Create an account and get 3 free clips per day.
An Overview of PET, MRI and PET/MRI | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
An Overview of PET, MRI and PET/MRI | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
Work-up for PAE | Nursing Management in Prostate Artery Embolization
Work-up for PAE | Nursing Management in Prostate Artery Embolization
Case 11: Bleeding Tracheostomy Site | Emoblization: Bleeding and Trauma
Case 11: Bleeding Tracheostomy Site | Emoblization: Bleeding and Trauma
aneurysmsangiogramarterybleedingBleeding from the tracheostomy siteblowoutcancercarotidcarotid arterychaptercontrastCoverage StentembolizationimageNonepatientposteriorpseudoaneurysmsagittalscreenstent
Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Below Knee Deep Vein Thrombosis As Part Of Ilio-Femoral DVT: How I Deal With It
Angio jet (Zelante)Angiojet (Solent)Catheter-directed thrombolysisConvatecDrain-fixev3 guidewire (Nitrex- Medtronic)IF DVTtherapeutic
Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks

- I wanted to discuss this topic because some of us are more sensitive to DNA damage than others. And it's a complicated ethical issue. I have a disclosure in that I developed a formulation to premedicate patients prior to CT and x-ray. We all know that we stand in fields of radiation for most of our careers,

and we also know that many of us have no hair for example on the outside of our left leg. This is a picture that a bunch of us took for fun demonstrating this. But this is in fact radiation dermatitis. We know that the founders of our field

suffered consequences from the chronic high doses that they received in the 1920's. And they lost digits, they lost ears, they lost noses any many of them died of cancers or cardiovascular disease. The mechanism of injury is the x-rays

impinge upon water molecules in our cells. They create free radicals. These free radicals bind with our DNA and then Oxygen binds with that site resulting in an oxidative injury which can be reduced by the use of anti-oxidants.

I studied this over the last eight or nine years and I looked at the issue of chronic low dose radiation. Now this is different from the data that we collect from Nagasaki and Hiroshima and from Chernobyl and elsewhere. There are cancer risks but there

are also cardiovascular risks. And there are risks from chronic inflammation from increased reactive Oxygen species circulating with our system. I've been in touch with the IAEA recently about this and they didn't actually

realize that we don't wear our badges. So they thought the data they were getting on the doses that we were receiving were accurate. So that was a very interesting conversation with them. So cardiologists have been known

to get lifetime doses of of over one Gray. There's a lot of literature on this in public health literature. For example for every 10 milliSieverts of low dose ionizing radiation and received by patients with acute MI's,

there's a 3% increase in age and sex adjusted cancer risk in the follow-up five years. There's an excellent paper from Kings College London demonstrating that when endovascular surgeons were studied with two specific immunofluorescence tests, P53 and H2 alpha,

they were able to demonstrate that some endovascular surgeons are more sensitive to radiation dose than others. So why would that be? Well it's interesting if you look at this genetically and you look at the repair mechanisms

and in this whole thing I think in fact the lens is kind of the canary in the coal mine. When you get radiation induced cataracts, it's in the posterior chamber of the lens not the middle or anterior, which is where age-related injury occurs.

And this is the germinal layer or reproductive layer. The growth layer in the lens itself. And this is where cataracts develop. And this is really kind of a harbinger I think of injury that occurs elsewhere in our system. We know that when we wear DLDs on our chest,

on our bodies, on our arms, that the dose to the left side of our head is six times higher than to the right. In fact they dosed the left lens as higher than the right. And most of us who have lens replacements have it of the left eye.

This literature from adjacent fields that we may no be aware of. In the flight safety literature for pilots and stewardesses. There's extensive literature on cosmic radiation to flight crews who's doses annually are in the same range as ours.

So when you look at medical staff, you have to look at the overall context of the human in the Angio suite. Many of our medical staff will not be well. They may have chronic cardiac disease. They may be on say drugs for auto

immune disease or Methotrexate. They may have other illnesses such as Multiple Myeloma. They may have antibiotics on board that alter the DNA repair ability like Tetracycline. And they have chronic stress and sleep dysfunction. Cigarettes and alcohol use.

All of these things decrease their ability to repair DNA damage. If you look at DNA repair mechanisms, there are constantly the terms BRCA1 and two, PARP, P53, and ATM that show up. And deficiencies in these,

I'm going to skip all this to show you, can result in increased injury from a same dose being received by two different individuals. Now who is at risk from this is well understood in adjacent fields.

Here are 37 references from the public health literature related to mutations and SNPs or polymorphisms in DNA structure known to cause increased sensitivity to radiation. So I would propose that in, and here are papers on that topic

in adjacent fields that we don't read. So when we talk about personalized medicine for our patients, we need to also think about personalized career choices based on our DNA repair ability when we decide what we do. This has to be done in the context

of empathetic compassionate approach. It may begin with screening based on family history and personal history, and then advance in the right context to genetic screening through mutations and SNPs that can decrease their ability

to repair DNA damage from our occupational exposure. I'll skip all this because I'm out of time. But one other issue to think about, mitochondrial DNA is inherited purely maternally. So maternal DNA damage, mitochondrial DNA damage could be transmitted across generations

in female interventionalists. Also screening is important. It's emotionally complex. It's ethically complex. But it's an important conversation to begin to have. Thank you.

positron emission tomography is the use

of a radioactive tracer in this case FD gee her fluorodeoxyglucose to assess the metabolic activity of ourselves ftg is tagged with glucose and glucose is used by our body for energy cancer cells are thought to be our Armour hypermetabolic

so if we inject FDG to our patients it goes to areas with hyper metabolic activity this area is called a hotspot and when a hotspot is noted in a PET scan its it's thought to be cancerous this is an example of a hyper metabolic

region noted in the pelvic area of the patient this patient is diagnosed of cervical cancer and what is MRI as you all know MRI is the use of radio frequency currents produced by strong magnetic fields to provide detailed

anatomical structures it is the preferred method for imaging soft tissue organs and there's no ionizing radiation present now what is pet MRI pet MRI is a combination of these two modalities instead of going to two scans using two

scanners we have one scanner that is able to obtain pet and MRI images simultaneously so why can't we just call this pet well we run through a few problems we have fdg-pet CT where it's a PET scan with low-dose CT accompanying

it and there's fdg-pet CT with diagnostic CT we're full sequences of CT is coupled with a scan and a pet MRI always has a diagnostic MRI done with it

- [Martin] Thank you so much for that introduction. I have no disclosures. The abdominal compartment syndrome and open abdomen treatment goes through a series of phases when you start recognize it as the first step and of course, the simple surgical treatment

is the next step is to open the patient. Then many people start thinking that maybe we should prevent this by not closing the abdomen in the first place if it's open repair. But there are really no strong data to suggest

that you help the patients by leaving them open unless they are difficult to close. Permissive hypotension, of course, is very important here, not to overload the patients with fluids. Massive transfusion protocols and early medical treatment

to reduce the risk of abdominal compartment syndrome. You will find a lot of data in the consensus definitions and updated clinical guidelines which were published in the Intensive Care Medicine, 2013. First author is Andrew Kirkpatrick from Calgary. We, Anders and me, we adapted those guidelines

to the vascular surgical patients and published those in the European Journal of Vascular and Vascular Surgery. Now, the abdominal compartment syndrome management, how it used to be was very easy and surgical. Either there was no ACS or there wasn't overt ACS

and then you opened the patient. However, it's become a bit more complicated. We first have to identify which other patients at risk and all the patients were up to AAA are at risk, high risk actually, and then the idea is that we should be proactive

and treat them for abdominal hypotension at an early stage by lowering the pressure and also targeted organ support. And this medical management can really make a very great difference and we're actually not focusing anymore

on the abdominal compartment syndrome but on the abdominal hypotension. This area between, an intra-abdominal pressure, between 12 and 20. What medical treatments are effective? Pain relief is extremely important.

Thoracic epidural catheter can often be given after a ruptured triple AAA. Maybe sometimes, you have to give thrombosites to persuade the anesthesiologist. But that's a very good measure. And then neuromuscular blockade is extremely effective.

It often reduces the pressure by half. We also combine positive and expiratory pressure, hypertonic albumin, and furosemide or renal replacement therapy. And with all these measures, actually, the compartment syndrome

and open abdomen treatment has become less common in our practice and this is a worldwide trend and this is very fortunate because as we demonstrated in a nationwide study, also published in the European Journal recently,

the mortality after ACS, after ruptured is still extremely high and here you see the survivor curves during the first year post-operative. So the mortality doubles if you get this complication. There was no difference if the primary treatment

was open or endovascular repair. We also developed a technique of treating the open abdomen by combining vacuum and mesh-mediated traction and this has become very popular all through Scandinavia and we merged data from six hospitals from three countries in Scandinavia

and published those recently, they're online, and here's the technique. We used the mesh to approximate the fascia towards the midline and that way we can close the patient quicker. Now, we had a 191 patients with open abdomen

after a AAA repair and as you can see, most of those were open, but there were also 49 in the vascular repairs and we achieved the primary delayed fascia closure rate at about 91% and only one patient had to be closed with a skin graft.

How to avoid hernias is a bit more complicated. You have to close as early as possible. Some suggest you should reinforce with the mesh. We never dared to do that because of the risk of infection and also the risk of gastrointestinal fistula. We remove all mesh and close the fascia meticulously instead

So, in conclusion ladies and gentlemen, recognize the problem, measure intra-abdominal pressure after both EVAR and open repair. It's important to close the patient's abdomen within two week

and a proactive strategy from the first day will help you. You may try this technique that we have developed. Thank you so much.

- [Narrator] I'd like to thank Dr. Veith and this symposium for being able to talk on this subject. I have no disclosures. When it was discussed in the last section, when we get this, preferentially in our institution, we attempt to repair ruptured aneurysms endovasucularly. And, as we all know, ruptured triple A's are,

they're a surgical emergency and a fatal surgical emergency at that with a overall mortality of approximately 80%. In the U.S., it ranks 12th to 15th, depending on the year, as the overall cause of death. Traditional treatment of ruptured aneurysms

has been open surgical repair, but over the last decade EVAR has become the preferred treatment modality. EVAR, as we all know, was introduced in the late 80s. Evolution of endovascular technology and increased surgeon comfort with EVAR

has made it the treatment of choice for ruptured triple A's in many institutions. Studies suggest that patients with EVAR for ruptured triple A's have higher secondary intervention rates both early and late. So, type two endoleaks after elective EVAR,

management is somewhat unclear. And the natural history is not all that well known. We don't know which type two endoleaks will go on to cause problems and which will not. The management of type two endoleaks is generally determined by the behavior of the aneurysm sac.

In the elective setting, delayed rupture of EVAR is rare. Approximately 80% of all type two endoleaks will spontaneously resolve in elective EVAR within six to twelve months. Type two endoleaks in a setting of an intact aneurysm are treated, generally, if the sac enlarges 5 millimeters

or if it persists for more than six months. Type two endoleak after EVAR for ruptured aneurysm is somewhat different. The aneurysm sac is disrupted in this situation and the blood is not contained within the aneurysm itself. The lack of aneurysm sac integrity can result

in expansion of a retroperitoneal hematoma in the presence of a type two endoleak. This can result in continued hemorrhagic shock or abdominal compartment syndrome. About 30% of EVARs ruptured triple A will have associated with them

a type two endoleak on completion angiography. Most type two endoleaks are treated at the time of repair or shortly after EVAR for ruptured aneurysms. Approximately one quarter of type two endoleaks will not be seen on completion angiogram, but would rather be visualized later on CT follow-ups.

We're missing a good 20% of them on completion 25% of them on completion angiogram. Treatment of type two endoleaks in EVAR for ruptured aneurysms prolongs operating time in the generally unstable, hypothermic, and coagulopathic patient.

These patients might be better served, rather than spending the extra time to embolize the type two endoleak, they might be better served in the ICU being rewarmed and resuscitated. Treatment of type two endoleaks should be reserved

for patients who deteriorate or have expansion of retroperitoneal hematoma or expansion of the excluded aneurysm sac. But, how often does this occur? We noted that practice is widely variable even in our own group as what we do

with type two endoleaks after ruptured aneurysm. So we decided to take a look at this. We did a retrospective review of EVARs ruptured aneurysms from two larges tertiary centers, the University of Michigan and Dartmouth. We took a look at comorbidities, anatomic variables,

and operative details and our primary outcomes were the presence of a type two endoleaks, reintervention, delayed aneurysm rupture, and aneurysm-related death. We had 56 patients over a 13 year period. The mean follow-up was 634 days. We found 21% had type two endoleaks on completion angiogram,

with an additional 7% detected on CTA later. The Iliolumbars were the source in the vast majority of cases. And of the 14 patients that went in immediate postop CTA, 43% had already sealed their type two endoleak and 36% underwent surgical embolization

upon surgeon preference. Only one patient for ongoing anemia. But in this group, there were no sac enlargement, delayed rupture, or the need for graft explantation in the entire cohort. These are our patient demographics

for patients with endoleaks and patients without endoleaks. There's no difference except for BMI. The larger the BMI the more likely you were to have a type two endoleak. Anatomic variables such as concurrent iliac aneurysm, thrombus at the IMA or at the level of the aorta,

or device did not correlate with the presence of endoleak after ruptured aneurysm. And the post operative variables, the only variable that came out was associated with type two endoleak after ruptured EVAR was pneumonia.

And the overall mortality was not different over the entire timeline of the cohort. Conclusions, type two endoleaks after EVAR is relatively common. The natural history of these appear to be surprisingly benign.

Early CTA prior to discharge may identify type two endoleaks that you may not see on completion angiogram. 50% of type two endoleaks for EVAR will spontaneously seal in the postoperative period and those that remain do not appear to increase the risk of sac expansion or rupture.

