- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- Thank you Professor Veith. Thank you for giving me the opportunity to present on behalf of my chief the results of the IRONGUARD 2 study. A study on the use of the C-Guard mesh covered stent in carotid artery stenting. The IRONGUARD 1 study performed in Italy,
enrolled 200 patients to the technical success of 100%. No major cardiovascular event. Those good results were maintained at one year followup, because we had no major neurologic adverse event, no stent thrombosis, and no external carotid occlusion. This is why we decided to continue to collect data
on this experience on the use of C-Guard stent in a new registry called the IRONGUARD 2. And up to August 2018, we recruited 342 patients in 15 Italian centers. Demographic of patients were a common demographic of at-risk carotid patients.
And 50 out of 342 patients were symptomatic, with 36 carotid with TIA and 14 with minor stroke. Stenosis percentage mean was 84%, and the high-risk carotid plaque composition was observed in 28% of patients, and respectively, the majority of patients presented
this homogenous composition. All aortic arch morphologies were enrolled into the study, as you can see here. And one third of enrolled patients presented significant supra-aortic vessel tortuosity. So this was no commerce registry.
Almost in all cases a transfemoral approach was chosen, while also brachial and transcervical approach were reported. And the Embolic Protection Device was used in 99.7% of patients, with a proximal occlusion device in 50 patients.
Pre-dilatation was used in 89 patients, and looking at results at 24 hours we reported five TIAs and one minor stroke, with a combined incidence rate of 1.75%. We had no myocardial infection, and no death. But we had two external carotid occlusion.
At one month, we had data available on 255 patients, with two additional neurological events, one more TIA and one more minor stroke, but we had no stent thrombosis. At one month, the cumulative results rate were a minor stroke rate of 0.58%,
and the TIA rate of 1.72%, with a cumulative neurological event rate of 2.33%. At one year, results were available on 57 patients, with one new major event, it was a myocardial infarction. And unfortunately, we had two deaths, one from suicide. To conclude, this is an ongoing trial with ongoing analysis,
and so we are still recruiting patients. I want to thank on behalf of my chief all the collaborators of this registry. I want to invite you to join us next May in Rome, thank you.
- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first
before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.
We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column
from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.
Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,
which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied
and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal
amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,
but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced
from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,
organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC
seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.
You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.
So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these
biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...
Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be
most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.
We have to work that out, I hope. Calcification is generally a very late feature in this process. Thank you very much.
- Thank you, and thank you Dr. Veith for the opportunity to present. So, acute aortic syndromes are difficult to treat and a challenge for any surgeon. In regionalization of care of acute aortic syndromes is now a topic of significant conversation. The thoughts are that you can move these patients
to an appropriate hospital infrastructure with surgical expertise and a team that's familiar with treating them. Higher volumes, better outcomes. It's a proven concept in trauma care. Logistics of time, distance, transfer mortality,
and cost are issues of concern. This is a study from the Nationwide Inpatient Sample which basically demonstrates the more volume, the lower mortality for ruptured abdominal aortic aneurysms. And this is a study from Clem Darling
and his Albany Group demonstrating that with their large practice, that if they could get patients transferred to their central hospital, that they had a higher incidence of EVAR with lower mortality. Basically, transfer equaled more EVARs and a
lower mortality for ruptured abdominal aortic aneurysms. Matt Mell looked at interfacility transfer mortality in patients with ruptured abdominal aortic aneurysms to try to see if actually, transfer improved mortality. The take home message was, operative transferred patients
did do better once they reached the institution of destination, however they had a significant mortality during transfer that basically negated that benefit. And transport time, interestingly did not affect mortality. So, regional aortic management, I think,
is something that is quite valuable. As mentioned, access to specialized centers decrease overall mortality and morbidity potentially. In transfer mortality a factor, transport time does not appear to be. So, we set up a rapid transport system
at Keck Medical Center. Basically predicated on 24/7 coverage, and we would transfer any patient within two hours to our institution that called our hotline. This is the number of transfers that we've had over the past three years.
About 250 acute aortic transfers at any given... On a year, about 20 to 30 a month. This is a study that we looked at, that transport process. 183 patients, this is early on in our experience. We did have two that expired en route. There's a listing of the various
pathologies that we treated. These patients were transferred from all over Southern California, including up to Central California, and we had one patient that came from Nevada. The overall mortality is listed here. Ruptured aortic aneurysms had the highest mortality.
We had a very, very good mortality with acute aortic dissections as you can see. We did a univariate and multivariate analysis to look at factors that might have affected transfer mortality and what we found was the SVS score greater than eight
had a very, very significant impact on overall mortality for patients that were transferred. What is a society for vascular surgery comorbidity score? It's basically an equation using cardiac pulmonary renal hypertension and age. The asterisks, cardiac, renal, and age
are important as I will show subsequently. So, Ben Starnes did a very elegant study that was just reported in the Journal of Vascular Surgery where he tried to create a preoperative risk score for prediction of mortality after ruptured abdominal aortic aneurysms.
He found four factors and did an ROC curve. Basically, age greater than 76, creatinine greater than two, blood pressure less than 70, or PH less than 7.2. As you can see, as those factors accumulated there was step-wise increased mortality up to 100% with four factors.
So, rapid transport to regional aortic centers does facilitate the care of acute aortic syndromes. Transfer mortality is a factor, however. Transport mode, time, distance are not associated with mortality. Decision making to deny and accept transfer is evolving
but I think renal status, age, physiologic insult are important factors that have been identified to determine whether transfer should be performed or not. Thank you very much.
- Relevant disclosures are shown in this slide. So when we treat patients with Multi-Segment Disease, the more segments that are involved, the more complex the outcomes that we should expect, with regards to the patient comorbidities and the complexity of the operation. And this is made even more complex
when we add aortic dissection to the patient population. We know that a large proportion of patients who undergo Thoracic Endovascular Aortic Repair, require planned coverage of the left subclavian artery. And this also been demonstrated that it's an increase risk for stroke, spinal cord ischemia and other complications.
What are the options when we have to cover the left subclavian artery? Well we can just cover the artery, we no that. That's commonly performed in emergency situations. The current standard is to bypass or transpose the artery. Or provide a totally endovascular revascularization option
with some off-label use , such as In Situ or In Vitro Fenestration, Parallel Grafting or hopefully soon we will see and will have available branched graft devices. These devices are currently investigational and the focus today's talk will be this one,
the Valiant Mona Lisa Stent Graft System. Currently the main body device is available in diameters between thirty and forty-six millimeters and they are all fifteen centimeters long. The device is designed with flexible cuff, which mimics what we call the "volcano" on the main body.
