- Thank you very much indeed and thank you again, Frank. The European Society guidelines, just to get things put surely, if you've had a major stroke and a large infarction with altered consciousness and drowsiness we recommend that surgery should be deferred and should not be urgently entered.
Similarly patients who present with stroke and evolution or crescendo TIAs are a very special subgroup, relatively small, and these should be treated with carotid surgery within 24 hours. So that gets rid of the two questions that somebody's going to ask afterwards.
What we're dealing with is how should you treat the non-disabling stroke or TIA. Now this is the natural history of early recurrent stroke after a TIA in patients with 50 to 99% stenoses and you can see that the early risks are really very high indeed, way higher than was reported
in the randomized trials. And that was because these patients never were included in the randomized trials. They'd suffered their stroke long before they had a chance to be treated. And we know from a meta-analysis of the pooled ECST,
NASCET, and VA data that the quicker you offer surgery the more strokes that you prevent in the long term, particularly in patients with severe stenoses. And so for that reason the ESVS recommended that wherever possible patients who have presented with a TIA or a non-disabling stroke,
they should undergo a carotid intervention within 14 days of onset, preferably as soon as possible. Now there's a lot of debate about the impact of if you operate early does that increase the procedural risk? Well there have been three big registries,
the Swedish with two and a half thousand patients, the UK with 23,000, and the German with 56,000. The study that captures eternal attention is the Swedish study with the 11% death and stroke rate within 48 hours. But while there was a small but modest increase
in the 48 hours complication rates with the UK and German databases, there were nowhere near as gross as the Swedish ones. The reality is it's quite difficult to get somebody with a non-disabling stroke into the operating theater within 48 hours.
The problem is in terms of whether you should do stenting or surgery is that the overviews of the randomized trials have shown that stenting is still associated with a threefold excess risk if you perform surgery within either seven days or eight to 14 days.
So the European Society recommended that if you are undergoing revascularization within the first 14 days it's preferable to offer carotid endarterectomy rather than carotid stenting, but as I will mention later, that might change
the next time the guidelines are published. And we also concluded that if you have, you do have comorbidities in recently symptomatic patients who make them high risk for surgery, and these are going to be careful about the definition of that. We recommend that an MDT needs to review that decision,
but if that is the case then stenting should be considered as an alternative. Now, I thought it useful also to point out that we recommend that early endarterectomy within 14 days should be considered after intravenous thrombolysis.
If the patient makes a rapid recovery the area of infarction is less than one-third of the MCA territory, a previously occluded middle cerebral mainstem is recanalized, and there is a significant stenosis and no evidence of any parenchymal hemorrhage
or significant brain edema. Now there is a careful caveat to this, and that is that you should withhold IV heparin and antiplatelet therapy for 24 hours after lysis completion, but then before you take the patient to theater
the patient should be restarted on antiplatelet therapy. So that will introduce a small delay, but if you don't the risks of hemorrhage are much higher. There are unanswered questions of course that the guidelines that Jean Baptiste and I chaired cannot answer.
First of all, do newer CAS technologies mean that it can be performed as safely as endarterectomy in the first seven to 14 days. And I'm notably referring to TCAR. Now I know there's a very large registry being published on the results of TCAR,
and I've reviewed it for the Journal of Vascular Surgery. And I heard Glenn Darling present it to the European meeting. But they cannot tell you what the death and stroke rates were when operations were performed within seven or 14 days of surgery,
and this is crucial. There's no point in saying that TCAR's fantastically good in asymptomatic patients or patients whose symptoms were three months ago. What we need to know is whether this offers a benefit in patients within the first seven to 14 days.
And the other big issue is whether following mechanical thrombectomy should a tandem internal carotid artery stenosis be treated by synchronous stenting or by deferred stenting to surgery. Now I was reviewing a lot of the literature
for a separate presentation yesterday, and the jury is out on that because there is not much published. But there do seem to be increased hemorrhagic complication rates where you have patients who undergo a synchronous mechanical thrombectomy
and synchronous carotid stenting. Thank you very much.
- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery
and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely
at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer
or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.
Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.
There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking
at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?
And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,
this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients
with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.
I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,
and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients
who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually
living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,
you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data
over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,
more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.
These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?
I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.
I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at
the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,
such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time
camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.
If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.
Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.
There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series
where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,
limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.
But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.
So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.
So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.
If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.
- Thanks Dr. Veith for the invitation. It's a privilege to be here. My only disclosure is that like Jo, I was a trauma surgeon before I became a vascular surgeon, so that informs part of this talk. As you know Dr. Veith promoted REBOA for aorta aneurysm ruptures long ago.
But there has been a resurgence of this as the military has seen that the majority of deaths on the battle field, preventable deaths on the battlefield is due to hemorrhage. And almost 90% of those were due to non-compressible torso hemorrhage,
not amendable to tourniquets. It's said necessity is the mother of invention and it was really the military vascular surgeons here today and John Eliason and Todd Rasmussen who wanted to prevent non-compressible hemorrhage and created an easy to use low profile catheter
that's have been called the ER-REBOA catheter in recognition of their contribution. It's also been the military vascular surgeons here today, Chuck Fox and Jo DuBose who have been the leaders in promoting and teaching this technology across the country and across the globe.
Like any new technology, however, it can lead to complications if used in an unexperienced hands. And the reported complication rate in the literature is only 5%. My belief is that this is vastly under reported.
It's predominantly performed by trauma surgeons currently. However, ER positions are increasingly using this wanting to use it for a non traumatic indications. However, the lack of experience of catheter and wire skills in these two groups can lead to devastating complications and errors in management.
And that can happen in every step along the way. You've seen some of these pictures earlier but we all can be placed in any number of places, any wars, any branch vessels. Here you see in ascending aorta, internal iliac, left carotid, left subclavian and these are
some of the great pictures from one of Jo's papers but I've seen this in several instances that I didn't think to take pictures myself. Additionally, if it's over inflated in a wrong location that can lead to a vessel rupture. And probably the most common complication
is the access site issues. So, if this is not recognized and dealt with earlier, it can lead to profound leg ischemia and ultimately end up in amputation which is a tragedy after you save the patient's life. Unfortunately, I've seen this in
more than one occasion already. Obviously, there is plenty of other complications including thrombosis, embolism, iliac dissection. I've seen aortic rupture, prolonged visceral and renal ischemia and balloon migration. A tragic example was given to me by
a prominent vascular surgeon who has consulted after a REBOA has been left in the aorta for 12 hours partially inflated which led to aorta, iliac complete thrombosis and despite revascularization had such a severe pelvic & lower extremity ischemia that ultimately led to the patient's death.
This is a shocking example of inexperience that can be prevented by involving people who know what they are doing. So, how can these complications be avoided? Well, certainly training and practice is critical. But also X-ray confirmation because misplacement is common
and it's important to recognize that all patients who have REBOA in place should go directly to the operating room because stopping at the CV scanner is not really an option. The patient is ischemic. You're on the clock.
And also teamwork is critical because while you're performing the procedure, you should have some other person ideally doing the trauma resuscitation because you need to focus entirely on the procedure to prevent complications. I have three basic recommendations for everyone.
One, is that, all trauma patients who are hypotensive should have femoral arterial line catheter placed. This is the longest and most difficult part of the procedure. But, once it is performed and if the patient remains hypotensive, you can easily upsize
to six, seven French sheath and then place REBOA if necessary. Secondly, use teamwork. This is a team effort and trauma surgeons are clearly at the tip of the spear and they are the boots in the ground who need to know
how to do this procedure. However, they do not have the vascular and endovascular experience that trauma surgeons all would've had. And, therefore, it's my recommendation that the vascular surgeons should be involved in 100%
of these cases after a ballon is placed. Especially, in centers that are not doing this very frequently. And it should trigger an automatic vascular consultation, the balloon should be taken down as soon as possible, and the sheath removed as soon as possible
and then bilateral ABIs should be performed because you need to act, you need to recognize complications early in order to prevent the onset of complications. Lastly, the military vascular surgeons have been the leaders in this,
promoting this technology and teaching it world wide and the rest of our civilian vascular surgeons need to step up and a take a leadership role. We need to learn and teach REBOA in our community. We need to help our hospitals to determine who should be credentialed.
And we need to evaluate all REBOA complications collectively, so we can learn from them and prevent them in the future.
- Thank you. These are my disclosures. So we know the traditional teaching is to wait 6 weeks after stroke for CEA to avoid hemmorhagic conversion. Of course improved imaging has allowed us to identify those people at risk, so that earlier intervention is safe.
And we just heard that most societies recommend that we intervene within 14 days. And that's because the highest risk of recurrent symptoms is within the first 4 weeks. Indeed, recent literature has shown that early stroke recurrence after the onset
of symptoms is higher than that was previously thought. And we have found, especially at our institutions, the stroke neurologists have become very aggressive in their insistence of early revascularization in the setting of symptomatic carotid disease, even to the point where they want it done within 48 hours.
So the goal of our study was to identify the postoperative risk associated with different timing intervals of carotid endarterectomy after stroke in effort to find the safest or earliest timing interval for repair. We queried the Vascular Quality Initiative
of all carotid interventions, all carotid endarterectomies performed on stroke patients between 2012 and 2017. And we excluded patients that were asymptomatic or had TIAs, emergency cases, carotid cavages, and occluded ipsilateral carotid arteries.
We stratified the patients into four groups, less than 48 hours, 3-7 days, 8-14 days, and greater than 15 days. Looked at major outcomes including perioperative stroke, death, stroke and death and MI, and then secondary outcomes such as cranial nerve injury,
reperfusion injury, and discharge Rankin scores. We identified 8404 patients. The demographic data was predominantly male, average age was 69, with obesity of 33%. 30% were current smokers, 82% were on aspirin at the time of their endarterectomy,
and 84% were on statin. This is just looking at the demographics. You can see that between the patients treated within 48 hours and the other groups, the early group had a lower instance of functionally dependent patients,
congestive heart failure, or statin use. The first two groups up to 7 days were less likely to be living at a nursing home, have renal insufficiency or COPD. These were the operative details. The majority of the patients had general anesthesia,
and most patients had heparin. You can see that there were some eversions but the majority of patients had a patch. And 61% had a shunt of which 45% were routine. 30% of the patients had EEG measured. And looking at the significant operative differences,
the patients treated within 48 hours had a higher shunt rate, higher dextran use and a higher re-exploration rate. So the primary endpoints, 30-day mortality was 1%. The in-hospital stroke rate was 2.1% and the stroke and death was almost 3%.
When you're looking at the differences by groups there was no difference in 30-day mortality. However, patients treated within 48 hours and then 2-7 days had a significantly higher in-hospital stroke rate, almost double that of the patients that waited.
And the perioperative stroke and death rate was again higher in the first two groups. Secondary endpoints, in-hospital TIA was .6%, cranial nerve injury was 3.2%, and reperfusion injury was .2. And there was no difference in the secondary endpoints
between all of the groups. This was the multivariate regression for perioperative stroke and death and interestingly, only less than 48 hours was a significant predictor. The rest of the timings were actually protective.
There was no timing difference for 30-day mortality. And for in hospital stroke, again it was the first 7 days that were negative predictors, and operating after 8 days was protective. And finally for post-operative complications, early intervention in less than 48 hours was significant.
So in summary, post-operative stroke and death was significantly lower in patients treated after 7 days. This is driven by a significantly lower post-operative stroke rate. Delay to 8 days or more gave a 1.5-fold decrease in the risk of stroke and death.
And timing surgery to 8 days or more significantly lowered the odds of post-operative stroke. Based on the VQI data, surgeons should make every attempt to avoid intervention in the first 48 hours following a stroke. The optimal window of surgery after stroke appears
to be 8-14 days as this significantly decreased the odds of post-operative stroke and death and other complications. Thank you.
