- 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.
- 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.
- 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.
- [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.
- In preparation for tonight's debate I thought I would take us back and look at something a little bit interesting, maybe not all that relevant, but uh but maybe, and that's the open vessel hypothesis, and the applicability to DVT. So here are my disclosures. What is the open vessel hypothesis? And of course I thought I'd be the first person to talk
about this related to veins but certainly I'm not, but maybe I'll be able to bring it to your attention. It really goes back to 1941, and um and it goes back to uh acute MI um experimentally in dogs was related to the duration of coronary artery occlusion. And the hypothesis back in 1941 was termed the
time-dependent open artery hypothesis, because it was postulated that the extent of myocardial damage was related to the time that was required to reopen the lesion at least experimentally. And it wasn't until about 1990, where the um M-I-T-I MITI trial demonstrated that patients who were given
t-PA, within 70 minutes of coronary symptoms had a 1% mortality compared to 10 times that, if in this case, thrombolytic agent was given after 70 minutes of symptom onset and of course, this is the whole reason there's so much emphasis on getting people to the cath lab quickly.
Well what does this have to do with DVT? Well I think if we look at the findings of the ATTRACT trial at least the findings that we know from presentations so far I think it can be explained in part by the open vessel hypothesis applied to veins, so ATTRACT, I won't go into this, we've already uh seen uh the results
but I will um give Tim Yates credit for talking about the open vein hypothesis, oh about six months ago, at New Cardiovascular Horizons. The um primary endpoint of ATTRACT, we saw that not different secondary findings though, again we saw some benefit and the benefit seem to be related
primarily to those patients with iliofemoral DVT. So now I'm going to take you back to the National Venous Registry. Mark Mewissen presented this and let's look at the extent of thrombolysis in the iliofemoral and femoropopliteal segments and more lysis is to our right.
And uh grade three is more lysis than grade two. Um, the bottom line of this was the acute resolution of the thrombus was almost identical for iliofemoral or femoropopliteal DVT. A little bit surprising to me, but something that was demonstrated uh almost 20 years ago.
And here is the patency, iliofemoral DVT uh after treatment uh 64% uh vs. 47% in the femoropopliteal segment that's at 12 months. Again, not all that surprising. So here's the open vessel hypothesis applied to veins. Symptoms will improve when the large vessels can be reopened
and when they remain open over the long term. And we're more successful in preserving, I won't say I won't emphasize restoring or preserving long term patency for the iliofemoral vs. the femoropopliteal segments and for this um uh reason, venous stents work quite well in the pr
work so well in the femoropopliteal system but for this reason the ATTRACT results may be a reflection of not so much what happens with thrombolysis um mechanical uh uh pharmacologic thrombectomy but what happens over the longer term with stents. And the speculation is the veins with acute DVT
can be recanalized equally well. Uh the availability of devices however for the iliofemoral reason to preserve iliofemoral region to preserve patency uh contrasts with no such devices at least right now for the more (inaudible) venous system. So the open vessel hypothesis is applied to veins over
two year follow-up, might explain the primary endpoint failure of ATTRACT and had the trial been conducted on the iliofemoral DVT population alone, I think it is uh evident
- 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.
- I'm humbled to be introduced by a man with your integrity, so thank you for sharing that case. I don't perform procedures and now I know why. - [Man] Maybe you should, having seen that? - (laughs) I don't have the heart for it, I think. So, okay, so you met me before but if you haven't, these are still my disclosures.
The first is an IVC filter company and the second is a company that makes, has all sorts of assets in the venous space. You're more than welcome to ask me about these if you feel the need to. So, a 50 year old man presents from an outside hospital
with left lower extremity swelling. His left lower extremity looks like this. And pulses, motor function and sensation are normal and symptoms started three days ago and are about the same despite anticoagulation. For those of you who were here in the previous session,
you've heard that he wants a procedure done and he wants this clot out. He has a common femoral vein clot and so, he underwent pharmacomechanical catheter-direct thrombolysis and a stent was deployed like you can see here.
So, the topic of my few minutes is how do we avoid stent thrombosis basically? What is the right thing to do now from a medical standpoint so we don't experience stent thrombosis or even thrombosis within a stent.
You know, even reduction in the luminal diameter within a stent. How do we make sure that these stents remain patent as best as they can be patent? Well, you know, whatever it is we're doing and I can tell you
that there isn't any surprise in this talk, there is no standardization to what we're doing but whatever it is we're doing is probably working because overall stent patency rates are quite high for the venous system. And there is much variability in care.
