe between each session? - [Dr. Saad] We play it by ear. So it's a minimum of four to six weeks. We do a CT before clinic visits CT make a decision on whether we need to proceed see the patient see how they're doing
how they-- if you take the wind out of 'em then we're gonna give it more time. If we see liquefaction, we'll give it a little bit more time without infection. With kids a lot of them are kids as well we actually work around the school schedule.
So we can actually do it in the summer when they're free spring break so there's a lot of other things that we kind of play along with. But at least four to six weeks. Okay very good. Any more questions?
Any more questions? Okay thank you very much. Thanks. (audience applause)
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
I can't stress, also, the importance of the nurses.
I again, like I told you, I've been in four to five universities in the United States. Uniformly, invariably, the nurses always feel that they're left out. They feel that they're a little bit on the side,
and they're not in the focus of the procedure. And unfortunately that's inevitable because you've got the physicians and the techs focusing on their monitors, while you're focusing on your monitors. They're talking technical plumbing stuff,
you're dealing with medicine. You are the people that are actually taking care and actually doing the medicine in this procedure, okay? You will highlight if there's a problem to the physician but primarily, you are actually taking off of this plane and landing this plane safely.
Taking care of these patients. You are actually the medical core of this procedure. The other guys are just doing the plumbings, okay? So that is very important as well. We need to always stress that. That you are an integral part.
You do feel left out, it's inevitable, because everybody's focusing on something that you're not focused on. If you're focusing on what they're focusing, that's not a good thing, okay? And so it is very, very important that we have
strong nurses, good nurses. Strong personality nurses that actually can step up and speak up when something's going wrong. And we do really appreciate that, especially as physicians as we mature and we actually see the input from all the members of the team.
Thank you very much.
- [Caron] Good morning again. It may seem mundane to talk about this topic after all the complex aortic talks. However, vascular surgeons are frequently asked to manage retroperitoneal hematomas that occur either spontaneously or following a arterial catheterization procedures.
The presentation of these patients and the risk factors predicting the need for intervention are not well defined in the literature. The majority of the literature consists of case reports and small review series that highlight the role for therapeutic
or operative endovascular intervention, when necessary, reversal of anticoagulation and supportive care. So with these issues in mind one of the fellows at our institution decided to do a study and review the presentation and management of patients identified as having
retroperitoneal hematomas over a three year period at our single institution. We attempted to identify predictive risk factors to aid surgeons and endovascular specialists in determining those patients who will benefit most from intervention.
These were diagnosed radiologically by CT scan over a three year period at our tertiary care center. Hematomas that occurred directly as a result of recent surgery, for example after a colectomy, or as the result of trauma were excluded. Demographics, risk factors, and management were reviewed.
So we came up from our radiology database with 89 patients, 35 were excluded for the reasons I mentioned, and we ended up coincidentally with 27 patients who had spontaneous RPH's and 27 who had undergone a recent
endovascular or percutaneous procedure. A little bit more than half the cohort was female, the mean age was 71 with a wide range of 33 to 94, most of our cases were diagnosed in the inpatient setting, nearly 70% with 12% having outpatient CT scans, and 19 percent diagnosed in the emergency room setting.
