- Thank you very much, Dr. Veith, and thank you to you and the organizing committee for inviting me to participate again this year in, really, the premiere vascular meeting. This morning, I'd like to talk about the contemporary management of carotid artery aneurysms. These are my disclosures.
Extracranial carotid artery aneurysms and pseudoaneurysms may result from a variety of causes, including trauma, fibromuscular dysplasia, atherosclerosis. They're associated with dissection, connective tissue disorders, mycotic aneurysms associated with infection.
We see patch aneurysms from prior carotid endarterectomy, as well as aneurysms associated with radiation, and those that occur spontaneously. Sequelae of these aneurysms are often distal embolization, potential for thrombosis, some patients experience compressive symptoms, and rupture may occur as well.
Treatment has traditionally been through open surgical repair, but there have been advances in endovascular treatments, including covered stents, woven stents, such as the pipeline stent in size-appropriate cases, bare stents with or without adjunctive coil embolization.
Open surgical repair has been time tested and it's proven to be very effective, but there are potential morbidities associated with challenges or surgical exposure, particularly in patients with prior surgery or radiation and those with anatomically-challenging lesions.
A very definitive review of this has been conducted by the surgeons at the Mayo Clinic, including Drs. Money, Bower, and Fowl, and they have described the treatment of 141 aneurysms in 132 patients. In the evolution of treatment with endovascular techniques, covered stents have been employed.
These eliminate aneurysm and pseudoaneurysm perfusion completely and immediately after deployment, but there have been reports of delayed thrombosis of these covered stents when they've been deployed in the cervical distribution. This is a patient of ours who has a large patch aneurysm, nearly four centimeters in size.
If you look on the CAT scan you'll see there's very limited, essentially no overlying soft tissues as a result of the previous radical neck dissection. In this case, we'd elected to use a covered stent to achieve exclusion of this patch aneurysm, and then used a bare metal stent distally to augment the treatment itself.
Our therapies progressed to the use of bare metal stents with associated coil embolization so-called stent, assisted coil embolization. As you can see, there are two sequential, very large, pseudoaneurysms of the internal carotid artery. Here's the carotid bifurcation.
Here, I hope you can see between these green arrows, is the stent that's been deployed. We use closed cell stents typically for these applications, and we can use a microcatheter cannulate that pseudoaneurysm and deploy large neuro-embolic coils to promote flow of cessation.
When we follow up with these patients, here's this patient's one-month post-operative duplex ultrasound, there's no flow in the pseudoaneurysm, and excellent flow in the internal carotid artery without stenosis. We've then progressed to the use of overlapping closed cell stents, and in doing so,
hoped to sort of simulate the pipeline woven stent configuration but have greater applicability in terms of diameter of the internal carotid. Here, you can see this internal carotid artery spontaneous pseudoaneurysm. We then go ahead and bring our initial stent into position
across the origin of the pseudoaneurysm. Here's after initial stent deployment on this static image. Here, after our second stent deployment, you can see very limited static flow within the pseudoaneurysm itself, and that's evidenced by, after the flowed out of the internal carotid artery,
there's still residual contrast within the pseudoanerusym. Here are the individual characteristics of the patients that we've treated using endovascular techniques. To summarize those data, the mean duration of follow up for these patients is 331 days.
But we have followed one patient out to eight years. The study's limited by the relatively small number of patients and the limited duration of follow up in these patients. But our technical success has been 100%, in terms of being able to deploy the endovascular
techniques, and maintain patency. We've had no patients who've experienced neurologic sequelae, including no strokes or TIAs. There've been no cases in which the aneurysm has expanded, in most cases, the aneurysm itself regresses and there's been no flow within those aneurysms or pseudoaneurysms.
Finally, we have been able to maintain 100% patency in these patients, as monitored using our standard follow up protocol with duplex ultrasound being performed every three months for the first year, and annually thereafter. In conclusion, extracranial carotid artery aneurysms and pseudoaneurysms may be treated effectively
using standard open techniques. However, surgical exposure and perioperative morbidity may present challenges for open repair. Endovascular approaches to aneurysm and pseudoaneurysm treatment have evolved progressively. The preliminary results of our analysis with mid-term
follow up suggest that these techniques are effective and durable, with limited procedural morbidity. Thank you very much.
- So PAD affects five million adults in the United States today, and we know the US population is aging. And 15 to 20% of folks 70 years and older have claudication, a minority of these progress to CLI, and the impact on lifestyle is often minimized, as demonstrated in decreased quality of life scores
in these patients. Now with active tobacco use, there is acceleration of disease towards claudication, and there are higher rates of amputation, MI, and death. But prior to open or endo intervention, the SVS Guidelines recommend supervised exercise,
medical therapy with statins, beta blockers, antiantiplatelets, and Cilostazol, and an aggressive multidisciplinary approach to smoking cessation, which should last no less than six months. But what if a patient can't stop smoking?
We've all had these patients. Should patients with lifestyle limiting claudication be denied open surgical or endo-revascularization? So let's look at the open literature. A meta-analysis performed in 2005 of 29 eligible studies. The results were that bypass graft failure
was three times that in smokers versus nonsmokers. There was a dose response relationship in smoking cessation prior to or after bypass, equalized patencies. A more recent study, published in JVS in September, queried the VSGNE, 1789 lower extremity bypasses, 971 were nonsmokers, 818 were smokers,
and what they found was that primary patency at two years was 48% in smokers, versus 61% in nonsmokers, and when they propensity matched these patients, there was even a greater difference. 10 year survival was also decreased. And in another article,
published in August of this year in JVS, again a VSGNE study, over 2,000 patients, almost 3,000 patients with lower extremity bypass for claudication. The results looked at MALE, amputation-free survival, limb loss, death, major limb events or death,
and they found that current smoking was a significant predictor of major adverse limb events, and major adverse limb events or death. But do active smokers have worse outcomes after endovascular interventions? So, let's look at the literature again.
And there is none. The only paper I could find was a Markov decision analysis, in which compared revascularization in active smokers to medical management, this was a retrospective study, and their results demonstrated better quality of life in smokers after revascularization versus medical therapy.
The quality of life was similar, after revascularization in nonsmokers and smokers, and there was no increase in amputation rates up to 36 months. Also, 26% of the folks that were revascularized, quit tobacco use after their quality of life was improved.
So we decided to do a small study at my hospital. The outcome of endovascular interventions in active smokers with lifestyle limiting claudication versus nonsmokers. This was retrospective. 138 total patients with endovascular intervention for claudication, 47 were current tobacco users,
91 were never or former smokers. The primary endpoints were reintervention, secondary endpoints, surgical bypass, limb loss, MI, stroke and death. And here you can see, as in most studies, the smokers were a younger population,
and anticoagulation, in our patient population, was more common. As far as comorbidities, they were more common, as in most studies, in the nonsmoking group. And in a mean followup of 3.6 years for both groups, there was no statistically significant difference
between the two groups for any of the outcome measures. So in conclusion, active smokers with lifestyle limiting claudication, we would advocate, of course, smoking cessation. Outcomes with respect to reintervention, surgical bypass and limb loss appear to be equivalent in these two groups.
