- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing
renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is
near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital
pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency
and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,
except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward
endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac
endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.
The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open
conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small
accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited
incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,
but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis
and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.
- Yeah now, I'm talking about another kind of vessel preparation device, which is dedicated to prevent the occurrence of embolic events and with these complications. That's a very typical appearance of an occluded stent with appositional stent thrombosis up to the femur bifurcation.
If you treat such a lesion simply with balloon angioplasty, you will frequently see some embolic debris going downstream, residing in this total occlusion of the distal pocket heel artery as a result of an embolus, which is fixed at the bifurcation of
the anterior tibial and the tibial planar trunk, what you can see over here. So rates of macro embolization have been described as high as 38% after femoral popliteal angioplasty. It can be associated with limb loss.
There is a risk of limb loss may be higher in patients suffering from poor run-off and critical limb ischemia. There is a higher rate of embolization for in-stent restenosis, in particular, in occluded stents and chronic total occlusions.
There is a higher rate of cause and longer lesions. This is the Vanguard IEP system. It's an integrated balloon angioplasty and embolic protection device. You can see over here, the handle. There is a rotational knob, where you can,
a top knob where you can deploy, and recapture the filter. This is the balloon, which is coming into diameters and three different lengths. This is the filter, 60 millimeter in length. The pore size is 150 micron,
which is sufficient enough to capture relevant debris going downstream. The device is running over an 80,000 or 14,000 guide-wire. This is a short animation about how the device does work. It's basically like a traditional balloon.
So first of all, we have to cross the lesion with a guide-wire. After that, the device can be inserted. It's not necessary to pre-dilate the lesion due to the lower profile of the capture balloon. So first of all, the capture filter,
the filter is exposed to the vessel wall. Then you perform your pre-dilatation or your dilatation. You have to wait a couple of second until the full deflation of the balloon, and then you recapture the filter, and remove the embolic debris.
So when to use it? Well, at higher risk for embolization, I already mentioned, which kind of lesions are at risk and at higher risk of clinical consequences that should come if embolization will occur. Here visible thrombus, acute limb ischemia,
chronic total occlusion, ulceration and calcification, large plaque volume and in-stent reocclusion of course. The ENTRAP Study was just recently finished. Regarding enrollment, more than 100 patients had been enrolled. I will share with you now the results
of an interim analysis of the first 50 patients. It's a prospective multi-center, non-randomized single-arm study with 30-day safety, and acute performance follow-up. The objective was to provide post-market data in the European Union to provide support for FDA clearance.
This is the balloon as you have seen already. It's coming in five and six millimeter diameter, and in lengths of 80, 120 and 200 millimeters. This is now the primary safety end point at 30 days. 53 subjects had been enrolled. There was no event.
So the safety composite end point was reached in 100%. The device success was also 100%. So all those lesions that had been intended to be treated could be approached with the device. The device could be removed successfully. This is a case example with short lesion
of the distal SFA. This is the device in place. That's the result after intervention. That's the debris which was captured inside the filter. Some more case examples of more massive debris captured in the tip of the filter,
in particular, in longer distance total occlusions. Even if this is not a total occlusion, you may see later on that in this diffused long distance SFA lesion, significant debris was captured. Considering the size of this embolus,
if this would have been a patient under CLI conditions with a single runoff vessel, this would have potentially harmed the patient. Thank you very much.
- Thank you very much. It's an hono ou to the committee for the invitation. So, I'll be discussing activity recommendations for our patients after cervical artery dissection. I have no relevant disclosures.
And extracranial cervical artery dissection is an imaging diagnosis as we know with a variety of presentations. You can see on the far left the intimal flap and double lumen in the left vertebral artery
on both coronal and axial imaging, a pseudoaneurysm of the internal carotid artery, aneurysmal degeneration in an older dissection, and an area of long, smooth narrowing followed by normal artery, and finally a flame-tipped occlusion.
Now, this affects our younger patients with really opposity of atherosclerotic risk factors. So, cervical artery dissection accounts for up to 25% of stroke in patients under the age of 45. And, other than hypertension, it's not associated with any cardiovascular risk factors.
There is a male predominance, although women with dissections seem to present about five years younger. And there is an indication that there may be a systemic ateriopathy contributing to this in our patients, and I'll show you some brief data regarding that.
So, in studies that have looked at vessel redundancy, including loops, coils, and in the video image, an S curve on carotid duplex. Patients with cervical artery dissection have a much higher proportion of these findings, up to three to four times more than
age and sex matched controls. They also have findings on histology of the temporal artery when biopsied. So one study did this and these patients had abnormal capillary formation as well as extravasation of blood cells between the median adventitia
of the superficial temporal artery. And there is an association with FMD and a shared genetic polymorphism indicating that there may be shared pathophysiology for these conditions. But in addition, a lot of patients report minor trauma around the time or event of cervical artery dissection.
So this data from CADISP, and up to 40% of cases had minor trauma related to their dissection, including chiropractic neck manipulation, extreme head movements, or stretching, weight lifting, and sports-related injuries. Thankfully, the majority of patients do very well after
they have a dissection event, but a big area of concern for the patient and their provider is their risk for recurrence. That's highest around the original event, about 2% within the first month, and thereafter, it's stable at 1% per year,
although recurrent pain can linger for many years. So what can we tell our patients in terms of reducing their risk for a recurrent event? Well, most of the methods are around reducing any sort of impulse, stress, or pressure on the arteries, both intrinsically and extrinsically,
including blood pressure control. I advise my patients to avoid heavy lifting, and by that I mean more than 30 pounds, and intense valsalva or isometric exercise. So shown here is a photo of the original World's Strongest Man lifting four
adult-sized males in addition to weights, but there's been studies in the physiology literature with healthy, younger males in their 20s, and they're asked to do a double-leg press, or even arm-curls, and with this exercise and repetitions, they can get mean systolic pressures,
or mean pressures up into the 300s, as well as heart rate into the 170s. I also tell my patients to avoid any chiropractic neck manipulation or deep tissue massage of the neck, as well as high G-force activities like a roller coaster.
There are some case reports of cervical artery dissection related to this. And then finally, what can they do about cardio? A lot of these patients are very anxious, they're concerned about re-incorporating exercise after they've been through something like this,
so I try to give them some kind of guidelines and parameters that they can follow when they re institute exercise, not unlike cardiac rehabilitation. So initially, I tell them "You can do light walking, but if you don't feel well,
or something's hurting, neck pain, headache, don't push it." Thereafter, they can intensify to a heart rate maximum of 70-75% of their maximum predicted heart rate, and that's somewhere between months zero and three, and then afterwards when they're feeling near normal,
I give them an absolute limit of 90% of their maximum predicted heart rate. And I advise all of my patients to avoid extreme exercise like Orange Theory, maybe even extreme cycling classes, marathons, et cetera. Thank you.
