- It's my pleasure on behalf of the Sentury Trial investigators to present the two year data on the BTG Novate Sentry filter. These are my disclosures. Well, as we have heard this afternoon, it's no surprise to anyone the topic of IVC filter placement is controversial.
We know that IVC filters can protect patients by preventing PE. We also know that retrievable filters that are not retrieved have been reported to have, be associated with some complications. And we talked about FDA advisory,
obviously that has resulted somewhat in a decrease in filter use in this country. Obviously complication rates we've also heard about increase with implant time and include tilting, migration, fracture, perforation and embolization. And retrieval success reduces with implant time.
What's not controversial, and we have heard also about this, is the frequency of PE in this country and the expense associated with it. Obviously, survival benefits have been shown in appropriate populations, that are selected based on known indications. And existing retrieval technology, unfortunately,
as we've heard from Dr. Askandari, has not met the needs of patients when up to 40 to 50 percent are not coming back for retrieval. That was sort of the impetus behind the design of the Sentry Bioconvertible IVC Filter, which is designed to protect patients at transient risk
from PE and reduce complications of existing technologies. It employs a stable frame with filter arms held together by a bioabsorbable filament and designed to provide PE protection during a transient risk period, reduce IVC filter complications, including tilting, migration, fracture, perforation and embolization.
And this just shows an example in vitro and with a CT scan of the filter in the so-called filtering configuration. The filter then automatically bioconverts after the PE risk period is past. That's guaranteed to be in the
filtering position for at least 60 days. It bioconverts by hydrolysis of the bioabsorbable element, which allows the filter arms to retract to the IVC wall, leaving a patent lumen and reducing the risk for IVC occlusion or thrombosis later on, and obviously, the cost of IFC filter retrieval.
Here you can see filters that are in the bioconverted configuration. This just shows the deployment. It's a simple pin and pull seven French delivery system. These stable arms allow this to be placed almost always without any tilting
and is quite easy and accurate to deploy. This is in an ovine modeled pre-clinical study shows in a bioconverted configuration all of the filter elements become endothelialized and in this angioscopic view, really can't even see any of the filter elements.
This is again sort of predicated on something that I believe we're not all that familiar with and that's when the timing of PE occurs. And you can see here, from the trauma literature, orthopedic literature, other literature, on 500,000 patients and in these groups you can see
that over 90 percent of PEs take place in less than 10 days after an initial event and 99 percent of PEs within 20 days. That led the FDA to write a position decision analysis paper, which recommend filter retrieval between
29 and 54 days after implantation. So, on s, 23 sites, 63 operators. You can see this was a relatively imaging-intense protocol with 24 month CT Venogram and CT Venograms also at one month and six months.
Long term follow up, 94 percent of the eligible subjects were imaged at 24 months. You can see that 67.5 percent of the subjects had current PE and/or DVT at the time of enrollment, and 100 percent had contraindication to anticoagulation for some or all of the protection period.
In terms of the composite primary endpoint, there was a high degree of technical success, 100 percent of the patients received the device. 100 percent freedom from new symptomatic PE to 60 days. Two patients had symptomatic caval thrombosis at 8
by angiojet, one by EKOS. And there was no tilting, migration, embolization, fracture or perforation. At 12 months there were no new symptomatic PEs and there were no device related complications out to 12 months.
And at 24 months, two new symptomatic PEs, days 581 and 632,in patients with fully bioconverted filters. There were no device related out to 24 months. Both of these were adjudicated by a clinical events committee as not being device related.
And again, you can see that the bioconversion rate of 96.5 percent compares favorably to published retrieval rates, and we've talked about that. So, in conclusion, the primary endpoint at six months was met with clinical success of 97.4 percent. No new symptomatic PEs at 12 months.
2.4 new symptomatic PEs at 24 months, but no tilting, migration, perforation, fracture or embolization. And the 96.5 percent bioconversion rate compares favorably to published retrieval rates. Thanks very much.
- Good afternoon, Dr. Veith, organizer. Thank you very much for the kind invitation. I have nothing to disclose. In the United States, the most common cause of mortality after one year of age is trauma. So, thankfully the pediatric vascular trauma
is only a very small minority, and it happens in less that 1% of all the pediatric traumas. But, when it happens it contributes significantly to the mortality. In most developed countries, the iatrogenic
arterial injuries are the most common type of vascular injuries that you have in non-iatrogenic arterial injuries, however are more common in war zone area. And it's very complex injuries that these children suffer from.
In a recent study that we published using the national trauma data bank, the mortality rate was about 7.9% of the children who suffer from vascular injuries. And the most common mechanism of injury were firearm and motor vehicle accidents. In the US, the most common type of injury is the blunt type
of injury. As far as the risk factors for mortality, you can see some of them that are significantly affecting mortality, but one of them is the mechanism of injury, blunt versus penetrating and the penetrating is the risk factor for
mortality. As far as the anatomical and physiological consideration for treatment, they are very similar to adults. Their injury can cause disruption all the way to a spasm, or obstruction of the vessel and for vasiospasm and minimal disruption, conservative therapy is usually adequate.
Sometimes you can use papevrin or nitroglycerin. Of significant concern in children is traumatic AV fissure that needs to be repaired as soon as possible. For hard signs, when you diagnose these things, of course when there is a bleeding, there is no question that you need to go repair.
When there are no hard signs, especially in the blunt type of injuries, we depend both on physical exams and diagnostic tools. AVI in children is actually not very useful, so instead of that investigators are just using what is called an Injured Extremity Index, which you measure one leg
versus the other, and if there is also less than 0.88 or less than 0.90, depending on the age of the children, is considered abnormal. Pulse Oximetry, the Duplex Ultrasound, CTA are all very helpful. Angiography is actually quite risky in these children,
and should be avoided. Surgical exploration, of course, when it's needed can give very good results. As far as the management, well they are very similar to adults, in the sense that you need to expose the artery, control the bleeding, an then restore circulation to the
end organ. And some of the adjuncts that are using in adult trauma can be useful, such as use of temporary shunts, that you can use a pediatric feeding tube, heparin, if there are no contraindications, liberal use of fasciotomy and in the vascular technique that my partner, Dr. Singh will be
talking about. Perhaps the most common cause of PVI in young children in developed countries are iatrogenic injuries and most of the time they are minimal injuries. But in ECMO cannulation, 20-50% are injuries due to
ECMO have been reported in both femoral or carotid injuries. So, in the centers are they are doing it because of the concern about limb ischemia, as well as cognitive issues. They routinely repair the ECMO cannulation site.
For non-iatrogenic types, if is very common in the children that are above six years of age. Again, you follow the same principal as adult, except that these arteries are severely spastic and interposition graft must accommodate both axial and radial growths of these arteries, as well as the limb that it's been
repaired in. Primary repair sometimes requires interrupted sutures and Dr. Bismuth is going to be talking about some of that. Contralateral greater saphenous vein is a reasonable option, but this patient needs to be followed very, very closely.
The most common type of injury is upper extremity and Dr. McCurdy is going to be talking about this. Blunt arterial injury to the brachial artery is very common. It can cause ischemic contracture and sometimes amputation.
In the children that they have no pulse, is if there are signs of neurosensory deficit and extremity is cold, exploration is indicated, but if the extremity is pulseless, pink hand expectant treatment is reasonable. As far as the injuries, the most common, the deadliest injuries are related to the truncal injuries and the
mechanism severity of this injury dictates the treatment. Blunt aortic injuries are actually quite uncommon and endovascular options are limited. This is an example of one that was done by Dr Veith and you can see the arrow when the stent was placed and then moved.
So these children, the long-term results of endovascular option is unknown. So in summary, you basically follow many tenets of adult vascular trauma. Special consideration for repair has to do with the fact that you need to accommodate longitudinal
and radial growth and also endovascular options are limited. Ultimately, you need a collaborative effort of many specialists in taking care of these children. Thank you.
- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent
secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results
in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different
in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,
or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,
PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus
or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk
of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,
but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.
and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.
Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.
So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.
Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.
In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,
and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide
a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.
And an E-portal is being developed for dissemination. Thank you very much.
- Thank you, it's a pleasure to be here. I'll address how the Indigo Thrombectomy technology can expand the reach of what you can do for your patients. It will preserve treatment options, improve patient outcomes, conserve hospital resources,
and perhaps most importantly, improve your day. The old treatment strategy, every time I had someone with acute limb ischemia I felt like I was shopping at this store. When I went to surgery, I wished I could put a drip catheter in, it lasts a little longer,
to mop up some di when I went to the angio suite, I wished I could cut down and remove some more macroscopic debris. I submit that the new Indigo technology
will provide a new strategy for treating acute arterial ischemia. On the same concepts are predicated STEMI, code stroke, Level I trauma alerts, we've instituted acute aorta, and piggybacked on that, an acute arterial ischemia protocol.