It's a pivotal connection. And it's a two wire pre-loaded system with a main system wire and a wire through the left subclavian artery branch. And this has predominately been delivered with a through and through wire of
that left subclavian branch. The system is based on the valiant device with tip capture. The left subclavian artery branch is also unique to this system. It's a nitinol helical stent, with polyester fabric. It has a proximal flare,
which allows fixation in that volcano cone. Comes in three diameters and they're all the same length, forty millimeters, with a fifteen french profile. The delivery system, which is delivered from the groin, same access point as the main body device. We did complete the early feasibility study
with nine subjects at three sites. The goals were to validate the procedure, assess safety, and collect imaging data. We did publish that a couple of years ago. Here's a case demonstration. This was a sixty-nine year old female
with a descending thoracic aneurysm at five and a half centimeters. The patient's anatomy met the criteria. We selected a thirty-four millimeter diameter device, with a twelve millimeter branch. And we chose to extend this repair down to the celiac artery
in this patient. The pre-operative CT scan looks like this. The aneurysm looks bigger with thrombus in it of course, but that was the device we got around the corner of that arch to get our seal. Access is obtained both from the groin
and from the arm as is common with many TEVAR procedures. Here we have the device up in the aorta. There's our access from the arm. We had a separate puncture for a "pigtail". Once the device is in position, we "snare" the wire, we confirm that we don't have
any "wire wrap". You can see we went into a areal position to doubly confirm that. And then the device is expanded, and as it's on sheath, it does creep forward a bit. And we have capture with that through and through wire
and tension on that through and through wire, while we expand the rest of the device. And you can see that the volcano is aligned right underneath the left subclavian artery. There's markers there where there's two rings, the outer and the inner ring of that volcano.
Once the device is deployed with that through and through wire access, we deliver the branch into the left subclavian artery. This is a slow deployment, so that we align the flair within the volcano and that volcano is flexible. In some patients, it sort of sits right at the level of
the aorta, like you see in this patient. Sometimes it protrudes. It doesn't really matter, as long as the two things are mated together. There is some flexibility built in the system. In this particular patient,
we had a little leak, so we were able to balloon this as we would any others. For a TEVAR, we just balloon both devices at the same time. Completion Angiogram shown here and we had an excellent result with this patient at six months and at a year the aneurysm continued
to re-sorb. In that series, we had successful delivery and deployment of all the devices. The duration of the procedure has improved with time. Several of these patients required an extension. We are in the feasibility phase.
We've added additional centers and we continue to enroll patients. And one of the things that we've learned is that details about the association between branches and the disease are critical. And patient selection is critical.
And we will continue to complete enrollment for the feasibility and hopefully we will see the pivotal studies start soon. Thank you very much
- Yeah, thank you Dr. Asher, and again, I want to give credit to Dr. Zheng, one of our fellows who put together this work. So duplex surveillance for lower extremity revascularization, I think we all do that for vein grafts. It's less well accepted for prosthetic grafts. It's controversial for peripheral stent grafts,
and it's very controversial for peripheral stents. If we had time, I'd like to poll all of you and ask how many of you do a duplex scan after you put in a peripheral arterial stent, but more importantly, how many would intervene if you find the velocities are increasing.
So why do it? Well, revision of failing stents may yield better patency rates than if you intervene after the stent has occluded. You may not be able to restore patency if the stent has already occluded, I mean,
some of you may think you can always do that, I know I can't always do that. And performing endovascular treatment is obviously easier than converting to open surgery. So we reviewed 172 stents in 30 iliac and 89 fempop arteries.
Some were overlapping stents, so we kind of said there were 119 segments that we analyzed. The treated length for the iliac artery was about seven and a half centimeters, and for fempop, was about 12 centimeters. And we did duplex surveillance
in our accredited vascular lab in our office. We measured the peak systolic velocity, and the PSV ratios, every two centimeters within the stent but also in the adjacent proximal and distal arteries. We considered it an abnormal duplex finding, I think pretty much consistent
with what you would do for a vein graft, also, if you had a focal PSV over 300, uniform PSVs throughout the stent less than 45, or a ratio more than three, we would say that probably corresponds with more than a 75% stenosis
and generally we would intervene. We did the duplex one week after we put in a peripheral stent, and then about every six months. The follow up averaged about two years. So of these 119 stented segments, about half of 'em stayed normal.
All of the duplex criteria stayed normal during the entire follow up, nothing needed to be done. But interestingly, of the other half, they developed at least one abnormal duplex criterion. 40 of the 57 cases we intervened on, but of the 17 other cases we did not intervene,
either due to patient refusal, or the surgeon felt, well, let's just keep an eye on it, five did remain patent for a short follow up, but 12 of the 17 went on to occlude. Of the 12 occluded segments, we found that if there was more than one
abnormal duplex finding and you did not treat, 70%, again the numbers are small, but 70% occluded, compared to if you had the normal duplex findings, only 3% occluded, and this was highly significant. So of the 12 occluded stents, what happened? Well six we didn't do anything,
they were just for claudication, and the patients chose not to have open surgery. But four, we did try to open 'em and could not, and they needed a bypass, mainly for limb salvage. But two, we couldn't do anything, and they ended up with amputations.
So the bottom line in this relatively small series was if a stent occluded, they didn't necessarily do well and you couldn't open 'em up. So in conclusion, duplex surveillance for lower extremity stents, and that's what we're talking about,
can significantly predict stent occlusion based on these criteria, and the absence of any criteria strongly predicted stent patency. We even have a little disagreement, frankly, in my own group about how aggressive to be for these.
I tend to be pretty aggressive and intervene. Maybe during the discussion we can talk about this. Thank you.
- Thank you again Rex. This is again my disclosure, the same. I think you agree with me that we all do not want these images and after the procedure in our patients or in followup. We might be able to keep this reconstructions patent by continuing accuracy ventricle relation
but there is somehow a disturbance of the venous flow. If we we advocate that 50% stenosis is significant. Flexibility is one reason why we have already the first generation of dedicated venous stents. These are the currently available, excuse me, currently available venous stents
in the European market and despite very different structures, geometries and characteristics they all want to combine the best balance between flexibility, radial force, crush resistance or porosity. So this is not a real scientific way to show
or to evaluate the flexibility but it shows you that there are really differences between the current dedicated venous stents regarding the flexibility and we have closed cell stent, we have open celled stent, we have woven stent, we have laser knitted stent,
we have hybrid or segmented stent. So let us go to one case from our center. We re-cannulized the left iliac tract as you can see here. We used the closed cell stent at the proximal part, lengthen it with a dedicated venous
open cell segmented stent below the ligament going into the common femoral vein as you can see here. So going into the axial plane with duplex we see a very nice cross sectional shape below the artery at the mitonal point. This stent performs very well here
but a few centimeters more distal we have a destroyed cross sectional shape. Going into the detail, the same patient in longitudinal evaluation with stent we see three different diameters and if we take the proximal diameter
you see again the same picture with a minimum diameter of 1.27 maximum diameter of 1.57 giving us a 1.57 square centimeters of area and this is a 1.23 aspect ratio. Taking the kink, the level of the kink, we have the destroyed picture.
