- Thank you very much Mr. Chairman. Thank you Frank, for this kind invitation again to this symposium. This is my disclosure. With the drug coated balloons it is important to minimize the drug loss during the balloon transit during the inflation of the balloon.
Because Paclitaxel has a high degree of cytotoxicity that may induce necrosis and increase inflammation in the distal tissue, and we know that even with the best technique, we can loose 70 - 80% of the drop to the distal circulation,
the inference by different factors between them and the calcification of degree of these blood cells. There are adverse events secondary to drug coated balloons that have been reported recently. In animal molders it has shown that Downstream Vascular Changes are more frequent with
Drug Coated Balloons than with Drug-Eluting Stents. In animal molders it has been also shown that there is no evidence of significant downstream emboli or systemic toxicity with DCB's than with patients with controls. This was a study presented yesterday by (mumbles)
with a very nice and elegant study with a good methodology that shows in animals that there are different concentrations of the drug in distal tissue depending on the balloon that you are using. In this case, the range in balloon (mumbles)
those ones have the lowest concentration in the distal tissue. In clinical experience in this meta-analysis amputations and wound healing rate are lower with this series with controls. But there is controversy because
Complete Index Ulcer Healing is higher in this series than with control patients. But there are lower wound healing index in patients compared with drug-eluting stents. In the debate, (mumbles) and also in the dialux which are clinical trials in diuretic patients with CLI,
there we no issues of safety and no impair of the wounds healing. But, remember the negative result of the IN PACT DEEP trial in which there were more amputation at six months that could be influenced, but in all their factors, the lack of standardized
wound care protocols. (mumbles) has also reported recently good survival to 100% in patient treated with DCB's compared with plain balloons and with lutonic balloons. So in our institution, we did a study with the objective to examine
patient outcomes following the use of the drug-coated balloons in patients with CLI and diuretic patients with Complex Real World lesions undergoing endovascular intervention below-the-knee with the Ranger balloon coated with Paclitaxel.
This is a Two-Center Experience that is headed by the National University of Mexico in 30 patients with strict followup. With symptomatic Rutherford four to six. With the Stenosis and occlusion of infrapopliteal vessels and many degrees of calcification.
It was mandatory for all patients to have Pre-dilation before the use of DCB. We studied some endpoints like efficacy. (mumbles) Limb salvage, sustained clinical improvement, wound healing rate
and technical success and some other endpoints of safety. This is an example of multi level disease in a patient that has to be approached by (mumbles) access with a balloon preparation of the artery before the use of the DCB, and after this, we treated the anterior artery
and even to the arch of the foot. This is the way we follow our patient with ultra sound duplex with an index fibular of no more that 2.4. All patients were diabetic with Rutherford 5-6. 77% have a (mumbles) at the initial of the study.
And as you can see there were longer lesions and with higher degree of calcification and stenosis only in two of them we produced (mumbles). There were bailout stent placements in five patients and we did retrograde access in 43 patients.
Subintimal angioplasty was done in 32 patients, and Complete Index Wound Healing was in 93 of our patients. This is our Limb Salvage 94%. The Patency rate was 96% with this Kaplan Meir analysis. And in some patients we did a determination of Paclitaxel concentration in distal tissue
with the High Pressure Liquid Chromatography method. We only did this in five patients because of the lack of financial support, and technical problems. As you can see in three of them we had Complete Wound Healing.
Only one we had major amputation. This was the patient with the higher concentration of Paclitaxel in the distal tissue, and in one patient, we could not determine the concentration of Paclitaxel. This is the way we do this.
They take the sample of the patient at the moment we do the minor amputation. During day 10 after the angioplasty, we also do a (mumbles) analysis of the patient we have a limb salvage we can see arterial and capillar vessel proliferation and hyperplasia of the
arteriole media layer. But, in those patients that have major amputation even when they have a good sterio-graphic result like in this case, we see more fibrinoid necrosis which is a bad determination. So in conclusion,
angioplasty with the (mumbles) balloon maintain clinical efficacy over time is possible. We didn't see No Downstream clinical important or significant effects and high rates of Limb Salvage in complex CLI patients is possible.
Local toxic effects of paclitaxel and significant drug loss on the way to the lesion are theoretical considerations up to now because there is no biological study that can confirm this. Thank you very much.
- 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 again, I'd like to thank Dr. Veith for the opportunity to participate in this interesting debate. So, I have been tasked with the position Intra-operative Completion Study is not mandatory, and in fact I will show you why a selective approach will actually provide better results for our patients. These are my disclosures related to ongoing
clinical research and clinical trials. So again, Professor Eckstein and his colleagues should be very significantly commended for getting the entire German vascular surgery community to look at their data in a very rigorous fashion. However, both he and his co-authors will acknowledge
within the manuscript that there are significant problems with this database. A very large number of 142,000 elective carotid endarterectomy procedures with very ballotable stroke and death rates of 1.4 and 2.5%. However, a typical criticism from outside the
vascular surgery community, these are all self-reported. These are not 30 day outcomes, they're actually in-hospital outcomes. And while in Germany that still may be four days, it's not the 30 days that we see. I'll show you a little bit later on within the Crest data.
And interestingly, within their own manuscript only 50% of the patients actually had neurologic assessment both pre- and post-procedural. So, how can we make a relevant decision in terms of thinking about how we're going to treat these patients if we only have neuro data on half of them.
