- Thank you very much Mr. Chairman. Thank you Frank, for this kind invitation again to this symposium. This is my disclosure. With the drug coated balloons it is important to minimize the drug loss during the balloon transit during the inflation of the balloon.
Because Paclitaxel has a high degree of cytotoxicity that may induce necrosis and increase inflammation in the distal tissue, and we know that even with the best technique, we can loose 70 - 80% of the drop to the distal circulation,
the inference by different factors between them and the calcification of degree of these blood cells. There are adverse events secondary to drug coated balloons that have been reported recently. In animal molders it has shown that Downstream Vascular Changes are more frequent with
Drug Coated Balloons than with Drug-Eluting Stents. In animal molders it has been also shown that there is no evidence of significant downstream emboli or systemic toxicity with DCB's than with patients with controls. This was a study presented yesterday by (mumbles)
with a very nice and elegant study with a good methodology that shows in animals that there are different concentrations of the drug in distal tissue depending on the balloon that you are using. In this case, the range in balloon (mumbles)
those ones have the lowest concentration in the distal tissue. In clinical experience in this meta-analysis amputations and wound healing rate are lower with this series with controls. But there is controversy because
Complete Index Ulcer Healing is higher in this series than with control patients. But there are lower wound healing index in patients compared with drug-eluting stents. In the debate, (mumbles) and also in the dialux which are clinical trials in diuretic patients with CLI,
there we no issues of safety and no impair of the wounds healing. But, remember the negative result of the IN PACT DEEP trial in which there were more amputation at six months that could be influenced, but in all their factors, the lack of standardized
wound care protocols. (mumbles) has also reported recently good survival to 100% in patient treated with DCB's compared with plain balloons and with lutonic balloons. So in our institution, we did a study with the objective to examine
patient outcomes following the use of the drug-coated balloons in patients with CLI and diuretic patients with Complex Real World lesions undergoing endovascular intervention below-the-knee with the Ranger balloon coated with Paclitaxel.
This is a Two-Center Experience that is headed by the National University of Mexico in 30 patients with strict followup. With symptomatic Rutherford four to six. With the Stenosis and occlusion of infrapopliteal vessels and many degrees of calcification.
It was mandatory for all patients to have Pre-dilation before the use of DCB. We studied some endpoints like efficacy. (mumbles) Limb salvage, sustained clinical improvement, wound healing rate
and technical success and some other endpoints of safety. This is an example of multi level disease in a patient that has to be approached by (mumbles) access with a balloon preparation of the artery before the use of the DCB, and after this, we treated the anterior artery
and even to the arch of the foot. This is the way we follow our patient with ultra sound duplex with an index fibular of no more that 2.4. All patients were diabetic with Rutherford 5-6. 77% have a (mumbles) at the initial of the study.
And as you can see there were longer lesions and with higher degree of calcification and stenosis only in two of them we produced (mumbles). There were bailout stent placements in five patients and we did retrograde access in 43 patients.
Subintimal angioplasty was done in 32 patients, and Complete Index Wound Healing was in 93 of our patients. This is our Limb Salvage 94%. The Patency rate was 96% with this Kaplan Meir analysis. And in some patients we did a determination of Paclitaxel concentration in distal tissue
with the High Pressure Liquid Chromatography method. We only did this in five patients because of the lack of financial support, and technical problems. As you can see in three of them we had Complete Wound Healing.
Only one we had major amputation. This was the patient with the higher concentration of Paclitaxel in the distal tissue, and in one patient, we could not determine the concentration of Paclitaxel. This is the way we do this.
They take the sample of the patient at the moment we do the minor amputation. During day 10 after the angioplasty, we also do a (mumbles) analysis of the patient we have a limb salvage we can see arterial and capillar vessel proliferation and hyperplasia of the
arteriole media layer. But, in those patients that have major amputation even when they have a good sterio-graphic result like in this case, we see more fibrinoid necrosis which is a bad determination. So in conclusion,
angioplasty with the (mumbles) balloon maintain clinical efficacy over time is possible. We didn't see No Downstream clinical important or significant effects and high rates of Limb Salvage in complex CLI patients is possible.
Local toxic effects of paclitaxel and significant drug loss on the way to the lesion are theoretical considerations up to now because there is no biological study that can confirm this. Thank you very much.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.
- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- Thank you Tal. It's a privilege again to take the podium here. No disclosures. Everyone in here in this audience understands how important Traumatic Aortic Injury is, the second leading cause of death, primarily due to blunt mechanisms,
that are well known to the trauma and vascular community. And, we've learned a lot about how to care for these patient's in the transition in the vascular age. And, that began with the American Association for the Surgery of Trauma Studies in 2008 and 2009, which showed that TEVAR was associated
with an improved mortality and decreased paraplegia compared to older modalities. And, these are the graphs at my old training grounds at UT Houston, which, I'm sure would be the same at most other centers. A gradual transition to almost completely TEVAR
for every patient who has appropriate anatomy. And, we now have over a decade worth of survival data to show the outcome comparisons are the same as the older modalities. But the question has become now, are we over treating some of these injuries?
We need an optimal algorithm and an optimal algorithm requires an optimal grading system. And, that grading system should determine the treatment we utilize, it should guide the timing of the treatment. And, should provide some prediction of the natural history
in those patient's that we do not immediately treat. The SVS in 2011 developed a very nice anatomical based grading system, however, this is a lesionology type algorithm if you will, and not incorporating any of the valuable information that the patient also may possess
in terms of associated injuries. There have been alternative proposals: Vancouver, the Harborview "Minimal Aortic Injuries" is one that is very familiar and commonly utilized in the literature. And, even the Baltimore Classification which includes some physiology elements.
And the reality is, there are also other elements of ongoing issues Blunt Thoracic Aortic Injury, including not only how to manage those Grade 1/Grade 2 injuries but the timing of repair. How do we prioritize repair in the context of other sev
rain Injury and other bleeding solid organs and what's the optimal follow up regimen for these patients? It was with those questions in mind that 3 years ago we developed the Aortic Trauma Foundation. This is a non-profit organization with a Multispecialty
International Medical Advisory Board and a Board of Directors. We really wanted to improve outcomes of patient's with Traumatic Aortic Injury through education and research. We started with several initial, kind of low hanging fruit exercises, the first of which was a practice pattern survey
from members of the SVS, trauma organization, thoracic surgery organizations in interventional radiology and we found that there were some contingents here, and some very interesting findings in this survey. In fact, a majority of providers who care for these injuries don't rely on any guidelines at all.
Just their own personal knowledge of literature and their experience over their practice lifespan. Likewise, these mid-grade injuries represent some significant controversy with almost half the providers thinking that these just need medical therapy and observation as an outpatient.
And the remainder treating them emergently with TEVAR. Or, urgently with TEVAR. And we also conducted a large Retrospective Multicenter Study, 382 patient's from US Level 1 Trauma Centers and we found the at TEVAR compared to Open Repair
was associated with lower transfusion, lower overall mortality, lower aortic related mortality. None of these were surprising findings. But again, this study identified some controversy here, particularly with the, there's no difference in outcomes with those Minimal BTAI patient's if they're treated
with TEVAR or undergo medical non-operative management. Which suggests at least that in some of these patient's we are actually over-treating them. We have, as ongoing effort, our Aortic Trauma Foundation International, Multicenter PROSPECTIVE Blunt Thoracic Aortic Injury Registry
designed to identify predictors of early rupture, develop some multi-specialty consensus guidelines on treatment and management and establish long term outcomes. Anyone in this audience can join this effort, we have always gotten good contribution from VEITH.
We have a region based involvement, mechanism to promote the not only ATF involvement but the prospective registry in the US and abroad. And, we've had some good results. This initial registry went live in 2016, as of 2018, we have 381 patient's
in 23 centers internationally. And we plan to do a feasibility report when we cross the 500 patient threshold. And we invite anyone who seeks to become a member of the Aortic Trauma Foundation and actively contributes to utilize this data.
We all want to as a community, identify and define optimal care practices. We are going to actively solicit and review proposals for use and we hope that this data will produce a foundational platform upon which we can develop some really meaningful multi-specialty guidelines
that are evidence and practice based. Thank you.
- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology
to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions
that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,
it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,
as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient
and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy
by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?
Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification
of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,
matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.
You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.
And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.
And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.
Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,
next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages
to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,
so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?
Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization
of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases
of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.
Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging
with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR
to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care
to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,
two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents
using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging
reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,
we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.
And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.
A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,
and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs
and improve clinical outcomes. Thank you.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
- Good morning everybody. Here are my disclosures. So, upper extremity access is an important adjunct for some of the complex endovascular work that we do. It's necessary for chimney approaches, it's necessary for fenestrated at times. Intermittently for TEVAR, and for
what I like to call FEVARCh which is when you combine fenestrated repair with a chimney apporach for thoracoabdominals here in the U.S. Where we're more limited with the devices that we have available in our institutions for most of us. This shows you for a TEVAR with a patient
with an aortic occlusion through a right infracrevicular approach, we're able to place a conduit and then a 22-french dryseal sheath in order to place a TEVAR in a patient with a penetrating ulcer that had ruptured, and had an occluded aorta.
In addition, you can use this for complex techniques in the ascending aorta. Here you see a patient who had a prior heart transplant, developed a pseudoaneurysm in his suture line. We come in through a left axillary approach with our stiff wire.
We have a diagnostic catheter through the femoral. We're able to place a couple cuffs in an off-label fashion to treat this with a technically good result. For FEVARCh, as I mentioned, it's a good combination for a fenestrated repair.
Here you have a type IV thoraco fenestrated in place with a chimney in the left renal, we get additional seal zone up above the celiac this way. Here you see the vessels cannulated. And then with a nice type IV repaired in endovascular fashion, using a combination of techniques.
But the questions always arise. Which side? Which vessel? What's the stroke risk? How can we try to be as conscientious as possible to minimize those risks? Excuse me. So, anecdotally the right side has been less safe,
or concerned that it causes more troubles, but we feel like it's easier to work from the right side. Sorry. When you look at the image intensifier as it's coming in from the patient's left, we can all be together on the patient's right. We don't have to work underneath the image intensifier,
and felt like right was a better approach. So, can we minimize stroke risk for either side, but can we minimize stroke risk in general? So, what we typically do is tuck both arms, makes lateral imaging a lot easier to do rather than having an arm out.
Our anesthesiologist, although we try not to help them too much, but it actually makes it easier for them to have both arms available. When we look at which vessel is the best to use to try to do these techniques, we felt that the subclavian artery is a big challenge,
just the way it is above the clavicle, to be able to get multiple devices through there. We usually feel that the brachial artery's too small. Especially if you're going to place more than one sheath. So we like to call, at our institution, the Goldilocks phenomenon for those of you
who know that story, and the axillary artery is just right. And that's the one that we use. When we use only one or two sheaths we just do a direct puncture. Usually through a previously placed pledgeted stitch. It's a fairly easy exposure just through the pec major.
Split that muscle then divide the pec minor, and can get there relatively easily. This is what that looks like. You can see after a sheath's been removed, a pledgeted suture has been tied down and we get good hemostasis this way.
If we're going to use more than two sheaths, we prefer an axillary conduit, and here you see that approach. We use the self-sealing graft. Whenever I have more than two sheaths in, I always label the sheaths because
I can't remember what's in what vessel. So, you can see yes, I made there, I have another one labeled right renal, just so I can remember which sheath is in which vessel. We always navigate the arch first now. So we get all of our sheaths across the arch
before we selective catheterize the visceral vessels. We think this partly helps minimize that risk. Obviously, any arch manipulation is a concern, but if we can get everything done at once and then we can focus on the visceral segment. We feel like that's a better approach and seems
to be better for what we've done in our experience. So here's our results over the past five-ish years or so. Almost 400 aortic interventions total, with 72 of them requiring some sort of upper extremity access for different procedures. One for placement of zone zero device, which I showed you,
sac embolization, and two for imaging. We have these number of patients, and then all these chimney grafts that have been placed in different vessels. Here's the patients with different number of branches. Our access you can see here, with the majority
being done through right axillary approach. The technical success was high, mortality rate was reasonable in this group of patients. With the strokes being listed there. One rupture, which is treated with a covered stent. The strokes, two were ischemic,
one hemorrhagic, and one mixed. When you compare the group to our initial group, more women, longer hospital stay, more of the patients had prior aortic interventions, and the mortality rate was higher. So in conclusion, we think that
this is technically feasible to do. That right side is just as safe as left side, and that potentially the right side is better for type III arches. Thank you very much.
- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want
in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis
is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied
and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple
aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention
adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,
the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that
there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions
a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.
In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure
with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle
and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis
needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.
Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.
In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,
regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate
without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.
An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis
and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.
This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more
in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.
But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.
The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.
Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion
because I have a flight in a few hours. Thank you very much.
- I just like the title 'cuz I think we're in chaos anyway. Chaos management theory. Alright, unfortunately I have nothing to disclose, it really upsets me. I wish I had a laundry list to give you. Gettin' checks from everybody, it would be great. Let's start off with this chaos, what has been published.
Again "Ul Haq et al" is a paper from Hopkins. Bleomycin foam treatment of malformations, a promising agent. And they had 20 patients, 21 Bleomycin procedures. (mumbles) sclerosants in a few other patients, 40% complication rate, 30% minor, 10% major.
On a per procedure basis it was a 29% with about 7% major. All patients had decrease in symptoms. But to say "I use Bleomycin" or "I use X" because a complication (mumbles) is nonsense, you're mentally masturbating. It ain't going to be that way, you're going to have complications.
Alright, the use of Bleomycin should be reserved for locations where post-procedure swelling would be dangerous. Well they used it, and one patient required intubation for four days and another patient 15 days. So, it can happen with any agent.
So I don't know why that statement was made. "Hassan et al", noninvasive management of hemangiomas and vascular malformations using Bleomycin again, this handles the plastic surgery a few years ago. 71% effectiveness rate, 29% failure rate,
14% complication rate, 5 major ulcerations. Ulcerations happen with any agent. You're not going to escape that by saying, "Oh, well I'm not going to use alcohol because (mumbles)." No you're going to get it anyway. You all in the literature.
"Sainsbury", intra-lesional Bleomycin injection for vascular birthmarks five year experience again, 2011. 82% effectiveness, 17.3 for failure. Compli- severe blistering, ulcers, swelling, infections, recurrences. Okay, everybody's reporting it.
"Bai et al" sclerotherapy for lymphatic, oral and facial region, 2009. 43% effectiveness, but they found if they used it with surgery they had a higher effectiveness rate. Good. But again that's their effectiveness.
"Young et al", Bleomycin A5 cervico-facial vascular surgery, 2011. 81% effectiveness rate 19% failure for macrocystic. 37% failure from microcystic disease. Complications: ulcerations, hematoma, bleeding, fevers, soft tissue atrophy.
"Zhang et al." Now this is a study. They're goin' head-to-head alcohol versus Bleo. Oh, isn't that a nice thing to do. Huh, funny how that can happen sometimes. There's another paper out of Canada
that doesn't matter, there's 17 pages and there's no statistical significance for that. 138 patients, you got a lot of statistics. "Zhang et al", 138 children. 71 of 75 patients, which is 95% of that serie, were either cured,
markedly effective, or effective, with alcohol. In the Bleo group 41 of 63, that is 65% of the patients, had effective treatment. That means no cures, no markedly effective, just effective. That's their head-to-head comparison. Difference between Ethanol and
the Bleo group again was statistically significant. Ethanol at 75 patients of 14 cases skin necrosis. Bleo group at 63 patients of 5 cases skin necrosis. And in that group they stated it is statistically superior to Bleo. 95 versus 60, that's a big deal.
Again, cured, disappearance post-treatment without recurrence. Markedly effective, meant that greater than 80% was ablated. Effective means about less that 80% reduction but improved. Ineffective, no change. That was their criterion on that paper.
