- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.
They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression
if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.
Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.
This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,
and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients
who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,
and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,
symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.
There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,
again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,
six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,
it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse
if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective
in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.
This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent
because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common
in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.
So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,
those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,
like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.
And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,
get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.
If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners
over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,
it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,
look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.
That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,
then I would do something endovascular. Thank you.
- Well Mr. Chairman, dear friends, last year was here on the same stage for discussion of the results of the EVAR 1 trial and trying to tell you that the results of the EVAR 1 trial were no longer valid and this year I'll try to do the same for the EVAR 2 trial. The EVAR 2 trial was a randomized control trial
conducted in the UK in 33 centers with enrollment between 1999 and 2004. It was a randomized trial in which the patients were randomized between conservative treatment and open treatment and the common ground for the study was that these patients were unfit for open repair.
What is unfit for open repair in the EVAR 2 trial? Well the decision was made from three criteria. Cardiac reasons were the main reasons to consider patients as being unfit. Respiratory and renal reasons are the criteria that were used.
There have been several publications on this trial showing a design of the trial, the preliminary results, the final results in our recently last year, the very long results with this trial. And what are the results? Well as you can see here, it was a statistically
significant difference in aneurysm related mortality between the patients treated with EVAR and those treated conservatively but there was no difference in overall total mortality and this led us to the conclusion that indeed there was not really a place in those EVAR in those patients unfit for open repair.
However, we might look more closely to these results. The first thing in this trial is that almost 10% or more than 10% of the 197 patients that were randomized for EVAR actually did not receive the EVAR procedure because they died prior to the intervention and what was the reason for this?
Well the mean time between randomization and EVAR in this study was two months and in a quarter of the patients, it was even three months. The nine ruptures that occurred before the intervention had taken place. Actually it'd be more than half of
the aneurysm related mortality in this group. Another striking observation was that those patients that had no intervention, 1/3 of these actually were treated with EVAR in the followup period. And when we look at the results, whether it's observation-influenced results,
well you see when we perform a vertical analysis, the difference in aneurysm related mortality was even bigger and also there was a clear trend towards improved overall survival. Although this was not significant and therefore, the author still remains to the conclusion
that there was no place for EVAR in these patients. Looking again closer to the results and looking specifically at the patients with no intervention, already in 2009, there was more than half of these patients in this group actually were patients that already had EVAR.
And even worse, in 2015, of the 13 patients in this group that still survived, there was only one, yes only one, that did not have an EVAR procedure. So it's clear for me that only patients with EVAR actually survive.
Why are the results no longer valid either? Well this study was performed in 1999 up to 2004 and it's clear from further studies, just one example, that the results in the meantime have clearly improved from 1999 to 2004. While it wasn't the Stone Age for EVAR,
it was not more than Middle Ages. Plus mortality clearly improved with time and then when you look at the results of this trial, the 5.7% operated mortality in the EVAR group are actually at this moment no longer standard of care when you compare to these three other studies
which actually use the same criteria for considering patients that's unfit for open repair. Also we've got longer term survival. The mortality of 40% after, no, no, 60% after 40 as in 80% off of JVS can no longer be considered really as up to date results and probably the reason for that
is also the fact that medical treatment upstream in these optimal patients as only 40% statins. So are EVAR 2 results still valid? I think it's clear they are not. It's an old study with old devices. The mortality is not conform to actual standards.
Medical treatment was not optimal. The delay in treatment caused preventable deaths. More than 1/3 of the patients crossed over and the statistical analysis does not reflect the actual treatments of the patients. Does this mean that we should operate on all patients?
Well, maybe not. This is a very recent study published earlier this year in logical patients and you see that when some, certainly once several of the risk factors were considered being unfit patients were present, that results were indeed worse,
especially when there is renal insufficiency. The IR for the SVS guidelines correctly state that it is just to inform high risk patients over their risk status and their mortality score and then making an informed decision whether we should proceed with aneurysm repair or not.