- Thank you. We've all heard that hypogastric artery occlusion can be not so benign as Dr. Snyder mentioned. It's not advancing, there we go. There's the systematic meta-analysis of 61 papers and showing that when you have bilateral occlusion you actually can have worse symptoms
of claudication, even erectile dysfunction. There are these known commercially available devices but should we be doing bilateral cases? There's certainly increased complexity inherent in this and anatomic limitations and cost. We choose to look at a multicenter experience
of 24 centers, 47 patients. Here are the contributing contributors. When we published our experience these are the 47 patients using the GORE IBE device both in Europe and the United States with 6.5 month follow up. The aortic diameters, some of the characteristics.
You can see here that 23% had exclusive iliac aneurysm treatment in the absence of a AAA. Four had aneurysmal or ectatic internal iliac arteries. These are sometimes treated by coil embolizing the first branch and extending the internal branch into a first order branch, there you can see.
But anatomic limitations persist and you can see especially with lengths. You need quite a long length for that ipsilateral side with its device in order to do the bilateral case. These are the IFUs, 165 for the contra and 195 for the ipsi. In our experience you can see that actually 194 on the ipsi
and 195 is what we found as a mean. This seems prohibitive. Some of the tips and tricks to accommodate the shorter lengths are shown here. We can maximize overlap, and we can see that from 195 we can drop this
by maximizing the overlap to 175. We can certainly cross the limbs, that eats up some length. Intrinsic tortuosity can eat up the distance. We can see we can recreate the flow divider, bring up the flow divider higher, match the two limbs. That also can cut down the distance.
Finally in some of these patients we had shorter bridging stents, the endurant stent in particular is a little shorter instead of the 100 millimeter Gore limb and that can also shorten the distance. More about the procedural outcomes. You can see here great technical success.
There were no type one or type three endoleaks. There were some adjunctive stenting in some patients, four patients, because of some kinking and distal dissection. One technical failure's worth pointing out. This is a patient who has heavy calcification
in the iliac system here. Couldn't cannulate, the internal iliac artery required coil embolization. You can see this patient, we had to sacrifice that internal and extend into the external. Complications at 30 days are very acceptable.
One groin infection. You can see that radiographing clinical follow up. One patient with new buttock claudications, a patient who lost the internal iliac artery as I'll mention to you in a minute. The other one was asymptomatic
but also one internal iliac artery lost. No aneurysm related deaths. You can see there's some type two endoleaks but not type one or three endoleaks. More about limb occlusions. This is the external iliac limb.
You can see there were three external iliac limb occlusions, two in the perioperative period and one at six months which presented with claudication requiring a Fem-Fem. The two in the perioperative period, one was a thrombectomy and stent that was treated nicely. The other one was really an iatrogenic limb occlusion
because the internal branch was deployed inadvertently high jailing the external and causing the operators to have to go back and essentially sacrifice that internal in order to preserve flow to the external. You can see that this a patient who in fact did have the claudication symptoms, this is that one patient.
As far as internal iliac limb occlusion in addition to the one we just described there was one asymptomatic incidental find of a limb occlusion at six months. This is a comparison of what Dr. Snyder just discussed, the pivotal trial with expanded access to the global experience I just presented.
You can see when you look at fluoroscopy time, for instance, contrast media used or procedural duration that there is, of course, some increase requirement in the bilateral cases but I would argue that this is not prohibitive. Cost, however, may in fact be an issue.
Certainly this can be a quite costly procedure when we start doing bilateral cases. There are, in fact, new procedure codes that Gore has provided that can offset some of this cost especially for the hospital cost, but nonetheless this is something to be considered.
So in conclusion, preservation of bilateral internal iliac artery with a Gore IBE can be performed safely with excellent technical results and short term patency rates. Only one new onset of buttock claudication occurred in that inadvertent limb jailing. Limb and branch occlusions are rare but can be treated
successfully with stenting most of the time. Some anatomic limitations exist but a number of maneuvers can permit technical success even in shorter length aortoiliac segments. Contrast fluoroscopy and length of case do not appear to be prohibitive.
However, cost remains an issue. Thank you.
- Thank you very much. I'd like to thank the organizers for inviting me. When I started working on this talk, I felt like I was coming to defend that climate change isn't occurring, despite increasing data that suggests it's occurring. - [Woman] (laughing)
- I wasn't quite sure where to take it and I actually wanted to just change the title a little bit, and say DOAC's, I feel, are not indicated for all cancer patients with VTE. I'm going to argue that Low Molecular Weight Heparins are still indicated for substantial
subset of patients with cancer and VTE. These are my disclosures, none of which are relevant to this session. Let's talk about these studies, because these studies give us some insights as we look at them.
This was the Hokusai VTE cancer trial, and showed that Dalteparin and Dioxeapan were the same essentially. But this was a combined outcome of thromboembolism and major bleeding. As Dr. Murley showed you, the patients did better
with the Edoxaban arm as far as preventing recurrent VTE, but there was an increase risk of bleeding in patients who received Edoxaban compared to Dalteparin. The important question then becomes are there subsets of patients that we can identify who we may not want to give Edoxaban to.
They had to go to the supplemental material in the paper to figure this out, and the group subsequently published it... Oops, sorry. Group has subsequently published this, which shows you that if those patients
who had Gastrointestinal cancers had a markedly increased risk of a major bleed, compared to those who received Dalteparin. In contrast, non-gastrointestinal cancers really had no difference. Suggesting that those patients with gastrointestinal cancers
should be looked at as people who probably would benefit more from being on a Low Molecular Weight Heparin. Now, is this specific to Edoxoban? No, the SELECT-D trial also was run. Rivaroxoban for Cancer-Associated VTE,
and as you have already seen, the primary outcome for recurrent VTE was better for Rivaroxoban compared to Dalteparin. However, again, we see this safety signal of increased bleeding in the group that received the Rivaroxoban compared to Dalteparin.
Now if you look as this group as far as which patients had cancers or where did they bleed, the sites of major bleeding, Gastrointestinal was twofold higher in the Riveroxaban arm compared to Dalteparin. Again, a GI cancer related issue.
If you look at clinically relevant non-major bleeding, you also see a threefold increase risk of bleeding in the Riveroxaban arm with GI type bleeding, genital urinary you don't see, genital urinary also had a markedly increased risk of bleeding with Riveroxaban.