We feel that these patients should not be denied endovascular intervention, and improved quality of life after intervention may result in an increase in smoking cessation in this patient population. Limitations are obvious, this was a very small study,
and retrospective, and we are actually extending this study to look at several hundred additional patients. So I thank you for your attention.
- I want to thank Dr. Veith for the invitation to present this. There are no disclosures. So looking at cost effectiveness, especially the comparison of two interventions based on cost and the health gains, which is usually reported
through disability adjusted life years or even qualities. It's not to be really confused with cost benefit analysis where both paramaters are used, looked at based on cost. However, this does have different implications from different stakeholders.
And we look, at this point, between the medical center or the medical institution and as well as the payers. Most medical centers tend to look at how much this is costing them
and what is being reimbursed. What's the subsequent care interventions and are there any additional payments for some of these new, novel technologies. What does the payers really want to know, what are they getting for the money,
their expenditures and from here, we'll be looking mainly at Medicare. So, background, we've all seen this, but basically, you know, balloon angioplasty and stents have been out for a while and the outcomes aren't bad but they're not great.
They do have continued high reintervention rates and patency problems. Therefore, drug technology has sort of emerged as a possible alternative with better patency rates. And when we look at this, just some, some backgrounds, when you look at any sort of angioplasty,
from the physician's side, we bill under a certain CPT code and it falls under a family of codes for reimbursement in the medical center called an APC. Within those, you can further break it down to the cost of the product.
In this situation, total products cost around 1400 dollars and the balloons are estimated to be 406 dollars in cost. However, in drug-coated balloons, there was an additional payment, which average, because they're such more expensive devices than the allotments and this had an additional payment.
However, this expired in January of this year. When you look at Medicare reimbursement guidelines, you'll see that on an outpatient hospital setting, there's a reimbursement for the medical center as well as for the physican which is, oops sorry, down eight percent from last year.
And they also publish a geometric mean cost, which is quite higher than we expected. And then the office based practice is also the reimbursement pattern and this is slated to go down also by a few percentage points.
When you look at, I'm sorry, when you look at stents, however, it's a different family of CPT codes and APC family also. Here you'll see the supply cost is much higher in the, I'm sorry, the stent in this category is actually 3600 dollars.
The average cost for drug-eluting stents, around 1500 dollars and the only pass through that existed was on the inpatient side of it. Again, looking at Medicare guidelines, the reimbursement will be going down 8 percent
for the outpatient setting and the geometric mean cost is 11,700. So, what we want to look at really is what is the financial impact looking at primary patency, target lesion revascularization based on meta analysis. And the reinterventions are where the real cost
is going to come into effect. We also want to look at, when it doesn't work and we do bailout stenting, what is the cost going to happen there, which is not often looked at in most of these studies. So looking at a hypothetical situation,
you've got 100 patients, any office based practice, the payee will pay about 5145. There's a pass through payment which averages 1700 dollars per stent. Now, if you look at bailout stenting, 18.5 percent at one year,
this is the additional cost that would be associated with that from a payer standpoint. Targeted risk for revascularization was 12 percent of additional costs. So the total one year cost, we estimated, was almost a million dollars
and the cost per primary patency limb at one year was 13 four. In a similar fashion, for drug-eluting stents, you'll see that there's no pass through payment, but although there is a much higher payer expenditure. The reintervention rate was about 8.4 percent
at one year for the additional cost. And you'll see here, at the one year mark, the cost per patent limb is about 12,600 dollars. So how 'about the medical center, looking at Medicare claims data, you'll see the average cost for them is 745,000,
the medical center. Additional costs listed at another 1500. Bailout renting, as previously, with relate to a total cost at one year of 1.2 million or at 16,900 dollars per limb. Looking at the drug-eluting stents,
we didn't add any additional costs because the drug-eluting stents are cheaper than the current system that is in there but the reinterventions still exist for a cost per patent limb at one year of 14 six. So in essence, a few other studies have looked
at some model, both a European model and in the U.S. where the number of reinterventions at two to five years will actually offset the additional cost of drug-eluting stents and make it a financially advantageous process.
And in conclusion, drug-eluting stents do have a better primary patency and a decreased TLR than drug-coated balloons or even other, but they are more expensive than conventional treatment such as balloon angioplasty and bare-metal stents.
There is a decreased reintervention rate and the bailout stenting, which is not normally accounted for in a financial standpoint does have a dramatic impact and the loss of the pass through makes me make some of the drug-coated balloons
a little more prohibitive in process. Thank you.
- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first
before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.
We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column
from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.
Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,
which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied
and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal
amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,
but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced
from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,
organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC
seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.
You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.
So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these
biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...
Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be
most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.
We have to work that out, I hope. Calcification is generally a very late feature in this process. Thank you very much.
- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent
flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue
but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using
a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient
and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta
and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once
the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide
and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug
over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect
of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve
and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.
This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft
to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing
in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment
of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)
- 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.
- My topic is status of left atrial appendage exclusion and we're going to go to the heart in this topic. This is my disclosures: atricure being the main one. The other disclosure is we actually have an annual meeting of left atrial appendage that takes over three days, so this is a very
extensive topic and I'm going to ask you to put your seat belts on because it's going to be a lot of topics to cover over five minutes. So, as you know, the left atrial appendage is the source of thrombus that comes from the heart in ninety percent of patients so patients
who have a stroke coming from the heart, ninety percent chances are the clot was in the left atrial appendage. If you look at just in the US, if we can take care of left atrial appendage in these patients, we can deal with 130,000 strokes.
It's a very substantial number. And this translates with the amount of money that the industry has put in this. Over half a billion dollars currently and it's increasing significantly. This is one of the fastest growing area
of devices worldwide in any specialty. Now left atrial appendage also excludes atrial fibrillation so besides dropping and reducing the stroke, it does also an electric isolation so it reduces the atrial fibrillation rate in patients
who have chronic AFIB so those are two main reasons why we close left atrial appendage in specific patients who have the indication for. Now I'm going to go over the talk if you look at patients who have an open heart surgery, they already know, based upon this recently
published journal publication from Mayo Clinic, that left atrial exclusion significantly reduces stroke. In these patients, they actually look at 75,000 patients, five percent of them had surgical exclusion and that that propensity analysis among patients who had AFIB and closure of appendage versus
the same patient population with similar risk who did not and they had significantly less stroke in patients who had exclusion of appendage, as you see here, and less mortality. There is a specific trial called ATLAS that is going to be given a more randomized study
but there is a lot of data already supporting that appendage reduces significant stroke. Now these are the two studies. This is one of the most important slides that I want you to remember. They are the Endocardial Trial Devices
and there are Epicardial Devices and I'm going to go over in the last slide what are the pros and cons of each one. What I'm going to talk about each of them at a time. Now endocardial is obviously transcatheter techniques. Epicardial is a clip that is typically placed
outside but it could be also endocardial, as well. So Watchman is the most common device that is placed endocardial. It's also the only one that is FDA approved currently. And it's probably the best device that we will place in an elderly patients or failed patients.