What you can see here is that people treat, by the way, obviously stenting can be done for various reasons and I'm talking about post-DVT, right? So, sometimes people treat with low molecular weight heparin to Coumadin. DOACs are being used more for varying durations.
Sometimes with and sometimes without a combination of an antiplatelet agent. So you know, all the options you can think of are basically being done and the outcomes are like I showed you before, pretty good overall.
Now despite variability, some consensus exists and to be honest with you, I'm not going to show you all these points of consensus. What this is, this graph shows is a result of a, sort of a, questionnaire that was sent to peers in no standardized fashion
and what these people, in some of these statements that there's consensus about, I didn't agree with, so I decided not to bring forward for this discussion. But basically, people say that anticoagulation is preferable to antiplatelet therapy and most people treat for six to 12 months
after such a procedure. Lifelong antiplatelet therapy is recommended if anticoagulation is stopped, people said. And following lysis and stenting, anticoagulation can be discontinued after six to 12 months and people said that it depended
on whether or not the patient has a known thrombophilia or a known reason for the thrombosis. So, you know, as I said, there's variability and despite that variability, things are going okay. What about whether or not we should use vitamin K antagonist or a DOAC such as Rivaroxaban?
Well this small series of 111 patients basically showed the p value was not significant and over two years, the patency rates were very similar. So, you know, given all that, and I'm not showing you data because there are no data to show you,
then what is my practice and what are the limitations of that? Well, what we do after these procedures is that we give a dual antiplatelet agent for one month after the procedure. We treat with one antiplatelet agent
typically aspirin lifelong afterwards. Anticoagulation is only if the indication was of a DVT and basically, we don't do the same thing for every patient. So if there was iliac vein compression that we are sure of as the reason for the thrombosis,
we treat for only three months post-procedure as if this was provoked event, but if the etiology is unclear, we do treat long-term per guidelines for DVT as the same way you would do for any other unprovoked DVT. So thank you again for the opportunity
and thank you for listening.
- I have no disclosures that are relevant to this discussion. What I would start off with is, maybe you don't do it at all. Be careful what you ask for. This is very unforgiving work and know that going into it. The technical considerations a
absence of arteriosclerosis, it's a small vessel diameter and as we heard Dr. Eslami talk about, very high risk of vasospasm. The local clinical experience, I'm going to credit Dr. Jeff Friedman
who's one of our local reconstructive plastic surgeons, 10 patients underwent open surgery for repairs, eight arterial, two venous injuries. The age range 36 weeks of gestation to 12 months, Eight of the nine patients, 13 weeks of age or less. 90% of the injuries,
and we saw that again in Dr. Eslami's talk, are injuries that are iatrogenic as a result of invasive procedures performed on the effe cardiac catheterizations, arterial line placement,
direct arterial ligation, femoral vein injury, intra-arterial infusion or trauma. Most of these are like I menti femoral arterial lines, any sort of umbilical catheterizations,
femoral catheterizations and so on. One of the most important things is to do a real thorough evaluation, so in 70% of these cases they had a color flow doppler examination. Six patients had operative intervention. Doppler results verified intraoperative results
or ultrasound results in all cases and in one patient with preoperative arteriogram demonstrating accuracy of the diagnosis as well. No significant limb loss in these 10 patients, of course a small series despite prolonged ischemia times and I think that's probably one of the primary lessons
to take home is that kids tolerate ischemia fairly well and so to follow these would kind of be expectant treatment. Only one patient had toe amputations. Seven of the 10 patients survived, one early postop mortality, one late postop mortality and one nonoperative mortality.
Functional results were good, two with limb growth discrepancies. This is just to identify what you're looking at, make sure you're doing a good intraoperative ultrasound exam and know what you're getting into. This is just some examples of one child,
with obviously an ischemic limb there, this was from access from catheterization. You can see what the arm looks like, the hematoma down around the brachial artery and a microvascular repair there as you see. Going down and a little fasciotomy
all the way down into the hand, with a reasonable result. Of course, a nasty scar but a functional hand. The diagnosis am, doppler evaluation we place heavy weight on, the color doppler examination,
real time assessment of vessel patency, determine the level of occlusion. And then acutely the treatme acute intervention if obvious injury, discontinue the local catheter that's caused the injury,
anticoagulation with heparin, if possible, and really wait about six to eight hours before going unless the limb is totally threatened, warm packs, elevation, intervention if no improvement. And so, the operati
wide proximal and distal control, as you saw in that one case that I presented, complete division of the affected vessel, usually it's severely injured from the catheterization, proximal and distal thrombectomy using a #2 Fogarty, direct vascular repair if possible, vein grafts rarely.
