- Thank you very much Neil. I would like to thank Dr. Veet for having placed this talk in the program. I have no disclosures. Duplex scan is a very cheap methodology. I'm always surprised how people are not using it more. We have a dedicated ultrasound machine
in the operating room, and that makes it much easier for us to use it. We also learned that it's extremely sensitive to low flow. It can detect bleeding vessels when the arteriogram shows an occluded vessel.
It's better than a CT also for low flow situations. There's several advantage for ultrasound guided interventions. There's no radiation. No nephrotoxic contrast material. Multi-planar, magnification,
and you can visualize the arterial wall in addition to the lumen. You can perform a balloon angioplasty, as we've shown and reported before, as well as stenting and arterectomies. Basically, if there is a complication,
you can also treat the complication on the ultrasound alone without requiring x-ray. At the end of the procedure, you can confirm the adequacy of your technique, both anatomically and hemodynamically. The arterial mapping is very important
because it reliably identifies in inflow and outflow vessels, whether it's an acute situation or chronic occlusion. It selects the best site for an anastomosis if you're going to do a bypass, because you can select the least calcified segment.
Identifies the causes of occlusion, and occluded popliteal aneurysm versus arterosclerotic occlusive disease, and visualizes a low flow patent arteries that are not seen by arteriogram. We have done over a thousand cases,
and we're going to concentrate on the femoral popliteals that we perform on the duplex scan alone. Basically, the same demographics as you have in your own practice, with the age being of 73. The technical success was 95% on these patients.
99.6% for stenoses and 87% for occlusions. We did have some complications. We're going to concentrate on the thromboembolic complication of these cases. We have 12 out of 237 cases. Also, we added another 15 cases for these presentations,
where we have done duplex guided procedures and patients did embolize or occluded. 12 are infainguinal arteries, and three were bypasses. The treatment was mechanical thrombectomy in 64% of the cases,
thrombolysis alone in 20%, mechanical thrombolysis in 8%. Thrombolysis, suction, thrombectomy, and a new stent in 8% of the cases. Overall results were excellent. 88% of the patients did not require any further study,
and any further methodology for visualization of the vessels. Here's an example of a patient that had an embolus at the the tibioperoneal trunk. We placed a catheter. We injected tPA and 20 minutes later,
we did a duplex scan and was widely patent. This was done, did not require any further studies. This patient had a impossible case, was a clot that formed on top of the balloon, as you see here. On top of the balloon the clot,
so injected tPA here approximately before we deflate the balloon, and then we waited again. Then after, once we deflate the balloon, there were no more clots. This patient had an embolus to the SFA
and the popliteal, and the entire SFA was occluded. We puncture on ultrasound guidance and you can see the wire going through. You can visual, I'm sorry. Can you work it up again? Next? There you go.
Sorry, he was just showing the area of the puncture. We're placing the wire and the sheet, of course. Over the wire, we're going to put a suction thrombectomy device without going below the popliteal. You can see clearly the tip of the wire.
And now, we bring the suction thrombectomy device all the way to most distal portion where the occluded segment occurred. Now we're doing suction thrombectomy after injecting tPA. First we did thrombolysis,
now we're doing suction thrombectomy. Now we can see that it's not perfect, because the volume flow is very low. The peak systolic is very low. Obviously, there's a stenosis somewhere and we detected the stenosis in the SFA.
We had a wire cross, so that was easy. We did a balloon angioplasty and stenting, because the balloon angioplasty alone was not enough. He required the lesion. You can see, even with the stent, there's an area of stenosis that needs to be re-ballooned.
Now we ballooned it and we're basically done. Now the volume flow and peak systolic velocity are great, as I show you here, and we're done with that procedure. Just to finalize. Just the stent that was occluded acutely, and here's the suction device.
Again, the same thing. Look at the power of the suction device. It's going to bring the stents together, actually. All the way and I'm sure Dr. Veet's going to stop my talk any moment now. Here we go and see, and basically it's done.
So, the conclusion's obvious. You avoid the nephrotoxic agents. You visualize the low flow arteries. You identify the cause of occlusion. Those are unique to duplex scanning. Patients with acute arterial ischemia of diverse etiology
can be safely treated by various endovascular procedures under duplex guidance alone. Thank you very much.
- I am not Walter's enemy. I can tell you that. I am against the motion. (man laughing) I will stick to the truth, to the facts. I don't like polemic, like you. I don't like to play, let's say games
of undermining what my opponent is saying. I'm just showing what I believe in because it is the truth, okay? (quiet laughter) I have nothing to disclose. Let's stick to the definition of 'cure.'
We all know that 'cure' means 'at least one year follow-up, angiographic follow-up after the, so-called, final angiography, that shows that malformation is gone.' Call it whatever you want.
Technical success, obliterated, trombosed, concluded, ablated, gone. Then at least one year follow-up on that. Angiographic to prove it's gone. The rest is just a scale on how you can evaluate the results.
Angiographically and clinically. The only way, for me, to speak to the truth is to find in a material where there is a chance to compare.
Hat to hat. Both type of treatments. Polymerizing versus alcohol. And, the only way to find such a place is to go to Wayne's place, because he's also constantly called
talking about salvaging this and salvaging that. I am very critical about what Wayne does. You can be assured about that. He's had 16 patients, I dig out there, and polymerizing agents they were failed.
Definitely, failed. Actually, they were salvaged, by Wayne. And, I'll show that to you. These are the patients. This is the time to which they've been treated. The usual type of distribution.
Young patients. All of them extensive. There is no, for a lack of an effort. There is no, for a lack of knowing how to use
the polymer. Onyx. How we can tell that, most of those is Onyx, some of them are glue. Or a combination. The median number of sessions
with this polymerizing agent is 8.5. Range from one to thirty. The other radiologists, the other experts, besides my honorable opponent, Doctor, Professor Wolgemuth,
they also know how to use Onyx. I can assure that. Sixteen patients, all symptomatic. They are all decompensated, showing three, four tier symptomatically. They have high cardiac output,
they have required repeated, repeated blood transfusions, infections, ulcers, disarticulation. To have disarticulation of vascular malformation means, oh, horrible bleeding, infected. There is no doubt,
they are symptomatic. Couple of examples. This is a young woman, extensive AVM in the foot, type four. Been treated five times with Onyx. And they know what they've done.
They've treated well. Yet, worsening symptoms, wheelchair bound, infected ulcer. Seventy-one session. Now, pay attention. Seventy-one sessions of ethanol/coils embolization. And, this woman is now running with her friends
after her amputation of couple of necrotic toes. Not because of the alcohol. Because of the malformation. Angiographically, not cured. Example of that. Okay.
This is malformation. This is not something in a tiny, little bitty thing. It's a malformation, no question about that. Before treatment. And, this is after treatment. We can all agree that,
this is not completely cured. It is a grade three it is 80 to 99 percent still left. But, clinically, she's running. She continues to be treated. Another example.
One year old girl with bleeding malformation from the lip. Admittedly only one Onyx being used because we didn't know what to do. Luckily, the little girl was close by so she came to Wayne and after,
it's intravenous predominant lesion. It's a type two lesion. Only after a six month treatment sessions, cured. This is before start of ethanol treatment. No question there is recurrence. We can not close that only by pushing
polymerizing agents somewhere in something called 'nidus.' But if you ablate the cells, ablate the nidus. You achieve cure.
And it's cured in one year angiographic follow-up. This is time and time and again. I will show these examples. This is the outcome. The outcome tells you six cured angiographically. Eight considerably improved, they improved.
None of them is failed in this. All failed polymerizing agent treatment. Then we can move on. Complication because that's where talking about how dangerous. Alcohol is very dangerous,
but so is knife in operating room. Take a knife and stab it somewhere in some artery, or in a pressurized vein, you'll have all this blood in your face and a shoot of blood doesn't taste very good in your mouth. So it's dangerous.
But, if you use it carefully, that's what you achieve, as a result. Where do we stand with these patients? Ongoing treatment, five. Cured, five, by summation.
One still waiting for a follow-up on angiographic follow-up. Improved on watchful observation is two. Lost to follow-up because schizophrenia. Lost to follow-up because of unknown reason, after two years of follow-up.
He's been doing well throughout these two years. One clinical failure. I will tell you that Wayne have, he's seen this person. Not clinical failure. Yeah, it's clinic.
By definition, is clinical failure. Angiographically, improved. Clinically, improved. The little boy was wheelchair bound, didn't want to continue with that and, therefore, went for amputation.
So it's a clinical failure. One. To summarize that, I highlight on this, venous predominant lesions. These are the ones these create.