It's 14 Fringe, has five sizes based upon a CT Scan. Sized pretty much like a anthracic aneurysm in how we measure actually, triple As. It's sized 10 o
and has 10 barbs in it. It's also approved in CE marks, as well. Now the FLX version of it is a new version that has been overworked right now but this study, this device is actually the most studied device. Protect-AF and Prevails are the typical two studies
and they have shown at four-year followup that the ischemic stroke and systemic embolization is significantly lower and comparable to coumadin and significantly lower bleeding rate, as well. But they are not perfect obviously. There is a lot of patients that cannot be treated
due to anatomic issues. There is also percent of patients will have leaks that will require additional anticoagulation. Now Amplatzer is not approved.
It's not a percutaneous endocardial device, that is CE marked, but I'm not going to spend time just because of the timing. Same applies to WaveCrest, Occulotech, and LAmbre. You can imagine these at the early time of EVARS and TVARS that we have initially one device on the market
and now more and more devices coming up. We have a similar one on the left atrial appendage. And these devices will come into market within the next few years. They are already in Europe available. But no randomized trials.
Now with all these endocardial devices there are multiple leak effects typically including leaking around it because as you know appendage orifices is not a perfect circle. It's not like a aorta, many aortas, at least. You could have an area that is very narrowed
and you could have what we call a really perivalval leak which cardiologists will name differently, a agofact in this case. Now one of the epicardial devices, these are devices that come from outside, is called the LARIAT.
This is 510K approved in the United States and also available in CE but has significant complications. Why? Because it's an endocardial device. That means you have to transvenous access and have a transeptal from right atrium going to the left atrium but also you have
to access the pericardium and pretty much put a loop around the left atrial appendage that connects over a magnet. It's actually a pretty neat device but it has significant issues with complications including tamponade and its the only device
that has actually a death rather compared to any other ones. Other ones have almost zero mortality rates. There is a leak option so if you close that appendage with a circular device, if you continues to have some blood going into it
this enlargened sac can actually open up again to orifices that's called the Gunnysack Effect. And one of the issues that, you know, Lariat has a failure rate. Plus, Lariat can be only applied for certain sizes of appendages that are small,
so that's important, as well. Now there are a lot of issues with surgical closures. I'm going to shorten this portion but to say the suture alone is not a perfect idea and for that reason, we actually use a clip for this that's called the AtriClip
that is FDA approved and this is how it looks like from inside the heart. You have an endocardial to endocardial apposition with less thrombogenesty. This is the AtroClip device again and we have option also to put that as a
thoracoscopic approach for patients who do not need open heart surgery. As you see at three month, the entire appendage dies off from ischemic event: it goes away, which is what we want. This is the prospective trial that showed
the safety of this device. And this is the left atrial appendage symposium that I mentioned to you. If you look at the Watchman device, the leak is a certain concern but it's the safest device for elderly patients, however, the epicardial
device are the safest with the lowest rate of leak and best outcome. Overall, this is my last slide, I think 100 percent of closing the left atrial appendage is important so that's the reason epicardial device right now are much more successful.
This is an important concept for patient with permanent AFib: it can cut down on the stroke risk by 90 percent and improves survival in patients and loved ones who has atrial fibrillation. Efficacy has been shown in multiple studies and in the safety, as well (mumbles).
If we have a heart-team approach, very similar like in the vascular approach, I think it takes away the specialty bias among the two various closure devices. Thank you very much.
- 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.
- 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.
- The FLEX Scoring Catheter is one of the new tools, which is dedicated to vessel preparation, either as a stent, as a therapy followed by plain balloon angioplasty, or preparing the vessel for drug-eluting balloons and stents. So, the background basically is that
we're more and more tackling chronic total occlusions, and these kind of lesions, they have an increased risk of being calcium-containing, creating dissections, perforations, embolization, and poor luminal gain. And for that purpose, this device, which is more or less
a kind of surgical device, was developed. It's a interventional tool which can be introduced via a six-French sheath. It's an over-the-wire system, running over a 14 or 18 thousandths guide wire. It's common in shaft lengths of
40 centimeters dedicated to AV, fistula treatment and 120 centimeters, and the device is exposed to the vessel wall with three atherotomes, with the indication for femoropopiliteal and AV fistula excess treatment. One size fits all is really the right description
of this device, except having two different shaft lengths, the device itself is coming in one size only. What does it result in? Well, it results in micro-incisions, as you can see it over here, also over here in an OCT image, and the depths of these incisions
is about 0.5 millimeters, the pressure which is applied to the surface is about one atmosphere, independent on the vessel size. So, the idea and the rationale for this device is to facilitate and increase the vessel compliance and to create an controlled environment for angioplasty.
There are, just recently, some specimen analysis performed by CBSET, what you can see over here, marked by arrows, these arrows indicate the FLEX-induced micro-incisions, and you can see that these incisions are really circumferential with controlled,
uniform depths of those incisions into the plaque or the vessel wall. This is a 150 times magnification and you can see these longitudinal micro-incisions, which are very much parallel, it's like using a cutting balloon,
the advantage, however, is that this device can be applied to even longer lesions, the limitation of a cutting balloon is the balloon length of 20 centimeters only. So what are the early results? I can present you the acute outcomes
of 100 patients' sample size, with chronic total femoropopliteal occlusions. We can see that the average lesion length was really significant, 191 millimeters, the range was up to 35 centimeters, and there was moderate to severe calcification
in almost 50% of those cases. The luminal gain post FLEX application was about 31%, and the following balloon opening pressure, which was documented within this registry, was four atmospheres only, which is a signal that really the vessel compliance
is significantly improved, considering the almost 50% of moderate to severe calcification of those lesions. There had been no emboli, there had been no flow-limiting dissections, nevertheless, the provisional stent use was still high with 19%.
This is one of two case examples I would like to share with you. This was an instant re-occlusion of the popliteal artery, 10 centimeters in length, this was passed with an 18 thousandths guide wire, three passes with the FLEX catheter had been performed,
as you can see over here. And this was then, this was the result after FLEX catheter application and this is post additional drug-coated balloon angioplasty, there was no dissection, there was no significant residual stenosis.
Another case example, unfortunately, the video will not run, this was a long distance flush occlusion of the SFA, and you can see the calcium here in the entire length of the lesion, this lesion was treated, again, with the FLEX catheter, here, the video is not running,
this is the final result after DCB application. So, in summary, there's a high degree of technical success in achieving consistent luminal gain post FLEX, there's a low opening balloon pressure, and the re-canalization of CTOs was possible with a low rate, zero rate of significant dissections
and the low provisional stent rate. Thank you very much.