And, a conservative approach to type two endoleaks in ruptured EVAR may be warranted. Thank you very much.

- [Lars] Thank you again Mr. Chairman. So, here are my disclosures. So the outline of the talk is here. And we need, that the need for radiation protection, it was evident already in 1928 when the ICRP was established. And according the European Union regulation

when it comes to radiation safety, you need practical training and also relevant competence in radiation protection. So in special case of the clinical use of new tecniques training is provided on these tecniques, or should be provided.

So what does that mean? That means, since interventional radiology, we have talked about it already, causes cancer and tissue effects, skin burns. And the new information around health effects has led to increased safety concerns.

We need to think more about this, how to implement this into our daily training for newcomers in radiation and the vascular world. So the comparison of risk in health care with other industries, health care is more like bungee jumping,

while actually the minimal risk is of commercial aviation and nuclear power. And they have a simulation training for years. So we know also that subclinical carotid atherosclerosis and early vascular aging is proposed due to low-dose ionizing radiation exposure.

So in the Cath lab we see that increased subclinical intimal medial thickness. And the telomere length is also shortened so that's essentially evidence that implies an accelerated vascular aging and early atherosclerosis among us.

And we know for sure that cataract especially among the cardiologists is a real problem. Also, many have talked about this, the work from St. George hospitals where radiation exposure during EVAR causes DNA damage in operators.

It's fantastic work by these guys, which actually shows that the lymphocytes have DNA damage. And also that we maybe need to protect our legs in order to be careful with this. So we have together with UKTS, these endovascular fellows who works together in UK

together with the Mentice Company developed some posters to be aligned with radiation safety awareness. Since simulation training is needed. And why is it so? Well is you get better quality.

You get reduced cost. You get better production along this. So simulation-based training is very important for this society and also for the health costs. So we know that we a competence in EVAR tecniques. We have worked with this

in Copenhagen with simulation training. In the upper corner there is the stroke group that we work with also for endovascular simulation training. To be with fast and with stroke, it's couple of new interventions there worldwide. And also we know from this paper here,

how to reduce radiation exposure during EVAR with Stephan Haulon and his friends. That the techniques to reduce radiation dose, it's important to train, not in the Cath lab, but in simulated setting. So you can integrate this to modern than work.

So what you can here can see, what you can do with endovascular simulators like the Mentice simulator, or Simulab simulator. You have a patient, you have an operating heat map. You can work with this, impact of table height and detector position.

You can train this with the fellows to see so they get a real figure immediately on the radiation dose. You can see how much radiation dose when you shoot angio. And you can also make marks on the floor where you get the most heating maps.

And this is even more important to use the shutters when you shoot your angio, which you can see on this as well, while it gets highlighted. And again, decreasing field of view increases also the dose as you can see.

So and also you have to avoid hostile angulation. This gives you a more practical training. Mandatory to have six hours, old PowerPoint presentation in European Union and in Denmark to get your license, but instead working with this in an interactive fashion,

together with a combined Laerdal manikin and a Mentice simulator will give you a much better way to train and you can also assess if they have reached the level of proficiency with this.

- [Speaker] Thank you very much. It is a great pleasure to be part of this debate, and this section that is very excellent. It's a tough task to debate with Germano, but I think today I will be able to push you over and to not to be a sissy puss anymore. I decided by intention not to mention

not to build up my presentation on the randomized trails because I was expecting we will have some information but, basically because, even the Cochrane Collaboration Group is not able to extract recommendation from these trials, so I bring you to Zurich, I will explain you why. This is a case we did October 2014.

You see, we have an anesthesiologist there, he is on backstage. We have no blood transfusion, we have just people working on the table. But in fact the patient has an inter-aortic balloon clamping

for 15 minutes because he's in shock, with a systolic arterial blood pressure of 65. He is vasoactive but we don't give to this patient any transfusion. And you have seen the procedure was done percutaneously and in 45 minutes.

This is in another patient, he came some weeks ago, two years old, he has a rupture perineal aneurysm. So, we fixed him with with a combined- reconstruction combining parallel grafts and the branched device. So we placed first a stent graft in the mesenteric artery

then we deployed the two branch device from Utech, then we parked and deployed a TAG graft, and then we deployed the chimney in the mesenteric artery the see-lec-tronk was already occluded and you see this the result. And what I have to tell to you

is this patient developed soon after the procedure, an acute coronary syndrome. He required a PCI for high-grade stenosis in the left anterior artery. So why I take you to Zurich? Because now we have 20 years experience with

EVAR in ruptured aneurysms. And what is important, you know, is we have the same method. We have an algorithm and we have the same methods in 20 years. We just implemented new tools when they emerge

we were thinking they are useful. Like this branched technology and parallel graft. We showed some years ago in a common paper, a Two-Center paper with Orebro, with Thomas Larzon. That the initial advantage was maintained through the years.

But now, let's go to our population. You see here we fixed the 227 patient in this time and we have 10 years of follow-up perspectively, a mean follow-up of five years of 40 percent survival. The killers, we have also heard this also from

Martin Beurkin before is, and from Janet Powell, the shock in this patient. This is what we know since a long time and the abdominal compartment syndrome that we do decompress in 20 years.

And you see in this table, this shows you t blue is open surgery, and the red is endo and the vertical axis is the time and you see that in the last eight years

we just treated 10 patient by open surgery, most by EVAR. There are cases where EVAR is not appropriate patients that are unstable, in shock. For example, this patient here we were required to introduce trans axially a balloon to stabilize it,

it's impossible to reconstruct for vessel in this time so we go for open surgery. When the patient has too many challenges to resolve to be accessible for endo. A new evolution is that we are training our patients specifically before we treat them.

So, we already use simulation for debriefing after our cases because the volume is decreasing of ruptured aneurysms so we simulated them. Now we wanted to look if we can do this preoperatively so we started last year. We made 10 cases with the Simbionix simulator.

You can see on the left is the simulation on the right down, this is the real case. So we are able to do this to be ready for the procedure in 20 minutes. So since we get the data from the CT, we need 20 minutes to be ready for simulation.

And it's highly useful to plan the position of the stent graft to be able to cannulate rapidly, or to anticipate natural tilting of the stent graft you put in, in angulated anatomies. So in conclusion I can say that

most ruptured aneurysms can be repaired by standard EVAR or advanced technique as chimney or FEVAR. But not all, and here is an interesting point: And, if I think about what Benjamin said with very high mortality,

I'm not sure what would happen with this population. But I think the survival and the outcomes will be very poor in this patient. I'm very curious how- now Germano will reply to me. Thank you very much for your attention.

- [Dr. de Vries] Thank you for the kind introduction. These are my disclosures. It's why do endografts sometimes need additional fixation with EndoAnchors? Well first, patients with multiple hostile neck parameters still suffer a substantial risk for type I endoleak and endoleak related mortality.

The second reason is that our deployment accuracy of the endograft is not as good as we think. We reviewed 85 consecutive cases in our own hospital and we saw that mainly do the slope of the endograft in the aortic neck, we lose some important apposition,

especially in the outer curve. So the preoperative neck length is not the same as our post-EVAR seal. And the third reason is that some other techniques, like FEVAR do have their limitations and some people are declined because of the branch arteries.

There are also some physiological conditions which is are not good enough for FEVAR. And of course open surgery, well per definition is more invasive and also patients will sometimes have their aneurysm repaired by endovascular means. So EndoAnchors really creates the stability

of a surgical anastomosin shown by David Dietz, and it really rivals the migration resistant of a hand sewn anastomosis. Of the global Anchor registry is captured real-world usage of the EndoAnchors and nowadays 770 patients have been enrolled worldwide.

The Primary Arm represents the majority of the patients in the Anchor Registry, 437 patients in the patients in the Primary Arm. It's not exclusive the Anchor Registry for the Medtronic devices, but also the workhorses like Gore and the Zenith endograft.

Of the prophylactic arm, the patients treated without any endoleak it carries 314 patients in this data slide. And you can see that the majority of those patients will hostile neck parameters. It's true in 91 percentage of the patient cohort.

The median neck length is 11 plus millimeters and also conicity substantial in more than 40% of the cases. What about procedural success? It's high, it's almost 95%. You need an average of around 5.5 EndoAnchors and the time to implant those EndoAnchors is 15 minutes,

and of course there is a learning curve. Core Lab adjudicated outcome, the two years outcomes, there is no new type Ia endoleak in this cohort and no endograft migration. In the Kaplan-Meier Estimates, especially the freedom from

aneurysm related mortality is 98.4% and freedom from secondary procedures at two years timeframe is 92%. There are no serious adverse events related to the implantation of the EndoAnchors itself. No aneurysm rupture and the aneurysm-related mortality

is due to cardiopulmonary comorbidity and not due to aneurysm rupture itself. There's one patient with a surgical conversion in this cohort. And the short neck indication that are patients in the Primary, 70 patients,

only placed with an Endurant in combination with the EndoAnchors and in a prophylactic setting or a patients with a type Ia endoleak. But the median neck length is now less than seven millimeters, so really challenging necks

and also conicity is substantial. It's also a clinical challenging patients cohort. A lot of patients with notable comorbidities and what is important to mention, 17% are patients with symptomatic aneurysm and also one patient with a ruptured aneurysm.

And the well the main treatment is then for prophylactic use but also 21% of the patient do have type Ia endoleak. Procedural results are 31 minutes fluoro time, but only 17 minutes to implant the EndoAnchors. This is the one year outcome. I think it's excellent.

Only one patient with a type I endoleak and he needed a secondary intervention. We had two other patients with a secondary intervention but it was due to a false aneurysm in the groin and a distal extension. No conversion to open surgery and no ruptures.

What about the cost effectiveness? Well you have to consider, it's not only the device cost, but also the level of resource utilization, and also clinical outcomes. And when you compare the short neck cohort, here the 70 patients to the fenestrated IDE study,

there's a cost differential of more than 5,000 U.S. dollars in benefits of the use of the EndoAnchors in those short and hostiles necks. So we can conclude that the Endurant stent graft in combination with the EndoAnchors for short neck indication is easy to use.

It's an off the shelf solution. It gives greater flexibility versus the alternatives. There is no need for renal arterial catheterization and it's really efficient. Thank you very much.

so we're just gonna like hop over to the clinic side and kind of discuss how we work up or what are the things we look for when we see the patients in clinic

so a lot of patients are referred to us by urologist so we have to have a urology on board to to better take care of this patient we can't treat this patient you know by ourselves so a lot of patients are referred to us by our

neurology team if they don't have a urologist we have to refer to them to erosions first before we can even work them up or PAE so we won't make sure that patient you know doesn't have any underlying cancer that we know of so we

want to make sure that we check their PSA levels because this high high patient can ask actually I predict a decent progression and actually our risk for acute urinary retention you want to make sure that you get

urinalysis a lot of patience wet with lots is not only due to pph you could also be secondary to UTI or if patient has some type of bladder tumor or bladder disorder so it's kind of good to know to understand some of the lingo

that urology uses so once they see the urologist they do some your dynamic studies and one of the popular ones are these non-invasive studies called euro flama tree and the post-void residual do you offer the Euro excuse me you heard

from a tree usually we will measure the flow rate and the volume of the patients so what they do is they they would pee in this special funnel and the final obviously they go in private but this final is connected to some machine that

can actually measures how fast and how much their voiding and so normally it's about 25 miles per second but if it's anywhere less than 13 to 15 it can suggest obstruction and use the obstructions usually due to BPH some of

us a very low flow rate such as like say less than ten or six you have you want to be a suspicious of some type of you to neutral structure after they do that usually what they'll do is they take a post void residual is basically scan so

they'll put that little probe above the bladder and they'll see how much is left in a bladder if it's 150 that she usually indicates in complete emptying someone who has greater than 200 that may suggest patients having some type of

bladder dysfunction so a lot of its patients to us at least woke up with some type of imaging and the ones that at least our physician selects is the MRI patient do get a CT angiogram which can also evaluate the pelvic Anatomy and

arteries however the process the mr process actually gives a better illustration of the prostate a tissue to see if there's any suspicious for cancer for example you can also display the president atomy and characteristic up

the gland so most patients do get MRI or at least we get them to get MRI to measure the actual volume in literature they will tell you that a patient can get a trance rectal ultrasound but I'm not sure how many

guys in here would like a probe stuck up their butt to get to get their prostate measured so unless you wanted to get pissed at you just supporter I am right so when we see the patient you obviously want to review their HMP more

importantly you'll want to check their comorbidities there's social history whether it is smoke or not because they're gonna that's gonna have an impact on how we stay patients and how you can predict their anatomies

obviously someone's died who is diabetic or who has a history of smoking you could expect for them to have a greater degree of atherosclerosis and again the first thing that we would get the patient why we walked in is we go in

that scoresheet the IPSS score and so that's gonna give us an idea of how bad this symptoms are so if they come in to us with a score of say you know they're mildly symptomatic I'm not sure how much to pee a procedure with would help them

because how much more lower can we get their scores down so a lot of patients we would treat are in the moderate to severe category and their quality of life score should be for the most part will be about three or higher you also

want to make sure the trusted results since this is Andrew Graham procedures you will make sure that they have a pretty decent renal function patients with lots a lot of them may have some degree of renal insufficiency so we have

to be careful make sure we watch that lab value so this is some of the screening criteria that a lot of us may use so patients who I have refractory to medications for the six months someone has a high IPSS core grain 13 or

qualifies score greater than three process volumes gotta be at least 40 grams we sometimes get patients with a high score but they're positive volumes around 30 we usually usually wouldn't treat those

patient because we can't basically treat or shrink the prostate any any lower than that you someone who has an abnormal urine Flo and someone who maybe refractor to medical therapy these are just a list of

exclusion criteria the ones that should my party set out someone who has prostatitis or current approximate infection you definitely want don't want to treat those patients chronic renal failure and relatively maybe coagulation