So that means when a patient like this presents with acute arterial ischemia, they get an algorithmic, systemic, trained, metered approach. They go past the holding room directly to the endovascular suite,
and all the processes happen in parallel, not in series. The call team is trained and dedicated, and while anesthesia is working up top with labs and lines, we use the duplex ultrasound to pick carefully our access sites. A faster time to reperfusion allows us to
do it and avoid general anesthesia, incision in hostile groins, and the exposure of lytic therapy, resulting in a decreased morbidity and mortality. Being able to treat the full spectrum of the arterial tree allows us to run options.
We preserve options by first mopping up more proximal clot, and then dripping distally when we need to, or, dripping distally to open up distal targets for surgical bypasses. As an example, this was a recent case
on a trauma CT scan, injured inthrelane aorta with emblogenic thrombus confirmed on intravascular ultrasound. We went in with a large bore system, a cath to aspirate the clot, and then used a cover stent to repair the aorta.
We shot an arteriogram the lower extremities, noticed that it embolized distally, and we used a Cat 6 to pluck out this clot and restore flow. Able to work up and down the full arterial tree. A learning curve for me was to understand that debris has to be corked to removal, which means no flow.
And most other worlds in vascular surgery, flow is good. No flow is bad. Also, you have to vacuum the clot out. Which means you have to uncross the lesion, which is counter intuitive for most of the precepts I've learned.
I've learned to use long sheaths to approach the lesion and to use larger catheters to remove more macroscopic debris. I rarely use the separator, I engage it and cork it for 90 seconds. That allows it to get a firm grip and purchase on it.
And I have to remember that no flow is good. This demonstrates how you approach the catheter with a large sheath. Under roadmap guidance you turn the aspiration vacuum on immediately before you cork it to minimize blood loss. And you use it like a vacuum by uncrossing the lesion
and let it slowly engage and aspirate the catheter. Ninety seconds allows it to get a firm grip and purchase so you can extract it without breaking it loose. I rarely use a separator, I use it only for large thrombus burdens, sub-acute clot, adherent debris,
or when the Indigo catheter is clogged. I strip out the catheter with the separator like a pipe cleaner, and then, every once in a while, on a subacute clot, I'll peck and morcellate it with a separator. Typically, in my lab, when I have new technology
I never have the team trained when I have just the right case, so I've learned over time, to train the team first. And with a trained team, they've taught me a lot. I've found with the Indigo catheter it's hard for me to watch the monitor,
work the catheter, handle the on-off switch, and watch the flow in the canister. So, what we do is we have a spotter who's not scrubbed. They taught me to take the on-off switch out, and then mechanically kink the tubing to make and on-off switch.
And they provide me feedback and just say fast, slow, or corked, so I can run the catheter and watch the monitor. I've learned to beware of the Cook Flexor sheaths, because they scuff up the tip. Use a check flow valve that unscrews from the
catheter if possible. I use coaxial catheters whenever possible, and I telescope them. You can telescope large catheters over small catheters. I use large sheaths and catheters whenever possible, using the preclose technique,
and then you can preserve options if you want to press more distally, you can cinch down, remove the large sheath, put in a 4 5 French, and then press ahead. I also, after I use a pulse technique, will occasionally use the Jungle Juice.
The team taught me the Jungle Juice is half strength contrast, some TPA and some nitroglycerine. When I lace the clot with Jungle Juice, I can observe fluoroscopically, the progress I'm making as I'm aspirating the clot. Thank you.
- Thank you so much. I have no disclosures. These guidelines were published a year ago and they are open access. You can download the PDF and you can also download the app and the app was launched two months ago
and four of the ESVS guidelines are in that app. As you see, we had three American co-authors of this document, so we have very high expertise that we managed to gather.
Now the ESVS Mesenteric Guidelines have all conditions in one document because it's not always obvious if it's acute, chronic, acute-on-chron if it's arteri
if there's an underlying aneurysm or a dissection. And we thought it a benefit for the clinician to have all in one single document. It's 51 pages, 64 recommendations, more than 300 references and we use the
ESC grading system. As you will understand, it's impossible to describe this document in four minutes but I will give you some highlights regarding one of the chapters, the Acute arterial mesenteric ischaemia chapter.
We have four recommendations on how to diagnose this condition. We found that D-dimer is highly sensitive so that a normal D-dimer value excludes the condition but it's also unfortunately unspecific. There's a common misconception that lactate is
useful in this situation. Lactate becomes elevated very late when the patient is dying. It's not a good test for diagnosing acute mesenteric ischaemia earlier. And this is a strong recommendation against that.
We also ask everyone uses the CTA angiography these days and that is of course the mainstay of diagnoses as you can see on this image. Regarding treatment, we found that in patients with acute mesenteric arterial ischaemia open or endovascular revascularisation
should preferably be done before bowel surgery. This is of course an important strategic recommendation when we work together with general surgeons. We also concluded that completion imaging is important. And this is maybe one of the reasons why endovascular repair tends to do better than
open repair in these patients. There was no other better way of judging the bowel viability than clinical judgment a no-brainer is that these patients need antibiotics and it's also a strong recommendation to do second look laparotomoy.
We found that endovascular treatment is first therapy if you suspect thrombotic occlusion. They had better survival than the open repair, where as in the embolic situation, we found no difference in outcome.
So you can do both open or endo for embolus, like in this 85 year old man from Uppsala where we did a thrombus, or the embolus aspiration. Regarding follow up, we found that it was beneficial to do imaging follow-up after stenting, and also secondary prevention is important.
So in conclusion, ladies and gentlemen, the ESVS Guidelines can be downloaded freely. There are lots of recommendations regarding diagnosis, treatment, and follow-up. And they are most useful when the diagnosis is difficult and when indication for treatment is less obvious.
Please read the other chapters, too and please come to Hamburg next year for the ESVS meeting. Thank You
- Afternoon. It's a privilege to be presenting this today. I have no disclosures. If you look at this, this is a picture of the last 10 IVC filters approved by the FDA. You'll notice that they all have some mechanism of removal most commonly hooks.
You may ask yourself, why is that? And the reason for this is basically one or two studies. Basically the PREPIC study which was originally published in 1998 with two-year data, followed by a publication in Circulation with eight-year data.
Now the PREPIC itself, the study itself was the first prospective, randomized trial comparing anticoagulation to IVC filters. It was performed from 1991 to 1995 in France. 400 patients with DVT that were considered at risk for PE were enrolled.
And they were randomized at first either unfractionated versus fractionated heparins, and then IVC filter versus no IVC filter. And the filters used are demonstrated here, the Greenfield, the Cardinal, LGM, and Bird's Nest. And all patients were anticoagulated with warfarin
at the time of discharge whenever possible. Primary outcome was pulmonary embolism. The secondary outcomes were DVT, death, major filter complications, and major bleeding. And again, the data was published at two and eight years. So the two-year results, the PREPIC study,
they presented first some data on unfractionated versus fractionated heparin, but then this table. And this table shows basically that there was no difference in symptomatic PE between groups. But there was a difference in recurrent DVT
with patients having a filter in place having a higher incidence of DVT than those that did not. And the thought was that this presence of the filter increased the risk of DVT. Now the data at eight years, published in Circulation, did show a difference between symptomatic pulmonary embolism
with patients having a filter having a lower incidence of recurrent PE. However, the symptomatic DVT remained elevated in patients that had filters in place. And this was statistically significant. Of note, there was a fairly significant number of patients
that had cable thrombosis in the group that had filters that may have contributed to this number. So if you want to be critical about the study, there are a few things that are a little bit unperfect I guess you could say. It's now thought as a study of filter randomization
in patients with DVT, but it was actually also a study looking at unfractionated and low molecular weight heparins. And this lends itself to be a fairly weak study designed to make conclusions on IVC filters, the performance of IVC filters, and it's underpowered really to make a definitive conclusion.
The other problem with this study is that there's a wide variety of filters, I mean a Bird's Nest and the Greenfield, they're very different filters. And that lack of standardization I think is problematic. These filters both can have different rates
of IVC thrombosis, which can affect the data. So the statistical analysis was less than perfect. They should have corrected for multiple comparisons which they did not. And it also showed that PE can occur remotely, and if you don't have a filter in place,
it's probably not protective, obviously. So a PREPIC study was recently published, the PREPIC 2 in 2015. And this asks the question, do patients with acute PE at high risk of recurrence benefit from IVC filter in addition to anticoagulation?