Minimum diameter 0.65, maximum diameter of 1.47 giving us only a 0.89 square centimeters and regarding the published and the aspect ratio is 2.3 and regarding this 2008 published paper which showed that area affects outcome and the recent work of Lowell Kabnick
which shows that not only the area but also the aspect ratio affects the outcome. We have to conclude that in this patient, of our center this kink might destroy or might affect the outcome. This is the literature you heard in the last session
already the patency rates of all stents but my message from this table is they included only a small number of patients with short followups as you can see ranging from 10 to 12 but despite very different flexibilities
which we have seen in the second slide we have no significant differences regarding the patency or the outcome and therefore whether more flexibility leads to a better clinical outcome remains still unclear. In conclusion, there is no doubt
that flexibility is important. The flexibility of majority of current venous stents seems to be enough. Till date with currently available studies we cannot answer how much flexibility we need. Where is the threshold
to say this is good and the other is bad? If more flexibility means really better outcome and it is not only the stent, it is more the pattern of disease which affects the outcome. So we started with arterial stents in the venous pathology, we improved to first generation of dedicated venous stents
but we are looking for best stents. Thank you very much.
- Thank you very much. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,
12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end
or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three
now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing
that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,
they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.
The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal
and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients
were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.
That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.
Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known
that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage
for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available
in about a month, thank you.
- So thank you for the kind introduction and thanks for professor Viet for the invitation again this year. So, if we talk about applicability, of course you have to check the eye views from this device and you're limited by few instructions for users. They changed the lengths between the target vessel
and the orifice and the branch, with less than 50 mm , they used to be less than 25 mm. Also keep in mind, that you need to have a distance of more than 67 mm between your renal artery cuff and your iliac bifurcation. The good thing about branch endografts
is that if you have renal artery which comes ... or its orifice at the same level of the SME, you can just advance and put your endorafts a bit more proximally, of course risking more coverage of your aorta and eventually risking high rate
of paraplegia or spinal cord ischemia. Also if your renal artery on one side or if your target vessel is much lower with longer bridging stent grafts which are now available like the VBX: 79 mm or combination of bridging stem grafts, this can be treated as well.
Proximally, we have short extensions like the TBE which only allows 77 or 81 mm. This can also expand its applicability of this device. The suitability has already been proven in.. or assessed by Gaspar and vistas and it came around plus 60%
of all patients with aortic aneurysms. Majority of them are limitations where the previous EVAR or open AAA repair or the narrow diameter reno visceral segment in case of diabetes sections. So, what about the safety of the T-branch device?
We performed an observational study Mister, Hamburg and Milner group and I can present you here the short term results. We looked at 80 patients in prospective or retro prospective manner with the t-branch as instructed for use.
Majority were aneurysms with the type two or type four Crawford tracheal aneurysms, also a few with symptomatic or ruptured cases. Patient characteristics of course, we have the same of the usual high risk cardiovascular profiling,
this group of patients that has been treated. Majority was performed percutaneously in 55%. The procedure time shows us that there is still a learning curve. I think nowadays we can perform this under 200 minutes. What is the outcome?
We have one patient who died post operative day 30, after experiencing multiorgan failure. These are 30 day results. No rupture or conversion to open surgery. We had one patient with cardiac ischemia, seven patients with spinal cord ischemia
and one patient has early branch occlusion. There was both renal arteries were occluded, he had an unknown heparin induced thrombocytopenia and was treated with endovascular thrombectomy and successfully treated as well. Secondary interventions within 30 days were in one patient
stent placement due to an uncovered celiac stent stenosis In one patient there was a proximal type one endoleak with a proximal extension. One patient who had paraplegia or paraparesis, he had a stenosis of his internal iliac artery which stem was stented successfully,
and the paraparesis resolved later on in this patient. And of course the patient I just mentioned before, with his left and right renal artery occlusion. So to conclude, the T-branch has wide applicability as we've seen also before, up to 80% especially with adjuvant procedures.
Longer, more flexible bridging stent grafts will expand the use of this device. Also the TBE proximal extensions allows aortic treatment of diameters for more than 30 mm and I think the limitations are still the diameter at reno visceral segment,
previous EVAR or open AAA repair and having of course multiple visceral arteries. Thank you.
- The FLEX Scoring Catheter is one of the new tools, which is dedicated to vessel preparation, either as a stent, as a therapy followed by plain balloon angioplasty, or preparing the vessel for drug-eluting balloons and stents. So, the background basically is that
we're more and more tackling chronic total occlusions, and these kind of lesions, they have an increased risk of being calcium-containing, creating dissections, perforations, embolization, and poor luminal gain. And for that purpose, this device, which is more or less
a kind of surgical device, was developed. It's a interventional tool which can be introduced via a six-French sheath. It's an over-the-wire system, running over a 14 or 18 thousandths guide wire. It's common in shaft lengths of
40 centimeters dedicated to AV, fistula treatment and 120 centimeters, and the device is exposed to the vessel wall with three atherotomes, with the indication for femoropopiliteal and AV fistula excess treatment. One size fits all is really the right description
of this device, except having two different shaft lengths, the device itself is coming in one size only. What does it result in? Well, it results in micro-incisions, as you can see it over here, also over here in an OCT image, and the depths of these incisions
is about 0.5 millimeters, the pressure which is applied to the surface is about one atmosphere, independent on the vessel size. So, the idea and the rationale for this device is to facilitate and increase the vessel compliance and to create an controlled environment for angioplasty.
There are, just recently, some specimen analysis performed by CBSET, what you can see over here, marked by arrows, these arrows indicate the FLEX-induced micro-incisions, and you can see that these incisions are really circumferential with controlled,
uniform depths of those incisions into the plaque or the vessel wall. This is a 150 times magnification and you can see these longitudinal micro-incisions, which are very much parallel, it's like using a cutting balloon,
the advantage, however, is that this device can be applied to even longer lesions, the limitation of a cutting balloon is the balloon length of 20 centimeters only. So what are the early results? I can present you the acute outcomes
of 100 patients' sample size, with chronic total femoropopliteal occlusions. We can see that the average lesion length was really significant, 191 millimeters, the range was up to 35 centimeters, and there was moderate to severe calcification
in almost 50% of those cases. The luminal gain post FLEX application was about 31%, and the following balloon opening pressure, which was documented within this registry, was four atmospheres only, which is a signal that really the vessel compliance
is significantly improved, considering the almost 50% of moderate to severe calcification of those lesions. There had been no emboli, there had been no flow-limiting dissections, nevertheless, the provisional stent use was still high with 19%.
This is one of two case examples I would like to share with you. This was an instant re-occlusion of the popliteal artery, 10 centimeters in length, this was passed with an 18 thousandths guide wire, three passes with the FLEX catheter had been performed,
as you can see over here. And this was then, this was the result after FLEX catheter application and this is post additional drug-coated balloon angioplasty, there was no dissection, there was no significant residual stenosis.