Here are our demographics again, and I will point out that comorbidities included end-stage renal disease in 7.8% of malignancy and 20% and known coagulopathy in 5%. A recent procedure involving vascular intervention had been involved and the most common
was cardiac catheterization as you can see here, although some of these patients underwent peripheral vascular or other types of interventions. 63% of the patients were on some sort of anticoagulation therapy with the most common indication being atrial fibrillation, and the most common agent
being intervenous heparin. 57.4% of the patients were on antiplatelet therapy. The indications for CT scans included pain, hypotension, or a drop hematocrit or other concern for bleeding. And you can see here actually the most frequent
indication for imaging was a physical examination or lab concern for hemorrhage. So the interventions, 15% of patients required an invasive procedure, five patients underwent endovascular intervention, with three consisting of covered stent placement,
and two consisting of coil embolization. Two patients underwent open surgical common femoral or external iliac artery repair, and one patient underwent open repair following failed endovascular coiling. We tried to see who would need this management
and we looked at the patients who had, had a catheterization versus the spontaneous hematomas, although there was a trend here, this was not statistically significant. Although nearly 20% of patients who had, had
an arterial intervention did require invasive management. We looked at anticoagulation and we found that actually the patients who were not on anticoagulation had a higher incidence of a need for invasive management, although this may be due to the fact that
anticoagulation was able to be reversed when it was present. So in summary, neither recent arterial intervention or the presence of anticoagulation helped us decide who would need intervention. I think it's very interesting to know that 17.8% of these patients expired on the same admission
on which the RPH was diagnosed, likely reflecting the comorbidities in this inpatient population. This was a retrospective review and it should be noted that vascular surgeons were not involved in the decision-making or management of all these patients.
The literature on RPH following PCI notes other predictive factors such as, sheath size, antiplatelet medications, or anticoagulation. And they also noted a high mortality in these patients of 13%. So in conclusion, most patients
with retroperitoneal hematomas was successfully managed through anticoagulation reversal, transfusion, and supportive care. However, a meaning proportion of these patients require invasive management and this is usually accomplished by and endovascular approach.
The unanticipated significant proportion of these patients who expired in the same hospitalization highlights that it often occurs in patients with significant comorbidities. Thank you for your attention.
Hypersplenism and portal hypertension, which is basically parenchymal reduction. I'm gonna-- how many minutes do I have? 10 minutes? 10 minutes, okay. So this is the other one, which is,
you're not trying to exclude aneurysms, you're not trying to impede flow, you're actually trying to kill spleen. You're trying to reduce splenic volume. This is an end artery splenic artery embolization. Completely different technique.
Completely different inventory except the microcath. HyperSplenism is basically splenomegally with reduction of blood cells. We usually do it for thrombocytopenia but it also could be neutropenia, okay? Neutropenia is actually a double-edged sword.
Sometimes we can't embolize because the white blood cell is so low that it's a high infection rate, so they actually have to boost up the white blood cells for us before we actually do the embolization to try to reduce the risk of infection.
Okay, so even in really bad thrombocytopenia, and there's actually neutropenia, we would actually have to wait. The hemooncologist would actually give drugs to increase and boost immunity, increase the white counts, so we can actually embolize the spleen.
Ideally, old school, you have to embolize at least 60-75% of the spleen. So, old school IRs would actually go in and whack the spleen 70-80%, once and for all. So usually, there are two ways to do this. One way is to actually just go to the splenic artery
and spray the spleen with particles, whether it's gel foam, any form of particles, PVA, embospheres, whatever. Bland particles. And actually just spray the spleen and hope for the best, that 25% of it's still alive.
Okay and you do it, you know, you play it by ear. Embolize a little bit, watch, repeat it and such. That's kind of one way of doing it. And that's also the way that you would actually have to be forced to have to do it if you can't reach the splenic branches.
Another way is to actually take out the lower 70-80% of the spleen, sparing the upper pole, and you usually try to spare the upper pole, because that's the closest to the lung. If there's a lot of pain involved, and there is a lot of pain involved with a spleen,
if the pain is higher up in the upper pole, you get a lot of splinting, they don't take a deep breath in you get atelectasis, you get fever, you get fever along with post-embolization syndrome, which also gives you fever, and now you're kind of in the fog of fevers and is this post-embolization?
Is this atelectasis? Is this splinting, or is it the worst of your fears, which is the spleen is dead and it's liquefied and you're getting infection and an abcess. So what we try to do is minimize the pain with the splinting and the atelectasis by sparing the upper pole.