Type four. (man speaking off screen) Tough. Couple of examples. Striking examples. This is venous predominant lesion, IIA.
I'm sorry. IIIa, IIIb being treated. Sorry. Can we go back to that? Any way I can go back on that?
This IIIa, IIIb, there's has been five. That's moves forward. Five surgery, Onyx, anything thrown in. Extensive malformation. Shoulder, arm, a no-flow into the lower arm
because of the. And it's moving forward. I'm sorry for that. But it was cured. And there was a follow-up, too. I believe there was something.
Twenty, 15, 17 months follow-up. So we have the next patient. Thirty-two year old female treated with glue in the past.
Twenty procedure including all vessels. Everything that can not be, could be embolized, was emolized. Ended up with the worsening and this is the typical example a IIIa malformation, typical example.
This was way back in the past. This is how Wayne has developed that. It took him, I heard, nine hours and another 100 coils, but he cured that.
- [Male] 298. - Two hundred ninety-eight. This is the follow-up, you know. Eighteen months later. To summarize on that. Nothing to do with my feelings for Wayne.
Nothing to do with Walter being my enemy. (quiet laughter) No, it's just a fact, a truth. Polymerizing agents, by definition, do not cure AVMs. Do not cure.
Sometimes, when used properly, still worsen the patient's symptoms. Ethanol cures AVM. Provided that you do that with precision and skills. How you acquire precision and skills? Ask the surgeons around here.
How do they lift up this face? How Max can lift out, you know, big time metastasis sections in liver? How do you do that? With skills.
How do you acquire skills? Learn. Thank you.
- Thank you Jose and Marcia. No disclosures. So the primary valve incompetence treatment techniques was started by Bob Kistner and the techinique involved a longitudinal internal valvuloplasty by longitudinal incision and tacking of the redundant valve edges.
And the next treatment available was a transverse valvuloplasty which was again under vision and the valves were tacked at the at the commissures but the incision was transverse. And a combination of the two techniques resulted in the technique of Sottiurai, the T internal valvuloplasty
which was later modified by Michel Perrin to be able to evaluate all aspects of the valve. Further to that, we developed the trapdoor internal valvuloplasty in which a trapdoor was created. All these techniques, the mainstay was reefing of the valve commissures.
On the left hand side, you can see a redundant valve, prolapsing cusps, and on the right hand side, a repaired valve after the reefing. But you can see that the commissure is quite heavily placated. So the possible disadvantage of reefing technique
is the resultant heaped up commissural junctions. This creates valvular rugal folds and obviously when healing occurs it will have increased cicatrization, it will occupy the space, and reduction of functional valve area. When we evaluated the various thrombosis results of
supra-valvular technique, modified T technique, and the trapdoor technique, we found that on an average, there was about a 4.5 to 9% incidence of valve thrombosis. And we also found that in another 6.1% patients there, the valve stations resolved. Cumulatively, these two complicates accounted
for almost 13% of all valvuloplasties. We published a new technique of reduction internal valvuloplasty on the lessons that we leared from Dr. Lugli's experience. And we wanted to quantify the repairs that we do by measuring intra valvular distances and
trans-commissural diameters preoperative as well as intra-operative by ultrasound. We used various techniques, we devised measuring forceps and this is how it's done, whereby we are able to excise the redundant valve and stitch it back onto the valve
and have no rugal folds at the end. And this can induce, this can reduce incision in high shear areas as well. And therefore, give you a good result. This is intra-operative result of competence where you can see the patient is doing valsalva
and you can see the two valve leaflets and this is the stripping technique. And a post-operative descending angiogram or venogram shows a competent valve. So when we looked at the relationship of reflux, valve repair, and ulcer healing,
we found that when we did single level repairs, we only found 50% ulcer healing. But when we did multiple level repairs, the healing was 100% in a short period of time. And the valve competency always did not correlate with ulcer healing.
In our case the valve competency levels were 87.5% and ulcer healing was 88.9% but mainly due to the single level repairs, that did not really work. So the Rival Technique in conclusion ladies and gentlemen is a complete departure from the reefing technique which has been the mainstay of valvuloplasties.
At two years, we've had 100% patency and about 87% competency of repaired valves, with a freedom from C6 ulcers at two years about 89%. Rival Technique has now replaced our technique, earlier techniques, and is the preferred technique in our center.
Thank you for your attention.
- Good afternoon. I have no disclosures. I was going to say that the bulk of this work was done by Johnston Moore who's a 3rd-year medical student with us and my partner, Ben Pearce does the novel work that's in this. As you all know there are a number of risk factors
for peripheral vascular disease and diabetes is certainly one of the more important ones. And that's what I'm going to talk about in this talk. This image here shows you the odds ratio increase for peripheral vascular disease with each of these risk factors.
Why should we care? If you look at this map in 1995, it was all yellow, in the 0-6.5% rate of diabetes and now much of the country is getting to look like Alabama, where we say we're in the heart of the biscuit belt.
This is the increasing rate of diabetes diagnosed in the country over a 50-year time span, over 50 years, and you can see that it seems to be ever increasing. The importance of limb preservation, I don't need to tell this group for patients
that get a higher level of amputation more often go to nursing homes and more often end up in a wheelchair. So limb preservation is very important. This slideshow is a functional outcome after amputation, which decreases with a higher level of amputation. And diabetes is known to be associated
with higher levels of amputation. As you may know, Hemoglobin A1C has been linked to lower extremity amputation in diabetic patients and worsened Hemoglobin A1C increases the risk of amputation and higher level of amputation. This is a nice meta analysis that shows multiple papers
that demonstrated that an increasing Hemoglobin A1C over 7 increases the risk of amputation by 26% for every 1% rise in A1C level. Another interesting paper about insulin-sensitizers. So these are the glitazone drugs and Metformin. There is some suggestion that patients
that are on a sensitizing agent in addition to insuin have a lower risk of amputation. They also have a lower risk of peripheral arterial disease in general. Comparison to patients that are on insulin only they have a lower risk of requiring revascularization
and a lower risk of amputation as I said. So we did a project at UAB, looking at these questions about A1C and a choice of diabetic control regimen, and thus impact on amputation and amputation-free survival. When we pulled patients who had A1C levels within three months of their procedure
we ended up with 306 limbs. And we looked at patients that had amputation and/or death, both endo and open revascularization. And what we found was a simple diagnosis of diabetes, and this is not new, increased the risk of amputation pretty significantly.
Here this is one year amputation-free survival, 78% of non-diabetics and 61% in diabetics. As I said, just a simple diagnosis of diabetes was actually the more important risk factors. But an insulin only diabetic was the most significant risk factor for amputation and increasing level of A1C
was approaching statistical significance. A multivariate logistic regression, Creatinine, insulin-only management, and age were associated with amputation. So in summary, the diagnosis of diabetes increases overall mortality, that's known.
Decreases amputation free survival and in a small cohort there was a trend towards higher amputation rates for poor glucose control measured by Hemoglobin A1C. The glycemic control strategy was significantly associated with amputation free survival. So those patients with only insulin control
had higher rates of amputation. The strongest predictor of poor amputation free survival, as I mentioned, is diabetes, but the modality of glycemic control does impact the outcome and insulin sensitizers may improve patient outcomes over time.
- This work has been done by in my hospital with collaboration of the University of Bologna in Italy. We have no financial disclosures. So all starts from the result of a new TECCO study, but it was published last year showing that stenting was equivalent or even be better in surgery for the de novo common femoral and deep femoral arterial stenosis.
This was a small randomized study of around 117 patients with common femoral artery stenosis. Interestingly enough, 86% of his patients were claudicants, so the applicability of a randomized control trial should be limited to claudicant. The primary outcome was on the patency,
but it was with complication. The combined rate of morbidity and mortality that was 26% in the open surgical arm, and 12.5% in the stent population, and this was just significant. After a median follow up of 24 months, the rates of primary
patency target lesions and system clinical improvement were similar in the two groups. There was no mortality in every group, but one stroke in the endovascular arm. Minor complication were more often seen in the surgical arm with hematoma, delayed wound healing, temporary lymphatic
leakage, paresthesia, but no infection of a graft. The follow up in this small study was not powered enough to assess secondary endpoint, and only 46 patients were available at 24 months for analysis. And the length of stay in the stent group were three days, and six days in the surgical group.
So if you go through the Vascular Quality Initiative published by (mumbling) last year, we find that the 30-day mortality was 1.6%. And the access site hematoma was 5.2%, with a risk of arterial dissection. We have a total rate of complication of nearly 10%.