Another case example, unfortunately, the video will not run, this was a long distance flush occlusion of the SFA, and you can see the calcium here in the entire length of the lesion, this lesion was treated, again, with the FLEX catheter, here, the video is not running,
this is the final result after DCB application. So, in summary, there's a high degree of technical success in achieving consistent luminal gain post FLEX, there's a low opening balloon pressure, and the re-canalization of CTOs was possible with a low rate, zero rate of significant dissections
and the low provisional stent rate. Thank you very much.
- Thank you very much for the kind introduction, and I'd like to thank the organizers, especially Frank Veith for getting back to this outstanding and very important conference. My duty is now to talk about the acute status of carotid artery stenting is acute occlusion an issue? Here are my disclosures.
Probably you might be aware, for sure you're aware about pore size and probably smaller pore size, the small material load might be a predisposing factor for enhanced thrombogenicity in these dual layer stents, as you're probably quite familiar with the CGUARD, Roadsaver and GORE, I will focus my talk a little bit
on the Roadsaver stent, since I have the most experience with the Roadsaver stent from the early beginning when this device was on the market in Europe. If you go back a little bit and look at the early publications of CGUARD, Roadsaver and GORE stent, then acute occlusion the early reports show that
very clearly safety, especially at 30 days in terms of major cardiac and cerebrovascular events. They are very, very safe, 0% in all these early publications deal with these stents. But you're probably aware of this publication, released end of last year, where a German group in Hamburg
deals with carotid artery stenosis during acute stroke treatment. They used the dual layer stent, the Roadsaver stent or the Casper stent in 20 cases, in the same time period from 2011 to 2016, they used also the Wallstent and the VIVEXX stent,
in 27 cases in total and there was a major difference, in terms of acute stent occlusion, and for the Roadsaver or Casper stent, it was 45%, they also had an explanation for that, potential explanations probably due to the increase of thrombogenic material due to the dual layer
insufficient preparation with antiplatelet medication, higher patient counts in the patients who occluded, smaller stent diameters, and the patients were not administered PTA, meaning Bridging during acute stroke patient treatment, but it was highlighted that all patients received ASA of 500mg intravenously
during the procedure. But there are some questions coming up. What is a small stent diameter? Post-dilatation at what diameter, once the stent was implanted? What about wall apposition of the stent?
Correct stent deployment with the Vicis maneuver performed or not and was the ACT adjusted during the procedure, meaning did they perform an adequate heparinization? These are open questions and I would like to share our experience from Flensburg,
so we have treated nearly 200 patients with the Roadsaver stent from 2015 until now. In 42 patients, we used this stent exclusively for acute stroke treatment and never, ever observed in both groups, in the symptomatic and asymptomatic group and in the group of acute stroke treatment,
we never observed an acute occlusion. How can we explain this kind of difference that neither acute occlusion occurred in our patient group? Probably there are some options how we can avoid stent thrombosis, how we can minimize this. For emergency treatment, probably this might be related
to bridging therapies, though in Germany a lot of patients who received acute stroke treatment are on bridging therapy since the way to the hospital is sometimes rather long, there probably might be a predisposing factor to re-avoid stent thrombosis and so-called tandem lesions if the stent placement is needed.
But we also take care of antiplatelet medication peri-procedurally, and we do this with ASA, as the Hamburg group did and at one day, we always start, in all emergency patients with clopidogrel loading dose after positive CT where we could exclude any bleeding and post-procedurally we go
for dual anti-platelet therapy for at least six months, meaning clopidogrel and ASA, and this is something probably of utmost importance. It's quite the same for elective patients, I think you're quite familiar with this, and I want to highlight the post-procedural clopidogrel
might be the key of success for six months combined with ASA life-long. Stent preparation is also an issue, at least 7 or 8 diameters we have to choose for the correct lengths we have to perform adequate stent deployment and adequate post-dilatation
for at least 5mm. In a lot of trials the Roadsaver concept has been proven, and this is due to the adequate preparation of the stent and ongoing platelet preparation, and this was also highlight in the meta-analysis with the death and stroke rate of .02% in all cases.
Roadsaver study is performed now planned, I am a member of the steering committee. In 2000 patients, so far 132 patients have been included and I want to rise up once again the question, is acute occlusion and issue? No, I don't think so, since you keep antiplatelet medication
in mind and be aware of adequate stent sizing. I highly appreciated your attention, thank you very much.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- [Speaker] Good morning everybody thanks for attending the session and again thanks for the invitation. These are my disclosures. I will start by illustrating one of the cases where we did not use cone beam CT and evidently there were numerous mistakes on this
from planning to conducting the case. But we didn't notice on the completion of geography in folding of the stent which was very clearly apparent on the first CT scan. Fortunately we were able to revise this and have a good outcome.
That certainly led to unnecessary re intervention. We have looked at over the years our usage of fusion and cone beam and as you can see for fenestrated cases, pretty much this was incorporated routinely in our practice in the later part of the experience.
When we looked at the study of the patients that didn't have the cone beam CT, eight percent had re intervention from a technical problem that was potentially avoidable and on the group that had cone beam CT, eight percent had findings that were immediately revised with no
re interventions that were potentially avoidable. This is the concept of our GE Discovery System with fusion and the ability to do cone beam CT. Our protocol includes two spins. First we do one without contrast to evaluate calcification and other artifacts and also to generate a rotational DSA.
That can be also analyzed on axial coronal with a 3D reconstruction. Which essentially evaluates the segment that was treated, whether it was the arch on the arch branch on a thoracoabdominal or aortoiliac segment.
We have recently conducted a prospective non-randomized study that was presented at the Vascular Annual Meeting by Dr. Tenario. On this study, we looked at findings that were to prompt an immediate re intervention that is either a type one
or a type 3 endoleak or a severe stent compression. This was a prospective study so we could be judged for being over cautious but 25% of the procedures had 52 positive findings. That included most often a stent compression or kink in 17% a type one or three endoleak
in 9% or a minority with dissection and thrombus. Evidently not all this triggered an immediate revision, but 16% we elected to treat because we thought it was potentially going to lead to a bad complication. Here is a case where on the completion selective angiography
of the SMA this apparently looks very good without any lesions. However on the cone beam CT, you can see on the axial view a dissection flap. We immediately re catheterized the SMA. You note here there is abrupt stop of the SMA.
We were unable to catheterize this with a blood wire. That led to a conversion where after proximal control we opened the SMA. There was a dissection flap which was excised using balloon control in the stent as proximal control.
We placed a patch and we got a good result with no complications. But considerably, if this patient was missed in the OR and found hours after the procedure he would have major mesenteric ischemia. On this study, DSA alone would have missed
positive findings in 34 of the 43 procedures, or 79% of the procedures that had positive findings including 21 of the 28 that triggered immediate revision. There were only four procedures. 2% had additional findings on the CT
that were not detectable by either the DSA or cone beam CT. And those were usually in the femoro puncture. For example one of the patients had a femoro puncture occlusion that was noted immediately by the femoro pulse.