- (speaks French) liver surgeon I perform hepatobiliary surgery and liver transplantation. Maybe I don't belong here, I so probably more rested than anybody in the room here. But today I will present about liver surgery and hepatectomy. I work at The Royal Free where I have the honor and pleasure to have seen Krassi. We are in the
little island in the North Sea. There is many things going wrong there including Brexit but, the guys uh, we have a major advantage. The NHS favors centralization. Centralization look there: London is bigger than New York Uh, eight million, 50 million greater London
and we drain about six millions of people with our HPB center. In the center we perform about 2,000 operations, of major surgery. In five years, half of them are liver surgery. And most of them have uh, benign, malignant tumor. A very small percentage have benign tumor.
I count here for complications uh, and mortality look there, 3.1% of only the malignant because the benign are young people and we perform a different strategy, they have no mortality. Today Hepatic Hemangioma, look there it is uh, 1898 is a key year. Not only the first description
of the lady that died after bleeding out in an autopsy but also, Hermann Pfannenstiel uh, Professor Pfannenstiel. I will introduce you to him. He described the first operation. Now, we're talking of congenital malformations, they uh, lesions occur in the liver and they may grow,
but only 20% they grow. They have a chaotic network of vessels and they have fibrotic, fibrotic development within it. I introduce you Hermann Pfannenstiel, he was a gynecologist, famous, famous, important incision that we still use today.
Remember him, we'll talk to him later. Microscopically, the microscopic is our well-circumscribed lesion, they're compressible. Important you see down there that they compress the liver that is normal close to it. This has an implication because if you operate,
you fill find a blood duct or a vessel and it will bleed or leak by. Microscopically, they are ectatic blood vessels and they are fed by arteries. This is also an important point, for therapy. Separated by fibrous septa, this is also important
because they become harder and they become bigger. And they have distorted blood vessels. They're more frequent uh, benign tumor. Prevalence up to 7%, they have non-neoplastic this must be clear, they are non-cancer. The proliferation of endothelial cells, women
have more and particularly pregnant women, more pregnancy or contraceptive. We divide them in cavernous and capillary and we'll have a word on that. Symptomatic being half of the cases, multiple in 10%, they rarely bleed and they rarely rupture.
Capillary Hemangiomas cells small, I show you an MRI here. The differential with HCC liver cancer is most important. They both are theorized but they continue to appear on late face. They are asymptomatic please, do not touch them, they do no harm.
And so we will not speak of them. We speak only of the cavernous hemangioma. And here, the cavernous hemangioma bleeds Oh my God, no, it's not true. There are 83 reports of bleeding since the report of Hermann Pfannenstiel. Uh, 97 cases, adenomas bleed more frequently.
Frequently, in the past they were confused. Hemangioma and adenoma, adenoma does bleed. There are only true cases, 46 in the literature. Size is not important and they are very rare in elderly people.
This is what we see when they are giant cavernous hemangiomas, they're serious, they are rather easy to diagnose. Diagnostic criteria, uh, look up typical for uh, cavernous hemangioma. How do you point here? Yep, you stop. If you then see that you have
an atypical hemangioma, you jump over to an MRI. MRI is too nowadays, diagnostic and uh, the important thing is you stop. Once you have the diagnosis with MRI, you stop, do nothing yet, do not follow, bye-bye. Treatment modalities surgery: Selective TAE, Radiotherapy, Medication: two classes,
Propranolol, to decrease the hyper circulation. Bevacizumab as a class of drugs of inhibitors of inferior growths and endories, eventually are cold. This is seminal paper, about 35 years ago "Do not treat asymptomatic patients." This is a key: do not bother with hemangioma.
If you do have the algorithm, you look at complaints that can present incidentally when they have complained, not complained, no treatment of abdominal pain. Unrelated to no treatment, we have to eventually make sure that the pain is not related to the cavernous hemangioma. If there is other futures
like compression giant, you can do surgery. If you have a doubt in diagnosis, today rare with MRI, then you can perform a biopsy. The surgical indication then remain progress, severe, disabling symptoms. Diagnostic uncertainty nowadays not the case, with MRI.
Consumptive coagulopathy or Kasabach-Merritt syndrome is a serious, we will see when you perform human transplants. Spontaneous rupture with bleeding as an emergency. Rapid growth in 25%. This is a paper that shows that the size of the cavernous hemangioma is here,
and you can see that operation has been performed for larger size, however, look that even in non-symptomatic or partially asymptomatic patients, you can reach sizes up to 15 centimeters. And this a review of the literature from a Chinese group where they revised a thousand to a hundred cases,
no mortality in the series and enucleation versus the anatomic resection is better. Less complications, less blood less, less time of surgery, and less hospital stay. So please, in this case of surgery, we do enucleation. I was asked by my society the HPBA to speak
about transplantation for liver tumor. You can that an indication is unresectable disease, severe symptoms and mass occupying effects. Pre-cancerous behavior is not for hemangioma only for adenoma differential diagnosis with HCC. And you have to be attentive that you avoid
liver insufficiency during your resection. So, in conclusion, for benign lesions, hemangioma technically is the only indication. And now the systematic review that shows around several emothing United States UNOS and the ELTR Several, several benign tumors but if you break down
for type of tumors you see that most of them are Polycystic disease or partly cavernous hemangioma are very low. 77 in Europe, out of 97,000 operation of transplantation. So, let's get an old paper. The pioneer of transplantation again, extremely low,
one out of 3,200. An extremely low percentage. It's my personal experience I was working at Essen, Germany. Almost a thousand transplants we performed. Unfortunately most of them I did and we never transplanted one hemangioma, my experience for transplantation is zero because it should not be done.
So, my advice for hemangioma. Biopsy not advised, see a liver surgeon in a serious center, diagnosis is done my MRI, observe doubt symptoms and observe. Let the patient beg you for surgery, if significant increase in size and symptoms, we can do surgery. Embolization is possible.
Sometimes it's harmful. The role of the surgeon is to confirm the diagnosis, differentiate it from cancer, exclude causes of other symptoms and avoid unnecessary surgery that's the main thing. Surgery for severe symptoms of Kasabach-Merritt. Only for complicated symptomatic lesions, or where the
diagnosis is uncertain. Ladies and gentleman, I will conclude with a couple of questions. If you have a daughter or son with a liver tumor, would you go to a center or a competent surgeon or to a gynecologist. Professor Pfannenstiel for instance or another doctor. If your car has a problem,
would you go to a good mechanic once for all, or to a small shop for 20-40 times. It is a matter of experience and a matter of costs. And with this, I am ready for your questions. - [Audience Member #1] When have you personally operated on these lesions?
- [Speaker] I am. And the experience that I have in the past I seemed young but I practiced for many years. When I started 25-30 years ago, we were operating many of these because we were not so certain. Then MRI came, and MRI basically made the diagnosis so easy and straight-forward and we started observing
patients. We still do operate today, but they are very large tumors and when I do personally, I avoid the androbolization before because you have more skylotec reaction, just (grainy sound effect) to peel it away from the normal parenchymal.