Lets for the moment assume we can call out those patients. How does this relate to clinical practice? Well the authors also admit that this is an observational study, and that even though there is some association, there clearly is no causal relationship
as my previous debater just admitted. And in fact, they argue that this is perhaps the best method to look at generating hypotheses for future randomized trials, much like Dr. Aborama has done with the use of carotid endarterectomy with patching. So, let's look a little bit more about the data
and see how relevant it is to your current practice. So in the Germany registry, a quarter of the patients are treated under local anesthetic. 40% have no type of neurologic monitoring, and over 40% are performed with aversion endarterectomy. Very, very different than the practice that we see
in our institution, and in the New England region. And I would argue that there's a lot of concern in terms of what the indications are for monitoring, what the indications are for shunt use. Again, that's 43%. But there's absolutely no data in this registry about
indications for shunting, when it was used, or when patients were re-explored and what they found at the time. And a little bit concerning is in 17% of the patients, there was no anti-platelet agent used in patients undergoing carotid endarterectomy.
And, I would argue that that number is just a little bit high. How about when we go to the univariate analysis? Once again, we see that there's a benefit of 0.4% decrease in stroke and death for a local anesthetic, although we are well aware that there are numerous other
perspectives that have looked at this and not shown that same relationship. Again, there's a benefit for aversion endarterectomy, but I would argue at least in the New England region and perhaps in the United States except for select centers, aversion endarterectomy is used the minority of the time
and that in fact is an indication in my mind to have a lower threshold for either angiogram or completion duplex. Most concerning, there was 0.3% difference in the stroke and death rate with the lack of an intraoperative completion study, but there was no data about indications, findings,
whether that resulted in an intervention, or what the result of that intervention was. And initially in the univariate analysis, neuro-psyche, physiologic monitoring was protective, but later on in the multivariate, it was not. Here is that same multivariate analysis that shows again
that in fact shunting and neuro-physiologic monitoring are increased risk factors for stroke. Certainly there's going to be some bias. My concern is I'm not convinced the authors are able to call out the co founding variables, even in their multivariate regression analysis.
And in fact, in their concluding paragraphs they state there's no information supplied on whether intraoperative completion studies caused an operative revision or not, and no information about cause of death. In fact, they don't even have information about
intraoperative heparin or protamine application. So I would argue I'd be very skeptical about making my final decisions based on this. Thinking about the technical aspects of angiography, there's no doubt that this is very helpful at times, but think about the details of where do you put the needle.
What type of imaging? Is it a C-arm, is it a flat plate? Who interprets it, and what are your thresholds for intervention? So, it certainly may be harmful, may be unnecessary, and may even give you false positives.
Similarly with Completion Duplex studies, there certainly is a false positive rate and then there's risk for re-clamping. I reached out to my friend and colleague Braglol to see if there was any data from Crest that would help us, and unfortunately other than the fact that stroke happens
up to 30 days after our initial endarterectomy, there was no data supporting that. So, perhaps the best study that we have is our current practice in New England where we had 6,000 patients, a third of whom received completion studies. We broke this down into rare, selective, and routine
duplex or angio studies. And in fact, in the selective group we had a very low rate of re-exploration versus the other group, and a much lower incidence of overall stroke and death. In fact, the only benefit that was statistically significant was a decrease one year rate of re-stenosis.
So in conclusion, I would argue that this is probably unnecessary, and in fact maybe harmful. Meticulous technique, intra-procedural monitoring with selective shunt use, and continuous wave doppler use may, in fact, be the way to go. But this does give us an opportunity for prospective,
randomized trial as part of another study to look for completion study indications. Thank you very much.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- Yeah, thank you Dr. Asher, and again, I want to give credit to Dr. Zheng, one of our fellows who put together this work. So duplex surveillance for lower extremity revascularization, I think we all do that for vein grafts. It's less well accepted for prosthetic grafts. It's controversial for peripheral stent grafts,
and it's very controversial for peripheral stents. If we had time, I'd like to poll all of you and ask how many of you do a duplex scan after you put in a peripheral arterial stent, but more importantly, how many would intervene if you find the velocities are increasing.
So why do it? Well, revision of failing stents may yield better patency rates than if you intervene after the stent has occluded. You may not be able to restore patency if the stent has already occluded, I mean,
some of you may think you can always do that, I know I can't always do that. And performing endovascular treatment is obviously easier than converting to open surgery. So we reviewed 172 stents in 30 iliac and 89 fempop arteries.
Some were overlapping stents, so we kind of said there were 119 segments that we analyzed. The treated length for the iliac artery was about seven and a half centimeters, and for fempop, was about 12 centimeters. And we did duplex surveillance
in our accredited vascular lab in our office. We measured the peak systolic velocity, and the PSV ratios, every two centimeters within the stent but also in the adjacent proximal and distal arteries. We considered it an abnormal duplex finding, I think pretty much consistent
with what you would do for a vein graft, also, if you had a focal PSV over 300, uniform PSVs throughout the stent less than 45, or a ratio more than three, we would say that probably corresponds with more than a 75% stenosis
and generally we would intervene. We did the duplex one week after we put in a peripheral stent, and then about every six months. The follow up averaged about two years. So of these 119 stented segments, about half of 'em stayed normal.