- Okay, is thermal ablation obsolete? No. My disclosures. Are nontumescent ablation procedures ready to take over? This is an article in 2014 by Michael Sadek and myself. No in 2014, no in 2019, and no in 2020, and I predict no in 2023. That's about as far as I can go.
So every time I hear this, I scratch my head, "oh my God." So, there's similar arguments regarding open surgery versus minimally invasive surgery. We know that they're both needed, in terms of different particular incidences of pathology. Risk/benefits, insurance coverage?
So if we look at everything, does size matter? And I would submit to you that right now, in terms of the non-thermals, size does matter. So if we look at 12mm or less, I think that's where the sweet spot for non-thermals are. If we look at trials, clinical correlation of success
in acute thrombotic of lower extremity endovenous thermal ablation, the subset showed that there was no real differences between RF and laser. If we look at this prospective study, looking at 1470 laser and radiofrequency, again, no difference.
If we look at this study, no difference, it all works. So in this particular paper by Professor Davies and his group, he looked at certain things and his summary for this article was thermal treatment with RFA and EVLA is the mainstay of varicose vein treatment at present.
Both RFA and laser appeared to have similar efficacies. If we look at this trial that was a pivotal trial in terms of cyanoacrylate and RFA, there's no inferior with regard to efficacy, etc. If we look at a multi-center randomized controlled trial comparing radiofrequency and mechanical occlusion
chemically assisted ablation of varicose veins, again, pain secondary to truncal ablation is less painful with MOCA than RFA with similar short-term technical and quality of life and safety outcomes. If we look at this trial we heard earlier today of partial exposing of this, mechanochemical ablation
versus cyanoacrylate adhesive for the treatment of varicose veins, study protocol for a randomized controlled trial, there is really no difference across the board. Just when you thought new RFA devices are now coming out. We know we talked earlier about
RFA continuous and segmental, and just understand that if it was obsolete, why would they come out? So Kabnick the fortune teller, better known as Carnac, is thermal ablation obsolete? I would submit to you in my crystal ball,
between the times of 2018 and 2023, the answer is no. And then I got my ouija board out, because I didn't understand what I was thinking about, and really the ouija board went "no." So ladies and gentlemen, in conclusion, as of now and 2023, there is not one perfect modality for
venous ablation, each has their sweet spot. Thermal long track records and larger veins, perforator approval, with thermal. Non-thermal, no tumescent, perhaps a shorter procedure and nerve sparing. Recommendation, most of us agree, if you can only
afford one device, I would do thermal. My recommendation would be to have thermal and non-thermal. Thank you very much.
- So PAD affects five million adults in the United States today, and we know the US population is aging. And 15 to 20% of folks 70 years and older have claudication, a minority of these progress to CLI, and the impact on lifestyle is often minimized, as demonstrated in decreased quality of life scores
in these patients. Now with active tobacco use, there is acceleration of disease towards claudication, and there are higher rates of amputation, MI, and death. But prior to open or endo intervention, the SVS Guidelines recommend supervised exercise,
medical therapy with statins, beta blockers, antiantiplatelets, and Cilostazol, and an aggressive multidisciplinary approach to smoking cessation, which should last no less than six months. But what if a patient can't stop smoking?
We've all had these patients. Should patients with lifestyle limiting claudication be denied open surgical or endo-revascularization? So let's look at the open literature. A meta-analysis performed in 2005 of 29 eligible studies. The results were that bypass graft failure
was three times that in smokers versus nonsmokers. There was a dose response relationship in smoking cessation prior to or after bypass, equalized patencies. A more recent study, published in JVS in September, queried the VSGNE, 1789 lower extremity bypasses, 971 were nonsmokers, 818 were smokers,
and what they found was that primary patency at two years was 48% in smokers, versus 61% in nonsmokers, and when they propensity matched these patients, there was even a greater difference. 10 year survival was also decreased. And in another article,
published in August of this year in JVS, again a VSGNE study, over 2,000 patients, almost 3,000 patients with lower extremity bypass for claudication. The results looked at MALE, amputation-free survival, limb loss, death, major limb events or death,
and they found that current smoking was a significant predictor of major adverse limb events, and major adverse limb events or death. But do active smokers have worse outcomes after endovascular interventions? So, let's look at the literature again.
And there is none. The only paper I could find was a Markov decision analysis, in which compared revascularization in active smokers to medical management, this was a retrospective study, and their results demonstrated better quality of life in smokers after revascularization versus medical therapy.
The quality of life was similar, after revascularization in nonsmokers and smokers, and there was no increase in amputation rates up to 36 months. Also, 26% of the folks that were revascularized, quit tobacco use after their quality of life was improved.
So we decided to do a small study at my hospital. The outcome of endovascular interventions in active smokers with lifestyle limiting claudication versus nonsmokers. This was retrospective. 138 total patients with endovascular intervention for claudication, 47 were current tobacco users,
91 were never or former smokers. The primary endpoints were reintervention, secondary endpoints, surgical bypass, limb loss, MI, stroke and death. And here you can see, as in most studies, the smokers were a younger population,
and anticoagulation, in our patient population, was more common. As far as comorbidities, they were more common, as in most studies, in the nonsmoking group. And in a mean followup of 3.6 years for both groups, there was no statistically significant difference
between the two groups for any of the outcome measures. So in conclusion, active smokers with lifestyle limiting claudication, we would advocate, of course, smoking cessation. Outcomes with respect to reintervention, surgical bypass and limb loss appear to be equivalent in these two groups.
We feel that these patients should not be denied endovascular intervention, and improved quality of life after intervention may result in an increase in smoking cessation in this patient population. Limitations are obvious, this was a very small study,
and retrospective, and we are actually extending this study to look at several hundred additional patients. So I thank you for your attention.
- Good morning. It's a pleasure to be here today and I wanted to let you know that a lot of this work that was being done earlier were really driven by physician need. As you can see, the trial as well as the EXCEL registry is finally on the way, so it's very exciting.
I'm not going to spend a lot of time on this but everybody knows the primary predictor of EVAR failure is really short necks and angulated necks. The first generations have been pretty good but they were really not intended for this type of anatomy. We see a lot of patients with really distorted anatomy
but they still have a relatively lengthy or 10 mm neck. In fact, about 80% of the EVARs treated in the United States have at least a 10 mm proximal neck. They may not be of the highest quality but they're there. So, how could be achieve better results? Basically we need to use every millimeter
of this landing zone, so that we can use the 10 mm neck to its fullest advantage and I believe when you do that, the results are fairly comparable to doing any type of above renal repair, like a fenestrated or branch graft. The stabilization of the device
during delivery is absolutely crucial. So essentially what you want to do is have a device that is able to utilize every neck angle and every millimeter of that available neck. And we know that 80% of all the patients, do have that neck. So, the new conformable endovascular device
has been around for the last five years or so but recently went into trial in December of last year. It's very different proximally than the current EXCLUDER in that the fixation system is single and it has a series of nested stents very similar to a conformable C-TAC device.
As you can see, this allows the device to conform to the anatomy, but not only that you're able to adjust the device inside too and that's actually Frank Veith's terminology, is that you're able to adjust this so that you can inch it up and utilize the entire neck.
16 French, proximal fixation, trunk length's a little bit longer than the current EXCLUDER at 5.5 to 6.5. This allows further treatment in the future going forward if you need to do a fenestrated device or branch graft device above it.
This device was designed to conform up to 90 degree angles and it's designed to seal at 10 mm necks. And, the most important aspect of it is, you're able to reposition the device once you deploy it. The mechanism is really one of being able to angle the device with a steering system
before the deployment and also afterwards and also be able to restrain the device up and down. Another major difference is that it has a 30% restraining secondary sleeve just like a ZFEN device so you're able to move this device up and down the angulated neck
and I'll show that with a case. The clinical trial in the U.S. began in December of last year and so far, I'll show you the update but unfortunately the FDA disallows us to give you any data. I can give you some of the demographics but I'll show you
that the preliminary results look excellent. The goal is to implant 80 patients in the short arm which is complete and 110 patients in the high neck arm is partially complete at almost 30 patients. The trial update objective is as outlined, there are 48 U.S. sites
and the current study enrollment is 106 patients, the short neck arm again I said is complete. Primary safety endpoints, not unlike any other device. Primary effectiveness endpoints, again freedom from all of these aspects. The first device was in 2017,
this was a relatively straightforward patient. The device performed well, this is a six month follow-up. The device had no migration issues, confirmed beautifully. But this is not really what the device was designed for. So, I'm going to give you a case of a patient that was enrolled in the high risk arm.
This patient had an 8.5 cm aneurism, 82 degree angulation, 11 mm proximal neck, turned down for EVAR or fenestrated at two other institutions in the New York City area and basically came for a third opinion as most New Yorkers do.
The aneurism looks like this and it's kind of a very angulated proximal neck with extremely torturous iliacs. This is the case that we did. You can see the device being configured here with the steering wire and when you do this,
you can see the device being able to be easily moved proximally and distally and the next portion of the video shows that steering wire kind of implanting the device into the lesser curve. - [Moderator] The device is deconstrained right? - Yes.
You can restrain it and it's a combination of being able to restrain it and open it which allows you the flexibility and as you can see with this maneuver, the device looks like it's perfectly opposed but in fact, the posterior aspect did not oppose very well.
So, we adjusted it further by increasing the posterior coverage and this is the post-op and we got a seal. There was no ballooning. This device, the ballooning is optional. So, the results have been excellent so far
with the highly angulated neck arm and we'll only see, there's only 30 patients so far but the results have been excellent so far. - [Panel Member] Rob and for you and for also Mark who presented that last case last week. When you deploy this device
it seems that you have a stiff wire, you're almost fighting the very advantage you're proposing. Do you ever consider swapping out for a floppier wire so you can then really get the native anatomy configuration? Because now that fusion image is presumably the pre-op fusion without the stiff wire.
So, I just wondered whether there's any value to that. - That's a great question. In fact, if you look at this video again, not this one but, let me see, this one, there's no wire, that the tip of the Amplatz wire is right at the tip of the device.
So that device is almost unsupported at this level, so you're able to freely flex that device back and forth without the constraints of a stiff wire. - [Panel Member] Is that your personal style or is that something that's part of it. - It's actually a recommended
and the part of the deployment process is to bring the floppy wire. So, you can use like a Glidewire Advantage or an Amplatz Super Stiff or whatever wire you like to use but it has to have a very floppy unsupported section in the proximal segments
to be able to get this kind of maneuverability. - [Moderator] So for the panel who've used this device, with all this manipulation of the proximal neck and especially in a diseased neck, is there any evidence of embolization of thrombus into the renals or distally?
- [Panel Member] Of course there is the potential for that but we haven't seen it yet and I think that the FDA IDE Trial and the registry will address that. I think that you should be careful. If there is a lot of neural thrombus in that neck
then this manipulation could be a potential risk. Actually what you're doing is, it's not that easy to get it into position in just one angulation. Sometimes you have to angulate, push it a little bit, restrain it again and reposition it to come in the perfect position,
especially for high angulation. - Yes. There's definitely a learning curve here but the learning curve actually can be achieved with just a couple of cases to be able to see how the device behaves
in the human anatomy.
- Thank you very much Frank and thanks for the invitation. My first thing is to deal with the patient who's awaiting CABG who's had a previous stroke or TIA. This is the only study of it's kind showing that if you proceed with isolated CABG, the risk of stroke is extremely high and if you look at the meta-analysis that we've done of whether you do endarterectomy or
stenting in symptomatic patients, this is all the literature there is. And what you can clearly see is that the death and stroke rates in patients undergoing CAS followed by CABG are much higher than after carotid and endarterectomy. And that lead us to recommend that a stage of
synchronous carotid intervention should be considered in CABG patients with a history of stroke or TIA and who have a 50 to 99% stenosis. But advise that for now, if you're going to do that such an intervention, surgery should probably be considered instead of stenting.