So it was a multicenter trial in France. They had about 400 patients that were randomized, half into filters, half into no filters. Their risk factors are listed, and they're quite broad. And all filters were removed at three months. And they had follow up at three and six months.
And this is the data. The data at three months shows that there was no difference in recurrent PE between the patients with filters and the patient without filters. And at six months this remained the same. And there was no difference in DVT
between groups at six months. So fact or fiction? Well I think the PREPIC studies are mostly fact with maybe a little bit of fiction thrown in. The data from PREPIC suggests that patients with IVC filters have an increased risk of DVT long term,
but a decreased risk of PE long term. PREPIC 2 suggests that IVC filters may not decrease the risk of PE in high-risk patients, and did not show an association between filters and recurrent DVT at six and three months. Thank you.
- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old
but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,
and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.
- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,
and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was
revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.
In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat
was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.
Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone
returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.
Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy
with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,
the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.
Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.
So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really
how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017
in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.
Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at
five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery
to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional
independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.
So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,
but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could
help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.
- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed
is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome
is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement
and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.
So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.
We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy
which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures
that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.
As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.
So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,
and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.
So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.
It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,
'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula
and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.
It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically
a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.
Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal
vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.
Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding
the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody
who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test
confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,
so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,
although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.
It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get
a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.
And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,
immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.
We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.
So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,
and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.
DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,
when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.
- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want
in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis
is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied
and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple
aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention
adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,
the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that
there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions
a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.
In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure
with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle
and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis
needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.
Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.
In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,
regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate
without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.
An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis
and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.
This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more
in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.
But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.
The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.
Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion
because I have a flight in a few hours. Thank you very much.
- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.
It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.
So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations
of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.
Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.
So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient
who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal
angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near
or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility
was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.
Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal
or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection
or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.
So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump
to prevent hip disarticulation. Thank you for much for your attention.
- Great, thank-you very much, a pleasure to be here. My disclosures. So, we've talked a little bit about obviously percutaneous and thrombectomy techniques. Obviously we have catheter-directed thrombolysis with TPA, but what happens when we can't use TPA
mechanical techniques? We've discussed several of them already in this session, I'm going to try to kind of bring them together and note the differences and how they evolved. And really look at fragmentation, rheolytic therapy, vacuum assisted devices, and vacuum and suction devices.
So when do we need these? Patients that can't tolerate thrombolysis, can't get TPA, that have a high risk of TPA, or maybe there is a situation we need a rapid response. We're trying to create flow and establish flow as much as possible and a lot of times we use this
in combination therapy if we've already hurt. What's the ideal device? I think there are multiple different characteristic's that could define the ideal device. Obviously we want it simple to use, We want it to be reproducible,
we want it to remove a lot of thrombus, but minimize blood loss and trauma to the vessels and to the blood cell. These are just some of them. There's a lot of mechanical thrombectomy devices right now on the market continuing to grow,
both in the arterial and venous system so I think this is going to be an evolution. We started really using mechanical fragmentation with a pig tail and spinning a pig tail. We used that. A lot of times the patient with severe massive pulmonary embolism.
These we're really small antidotes, small case reports. Will Kuo, looked at these in the 2009 and basically saw over all clinical success, about 86% using these mechanical devices. Then we had some that were even more automated.
All these did was break up the clot. So you have the Trerotola Device , Cleaner Device, really almost in the dialysis space. Rheolytic Throbectomy, we've already heard about. Some of how it works and the advantages. Really I think this is the first time we've saw
a system which would try to aspirate and remove some of that thrombus as it got broken up. The PEARL registry really showed for the first time, maybe we can get this done within 24 hours, can we get this done in one session? Unfortunately in this registry only about three or
four percent of patients actually had just rheolytic therapy alone without any TPA. We've discussed a little bit about the use of Ango and this type of device in terms of bradyarrhythmia's and that may be a limitation. But I think we can still use it particularly
outside of the chest. So What about suction devices? You can have a catheter, I think a catheter suction device is very limited. We use that in the arterial tree when there is a small thrombus, a small embolus, I think
we're very limited, not only in the amount of thrombus we can remove but the amount of suction we can apply. Other types like almost mechanical, very simple to use systems is the aspire device. Well you can basically create and suction a
limited area and then help you aspirate the thrombus. And then to the other extreme. We're going to hear my next speaker talk about Angiovac, again a different system, a different system requires a patient on bypass large 26 french devices.
Where we can actually go in and deal with a large amount of thrombus, like this patient had a thrombus cave on both iliac veins. And to be able to basically come with this vacuum aspiration system over wires and kind of pulling them out and you get these little canisters,
seeing what you've actually removed. Very gratifying. But takes a lot of work to get it going. We've heard a little bit about vacuum assisted with the Indigo system. With a system of creating a constant continuous vacuum.
We now have eight french catheters with incredible aspiration volume, almost 20cc's, I'm sorry you can get up to 140cc's of thrombus in a minute can be aspirated quickly. Here is a patient, 80 years old, colorectal CA. You can see the thrombus in the right leg.
There was actually a mass invading this vein. That is where we wanted to use thrombolysis, really went a head and you can see the amount of thrombus. Cleared this out with some passage. You can see this here, the separator. You started seeing thrombus especially when
its acute it kind of looks like this. It's kind of gelatinous, things that we've already seen, and then went ahead and placed a stent, dilated that stent. Had to clean up some more with the device
on top of the stent, but with a good result without needing any TPA. Other types of extraction devices we've seen the Inari device, again this is like a stent Triever device, a nitinol ring we can use this in the pulmonary arteries.
And we've already seen previous and talked about the ClotTriever device Again remove that thrombus, put it into a bag and remove it. So again, capture and removal of thrombus. And this is a solution without the need of TPA. New kid in the block the JETi device
Again very similar to aspiration Indego device, but at the same time it has a jet to macerate the clot and kind of break up the clot a little to smaller areas so we can able to thromb and take more out. I think really here what I've seen and Dr. Razavi
showed me this case. Being able to treat a patient quickly, treat that patient very quickly you can see the amount of thrombus being able to, within about an hour and 15 minutes, get all that thrombus, then create patency in that vein and he showed
some early initial good data. Over the last year we did have a paper that was presented here and published this year in the Journal of Vascular Surgery, venous and lymphatic disorders and again pulled multiple patient's, again showing that
it affective and safe. We still need better data. We need to figure out which patients are best treated with which devices and which again will be affective. Thank-you very much.
- Thank you very much both. It was a great pleasure to see you. I continue to be grateful for the guidance you have given me over the years. Thank you to the organizers for advising me to speak. These are my disclosures. So really there are two questions posed by this topic.
One is, is the patent popliteal vein necessary? I would assume from this is it necessary for patency and symptom relief to be achieved in treating patients with both acute DVT and potentially chronic. And has the evolution formic mechanical therapy
led to over stenting. Which means we have to ask the question what is an appropriate rate for stenting. I am not sure we know the answer to that. So being able to answer over stenting requires us to know how many patients
actually need the stent in the first place in acute DVT treatments. The problem is essentially this. Is that when we form lithic therapies and this is a classic case of treatment formed with formic and mechanical device
but without a follow up using lithic in the patient for whom lithic was not feasible. You end up opening up a vessel but you can see from the image on the left hand side that there is a degree still of luminol contrast deficit suggesting some cult left behind
in the external iliac vein. Well there is obviously a May-Thurner legion at the top. The question of over stenting is one of do we just stent the May-Thruner and extend it down into the external iliac vein to trap that thrombus
or would a period of time of lithic have resulted in this clot resolving and not needed a stent at the end of it. To get to the question of how many people should be stented. The only way we can really do this
is try and exstipulate from the literature to some extent. This is the short and long term outcome from the Kevin study. Where there is ultrasound follow up of patients underwent standard treatment only.
And a additional group in the patients had catheter-directed thrombolysis. We can see there that the patients did six months in catheter-directed thrombolysis group is around 60%. And the patency seen with the non treated group
is around 40%. If we kind of use these numbers as a guide we probably expect therefore that the stent rate would be somewhere between 40 and 60 percent. To account for treating the outflow structure that presumably patients see at six months.
But this is clearly not a very rebost method of being absolutely clear on who needs stents. Additional method is we don't really have and answer for who should be stented at the end of a procedure. So if you look at the massive variability
in the other studies. We see that attract stent rate is approximately 28% for the study. Which is obviously a operative discretion and has been criticized for that reason. But there is no comment on the Popliteal vein
or Popliteal vein patency. Cavent did an stent rate of 15% again with no real comment on whether the Popliteal vein was open and it wasn't a prerequisite for treatment in the study. This contrast with the Ansberg Aspirex Registry.
