- Thanks, so we've talked about open techniques, and as Marsham mentioned, wouldn't it be nice if we could develop some type of endovascular valve replacement or any reflux procedure. There are a subset of patients that require this, as we get out in these more severe disease severity, is when start seeing more
of a higher prevalence of deep venous incompetence. This tends to be a mix of primary deep venous incompetence and post-thrombotic, which also gives you a mix of the pathology of reflux and obstruction along the axial vein tree. And really, it's to find the most critical
site of disease for repair. As you've heard, the open surgical techniques have been the mainstay now, conservative would be compression, and we're now going to talk about implantable valves. Kistner, as we know, has been the father of this,
and really, his concept has been that in the deep axial system, that we have the, really, the external iliac, 25% percent of the time, has one valve. But, in general, the iliac system is valveless. But, we're choosing the common femoral vein,
the femoral vein profunda, or popliteal, that we need one competent valve somewhere along those axial segments to get the control of venous hypertension. That's really the goal. We've heard about external repair, or reefing,
that's available if the valve is intact. However, if the valve is not intact, and destroyed, then you need to bring in a new valve, either transplanted from the axillary, or transposing from good valve, to an axial segment. And really, this has been the data with open repair.
Yes, you can get ulcer healing, but there's a pretty rapid fall off at about three to five years with all these open techniques, with valve fatigue, or scarring, or enamel hyperplasia, or thrombosis. This is really, so Dusan Pavcnik at Dotter Institute
in Oregon, has been working on this for a while, the bioprosthetic valve. The first-generation, he was using sub intestinal submucosa, which basically gave you a collagen skeleton, with growth factors sewn onto a metal frame.
And then that gets implanted, and the idea was that hopefully, it'll repopulate with endothelial cells and mimic a human valve. The problem with this one was mostly tilting of the frame in vivo.
And this is kind of what it looks like, developed, delivered through its delivery system. The second-generation valve, they worked more on the frame, and still, you know, with a prosthetic in here, you do see good incorporation of the bioprosthetic valve in a vein wall with population of endothelial cells.
They've also looked at transplanting native valve to native valve on a frame, so using jugular of one side, taking it out, sewing it onto a frame, and placing it on the other side in sheep.
And that was mixed with a variety of problems, as always enamel hypoplasia and thrombosis are the main two actors that cause these to fail. Then the last thing that I've seen, that I haven't seen any results on, was this idea of the autologous endothelial monolayer
on a valve, which, when you then put it in the circulation, then you've got flow conditions, and then you worry about the sheer and the flow disrupting the populated cells from the valve. So, I asked Tim Liem, who's,
whom you've met earlier, he's out there in Oregon, and knows the Dotter institute, and I wanted to see the fate of these valves that we just talked about, with autologous, and they've implanted some in Korea and Europe. They lasted for about three months
and they all go on to fibrose or thrombose. So, it's been a challenge with the autologous valves. We've heard about neovalves already, which again is open monocusp, and now there's an endovascular system under development, where they use
intra-vasc or ultrasound mounted on a catheter, a blade, and a balloon, to create an endovascular monocusp valve. So, that's been under development for a while. But, in conclusion, a percutaneous valve is an unmet need in a small subset of patients
who come to us with wide open deep venous incompetence, ulceration, and a miserable quality of life, and currently there's not a great option, except for open surgery, which doesn't last more than five years or so. Thank you.
- I am not Walter's enemy. I can tell you that. I am against the motion. (man laughing) I will stick to the truth, to the facts. I don't like polemic, like you. I don't like to play, let's say games
of undermining what my opponent is saying. I'm just showing what I believe in because it is the truth, okay? (quiet laughter) I have nothing to disclose. Let's stick to the definition of 'cure.'
We all know that 'cure' means 'at least one year follow-up, angiographic follow-up after the, so-called, final angiography, that shows that malformation is gone.' Call it whatever you want.
Technical success, obliterated, trombosed, concluded, ablated, gone. Then at least one year follow-up on that. Angiographic to prove it's gone. The rest is just a scale on how you can evaluate the results.
Angiographically and clinically. The only way, for me, to speak to the truth is to find in a material where there is a chance to compare.
Hat to hat. Both type of treatments. Polymerizing versus alcohol. And, the only way to find such a place is to go to Wayne's place, because he's also constantly called
talking about salvaging this and salvaging that. I am very critical about what Wayne does. You can be assured about that. He's had 16 patients, I dig out there, and polymerizing agents they were failed.
Definitely, failed. Actually, they were salvaged, by Wayne. And, I'll show that to you. These are the patients. This is the time to which they've been treated. The usual type of distribution.
Young patients. All of them extensive. There is no, for a lack of an effort. There is no, for a lack of knowing how to use
the polymer. Onyx. How we can tell that, most of those is Onyx, some of them are glue. Or a combination. The median number of sessions
with this polymerizing agent is 8.5. Range from one to thirty. The other radiologists, the other experts, besides my honorable opponent, Doctor, Professor Wolgemuth,
they also know how to use Onyx. I can assure that. Sixteen patients, all symptomatic. They are all decompensated, showing three, four tier symptomatically. They have high cardiac output,
they have required repeated, repeated blood transfusions, infections, ulcers, disarticulation. To have disarticulation of vascular malformation means, oh, horrible bleeding, infected. There is no doubt,
they are symptomatic. Couple of examples. This is a young woman, extensive AVM in the foot, type four. Been treated five times with Onyx. And they know what they've done.
They've treated well. Yet, worsening symptoms, wheelchair bound, infected ulcer. Seventy-one session. Now, pay attention. Seventy-one sessions of ethanol/coils embolization. And, this woman is now running with her friends
after her amputation of couple of necrotic toes. Not because of the alcohol. Because of the malformation. Angiographically, not cured. Example of that. Okay.
This is malformation. This is not something in a tiny, little bitty thing. It's a malformation, no question about that. Before treatment. And, this is after treatment. We can all agree that,
this is not completely cured. It is a grade three it is 80 to 99 percent still left. But, clinically, she's running. She continues to be treated. Another example.
One year old girl with bleeding malformation from the lip. Admittedly only one Onyx being used because we didn't know what to do. Luckily, the little girl was close by so she came to Wayne and after,
it's intravenous predominant lesion. It's a type two lesion. Only after a six month treatment sessions, cured. This is before start of ethanol treatment. No question there is recurrence. We can not close that only by pushing
polymerizing agents somewhere in something called 'nidus.' But if you ablate the cells, ablate the nidus. You achieve cure.
And it's cured in one year angiographic follow-up. This is time and time and again. I will show these examples. This is the outcome. The outcome tells you six cured angiographically. Eight considerably improved, they improved.
None of them is failed in this. All failed polymerizing agent treatment. Then we can move on. Complication because that's where talking about how dangerous. Alcohol is very dangerous,
but so is knife in operating room. Take a knife and stab it somewhere in some artery, or in a pressurized vein, you'll have all this blood in your face and a shoot of blood doesn't taste very good in your mouth. So it's dangerous.
But, if you use it carefully, that's what you achieve, as a result. Where do we stand with these patients? Ongoing treatment, five. Cured, five, by summation.
One still waiting for a follow-up on angiographic follow-up. Improved on watchful observation is two. Lost to follow-up because schizophrenia. Lost to follow-up because of unknown reason, after two years of follow-up.
He's been doing well throughout these two years. One clinical failure. I will tell you that Wayne have, he's seen this person. Not clinical failure. Yeah, it's clinic.
By definition, is clinical failure. Angiographically, improved. Clinically, improved. The little boy was wheelchair bound, didn't want to continue with that and, therefore, went for amputation.
So it's a clinical failure. One. To summarize that, I highlight on this, venous predominant lesions. These are the ones these create.
Type four. (man speaking off screen) Tough. Couple of examples. Striking examples. This is venous predominant lesion, IIA.
I'm sorry. IIIa, IIIb being treated. Sorry. Can we go back to that? Any way I can go back on that?
This IIIa, IIIb, there's has been five. That's moves forward. Five surgery, Onyx, anything thrown in. Extensive malformation. Shoulder, arm, a no-flow into the lower arm
because of the. And it's moving forward. I'm sorry for that. But it was cured. And there was a follow-up, too. I believe there was something.
Twenty, 15, 17 months follow-up. So we have the next patient. Thirty-two year old female treated with glue in the past.
Twenty procedure including all vessels. Everything that can not be, could be embolized, was emolized. Ended up with the worsening and this is the typical example a IIIa malformation, typical example.
This was way back in the past. This is how Wayne has developed that. It took him, I heard, nine hours and another 100 coils, but he cured that.
- [Male] 298. - Two hundred ninety-eight. This is the follow-up, you know. Eighteen months later. To summarize on that. Nothing to do with my feelings for Wayne.
Nothing to do with Walter being my enemy. (quiet laughter) No, it's just a fact, a truth. Polymerizing agents, by definition, do not cure AVMs. Do not cure.
Sometimes, when used properly, still worsen the patient's symptoms. Ethanol cures AVM. Provided that you do that with precision and skills. How you acquire precision and skills? Ask the surgeons around here.
How do they lift up this face? How Max can lift out, you know, big time metastasis sections in liver? How do you do that? With skills.
How do you acquire skills? Learn. Thank you.
- Thanks, I appreciate the invitation. MR imaging of vascular malformations poses some challenges primarily related to the heterogeneous spectrum of the lesions. The primary distinction to be made with imaging is between low flow and high flow abnormalities. This distinction, however, can often be made clinically
and so the real value in MR is in determining the malformation extent and the associated involvement of adjacent normal structures. The basic MR evaluation of vascular malformations should of course be multiplanar in two or three orthogonal planes, and in each of those planes,
there should be T1 and T2 weighted imaging. There's some debate about the value of contrast-enhanced scans. Certainly contrast-enhanced scanning will show things like arteriovenous shunting and lesion perfusion, but mostly the value of contrast-enhanced scanning
is in making the diagnosis of the abnormality rather than in guiding specific treatment. So let's talk about the various imaging sequences and go through a few examples. On T1 weighted images, we see the anatomy of the limb or of the area in question quite clearly.
But what you notice is that there's a signal similarity between the normal tissues and the adjacent malformation, such that they blend together. That means that assessment of lesion extent is poor on T1 weighted images. Now this is in distinction from T2 weighted imaging
where malformation images tend to stand out quite dramatically from the adjacent surrounding normal tissue, making assessment of lesion extent quite good, with the following caveat that on these bright water-type sequences, edema, when present, especially in high-flow lesions
or in low-flow lesions following embolization, it can result in overestimation of lesion extent. Many people routinely include contrast-enhanced imaging for malformation evaluation. I think it's probably not necessary and doesn't actually provide that much
additional information beyond making the actual diagnosis. Now that said, that's to be distinguished from dynamic time resolved imaging, which is a newer type of contrast-enhanced imaging using faster acquisition. It has what's called a higher temporal resolution and we can clearly differentiate
inflow arteries from draining veins and this can be valuable in treatment planning as well. Here we see pre- and post-contrast images and you'll notice that on the post-contrast images, there's slightly better visualization of the malformation, but the difference between the two is really modest
and probably not clinically relevant. Now that's to be distinguished from time resolved imaging, which will allow us to see arterial, parenchymal, and venous phases, and these can be stitched together to create a movie that really does look quite a bit like a catheter-based angiogram.
The difference between high and low flow malformations is primarily made based on structural characteristics, rather than MR signal abnormalities. So, low flow lesions will usually have minimal mass effect. Here we see signal abnormality with almost no mass effect. When a mass is present, it sometimes has
hamartomatous stromal elements that look like septations running through the mass. When a mass is not present, the lesion tends to be pretty infiltrative. Without any mass effect, sometimes the degree of infiltration is amazingly intimate, as in, case like this.
When we see phleboliths, which are routinely identified on radiographic images, we have confidence that we're dealing with a low flow lesion. But in fact, MRI imaging can identify phleboliths pretty consistently, and here you see they appear as rounder, oval, low signal images
on all imaging sequences, and of course, they don't enhance. Now, these findings are in distinction to high flow lesions, which demonstrate no well-defined mass ever, and in fact, if you see a well-defined mass it should make you think that you're dealing with a tumor rather than a malformation.
But they will demonstrate characteristics of enlarged feeding arteries, enlarged draining veins, and these infiltrative masses will often be riven through with multiple flow voids, and the degree of infiltration can be really, pretty impressive.
There are some signal characteristic differences between the various malformations. It's a long and involved topic, and probably something that doesn't make sense to go into here at this point, but I think the utility of MR in vascular malformations is primarily related to defining the anatomic
characteristics of the malformation, assessing what normal structures are involved or immediately adjacent, and this allows us to mitigate risk and plan the procedures. Now this is different from post-treatment evaluation of MRI, where there's definitely differences between how low flow and high flow lesions respond.
In low flow images, post-embolization we see significant signal changes. In high flow lesions, post-embolization we see anatomic changes. One important caveat to remember is when imaging and malformation within three months of an embolization,
it can be difficult to interpret related to the post-embolization inflammatory reaction. So on T1 weighted imaging post-embolization, we see bright signal, representing thrombus is the treated area as opposed to lack of bright signal, in the non-treated area.
On T2 weighted images, where the malformation generally appears bright, post-embolization we see dark areas in the treated zoned, representing scar. I personally prefer evaluating these with T2 weighted images. I think the distinction between treated and
untreated is greater and more consistent. Another example, scar forming, T2 weighted images. Again, I think the distinction is pretty clear. Although, contrast-enhancement isn't all that valuable in pre-treatment planning. Actually, can I get this video to go?
There we go. Although contrast-enhanced scanning isn't generally valuable in pre-treatment planning, there can be some utility in post-treatment evaluations. Specifically, dynamic time-resolved imaging or virtual angiography can be applicable to high flow malformations.
As you can see here, when the post-treatment evaluation and assessment of residual arteriovenous stunting is an important end point. Thank you. (applauding) - [Announcer] Any questions from the audience?