At least in theory. An interesting paper came out and they actually showed how much of the spleen they took out, and what the results were. So when you take out more than 70%, which is by the book, old school way of doing it,
which is the majority of the IRs that you work with are gonna be doing this. They're gonna be taking a whack of the spleen 70-80%, biting the bullet, and then seeing what happens. You get a 50% complication rate.
Complications could be pain, it could be fever, it could be liquefaction. But you get very good results with neutropenia. Okay? If you do 50-70% you still get pretty good results with lower complications.
If you embolize less than 50%, you get okay response but it's not durable. It's only for six months and you get no complications. So here's my school. Here's the new school. What we do is we actually reach that 75%
but we reach it through two to three sessions. We take it bit by bit. What we do is we do a first session, 25-30%, where we take a whack of the lower pole, not the upper pole, so we can bring them back again. Because if you give it to them at the top,
and they really hurt, they'll never come back. (laughs) So you make sure they come back, at least for another session. Okay, so you take the lower pole out first. Some people, and I'll show you an example,
they'll take the middle portion out first, and then they'll take the lower pole and the last top pole at the very end. But another way is take the lower pole, then you take the upper pole. And then if you need to do some more,
you take a part of the middle portion. Okay, and this is an example of a very large spleen. I'm just running it through for ya. Going for the lower branches, lower pole, to-- actually, sorry, we went for the middle portion first,
this is the example of the middle portion. Took that out. And this is kind of your post. After the first session. Second session we took out more. Which is the lower pole.
Third session, we went for the upper pole and we took out the upper pole. Then we did-- and I'll show you the results, and this is what you see. So first time, it's 100% baseline of the parenchyma, we took it down to 62% residual, 46% residual,
and after the third time we actually brought it down to 25%, no complications, no pain, they keep coming back after a month and a half, and they were very well stabilized. And this is actually the same patients with the results. Platelet counts go up as the splenic volume goes down.
We're taking it gradually, piecemeal, instead of taking just one bite at it originally. The same thing with portal hypertension. I don't have time to talk about portal hypertension, but it's the same kind of technique, the same kind of approach.
It is phased or staged and it's basically going after the parenchyma. Thank you very much. (audience applause)
- [Chris] Frank and Jim, thank you very much, and it's an honor to be here at Veith, and in this session to talk to you about low-profile endografts and how they may expand treatment options in poor iliac vessels and even bad necks as is the topic of this session. We know that access is a major determinant of the amenability of a patient to EVAR and that more of these
procedures are being done percutaneously without general anesthesia. Lower profile systems may increase the number of patients that we can treat and potentially reduce hospital costs and lengths of stay. The premise of the fast-track EVAR has been looked at, where
we move away from the traditional EVAR with cut-downs and general anesthesias and longer stays to the procedure being done more percutaneously without general anesthesia, no ICU stay and next-day discharge, which is our standard of care for most of 'em. This fast-track premise has been perspectively studied in
the LIFE registry. This was 250 patients which have already been completed and published most of them could complete the fast-track protocol. And what you see is a significant cost advantage to that, but more than 21,000 dollars per patient.
And as importantly, the procedure time, length of stay and 30 day resubmissions were significantly reduced compared to the traditional EVAR and the premier data, with significantly less major events and no ICU stays in addition to the cost savings. There's a newer device almost completed enrollment here in
the IDE trial, only requiring a 7 millimeter neck, with a low profile system and at 7 millimeters, this can be placed very accurately and aggressively to the renal arteries appropriate for this session. Now I'm going to show you three cases where this may be of particular benefit.
This is a gentlemen with a lot of comorbidities and rapidly expanding, symptomatic aneurysm and you'll see by the CT angiogram, not only did he have some juxtarenal angulation, but really severe iliac tortuosity. And you can see it's a fairly large neck right at the level of the lower-left renal artery and this is a
big expanding aneurysm. Here is that procedure, again you see the juxtarenal angulation and fairly large diameter neck at the renals. But more importantly you see absolutely, severely tortuous iliac vessels.