However, genital urinary cancers as a whole, were not necessarily associated with the increased risk of bleeding. In contrast, esophagogastric cancers were associated with an increased risk of bleeding. There's also a lot of subsets of patients
with cancer and VTE who are treated. This was an interesting study that just came out looking at Rivaroxoban for central venous catheter associated venous thromboembolism. The enrolled patients greater than 18 years of age, active malignancy and symptomatic proximal,
upper extremity DVT, treated them with Rivaroxoban, this was a prospect of single arm trial, 15mg twice a day for three weeks, and 20mg daily for nine weeks. Primary outcome was achieved,
all of these folks had line preservation at 12 weeks. Interestingly, there was one recurrent event, it was a fatal PE at six weeks, but again the bleeding signal is what stood out. This is the risk of bleeding, you can see by 40 days, slightly more than one month.
About 13% of people had sustained a major bleed or clinically relevant non-major bleed. Again this bleeding issue pops up. Importantly, it wasn't bleeding around the catheter, it was bleeding from GI, GU, and GY insights. Okay?
Again, the bleeding issue becomes important. Gastrointestinal tumors become important. Now if bleeding is an issue, what about Thrombocytopenia? Should we be using this in patients who have Thrombocytopenia,
which is a common problem in the cancer patient population. Now patients with platelet counts less than 50 times 10 to the 9th per liter were excluded from participation in Hokusai VTE Cancer, and SELECT-D required adequate hematologic function.
Both of these trials did have protocols in place for what to do if the platelet count dropped. Never the less, what's come out from the SSC group from the International Society on Thrombosis and Hemostasis is that the data on the use of the DOAC's in cancer associated thrombosis patients with severe thrombocytopenia
that less than 50,000 is lacking. The DOAC's may therefore may not be appropriate for most patients with cancer associated thrombosis and platelet counts less than 50,000. Now the last group, and the last thing that you need to think about
which was also just briefly mentioned in one of Dr. Murley's slides was this drug-drug interaction with the DOAC's. This is important because certain drugs do interact with the DOAC's and these are some of the chemotherapy agents.
In fact, certain classes of chemotherapeutic agents interact with CYP3A4, P-glycoprotein, or both. Drugs that interact with these mechanisms can interfere with the effect of the direct oral anticoagulants and potentially cause it to be cleared faster or accumulate.
These included the antimitotic microtubule inhibitors. The taxanes, it included the TKI's which are used in CML and it included a series of immune-modulating agents, including steroids. So in conclusion, who to favor for a Low Molecular Weight Heparin, gastrointestinal malignancy,
severe thrombocytopenia, selected chemotherapies, and then some considerations for following scenarios. Thank you very much.
- Thanks Frank, for inviting me again. We know very well that CAS and CEA are, and will remain, emboli-generating. This is an algorithm in which we can see the microembolic profile during unprotected carotid stenting. But I am a vascular surgeon, oriented to an endovascular approach, and I believe strongly
in carotid artery stenting renaissance, when we use tips, tricks and new devices. So the real difference between the two procedures are between 0 and 30 days, and this is demonstrated by the result of 10 year by CREST and by ACT 1. So, but the procedure must be protected.
Because as the Kastrup metanalisys said, the unprotected procedure are three, four-fold increase for cerebral protection embolic. And these are the recommendations from European Society of Cardiology and American Heart Association, regarding
the use of embolic protection devices. But what kind of embolic protection device? We know very well that the cerebral distal protection have some strengths and some weaknesses. And the same is for the cerebral proximal protection with the strengths and weaknesses.
So, but this is rarely used, both in the rest of Europe and in Italy. But what about dissent? We are four studies with only prospective, including a population cohort larger than 100 patients. From Italy, from Germany, from Piotr Michalik,
from Poland, again from Italy. As these are the results that are near with the rod centered stent, with very satisfactory results. With very low rate of... This is the CLEAR-ROAD study, with very low rate of complication.
This is a total of 556 patients who underwent stenting with the new generation of stent. This is the incidence of adverse events at 30 days. So, how we can apply the benefit to our procedures with OCT? And OCT demonstrated the safety of new stent design. And why I use OCT in carotids?
With two main issues. A high definition of carotid plaque, and the correct interaction between plaque and stent. With the high definition of carotid dark in order to identify the plaque type. The degree and area of stenosis,
the presence of ulceration, and the thrombus. I study the interaction between plaque and stent. In order to study the stent apposition, the stent malapposition, the fibrous cap rupture, and the plaque micro-prolaps. So this data I published last year on
EuroIntervention, with the conclusion that in relation to the slice-based analysis, we have the correct comparison with conventional stents, and the incidence of plaque prolapse was absolutely lower. So in conclusion, why I strongly believe in a reinvigoration of carotid stenting?
For the use of better embolic protection device. For the use of newer mesh covered stents, and definitively, OCT proves it as shown. Thank you for your attention.
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.
Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.
Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care
over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.
Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.
And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed
with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better
treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?
That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents
shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,
deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.
Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.
Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.
Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same
that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?
More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article
a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.
- 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.
- 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.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed 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.
- Good morning. Thank you for the opportunity to speak. So thirty day mortality following unselected non-cardiac surgery in patients 45 years and older has been reported to be as high as 1.9%. And in such patients we know that postoperative troponin elevation has
a very strong correlation with 30-day mortality. Considering that there are millions of major surgical procedures performed, it's clear that this equates to a significant health problem. And therefore, the accurate identification of patients at risk of complications
and morbidity offers many advantages. First, both the patient and the physician can perform an appropriate risk-benefit analysis based on the expected surgical benefit in relation to surgical risk. And surgery can then be declined,
deferred, or modified to maximize the patient's benefit. Secondly, pre-operative identification of high-risk patients allows physicians to direct their efforts towards those who might really benefit from additional interventions. And finally, postoperative management,
monitoring and potential therapies can be individualized according to predicted risk. So there's a lot of data on this and I'll try to go through the data on predictive biomarkers in different groups of vascular surgery patients. This study published in the "American Heart Journal"
in 2018 measured troponin levels in a prospective blinded fashion in 1000 patients undergoing non-cardiac surgery. Major cardiac complications occurred overall in 11% but in 24% of the patients who were having vascular surgery procedures.