I think it's important to note, you mentioned the importance of T2 weighted imaging. And it is crucial, particularly for venous and lymphatic, or mixed lesions. But I think it's also important to state with T2 imaging, that you have to have fat suppression,
'cause fat also has bright signal and can be confused with malformation. - [Scott] Yeah, exactly, and there's really a broad range of T2 weighted images. What we rely on mostly is this short towen version recovery which,
- [Announcer] Now that's different, yeah. - [Mark] Yeah that's going to be. - I was going to write next. - [Mark] Yeah, so the, T2 fat suppressed images are, of course, critical, and should be obtained in every plane. We actually also obtain stir imaging in every plane. Yes, question?
- [Audience Member] So is the T2 full, (mumbling) what time do you need. - [Mark] I'm sorry, can you repeat that? - [Audience Member] What time do you need to continue to use of a full of T2 for (mumbling) - [Mark] Well, it depends on what you're looking for.
If you're trying to assess for complications, you can image any time. But, the challenge in interpreting is that the diagnostic radiologist won't necessarily know exactly where you've treated, and the lesion may appear abnormal in ways that aren't understood.
So, as the interventionalist who's doing the procedure, you really need to sit with the radiologist and help them understand what you did within that short timeframe. Now, if you're talking about imaging after three months, it's much easier to interpret signal changes have moderated, and that post-embolization inflammatory
phase has resolved. - [Audience Member] After two or three months? - [Mark] After three months, yeah. - [Announcer] Okay, thank you so much. - [Mark] Thank you.
- I like this title because I do think this is probably the final study we're going to see on a large scale for pharmacomechanical thrombectomy and catheter-directed thrombolysis for acute DVT treatment. These are my disclosures. So, the CaVenT trial came on the heels
of a number of smaller single center series and sort of case studies on catheter-directed thrombolysis. And of course this was a randomized study in 24 different Norway hospitals that showed a patency advantage and a reduction in PTS on both early and late term, even out to five years
in patients treated with catheter-directed thrombolysis rather than anticoagulation alone. The ATTRACT trial of course is the follow up to this study in a sense, it was a large US trial, an NIH-funded multicenter trial that used a strategy of thrombus removal with
adjunctive catheter-directed thrombolysis for acute DVT and essentially this accrued over 50 or so hospitals throughout the US. Using either pharmacomechanical thrombectomy and/or catheter-directed thrombolysis versus standard treatment of anticoagulation.
Enrollment completed in 2014 was presented at SIR and has been published in a New England Journal article I show there. Inclusion criteria essentially involved acute DVT's defined as symptomatic DVT of less than 14, or less than or equal to 14 days duration
including the femoropopliteal and iliofemoral segment and I think that's kind of important, these two locations, so you could have isolated femoropopliteal disease. Randomization was a one to one between anticoagulation versus pharmacomechanical thrombectomy plus anticoagulation
and the analysis was stratified by plus or minus common femoral involvement. So you could have a group stratified to no iliac and no common femoral involvement. The PMT treatment was basically infusion first for IVC or popliteal vein thrombosis,
but everything else was treated with an attempt at single session pharmacomechanical thrombectomy followed by lytic therapy if needed to clear residual thrombus for up to 24 hours with adjunctive measures afterward including stunting, et cetera.
No IVIS imaging or any of that was prescribed. These are the primary efficacy and secondary efficacy endpoints, and these are important, I think, because it effects the outcome of our perception of the results of this trial. The primary efficacy endpoint was a binary presence of PTS
at any time point between six and 24 months. Defined as Villalta score of greater than five or a venous ulcer. Whereas secondary endpoints were not binary so much, but continuous, so severity of PTS, proportion of patients with moderate to severe, et cetera.
And then of course there are some quality of life measures, as well as symptoms: leg pain and leg size. These are the primary safety endpoints, primarily episodes of, issues of bleeding, recurrent thromboembolism, and death. So looking at the sort of meat of the study,
or the primary efficacy endpoint, this was considered a negative trial in the sense that this primary endpoint of reduction of the incidents of PTS did not occur in those patients undergoing pharmacomechanical thrombectomy or thrombolysis, and so there's no difference
between these two groups in this regard. On an other hand, there was an unfortunate increase in bleeding risk, both early on as well as any bleeding. So early major bleeding, and any bleeding within the first ten days.
So this was a finding that lead to, or, these two findings lead to the conclusion in the paper, that among patients with acute proximal deep-vein thrombosis, the additional pharmacomechanical catheter-directed thrombolysis to anticoagulation did not result in a lower risk of post-thrombotic syndrome.
And did in fact lead to higher bleeding rates. So this is real and true, but looking deeper into the study, I would say that there are some other important secondary efficacy endpoints, and if you look at this, you see that along the continuous variables, and if you look at severity of PTS,
this was favored in the more aggressively treated arm across all time points. And so, if we're looking at degree of PTS, I think there's quite a difference. It's also true that there was a difference in leg pain severity, so subjective reporting of
pain as well as the actual index limb circumference. If you look at some other secondary endpoints, even though there was no difference in the binary metric of any PTS, across all-comers, if you looked at moderate to severe PTS, there was a significant difference, and this seemed to be more true in the patient
with the proximal iliofemoral DVT, rather than those patients with simply femoropopliteal DVT. So I think there are a lot of criticisms of the ATTRACT trial that we've probably heard and discussed. Large selection bias, large number of patients screened for those who were randomized, devices changed
over the course of time, no IVIS in the protocol, no patency assessment in majority of subjects, and probably the biggest issue is inclusion of femoropopliteal DVT, which is done largely to drive enrollment. And I would argue these issues are common to all
randomized trials, randomized trials do strike a balance between broad applicability to different patient populations while trying to still answer specific questions that are manageable. And so I think these are reasons why we have to look deeper into the trial results with some of the secondary endpoints,
rather than just focusing on that major headline. So I would say that in terms of lessons learned, the ATTRACT trial does confirm that this aggressive strategy of thrombus removal may not be appropriate for all patients with iliofemoral and femoropopliteal DVT
in part because of this increased risk of bleeding. I think this something that we know, and ATTRACT has confirmed that. Finally, this bleeding risk is extraordinarily low overall, so that makes me believe there are some patients who very much warrant it due to their symptoms
and their active status. And I do think it did show that the results in less severe PTS in those patients treated with aggressive strategies of thrombus removal. So this is what we want to avoid, a patient like this, who is very symptomatic,
very young, and very active, who has never had any discussion of thrombolytic therapy offered to him, and then referred only three months later or six months later, when there's really not as much we can do about that patient. So it's in conclusion the ATTRACT trial was well-designed
and rigorous with broad clinical scope. It confirms that decision to offer aggressive strategies of thrombus removal continue to require us to make artful clinical decisions in a patient specific manner. And I think it does illustrate that a certain subset of patients,
especially those younger active patients, probably do warrant thrombolytic therapy, thanks.
- Thanks Gustava, Fred. Thanks Frank for the opportunity. These are my disclosures. So, why are talking about aortic septotomy, and when is it necessary? It's really for treating complicated TADs with malperfusion, planning an EVAR or TEVAR when you don't have
adequate landing zones. So, certainly trying to bail out from a complication or EVAR, TEVAR. This was my first case in 2006. It was an elective case, a clot client who came with an aortic dissection.
And what I ended up doing at the time, was going from true to the false lumen at the aortic bifurcation, marching up the aorta, snaring a stent, snaring a wire from true to false lumen, and then essentially created a place where from the femoral approach, we could just apply
gentle downward traction to tear the septum. I'll show you exactly what this. The two wires come out on the femoral, from the femoral side. You essentially pull down gently and this is simply glide wire,
you could use a variety of wires. So this is something we've implemented in 2006. And of course this experience has grown. We've used it in a lot of different circumstances. Here's a completion angiogram for this case. So, what else can we do?
We can certainly do septotomies. We can put in stentgrafts or just bare metal stents to connect the true to the false lumen. The trouble with this is when aneurysms expand. These stents are really difficult to deal with.
And I'm not a big fan of putting stents in, bare metal stents across a paravisceral aorta. So, for that reason aortic septotemy is very helpful. Certainly can be used when you have infrarenal aortic aneurysms, following up with the thoricoabdominic dissections and you need
to create better landing zones. Once again, true to false lumen snare, gentle downward traction, creating single barrel lumens where you have adequate proximal and distal landing zones to obtain seals. I'll show you through a complication of a TEVAR.
Here's a patient who came in. Sudden onset chest, back pain and left foot rest pain. At the time we went in, and thought just simply getting in through the true lumen, and deploying the stentgraft all the way from the descending thoracic aorta.
From the left subclavian to the descending thoracic aorta would have been sufficient and it seemed like it was. And I think most would treat it this way. The trouble was as soon as the stentgraft was deployed, the paravisceral aorta collapsed. It was an acute dissection and now we have a very
difficult situation where the entire paravisceral aorta has really collapsed from the septum. So in this particular case, we were able to protect the celiac and the SMA with the wires that you see, where the red arrows are. And once again, put a catheter from the true to the false
lumen, snare in the descending thoracic aorta, apply gentle downward traction, to unfold and drag the septum down to the aortic bifurcation, knowing very well, as much as we were going to be able to profuse the visceral arteries, which we were able to,
we now have to deal with an occluded infrarenal aorta. And you have to be ready to do these things, especially if you are using septotomy techniques. And this particular case, we just did kissing stentgrafts, to manage this. Other scenarios could be delayed complications.
This is a patient who initially came in with a thorical dinaric dissection, which expanded into an aneurysm and underwent endovascular repair. Fairly straightforward, the coil embolisation of the false lumen. Everything went uneventful, except the patient
shows up a few days later with saddle paresthesias, bilateral lower extremity weakness, urinary incontinence, only when he ambulated. At rest, he was completely normal. This is, I think, the first case of transient ischemia and cauda conus syndrome following TEVAR.
Of course it was a daunting situation, and what we found is that the obvious dissections extended all the way to the iliac bifurcation. And this particular case, once again, going in from the right and left, true and false lumen from both sides,
I was able to snare wires and catheters into the mid aorta and you'll see this play out in the segment, and once again, gentle downward traction, create a septotomy extending to the left iliac bifurcation and to the right iliac bifurcation, and once again you see that right external iliac artery
has a prolapse septum which we treated with a stentgraft. So, there's a lot of different ways of managing these problems, and this patient's symptoms actually resolved and he recovered immediately. And I think what we need to do is be ready to deal with all sorts of potential complications that occur.
Many others have started to report on these findings as well. And obviously, there's a lot of benefit and right now, Ramon Berguer, Juan Parodi has a septotomy catheter that is currently under trial. So I think, my personal suggestions are,
this is not necessarily simple, but you have to be able to be ready to deal with all potential complications if you do aortic septotomy. And it is a very useful technique in managing complex aortic dissections.
Frank, Jackie, and the team, thank you very much. We love being in New York City at this time.
- Thank you, Mr. Chairman. Thank you, Dr. Vieth for the kind invitation to be here. My disclosures, so Angiotomagraphy show us zoozataous To choose the better approach our technical approach to our patients, length, diameters, localization of the aneurism sac, so neck diameters less than 4mm suggest us
that no adjunctive technique could be necessary only embolization. Dome-to-neck ratio less than 1.2 suggest us that stent-assisted technique or remodel technique with balloon probably will be necessary as we do prefer our technical approach so is general anesthesia
to get a panea to get a nice image transfemoral or transbraquial says transaxial says covered stents after heparin initial aortogram to do super selective catheterization of our vessels in coaxial technique to do super selective catheterization
to get the vascular disdel belt road-mapping and scaffolding technique to do the compactation of the coils. Dual Antiplatelet Therapy 5 days before the procedure so the goal of the treatment is to prevent aneurysm expansion by excluding
it from the arterial circulation, saving branches, patency, and freedom from rupture. The radial shows the stent in red deployed, and the microcatheter inside the aneurysm sac in this Intraparenchymal Aneurysm The CT control.
So the materials that we use when necessary The enterprise, solitaire stents, detachable coils-axium 3D to get more volume inside the aneurysm sac and solaris as a new Brazilian stent graft. Another case to explain Intraparenchymal Aneurysms to treat distill one the stent are deployed,
the microcatheter inside the aneurysm sac the stent avoid migration or animation of the coils that's a nice compaction. So the prosmo one Same technique and the normal flow to the spleen. So in seven years, we treated 26 cases
in 21 patients electively. Coiling alone in 65% of experience in wide-neck case coiling with stent, 25% and balloon with remodeling technique in 10% as we are doing more nowadays. Follow up 1-3-12 months with ourdoplar
To show us aneurysm exclusion. So are main results are complete regression of all aneurysm sac, with no evidence of recurrences up to now. No deaths, no secondary interventions and 1 Retroperitoneal Hematoma, our major complication
threethirty consecutively. You use covered stents when we have large arteries, notruousity, youresilitus mojor impact, stent graft available now visible so in this case a large right renal artery aneurysm is treated with covered stent with a nice result.
Another case, you can see the exclusion of the aneurysm sac in the basilar branches. Superormedial aneurysm case is treated with multilayer, the final result show a exclusion of the aneurysm sac and the patency branches inside of the device.
So in conclusion, ladies and gentlemen it's a feasible, safe, and should be done with low risk in our opinion. For the treatment of visceral artery aneurysms planning is necessary to get positive result individualizing all cases.
Endovascular treatment is the first line of option in our opinion to treat our patients, but don't forget we are vascular surgeons and if there are technical or anatomical restrictions do open access those publications about these issues, thank you about your attention
- Just going to do a little bit of a deeper dive into the types of nutcracker syndrome. I think most everyone knows this one. The anterior nutcracker syndrome in which the left renal vein is compressed as it passes between the aorta and the SMA, and this is definitely the most common
and certainly the most written about, but there's also posterior nutcracker syndrome in which there's a left renal vein which is retroaortic, and in this case it's compressed between the aorta and the spine, and then even more rare is the atypical nutcracker
in which there is a truncular vascular malformation trapping the left-sided IVC and renal vein between the SMA and aorta. Why do I mention these? I mention these because they inform the decision for open surgical repair when necessary.