All of the duplex criteria stayed normal during the entire follow up, nothing needed to be done. But interestingly, of the other half, they developed at least one abnormal duplex criterion. 40 of the 57 cases we intervened on, but of the 17 other cases we did not intervene,
either due to patient refusal, or the surgeon felt, well, let's just keep an eye on it, five did remain patent for a short follow up, but 12 of the 17 went on to occlude. Of the 12 occluded segments, we found that if there was more than one
abnormal duplex finding and you did not treat, 70%, again the numbers are small, but 70% occluded, compared to if you had the normal duplex findings, only 3% occluded, and this was highly significant. So of the 12 occluded stents, what happened? Well six we didn't do anything,
they were just for claudication, and the patients chose not to have open surgery. But four, we did try to open 'em and could not, and they needed a bypass, mainly for limb salvage. But two, we couldn't do anything, and they ended up with amputations.
So the bottom line in this relatively small series was if a stent occluded, they didn't necessarily do well and you couldn't open 'em up. So in conclusion, duplex surveillance for lower extremity stents, and that's what we're talking about,
can significantly predict stent occlusion based on these criteria, and the absence of any criteria strongly predicted stent patency. We even have a little disagreement, frankly, in my own group about how aggressive to be for these.
I tend to be pretty aggressive and intervene. Maybe during the discussion we can talk about this. Thank you.
- Thank you for asking me to speak. Thank you Dr Veith. I have no disclosures. I'm going to start with a quick case again of a 70 year old female presented with right lower extremity rest pain and non-healing wound at the right first toe
and left lower extremity claudication. She had non-palpable femoral and distal pulses, her ABIs were calcified but she had decreased wave forms. Prior anterior gram showed the following extensive aortoiliac occlusive disease due to the small size we went ahead and did a CT scan and confirmed.
She had a very small aorta measuring 14 millimeters in outer diameter and circumferential calcium of her aorta as well as proximal common iliac arteries. Due to this we treated her with a right common femoral artery cutdown and an antegrade approach to her SFA occlusion with a stent.
We then converted the sheath to a retrograde approach, place a percutaneous left common femoral artery access and then placed an Endologix AFX device with a 23 millimeter main body at the aortic bifurcation. We then ballooned both the aorta and iliac arteries and then placed bilateral balloon expandable
kissing iliac stents to stent the outflow. Here is our pre, intra, and post operative films. She did well. Her rest pain resolved, her first toe amputation healed, we followed her for about 10 months. She also has an AV access and had a left arterial steel
on a left upper extremity so last week I was able to undergo repeat arteriogram and this is at 10 months out. We can see that he stent remains open with good flow and no evidence of in stent stenosis. There's very little literature about using endografts for occlusive disease.
Van Haren looked at 10 patients with TASC-D lesions that were felt to be high risk for aorta bifem using the Endologix AFX device. And noted 100% technical success rate. Eight patients did require additional stent placements. There was 100% resolution of the symptoms
with improved ABIs bilaterally. At 40 months follow up there's a primary patency rate of 80% and secondary of 100% with one acute limb occlusion. Zander et all, using the Excluder prothesis, looked at 14 high risk patients for aorta bifem with TASC-C and D lesions of the aorta.
Similarly they noted 100% technical success. Nine patients required additional stenting, all patients had resolution of their symptoms and improvement of their ABIs. At 62 months follow up they noted a primary patency rate of 85% and secondary of 100
with two acute limb occlusions. The indications for this procedure in general are symptomatic patient with a TASC C or D lesion that's felt to either be a high operative risk for aorta bifem or have a significantly calcified aorta where clamping would be difficult as we saw in our patient.
These patients are usually being considered for axillary bifemoral bypass. Some technical tips. Access can be done percutaneously through a cutdown. I do recommend a cutdown if there's femoral disease so you can preform a femoral endarterectomy and
profundaplasty at the same time. Brachial access is also an alternative option. Due to the small size and disease vessels, graft placement may be difficult and may require predilation with either the endograft sheath dilator or high-pressure balloon.
In calcified vessels you may need to place covered stents in order to pass the graft to avoid rupture. Due to the poor radial force of endografts, the graft must be ballooned after placement with either an aortic occlusion balloon but usually high-pressure balloons are needed.
It usually also needs to be reinforced the outflow with either self-expanding or balloon expandable stents to prevent limb occlusion. Some precautions. If the vessels are calcified and tortuous again there may be difficult graft delivery.
In patients with occluded vessels standard techniques for crossing can be used, however will require pre-dilation before endograft positioning. If you have a sub intimal cannulation this does put the vessel at risk for rupture during
balloon dilation. Small aortic diameters may occlude limbs particularly using modular devices. And most importantly, the outflow must be optimized using stents distally if needed in the iliac arteries, but even more importantly, assuring that you've
treated the femoral artery and outflow to the profunda. Despite these good results, endograft use for occlusive disease is off label use and therefor not reimbursed. In comparison to open stents, endograft use is expensive and may not be cost effective. There's no current studies looking
into the cost/benefit ratio. Thank you.
- 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.
- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.
The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,
however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,
defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought
to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.
I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have
right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.
This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,
small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have
SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented
five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.
The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by
a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of
atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for
inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries
are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.