It's my personal opinion though that clinical judgment is probably the most important factor in this decision making process. Thank you for your attention.
- [Presenter] Thanks Bill. And again I have no disclosures to make on this particular presentation. So, in terms of variance, the anterior accessory GSV is not a variant. It's present in most of us, but it's an unusual cause of primary varicose veins,
although a very common cause of secondary varicose veins after primary treatment. It runs parallel to the great saphenous vein, in the saphenous space, and courses a bit more anteriorly in the thighs, so that on ultrasound, you'll see a lining here,
in this case inside the saphenous space, aligning with the superficial femoral artery and the femoral vein. In some cases, it can be the primary saphenous vein along the medial aspect of the thigh, in association with hypoplasia of the great saphenous vein
as listed on the left, and the right picture with aplasia of the great saphenous vein. And many times physicians are treating what they think is the great saphenous vein, and really it's this embryologic variant,
the anterior accessory vein, with a different takeoff. A different vein to talk about in terms of variance is the superficial accessory saphenous vein. It's present in many patients. It's really a tributary of the great saphenous vein,
running in the subcutaneous fat outside the superficial fascia that eventually joins into the great saphenous vein. So on this longitudinal view, it creates this sort of appearance with the great saphenous vein below its entry
as a smaller caliber vein. Consequently, it has the name of the H-vein, and on ultrasound, below the level of its joining with the great saphenous vein, the great saphenous vein is small,
and in this particular case with varicose veins, associated with reflux in the superficial accessory saphenous vein. It's a larger caliber, and then up higher, you can see that it drains into the great saphenous vein, and it's no longer visible.
The small saphenous vein has a lot of variability related to the differences in its termination on the posterior aspect of the calf and the thigh. Many patients have what we can call saphenopopliteal junction dominant drainage, and other patients have what we might consider
thigh extension dominant drainage. It's a spectrum, most patients have these connections, and if you look carefully, you'll find the thigh extension connection even in the majority of patients that have primarily saphenopopliteal junction termination.
The termination higher on the thigh can be into a perforator on the back of the thigh, it can be into the gluteal venous system in the pelvis, and it can travel up through an intersaphenous or Giacomini vein toward the inner thigh,
and sometimes to the great saphenous vein. Duplications of the deep system are very common, particularly in the femoral vein in up to 20% of the patients. Isolated popliteal vein duplications are uncommon, but in association with femoral duplications
occur in up to 6% of the variations. These duplications all travel through the adductor canal and follow the normal course of the vein. In contrast, remnants of the sciatic vein can introduce different variants. The sciatic vein is an embryonic vein
that was the primary drainage of the lower limb in a very small fetal stage. At some point, most of it regresses, and so the popliteal vein, which is the sciatic vein remnant, eventually connects up with the pelvic circulation
through the common femoral vein and the external iliac vein which develop later. The saphenous remnants regress, with the exception of the popliteal vein, and portions of the internal iliac vein. A true sciatic vein variant is a less common variant,
where the popliteal vein is in continuity with a large caliber vein that follows the sciatic nerve up into the pelvis, draining into the internal iliac vein. But in contrast, sciatic vein remnants are not uncommon,
and it's not unusual for one to find the primary drainage of the popliteal vein not going through the adductor canal, but to ascend upward variable lengths along the course of the sciatic vein, to eventually terminate either in the femoral vein directly
or into the deep femoral vein up higher, with or without hypoplasia, or in rare cases, aplasia of the femoral vein. And so it's important to recognize these variants in distinction to post-thrombotic changes
in the femoral vein. When you have a small vein, that small vein can be normal anatomically by all other features, and may represent a variant rather than a post-thrombotic complication.