All treatment options for nutcracker are directed to reduce venous hypertension, and we have the generally armamentarium of vascular procedures as I've listed here. Today my task is to discuss the open surgical options and really the two most important ones
are the versions of left renal vein transposition that I've listed here and have been discussed by Dr. Gloviczki and then gonadal vein transposition which, in our institution, is preferred if the anatomy is suitable. So since I'm following Dr. Gloviczki
I had to list all the papers from his institution, but this is the one that's most (mumbles) to my talk. This is their experience with left renal vein transposition versus conservative management in 23 patients, about 50/50, and what they found, if you look at their results and the characteristics of the patients that they treated,
were that if they selected their patients well, and by that I mean patients with appropriate anatomy and appropriate symptoms, they had excellent results when using left renal vein transposition to treat nutcracker syndrome. This is the other manuscript that Dr. Gloviczki mentioned,
so this is a version of open repair that includes stenting plus left renal vein transposition with suturing the stent in place that I think they hope will deal with the issues of migration in renal vein stenosis. So far their early results are excellent.
And then this is a meta-analysis, also mentioned by Dr. Gloviczki, and one of the elements of this meta-analysis was a surgical arm, if you will, although it wasn't really an arm since it's not a study, but they describe those patients
that were treated surgically. So what did that look like? Well in this meta-analysis they found that open surgical approach was associated with resolution of symptoms in the majority of patients, there were very few complications,
no renal failure or mortality, few postoperative complications in this manuscript as well as in our experience. By far (mumbles) the most common postoperative complications are ileus and hematoma, and freedom from re-intervention was fairly good.
75% at a year and 70% at 12 months. So with regard to surgery, I think the selection of the surgical approach needs to based on the patient anatomy and the patient clinical characteristics. Ideally, master all techniques
so you can offer all of them to the patient. I'd like to highlight my favorite operation for this condition which is gonadal vein transposition. I'll go over how to do it in just a moment, but the idea is that you transect the gonadal vein. You mobilize it completely from
the pelvis to the left renal vein, and you transpose it onto the inferior vena cava, and this both achieves a decrease in pelvic hypertension and it decompresses the left renal vein beautifully but doesn't put the left renal vein itself at risk for thrombosis.
It also, which is important in young people, does not require a great saphenous vein harvest which sometimes may be necessary in certain versions of the left renal vein transposition. So here's the technique. You make a mini-laparotomy,
do standard retroperitoneal exposure, mobilize the gonadal vein, and implant it onto the IVC. Here is a case of posterior nutcracker syndrome. You can see that renal vein transposition would be really hard here. There's the gonadal vein.
This patient was successfully treated, and then another patient with atypical anatomy who was successfully treated with a right gonadal vein transposition, and we actually wrote this up in case reports. So lastly, I just wanted to quickly review our experience.
We've done 15 gonadal vein transpositions. We've had excellent success, 100% technical and 93% clinical. The caveat with that is we have a really short follow-up, so it's hard to say yet whether we'll have the problems with clinical recurrence and restenosis.
So in summary, I think we are waiting a good renal stent, but gonadal vein transposition currently, I think if it's a large gonadal vein, is the treatment of choice if you're going to go this surgical route. Thank you.
- Thank you Lowell. - Good morning, and thanks Lowell and Jose, for the invitation to come back this year. I don't have any disclosures. Well, what we're going to talk is imaging the female pelvic veneous system. And the female pelvic venous system is a complex arrangement
of four interconnected venous systems, and really you have to understand the anatomy to understand the keys to imaging it and treating it, and that's the connections between the renal vein, both the left and the right ovarian veins, the tributaries of the internal iliac veins,
and the superficial veins of the lower extremity through the saphenofemeral junction. And central to all of this are the tributaries of the internal iliac vein. Which functions as a gateway between the pelvis and the leg, and really are exactly analogous to perforating veins,
connecting the deep veins of the pelvis to the superficial veins of the leg, and you have to have an intimate knowledge of this anatomy both to image it adequately, as well as to treat it. So classically, the internal iliac vein is thought as the confluence of three tributaries.
That is, the obturator vein anteriorly, tributaries of the internal pudendal vein, sort of in the middle of the pelvis, and the superior and inferior gluteal veins, and these communicate with the legs through four escape points
that the anatomists describe anteriorly as the obturator point or the "O" point, where the round ligament vein comes through the abdominal wall, the "I point. And medially in the thigh, pudendal or the "P" point, and posteriorly the gluteal point,
which communicates both with the posterior thigh as well as with the sciatic nerve and gives rise to sciatic varices. (coughs) From our standpoint today, I'm more interested in atypical, varices, that is, pelvic source lower extremity varices,
arising from the pelvis, anteriorly for the obturator vein, and from the round ligament vein, which communicate with the vulva, branches of the internal pudendal vein, which communicate with the perineum, and the medial thigh, and posteriorly, with branches of the superior and inferior gluteal vein.
So as far as imaging goes, we're interested primarily in two clinical scenarios which the imaging requirements are somewhat different. That is, atypical pelvic source varices without any pelvic symptoms, and atypical varices with pelvic pain, and the way that we study these with venography
are quite different. Although some people do pursue blind sclerotherapy from below, I do think imaging with venography adds substantially to both the control of the sclerosant, as well as how thoroughly you're able to embolize the pelvic tributaries.
And I personally like to do sclerotherapy of the varices with venography, and use direct puncture venography using either a 23 or a 25 gage butterfly needle, that's placed under ultrasound guidance. Contrast is then injected to calibrate both
the variceal bed as well as to track the tributaries, as I'll show a minute, up into the pelvis, and usually you can embolize about to the level of the broad ligament. Simultaneously, foam sclerotherapy is performed, using a combination of Sotradecol,
and Ethiodol as a contrast media, and then is followed both by Flouroscopy, using a reverse road mapping technique to subtract the bone and other things out, and follow the contrast through as well as with ultrasound as shown here.
And just as an example, here's some vulvar varicosities, that communicate both with the obturator vein up here, with the round ligament vein through the "I" point, as well as with the saphenofemoral junction here. And although you could do this blindly, I do think you get a much better understanding
of the anatomy and the volume of sclerosant required, doing it with venography. These are posterior thigh varicosities, that communicate through the "G" point here, and you can actually see the contrast refluxing into the inferior gluteal vein shown here,
and all of this can be treated with sclerosant. The second clinical scenario, is that of atypical varices with pelvic pain, in which case you do want to make sure you treat the pelvic variceal bed completely. And for this, the venography techniques are
balloon occlusion venography performed from above. My preference is right internal jugular vein approach, because it's easier to place the occlusion balloon into the right and left internal iliac veins, which a sequentially selected, and then I use a Berenstein occlusion balloon
and then place it just below the confluence of the internal iliac vein and the external iliac veins, inflate the balloon, inject contrast, which both blocks antegrade flow, and allows reflux into the varices. Most of the time you can't see these varices if you don't have an occlusion balloon,
and then as you see the varices, sequentially select more distal tributaries with a glide wire, put the balloon down, inflate it, and perform sclerotherapy and occasionally, depending on the size of the vein, use coils if you need to. Here is an example of the balloon
in the internal iliac vein, you see the "O" point. We've already sclerosed the contralateral obturator vein, and you see this classical obturator hook here, which is classical for the obturator vein. Here the occulsion balloon is in tributaries of the internal pudendal vein,
you see it communicating through the "P" point with varices in the medial thigh, and then with the great saphenous vein here, with a type two junction. Here the balloon is in the inferior gluteal vein. You see communication with the "G" point here,
as well as communication with sciatic varices, this classic horsetail look shown here. So in conclusion, understanding anatomy is critical to the treatment of pelvic venous disorders, you do clearly have to understand the anatomy of the internal iliac vein, as well as the escape points,
and vary your venographic technique, based on the patient's symptoms. Thank you very much.
- Thanks very much Ali, and good morning. Kommerell was a German radiologist who made the first clinical diagnosis of this lesion in 1936, however, anatomically the existence of this anomalous right subclavian artery was first described
in the middle of the 1700s. One can see in some cases where these lesions attain a very large size why as they course behind the esophagus swallowing difficulties can be a prominent clinical symptom. The abnormal course of this vessel
is behind the esophagus in the vast majority, about 80%. Between the trachea and the esophagus, in 15%, and in front of the trachea occasionally, 5%. The diverticulum is a remnant of the embryonic dorsal aorta and it is always, by definition, associated with an aberrant subclavian artery.
One cannot exist with the other. To take home this is the easiest, best way to remember on these things. There are essentially two types of comorals. K type one is the one associated with a normal anatomy, aortic arch but an anomalous,
a bearing right subclavian artery. In the endovascular era it is relatively straightforward to treat this. As you can see they are excluding from within the aorta with an endograft and closing off the subclavian artery
beyond the diverticular, either surgically or endovascularly. A new iteration that is quite interesting to me, and we've had an opportunity to use it once, is Mario Lachat's periscope technique that actually can be used very well anatomically
from a transfemoral approach as you can see for this configuration. Comoral type two is a different animal altogether. Associated with a totally abnormal anomalous aortic arch anatomy, so-called right-sided, or right side aortic arch.
More rare certainly than the type one. And this is complex of course, but it is a type two, right-sided arch that we see with certain regularity than the one that we are talking about and usually associated with the comorals diverticulum
associated with a bearing left subclavian artery in such a case. It is amazing that almost every time we have seen a case like this the anatomy is essentially identical. This is the configuration that we see
on a regular basis. We had an opportunity to treat about seven such cases between the two in the last decade. And this is a good case in point, a patient presenting with a very large comoral type two. A cardiothoracic surgeon had attempted to approach this
from a right thoracotomy approach six months previously. Not clear what his thinking had been but thank goodness he bailed out before doing too much damage or killing the patient. He recovered from that.
We treated him. Here's the anatomy by the way which again is extremely consistent in everyone of these cases. Almost always almost identical to what you see there. K type two.
We treated this in a staged fashion. One of the main difficulties in dealing with this endovascularly is that invariably the aortic arch is sharply angulated so navigating and deploying things across that anatomy can be difficult,
- I try to dissect this convoluted title into two questions, basically, when is endovascular treatment of post coarctation aneurysm best, and when is an open surgical intervention required. A couple of years back in time, we looked at predictors
of aneurysmal formation in patients after surgical correction of coarctation, and we found essentially two predictors, which is previous surgical patch repair, and the age at the surgical repair, as predictors for the evolution of
a post coarctation aneurysm. In other words, these two predictors could actually become important for the selection of patient for open surgery. I come to this in a moment.
A year later, we could publish the feasibility of percutaneous endovascular repair of those post coarctation aneurysm, post surgical aneurysm, easily by a customized
or off the shelf stent graft. So that is basically accepted in the community, and reflected in guidelines, that basically come to the conclusion to the question, when is endovascular treatment
of post coarctation aneurysm best. In the case of a risk-benefit ratio high for open surgery, which is in case it's a redo surgery, of course, in presence of extensive collaterals, with a significantly increased bleeding risk,
adult patients above the age of 13.5 years, according to the statistical analysis, and when end to end anastomosis is not feasible, and of course, patients need to be suitable for an endovascular approach.
Patient preference may play a role, most recently, and of course, is conclusion of endo first should be executed in dedicated centers that have options to treat the patient even openly.
The second part of my title, or the second question is basically to the preferred use of open stents or covered stents, and in order to show our recent analysis on this, I had the privilege to compare
a group of patients from my previous institution that used self-expanding open stents, and with my current position in another place, that uses CP stents, or covered balloon expandable stent grafts
in the setting of coarctation as the first and only option. So we have no data from two different hospitals that show similar patient sets, a total of 52 in each group, that do not show any demographic differences
over a time of 10 years, collected over 10 years. Clinical presentation of comorbidities are essentially the same, so we're dealing with a comparable set of patients
and two different concepts of treating primary coarctation. The post interventional vascular events are also similar, no significant differences between the two concepts from two different sites,
with a trend towards more re-stenosis in the setting of ballon expandable stents being used as the first approach, but not significantly more. Even in hospital complications, comparing these two groups of 52 patients,
age didn't show any significant difference, with a trend for longer hospitalization in patients treated with the CP stent or covered stent. Maybe this is only a coincidental finding and a more cultural event
rather than medically driven. If you look at the outcome curves between both groups, with no mortality in either group, there is a similar shape of the Kaplan-Meier curves
over up to 90 months, with an interesting difference in the first post interventional phase, with three asymptomatic localized dissection in the balloon expandable stent graph group, however, no significant difference over time.
This next slide summarizes the ballon expandable procedure with the CP stent. After obtaining lumen and connection between this ectatic aorta, it was possible to stent the segment
with a covered CP stent very nicely. You see the result on the lower right corner. The other concept is a bare self expanding Nitinol stent placed first after recanalization of the coarctation and then potential post ballooning
to obtain an appropriate dimension and the lumen. In summary, comparing those two approaches and answering the question, when is an open operation still required, I think it's fair to say that in adult coarctation,
and endo approach should be chosen first, and bare, self-expanding Nitinol are relatively safe as a concept, and durable solution, without the risk of side branch obstruction, whereas covered ballon expandable CP stents
are also safe, and offer a durable solution, but have to respect the LSA anatomy. An open surgery I think should be reserved for infants and children younger than 13.5 years, only in view of an end-to-end anastomosis.
Thank you very much.
- Thank you so much. Seattle, like many other cities in the U.S. is facing a terrible, heroin epidemic crisis. We are the safety net for these patients. I was honored, when I was asked to came and share with you how we manage these patients at Harrow View Medical Center. Over the last few years, we have educated our ED doctors,
in order to avoid over-head page to vascular surgery. That they don't do any I&Ds at the bedside. If a patient with a history of IV drug use present with induration or pain on the groin. On those patients, they get triaged for sepsis, they get an IV access, can take some time.