And interestingly enough in this Siracuse study, was where mostly claudicants were taken care of. You see that the result depends on the symptomatology. If you have a patient with critical infracting ischemia, you have real operation and bad result with the endo first technique.
We have studied our result. In a retrospective study of nearly 150 open revascularizations, half claudicants, half rest pain, and our 30-day result we had 98% of primary patency, three occlusion, 1.7% of mortality at 30 days, 1.4% of cardiovascular complication MI,
groin wound complication was seen in five percent of cases, and in multivariate analysis, only tissue loss and infection, wifi three-four was a predictive factor for wound complication at the groin. This is perhaps the most important aspect of the study. This is what we're seeing in these patients.
As you see here, most of the lesion were at the orifice of a deep femoral artery in more than 73% of the cases. So if you do endo in this application, you can jail or covered the deep femoral artery. Inside of this by open surgery you can clean both artery and leave a good vascularization.
In our practice result in claudicants are excellent, are shown here. They are not so good in patient with rest pain and gangrene because obviously these patients with CLTI and occlusion of the popliteal and infrapopliteal artery needs a popliteal or tibial revascularization
in addition to that of a deep femoral artery to save a foot. So we think that until now open surgery is still the best option in most cases. Thank you.
- The proposition is polymerizing agents can and do cure AVMs and are now the agents of choice, ethanol is too dangerous. When I saw what Wayne had asked me to talk about, I immediately called him. And I said there are two words in this proposition
which are giving me some trouble. The first word is dangerous. In IR we do dangerous every day, especially in July. And with respect to cure in IR, mostly we just try to fix things.
Nonetheless, there are proper uses of ethanol. There are, however, some risks to the use of ethanol in medicine. First off, ethanol is a sclerosing agent and it is toxic to tissue. It denatures the proteins
of the endothelium, activates the coagulation system and produces blood clots. While we are trying to do that, when we're trying to control an AVM, it does also generate acetaldehyde and reactive oxygen species
which damage healthy tissue. It can result in endotoxin leakage, inflammatory cytokine release, and modification of signal transduction in the cell membrane and when we deliver alcohol, unless we dilute it with contrast,
we really cannot see where it goes. There are some other issues with ethanol. The first is that it's known to impair wound healing. If ulcers occur with ethanol use, they are difficult to heal. If you place skin grafts on these lesions,
they typically fail. And if you use ethanol in an area of prior surgical scar, there is a high risk of skin injury. In addition, the use of ethanol is associated with pain, it's a painful procedure.
If you deliver ethanol in proximity to a nerve, you will develop nerve injury and if you have sciatic nerve injury, that can be devastating which can take months if it all to heal. The other issue relates to the dosing
and the volume of ethanol that's delivered. If you deliver high doses of ethanol at one sitting, you can get systemic effects. Now, a slightly tipsy patient post-embolization is not necessarily a big problem, however, if the patient develops hemoglobinuria,
that can be significant. If you use low volumes of ethanol with each treatment, it requires multiple treatments. You can also get cardiopulmonary problems with ethanol. The ethanol can induce arrhythmias, it can induce bronchiospasm,
it can precipitate pulmonary emboli because of the sludge that migrates up to the lungs and you can get cardiovascular collapse with the use of ethanol. Fortunately that is rare. Other polymers such as the cyanoacrylates
or liquid embolics and their viscosity can be altered. The downside in our experience with the cyanoacrylates is that they're difficult to control, they tend to spatter.
And our long-term experience with the cyanoacrylate shows that it is not permanent and it does degrade. The ethanol vinyl alcohol copolymer or Onyx behaves as a filler. It induces a mild inflammatory reaction.
It's associated with minimal pain post-procedure and skin injury is infrequent and it is in our experience a permanent agent. There may be difficulty getting it to travel deep into the nidus and that can be a big problem,
if you just deliver the Onyx in just a push away, it will not go very far and you will leave your nidus untreated which can lead to recanalization. So, we dilute our Onyx 18 with DMSO
which makes it more easier to spread out into the distal portion of the malformation. It is somewhat harder to see when it is diluted. We also use a glue roadmap. This will reduce our radiation dose
and we don't deliver the Onyx the way the neuro-interventionalists do, we tend to deliver it much faster than the neuro people do. And if you have obscuration of your vessels by prior Onyx placement, the glue roadmap can help.
When we use Onyx without operative resection, it is an off label use. But nonetheless, when used, it does facilitate operative resection and you just have to remind your surgeons to use a bipolar bovie otherwise you will get sparking.
With respect to cure. I think cure, when we talk about it, it really depends upon our definition of cure. Polymer occlusion will result in relief of AVM symptoms. And it can cure some lesions.
Whether we are able to remove all shunting in large lesions I think is doubtful, but nonetheless, Onyx copolymer is associated with lower morbidity than alcohol. And when we look at ethanol versus polymers, the ethanol is a one-generation agent.
Whereas if we look at polymers, if we consider cyanoacrylate as a first generation and Onyx as a second generation, and squid maybe as a third, the future is pretty much unlimited for us because you can prepare polymers which will contain drugs
or other agents. So, I think the choice is you have to determine whether you want to use ethanol, or whether you want to use a polymer. Thank you.
- So these are my disclosures. So I tried to divide this talk up into four areas that are common that occur in our practice at Mayo. One will cover guidelines. What do the chest guidelines and SIR guidelines show?
And a statement by the AHA, and then patients with PE that are presenting in different phases, and then patients that have a subset of CHF and then obviously special patients such as pulmonary embolectomy.
And so let's talk about the guidelines. And I think it's really important to understand a few factors when you're considering putting filters in. One is obviously the workup of the patient, and what are their anatomical considerations?
Number two the extent of clot burden, and then number three the hemodynamics of the patient for their age and how did they get to you? And then fifth you can look at the guidelines to help you.
So, what is the circumstances that a provoked DVT, unprovoked DVT, with and without malignancy, what is their age? I'm not going to cover that, but that's in the setting of what you should be considering as you think about that.
So these are the guidelines the chest guidelines are on the top, and then the SIR guidelines and there's pretty good uniformity between the two guidelines at least for placement of filters and I've highlighted those.
For example acute proximal DVT if you can't anticoagulate because of risk of bleeding. So that's a 1C recommendation. Part C there is in the treatment of PE acute PE if anticoagulation is not possible because of risk of bleeding.
And then SIR guidelines recommend absolute indication for proven VTE, recurrent VTE despite anticoagulation or contraindication to anticoagulation. So these are really guidelines to help us think about how we would manage these patients
and where we would place filters. And again the other thing that we have to remember is that some of these guidelines were written when we were still doing a fair bit of permanent filters and now with the FDA recommendations
for temporary filters if you put a temporary filter in, or an optional filter you're obligated to schedule the patient for a return to your office to come back for removal. And that creates another set of challenges
for our patient. How do you get em back? How do you schedule em for a return? When do you schedule em for a return? And then obviously does every patient need a filter removal?
Does a 90 year old patient with a optional IVC filter need an aggressive treatment for filter removal than a 50 year old for example. And so these are the guidelines. And these are the relative indications.
If you're not sure, these are sort of on the... Depending on where you're at for example large free-floating proximal DVT ilio clot in transit gets a filter placed as well. So I want to talk about a scientific statement
that Mike, Dr. Jaff co-chaired. And this was a statement from American Heart, and it really also provided some guidelines also for IVC filters in the setting of acute PE, and it listed different scenarios
of when you might place a filter. Adult patients with an acute PE very similar to what the SIR guidelines and AACP were. This was class one level B that could not be contraindicated or anticoagulated
due to excessive bleeding. Number two was anticoagulation should be assumed in patients with an IVC filter once contraindications to anticoagulation or active complications have been resolved. And we're going to talk a little bit about
how they got to this. And then patients who have retrieval filters should be evaluated periodically. That's very important I sort of alluded to this. If you place a filter, you need to somehow have a mechanism in place to bring em back.
In our facility every patient that gets an optional filter placed, has a nurse assigned to making sure once their care has resolved and they're ready for filter removal that they're scheduled for a return with an office visit.
And then number four recurrent acute PE despite therapeutic anticoagulation. It's reasonable to place an IVC filter very similar to the chest guidelines, and I won't repeat the rest. So how did we get here?
So this is the first paper that I'm going to review. This was a clinical trial of permanent filters in patients with proximal DVT. So permanent filter this was 200 patients randomized to permanent filters for preventing clots.