Again with the lower profile system 16 and 14 french sheaths can be advanced fairly easily. This is all after pre-closing. And just as importantly you can aggressively position so that you can see fabric being placed just at the renal artery, and then you can actually hold it in place as the
polymer rings form and conform to this angulated neck. And here's the completion angiograms that you can see are actually well-preserved and there's no endoleak. And the 30 day on that one year CT angiogram looks very good in terms of the iliacs and no endoleaks. Second case I was asked by a CT surgeon in our facility that
used to do these to come and help, he'd already done a cutdown on the right and was having trouble on the left ... And we worked together. Here you can a little bit of a reverse conical neck and small iliac vessels. This is the cutdown and even then the 12 and 14 french
dilators couldn't go very easily and so we had to change the initial plan which was we were going to require a 20 french sheath to the lower profile systems and again can aggressively deploy this to the reverse conical neck and complete the procedure fairly easily. And then finally, we often run into the scenario where we're
treating both the expanding aneurysmal disease and iliac obstructive disease. Here you can see common iliacs disease and a left external iliac CTO. Here's actually crossing this from the arm into the proximal common femoral artery.
And treating the external iliac vessel first with Nitinol stents. The initial plan was to go ahead and treat everything in the same setting and cover this with our endograft. Maybe not the greatest idea with the Nitinol stent going down as low as it did.
But we very carefully got access with road mapping and vascular ultrasound below that, and pre-close it. Although you can see here that with an 8 french sheath, with the new stent we lifted that up. So we changed plans and fixed that and then just did ... You can see the common iliac artery extends here,
and here. And then brought him back in two months to complete the EVAR procedure. Here we used a combination of road map and vascular ultrasound from micro-acupuncture access. And now, pre-closed and very carefully took a dilator
through the Nitinol stents, able to get the 12 french sheath systems up through the stents very carefully. 14 french sheath on the right, carefully through those stents and then able to complete the procedure very nicely. So in conclusions, I think there's a trend across the
spectrum of companies to move towards a lower profile EVAR systems. I think that these have the potential to increase the number of patients that we can treat. And both in terms of iliacs and maybe even neck and also reduce hospital costs on lengths of stays and
appropriate patients. Thank you very much.
Moving on to percutaneous decompression techniques for the discs, we can have decompression and we can have regeneration techniques for the discs. Specifically for the decompression techniques we can have thermal techniques using laser, continuous or pulsed radiofrequency and plasma energy ablation.
We can have mechanical decompression using a wide variety of devices and we can have chemical decompression by means of Discogel or ozone intradiscal injections. All these techniques, what they are actually based on is that fact that a intervertebral disc is a closed hydro-ablic space and when you are removing a small
part from the nucleus, you are actually causing a significant decrease in the intradiscal disc and this disc pressure actually is what makes the herniation move inwards. And we have these techniques from back in the 1940s. The indications for these kind of treatments
in the intervertebral discs include patients who are capable of providing consent with a symptomatic small to medium-sized herniation and when we are speaking about the size of the herniation, if you have a theoretical line between the facet joints, all herniations which do not cross this line,
they can be percutaneously treated. And when we are speaking about symptomatic cases, symptoms should be consistent with the segmental level where the herniation is located on the MR imaging. For example, if you have a left L4-L5 foraminal herniation, you are expecting the patient
to report a left L4 root neuralgia. Absolute contraindications include sphincter dysfunction, extreme sciatica and progressive neurologic deficit. And actually all these are indications for surgery. Additional absolute contraindications include sequestration or the presence
of asymptomatic herniation, local or systemic infection, spondylosthesis and stenosis of the vertebral canal, anticoagulants, coagulation disorders and the patient refusing to provide informed consent. Most of these techniques are performed under fluoroscopy so we (mumbles) projection with 45-degrees angulation
of the fluoroscopy beam and as far as the lumbar spine is concerned, we perform a direct posterior lateral (mumbles) in the disc. In the final position, we need to have the needle in the anterior third of the disc in the lateral projection towards the midline in the AP projection and you can see
how important the technologist is because we need to have good visualization of what we are doing. Once you are there, you have access to the disc and you can insert any kind of product that you are familiar with, starting from thermal, going to mechanical or chemical decompression.