The DSA accounts for approximately 20% of our total radiation dose. However, it allows us to eliminate CT post operatively which was done as part of this protocol, and therefore the amount of radiation exposed for the patient
was decreased by 55-65% in addition to the cost containment of avoiding this first CT scan in our prospective protocol. In conclusion cone beam CT has allowed immediate assessment to identify technical problems that are not easily detectable by DSA.
These immediate revisions may avoid unnecessary re interventions. What to do if you don't have it? You have to be aware that this procedure that are complex, they are bound to have some technical mistakes. You have to have incredible attention to detail.
Evidently the procedures can be done, but you would have to have a low threshold to revise. For example a flared stent if the dilator of the relic gleam or the dilator of you bifurcated devise encroach the stent during parts of the procedure. Thank you very much.
- Thank you very much. These are my disclosures. So, infected aorta, in terms of the primary infected aorta and secondary infected stent grafts is a difficult problem, and its instance is probably increasing the more we treat. These patients present late, they're often very malnourished,
and they have significant comorbidity. One place where endovascular therapy is definitely effective is in the emergency situation, both the primary infected aortas, like this case on the right hand side, and also for primary aorto-enteric fistula in an emergency.
This is a young man who had obesity surgery and leaked from his gastric anastomosis. He had an esophageal stent, which then caused a significant infection in the mediastinum and eroded through his aorta. He came in in extremis bleeding
and a short stent to cover that saves his life and gives you an opportunity for later on. It's also effective in secondary infections. This is a young lady who had an aortobifemoral bypass, who is bleeding in the retroperitoneum, and you can cover that with a stent graft
and think about further treatment later. Certainly in the short term, endovascular results from treating primary mycotic aneurysms are good. Our series on the left hand side, we had only one death in our endovascular group. In further case series and in systematic reviews,
the 30 day mortality is consistently somewhere between 10% and 15% in the early stage. Long term results from primary mycotic aneurysm treatment are not that bad. This is the biggest paper, I think, in circulation, showing the three, four, five year results
which are acceptable, but you have to remember that success was gained in this group. In those without persistent sepsis, in those without aortoenteric fistula, and probably in some bacterial types, particularly salmonella, which can be treated
well before the endograft is implanted. The secondary graft infection we have to remember, though, has a significant early mortality. This is our series from Imperial, our open graft excision surgery, for urgent and emergency cases included, is 25%,
but for that you swap an excellent five year mortality. Only a few patients die in that long period. If you're putting an endograft in for secondary graft infection and aortoenteric fistula, we can look to this systematic review which I was good to join in with Steve Kakkos.
The results for endovascular treatment are poor. The rate of current sepsis at two years is 42% in the endovascular group, far worse than that for excisional surgery, so they don't do well. I've got significant concerns for endovascular treatment, and we need to worry about these if we're going to put
endovascular grafts in and leave them in. The first is of antimicrobial resistance, there are more and more resistant bugs occurring in our practice, and it's certainly been our practice in our series. Over the last three years, the number of patients with resistant bugs is up to about 50%.
This is a young man who had infective endocarditis with a fungal disease, a multi-resistant fungus. This is the state of his aorta in the top left hand panel. Of course he needs a deep venous reconstruction, which we then cover with Omentum, and he did well after that.
For aortoenteric fistula, if you're going to put an endograft in, in our experience, these get reinfected and rupture, and they probably do need definitive treatment. In secondary graft infection, aortoenteric fistula, remember, is present in 1/3 of patients,
and you need to consider this. You're only going to find that at surgery if you're placing a stent graft in. Again, we discussed earlier in this session, further interventions: graft infection
is more commonly associated with multiple interventions, and it provides a further nidus for infection. So, when is endovascular therapy effective? Well, endovascular treatments in the emergency cases are life-saving and I think they are effective. For primary aortic infection, it's effective
when there is clearance of sepsis, a low -virulence microorganism, and no fistula. Then, the results are acceptable. For secondary cases treated with Endo techniques, the long term recurrence of sepsis is significant, and they really need definitive graft excision,
or you need to accept they have antibiotics and accept palliation. Thank you very much.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- Thank you Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try
to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.
And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,
secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group
is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted
by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.
And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use
those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,
but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.
For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions
for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,
and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.
But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,
so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at
the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions
at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR
predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive
of iliac limb reinterventions. Thank you very much.
- So I have the honor to provide you with the 12-month result of the TOBA II trial. I guess we all confirmed that this action is the primary mechanism of angioplasty. We all know that lesions of dissection have a TLR rate of 3.5 times higher than lesions without dissection.
The current tools for dissection repair, these are stents. They have limitations, really a large metal load left behind causing inflammation. This is leading to in-stent restenosis. So the Tack Endovascular System.
It's a delivery system over six French catheter. This is for above the knee with six implants pre-loaded on a single catheter. The Tack implant itself, it has an adaptive sizing, so it adapts to the diameter of the vessel from 2.6 up to 6.0 for SFA and PPA usage.
It's a nitinol implant with gold radiopaque markers for visibility. Has a unique anchoring system, which prevents migration, and a deck which is deployed in six millimeter in length. So with regard to the TOBA II study design,
this was a prospective multi-center single-arm non-blinded study at 33 sites in US and Europe. We enrolled 213 subjects. These were all subjects with post-PTA dissection. So only with a dissection visible on the angiogram, the patients could be enrolled into this study.
We had the usually primary safety end point, primary efficacy end points, which we are familiar from other trials and other studies so far. With regard to the inclusion criteria, I just want to look at this very briefly.
Mainly we had de novo or non-stented restenotic lesions in the SFA P1. If it was a stenosis, the lesion length could be up to 150 millimeter. If it was a total occlusion, the length was up to 10 centimeters.
They had to be the presence of at least one target run of vessel to the foot. They had to be a post residual, post-PTA residual stenosis of lower than 30%, and the presence of at least one dissection Grade A to F. With regard to the key lesion characteristics,
baseline for the different patients, there was not a big difference to other studies out there. The only difference was maybe we had slightly more patients with diabetes. The lesion, the target lesion length, the mean target lesion length was up to 74 millimeters.
We also had patients with calcification, mainly moderate but also some with severe calcification. There were two met the primary end points. The 30-day freedom from major adverse event, and also the primary efficacy end point at 12 months, which was a freedom from clinical driven TLR,
and freedom from core lab adjudicated duplex ultrasound derived binary restenosis. Now, with regard to patency in a patient cohort, where we really had 100% dissected vessel at 100% dissected vessel population, we had primary patency at 12-month of 79.3%
and a freedom clinical driven TLR of 86.5%. There was with regard to dissection severity, we had 369 total dissections we were treating. The number of dissections per subject was 1.8. The mean dissection length was two centimeters. So around 70% of subjects had a dissection of
Grade C or greater before using the Tack. In 92.1% of all dissections, this could be completely resolved with a Tack. With regard to the Tack stability and durability, in total, 871 Tacks have been deployed. So that was a number of 4.1 Tacks per subject.