And what this paper showed was that if you had an iliofemoral DVT and a clot and you got a filter, that it put you at a higher risk for filters and really didn't prevent PE. And so this is number one paper that's
very important that we should recognize. So this is again permanent filters four different types of filters that are basically not used that often. One of them is the Bird's Nest. And this was a New England Journal paper
a PREPIC 1 trial, and this is what the age group were and the filters are very well matched. This was the gender as you can see the baseline characteristics very well matched. And this is table two this was the endpoint
within the first 12 days. And if you look at the filter group, you'll see that there was PE: two symptomatic in the filter group, five in the non-filter group P value 0.03, major bleeding was about the same
nine in the filter group versus six. So again, filter plus anticoagulation versus filter alone. And then there's death no difference in death. And so this really helped set the stage in the early or late 90s early 2000s
of how to manage permanent filters. And this is principle endpoints at two-year follow-up in the filter group versus non-filter group. And you can see symptomatic PE no difference. Recurrent DVT there was a difference,
and this sort of changed the way we managed filters and our temporary filters. We used this data set to help us with iliofemoral DVTs for example, and this is major bleeding and death. So again, no difference between
filter and no filter. And this is within 12 days. This is the principle endpoint within first 12 days after randomization. Between Heparin and Unfractionated Heparin because patients were treated with either
of the therapy again showing no difference. And this is the last table from that paper which is endpoints during the two-year follow-up of Low-Molecular Weight Heparin again showing no differences between Low-Molecular Weight Heparin
and Unfractionated Heparin. How about retrievable filters? The French group the same set of authors looked at the same problem, but looked at it with retrievable IVC filters. And what they wanted to do is evaluate
the efficacy and safety of retrievable IVC filters plus anticoagulation versus anticoagulation alone for preventing PE. In patients who were at risk for acute PE and a high risk for, or had acute PE and were at a high risk.
So this is retrievable IVC filters, and what is this study shows. So this was a study again done outside the US. It was randomized, open label, blinded endpoint, PREPIC2 with a six-month follow-up. Took seven years to enroll 400 patients.
Patients had to have an acute symptomatic PE with a lower limb DVT, and have at least one criteria for severity. They were assigned to retrievable IVC filter implantation plus anticoagulation or anticoagulation alone,
and they had to have a planned retrieval of filter at three months, six month follow-up data. The primary endpoint was symptomatic recurrent PE at three months and secondary outcomes were recurrent PE
at six months, symptomatic DVT, major bleeding, death at three and six months and filter complications. And the results showed that in the filter group the filter they had a few patients that couldn't get the filter so they
could have placed 193 filters out of 200, and they were retrieved 153 were retrieved of the 164 in which retrieval was attempted. So again you're seeing patients not getting filters retrieved. By three months recurrent PE had occurred
in six patients in the filter group versus three. So you saw a prevention of recurrent PE in patients with a filter, and the results were very similar at six months. So you see the confidence intervals there. There was no difference observed among
the two groups regarding the other outcomes. And filter thrombosis occurred again in three patients. So what about IVC filter and PE plus or minus thrombolysis? So I'm going to show you a couple of studies
that suggest that patients that are with PE and thrombolysis may do better with a filter. And these are large databases. The first one was alluded to by our previous speaker is Paul Stein
Paul Stein's group. And they looked at in hospital all-cause fatality rate according to the use of vena cava filters as determined using the nationwide in-patient sample, and patients across the US.
And this is very interesting. As I was getting ready for this talk, this was an interesting observation that they made. So this is all-cause mortality in patients with PE across the country,
and patients were either categorized according to unstable or stable and you can see that across the X axis, and whether or not they got lytic therapy or not. And on the Y axis you can see fatality, in the hospital fatality based on filter
and non filter. And as you look across the different groups if you had an unstable patient who did not get lytic therapy, patients with filters did better than patients without filters.
If you had an unstable patient who had planned lytic therapy, unstable patients did better with filters than not. And even in the stable lytic group there was a difference in the groups.
So this suggests that there is a treatment benefit for patients with PE that are stable or unstable that are getting planned lytic therapy or not getting planned therapy. There is no difference if you are stable
with no lytic therapy. So it's implying that there may be an effect from the lower extremity or clot outside of where you're treating that may be contributing to the fatality. Here's another paper from the same group.
And this is using a premier health care database over 2010 to 2014, and they classified patients into similar groups based on ICD 9 codes and whether they were unstable or stable. So these were patients with PE
and an admitting diagnosis of PE, as well as a primary diagnosis of PE. And they used a time-dependent analysis according to the date of insertion of the IVC filter to control for the immortal time bias.
I don't understand all that but this is what the authors showed. So they had 266,000 patients with PE. 4,200 were unstable, PE admitting and primary diagnosis was down to 479 and those were divided
into thrombolytics versus non thrombolytics and if you saw if you got a filter eight patients died versus in the first group in thrombolytic group versus 42. Again in the non thrombolytic group, less patients died 27 versus 80.
So again showing a protection in patients with PE who are getting, who are unstable and who are getting admitted with filters. So there are other subsets, I'm not going to speak about them.
But I want the audience to understand there's patients with heart failure that may be that filters may be protective for. So if you present with heart failure in the setting of PE, that there is a large paper
large data set showing that patients should receive filters. And another sub special group patients undergoing pulmonary embolectomy that filters may also be protective for. So I want to be cognizant of the time,
and I'm going to stop there. 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
- Alright-ey, hands put up. Who is for Onyx? Put your arms up. - [Male Audience Member] Who supports the Onyx Motion? - Onyx Motion, that's correct. He should've gone to law school. Who supports the alcohol motion?
Who supports the motion in the ocean? Alright, thank you I think we covered a lot of territory today. We want to have theses things and we are so glad that everybody came. I think this is Tony's first time,
Walter's first time here, Loronze and we really learned a lot today. I'm really glad Pletio Rossi was here because without him and his development of selective catheterization, I mean where would we be
sticking needles in every artery like that, trying to do angiograms, much less advanced sheaths or anything else. Pletio was wonderful having him here, one of my hero's. Anybody like to say anything?
Anybody got any questions or anything? - [Female Audience Member] The HHT scientific meeting's in June in Puerto Rico if you want some more good-- - Do they have electricity there yet? - [Female Audience Member] I hope so, I knew it looked nice before.
- Oh, okay, okay. Alright, well thank ya'll so much and we'll see you next year. (Clapping)
- 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, 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.
- Good afternoon to everybody. This is my disclosure First of all, literature. In literature I found only four cases, single cases, of dorsalis pedis artery entrapment. Claudication, in case of active dorsiflexion, blue toe syndrome by extrinsic compression
of the extensor hallucis brevis tendon, claudication, forced plantar flexion, anterior tarsal tunnel syndrome with DPA thrombosis. So few single-case reports, heterogeneous. Now I think that the reason more common situation of
dorsalis pedis artery entrapment, this was my first case. It was a patient with critical limb ischemia, with occlusion of anterior tibial artery. I tried to do balloon intimal angioplasty of the anterior tibial artery,
and was about to find residual dorsalis pedis artery. But despite the multiple inflation of balloons there at this level, the stenosis always remained. Then suddenly the patient spontaneously
changed the position of the foot. The stenosis disappeared. So I understood that this was a functional obstruction observed in plantar flexion of the foot and released in standard position.
I started to look at the patient, and this is a baseline angio, so it's not related to a subintimal angioplasty or something like that. With the plantar flexion, there is stenosis,
and here the stenosis released. So the subintimal entrapment is an anatomical condition and is not related to the endovascular treatment like spasm dissection. This is another the case, and you can see that here
we have an occlusion, so DPA-E can lead to functional total occlusion. This is another patient with perfect entrapment, and you can see that the entrapment is stuck in this position by
something compressing the artery. So DPA-E is a rare anatomical condition that can affect pedal and tarsal arteries. It must be considered when there is a focal stenosis at the passage of the anterior tibial and dorsalis pedis artery,
and the patients has a plantar flexion of the foot. In the majority of the cases the dynamic obstruction is in correspondence of the distal astragalus. In some cases, is higher at the ankle level, like in this case.
Now what is the prevalence of this condition in the population? We decided to do duplex scan flow dynamic evaluation in more than 200 patients with asymptomatic legs. We measured at 90 degree ankle joint
and in forced plantar flexion, the blood flow to the dorsal pedis artery. Five patients, we found functional obstruction which resembled dorsal pedis artery entrapment condition. So in the general population, it seems that about two percent of people
has an asymptomatic entrapment of the pedal artery. The problem is, can this entrapment become symptomatic, because many patients, especially bedridden and neuropathic patients assume a plantar flexion as the resting position
while lying on the bed. In these patients, we cannot exclude that DPA-E could play a role in developing or maintaining CLI. In my last six years I made about 4,000 angios on CLI patients,
and I found that in 15 cases, this dorsal pedis artery entrapment, so zero point four percent. This is an example of a patient, I studied this patient for critical limb ischemia. We have a long occlusion of the superficial femoral artery.