This is our experience. - [Audience] Thank you. - [Speaker] Thank you very much, yes? - [Audience Member #2] Yes, one question. When you operate, and with all of the experience you have, what are the complications of
(mumbles) - [Speaker] The main, so first of all, there has been also an evolution in the type of operation we don't do anymore the resections where you have some bi-leaks. If you operate correctly, it's bleeding and one infection not one born. If you have to watch bi-leak is the one
that you have to watch and that's because the tissue is pushed away and you may miss something during the enucleation.
- 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.
- Relevant disclosures are shown in this slide. So when we treat patients with Multi-Segment Disease, the more segments that are involved, the more complex the outcomes that we should expect, with regards to the patient comorbidities and the complexity of the operation. And this is made even more complex
when we add aortic dissection to the patient population. We know that a large proportion of patients who undergo Thoracic Endovascular Aortic Repair, require planned coverage of the left subclavian artery. And this also been demonstrated that it's an increase risk for stroke, spinal cord ischemia and other complications.
What are the options when we have to cover the left subclavian artery? Well we can just cover the artery, we no that. That's commonly performed in emergency situations. The current standard is to bypass or transpose the artery. Or provide a totally endovascular revascularization option
with some off-label use , such as In Situ or In Vitro Fenestration, Parallel Grafting or hopefully soon we will see and will have available branched graft devices. These devices are currently investigational and the focus today's talk will be this one,
the Valiant Mona Lisa Stent Graft System. Currently the main body device is available in diameters between thirty and forty-six millimeters and they are all fifteen centimeters long. The device is designed with flexible cuff, which mimics what we call the "volcano" on the main body.
It's a pivotal connection. And it's a two wire pre-loaded system with a main system wire and a wire through the left subclavian artery branch. And this has predominately been delivered with a through and through wire of
that left subclavian branch. The system is based on the valiant device with tip capture. The left subclavian artery branch is also unique to this system. It's a nitinol helical stent, with polyester fabric. It has a proximal flare,
which allows fixation in that volcano cone. Comes in three diameters and they're all the same length, forty millimeters, with a fifteen french profile. The delivery system, which is delivered from the groin, same access point as the main body device. We did complete the early feasibility study
with nine subjects at three sites. The goals were to validate the procedure, assess safety, and collect imaging data. We did publish that a couple of years ago. Here's a case demonstration. This was a sixty-nine year old female
with a descending thoracic aneurysm at five and a half centimeters. The patient's anatomy met the criteria. We selected a thirty-four millimeter diameter device, with a twelve millimeter branch. And we chose to extend this repair down to the celiac artery
in this patient. The pre-operative CT scan looks like this. The aneurysm looks bigger with thrombus in it of course, but that was the device we got around the corner of that arch to get our seal. Access is obtained both from the groin
and from the arm as is common with many TEVAR procedures. Here we have the device up in the aorta. There's our access from the arm. We had a separate puncture for a "pigtail". Once the device is in position, we "snare" the wire, we confirm that we don't have
any "wire wrap". You can see we went into a areal position to doubly confirm that. And then the device is expanded, and as it's on sheath, it does creep forward a bit. And we have capture with that through and through wire
and tension on that through and through wire, while we expand the rest of the device. And you can see that the volcano is aligned right underneath the left subclavian artery. There's markers there where there's two rings, the outer and the inner ring of that volcano.
Once the device is deployed with that through and through wire access, we deliver the branch into the left subclavian artery. This is a slow deployment, so that we align the flair within the volcano and that volcano is flexible. In some patients, it sort of sits right at the level of
the aorta, like you see in this patient. Sometimes it protrudes. It doesn't really matter, as long as the two things are mated together. There is some flexibility built in the system. In this particular patient,
we had a little leak, so we were able to balloon this as we would any others. For a TEVAR, we just balloon both devices at the same time. Completion Angiogram shown here and we had an excellent result with this patient at six months and at a year the aneurysm continued
to re-sorb. In that series, we had successful delivery and deployment of all the devices. The duration of the procedure has improved with time. Several of these patients required an extension. We are in the feasibility phase.
We've added additional centers and we continue to enroll patients. And one of the things that we've learned is that details about the association between branches and the disease are critical. And patient selection is critical.
And we will continue to complete enrollment for the feasibility and hopefully we will see the pivotal studies start soon. Thank you very much
- 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.
- 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.
- 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. 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.
- 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.
- Few aspects of vascular surgery are more controversial than the management of neurogenic TOS as you heard earlier from Dr. Illig. I will propose that recurrent neurogenic TOS and persistent neurogenic TOS are even more of a challenge to deal with. Persistent neurogenic TOS
occurs in 10 to 15% of patients, and it's really the individual who fails to show any improvement following decompression. Recurrent, 15 to 30% of individuals who have some degree of partial or complete relief after the initial decompression.
This may be insidious or acute, and most often occurs somewhere within a two-year time frame. It could be a missed original diagnosis. Or it may be a secondary insult, a new stretch injury to the plexus,
incomplete rib resection, ectopic bands, scar tissue formation around the plexus, or pec minor syndrome. Pec minor syndrome is a frequent cause of recurrent and/or persistent neurogenic symptoms.
Its co-existence is over 50% of patients with neurogenic TOS. Sanders recognized in 2003 that pec minor causes the majority of recurrent neurogenic TOS symptoms. What is it?
Well the pec minor originates in the second, third, fourth, and fifth ribs, inserting on the coracoid process, which is part of the scapula. Muscle hypertrophy, spasm, and fibrosis will constrict those structures underneath,
which would be the axial artery vein and posterior to that will be your plexus. This was first described in '45 by Wright. Lord and Stone did five decompressions for what they defined as "hyperabduction syndrome." It was lost at some point,
rediscovered by Thomas then Doctor Sanders in 2004, who studied it prolifically, defined it as a sub-set of neurogenic TOS. There's a plethora of literature in this present day and age supporting pec minor syndrome.
Etiology: majority of people have trauma, most often in motor vehicle accident with a whiplash type of injury. Repetitive shoulder strain and spontaneous events can occur, inducing hyper-induction of the shoulder. Clinical symptoms are similar
between neurogenic and pec minor: weakness, pain in the neck, clavicular, anterior chest wall, trapezius region and then paresthesias, most often in the ulnar distribution. Isolated pec minor does happen. Typically these individuals
have fewer head and neck symptoms. And you'll notice the intensity of symptoms are significantly less. On your examination it's your standard TOS examination. Unfortunately provocative maneuvers are not as rewarding. You'll find that with isolated pec minor,
these individuals have fewer head and neck symptoms, typically with rotation, tilt, scalene compression. There's nothing really to see. But they do have point tenderness over the infraclavicular region, directly on top of the pec minor.
And you'll notice that with contraction of the pec major, the symptoms will be minimized. Sanders noted the three most common findings with pec minor syndrome are: tenderness to palpation in the subcoracoid space, ULTT and EAST.