But 96% of all interventions of the CABG and carotid variety are in asymptomatic patients, so what about them? Well, this is all the literature there is on stroke risk in patients undergoing isolated CABG with a unilateral asymptomatic stenosis of 70 to 99 or 80 to 99 and you can see there is an awful lot of zeroes
in that table and if you go at patients with bilateral significant disease, the death and stroke rate is much higher but again there is not too many strokes here. And if you look critically at the literature and ask yourself okay we've had so many strokes, how many of them can be attributable to underlying
carotid disease by looking at the CT scans or the distribution of lesions, you'll see that between 85 and 95% of all strokes cannot be attributed to an underlying significant carotid stenosis. And if you look at all the death and stroke rates and this is a multiple meta-analysis that our
group have done over the last 15 years, these are the death and stroke rates depending on how you treat the patients, and 80% of these are asymptomatic and 80% have got unilateral stenosis and the death and stroke rates are far in excess of the risk of stroke if you just perform an
isolated CABG in patients with unilateral asymptomatic disease. There have been two randomized trials. This is one, the Iluminati trial that Jean-Baptiste was involved in, 30-day death and stroke rates not significantly different.
There is quite an astonishing trial from Germany, which was again unilaterally asymptomatic stenosis with a near 20% death and stroke rate with synchronous carotid CABG and a 10% definite stroke rate with medical therapy, ah isolated CABG, sorry. So the ESVS have advised that a staged synchronous
carotid intervention is not recommended in CABG patients with an asymptomatic unilateral, 70 to 99% stenosis for preventing stroke after CABG. A staged synchronous intervention may be considered in patients with bilateral disease, the evidence is not brilliant but it's such a rare thing that it's
probably not worth arguing about. Now what about patients who are undergoing non-cardiac surgery? This is quite an interesting group, because if say, a gastrectomy, a hip replacement or whatever, if they've had a previous history of stroke or TIA
they should undergo carotid imaging and if they've got a significant stenosis they should undergo prior carotid revascularization prior to undergoing their gastrectomy et cetera. But what about the asymptomatic patient? This is quite interesting.
First of all, let's just look at a very large study by Jorgensen, 4 nearly 500,000 elective non-cardiac operations and 7,000 had suffered a prior stroke or TIA, and the most important thing was, the stroke risk was directly related to the time from the onset of the TIA to doing the operation.
So if you did it within three months of the stroke or TIA there was a 12% peri-operative stroke rate, but if you managed to get out to six months, the stroke rate was only 0.1% so the lesson learned there is that if it's possible to delay surgery in patients who've had a prior stroke or TIA
or a recent one, you should delay it for six months. Only two studies have looked at whether asymptomatic carotid stenosis increased the stroke risk in patients undergoing non-cardiac operations. Ballotta did a randomized trial, and Sonny, which is a very large observational study,
looked at the impact of asymptomatic carotid stenosis on outcome and found that there was no evidence that a pre-existing carotid stenosis increased the risk of stroke in patients undergoing major non-cardiac surgery. Similarly, in a huge study on TAVI patients,
no evidence that carotid disease was a risk factor for perioperative stroke. So in our recommendations we advised routine carotid imaging in asymptomatic patients undergoing major non-cardiac surgery is not recommended and prophylactics and arterial stenting is not
recommended in patients with asymptomatic carotid stenoses undergoing non-cardiac/vascular procedures. And if you'd like to look at all the literature and data that we came to in using to our conclusions, the guidelines are free to access on the internet.
Thank you very much.
- 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, thank you. Dear Colleagues, I have no Financial Disclosures. If we look at the old randomized stroke trials, mainly NASCET and ECST, we had a combined any stroke and death rate within 30 days of 7%, and there were some clinical and morphological arrivals that were associated
with an higher or a lower risk. The Carotid Stenosis Trialists' Collaboration was established to perform pooled individual patient data analysis from the major carotid randomized trials of the last year, ICSS, SPACE, EVA-3S, CREST and now also GALA.
And the aim of this study was to look at the impact of clinical characteristics and perioperative measures on the 30-day risk of stroke and death, and whether the risk of CEA for symptomatic patients has changed since since ECST and NASCET. And I'll jump directly into the results,
the primary outcome, any stroke or death within 30 days occurred in 4.3% of the patients, disabling stroke and death, 2.1, any stroke 4%, all-cause death 0.8%. If we looked at the multi-variable analyses, these are the impact of the clinical characteristics,
no clinical factor was associated with the lower or bigger risk, with the exception of a contralateral stenosis or occlusion. This was statically significant, with an risk increase of almost 60% relative risk increase. We looked at the clinical signs of the patients.
There was a tendency that stroke patients had a bit worse results, but again, statistically not significant, however patients who had an disabling stroke, namely a modified Rankin scale of 3 to 5, had a significantly higher risk of a repetitive stroke or death.
Time interval didn't play a role, at any time interval, nothing there, and also the in-trial center volume. The techniques, a tendency that CR without patch, and interestingly Eversion-CEA had worse results in this big data cohort, but again, statistically not significant.
Shunt use was a bit biased, that was associated with an increased risk, and we looked also at the type of anesthesia, this is I think the most important result of this study, and we were able to show that local anesthesia had better outcomes as compared
to general anesthesia, with a 30% relative risk reduction in these patients. So, summing up and comparing the data with the ECST and NASCET trial, we had a reduction from 7% down to 4.3% and also for the other single end points, disabling stroke, death, any stroke, all-cause death, et cetera.
There was a reduction in the overall complication rate with the exception of, in most cases Passager cranial nerve palsy. So in conclusion, we found a higher surgical risk in patients with a contralateral high grade stenosis or occlusion, we also found a higher risk in patients
with a modified Rankin Scale of 3 to 5 at randomization, so disabling strokes. Lower surgical risk if surgery was done under loco-regional anesthesia, and no significant effects for surgical technique, co-morbidities, gender or age. Thank you very much for your attention.
- Thank you. I have no conflict of interest. Now the first burning question in carotid artery disease management. I agree with the previous speaker somewhat. Is that is who if anyone with asystematic Carotid Stenosis is likely to benefit from a carotid procedure
in addition to current optimal medical intervention? Where I have to ask this question because of significant advances in medical revascularization over the last three to four decades. Particularly since ACAS was published.
Now at most about 4% of persons with asystametic cartonied stenosis will have a stroke caused by the lesion as explained on Tuesday. We just know that its overall harmful and wasteful to do a procedure on all of them.
But stoke risk stratification cannot identify those who now benefit from carotid endocardectomy and stenting is overall more harmful than endocardectomy. There are many proposed markers of high stroke risk in asymptomatic carotenosis patients given just medical treatment.
Including those some of the European society vascular surgeons. But we already know that each of these markers used in isolation they lack sufficient specificity to identify those most likely to benefit from a procedure. In other words they are to common.
And also the event rates with these individual markers are too low. Particularly considering that all of these studies of these markers were done with suboptimal medical treatment. The second burning question.
Is will prevailing carotid trails find a current procedural indication in stroke prevention? Well the answer with respect to ACST-2 is no. Because its just a trail of stinted verse endocaretomy There is no medical treatment only arm. So its not testing the efficacy of these procedures.
It will help to measure harm of one procedure versus another. But this is of little value without a procedurual indication in the first place. The answer of CREST-2 is not too. Because unfortunately there randomizing
average risk patients like those in ACAS. And we already know that to do a procedure on all of these people is going to be futile and harmful. There's no stroke risk stratification before recruitment. An although they are doing some sub group analysis with markers.
Are these powered sufficiently? I haven't seen that is the case so far. If you look at the CREST-2 sample size. There is approximately 85% power to detect differences in peri-procedural stroke or death or later ipsilateral stroke with endocardectomy versus stent
or stenting versus medical treatment. If the average annual event rate in the medical intervention arm is greater than 2.1 or less than .2 compared to .9 in those procedural arms. Now we know from CREST-1 that they did achieve and average annual event rate of .9 with endocardectomy
but not with stenting. The risk there was about twice as high at 1.6. And its highly likely that they will get an annual event rate in the medical intervetion arm within that range. So that means that the overall role
CREST is most likely to show that stenting causes harm and endocardrectomy knows significant difference with the respect to medical intervention on its own. In other words no procedural indication because if stenting is more harmful we won't do it. And if endocardectomy adds no benefit we won't do it.
The same response for ESCT-2 because like CREST-2 its randomizing average surgical risk patients. No stroke risk stratification before recruitment. Not pre-powered for high stroke risk markers that we have been talking about. ACTRIS has the best chance of finding a procedural role
in asystematic carotid stenosis because they are doing stroke restratification before recruitment. Using embolize detection, errands of impaired to cerebral vascular reserve, errands of intraplaque hemorrhage on MRI
and errands of rapid and severe stenosis progression. But the outcome of this will depend on how the data is analyzed. For example these markers be tested separtly or combined. We already know that markers individually lack specificity. And at the moment the trail does appear to underpowered
with the total of only 700 total patients expected. Mean while TCAR is being accessed only in registries plus or minus input in CREST-2. So it appears we have absent or underpowered comparisons with current medical intervention.
So a clinical indication is unlikely to be established with the current research that is planned. Actually procedural trails are premature when it comes to asystametic cartonid stenosis. What we should be doing is first defining current optimal medical treatment.
Measuring its impact. Risk stratifying people. Using procedural trials only if we find a sub group with an ipsilateral stroke rate that is high enough despite current optimal medical treatment. So if anyone would like to help on this path.
Please speak to me afterwards.
- Good afternoon. On behalf of my co-author Danielle Lyon I'd like to thank Dr. Veith for allowing us to present our data. No disclosures are relevant to this talk. So, why a small incision carotid endarterectomy? I actually came on to it maybe a decade ago when in debates for carotid stenting versus
carotid endarterectomy my interventional colleagues would show pictures like this. And pictures like this, with big incisions which is how I was trained from sternal notch to the angle of the mandible and above. Then I started thinking you know, maybe this could be done
through a smaller incision safely. So it's a smaller incision, it's cosmetically much more acceptable especially in ladies. Endarterectomy typically only involves about three centimeters of artery anyways. And, there's decreased tissue trauma
with a smaller incision. All of my patients are operated on clopidogrel and aspirin and we also operate on patients on full warfarin anticoagulation without reversal which we published in the annals a few years ago. So first, rely on the preoperative imaging.
So I always get a CTA to confirm the duplex ultrasound. Here you can see a very focal plaque in the proximal internal carotid artery. Here's a more heterogeneous plaque and opposite a carotid stint. I typically do these with,
under general anesthesia with EEG monitoring. The self-retaining retractor I use to stretch the incision would be, I think, a challenge in an awake patient. I image the carotid bifurcation, just like our previous speaker, with ultrasound ahead of time. Just a regular Site-Rite ultrasound,
you don't need a duplex. I typically call my friend Russell who comes with the ultrasound, and doing both longitudinal and transverse views to identify the carotid bifurcation and confirm the extent of the plaque. The incision is typically around three centimeters,
but clearly less than four centimeters, and it's centered over the previously marked carotid bifurcation. I use a standard incision along the anterior border of the sternomastoid muscle. And then use a self-retaining retractor to stretch the incision a bit.
This is a pediatric omni retractor which works really well for this purpose. It's very important, especially for the more-sef-full-ab blade to make sure that you identify the hypoglossal nerve as you can put a fair bit of traction on that upper blade and sometimes the incision is small enough that I actually
make a little counter incision for the proximal clamp. I've found that the use of a shunt can be challenging with this technique. There's one case out of 124 that I had to extend more proximally in order to safely put a shunt. I do, though, use acute ischemic preconditioning.