The magic number for all these techniques concerning success rate is around 80%. The complication rate is very low, between 0.5%. What we do know so far from the literature is that there are no studies of evidence of superiority of one technique over the other.
As we've already said, complications are really rare. Spondylodiscitis is the most fearsome one with a percentage of 0.24% per patient.
- 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.
This is another example. This is a complex aneurysm. This is an aneurysm that's actually involved the common trunk of the SMA and the splenic artery. So we can't embolize the splenic artery. That's not a good thing.
This shows you a lot of teaching points, a lot of technical teaching points about the management of these complex aneurysms. So this is a complicated... This is a complicated aneurysm. It involves the common trunk of the SMA and the celiac axis.
So the plan is, we need, going down low, is actually the SMA, so what we need to do is to embolize the splenic artery, proximal as possible, okay, to allow as much collateral as possible to go to the spleen. Do a stint graft from the aorta into the SMA to exclude the aneurysm and then thrombose it.
The embolizing material in this case, plugs, it could be coils as well, would do the same principle of preventing back bleeding into the aneurysm. So you're kinda seeing all these principles being put together in this complex procedure.
So the first thing, we went up to the splenic artery and we embolized it with plugs, okay and that's kind of embolized, and then we went into the SMA and put balloon expandable stints and excluded the aneurysm. Here you see the aneurysm with the eggshell calcification,
see this anatomy perfectly, almost on the dead lateral. We put the stint grafts. On our follow up CT, the aneurysm had shrunk partially thrombosed, but still there is still more flow in the aneurysm. So this most likely kind of like a type 1 endo leak
into the aneurysm. The patient was on Plavix and on Aspirin. So technically, what you can do is to put another stint proximally and close that kind of type 1 endo leak. What we chose to do is actually stop the Plavix and stop the Aspirin, just stop it,
'cause they're anticoagulants, stop it for a month and follow up CT. That helps actually thrombose it. Okay so instead of subjecting a patient to another procedure, you just stop the Aspirin and Plavix for a month. Maybe that's enough to help it thrombose.
Then resume the Aspirin and Plavix, and that's all we needed to do is just stop the Aspirin and Plavix. Kind of several technical and medical teaching points
This you can actually apply these principles you can actually apply to all visceral aneurysms, especially all branches coming out of the celiac axis.
You can do that with the spleen, you can do that with the hepatic artery, for example. So here you've got a splenic artery aneurysm. Yeah. So ideally, what you wanna do with a splenic artery aneurysm is to actually exclude the aneurysm itself while
maintaining maximum flow to the spleen so you don't kill the spleen, okay? The best approach to that, if you can do that, which is not common, actually quite rare, is to actually put a stint graft across the splenic artery, excluding the aneurysm itself,
and letting it thrombose. That's the ideal situation, which is the rare situation. Rarely you can actually do that. This is more common with older people, middle-age to older people. It is also more common with women,
in childbearing or later stages in life age. With age, our splenic artery actually toils and turns more and more, it actually becomes more and more redundant and ectatic, and becomes more coiled. And it's more common to find coiling and difficult anatomy with women as well.