Again, 30 cases, superficial VMs effective rate was 95% in the Ethanol group and the deep group 94%. Okay. What was in the Bleo group? 68% superficial, 56% of deep group. So that's a statistical significance
of failure, between the two agents, comparing head-to-head in anatomic areas. Ethanol VM papers, let's go on to that, we're goin' to do other stuff. "Lee et al", advanced management, 2003, midterm results. 399 procedures in 87 patients,
95% significant or complete ablation, 12.4% complication. "Johnson et al", Kansas. University of Kansas med center, 2002. 100% success rate in tongues. One patient had a massive tongue and had breathing difficulties prior to treatment
remained intubated 5 days and then uneventfully discharged, that was their only complication. "Su et al", ethanol sclerotherapy, face and neck. Again, these are complex anatomies with complex issues of cranial nerves as well as airway control. 2010, 56 of 60 procedures, 90%, four minimal residual,
no skin necrosis, no nerve injuries. "Orlando", outpatient percutaneous treatment, low doses under local anesthesia. This is a very interesting paper out of Brazil. They did 'em under IV sedation, just a little bit by little bit.
They said they had trouble gettin' general so they had to figure another way. Smart, I like people thinkin' things out. Who here doesn't have a problem with anesthesia? Gettin' 'em not to quit before two o'clock? (laughs)
Alright, used local only 39 patients extremity VMs, main symptoms of pain. Cure or significant improvement in 94%. One ulcer, 3 transient paresthesias. "Lee et al", sclerotherapy craniofacial again, 2009. 87 patients, 75% were reductions.
71 of 87 excellent outcomes. One patient transient, tongue decreased sensation. One transient facial nerve palsy, no skin injuries. "Vogelzang" is a very important paper of a single center. Is that author- anybody here? Again, they did VMs and AVMs in this series
and then a per patient complication rate is 13.3, in AMVs 9.7 per patient, but I think what also is important is to do things with regards to procedures. And they listed both. So we'll just, it's about time to quit. This is our embolization series.
And neck, upper extremity, all the anatomies. And we're about a 10 to three ratio with regards to VM/LMs to AVMs in numbers. I think everybody's pretty much like that, a third of their practice. Again, our minor complications are that.
Major complications are these. Summary, what we found in the literature is that Ethanol publications state its efficacy rate routinely at 90 to 100%. And all other second tier sclerosants are 60 to 80%. So I think that's the take home message.
- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.
Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance
between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.
Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.
Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100
consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any
stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria
having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this
on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher
than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of
the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,
you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because
the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity
because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish
this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,
regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. Thank you very much.
- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification
for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,
also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of
a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,
and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct
arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,
and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding
the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,
mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from
multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views
on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied
by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?
IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.
This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way
to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,
but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.
Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?
And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,
the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.
So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.
Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.
So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,
and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described
in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,
so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example
50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System
is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.
Thank you very much.
- (speaks French) liver surgeon I perform hepatobiliary surgery and liver transplantation. Maybe I don't belong here, I so probably more rested than anybody in the room here. But today I will present about liver surgery and hepatectomy. I work at The Royal Free where I have the honor and pleasure to have seen Krassi. We are in the
little island in the North Sea. There is many things going wrong there including Brexit but, the guys uh, we have a major advantage. The NHS favors centralization. Centralization look there: London is bigger than New York Uh, eight million, 50 million greater London
and we drain about six millions of people with our HPB center. In the center we perform about 2,000 operations, of major surgery. In five years, half of them are liver surgery. And most of them have uh, benign, malignant tumor. A very small percentage have benign tumor.
I count here for complications uh, and mortality look there, 3.1% of only the malignant because the benign are young people and we perform a different strategy, they have no mortality. Today Hepatic Hemangioma, look there it is uh, 1898 is a key year. Not only the first description
of the lady that died after bleeding out in an autopsy but also, Hermann Pfannenstiel uh, Professor Pfannenstiel. I will introduce you to him. He described the first operation. Now, we're talking of congenital malformations, they uh, lesions occur in the liver and they may grow,
but only 20% they grow. They have a chaotic network of vessels and they have fibrotic, fibrotic development within it. I introduce you Hermann Pfannenstiel, he was a gynecologist, famous, famous, important incision that we still use today.
Remember him, we'll talk to him later. Microscopically, the microscopic is our well-circumscribed lesion, they're compressible. Important you see down there that they compress the liver that is normal close to it. This has an implication because if you operate,
you fill find a blood duct or a vessel and it will bleed or leak by. Microscopically, they are ectatic blood vessels and they are fed by arteries. This is also an important point, for therapy. Separated by fibrous septa, this is also important
because they become harder and they become bigger. And they have distorted blood vessels. They're more frequent uh, benign tumor. Prevalence up to 7%, they have non-neoplastic this must be clear, they are non-cancer. The proliferation of endothelial cells, women
have more and particularly pregnant women, more pregnancy or contraceptive. We divide them in cavernous and capillary and we'll have a word on that. Symptomatic being half of the cases, multiple in 10%, they rarely bleed and they rarely rupture.
Capillary Hemangiomas cells small, I show you an MRI here. The differential with HCC liver cancer is most important. They both are theorized but they continue to appear on late face. They are asymptomatic please, do not touch them, they do no harm.
And so we will not speak of them. We speak only of the cavernous hemangioma. And here, the cavernous hemangioma bleeds Oh my God, no, it's not true. There are 83 reports of bleeding since the report of Hermann Pfannenstiel. Uh, 97 cases, adenomas bleed more frequently.
Frequently, in the past they were confused. Hemangioma and adenoma, adenoma does bleed. There are only true cases, 46 in the literature. Size is not important and they are very rare in elderly people.
This is what we see when they are giant cavernous hemangiomas, they're serious, they are rather easy to diagnose. Diagnostic criteria, uh, look up typical for uh, cavernous hemangioma. How do you point here? Yep, you stop. If you then see that you have
an atypical hemangioma, you jump over to an MRI. MRI is too nowadays, diagnostic and uh, the important thing is you stop. Once you have the diagnosis with MRI, you stop, do nothing yet, do not follow, bye-bye. Treatment modalities surgery: Selective TAE, Radiotherapy, Medication: two classes,
Propranolol, to decrease the hyper circulation. Bevacizumab as a class of drugs of inhibitors of inferior growths and endories, eventually are cold. This is seminal paper, about 35 years ago "Do not treat asymptomatic patients." This is a key: do not bother with hemangioma.
If you do have the algorithm, you look at complaints that can present incidentally when they have complained, not complained, no treatment of abdominal pain. Unrelated to no treatment, we have to eventually make sure that the pain is not related to the cavernous hemangioma. If there is other futures
like compression giant, you can do surgery. If you have a doubt in diagnosis, today rare with MRI, then you can perform a biopsy. The surgical indication then remain progress, severe, disabling symptoms. Diagnostic uncertainty nowadays not the case, with MRI.
Consumptive coagulopathy or Kasabach-Merritt syndrome is a serious, we will see when you perform human transplants. Spontaneous rupture with bleeding as an emergency. Rapid growth in 25%. This is a paper that shows that the size of the cavernous hemangioma is here,
and you can see that operation has been performed for larger size, however, look that even in non-symptomatic or partially asymptomatic patients, you can reach sizes up to 15 centimeters. And this a review of the literature from a Chinese group where they revised a thousand to a hundred cases,
no mortality in the series and enucleation versus the anatomic resection is better. Less complications, less blood less, less time of surgery, and less hospital stay. So please, in this case of surgery, we do enucleation. I was asked by my society the HPBA to speak
about transplantation for liver tumor. You can that an indication is unresectable disease, severe symptoms and mass occupying effects. Pre-cancerous behavior is not for hemangioma only for adenoma differential diagnosis with HCC. And you have to be attentive that you avoid
liver insufficiency during your resection. So, in conclusion, for benign lesions, hemangioma technically is the only indication. And now the systematic review that shows around several emothing United States UNOS and the ELTR Several, several benign tumors but if you break down
for type of tumors you see that most of them are Polycystic disease or partly cavernous hemangioma are very low. 77 in Europe, out of 97,000 operation of transplantation. So, let's get an old paper. The pioneer of transplantation again, extremely low,
one out of 3,200. An extremely low percentage. It's my personal experience I was working at Essen, Germany. Almost a thousand transplants we performed. Unfortunately most of them I did and we never transplanted one hemangioma, my experience for transplantation is zero because it should not be done.