Which is a registry of a purely mechanical device to aspirex clot and the stent rate is 100%. Baekgaard Copenhagen used a catered-directed thrombolysis with a mandated open popliteal vein for purpose to be in the study. He has a stent rate of 60%.
My own personal experience of 160 odd patients is that were stenting around 80% of patients with outflow legion at the end of treatment. And were not really bothered by whether the popliteal vein is clear or not. But that doesn't necessarily answer the question
whether it makes a difference in the long run. So its very difficult even looking at the data we have because there is no standard definition of what a outflow stenosis is. There is no objective measure for an outflow stenosis. So stenting becomes and operative discretion decision.
But you would have to say that if your taking purely mechanical devices and the stent rates are going up to 100% that the inclination would be that there is potential for formic mechanical therapy to lead to overstenting and increase use
for stents for sure. In our experience then we had 81 patients who had CDT alone verse 70 patients who had AngioJet Thrombectomy. The basic characteristics of the group are pretty much identical.
With similar ages and no difference between whether the thrombus with left side or right side of body or so on. And these are the patency curves for the different groups with equivalent primary, primary assisted and secondary patency over two yeas.
We had no difference in stent rates with the median stenting of 80% in both groups with two stents used in average for each of those patients. However in our practice AngioJet is rarely used alone. So we had 70 patients for whom AngioJet was used. 24 of those where AngioJet was used up front
as the first line of treatment followed by some CDT. We have tended find that if we wanted full clock clearance. We have always had omit to some extent. And single stage therapy is quite difficult to achieve unless you spent a lot of time in it.
Patency in the popliteal vein is clearly affected by some extent. These are our follow up results if we don't have a patent popliteal vein at the end. It does drop off in stent patency. So the conclusions then I think.
Is that patent popliteal vein is necessary for long term results. But you can still treat patients that have acute popliteal vein for larsons that is not a contraindication. Pure mechanical therapies may well lead to higher stent rate.
But is this a bad thing or a good thing? We don't really know this at this stage as to what the long term outcomes will be. Thank you very much.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
- Thank you and thanks again Frank for the kind invitation to be here another year. So there's several anatomic considerations for complex aortic repair. I wanted to choose between fenestrations or branches,
both with regards to that phenotype and the mating stent and we'll go into those. There are limitations to total endovascular approaches such as visceral anatomy, severe angulations,
and renal issues, as well as shaggy aortas where endo solutions are less favorable. This paper out of the Mayo Clinic showing that about 20% of the cases of thoracodynia aneurysms
non-suitable due to renal issues alone, and if we look at the subset that are then suitable, the anatomy of the renal arteries in this case obviously differs so they might be more or less suitable for branches
versus fenestration and the aneurysm extent proximally impacts that renal angle. So when do we use branches and when do we use fenestrations? Well, overall, it seems to be, to most people,
that branches are easier to use. They're easier to orient. There's more room for error. There's much more branch overlap securing those mating stents. But a branch device does require
more aortic coverage than a fenestrated equivalent. So if we extrapolate that to juxtarenal or pararenal repair a branched device will allow for much more proximal coverage
than in a fenestrated device which has, in this series from Dr. Chuter's group, shows that there is significant incidence of lower extremity weakness if you use an all-branch approach. And this was, of course, not biased
due to Crawford extent because the graft always looks the same. So does a target vessel anatomy and branch phenotype matter in of itself? Well of course, as we've discussed, the different anatomic situations
impact which type of branch or fenestration you use. Again going back to Tim Chuter's paper, and Tim who only used branches for all of the anatomical situations, there was a significant incidence of renal branch occlusion
during follow up in these cases. And this has been reproduced. This is from the Munster group showing that tortuosity is a significant factor, a predictive factor, for renal branch occlusion
after branched endovascular repair, and then repeated from Mario Stella's group showing that upward-facing renal arteries have immediate technical problems when using branches, and if you have the combination of downward and then upward facing
the long term outcome is impaired if you use a branched approach. And we know for the renals that using a fenestrated phenotype seems to improve the outcomes, and this has been shown in multiple trials
where fenestrations for renals do better than branches. So then moving away from the phenotype to the mating stent. Does the type of mating stent matter? In branch repairs we looked at this
from these five major European centers in about 500 patients to see if the type of mating stent used for branch phenotype grafts mattered. It was very difficult to evaluate and you can see in this rather busy graph
that there was a combination used of self-expanding and balloon expandable covered stents in these situations. And in fact almost 2/3 of the patients had combinations in their grafts, so combining balloon expandable covered stents
with self expanding stents, and vice versa, making these analyses very very difficult. But what we could replicate, of course, was the earlier findings that the event rates with using branches for celiac and SMA were very low,
whereas they were significant for left renal arteries and if you saw the last session then in similar situations after open repair, although this includes not only occlusions but re-interventions of course.
And we know when we use fenestrations that where we have wall contact that using covered stents is generally better than using bare stents which we started out with but the type of covered stent
also seems to matter and this might be due to the stiffness of the stent or how far it protrudes into the target vessel. There is a multitude of new bridging stents available for BEVAR and FEVAR: Covera, Viabahn, VBX, and Bentley plus,
and they all seem to have better flexibility, better profile, and better radial force so they're easier to use, but there's no long-term data evaluating these devices. The technical success rate is already quite high for all of these.
So this is a summary. We've talked using branches versus fenestration and often a combination to design the device to the specific patient anatomy is the best. So in summary,
always use covered stents even when you do fenestrated grafts. At present, mix and match seems to be beneficial both with regards to the phenotype and the mating stent. Short term results seem to be good.
Technical results good and reproducible but long term results are lacking and there is very limited comparative data. Thank you. (audience applauding)
- Thank you, and thank you Dr. Veith for the opportunity to present. So, acute aortic syndromes are difficult to treat and a challenge for any surgeon. In regionalization of care of acute aortic syndromes is now a topic of significant conversation. The thoughts are that you can move these patients
to an appropriate hospital infrastructure with surgical expertise and a team that's familiar with treating them. Higher volumes, better outcomes. It's a proven concept in trauma care. Logistics of time, distance, transfer mortality,
and cost are issues of concern. This is a study from the Nationwide Inpatient Sample which basically demonstrates the more volume, the lower mortality for ruptured abdominal aortic aneurysms. And this is a study from Clem Darling
and his Albany Group demonstrating that with their large practice, that if they could get patients transferred to their central hospital, that they had a higher incidence of EVAR with lower mortality. Basically, transfer equaled more EVARs and a
lower mortality for ruptured abdominal aortic aneurysms. Matt Mell looked at interfacility transfer mortality in patients with ruptured abdominal aortic aneurysms to try to see if actually, transfer improved mortality. The take home message was, operative transferred patients
did do better once they reached the institution of destination, however they had a significant mortality during transfer that basically negated that benefit. And transport time, interestingly did not affect mortality. So, regional aortic management, I think,
is something that is quite valuable. As mentioned, access to specialized centers decrease overall mortality and morbidity potentially. In transfer mortality a factor, transport time does not appear to be. So, we set up a rapid transport system
at Keck Medical Center. Basically predicated on 24/7 coverage, and we would transfer any patient within two hours to our institution that called our hotline. This is the number of transfers that we've had over the past three years.
About 250 acute aortic transfers at any given... On a year, about 20 to 30 a month. This is a study that we looked at, that transport process. 183 patients, this is early on in our experience. We did have two that expired en route. There's a listing of the various
pathologies that we treated. These patients were transferred from all over Southern California, including up to Central California, and we had one patient that came from Nevada. The overall mortality is listed here. Ruptured aortic aneurysms had the highest mortality.
We had a very, very good mortality with acute aortic dissections as you can see. We did a univariate and multivariate analysis to look at factors that might have affected transfer mortality and what we found was the SVS score greater than eight
had a very, very significant impact on overall mortality for patients that were transferred. What is a society for vascular surgery comorbidity score? It's basically an equation using cardiac pulmonary renal hypertension and age. The asterisks, cardiac, renal, and age
are important as I will show subsequently. So, Ben Starnes did a very elegant study that was just reported in the Journal of Vascular Surgery where he tried to create a preoperative risk score for prediction of mortality after ruptured abdominal aortic aneurysms.
He found four factors and did an ROC curve. Basically, age greater than 76, creatinine greater than two, blood pressure less than 70, or PH less than 7.2. As you can see, as those factors accumulated there was step-wise increased mortality up to 100% with four factors.
So, rapid transport to regional aortic centers does facilitate the care of acute aortic syndromes. Transfer mortality is a factor, however. Transport mode, time, distance are not associated with mortality. Decision making to deny and accept transfer is evolving
but I think renal status, age, physiologic insult are important factors that have been identified to determine whether transfer should be performed or not. Thank you very much.