factors that could be patient dependent sometime sometimes we could optimize them to get this arteriogram procedure and prostate and bladder malignancy also this somewhat also relative we do treat patients with prostate cancer it just

depends on what course of treatment they're on currently so once we had screen the patients and and deemed them to be a candidate we reviewed the patient we review in detail the procedure with the patient so you want

to let them know that it's a our angiogram procedure that will go through the either the growing or sometimes the radio and the procedure itself you can take anywhere from one for one to four hours and sometimes longer depending on

how complicated their arteries feeding the prosthetist more importantly we want to educate them about the side effects okay we have to let them know that a lot of their symptoms might actually worsen during the first few days after the

procedure so if they have the Syria now urinary continence they actually may get really worse especially for the first few days okay we have to go over the complication with the patients that can include a public infection ischemia or

any vessel related complications that pseudoaneurysm or bleeding so we have to basically have a basic knowledge of how do we combat this side effects and these are just some of the list of side effects that

are mentioning or at least we also used a PI radium it helps I guess to numb up the prostate urethra we have to educate the patient that this can change the color of the urine so we always make a note to our patients that if you are

going to take this medication please call us that way we don't kind of shock you and we also know that the change of color is from the pair radium and not from anything else the tripping or oxybutynin

it helps reduce bladder spasm we would normally use it for a patient who go somewhere to Foley our patients would go some Foley tends to have a great degree of bladder spasm Coley's a lot of spatially get constipated for multiple

reasons being better that or they and she is soft and there's also the over-the-counter azem so this is just a sum of the standard medications that we would give all our patients all of them will get about cipro for seven days

we'll give them some type of anti-inflammatory Asia usually is ibuprofen were prescribed 800 a tid if needed anti-acids since it's just to protect your belly or their stomach from the ibuprofen minimum we'll get a stool

softener at least for the first three days or if they got developed loose toast and we would ask them to stop it and the medications for pain that we would get them as Norco just in case and I would say like more than half these

patients don't even need Norco at best they'll probably use ibuprofen you know just to minimize the inflammatory side effects that I get it also helps out with post embolization that sometimes we'll get and I believe so I don't I'm

not sure if I'm messing about post embolization syndrome patient do can get these symptoms and a lot of symptoms can vary they can get some body slug or fever malaise and the degree the symptoms were may bear from patient to

patient and a lot of symptoms are described kind of like a flu-like symptoms and we also want to reiterate a patient that the symptoms are temporary and it should get better over to at least at first week or so so patients on

warfarin we have a lot of patients on warfarin for whatever reason whether they had a recent cardiac intervention we want to assure that we stop those medications at least before the edge ground procedure so it's very important

that you have a good rapport or whoever and have prescribed him the coumadin whether it's a cardiologist or the surgical team and a lot of dissipation may need to be crossover outside like a short-acting

anticoagulation such as Lobo Knox at least in our practice we ask the patient to this condition discontinue your aspirin unless they're you know they have a recent cardiac intervention we may leave it leave them

on aspirin metformin as very important since we did it is a natural procedure we want to at least hold have the patient hold the metformin the morning of the procedure and maybe a couple of days after and someone who are

allergic to contrasts we will make sure that we're prepared to premedicate a patient and also be prepared in case there's a severe reaction and the pre medication as we know will give them some type of a standard metal prednisone

will they'll take it like twelve seven or one hour before and they also gets unbearable and preoperatively or one hour before the procedure and during the clinic we also determine the level of anesthesia so since this procedure

usually takes a long time we always get it with our anesthesia team is just more for patient comfort it's not really for pain okay I couldn't imagine laying a table for several hours at the time so we all shop anesthesia on board just

really for patient comfort so we're just

my last case here you have a 54 year old patient recent case who had head and neck cancer who presents with severe bleeding from a tracheostomy alright for some bizarre reason we had two of these

in like a week all right kind of crazy so here's the CT scan you can see the asymmetry of the soft tissue this is a patient who had had a neck cancer was irradiated and hopefully what you can notice on the

right side of the screen is the the large white circles of contrast which really don't belong there they were considered to be pseudo aneurysms arising from the carotid artery all right that's evidence of a bleed he was

bleeding out of his tracheostomy site so here's a CTA I think the better image is the image on the right side of the screen the sagittal image and you can see the carotid artery coming up from the bottom and you can see that round

circle coming off of the carotid artery you guys see that so here's the angiogram all that stuff that is to the right to the you know kind of posterior to the right of the screen there it doesn't belong there that's just

contrast that's exiting the carotid artery this is a carotid blowout we'll call it okay just that word sounds bad all right so that's bad so another question right what do you want to do here

I think embolization is reasonable but probably not the thing we can do the fastest to present a patient to treat a patient is bleeding out of the tracheostomy site so in this particular case this is a great covered stent case

alright and here's what it looked like after so we can go right up and just literally a cover sent right across the origin of that pseudoaneurysm and address the patient's bleeding alright

- [Clark] Well, dear chairmen, Frank, thanks for the invitation. In this talk, I'd like to focus on the role of calcifications in the aortic wall, and whether we could use it for clinical risk assessment. My disclosures. Well, an aortic calcification is, of course,

a clear anatomical entity. It's not that difficult to visualize it. Obviously, for a meaningful assessment, we need to quantify it. This can be done by a simple, abdominal aortic calcium score, AAC 0.8.

The severity of calcification is measured in points assigned to the presence of high-density signaling on the anterior and posterior walls of the aorta between the first and the fourth lumbar vetrabra. The cumulative points of both anterior and posterior walls represent the AAC 0.8 score.

This is a cut from (mumbles) for event-free survival in 2 1/2 thousand individuals, and it shows the prognostic value of AAC for cardiovascular outcomes. A high AAC score predicts future events, and it says something about overall survival.

Now, occlusive and aneurysmal disease are not the same, but calcifications also occur in the aneurysmal wall, and they can be assessed with CTA, quite simply. The effects of calcification are unclear, and we don't know whether it's protective or it's generative.

To verify the roles of these calcifications, patients with an aneurysm confirmed by CT in a six-year period were included. Three groups were distinguished on the likelihood of rupture. The elective group were patients,

who had received elective surgery. Acute aneurysms were either symptomatic, nonruptured, or ruptured confirmed CTA. Doing so, significant differences in diameter and calcification were found between ruptured and elective patients.

Using the AAC score, symptomatic patients were significantly more calcified than elective ones. Then after logistic regression, comparing elective versus nonelective aneurysms, female gender came out as the most important risk factor. Compared to diameter, the AAC was better able to distinguish

acute from elective aneurysms. Now, it's obvious that the conclusions of the few studies we have on the prognostic value of calcification in triple A, directly linked to reliability of the methods of measuring the extent of calcification.

Fully quantitative measurements are considered to be best. Mass and volume and several software tools are currently being used, but without exact knowledge on accuracy or, ultimately, use of these tools. This one, we used the Phantom with calcium rods

of pre-established, massive volumes, which were scanned with the specifics D protocol for coronary arteries and one for the abdominal aorta. This was done to see whether calcification tools tested on coronary arteries can be directly applied to the aorta without adjustments.

Five CT scans for each protocol were performed, and the Phantom was moved two to five millimeters in a random direction between each scan to mimic patients' movement. For each measurement tool and for both scanning protocols, the mass and volume were greatly overestimated.

It appears that the error and the variability of the results increased, when the size and the mass of the calcium element decreased. Also, the presence of contrast has a significant effect on aortic calcification's course. To assess the size of this effect

on the clinical conditions, 50 four-phased liver CT scans were retrospectively collected and analyzed in patients over 65 years of age. The first phase was with contrast, followed by three... No, without contrast followed by three contrast

and have phases of different intensity. Here we saw that measuring calcifications under contrast-enhanced conditions overestimated the calcium volume by a significant margin, yet it underestimated the mass of calcification significantly.

As the results, there's no provision factor to adjust for the error. Clinically-relevant small calcifications are most erroneously measured. Tools validated for coronary arteries that can now be extrapolated to the abdominal aorta,

and patients will need two instead of one CT scan, so, with and without contrast. Most striking, I believe, the previous research using calcification scoring tools on the abdominal aorta, especially with contrast, should be highly scrutinized. As a final conclusion, I think it's clear

that before future studies are implemented, we should first harmonize protocols and software packages to get reliable calcium measurement results. Thank you for your attention.

- [Narrator] Thank you, I'd like to thank Doctor Veith for the privilege of the podium and the long title of my talk. I have nothing to disclose financially but I will say that one of my disclosures is that I've actually never implanted an Endologix device but I have

removed a large number of them and treated a large number of type three endoleaks as a result of them. The AFX graft is a unibody stent design. It is a single component designed to sit on the aortic bifurcation.

The company calls that anatomic fixation. It has an endoskeleton which is a unique design compared to many of the other devices available. And it is coated in a second generation PTFE polymer. The advantage is that it avoids a need for contralateral gate cannulation

and the goal is to place the device at the aortic bifurcation and then gradually build up to the infrarenal neck. Over time the device was used for broader and broader indications with larger and larger proximal cuffs being placed

to treat wider infrarenal necks. Even to the point that a whole generation of cases called Topper cases was developed where very large aortic cuffs were crammed down into the main body of the device and even thoracic endograft proximal cuffs

were placed within this device to achieve a seal and relatively large necks. Our experience is that two large tertiary hospitals here in New York, these are both 800 bed hospitals and we looked at our experience from a period of 2013 to 2015 when we implanted

approximately 80 of these devices. Over that period of time we encountered 11 type three endoleaks, four of those patients presented ruptured and three of those patients had died from aneurysm-related deaths. As is evident in many of these published pictures

the problem occurs at the connection point between the main body of the device and the upper proximal component leading to a type three endoleak. In a fantasy world where all the aneurysms are perfectly vertical, up and down,

the force vector of the blood flow is transmitted along the center-line of the device down to the aortic bifurcation. So conceptually placing the device on the aortic bifurcation makes a lot of sense. However in the real world most aneurysms

are angulated, usually to the left, resulting in a different vector of force leading toward the blood being pushed toward the outer wall of the aorta. My argument is that if you are sitting on the aortic bifurcation that acts as a fulcrum point

because the vector of force is now off to the side of the aneurysm, the lower part of the device has nowhere to go and is basically seated on the aortic bifurcation. So the idea is that if you have good proximaL fixation and now you have good,

a distal fulcrum, the only area where the device can then relieve that pressure is in the mid-component between the proximal cuff and the distal component. And as you add larger and larger sac diameters the room for that disconnection becomes larger.

And this was evident in some later papers. Furthermore in these Topper cases where a very large cuff is being sandwiched inside of a smaller device, you see this instability in this junction where you have a watermelon seeding effect where

this large device which is being crammed down there actually will pop out. This we see when there are different manufactured components for the proximal device as well as these large thoracic cuffs. I would argue that this is a danger zone.

Here you can see two examples. Here on the left side you can see a very large cuff being crammed down into a very small main body device. In the second panel you can see the similar situation, you can expect

that this is not a long-term stable situation. This was published by Gary Lemmon in 2016 where they did a retrospective review of their experience with a variety of devices, not just the Endologix device. But they were specifically looking at type three endoleaks.

They divided the cohort into two groups, Endologix and everybody else. And there was a substantially increased risk of post-implant rupture and the need for re-interventions in the Endologix group. Ultimately concluding that the uncoupling

of these components is a big problem and that you should not use these oversized aortic cuffs. Once these disconnections do happen there are significant challenges to secondary intervention. These devices have internal wireframes which make negotiation difficult

and the severe angulation that you can see evident in this picture here makes bridging the gap very challenging. Duplex ultrasound is not adequate for following these devices because as the disconnections occur there's not much to see of duplex.

So I believe that serial radiography needs to occur. The IFU was changed in 2015 to recommend not placing proximal devices that are significantly enlarged in this device. So in conclusion, I would say, should we prophylactically reline these devices?

I believe to some degree many of these devices out there are essentially ticking time bombs. The devices don't present themselves until a rupture has already occurred in many instances, and these are the patients that are significantly at risk.

So in summary, component separation remains a significant problem with this device. It's associated with a significant risk of rupture and death especially in patients with large aortic sacs. Vigilant surveillance is definitely

required and prophylactic relining of the device should be considered. Thank you.

- [Jes] Here are my potential disclosures, I have none. Research in non-aneurysm screening programs points to the risk of more or less severe negative, psychological side effects. It is feelings of stigmatization, fear, aggression, psychosomatic reactions, social isolation, nocebo effects, that's the completely opposite than placebo.

It causes illness and blame the victim reactions in lifestyle mediated diseases. And I ... Expose the psychological side effects, also in my first screening trial, and concluded that the offer of screening

causes transient psychological stress in subjects, found to have no aneurysm. But more seriously, diagnosis of an aneurysm seems to impair quality of life progressively, in conservatively treated cases. And this impairment

seems completely reversible by operation. And that is just what the UK SAT Trial also reported. But it couldn't confirmed in the MASS trial by Theresa Marteau. She is one of the leading experts in psychometrics.

And she is exceptionally critical on screening. She couldn't show any significant reaction or states compared to the non-invited controls, except a short and transient reaction on those having surgery. In all the differences if any were small, she concluded.

Neither could I in my second randomized trial, but this time I was aware of the side effects, and carefully instructed on how to inform the screened positive men. The MASS trial was also the second trial of Mr. Alan Scott. He was experienced from the Chichester trial,

and may have done the same experiences. And qualitative studies in recently initiated programs also conclude the need for proper information. So I'll tell you one message today, is let the patients know, "The danger of an aneurysm is not knowing you have one."