- Thank you, Dr. Ascher. Great to be part of this session this morning. These are my disclosures. The risk factors for chronic ischemia of the hand are similar to those for chronic ischemia of the lower extremity with the added risk factors of vasculitides, scleroderma,
other connective tissue disorders, Buerger's disease, and prior trauma. Also, hemodialysis access accounts for a exacerbating factor in approximately 80% of patients that we treat in our center with chronic hand ischemia. On the right is a algorithm from a recent meta-analysis
from the plastic surgery literature, and what's interesting to note is that, although sympathectomy, open surgical bypass, and venous arterialization were all recommended for patients who were refractory to best medical therapy, endovascular therapy is conspicuously absent
from this algorithm, so I just want to take you through this morning and submit that endovascular therapy does have a role in these patients with digit loss, intractable pain or delayed healing after digit resection. Physical examination is similar to that of lower extremity, with the added brachial finger pressures,
and then of course MRA and CTA can be particularly helpful. The goal of endovascular therapy is similar with the angiosome concept to establish in-line flow to the superficial and deep palmar arches. You can use an existing hemodialysis access to gain access transvenously to get into the artery for therapy,
or an antegrade brachial, distal brachial puncture, enabling you treat all three vessels. Additionally, you can use a retrograde radial approach, which allows you to treat both the radial artery, which is typically the main player in these patients, or go up the radial and then back over
and down the ulnar artery. These patients have to be very well heparinized. You're also giving antispasmodic agents with calcium channel blockers and nitroglycerin. A four French sheath is preferable. You're using typically 014, occasionally 018 wires
with balloon diameters 2.3 to three millimeters most common and long balloon lengths as these patients harbor long and tandem stenoses. Here's an example of a patient with intractable hand pain. Initial angiogram both radial and ulnar artery occlusions. We've gone down and wired the radial artery,
performed a long segment angioplasty, done the same to the ulnar artery, and then in doing so reestablished in-line flow with relief of this patient's hand pain. Here's a patient with a non-healing index finger ulcer that's already had
the distal phalanx resected and is going to lose the rest of the finger, so we've gone in via a brachial approach here and with long segment angioplasty to the radial ulnar arteries, we've obtained this flow to the hand
and preserved the digit. Another patient, a diabetic, middle finger ulcer. I think you're getting the theme here. Wiring the vessels distally, long segment radial and ulnar artery angioplasty, and reestablishing an in-line flow to the hand.
Just by way of an extreme example, here's a patient with a vascular malformation with a chronically occluded radial artery at its origin, but a distal, just proximal to the palmar arch distal radial artery reconstitution, so that served as a target for us to come in
as we could not engage the proximal radial artery, so in this patient we're able to come in from a retrograde direction and use the dedicated reentry device to gain reentry and reestablish in-line flow to this patient with intractable hand pain and digit ulcer from the loss of in-line flow to the hand.
And this patient now, two years out, remains patent. Our outcomes at the University of Pennsylvania, typically these have been steal symptoms and/or ulceration and high rates of technical success. Clinical success, 70% with long rates of primary patency comparing very favorably
to the relatively sparse literature in this area. In summary, endovascular therapy can achieve high rates of technical, more importantly, clinical success with low rates of major complications, durable primary patency, and wound healing achieved in the majority of these patients.
- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old
but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,
and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.
- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,
and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was
revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.
In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat
was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.
Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone
returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.
Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy
with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,
the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.
Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.
So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really
how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017
in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.
Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at
five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery
to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional
independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.
So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,
but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could
help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.
- Good morning. I'd like to thank everybody who's in attendance for the 7 A.M. session. So let's talk about a case. 63 year old male, standard risk factors for aneurismal disease. November 2008, he had a 52 mm aneurism,
underwent Gore Excluder, endovascular pair. Follow up over the next five, relatively unremarkable. Sac regression 47 mm no leak. June 2017, he was lost for follow up, but came back to see us. Duplex imaging CTA was done to show the sac had increased
from 47 to 62 in a type 2 endoleak was present. In August of that year, he underwent right common iliac cuff placement for what appeared to be a type 1b endoleak. September, CT scan showed the sac was stable at 66 and no leak was present. In March, six months after that, scan once again
showed the sac was there but a little bit larger, and a type two endoleak was once again present. He underwent intervention. This side access on the left embolization of the internal iliac, and a left iliac limb extension. Shortly thereafter,
contacted his PCP at three weeks of weakness, fatigue, some lethargy. September, he had some gluteal inguinal pain, chills, weakness, and fatigue. And then October, came back to see us. Similar symptoms, white count of 12, and a CT scan
was done and here where you can appreciate is, clearly there's air within the sac and a large anterior cell with fluid collections, blood cultures are negative at that time. He shortly thereafter went a 2 stage procedure, Extra-anatomic bypass, explant of the EVAR,
there purulent fluid within the sac, not surprising. Gram positive rods, and the culture came out Cutibacterium Acnes. So what is it we know about this case? Well, EVAR clearly is preferred treatment for aneurism repair, indications for use h
however, mid-term reports still show a significant need for secondary interventions for leaks, migrations, and rupture. Giles looked at a Medicare beneficiaries and clearly noted, or at least evaluated the effect of re-interventions
and readmissions after EVAR and open and noted that survival was negatively impacted by readmissions and re-interventions, and I think this was one of those situations that we're dealing with today. EVAR infections and secondary interventions.
Fortunately infections relatively infrequent. Isolated case reports have been pooled into multi-institutional cohorts. We know about a third of these infections are related to aortoenteric fistula, Bacteremia and direct seeding are more often not the underlying source.
And what we can roughly appreciate is that at somewhere between 14 and 38% of these may be related to secondary catheter based interventions. There's some data out there, Matt Smeed's published 2016, 180 EVARs, multi-center study, the timing of the infection presumably or symptomatic onset
was 22 months and 14% or greater had secondary endointerventions with a relatively high mortality. Similarly, the study coming out of Italy, 26 cases, meantime of diagnosis of the infection is 20 months, and that 34.6% of these cases underwent secondary endovascular intervention.