- I think we have time. If there are any questions, please come up to the microphone and any of the panels have questions for each other. I have a number of questions I could ask but I just see if anyone wants to start out. Claudio?
- I have a question Doctor Mark. He show us very nice utilization of this device for occluded limbs. My question is, do you protect in any way the other side? If not, don't you have, you're not concerned
or you're not afraid of pushing clots from one side to the other one when you're manipulating the device? And the second one, do you do this percutaneously? And if that's the case, do you have any concern about having destabilization?
Because once you start to manipulate the clot that is occupying the entire graft, and there is reestablishment of flow in an antegrade flush, and you may have some of that clot dislodge and embolize distant. - Yeah, as I mentioned,
nobody wants to be the guru of limb occlusions. However, we have seen them and we always go retrograde ipsilateral, not seen emboli once from those seven cases and in fact, the 73 we presented at the midwest there was only two instances of embolization
when we utilized this device. And both times we were able to extract those just by going further down with the cat six and both of them was below the knee popliteal. In particular, the acute ones, it's soft and it's no different than watching it in vivo
or in vitro model, as you know better than I, comes out quite easily. - Let's take our question from the audience. - [Scott] Hi, Scott Tapart from Stuart, Florida. So I'd like to poll the panel there about are you doing every single
acute limb ischemia percutaneously? The pictures are elegant, the techniques are elegant, but the last speaker touched on the profoundly ichemic Rutherford 2B patient, where you're most likely going to have to do a fasciotomy. Are you going to the OR
or are you doing this percutaneously and then watching and waiting and seeing about fasciotomy? Or has this changed your fasciotomy approach? - So since we have a number of people, that's a great question. Why don't we start at the end
and let's just go kind of rapid fire, maybe one or two sentences, how do you choose your patients and what do you do with those 2Bs and we'll try to get through everybody. - Sure, so, to reiterate the last slide of the presentation,
essentially anybody with a significant motor or neutral deficit is somebody I tend to do in an open fashion. And if I'm the least bit concerned about doing a fasciotomy or there's evidence of compartment syndrome I do that patient open.
- We try to start endovascular, and if we can clean and reestablish antegrade flow, that would take care of the problem. And of course, I'm a radiologist, so I always consult with my colleagues in surgery and they decide if a fasciotomy needs to be done or not.
And it's that at the end. - Okay, I have to be honest, we start with the selective indication but now we move maybe to 90% of our patients doing percutaneously. We will adjust patients with probably an embolization,
a huge embolization, into the common femoral artery for open surgery. Of course, in our mind, also in the registry, we have some cases of fasciotomy after percutaneous approach so it's not a limitation. - The advantage of acute arterial protocol,
as they all go to the end of asher suite and they all run along our protocol but you can run the option. You get them to treatment quicker because they don't dilly-dally around in the holding room. But then according to how the patient's doing
you can mop up as much clot as you can with the percutaneous technique and then do the fasciotomy when you're done or press head and drip more if you need to. So I think to have an algorithm where you can treat the full spectrum
is what's best for the patient. - I think it depends on the time as well because I did two weeks ago a patient who needed a fasciotomy directly so I performed that first and then it rules out any traumalitic therapy
or whatever that you want to do. And actually, if I do antivascular techniques I usually give a shot or RTPA or something and then go further with it. But anomerization of this patient's arteries as well so prefer actually if it's really a case
that needs fasciotomy just to perform surgical thrombectomy. - Yeah, percutaneous eight French up and over and almost always, you're going to be done with your thrombectomy within about 30 to 45 minutes. I don't think you're adding that much time
and for us, by the time we get anesthesia in him assuming anesthesia's anesthesia no matter what part of the world you're in, so you can get to the hybrid room quicker and then if it's going to fail then you're going to call in the OR or call an anesthesiologist.
- I wouldn't have much else to add. I do think there is some patient selection, if you have an entire SFA, 30 centimeter clot, that's going to take you hours to do so for these thromboembolic things that are 10 centimeters or shorter
lodged in the popliteal TP trunk, this method works really well. I think for the longer patients, you might think about something else. - But just a comment on the general anesthesia. If a patient is in real or really pain,
he can't lie down for 30 minutes, even. I mean, they are rolling in pain and I would do the fasciotomy first because general anesthesia is needed because there is so much pain or, yes, so yeah.
- So, let me say, does that answer it, Scott? So let's, since we have a number of panelists and we're running out of time, how about if we ask each person going down the room, you heard a whole bunch of different speakers here with a lot of experience
and if you haven't used this, there is a learning curve. The learning curve is pretty shallow. Really, a lot of it has to do with controlling your blood loss. But if we ask each person for just one tip
and we'll see if we can get through everybody. If you telling people who hadn't done a lot of this, one tip or one trick, let's see if we can get seven or eight tips and tricks out. So, I'll go last. Let's start back down at that end
and we'll end up at this end. - Sure. Use the largest catheter that the vessel will comply to. - Amen, brother. - I agree with that.
And the way I do it, in order to avoid too much blood loss, I like to engage with a syringe. So I come with my catheter, I hook a syringe in the bag, 20cc or sometimes even larger, and when I have the fish at the end of my line, then I connect to the pump and I continue.
That way if I'm aspirating, I'm not going to aspirate a large volume so I want to engage the clot. And then I bring the clot out. That's my trick. - Okay.
Very nice comment. Of course, I agree with the previous colleagues but I will say that first the trick is really the largest catheter is better, then my idea that I developed during my learning curve is the use of separate to cut away.
I probably use now in 95% of cases because it just makes everything quicker and faster and better. - I use the perclose device for large-bore catheters often and that allows me to pull the plug out, especially if it's fibrous plugs,
safe from the heart without shearing it off on the end of the catheter. I've got one question for Claudio, on that case of the carotid subclabian with the acute carotid occlusion, do you think the nitroglycerin would have helped?
- For the doctor? - For the surgeon. - Absolutely. - And then, change the diapers. - Well, I would advise if you do a surgical embolectomy do it also on the hybrid room
and try to do it also over the wire. Especially be careful if you do it below the knee. I would suggest do it open below the knee, even. - I would say don't afraid to use an eight French for ALI and that closure devices are your friends here. But you can use an eight all the way down to the pop
and then for us, the tibials, we'll use a six. - Yeah, I would agree with that. So I guess my tip would be, I agree with everything everyone said, although I don't use the separator very often in the arterial side, I do in the veins.
But one tip is, if you're not going to use a separator, if you're going to start without it, let's say you want to give it a try, I don't work through a 2E borst because the angle, the eddy currents that form around that 2E borst
trap clots and you constantly have to clean that 2E out so if you're going to start with a focal embolis in the artery my recommendation is take the 2E off, hook up to the vacuum directly, and you'll get less clot stuck in the 2E. If you want to go to the separator
then you can always add that on at the back end. - So I have a question for Fennel. I used a penumbra like a few weeks ago and it ended up really bad because the surrounding catheter from the penumbra, everything got, you know, clotted
and then I didn't have any outflow did I choose the wrong size or what is it that happened, did you see it ever? - We have not had that problem. We're usually working on heparinized patients and have not seen that happen.
- She was heparinized. No? Okay. - Okay. Any other comments? Otherwise, we'll end one minute early
on a nice, long day.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- And thanks to Dr. Veith for the opportunity to get involved. Here's my disclosures. Like so many in the audience, for years and years we've had awesome results with the AngioJet from Boston Sci. We know that this rheolytic system works quite well.
However it has a black box warning for PE due to the hemolysis and the adenosine that can be extruded out. It's oftentimes not stand alone. It's not used for stroke and there can be some renal issues. But we've had excellent results with it over the years,
but at the end of the day often times you still need lytics. And I think Professor Davies just eluded to the potential problems not only medical, but legal as well of lytics. Therefore for the past four plus years we've utilized this as well as other thrombectomy devices.
This is the Indigo device from Penumbra. I'm certain by now most of your are familiar with it, but if not what it is it's a braided catheter that's very atraumatic and soft at the tip. It can come straight in or torqued so you can have some directionality to it.
And then what it also has is this separator technology which is really just like a glorified pipe cleaner to be honest. You're going to go in and out with this device as I'll show you here in a second, to clear the lumen while you're
allowing for continuous aspiration through this system. We learned from our neurosurgery colleagues who utilized typically the CAT five, sometimes six for their stroke patients, but now there's CAT three, five, six, and eight. And within the next probably three to four months
there's going to be CAT 10 or possibly even 12 out there. This is what you have. It's all pretty simple. You cross your lesion with the wire. You then bring your catheter across. You connect it to this suction device,
hit the green button and away you go. You get maximal aspiration. And what's nice about it is in particular for the CAT eight with the XTORQ, as you can see you can get out to vessel 25 millimeters in diameter.