The bailout stent rate was very low, just one. The freedom from Tack fracture at 12 months, 100%, and there was one minor Tack migration at 12 months with education by the core lab so the Tack was not seen at the same place as six months or 12 months before.
There was significant clinical improvement with Rutherford category improvement in 63%, which improved of up to two classes. There was also an improvement in ABI, walking impairment questionnaire. So just to conclude, TOBA II is a unique trial.
First to enroll 100% dissected vessels. Successfully met the primary efficacy and safety end points, and demonstrated the Tack is an efficient repair system for dissections after POBA or DCB with minimum metal left behind, low radial force, stable and durable design,
and preservation of future treatment options. There was only a very, very low bailout stent rate. This in combination with high patency rate and high freedom from clinical TLR. Thank you very much.
- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide
and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter
is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues
that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement
of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side
and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,
then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,
coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,
and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques
with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation
of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.
We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go
so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side
or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.
Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.
On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded
and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.
Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.
Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,
despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients
to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,
and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,
and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.
- Thank you, chairman. Good afternoon, ladies and gentlemen. I've not this conflict of interest on this topic. So, discussion about double-layer stent has been mainly focused about the incidence of new lesions, chemical lesions after the stenting, and because there are still some issue
about the plaque prolapse, this has still has been reduced in a comparison to conventional stent that's still present. We started our study two years ago to evaluate on two different set of population of a patient who underwent stent, stenting,
to see if there is any different between the result of two stents, Cguard from Inspire, and Roadsaver from Terumo in term of ischemic lesion and if there is a relationship between the activity of the plaque evaluated with the MRI
and new ischemic lesion after the procedure. So, the population was aware of similar what we found, and that there's no difference between the two stent we have had, and new ischemic lesions is, there's a 38%, for a total amount of 34 lesions,
and ipsilateral in 82% of cases. The most part of the lesion appeared at the 24 hours, for the 88.2% of cases, while only the 12% of cases, we have a control at our lesion. According to the DWI, we have seen that
the DWI of the plaque is positive, or there is an activity of the plaque. There's a higher risk of embolization with a high likelihood or a risk of 6.25%. But, in the end, what we learned in the beginning, what there have known,
there's no difference in the treatment of the carotid stenosis with this device, and the plaque activity, when positive at the DWI MR, is a predictive for a higher risk of new ischemic lesions at 24 hours. But, what we are still missing in terms of information,
where something about the patency of the stents at mid-term follow-up, and the destiny of external carotid artery at mid-term follow-up. Alright, we have to say we have an occlusion transitory, occlusion of the semi-carotid artery
immediately after the deployment of the Terumo stent. The ECA recovery completely. But in, what we want to check, what could happen, following the patient in the next year. So, we perform a duplicate ultrasound, at six, at 12, and 24 months after the procedure,
in order to re-evaluate the in-stent restenosis and then, if there was a new external carotid artery stenosis or occlusion. We have made this evaluation according to the criteria of grading of carotid in-stent restenosis proposed on Stroke by professors attache group.
And what we found that we are an incidence of in-stent restenosis of 10%, of five on 50 patient, one at six month and four at one year. And we are 4% of external carotid artery new stenosis. All in two patient, only in the Roadsaver group.
We are three in-stent restenosis for Roadsaver, two in-stent restenosis for Cguard, and external new stenosis only in the Roadsaver group. And this is a case of Roadsaver stent in-stent restenosis of 60% at one year. Two year follow-up,
so we compare what's happening for Cguard and Roadsaver. We see that no relation have been found with the plaque activity or the device. If we check our result, even if this is a small series, we both reported in the literature for the conventional stent,
we've seen that in our personal series, with the 10% of in-stent restenosis, that it's consistent with what's reported for conventional CAS. And the same we found when we compared our result with the result reported for CAS with conventional stent.
So in our personal series, we had not external carotid artery occlusion. We have 4% instance, and for stenosis while with conventional CAS, occlusion of external carotid artery appear in 3.8% of cases.
So, what can we add to our experience now in the incidence, if, I'm sorry, if confirmed by larger count of patient and longer study? We can say that the incidence of in-stent restenosis for this new double-layer stent and the stenosis on the external carotid artery,
if not the different for all, with what reported for conventional stent. Thank you.
- [Professor Veith] Laura, Welcome. - Thank you Professor Veith, thank you to everybody and good morning. It's a great pleasure, to have the possibility to present the result of this randomized trial we performed near Rome in Italy.
Risk of CAS-related embolism was maximal during the first phases of the second procedure, the filter positioning predilation and deployment and post dilatation. But it continues over time with nithinol expansion so that we have an interaction between the stent struts
and the plaque that can last up to 28 or 30 days that is the so called plaque healing period. This is why over time different technique and devices have been developed in order to keep to a minimum the rate of perioperative neurological embolization.
This is why we have, nowadays, membrane-covered stent or mesh-covered stent. But a question we have to answer, in our days are, "are mesh covered stents able to capture every kind of embolism?" Even the off-table one.
This is why they have been designed. That is to say the embolism that occurs after the patient has left the operating room. This is why we started this randomized trial with the aim of comparing the rate of off-table subclinical neurological events
in two groups of patients submitted to CAS with CGuard or WALLSTENT and distal embolic protection device in all of them. We enrolled patient affected by asymptomatic carotid stenosis more than 70% and no previous brain ischemic lesion
detected at preoperative DW-MRI. The primary outcome was the rate of perioperative up to 72 hour post peri operatively in neurological ischemic events detected by DW-MRI in the two CAS group. And secondary outcome measure were the rise of (mumbles)
neuro biomarker as one on the better protein in NSE and the variation in post procedural mini mental state examination test in MoCA test score We enrolled 29 patients for each treatment group. The study protocol was composed by a preoperative DW-MRI and neuro psychometrics test assessment
and the assessment of blood levels of this two neuro biomarkers. Then, after the CAS procedure, we performed an immediate postoperative DW-MRI, we collect this sample up to 48 hours post operatively to assess the level of the neuro biomarkers
then assess 72 hour postoperatively we perform a new DW-MRI and a new assessment of neuro psychometric tests. 58 patient were randomized 29 per group. And we found one minor stroke in the CGuard group together with eight clinically silent lesion detected at 72 hours DW-MRI.