As underset, we can calculate that it takes approximately two elective repairs to prevent one rupture. It may sound quite acceptable, but you can also formulate it this way, that approximately half of those referred for elective repair,

they risk complications and death for conditions that they never would have trouble with if it was left unrepaired. This is a serious and an ethical dilemma which can't be solved currently. Not for screen detected cases,

not for randomly detected cases. We simply need better tools. Nevertheless, screening and preventive repairs still saves more lives and it doesn't cause more postoperative death, and complications because it prevents emergency procedures.

And the fact that treating screen detected cases are much less dangerous than treating incidentally detected cases. Screen detected cases actually are treated with one third the risk of those detected incidentally. So when the randomized clinical trials,

are weighted in a population based view, using gained, quality adjusted living years and its costs, early detection shows to be efficient and cost effective, but it doesn't take into account other psychological costs. Diagnoses without benefit and harm against people who would never have problems if they were left alone.

But who is to decide what's best for the individual? I know a lot of ... people who want to play God and take the decision on other people, but I strongly believe that men age 65 are old enough to make a decision on their own.

Thank you very much.

- [Gerry] These are my disclosures. When it comes to ilio-femoral deep vein thrombosis, many of us feel that is the most important area to treat. And some of us feel that the inflow is very important, in which case, you've got to worry about it. But if you feel that the inflow doesn't matter at all, then you can forget about it.

So that's for those of you who aren't from New York, that was my Irish accent on a New York, forget it. This is one of the ways to get into the below-knee veins, posterior tibial venous access. It looks quite easy, it's not quite so easy. Although there's two veins side by side,

you typically only get one chance at one vein because the other one goes into spasm. Pardon me, very sensitive mouse, like myself. You choose your wire of choice. I quite like the ED3 Nitrex. And then confirm that you are inside the veins,

because that happens all of the time to me. Those are funny looking veins because I've managed to puncture the artery. And which brings up one of the pitfalls, try not to puncture the artery. If you do manage to get into the vein,

you then insert a catheter and a catheter-directed thrombolysis after that is fairly standard. There's a few little tips and tricks in terms of stitching it in, using a small sheath is possible.

Heparin through the sheath, and then TPA through the infusion catheter. If you are fortunate enough to have the right length of catheter for the thrombus, then you can leave it at that length. Otherwise, you can pull it back

by 10 or 15 centimeters per day. And it typically takes three days to perform catheter-directed thrombolysis in this region. We always put on compression stockings, which sounds fairly basic, but it's important because it means that things don't get pulled.

And curious house officers and doctors don't have a good look at it and pull the whole thing out. Or the patient, for that matter. That's posterior tibial vein access, fiddley, tricky, easy to get into the artery, spasm is coming. You can do it with pharmaco-mechanical thrombectomy

using a 6 French device. The only one that I'm familiar with would be the AngioJet Solent, and not the newer Zelante. Views of the West of Ireland, not from this morning. Then if you want to switch tracks, how else can you get into the deep veins

of the lower extremities? Well, we're talking about improving the inflow, so we're going to now try and go from above and below. This is a patient with massive deep vein thrombosis. You'll see in just a second now. Thrombus starting here,

occlusive thrombus going to the profunda, occlusive thrombus down into the femoral, duplicated femoral vein, and then, most importantly, it goes into the below-knee popliteal. You might say why does this matter? Why do you care about the popliteal at all?

Well, I'm a bit old-school. I do believe that inflow matters quite a lot. Pardon me. So you can see a thrombus starts just here, a rather unusual place for a thrombus to start. Typically it starts much higher in the common iliac vein.

You can see it goes into the profunda femoris here. That's quite important technically, because the profunda is a very important vein in terms of long-term patency of the segment. And you can also see, lordy me, that it goes into the below-knee here as well.

This is what we call criss-cross. Fairly standard, fairly straight-forward, back of the knees, catheters into the popliteal vein from above and below. It sounds very easy, it's actually surprisingly difficult. The problem is that although you start very far apart, your two needles tend to approach

and you tend to puncture the vein in almost identical position, time and time again. So you have to start what feels like an awfully long way apart, in order to get some clearance between the two catheters. This is what you look like

when you're going to start catheter-directed thrombolysis. And what we're doing now, is we start catheter-directed thrombolysis at the bottom end, while working on the top end. The bottom sheath, rather the sheath facing inferiorly, is 6 French, with an infusion catheter

which is typically 20 centimeters long. And then this is a 10 French sheath going north. And through that you can perform AngioJet or whatever your thrombectomy device de jour is. Now this is an initial venogram of the below-knee veins and you can appreciate that there's very little inline flow

going from south to north. And you're seeing a whole lot of collaterals and very little flow going north at all. Pardon me. AngioJet works well here, although there are a variety of thrombectomy devices.

Then I must say I'm a big believer in aspiration. And you can get quite aggressive with a curved 8 French catheter. It sounds very basic, works very well. It's particularly useful, again, to go back to the profunda femoris inflow,

as well as the internal iliac. So this is what it looks like after aspiration. And you can see a rather unusual stenosis. And then, obviously, you need to go on to treat that. We start with our stent at the top to cover the iliac vein compression point,

and then carry on down here, and add a further stent down at the bottom. The inguinal ligament, I don't think is nearly as important as others feel. I think you you have to stent from flow to flow. And you can see that the final flow we've got here

at the end is quite satisfactory. Now this is when I say at the end, this is the end of the above-knee treatment. 'Cause you still haven't dealt with the below-knee veins. So you get your catheters running overnight, and you've got thrombolysis going north and south.

So this is your sort of set-up, your 10 French sheath going north with a catheter through it. A drain fix is quite useful for those of you who have access to that, to keep the catheter in position. And similarly going south, like this.

And this is what it looks like below beforehand, and this is what it looks like afterwards. You might think well, that doesn't really matter very much, but the popliteal vein will guarantee the success of your treatment. If you do not have a patent popliteal vein, in my view,

your success long-term is going to be much more guarded. And then, this is what it looks like from below, and the next morning. You can also appreciate that there's quite significant inflow now from the profunda. You can see the mixing just there, at the top up here.

So you've now guaranteed an inflow from above and below, but it takes two days, typically, because you've got to work one day on the above-knee segment and the second day on the below-knee segment. So could you move it on a bit?

Again, Galway, but not this morning because it was raining. You can do it as a single session criss-cross, so this is very similar to many of the arterial thrombectomies that you perform. I specialize in big, swollen, purple legs,

save the Speedos, they're not mine. But he's got a very, very swollen right leg. Rather unusual when somebody presents with a right leg tense phlegmasia. It starts to get me wondering, why should he have a right leg phlegmasia?

No specific reason. Left, obviously, would be straightforward. A CTV again, heading south here. Nothing really specific there, but you can appreciate this leg is very tense indeed. And there's thrombus in the femoral,

and most importantly, it goes down below-knee again. So you've got no inflow into your popliteal segment. If that popliteal vein is opened, it's a straightforward one hour, one and a half hour procedure. With a thrombosed popliteal vein, it's more difficult.

So here's the view of the external iliac vein, and here's the longitudinal curl reformat, showing A, a very swollen limb, and B, the length of the thrombus. In this case, again, you'd use the same criss-cross technique.

But this time, we were going to attempt a thrombectomy above and below. And starting off, you put a little catheter in here. Niggle it down as far down as you can, and just flush inject five, 10 milligrams of TPA while you're setting up your thrombectomy device.

That usually takes a few minutes. And in that meantime, you then can get to work. And this is just after five to 10 minutes of tissue plasminogen activator. You opened up some segment here. Then you get to work

with, as it happens in this case, the AngioJet. Not perfect, because our puncture points are very close to each other, but you can appreciate that we do have rapid inline flow. And this is over the course of 45 minutes or so. We're now up to about an hour

with, I think that's a Cook Zilver venous stent going from south to north. And this is his CTV, with a filter in situ. At six months, he has a widely patent vein. And the same on the sagittal reformat. You can appreciate that the stent is widely open.

In summary, there's pros and cons to both. First of all, you have to believe that the popliteal vein matters in terms of inflow. I do, I believe that inflow matters in terms of most vascular procedures. CDT is less labor intensive but costs more,

and there are the risks of thrombolysis. Pharmaco-mechanical thrombectomy is faster, and you can do all of your work in one go. But it certainly takes two hours of your time. Posterior tibial vein is more difficult than it it looks. There's lots of ways to skin this particular cat

and Fabritzio and I wrote a little book last year. If you're interested, you can learn more. Thank you so much.

- Thank you very much. I'd like to thank Dr. Veith for the opportunity to be here and give a quick smattering in four minutes and a quarter. I have no disclosures. So despite the well-documented benefits of straightforward catheter-directed thrombectomy, it remains slow. It can several days and we need speed.

So, devices for physical removal of clots, disruption of clot, large volume removal, and/or combinations of above have certainly been developed. So, with regards with physical removal, aspiration devices, the number of which we'll have several speakers following, the CAT series is by far the

best example of it, if you will. Suction device connected to a continuous pump. Unfortunately, if offers poor transition into the wire. You have to advance in bare. Particularly when you're doing arteries, this can be concerning.

As you advance the thing, you can't tell if the clot is actually removed or not removed, so sometimes you can push it forward. If you've ever used the device, you've seen this. And clogging requires the entire remov

and thus, and you have to put it back through the artery and start all over again. And the concept of continuous removal with a pump is good for suction, but unfortunately, you can remove up to 160 cc's with just 20 seconds of using the device, as it doesn't have a reperfusion system.

The Aspire Mechanical is sort of a low-tech version, a manual aspiration device, where you have a pump that you manually pump up to start negative pressure. You can advance the catheter. The nice thing, you can connect it to literally anything.

If you can get a catheter in there, you screw it in and away you go. You're less likely to have extreme blood loss. You're unable to adjust the suction, unfortunately. And it's not really clear if the suction is actually working or not working.

The pump is on, you know that. But if you pumped it two or three times, is it sucking or not sucking? There's no actual feedback. The AngioVac is the most powerful or large-volume aspiration system.

It's filtered through a veno-veno extracorporeal pump. You can get a big circuit in there. You can do vena cavas, you can do iliacs, it's great. But you have to set up this very complex system. You require, what I'm going to put here as massive sheaths. So if you ever think about doing this in arteries,

you really can't do it. You need a 24-french sheath to put the device in, and then you need at least an 18 or a 20 to put the volume back in. So unfortunately, for arteries, you're going to have to put a conduit in,

and you're going to have to advance it bare through an artery. The extracorporeal filter pump is very expensive and it's not reimbursed. A lot of institutions will either let you use it a few times until they realize how much it costs, and then you're only going to be reimbursed for a thrombectomy.

With regards with mechanical, the Arrow-Trerotola is probably the most powerful and classic mechanical clot disrupter. It's got a spinning cable that looks like this, the new version. And it can damage native vessels,

so it's designed only for grafts. However, it can also get entangled in wires and stents, so even though the black box warning says don't do it, it doesn't keep people from trying it and having multiple attempts. And this is something that we had to remove once

from a graft because it was all entangled in the wire, and it could neither be pushed in or pulled out. It causes embolic materials. It spins inside, and we've never really manned up or womanned up and looked at what happens to the lungs when we fracture all this stuff.

Combination systems, like the Angiojet, is nice 'cause it can shoot out TPA and spray out a saline and break things up. And also, it has a negative pressure, which causes Bernoulli effect to extract clot. The upside is that it removes soft clot

through small side holes. We love it. It's fast, it sprays saline. However, it can also damage vessel walls. At some point, we've read and/or done ruptured in a thin vessel.

And of course, there's a black box warning against pulmonary. But also, if you've ever used it in a cadaveric graft, you'll do it once, and then they'll come back a month later, and now you have this diffused aneurysmal destruction of your bypass.

It also causes hemolysis. Typically, if you look at a Foley catheter, this is what your urine starts with at the bottom and what your urine ends with at the end. And both my group and Dr. Kashyap, who will be following, have assumed that it may not be good for the kidney.

I'll let him continue with that. So in summary, be judicious when you're choosing your approach. Continue to consider the potential downsides of each product. Risk/benefit ratio based on the patient.

Patient has renal dysfunction, limited outflow, sheath size. Old school lysis may be the way to go. Just look at it and maybe you don't have to do a fancy device every time. Or, actually, go with an open thrombectomy.

Mechanical thrombectomy is thus not like a car. When you're looking at these different options and say, "Gosh. You know, maybe it is faster, but perhaps I should think about it." But if somebody offers you this, there's no conceivable downside.

I would go with it. Thank you very much.

- [Germano] Thank you very much Mr. Chairman. Let me please thank Dr. Veith for his invitation, for his great hospitality and for being my friend and the mentor for many, many years. Thank you Frank. So, I also would like to thank Mario

for making a very interesting point that the EVAR is very appropriate unless it's not appropriate. And I certainly do acknowledge the value of EVAR. It's a great technique when it's appropriate. However, the problem is,

should it be considered the only choice? And this could be the case if it offered better results, if it was always feasible and maybe cheaper. So, as far as better results are concerned, we've already heard about all the randomized trials not significant.

There's a meta-analysis on over 80,000 patients that also showed no significant difference in mortality. And regarding feasibility, I think we all agree that there are anatomic limitations of EVAR and cases that are really tough with EVAR are really straightforward with surgery.

And this also applies to access vessels. And it also applies to anomalies of the kidneys, for example, saw a pelvic kidney here with its surgical solution. A horseshoe kidney here. And also there are clinical limitations,

are not many common, but certainly we don't want to treat an infection or a fistula with EVAR. And we know that large hematomas are a problem if we don't open the belly and raise a surgical solution for this.