So essentially a cava. This shows you how powerful this is. This is one of my patient's with a standard nitinol stent. A Zilver PTX was occluded and you can see how powerful this device
is with maximal aspiration. Turn it off and obviously the self expanding stent goes right back to normal. So after our results with the ALI patients, and we presented our data at the Midwest meeting in St. Louis earlier this fall,
we start looking at our DVT patients and here you can see an effort thrombosis. Somebody here. We went eight French basilic. Ultrasound guided. Put an eight French Indigo in and with no lytics,
were able to clean this out. We then went on to, I put him on a DOAC. Today I'd probably use Lovenox for two weeks. And then he went home. He's a 32 year old.
Went to Disney World with his family and then came back later on for is infraclavicular rib excision. Here's another one of my patients, Lena. She's a 19 year old who started her OPCs on the way back to Bellarmine College in Louisville.
And as you can see here, she is a likely underlying May Thurner lesion. Extensive of femoral DVT. As you look over here to the screen left to screen right, you can see that we crossed it, put our catheter up in the common iliac vein,
as as you can see we're twisting it around to get to the edges of the vessel, the whole iliofemoral system. Here's what you get afterwards. You get antegrade flow. Certainly there's no device yet that's perfect at this.
For this particular patient we gave her 14 milligrams of lytics then did our IVUS then did our wallstent. And she's done quite well. We use it for arms. We use it for legs.
We use it for filters as well as you can see here with this occluded filter. And often times the picture you're going to get is an underlying acute on chronic thrombosis here. And we later on came back and took that filter out. So I think there's no question there's less lytics with it.
Earlier this year we presented at the American Venous Forum in Tucson. Our initial experiences with vacuum-assisted thrombectomy for DVT. And what showed is that often times you can get antegrade flow as I'll show you here.
Some of them are single sessions. But more importantly just as efficacious as it is it's safe. You can see here that we had minimal blood loss, low transfusions, and here's our breakdown. As we use it for all venous pathologies as you can see.
So at the time when we looked at our first 20, you can see that there were some that were single session therapy. And that's before. We've now added the turbo pulse technique where you're going to lace it with
14 milligrams of TPA through a unifused catheter, wait 20 minutes, go around get some coffee, whatever you need to do, come back and then use the Indigo. So at the end of the day, I think as Professor Davies eluded to, there are major complications with lytics.
This is not what we need for our patients. So in 2018 we can either continue to load with dangerous lytics or minimize lytics, adopt continuous aspiration thrombectomy. It's your all's choice. So thanks so much.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- [Speaker] Thank you. My disclosures. So upper extremity dvt occurs in 4-10% of all causes of venous thrombosis. And while a minority, dvt in the upper extremity can often be caused by thoracic outlet syndrome, effort thrombosis, occasionally
idiopathic venous thrombosis. The majority is more likely related to central venous catheters, pacemakers, cancer, etc. This is some of the presentation of someone with Paget Schroeder or venous thoracic outlet syndrome, we're all well aware of this.
Some features of this can be sudden onset of pain, discoloration and some of this subcutaneous collateral veins that we note. Initial treatment of this is traditionally with venous thrombolysis. Although the results are good, this thrombolysis can
be associated with bleeding complications, potential for renal insufficiency, prolonged dwell times, and increased cost. I think it's important that this is not just a talk about a technique but a technique in the context of an operation this is soon to come.
Whether you choose to take out the rib at the same setting or you choose to delay the operation by a week or two, by and large the complications associated with that venous thrombolysis are going to come back and haunt you in the next operations. I think that's the context of this talk.
One of the risks I just mentioned about some of these techniques is, that's sort of curious to me, is the acute kidney injury after AngioJet venous thrombolysis. You see here, this paper, of a hundred patients, 50 AngioJet, 50 catheter directed thrombolysis, shows a statistical significantly
increased risk of acute kidney failure in the AngioJet group. Eight fold odds ratio. The Indigo system enables operators to remove the thrombus in a single setting, while potentially reducing or eliminating the need for thrombolysis.
This has already been discussed by some of the prior speakers, you see the different iterations first introduced in 2014. The CAT8 is the largest device and you can see some of the features of this proprietary technology with the separator and the directional sheaths that
allow us to aspirate nicely. This continuous suction you see here, can be very nicely controlled with an on-off switch that minimizes blood loss. It's single operator design, very easy to set up, hands free aspiration, a very simple set up.
You also heard just recently about the volume that can be aspirated in 20 seconds you see, especially with the larger profile devices, quite impressive amount of thrombus can be removed. Again, with the careful control for blood loss. The directionality of the sheath is also important,
and you can see some of the different directionality sheaths. Here's a couple case examples of a Paget-Schroder patient comes in with an acute sudden onset of arm pain and swelling discoloration, and you can see the penumbra device being used to clean out that vein.
This is another example, a 25-year old male with acute right arm swelling, sort of a body lifter type, and you can see here, this is the separator that's being moved forward and backwards, in and out to help break out the thrombus. This is the CAT8 device.
The pre-intervention picture seen here, we're crossing the lesion with a wire and and you can see the post-intervention on the right. You, of course, have the venous compression from the first rib, thoracic outlet, but the vein is widely open and now we can go ahead and see
the specimen that's retrieved as you've seen other videos in the prior presentations. This, of course, is what we're left with at the time of surgery. I only bring this up to remind us that there is a second stage to this treatment,
which is the rib resection. A combined experience that I just want to put together, very small numbers of course but, 16 patients with thoracic outlet who presented and were treated with the Penumbra system. You can see here, some of the demographic data.
I'll just point out the symptoms, of course, pain, swelling in these patients, imaging mostly venous duplex, occasionally CT or MR venogram. They all of course get venography at the time of procedure. The extent of the thrombus in all of them was complete occlusion and you can see some
of the extent in the subclavian axillary veins. Site of access can be the brachial or the basilic vein. The operative details as well, shown here, and I'll just point out the estimated blood loss, it can be very reasonable, especially with some experience you can sort of control that
on-off valve and minimize blood loss with this technique. Adjunctive therapies are shown here and of course, maybe because we're a little bit stuck on our ways, we did have a fair number of adjunctive lytic therapy. There were only three patients who had overnight lysis. A lot of venoplasty done at the time of the procedure.
All veins remained patent until the day of the rib resection but I will point out that one of these patients did develop a significant complication with hemothorax. This is one of those patients who had overnight lysis. And I point that out to stress that perhaps
this is what we're trying to move away from. So, in conclusion, mechanicothrombectomy using Indigo device shows promising initial results. Minimal blood loss, one complication of the hemothroax with the overnight lytics. No renal insufficiency or distal embolization.
The practice pattern, I think, need to adjust away from routing lytics to additionally minimize complications prior to surgery. Thank you.
- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,
valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction
but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique
to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the
sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness
but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have
smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.
Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse
and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap
we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid
valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility
to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put
in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction
disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.
- You already heard about different devices which can finish the treatment of acute DVT in the lab and I would like to add one of the devices which is quite widespread in Europe. And share the first study on this device. This is called the Aspirex device. So what is the objective?
Post traumatic syndrome after proximal DVT, I think that's clear. 25% of the patient are at risk for developing post traumatic syndrome. I think that is clear and some of these patient even expect severe post traumatic syndrome.
We already saw this ATTRACT trial outcome and we learned that especially patient with Iliofemoral DVT might benefit from treatment, invasive treatment of Iliofemoral DVT but of course, we need to know that is catheter-directed thrombolysis causes issues
and therefore our way should be to go away from thrombolytic therapy to a pure mechanical thrombectomy approach. This is a typical case example of a patient, 20 year old female patient who came to the emergency room with that leg on the left side in the morning,
back pain in the evening and this is clear that it is a descending Iliofemoral DVT in that patient caused by May-Thurner syndrome. So, with modern devices like this Aspirex, mechanical thrombectomy device, the 10 French device is able to aspirate up to 130 millimeter,
ml per minute of clots. You see that this can be effectively treated and then stinted within the May-Thurner syndrome within one session approach. So, but, what is clear of course that we need to get data
for these modern Mechanical Thrombectomy devices and therefore, we conducted clinical follow-up study to evaluate safety and efficiency of that Aspirex Mechanical Thrombectomy device. This device is based on the Archimedic principle which you can see here it comes with six up
to 10 French systems and with that you are able, as I already showed to sac 130ml of thrombus per minute. So these are the study details I want to show you. We treated 50 psychs, 56 patients with acute, subacute and acute on chronic which means up to 3 months of symptoms patients with Iliofermal DVT.