You can see here that among vascular surgery patients there was a really high prevalence of elevated troponin levels preoperatively. And again, if you look here at the morbidity in vascular surgery patients 24% had major cardiac complications,
the majority of these were myocardial infarctions. Among patients undergoing vascular surgery, preoperative troponin elevation was an independent predictor of cardiac complications with an odds ratio of 1.5, and there was an increased accuracy of this parameter
in vascular surgery as opposed to non-vascular surgery patients. So what about patients undergoing open vascular surgery procedures? This is a prospective study of 455 patients and elevated preoperative troponin level
and a perioperative increase were both independently associated with MACE. You can see here these patients were undergoing a variety of open procedures including aortic, carotid, and peripheral arterial. And you can see here that in any way you look at this,
both the preoperative troponin, the postoperative troponin, the absolute change, and the relative change were all highly associated with MACE. You could add the troponin levels to the RCRI a clinical risk stratification tool and know that this increased the accuracy.
And this is additionally shown here in these receiver operator curves. So this study concluded that a combination of the RCRI with troponin levels can improve the predictive accuracy and therefore allow for better patient management.
This doesn't just happen in open-vascular surgery patients. This is a study that studied troponin levels in acute limb ischaemia patients undergoing endovascular therapy. 254 patients all treated with endovascular intervention
with a 3.9% mortality and a 5.1% amputation rate. Patients who died or required amputation more frequently presented with elevated troponin levels. And the relationship between troponin and worse in-hospital outcome remains significant even when controlling for other factors.
In-hospital death or amputation again and amputation free survival were highly correlated with preoperative troponin levels. You can see here 16.9% in patients with elevated troponins versus 6% in others. And the cardiac troponin level
had a high hazard ratio for predicting worse in-hospital outcomes. This is a study of troponins just in CLI patients with a similar design the measurement of troponin on admission again was a significant independent predictor
of survival with a hazard ratio of 4.2. You can see here that the majority of deaths that did occur were in fact cardiac, and troponin levels correlated highly with both cardiac specific and all-cause mortality. The value of the troponin test was maintained
even when controlling for other risk factors. And these authors felt that the realistic awareness of likely long term prognosis of vascular surgery patients is invaluable when planning suitability for either surgical or endovascular intervention.
And finally, we even have data on the value of preoperative troponin in patients undergoing major amputation. This was a study in which 10 of 44 patients had a non-fatal MI or died from a cardiac cause following amputation.
A rise in the preoperative troponin level was associated with a very poor outcome and was the only significant predictor of postoperative cardiac events. As you can see in this slide. This clearly may be a "Pandora's box".
We really don't know who should have preoperative troponins. What is the cost effectiveness in screening everybody? And in patients with elevated troponin levels, what exactly do we do? Do we cancel surgery, defer it, or change our plan?
However, certainly as vascular surgeons with our high-risk patient population we believe in risk stratification tools. And the RCRI is routinely used as a clinical risk stratification tool. Adding preoperative troponin levels to the RCRI
clearly increases its accuracy in the prediction of patients who will have perioperative cardiac morbidity or mortality. And you can see here that the preoperative troponin level had one of the highest independent hazard ratios at 5.4. Thank you very much for your attention.
- Good afternoon to everybody, this is my disclosure. Now our center we have some experience on critical hand ischemia in the last 20 years. We have published some papers, but despite the treatment of everyday, of food ischemia including hand ischemia is not so common. We had a maximum of 200 critical ischemic patients
the majority of them were patient with hemodialysis, then other patients with Buerger's, thoracic outlet syndrome, etcetera. And especially on hemodialysis patients, we concentrate on forearms because we have collected 132 critical ischemic hands.
And essentially, we can divide the pathophysiology of this ischemic. Three causes, first is that the big artery disease of the humeral and below the elbow arteries. The second cause is the small artery disease
of the hand and finger artery. And the third cause is the presence of an arterial fistula. But you can see, that in active ipsillateral arteriovenous fistula was present only 42% of these patients. And the vast majority of the patients
who had critical hand ischemia, there were more concomitant causes to obtain critical hand ischemia. What can we do in these types of patients? First, angioplasty. I want to present you this 50 years old male
with diabetes type 1 on hemodialysis, with previous history of two failed arteriovenous fistula for hemodialysis. The first one was in occluded proximal termino-lateral radiocephalic arteriovenous fistula. So, the radial artery is occluded.
The second one was in the distal latero-terminal arteriovenous fistula, still open but not functioning for hemodialysis. Then, we have a cause of critical hand ischemia, which is the occlusion of the ulnar artery. What to do in a patient like this?
First of all, we have treated this long occlusion of the ulnar artery with drug-coated ballooning. The second was treatment of this field, but still open arteriovenous fistula, embolized with coils. And this is the final result,
you can see how blood flow is going in this huge superficial palmar arch with complete resolution of the ischemia. And the patient obviously healed. The second thing we can do, but on very rarely is a bypass. So, this a patient with multiple gangrene amputations.
So, he came to our cath lab with an indication to the amputation of the hand. The radial artery is totally occluded, it's occluded here, the ulnar artery is totally occluded. I tried to open the radial artery, but I understood that in the past someone has done
a termino-terminal radio-cephalic arteriovenous fistula. So after cutting, the two ends of the radial artery was separated. So, we decided to do a bypass, I think that is one of the shortest bypass in the world. Generally, I'm not a vascular surgeon
but generally vascular surgeons fight for the longest bypass and not for the shortest one. I don't know if there is some race somewhere. The patient was obviously able to heal completely. Thoracic sympathectomy. I have not considered this option in the past,
but this was a patient that was very important for me. 47 years old female, multiple myeloma with amyloidosis. Everything was occluded, I was never able to see a vessel in the fingers. The first time I made this angioplasty,
I was very happy because the patient was happy, no more pain. We were able to amputate this finger. Everything was open after three months. But in the subsequent year, the situation was traumatic. Every four or five months,
every artery was totally occluded. So, I repeated a lot of angioplasty, lot of amputations. At the end it was impossible to continue. After four years, I decided to do something, or an amputation at the end. We tried to do endoscopic thoracic sympathectomy.
There is a very few number of this, or little to regard in this type of approach. But infected, no more pain, healing. And after six years, the patient is still completely asymptomatic. Unbelievable.
And finally, the renal transplant. 36 years old female, type one diabetes, hemodialysis. It was in 2009, I was absolutely embarrassed that I tried to do something in the limbs, inferior limbs in the hand.
Everything was calcified. At the end, we continued with fingers amputation, a Chopart amputation on one side and below the knee major amputation. Despite this dramatic clinical stage, she got a double kidney and pancreas transplant on 2010.
And then, she healed completely. Today she is 45 years old, this summer walking in the mountain. She sent to me a message, "the new leg prostheses are formidable". She's driving a car, totally independent,
active life, working. So, the transplant was able to stop this calcification, this small artery disease which was devastating. So, patients with critical high ischemia have different pathophysiology and different underlying diseases.