They take labs, including blood cultures. If we can, we do ABIs, this is during the day, and we start the patient on broad-spectrum antibiotics. After that, the patient goes for a CAT Scan. The CAT Scan is really useful for us, it help us not only see the anatomy,
see if the cell is coming close to the external iliac or close to the bifurcation. But maybe even more important, it help us, and you can see the upper emissions, find a lot of needles that have broke and left over by the patients that --
It's a huge hassle for your team in the operating room. So once we have the CAT Scan. We go to the operating room, we get the patient under general anesthesia, we puncture the contralateral side, and this is our preferred method to
take care of this patient. We go up and over, we put the sheath at the end of the external iliac artery, we give some heparin, we do an angiogram that shows exactly where is the injury and we put an occlusion balloon,
usually like a 7 by 60 does the job. Once we have the ballon, we can then ride directly in the pseudoaneurysm. When you open, you take out all the clot and puss and all that tissue. And once you irrigate and debride,
you will see at the bottom, your wound. Usually you see the balloon inside the artery, with a rupture wall, and the proximal ends of the artery. So what we do with with arterial ligation, we resect to help the artery until we gain control, we paralyze vessel loops, remove the balloon
and we do the ligation both the stems and usually we try to preserve the bifurcation. It is a long puncture, it's not possible, we try to preserve our zincuflex, so the patient will have a collateral pathway to their leg. After that, we try to approximate the tissue on top,
or we do an sartorius flap. Now our patient that use black tar heroine, sometimes there's too much inflammation, too much puss, we just put the dressing and we come back in a couple of days for a wash out, to take care of the wound.
After that, the patient goes to intensive care unit, and you will notice that I didn't mention, we ever raise the foot. We don't put any pulse oximeters or do any studies. The foot is going to be okay. The patients usually have some kind of chronic compression
previously and they will tolerate ischemia pretty well. Patient goes to the ICU and the first thing that we do, we avoid hypotension, but we call ID and Pain Service. This patient's outcomes are going to be better if the pain is going to be well controlled, because they will be compliant with the treatment.
ID recommends that antibiotics treatment and helps with management other comorbidities. I know we're starting to have a lot of patients that have PE's during admission, so we try to rule out DVT study and we'll start the patients in treatment.
When we look at our cases, we have more than 50% patient that present with bacteremia, and of those, almost 40% was due to MRSA, so it's a very severe condition that the patient require several weeks of IV antibiotics. Post OP ABI, immediately,
we have a median of 0.41, so the leg is viable. And our amputation rate for these patients is very low. We have only lost 4 legs and of those 4 legs that we have to amputate, 2 patients we revascularized the immediate post-op period and both were infected.
So we actually avoid actively doing revascularizations in the accurate period. In conclusion, the vascular emergencies due to IV drug use are increasing and we as vascular surgeons should be prepared to deal with this and educate our colleagues
on how to treat them. Femoral artery ligation is well tolerated and we recommend not performing an immediate revascularization. The amputate rate is low and ID and Pain Service collaboration is essential for these procedures. Thank you so much.
- Symptomatic post-thrombotic disease affect at least 30-50% of patients with deep vein thrombosis. Regular wearing of individually selected compression garments with regular follow-up alleviate symptom in many patients. However, compression therapy doesn't eliminate chronic structural post-thrombotic changes,
implies lifelong treatment, ineffective of many cases, and low overall patient compliance remain a serious challenge. Raju S. Et., alia Asia. Percutaneous balloon angioplasty and stenting of iliofemoral venous segment have recently improved
the outcomes for patients with severe PTS, related to venous outflow obstruction. Postinflammatory vein wall remodeling and destruction of the venous value is considered to be the morphological substrate for PTS. Auto transplantation of valve-containing venous segment
demonstrated good five year results of half of patients, 50%. Maletti., Perrin., 10 years ago. However, there is currently low correlation between hemodynamic effect and clinical success of deep vein surgery in published literature.
The main goal of this study is to develop a novel surgical technique on venous neo-valve formation to correct deep axial reflux and improve venous outflow in post-thrombotic disease We perform the first series of in vitro experiments
using methods of mathematical modeling to develop a novel surgical technique on venous neo-valve formation. Five macroscopically intact common femoral veins were taken out autopsies from individuals without history of venous thrombosis.
And five common femoral veins were taken off autopsies from individuals with PTS. It was very difficult. The surgical technique involves complete transection of the common femoral vein, eversion of the proximal end of the vessel
with simultaneous endo-phlebectomy and creation of neo-leaflets from the inverted vein wall by interrupted sutures. Transection of the femoral vein and eversion of the approximal end of the vessel. During mathematical modeling appropriate dimensions
of the neo-valve were determined to resemble morphology of a native valve. An optimal vein wall thickness for neo-leaflets was determined to enable appropriate elasticity and coaptation. The hydraulic probe demonstrated good competency
of the neo-valve at 1.5 atmospheric in vitro. The absence of outflow obstruction was predicted as less than 20% stenosis during the maximal valve leaflets separation. In conclusion: A novel experiment model was autologous deep
venous neo-valve was created and evaluated in vitro. In vivo experiments to evaluate hemodynamic effect, thrombosis risk, and long term hemodynamic effect. Thank you very much.
- Alright-ey, hands put up. Who is for Onyx? Put your arms up. - [Male Audience Member] Who supports the Onyx Motion? - Onyx Motion, that's correct. He should've gone to law school. Who supports the alcohol motion?
Who supports the motion in the ocean? Alright, thank you I think we covered a lot of territory today. We want to have theses things and we are so glad that everybody came. I think this is Tony's first time,
Walter's first time here, Loronze and we really learned a lot today. I'm really glad Pletio Rossi was here because without him and his development of selective catheterization, I mean where would we be
sticking needles in every artery like that, trying to do angiograms, much less advanced sheaths or anything else. Pletio was wonderful having him here, one of my hero's. Anybody like to say anything?
Anybody got any questions or anything? - [Female Audience Member] The HHT scientific meeting's in June in Puerto Rico if you want some more good-- - Do they have electricity there yet? - [Female Audience Member] I hope so, I knew it looked nice before.
- Oh, okay, okay. Alright, well thank ya'll so much and we'll see you next year. (Clapping)
- Thanks again to the organizing committee for inviting me. There has been an extensive session this morning on ascending endografting. I think almost everything was said and will be repetition, but we'll still do so. What we learned in ascending endografts is that post surgery legions
are probably the best indications when we have pseudoaneurysm or bleeding in the ascending. Type A dissection is a rare indication, and ascending aneurysm actually doesn't work very well due to the fusion form type of these anatomies. Our experience is lended to 24 cases until 2017,
and you will notice that most of those cases were emergent, they were usually referred by a cardiothoracic surgery to our unit in order to treat those patients in a rather emergency situation. And in these cases we have mainly taken transfemoral approaches,
but you see that from transapical and trans subclavian also have been applied. There's some significant mortality tied to this treatment option, and this is due to the emergent character of the treatment. There were a lot of, a few type A dissections,
ruptures, bleedings, et cetera. Our device of choice has been the cook ascent device, which has been first published here, to be used in acute type A dissection, and is not current, not commercially available. We've also used a lot of customized grafts,
which is especially helpful when you need to tapered graft with a different proximal and distal diameters, and there you can use tapered grafts and just cut them to length that is, that fits well. There have been reports with these kind of customized
or off the shelf grafts that are commercially available, and trimmed to the length that is needed and experiences have been mainly very good. Main issue remains in over sizing and that is especially an issue because the type of CT for which they,
which is used for measuring the aorta is quite different. You need to know whether it's native or its graft, its gated or non-gated, systolic, diastolic, gated CT, the age and blood loss play a role in the pulsatility of the vessel, but generally I would like to say
that 20% over sizing's probably the right number, and this is mainly due to that already the pulsatility of this area of the aorta is, within 15%, relatively high. This is a case with the type A aortic dissection, you see that at the greater curvature, how the contrast goes into the dissection.
There's a cook ascent device that is delivered from transfemoral route, and you see here on the completion angiogram it looks quite nicely sealed, but what you also see is a problem that we frequently see is that the bare struts go into the valve
and cause a valvular insufficiency in this patient, so the patient required a TAAD that was done transapically, but the target valve did not stay where it was suppose to so it needed to be snared into a better position, and then again treated with an ascending TEVA. This time from the transapical
because we already had that access. And when this was done the patient could receive his, um, let me go back. Could receive this uh, Edwards, uh valve. Just to show you
that you can put a lot of these materials into one patient and maybe he would have been better off with open surgery, but I'm sure there was a reason why he was preferred for endo treatment. One of the big issues is inner curve apposition,
because the device is proximity, quite often not perpendicular, what is necessary in order to give them the radiant force to seal. And you see this from the, come picture this, images I got from other colleagues,
are about the Gore ARISE Studies. And what Gore is, um, is uh, is using here is a mechanism to meet this problem of the inner curvature, which I think is very helpful. We've been doing similar,
and been presented here ten years ago at the Veith-Symposium. We called it in situ bending, a bowden-cable principle to shorten the curve, the inner curvature. Medtronic has been working, Ali Khoynezhad is in the room.
He's been doing the physician sponsored IDE trial on this with really good results, and we hope to hear more from him. But if I look at the images, there's also the same issue of perpendicularity of the device, the approximate part,
and you see the same in other publications. Here from us, and again you see that the devices don't really deploy well at the inner curvature. I think I jumped over this case, which is about a transapical bridging stent,
because I have run out of time, I apologize for that. This is also imported for Martin Czerny, who has been on the podium showing today, the combination of Bolton NBS ascending graft, because its really what we need
in order to treat those patients, in order to get a safe landing zone. And to summarize, in my belief, the endovascular treatment of the ascending aorta is already beneficial in selected high risk patients, and those surgery lesions are the best aneurysms
will not work without having a valve attached to the ascending graft. Transfemoral delivery may not be the right route, in my belief the transapical was much more promising, and we see a significant process in the device development. Thank you very much.
- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification
for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,
also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of
a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,
and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct
arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,
and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding
the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,
mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from
multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views
on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied
by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?
IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.
This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way
to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,
but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.
Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?
And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,
the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.
So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.
Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.
So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,
and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described
in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,
so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example
50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System
is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.
Thank you very much.
- Folks always ask if you can do saphenous vein ablation in the presence of Deep Venous Obstruction. So, we'll talk about that a little bit. So, deep vein thrombosis, as we know, acutely, the danger, or the pulmonary embolus
is what we worry about anti-coagulation is the standard for that, but the longer fate of a DVT may be the post-thrombotic syndrome of which this is from scarring and valve damage, as we know. Mark Meissner showed us in this study back in '97
that more proximal DVT, femoral DVT fares worse than calf vein DVT as far as symptoms, and that goes out to about four years in this study. And we know that the worse actor of all is probably ileo femoral DVT,
so the more progressable the deep vein thrombosis, the greater the obstruction, the greater the symptoms. So, I always show, I like this study by Lois Killewich that she did back in 1989 basically showing the recanalization of deep vein thrombosis on a timeline.
And the message here is, that around three months, 86% of the recanalization has occurred. So, that's kind of my trigger as far as the earliest that I would even consider doing intervention on a post-thrombotic, would be at least three months to allow recanalization to occur.
We know that folks with, post thrombotic folks, do worse as far as receipt scores at five years if you compare primary deep veinous disease with post thrombotics, the post thrombotics fare poorly. And that's really the rationale between these
clot removal strategies in the ileo femoral segment to try and mitigate post-thrombotic syndrome. So, when you have a patient in front of you, the way I kind of line these things up, there going to be either obstruction dominant or reflux dominant.
You're not going to get a limb assymetry. A big, you know, one leg just clearly, larger than the other from saphenous vein reflux. It's just not going to happen. So, if you got true limb assymetry, and a saphenous vein that's 10mm and incompetent,
you're not going to improve their limb assymetry from saphenous vein ablation. So, you got to look at your indications. This patient should be looking for something ileo femoral that you can stent, but I don't think the saphenous is going to be much of a contribution.
The other thing, these folks don't have a lot of vericose veins they have more advanced skin damage. Whereas with reflux dominant, saphenous vein incompetent patient will usually present with vericose veins,
they won't have the limb assymetry, and that's why the C-3 gets a little hazy. It's swelling from superficial vein disease. It's usually just some fullness in the malleolus, maybe around the ankle, but you're not going to get full-blown edema
from saphenous vein incompetence. So, know why you're doing saphenous vein ablation. Not all refluxing saphenous veins need to be treated. Can you do saphenectomy in the presence of deep vein obstruction? We've shown this before.
This old Raju study that he did saphenectomy stripping in two groups, those with and without previous thrombosis, and they both did fairly well, did not seem to be impaired by the presence of obstruction.
This study by Puggioni on RFA ablation. She looked at some patients with DVT in a larger group that were all treated with RF ablation, and the bottom-line of her study was that RF ablation in patients with previous DVT is safe. Again, I wouldn't do it until after three months.
Does prophylactic anti-coagulation have any effect on post-thrombosis rates after saphenous vein ablation? Well, not in the study by Knipp. They used low molecular-weight heparin in folks going saphenous vein ablation, and it just increased the risk of bleeding,
and it had no effect on thrombosis. Can you do combined iliac vein stenting and saphenous vein ablation in the same setting? This is another iconic study by Neglen showed that, yes, you can. Patients with advanced disease
that underwent iliac vein stenting and saphenous vein ablation in the same operation had good symptom relief and very few complications. So, in conclusion, saphenous vein ablation may benefit
patients with previous DVT. Clearly, you're not going to do this in the acute phase of the DVT. When is it safe? I'd say the earliest you would do it, or even consider it is three months
because that's when recanalization starts to peak out. Limbs with concomitant superficial vein reflux and deep vein obstruction can be safely treated by combined treatment, at least in the Neglen series, and the DVT prophylaxis should be
administered at the surgeon's discretion. Thanks.