So typically the mean blood pressure is 90 or above, the patient's fully anticoagulated. I'll clamp the distal internal carotid artery and if there are EEG changes I'll unclamp it, raise the pressure just a little bit more and in most occasions the second or sometimes third time the internal
carotid artery is clamped the EEG does not change. And again, you can extend the incision if necessary as patient safety is absolutely paramount. So the technique is safe. In 124 consecutive patients there were no strokes or deaths.
There was one temporary cranial nerve injury which was the marginal mandibular. A complete endarterectomy can be achieved. Again, no increase in cranial nerve injury compared with a standard incision. And it really is a superior cosmetic result.
So here's a photo that I received from silk road, you probably did too. So here's the TCAR incision compared with a standard carotid endarterectomy incision on the other side. Here's a couple of my recent patients, so you can do this operation with an incision
that is about the same size as that utilized for TCAR. Thank you.
- [Narrator] Calcium is a big challenge for hope in intervascular procedure. In particular, it can increase the risk of complications and also reduce the efficacy of drug-coated balloons. The presence of calcium will reduce the vessel compliance, so it is barrier for the optimal dilatation.
And also reduce the tissue permeability, and is a barrier for optimal drug uptake. Different studies, in-vivo and ex-vivo, confirm that circumferential distribution is more important than longitudinal. When we have a complete circumferential
distribution of calcium, drug uptake is less. The effect of calcium on drug uptake is confirmed by this study. They have evaluated the tissue concentration of paclitaxel before and after atherectomy in calcified and non-calcified lesion.
In the absence of calcium, you can see that there was not a big difference in terms of tissue concentration before and after atherectomy. On the opposite, tissue concentration of paclitaxel was higher after atherectomy
in case of heavy calcified lesion. There is not a consensus on calcium definition. Nowadays, we have five different classifications, but all of them say the importance of bilateral or circumferential distribution to define the calcium severity.
If we analyze the five most common trials on DCBs, we can observe that calcium-related exclusion criteria are very similar. Generally, DCB trials do not include severe calcifications. For example, the IN.PACT-SFA, LEVANT 2 and ILLUMENATE European reported,
more or less, 10% of severe calcified lesions. On the contrary, more that 40% of severe calcium have been included in the ILLUMENATE US and ILLUMENATE GLOBAL. If we analyze the one year primary patency of these studies, we observe, more or less, the same outcome.
However, keep in mind that two of them, the ILLUMENATE GLOBAL and the ILLUMENATE US, included more that 40% of patients with severe calcification. To increase the efficacy of drug-coated balloons in heavily calcified lesions,
vessel preparation is mandatory. Different devices can be used for vessel prep. We can use a simple PTA balloon. We can use a special balloon, like cutting or scoring. We can use atherectomy or also lithoplasty. Very good data have been reported
by the Definitive AR study, where atherectomy was used in combination of DCB in long, calcified lesions. Also, scoring balloon plus DCB can improve the permanent patency rate, as reported by the PANTHER registry. Matching data has been reported
with the use of lithotripsy in complex, calcified lesions. The DISRUPT PAD II study reported very good results, especially in terms of primary patency and clinical driven TLR after one year, in such complex lesions.
In conclusion, calcium limits the optimal dilatation. Circumferential or bilateral distribution increased the complexity of the lesion. Circumferential distribution reduced the drug uptake. In case of complex lesion, proper vessel prep is mandatory. And what we are looking forward in the near future,
is a consensus that can be reached to define calcium grading. Thank you for your attention.
- Few aspects of vascular surgery are more controversial than the management of neurogenic TOS as you heard earlier from Dr. Illig. I will propose that recurrent neurogenic TOS and persistent neurogenic TOS are even more of a challenge to deal with. Persistent neurogenic TOS
occurs in 10 to 15% of patients, and it's really the individual who fails to show any improvement following decompression. Recurrent, 15 to 30% of individuals who have some degree of partial or complete relief after the initial decompression.
This may be insidious or acute, and most often occurs somewhere within a two-year time frame. It could be a missed original diagnosis. Or it may be a secondary insult, a new stretch injury to the plexus,
incomplete rib resection, ectopic bands, scar tissue formation around the plexus, or pec minor syndrome. Pec minor syndrome is a frequent cause of recurrent and/or persistent neurogenic symptoms.
Its co-existence is over 50% of patients with neurogenic TOS. Sanders recognized in 2003 that pec minor causes the majority of recurrent neurogenic TOS symptoms. What is it?
Well the pec minor originates in the second, third, fourth, and fifth ribs, inserting on the coracoid process, which is part of the scapula. Muscle hypertrophy, spasm, and fibrosis will constrict those structures underneath,
which would be the axial artery vein and posterior to that will be your plexus. This was first described in '45 by Wright. Lord and Stone did five decompressions for what they defined as "hyperabduction syndrome." It was lost at some point,
rediscovered by Thomas then Doctor Sanders in 2004, who studied it prolifically, defined it as a sub-set of neurogenic TOS. There's a plethora of literature in this present day and age supporting pec minor syndrome.
Etiology: majority of people have trauma, most often in motor vehicle accident with a whiplash type of injury. Repetitive shoulder strain and spontaneous events can occur, inducing hyper-induction of the shoulder. Clinical symptoms are similar
between neurogenic and pec minor: weakness, pain in the neck, clavicular, anterior chest wall, trapezius region and then paresthesias, most often in the ulnar distribution. Isolated pec minor does happen. Typically these individuals
have fewer head and neck symptoms. And you'll notice the intensity of symptoms are significantly less. On your examination it's your standard TOS examination. Unfortunately provocative maneuvers are not as rewarding. You'll find that with isolated pec minor,
these individuals have fewer head and neck symptoms, typically with rotation, tilt, scalene compression. There's nothing really to see. But they do have point tenderness over the infraclavicular region, directly on top of the pec minor.
And you'll notice that with contraction of the pec major, the symptoms will be minimized. Sanders noted the three most common findings with pec minor syndrome are: tenderness to palpation in the subcoracoid space, ULTT and EAST.
You'll notice that in some of these patients who do have persistent or recurrent symptoms, quite likely, pec minor tenderness was missed in the original diagnosis. A thorough history and physical certainly is beneficial. Unfortunately there's no test or exam
that is pathognomonic for this. Appropriate imaging should be completed to rule out other pathology. And then a selective pec minor muscle block not a plexus block, but a minor block, a muscle minor block,
should be considered. EMG testing has mixed results. When you look at your muscle block, typically done with a baseline examination, you'll then inject lidocaine 4 cc with ultrasound guidance 45 degree angle to avoid dropping in the lung.
Inject in a two to three centimeter area. And what you're looking for is resolution of your tenderness, improvement of your symptoms, at rest and with provocative maneuvers. For those ones who have an unsuccessful block
you may want to consider repeating it, or consider performing a scalene block. For those individuals that do have pec minor syndrome, conservative therapy, which is range-of-motion and stretching, tends to work well, 50% resolution in eight-week window.
For those individuals who fail pec minor tenotomy, low-risk out-patient procedure, relatively quick recovery time. A variety of approaches have been defined in the literature. Here's one approach with a patient
previously undergoing neurogenic decompression with a superclavicular approach, this is the anterior axillary approach, with a two to three centimeter vertical incision in the anterior axillary line. The subcutaneous divide at the pec fascia
is open and the muscle is elevated with a Deaver retractor. You'll trace this up to the coracoid process, and with that being the case, you'll transect two to three centimeters of the pectoralis minor muscle,
and then release any fascial bands or accessory muscle around the neurovascular bundle. These patients have done well. With isolated tenotomy you'll see that there's an improvement anywhere from 90 to 100%. However, you need to take into consideration
a good number of these people have combined neurogenic TOS and pec minor syndrome. And with that being the case, the success may be a little bit less. So in summary, pec minor syndrome is a frequent cause
of recurrent or persistent neurogenic TOS. Isolated pec minor tends to have fewer head and neck symptoms. Diagnosis is aided with a block. And tenotomy appears to be safe and effective. Thank you.
- I'd like to thank Dr. Veith for this kind invitation and the committee as well. So these are my disclosures, there's none. So for a quick background regarding closure devices. Vascular closure devices have been around
for almost 20 years, various types. Manual compression in most studies have always been shown to be superior to vascular closure devices mainly because there's been no ideal device that's been innovated to be able
to handle all sorts of anatomies, which include calcified vessels, soft plaque, etc. So in this particular talk we wanted to look at to two particular devices. One is the Vascade vascular closure device
made by Cardiva and the other is the CELT arterial closure device made by Vasorum in Ireland. Both these devices are somewhat similar in that they both use a disc. The Vascade has a nitinol disc
as you can see here that's used out here to adhere to the interior common femoral artery wall. And then once tension is applied, a series of steps is involved to deploy the collagen plug
directly on to the artery which then allows it to expand over a period of time. The CELT is similar in that it also uses a stainless steel disc as you can see here. Requires tension up against the interior wall of the common femoral artery.
Nice and tight and then you screw on the top end of the device on to the interior wall of the artery creating a nice little cylinder that compresses both walls of artery. As far as comparability is concerned between the two devices you can see
here that they're both extravascular, one's nitinol, one's stainless steel. One uses a collagen material, the other uses an external clip in a spindle-type fashion. Both require about, anywhere between three to seven minutes of pressure
to essentially stop the tract ooze. But the key differences between the two devices, is the amount of time it takes for patients to ambulate. So the ambulation time is two hours roughly for Vascade, whereas for a CELT device
it's anywhere from being immediate off the table at the cath lab room to about 20 minutes. The data for Vascade was essentially showing the RESPECT trial which I'll summarize here, With 420 patients that was a randomized trial
to other manual compression or the device itself. The mean points of this is that the hemostasis time was about three minutes versus 21 minutes for manual compression. And time to ambulation was about 3.2 hours versus 5.7 hours.
No major complications were encountered. There were 1.1% of minor complications in the Vascade versus 7% in the manual compression arm. This was actually the first trial that showed that a actual closure devices
had better results than manual compression. The main limitations in the trial didn't involved complex femoral anatomy and renal insufficiency patients which were excluded. The CELT ACD trial involved 207 patients that were randomized to CELT or to manual
compression at five centers. Time to hemostasis was anywhere between zero minutes on average versus eight minutes in the manual compression arm. There was one complication assessed at 30 days and that was a distal embolization that occurred
early on after the deployment with a successfully retrieved percutaneously with a snare. So complication rate in this particular trial was 0.7% versus 0% for manual compression. So what are some pros and cons with the Vascade device?
Well you can see the list of pros there. The thing to keep in mind is that it is extravascular, it is absorbable, it's safe, low pain tolerance with this and the restick is definitely possible. As far as the cons are involved.
The conventional bedrest time is anywhere between two to three hours. It is a passive closure device and it can create some scarring when surgical exploration is necessary on surgical dissections.
The key thing also is you can not visualize the plug after deployment. The pros and cons of the CELT ACD device. You can see is the key is the instant definitive closure that's achieved with this particular device, especially in
calcified arteries as well. Very easy to visualize under fluoroscopy and ultrasound. It can be used in both antegrade and retrograde approaches. The key cons are that it's a permanent implant.
So it's like a star closed devised, little piece of stainless steel that sits behind. There's a small learning curve with the device. And of course there's a little bit of discomfort associated with the cinching under the (mumbles) tissue.