Don't give up and try to find for everyone the proper solution. Thank you very much for your attention.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent
secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results
in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different
in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,
or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,
PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus
or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk
of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,
but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.
and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.
Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.
So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.
Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.
In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,
and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide
a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.
And an E-portal is being developed for dissemination. Thank you very much.
- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.
And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.
Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,
it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized
due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage
of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,
which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal
in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak
which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.
And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success
is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent
Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,
an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,
retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered
balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.
At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed
if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.
The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR
combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,
and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.
- Our group has looked at the outcomes of patients undergoing carotid-subclavian bypass in the setting of thoracic endovascular repair. These are my obligatory disclosures, none of which are relevant to this study. By way of introduction, coverage of the left subclavian artery origin
is required in 10-50% of patients undergoing TEVAR, to achieve an adequate proximal landing zone. The left subclavian artery may contribute to critical vascular beds in addition to the left upper extremity, including the posterior cerebral circulation,
the coronary circulation if a LIMA graft is present, and the spinal cord, via vertebral collaterals. Therefore the potential risks of inadequate left subclavian perfusion include not only arm ischemia, but also posterior circulation stroke,
spinal cord ischemia, and coronary insufficiency. Although these risks are of low frequency, the SVS as early as 2010 published guidelines advocating a policy of liberal left subclavian revascularization during TEVAR
requiring left subclavian origin coverage. Until recently, the only approved way to maintain perfusion of the left subclavian artery during TEVAR, with a zone 2 or more proximal landing zone, was a cervical bypass or transposition procedure. As thoracic side-branch devices become more available,
we thought it might be useful to review our experience with cervical bypass for comparison with these newer endovascular strategies. This study was a retrospective review of our aortic disease database, and identified 112 out of 579 TEVARs
that had undergone carotid subclavian bypass. We used the standard operative technique, through a short, supraclavicular incision, the subclavian arteries exposed by division of the anterior scalene muscle, and a short 8 millimeter PTFE graft is placed
between the common carotid and the subclavian arteries, usually contemporaneous with the TEVAR procedure. The most important finding of this review regarded phrenic nerve dysfunction. To exam this, all pre- and post-TEVAR chest x-rays were reviewed for evidence of diaphragm elevation.
The study population was typical for patients undergoing TEVAR. The most frequent indication for bypass was for spinal cord protection, and nearly 80% of cases were elective. We found that 25 % of patients had some evidence
of phrenic nerve dysfunction, though many resolved over time. Other nerve injury and vascular graft complications occurred with much less frequency. This slide illustrates the grading of diaphragm elevation into mild and severe categories,
and notes that over half of the injuries did resolve over time. Vascular complications were rare, and usually treated with a corrective endovascular procedure. Of three graft occlusions, only one required repeat bypass.
Two pseudoaneurysms were treated endovascularly. Actuarial graft, primary graft patency, was 97% after five years. In summary then, the report examines early and late outcomes for carotid subclavian bypass, in the setting of TEVAR. We found an unexpectedly high rate
of phrenic nerve dysfunction postoperatively, although over half resolved spontaneously. There was a very low incidence of vascular complications, and a high long-term patency rate. We suggest that this study may provide a benchmark for comparison
with emerging branch thoracic endovascular devices. Thank you.
- 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.
- I just like the title 'cuz I think we're in chaos anyway. Chaos management theory. Alright, unfortunately I have nothing to disclose, it really upsets me. I wish I had a laundry list to give you. Gettin' checks from everybody, it would be great. Let's start off with this chaos, what has been published.
Again "Ul Haq et al" is a paper from Hopkins. Bleomycin foam treatment of malformations, a promising agent. And they had 20 patients, 21 Bleomycin procedures. (mumbles) sclerosants in a few other patients, 40% complication rate, 30% minor, 10% major.
On a per procedure basis it was a 29% with about 7% major. All patients had decrease in symptoms. But to say "I use Bleomycin" or "I use X" because a complication (mumbles) is nonsense, you're mentally masturbating. It ain't going to be that way, you're going to have complications.
Alright, the use of Bleomycin should be reserved for locations where post-procedure swelling would be dangerous. Well they used it, and one patient required intubation for four days and another patient 15 days. So, it can happen with any agent.
So I don't know why that statement was made. "Hassan et al", noninvasive management of hemangiomas and vascular malformations using Bleomycin again, this handles the plastic surgery a few years ago. 71% effectiveness rate, 29% failure rate,
14% complication rate, 5 major ulcerations. Ulcerations happen with any agent. You're not going to escape that by saying, "Oh, well I'm not going to use alcohol because (mumbles)." No you're going to get it anyway. You all in the literature.
"Sainsbury", intra-lesional Bleomycin injection for vascular birthmarks five year experience again, 2011. 82% effectiveness, 17.3 for failure. Compli- severe blistering, ulcers, swelling, infections, recurrences. Okay, everybody's reporting it.
"Bai et al" sclerotherapy for lymphatic, oral and facial region, 2009. 43% effectiveness, but they found if they used it with surgery they had a higher effectiveness rate. Good. But again that's their effectiveness.
"Young et al", Bleomycin A5 cervico-facial vascular surgery, 2011. 81% effectiveness rate 19% failure for macrocystic. 37% failure from microcystic disease. Complications: ulcerations, hematoma, bleeding, fevers, soft tissue atrophy.
"Zhang et al." Now this is a study. They're goin' head-to-head alcohol versus Bleo. Oh, isn't that a nice thing to do. Huh, funny how that can happen sometimes. There's another paper out of Canada
that doesn't matter, there's 17 pages and there's no statistical significance for that. 138 patients, you got a lot of statistics. "Zhang et al", 138 children. 71 of 75 patients, which is 95% of that serie, were either cured,
markedly effective, or effective, with alcohol. In the Bleo group 41 of 63, that is 65% of the patients, had effective treatment. That means no cures, no markedly effective, just effective. That's their head-to-head comparison. Difference between Ethanol and
the Bleo group again was statistically significant. Ethanol at 75 patients of 14 cases skin necrosis. Bleo group at 63 patients of 5 cases skin necrosis. And in that group they stated it is statistically superior to Bleo. 95 versus 60, that's a big deal.
Again, cured, disappearance post-treatment without recurrence. Markedly effective, meant that greater than 80% was ablated. Effective means about less that 80% reduction but improved. Ineffective, no change. That was their criterion on that paper.