We performed IVIS on all these patients. We found May-Thurner syndrome in at least half of these patients as a reason for the Iliofermal DVT. You see the patient demographics. Some of the patients had even malignancy condition. A lot of patients were on oral contraceptives.
Here are the clinical symptoms within our cohort. Most of the patients came with swelling and rest pain. The rVCSS at the beginning was 4.5 within this cohort. Most of the traumatic lesions were on the left side involving even the profunda and the common femoral vein in this cohort.
You see here the excess which we used for treating these Iliofermal DVT, we used in the main part of the cohort, the left popliteal vein access or left femoral vein access. 84% were treated with 10 French system, the Aspirex device. As I mentioned we used IVIS
to analyze underlying pathologies. We found in most of the patients underlying pathologies and this explains why we implanted stents in 100% of the patients. You see the treatment duration which was in mean 94 minutes within this treatment cohort.
These are the patency analysis within one year. You see patency at 12 months, 87% percent in these patients, which we could follow up after 12 months. Here you see the Post-thrombotic syndrome analysis after 12 months so only low PTS
and some kind of moderate PTS were seen in these patients. There were no severe Post-thrombotic syndrome. Most of the patients just had a little bit of swelling after that procedure. Of course, it's important to mention safety and those end points.
There were just some small punctures associated, site being complicationS. Of course re-hospitalization is a severe adverse event which you can see here. But there were of course no bleeding events in this cohort. And to follow up
on this much more multicentric perspective trial, we just started a multicenter trial on this and we'll follow up patients up to five years within this just initiated multicenter registry. And I think we can show some preliminary data next year. Thank you very much.
- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations
related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,
and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be
a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation
of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest
as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher
patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.
The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence
that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization
versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,
in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,
one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients
who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored
superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months
for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.
But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear
to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.
Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.
- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.
You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience
the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,
as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.
If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.
We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.
Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.
No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time
of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities
and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice
In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases
due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.
We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.
So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed
with multi-institution trial and longer follow-up
- Jim, thanks so much, and thanks to Doctor Veith for the opportunity to get involved. Here's my disclosure. So, certainly you don't want to be an expert on limb thromboses, however, it happens. And so, when you see these patients, no longer are we looking at fem-fem,
or even lytics, catheter-directed lytics. So how do we get from screen left to screen right in a single session therapy? Well, as we know, when these patients present, there's several different management options. You can do open thrombectomy with or without
a fem-fem, pharmacomechanical thrombectomy. There's catheter delytic and ultrasound accelerated thrombolytics, and then now, today, we have vacuum-assisted thrombectomy, as we've heard throughout this session, or continuous aspiration thrombectomy,
however you want to mention it. Regardless, when you end up with lytics, this is exactly what you're dealin' with. You're playing with fire, and if we do it long enough, you're going to see this complication. So we've really adopted a clot extraction
instead of a clot dissolution policy at our institution. I think Jim just showed you this technique that is afforded to us by the Indigo thrombectomy system, as you can see here in a Vivo model, this catheter actually does work extremely well.
It'll remove this soft thrombus, as you can see here. My first experience with this was actually for an occluded popliteal stent, as you can see here. We had a occlusion of the standard nitinol stent. This aspiration power was incredibly surprising to me. As you can see, it collapsed the standard nitinol stent.
So at that point, several years ago, we realized how good this device was, and how we want to minimize lytics for our folks. So we started in 2014 and recently this year at the Midwest Vascular forum in Saint Louis, we presented our data.
At that time, we had 73 patients over the years with acute limb ischemia. And here you can see the breakdown. For this presentation I'm going to focus on this cohort here, which is seven. But as you can see, like my panelists here,
we use it for occlusions, for not only occlusions but emboli as well, and also we had one case of an upper extremity embolism that we were able to successfully treat with this device. At that time, again, looking at all 73 patients,
you can see here that it's a very efficacious device. There were a couple folks who needed transfusion and perhaps the blood loss was a little higher than 300. However, as you can see here, the folks who had a blood loss, all five had open adjunctive interventions as well, and the ones who needed transfusion
all had catheter directed lytics as adjunctive therapy. As far as our efficacy endpoints, what we looked at was antegrade flow. As you can see here, oftentimes with your vacuum system thrombectomy, you're able to get antegrade flow. However, intermittently there's also other
adjunctive therapies that we had to use frequently as well. Going back to what, you know, my topic for today, how do you go from screen left to screen right, where here you can see one of our patients who came in. We did a retrograde ipsilateral stick,
crossed the lesion with the wire, then we delivered our eight french Indigo catheter and were able to get, in a single session, as you can see here, antegrade flow. So here's another, all this in one single session therapy. Here's another patient of ours.
As you can see to the left, one of our Gore Excluder limbs had occluded, and again, with single session therapy we were able to provide patency to that occluded right limb. Another case here, you can see one of our other Medtronic grafts.
And what you'll see here as you're looking to the right, here we are with our eight french Indigo catheter, is the separator, which is like a pipe cleaner. And we were able to clear out this clot and provide patency to this
all in a single session therapy. And again, here you can see from left to right how we were able to thrombectomize that limb. So over the years, the last three years, we do about 80 to 90 EVARs a year. During that time period, we have seven patients
come in with limb occlusions. And as you can see here, four of them were chronic, three claudicants and one res-pain, and three of them were acute limb Rutherford one, two A or two B. As you can see here, 42% of the time for these
occluded limbs, we were able to do it with no lytics, not even a pulse spray, nothing, not one drop of lytics. As you can see here, some of them we did have to do it in a single session. What we do is use a McNamara catheter.
We would squirt out, you know, anywhere from, as you can see, 14 to 18 milligrams of lytics, go get a cup of coffee, go make rounds, come back 20 minutes later, then utilize your device. And again, you can see, in a single session therapy we were able to afford patency.
And then finally, you can see here the blood loss was minimal. So this is a safe device. So in conclusion, I think that single session therapy is safe. It can facilitate achieving antegrade flow
in the management of stent graft limb occlusions. And single session therapy is the future of not only stent graft limb occlusions but all acute limb ischemia. Thanks so much.
- Thank you, thanks for the opportunity to present. I have no disclosures. So, we all know that wounds are becoming more prevalent in our population, about 5% of the patient population has these non-healing wounds at a very significant economic cost, and it's a really high chance of lower extremity amputation
in these patients compared to other populations. The five-year survival following amputation from a foot ulcer is about 50%, which is actually a rate that's worse than most cancer, so this is a really significant problem. Now, even more significant than just a non-healing wound
is a wound that has both a venous and an arterial component to it. These patients are about at five to seven times the risk of getting an amputation, the end patients with either isolated venous disease or isolated PAD. It's important because the venous insufficiency component
brings about a lot more inflammation, and as we know, this is associated with either superficial or deep reflux, a history of DVT or incompetent perforators, but this adds an increasing complexity to these ulcers that refuse to heal.
So, it's estimated now about 15% of these ulcers are more of a mixed etiology, we define these as anyone who has some component of PAD, meaning an ABI of under point nine, and either superficial or deep reflux or a DVT on duplex ultrasound.
So we're going to talk for just a second about how do we treat these. Do we revascularize them first, do we do compression therapy? It has been shown in many, many studies, as with most things, that a multi-disciplinary approach
will improve the outcome of these patients, and the first step in any algorithm for these patients involves removing necrotic and infected tissue, dressings, if compression is feasible, based on the PAD level, you want to go ahead and do this secondary, if it's not, then you need to revascularize first,
and I'm going to show you our algorithm at Michigan that's based on summa the data. But remember that if the wounds fail to heal despite all of this, revascularization is a good option. So, based on the data, the algorithm that we typically use is if an ABI is less than point five
or a toe pressure is under 50, you want to revascularize first, I'll talk for a minute about the data of percutaneous versus open in these patients, but these are the patients you want to avoid compression in as a first line therapy.