So, my advice for hemangioma. Biopsy not advised, see a liver surgeon in a serious center, diagnosis is done my MRI, observe doubt symptoms and observe. Let the patient beg you for surgery, if significant increase in size and symptoms, we can do surgery. Embolization is possible.
Sometimes it's harmful. The role of the surgeon is to confirm the diagnosis, differentiate it from cancer, exclude causes of other symptoms and avoid unnecessary surgery that's the main thing. Surgery for severe symptoms of Kasabach-Merritt. Only for complicated symptomatic lesions, or where the
diagnosis is uncertain. Ladies and gentleman, I will conclude with a couple of questions. If you have a daughter or son with a liver tumor, would you go to a center or a competent surgeon or to a gynecologist. Professor Pfannenstiel for instance or another doctor. If your car has a problem,
would you go to a good mechanic once for all, or to a small shop for 20-40 times. It is a matter of experience and a matter of costs. And with this, I am ready for your questions. - [Audience Member #1] When have you personally operated on these lesions?
- [Speaker] I am. And the experience that I have in the past I seemed young but I practiced for many years. When I started 25-30 years ago, we were operating many of these because we were not so certain. Then MRI came, and MRI basically made the diagnosis so easy and straight-forward and we started observing
patients. We still do operate today, but they are very large tumors and when I do personally, I avoid the androbolization before because you have more skylotec reaction, just (grainy sound effect) to peel it away from the normal parenchymal.
This is our experience. - [Audience] Thank you. - [Speaker] Thank you very much, yes? - [Audience Member #2] Yes, one question. When you operate, and with all of the experience you have, what are the complications of
(mumbles) - [Speaker] The main, so first of all, there has been also an evolution in the type of operation we don't do anymore the resections where you have some bi-leaks. If you operate correctly, it's bleeding and one infection not one born. If you have to watch bi-leak is the one
that you have to watch and that's because the tissue is pushed away and you may miss something during the enucleation.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- I think by definition this whole session today has been about challenging vascular access cases. Here's my disclosures. I went into vascular surgery, I think I made the decision when I was either a fourth year medical student or early on in internship because
what intrigued me the most was that it seemed like vascular surgeons were only limited by their imagination in what we could do to help our patients and I think these access challenges are perfect examples of this. There's going to be a couple talks coming up
about central vein occlusion so I won't be really touching on that. I just have a couple of examples of what I consider challenging cases. So where do the challenges exist? Well, first, in creating an access,
we may have a challenge in trying to figure out what's going to be the best new access for a patient who's not ever had one. Then we are frequently faced with challenges of re-establishing an AV fistula or an AV graft for a patient.
This may be for someone who's had a complication requiring removal of their access, or the patient who was fortunate to get a transplant but then ended up with a transplant rejection and now you need to re-establish access. There's definitely a lot of clinical challenges
maintaining access: Treating anastomotic lesions, cannulation zone lesions, and venous outflow pathology. And we just heard a nice presentation about some of the complications of bleeding, infection, and ischemia. So I'll just start with a case of a patient
who needed to establish access. So this is a 37-year-old African-American female. She's got oxygen-dependent COPD and she's still smoking. Her BMI is 37, she's left handed, she has diabetes, and she has lupus. Her access to date - now she's been on hemodialysis
for six months, all through multiple tunneled catheters that have been repeatedly having to be removed for infection and she was actually transferred from one of our more rural hospitals into town because she had a infected tunneled dialysis catheter in her femoral region.
She had been deemed a very poor candidate for an AV fistula or AV graft because of small veins. So the challenges - she is morbidly obese, she needs immediate access, and she has suboptimal anatomy. So our plan, again, she's left handed. We decided to do a right upper extremity graft
but the plan was to first explore her axillary vein and do a venogram. So in doing that, we explored her axillary vein, did a venogram, and you can see she's got fairly extensive central vein disease already. Now, she had had multiple catheters.
So this is a venogram through a 5-French sheath in the brachial vein in the axilla, showing a diffusely diseased central vein. So at this point, the decision was made to go ahead and angioplasty the vein with a 9-millimeter balloon through a 9-French sheath.
And we got a pretty reasonable result to create venous outflow for our planned graft. You can see in the image there, for my venous outflow I've placed a Gore Hybrid graft and extended that with a Viabahn to help support the central vein disease. And now to try and get rid of her catheters,
we went ahead and did a tapered 4-7 Acuseal graft connected to the brachial artery in the axilla. And we chose the taper mostly because, as you can see, she has a pretty small high brachial artery in her axilla. And then we connected the Acuseal graft to the other end of the Gore Hybrid graft,
so at least in the cannulation zone we have an immediate cannualation graft. And this is the venous limb of the graft connected into the Gore hybrid graft, which then communicates directly into the axillary vein and brachiocephalic vein.
So we were able to establish a graft for this patient that could be used immediately, get rid of her tunneled catheter. Again, the challenges were she's morbidly obese, she needs immediate access, and she has suboptimal anatomy, and the solution was a right upper arm loop AV graft
with an early cannulation segment to immediately get rid of her tunneled catheter. Then we used the Gore Hybrid graft with the 9-millimeter nitinol-reinforced segment to help deal with the preexisting venous outflow disease that she had, and we were able to keep this patient
free of a catheter with a functioning access for about 13 months. So here's another case. This is in a steal patient, so I think it's incredibly important that every patient that presents with access-induced ischemia to have a complete angiogram
of the extremity to make sure they don't have occult inflow disease, which we occasionally see. So this patient had a functioning upper arm graft and developed pretty severe ischemic pain in her hand. So you can see, here's the graft, venous outflow, and she actually has,
for the steal patients we see, she actually had pretty decent flow down her brachial artery and radial and ulnar artery even into the hand, even with the graft patent, which is usually not the case. In fact, we really challenged the diagnosis of ischemia for quite some time, but the pressures that she had,
her digital-brachial index was less than 0.5. So we went ahead and did a drill. We've tried to eliminate the morbidity of the drill bit - so we now do 100% of our drills when we're going to use saphenous vein with endoscopic vein harvest, which it's basically an outpatient procedure now,
and we've had very good success. And here you can see the completion angiogram and just the difference in her hand perfusion. And then the final case, this is a patient that got an AV graft created at the access center by an interventional nephrologist,
and in the ensuing seven months was treated seven different times for problems, showed up at my office with a cold blue hand. When we duplexed her, we couldn't see any flow beyond the AV graft anastomosis. So I chose to do a transfemoral arteriogram
and what you can see here, she's got a completely dissected subclavian axillary artery, and this goes all the way into her arterial anastomosis. So this is all completely dissected from one of her interventions at the access center. And this is the kind of case that reminded me
of one of my mentors, Roger Gregory. He used to say, "I don't wan "I just want out of the trap." So what we ended up doing was, I actually couldn't get into the true lumen from antegrade, so I retrograde accessed
her brachial artery and was able to just re-establish flow all the way down. I ended up intentionally covering the entry into her AV graft to get that out of the circuit and just recover her hand, and she's actually been catheter-dependent ever since
because she really didn't want to take any more chances. Thank you very much.
- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old
but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,
and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.
- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,
and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was
revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.
In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat
was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.
Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone
returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.
Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy
with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,
the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.
Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.
So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really
how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017
in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.
Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at
five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery
to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional
independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.
So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,
but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could
help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.
- Thank you very much for the kind introduction, and I'd like to thank the organizers, especially Frank Veith for getting back to this outstanding and very important conference. My duty is now to talk about the acute status of carotid artery stenting is acute occlusion an issue? Here are my disclosures.