And in the distality, we have a part in the anterior tibial artery, and here I have seen this condition. So I started to think about, but critical limb ischemia, why we have only superficial femoral artery occlusion,
a good popliteal artery, anterior tibial artery is good, we have a good foot vessel. And here, we have this small entrapment, the typical entrapment. So I decided to start to treat the superficial femoral artery.
It seems a bad question, this one. But look at the foot. After the opening of the superficial femoral artery, we have not one red blood cell going into the foot. Because the foot is in a plantar flexion position. What to do in this case?
The only thing to do is to say to the patient, please rise your foot. And you can see that immediately, this ligament or something, I don't know, I was a cardiologist, not a vascular side but there is something there compressing the artery.
So in the typical position, so what to do? I think that in DPA-E patients, heel protectors can save the heel and the patency. Thank you very much for your attention.
- [Tarek] Good morning. First of all I would like to thank Professor Yakes who allowed me to be with you for the second year. I'm getting used to, for something different, which is a story, how we build our Vascular Malformation Program with a 13-year experience in Cairo's International Medical Center.
This my disclosures. Always we have another diagnostic and treatment dilemma with vascular malformation in Egypt. They usually misdiagnose, for one case, you seen someone did a foreign lesions, the neck, many investigation unnecessary,
duplex ultrasound, MR with contrast, CT angio, direct angiography and venography, ending with the same result, probably vascular malformation. But after discussion with Wayne, he told me, "I realize now that "every country in the world has
"the same problem, not only Egypt." They usually left untreated infantile hemangioma, told by the doctor, leave it alone, it will disappear, and never happen. Or, in this 30-year gentleman, extensive venous malformation, left it untreated because
there is no hope for treatment. Or, mistreated, just laser repair for a capillary malformation, mark left alone. This one was a terrible case as we noted that having a misdiagnosis intranatally as an enteratoma mistreated in his first day of life
with extensive surgery, complete facial denervation. When you do the MRI and clinically it is just venolymphatic and need to treatment and you don't know to treat the lesion or treat the complication. So even cases were sent to some centers abroad
with no valuable outcomes. So my dream was to having a new treatment strategy based on a multidisciplinary approach with full integration of the endovascular therapy to improve the patient outcome. So this came true with Professor Yakes in 2005
with a dedicated team and a patient database following the ISSVA classification. We started with patient and family teaching and counseling. They are happy now. And spread of the knowledge to the vascular surgeon of Egypt by publication of Professor Yakes in our
Egyptian Journal for Vascular and Endovascular Surgery. In 2008 we have the first case in Egypt treated with propranolol. As the same year was the discovery for treatment of the infantile angioma. And then nine-months age child
treated with propranolol for two years and then for six year follow-up with good result. We also published this for the knowledge spreading. We picked this case from her neurosurgeon before undergoing an heroic operation at the age of three months age
treated with propranolol oral for one year and with very good recovery. Also publication for spreading the knowledge. Then we start to do that but increase the public awareness by some TV program. On that was Professor Yakes that he shared
in this program also shows that normal people in Egypt can now know that how we diagnose, how we pick the cases and what is the way of treatment. Also spreading of the knowledge between the vascular surgeon in Egypt
and I acknowledge Professor Rahmat Saad is here and he is with us. So most of the vascular surgeon in Egypt now knows that how we pick and how we treat the cases. Also getting Professor Yakes in these meetings. We attracted Professor Vogelzang
all we know, well published in the literature, Professor Evan Seev, the father of EVAR and directed the beginning of the vascular malformation treatment in Sweden, Hamburg and London. I don't know why he's feeling sick.
(audience laughs) Okay, they have been interesting to visit our developing center. But also active, very active, sorry I'll get one, very active, one of the cases he came to us with history of some bleeding from the skull ligation of the external carotid artery
before we put in his sleep. We need six hands to stop the bleeding until all the three professors worked on him with six hours to stop the bleeding and to embolize him. Right carotid venous was shown to some stage. Making of coils from just simple wires
at 2 a.m. in the morning, we done everything. This is a left vertebral using these coils and directional injections and this I the end of the one-hour stage of the treatment until in the morning we can see at least now the scalp itself, now we can see.
And this, four days before he go home for follow-up treatment. At one of the occasion we seen 17 new cases in the outpatient clinic, seven and a half p.m. after a long day we start the clinic to see 70 cases.
Our center now is known as a center of excellence in Egypt for diagnosing and treating the vascular malformation, picking the cases not only from Cairo, Egypt but also from the surrounding countries. We seen patient from everywhere around us. This is vascular malformation workload since 2005
starting only with four cases with Professor Yakes and after proper spread of the knowledge to the public and the doctors in Egypt we, in last September, we treated 110 cases in continuous three and a half days working. This is the distribution of the case.
We see now, at least between three and four cases every week. Now the current situation in Egypt is that, misdiagnosis and mistreated are avoided, early pick up of de-novo case, we have one center of excellence
engaged with the larger malformation patient population and a full experienced expert attending on regular basis which allow for a faster ramp-up experience and, decreasing the complication rates. Now I would like you to come and visit Egypt so you can see the pyramids, Sphinx,
you may go up to Abu Simbel, Luxor, see Ramses temple but if you come closer, you might see Yakes and Radwan. Thank you. (audience laughter)
- I've made this agent comparison chart, just sort of summarizing the areas where I think that Onyx is better as compared to ethanol. I think things to come, oops, sorry, I got to go back. I think the items to be commented on are one, that there's less skin necrosis with the polymers.
It's a less painful procedure, and the Onyx, in our experience, is durable. But in the treatment of any type of AVM, you have to get your agent into the nidus of the malformation. If you don't do that,
then you're just doing a proximal occlusion. And we know from the surgical literature that that does not work. They will simply, the angiogenic stimulus, whatever triggers it, will continue. And that gets me to another point.
I really don't think that we really know what stimulates these malformations to grow. We think it may have something to do with a resistance in the flow, but we have some pelvic AVMs who have been stable for 30 years.
We're not touching them, and we have no intention of touching them, whereas we have children who will present with an AVM at age four and then by age seven, they are unable to ambulate. So in any event, I think that
polymers represent the future. And I just want to quote from this old movie, The Graduate. "Plastics," thank you.
- 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.
- Alright, that's our beautiful city by our inland freshwater ocean. I'm against the proposal because, in my opinion, ONYX and the polymerizing agents don't do what they're supposed to do, which is cure. You know, we could talk about this, but in preparation for this, I looked at the
relatively sparse, but available, literature on ONYX, and the fact of the matter is, repeatedly when one looks at what is in the literature, ONYX does not cure with a few exceptions. For example, this is the curative exception. This is a mandibular AVMs, three of them cured
at one year angiographic followup. Now, I consider cure a very simple metric: is it gone at one year followup angiography or imaging? And this meets that criteria, but again, we know that mandibular AVMs, as Dr. Fannis has so nicely shown, this is a bone cyst, essentially,
fill it with anything, it'll get cured. All venous predominant legions, three A. So, yes, cure is possible in isolated circumstances. I think Walter has acknowledged that. But, all the other data, including Dr. Loglos' own data, is that there is no angiographic
followup, short clinical followup. Other papers, Embolization of peripheral high-flow AVMs by Kilani et. al, surgical excision in nine out of 19. Right, that's not the same thing, but it is one aspect of doing it, and there's no angiographic followup. And we see this again and again and again.
Very short clinical followup. So paper after paper refused to tell us that we don't really know what the behavior of ONYX is, as defined by the very simple metric of cure. Although complete, in this paper for example, although complete angiographic exclusion of the nidus
is obtained in a minority, 36 percent, of cases, there's no angiographic followup, so the exclusion is presumably based on immediate post-embolization angiography. In other words, ONYX looks good, acts bad. Other embolization agents in this paper also used,
probably some of them ethanol, which actually got the job done. And then finally, another paper with zero clinical or angiographic followup. So the answer is obvious: ONYX, while it is used copiously by some of the participants in this debate, does not cure,
and I, as my Chinese friends said, think ONYX is garbage. I don't think it works. Few examples of that, here's a young woman, a patient of Dr. Yakes, who, 12 years old, extensive facial maxillary scalp AVM, nine ONYX embolizations, left blind in the right eye
with persistent massive oral and nasal hemorrhage, and after appropriate embolizations, patient was stabilized clinically, and the ONYX was resected. She's stable now, not cured, but she's actually had an excellent clinical result. And you can see that's what it looks like.