Seven patient presented in WALLSTENT group silent 72 DW-MRI lesion were no difference between the two groups but interestingly two patients presented immediately postoperatively DW-MRI lesions. Those lesion were no more detectable at 72 hours
this give doubts to what we are going to see with DW-MRI. When analyzing the side of the lesion, we found four ipsilateral lesion in the CGuard patient and four contra or bilateral lesion in this group while four ipsilateral were encountered in WALLSTENT patient and three contra or bilateral lesion
in the WALLSTENT group were no difference between the two groups. And as for the diameter of the lesion, there were incomparable in the two groups but more than five lesion were found in five CGuard patients, three WALLSTENT patient
with no significant difference within the two groups. A rise doubled of S1 of the better protein was observed at 48 hours in 24 patients, 12 of them presenting new DW-MRI lesions. And this was statistically significant when comparing the 48 level with the bars of one.
When comparing results between the two groups for the tests, we found for pre and post for MMSE and MoCA test no significant difference even if WALLSTENT patients presented better MoCA test post operatively and no significant difference for the postoperative score for both the neuro psychometric test between the two groups.
But when splitting patients not according to the treatment group but according to the presence of more or less than 5 lesion at DW-MRI, we found a significant difference in the postoperative score for both MMSE and MoCA test between both group pf patients.
To conclude, WALLSTENT and CGuard stent showed that not significant differences in micro embolism rate or micro emboli number at 72 postoperative hours DW-MRI, in our experience. 72 hour DW-MMRI lesion were associated to an increase in neuro biomarkers
and more than five lesion were significantly associated to a decrease in neuro psychometric postoperative score in both stent groups. But a not negligible number of bilateral or contralateral lesions were detected in both stent groups This is very important.
This is why, probably, (mumbles) are right when they show us what really happened into the arch when we perform a transfer more CAS and this is why, maybe,
the future can be to completely avoid the arch. I thank you for your attention.
- Thank you very much indeed, Chairman. Ladies and gentleman, thank you very much for the podium. Right, my opponent Professor Hogan, has just given his statement asking you to abandon two fenestrated endovascular repairs in favor of three and four fenestrations, but this picture proves to you that during his spare time,
he's actively promoting single fenestration devices, actually. Just keep that in mind. My contention is that three and four branch fenestrated EVARs result in higher complications and higher mortality, which means that they should be avoided if at all possible.
What exactly are the critical issues that are at question here? Do four fenestrated endovascular repairs carry higher risk of complications compared to simpler devices? If they do, are the worth it? However, my opponent is also one of the world's
experts in this area. We've definitely learned quite a lot from him in the early stage of our program about 10-13 years ago. So, he usually has something sensible to say, has he got a point? My plan for this debate is to give you a very balanced view
based on multicenter data. Don't forget, the very compelling data Eric showed you are his single-center series. It is not easy to replicate his results in most other centers. I also would like to keep the debate clean.
Now, coming to the facts, four fenestrated repairs, beyond a doubt, just take more operating time than simpler devices. They're also technically one of the most challenging of aneurysm repairs that you do. They do test your center and team's experience.
Definitely in extricating oneself from intra-operator difficulties, and also, experience gives you the confidence through the operation that you will see the day through. It's also the case that the greater length of aorta is covered by stent graft fabric,
the more lumbars are taken, compromising the spinal cord blood supply further, which is a significant factor. This is a multicenter series from UK, from Terumo Aortic, their Anaconda Fenestrated platform multicenter series of their first 101 devices.
You notice that when the seals are extended to above celiac axis, which means four fenestrated devices, they had a much higher mortality compared to simpler devices. There's also the British Society of Endovascular Therapies Globalstar registry, which I run, currently has got
just over 850 patients registered, and we had data adequate for analysis in 533 patients. Being a much more spread out multicenter series, the results are worse. And you notice that three and four fenestrated devices in this pragmatic multicenter nationwide series
have got a much higher, substantially higher, death rate compared to simpler devices, which is statistically significant. In the long run, up to about four to five years, you notice that four fenestrated do carry a higher, slightly higher risk of re-intervention,
but the overall mortality is not hugely different. The numbers do dwindle. There are very few numbers up to ten years. So, it's not worth looking after 40 years of research. Paraplegia, the Globalstar registry had a total of six paraplegia occurrences reported.
Five of those are in patients who had four fenestrated devices put in. This is definitely worth remembering. It is a complication that really sinks you hard. So, in conclusion, the complexity of device should actually not be compared
without the context of anatomy. Frequently, to get an adequate and durable seal, you do need four fenestrations. However, remember, multicenter series do conclusively show that four fenestrateds are definitely more dangerous compared to the simpler of the devices.
However, this increased risk has to be compared against the perceived risk of alternative treatments such as open repair. So to conclude, Chairman, ladies and gentlemen, the primary aim of fenestrated repair is actually to achieve satisfactory seal zone, which I would say,
which I would say probably at least 20 millimeters of aorta, which is relatively free from calcification or thrombus. That is the bare minimum we should be looking at to get a durable seal. While that is the primary concern, and we need to incorporate as many number of fenestrations
as are technically required depending on your platform that you wish to use. The number of fenestrations themselves are, in fact, secondary and less important. However, if you are able to achieve such a good durable seal without using three or four fenestrations,
more complex devices are certainly not worth it. Thank you very much for your attention.
- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology
to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions
that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,
it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,
as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient
and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy
by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?
Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification
of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,
matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.
You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.
And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.
And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.
Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,
next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages
to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,
so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?
Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization
of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases
of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.
Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging
with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR
to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care
to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,
two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents
using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging
reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,
we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.
And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.
A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,
and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs
and improve clinical outcomes. Thank you.
- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,
it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.
And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication
what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies
to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging
that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,
with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures
to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit
in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is
based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,
and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.
Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system
that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress
and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform
a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.
I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient
before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.
But we hope to present on that more solid data next year. Thank you very much.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.
The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,
however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,
defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought
to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.
I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have
right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.
This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,
small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have
SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented
five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.
The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by
a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of
atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for
inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries
are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.
- I'm going to take it slightly beyond the standard role for the VBX and use it as we use it now for our fenestrated and branch and chimney grafts. These are my disclosures. You've seen these slides already, but the flexibility of VBX really does give us a significant ability to conform it
to the anatomies that we're dealing with. It's a very trackable stent. It doesn't, you don't have to worry about it coming off the balloon. Flexible as individual stents and in case in a PTFE so you can see it really articulates
between each of these rings of PTFE, or rings of stent and not connected together. I found I can use the smaller grafts, the six millimeter, for parallel grafts then flare them distally into my landing zone to customize it but keep the gutter relatively small
and decrease the instance of gutter leaks. So let's start with a presentation. I know we just had lunch so try and shake it up a little bit here. 72-year-old male that came in, history of a previous end-to-side aortobifemoral bypass graft
and then came in, had bilateral occluded external iliac arteries. I assume that's for the end-to-side anastomosis. I had a history of COPD, coronary artery disease, and peripheral arterial disease, and presented with a pseudoaneurysm
in the proximal juxtarenal graft anastomosis. Here you can see coming down the thing of most concern is both iliacs are occluded, slight kink in the aortofemoral bypass graft, but you see a common iliac coming down to the hypogastric, and that's really the only blood flow to the pelvis.