Probably you might be aware, for sure you're aware about pore size and probably smaller pore size, the small material load might be a predisposing factor for enhanced thrombogenicity in these dual layer stents, as you're probably quite familiar with the CGUARD, Roadsaver and GORE, I will focus my talk a little bit
on the Roadsaver stent, since I have the most experience with the Roadsaver stent from the early beginning when this device was on the market in Europe. If you go back a little bit and look at the early publications of CGUARD, Roadsaver and GORE stent, then acute occlusion the early reports show that
very clearly safety, especially at 30 days in terms of major cardiac and cerebrovascular events. They are very, very safe, 0% in all these early publications deal with these stents. But you're probably aware of this publication, released end of last year, where a German group in Hamburg
deals with carotid artery stenosis during acute stroke treatment. They used the dual layer stent, the Roadsaver stent or the Casper stent in 20 cases, in the same time period from 2011 to 2016, they used also the Wallstent and the VIVEXX stent,
in 27 cases in total and there was a major difference, in terms of acute stent occlusion, and for the Roadsaver or Casper stent, it was 45%, they also had an explanation for that, potential explanations probably due to the increase of thrombogenic material due to the dual layer
insufficient preparation with antiplatelet medication, higher patient counts in the patients who occluded, smaller stent diameters, and the patients were not administered PTA, meaning Bridging during acute stroke patient treatment, but it was highlighted that all patients received ASA of 500mg intravenously
during the procedure. But there are some questions coming up. What is a small stent diameter? Post-dilatation at what diameter, once the stent was implanted? What about wall apposition of the stent?
Correct stent deployment with the Vicis maneuver performed or not and was the ACT adjusted during the procedure, meaning did they perform an adequate heparinization? These are open questions and I would like to share our experience from Flensburg,
so we have treated nearly 200 patients with the Roadsaver stent from 2015 until now. In 42 patients, we used this stent exclusively for acute stroke treatment and never, ever observed in both groups, in the symptomatic and asymptomatic group and in the group of acute stroke treatment,
we never observed an acute occlusion. How can we explain this kind of difference that neither acute occlusion occurred in our patient group? Probably there are some options how we can avoid stent thrombosis, how we can minimize this. For emergency treatment, probably this might be related
to bridging therapies, though in Germany a lot of patients who received acute stroke treatment are on bridging therapy since the way to the hospital is sometimes rather long, there probably might be a predisposing factor to re-avoid stent thrombosis and so-called tandem lesions if the stent placement is needed.
But we also take care of antiplatelet medication peri-procedurally, and we do this with ASA, as the Hamburg group did and at one day, we always start, in all emergency patients with clopidogrel loading dose after positive CT where we could exclude any bleeding and post-procedurally we go
for dual anti-platelet therapy for at least six months, meaning clopidogrel and ASA, and this is something probably of utmost importance. It's quite the same for elective patients, I think you're quite familiar with this, and I want to highlight the post-procedural clopidogrel
might be the key of success for six months combined with ASA life-long. Stent preparation is also an issue, at least 7 or 8 diameters we have to choose for the correct lengths we have to perform adequate stent deployment and adequate post-dilatation
for at least 5mm. In a lot of trials the Roadsaver concept has been proven, and this is due to the adequate preparation of the stent and ongoing platelet preparation, and this was also highlight in the meta-analysis with the death and stroke rate of .02% in all cases.
Roadsaver study is performed now planned, I am a member of the steering committee. In 2000 patients, so far 132 patients have been included and I want to rise up once again the question, is acute occlusion and issue? No, I don't think so, since you keep antiplatelet medication
in mind and be aware of adequate stent sizing. I highly appreciated your attention, thank you very much.
- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery
in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,
but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase
and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,
and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast
in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.
So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,
it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause
of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.
So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes
and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,
and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR
might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement
without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac
Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,
to save our country from a type II endoleak, and I thank you for your attention.
- Good morning, thank you very much to Dr. Veith and Professor Veith and the organizers. So this is real holography. It's not augmented reality. It's not getting you separated from the environment that you're in. This is actually taking the 3D out of the screen
so the beating heart can be held in the palm of your hand without you having to wear any goggles or anything else and this is live imaging. It can be done intra-procedure. This is the Holoscope-i and the other one is the Holoscope-x
where in fact you can take that actually 3D hologram that you have and you can implant it in the patient and if you co-register it correctly then you can actually do the intervention in the patient
make a needle tract to the holographic needle and I'm going to limit this to just now what we're actually doing at the moment and not necessarily what the future can be. This is ultimate 3D visualization, true volumes floating in the air.
This is a CT scan. So it started working, So we get rid of the auto-segmented and you can just interact. It's floating 45 centimeters away from you and you can just hold the patient's anatomy here and you can slice into the anatomy.
This is for instance a real CT of an aorta with the aortic valve which they wanted to analyze for a core valve procedure. This is done by Phelps. If you take the information
and they've looked at the final element analysis and interaction between the stem and the tissue. So here you can make measurements in real time. So if you did the 3D rotation and geography and you had the aorta and you wanted to put in a stent graft EVAR TVAR, and you would see,
and you could put in a typical tuber that you would do, and you could see how it, and this is a dynamic hologram, so you can see how it would open up, you can mark where your fenestration's chimney is and all that type of stuff would be. And you can move it around, and you have
a complete intuitive understanding of a, can we go to the next slide please, I can't, it seems to be clicking, thank you. So how do we do all this? Well, to create a hologram, what you need to do is just conceptualize it as printing in light.
Like if you had plastic and you took the XYZ data and you just put it into a 3D printer, and it would print it for you in light, then you'd go, Okay, so I understand, if it was printed for you in plastic then you'd understand. But imagine it's printing in light.
So we have every single piece of light focused, each photon is focused so that you can see it with a naked eye, in a particular place, but the difference is that it's totally sterile, you don't have to take off your gloves, you don't have to use a mouse,
you can interact with it directly. And all the XYZ data is 100% in place, so we've just seen a beautiful demonstration of augmented reality, and in augmented reality, you have to wear something, it isolates you from the environment that you're in, and it's based on
stereoscopy, and stereoscopy is how you see 3D movies, and how you see augmented reality, is by taking two images and fusing them in one focal plane. But you can't touch that image, because if you look at me now, you can see me very well, but if you hold your finger up 45 centimeters
and you focus on your finger, I become blurred. And so, you can only focus in one plane, you can't touch that image, because that image is distant from you, and it's a fused image, so you have the focus plane and you have the convergence plane, and this is an illusion
of 3D, and it's very entertaining, and it can be very useful in medical imaging, but in intra-operative procedures it has to be 100% accurate. So you saw a very beautiful example in the previous talk of augmented reality, where you have gesturing, where you can actually gesture with the image,
you can make it bigger, you can make it smaller. But what RealView does by creating real holography, which is all the XYZ data, is having it in the palm of your hand, with having above 20 focal planes, here, very very close to your eye, and that in another way, of having all those focal planes not only actually lets you
do the procedure but prevents nausea and having a feeling of discomfort because the image is actually there as of having the illusion of the images there. So just to go back, all RealView imaging is doing, is it's not changing your 3D RA cone, BMCT, MRI,
we can do all those XYZ datas and we can use them and we can present them, all we're doing, so you use your acquisition, we're just taking that, and we're breaking open the 3D displays and seeing all that 3D data limited in the 2D screen, let's set it free and have it floating in the air.
So we have the holoscope-i for structural cardiology and electrophysiology, and obviously the holoscope-x, which makes the patient x-rayed, completely visible. So its an over the head, this is now, obviously, free-standing when somebody buys us like Phillips or Siemens, it will be integrated into your lab,
come down from the ceiling, it's an independent system, and you just have a visor that you look through, which just goes up and down whenever you want to use it. You can interact with it the same as you do with your iPhone you can visualize, you can rotate, you can mark, you can slice, you can measure, as I showed you
some examples of it, and you can do this by voice as well, you just talk to it, you say slice and you slice it with your hand, it recognizes everybody's hand, there's no delay for whatever you're imaging. So structural cardiac procedures, this is what
a mitral valve will look like, floating in the air in front of you, you can see the anterior leaflet, the posterior leaflet. And once the catheter is inside and you're guiding the catheter inside the procedure, you can turn on your doppler, you'll be able to see that the catheter
movements, so for someone doing a mitral clip, or whatever, this would be very very useful. This is an electrophysiological procedure, and you can see how the catheter moves, when the catheter will move, and obviously, as my previous speaker was saying, you are appreciating 3D in a 2D screen,
so it's very difficult to appreciate, you'll have to take my word for it. But I think you can see dynamic colography at this quality, that you can interact with, that is something that is very special, we've presented at a number of conferences,
including at Veith, and we've already done a first in man, and the most exciting thing for now, is just this week, the first machine was installed at Toronto general, at the Peter Munk Cardiac Center, and they've done their first case, and so now we are launching and clinical trials in 2018, and hopefully,
I'll have something which is more vascular relevant, at the next time, Veith 2019, thank you very much.