If you have more moderate PAD, like in the point five to point eight range, you want to consider compression at the normal 40 millimeters of mercury, but you may need to modify it. It's actually been shown that that 40 millimeter of mercury
compression actually will increase flow to those wounds, so, contrary to what had previously been thought. So, revascularization, the data's pretty much equivocal right now, for these patients with these mixed ulcers, of whether you want to do endovascular or open. In diabetics, I think the data strongly favors
doing an open bypass if they have a good autogenous conduit and a good target, but you have to remember, in these patients, they have so much inflammation in the leg that wound healing from the surgical incisions is going to be significantly more difficult
than in a standard PAD patient, but the data has shown that about 60% of these ulcers heal at one year following revascularization. So, compression therapy, which is the mainstay either after revascularization in the severe PAD group or as a first line in the moderate group,
is really important 'cause it, again, increases blood flow to the wound. They've shown that that 40 millimeters of mercury compression is associated with a significant healing rate if you can do that, you additionally have to be careful, though,
about padding your bony areas, also, as we know, most patients don't actually keep their compression level at that 40, so there are sensors and other wearable technologies that are coming about that help patients with that, keeping in mind too, that the venous disease component
in these patients is really important, it's really important to treat the superficial venous reflux, EVLT is kind of the standard for that, treatment of perforators greater than five, all of that will help.
And I'm not going to go into any details of wound dressings, but there are plenty of new dressings that are available that can be used in conjunction with compression therapy. So, our final algorithm is we have a patient with these mixed arterial venous ulcers, we do woundcare debridement, determine the degree of PAD,
if it's severe, they go down the revascularization pathway, followed by compression, if it's moderate, then they get compression therapy first, possible treatment of venous disease, if it still doesn't heal at about 35 weeks, then you have to consider other things,
like biopsy for cancer, and then also consider revacularization. So, these ulcers are on a rise, they're a common problem, probably we need randomized control trials to figure out the optimal treatment strategies.
- Great, thank you Tim and Dan, and thank you Dr. Veith, this is the first time actually we're presenting this. This is work that's been done between my fellow who's really the sophisticated one with this with his PhD, Luka Pocivavsek. Here's my disclosures, Luka doesn't have any.
Really three goals in mind when we looked at this methodology to try to assess the value and efficacy of long-term durability of necks. To identify patients that are high risk for device failure, potentially type one endoleak, device migration, failure of our proximal seal zone.
This is an example that this patient will come up through this entire presentation but someone that I treated with a rupture. Initially successful result, then developed a dilation of the neck and then needed an additional procedure
to treat a type one endoleak. Second goal is maybe to look at appropriate device selection and sizing so we can prevent these complications from happening. So as an example, I'll show you this case, which for many of us is challenging
to select the right size proximal aortic endograft. You have a reverse taper of this neck, the cone, trying to figure out whether a 36 device is best because of the 32 diameter, but you're 23 proximally and maybe this technology will be able to help us identify which devices
will do better in certain anatomy. And finally evaluate the mechanisms of the interface, the adhesion that we see between the device and aortic wall for the current technology and potentially evaluate new device development. So what is this?
What we did is extrapolate from what was known from finite element analysis and this patient, as I mentioned earlier, presented with a rupture. We were able to look at her pre-rupture CT scan and with our technique predict the area of rupture
which is what we saw on CT scan and you can see this high-stress area. So we were able to define the aortic wall that was in the danger zone for rupture, and then took that analysis and started to extrapolate that understanding to looking
at the interface between the device and the aortic neck. So what we see here is post-implant with slightly challenging anatomy. A short neck, a little bit of angulation, and with Luka's expertise, we were able to really start doing
what we call this cohesive zone method and look at doing a really statistical analysis of what happens with the device and I'll show you that a little bit more. So when you look at this equation, it tells you what is the available literature
that we know for device displacement looking at the displacement of the interface of the graft to the aortic wall, and then the contact zone. And we can alter that in the computer model to change the Newton force that exists
and get a lower adhesion and then a stricter tight adhesion between the device and the wall and see the impact that has. So this is just showing you from the CT scan looking at the vector of stress and strain that we're able to look at in this model.
And then specifically what we see when there's separation of the device and the wall, there's areas that are higher strain and stress and you can see the vector differences here versus this area where there's a stiff contact and we're able to create,
it's much less and the risk of separation of device and wall is much lower. So we're able to take certain understandings and look at different geometries, change our pressurization, have the boundary conditions appropriate
and then start to really look at the zone mechanics. So what this looks like is you have two different adhesion models here. One is with weak adhesions of the device to the wall and one is where we can specifically create stronger adhesion and how this would be done down the road
would be potentially something that you could look at with device design, development, and with the weak adhesion you can see how the device basically falls out of the this challenging anatomy and with strong adhesion it does a little bit better.
There is some migration but not to the same extent. So what we're trying to predict is who has loss of seal and can we prevent this? And one of the mechanisms that we've started to look at is whether or not when you add endoanchor technology to the proximal seal zone to prevent that migration
if we can prevent this loss of seal. This is way too complicated but you get it, this is what we're looking at computationally, and this is what we see clinically. This patient who a year and a half later, develops a type one endoleak,
it's systolic pressures that are elevated, it's more extreme, and we think that there's some loss of seal that happens just when patients' pressure goes up too high. So in conclusion, we think that this is a nice extrapolation
of what we know from finite element analysis. Can be applicable to not just understanding if we've successfully treated patients but to potentially even size appropriately and evaluate new devices. Thank you.
- Thank you very much for the very kind invitation, and I promise I'll do my best to stick to time. The answer is probably to this audience I don't really need to say very much about the ATTRACT trial, but I think it is quite important to note that the ATTRACT trials have now been out for some time, and it is constantly being
talked about in its various dimensions. So I'm going to just spend a few seconds really talking about the ATTRACT trial. A large number of patients screened. One in 41 patients were actually recruited into it and it was a trial that ran for a long time.
Wasn't really with respect to the primary endpoint any particularly good evidence, but for those people who had moderate or severe post-thrombotic syndrome, it probably was of benefit. And if you looked at the Villalta score
and the VCSS scores there was some evidence to support it. So overall, probably some positive take-home messages, but not as affirmative as people would have thought. Now the reason that I've dwelled a little bit on that is that actually, what do we mean when we talk about the post-thrombotic syndrome?
Because I would say in the upper limb, because I have never personally seen an ulcer in the upper limb. Has anybody seen an ulcer in the upper limb due to venous disease? No.
So in a way we are talking about a slightly different entity. We are talking about a limb that has undoubtedly much more finer movements. And there was depression by some people with the results of the ATTRACT trial.
But when you look at the five year results from the CaVenT trial, there was some evidence to suggest that actually, as you get further out, there may be some benefit. If you look at this summation analysis, and I completely accept this is related to the leg,
again, there may be some benefit from the CDT. Now, this is a case of mine. Now I wonder if any of you can tell me how many stages may have been involved from going from the right, to having a ballonplasty in the vein. Pick a number, anywhere between five and ten.
The answer is you have numerous checks of the thrombolysis, you may have a venoplasty, you might have a first rib excision. You may then have occlusion and then realize this before you go on and do the first rib. So all I'm suggesting to you that this is not
a cheap treatment to offer patients treatment to the upper limb. Then we looked forward to some help from the guidelines. Well we look at the American guidelines and give or take, I think the answer is we probably shouldn't be doing it and that we should be only offering anticoagulation.
So do the Brits help? Well actually if you look at the Brits, it sort of says well, you can think a bit about doing decompression, but really if I was standing up in a court of law, I really wouldn't want much support from this guideline
that I had done the right thing. And then the International Society of Thrombolysis and Hemostasis really says well, you can do a little bit of this that thoracic outlet syndrome may be a risk factor. But give or take, surgeries still are a little bit dubious.
So, really there's one good review out there, and this is the review of Vasquez that basically looked at 146 articles, and they found some data on just under 1300 patients. And they postulated and chose some evidence to suggest that there was some evidence
that first rib excision and thrombolysis reduce PTS, and that anticoagulation alone was not enough for the majority of the patients. Very difficult to work out how you selected which patients you should or should not intervene on. Now, I'm sure everybody is rather sick and tired
of me talking about money, and I accept it doesn't really apply here. But money is actually quite important. Five interventions to prevent something that may not happen and at worst may be just a few collateral veins across the chest.
So ladies and gentlemen, I would want you to think very hard, is it actually cost-effective to be offering all patients presenting with an early auxiliary vein thrombosis thrombolysis, and then subsequently first rib excision? These are some of the truths, I think the answer is
it does seem to work. You do need to recognize and make the diagnosis. Usually delayed thrombolysis doesn't work, but there are lots of questions that are unanswered. And how would you defend what you have done in a court of law?
Somebody has a stroke, you then do the first rib, they get a large hemothorax, and they then die because there had been too much TPA on board. Yes, give it some thought. So ladies and gentlemen, I'm afraid I haven't actually answered the question,
but I think you need to give it careful consideration, what are the indications and merits? Thank you very much.
- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent
flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue
but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using
a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient
and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta
and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once
the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide
and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug
over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect
of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve
and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.
This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft
to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing
in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment
of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)
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