And this was recognized by Dr. Raju in 1991 in a publication where he demonstrated venograms in a patient with a post-thrombotic femoral vein, and well-formed collaterals between the popliteal vein and the profunda, in contrast to this patient,
which had no post-thrombotic changes in the femoral vein, but well-defined congenital variation connections between the popliteal vein and the deep femoral vein. So in summary, superficial venous variability is related to the variable terminations
of the small saphenous vein, the anterior accessory saphenous vein, which is inside the saphenous sheath, superficial accessory saphenous veins, which are outside the saphenous space. It's important to recognize deep vein variablity,
'cause you want to avoid false negative diagnoses of acute deep vein thrombosis by not recognizing thrombosis in a duplication, and you want to avoid false positive diagnoses of post-thrombotic syndrome
- So this talk is similar to Professor Vermossin in that we're trying to establish again the idea that EVAR is really the choice of treatment here, especially for patients who can't undergo an Open Repair. I have no disclosures. So why does this even come up? Well, as we know the DREAM trial very nicely elegantly
show that early on there was a mortality benefit of EVAR over Open Repair, but out to two years that mortality benefit was lost and the curves began to meet and equilibrate. And when you look at the EVAR 1 study, when you get out to eight years,
those curves actually invert and the all cause mortality for Open Repair was actually beneficial as compared to EVAR. And so it becomes a question, based on somebody's RCT or whether or not Open Repair is really the better way to go. But at least for this discussion we're talking about
a select group of patients. Those patients who are unfit for Open Repair. Multiple comorbidities, high frailty index. Totally different population than the overall cohort. And so when you go back to EVAR 1 and you look at it, these patients, these frail patients,
lot of comorbidities. They're the ones who would exactly benefit from that early aneurysm or early all cause mortality benefit from EVAR, 'cause these are the patients that may not life to meet that eight year crossover point.
In addition, there's been a lot of temporal changes in terms of EVAR. There's evolving technology and there's evolving techniques. The devices are lower profile. They have better durability.
It's easier and more precise in terms of delivery and implantation for these devices as well now. Moreover the techniques have evolved significantly. We're doing almost all these percutaneously. There's very rarely a situation where you need to cut down. The procedures are done very quickly now.
A lot of them are done in less than an hour. And there's avoidance at least of major pitfalls, I mean, the last time I've heard about an iliac artery disruption was probably five or six years ago. This type of large complication rarely occurs anymore. And this study from the Mayo Clinic corroborates this.
When they look at their series of patients who had Open Repair and EVAR, the top graph is basically those patients who were treated from 2006 or earlier. The bottom graph is the patients treated from 2005 or later. And you can see the mortality benefit from Open Repair basically disappears in the lower graph
and that cohort that's treated later. Again, kind of corroborating that techniques and devices have changed, improving EVAR's survivability. And this paper looks at the NSQIP database and says basically the same thing. That contemporary 30 day mortality after EVAR
in high risk patients is substantially lower than that reported in EVAR 2 trial. So gain, demonstrating and showing a picture of EVAR with better survivability and the data that's come out from these earlier trials in terms of EVAR mortality is not necessarily translatable to current day.
So, what we are expecting for EVAR? Well, I think really, two things. You want prevention of death from the aneurism and you want a quality of life. I mean, quality of life is important. These patients come in and expect to be able
to be back on their feet shortly after the procedure. And when you look at the EVAR 2 long term survival, aneurism related mortality is improved over Open Repair out to 12 years. And then when you look at the improved data, the quality of life was significantly better
for EVAR versus that of Open Repair. But I wanted to just kind of get you to shift and look at it from a different perspective and not just see it from what EVAR is in terms of beneficial, how it's changed and how the survivability is improved.
But really what are the expectations in terms if Open Repair? What is the patient tolerance? What are the training and what are the volume paradigms in today's day and age? Well clearly, when you look at these two things
percutaneous, especially the access to the groin, is going to be infinitely better tolerated than an open incision, whether it be transperitoneal or retroperitoneal. So clearly there's a benefit of EVAR in terms of that. But more importantly, we know that the,
historically we've shown that high volume centers and high volume surgeons have better results for Open Repair. And without question, the more you do, the better you're going to get at it. And so, when you look at that in conjunction
with these types of data where clearly the numbers of Open Repair through the country are reducing dramatically and continue to decline. We looked at this and this was a slide of EVAR, which was the positive slope, and Open Repair, which is a negative slope,
in terms of trainees graduating. And that ended in 2010. That slope continued to be negative. When you put those two together, you realize that people are coming out with less and less Open training.