And then there are logistic limitations, of course especially if you tried to treat most of the cases you need advanced techniques for at least a quarter of these cases, as shown by Mario (mumbles), and to do so you need

of course round the clock availability of highly trained endo team and everything else. Including, a large warehouse of gadgets. This is Mario's warehouse for all his wires and things. And actually this debate has been going on

for several years now. So, I've been trying to search the literature a little bit to see if there's anything new about it. And there's actually a couple of interesting, a few interesting new papers. Such as this one from Sweden,

from Anders and his colleagues, that show that very interesting change in the epidemiology of triple A's. Which is related to the introduction of EVAR, to the screening of the population, to the reduced prevalence of triple A's.

And we also saw these from the data that Mario showed in the first years of his cases. It was 30, 20, and now in the last years he's showing about 10 cases per year. We've all been seeing this. And this results, of course, in increased incidence

of intact triple A's, reduced incidence in ruptured triple A's and improved survival for both. And Warner and co-workers show that regionalizations of emergent ruptured aneurysms repaired to tertiary centers decreased the mortality by 20%. And transfer did not impact the mortality.

I think that Bam showed to us very beautifully how this can be achieved in a very scientific and sophisticated way. And we do have an update. This year update of the Cochrane Review that includes all four randomized trials.

And once again, there's no difference in 30-days mortality shown and neither there's a difference in 6 and 12 months outcomes. This last literature paper from Siracuse and co-workers, on behalf of the American College of Surgeons,

showed the registries of over 400 patients treated by open repair in the United States, so it shows that this is still commonly done. And the overall mortality was 35%, which is somehow lower than previous historic data. So regarding training, I think we should consider

that if a center does 90% or more of the elective case endovascularly there is very little or no chance to train new generations to open surgeries. So, for these kind of centers the boat has sailed already and this ability has been lost for the future generations.

So, we should consider this very carefully when we decide what we want to do with our patients. In conclusion, dear colleagues, Chairman, Mario, I believe that the present evidence is that EVAR for ruptured aneurysm is not superior, feasibility is not 100% and therefore,

there is still a justification to have a selective approach for these patients. Thank you.

- [Presenter] Thank you Mr. Chairman. I'm going to give this presentation on behalf of Professor Richter, who had to leave earlier to go back to Germany. So, there is a very interesting paper that was published just very recently regarding the radiation damages on the DNA of the operator performing EVAR.

And this has stressed the concept that every time we are working the cath lab we have to protect ourself. And also we have to use all the systems available to reduce the exposure, not only for the patient, but especially for the operators.

And you know that especially in Europe starting from next year there will be a tremendous reduction of the maximum dose for the operators. There are no disclosures for this. When we talk about radiation dose,

there are four key points. First of all, obviously, is the patient. If we have an obese patient we can increase the amount of radiation. The hardware, software, and also the skills of the operators.

But the software is where we're at now. More information and more progress regarding guidance and also virtual reality. This is the system that is acclimated to the Siemens machine and it's pretty easy. You have just to upload a CD

with all the high quality CT scan. And the system by itself creates in a couple of seconds a vessel modeling that you can use to perform your procedures. Also in the previous sessions, you have seen a lot of these examples.

Once the system creates the model you have just to put some dots and some lines just to add a better overview and convey the angulation of the anatomy. And using this mask obviously we can reduce tremendously the amount of radiation, not only again for the patients

but also for the operators. Just to give you an idea, this was a case that they did in Stuttgart with an EVAR plus a renal artery stent you can see that the final sum of exposure was around 2800 milligrees. That is generally reported as a very low if you compare

to the mean dose in the EVAR German Registry, they're was around twelve thousand. So four or five times less. This is pretty important, especially for high volume centers where the operators are in the cath lab and the operating theater

for many times during the week. Just to give you also some information from a technical point of view that the system is pretty accurate because once we have this sort of mask and we introduce the EVAR, obviously there is a sort of modification

of the anatomy, you can see that we can do just a small correction on the 2D and 3D plan, just tilting the table and the C arm and then we can replace completely, the side called, the level of the renals or SMA or the celiac track.

This is just again another example to show you how we can create a track and it's very important you can see the aorta is comparative when with the standard angiography. And again you can see also in this case there was a very low amount of radiation

with just 40 minutes of cytoscopy. Obviously this reduction of dose is also related to a reduction of contrast media. Just to confirm you the accuracy of the system, you can see here that we have a blue circle that are showing the origin of the vessel

and then the green circle is the landing zone. In this case there was the curiosity that the landing zone for the SMA was higher than the origin but if we go to the angio, you can see the anatomy that was pretty unusual with the SMA going in the higher portion

senior to what was reported on the navigator. And this is also another blue projection to conform the origin of all the branches and this in you know the final with was a pretty complex case with the four branches that was deployed in the cardiac way.

So again some of the images. And all this can be performed with a low amount of contrast because it just to press the paddle for a couple of seconds, release the paddle and the images fix and you can use as a trace to deploy the stengraft and also to do some complex branches EVAR

often that is the procedure. And again also in this complex, more complex situation the advantage is more and more evident because you can see that again the dose was just for 43 minutes of cytoscopy and there was them 10,000 milligrees that you know is less than was

reported in the German Registry. They compare also 10 patients you know without guidance and with guidance and there was a reduction of more or less four or five times less than the regular one. So in conclusion definitely this is something

that is very helpful but we have also to remember that it is not only the technology helping us, we have a lot of gadgets as you know, that we can use in our daily activity. Thank you for your attention.

- [Julio] And I appreciate the invitation from Dr. Veith. Those are my disclosures. The first time that I use a aortic occlusive balloon, it was actually not for endoluminal repair, it was done for a open repair, and that's important to know, because for those that believe that open repair is the way

to deal with ruptures, then this a tool that you can use to avoid decompensation on a patient. In my case, it was a life-saving technique. So the scenario of a rupture is really a challenging one. It demands quick and precise steps to avoid decompensation, and if you're planning

on using a aortic occlusion balloon, that might be time-consuming. So some tips to a streamlined decision and technique might be helpful here. Now, the first question is, since sometimes the placement of the balloon could turn into a difficult

and time-consuming task, a time to deal with small, calcified or tortuous iliac, we need to know who really need it. There is no guidelines available to assist you in that determination. However, we like to use the coronal view

of the CT scan because it give you immediately a glance of the magnitude of the retroperitoneal bleeding. We did a study in which we want to correlate this hematoma with the probability of survival and also to look into incidence of decompensation during the procedure, so we take this coronal view

and we divide this abdominopelvic region in nine segment. A line above the sac of the aneurysm, one at level of the bifurcation, and two vertical lines just crossing the psoas, a very quick determination that can be done. So we defined the small hematoma every time

the less than four segments of the bleeding is presented, and we found 20 patients with that category. The medium-size hematoma, four to six segment, and those we found 22 patient. The large hematoma was defined by seven to nine segments, and we included 15 patients in that category.

So besides that, we look into the condition of the patient, hemodynamically speaking at arrival, what was their response to the induction of anesthesia, and what kind of events we have during the procedure, talking about hypotension, shock, or even arrest. Although I don't have time enough to go in details

of the whole study, but I can forward to you the conclusion. The small hematoma, we don't see or witness any particular events of hypotension, so our conclusion is no balloon support is needed for this group. However, the large hematoma, we have events

that goes from hypotension to code arrest, so those patients always has to be supported, and I recommend that you use the balloon even from the very beginning. The medium-size hematoma, however, was an unpredictable group.

However, those that came with a hematocrit of less than 24, even though it seems to be hemodynamically stable and has no adequate volume resuscitation prior, I'm talking about here blood transfusion, those need to be supported as well. So once your determination on who should get the balloon,

the access has been presented before can be done under local anesthesia. And even though the ultrasound-guided technique becoming very popular, one of the technique that I use for many years is just do a small cut-down, a blunt dissection with my finger

getting to the anterior surface of the artery at puncture the vessel, but I can get to know that many patient with hypotension without palpable pulses, you can use ultrasound very well with those cases. The decision of going brachial versus common femoral

should be done beforehands by looking at the CAT scan. But in any case, a quick angiogram can be done in doubtful iliacs. Consider for those patients with the small iliacs, place the aortic occlusive balloon over the stiff wire. Never use a floppy or hydrophilic wire

because you will have your balloon pushed down by the pressure. The best iliac should be reserved for the EVAR unless the decision was made to open the patient. Immediately exchange for a quick stiff wire like the Lunderquist wire, and I believe

the long, stiff sheath should be at level of the visceral branches. That allow you for support and prevent the balloon to being pushed down by the aortic pressure. We believe that the preferred location for the balloon is the supraceliac position.

That allows for quick stabilization, and also it give you adequate room for the completion of the endografting. Once you've deployed the main body, a quick maneuver of moving the balloon from contralateral to ipsilateral side can be done.

In those that doesn't tolerate the deflation of the balloon because become unstable, avoid decompensating by using double balloon technique. A second puncture can be done in the groin to introduce a new balloon as well. Make sure that the patient is hemodynamically stable

before removal of the balloon, and having the sheath beyond the top of the graft is advantageous because prevent the endograft can get cuts by the hooks, the barbs of the bare metal of the endograft. Remember, the best outcome occurs

when the institution has in place an algorithm to deal with rupture aneurysms. Thank you very much.

- [Dr. Vikram Kashyap] Thanks to Dr. Viets for the kind invitiation. Dr. Hotze and Dr. Calgoro, and thank you Dr. Escobar for that great introduction. Obviously, percutaneous mechanical thrombectomy's something that we all use. It hastens treatment, and we use it regularly

for both venous and arterial thrombosis. However, PMT has been linked to cases of reversible post-operative acute kidney injury. It's thought to be due to either the hemolysis and the deposition of red corpuscle elements into the kidney parenchyma, and it may actually also

potentiate contrast-induced nephrotoxicity. Clearly, PMT leads to mechanical breakdown, but the intravascular hemolysis is perhaps the concern. And as Dr. Escobar illuminated, clearly can reduce the time for catheter-directed thrombolysis

or overall thrombectomy, period. Catheter-directed thrombolysis on the other hand, chemical breakdown through, usually, the plasminogen system, with converting to plasma, and then fibrinolysis. But clearly, because of the risk of bleeding, we think about using PMT to decrease the CDT time.

Our hypothesis was that there is an increased incidence of renal dysfunction in patients undergoing PMT for treatment of an acute thrombus, compared to patients undergoing CDT alone. So this is a report- a single-center, retrospective study. 227 patients were reviewed.

145 patients were included into the study analysis. The excluded patients included patients that had acute kidney injury before their intervention, patients that were already end-stage renal patients on dialysis, and patients who that either inadequate or no follow-up data.

So of those 145-odd patients, one-third had arterial thrombosis, two-thirds had venous thrombosis, and as you can see in this pie graph, about half the patients had combination catheter directed thrombolysis

and percutaneous mechanical thrombectomy. 12 percent had CDT alone. 10 percent had PMT alone. And then 29 percent had PMT with pulse spray tPA in a single-setting intervention. We used the RIFLE Criteria to characterize

the severity of renal dysfunction after intervention. And in the RIFLE Criteria, you can see in these rows risk, injury, and failure. There's an increase in creatinine or a decrement in GFR and Loss and ESRD are obviously patients that go on to either temporary or permanent dialysis.

This was the incidence of renal dysfunction in this group. 20 percent in the patients that had PMT alone. With power pulse PMT TPA - 21 percent. With the combination PMT and catheter-directed thrombolysis - 14 percent. And with catheter-directed thrombolysis alone - zero percent

These were highly significantly different between these two groups and the CDT group with values as you can see here on the lower right. If we look at the RIFLE Criteria, none of these patients went on to permanent dialysis. They all had risk, injury, or failure,

which were decrements in GFR, or escalations in creatinine. In fact, all the patients were covered to their baseline renal function, but it took an average of 5.1 days. This lengthened their hospitalization. And all 22 patients that had renal dysfunction

had either PMT alone or PMT combination therapy. If you look at the procedural of variables in this table, you can see that the length of admission's actually fairly similar. Importantly, the total TPA dose was similar, and the total contrast volume

between these two groups was also similar. If you look at other post-procedure outcomes, luckily, none of these patients that had renal dysfunction had long-term harm. There was similar six month mortality, six percent versus five percent.

Other complications were very similar. Limb salvage was 92 and 95 percent and there was no increased readmission rate for DVT or arterial thrombosis. So, ladies and gentlemen, in conclusion, the use of PMT as a treatment for venous

or arterial thrombosis is associated with acute renal dysfunction, but is not associated with adverse six month clinical outcomes. We still use this to hasten thrombolysis time and decrease time in the hospital,

but I think it necessitates that we have post-operative, post-procedure vigilance, and renal protective measures as much as possible to decrease the likelihood of renal dysfunction. Thank you very much.

- [Lu] I have no disclosures. And we know, from the clinic outcome of multilayer flow-modulating bare stents was good but not good enough. Aneurysm expansion and rupture were reported and the indication was limited. - From our experience, we find the short-sac entrance

aneurysm manifested a quicker thrombosis compared with the wide sac entrance ones. So what's the sac entrance? It's the length of the flow entrance into the sac of aneurysm.

So, we have some idea that's the joint procedure and then the length of aneurysm sac entrance could be artificially shortened by a stent-graft covering part of it, and followed by multiple layers of uncovered stents to cover the residual sac entrance.

So stent-grafts used to cover non-branch zone of aneurysm, shortening the sac entrance And then, the uncovered stents used to cover the reno-visceral segment of aorta, and the preserving the visceral branches. We treat clinical practice with shape Type V

thoracic abdominal aneurysm, and Type I, Type II, Type III, even Type IV thoracic abdominal aortic aneurysm. For example, this Type V, this is the pre-operation CTA find that, and the step one is pre-stenting angiogram to confirm the size and location of the aneurysm.