So we looked at our own experience with both devices at the Christie Clinic. We looked at Vascade with approximately 300 consecutive patients and we assessed their time to hemostasis, their time to ambulation,
and their time to discharge, as well as the device success and minor and major complications. And the key things to go over here is that the time to hemostasis was about 4.7 minutes for Vascade, at 2.1 hours for ambulation, and roughly an average
of 2.4 hours for discharge. The device success was 99.3% with a minor complication rate of .02% which we have four hematomas and two device failures requiring manual compression. The CELT ACD device we also similarly did
a non-randomized perspective single center trial assessing the same factors and assessing the patients at seven days. We had 400 consecutive patients enrolled. And you can see we did 232 retrograde. We did a little bit something different
with this one, we did we 168 antegrade but we also did direct punctures to the SFA both at the proximal and the mid-segments of the SFA. And the time to hemostasis in this particular situation was 3.8 minutes,
ambulation was 18.3 minutes, and discharge was at 38.4 minutes. We did have two minor complications. One of which was a mal-deployment of the device requiring manual compression. And the second one was a major complication
which was an embolization of the device immediately after deployment which was done successfully snared through an eighth front sheath. So in conclusion both devices are safe and effective and used for both
antegrade and retrograde access. They're definitely comparable when it comes, from the standpoint of both devices (mumbles) manual compression and they're definitely really cost effective in that they definitely do increase the
throughput in the cath lab allowing us to be able to move patients through our cath lab in a relatively quick fashion. Thank you for your attention.
- Thank you much, Mr. Chairman, and I think that you have seen a lot of stuff that's not correct. That's my disclosure, doesn't affect any part of my talk today. Use of Patches in Large Trials. In NASCET and ECST,
patching was left to operator preference. In the NASCET, 83% of patients had primary closure, 9% had vein patch closure and 8% had synthetic patch closure. We've been trained to do the primary closure for all our patients,
and we were happy with that until the new relation came up by Professor Aborahma, and he told us that we have to start putting patches. So, we'll put a Dacron patch or we'll put a Vascu-Guard patch or we start doing a lot of eversion endarterectomy.
The only trick in all of that is the hemostasis that you have to put a lot of time in it because there's no different between the three of them. Then the systemic review of randomized control trial being published about the different part of patch and what we discovered,
that selective patching in narrow arteries hasn't been studied in any randomized control trials. There is no clear indication for selective patching. Despite limitation of data, results of the review support a recommendation in favor of routine patching. We couldn't find anything, but we just said to go, so...
Surgeon always understand the evidence differently, and it's up to the surgeon to decide whether to patch or not. A Cochrane review level one evidence, quality of trial were generally poor, and believe it or not,
this is how the guidelines have been built on in 2011 for the SVS and 2017 for the European Society. Carotid vein patch do rupture with potentially fatal consequences. Synthetic material are vulnerable to infection. And later on, variation of eversion
of carotid endarterectomy in the regional variation of the vascular quality initiative showed that there's 1% eversion (mumbles) up to 23% in primary closure, and the use of patch varied between 87 to 99 depend on the surgeon preference.
Bovine pericardium. Bovine pericardium demonstrates statistically significant decrease in intraoperative suture line bleeding compared with Dacron. I have no problem with that. Handling characteristics were judged by the surgeon
to be superior and we believe it's an alternative to Dacron in all cases of carotid endarterectomy as the previous presenter have shown. However, in 2007, the publication was that Never to bovine carotid patch in symptomatic patients or the young because of the catastrophic complications.
So the group in Yale under Alan Dardik decided to study this by getting the patch put in antibiotic to prevent this reaction, and the whole idea of macrophage and arterial stem cell infiltrates bovine patch, they hypothesized that antibiotic pre-treatment
of the patch before implantation would decrease infiltrating cells and prevent neointimal formation. However, they found that low level of antibiotics adsorbed and have off-target effect and didn't make any difference. And then we looked again and again.
Long-term clinical results reported several alarming issues regarding the bovine patch, mainly accelerated restenosis, patch rupture, cartilaginous metaplasia, pseudoaneurysm infection and acute thrombosis. Moreover, later on, the 10 years follow-up
have shown that post-operative complication were 6% in bovine pericardium with 2% aneurysmal dilatation. And in 2018, something very interesting, if you got a bovine patch in your neck, you're more likely to die rather than having any other patch
at 38 versus 45%. Then they compare the bovine patch to other type of patches, and what they find, that when you put the bovine patch in your neck, you have 6% re-exploration if using the Vascu-Guard. You have shown that,
but you didn't show that the bovine patch, the publication depended on only 149 patients for the whole meta-analysis. And additional randomized trials with adequate follow-up periods are needed to compare its effect.
And let's look at the prospective randomized control trial of the Hemashield versus the PTFE. There was higher restenosis in the Hemashield Finesse patch and, later on prospective (mumbles) of ACUSEAL was Professor Aborahma. Mean hemostasis time was higher for ACUSEAL
but Vascu-Guard bovine patch had more re-exploration for neck, as previously shown. And then, the long-term effect of prosthetic material disintegration with failure in the absence of infection, and moreover, seromas and tissue reaction
related to Dacron with no evidence of infection. So, start looking at our own experience and what we found, that if we do a primary closure, the stenosis rate is 4%. If we used a bovine patch, the stenosis rate is 43% and 1/3 of that goes for carotid angioplasty and stenting. And if you'd like to know more, this is our publication.
Never reach out your hand unless you are willing to extend an arm. Never to do that in patient coming through your practice ever. This is a patient that came to us with a meta-cartilaginous problem,
and we have to excise it completely. He had a bovine pericardial patch, and as you can see in here, that huge amount of reaction, and when you open it, after putting a hemoband into the common carotid to the ICA in order to control that, the dissection is so difficult and sometimes impossible.
And we replaced that later on with a reverse saphenous vein in order to get the blood flow going back. Mr. Chairman, ladies and gentleman, there is no evidence of superiority of any patch type. Late catch up phenomena of patch disintegration is a call for a concern.
Bovine patches had shown accelerated restenosis rate in diabetic symptomatic young women. Vascular surgeon must get better at eversion endarterectomy. Primary closure is an alternative option in the five millimeter ICA or larger and only if we use 7/0 proline.
I advise you that this is the commonest procedure that we do. However, there's no evidence for superiority for any closure method for the most performed that we ever have done. Thank you so much for the opportunity to present today.
- This is a little bit more detailed explanation of the pathophysiology behind Type IV AVM's. Medical disclosures are none. And this is the Yakes classification and this is Type IV lesion we are going to talk about now. So, this angioarchitecture has not been described before, and was first described in the Yakes classification.
What is so unique? It has multiple arteries, arterioles, but these arterioles form innumerable fistulas that are of a microsize, and they infiltrate the affected tissue. So, this is, this can affect every kind of tissue,
skin involvement and muscle involvement, and other than brain AVM, bleeding occurs if mucosa involvement is present or if an ulcer is present. So, we have to think about the definition of an AVM, which is an artery to vein connection
without an intervening capillary bed. But, what applies in Type IV? As you can see here, very nice example of this infiltrating type is that the tissue where the AVM is located is also viable, so the assumption is that
normal capillary beds are interspersed into these innumerable AVMs existing next to the malformed AVM fistulas, and this is a new definition of AVM. So, how to access this lesion? Of course, transarterial is possible
with a catheter or micro catheter. If anatomy doesn't allow transarterial approach, direct puncture is an option. Also, as you can see, in the direct puncture in the lower video, you can see the venus drainage of these fistulas,
and direct puncture of the vein compressed to reflux ethanol into the fistulas is also an approach. But, what is the challenge here? If you want to treat this lesion, you have to keep in mind
that you don't want to occlude the capillaries that are supplying the tissue. So, to find the right treatment approach, the physiologic concept is often important to understand that the arteriovenous fistulas drain into multiple veins and arterialize these veins
so we have a high pressure on this venus outflow site. The normal capillaries have a normal outflow too but this is of lower pressure, and this comes to competition between the arterialized veins and the normal venus outflow, which is, which is inferior to the normal capillary outflow.
So, what follows is a restriction of normal tissue flow with back-up to the capillaries, and backing up into the arterial inflow. So, we have the situation that the arterial venus fistulas have a lower pressure, lower resistance, and an increased arterial flow
compared to the normal capillaries, and this has to be taken into advantage for treatment. How can this be achieved? Thicken the fluid and dilute the ethanol by creating a mixture of 50/50 contrast and ethanol. So, this mixture will follow the preferential flow
into the arteriovenous fistulas in transarterial injections bearing the normal capillaries. So, if it's possible to puncture into the fistulas, pure ethanol can be used, but especially in transarterial access where normal nutrient vessels can be filled,
50:50 mixture contrast is the key to treat a Type IV AVM, Type IV Yates AVM, and here, you can see, using this approach, how this AVM can partly be treated in many several treatment sessions. And here you can see the clinical result. So, this huge ulcer, after seven treatments, healed
because of the less venus hypertension in the lesion. So the additional benefit of 50/50% ethanol contrast mixture is that your injection is visible on flouroscopy so you can see if which vessels you are including. You can react and adjust the pressure you're injecting. So, it also has to be considered
that the more you give diluted, the more total ethanol can be needed, but it's not efficient in larger vessels. This is also the advantage that you just treat the microfistulas. It's of importance that you use non-ionic contrast
as ionic contrast precipitates in the mixture. So here, you can see again, see the Type IV AVM of the arm and hand, which I already showed in my first talk, and here, you see the cured result after multiple sessions showing good arterial drum without fistulas remaining.
So, the conclusion is that Yakes Type IV is a new entity. It's crucial to understand the hemodynamics and the concept of 50/50 contrast ethanol mixture to treat this lesion with also a curative approach. Thank you very much.
- Thank you, thank you for the opportunity to talk. And I'm going to go quickly through some of the background slides 'cause we've heard some of this. I have no disclosures. So we've heard a little bit about popliteal entrapment already.
The population it affects. But where I'm going to point out that I think IVUS and some of these newer techniques may be more useful are in these patients because they, if they get repetitive compression they can get occlusion, embolism, and aneurysm.
So I think in these functional patients that we just heard about and in some of these patients who have maybe more subtle findings than a standard type one or type two, that's where I think these techniques are particularly helpful.
Additionally, we have seen a huge rise in women, female athletes over the past decade like you saw on the last slide. They seem to be the more predominant type. And functional, we, Doctor Ali just reviewed all of this. But functional seems to be a more common type.
And that's where, at least at Michigan, we find IVUS to be most useful. For that, and then also for type three, where the muscle, accessory muscle slip may not be as visible on conventional imaging. So, we just heard again about functional entrapment,
I'm also going to talk about at Michigan how we distinguish that between recurrent compartment syndrome, which is another common diagnoses that we see a lot of people coming in with. But it's important to mention too
that all these diagnostic tests are positive in a certain percentage of normal patients. So you really have to be looking at the specific patient population that has these symptoms before you're kind of pursuing this diagnostic algorithm. So our typical work-up and diagnosis,
again, is not always straightforward. We usually start with exercise ABIs. If that's abnormal we have an MRA protocol. And provocative angio that we will pursue. If it's normal, we'll typically do a duplex as has been shown up here previously
to help us distinguish between chronic compartment syndrome and functional entrapment. But it's important also to think of some of the other causes like cystic adventitial disease, endofibrosis, and some other things that can present with similar symptoms.
This is just showing a provocative MRA, which is sort of the next thing in our algorithm. We have patients do active plantar flexion, although, as has been reported in lots of literature, there's a really high false negative rate here because it's very dependent on the protocol.
Patients have to hold this plantar flexion for a long period of time. And so it can be very easy to miss these type three, type four, and functional on the MRA. And we see that quite a bit at Michigan. So we often then proceed to provocative angiogram,
which is shown here in one of our swimmers. He's in neutral position here, and then in this second angiogram you can see he's in active plantar flexion. We often have to use vasodilators in these patients to sort of simulate the amount of exercise
that they're used to getting. But again, these, we only go to this step if we're really convinced that the symptoms are specific for this diagnoses. Now where I think IVUS is particularly useful is these long segments, like you can see over here,
where you can't identify the exact compression point. That's where we're using it. So, again, kind of in these type three, four, and six. But we found it to be a very good adjunctive tool. We're using it all the time in these patients now. And it helps us both identify the exact location
of compression, what specifically is compressing, and it allows us to do a more precise surgical approach and completely identify that area and resect it. And we're also using it postoperatively to confirm that we have indeed relieved all of the compression.