Once again, a relatively high mortality at 38.4%. Study out of France, 11 institutions, 33 infective endographs, time of onset of symptoms 414 days, 30% of these individuals had undergone secondary interventions. In our own clinical experience of Pittsburgh,
we looked at our explants. There were 13 down for infection, and of those nine had multiple secondary interventions which was 69%, a little bit of an outlier compared to the other studies. Once again, a relatively high mortality at one year. There's now a plethora of information in the literature
stating that secondary interventions may be a source for Bacteremia in seeding of your endovascular graft. And I think beyond just a secondary interventions, we know there's a wide range of risk factors. Perioperative contamination, break down in your sterile technique,
working in the radiology suite as opposed to the operating room. Wound complications to the access site. Hematogenous seeding, whether it's from UTIs, catheter related, or secondary interventions are possible.
Graft erosion, and then impaired immunity as well. So what I can tell you today, I think there is an association without question from secondary interventions and aortic endograft infection. Certainly the case I presented appears to show causation but there's not enough evidence to fully correlate the two.
So in summary, endograft infections are rare fortunately. However, the incidence does appear to be subtly rising. Secondary interventions following EVAR appear to be a risk factor for graft infection. Graft infections are associated without question
a high morbidity and mortality. I think it's of the utmost importance to maintain sterile technique, administer prophylactic antibiotics for all secondary endovascular catheter based interventions. Thank you.
- 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)
- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.
It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.
So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations
of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.
Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.
So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient
who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal
angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near
or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility
was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.
Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal
or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection
or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.
So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump
to prevent hip disarticulation. Thank you for much for your attention.
- 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.
- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro
or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire
because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,
or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,
very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D
in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--
radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about
to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.
So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where
the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist
to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here
to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric
reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I
mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic
close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to
understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.
Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use
Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.
We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.
You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.
Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial
phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,
the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,
very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone
and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.
In other words can offer higher value in patient care. Thank you.
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. Thank you.
- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide
and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter
is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues
that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement
of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side
and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,
then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,
coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,
and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques
with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation
of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.
We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go
so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side
or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.
Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.
On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded
and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.
Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.
Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,
despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients
to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,
and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,
and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.
- Good morning, for all of you who got up early. It's a pleasure to be here, thank you Frank for the invitation. I'm going to talk about a problem that is extremely rare, and consequently can only be investigated by putting together databases from multiple institutions, called adventitial cystic disease.
Okay, I have no conflicts. So adventitial cystic disease is an extremely uncommon problem, but it's important because it occurs often in young people. Virtually all series of adventitial cystic disease have fewer than five patients in it,
so they essentially become case reports. And yet it's a very treatable problem. There are several theories about why it occurs, you can see this picture here. The mucin-assisting material that occurs in the popliteal artery region most commonly.
The etiology of that and the origin of that is debated, whether it comes from the joint space, whether it comes from rest, whatever. But it's not really known. In addition, what's not known is the best treatment. There are several options.
Some would advocate just simple aspiration of the cystic material, although it's very viscous. Others simply excising the cyst and leaving the vessel in place. Some both excising and either doing
an interposition graft or a bypass. Early results with every one of these options have been reported, but they're quite variable as far as the outcome. And therefore, we really don't know not only the optimal approach,
but also the best outcome. For that reason, we did a study with 13 institutions on adventitial cystic disease using a technique called vascular low-frequency disease consortium.
Where everybody uses a standardized database and similar collection to act like a single institution. The aim of this study, which is one of 20 that we've conducted over the last 15 years, was to determine first of all what people were doing
as far as current practice patterns, and then look at the outcomes with the different treatment options. And this was published in the Journal of Vascular Surgery. Adventitial cystic disease of any site was identified using both the CPT ICD-9 physician logbooks,
pathology databases, and procedure codes. And then we collected epidemiologic data as well as operative and follow-up data, with our primary endpoints being vessel patency and the need for re-intervention, since amputation is extremely uncommon and rare.
This is the process for the low-frequency disease consortium. Where not only is a standardized database used, but each institution collects their data after getting IRB approval. And then deidentifies it
before sending it to a central server. So there's no way that there could be a security breach. And then we do an analysis of the data. The results of this study were that in the small number of institutions, 15 institutions, 47 patients were identified.
The majority were male, and the majority were smokers. What was interesting to us was that not all are in the popliteal region. And actually there were several patients as you can see, who had upper-extremity adventitial cystic disease, although it's far more common in the popliteal space.
And also there was actually one patient who had adventitial cystic disease of the femoral vein. The symptoms were typically claudication, and ischemic rest pain or tissue loss were quite rare. If you look at the risk factors, smoking, which was probably a comorbidity
and would not be claimed to be the etiology but was present. Other than that, this is a typical distribution of patients with vascular disease. As far as imaging here, you can see a duplex ultrasound
showing the cystic mass and how it typically looks. The majority of patients had a duplex, but also they often had an MRA or CTA as well as an angiogram. And the angiogram was typically part of the treatment paradigm.
This is just the typical appearance of an MRA showing what some people would call the scimitar sign, which is that it's not a typical plaque. And this is a picture of a CT angiogram showing a similar view of a vessel. The results,
so there were some that did not treat only the cyst, but also resected the artery. And either bypassed it, as you can see here, or did an interposition graft,
here's just a picture of one of those. And there were others that just treated the cyst, and either aspirated it alone or resected the cyst and patched the artery. Or did cyst drainage and nothing else to the vessel. If you look at the typical incision of these patients,
this is a posterior approach of the popliteal region. And the small saphenous vein as you can see is marked, and uses the conduit for bypass. The outcomes of these patients were similar as far as length of stay, complications. The one you'll notice is that
two of the five with cyst resection had a complication, so that's a little bit higher. But otherwise they're quite similar as far as the short-term outcomes and results. The main problem, and also if we look at the improvement in ABI,
although cyst resection with bypass had a higher increase in ABI, the rest of the treatments were similar. In other words, the initial outcome was similar with any of those different options.