I think Dr. Singh also mentioned that primary repair is better and we certainly believe the same way. And then fasciotomy is used liberally, postoperative anticoagulation again if possible.
suture usually with a microscope, interrupted sutures are a mainstay, papavarin and nitroglycerin generally work fairly well for vasospasm, again back to the ultrasound and then determine the appropriateness for operative intervention. You kind of need to know that going into it.
Operative intervention only in the case of no improvement and venous injuries are usually a little more difficult to treat and often surgical intervention gives poor results. If you just look at t am and doppler, suspected spasm or thrombosis,
conservative management first, if fails, six to eight hours eventually go to the operating room, if it resolves, obviously no care after that. In the future I think development of a team approach with plastic surgery, pediatric cardiology, pediatric surgery and neonatology is important,
establish early intervention program, and determine the possibility avoiding long term sequelae. Thank you very much.
- 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.
- 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.
- 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.
- 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,
- 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
- Thank you very much. Thank you, Frank, for inviting me again. No disclosures. We all know Onyx and the way it comes, in two formulas. We want to talk about presenter results when combining Onyx with chimney grafts. The role of liquid embolization or Onyx is listed here.
It can be used for type I endoleaks, type II endoleaks and more recently for treatment of prophylaxis of gutters. So what are we doing when we do have gutters? Which is not quite unusual. We can perform a watchful waiting policy, pro-active treatment in high flow gutters,
pro-active treatment low flow gutters, or we can try to have a maximum overlap, for instance with ViaBahn grafts 15 centimeters in length or we can use sandwich grafts in order to reduce these gutters in type I endoleaks. Here, a typical example of a type I leak treated with Onyx.
And here we have an example of a ruptured aneurysim treated with a chimney graft. And here is what everybody means when they're talking about gutters. Typical examples, this is what you get. You can try to coil these
or you can try to use liquid embolization. Here's the end result after putting a lot of coils into these spaces. What are these issues of the chimney-technique type I endoleak? Which are not quite infrequent as you see here.
Most of these resolve, but not all of them. So can we risk to wait until they resolve? And my bias opinion is probably not. Here, the incidents of these type endoleaks is still pretty high. And when you go up to the Arch
the results can even be different. And in our own series published here, type I endoleak at the Arch were as high as 28%. A lot of these don't resolve over time simply because it's a very high flow environment. Using a sandwich technique is one solution
which helps in a lot of cases but not all of these simply because you have a longer outlet compared to a straightforward chimney graft. You can't rely on it. So watchful waiting? There are some advocates who
prefer watchful waiting but in high flow gutters this is certainly not indicated. And the more chimneys you have, like in a thoracoabdominal aneurysm with four chimneys, the less you can wait. You have to treat these very actively,
like you see here, in these high flow areas. Here a typical example, again symptomatic aneurysm with sealing. Here Onyx was used but without any success. So what we did is we had to add another chimney and plus polymer sealing and then we had a good result.
Here some results, only small serious primary gutter sealing using Onyx with good results in a type I leak. But again, this is only a small series of patients. Sandwich technique already mentioned. When you use, like we did here for chimney grafts in the arteries, you do need Onyx otherwise you
always get problems with these gutters and they do not seal over time. Another example where liquid polymer was used. And here again, you see the polymer. The catheter in order to inject the polymer is very difficult to see but with a little bit of experience
you know where you are. And again, here it is, the Onyx, a typical example. Here another example of the Arch, bird beacon effect, extension, chimney graft. Again the aneurysm gets bigger. And so a combination of using proximal extensions
plus chimneys plus liquid embolization solves this problem after quite a long period of time. And here typically is what you see when you inject the Onyx. This does not work in all cases. Here we used Onyx in order to seal up the origin of the end tunnel.
This works very nicely but there is so ample space for improvement and in some cases it's probably better to use a fenestrated branch graft or even the opt two stabler instead of using liquid embolization. Thank you very much.
- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,
but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody
with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?
And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy
for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,
thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world
for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and
patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt
to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize
what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,
and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,
it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would
ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a
experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,
but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,
it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,
place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,
any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution
using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation
and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology
and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,
it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,
and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a
single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,
and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,
a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at
alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,
and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.