- This, yeah, I'm not quite sure why I seem to always get this talk. Maybe its because I do have more screw-ups or just show them in a more ridiculous fashion. There's no significant disclosures relative to this, apart from the fact that I'm seriously embarrassed. I'm actually not going to talk about stent migration,
because in the last year or two there's an absolute epidemic of stents being reported in the right atrium, pulmonary artery, floating in the IVC. In one state alone, there's been a 10,000, sorry 1,000% increase in the amount of venous stents placed in the past year,
or past two years. So that is somewhat worrying to me. I'm frankly amazed when iliac stents migrate and I'm always amazed when renal stents don't migrate. And there's a nice image of an echo of, I think that's a wall stent in the right atrium.
That heart doesn't look so good. And here's one being fished out very cleverly out of a pulmonary artery. How they ever got there is kind of amazing. I think patients either with no stenosis or totally mis-sized stents were being used.
No, I'm going to talk about something even worse, and that is, not worse in terms of patient outcome, but it is more embarrassing. So typical patient that we see who was managed conservatively with an iliofemoral deep vein thrombosis and presented about nine months later
with weight gain, venous claudication for which we have no objective measure. But no ulcers and no visible post-thrombotic syndrome. And for reasons that known only to myself and I don't know why I did it, I decided to go up and over from the right groin to try and cross
this left iliofemoral venous obstruction. And I'm not sure how well it projects, but essentially we're getting a TriForce Cook device and a roadrunner wire down here, and in due course we crossed the lesion, and we did a videogram And that looks pretty good.
And so we go on, pardon me, I'll try and go on. And this is a venogram from an oblique view. And again, nothing difficult about this. This is all fairly straightforward. We do a balloon dilatation and there is our final completion stent.
And I'm feeling fairly good. She was feeling quite uncomfortable because the urethral catheter we had difficulty getting in and it's possibly a little bit not concentrating hard enough on that. And so I saw the next day as per standard practice
and was doing my ultrasound. But her leg clinically hadn't improved much at all. And I was, I just wasn't happy with the ultrasound. There wasn't, I couldn't figure out exactly what was wrong. There was certainly flow in the stents and there was flow below.
But it just didn't look right. So I did a CT and admittedly there is a radiation cost here, but just we'll have a little look at this and, yeah, okay. So we'll look at that again, because it isn't quite humiliating enough the first time around. Let's just concentrate just in here, um, yeah.
This is one of these unusual Irish patients where the femoral vein in fact passes posterior to the inferior pubic ramus, otherwise known as the obturator vein. Somewhat embarrassing, and on a sagittal reformatted, it looks just even that bit better. So, you can see it coming in beautifully,
right out the back here. So she was actually incredibly cool about it, I just said, you know, I've screwed up and we've made a mess here. And that's a single shot of it there. You can see that I've placed it into the obturator vein.
And, so then at that stage I go from above and its partially thrombosed. I puncture from below and get access to the stent. And then you can see here we've gone in the correct access here, through the interstices, and now we have actually a straight shot
and then I'm snaring my wires so you're back to first principles and just do things properly after that. And then ballooning here and now this is the only same time you'll see a bifurcated stent of this fashion. And you can see here that we have eventually good flow
in a correct orientation. I've taken out my little sheath here, so there's a small leak here. This is what cone-beam CT looks like. You've got a double stent system here, which then splits right there into the occluded obturator
and the patient common femoral. And she's actually done very, very well since that time. And this her own follow-up and you can see the stent is widely patent. So, although the stent didn't get away, it certainly was misplaced.
Lessons for me, trust your gut. If you think there's something wrong, there is usually is. And I remember Mike Dick years and years ago saying, "Just sit down, take off all your leads, and go into your room, and just think for a few minutes,
before you do the next step." And I wish I had done that at the time. Thank you very much.
- Thank you Doctorr Veith for asking me back. So as we know, end-stage renal disease prevalence has been increasing, and the last year we have is 2015 even though the costs seem to have plateaued which is in keeping with aggressive efforts
to keep costs in check. Value is like beauty. It's in the eye of the beholder, and then you have these two good-looking guys here, and I would submit to you that probably, what would be personal preferences,
you might find one more likable than the other. But my point here is that value has many, it's in the eye of the beholder in that you have a payer who has different sense of value than the patient,
the nephrologist, the hospital, and the private practice. This is from Dr. Porter's article. Michael Porter in New England Journal of Medicine which is a great article to read, actually.
Atually Prebier suggested that I read this, and it's really quite insightful, looking at value as healthcare outcomes that matter to patients over the costs for delivering that particular outcome. And indeed is there a long term value for stent-grafting
in view of all these other procedures that we have? We're not going to talk about drug-coated balloons because we don't really know what that is going to show. Stent grafts have conceptual, clinical, and economic benefits. As you might imagine it excludes disease
like intimal hyperplasia. It helps with flow disturbances. And there has never been, in any study, where stent grafts were compared with balloon angioplasty, where stent-grafts performed inferiorly. So if you have increased patency, primary patency,
if you have a decreased number of interventions, it would seem only logical that you might have an economic value signal there. We're going to address these. They have been addressed previously in a revised trial, and other randomized trials.
We now present some of our Revise Two data. This, of course is the Flair trial which looked initially with the Bard's Flair device showing improved primary patency in both the target lesion and in the access circuit.
Ted was remiss of me last time when I spoke about the RENOVA trial without showing this Flair because he didn't see his name there, as Ted was one of the authors. This is for you Ted, thank you.
At 24 months showed similarly, almost twice as good primary patency over the group. Bart Dolmatch earlier this year in the JVIR did a theoretical construct, looking at the Bard data from Flair and RENOVA and proposed a theoretical projections
where one was decreased bare-metal stent use plus increased stent grafts. And the other was increasing angioplasty, decreased bare-metal stents use. And basically what he showed was, over time these negative values here
or points of value from both the payer right, Medicare, and from the point of care, device-related costs, there was value over time as you decrease bare-metal stent use. And these predicted reductions
in total Medicare payments ranged from .3 to 1. And here we have a little bit of a blip from the point of care, which was minimally not cost savings. But, in general, these were in the in-stent restenosis group.
This was in the anastomotic group. The use of stent-grafts for AV graft anastomotic stenosis appear to be economically favorable. The conclusion, now this may sound like a little bit of a commercial bias, but really I only had access to the revised trial data
as one of the authors. And as you know, there's a 50% increase in patency over angioplasty at two years. In the Kaplan-Meiers, 50% increased patency over angioplasty for the primary, for the circuit at two years.
So again, if you know you're having increased patency it seems logical that you might have increased value. Poorer results for the thrombotic group versus the non-thrombotic group. But the relationship of better results with the stent-graft were preserved.
Now, let's look. Reduction in Interventions Over 24 Months- A Study Population. Again, over 24 months all groups better for the stent-grafts, okay? We looked at the stenosis group and the thrombosis group.
The revised trial had the advantage of being able to present these groups and look at both of them, unlike other trials, the treatment with randomization, and then we followed them over 24 months. All reinterventions better with the angioplasty. For the thrombotic group was the most number
of interventions compared to the stent-grafts, more by 40%, 16% with the non-thrombosed group better for stent-grafts. Forty-four percent was decreased reinterventions-per-subject with angioplasty alone, how many patients had to come back for angioplasty alone?
Well, 44% less in the thrombosis group. Thirty-six percent less for thrombotic reinterventions for thrombolysis again, with an advantage to the stent-grafts in the thrombosed group. Stent reinterventions, although they were about the same
because it was difficult to look at this group because the investigators were not required to do stent-grafts, the bare-metal stents and everything else is in there as well. Let me skip ahead a little bit here, cause we want to get to the meat of these things.
All reintervention types, okay, decreased number with stent-grafts. Am I going forward or am I going backwards? I'm terribly sorry. (laughing) The audience gets to vote again.
What about the time to the first intervention? This is more of a quality control, or quality measure-of-life study for the dialysis patients, how many times they have to come back. Viabahn stent-grafts in the stenosis group have longer time than any of the others.
But again, look at the thrombosed group, Viabahn stent-graft 76 versus 56 days, time to first reinterventions in the access circuit with stent-grafts are used for the index procedure, again, better results for stent-grafts: 35% versus 47. First thrombosis after the initial procedure:
36% longer time, versus 19%, okay? And time to first occlusion again, is better for the stent-graft group that was thrombosed. What about costs? What about the money?
Thirty-eight percent lower reintervention costs when using Viabahn as an index of the thrombosed grafts. The lines cross over at 18 months for stent-grafts less than angioplasty. So if we can keep these folks going to 18 months, is when you start to see the value.
Index costs were higher for stent-grafts of course. But at 15 months, particularly in the thrombosed group, things crossed over and you had more value. So we're back to the equation again. Dramatic reduction in reintervention costs drives total cost significantly at two years
with fewer interventions and improved patency. And in the dysfunction-but-not-thrombosed group, those was cost parity but fewer interventions. So John, you've been at this. What can I take away from this talk? This is it.
The data of the trials, not only revised, but the others, shows that thrombosed and failing grafts and other recent economic studies strongly suggest that there is clinical value obtained by treating thrombosed grafts with stent-grafts. The revised trial allowed this opportunity
to look at both groups: among thrombosed circuits the value was even larger. So if you have folks come and present to you with thrombosed it may be a serious consideration for placing a stent-graft. And of course, we all welcome you to Methodist Hospital
in May for the Vasa Annual Practicum. Thank you.
- This work has been done by in my hospital with collaboration of the University of Bologna in Italy. We have no financial disclosures. So all starts from the result of a new TECCO study, but it was published last year showing that stenting was equivalent or even be better in surgery for the de novo common femoral and deep femoral arterial stenosis.
This was a small randomized study of around 117 patients with common femoral artery stenosis. Interestingly enough, 86% of his patients were claudicants, so the applicability of a randomized control trial should be limited to claudicant. The primary outcome was on the patency,
but it was with complication. The combined rate of morbidity and mortality that was 26% in the open surgical arm, and 12.5% in the stent population, and this was just significant. After a median follow up of 24 months, the rates of primary
patency target lesions and system clinical improvement were similar in the two groups. There was no mortality in every group, but one stroke in the endovascular arm. Minor complication were more often seen in the surgical arm with hematoma, delayed wound healing, temporary lymphatic
leakage, paresthesia, but no infection of a graft. The follow up in this small study was not powered enough to assess secondary endpoint, and only 46 patients were available at 24 months for analysis. And the length of stay in the stent group were three days, and six days in the surgical group.
So if you go through the Vascular Quality Initiative published by (mumbling) last year, we find that the 30-day mortality was 1.6%. And the access site hematoma was 5.2%, with a risk of arterial dissection. We have a total rate of complication of nearly 10%.
And interestingly enough in this Siracuse study, was where mostly claudicants were taken care of. You see that the result depends on the symptomatology. If you have a patient with critical infracting ischemia, you have real operation and bad result with the endo first technique.
We have studied our result. In a retrospective study of nearly 150 open revascularizations, half claudicants, half rest pain, and our 30-day result we had 98% of primary patency, three occlusion, 1.7% of mortality at 30 days, 1.4% of cardiovascular complication MI,
groin wound complication was seen in five percent of cases, and in multivariate analysis, only tissue loss and infection, wifi three-four was a predictive factor for wound complication at the groin. This is perhaps the most important aspect of the study. This is what we're seeing in these patients.
As you see here, most of the lesion were at the orifice of a deep femoral artery in more than 73% of the cases. So if you do endo in this application, you can jail or covered the deep femoral artery. Inside of this by open surgery you can clean both artery and leave a good vascularization.
In our practice result in claudicants are excellent, are shown here. They are not so good in patient with rest pain and gangrene because obviously these patients with CLTI and occlusion of the popliteal and infrapopliteal artery needs a popliteal or tibial revascularization
in addition to that of a deep femoral artery to save a foot. So we think that until now open surgery is still the best option in most cases. Thank you.
- Thank you Jose and Marcia. No disclosures. So the primary valve incompetence treatment techniques was started by Bob Kistner and the techinique involved a longitudinal internal valvuloplasty by longitudinal incision and tacking of the redundant valve edges.
And the next treatment available was a transverse valvuloplasty which was again under vision and the valves were tacked at the at the commissures but the incision was transverse. And a combination of the two techniques resulted in the technique of Sottiurai, the T internal valvuloplasty
which was later modified by Michel Perrin to be able to evaluate all aspects of the valve. Further to that, we developed the trapdoor internal valvuloplasty in which a trapdoor was created. All these techniques, the mainstay was reefing of the valve commissures.
On the left hand side, you can see a redundant valve, prolapsing cusps, and on the right hand side, a repaired valve after the reefing. But you can see that the commissure is quite heavily placated. So the possible disadvantage of reefing technique
is the resultant heaped up commissural junctions. This creates valvular rugal folds and obviously when healing occurs it will have increased cicatrization, it will occupy the space, and reduction of functional valve area. When we evaluated the various thrombosis results of
supra-valvular technique, modified T technique, and the trapdoor technique, we found that on an average, there was about a 4.5 to 9% incidence of valve thrombosis. And we also found that in another 6.1% patients there, the valve stations resolved. Cumulatively, these two complicates accounted
for almost 13% of all valvuloplasties. We published a new technique of reduction internal valvuloplasty on the lessons that we leared from Dr. Lugli's experience. And we wanted to quantify the repairs that we do by measuring intra valvular distances and
trans-commissural diameters preoperative as well as intra-operative by ultrasound. We used various techniques, we devised measuring forceps and this is how it's done, whereby we are able to excise the redundant valve and stitch it back onto the valve
and have no rugal folds at the end. And this can induce, this can reduce incision in high shear areas as well. And therefore, give you a good result. This is intra-operative result of competence where you can see the patient is doing valsalva
and you can see the two valve leaflets and this is the stripping technique. And a post-operative descending angiogram or venogram shows a competent valve. So when we looked at the relationship of reflux, valve repair, and ulcer healing,
we found that when we did single level repairs, we only found 50% ulcer healing. But when we did multiple level repairs, the healing was 100% in a short period of time. And the valve competency always did not correlate with ulcer healing.