The one thing you can see circled in red is the patients who had simple cyst aspiration. It was not durable, and consequently they often had to have a second procedure. And the resection of the artery was generally, or bypass of the artery,
generally had better long-term outcomes. The follow-up was 20 months, and here you can see the recurrence and the types of modality of follow-up. So I just conclude by saying that our experience from multiple institutions
is that this is an uncommon problem, that cyst recurrence is very high if aspiration alone is used, and either interposition or bypass is the optimal treatment. Thanks very much for your attention.
- Thank you again Rex. This is again my disclosure, the same. I think you agree with me that we all do not want these images and after the procedure in our patients or in followup. We might be able to keep this reconstructions patent by continuing accuracy ventricle relation
but there is somehow a disturbance of the venous flow. If we we advocate that 50% stenosis is significant. Flexibility is one reason why we have already the first generation of dedicated venous stents. These are the currently available, excuse me, currently available venous stents
in the European market and despite very different structures, geometries and characteristics they all want to combine the best balance between flexibility, radial force, crush resistance or porosity. So this is not a real scientific way to show
or to evaluate the flexibility but it shows you that there are really differences between the current dedicated venous stents regarding the flexibility and we have closed cell stent, we have open celled stent, we have woven stent, we have laser knitted stent,
we have hybrid or segmented stent. So let us go to one case from our center. We re-cannulized the left iliac tract as you can see here. We used the closed cell stent at the proximal part, lengthen it with a dedicated venous
open cell segmented stent below the ligament going into the common femoral vein as you can see here. So going into the axial plane with duplex we see a very nice cross sectional shape below the artery at the mitonal point. This stent performs very well here
but a few centimeters more distal we have a destroyed cross sectional shape. Going into the detail, the same patient in longitudinal evaluation with stent we see three different diameters and if we take the proximal diameter
you see again the same picture with a minimum diameter of 1.27 maximum diameter of 1.57 giving us a 1.57 square centimeters of area and this is a 1.23 aspect ratio. Taking the kink, the level of the kink, we have the destroyed picture.
Minimum diameter 0.65, maximum diameter of 1.47 giving us only a 0.89 square centimeters and regarding the published and the aspect ratio is 2.3 and regarding this 2008 published paper which showed that area affects outcome and the recent work of Lowell Kabnick
which shows that not only the area but also the aspect ratio affects the outcome. We have to conclude that in this patient, of our center this kink might destroy or might affect the outcome. This is the literature you heard in the last session
already the patency rates of all stents but my message from this table is they included only a small number of patients with short followups as you can see ranging from 10 to 12 but despite very different flexibilities
which we have seen in the second slide we have no significant differences regarding the patency or the outcome and therefore whether more flexibility leads to a better clinical outcome remains still unclear. In conclusion, there is no doubt
that flexibility is important. The flexibility of majority of current venous stents seems to be enough. Till date with currently available studies we cannot answer how much flexibility we need. Where is the threshold
to say this is good and the other is bad? If more flexibility means really better outcome and it is not only the stent, it is more the pattern of disease which affects the outcome. So we started with arterial stents in the venous pathology, we improved to first generation of dedicated venous stents
but we are looking for best stents. Thank you very much.
- Thank you very much and I would like to thank Dr. Veit for the kind invitation, this is really great meeting. Those are my disclosures. Percutaneous EVAR has been first reported in the late 1990's. However, for many reasons it has not been embraced
by the vascular community, despite the fact that it has been shown that the procedure can be done under local anesthesia and it decreases OR time, time to ambulation, wound complication and length of stay. There are three landmark papers which actually change this trend and make PEVAR more popular.
All of these three papers concluded that failure or observed failure of PEVAR are observed and addressed in the OR which is a key issue. And there was no late failures. Another paper which is really very prominent
is a prospective randomize study that's reported by Endologix and published in 2014. Which revealed that PEVAR closure of the arteriotomy is not inferior to open cut down. Basically, this paper also made it possible for the FDA to approve the device, the ProGlide device,
for closure of large bore arteriotomies, up to 26 in the arterial system and 29 in the venous system. We introduced percutaneous access first policy in our institution 2012. And recently we analyzed our results of 272 elective EVAR performed during the 2012 to 2016.
And we attempted PEVAR in 206 cases. And were successful in 92% of cases. But the question was what happened with the patient that failed PEVAR? And what we found that was significantly higher thrombosis, vessel thrombosis,
as well as blood loss, more than 500 cc in the failed PEVAR group. Similarly, there was longer operative time and post-operative length of stay was significantly longer. However, in this relatively small group of patients who we scheduled for cut-down due to different reasons,
we found that actually there was no difference between the PEVAR and the cut-down, failed PEVAR and cut-down in the terms of blood loss, thrombosis of the vessel, operative time and post-operative length of stay. So what are the predictors of ProGlide failure?
Small vessel calcification, particularly anterior wall calcification, prior cut-down and scarring of the groin, high femoral bifurcation and use of large bore sheaths, as well as morbid obesity. So how can we avoid failures?