- [Speaker] Good morning everybody thanks for attending the session and again thanks for the invitation. These are my disclosures. I will start by illustrating one of the cases where we did not use cone beam CT and evidently there were numerous mistakes on this
from planning to conducting the case. But we didn't notice on the completion of geography in folding of the stent which was very clearly apparent on the first CT scan. Fortunately we were able to revise this and have a good outcome.
That certainly led to unnecessary re intervention. We have looked at over the years our usage of fusion and cone beam and as you can see for fenestrated cases, pretty much this was incorporated routinely in our practice in the later part of the experience.
When we looked at the study of the patients that didn't have the cone beam CT, eight percent had re intervention from a technical problem that was potentially avoidable and on the group that had cone beam CT, eight percent had findings that were immediately revised with no
re interventions that were potentially avoidable. This is the concept of our GE Discovery System with fusion and the ability to do cone beam CT. Our protocol includes two spins. First we do one without contrast to evaluate calcification and other artifacts and also to generate a rotational DSA.
That can be also analyzed on axial coronal with a 3D reconstruction. Which essentially evaluates the segment that was treated, whether it was the arch on the arch branch on a thoracoabdominal or aortoiliac segment.
We have recently conducted a prospective non-randomized study that was presented at the Vascular Annual Meeting by Dr. Tenario. On this study, we looked at findings that were to prompt an immediate re intervention that is either a type one
or a type 3 endoleak or a severe stent compression. This was a prospective study so we could be judged for being over cautious but 25% of the procedures had 52 positive findings. That included most often a stent compression or kink in 17% a type one or three endoleak
in 9% or a minority with dissection and thrombus. Evidently not all this triggered an immediate revision, but 16% we elected to treat because we thought it was potentially going to lead to a bad complication. Here is a case where on the completion selective angiography
of the SMA this apparently looks very good without any lesions. However on the cone beam CT, you can see on the axial view a dissection flap. We immediately re catheterized the SMA. You note here there is abrupt stop of the SMA.
We were unable to catheterize this with a blood wire. That led to a conversion where after proximal control we opened the SMA. There was a dissection flap which was excised using balloon control in the stent as proximal control.
We placed a patch and we got a good result with no complications. But considerably, if this patient was missed in the OR and found hours after the procedure he would have major mesenteric ischemia. On this study, DSA alone would have missed
positive findings in 34 of the 43 procedures, or 79% of the procedures that had positive findings including 21 of the 28 that triggered immediate revision. There were only four procedures. 2% had additional findings on the CT
that were not detectable by either the DSA or cone beam CT. And those were usually in the femoro puncture. For example one of the patients had a femoro puncture occlusion that was noted immediately by the femoro pulse.
The DSA accounts for approximately 20% of our total radiation dose. However, it allows us to eliminate CT post operatively which was done as part of this protocol, and therefore the amount of radiation exposed for the patient
was decreased by 55-65% in addition to the cost containment of avoiding this first CT scan in our prospective protocol. In conclusion cone beam CT has allowed immediate assessment to identify technical problems that are not easily detectable by DSA.
These immediate revisions may avoid unnecessary re interventions. What to do if you don't have it? You have to be aware that this procedure that are complex, they are bound to have some technical mistakes. You have to have incredible attention to detail.
Evidently the procedures can be done, but you would have to have a low threshold to revise. For example a flared stent if the dilator of the relic gleam or the dilator of you bifurcated devise encroach the stent during parts of the procedure. Thank you very much.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. Thank you.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- I'd like to thank Dr. Veith and the committee for the privilege of presenting this. I have no disclosures. Vascular problems and the type of injuries could be varied. We all need to have an awareness of acute and chronic injuries,
whether they're traumatic, resulting with compression, occlusion, tumoral and malformation results, or vasospastic. I'd like to present a thoracoscopic manipulation of fractured ribs to prevent descending aortic injury
in a patient with chest trauma. You know, we don't think about this but they can have acute or delayed onset of symptoms and the patient can change and suddenly deteriorate with position changes or with mechanical ventilation,
and this is a rather interesting paper. Here you can see the posterior rib fracture sitting directly adjacent to the aorta like a knife. You can imagine the catastrophic consequences if that wasn't recognized and treated appropriately.
We heard this morning in the venous session that the veins change positions based on the arteries. Well, we need to remember that the arteries and the whole vascular bundle changes position based on the spine
and the bony pieces around them. This is especially too when you're dealing with scoliosis and scoliotic operations and the body positioning whether it's supine or prone the degree of hypo or hyperkyphosis
and the vertebral angles and the methods of instrumentation all need to be considered and remembered as the aorta will migrate based on the body habits of the patient. Screws can cause all kinds of trouble.
Screws are considered risky if they're within one to three millimeters of the aorta or adjacent tissues, and if you just do a random review up to 15% of screws that are placed fall into this category.
Vertebral loops and tortuosity is either a congenital or acquired anomaly and the V2 segment of the vertebral is particularly at risk, most commonly in women in their fifth and sixth decades,
and here you can see instrumentation of the upper cervical spine, anterior corpectomy and the posterior exposures are all associated with a significant and lethal, at times, vertebral artery injuries.
Left subclavian artery injury from excessively long thoracic pedicle screws placed for proximal thoracic scoliosis have been reported. Clavicular osteosynthesis with high neurovascular injury especially when the plunge depth isn't kept in mind
in the medial clavicle have been reported and an awareness and an ability to anticipate injury by looking at the safe zone and finding this on the femur
with your preoperative imaging is a way to help prevent those kinds of problems. Injuries can be from stretch or retraction. Leave it to the French. There's a paper from 2011 that describes midline anterior approach
from the right side to the lumbar spine, interbody fusion and total disc replacement as safer. The cava is more resistant to injury than the left iliac vein and there's less erectile dysfunction reported. We had a patient present recently
with the blue bumps across her abdomen many years after hip complicated course. She'd had what was thought to be an infected hip that was replaced, worsening lower extremity edema, asymmetry of her femoral vein on duplex
and her heterogeneous mask that you can see here on imaging. The iliac veins were occluded and compressed and you could see in the bottom right the varicosities that she was concerned about. Another case is a 71-year-old male who had a post-thrombotic syndrome.
It was worsened after his left hip replacement and his wife said he's just not been the same since. Initially imaging suggests that this was a mass and a tumor. He underwent biopsy
and it showed ghost cells. Here you can see the venogram where we tried to recanalize this and we were unsuccessful because this was actually a combination of bone cement and inflammatory reaction.
Second patient in this category, bless you, is a 67-year-old female who had left leg swelling again after a total hip replacement 20 plus years ago. No DVTs but here you can see the cement compressing the iliac vein.
She had about a 40% patency when you put her through positioning and elected not to have anything done with that. Here you could see on MR how truly compressed this is. IVA suggested it was a little less tight than that.
So a vascular injury occurs across all surgical specialties. All procedures carry risk of bleeding and inadvertent damage to vessels. The mechanisms include tearing, stretching, fracture of calcific plaques,
direct penetration and thermal injury. The types of injuries you hear are most common after hip injuries, they need to be recognized in the acute phase as looking for signs of bleeding or ischemia. Arterial lesions are commonly prone then.
Bone cement can cause thermal injury, erosion, compression and post-implant syndrome. So again, no surgery is immune. You need to be aware and especially when you look at patients in the delayed time period
to consider something called particle disease. This has actually been described in the orthopedic literature starting in the 70s and it's a complex interaction of inflammatory pathways directed at microparticles that come about
through prosthetic wear. So not only acute injury but acute and chronic symptoms. Thank you for the privilege of the floor.