Their experience with Open Repair is only declining and when you contrast that with EVAR, which is improving technology and techniques, it becomes obvious that in certain circumstances I think the randomized control data can no longer be looked at and you have really just think about
EVAR as the best treatment for these patients. Thank you.
- Well thank you and um, it's kind of a how to do it, how to tie your shoes type talk. And clearly now that these venous assessment tools have been present for more than two decades. It has created a common landscape for communication, for comparing outcomes.
And with that common language we really have a good guide of what to use. So. From a favorable standpoint you know the CEAP. And this is the revision from 2004. Really established good classification
across the clinical, etiologic, anatomic, pathophysiologic categories. And certainly with the clinical side of things, that really has taken off. Where the EAP has been more on the research side. But with this common language has come the ability
to communicate like versus like. And clearly if you look at the clinical classifications system. There's a clear line drawn really from C4 and greater, and some would include C3. Versus the C 1&2 in terms of disease severity.
And I think we're all familiar with classifications. But these are very categorical type classifications. And you know if you look at population based studies, certainly the c1 2 category counts for most. Where C3 is about 15% of population, and C4 grade are anywhere from 3-5% of the population.
You know the upsides of CEAP it's really proven to be effective in assisting in evaluation of various treatment modalities. Allows comparison of results from different institutions using universal language. It's really enhanced our understanding with these categories
of potential etiologic factors. And by doing so it's improved the scientific standards in the evidence. And allows for meaningful research and comparison of cohorts. Bu there's certainly some limitations to CEAP.
There's a degree of complexity that makes utilization difficult across all spectrums of clinical care. It's limited as a severity classification system, in that it's relatively static. And then even with improvement there's sometimes a little change that happens within the categories.
There's lack of reversibility. There's some problems with differentiation especially when you look at the clinical categories. Varicose veins, edema, and such. Clinical use of C category has been widely adapted. Where there's more limited use of EAP.
And really has raised the need and question to freshen up CEAP with reclassification. So over the last year or so, there's an American VF formed task force. Which has been tasked with revising CEAP. And I apologize I can't present the information just yet.
Because it's still under modification and maybe next year we'll have the revised CEAP classification to promote. With that in mind the Venous Clinical Severity Scoring came in behind CEAP. As a more sensitive scale to determine changes in treatment,
and it's really meant as a compliment to CEAP. And it has both clinical utility and research applications most recently revised in 2010. And again most of us are familiar with VCSS. In that it's several attributes that are rated across the spectrum of severity from 0-3.
From the standpoint of the revised system. It has been studied and it has been shown to have good inter and intra user reproducibility. Which is important in that it makes it consistent across users. And if you look at Michael Vasquez's publication here.
It shows a good practical use of both CEAP and VCSS. And that in this particular patient with some hemosiderin, a pigment change, a C4 category. When you plug in the VCSS it's a 15. And then after treatment there's still a C4,
but there VCSS fell to 11. And similarly the same patient here who starts with a CEAP of six and VCSS of 27. And then across the spectrum of treatment, still is a V6 about mid-treatment, but has improved to VCSS of 19.
And then after completion of treatment the best they can get is going from a C6 to a C5. But they're VCSS is now 5. And most of the benefit comes with pain, varicosity, and edema.
That's where you see most of the change in VCSS. And certainly the guidelines support the use of CEAP. This is varicose vein guidelines where the basic of more for clinical practice than the full CEAP for research. And same thing with the venous ulcer guidelines.
And I'll just leave you with this app which you can pull up on your phone. SVS iPG. Which actually has CEAP and VCSS embedded so you can have it at the bedside. Or you can embed it in your clinical templates.