Now that's hideous, that's not going to work. And it also, I think, points out what Dr. Walgramuth has actually admitted to, which is it's very difficult to see through this stuff. Radiation dose is increased, and identifying what to do and where to go is a real challenge.
Another such example, I think, suffice it to say a picture is worth a thousand words is this illustrative case of an extensive pelvic AVM, treated with what appeared to be gallons of ONYX, with very little benefit, and an enlarging ulcer. This was later treated by direct alcohol injection
with cure and improvement resolution of that ulcer. So, in summary, it's real simple, folks. There's no evidence in the literature that polymerizing agents have cured AVMs with an exception of a few venous predominant legions. And as I said, you could probably put Jello
in the outflow of those things and it'd work. My own personal experience is repeatedly had ONYX failures, and importantly, many patients are worsened by this treatment, and actually, their subsequent curative treatments are hampered. Thanks very much.
- [Moderator] Anybody have any burning questions? So Enrico, who do you not do duplex-guided interventions on? - [Enrico] Ah that's a very good question. When I don't have somebody adept to help me. If I'm doing it by myself, I'm not going to do it at this point. Hopefully there's a couple of companies
that are working on devices where you'll be able to do it by yourself. But at this point, you need someone that's going to handle the probe while you handle the catheter so. And the second contraindication
would be a severely calcified, sicofriend calcified vessel. If you have this calcification for about two centimeters and the rest you can see, segmentally it's okay, but if it's a long calcified occlusion
where you cannot see anything, of course it's not going to be acceptable to do on the ultrasound guidance. - [Panelist] I have a question for Dr. Rico. But is the problem here is that so many of those groins have been used and abused forever
with closure devices and all that. So when you go back to that groin, it looks like it been operated four times. There's a lot of inflammation around. I realized that my fellow is staying away from those groins now.
He call in sick when I tell him tomorrow we have a groin to do. So do you think that the results just, I understand first time around, but for those patient with much pulled sticks before and devices.
Should we consider a stand instead? - I have no scientific argument to answer to you, because what we have done these of novel groin incision. If you have a patient with a very fat weave of free producent divention of the groin.
This could be a problem, but in this case I mean if you have a careful surgical technique I mean you kind of already have a complication growing infection (mumbling) like this. I think it's alright if you're really safe even.
But you have to take time and to do everything right. I think to put a (mumbles). When you see oh important is deep feminal aheartery. I think it's quite dangerous. And if it jail. And if he trembles.
I mean you are really in a bad situation. - Okay I think that wraps it up.
- I have nothing to disclose but what I will tell you is that the only way for me to learn the mechanics of treating low-flow malformations has been to learn from Wayne, follow what he's doing, and basically what I've done is I've filmed every single step he's taking,
dissect that, and then present you the way that he's doing it. The best way to do that is not listen to Wayne, but to film him, and just to check that afterwards. And he goes regularly to Cairo, this is the place of Dr. Rodovan sitting here
in front of us, and with Dr. Alaa Roshdy. I've learned a lot there from Wayne. This is Wayne's techniques, so normally if you look at puncture, the low flow malformations here then you get return or you aspirate so this is what happens, they inject contrast then they find volume
and inject whatever agent you prefer to inject. It happens to be alcohol but that is not essential. More often than not, there is no return. What to do then? There is a technique that Wayne has developed. Stab-Inject-Withdraw, just under high modification inject,
identify that you're not outside the vessel, get the vessel, start to fill slowly, and identify that and inject the alcohol. Of course you can do that under exposure just to see the effect of the alcohol thrombosing, et cetera.
Another example of no return is to subcutaneously certainly show that there is a low pressure system, and again, Stab-Inject-Withdrawal, and there is a cyst. Is it extravasation or is the malformation aspirate? And if it collapses, that's the malformation.
And then continue to fill in with contrast, define how big the malformation is, and then accordingly inject the amount of abrasive agent that you're using. Lymphatic malformation is very difficult to treat because the vessel's so small, would say microscopic,
and again, Stab-Inject-Withdraw, identify that it's not extravasating but it is the vessel, and start slowly, slowly to fill and any time in doubt that should there, just do a run, identify, and that is the vessel, or the network of the vessels and
start to fill that with the agent you're using. But there are certain zones that just don't inject anything, and these are the arteries. How often do arteries occur? When you puncture them. I just directly looked at all these 155 patients I've seen Wayne treat there a matter of,
I would say, 100 patients in three days. 30 patients per day, that's about six percent. And you see the artery by pulsating flow depending on the pressure that you apply. And we see again the artery pulsating and we have no doubt about that.
However, it could be difficult to see. Depending on how much you push in the contrast and you see these being ornery so there's a No-Go-Zone, no injection of any agent and again, a tiny bit of lottery there in the foot could be disastrous.
You inject any agent, any, you will have ended up with necrosis of course if you don't inject inhibitors, but not yet. The humorous may not end up with necrosis when all the mysticism with puncture will be gone. So we have extravasation, when you say extravasation
like starting injecting, still good, looking good, but you see how the extravasation even blows up and at the end it bursts, again under pressure they should apply, so pressure is really important to control and then you stop and don't inject any more.
Extravasation, you see how its' leaking in the back there, but you correct the position of the needle, identify all the vessels, the tiny little vessels, just have to be used to identify the pattern and then you start to inject the agent again.
Control is very essential. Here is the emphatic malformation labia and though there is this tiny little bity extravasation you continue because there is you know, run-off, it is filling the system and you can safely inject the alcohol.
Intraarticular could be malformation there and this is definitely safe pla however, if it is in the free space in the the joint, that's again, it's No-Go-Zone. How you see that is just be used to
the pattern recognition and you find that this is free. It's around the condyle there so there is no injection. Compression is again good to note to control by compression where the agents go. This is a normal vein, certainly at risk of getting with alcohol, whatever agent
you're using deep in the system, avoid that by compression. Compression can be applied manually and then that gives you a chance to fill the malformation itself and not strike connection too deep in the system. Intraosseous venous malformation,
low-flow malformations can occur anywhere, here in the spine and the axis is transpedicular patient prone because it's soft. The malformation has softened up the bone. You can just use a 21-gauge needle and identify the malformation and follow
by the agent you're using. Peculiar type of venous malformation called capillary venous malformation. Basically it's a low-flow malformation without any shunt here in the sciatic notch of the patient and geography shows that there is no shunt
there is just big veins and intense pacification. And identify the veins by indirect puncture again, see the pattern of that and inject alcohol and following geography we can see that there has decreased the density but it is a lot more left to be done.
In conclusion, direct puncture is the technique in this low-flow malformation but Stab-Inject-Withdraw is the really helpful technique for successful treatment of microvascular, microcystic lesion. No-Go-Zones for certain when you see arteries
and anytime in doubt you just have to do a run to identify if they're arteries or not. Intraarticular free space and extravasation and normal veins, similarly, No-Go-Zone. Capillary venous, intraosseous malformations can be treated successfully. Thank you.
(audience applause) - [Facilitator] Thank you, Crossey. Excellent talk, very practical and pragmatic. Any comments or questions? Dr. Yakes. - [Dr. Yakes] We have been to many meetings and people have talked about doing
other ultrasound guides, accessing the malformations. You'll never see those arteries by ultrasound. - [Facilitator] That's absolutely correct. I concur. I concur and I think some of the disasters we've seen where suddenly something falls off
have been in these situations because they don't understand or in expansile foam-based therapies, I've seen that. I've seen plenty of these, so it's always present, potentially.
- [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.
- My rebuttal is short and sweet. I think that those of us who have seen both agents, seen it in a fair comparison, understand that while ethanol has an appearance of difficulty to use, have come to the conclusion that it is actually safe. It has to be applied in the right spot. If it is such it will absolutely cure
and in it's very, very safe fashion. I think Walter mentioned the four deaths that I referred to. I agree, tragic, terrible, but we learn. Haven't had any deaths since, because I understand now the mistake I made and how to use ethanol.
I think the same thing is true. Max will tell you that there were enumerable deaths during the development of transplanting these difficult operations. No longer, all controlled, it's all because of learning. Thanks.