- Thank you very much and thank you Dr. Veith for the kind invite. Here's my disclosures, clearly relevant to this talk. So we know that after EVAR, it's around the 20% aortic complication rate after five years in treating type one and three Endoleaks prevents subsequent
secondary aortic rupture. Surveillance after EVAR is therefore mandatory. But it's possible that device-specific outcomes and surveillance protocols may improve the durability of EVAR over time. You're all familiar with this graph for 15 year results
in terms of re-intervention from the EVAR-1 trials. Whether you look at all cause and all re-interventions or life threatening re-interventions, at any time point, EVAR fares worse than open repair. But we know that the risk of re-intervention is different
in different patients. And if you combine pre-operative risk factors in terms of demographics and morphology, things are happening during the operations such as the use of adjuncts,
or having to treat intro-operative endoleak, and what happens to the aortic sac post-operatively, you can come up with a risk-prediction tool for how patients fare in the longer term. So the LEAR model was developed on the Engage Registry and validated on some post-market registries,
PAS, IDE, and the trials in France. And this gives a predictive risk model. Essentially, this combines patients into a low risk group that would have standard surveillance, and a higher risk group, that would have a surveillance plus
or enhanced surveillanced model. And you get individual patient-specific risk profiles. This is a patient with around a seven centimeter aneurysm at the time of repair that shows sac shrinkage over the first year and a half, post-operatively. And you can see that there's really a very low risk
of re-intervention out to five years. These little arrow bars up here. For a patient that has good pre-operative morphology and whose aneurysm shrinks out to a year, they're going to have a very low risk of re-intervention. This patient, conversely, had a smaller aneurysm,
but it grew from the time of the operation, and out to two and a half years, it's about a centimeter increase in the sac. And they're going to have a much higher risk of re-intervention and probably don't need the same level of surveillance as the first patient.
and probably need a much higher rate of surveillance. So not only can we have individualized predictors of risk for patients, but this is the regulatory aspect to it as well.
Multiple scenario testing can be undertaken. And these are improved not only with the pre-operative data, but as you've seen with one-year data, and this can tie in with IFU development and also for advising policy such as NICE, which you'll have heard a lot about during the conference.
So this is just one example. If you take a patient with a sixty-five millimeter aneurysm, eighteen millimeter iliac, and the suprarenal angle at sixty degrees. If you breach two or more of these factors in red, we have the pre-operative prediction.
Around 20% of cases will be in the high risk group. The high risk patients have about a 50-55% freedom from device for related problems at five years. And the low risk group, so if you don't breach those groups, 75% chance of freedom from intervention.
In the green, if you then add in a stent at one year, you can see that still around 20% of patients remain in the high risk group. But in the low risk group, you now have 85% of patients won't need a re-intervention at five years,
and less of a movement in the high risk group. So this can clearly inform IFU. And here you see the Kaplan-Meier curves, those same groups based pre-operatively, and at one year. In conclusion, LEAR can provide
a device specific estimation of EVAR outcome out to five years. It can be based on pre-operative variables alone by one year. Duplex surveillance helps predict risk. It's clearly of regulatory interest in the outcomes of EVAR.
And an E-portal is being developed for dissemination. Thank you very much.
- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.
And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.
And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,
but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.
The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.
And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,
or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.
And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome
occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity
Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,
such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.
When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.
We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.
And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.
Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.
Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial
And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05
and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options
that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.
- Thanks Fieres. Thank you very much for attending this session and Frank for the invitation. These are my disclosures. We have recently presented the outcomes of the first 250 patients included in this prospective IDE at the AATS meeting in this hotel a few months ago.
In this study, there was no in-hospital mortality, there was one 30-day death. This was a death from a patient that had intracranial hemorrhage from the spinal drain placement that eventually was dismissed to palliative care
and died on postoperative day 22. You also note that there are three patients with paraplegia in this study, one of which actually had a epidural hematoma that was led to various significant and flacid paralysis. That prompted us to review the literature
and alter our outcomes with spinal drainage. This review, which includes over 4700 patients shows that the average rate of complications is 10%, some of those are relatively moderate or minor, but you can see a rate of intracranial hemorrhage of 1.5% and spinal hematoma of 1% in this large review,
which is essentially a retrospective review. We have then audited our IDE patients, 293 consecutive patients treated since 2013. We looked at all their spinal drains, so there were 240 placement of drains in 187 patients. You can see that some of these were first stage procedures
and then the majority of them were the index fenestrated branch procedure and some, a minority were Temporary Aneurysm Sac Perfusions. Our rate of complication was identical to the review, 10% and I want to point out some of the more important complications.
You can see here that intracranial hypotension occurred in 6% of the patients, that included three patients, or 2%, with intracranial hemorrhage and nine patients, or 5%, with severe headache that prolonged hospital stay and required blood patch for management.
There were also six patients with spinal hematomas for a overall rate of 3%, including the patient that I'll further discuss later. And one death, which was attributed to the spinal drain. When we looked at the intracranial hypotension in these 12 patients, you can see
the median duration of headache was four days, it required narcotics in seven patients, blood patch in five patients. All these patients had prolonged hospital stay, in one case, the prolongation of hospital stay was of 10 days.
Intracranial hemorrhage in three patients, including the patient that I already discussed. This patient had a severe intracranial hemorrhage which led to a deep coma. The patient was basically elected by the family to be managed with palliative care.
This patient end up expiring on postoperative day 21. There were other two patients with intracranial hemorrhage, one remote, I don't think that that was necessarily related to the spinal drain, nonetheless we had it on this review. These are some of the CT heads of the patients that had intracranial hemorrhage,
including the patient that passed away, which is outlined in the far left of your slide. Six patients had spinal hematoma, one of these patients was a patient, a young patient treated for chronic dissection. Patient evolved exceptionally well, moving the legs,
drain was removed on postoperative day two. As the patient is standed out of the bed, felt weakness in the legs, we then imaged the spine. You can see here, very severe spinal hematoma. Neurosurgery was consulted, decided to evacuate, the patient woke up with flacid paralysis
which has not recovered. There were two other patients with, another patient with paraplegia which was treated conservatively and improved to paraparesis and continues to improve and two other patients with paraparesis.
That prompted changes in our protocol. We eliminated spinal drains for Extent IVs, we eliminated for chronic dissection, in first stages, on any first stage, and most of the Extent IIIs, we also changed our protocol of drainage
from the routine drainage of a 10 centimeters of water for 15 minutes of the hours to a maximum of 20 mL to a drainage that's now guided by Near Infrared Spectroscopy, changes or symptoms. This is our protocol and I'll illustrate how we used this in one patient.
This is a patient that actually had this actual, exact anatomy. You can see the arch was very difficult, the celiac axis was patent and provided collateral flow an occluded SMA. The right renal artery was chronically occluded.
As we were doing this case the patient experienced severe changes in MEP despite the fact we had flow to the legs, we immediately stopped the procedure with still flow to the aneurysm sac. The patient develops pancreatitis, requires dialysis
and recovers after a few days in the ICU with no neurological change. Then I completed the repair doing a subcostal incision elongating the celiac axis and retrograde axis to this graft to complete the branch was very difficult to from the arm
and the patient recovered with no injury. So, in conclusion, spinal drainage is potentially dangerous even lethal and should be carefully weighted against the potential benefits. I think that our protocol now uses routine drainage for Extent I and IIs,
although I still think there is room for a prospective randomized trial even on this group and selective drainage for Extent IIIs and no drainage for Extent IVs. We use NIRS liberally to guide drainage and we use temporary sac perfusion
in those that have changes in neuromonitoring. Thank you very much.
- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years
of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).
It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,
it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases
that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it
was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.
And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted
inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted
selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.
In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients
stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.
This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,
and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,
and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.
- So this is what I've been assigned to do, I think this is a rich topic so I'll just get into it. Here are my disclosures. So I hope to convince you at the end of this talk that what we need for massive PE when we're talking about catheter based therapy is a prospective registry. And what we need for catheter based therapy for
submassive PE is a randomized controlled trial. So we'll start with massive PE and my rational for this. So you know, really as you've heard, the goal of massive PE treatment is to rescue these patients from death. They have a 25 to 65% chance of dying
so our role, whatever type of physician we are, is to rescue that patient. So what are our tools to rescue that patient? You've heard about some of them already, intravenous thrombolysis, surgical embolectomy, and catheter directed therapy.
The focus of my talk will be catheter directed therapy but let's remember that the fastest and easiest thing to do for these patients is to give them intravenous thrombolysis. And I think we under utilize this therapy and we need to think about this as a first line therapy for massive PE.