Theories behind that is pregnancies, estrogen, being kind of a relaxant to muscles, and actually causes more ectasia to the splenic artery. So the older you are, the more likely-- the patient is a woman, the more likely there would be actually tortuosities and this makes it very difficult to
put a stiff platform up there for a stint graft to actually cross over and actually purely exclude the aneurysm and maintaining full flow to the spleen
- [Neal] Thank you, I'd like to start this afternoon by thanking Dr. Veith. I'm not sure if you're here, but you really have been a true mentor and role model to me over the years, and thank you for that. This afternoon my charge was to discuss the role of 3D Fusion imaging and guidance with
the Siemens Artis Zeego System for Complex Vascular Interventions. So the Zeego 3D Fusion software helps link the preoperative CTA to live fluoroscopy. It uses markers and overlay to visualize the location, position, and position of the arteries
and arterial branches, and while I use 3D Fusion for most of my complex cases, I'm going to focus somewhat on FEVAR for this short five-minute talk, and I will also introduce you to the iGuide if you haven't seen it,
which I mostly use for trans-lumbar access for gluing to treat Type 2 endoleaks. There are two types of Fusion, there's 2D/3D Fusion, which uses two fluoroscopic projections, and there's 3D/3D Fusion, which uses a more detailed DynaCT spin.
In my experience, this is more accurate, and I've been using it, and I will show you how it works. Before the patient is prepped and draped, we do a quick spin. Then, while we're prepping and draping, the tech goes into the back room
and fuses that CT data with the preoperative CTA. Once that is performed, you can mark almost anything you want, and just for demonstration purposes, this is the techs marking the infrarenal aorta, and what you'll see on the actual fluoroscopy screen is what you see here in the middle,
and there's some parallax, and without giving contrast, if this were just the plain EVAR, you can adjust and get rid of the parallax, just based on this marking. Here's a nice case of a fenestrated case using the CTA as an overlay, and I put some nice circles
on to show you where the fenestrations are, and you can see how nicely and easily the fenestrations can line up with the renal vessels on the left and the mesenteric vessels on the right, and this really simplifies the case and it decreases operative time, contrast,
and makes the cases quite simple. If you don't like the overlay, you can use these little circles that can mark the origins of the vessels and also give you the direction of the vessels in a circumferential 3D kind of way. The two images are from our unit,
and the image in the middle is from Siemens. It's the new pheno software. The overlay can also help you identify the bifurcation, which is important for contralateral limbs, and it will show you before giving any contrast the exact angle for the hypergastric arteries
when you're landing your distal limb. So the advantages of 3D Fusion are multiple. It helps you see the location and position of arterial branches before giving any contrast. You can correct for parallax again without giving any contrast.
There certainly is shorter cannulation and case time. There's less radiation, less contrast. I think more accurate deployment, and I think all these things account for better outcomes. What about limitations? I think most of the limitations come from misalignment
of the overlay and the anatomy, and how can that happen? Well, it could be Fusion error. The tech may not fuse it correctly. The patient can move if you're doing cases awake. There can be respiratory variation.
This actually is probably most impressive when you're trying to occlusive cases of the celiac and SMA, and stiff wires alter anatomy, and they are trying to make new software that can help with that. If the overlay does not align,
you can simply shoot an angiogram as you see on the right, and the techs can actually go and adjust that overlay. Lastly, I'm going to discuss the iGuide, which I use for Type 2 Embolization, to be a trans-lumbar route. You would perform a spin as you've seen before,
and they would fuse. Remember the patient would be prone, and then I'll show you how you can pick the endoleak target and skin entry point. So, here's the endoleak target, and if you can see on the upper left you're going to pick
the entry point to the skin, and then the computer generates a direct path to make sure you're not going to hit anything on the way in, and once you like that path, this is what you see on the screen. You see your destination as the circle in the middle,
and then a dotted line to show you how to get there, and you can see in multiple views. Here's a lateral oblique and oblique, and it makes the procedure fairly easy. You almost will always get adenitis if it's there, and ideally you see dripping blood as you do here.
You can inject some contrast. If you're happy you can inject your glue, and I thank you for your attention this afternoon.