I think that the key issue is access. So we recommend that all access now or we demand from our fellow that when we're going to do the operation with them, cut-down during fluoroscopy on the ultra-sound guidance, using micropuncture kits and access angiogram is actually mandatory.
But what happened when there is a lack of hemostasis once we've deployed two PEVARs? Number one, we try not to use more than three ProGlide on each side. Once the three ProGlide failed we use the angioseal. There's a new technique that we can have body wire
and deployed angioseal and still have an access. We also developed a technique that we pack the access site routinely with gelfoam and thrombin. And also we use so-called pull and clamp technique, shown here. Basically what it is, we pull the string of the ProGlide
and clamp it on the skin level. This is actually a very very very good technique. So in conclusion, PEVAR first approach strategy successful in more than 90% of cases, reduced operative time and postoperative length of stay, the failure occurred more commonly when the PEVAR
was completed outside of IFU, and there was no differences in outcome between failed PEVAR and planned femoral cut-down. Thank you.
- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.
Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.
Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care
over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.
Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.
And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed
with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better
treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?
That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents
shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,
deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.
Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.
Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.
Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same
that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?
More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article
a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.
- Thank you, 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.
- Have nothing to disclose. This is a question we see everyday, we start off with the toe on the left we hope to end up with this, not this and this. And the question is, can we have some
or do we have something in our toolbox that can tell us this will end up here, not here and not here. So, when you look in the literature and most armor materials of vascular oxygen,
we have physical exam the most basic as the ankle break you index which is historically and currently can be inaccurate based on the calcium changes in the diabetic digital pressures are supposed to be
less affected by the cost of five changes in the diabetic, we also duplex which some people use as well as the velocities or the waveform patterns to help to determine blood flow to the foot contrast based imaging although use essentially on all patients with limb savage
really has not provided accurate measurements of whether or not the patient will heal. Over 20 years ago, there was some data to look at two pressures to determine whether or not you heel the toe or in the foot.
At this point, it was felt to be somewhere in the 50 to 60 millimeters of mercury. You saw patients healed statistically better. However, you still see people heal on this side who are under the 50% 50 millimeters of mercury range.
Perspective data has been seen in the literature. This is a paper that it looked at whether or not monitor healing monitoring amputations would heal the toe pressure, the odds ratio was calculated and as you can see
every millimeter of increase in the toe pressure the risk of monitor for an amputation progressing to hire amputation was decreased, and the toe brachial pressure index was also very important in the term of whether or not the patient would heal. This is a meta analysis of the literature
looking at all the different studies that have been used to determine whether or not two blood pressure and to break your index could show predictive value of healing. Unfortunately,
there are a lot of variations in the way these studies are performed. However, it is felt there are some predictive values. One of the things the reason we looked at our data is some people use Doppler waveform. Some of our colleagues,
instead of looking at the actual pressure reading at the level to toe will look at velocities and waveforms and try to use that as a predictive value. In this particular study,
it has been shown in patients on dialysis, looking at their waveform and without wombs, whether or not they'll go on eventually have a major amputation. And in this setting, it may have some impact
but these are patients with wounds but these are patients that you are following who are on dialysis, and waveforms can predict future amputation. Trans cutaneous oximetry and some institutions are readily available.
however, sorry, however, most institutions that I've worked at it's only available in wound healing center and is not readily available in the vascular lab
although this is based on oxygen tension, the numbers are pretty similar to what we expect to find with healing potential with a digital blood pressures. Our experience we looked at this several years ago we presented a vest and also is published in the annuals of vasculature surgery,
we tried to look at whether or not the velocities within the tibia Walgreens the waveforms within the the tibia Walgreens, and or was there a number that was the best number to predict whether or not the patient would heal.
Similar to what is taught in most educational institutions, around 50 millimeters of mercury was statistically significant and that over 90 or close to 90% of patients healed at that level of perfusion. Unfortunately, under 47,
you still had 70 some percent of the people healed. We looked at this when I was in Tampa and fellowship, we had over 90% predictive value whether or not you could heal in the foot or mid foot based on toe pressures.
However, it really doesn't help us that much because there's still a significant portion of patients who will heal in the 30 to 50 millimeter range. Overall, what does all this mean? I'm unsure.
One of the most difficult things we see with patients that we're going to plan amputation and we can improve the revascularization strategies is in the patient who have two pressures in the zero to 20
since we do not going to heal and proceed with major amputation versus those who are in the 30 to 50 it's essentially a coin toss whether or not they will heal and then over 50 is still not a for sure thing.
Like to thank the opportunity to share information. Thank you.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- 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.
- These are my disclosure, did not influence my work. I would like to thank you for Dr. Weith for the invitation. And I think this is time we cannot ignore anymore one of our major complication during the procedures not just TAVIing with any other surgeries. My tool is the transcranial doppler and I just call it the
stethoscope to the brain because it's really listen to the flow, measure the speed of the flow, measure the direction of the flow. But it also tells me by the resistance if the vessel in the brain occluded or open.
So this is the example how an embolus traveling in the middle cerebral artery or the ACA look like. And again there's not many of those good emboli. The only good emboli we using for PFO testing. But-- sorry--
My pointer would like to show you that on the right bottom corner this is how an MC occlusion looks like real time when a waveform just disappears. This is the example also a teaching tool that you can was the contrast injection and how the lots of air with the contrast injection look like.
But again going back to the TAVI, you can see that the cerebral DWI lesion 90, 80 almost 86 percent, it's a really high number for this procedure. And when you divide them by the transcranial doppler you can see the balloon valvuloplasty and the placement
of the valve comes with the highest emboli count. During their study in Houston this is how they divided the procedure to different phases. And I just want to walk you through a procedure. And this is one of the first challenge, just crossing the valve.