In our case the valve competency levels were 87.5% and ulcer healing was 88.9% but mainly due to the single level repairs, that did not really work. So the Rival Technique in conclusion ladies and gentlemen is a complete departure from the reefing technique which has been the mainstay of valvuloplasties.
At two years, we've had 100% patency and about 87% competency of repaired valves, with a freedom from C6 ulcers at two years about 89%. Rival Technique has now replaced our technique, earlier techniques, and is the preferred technique in our center.
Thank you for your attention.
- Good afternoon, Mr. Chairman. Thank you for allowing me present on the topic of importance and prevention of treatment of complications of TAVR. And TAVR and TAVI are the same, transcatheter aortic valve replacement versus implantation.
So VARC stands for Valve Academic Research Consortium and they defined specifically specific details of various complications of TAVR and major vascular complications are actually one of them. This is one of the earlier publications looking at all of the outcomes, but you see
the number of, or the significant percentage of vascular complications, meaning many of them led to issues with mortality. I remember initially when we started to do TAVRs, about almost 10 years ago, it was, we had a lot of iliac ruptures.
I remember at least two or three abdominally aortic fractures that required EVAR. Those were very common. Part of it was because the devices was much larger, the profile was much bigger. We had to deal with some narrow vessels.
There was some excessive calcification, tortuosity, and we learned early on with the TEVAR as well and that you can overcome one or two of those, but it's hard to tackle when you have all the three conditions existing in a patient. Obviously, wire management was also something
that the cardiologist had to learn because many of them were not used to large devices while vascular surgeons, some of the intervention cardiologists in Europe who do a lot of EVARs and TEVARs were familiar with wire management and type of wire is very important.
Myself, as someone who was not placing many wires inside the ventricle region, we learned as well what kind of wires we need and how the wire has to be shaped and placed inside a ventricle to avoid any complications within the ventricle as well.
One of the things we learned to improve outcomes are really access management, which is critical. Many of these are done percutaneously, as you know, and having an ultrasound guided and access to this area is very important. And fluoroscopy, while being helpful in many patients,
especially with palsis femoral arteries, many people feel that the ultrasound adds additional accuracy to avoid high or low stick. But this usually with a micro-puncturist, I usually do an angiogram, confirm that we don't have a high or low stick
and that's particularly upgraded to 035 in a you know five or eight French sheath, depending on. Next thing particularly is following the wires for unfavorable tracking, like you see in this case, for example. That depends, it mostly has to do with the wire you choose
to track this device over, but also sometimes anatomy and vessel consistency. Now direct iliac access has been used in the past, and I think there is a useful for certain number of patients as an alternative, but today rarely used for any TAVR
just because of the profile going down. Exo-conduit is very commonly used and I think is a good and helpful situation for patients requiring large device. And most of its ations is actually, I used to leave the ilio-femoral artery bypass,
because it hopes not only provide profusion to that leg, but also can be helpful for future re-intervention of that patient. Now endo-conduit has become also popular, which means basically we go in from inside with an Igor or similar devices,
we crack open the iliac arteries and this may be an opportunity as well. Having said that if you have a graft past iliac inguinal canal, that may or may not be good because it tends to bend in that area. Dissections we have seen frequently with TAVR,
and that's typically treated with stents as well. With percutaneous options with TEVARs and EVARs, we see a lot of femoral artery stenosis that needs to be followed up with these patients. So the position of these devices are very important when you do a perclose and tuberclose devices.
Dissections, fistula, we talk about pseudo-aneurysm and other issues can happen with TAVR and those need to be monitored and watched for, obviously, as well. Same thing with embolization of some closure devices. But open surgical repair has its own issues as well.
We can have lymphocelle. We can have venous obstruction, arterial stenosis, neuropathy, infection. So none of this exposure, either percutaneous or open is without complication, and we've got to keep an eye on those particularly.
Retrograde dissection, I've put on. It's mostly a complication of TEVAR, but as we described already with TAVR, with the TAVR as well, you have, predictably, especially with devices who have bare wires in the STJ area can cause localized,
penetrative, aortic lesions, but also dissections that needs to be watched for and cared for. And sometimes the echo, the trans-thoracic echo, will fail to show that because you pass the lesion site,
where the echo will show. So if you pass a certain area, you may not be able to see with the trans-thoracic echo, but he hopefully should show it. But if not, an angiogram or intravascular ultrasound should be an alternative.
And there's a couple of ways to deal with this, obviously, besides, using ascending stent graft is also. Hemiarch replacement, or what we did in the past extra-anatomic bypass in a zone zero. Make it a zone zerotitus. With that said, I want to say the TAVR has
significant complications that has thankfully reduced, but they are a major source of complications and mortality within this patient population. Thank you.
- I want to talk to you today about the MobiusHD device. And the question is can we modulate hypertension through the carotid bulb? My only disclosure is that I'm the site principle investigator for the CALM-2 trial at our site at SIU. Well cardiovascular death risk doubles with each
10/20 increase in blood pressure. And we know that hypertension causes or contributes to 60% of cerebrovascular disease, ischemic heart disease, as well as renal disease. And pharma has not really solved this problem for us. First off lifestyle modifications are usually inadequate,
patients often aren't compliant with their drugs. Drugs only work for as long as they're taken. And we know from our own clinical practice only about a third of patients actually have their hypertension adequately controlled. As well, 15 to 20 percent are resistant
to maximal medical therapy in the first place. And say, average effect of any single drug is a reduction only of only about 10/5. So, the question is what if there was a one time treatment with a durable effect? So, we're all familiar with
the carotid sinus baroreceptors. That may be a little bit of a misnomer because they don't actually sense pressure, they're responsive to stretch rather than pressure itself. But that's a surrogate for pressure.
And we know, or have learned that sustained activation only occurs if you have pulsatile stretch. Hence the concept of the MobiusHD device. This is a Nitinol self expanding internal carotid implant that goes into the carotid bulb. And the concept is that it changes the shape
of the carotid sinus in the diastolic phase. So, several different sizes of this. Its sized specifically to exert just enough radial force on the vessel to reshape it in diastolically, but prevent migration in systolically. And reshaping this vessel increases
mathematically the differential strain and therefore stretch. Which is what's measured by the baroreceptors. The device is similar to many of the implants we use. It has delivery system. Here you can see it prior to deployment.
It can be partially deployed and then recaptured and repositioned if necessary to get it in exactly the proper position where you want it. So, the first-in-man trials. So, the first-in-man trials.
So, these were performed in Europe. The feasibilies if you wish. 30 patients with multidrug resistant hypertension with an average of 4.4 antihypertensive drugs, all had successful insertion of the device. And there were five SAE's in four patients.
Interestingly, two of those SAE's were actually hypotension. Symptomatic hypotension, which may in fact speak to the efficacy of the implant. So, heres some of the data from that if you look at office blood pressures. The mean office blood pressure at the beginning
was 184/109 in these groups. And you can say statistically significant reductions in both systolic and diastolic office blood pressures out at to six months here. What about ambulatory blood pressure? Same thing here you can see significant reductions
at three and six months in ambulatory blood pressure in these patients reduced by an average of 21/12 millimeters of mercury in these populations. But does it have any kind of a long term effect? Well, as you can see the numbers get pretty low, the further out you get on this.
But nonetheless, it does appear to have a sustained, durable effect on reduction of blood pressure and this. And the other interesting thing is the concept of the DDD, which is the daily defined dose. So, not only are the blood pressures being lower,
but the amount of medications that these patients are having to take is also being reduced somewhat as well. So, hence after the feasibility trial on these results, the company has decided to launch what is being named the CALM-2 trial. I'm proud to report that SIU randomized the first patient
in this trial on July fifth 2018. So, the trials still very much in the early phases. The trial will enroll 300 patients at up to 75 European and US centers, with a 1:1 randomization to a sham procedure. The sham patients actually get a sixth French sheath
in the carotid artery. Get their full angiographic evaluation and then they are randomized on the table. And there's a script we go through if they randomize to nothing. And if they randomize to the device
obviously we proceed and implant the device. There's a primary effectiveness endpoint at six months. And that will be assessed by the ambulatory blood pressure and a safety endpoint at three months of the composite cardiac and neuro events. So, in conclusion then, mechanical stimulation
of the carotid sinuses been demonstrated to effectively lower blood pressure. At least in the short term. And the clinical applicability of this we hope to get more information from in this trial. Thank you very much.
- [Presenter] Okay, so you've heard two aspects of the valve, so going to give you actually two, what's called the sail valve and also the VenoValve, two other options that are out there. These are my disclosures. So if you look, these are our options in 2017,
but we really talking about these three, Amrit's already spoken about the Neovalve. All these are the indications for secondary venous problems, and usually monocusp, can be bicuspid, usually monocusp, but can be bicuspid also, and this is monocusp as well.
So want you to get the idea, a lot of monocusp is coming around even though we think theoretically, bicuspid works better, but maybe not, in terms of prosthetic valves. So this is what's known as a sail valve.
Its percutaneous is a monocusp valve. It's almost not a valve. It functions in a slightly different way. It does have a physiologic leak and it's a thin piece of PTFE and what happens is if the blood is going from here up,
when it goes up these slits become larger and when the blood wants to reflux back these become smaller slits and it's like a billowing sail so it's a self-cleaning type of valve. You don't get much on the PTFE itself and it's obviously percutaneous.
So they have done 10 pigs placed in their iliac veins. Access is six French, deployment was 100% and it expands to a 10 millimeter diameter which most of us working in this space think you need about an eight to 10 millimeter size of a stent if you're going to use a stent.
Some of the results at four weeks did ascending venography on these pigs, not patients and they were all patent and then they did some descending of venography and eight of them, five were competent, 1 was partially competent, and two were incompetent. That was due to what they said malpositioning
or maybe it's tilting itself. More importantly at least on Histology, in pigs, not humans, there was really no microscopic thrombis on the valves so that was kind of encouraging. That is the sail valve. Then the second one that to complete the whole cycle during this segment is the VenoValve
which is a porcine derived valve. It's monocusp but it is an open insertion and it's based upon heart valve technology. One of the nice things is and that's another nice thing about the Blueleaf, you don't have a size mismatch. The Blueleaf you're doing it in the native vessel
and here you can tailor the inflow and outflow and papers show that that's really clearly important. You can't put a small valve if you have a big inflow and small outflow et cetera. You need a nice tapering so this will allow you to, when you do it open to tailor the size.
This is what it looks like. Here it's a monocusp valve that's mounted on a metal alloy frame. This is placed in the jugular veins of sheep and it's an open insertion. Clearly you suture it closed with some 7-0 sutures and then you affix it to the vein wall so it doesn't migrate also with some 7-0 sutures
and you can test it. This is a decent ascending venogram so head is up here, neck is down here in the jugular vein of the sheep. Then we can do a descending venography as well. So descending injecting from here, and there's not much leak going down.
So the FDA is submittal and hopefully do some sheep. They want to be sacrificed in 30 or 90 days and hopefully start a inhuman trial within the future. So this really goes back to the axillary valve transplant which is where I kind of started, believe it or not, 35 years ago as a, 37 years ago,
as a surgical resident doing axillary valve transplants. This is monocusp. It's an open insertion. It helps you do better inflow and outflow. But the challenges of all these are going to be, as Amrit already said it's a specialized area. And Mike (unintelligible) also.
Who needs this? Is this the first line or the final line of care in these patients and where do we place the valves or where to create the valves? Is it in the popliteal, the femoral region, or the common femoral?
Maybe some of it depends upon the profunda vein status. We've been doing this for 35 years when I was a surgical resident and I'm glad that we're finally getting to the point where we have a lot of nice options and see which ones pan out
because it'd be great for these patients. Thank you.
- Thank you very much, thank you Cees, that was really interesting, it's um, it's a topic close to my heart and I think that there's a great deal of work about pneumatic compression that we can learn from. These are my disclosures. Your stent choice, well,
we talk an awful lot about stents, but it is really only one part of the entire spectrum of factors that get it right. And when you get it right, you have an open vein and we believe that the open vein works, although the open vein hypothesis
seems somewhat compromised, considering where it came from in terms of open arteries. But your stent choice is just one of the factors that goes into it, and your inflow, and your outflow generally we can improve upon. Your muscle pump we'd like to improve
by using pneumatic compression boots, and then obviously getting your anti-coagulation right, as Dr. Weinberg explained, is really really key afterward. So, stent choice is one of the aspects, but it's certainly not the only aspect. You're familiar, and probably sick of these diagrams
showing the differences between radial force, crush resistance, and the trade-offs between stent flex, strengths, rather, and when I use strength it's a fairly generic term, and flexibility. And obviously in Europe, we have access to a wide variety of stents.
The Cook Zilver Vena first came out in 2010. Bard Venovo was, I think, 2016. The ABRE was just last December, but it's commercially available. The Optimed Sinus-Venous has been around for quite some time, I'm going to say 2011 if I'm correct.
And the Sinus Obliquus, then it was a little bit later, maybe 2014, 2015, and for those of you who haven't seen this before, this has got a, a closed-cell design at the top which is quite rigid, if I may, and then a very flexible sinus,
or rather open-cell design at the inferior portion, the top portion is angled to address the IVC confluence. And then the Veniti Vici, which is, (coughs) excuse me, was extensively studied in the VIRTUS trial, and this is a more closed-cell, but there's still a considerable flexibility.
So, like everything else in life, you know, you can go for the old broad who's got loads of money, or you can go for the young hot chick, and you know, she's broke. And you know, life is like that, and stents are like that too.
You know, what you get in one you lose in the other. And like a lot of the other things, you have to get everything right to make the stent work. That analogy certainly does not apply to women. But the closed-cells generally have higher force but they're slightly more rigid.