And the etiology of this is numerous, it's diagnosis of exclusion, it's diagnosed in less than 1.5% of liver transplants in the United States and Japan. For some reason it is diagnosed at 25% in Germany, so somebody's overcalling it and somebody's undercalling it.
Over the years, I can tell you, 10 years ago, most transplant surgeons in the United States did not believe in it. Now they're believing it more and more, they're calling it more and more. It probably is happening in 1-2% of transplants
in the United States, not 25%. This is a perfect example where the hepatic artery is open, the hepatic artery is so slow that the actual splenic vein catches up with it. The splenic vein actually catches up with the flow in the hepatic artery.
That's how slow and stagnant that hepatic arterial flow is. Your differential diagnosis is a fistula. It's that there's a fistula between the hepatic artery, that's kind of differential diagnosis. However, this is truly a splenic phase. You see the spleen.
Contrast has gone right through the spleen up, down the splenic vein and caught up with the hepatic artery, so this is a true, slow flow in the hepatic artery in a transplant. Initially, we thought that the best way to deal with this is to actually embolize the spleen and there are two types.
There's a GDA spleen, and a splenic artery steal. So there's a GDA steal, which is even rarer, and a splenic artery steal. So initially we thought that the best way to deal with this is just to embolize the spleen, because this is splenic steal.
The spleen is stealing flow from the hepatic bed. Simple, simple thought process. Embolize the spleen, or embolize the GDA in case if it's a GDA. But it's actually a lot more complicated than that.
- [Gianluca] Thank you, Mr. Chairman. Thanks to Frank (mumbles) for the very kind invitation. I have nothing to disclose regarding this presentation and silent cerebral infarct is a small, radiologically detected infarction with no history of acute neurological dysfunction given by the lesion.
And they are usually associated with the degree of carotid stenosis, the number of microemboli at TCD and the plaque histology. In the general population, they affect almost 20% of the population
and they are significantly associated with early stroke and long term stroke rate. For that reason, the presence of silent cerebral infarcts is considered an adjunctive risk in patients that undergoing carotid endarterectomy.
And this was already demonstrated by this work by Cao, in which patient with the presence of silent cerebral infarct had a higher risk of postoperative stroke and long term stroke incidence after carotid endarterectomy.
When we looked at a series of patients, both symptomatic and asymptomatic, after carotid endarterectomy. We saw that the presence of brain infarcts was one of the carotid risks that associated with increased stroke rate after endarterectomy,
no matter where the infarct was located, as you can see from this table. So for that reason, we further expanded our analysis to only asymptomatic patients admitted to carotid endarterectomy with this work. And again we saw that silent cerebral infarcts
are significantly associated with early postoperative stroke and that was an independent factor of postoperative stroke in this series of patient. And this effect was sustained at long term either for ipsilateral stroke and combined stroke and death.
And again, this was an independent risk factor of long term stroke rate after carotid endarterectomy. What about carotid stenting? Actually, the literature, there are no paper dealing specifically with this topic.
So we made an analysis on 420 consecutive carotid stenting patient treated for asymptomatic stenosis and all those patients were evaluated with a preoperative CT scan. And if you look at this graph,
you see that there was no difference in patient submitted to stenting with or without the present of silent cerebral infarct. If we look at the two groups of patient, patient with positive presence, the presence of carotid lesion
before endarterectomy and stenting, there was no difference in the two groups. Whereas, if we look at the patient with no evidence of infarction before endarterectomy or stenting, there was a trend toward greater incidence of stroke
in patient undergoing stenting. So, in conclusion, silent cerebral infarcts increase the risk of postoperative events after carotid endarterectomy and this risk should be considered in indication to revascularization of our patient.
In the stenting group, this effect is less pronounced, but this is probably due to the higher overall risk of neurologic event after stenting. In conclusion, to answer to the answer at the beginning, should all asymptomatic carotid stenosis patients
get head CT scan? The question is definitely yes. Thank you.