Again, 30 cases, superficial VMs effective rate was 95% in the Ethanol group and the deep group 94%. Okay. What was in the Bleo group? 68% superficial, 56% of deep group. So that's a statistical significance
of failure, between the two agents, comparing head-to-head in anatomic areas. Ethanol VM papers, let's go on to that, we're goin' to do other stuff. "Lee et al", advanced management, 2003, midterm results. 399 procedures in 87 patients,
95% significant or complete ablation, 12.4% complication. "Johnson et al", Kansas. University of Kansas med center, 2002. 100% success rate in tongues. One patient had a massive tongue and had breathing difficulties prior to treatment
remained intubated 5 days and then uneventfully discharged, that was their only complication. "Su et al", ethanol sclerotherapy, face and neck. Again, these are complex anatomies with complex issues of cranial nerves as well as airway control. 2010, 56 of 60 procedures, 90%, four minimal residual,
no skin necrosis, no nerve injuries. "Orlando", outpatient percutaneous treatment, low doses under local anesthesia. This is a very interesting paper out of Brazil. They did 'em under IV sedation, just a little bit by little bit.
They said they had trouble gettin' general so they had to figure another way. Smart, I like people thinkin' things out. Who here doesn't have a problem with anesthesia? Gettin' 'em not to quit before two o'clock? (laughs)
Alright, used local only 39 patients extremity VMs, main symptoms of pain. Cure or significant improvement in 94%. One ulcer, 3 transient paresthesias. "Lee et al", sclerotherapy craniofacial again, 2009. 87 patients, 75% were reductions.
71 of 87 excellent outcomes. One patient transient, tongue decreased sensation. One transient facial nerve palsy, no skin injuries. "Vogelzang" is a very important paper of a single center. Is that author- anybody here? Again, they did VMs and AVMs in this series
and then a per patient complication rate is 13.3, in AMVs 9.7 per patient, but I think what also is important is to do things with regards to procedures. And they listed both. So we'll just, it's about time to quit. This is our embolization series.
And neck, upper extremity, all the anatomies. And we're about a 10 to three ratio with regards to VM/LMs to AVMs in numbers. I think everybody's pretty much like that, a third of their practice. Again, our minor complications are that.
Major complications are these. Summary, what we found in the literature is that Ethanol publications state its efficacy rate routinely at 90 to 100%. And all other second tier sclerosants are 60 to 80%. So I think that's the take home message.
- Thank you Dr. Asher. What an honor it is to be up here with Dr. Veith and Dr. Asher towards the end. You guys are leading by example being at the end of the meetings. So, thank you for allowing me to be up and talking about something
that not a lot of vascular surgeons have experience with, including me. I have no disclosures. On your left, I have listed some of the types of diseases that we most commonly see in the vertebral artery, and there are quite a lot.
And on the right, the standard types of treatment that we pursue in vascular surgery or as a vascular specialist. And often, in the vertebral artery, if we are going to pursue treatment, it's the endovascular route.
But I'll talk a little bit about open surgery. The clinical presentation is often vague. And the things I wanted to point out here in this long list are things like alternating paresthesias, dysphagia, or perioral numbness may be something in the history to look for
that you may not be thinking about when you're thinking about vertebral basilar disease. The anatomy looks straightforward in this picture, with the four segments, as you can see. It gets a little more complicated with just the arterial system,
but then when you start looking at all these structures, that you have to get out of of the way to get to the vertebral artery, it actually can be a difficult operation, particularly even in the V1 segment. The V1 typically is atherosclerotic disease.
V2 is often compression, via osteophyte or musculo-tendon structures. And V3 and V4, at the top, are typically from a dissection injury from sort of stretch or trauma injury. The pathophysiology isn't that well understood.
You have varying anatomy. It's very difficult to access this artery. Symptoms can be difficult to read, and treatment outcomes are not as reliable. But I'm going to take you through a very quick path through history here in the description
of the V1 segment exposure by Dr. Rentschler from 1958. And I love these pictures. Here is a transverse incision over the sternocleidomastoid, just above the clavicular head on the right side. And once you get the sternoclavicular head divided, you can see the longus colli muscle there.
Anteromedial is the carotid. Of course, you surround that with a Penrose drain. And then once you do that, you can separate your longus colli, and deep to that, the vertebral artery just easily slips right up, so you can do your transposition.
It's not quite that easy. I've done one of these operations, and it was difficult finding t e. And, again, here is on the opposite side, you can see the transposition in this cartoon.
Dr. Berguer is the world's expert, and a lot of this open surgical work comes out of the University of Michigan. Here is a study looking at 369 consecutive extracranial vertebral artery reconstructions. You can see the demographics of clinical presentation.
And note that about 34% of patients are presenting with hemispheric symptoms, with 60% in the vertebral basilar distribution. 300 of these reconstructions were for atherosclerosis. And the outcomes were pretty good. Before 1991, there wasn't really a protocol in place
in assessing and doing these procedures. And you can see the stroke and death rates of 4.1 and 3.2% respectively. And then the outcomes after 1991 are considerably better with a five year patency rate of 80%. So, in summary, vertebral artery disease is,
I think if you review this, is somewhat under diagnosed. Revascularization is a viable option. Most often, it's endovascular. But if you have endo-hostility, then an open, particularly for the V1 segment, may be a better option.
And this requires people with good operative experience. 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.
- Thank you, ladies and gentlemen. And our faculty here. Thank you so much for having me, and I'm thrilled to be here as I think some of the few interventionalists who are here. So, the idea was, what is the, is the stance
being overused after the Orbita Trial? And I bring it up because what is the Orbita Trial? This was a trial that really got a lot of, a lot of attention and I think it's important for you to kind of think about it.
It was actually the very first sham-controlled study of 230 patients who were enrolled, 200 who were randomized. Comparing actually PCI to placebo in patients with severe single vessel disease who were medically optimized but were stable.
Very, very interesting. They followed up these patients and the, based, looked at the change in exercise time in these patients and found absolutely no benefit for PCI in changing the exercise time.
So they said, in medically, in patients with medically-treated angina and severe coronary artery stenosis, PCI did not increase exercise time by by, in any difference from placebos. So, this really, really brought up so much attention
and that we were really, really doing unnecessary procedures and the last thing we heard is the last nail in the coffin of PCI. And so, I think it's important to think about what were the issues with that important disease and where we are with the scope of coronary disease.
Which is not insignificant. At the moment, with 326 million patients in the United States, and prevalence of CAD at 16.5, PCI is being performed in 667,000 patients per year. And I think it is important to note
that for the most part, about 50% of this is for acute coronary syndromes, which is not all the Orbita Trial. It's supportive evidence for routine revascularization with guideline-based therapy, directive therapy.