Look at those white lines on the TCD real time while your wire trying to cross your valve. Those are all microemboli. During the BAV you can see there's a hypoperfusion. So hypoperfusion the brain really doesn't like hypoperfusion too much.
So but when you see the folly sword you can see the microemboli too. So again not just the microembolization but the hemodynamics, how your hypoperfusion is really important. And a successful BAV and a valve placement shows that you
have end diastolic flow. Here comes the arch crossing by the TAVI. And you can see just crossing the arch it's also comes with embolization. And why your positioning? The positioning itself again comes
with a shower of microembolization. And it also see that the diastolic profusion is also suffers. And a low diastolic profusion is hyperprofusion again. And why the placement you see the rapid pacing, this is comes with again hyperprofusion and microemboli.
Those are the incidents how we can see by deflating the balloon you're going to see the incidents of microembolization. The different valves again results of no flow pattern. And this is again, in this moment you can see the flow is gone.
Your concern is this something that we just lost a signal. The flow comes back and these are lack of signals and lack of flow of temporarily. But we can also assess how the AI is treated when there's no diastolic flow. That's not good,
that's correlating nicely. And the final results when finally you have a good end diastolic flow pattern that tells you that your surgery's successful. Again different devices can be studied by the DCD, a low deployment versus the balloon deployment.
And this is my most scary picture when you see that the valve is crossing the arch and one of the signals you're going to see and disappear. So this is why we encourage bilateral signal, bilateral MCM monitoring. And here when the microemboli comes,
your signal disappearing, that resulting in a stroke. And you can again act and go to the neuro angio suite. So our data also showed that despite that we have a really low number of stroke and TIA's, we didn't see too much difference.
But phase five, this is when the deployment happens with the high emboli count. But also you cannot ignore that the phase two, when you just moving your catheter causing the valve come through the high emboli count as well.
And just a different way of showing you that majority of the HITS again comes with the valve deployment. But also the low flow stages when we have hyperprofusion we just cannot ignore. Thank you so much for your attention.
- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.
Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance
between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.
Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.
Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100
consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any
stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria
having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this
on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher
than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of
the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,
you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because
the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity
because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish
this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,
regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. 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 Mr. Chairman, good morning ladies and gentlemen. So that was a great setting of the stage for understanding that we need to prevent reinterventions of course. So we looked at the data from the DREAM trial. We're all aware that we can try
to predict secondary interventions using preoperative CT parameters of EVAR patients. This is from the EVAR one trial, from Thomas Wyss. We can look at the aortic neck, greater angulation and more calcification.
And the common iliac artery, thrombus or tortuosity, are all features that are associated with the likelihood of reinterventions. We also know that we can use postoperative CT scans to predict reinterventions. But, as a matter of fact, of course,
secondary sac growth is a reason for reintervention, so that is really too late to predict it. There are a lot of reinterventions. This is from our long term analysis from DREAM, and as you can see the freedom, survival freedom of reinterventions in the endovascular repair group
is around 62% at 12 years. So one in three patients do get confronted with some sort of reintervention. Now what can be predicted? We thought that the proximal neck reinterventions would possibly be predicted
by type 1a Endoleaks and migration and iliac thrombosis by configurational changes, stenosis and kinks. So the hypothesis was: The increase of the neck diameter predicts proximal type 1 Endoleak and migration, not farfetched.
And aneurysm shrinkage maybe predicts iliac limb occlusion. Now in the DREAM trial, we had a pretty solid follow-up and all patients had CT scans for the first 24 months, so the idea was really to use
those case record forms to try to predict the longer term reinterventions after four, five, six years. These are all the measurements that we had. For this little study, and it is preliminary analysis now,
but I will be presenting the maximal neck diameter at the proximal anastomosis. The aneurysm diameter, the sac diameter, and the length of the remaining sac after EVAR. Baseline characteristics. And these are the re-interventions.
For any indications, we had 143 secondary interventions. 99 of those were following EVAR in 54 patients. By further breaking it down, we found 18 reinterventions for proximal neck complications, and 19 reinterventions
for thrombo-occlusive limb complications. So those are the complications we are trying to predict. So when you put everything in a graph, like the graphs from the EVAR 1 trial, you get these curves,
and this is the neck diameter in patients without neck reintervention, zero, one month, six months, 12, 18, and 24 months. There's a general increase of the diameter that we know.
But notice it, there are a lot of patients that have an increase here, and never had any reintervention. We had a couple of reinterventions in the long run, and all of these spaces seem to be staying relatively stable,
so that's not helping much. This is the same information for the aortic length reinterventions. So statistical analysis of these amounts of data and longitudinal measures is not that easy. So here we are looking at
the neck diameters compared for all patients with 12 month full follow-up, 18 and 24. You see there's really nothing happening. The only thing is that we found the sac diameter after EVAR seems to be decreasing more for patients who have had reinterventions
at their iliac limbs for thrombo-occlusive disease. That is something we recognize from the literature, and especially from these stent grafts in the early 2000s. So conclusion, Mr. Chairman, ladies and gentlemen, CT changes in the first two months after EVAR
predict not a lot. Neck diameter was not predictive for neck-reinterventions. Sac diameter seems to be associated with iliac limb reinterventions, and aneurysm length was not predictive
of iliac limb reinterventions. Thank you very much.
- So I'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.
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