Let me give you another layer of complexity to what's going on with the hemodynamics of this. This is actually a balance of two things: think of it as a pivot or a balance on two aspects. One pivot is on the arterial side of the house. This is actually a balance between the hepatic arterial
resistance and the splenic arterial resistance. Things that would increase the hepatic artery resistance will give preferential flow to the spleen. So it may not be a splenic problem, it could be actually a liver problem. A stiff graft is a problem.
A poor graft is a problem. A huge subcapcillar hematoma in the liver that's compressing the liver, increasing the resistance of the spleen, of the liver, would cause hepatic arterial flow to go towards, preferentially, towards the spleen. So it's a balance between hepatic and splenic arterial beds.
The other side of the house is the veinous side, which is what we talked about a little bit before. It's either the quality or size of the graft versus the amount of portal flow there is. If the portal flow is increased, with a good graft, or is it a poor graft with normal portal flow?
So this is a balance between two things. This is quite a complex procedure. Quite a complex hemodynamics and causes. Be as it may, that's all academic.
- [Santi] Mr. Chairman, dear colleagues, thanks to Professor Veith for the kind invitation. Be in New York one more time is always so great. So, let's talk a little bit about the Gore C-TAG. These are my disclosure. So now it's already clear that this type of endograft perform nicely in many different scenarios
at the level of the thoracic aorta. It works nicely in a descending aneurysm, works nicely in acute B dissection, works nicely also in those forms of B dissection that be in the subacute or even, in the early chronic phase favoring
a pretty good remodeling. But works nicely and conform perfectly I would say some case also of EA affected by intramural hematoma or a penetrating aortic rupture. And in addition is also one of the typical graft that are used in our practice for treating PAU patients.
So in order to know a little bit more in terms of long term results of such graft, we are querying the GREAT registry, which is a post-market Gore registry, which aim is to report about long-term durability of aortic endograft after 10 years follow up.
So 5,000 patient has been enrolled, and regarding to the thoracic section, we have 963 patients enrolled and subdivided as you can see in this slide. In total, at the thoracic level, there are 21% of the entire cohort mostly are men,
as always, in this disease. Look a little bit more for aneurysm, patients are a little bit more than 300. The reason for treatment was primary procedure, in the vast majority of the case, 86%. But also reintervention after other endovascular
or previous endovascular procedure or previous open surgical repair. More than 50% of the cases, the proximal landing zone in these ranges was zone three, and then zone four as you can see. And branch vessel procedure were necessary
in almost one fourth of these patient. If we look about the long-term result, at least those that are available at this point, we can see that the results are pretty good in terms of aortic related mortality, and also in terms of freedom from any reintervention.
But we have to also say that the previous report by Professor Ferman told us very interesting, that in order to wait a little bit more before to be sure about the durability of any endograft. But the results still are good also in terms of device-related intervention.
Another recent evaluation using the same registries related to those patients that were treated for dissection. This is a paper that has been run by Ali Azizzadeh and the group who takes care about these patients. They considered both acute and chronic setting,
results are pretty good in terms of mortality, in terms of aortic mortality, as you can see over here. And also the results at middle term follow up are very satisfactory, and are basically related to the preoperative condition of these patients.
Very recently we are analyzing only those acute, and we are comparing those who presented with the complicated versus uncomplicated initial clinical status and also in this case, results are very satisfactory. If we look about the midterm results,
we can say that when we compare acute uncomplicated versus all the other types of B dissection, means complicated plus chronic, results are in evident way, in favor of those that were treated in uncomplicated status. So coming quickly back to the conclusion,
we can say that Gore C-TAG perform nicely in TEVAR, in very wide, say, in several scenarios as we have seen previously. And C-TAG performs also nicely in terms of midterm results, both for problems related to aortic mortality, all cause mortality, and freedom from related to the device.
In addition, we have also to underline one more time, that these registry gave us also the chance to look into some very strange situation, as you can see over here. Thank you very much for your attention.
Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.