Then, the first uncovered stent was deployed to cover the entire aneurysm zone, providing circumferential bearing support for the subsequent stents. Then, a stent-graft was placed within the first bare stent to cover the most part of the sac entrance,

leaving a residual sac entrance in the reno-visceral segments. And step four is the second that can uncovered stent was deployed overlapping to cover the residual sac entrance at the reno-visceral zone. And just to follow-up, complete the thrombosis

and the shrinkage of the aneurysm sac, and patent all the collaterals. We also use the Type I stent-grafts covering proximal aneurysm sac, and the multilayer bare stents covering reno-visceral segment. Follow-up CTA should complete thrombosis

of the aneurysm sac and the patent side branches. Under the Type II, we used that the same, the stent-graft covering proximal and distal aneurysm sac, and the multilayer bare stent covering reno-visceral segment and CTA showed the thrombosis or aneurysm sac and the patent side branches.

The Type III, it's the same, cover the proximal and distal aneurysm with the stent-graft, and then the multilayer covering the reno-visceral segment. And the thrombosis doing a follow-up, and all the branches patent. And this shows the Type V,

we used the stent-graft supposedly covering the distal aneurysm sac, then use the multilayer bare stent covering the reno-visceral segment. That's the follow-up, we find all the aneurysm sac thrombosis and all the side branch patent.

For now we did 34, the patients, and Type I, 19, Type II, two cases, Type III, two cases, and Type IV, four cases, and Type V, seven cases.

And the diameter, the most larger, the largest is the 112 millimeter. And we follow-up an shrink, 19 patients stabilization in 15 patients and one aneurysm expansion. And then we've, discussion was the changing flow pattern

we find that it's could change greatly after the joint procedure. You again find form this, the movie, you can find change a lot. And we compared that, we find a joint, we compared a joint procedure and compared with the

only uncovered stents, we find quick, quicker thrombosis and a more diameter decreased ratio. So our indication, I mentioned that the largest, that is the 112 millimeter of diameter, but there are also some limitation. For example, this patient after 4 years,

we find a separated bare stents with the stent-graft so it's joint limitation. And the part that we put now, the stent-graft and the bare stent after six months, thrombosis all the segment. So, my conclusion is

joint procedure might be a modified concept for the flow-modulating with better outcome, but in the, it's need a new designed joint stents to overcome the limitation. Thank you very much.

- [Narrator] Thank you, thank you Dr. Veith and the committee for the kind invitation. No related disclosures. Carotid webs are rare, noninflammatory arteriopathy that are also known as pseudovalvular folds, as well as other pseudonyms for this. They are small, shelf-like linear filling defects,

arising posteriorly from the posterior proximal-most ICA and project superiorly into the lumen. They're generally regarded as a developmental anomaly of the brachiocephalic system, and histopathology lacks atheromatous changes and inflammation of the tunica intima.

They may be associated with FMD, or be considered an atypical form of intimal fibroplasia, and generally arise from dysplasia within the media. They will as we will see, carry a considerable stroke risk based on laminar flow disruption and irregular shear profile.

This is the mechanism by which they produce strokes, seen clockwise from the top upper-left. There are areas of stasis in which thrombus can develop behind the web. The thrombus can enlarge and eventually embolize. Operative findings and pathologic findings include

these webs seen here behind this nerve hook, and generally smooth muscle with extensive myxoid degenerative changes. Over the last several years we have treated 10 patients with carotid endarterectomy for symptomatic webs. The mean age of these patients

is generally quite young, in the 40s. The majority are female, one patient had a bilateral web and 70% of these patients had no atherosclerotic risk factors whatsoever. The mean maximum peak systolic velocity on duplex was 77 centimeters,

and five of the cases were closed primarily without a patch. There were no strokes perioperatively in this group, no mortalities, and there have been no new neurological events nor restenosis. Several other groups have looked at this phenomenon as well,

this is a case series of which 7 patients were identified prospectively having had an ischemic stroke. Again, the mean age was young. Of note, five of these patients had a recurrent ipsilateral stroke to the web. No FMD was seen throughout the other vascular beds

and four out of five of these patients, the recurrent patients had CEAs with no recurrence at approximately a year. Another review identified 33 patients who had excellent CAT scan imaging. These were younger patients over a six year period,

with cryptogenic stroke. The prevalence of webs within that group was 21%. Symptomatic patients within that group with webs were 7 patients out of 33 and again you see a young age, predominance of women,

in this study of predominance of African American patients 3 bilateral webs, all patients had MCA infarcts. And oh, 1.6% of the webs in the control group were without a stroke. Another case-control study looked at 62 cases over four years.

They were able to match 53 of these patients with other cerebrovascular pathology, webs were found in 9% of the cases, but only 1% of the controls. And again of the webs, predominance of young patients

and women with two bilateral strokes. So what about diagnosis? Even large webs generally do not meet the velocity criteria for significant stenosis, and while you may see a filling defect, you're generally dependent on B mode imaging,

and having a high level of suspicion, for identifying this process. CTA is the gold standard, it's got rapid, high-resolution imaging, reformatting across planes, makes this an excellent modality

in associated findings of thrombus, and atherosclerosis can also be detected. Angiogram again, as always, gives you a good view of flow dynamics, intra and extra cranial pathology, and in general the finding is of contrast pooling,

which you have to look for behind the web. MRA is one method that's been used to characterize this, in this modality you can see slowed blood flow distal to the web, blood pooling distal to the web, and generally this all leads to an atypical pulsatility, of the carotid wall near the area of the web,

suggesting impaired hemodynamics in this condition. Management is with a carotid endarderectomy which has been the preferred treatment, although some have advocated medical management with formal anticoagulation, patients have had strokes

while on anti platelet therapy, and there are several case series now appearing of acute stroke treated with stents, these are generally delayed following thrombectomy. There's one latrogenic dissection in these groups. These patients have few atherosclerotic risk factors,

in the same demographics as noted above. So in conclusion, these are associated with FMD and intimal fibroplasia. The prevalence is low. The prevalence may be increasing but it's not clear whether this is a true prevalence increase,

or simply increased detection. They're associated with recurrent symptoms even in the setting of adequate medical therapy and is an underappreciated cause of stroke, and are now becoming a recognized, and rather than a cryptogenic cause of stroke.

They are generally not identified by current duplex criteria in asymptomatic patients, and duplex may miss them entirely. Axial imaging is essential and currently we don't stratify these based on either legion characteristics or demographics.

So while the optimal management is not completely defined given the recurrent stroke risk CEA seems prudent especially in young, medically fit patients with or without patch angioplasty, which may have some impact on quality metrics

at least in the United States. We've treated patients with three months of antiplatelet therapy, aspirin indefinitely. Right now the role of statins is undefined, and the durability and role for endovascular approaches remains also undefined.

Thank you.

- [Instructor] Thank you very much. So, you saw some of the issues that our, oh, this is the slightest cut, but that's okay. Some of the issues that we've seen with these percutaneous mechanical devices, and, back in the 90's, and perhaps even more than a decade ago, there were a lot of these.

And this space gets hot and cold, and one of the problems is that the level of evidence for doing these is very low, and when it is done, it wasn't done well. And this is a nice registry, a lot of patients enrolled, unfortunately we didn't learn

what we had to learn from these types of registries, because of just the study wasn't done well. So the level of evidence is low, and when we did have them, they didn't really work. And you saw some of the problems, that these devices can cause.

And here's another problem that wasn't discussed. You can see the DVT, iliofemoral DVT in here, and a device is pushed a few times up and down, and sort of aspiration, a Bertoulli, that type of thing. And this looks, oh wow, well this looks good,

maybe the thing is working, except all the clot is up here. So, these devices tend to push the clot around. So the issue is, enter now more recently, these are some of the more recent ones. Note that the AngioVac is not here, I don't consider that a practical thrombectomy device,

and so, it's not here. So, we're going to be talking about JETi. This is a system that is an aspiration system with a jet that comes inside the catheter, therefore the clot is engaged and pulled in and broken down by the jet, therefore there's no hemolysis.

And this demonstrated in this case, which is acute and chronic 17 year old multiple DVTs in the past, the iliofemoral segments are stented, as you can see here, this segment is somewhat fresh clot but these, as you can see, are subacute clot. Look at this, so the system now is designed

for over the wire, but for DVT you can use it without the wire, because it works a lot better. As you can see it can really aspirate the clot, in before your eyes. Now this I have passed the device in here once, and you can see the fresh clot is gone,

we have some residual debris in there, we have not established flow yet, and then I turn the device on... and it pulls the whole thing in, okay? So, very powerful aspiration method. So, and as you can see here, we don't have

a flow establish, outflow established yet. Therefore, when you turn it on, you have a vacuum created right here, and so this tells you how strongly this device can aspirate and work. And this isn't on the table.

After a pass here, two passes here, some residual clot in here, obviously there's residual clot there. So we pass it around these areas once more, and this segment obviously needs to get stented and on the table, re-establish antegrade flow. Since May, we've had 19 patients treated, most of them DVT.

And, based on our assessment, 17 of the 19 patients at a total time of 90 minutes on the table, had better than 90% clot retrieve. We have 30-day patency data on only 16 of those patients, because this is really since this May. And 15 of those were open, one re-thrombosed

and we had to retrieve again. Conclusion, so preliminary experience indicates that this is an effective device. There were no safety issues, we don't see any hemolysis, we don't see any pushing around of the clot, but there is a learning curve to it,

and for best application, thank you.

- [Presenter] Thank you very much. This is Jordan. It's my pleasure to share this panel with endoanchors believers, I'm one of them. So, there's my disclosures. The scope of the problem about the proximal migration starts

in order to think about the durability of thoracic endografting, because it still is a concern. The cranial migration from the distal attachment is part of this particular concern, especially when the distal neck length is less than three centimeter.

I think this is a under-reported complication in these areas. That is, what has happened, after some kind of follow-up, after four years follow-up, the distal part of the aorta, or the distal part of the endograft is dis-attached from the primary landing zone.

Because all the forces in the ascending thoracic aorta acting in the up cranial fashion. So when you are virtually sure there some kind of migration rate of two years but also have some kind of cranial migration from the distal part of the aorta at the one year is 1.2%

for the VALOR trial and 1% in one year also for the TX2 trial. In our experience, before 2006, for distal neck length, between 1.5 to 3 centimeter in length, 60% of cranial migration rate was registered at five years follow-up. So what's a lot of percent about that we try to perform

a different kind of approach for those particular short or no short, nice distal neck of thoracic aorta. So cranial migration as previously mentioned is under-reported. The upside for the abdominal aorta with the forces acting in the downstream anteriorly in the thoracic one is

posteriorly a cranial and also a cranial migration course. And this kind of phenomenon kind of course in the long run follow-up. These connections and also cranial migration. About the preventative actions there are different kind of creative alternative in order to prevent that,

but let me to focalize my attention and your attention to endoanchors philosophy that is part of our current approach. For a regular neck of more than three centimeters we can use regular endograft but sometimes when it's not so regular it's not so straight, we prefer to use in combination

with endoanchors. When you have a regular straight but between 1.5 and 3 centimeter we prefer to use distal scalloped endograft plus endoanchors as you cam see here. That is what the speakers talk about very extensively but this is just a case in order to see

what happened after two years follow-up in this lady when it has this distal type one endolink we apply the endoanchors and after three years the endoanchors remain in the same position, as you can see here, without any kind of further complications.

So another example, in combination with scalloped devices, scalloped thoracic endograft, just in order to be sure, that the movement in the distal part doesn't occur or even weaken over time. For sure, when you have very short neck length,

that means less than 1.5 centimeter, then we need to switch to another kind of solution like this fenestrated or branched endograft, like you can see here in this example. So in summary, the durability of thoracic endografting remains a concern when cranial migration is a consequence

of biomechanical forces of the thoracic aorta and it is under-reported. The proximal and distal necks deserve equal attention. And many different approaches have been suggested to avoid cranial migration. And endoanchors in combination with the scalloped,

fenestrations and branched endografts should be applied more often. Thank you very much.

[Mark] - Thanks Evan, thanks Dr. Veith for inviting me again this year. These are my disclosures as it pertains really to this talk, a major one being Centerline Biomedical. You know, what's all the really talk about why is there a whole session dedicated to this? Well this really has come about, this is a paper about

brain tumors for cardiologists that came up and there's really a call of an alarm. What is our exposure as interventionalists and what is our risk? If you look at things that have gone on, you can look at the explosion of endovascular procedures done by

vascular specialists. Those of us that do it a very wide, varied practice, are going to be different than those who do disease specific practices, and you can see there the amount of EVAR change has grown significantly over the years, not only for EVAR but also for Thoracic disease.

But really what we're talking about is what is our exposure risk, and you heard Lars talk to us about exposure in the operating room. The biggest portion of that exposure is scatter radiation from the beam as it comes off the patient. And you need to learn how to protect yourself and consider

its importanty. Obviously as the complexity of the procedure increases, that will increase as the body habitus of the patient changes that number increases. The more you get to an angled radiation exposure, that matters.

Now you can do some things to protect yourself. Obviously, the further you're away from the radiation source the lower it's going to be. But also the proper imaging can make a difference if you have your imaging intensifier upside down, and yes it does happen, I've been at places where this is.

You see how much significantly in the middle panel there, it increases your exposure. Not having the image collector down as far on the patient is a difference, and having appropriate lead shielding on the ground as you see on the far right, hanging all the way to the floor makes a difference in your exposure.