So here's, you saw a video of this already, but here's a patient essentially in neutral position, you can see the artery. When they go into plantar flexion you can see how this is being compressed here. And we will run this down the whole way
and find the maximal areas of compression. And as you can see over here, we'll kind of mark them based on bony landmarks with angiography pictures so that we can identify these exact areas. And then we'll pull that up when we're doing our operative treatment.
So we will also then, after we have done whatever operative treatment we're doing, we will then wake them up, have them do a provocative angio again with us and an IVUS just to confirm before we leave the operating room that we have indeed relieved all of the compression.
And this, we've found, has really significantly minimized the amount of patients that don't get relief postoperatively. So this is a very busy slide, but it's basically just our algorithm at University of Michigan for these patients.
They all come in, they get exercise ABIs. Depending on if they're normal or abnormal they sort of go toward the MRA protocol. As you can see, unless they have a clear type one or type two entrapment, they're all getting this provocative angio and IVUS.
In patients that are a little less clear, they're all getting exercise compartment pressures, meaning that they're running prior to getting compartment pressure measurements. If it's greater than 25 they're getting a fasciotomy. If their results are positive,
depending on whether we think it's functional or true popliteal entrapment, we'll either do a standard posterior release or a musculotendinous resection. But again, this technology, I think, is very useful. We need to be more vigilant in diagnosing these patients.
And I think newer technologies will also aid in this. Thank you.
- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years
of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).
It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,
it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases
that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it
was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.
And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted
inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted
selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.
In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients
stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.
This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,
and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,
and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.
- Thank you very much, it's an honor to be here. I want to thank Professor Veith for his help with all EVTM movement and everything we're doing in the committee. Thank you very much. I would speak shortly about the trials. We can look at REBOA and what happened in last years and this is a map that's actual around two years ago.
And two years ago there were very few places that did REBOA even few places in the US if I might say, that did these aortic balloon occlusion. These numbers are doubled now, many countries and many institutes are doing it. REBOA is increasing like aortic balloon occlusion
is increasing not only in trauma. There are mainly case serious observation but there is not a lot of data. The new sheaths came, they are much smaller seven french and six french, and it changed the way we use these methods.
And the indications and contra-indications they are not really clear, I have to say. There are new methods, like using partial REBOA or intermittent REBOA on off, it might be better but we don't really know yet. And we know that total REBOA ischemia burden
is more clear than ever. We know that it's invasive method to close the aorta for long time. I think my view is there are more complications of REBOA than reported, around three to five percent and REBOA as a resuscitation tool and part of
endovascular resuscitation and trauma management. If we look at what's published in general we can see there are a lot of case series reviews. Some animal studies, some guidelines, like the pelvic guidelines from the World Surgical Association. Now it's nailed inside,
it's in the guidelines and you can use it. And some registry data, and I will name a bit about it. Currently, I know about more than 300 centers that are using REBOA for trauma. We know that there were done around 34 cases military, pure military REBOA.
Around 18 cases pre-hospital civilian REBOA. And of course, there are a lot of non-trauma that's done and we don't know how many are done. We know it's doable and we know that when you use REBOA you increase the systolic blood pressure and this is very important.
We know that you can do it from the pre-hospital to the ICU, and it's been done in the city in the ICU in different places. About the mortality and thoracotomy, I don't know really if you can compare these things, but used in specific patients, probably better than thoracotomy,
this is controversial. Relative few complications as I mentioned, but I think there are more complication than reported. And as I mentioned, there is severe metabolic effect of prolonged REBOA, if you use a total REBOA for example. This is the ABO Trauma Registry, and this registry is
a multinational or international corporation. The idea is, that people report to this registry the data, trauma REBOA, and can use this data. So this does not belong to me, this belongs to this group reporting in, and you can use it and report from it. It's very interesting what data is coming in.
This is how it looks like, and you can put also photos, cases, not only the report itself. It's quite astonishing what you can see in this. If we look at the two years result that we reported on 28 patients, it was very high ISS, mostly blunt trauma
which is very exciting because these are blunt trauma patients mainly, getting the REBOA and we know what happen if you compare them to thoracotomy. If you do thoracotomy for blunt injuries we know the results are very bad. Interestingly enough, the access was done mainly blindly
and succeeding with one to three attempts. And people sometimes ask, how can you do on a CPR patient the access, but we manage to do it and it worked. And the survival from the ED was 82%, 30 day survival 43%. I just want to show this slide talking about with 138 patients, currently 212 patients.
Even if you divide into impending cardiac arrest, people that have no palpable pulse or going through CPR even some of them can be saved using the balloon and some of them will get blood pressure when using this method, even survival as seen here, down here.
I will speak briefly about the other studies. This is Japanese Registry, they have included some numbers of patient and analyzed it in its published perspective study that will start soon. This is the UK REBOA trial, which is a prospective randomized trial that has now currently
as I know, 24 patients has been included. This is a very special and very exciting trial we will see what it will lead to. I will not report a lot about the AAST study Joe DeBose that sits here is the manager of this and he can report a bit more, but what I would like to say
that probably there is a survival benefit for REBOA, especially as the claim it might be particularly good if performed prior to arrest. The problem with clinical trials, we know this is not homogenous data, and I'm not sure we will ever get evidence.
And the solution in my world would be maybe to have the methods in a virgin teritory and see if you get better results. Thank you very much for being here and have an opportunity to talk. Thank you.
- Thank you chairman, thank you again to Dr. Veith for this kind invitation. Ladies and gentlemen I have no disclosure. Actually I have a problem with my mouse, it doesn't really go. Yes I know it is the green button but it doesn't work, okay now it works.
I'm sorry, okay. So again, one year ago we published a paper to evaluate the impact of cerebral lesions and their volume on carotid revascularization outcome. In that paper, not only we looked at the presence of cerebral ischemic lesion but also
we measure the volume of that lesion. While there was no effect of the presence of the cerebral ischemic lesion in the outcome of those patients, if we look at the patient who suffered a post operative stroke, we saw that the amount of the volume of the
lesion was significantly greater compared with patient with no post operative event. And also by combining stroke and death in those populations, the volume was still greater than the other patient. ROC analysis, the cut off point was set
at 4,000 cubic millimeters in that population. BY examining patients with ischemic lesion volume greater than 4,000 cubic milimeters the incidence of post operative stroke was significantly higher compared with patient with a smaller lesion. A multivariate analysis, a volume greater than
4,000 cubic millimeter was an independent predictor of post operative stroke in that population. So the conclusion of this study was that the presence of a cerebral ischemic lesion has no overall effect on the revascularization outcomes. However, if the cerebral ischemic lesion volume
is greater than 4,000 cubic millimeter then the risk of stroke is significantly increased. We wanted to further expand these conclusion and we look at the benefit of a deferred carotid revascularization only in patient with a moderate disabling stroke.
We presented this data at the last ESVS meeting in Spain. So the study endpoint where perioperative 30-day stroke death after endoctorectomy just in patient with a large cerebral ischemic lesion and we investigated the best timing to reduce the post operative complication rate.
So we just extrapolated a small portion of our patient, 126 patient with moderate disabling stroke and a very large ischemic lesion. As you can see from the table here, the volume of the ischemic cerebral lesion in that population was pretty high.
Overall stroke and death in that population was 70.1% and time from symptoms to revascularization was a mean of 7 weeks. ROC analysis, the cut off point was set at four weeks in which you add the maximum differences in the result. So looking at patient operated within four weeks
and after four weeks from symptoms we didn't find any difference in the two groups. However, stroke and death was significantly greater in the patient operated within four weeks compared with patients operated later. And the multivariate analysis, timing to endorectomy
less than four weeks was an independent predictor of stroke after endoctorectomy. So, endoctorectomy after disabling stroke has a high risk of post operative major adverse event which was 7.1% in our series but can be as high as 26% in the literature.
The take home message is that the patient with large cerebral lesions greater than 4,000 cubic millimeters have a better outcome if operated four weeks after symptoms. Thank you for your attention.
- Thank you, I have no conflict of interest. Although less represented in studies, it has been clearly shown that women are less likely to benefit and more likely to suffer carotid procedural stroke or death compared to men. So let's look at procedural benefit for women in particular first, carotid endarterectomy first.
The only women with carotid stenosis who have been shown to receive a statistically significant overall benefit from carotid endarterectomy have been symptomatic women with 70 to 99% NASCET stenosis without near occlusion who had carotid endarterectomy performed within two
to three weeks of their last cerebral event. They also had to satisfy all the trial inclusion and exclusion criteria. So, symptomatic women in the randomized trials did not receive a benefit from endarterectomy compared to medical treatment on its own
if they had 70 to 99% NASCET stenosis, and endarterectomy was performed more than two to three weeks from the last cerebral event. Or if they had 50 to 69% NASCET stenosis no matter the timing of the endarterectomy. Now, symptomatic men in the
randomized trials had more benefit. Symptomatic men with 70 to 99% NASCET stenosis actually had an overall statistically significant benefit from endarterectomy up to at least three months after their last cerebral event. And I haven't seen it published exactly
when that benefit period finished. Also, men with 50 to 69% NASCET stenosis had overall benefit from endarterectomy, but only if the surgery was performed within two to three weeks of their last cerebral ischemic event. With respect to asymptomatic women,
there's been no clear benefit from endarterectomy in randomized trials. So they did not benefit in ACAS, and the closest to benefit ACST were aged less than 75 years of age. But this was only borderline statistically significant. Asymptomatic men also had more benefit in the randomized
trials of endarterectomy versus medical treatment. So, overall, they had a benefit if they had at least 60% NASCET stenosis, and they were aged less than 75 to 80. What about transfemoral, transaortic stenting? Women and men have not been shown to benefit from stenting
compared to medical intervention alone or endarterectomy. Now, I've head some rumors that women in ACT-1 trial had less harm from stenting compared to endarterectomy. But I haven't seen that result published yet. And when it is published they need to include the peri-procedural risk of stroke and death.
Of course, women and men are much less likely to benefit from any carotid procedure now due to advances in medical intervention. What about procedural harm, endarterectomy? Well, in the randomized trials of endarterectomy versus medical treatment and other studies women
are more likely to have peri-operative stroke and death compared to men. That's seen in randomized trials, but also in non-randomized trials. What about trans-femoral/aortic stenting? Randomized trials and other studies
have been underpowered to compare outcomes with stenting in symptomatic women versus men, but across both sexes stenting has significantly more harm associated with it. In a meta-analysis of randomized trials symptomatic women had one and a half times more peri-procedural stroke
and death with stenting compared to endarterectomy. Again, for asymptomatic patients the trials have been underpowered, but a trend to more harm with stenting. And, also, seen in CREST with combined symptomatic and asymptomatic women.
As Cosmas mentioned, more harm with stenting. TCAR, doesn't look like we're planning to do adequate comparisons with current medical treatment, so no current indication. In summary, overall, the only women shown to benefit from endarterectomy were symptomatic
with 70 to 99% stenosis with endarterectomy within two to three weeks of the last event. Overall, all women are more likely to be harmed by endarterectomy compared to men, and to be harmed by stenting compared to endarterectomy. Everyone is less likely to benefit
from these procedures now. So given all this information, why are we doing so many procedures in women? Thank you.
- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.
And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,
as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,
presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,
as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.
So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.
Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,
and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.
Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there
in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,
but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,
but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,
but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion
that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer
and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.
And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.
And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,
treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.
And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.
We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat
with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,
and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.
So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.
Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen
and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.
(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.
Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.
And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily
arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,
it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this
florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.
We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation
in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,
which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen
of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.
- [Narrator] Okay, very interesting hypothesis.