The open-cells are, perhaps, slightly weaker, but there's infinite varieties of imaginations and changes that can be made to those two very generic statements. For instance, in the newer stents, if you cut off a larger, laser cut a Nitinol tube,
you will intrinsically get thicker struts, and therefore slightly larger sheath size, but ultimately slightly more strength at the expense of slightly less flexibility. I think for me, the thing that I've learned the most about the newest venous stents,
or using the newer venous dedicated stents, is that you must do very aggressive balloon dilatation pre and post, that's absolutely essential. Regardless of what stent you use. And I'm horrified to see some of the Twitter handles of people using pre-dilatation
with an eight millimeter balloon, then putting in a 20 millimeter Wallstent and then ballooning it again to 14. Absolutely no logic to any of that. So I think you should balloon to the nominal diameter of the stent.
And it is interesting that you get a much higher force when you get that stent to the nominal diameter. The actual physical properties of the stent change when it hits that diameter. So not getting to the diameter of the stent is a huge mistake.
Now, do fractures really matter? We've been looking extensively at this in a variety of the different trials, and it's hard to know. Certainly, luminal reduction does. Fractures, not so sure about. Fractures sound like they're easy to diagnose.
They're actually very difficult. And compression at the inguinal ligament, is it real? It seems to be real. It seems to be more real than I certainly believed, in a certain proportion of patients. Typically skinnier ones, in my experience,
again, skinny females. Flexibility is obviously a big, big issue, and when you think of where your knee goes in relation to your shoulder if you're doing your yoga class, or anything else for that matter, tying your shoelaces,
there's a lot of bend required. And if you think of where we are now in aortic stent grafting compared to where we were when I last had hair, everything has changed. All of the devices have changed.
We went from Ancure, which had 64 steps, through AneuRx, and now, you know, things have moved on way past 2010 as well. So, in terms of my choices, in the USA you've got two choices, you got Wallstent and Z stent.
And if you got a rupture, use a Gore or something like that. In Europe, it's a much more, nuanced and challenging to try and figure out which ones you do. And these are just my choices. Is there any evidence to back them up?
None whatsoever. Have I had problems with most of the stents? Yes. Most of those problems were probably self-induced. I've certainly learned that pre-dilatation and post-dilatation are the essentials.
And flexibility is a lot more important than I would've thought if you had asked me five years ago. Thank you very much.
- So this is what I've been assigned to do, I think this is a rich topic so I'll just get into it. Here are my disclosures. So I hope to convince you at the end of this talk that what we need for massive PE when we're talking about catheter based therapy is a prospective registry. And what we need for catheter based therapy for
submassive PE is a randomized controlled trial. So we'll start with massive PE and my rational for this. So you know, really as you've heard, the goal of massive PE treatment is to rescue these patients from death. They have a 25 to 65% chance of dying
so our role, whatever type of physician we are, is to rescue that patient. So what are our tools to rescue that patient? You've heard about some of them already, intravenous thrombolysis, surgical embolectomy, and catheter directed therapy.
The focus of my talk will be catheter directed therapy but let's remember that the fastest and easiest thing to do for these patients is to give them intravenous thrombolysis. And I think we under utilize this therapy and we need to think about this as a first line therapy for massive PE.
However, there's some patients in whom thrombolytics are contraindicated or in whom they fail and then we have to look at some other options. And that's where catheter directed therapy may play a role. So I want to show you a pretty dramatic case and this was an eye-opening case for me
and sort of what launched our PERT when I was at Cornell. It's a 30 year old man, transcranial resection of a pituitary tumor post-op seizures and of course he had a frontal lobe hemorrhage at that time. Sure enough, four or five days after this discovery
he developed hypertension and hypoxia. And then is he CT of the chest, which I still remember to this day because it was so dramatic. You see this caval thrombosis right, basically a clot in transit
and this enormous clot in the right main pulmonary artery. And of course he was starting to get altered, tachycardiac and a little bit hypotensive. So the question is, what to do with this patient with an intracranial hemorrhage? Obviously, systemic thrombolytics are
contraindicated in him. His systolics were in the 90 millimeter of mercury ranged, getting more altered and tachycardiac. He was referred for a CDT and he was brought to the IR suite. And really, at this point,
you could see the multidisciplinary nature of PE. The ICU attending was actively managing him while I was getting access and trying to do my work. So this was the initial pulmonary angiogram you can see there's absolutely no flow to the right lung even with a directed injection
you see this cast of thrombus there. Tried a little bit of aspiration, did a little bit of maceration, even injected a little TPA, wasn't getting anywhere. I was getting a little bit more panicked as he was getting more panicked
and I remembered this device that I had used in AV fistula work called the Cleaner. Totally off label use here, I should disclose that and I have no interest in the company, no financial interest in the company. And so we deployed this thing, activate it a few times,
it spins at 3,000 rpm's, he coughed a little bit, and that freaked us all out also. But low and behold we actually started seeing some profusion. And you can see it in the aortogram actually in this and that's the whole point of massive PE treatment with CDT,
is try to get forward flow into the left ventricle so that you have a systemic blood pressure. Now, you know, when we talk about catheter based therapies we have all sorts of things at our disposal. And my point to you is that you know really, thank you...
You guys can see that, great. So really, the point of these catheter therapies is that you can throw the kitchen sink at massive PE because basically your role is to try to help this patient live. So, if I can get this thing to show up again.
There we go. It's not working very well, sorry. So, from clockwise we have the AngioVac circuit, you have, let's see if this will work again, okay. Nope, it's got a delay. So then you have your infusion catheter,
then you have the Inari FlowTriever, you saw the Cleaner in the previous cast, and you have the Penumbra aspiration device the CAT 8. And some of these will be spoken about in more detail in subsequent talks. But really, you can throw the kitchen sink at massive PE
just to do whatever it takes to get profusion to the left side. So, the best analysis that has been done so far was Will Kuo in 2009. He conducted a meta-analysis of about 594 patients and he found this clinical success rate of 86.5%.
This basically meant these patients survived to 30 days. Well, if that we're the case, that's a much lower mortality than we've seen historically we should basically be doing catheter directed therapy for every single massive PE that comes into the hospital. But I think we have to remember with this meta-analysis
that only 94 of these patients came from prospective studies, 500 came from retrospective, single center studies. So even though it was a very well conducted meta-analysis, the substrate for this meta-analysis wasn't great. And I think my point to you is that
we really are going to have a hard time studying this in a prospective fashion. So what is the data, as far as massive PE tell us and not tell us? Techniques are available to remove thrombus, it can be used if systemic lysis is contraindicated,
but it doesn't tell us whether catheter based therapies are better than the other therapies. Whether they should be used in combination with them and which patients should get catheter based therapy, which should get surgery and which techniques are most effective and safe.
Now, I think something we have to remember is that massive PE has a 5% incidence which is probably a good thing, if this was even higher than that we would have even more of an epidemic on our hand. But this is what makes massive PE very difficult to study.
So, if you looked at a back of the envelope calculation an RCT is just not feasible. So in an 800 bed hospital, you have 200 PE's per year, 5% are massive which means you get 10 per year in that hospital, assume 40% enroll which is actually generous,
that means that 4 massive PE's per year per institution. And then what are you going to do? Are you going to randomize them to IV lytics versus surgery versus interventional therapy, a three arm study, what is the effect size, what difference do you expect between these therapies
and how would you power it? It's really an impossible question. So I do want to make the plug for a Massive PE Prospective Registry. I think something like the PERT consortium is very well-suited to run something like this
especially with this registry endeavors. Detailed baseline characteristics including all these patients, detailing the intervention and looking at both short and long-term outcomes. Moving on to submassive PE. As you've heard much more controversial,
a much more difficult question. ICOPER as you already heard from the previous talk, alerted the world to RV dysfunction which this right ventricular hypokinesis conferring a higher mortality at 90 days than no RV dysfunction. And that's where PEITHO came in as you heard.
This showed that the placebo group met the primary endpoint of hemodynamic decompensation more commonly than the Tenecteplase group. Of course, coming at the risk of higher rate of major bleeding and intracranial hemorrhage. So I just want to reiterate what was just said
which is that systemic thrombolysis has a questionable risk benefit profile and most patients with submassive PE, as seen in the guideline documents as well. So that sort of opens a sort of door for catheter directed therapy.
Is this the next therapy to overcome some of the shortcomings of systemic thrombolysis? Well what we have in terms of CDT is these four trials, Ultima, Seattle II, Optalyse, and Perfect. Three of these trails were the ultrasound assisted catheter, the Ekos catheter.
And only one of them is randomized and that's the Ultima trial. I'm going to show you just one slide from each one of them. The Ultima trial is basically the only randomized trial and it showed that if you put catheters in these patients 24 hours later their RV to LV ratio will be lower
than if you just treat them with Heparin. Seattle II is a single arm study and there was an association with the reduction in the RV to LV ratio at 48 hours by CTA. PERFECT, I found this to be the most interesting figure from PERFECT which is that you're going to start it at
systolic pulmonary artery pressure of 51 and you're going to come down to about 37. Optalyse, a brand new study that was just published, four arms each arm has increasing dose associated with it and at 48 hours it didn't matter, all of these groups had a reduction in the RV to LV ratio.
And there was no control group here as well. What is interesting is that the more thrombolytics you used the more thrombus you cleared at 48 hours. What that means clinically is uncertain at this point. There is bleeding with CDT. 11% major bleeding rate in Seattle II,
no intracranial hemorrhages. Optalyse did have five major bleeds, most of the major bleeds happened in the highest dosed arms. So we know that thrombolytics cause bleeding that's still an issue. Now, clot extraction minus fibrinolytic,
this is an interesting question. We do have devices, you're going to hear about the FLARE trial later in this session. EXTRACT-PE is ongoing which we have enrolled about 75 patients into. What the data does and does not tell us
when it comes to CDT for submassive PE it probably reduces the RV to LV ratio at 24 hours, it's associated with a reduction at 48 hours, major bleeding is seen, we do not know what the short and long-term clinical outcomes are
following CDT for submassive PE. Whether it should be routinely used in submassive PE and in spite of the results of Optalyse this is a preliminary trial, we don't know the optimal dose and duration of thrombolytic drug. And even is spite of these early trials
on these non-lytic techniques, we don't know their true role yet. I'd liked to point out that greater than 1,600 patients have been randomized in systemic lytic trails yet only 59 have been randomized in a single, non-U.S. CDT trial.
So this means that you can randomize patients with submassive PE to one treatment or the other. And we want to get away from this PERT CDT roller coaster where you get enthusiasm, you do more cases, then you have a complication, then the number of cases drops.
You want that to be consistent because you're basing it on data. And that's where we're trying to come up with a way of answering that with this PE-TRACT trial. Which is a RCT of CDT versus no-CDT. We're looking at clinical endpoints
rather than radiographic ones greater than 400 patients, 30 to 50 sites across the country. So in summary I hope I've convinced you that we need a Prospective Registry for massive PE and a Randomized Controlled Trail for submassive PE. Thank you.
- Good afternoon. So as we've already heard, traumatic injuries are the leading cause of death and disability in children over the age of one. Fortunately, these types of injuries are relatively infrequent, most commonly involving the lower extremities, for example femur fractures,
causing disruption of the SFA or popliteal artery, or the upper extremities, supracondylar humeral fractures will cause damage to the axial or to the brachial artery. Retrospective review of a children's registry from 1993-2005 with 103 patients all of whom were under the age of 18, most were males.
The majority are penetrating wounds. And most frequently, the extremities were involved. Open surgical repair was favored, primary repair when possible, vein patches for use for those under the age of six, and an interposition graft or bypass was used
for those over the age of 12. Non-operative management was selectively chosen in about 10%, and the outcome in this cohort, 10% mortality, 11 amputations, and limb length discrepancy did become a problem over time, necessitating revascularization in 23%.
A nationwide Swedish registry from 1987-2013 looked at 222 patients, children under 15. In this scenario, 2/3 were male, 2/3 had blunt trauma. Once again, upper extremity injuries were more commonly seen in those under 10. Lower extremity injuries more frequently seen
in those between the ages of 11-15. With that cohort that we talked about, 96% were treated with open surgical repair, similar to what we saw before. Interposition grafts, vein patches for the young, and primary repair whenever possible. However, endo therapy was introduced in this scenario,
with eight patients undergoing intervention for axillary, subclavian artery, iliac, and aortic trauma. A summary of four large series was pooled here, and essentially shows you once again the majority of the injuries are in the extremities. The gold standard to date remains open surgical repair,
either with patch, endo anastomosis, or interposition graft, depending on the age and the location. Lajoie presented this abstract, which is a single center retrospective review, nine years, 60 patients, all under the age of 18. And once again with vascular trauma pediatric group,
majority of treatment is with open, however 16% underwent endovascular intervention with embolization, stents, and stent grafts utilized. None of the stents were implanted in anyone under the age of 13. Follow-up six weeks showed no difference
in the amputation rates or the mortality rates, however reinterventions were certainly higher in those who underwent endovascular therapy. National Trauma Databank from 2007-14 of pediatric trauma under the age of 16. 35,000, so it's a very large cohort.
And you're going to see here, it's not just a trend. This was statistically significant. There is an increase endovascular therapy utilization across the board in that time frame, and specifically for blunt trauma, increasing from 5.8% up to 15.7%.
And what you can take away from this is that the increased endovascular therapy was utilized in children over 12, larger hospitals, level one trauma centers, and those who resided in northeast. In addition to that, those who had a higher
injury severity score also underwent endovascular therapy. The most common procedures, embolization of the internal iliac, and TEVAR for blunt aortic trauma. Unfortunately, despite this, the in-hospital survival failed to improve.
So now there's a plethora of data out there, and multiple single-site institutional reviews of their own experience. Here's what I can say. I think there are some select indications for which endovascular therapy appears to be advantageous.