So in conclusion yes they're helpful. There is no one universal tool but certainly both CEAP and VCSS used together, do achieve the needs of what they're intended to do. There's certainly some improvements that will be forthcoming with CEAP.
And I thank you.
- Thank you very much for the presentation. Here are my disclosures. So, unlike the predecessor, Zenith Alpha has nitinol stents and a modular design, which means that the proximal component has this rather gentle-looking bear stents and downward-looking barbs.
And the distal part has upward-looking barbs. And it is a lower-profile device. We reported our first 42 patients in 2014. And now for this meeting we updated our experience to 167 patients operated in the last five years.
So this includes 89 patients with thoracic aneurysms. 24 patients in was the first step of complex operations for thoracoabdominals. We have 24 cases in the arch, 19 dissections, and 11 cases were redos. And this stent graft can be used as a single stent graft,
in this case most of the instances the proximal component is used or it can be used with both components as you can see. So, during the years we moved from surgical access to percutaneous access and now most of the cases are being done percutaneously
and if this is not the case, it's probably because we need some additional surgical procedures, such as an endarterectomy or in cases of aorto-iliac occlusive disease, which was present in 16% of our patients, we are going to need the angioplasty,
this was performed in 7.7% of cases. And by this means all the stent grafts were managed to be released in the intended position. As far as tortuosity concerned, can be mild, moderate, or severe in 6.6% of cases and also in this severe cases,
with the use of a brachio-femoral wire, we managed to cross the iliac tortuosity in all the cases. Quite a challenging situation was when we have an aortic tortuosity, which is also associated with a previous TEVAR. And also in this instances,
with the help of a brachio-femoral wire, all stent grafts were deployed in intended position. We have also deployed this device both in chronic and acute subacute cases. So this can be the topic for some discussion later on. And in the environment of a hybrid treatment,
with surgical branching of the supoaortic tranch, which is offered to selected patients, we have used this device in the arch in a number of cases, with good results. So as far as the overall 30-day results concerned, we had 97.7% of technical success,
with 1.2% of mortality, and endoleaks was low. And so were reinterventions, stroke rate was 1.2%, and the spinal cord injury was 2.4%. By the way we always flash the graft with CO2 before deployment, so this could be helpful. Similar results are found in the literature,
there are three larger series by Illig, Torsello, and Starnes. And they all reported very good technical success and low mortality. So in conclusion, chairmen and colleagues, Zenith Alpha has extended indications
for narrow access vessels, provide safe passage through calcified and tortuous vessels, minimize deployment and release force, high conformability, it does retain the precision and control of previous generation devices,
however we need a longer term follow up to see this advantages are maintained over time. Thank you very much.
- So thank you to the organizers and to Dr. Veith, and thank you to Dr. Ouriel for giving me the introduction of the expense of an unsuitable procedure for pain patients. We have no disclosures.
I think when you look at MRV or Venous interventions, you can look at it as providing you a primary diagnosis, confirming a diagnosis if there's confusion. Procedural planning, you can use it as a procedural adjunct,
or you can use it as a primary procedural modality. In general, flow-dependent MRI has a low sensitivity and a slow acquisition time, making it practically impractical. Flow-independent MRI has become more popular, with sensitivity and specificities
rounding at 95 to 100%. There's a great deal of data on contrast-enhanced MRI, avoiding adanalenum using the iron compounds, and you'll hear later from Dr. Black about Direct Thrombus Imaging. There has been significant work on Thrombus Imaging,
but I will leave it up to him to talk about it. MR you can diagnose a DVT, either in both modalities, and you can see here with the arrows. It will also provide you data on the least inaccessible areas for duplex and other modalities,
such as the iliac veins and the IVC, as can be seen here. It is also perhaps easier to use than CTV, because at least in my institution CTV always comes out as a CTA, and I can't help that no matter what happens.