- Ladies and gentlemen, I would like to thank Professor Veith for his kind invitation. A minimally invasive carotid endarterectomy. I have nothing to disclose. Here you can see the same patient operating with the classic carotid endarterectomy with normal incision and on the other side,
you will see the patient, the same patient after the minimal incision carotid endarterectomy. So ladies and gentlemen, if one can safely perform carotid endarterectomy by minimal incision, let's do it routinely. The technique of minimal incision carotid endarterectomy.
The incision must be done over a carotid bifurcation. In slim patient, it is easy to determine the location just by the palpation. By routinely, I advise to mark bifurcation by using ultrasound. Reaching the artery by tissue separation
along the border of sternocleidomastoid muscle. Once the artery is visualized, apply the vessel loop on the external carotid artery. If it is needed, on the thyroid artery. Pulling the external carotid artery vessel loop up to the opposite side,
and releasing posterior part of bifurcation enables visualization and applying vessel loop on the common carotid artery, about 15 millimeter down the bifurcation. Pulling the external carotid artery vessel loop down into the opposite side reveals anterior and posterior
portion of internal carotid artery. What is the most important? The vessel loop on the internal carotid artery must be located above atherosclerotic plague. Temporary clamping of internal carotid artery for 30 seconds should show if the shunt is needed.
If there is no neurological signs, we continue pulling all vessel loops to elevate the artery to the level of the skin. Typically, longitudinal incision from common carotid artery to internal carotid artery is performed. The main important maneuver
that led to perform this operation correctly and safely, this is eversion-like movement. After arteriotomy, I squeeze the artery, internal carotid artery, usually on the level of the end of the atherosclerotic plague, usually using the forceps.
I make eversion-like movement. This led me easily and safely remove that atherosclerotic plague from the internal carotid artery. Always allow one two second backflow from internal carotid artery
to remove potential debris by the blood flow. The same, unclamping common carotid artery for a short period of time to remove potential debris from the proximal part. Should a shunt be indicated, it is easy and quick to insert.
As a first step, the shunt is inserted into internal carotid artery. It is necessary to slightly loosen internal carotid vessel loop. In the same way, I put the shunt into the common carotid artery if it is needed.
Continued suture usually close the arteriotomy. If the diameter of the internal carotid artery is smaller than two millimeter, artificial patch can be easily used. Redon drainage is always used. I make another small incision for the Redon drain
due to very, very small incision for endarterectomy. And continued suture usually closes the wound for good cosmetical effort. Here, you can see the operation step-by-step. What I will now emphasize this group of patient.
This is symptomatic patient with a very soft atherosclerotic plague. In this series, our experience. This is 165 patients allocated into two groups. 122 patients in the minimal incision carotid endarterectomy group,
and 43 patients in classic endarterectomy group. Patients randomly allocated. Here, you can see the results three months, up to three months results. I will like to emphasize there were no nerve injury. Hoarseness and shunt was used in 12%
in minimal incision carotid endarterectomy group. Here, you can see in the first and second column, the results up to September 2017. Third and fourth column, the results up to September 2018. Here you can see some examples. Here you will see some more examples.
Here you will see the scar that is after the operation. So nearly no limitation in neck movement, quick wound healing, short hospital stay, and perfect cosmetic effect. So to conclude, ladies and gentlemen, this is the low risk operation.
This is the operation of quick recovery. Precautions and contraindication, according to my experience seems to be same as for classic carotid endarterectomy. Of course, further study is required. Minimal incision, I also used during the
aortobifemoral and femoropopliteal operations. I hope to show it next year. Ladies and gentlemen, when I was a young surgeon, it was said that big surgeon, big incision. I'd rather suggest, good surgeon should try to make the smallest incision possible.
Data and presented technique will be published. Thank you very much for your attention.
- [Speaker] Thanks for the opportunity to present today. I'm going to talk about a specific complication of REBOA, a spinal cord injury. These are my disclosures. REBOA utilization for trauma and hemorrhagic shock has really increased greatly over the last decade, as you've heard.
Comparative data with resuscitative thoracotomy, although not easy to do, appears favorable. Case series and some meta-analyses have suggested that there is a clinical benefit, as Dr. Hur also stated, an ideal time for balloon occlusion though is not clear. Less is better, but what is the optimal time frame?
Many reports don't even include occlusion times, although that's getting better as data matures. Animal studies have suggested a significant morbidity mortality with end-points increased at 60-and 90-minute occlusion times. In human studies, when balloon occlusion times have
been compared, they're shorter in survivors than in patients who died. We know that surgical cross-clamp of the aorta has long been associated with spinal cord ischemia risk. In a large metanalysis of blunt traumatic aortic injury repaired with open surgical techniques
and no distal perfusion adjunct, there was 19% risk of paralysis in humans. In porcine studies and sheep studies, prolonged REBOA has been associated with spinal cord injury as well. But rarely reported in humans and whether
that's a reporting bias because of mortality it's not clear. The advantage of studying defined times for REBOA in a non-human primate model were why we undertook this study. The bipedal model really analogous to human
in most respects with the spinal cord anatomy being very similar and the coagulation cascade being the same. Here was our design. We had three groups, one was an initial survival study and model development phase.
Group two and group three were comparing 60- and 30-minute REBOA in the olive baboon with a ten-day survival and particular intent to look at the end point of spinal cord ischemia. This is an example of a pre and during balloon inflation.
You can see the brachial and femoral pressures on the screen on the left show very low blood pressures and soon after balloon inflation you get restoration of normal tension in the brachial arterial line. For our study, we saw these end points that in the
60-minute balloon inflation that animals become quite hypertensive rather than normal tensive. First 30 minutes we had no animals that were in hypertension phase. There was a significantly higher metabolic price to pay with prolonged balloon inflation at
60 minutes with the average base deficit delta of about 18 per millimoles liter. We also saw elevated troponins in the 60-minute occlusion group compared to the 30-minute group. Some had values even over five nanograms per milliliter as well as systolic evidence of myocardial injury.
All animals in the 60-minute REBOA group had histological evidence of renal injury, although none of them had creatine elevated of greater than 1.5 base line at the 10-day end point. Thirteen percent of the animals had histologic and laboratory evidence of myocardial injury.
And 50% of the animals in the 60-minute group had paralysis and histologic evidence of spinal cord injury. These are some representative images that show cavitation in the ventral horns of the spinal cord with severe inflammatory infiltrate. These are some more unexpected findings that show
ischemic injury to the dorsal horns as well as the dorsal columns in some of the animals. Wide spread spinal cord injury are not confined to the anterior spinal artery distribution. In summary, 60-minutes of REBOA balloon inflation after profound hemorrhagic shock in a
nonhuman primate model has high survival, but high morbidity. Fifty percent spinal cord ischemia, metabolic derangement, myocardial strain and injury and renal histologic injury. But in this study, all of these major morbidities
were essentially mitigated by limiting balloon inflation time to 30 minutes. With this in mind, we recommend that zone 1 REBOA be limited to 30 minutes in humans and after 30 minutes, every effort should be made to intermittently deflate the balloon as tolerated to allow
some reperfusion to occur. Thank you so much.
- Talk to you a little bit about again a major paradigm shift in AVMs which is the retrograde vein approach. I mean I think the biggest benefit and the biggest change that we've seen has been in the Yakes classification the acknowledgment
and understanding that the safety, efficacy and cure rate for AVMs is essentially 100% in certain types of lesions where the transvenous approach is not only safer, but easier and far more effective. So, it's the Yakes classification
and we're talking about a variety of lesions including Yakes one, coils and plugs. Two A the classic nidus. Three B single outflow vein. And we're talking now about these type of lesions. Three A aneurysmal vein single outflow.
Three B multiple outflows and diffuse. This is what I personally refer to as venous predominant lesions. And it's these lesions which I think have yielded the most gratifying and most dramatic results. Close to 100% cure if done properly
and that's the Yakes classification and that's really what it's given us to a great degree. So, Yakes one has been talked about, not a problem put a plus in it it's just an artery to vein.
We all know how to do that. That's pulmonary AVM or other things. Yakes two B however, is a nidus is still present but there is a single outflow aneurysmal vein. And there are two endovascular approaches. Direct puncture, transarterial,
but transvenous retrograde or direct puncture of the vein aneurism with the coil, right. You got to get to the vein, and the way to get to the vein is either by directly puncturing which is increasingly used, but occasionally transvenous. So, here's an example I showed a similar one before,
as I said I think some of these are post phlebitic but they represent the archetype of this type of lesion a two B where coil embolization results in cure, durable usually one step sometimes a little more. In the old days we used to do multiple
arterial injections, we now know that that's not necessary. This is this case I showed earlier. I think the thing I want to show here is the nature of the arteriovenous connection. Notice the nidus there just on this side of the
vein wall with a single venous outflow, and this can of course be cured by puncture, there's the needle coming in. And interestingly these needles can be placed in any way. Wayne and I have talked about this.
I've gone through the bladder under ultrasound guidance, I've gone from behind and whatever access you can get that's safe, as long as you can get a needle into it an 18 gauge needle, blow coils in you get a little tired, and you're there a long time putting in
coils and guide wires and so on. But the cures are miraculous, nothing short of miraculous. And many of these patients are patients who have been treated inappropriately in the past and have had very poor outcomes,
and they can be cured. And that a three year follow-up. The transcatheter retrograde vein is occasionally available. Here's an example of an acquired but still an AVM an acquired AVM
of the uterus where you see the venous filling on the left, lots of arteries. This cannot be treated with the arterial approach folks. So, this one happened to be available
and I was having fun with it as well, which is through the contralateral vein in and I was able to catheterize that coil embolization, cured so. Three A is a slightly different variant but it's important it is different.
Multiple in-flow arteries into an aneurysmal vein wall. And the important identification Wayne has given us is that the vein wall itself is the nidus and there's a single out-flow vein. So, once again, attacking the vein wall by destroying the vein, packing
and thrombosing that nidus. I think it's a combination of compression and thrombosis can often be curative. A few examples of that this was shown earlier, this is from Dr. Yake's experience but it's a beautiful example
and we try to give you the best examples of a singular type of lesion so you understand the anatomy. That's the sequential and now you see single out-flow vein. How do you treat this?
Coil embolization, direct puncture and ultimately a cure. And that's the arteriogram. Cured. And I think it's a several year follow-up two or three year follow-up on this one.
So a simple lesion, but illustrative of what we're trying to do here. A foot AVM with a single out-flow vein, this is cured by a combination of direct puncture right at the vein. And you know I would say that the beauty of
venous approach is actually something which it isn't widely acknowledged, which is the safety element. Let's say you're wrong, let's say you're treating an AVM and you think okay I'm going to attack
from the vein side, well, if you're not successful from the vein side, you've lost nothing. The risk in all of these folks is, if you're in the artery and you don't understand that the artery is feeding significant tissue,
these are where all the catastrophic, disastrous complications you've heard so much about have occurred. It's because the individuals do not understand that they're in a nutrient artery. So, when in doubt direct puncture
and stay on the venous side. You can't hurt yourself with ethanol and that's why ethanol is as safe as it is when it's used properly. So, three B finally is multiple in-flow arteries/arterioles shunting into an aneurysmal vein
this is multiple out-flow veins. So direct puncture, coils into multiple veins multiple sessions. So, here's an example of that. This is with alcohol this is a gentleman I saw with a bad ulcer,
and this looks impossible correct? But look at the left hand arteriogram, you can see the filling of veins. Look at the right hand in a slight oblique. The answer here is to puncture that vein. Where do we have our coil.
The answer is to puncture here, and this is thin tissue, but we're injecting there. See we're right at the vein, right here and this is a combination arteriogram. Artery first, injection into the vein.
Now we're at the (mumbles), alcohol is repeatedly placed into this, and you can see that we're actually filling the nidus here. See here. There's sclerosis beginning destruction of the vein
with allowing the alcohol to go into the nidus and we see progressive healing and ultimately resolution of the ulcer. So, a very complex lesion which seemingly looks impossible is cured by alcohol in an out-flow vein.