Now there are protective strategies, whether that's protective equipment, drapes or shielding. In the last session, you can see in the bottom middle, the red pad which are fairly inexpensive compared to some, that makes a difference. The anesthesiologist having a full lead shield there all

the way in front of them, makes a significant difference for them. In our institution, I do use a zero gravity suit. But what people also don't understand is that even not using the appropriate equipment the right way makes a difference. If you do not have side shields on your glasses, about 21%

of the exposure is going to come around the sides of those glasses, and in. And you can consider that a window into your brain, in terms of potential exposures. So you need to make sure that you have appropriate fitted glasses, and there are side shields on your glasses,

to protect yourself. Not only against cataracts, but also radiation exposure the the brain. Now as there have been studies on zero gravity, we actually had two zero gravities, one for myself and one for my partner which is typically the fellow on the other side

of the table when we do complex procedures. But they've looked at the 122 procedures here in zero gravity versus lead apron. And those people not familiar with zero gravity suit, it's a 75 pound lead suit suspended from a boom above you, so you're not wearing any lead when you don't need it,

and there's no weight on your neck and shoulders for the case, and it's much more extensive protection that covers you all the way from above your head, down to your ankles. And you can see here the decrease in exposure in the middle panel. The fold is anywhere from two to about five fold decrease

in radiation exposure. The problem if you talk to physicists, it's hard to prove because they make us wear our badges on the outside of the zero gravity suit, and if you do a double badge situation, it's 11% of your inner badge and 89% of your outer badge, so the most you could prove from a physicist is

a reduction of 11%. Now what about modern day badges? We are in the habit of not knowing about our radiation exposures until a month later, so what were you doing wrong, and when were you doing it wrong, gets to be a problem. Now with modern day badges that detect an early warning,

this is what happens. You can track your cases over time, you can see which day you had a higher exposure rate, and so these real time dose monitorings, allow you to adjust what you're doing in the operating room that can give you direct feedback, in terms of standing too close, standing on the foot pedal

too long for the radiation exposure, and changing your angle or not coning out your images makes a difference. But also we need to consider about a better way to do things. Center line imaging or center line biomedical has now a new system which they're developing.

Our current paradigm is ionizing radiation in 2d visualization. We need to consider moving to intraoperative positioning system, with a 3d interactive image and electromagnetic navigation. Catheters and wires will have censors on them, will allow

you to locate your wires and catheters inside the patient by using electomagnetic panel that sits below the patient. This is a porcine model where you take your CT scan preoperatively, fuse it just like you currently do with technology, but you take that image and you place it into a display imaging system.

This display imaging system connects in with electromagnetic navigation, and you can then track your catheters throughout the body and look at any view you want. In this case we're catheterizing the left renal artery, in a porcine model. From that, you can then do a final conformation angiogram

as you see here, to prove that you're in your left renal artery. So in conclusion, current advancements in vascular therapy significantly increase the exposure of aortic specialist to the harmful effects of ionizing radiation. Maximal efforts should be employed by proceduralists to

protect themselves. And future research should be directed at identifying non-ionizing methods for navigation and device implantation. Thank you.

- [Sakalihasan Natzi] This my disclosure. We know that aneurysm rupture occurs when the mechanical stress acting on the wall exceeds the strength of the wall We know also the rupture of an AAA occurs at the hot spot characterized by an increased local metabolic activity as we find in our case. And we know also the degradation of the aortic wall

as we can see here, we didn't find any small muscle cells at the side of the rupture. During several years in, we observed significant association increased FDG uptake at the aortic wall and the rupture, especially side of the rupture. It is not a best fit for AAA and we can observe similar

results at thoracic aortic aneurysm also. Recently, one group from Japan, they observed a similar study and recently their paper was published. A beautiful study performed by Gilbert Upchurch in their laboratory on their animal model, they used FDG uptake and they also observed association between increased FDG

uptake and the site of the rupture. During several studies, we observed significant correlation between the increased FDG uptake in dark gray here and the presence of inflammatory cells, especially macrophages. Recently, during open surgery, we gathered abdominal

samples at the positive PET/CT and negative side. You can see here, easily, we are observing an increasing number of inflammatory cells at the positive side compared to negative side. And more interestingly, more important, we are observing degradation of small muscle cells in positive side

compared to negative side in the same abdominal wall. And during this study also, we observed the association with positive PET/CT and the presence of inflammatory cells, as MMP1 and MMP13 and some gimocans. We also studied the association between wall sheer stress

and uptake of the FDG, and we also once again find in some patients the association 18F-FDG uptake and increased wall sheer stress. And we a udd from the United Kingdom also found similar results that there are

observed association between increased FDG uptake and increased sheer stress. We also stressed with the MRI and we used a superparamagnetic particle of iron oxide, SPIO, and once again we observed the association between increased SPIO uptake at the liminal part of the

thrombus and the presence of the inflammatory cells. And during the Ex Vivo study we have found simliar results. Once again, we observed significant association between SPIO uptake and the presence of increased metabolic activity in the level of the aortic wall. We wanted to perform the largest cooperative study

but unfortunately Gilbert's company stopped the production of SPIO. And when we look after the publication of literature, we found only three publications on the relationship between SPIO and ultrasmall SPIO and abdominal disease. In their paper, the authors from the United Kingdom

concluded that there are significant correlation between ultrasmall SPIO uptake and the rapid growth of inflammatory cells. And the same authors set up a multi-anthrocourse study in Scotland, and they were expected to report their results during 2017.

But unfortunately I didn't find the results and we hope to have their results of this very interesting study very soon. In conclusion ladies and gentlemen, our results reinforce the hypothesis that there is a correlation between 18-FDG uptake by the aneurysmal aortic wall and the

triggering processes leading to aortic aneurysm rupture. This uptake is correlated to the abundance of inflammatory cells and could reflect the protease release within the thrombus and aneurysmal aortic wall. There is a potential link between accelerated metabolism in the aneurysmal aortic wall and high mechanical stresses

experienced by the wall. And aortic MRI using SPIO and/or USPIO could predict AAA rupture in some patients. However, further studies on larger populations of patients are needed to confirm these findings. Thank you very much for your attention.

(audience applause)

- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company

for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.

The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the

middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,

which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up

in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.

Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,

embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,

we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,

which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.

We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,

excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success

just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and

no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.

We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,

and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.

We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,

post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch

blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it

through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,

we actually have several publications out, demonstrating safety and ethicacy. Thank you.

- [Dr. Cho] Thank you very much, thank Frank, for the invitation and for the opportunity to speak on the carbon dioxide angiography. Disclosures, none. Here are three images taken, obtained from the carbon dioxide, and MRA, and CTA.

If you look at the CO2 images, it's quite comparable to the MR and CTA, and MR requires gadolinium, which can cause nephrogenic systemic fibrosis. And if you inject the contrast for the CTA there's a risk of the contrast-induced nephropathy.

So, there's many additional advantages using CO2. First of all, CO2: non-allergenic. So, if you have the contrast allergy history of patient, you do not need a sterile preparation. And CO2 is non-nephrogenic,

therefore you can inject the unlimited volume of the procedure, particularly in a complex procedures, and you can use CO2 for both patient, with, without the renal failures. And the CO2 has a very low viscosity.

We talk more about this, this is unique property to allow you to inject CO2 with small pore system, even 25 gauge needle and three French microcatheter. They give a tremendous flexibility when you're doing a procedure. And central reflux,

central reflux, that means, if you inject it distally and CO2 flow backward, the CO2 flow two direction, antegrade as well as retrograde, whereas contrast flow is only antegrade. So that give you additional information

you will see for endovascular interventions. And CO2 is very inexpensive. The tank costs $600, which will last three, four years, but if you use contrast, it may take several million dollars for the contrast budget. And we currently using the plastic bag system.

The bag is filled with CO2 from the tank. You have to have a clean tank, not large, laboratory tanks. CO2 USP, and fill up, then empty several times through the micro filters, and they have connecting system

that have multiple one-way valves. You make two connection between the bag and the collecting system right here, and also here. Those two connections be made by operators, but if you're doing this, you have to make sure these two connections properly connected.

If you have misconnection or disconnection during the procedure, basically you are sucking the air from the room, and then you can get a catastrophe. So it's very important to check them. The way you check, you close the stopper here and aspirate the injection syringe,

you should not be able to fill the syringe. And if you do this, absolutely safe techniques. And there's another device called CO2mmander available on the markets. This is FDA approved and also convenient.

And you can see CO2 floating, called buoyancy. This is CO2, about 20cc in the aorta. You can see, only you'd see about 30% of the ante part of the lumen. Here is the artist's rendition, you can see the renal artery will not fill

because of buoyancy, that's where you turn the patient from side to side depending upon the location of the renal arteries to fill it. And you can take advantage of the buoyancy on the median arcuate ligament compression syndrome,

because celiac SMA originated from the ventral aspect, so the CO2 naturally fills those branches. You need about 10 to 15cc. Here median arcuate ligament compression during expiration, and then inspiration give relief. So CO2 is much better way

to evaluate median arcuate ligament compression syndrome than contrast. We take close-up lateral view. If we inject the contrast in celiac stenoses, you see the flow defect from GDA because reversal, but if you inject the carbon dioxide,

you should get the antegrade flow. That's why the CO2's very (mumbles), and you can see both vessel, antegrade and retrograde. So, when you do CO2 renal angiogram, you already see to some positional change. In this case, you have the left side up

to fill the left renal artery. Sometimes you inject selective injection retrograde flow, but you can do even extreme cases of the left side up, completely, and then take closer lateral view to visualize. When you do CO2 angiogram for the patient

with the aneurysm, the aortic aneurysm, watch out for the trap. Once it's trapped and becomes high, CO2 partial pressure gas exchange takes place between nitrogen and carbon dioxide. You can potentially occlude your diameter

with nitrogen, causing ischemic colitis. In the aortoiliac occlusion, you can see beautiful pictures. CO2 flow backward, antegrade, you can see outflow studies and you can inject the CO2 into the SFA in retrograde so you can see the proximal vessels,

and when you do renal arteriogram, you'd advance the microcatheter more distally and then try reflux back toward the orifice to visualize renal arteries. And when you have motion artifact like this from peristalsis,

you can do a focal new mask, and you can get clean up the vessel with post-processing. When there are multiple irregularities with redundant tortuous (mumbles) to tend to flow more, dependent, non-dependent part, you do stacking technique, you can get beautiful pictures.

If you don't know how to do this, everybody will complain, "the CO2 (mumbles) is bad." And when you have multiple stenoses like this, it looks like a stenosis in frame orientation of the gas, we can do stacking here,

continuous column with the CO2, so you get the post-processing to make a better pictures. And CO2 guided intervention, for the SMA stent is good, renal stentings, and renal transplant, and the femoral artery occlusions

with the CO2 guided intervention, you can do all this with CO2 guided without any contrast. Many of these, at present, high risk. And one of my colleagues doing it at the University of Michigan, you can do a CO2 guided EVAR procedures shows very...

So I'd like to summarize that my presentation is giving the tips and trick for CO2 intervention angiography, you can see all this. Do not use CO2 above diaphragm. Do not inject cerebral coronary in the thoracic aorta.

And use closed system, and CO2, use end-hole catheter for delivering. You don't need a pigtails. And inject more selectively to get a better pictures, and reduce motion and taking fast exposure, get additional mask for the subtraction, using new mask,

and elevate the imaging area, so you can use a vasodilator for the lower extremities, and use the CO2 reflux technique, they will give a much better picture when you inject more antegrade. And the postprocess with new mask and stacking

is very important. Thank you.

- [Doctor] Mr. Chairman, dear colleagues, I have nothing to disclose. My only disclosure is that I might be recognized as being ambassador of one of the most beautiful region of the world. So ruptures of abdominal aortic aneurysms into the vena cava or into the iolaco veins

are rare clinical entities. The symptoms are those of ruptured aneurysms together with signs of congestive heart failure, or leg swelling. The diagnosis is often made clinically or confirmed by CT scan, as in this example.

The reported results of treatment were earlier more focused on open repair. During the last years, more and more papers advocated endovascular treatment showing lower mortality, but all these studies performed as cohort analyzers or in case reporters have poor evidence level.

The recommendation, however, seem to favorize clearly the endoscopic option showing lower mortality rates overall. If you treat an aortic AV fistula as in this example, with a shunt into the left iliac vein using a first step, a unilateral left sided

bifurcated scent craft. Here you see the case. And then the reconstruction after two days with the contralateral bifurcated graft, and an aortal biolextent graft, and the postop CT scan, then shows no evidence of Type I endoleak,

and no persistent AV fistula. The problem of course, seems to be resolved. You have no persistent AV fistula. But not in all cases, as shown in this example, the eventual Type II endoleak are isolated from the AV fistula, so if you have

the situation with the successfully fixed aneurysm on one hand, but a Type II endoleak in combination with the fistula in the cable vein or in the aortic vein on the other hand, what are you doing now? In the persistent AV fistula,

for Type II endoleak, in this very special situation, really is this really a bad thing or is it eventually helpful for aneurysm shrinking, and what about the clinical evidence of ongoing AV shunt? This is such an example of a patient with chest pain having had a syncope

with a CT scan showing the contrast media in the vein already in the early phase, as shown in this picture. In the lateral view and also in the transverse section, you see the fistula, obviously, despite very kinked aortic arteries in this example.

This was all done by IVAR pEVAR, and beside these very kinked arteries on both sides, the intervention could be done successfully by percutaneous approaches on both side. The intraoperative angiography, as you might see on the next slide,

showed initially the fistula in the vena cava and finally the Type II endoleak is still visible. Ilioac and lumber arteries, and the inferior mesenteric artery were responsible for the endoleak, as you can see here, but the patient showed an immediate relief

of all symptoms, and he could be discharged. After three months, the aneurysm sack shrinking was remarkable, and this continued also after nine months. It was shown that still the endoleak was obvious and the fistula was persistent, but the patient had no symptoms.

So what about these persistent AV fistulas? Should we treat them, for example, by venous sealing, as recommended by a few authors? No complication of strombosis of the venous stent grafts are reported, and together with other groups, we recommend clearly not to do this,

and to make any effort and not to make any efforts to close the fistula when it's in combination with an endoleak Type II. The same observation was made here by Ferhaugae, a few years ago, and in this further study by Malina, one year ago.