The aneurysm itself actually extended close to the renal, so we felt we needed to do a fenestrated graft. We came in with a fenestrated graft. Here's the renal vessels here, SMA. And then we actually came in from above in the brachial access and catheterized
the common iliac artery going down through the stenosis into the hypogastric artery. With that we then put a VBX stent graft in there which nicely deployed that, and you can see how we can customize the stent starting with a smaller stent here
and then flaring it more proximal as we move up through the vessel. With that we then came in and did our fenestrated graft. You can see fenestrations. We do use VBX for a good number of our fenestrated grafts and here you can see the tailoring.
You can see where a smaller artery, able to flare it at the level of the fenestration flare more for a good seal. Within the fenestration itself excellent flow to the left. We repeated the procedure on the right. Again, more customizable at the fenestration and going out to the smaller vessel.
And then we came down and actually extended down in a parallel graft down into that VBX to give us that parallel graft perfusion of the pelvis, and thereby we sealed the pseudoaneurysm and maintain tail perfusion of the pelvis and then through the aortofemoral limbs
to both of the common femoral arteries, and that resolved the pseudoaneurysm and maintained perfusion for us. We did a retrospective review of our data from August of 2014 through March of 2018. We had 183 patients who underwent endovascular repair
for a complex aneurysm, 106 which had branch grafts to the renals and the visceral vessels for 238 grafts. When we look at the breakdown here, of those 106, 38 patients' stents involved the use of VBX. This was only limited by the late release of the VBX graft.
And so we had 68 patients who were treated with non-VBX grafts. Their other demographics were very similar. We then look at the use, we were able to use some of the smaller VBXs, as I mentioned, because we can tailor it more distally
so you don't have to put a seven or eight millimeter parallel graft in, and with that we found that we had excellent results with that. Lower use of actual number of grafts, so we had, for VBX side we only had one graft
per vessel treated. If you look at the other grafts, they're anywhere between 1.2 and two grafts per vessel treated. We had similar mortality and followup was good with excellent graft patency for the VBX grafts.
As mentioned, technical success of 99%, mimicking the data that Dr. Metzger put forward to us. So in conclusion, I think VBX is a safe and a very versatile graft we can use for treating these complex aneurysms for perfusion of iliac vessels as well as visceral vessels
as we illustrated. And we use it for aortoiliac occlusive disease, branch and fenestrated grafts and parallel grafts. It's patency is equal to if not better than the similar grafts and has a greater flexibility for modeling and conforming to the existing anatomy.
Thank you very much for your attention.
- Good afternoon, Dr. Veith, organizer. Thank you very much for the kind invitation. I have nothing to disclose. In the United States, the most common cause of mortality after one year of age is trauma. So, thankfully the pediatric vascular trauma
is only a very small minority, and it happens in less that 1% of all the pediatric traumas. But, when it happens it contributes significantly to the mortality. In most developed countries, the iatrogenic
arterial injuries are the most common type of vascular injuries that you have in non-iatrogenic arterial injuries, however are more common in war zone area. And it's very complex injuries that these children suffer from.
In a recent study that we published using the national trauma data bank, the mortality rate was about 7.9% of the children who suffer from vascular injuries. And the most common mechanism of injury were firearm and motor vehicle accidents. In the US, the most common type of injury is the blunt type
of injury. As far as the risk factors for mortality, you can see some of them that are significantly affecting mortality, but one of them is the mechanism of injury, blunt versus penetrating and the penetrating is the risk factor for
mortality. As far as the anatomical and physiological consideration for treatment, they are very similar to adults. Their injury can cause disruption all the way to a spasm, or obstruction of the vessel and for vasiospasm and minimal disruption, conservative therapy is usually adequate.
Sometimes you can use papevrin or nitroglycerin. Of significant concern in children is traumatic AV fissure that needs to be repaired as soon as possible. For hard signs, when you diagnose these things, of course when there is a bleeding, there is no question that you need to go repair.
When there are no hard signs, especially in the blunt type of injuries, we depend both on physical exams and diagnostic tools. AVI in children is actually not very useful, so instead of that investigators are just using what is called an Injured Extremity Index, which you measure one leg
versus the other, and if there is also less than 0.88 or less than 0.90, depending on the age of the children, is considered abnormal. Pulse Oximetry, the Duplex Ultrasound, CTA are all very helpful. Angiography is actually quite risky in these children,
and should be avoided. Surgical exploration, of course, when it's needed can give very good results. As far as the management, well they are very similar to adults, in the sense that you need to expose the artery, control the bleeding, an then restore circulation to the
end organ. And some of the adjuncts that are using in adult trauma can be useful, such as use of temporary shunts, that you can use a pediatric feeding tube, heparin, if there are no contraindications, liberal use of fasciotomy and in the vascular technique that my partner, Dr. Singh will be
talking about. Perhaps the most common cause of PVI in young children in developed countries are iatrogenic injuries and most of the time they are minimal injuries. But in ECMO cannulation, 20-50% are injuries due to
ECMO have been reported in both femoral or carotid injuries. So, in the centers are they are doing it because of the concern about limb ischemia, as well as cognitive issues. They routinely repair the ECMO cannulation site.
For non-iatrogenic types, if is very common in the children that are above six years of age. Again, you follow the same principal as adult, except that these arteries are severely spastic and interposition graft must accommodate both axial and radial growths of these arteries, as well as the limb that it's been
repaired in. Primary repair sometimes requires interrupted sutures and Dr. Bismuth is going to be talking about some of that. Contralateral greater saphenous vein is a reasonable option, but this patient needs to be followed very, very closely.
The most common type of injury is upper extremity and Dr. McCurdy is going to be talking about this. Blunt arterial injury to the brachial artery is very common. It can cause ischemic contracture and sometimes amputation.
In the children that they have no pulse, is if there are signs of neurosensory deficit and extremity is cold, exploration is indicated, but if the extremity is pulseless, pink hand expectant treatment is reasonable. As far as the injuries, the most common, the deadliest injuries are related to the truncal injuries and the
mechanism severity of this injury dictates the treatment. Blunt aortic injuries are actually quite uncommon and endovascular options are limited. This is an example of one that was done by Dr Veith and you can see the arrow when the stent was placed and then moved.
So these children, the long-term results of endovascular option is unknown. So in summary, you basically follow many tenets of adult vascular trauma. Special consideration for repair has to do with the fact that you need to accommodate longitudinal
and radial growth and also endovascular options are limited. Ultimately, you need a collaborative effort of many specialists in taking care of these children. Thank you.
- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.
You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience
the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,
as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.
If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.
We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.
Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.
No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time
of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities
and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice
In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases
due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.
We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.
So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed
with multi-institution trial and longer follow-up
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- Thank you 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.
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