There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,
Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.
Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings
in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?
I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,
you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.
So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,
we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.
- 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.
- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.
They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression
if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.
Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.
This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,
and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients
who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,
and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,
symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.
There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,
again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,
six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,
it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse
if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective
in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.
This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent
because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common
in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.
So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,
those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,
like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.
And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,
get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.
If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners
over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,
it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,
look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.
That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,
then I would do something endovascular. 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.
- 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.
- 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.
- 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.
- 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.
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.
- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.
Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates
an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.
You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't
or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.
CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,
we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.
She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.
So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.
Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.
It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign
and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there
but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?
Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy
and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.
So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,
a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,
gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection
it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible
before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains
in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low
or cut out the super renal fixations so you can take them out a little easier. 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.
- Jim, thanks so much, and thanks to Doctor Veith for the opportunity to get involved. Here's my disclosure. So, certainly you don't want to be an expert on limb thromboses, however, it happens. And so, when you see these patients, no longer are we looking at fem-fem,
or even lytics, catheter-directed lytics. So how do we get from screen left to screen right in a single session therapy? Well, as we know, when these patients present, there's several different management options. You can do open thrombectomy with or without
a fem-fem, pharmacomechanical thrombectomy. There's catheter delytic and ultrasound accelerated thrombolytics, and then now, today, we have vacuum-assisted thrombectomy, as we've heard throughout this session, or continuous aspiration thrombectomy,
however you want to mention it. Regardless, when you end up with lytics, this is exactly what you're dealin' with. You're playing with fire, and if we do it long enough, you're going to see this complication. So we've really adopted a clot extraction
instead of a clot dissolution policy at our institution. I think Jim just showed you this technique that is afforded to us by the Indigo thrombectomy system, as you can see here in a Vivo model, this catheter actually does work extremely well.
It'll remove this soft thrombus, as you can see here. My first experience with this was actually for an occluded popliteal stent, as you can see here. We had a occlusion of the standard nitinol stent. This aspiration power was incredibly surprising to me. As you can see, it collapsed the standard nitinol stent.
So at that point, several years ago, we realized how good this device was, and how we want to minimize lytics for our folks. So we started in 2014 and recently this year at the Midwest Vascular forum in Saint Louis, we presented our data.
At that time, we had 73 patients over the years with acute limb ischemia. And here you can see the breakdown. For this presentation I'm going to focus on this cohort here, which is seven. But as you can see, like my panelists here,
we use it for occlusions, for not only occlusions but emboli as well, and also we had one case of an upper extremity embolism that we were able to successfully treat with this device. At that time, again, looking at all 73 patients,
you can see here that it's a very efficacious device. There were a couple folks who needed transfusion and perhaps the blood loss was a little higher than 300. However, as you can see here, the folks who had a blood loss, all five had open adjunctive interventions as well, and the ones who needed transfusion
all had catheter directed lytics as adjunctive therapy. As far as our efficacy endpoints, what we looked at was antegrade flow. As you can see here, oftentimes with your vacuum system thrombectomy, you're able to get antegrade flow. However, intermittently there's also other
adjunctive therapies that we had to use frequently as well. Going back to what, you know, my topic for today, how do you go from screen left to screen right, where here you can see one of our patients who came in. We did a retrograde ipsilateral stick,
crossed the lesion with the wire, then we delivered our eight french Indigo catheter and were able to get, in a single session, as you can see here, antegrade flow. So here's another, all this in one single session therapy. Here's another patient of ours.
As you can see to the left, one of our Gore Excluder limbs had occluded, and again, with single session therapy we were able to provide patency to that occluded right limb. Another case here, you can see one of our other Medtronic grafts.
And what you'll see here as you're looking to the right, here we are with our eight french Indigo catheter, is the separator, which is like a pipe cleaner. And we were able to clear out this clot and provide patency to this
all in a single session therapy. And again, here you can see from left to right how we were able to thrombectomize that limb. So over the years, the last three years, we do about 80 to 90 EVARs a year. During that time period, we have seven patients
come in with limb occlusions. And as you can see here, four of them were chronic, three claudicants and one res-pain, and three of them were acute limb Rutherford one, two A or two B. As you can see here, 42% of the time for these
occluded limbs, we were able to do it with no lytics, not even a pulse spray, nothing, not one drop of lytics. As you can see here, some of them we did have to do it in a single session. What we do is use a McNamara catheter.