Very, very important that observational data does show a very important relationship between ischemia and death and MI. Revascularization relieves ischemia and that is what it's supposed to do. Large scale studies have shown
a reduction in spontaneous MI, following revascularization versus guideline-directed therapy. And importantly, continued improvement in both PCI and CABG techniques have really shown excellent relief of symptoms
and that we are not here to really, really think about death and MI in the big, big picture. But more immediate reductions as preferred by patients and importantly, we have to note that ischemia directed therapy with revascularization can have important issues.
Regarding whether or not there is an overuse of PCI's, let me just take a, show you the map of the United States. The heat map. The hotter, the more PCI's. And you can see, it really is very much variable and that there is important appropriate use criteria
for coronary revascularization that continues to be updated on a very, very important issue. And there's no question that the media loves the hysteria about overuse of PCI. But I wanted to put that into the context
of what we were doing. In PCI, we are using FFR guidance and physiology guided PCI to show an enhanced outcome. And more and more, we're incorporating that into the armamentarium of both AUC, Appropriate-Use Criteria, as well as evaluating
the valuable patients. And it is important for you to take a look at what have we shown. So far, based on revascularization versus optimal medical therapy in relieving angina and has been a very, very important
improvement in exercise capacity. Albeit, that the one and only trial of the sham procedure didn't show a change in exercise, but there are a lot of issues in this underpowered study that shouldn't really, really turn you away.
For the fact that PCI does relive symptoms. Because there's a tremendous amount of evidence in, in view of reducing angina with a really, really good p value of 12 randomized clinical trials in this area. It is also important that the freedom of angina is shown.
Not just within the Orbita Trial that actually did show a reduction in angina, but very similar to previous studies. And the guidelines are telling us a very, very important Class 1A indication for patients with CID for both
prognosis and treatment. There is an upcoming ischemia trial in ischemic heart disease that will show in 8,000 patients on their NHLBI, with evidence of ischemia hopefully that we could show
that there is benefits. So to conclude, the current guidelines recommend use of revascularization for relief of symptoms with patients with ischemic, a stable ischemic disease. And while placebo remains an important aspect of this medical management up front,
and making sure that there is an important management, we should really, really understand that there's no question that optimal medical therapy has to stay in the background. And the use of PCI is, continues to be of important value.
Thank you for your attention.
- [Doctor] Thank you Tom and thanks Dr Veith for the invitation to be here again. These are my disclosures, so hypogastric embolization is not benign, patients can develop buttock claudication, higher after bilateral sacrifice, it can be persistent in up to half of patients. Sexual dysfunction can also occur, and we know that
there can be catastrophic complications but fortunately they're relatively rare. So now these are avoidable, we no longer have to coil and cover in many patients and we can preserve internal iliac's with iliac branch devices like you just heard. We had previously published the results of looking from
the pivotal trial, looking at the Gore IBE device with the six month primary end point showing zero aneurysm-related morality, high rates of technical success, 95% patency of the internal iliac limb, no type one or type three endoleaks and 98% freedom from reintervention. Importantly on the side of the iliac branch device, there
was prevention of new-onset of buttock claudication in all patients, and importantly also on the contralateral side in patients with bilateral aneurysms that were sacrificed, the incidents in a prospect of trial of the development of buttock claudication was 28%, confirming the data from those prior series.
And this is in line with the results of EVAR using iliac branch device published by many others showing low rates of mortality, high rates of technical success and also good patency of the devices. In press now we have results with follow-up out through two years, in the Gore IBE trial, we also compared
those findings to outcomes in a real world experience from the great registry, so 98 patients from the pivotal and continued access arm's of the IBE trial and also 92 patients who underwent treatment with the Gore IBE device in the great registry giving us 190 patients with 207 IBE devices implanted.
Follow-up was up to three years, it was an longer mean follow-up in the IDE study with the IBE device. Looking at outcomes between the clinical trial and the real world experience, they were very similar. There was no aneurysm-related mortality, there was no recorded new-onset ipsilateral buttock claudication,
this is all from the IDE trial since we didn't have that information in the great registry, and looking at the incidence of reinterventions, it was similar both in the IDE clinical trial experience and also in the great registry as well. Looking at patency of the internal iliac limb, it was
93.6%, both at 12 months and 24 months in the prospective US IBE pivotall trial and importantly all the internal iliac limb occlusions occurred very early in the experience likely due to technical or anatomic factors. When we look at the incidence of type two endoleaks, we had previously noted there was a very high incidence of
type two endoleaks, 60% at one month, this did tail off a bit over time but it was still 35% at two years. A total of five patients in the pivotal IBE trial had a reintervention for type two endoleak through two years, and despite that high incidence of type two endoleak, overall the incidence of aortic aneurysm sac expansion
of more than five millimeters has been rare and low at two and nine percent at 12 and 24 months, and there's been no expansions of the treated common iliac artery aneurysm sac's at either 12 or 24 months. Freedom from reintervention has been quite good, 90.4% through two years in the trial and most of these
re-interventions were type two endoleaks. We now have some additional data out through three years in about two thirds of the patients we have imaging data available now through three years in the pivotal IBE trial, there have been no additional events, device related events reported since the two year data and through three years
we have no recorded type one or type three endoleaks, no aneurysm ruptures, no incidences of migration, very high rates of patency of the external and internal iliac arteries, good freedom from re-intervention and good freedom from common iliac artery aneurysm sac enlargement. And I think, in line with these findings, the guidelines
now from the SVS are to recommend preservation of the internal iliac arteries when ever present and that's a grade 1A recommendation, 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.
- Thanks Fieres. Thank you very much for attending this session and Frank for the invitation. These are my disclosures. We have recently presented the outcomes of the first 250 patients included in this prospective IDE at the AATS meeting in this hotel a few months ago.
In this study, there was no in-hospital mortality, there was one 30-day death. This was a death from a patient that had intracranial hemorrhage from the spinal drain placement that eventually was dismissed to palliative care
and died on postoperative day 22. You also note that there are three patients with paraplegia in this study, one of which actually had a epidural hematoma that was led to various significant and flacid paralysis. That prompted us to review the literature
and alter our outcomes with spinal drainage. This review, which includes over 4700 patients shows that the average rate of complications is 10%, some of those are relatively moderate or minor, but you can see a rate of intracranial hemorrhage of 1.5% and spinal hematoma of 1% in this large review,
which is essentially a retrospective review. We have then audited our IDE patients, 293 consecutive patients treated since 2013. We looked at all their spinal drains, so there were 240 placement of drains in 187 patients. You can see that some of these were first stage procedures
and then the majority of them were the index fenestrated branch procedure and some, a minority were Temporary Aneurysm Sac Perfusions. Our rate of complication was identical to the review, 10% and I want to point out some of the more important complications.