So the Yakes classification of AVMs is the only one in which architecture inform treatment and produces consistent cures. And venous predominant lesions, as I've shown you here, are now curable in a high percentage of cases
when the underlying anatomy is understood and the proper techniques are chosen. Thanks very much.
- Thank you Dr. Asher. What an honor it is to be up here with Dr. Veith and Dr. Asher towards the end. You guys are leading by example being at the end of the meetings. So, thank you for allowing me to be up and talking about something
that not a lot of vascular surgeons have experience with, including me. I have no disclosures. On your left, I have listed some of the types of diseases that we most commonly see in the vertebral artery, and there are quite a lot.
And on the right, the standard types of treatment that we pursue in vascular surgery or as a vascular specialist. And often, in the vertebral artery, if we are going to pursue treatment, it's the endovascular route.
But I'll talk a little bit about open surgery. The clinical presentation is often vague. And the things I wanted to point out here in this long list are things like alternating paresthesias, dysphagia, or perioral numbness may be something in the history to look for
that you may not be thinking about when you're thinking about vertebral basilar disease. The anatomy looks straightforward in this picture, with the four segments, as you can see. It gets a little more complicated with just the arterial system,
but then when you start looking at all these structures, that you have to get out of of the way to get to the vertebral artery, it actually can be a difficult operation, particularly even in the V1 segment. The V1 typically is atherosclerotic disease.
V2 is often compression, via osteophyte or musculo-tendon structures. And V3 and V4, at the top, are typically from a dissection injury from sort of stretch or trauma injury. The pathophysiology isn't that well understood.
You have varying anatomy. It's very difficult to access this artery. Symptoms can be difficult to read, and treatment outcomes are not as reliable. But I'm going to take you through a very quick path through history here in the description
of the V1 segment exposure by Dr. Rentschler from 1958. And I love these pictures. Here is a transverse incision over the sternocleidomastoid, just above the clavicular head on the right side. And once you get the sternoclavicular head divided, you can see the longus colli muscle there.
Anteromedial is the carotid. Of course, you surround that with a Penrose drain. And then once you do that, you can separate your longus colli, and deep to that, the vertebral artery just easily slips right up, so you can do your transposition.
It's not quite that easy. I've done one of these operations, and it was difficult finding t e. And, again, here is on the opposite side, you can see the transposition in this cartoon.
Dr. Berguer is the world's expert, and a lot of this open surgical work comes out of the University of Michigan. Here is a study looking at 369 consecutive extracranial vertebral artery reconstructions. You can see the demographics of clinical presentation.
And note that about 34% of patients are presenting with hemispheric symptoms, with 60% in the vertebral basilar distribution. 300 of these reconstructions were for atherosclerosis. And the outcomes were pretty good. Before 1991, there wasn't really a protocol in place
in assessing and doing these procedures. And you can see the stroke and death rates of 4.1 and 3.2% respectively. And then the outcomes after 1991 are considerably better with a five year patency rate of 80%. So, in summary, vertebral artery disease is,
I think if you review this, is somewhat under diagnosed. Revascularization is a viable option. Most often, it's endovascular. But if you have endo-hostility, then an open, particularly for the V1 segment, may be a better option.
And this requires people with good operative experience. Thank you very much.
- Thank you Mr. Chairman, thank you Dr. Veith for the kind invitation. I have no disclosures relevant to this particular lecture. But I think we ought to talk about what critical limb ischemia is. Obviously it's what we call Rutherford four through six. It's most commonly associated with multi-level disease.
About 1/3 or so of the cases are infrapopliteal only, mostly in diabetic patients. There's very poor overall life expectancies. We look at this group of patients in multiple studies, it ranges somewhere between three and four years of average life expectancy,
and there are substantial differences in outcomes within critical limb ischemia, with far worse outcomes in those with poor overall health, advanced stage presentation, or poor runoff at the level of the foot. Now, what is the rationale for endovascular therapy
in critical limb ischemia? Well first, patients are often old and infirmed, and many aren't really considered candidates for open surgery because of poor overall health. Surgery requires inflow, usually attainable. Outflow, not always so easy.
A conduit, which typically should be vein, if we want durable results, and an incision. Active infection is problematic, as there may be graft infection or sepsis. Extensive surgical scarring may compromise future rescue intervention,
and this is a progressive disease, that often requires additional treatment. Now, there have been multiple publications, and this is just a recent one, which came out in the Journal of the American Heart Association. It's a multidisciplinary,
retrospective analysis of Medicare data in people who had presented with critical limb ischemia. This is not perspective, it's not sited in many areas, but I ask you to look at this conclusion. It was there was lower major amputation rates following endovascular therapy.
Both surgery and endovascular did better than primary amputation, in terms of outcomes. But again, this is not a perfect study. Now, we have many publications which have shown very good limb salvage rates in patients using interventions.
Here we see this from Faglia, again showing very low major amputation rates. This from Sam Ahn, once again, very good limb salvage rates. But in truth, we have only one randomized, control trial, level one data, comparing intervention with surgery. And that was the BASIL Trial.
The BASIL Trial is an old trial, it's criticized, appropriately, because the only treatment used was sub-intimal angioplasty. And with sub-intimal angioplasty, often, the sub-intimal tract in crossing is far greater than the area of total occlusion,
resulting in much longer treatment zones. In addition, this trial did not allow some of the new and better treatments that are now available for having better patency to be performed. Nonetheless, in the BASIL Trial, despite very primitive treatment,
that being only sub-intimal angioplasty, we can see that one year out, and in fact out to two years, angioplasty and surgery were relatively equal in terms of limb salvage. At five years, there seemed to be a major advantage to surgery,
in terms of both quality of life, and in terms of less need for reintervention. So then we have to ask, what has changed since BASIL? Well now we have far better crossing. We have re-entry tools that stop us from having to go 10 centimeters
beyond the area of occlusion to get back in. Dedicated crossing tools, better wires, retrograde access, this is important, we have markedly improved patency, with drug coated balloons, drug-eluting stents, wire interwoven nitinol stents, and stent grafts, which have shown in the SFA all of these things,
better SFA patency, and if indeed, we can maintain SFA patency in multi-level disease, often, if there's recurrence, the patients do well. We also have improved Tibial patency in the proximal tibial vessels. However, we do not yet have a great endovascular solution
for long distal tibial vessel occlusions, and that's just the truth. I have to go back here, one, but we have better medical therapy too. As we look at PCSK9 inhibitors, in the GLAGOV Trial, we see in other parts of the body,
a 30% reduction in atherosclerotic volume out at 70 weeks, indeed will this change what we're doing. This has launched this decade of endovascular interventions. So what about this taking away surgical options? BASIL, I think, doesn't apply because the sections went far beyond where they should.
That's bad technique. Stenting across the common femoral or patent popliteal, in my opinion, bad technique. Distal embolization, we've not done enough preparation. I will also caution that sometimes, surgery has bad outcomes as well.
So, the rationale is we really don't want to perform anything that hurts a patient. Entire procedures performed via a sheath, remote from the site, there's less pain, shorter recovery, no extensive scar, and the argument that intervention
takes away surgical options, I think is no longer so valid. Bad intervention or bad surgery, take away options. Where is distal bypass indicated? In large non-healing ulcers in patients with good life expectancy, good quality vein, good outflow, and excellent surgical expertise.
Densely calcified long segment infrapopliteal disease, or disease from the common femoral all the way to the ankle. I think these clearly are going to do better with surgery, certainly in today's world. But even these areas may change. If more effective tools solve the patency problems,
with long segment infrapopliteal disease, and there are trials now aiming at this, such as SAVAL, DCB trials, and Lithoplasty. I thank you for your attention.
- 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 very much. I appreciate the opportunity to present and I'd like to thank the program committee and Doctor Veith. I have no disclosures. So Traumatic Limb Ischemia is uncommon. Demtriades looked at this with the national trauma database and found that it only occurred in about one point six
percent of patients. And the majority, or 51 percent, are penetrating injuries. These are often managed by the trauma surgeons at tertiary centers. But with the change in training paradigms, with general surgeons not doing as much vascular procedures
and open vascular surgery not being done as much by many of the trauma surgeons. Vascular surgeons are being called upon to do this, more and more often. The objective of our study is to describe a contemporary series of patients with acute limb ischemia
secondary to trauma that were managed by the vascular surgeon. In identified factors that were accossiated with limb salvage and functional outcomes. We did a retrospective review of our institution over a three year period and looked at several factors,
including the preoperative imaging the level of aclusion, limb salvage, and functional limb outcomes. We identified 68 patients in our study and the majority of these patients had moderate ISS scores and Rutherford Class two ischemia. 53 percent were from an outside hospital
and 62 percent had blunt injury, while 38 percent suffered penetrating injury. If you look at the mechanism again, the majority were motor vehicle accidents for the blunt and gunshot wounds and stab wounds for the penetrating injuries.
Median ages would be expected as fairly young with at 36 and 46 and the majority of these people are males. As is the cases with most trauma series. 58 percent were transferred from an upper, from another hospital in the upper extremity series and 51 percent in the lower extremity series.
With a median time of transfer about three hours. The median time to the operating room was about four and a half hours in this patient population. And most of these patients did receive some kind of preoperative imaging, either a CAT scan with 55 percent of the upper extremity
and 68 in the lower extremity. And the Rutherford classification of ischemia was, generally, two B and below. We looked at the location and the majority in the lower extremity were the Femoropopliteal region and in the upper extremity where the Axillary
and Brachial artery region. So, looking at the number of operations these patients underwent, and the upper extremity and lower extremity both of them underwent a median number of three operations and 84 percent of the patients upper extremity injuries went an open procedure
and 69 percent in the lower extremity. So, open procedures are the modality of choice for repair of these injuries. 58 percent of the lower extremities went on to have Fasciotomies, as well. In some of the details, the open repair
was a dominant treatment as stated. Shunts were only utilized in two of our patients, with Fasciotomies only occurring in 25 percent 58 percent of the lower extremity injuries. And we think about some of the details, we had eight patients who underwent Fasciotomies
during the first operation with dead muscle encountered in three of those patients. Three patients underwent a delayed Fasciotomy with dead muscle encountered in one of those patients. Limb salvagery overall is 94 percent in the upper extremity and 78 percent in the lower extremity.
And again, with the amputation patients, we had 12 patients that underwent an amputation, one primary amputation. The overall limb salvage was 94 percent for upper extremity and 78 percent for lower extremity. The predictors or amputation of functional limb,
in a functional limb where the number was a Rutherford Classification and the number of procedures these patients undergo. The length of stay was 11 days, 25 percent were discharged to a skilled nursing facility and follow up occurred in 59 percent of the patients, as the case
with many of the trauma type studies. When you think about functional deficits, the patients that had no functional deficits in the upper extremity were about 57 percent and the lower extremity 68 percent. But major deficits occurred in one third of the patients
with an upper extremity injury versus six percent. Whereas amputation occurs much more frequently in the lower extremity versus the upper extremity. So, Traumatic Acute Limb Ischemia is uncommon outside of trauma centers, vascular surgeons are extremely well equipped
to deal with this, majority of extremities can be salvaged, transfer times to a tertiary center may explain some of the correlation with limb salvage, and rehabilitation and follow up can be difficult in this patient population. Again, we only had 59 percent follow up, you know,
in the literature it's around 60 and 66 percent in this patient population. It can be managed with very high rates as limb salvage by vascular surgeons. So I think that we can do this and we do it quite well. Limb salvage doesn't equate to functional outcomes,
particularly in the upper extremity. And in the future, I think that we need to probably get better about the follow up and identify some patient centered functional status and quality of life questionnaries post salvage, to see truly what the outcome is and the functional status
is of these patients. Thank you very much. (applause)
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