- Thank you Robbie, and I'd like to thank the meeting organizers and especially Dr. Veith for the generous invitation. As Dr. Norm Rich would say, war is my rule, conflict of interest but I am a consultant for Prytime Medical. Despite compelling research by Morrison and others
on translational research demonstrating effectiveness of aortic balloon occlusion in controlling pelvic hemorrhage. Introducing change is not easy in an institution and we are going to go into a little bit about how to implement those changes in practice.
We want to describe a process for the implementation of REBOA technology into modern practice. And our approach was several steps. We identified key innovators and early adopters in our own institution, conducted a literature review of best evidence,
outline criteria for proficiency and credentialing, and performed an analysis of our consecutive patients, and finally define measurements of success. It's important to research the literature before adopting a new technology and my partners and I published what we perceive to be our role
in controlling exsanguinating torso hemorrhage. And reported that it's important that this new technique be evaluated rigorously and transparently evaluated before widespread adoption. We developed a box where we thought this was the safest indications,
patients in shock with a torso hemorrhage, and pasted that to our cart of supplies and enlisted the support of the nursing staff in our emergency department. And then taking what we learned from John Eliason and Todd Rasmussen in the E Stars program,
developed our own workshop locally to advance the skillsets of our trauma surgeons to ensure that they were comfortable performing ultrasound guided access. This included an eight hour workshop at the Center for Surgical Innovation
at the University of Colorado. We focused our emphasis on ultrasound guided techniques using micropuncture sets and spent a considerable amount of time with emphasis on simulation training. We expanded those simulator trainings
to include knowledge of the zones of the aorta and careful placement of the balloon and measuring to avoid unintended zone placement. And then transition to a live animal model technique where we feel as we learned in the E Stars program that having live tissue gives proper feedback
for introducing sheaths and wires and catheters and such into the femoral vascular tree. At the time we began our course, we used the CODA with a Glidewire advantage and as soon transitioned. We felt that the best patient cohort
was the patients that we studied the most in Denver. Over a 10 year period, we saw almost 2,000 patients, 6% were in severe shock, and we predominantly pack and take those patients to the O.R. for external fixation. We expanded REBOA to include it
in our clinical practice guidelines for refractory shock. And our clinical experience is that we place this under strict ultrasound guidance under proctoring and mentoring with an attending that's attended this course. And we confirm the zone of placement in the operating room,
correction in the emergency department, with a digital X-ray. The balloon occlusion mean time is approximately 30 to 45 minutes. These patients are going expeditiously to the operating room for prepared neopolic packing
and external fixation and their mortality is significant. Despite that, our outcomes amongst the last 75 cases had a survival rate of 72%. A subgroup analysis of just pelvic injuries was a mortality of approximately 21%. We mostly use the balloon for blunt abdominal pelvic trauma
but we have done this for a few ruptures and penetrating injuries as well. As I mentioned, we transitioned from the older system, which required a 12 French sheath and femoral artery repair. And that has probably broadened the use of this catheter now that it's a seven French fluoroscopy-free
and wireless system with a balloon of 32 millimeters. We take caution to teach to avoid unintended zones of placement. Our average length is 28 to 29 millimeters and we inflate to eight, taking care not to overinflate the balloon.
This is our current adoption curve where we see a doubling over the last three years of its use. And the potential problems will be spoken to by Dr. McGee who's put together a talk on complications but we've essentially seen this
in almost every branch vessel. The key to success is partnership with the trauma surgeons and having a senior mentor who understands innovation. And in summary, I'd say there needs to be a commitment for the innovation, training and proctoring, credentialing, and clinical practice
guidelines for safe use. Thank you for your attention.
- I think it's unfair to have Wayne here with all his expertise and knowledge and throwing all these combative comments, vulgar attack, et cetera. But the bottom line is all these types, no matter how you define them, they are mixed.
They are mixed, they are not, with the exception for HDT. You have Type 1 in a midst of Type 2. You have Type 2A and then 3B, type something. I don't even know what they are, except that you say venous predominance, yes. Can be multiple venous predominance, yes.
Then you can have Type 4, these are the major groups. But to have a filler that occupies a space, can be Onyx, it's fine. It doesn't cure. You have to do something to these cells. You have to compress them.
You have to ablate them. You have to take them out. And a filler doesn't do that. The filler recolonizes on top of that, as you've put it already, from Molly. Recolonizes.
You can use it as a filler, but the cure, the ablation, has to be something that's powerful. Like a knife, even worse than knife, burn injuries, burn it to the bottom. That's how you achieve a cure. If you don't believe me, just look at ...
Can you play us that clip that was rotating constantly as Walter was talking, here, how Onyx is wonderful? This is the girl that you show on the pictures from Bob. Can you look at that? It's a ton of extras placed into the veins,
arteries, everywhere. She continues to bleed. On top of that, it's horrendous, how to treat it. Wayne managed to stop and control the bleeding, but this is an example.
This is the most scary sample of what Onyx cannot do. So back to the motion. Polymerizing Onyx can cure, and it's the material of choice to use? The answer is no. Alcohol is dangerous, personally,
I say yah, very dangerous, if you drive and you don't know how to use it. But so is everything else. But if you know, you can cure them. Thanks.
- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --
- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.
But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,
is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy
in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.
The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation
so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later
that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low
and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse
even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean
as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques
different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between
pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients
are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system
you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because
this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out
now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference
between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing
a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is
the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories
and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here
again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result
and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not
fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again
look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as
the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here
This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you
- Thanks a lot for again for inviting me because you know, (laughs) I'm in very hostile territory, (audience laughs) but, I will tell you the truth now, (audience laughs) and being in hostile territory and telling the truth can
be totally different things and I, I'm also never in any way, you know I'm totally scientific type, I will never be polemic, like you are. (audience laughs) Okay, so let's start with the truth, start with the truth, I show you two typical cases, this is a typical ethanol case
here with couple of, it was successful, at least in losing it's toes, and I'll show you another example again, a foot AVM, this is one session, one session, in fact its 14 vials of squid in this case, and it's done. so, this is not statistic, but I always
see, and I've seen it today in a couple of talks, Onyx used as glue. And that doesn't work, you have, if you start to treat a patient, you have to really treat him and it's not something you inject, and that it's gone, you have to fill all the AV shunts, you have to fill the whole lesion.
And if you don't do it, of course you see a lot of failed on ex-patients and if its used improperly, and that's the only thing I, I wouldn't say I agree with you, I would say I'm thinking in the same direction, yeah, that's if you use Onyx in the wrong way, you have a very good chance to make thing worse.
So, its a technical thing, and if people start to use Onyx, and they inject something, and then its something like putting in some coils, that's not worthwhile, it makes no sense to include some arterial feeders, we know this since, I think more than 20 years, it's like making a surgical ligation of the feeding
artery, it's totally senseless. You have to completely occlude the area of the arteriovenous shunting, apart from the predominantly venous one, where you can just occlude the venous outflow, by whichever thing you use, and the area of arteriovenous shunting is always bigger than you see it in a normal DSA,
because the blood does the same as the contrast medium does, it flows along the route of the least flow resistance. And so, at the end, if you want to be sure that you have to completely occluded the AVM, you will end up with a cast which is much bigger than what you see at the beginning of a DSA, yep, it was agreed, see.
- [Audience Member] You know I'm shaking my head as you talk. - Yeah, yeah, your getting tired. (laughs) Here we go, So, and this is only the really scientific slide in my talk, because when people die when you inject ethanol
in vascular malformation treatment, its something, its banal, all of us have seen it many times, but there was a scientific question, why do people die on the table if you inject ethanol in AVM treatment on vascular malformation treatment? And there's one scientific publication here, because we
all thought do they die because of complete vasoconstriction in the pulmonary arterial system, or is it, are they dying due to the thrombi? That, you know ethanol, it uses small slatch or big thrombi and they go to the pulmonary circulation and they die. So, is it the vasospasm, induced by ethanol, or is it the
thrombi induced by ethanol, that they die is clear. So, there was a very nice publication out there in 2012, was presented in Malibu, at the IFSA meeting, it was about four patients, which three of them died, two were just after injecting of between five and 12 milliliters of ethanol, one was a direct puncture pelvic AVM, and it was caused,
that this was nicely stated there, it was caused by multiple small peripheral emboli. So it's not vasospasm that kills the people, it's the thrombus, and I think this was a very very worthwhile contribution to all our knowledge and really thank you Bob for this paper, thank you
very much, now we know why they died. I haven't, unfortunately I can't contribute to this discussion with Onyx because there wasn't any patient dying on the table during my embolization's and I've done now, we're preparing the paper of 160 AVM patients with I don't know, 400 sessions and well maybe if we wait
40 years more, 50% will have died but, (audience laughs) from natural cause, so I can tell you again this is the truth, we will talk about the truth here, and this is, ethanol can be worthwhile even in AVM's, I don't deny that and maybe it will have its place for a couple of more years
before we do Onyx and MEK1-Inhibitors, so there is for couple of more years, this is a role for ethanol, but it's somewhere deep down there, and this is a slide I show for the third time now just for you Wayne, please and I show it because you should start to publish your classification.