You'll notice that in some of these patients who do have persistent or recurrent symptoms, quite likely, pec minor tenderness was missed in the original diagnosis. A thorough history and physical certainly is beneficial. Unfortunately there's no test or exam
that is pathognomonic for this. Appropriate imaging should be completed to rule out other pathology. And then a selective pec minor muscle block not a plexus block, but a minor block, a muscle minor block,
should be considered. EMG testing has mixed results. When you look at your muscle block, typically done with a baseline examination, you'll then inject lidocaine 4 cc with ultrasound guidance 45 degree angle to avoid dropping in the lung.
Inject in a two to three centimeter area. And what you're looking for is resolution of your tenderness, improvement of your symptoms, at rest and with provocative maneuvers. For those ones who have an unsuccessful block
you may want to consider repeating it, or consider performing a scalene block. For those individuals that do have pec minor syndrome, conservative therapy, which is range-of-motion and stretching, tends to work well, 50% resolution in eight-week window.
For those individuals who fail pec minor tenotomy, low-risk out-patient procedure, relatively quick recovery time. A variety of approaches have been defined in the literature. Here's one approach with a patient
previously undergoing neurogenic decompression with a superclavicular approach, this is the anterior axillary approach, with a two to three centimeter vertical incision in the anterior axillary line. The subcutaneous divide at the pec fascia
is open and the muscle is elevated with a Deaver retractor. You'll trace this up to the coracoid process, and with that being the case, you'll transect two to three centimeters of the pectoralis minor muscle,
and then release any fascial bands or accessory muscle around the neurovascular bundle. These patients have done well. With isolated tenotomy you'll see that there's an improvement anywhere from 90 to 100%. However, you need to take into consideration
a good number of these people have combined neurogenic TOS and pec minor syndrome. And with that being the case, the success may be a little bit less. So in summary, pec minor syndrome is a frequent cause
of recurrent or persistent neurogenic TOS. Isolated pec minor tends to have fewer head and neck symptoms. Diagnosis is aided with a block. And tenotomy appears to be safe and effective. 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.
- So thank you ladies and gentleman, thank you Doctor Veith for inviting me again this year. These are my disclosures. So more effective thrombolysis by microbubbles and ultrasound has been proven actually effective in earlier studies, treating a myocardial infarction or acute ischemic stroke.
But what are these microbubbles? These are 1 to 10 micrometers, gas-filled bubbles with a lipid shell. It oscillate when subjected to low intensity ultrasound, and can cavitate when subjected to high intensity ultrasound. Initially they were designed for diagnostic use
as intravascular contrast enhancers. However, they have many advantages, non-specifical mechanical effects, to induce thrombus breakdown due to mechanical force of microbubbles if they are subjected to ultrasound. So we conducted the first human trial
in peripheral arterial diseases in Microbubbles and UltraSound-accelerated Thrombolysis, the MUST study for peripheral arterial occlusions. Which is a single phase two trial for actually safety and feasibility study. The MUST-TRIAl consist out of 20 patients
for safety and feasibility, which in 10 patients will be treated with Urokinase, and 10 with Alteplase. And then added, for the first hour, microbubbles and we evaluated the VAS pain scores, duplex echography for circulation or revascularization, microcirculation and daily angiography as usual.
Included were men and women 18 to 85 years. A maximum of two weeks of symptoms of lower limb ischaemia due to thrombosed or occluded lower limb peripheral native arteries or venous or prosthetic bypass grafts. And Rutherford class 1 or 2A. They have to understand the nature of the procedure
and written informed consent. And excluded were all known factors that exclude standard thrombolysis therapy, hypersensitivity to contrast enhanced agents, a recent acute coronary syndrome. Endpoints, again, it's a safety
and then a technical feasibility trial. Also we looked at the organisation, and the treatment duration for technical, angiographic, and clinical success. We looked at the severe adverse event and mortality rates, VAS-pain scores and microcirculation.
If the patients came in, we inform them about the MUST trail, we performed an ECG analysis and informed consent. They fill out some questionnaires and when they come in to the angio-room, we started a thrombolysis with a catheter, the Mc Nemara.
And the first group, the Urokinase 10 patients, we treated with 500 units of bolus and then continued with a 50,000 units of Urokinase per hour. The Alteplase group had started with a 5 milligram bolus and then they continued with 1 milligram per hour
for the first 24 hours. And then, the ultrasound room, they got a bubble infusion for the first hour of treatment. Then we would continue with thrombolysis on a surgical ward, every sixth hour we'd look at if there was revascularization at the duplex ultrasound.
And if signs of revascularization are observed on the duplex ultrasound or on the next day, we routinely perform the angiography. Then we could cessate the thrombolytic therapy, and if necessary, acute or elective additional intervention to correct underlying lesions,
or to establish patencies. We check the wound and then we follow-up these patients every six weeks, three months, 6 months, and one year after thrombolytic therapy. So these are the patient characteristics, mostly of these were male, 70 years,
and five of them were native bypass, and five were a bypass occlusion, venous or prosthetic. And two of them had multiple occlusions, whether Rutherford class 1 or 2A. And these were the first 10 patients that were treated with Urokinase and I will present here
the results of these 10 patients first. So, very important, there were no deaths, no severe adverse events, and it was technical feasible. The flow at the duplex examination was there after 24 hours, but most of our patients actually had it already after 6 hours.
The amputation rate, right now, is zero. And also no bypasses were now needed. So we will continue this MUST trial right now and January we probably will have the inclusion of the group with the Alteplase, which I'll present next year.
And we think that microbubbles with Urokinase is a safe combination right now. We will further include the groups of adults placed and further optimalisation of the microbubbles technique with nanobubbles. Had a talk about that yesterday, so you can look it up.
And nanobubbles are nanoparticles of 5 to 500 nanometers, which are very small, they do not penetrate the endothelial barrier of the doubt and it damage. And it can carry the thrombolytics actually to the side the aorta catheter need it. You can also make the magnetic paste,
which means you can paste these patients on the MRI. Then you can have local treatment of thrombolytic therapy. So thank you for your attention.
- Thank you, thanks for the opportunity to present. I have no disclosures. So, we all know that wounds are becoming more prevalent in our population, about 5% of the patient population has these non-healing wounds at a very significant economic cost, and it's a really high chance of lower extremity amputation
in these patients compared to other populations. The five-year survival following amputation from a foot ulcer is about 50%, which is actually a rate that's worse than most cancer, so this is a really significant problem. Now, even more significant than just a non-healing wound
is a wound that has both a venous and an arterial component to it. These patients are about at five to seven times the risk of getting an amputation, the end patients with either isolated venous disease or isolated PAD. It's important because the venous insufficiency component
brings about a lot more inflammation, and as we know, this is associated with either superficial or deep reflux, a history of DVT or incompetent perforators, but this adds an increasing complexity to these ulcers that refuse to heal.