They all stated despite, you could also say, it was rather mean, thanks to the AV fistula that was shrinking. So in conclusion, Mr. Chairman, after own experience, and after studying the literature. Can you go back, sorry?

And studying the literature, we are all convinced that EVAR as the preferred option in ruptured triple a with AV fistula, venous ceiling on treating the endoleak Type II should not be aimed. In contrary, in endoleak Type II persistent AV fistula might be helpful for aneurysm sack shrinking,

and peak pressurization of the aneurysm. Thank you.

- [Lu Qingsheng] I have no disclosures. We know for indication of EVAR we need favorable proximal neck anatomy but if it not unfavorable maybe we are some Type 1a endoleak it's a serious complication for EVAR. So for prevent and treat Type 1a endoleak

especial for some juxtarenal aneurysm maybe we use the chimney fenestration branch and some sac bag. Could we find a simple safe cheap and effective method? So we find from open surgery we were introduced this fibrin glue

means its complex of thrombin and fibrinogen, it's used hemostasis in open surgery so we put that into inject that into the sac, we call it fibrin glue sac embolization. I will show you some cases.

For this case is very short neck and not quality of deck and after deploy the stent graft, of course very serious Type 1a endoleak. But fortunately, we put a catheter before we deploy the stent graft so this catheter is into the sac of the aneurysm

then we use up a long controlled blood flow and we inject from the catheter into the sac of the aneurysm and we inject the fibrin glue. And you can find the contrast not moved after we withdraw balloon. Then we do the angiogram.

We find no any endoleak. Another case showed is angulated neck as this patient. Of course after we deployed stent graft have a lot of endoleak. And we do again this technique. And control the balloon, control the blood flow,

then inject the fibrin glue, and we check all that and withdrew the balloon, there are no any movement about the sac. And we do the angiogram and no any endoleak. Till now, we did, we begin this technique 2002, so we follow long time that we can show it's safe.

So till now we treat 156 cases and proximal less then short proximal neck is 75 cases even some of less than 10 millimeters. And angulation more than 60 degree even some cases more than 75 degree.

Most of them more than 98% of patients' endoleak was resolved. And during our follow up, the mean time more than 100 months, only three patients died of aneurysm related sac enlargement.

The mean maxim aneurysm diameter decreased and no recurrent Type 1 endoleak so we have confidence that it's safe and no any sealant-related complication for example renal failure and aplasia other things. So we discuss the mechanism

it's not only embolization for endoleak but also coagulating all sac of aneurysm like this in shows how it worked. And we also measure the pressure in the sac. Intrasac pressure decreased significantly in treated cases. And how about that technique we need occlusion

proximal blood flow and protect branch ateliers and prevent distal embolization. And we also treated into the rupture aneurysm and it can treat any type of endoleak as these cases it's a rupture aneurysm we do the EVAR emergency.

And after we deploy this devices, we find this endoleak. We don't make sure which kind of endoleak but anyway we just do that, control the blood flow use the balloon then inject the fibrin glue in that.

And all the sac of aneurysm. Then we do the angiogram and endoleak disappeared. We'll be treat any type endoleak of the rupture EVAR we prevent rupture post-EVAR and we decreased abdominal compartment syndrome. So the conclusion is

fibrin glue sac embolization is a simple and effective treatment method. And this method could expand the current indication of EVAR. For selective the length maybe can to the 5 millimeters, angle maybe can to the 90 degree,

and for emergency we seen it should be into the older EVARs for rupture aneurysms. Thank you very much.

- [Janet] Thank you very much indeed and again thank you to Dr. Veith for this invitation. On many debates, just try and mock the opponent, well I wouldn't dream of doing that to this opponent. Besides, I want to be straight and I just want to play a straight bat and tell you what the results are. And tell you what's new, the results have

actually been published during the course of this meeting on Tuesday in the British Medical Journal. You can read them if you don't want to listen to me. No disclosures. Despite what Thomas Larsen said, the patients who entered this trial were completely unselected.

The only selection criteria was that they might have a chance of being saved with a repair. They were diagnosed therefore before CT scan and therefore before the diagnosis of rupture could be confirmed. We had about 300 patients in each group

and we used an endovascular strategy since we haven't yet ascertain that these patients would be suitable for endovascular repair. In fact, about 2/3 of them were. Inavertibly some of these patients did not have a rupture, although 98% of the patients did have an aneurysm.

And the mean diameter of the aneurysms in each group was about eight and a half centimeters, they were large. The primary outcome was survival. And these are the survival curves shown here to six years, endovascular strategy in blue, open repair in red. At about three years, the survival curves

have the maximum differentiation. And at three years, 56% of the patients doing endovascular strategy was still alive, versus only 48% in the open repair group. That's for the 613 patients. If you take those patients that didn't die

before a repair and had a repair, the odds ratio now reduces to 0.62, a highly significant finding in favor of the endovascular strategy. Dr. Larsen complained about the crossovers. This was an emergency pragmatic trial. About 10% crossovers from each arm.

And the compliance analysis, the results are very similar to those for the 502 rupture repairs. As 30 days, at three years, the endovascular strategy remains much better for women. You can see that at 30 days, the mortality after EVAR in women was 24% versus 52% for open repair,

a much bigger differential than in men. And this early survival advantage for women is maintained at three years. What about re-interventions? The achilles heel of endovascular repair? Time to first re-intervention shown on the left.

Obviously, a rapid rate immediately after repair. But then it's a steady rate out to three years. And if you look at the time to the first re-intervention for a life threatening condition shown on the right, again a steady rate in the midterm, but if anything, slightly higher in the open repair group

than the endovascular strategy group. So the endovascular strategy group does not cost more in re-interventions. At a cumulative level over the three years, the endovascular strategy group also gains in quality of life, enhanced qualities.

This means that the endovascular strategy at three years costs less and is highly cost affective, far more cost effective than we first reported after 12 months. So in summary, at three years, it's becoming clear that the endovascular strategy is better than open repair with respect to mortality, similar

re-intervention rates, they gain in qualities, costs less, and is highly cost effective. How do we interpret these rather unexpected data? Well firstly I think immediately these unselected patients come in, shock kills. The endovascular strategy patients

get patients out of hospital quickly and we all know how good that is. We think that perhaps longest days on intensive care with a greater need for renal support is what increases the midterm mortality in the open repair group.

We would like to stress that an endovascular strategy still means EVAR for suitable anatomy. And if you do endovascular repair outside liberal IFU and particularly if you need a conversion to open repair, this is dangerous. And, as ever, always follow patients in the longer term.

There may be surprises. Thank you very much. (audience applauding)

now that you all have an overview and a refresher of nursing school and how these medications work in our body I want to now go over our practice

guidelines and the considerations that we take into place so as you know I'm not going to go over into detail the patient populations that are prescribed these meds but kind of knowing that these are the

patients that we see in our practice that for example are on your direct direct vector 10a inhibitors patients with afib or artificial valves or patients with a clock er sorry a factor v clotting disorder these oral direct

thrombin inhibitors patients with coronary artery thrombosis or patients who are at risk for hit in even patients with percutaneous coronary intervention or even for prophylaxis purposes your p2 y12 inhibitors or your platelet

inhibitors are your cabbage patients or your patients with coronary artery disease or if your patients have had a TI AR and mi continued your Cox inhibitors rheumatoid arthritis patients osteoarthritis vitamin K antagonists a

fib heart failure patients who have had heart failure mechanical valves placed pulmonary embolism or DVT patients and then your angiogenesis inhibitors kind of like Kerry said these are newer to our practice these are things that we

had just recently really kind of get caught up with these cancer agents because there really aren't any monitoring factors for these and there is not a lot of established literature out there knowing that granted caring I

did our literature review almost two years ago now so 18 months ago there is a lot more literature and obviously we learned things this morning so our guidelines are reviewed on a by yearly basis so we will be reviewing these too

so there is more literature out there for these thank goodness so now we want to kind of go into two hold or not to hold these medications so knowing that we have these guidelines and we'll be sharing you with you the tables that

tell us hold for five days for example hold for seven days some of these medications depending on why the patient is taking them are not safe to hold so some of the articles that we reviewed showed that for sure there's absolutely

an identified risk with holding aspirin for example a case study found that a patient was taking aspirin for coronary artery disease and had an MI that was associated with holding aspirin for a

radiology procedure they found that this happened in 2% of patients so 11 of 475 patients that sounds small number but in our practice we do about 400 procedures in a week so that would be 11 patients in one week that would have had possibly

an adverse reaction to holding their aspirin and then your Cox inhibitors or your NSAIDs as Carrie already mentioned it's just really important to know that some of those the Cox inhibitors have no platelet effects and then your NSAIDs

can be helped because their platelet function is normalized within 24 to 48 hours Worf Roman coumadin so depending on the procedure type and we'll go into that to here where we have low risk versus moderate to high risk

we do recommend occasionally holding warfarin however we need to verify why the patient is absolutely on their warfarin and if bridging is an option because as you learn bridging is not always on the most appropriate thing for

your patient so when patients on warfarin and they do not have any lab values available that's when you really need to step outside of guidelines and talk with your radiologists your procedure list and potentially have a

physician to physician discussion to determine what's best for a particular patient this just kind of goes into your adp inhibitors and plavix a few of the studies that we showed 50 are sorry 63 patients who took Plex within five days

of their putt biopsy they found that there was of those one bleeding complication during a lung biopsy so minimal so that's kind of why we have created our guidelines the way we did and here's just more information

regarding your direct thrombin inhibitors as cari alluded to products is something that we see very commonly in our practice and then your direct vector 10a inhibitors this is what we found in the literature

- [Jean] Thank you, Will, thank you again, Frank, for inviting me to your symposium. I'm going to talk to you about this concept of the value of EndoAnchors and TEVAR, and if you talk about that, basically, you need to figure out if we can predict TEVAR failure. So we published, last year, the creation of a novel

that makes a severity grading score to assess thoracic aneurysm and see if we can actually predict the patient that will not behave nicely with a simple TEVAR. Here's an example of two scores. Patient with an ASG score of 24

and the other one with an ASG score of 43. And the top of the ASG score is all the way up to 57 if you have all the worst characteristic that is applied to the different region of the thoracic aorta. So we found by doing a ROC Curve analysis

that an ASG score of 24 was actually the cut off, and below 24 was the low score group. And 24 and higher were patients with the really bad, challenging anatomy. And those patients had only a 69% freedom

from postoperative endoleak, requiring re-intervention at two years. So this novel anatomic severity grading score can actually really successfully identify patients that are at increased risk of endoleak requiring re-intervention

and then it would make sense in those patients to potentially apply for prophylactic EndoAnchors. And this is what we did in this next study where we looked at only patients with a high ASG score. So we had 63 patients with those high scores. 40% had only TEVAR and under the 20 patients

had TEVAR and prophylactic EndoAnchors as well. And if you look at those patients that only had TEVAR and bad anatomy, we had a 58% chance of freedom from aortic related re-intervention at three years. The 62% freedom from Type I endoleak at three years.

But when you place prophylactic EndoAnchors you end up with an excellent result with 95 to 100% survival free from any of those two kind of problem. So this would be the value in using EndoAnchors and these are better to me now. The technique for the thoracic EndoAnchor

and compared to the abdominal is that we have the selection of three potential active guide size, 22, 32, 42. And we size it according to the size of the endograft. I say as an example of a patient with challenging anatomy that was the patient with the ASG score of 43. This patient had a hemiarch debranching

and then we went ahead and deployed the endograft and deployed the EndoAnchor at the inner arch. This is the completion angiogram after those prophylactic EndoAnchors. And there is no endoleaks at two years. This patient is now currently at over three year follow-up

no migration and no endoleak, despite an extremely challenging anatomy. You can also have another prophylactic indication is to prevent upward migration. If you look at the tapering of the thoracic endograft right above that celiac artery,

this is really an area that in fact in the Valor II trial, has really showed that a lot of patient have Type 1B endoleak after a few years. And by using circumferential placement of those EndoAnchors at the distal end of the TEVAR,

you can really prevent this upward migration and endoleak 1B formation. Now the technique it's really about the angle of attack. I think if you have a bad angle of attack, you will not be able to deliver properly. But when you have a real 90 degree perpendicular attack

of the endograft this is how you can safely deploy those EndoAnchors in the thoracic aorta. This is a deployment of the ascending aorta in an RAO view, so you can not only deploy at the inner curve, but you can also deploy EndoAnchor on the interior or posterior aspect of the arch

by deploying anchors with these special view with the barrel. When you look at the outer curve of the arch, this is an easy Zone 1 delivery. This is a more tricky Zone 1 delivery, but it also possible to deploy EndoAnchors

in the outer curve. Same thing when we have the sternum open to do a total arch debranching, we can deploy EndoAnchors in an antegrade fashion in Zone 0 and obtain also great result. Top 10 tips for EndoAnchors.

First is take the time for preoperative planning. Second one is wishful thinking will not create the landing zone. Sometimes you have to do some debranching to obtain a landing zone. Deliver the endograft accurately.

Do the aortic balloon molding first. You have to size the Aptus guide according to the endograft size. You have to undersize it when you want to use it at the level of the outer curve of the arch. You deploy two rows in TEVARs.

I always deploy three rows in arch because of the increase in hemodynamics at that level. I think a good place to learn to do TEVAR and EndoAnchors is the distal end near the celiac artery. And never start a challenging TEVAR case without EndoAnchors.

So in summary, EndoAnchors in TEVAR are done in imperfect landing zones, improve outcomes by decreasing Type I endoleaks and the need for aortic reinterventions. Safe and effective deployment of EndoAnchors really relies on simple techniques, device selection,

and the knowledge of the failure modes of doing TEVAR in those challenging zones. Thank you.

Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.