I didn't use it because there is no paper there, please publish it then I will always classify according to your classification. - [Audience Member Cheers] - Thank you for your attention, thank you for giving me the chance to talk about the truth here in this seminary
and please don't do anything stupid with ethanol.
- 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.
- Now we all have seen one thing. We have to treat AVM's according to their classification angio anatomy. If you have something like, direct arterial venous communications, like pulmonary HHT patients, like the rare patients with inborn arterial venous fistulas,
you will never use ethanol. That's my opinion. That's an opinion. But I think most of us will agree on that. Will you? - [Audience] Yes.
- I think many of us will agree. So would you just do it for a HHT pulmonary patient, you would inject ethanol? - [Audience] No. - So, okay. And the direct arterial venous communications inborn,
they are very rare and they can be beautifully treated with plugs and whatever. These are one part on the AVM patients. Second part is predominantly venous outflow. However you say it's 2B, 3A or whatever. It's a dominant venous outflow
and you can cure them and I say cure, even in my paper there is imaging of follow up, but it's not in the abstract bar. (smiling) So you just, - (laughing)
- So you just occlude the venous outflow, as close to the nidus as you can. So I don't need ethanol for that. I don't need to take the risk for my patient. And so that leaves the type 4 small vessel AVM's. They are, even in my opinion,
not treatable with a polymerizing agent. There is a real place for ethanol. And then you you go to these difficult, more net-like, type 3 or whatever, AVM's, then my opinion is, I do it as long as possible,
with a safe agent. Like pushing in tons of onyx. And if there is something left over, or if there comes something in follow up, because we all need follow up for these patients, then you can finish it with ethanol.
That's my statement. Thank you.
- Thanks, I appreciate the invitation. MR imaging of vascular malformations poses some challenges primarily related to the heterogeneous spectrum of the lesions. The primary distinction to be made with imaging is between low flow and high flow abnormalities. This distinction, however, can often be made clinically
and so the real value in MR is in determining the malformation extent and the associated involvement of adjacent normal structures. The basic MR evaluation of vascular malformations should of course be multiplanar in two or three orthogonal planes, and in each of those planes,
there should be T1 and T2 weighted imaging. There's some debate about the value of contrast-enhanced scans. Certainly contrast-enhanced scanning will show things like arteriovenous shunting and lesion perfusion, but mostly the value of contrast-enhanced scanning
is in making the diagnosis of the abnormality rather than in guiding specific treatment. So let's talk about the various imaging sequences and go through a few examples. On T1 weighted images, we see the anatomy of the limb or of the area in question quite clearly.
But what you notice is that there's a signal similarity between the normal tissues and the adjacent malformation, such that they blend together. That means that assessment of lesion extent is poor on T1 weighted images. Now this is in distinction from T2 weighted imaging
where malformation images tend to stand out quite dramatically from the adjacent surrounding normal tissue, making assessment of lesion extent quite good, with the following caveat that on these bright water-type sequences, edema, when present, especially in high-flow lesions
or in low-flow lesions following embolization, it can result in overestimation of lesion extent. Many people routinely include contrast-enhanced imaging for malformation evaluation. I think it's probably not necessary and doesn't actually provide that much
additional information beyond making the actual diagnosis. Now that said, that's to be distinguished from dynamic time resolved imaging, which is a newer type of contrast-enhanced imaging using faster acquisition. It has what's called a higher temporal resolution and we can clearly differentiate
inflow arteries from draining veins and this can be valuable in treatment planning as well. Here we see pre- and post-contrast images and you'll notice that on the post-contrast images, there's slightly better visualization of the malformation, but the difference between the two is really modest
and probably not clinically relevant. Now that's to be distinguished from time resolved imaging, which will allow us to see arterial, parenchymal, and venous phases, and these can be stitched together to create a movie that really does look quite a bit like a catheter-based angiogram.
The difference between high and low flow malformations is primarily made based on structural characteristics, rather than MR signal abnormalities. So, low flow lesions will usually have minimal mass effect. Here we see signal abnormality with almost no mass effect. When a mass is present, it sometimes has
hamartomatous stromal elements that look like septations running through the mass. When a mass is not present, the lesion tends to be pretty infiltrative. Without any mass effect, sometimes the degree of infiltration is amazingly intimate, as in, case like this.
When we see phleboliths, which are routinely identified on radiographic images, we have confidence that we're dealing with a low flow lesion. But in fact, MRI imaging can identify phleboliths pretty consistently, and here you see they appear as rounder, oval, low signal images
on all imaging sequences, and of course, they don't enhance. Now, these findings are in distinction to high flow lesions, which demonstrate no well-defined mass ever, and in fact, if you see a well-defined mass it should make you think that you're dealing with a tumor rather than a malformation.
But they will demonstrate characteristics of enlarged feeding arteries, enlarged draining veins, and these infiltrative masses will often be riven through with multiple flow voids, and the degree of infiltration can be really, pretty impressive.
There are some signal characteristic differences between the various malformations. It's a long and involved topic, and probably something that doesn't make sense to go into here at this point, but I think the utility of MR in vascular malformations is primarily related to defining the anatomic
characteristics of the malformation, assessing what normal structures are involved or immediately adjacent, and this allows us to mitigate risk and plan the procedures. Now this is different from post-treatment evaluation of MRI, where there's definitely differences between how low flow and high flow lesions respond.
In low flow images, post-embolization we see significant signal changes. In high flow lesions, post-embolization we see anatomic changes. One important caveat to remember is when imaging and malformation within three months of an embolization,
it can be difficult to interpret related to the post-embolization inflammatory reaction. So on T1 weighted imaging post-embolization, we see bright signal, representing thrombus is the treated area as opposed to lack of bright signal, in the non-treated area.
On T2 weighted images, where the malformation generally appears bright, post-embolization we see dark areas in the treated zoned, representing scar. I personally prefer evaluating these with T2 weighted images. I think the distinction between treated and
untreated is greater and more consistent. Another example, scar forming, T2 weighted images. Again, I think the distinction is pretty clear. Although, contrast-enhancement isn't all that valuable in pre-treatment planning. Actually, can I get this video to go?
There we go. Although contrast-enhanced scanning isn't generally valuable in pre-treatment planning, there can be some utility in post-treatment evaluations. Specifically, dynamic time-resolved imaging or virtual angiography can be applicable to high flow malformations.
As you can see here, when the post-treatment evaluation and assessment of residual arteriovenous stunting is an important end point. Thank you. (applauding) - [Announcer] Any questions from the audience?
I think it's important to note, you mentioned the importance of T2 weighted imaging. And it is crucial, particularly for venous and lymphatic, or mixed lesions. But I think it's also important to state with T2 imaging, that you have to have fat suppression,
'cause fat also has bright signal and can be confused with malformation. - [Scott] Yeah, exactly, and there's really a broad range of T2 weighted images. What we rely on mostly is this short towen version recovery which,
- [Announcer] Now that's different, yeah. - [Mark] Yeah that's going to be. - I was going to write next. - [Mark] Yeah, so the, T2 fat suppressed images are, of course, critical, and should be obtained in every plane. We actually also obtain stir imaging in every plane. Yes, question?
- [Audience Member] So is the T2 full, (mumbling) what time do you need. - [Mark] I'm sorry, can you repeat that? - [Audience Member] What time do you need to continue to use of a full of T2 for (mumbling) - [Mark] Well, it depends on what you're looking for.
If you're trying to assess for complications, you can image any time. But, the challenge in interpreting is that the diagnostic radiologist won't necessarily know exactly where you've treated, and the lesion may appear abnormal in ways that aren't understood.
So, as the interventionalist who's doing the procedure, you really need to sit with the radiologist and help them understand what you did within that short timeframe. Now, if you're talking about imaging after three months, it's much easier to interpret signal changes have moderated, and that post-embolization inflammatory
phase has resolved. - [Audience Member] After two or three months? - [Mark] After three months, yeah. - [Announcer] Okay, thank you so much. - [Mark] Thank you.
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