We would squirt out, you know, anywhere from, as you can see, 14 to 18 milligrams of lytics, go get a cup of coffee, go make rounds, come back 20 minutes later, then utilize your device. And again, you can see, in a single session therapy we were able to afford patency.
And then finally, you can see here the blood loss was minimal. So this is a safe device. So in conclusion, I think that single session therapy is safe. It can facilitate achieving antegrade flow
in the management of stent graft limb occlusions. And single session therapy is the future of not only stent graft limb occlusions but all acute limb ischemia. Thanks so much.
- Thank you Louie, that title was a little too long for me, so I just shortened it. I have nothing to disclose. So Takayasu's arteritis is an inflammatory large vessel vasculitis of unknown origin. Originally described by Dr. Takayasu in young Japanese females.
The in-di-gence in North America is fairly rare. And its inflammation of the vessel wall that leads to stenosis, occlusion or aneurysmal formation. Just to review, the Mayo Clinic Bypass Series for Takayasu's, which was presented last year, basically it's 51 patients, and you can see
the mean age was 38. And you can see the breakdown based on race. If you look at the early complication rate and we look at specific graft complications, you had two patients who passed away, you had two occlusions, one stenosis, one graft infection.
And one patient ruptured from an aneurysm at a distant site than where the bypass was performed. If you look at the late complications, specifically graft complications, it's approximately 40%. Now this is a long mean follow up: this is 74 months, a little over six years.
But again, these patients recur and their symptoms can occur and the grafts are not perfect. No matter what we do we do not get superb results. So, look at the graft outcomes by disease activity. We had 50 grafts we followed long-term. And if you look at the patency, primary patency
right here of active disease versus non-ac it's significantly different. If you look at the number of re-interventions it's also significantly different. So basically, active disease does a lot worse
than non-active disease. And by the way, one of our findings was that ESR is not a great indicator of active disease. So we're really at a loss as to what to follow for active or non-active disease. And that's a whole 'nother talk maybe for another year.
So should endovascular therapy be used for Takayasu's? I'd say yes. But where and when? And let's look at the data. And I have to say, this is almost blasphemy for me
to say this, but yes it should be used. So let's look at some of the larger series in literature and just share them. 48 patients with aortic stenosis fro all were treated with PTA stenting.
All were pre-dilated in a graded fashion. So they started with smaller balloons and worked up to larger balloons and they used self expanding stents in all of them. The results show one dissection, which was treated by multiple stents and the patient went home.
And one retro-paret-tin bleed, which was self limiting, requiring transfusion. Look at the mean stenosis with 81% before the intervention. Following the intervention it was 15%. Systolic gradient: 71 milligrams of mercury versus 14. Kind of very good early results.
Looking at the long term results, ABI pre was .75, increased to .92. Systolic blood pressure dropped significantly. And the number of anti-hypertensive meds went from three to 1.1. Let's look at renal arteries stenosis.
All had a renal artery stenosis greater than 70%. All had uncontrolled hypertension. They were followed with MRI or Doppler follow up of the renal arteries. So, stents were used in 84% of the patients. Restenosis occurred in 50% of them.
They were, all eight were treated again, two more developed restenosis, they ended up losing one renal artery. So at eight years follow up, there's a 94% patency rate. What about supra-aortic lesions? And these are lesions that scare me the most for endovascular interventions.
Carotids, five had PTA, two had PTA plus stent. Subclavian, three PTA, two PTA. One Innominate, one PTA plus stent. One early minor stroke. I always challenge what a minor stroke is? I guess that's one that happens to your ex mother-in-law
rather than your mother, but we'll leave it that way. Long term patency at three years, 86%. Secondary patency at three years, 76%. Fairly good patency. So when Endo for Takayasu's, non-active disease is best. The patient is unfit for open surgery.
I believe short, concentric lesions do better. In active disease, if you have to an urgent or emergent, accept the short term success as a bridge to open repair. If you're going to do endovascular, use graded balloons or PTAs, start small. Supra-aortic location, short inflation times
I think are safer. And these three, for questions for the future. I guess for the VEITHsymposium in three years. Thank you.
- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want
in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis
is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied
and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple
aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention
adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,
the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that
there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions
a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.
In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure
with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle
and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis
needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.
Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.
In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,
regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate
without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.
An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis
and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.
This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more
in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.
But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.
The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.
Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion
because I have a flight in a few hours. Thank you very much.
- 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.
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