You can see here that intracranial hypotension occurred in 6% of the patients, that included three patients, or 2%, with intracranial hemorrhage and nine patients, or 5%, with severe headache that prolonged hospital stay and required blood patch for management.
There were also six patients with spinal hematomas for a overall rate of 3%, including the patient that I'll further discuss later. And one death, which was attributed to the spinal drain. When we looked at the intracranial hypotension in these 12 patients, you can see
the median duration of headache was four days, it required narcotics in seven patients, blood patch in five patients. All these patients had prolonged hospital stay, in one case, the prolongation of hospital stay was of 10 days.
Intracranial hemorrhage in three patients, including the patient that I already discussed. This patient had a severe intracranial hemorrhage which led to a deep coma. The patient was basically elected by the family to be managed with palliative care.
This patient end up expiring on postoperative day 21. There were other two patients with intracranial hemorrhage, one remote, I don't think that that was necessarily related to the spinal drain, nonetheless we had it on this review. These are some of the CT heads of the patients that had intracranial hemorrhage,
including the patient that passed away, which is outlined in the far left of your slide. Six patients had spinal hematoma, one of these patients was a patient, a young patient treated for chronic dissection. Patient evolved exceptionally well, moving the legs,
drain was removed on postoperative day two. As the patient is standed out of the bed, felt weakness in the legs, we then imaged the spine. You can see here, very severe spinal hematoma. Neurosurgery was consulted, decided to evacuate, the patient woke up with flacid paralysis
which has not recovered. There were two other patients with, another patient with paraplegia which was treated conservatively and improved to paraparesis and continues to improve and two other patients with paraparesis.
That prompted changes in our protocol. We eliminated spinal drains for Extent IVs, we eliminated for chronic dissection, in first stages, on any first stage, and most of the Extent IIIs, we also changed our protocol of drainage
from the routine drainage of a 10 centimeters of water for 15 minutes of the hours to a maximum of 20 mL to a drainage that's now guided by Near Infrared Spectroscopy, changes or symptoms. This is our protocol and I'll illustrate how we used this in one patient.
This is a patient that actually had this actual, exact anatomy. You can see the arch was very difficult, the celiac axis was patent and provided collateral flow an occluded SMA. The right renal artery was chronically occluded.
As we were doing this case the patient experienced severe changes in MEP despite the fact we had flow to the legs, we immediately stopped the procedure with still flow to the aneurysm sac. The patient develops pancreatitis, requires dialysis
and recovers after a few days in the ICU with no neurological change. Then I completed the repair doing a subcostal incision elongating the celiac axis and retrograde axis to this graft to complete the branch was very difficult to from the arm
and the patient recovered with no injury. So, in conclusion, spinal drainage is potentially dangerous even lethal and should be carefully weighted against the potential benefits. I think that our protocol now uses routine drainage for Extent I and IIs,
although I still think there is room for a prospective randomized trial even on this group and selective drainage for Extent IIIs and no drainage for Extent IVs. We use NIRS liberally to guide drainage and we use temporary sac perfusion
in those that have changes in neuromonitoring. Thank you very much.
- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,
both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,
and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms
non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches
versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,
that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require
more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage
than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased
due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations
impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion
during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion
after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing
the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials
where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this
from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph
that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents
with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,
whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.
And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent
also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,
and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.
So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,
always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.
Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)
- Thank you, Ulrich. Before I begin my presentation, I'd like to thank Dr. Veith so kindly, for this invitation. These are my disclosures and my friends. I think everyone knows that the Zenith stent graft has a safe and durable results update 14 years. And I think it's also known that the Zenith stent graft
had such good shrinkage, compared to the other stent grafts. However, when we ask Japanese physicians about the image of Zenith stent graft, we always think of the demo version. This is because we had the original Zenith in for a long time. It was associated with frequent limb occlusion due to
the kinking of Z stent. That's why the Spiral Z stent graft came out with the helical configuration. When you compare the inner lumen of the stent graft, it's smooth, it doesn't have kink. However, when we look at the evidence, we don't see much positive studies in literature.
The only study we found was done by Stephan Haulon. He did the study inviting 50 consecutive triple A patients treated with Zenith LP and Spiral Z stent graft. And he did two cases using a two iliac stent and in six months, all Spiral Z limb were patent. On the other hand, when you look at the iliac arteries
in Asians, you probably have the toughest anatomy to perform EVARs and TEVARs because of the small diameter, calcification, and tortuosity. So this is the critical question that we had. How will a Spiral Z stent graft perform in Japanese EIA landing cases, which are probably the toughest cases?
And this is what we did. We did a multi-institutional prospective observational study for Zenith Spiral Z stent graft, deployed in EIA. We enrolled patients from June 2017 to November 2017. We targeted 50 cases. This was not an industry-sponsored study.
So we asked for friends to participate, and in the end, we had 24 hospitals from all over Japan participate in this trial. And the board collected 65 patients, a total of 74 limbs, and these are the results. This slide shows patient demographics. Mean age of 77,
80 percent were male, and mean triple A diameter was 52. And all these qualities are similar to other's reporting in these kinds of trials. And these are the operative details. The reason for EIA landing was, 60 percent had Common Iliac Artery Aneurysm.
12 percent had Hypogastric Artery Aneurysm. And 24 percent had inadequate CIA, meaning short CIA or CIA with thrombosis. Outside IFU was observed in 24.6 percent of patients. And because we did fermoral cutdowns, mean operative time was long, around three hours.
One thing to note is that we Japanese have high instance of Type IV at the final angio, and in our study we had 43 percent of Type IV endoleaks at the final angio. Other things to notice is that, out of 74 limbs, 11 limbs had bare metal stents placed at the end of the procedure.
All patients finished a six month follow-up. And this is the result. Only one stenosis required PTA, so the six months limb potency was 98.6 percent. Excellent. And this is the six month result again. Again the primary patency was excellent with 98.6 percent. We had two major adverse events.
One was a renal artery stenosis that required PTRS and one was renal stenosis that required PTA. For the Type IV index we also have a final angio. They all disappeared without any clinical effect. Also, the buttock claudication was absorbed in 24 percent of patients at one month, but decreased
to 9.5 percent at six months. There was no aneurysm sac growth and there was no mortality during the study period. So, this is my take home message, ladies and gentlemen. At six months, Zenith Spiral Z stent graft deployed in EIA was associated with excellent primary patency
and low rate of buttock claudication. So we have most of the patients finish a 12 month follow-up and we are expecting excellent results. And we are hoping to present this later this year. - [Host] Thank you.
- 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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