So, it's estimated now about 15% of these ulcers are more of a mixed etiology, we define these as anyone who has some component of PAD, meaning an ABI of under point nine, and either superficial or deep reflux or a DVT on duplex ultrasound.
So we're going to talk for just a second about how do we treat these. Do we revascularize them first, do we do compression therapy? It has been shown in many, many studies, as with most things, that a multi-disciplinary approach
will improve the outcome of these patients, and the first step in any algorithm for these patients involves removing necrotic and infected tissue, dressings, if compression is feasible, based on the PAD level, you want to go ahead and do this secondary, if it's not, then you need to revascularize first,
and I'm going to show you our algorithm at Michigan that's based on summa the data. But remember that if the wounds fail to heal despite all of this, revascularization is a good option. So, based on the data, the algorithm that we typically use is if an ABI is less than point five
or a toe pressure is under 50, you want to revascularize first, I'll talk for a minute about the data of percutaneous versus open in these patients, but these are the patients you want to avoid compression in as a first line therapy.
If you have more moderate PAD, like in the point five to point eight range, you want to consider compression at the normal 40 millimeters of mercury, but you may need to modify it. It's actually been shown that that 40 millimeter of mercury
compression actually will increase flow to those wounds, so, contrary to what had previously been thought. So, revascularization, the data's pretty much equivocal right now, for these patients with these mixed ulcers, of whether you want to do endovascular or open. In diabetics, I think the data strongly favors
doing an open bypass if they have a good autogenous conduit and a good target, but you have to remember, in these patients, they have so much inflammation in the leg that wound healing from the surgical incisions is going to be significantly more difficult
than in a standard PAD patient, but the data has shown that about 60% of these ulcers heal at one year following revascularization. So, compression therapy, which is the mainstay either after revascularization in the severe PAD group or as a first line in the moderate group,
is really important 'cause it, again, increases blood flow to the wound. They've shown that that 40 millimeters of mercury compression is associated with a significant healing rate if you can do that, you additionally have to be careful, though,
about padding your bony areas, also, as we know, most patients don't actually keep their compression level at that 40, so there are sensors and other wearable technologies that are coming about that help patients with that, keeping in mind too, that the venous disease component
in these patients is really important, it's really important to treat the superficial venous reflux, EVLT is kind of the standard for that, treatment of perforators greater than five, all of that will help.
And I'm not going to go into any details of wound dressings, but there are plenty of new dressings that are available that can be used in conjunction with compression therapy. So, our final algorithm is we have a patient with these mixed arterial venous ulcers, we do woundcare debridement, determine the degree of PAD,
if it's severe, they go down the revascularization pathway, followed by compression, if it's moderate, then they get compression therapy first, possible treatment of venous disease, if it still doesn't heal at about 35 weeks, then you have to consider other things,
like biopsy for cancer, and then also consider revacularization. So, these ulcers are on a rise, they're a common problem, probably we need randomized control trials to figure out the optimal treatment strategies.
- 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.
- 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.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- 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)
- 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.
- Good afternoon, I'd like to thank the moderators and Dr. Veith for inviting me to discuss our experience with using coronary drug eluting stents to salvage failed or failing vein grafts. Vein graft stenosis is the major cause of delayed graft failure after infrainguinal bypass.
It affects one-third of bypasses and reduces primary patency. Obviously the gold standard is open revision, but there isn't always conduit for that. It requires a general anesthesia. The result of endovascular interventions
have been largely disappointing. In particular, conventional peripheral stents are way too large to treat most saphenous vein bypass grafts. Coronary drug eluting stents are a better match from a size standpoint
to saphenous vein bypass grafts and they have a mechanical advantage, or many mechanical advantages over balloons, especially with regard to watermelon seeding. The scaffold of the stent prevents the balloon from slipping proximately
or distally when your dilating the stent. Finally, the mechanism of vein graft stenosis, especially at anastomoses, is neointimal hyperplasia, so the drug eluding stent is rational and obviously it's been proven in saphenous vein grafts used for
coronary artery bypass grafting when compared to angioplasty and bare metal stenting. So this is a case of proximal stenosis of a bypass graft arising from the femoral artery, which we treated with a balloon mounted coronary drug eluting stent
with an excellent technical result. We retrospectively looked at our experience doing this from 2012 to 2017 and we looked at the following outcomes. Primary stenosis-free patency, assisted graft patency, graft occlusion,
amputation, and then I'll talk about this briefly, comparison to standard endovascular interventions on the same patients in the same bypasses. We put 21 drug eluting coronary stents and 19 lesions in 17 patients bypasses. All of these bypasses were either
baloney popliteal bypasses or tibial bypasses using saphenous vein bypass graft. The lesions were most likely or most often just distal to the proximal anastomosis or at the proximal anastomosis, although three of them were at the distal anastomosis.
Twelve of them were performed after failure of angioplasty at the same operative setting. The others were performed as a primary intervention in a single setting. Operative technical success was 100%, primary stenosis-free patency
and assisted graft patency were good at six months and declined from there, as you might expect. Five patients occluded their grafts during follow up and that resulted in four amputations, but twelve bypasses, or 70%, were still open at the end of the follow up.
We compared the 21 coronary drug eluting stent interventions to 23 more standard endovascular interventions for lesions of saphenous vein bypass grafts. When we compared the two approaches for all lesions, we didn't see any difference in primary stenosis-free patency
between the coronary drug eluting stents and the more standard endovascular interventions. Similarly, for recurrent lesions we didn't see any difference. But for primary treatment of initial lesions in saphenous vein bypass grafts,
there was better primary stenosis-free patency for the coronary drug eluting stents then for the standard endovascular interventions. So a couple of caveats. This is a single institution experience, it's a small sample size.
However for these tough lesions threatening bypass grafts, we saw that the majority of coronary drug eluting stents placed after immediate PTA failure were technically successful. Half of them were placed for recurrent lesions
and we did see a kind of patency that was at least comparable to standard vascular interventions. Here's a woman who was in a lot of trouble when she originally came to us. She had had bilateral knee arthroplasties
with a tourniquet, but she had popliteal aneurysms bilaterally that the orthopedic surgeon didn't recognize. So she thrombosed both her popliteal aneurysms. She only had enough conduit for a bypass on one side
so she got an above knee amputation on the other side. But the one side had kind of a not so great of saphenous vein and not so great of perineal artery, but we performed the bypass
and I then had to intervene on this bypass graft a number of times to keep it patent. And here you can see a stenosis at our distal anastomosis and some disease in her perineal artery that we treated with a drug eluting coronary stent
with an excellent technical result and this leg is still attached and she's walking. So again, in a small cohort at a single institution, I think this experience demonstrates that coronary drug eluting stents
provide durability at least comparable to standard endovascular interventions for the treatment of infrainguinal bypass graph stenosis that threaten bypasses and coronary drug eluting stents definitely performed better than
standard endovascular interventions in initial lesions. I think these results warrant further clinical investigation. Thanks.