Without question, as you've heard already, the blunt thoracic aortic trauma. Here's a 17-year-old, fell from a seven-story building and successfully underwent endovascular intervention. Another case, a 16-year-old gunshot wound to the thigh, injury to the profunda femoris was a large
false aneurysm in the anteromedial thigh, who underwent coil embolization successful exclusion of this area where the pseudoaneurysm happened to be, but maintained perfusion through the SFA and the remaining branches of the profunda. Is there a role here for blunt femoral trauma in the child?
Well, I'm not a big fan of it, doing it in adults, but there is a paper on it. 13-year-old popliteal artery trauma, high ISS score, this occlusion was recanalized and a self-expanding stent placed. And I will note that a bridging technique was utilized.
Once the other injuries were addressed, the patient underwent bypass. 12-year-old with polytrauma, iatrogenic orthopedic screw injury to the SFA, successfully treated with a Jomed stent, and then planned bridging procedure,
who underwent open repair a few days later with an interposition vein graft from the contralateral leg. One more case, 14-year-old polytrauma, self-expanding covered stent placed for an axillary artery injury, and this was a planned procedure as a bridging technique. He, unfortunately expired prior to that opportunity
to perform the bridging technique on him with a bypass. So, in summary, I do think pediatric vascular injuries are uncommon. Open repair, once again, remains the gold standard. Endovascular therapy appears to be increasing, especially TEVAR and embolization.
Endovascular therapy in the extremities is an option as a bridge in older people over 12 who have higher ISS scores. And a nationwide pediatric database for arterial trauma would be beneficial. Thank you.
So I'm a consultant for both of those. Okay, so repair of coarctations. So surgical repair is effective, has a low procedural mortality and morbidity, and so does stent implantation. But the mortality is very, very low with stents, and the morbidity is also lower in general.
Whatever method you choose, though, both methods are going to be complicated by hypertension, re-intervention for stenosis and aneurysm formation, which is normally just a question of time if you follow up the patient for long enough because the post-stenotic dilatation,
cystic medial necrosis, calcification, it's a sick wall. So the potential advantages of using a covered versus a bare stent versus angioplasty is that the angioplasty just tears, and we don't do angioplasty on native coarctations. But you put a stent in and you get this creation
of a longitudinal framework, and if you have a covered stent you're going to control the integrity of the vessel at the coarctation and below it, which is normally a very dangerous area, the poststenotic dilatation area. And they're particularly useful using covered stents
when there's an aneurysm which is present. However, there's no good studies to say that's really the right thing to do. So recently Tretter and McElhinney, they looked at all the reports that had been done for endovascular therapy for aortic coarctation,
and they noted that aortic rupture was particularly rare, less than 1%. Acute aneurysm formation, when intervening for endovascular therapy, was about up to 13% for angioplasty, up to 5% for bare metal,
and less than 1% after covered stents. But it depends on the reporting bias and there's a lot of inconsistent definitions. And overall, the acute wall injury seems to be going down for coarctation due to better delivery systems, more use of covered stents.
And there are really only three covered stents, which are balloon expandable, and the CP covered stent, which comes bare and covered, and it's stuck on quite loosely, the Atrium V12LD which is not available for the last two years,
which goes up to 22 millimeters, and the aortic BeGraft which comes in a whole range of sizes and covered. This is the Atrium V12LD with stainless steel covering the inside and the outside, and the BeGraft is chromium cobalt
and it's covered on just the outside. So, when you're doing the covered stents, you need to consider the vascular access damage that can be done because you need a relatively large delivery system, and I'm a pediatric cardiologist,
so using these in small kids you have to be very careful, and the CP stent can take even 11 to 12-French system. The stent integrity, because the CP Platinum-Iridium stents tend to fracture, the Atrium has a problem of infolding, and the Bentley is quite a strong stent and I've had no problems with it,
but it's early days yet. And the other thing is the covering integrity. The CP is incomplete while the Atrium and the Bentley seem to have a better cover. So looking at the COAST I study, which was a look at the CP stent,
which was a bare stent, they did 105 patients underwent attempted implantation, and just looking at sort of the aneurysm, the aortic wall injury, they did balloon dilatations just for some compliance testing, which I never do, and they generated some small
aortic aneurysms showing that that area is a problem. And in intermediate followup when they put in bare stents, they had a total of six aortic aneurysms, five were successfully treated with a covered stent placement and one resolved without intervention,
and they had some stent fractures. Then what they did, they did a COAST II study, which was looking at the CP covered stent, which was used, and they used it in a total of 158 patients. 83 had had previous intervention and had some aortic wall injury.
And when they were using that stent, complete coverage of the pre-existing aortic wall injury was achieved only in 92% of the patients, and seven patients had minor endoleaks. The other thing is, so that shows that the covering wasn't that good.
The other thing was is it takes a large delivery system four patients experienced important vascular site injury. In the Advanta trial the covered stents were very good, in general, for getting the blood pressure down, getting the gradient down, and increasing the diameter. And also, comparing sort of the long-term followup,
we followed the blood pressure for three years, the blood pressure stayed down and we had a very good result. The major problem was they had very small problems with femoral artery occlusion only in one patient compared to the four in the CP stents.
So there was one small aortic hematoma treated with a second stent, but the major problem was the stent wasn't robust enough in the aorta and had infolding. Two of which required urgent reintervention. The Bentley, which is a relative,
and we've had it since January 2017, so this is, let's say, a complex native coarctation. So we treated that with a BeGraft. And here you can see this is another patient, a little Bedouin girl, that had an endovasculitis and a coarctation,
and she was treated with a CP stent, which was covered, but you can see the aneurysm stayed. We put the, another Bentley stent in there. So you can see that the covering, even when using covered stent, is not necessarily always the right thing.
We've done now 22 patients with a Bentley BeGraft. You can see the median age and all different types of coarctations which have been previously treated or native. Overall, it gets down the gradient and the coarctation diameter stays up.
We had no acute wall injury and no other immediate complications. Patients that had pre-existing aneurysms, ones which you saw, was successfully treated, and at median followup things look good. So in conclusion, surgery, in my institution,
is the primary choice of intervention in patients who endovascular stenting is not possible. So infants and small children we won't do a balloon angioplasty because it tears the intima and they have aneurysms afterwards. If we can put in a covered stent,
that's our first choice. Safe and effective acute treatment of coarctation and associated with less aortic wall injury than bare metal and balloon angioplasty, but you need a lot of reintervention. The choice of the covered stent,
you need to consider delivery system, the maximum diameter of the stent, the stent integrity, whether it's going to fracture or infold, and the covering integrity. And when all is said and done we still need to have long-term followup imaging.
Thank you very much.
- Good morning. Happy to discuss with you some of the issues of the currently available stents. Nutcracker Syndrome patients most frequently present with left flank pain, pelvic pain, hematuria, usually due to a significant narrowing in front of the aorta between the aorta and the superior mesenteric artery.
Open surgical treatment has been kind of a gold standard. Left renal vein transposition done most frequently followed by gonadal vein procedures or even renal auto-transplantation. Renal vein stenting, in this country, has been done using Wallstents or SMART stents.
In our experience, where we reported 37 surgical patients. We used stents only for secondary procedures. Three of the six stents had problems of either migration or in-stent restenosis. There is a systematic review in the JVS-VL, recently published, 180 patients, 7 series.
Interestingly, 175 were treated in China with good clinical results in 6-126 months. Stent migration was observed from 0 to 6.7%, depending on the series. We have seen stent migration, sometimes it's immediately during t
and that's obviously the easiest to take care of. Or immediately after, before any healing, that is also a more favorable situation. The problem is when it travels to the heart. It is not frequent, but it happens.
This is the largest series, 75 patients, stented, 5 of them had migration. Two of them to the right atrium, one of them required a medium sternotomy to remove it. Stents not only migrate, although again it's rare,
but even one patient is too frequent in this series that usually involves young, female patients. Stents in this position unfortunately can also fracture. If they don't fracture, they can thrombos. If they don't thrombos, they can be compressed.
If they don't compress, that's a stiff stent, it practically always will perforate their renal vein because of the arching configuration of the renal vein and because the unavailability of less than four centimeter long stance. So it is a problem.
It can actually cause significant, severe migration, completely occluding the inferior vena cava together with perforation of the renal vein. Obviously these cases require open surgical repair,
and have a chance to remove a few of these stents. Percutaneous retrieval, fortunately, is possible in about 90% of the cases, and sometimes, if it doesn't cause significant cardiac injury even from the heart or the pulmonary artery and
we had several case reports, of stents, especially after the TIPS procedure, early on, that migrated into the central circulation that would be removed with different types of techniques, of snaring and pulling the lost stent into a large sheath,
whether you snare it at the end or you snare it in the middle. There are good case reports. This patient that we had, we could use a balloon, pull it down to the vena cava, and then from above and below, we could remove it
with a large sheath. Current stents, if you really don't want it to migrate, the only option we see is transposition patch and using hybrid procedure to fix the stents in the renal vein.
So, in general, open surgery remains the first line of intervention. Stents have a reported high mid-term success rate but migration, fracture, perforation, thrombosis, restenosis are problems and if you go to the FDA website, you see that there are much more cases than
those that are reported. So what do we need? We need dedicated renal vein stents that are short, flexible, resist fracture and migration, and we need them urgently. Thank you.
- My disclosures are not relevant. Joe showed this slide, this is the original SVS guidelines, which really, as he mentioned, is a lesion-based evaluation of what the trauma looks like. And, for the purposes of this discussion, we'll be focusing on grade three injuries. Which really means there's blood outside the aortic wall.
There is loss of integrity of all layers and there's a pseudoaneurysm. We've all transitioned to delayed TEVAR for grade one and two. But, what do we do with these grade three injuries? Where's the boundary between medical therapy
that puts the patient at risk of interval rupture and early repair? Which may, as I'll show, put them at risk of other problems. This is a pretty widely adopted prac the idea of treating traumatic pseudoaneurysms,
at least initially, with some medical therapy. This is a review of 18 studies, almost 1,000 patients. It showed really one in five were managed non-operatively. There is a very low rate of aorta-related mortality which will be a recurring theme on all the data I show you. And, there's a really low rate
of required late interventions. As true for many of our trauma-related literature, there's a really poor long-term follow-up rate. The AAST studies have shown us that delayed repair really can improve outcomes. There's a significant selection bias in
these are non-randomized trials for, I think, exclusively. But the reality is, if a patient can wait until stabilization of their other injuries, they do better if you can wait on repairing the aorta, both mortality and the paraplegia rates are lower.
But, it's not just completely a selection bias. There are maybe some other benefit here. And, one of the things that plays into play is: What are their other injuries like? What is their traumatic brain injury look like? And, we use this as a defining point at Grady
about figuring out whether someone really should be figured for early repair or not. If you look at this series of 300 patients with traumatic aortic injury, 248 had a concomitant brain injury, and those are obviously of a variety of different grades,
from a little blip on the CT scan to a potentially devastating neurologic insult. But, it's not uncommon to have to manage both injuries at the same time. That is the rule rather than the exception. They can be pretty significant
and, again, there's significant selection bias in this series out of Maryland. But, there's about a one third, one third, one third early repair, delayed repair or non-operative strategy. If you look at the non-op patients and the delayed patients, you can see
that we get to that very, very low mortality rate. The early repair patients, as you can imagine, are often associated with a fatal outcome. Now, that fatal outcome is not always a it is usually related to something else
and highlights the selection bias of series like this one, that show us that if you're sick when you come in with an aortic tear, you're going to continue to be sick regardless of whether we fix your tear or not. But, there is some other benefit, potentially. The traumatic brain injury is one piece that I've mentioned,
but it's not uncommon, I think we've all experienced situations like this where the trauma physician and the orthopedic physician and everyone who is taking care of these patients is really focused on a grade three aortic injury. And, it oftentimes allows for neglect
or missing of other injuries that may be more life-threatening. How do we avoid delay? There's a few areas where we can think about intervening. The first thing is getting a good radiographic grade, as Joe alluded to, and there's a variety
of different scoring systems. This ultimately amounts to a simplification of the Harborview scoring system which is the one that I personally have gravitated to over the last two years. Which demonstrates that for the old grade one and two
there is probably no benefit of repeat imaging, there is probably no benefit of intervention, and pseudoaneurysms should be fixed when they are stable and severe ongoing-rupture patients should be fixed right away. That assessment of stability is an important part of this.
Part of Dr. Crawford's interest, in particular, was evaluating the size of the pseudoaneurysm and the size of the hematoma. And so, all of these are things that we've seen before but they all probably behave a little bit differently. So, how do we look and see:
Are there specific types of injury that are more prone to rupture with non-operative therapy? And one of the things that's been assessed is the diameter ratio. I think Joe showed this data a second ago. Another is the size of the periaortic hematoma.
In this large series, if you had two of these three factors: a lactate greater than four, a mediastinal hematoma greater than 10 millimeters or a lesion to normal aortic ratio of greater than 1.4. That was 90% accurate in terms of theoretically predicting early rupture.
Which, if you just look at clinical judgment alone, goes down to 65%. Keeping in mind that clinical rupture, true rupture is very often a fatal event. There is a lot of value in moving that number from 65 to 90. If we can get good modeling that tells us
who is at particularly high risk of rupture in this selected group, there is a lot of potential benefit. Just as importantly, as I've mentioned earlier, if you have a higher aortic grade of injury, you are more likely to die but it does not predict aorta-related mortality.
Much of that is the selection bias that people with higher grades of aortic injury are fixed sooner and therefore are not candidates to die from aorta-related mortality. Let's skip through this. And then again, (audience member coughing)
the idea that we need additional information and we need better imaging, better physiologic data that predicts the need for early repair is the take-home message. The answer, as you can imagine, is more information. Part of what the Aortic Trauma Foundation is doing
is going to be evaluating: Are patients really going to do better with non-operative therapy if they have very specific criteria that allows them to be selected out? Are there high-risk criteria that we can figure out besides just eyeballing the CT scan and saying:
This is someone who's not going to do well if we sit on them. Thank you very much.
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