However, there's some patients in whom thrombolytics are contraindicated or in whom they fail and then we have to look at some other options. And that's where catheter directed therapy may play a role. So I want to show you a pretty dramatic case and this was an eye-opening case for me
and sort of what launched our PERT when I was at Cornell. It's a 30 year old man, transcranial resection of a pituitary tumor post-op seizures and of course he had a frontal lobe hemorrhage at that time. Sure enough, four or five days after this discovery
he developed hypertension and hypoxia. And then is he CT of the chest, which I still remember to this day because it was so dramatic. You see this caval thrombosis right, basically a clot in transit
and this enormous clot in the right main pulmonary artery. And of course he was starting to get altered, tachycardiac and a little bit hypotensive. So the question is, what to do with this patient with an intracranial hemorrhage? Obviously, systemic thrombolytics are
contraindicated in him. His systolics were in the 90 millimeter of mercury ranged, getting more altered and tachycardiac. He was referred for a CDT and he was brought to the IR suite. And really, at this point,
you could see the multidisciplinary nature of PE. The ICU attending was actively managing him while I was getting access and trying to do my work. So this was the initial pulmonary angiogram you can see there's absolutely no flow to the right lung even with a directed injection
you see this cast of thrombus there. Tried a little bit of aspiration, did a little bit of maceration, even injected a little TPA, wasn't getting anywhere. I was getting a little bit more panicked as he was getting more panicked
and I remembered this device that I had used in AV fistula work called the Cleaner. Totally off label use here, I should disclose that and I have no interest in the company, no financial interest in the company. And so we deployed this thing, activate it a few times,
it spins at 3,000 rpm's, he coughed a little bit, and that freaked us all out also. But low and behold we actually started seeing some profusion. And you can see it in the aortogram actually in this and that's the whole point of massive PE treatment with CDT,
is try to get forward flow into the left ventricle so that you have a systemic blood pressure. Now, you know, when we talk about catheter based therapies we have all sorts of things at our disposal. And my point to you is that you know really, thank you...
You guys can see that, great. So really, the point of these catheter therapies is that you can throw the kitchen sink at massive PE because basically your role is to try to help this patient live. So, if I can get this thing to show up again.
There we go. It's not working very well, sorry. So, from clockwise we have the AngioVac circuit, you have, let's see if this will work again, okay. Nope, it's got a delay. So then you have your infusion catheter,
then you have the Inari FlowTriever, you saw the Cleaner in the previous cast, and you have the Penumbra aspiration device the CAT 8. And some of these will be spoken about in more detail in subsequent talks. But really, you can throw the kitchen sink at massive PE
just to do whatever it takes to get profusion to the left side. So, the best analysis that has been done so far was Will Kuo in 2009. He conducted a meta-analysis of about 594 patients and he found this clinical success rate of 86.5%.
This basically meant these patients survived to 30 days. Well, if that we're the case, that's a much lower mortality than we've seen historically we should basically be doing catheter directed therapy for every single massive PE that comes into the hospital. But I think we have to remember with this meta-analysis
that only 94 of these patients came from prospective studies, 500 came from retrospective, single center studies. So even though it was a very well conducted meta-analysis, the substrate for this meta-analysis wasn't great. And I think my point to you is that
we really are going to have a hard time studying this in a prospective fashion. So what is the data, as far as massive PE tell us and not tell us? Techniques are available to remove thrombus, it can be used if systemic lysis is contraindicated,
but it doesn't tell us whether catheter based therapies are better than the other therapies. Whether they should be used in combination with them and which patients should get catheter based therapy, which should get surgery and which techniques are most effective and safe.
Now, I think something we have to remember is that massive PE has a 5% incidence which is probably a good thing, if this was even higher than that we would have even more of an epidemic on our hand. But this is what makes massive PE very difficult to study.
So, if you looked at a back of the envelope calculation an RCT is just not feasible. So in an 800 bed hospital, you have 200 PE's per year, 5% are massive which means you get 10 per year in that hospital, assume 40% enroll which is actually generous,
that means that 4 massive PE's per year per institution. And then what are you going to do? Are you going to randomize them to IV lytics versus surgery versus interventional therapy, a three arm study, what is the effect size, what difference do you expect between these therapies
and how would you power it? It's really an impossible question. So I do want to make the plug for a Massive PE Prospective Registry. I think something like the PERT consortium is very well-suited to run something like this
especially with this registry endeavors. Detailed baseline characteristics including all these patients, detailing the intervention and looking at both short and long-term outcomes. Moving on to submassive PE. As you've heard much more controversial,
a much more difficult question. ICOPER as you already heard from the previous talk, alerted the world to RV dysfunction which this right ventricular hypokinesis conferring a higher mortality at 90 days than no RV dysfunction. And that's where PEITHO came in as you heard.
This showed that the placebo group met the primary endpoint of hemodynamic decompensation more commonly than the Tenecteplase group. Of course, coming at the risk of higher rate of major bleeding and intracranial hemorrhage. So I just want to reiterate what was just said
which is that systemic thrombolysis has a questionable risk benefit profile and most patients with submassive PE, as seen in the guideline documents as well. So that sort of opens a sort of door for catheter directed therapy.
Is this the next therapy to overcome some of the shortcomings of systemic thrombolysis? Well what we have in terms of CDT is these four trials, Ultima, Seattle II, Optalyse, and Perfect. Three of these trails were the ultrasound assisted catheter, the Ekos catheter.
And only one of them is randomized and that's the Ultima trial. I'm going to show you just one slide from each one of them. The Ultima trial is basically the only randomized trial and it showed that if you put catheters in these patients 24 hours later their RV to LV ratio will be lower
than if you just treat them with Heparin. Seattle II is a single arm study and there was an association with the reduction in the RV to LV ratio at 48 hours by CTA. PERFECT, I found this to be the most interesting figure from PERFECT which is that you're going to start it at
systolic pulmonary artery pressure of 51 and you're going to come down to about 37. Optalyse, a brand new study that was just published, four arms each arm has increasing dose associated with it and at 48 hours it didn't matter, all of these groups had a reduction in the RV to LV ratio.
And there was no control group here as well. What is interesting is that the more thrombolytics you used the more thrombus you cleared at 48 hours. What that means clinically is uncertain at this point. There is bleeding with CDT. 11% major bleeding rate in Seattle II,
no intracranial hemorrhages. Optalyse did have five major bleeds, most of the major bleeds happened in the highest dosed arms. So we know that thrombolytics cause bleeding that's still an issue. Now, clot extraction minus fibrinolytic,
this is an interesting question. We do have devices, you're going to hear about the FLARE trial later in this session. EXTRACT-PE is ongoing which we have enrolled about 75 patients into. What the data does and does not tell us
when it comes to CDT for submassive PE it probably reduces the RV to LV ratio at 24 hours, it's associated with a reduction at 48 hours, major bleeding is seen, we do not know what the short and long-term clinical outcomes are
following CDT for submassive PE. Whether it should be routinely used in submassive PE and in spite of the results of Optalyse this is a preliminary trial, we don't know the optimal dose and duration of thrombolytic drug. And even is spite of these early trials
on these non-lytic techniques, we don't know their true role yet. I'd liked to point out that greater than 1,600 patients have been randomized in systemic lytic trails yet only 59 have been randomized in a single, non-U.S. CDT trial.
So this means that you can randomize patients with submassive PE to one treatment or the other. And we want to get away from this PERT CDT roller coaster where you get enthusiasm, you do more cases, then you have a complication, then the number of cases drops.
You want that to be consistent because you're basing it on data. And that's where we're trying to come up with a way of answering that with this PE-TRACT trial. Which is a RCT of CDT versus no-CDT. We're looking at clinical endpoints
rather than radiographic ones greater than 400 patients, 30 to 50 sites across the country. So in summary I hope I've convinced you that we need a Prospective Registry for massive PE and a Randomized Controlled Trail for submassive PE. Thank you.
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,
but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody
with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?
And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy
for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,
thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world
for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and
patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt
to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize
what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,
and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,
it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would
ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a
experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,
but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,
it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,
place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,
any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution
using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation
and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology
and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,
it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,
and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a
single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,
and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,
a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at
alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,
and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.
There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,
Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.
Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings
in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?
I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,
you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.
So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,
we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.
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