- I'd like the thank Doctor Veith for inviting me back to speak. I have no disclosures, we will be discussing some slight off-label use of the anitcoagulants. As we all know, acute limb ischemia occurs as a result of acute thrombosis of a native artery or bypass graft or embolism from a proximal
source, dissection, or trauma. The incidence is not insignificant, 15 cases per 100 000 persons per year, or interestingly about 10 to 16% of our vascular workload. Despite the relative frequency of this condition, there are relatively few guidelines to
guide us for anticoagulation therapy. The last set of guidelines for the American College of Chest Physicians regarding PAD gives some very brief, generic recommendations from 2012. They state, suggest immediate systemic anticoagulation with unfractionated heparin.
We suggest reperfusion over no reperfusion, which seems pretty obvious to an audience of vascular specialists. One of the challenges with acute limb ischemia is that it is a fairly heterogenous group. It can be thrombosis or embolism to the aorticiliac segments to the infrainguinal segments, and
there's also the patients who develop ALI from trauma. So we actually looked at the various phases of anticoagulation for acute limb ischemia and then we do, as with many institutions, utilize intravenous heparin at the time of the diagnosis, as well as obviously at the time of surgery,
but we found that there was a significant variation with regard to the early, post-operative anticoagulation regimens. One option is to give therapeutic intravenous heparin on an adjusted dose, but what we found in a significant minority of patients across the country actually,
is that people are giving this fixed mini-dose 500 unit an hour of heparin without any standardization or efficacy analysis. Then, obviously you go the long-term anticoagulation. We reviewed 123 patients who had ALI at our institution, who underwent surgical revascularization.
And they had the typical set of comorbidities you might expect in someone who has PAD or atheroembolism. In these patients, the Rutherford Classification was viable or marginally threatened in the majority, with about 25% having immediately threatened limb.
Various procedures were performed for these patients, including thromboembolectomy in the majority, bypass operations, angioplasty and stenting was performed in the significant minority and then primary amputation in the various selects few. We divided these patients into
the first four days of anticoagulation. Therapeutic with unfractionated heparin early on versus subtherapeutic or this mini-dose unfractionated heparin and we found that 29% of our patients were receiving the mini-dose unfractionated heparin, again without much efficacy analysis.
We used the International Society for Thrombosis and Haemostasis Anticoagulation Outcome Guidelines to look at the ischemic complications, as well as major and minor bleeding for these patients, and we identified actually not a significant rate of difference between the
subtherapeutic category and the therapeutic category of patients, with regard to mortality, with regard to recurrent limb ischemia, MI, VTE, or stroke, major amputation, and we actually didn't find because it's a fairly small study, any significant difference in major or minor bleeding for these patients.
So, we do feel that this small study did justify some efficacy of mini-dose unfractionated heparin because we didn't find that it was causing recurrent lower extremity thromboembolsim in these patients. Now on to long-term anticoagulation, for these patients, after that first three or four days
after the surgery, the options are long-term vitamin K antagonists, the DOAC's or vitamin K antagonists if you have atrial arrhythmia, or in the patients who had no other comorbidities, there really is not much guidance until recently. The compass trial was recently published in 2018
in stable PAD and carotid disease patients, identifying that rivaroxaban plus aspirin had a significant benefit over aspirin alone in patients who had stable PAD. And then, an upcoming trial, which is still ongoing currently in patients who underwent recent
revascularization, whether open or endo, is hopefully going to demonstrate that rivaroxaban, again has a role in patients with lower extremity ischemia. So in conclusion, there is relatively a scarcity of clinical data to help guide anticoagulation after acute limb ischemia.
Unfractionated heparin pre and intraop are standardized, but postop anticoagulation is quite variable. The mini-dose, we consider to be a reasonable option in the first few days to balance bleeding versus rethrombrosis, and fortunately we are having larger randomized clinical trials to help demonstrate the benefit of the DOACs and
aspirin in patients who are stable or post-revascularization for PAD, thank you.
- Thank you, Dr. Veith, for this kind invitation. Aberrant origin of the vertebral artery is the second most common aortic arch anomaly. It is more common in patients with thoracic aortic disease when compared to the general population. It's usually of no clinical significance,
except when encountered while treating cerebro-vascular disease or aortic arch pathology. And that's when critical decision-making to preserve its perfusion becomes necessary. This picture illustrates the most common
types of aortic arch anomalies. Led by bovine arch, isolated vertebral artery, and aberrant right side. In this study, it shows a significant correlation with thoracic aortic disease. We first should evaluate the origin
of the vertebral artery. On the right side of the screen you can see the most common type and it's when it's between the left subclavian and the left common carotid artery origin. This is an example of the left vertebral artery
aberrant associated with a mycotic aneurysm of the aortic arch. And this one is a right aberrant vertebral artery associated with a descending thoracic aneurysm and center retroesophageal location. We then look at the variation of
the vertebral artery and posterior circulation. Most commonly dominant left or hypoplasia of the right vertebral artery as shown in the picture. For termination in the posterior inferior cerebellar artery, or PICA.
Or occlusive lesion on the right side, which necessitates perfusion of the left side. This study shows that vertebral artery variations that could need perfusion is up to 30% of patients
with thoracic aortic disease. There are, unfortunately, minimal literature in the vascular, mostly case reports or series. And most of this says procedure data comes from the neurosurgical literature for occlusive disease that shows in this study,
for example, low morbidity, mortality. Complications include thoracic duct injury, recurrent laryngeal nerve, Horner's and CVAs. And they showed high patency rates. The SVS guidelines for left subclavian revasculatization, although low quality,
shows they indicated routine revascularization and they mention some of the indications for left vertebral artery revasculatization. And extrapolating from that, from those guidelines, we summarize the indications for vertebral artery
revascularization dominant ipsilateral left or hypoplastic right. Incomplete circle of Willis, or termination of the left in the PICA artery. Diseased or occluded contralateral vertebral artery.
Extensive aortic coverage or inability to evaluate the circle of Willis prior to intervention. Some technical tips, we use a routine supraclavicular incision. We identify the vertebral artery posterior-medial
location to the common carotid. We carefully preserve the recurrent laryngeal nerve or non-recurrent laryngeal nerve, which is common in aortic arch anomalies. Thoracic duct on the left side. Transpose it to the posterior surface
of the common carotid. And then clamp distal to the anastomosis and to avoid prolonged ischemia to the posterior circulation. This is a completion aortagram that shows patent left vertebral artery transposed
to the common carotid. And then one month follow-up shows that the left vertebral artery is patent with a complete repair of the aorta. So in our experience, we did six vertebral transpositions over
the last couple years, four on the left, two on the right. No perioperative complications. One lost follow-up. And up to 27 months of the patent vessels. In summary, aberrant vertebral artery is uncommon
finding, but associated with thoracic aortic disease. The origin and the course of the vertebral artery should be thoroughly evaluated prior to treatment. Revascularization should be considered in certain situations to avoid
posterior circulation ischemia. But more data is needed to establish guidelines. Thank you.
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