MR can also show you collaterals, which may be very important as you are trying to diagnose a patient. And in essence it may show you the smaller vein that you're more interested in, particularly in pelvic congestion syndrome,
such as this patient with an occluded internal iliac vein. It can also demonstrate, for those of you who deal with dialysis access, or it's central line problems, central venous stenosis and Thrombus. But equally importantly
it may show you that a stenosis is not intrinsic to the wall, but it's actually intrinsic to extravascular inflammation, as in this patient with mediastinal fibrosis, and which will give you a different way of what you wish to do and treat.
The European guidelines have addressed MR in it's future with chronic venous disease and they give it a 1C rating, and they recommend that if doesn't work you should proceed to Ibes. It can be used for the diagnoses of pulmonary embolism,
it can eliminate the use of ECHO, one can diagnose both the presence of the Thrombus, the dilatation of the ventricul, and if one is using Dynamic MR Imaging one can also see mcconnell sign or the equivalent on the septum between the two ventricles.
More interestingly it can also be used now in the chronic thrombuc, pulmonary hypertension, where it can show both the legions that are treatable and untreatable, as some of you may have heard from Dr. Roosevelt
earlier in the day, where they're now treating the outlying lesions with balloon angioplasty serial sessions. It can also look at the ventricul and give you some idea of where the ventricul stands with regard to it's performance,
we're looking at and linking this to the lungs. It can also show you the unusual, such as atresia of the IVC or it can help with you the diagnosis of Pelvic Congestion Syndrome. And it is extremely valuable
in dealing with AVM's, although it may take one, two, or three sessions with differing contrast bulosus to identify both the arterial, the intrinsic lesion, and the outflow lesions,
but a very valuable adjunct. In renal carcinoma it has two values, one is that it can may diagnosis venous invasion, and it may also let you understand whether or not you are dealing with bland thrombus or tumor thrombus,
which can change the staging for the patient and also change the actual intervention that you may perform. If you use flash imaging one will get at least an 89% sensitivity of the nature of thrombus,
whether it's bland or tumor thrombus, which may change what you need to do during the procedure. It could also tell you whether there's actual true wall invasion, which will require excision of the IVC
as opposed to the simple thromboendarterectomy. And this can run up to a specificity of 88% to exclude it. In the brain it's commonly used to diagnose the intra tumor vasculature. Diagnosing between veins and arterial systems, which can be helpful
particularly if one is considering percutaneous or other interventions. With regard to central venous stenosis there is some data and most people are now using an onlay technique where they take the MRI,
they develop the lines for the vessels and then use that as guide in one or two dimensions with fusion imaging to achieve access with a wire, catheter and balloon, as opposed to a blind stick technique.
There is data to show that you can image with the correct catheter balloons within the vessels and do serial MR's to show that it works. And finally with guidance catheters EP is now able to guide the catheter further and further in to achieve from the,
either the jugular or the venous access across the septum and to burn the entrium as appropriate. And finally, one can use MR to actually gain access, burn, and then actually use the MR to look at the specific tissue,
to show that you've achieved a burn at the appropriate area within the cardiac system and thus prove that your modality has achieved it. So in summary, we can use it for primary diagnosis, confirmatory diagnosis,
procedural planning, and procedural adjunct, but we're only still learning how to use it as a primary procedural modality. Thank you so much.
- Rifampin-soaked endografts for treating prosthetic graf y work? I have no conflicts of interest. Open surgery for mycotic aneurysms is not perfect. We know it's logical, but it has a morbidity mortality of at least 40% in the abdomen and higher in the chest.
Sick, old, infected patients do poorly with major open operations so endografts sound logical. However, the theoretical reasons not to use them is putting a prosthetic endograft in an infected aorta immediately gets infected. Not removing infected tissue creates
an abcess in the aorta outside the endgraft and of course you have to replace the aorta in aorto-enteric fistulas. So, case in point, saccular aneurysm treated with a TEVAR and two weeks later as fever and abdominal pain.
You start out like this, you put an EVAR inside you get an abcess. Ended up with an open ilio-celiac open thoraco with left heart bypass. Had to sew two arches together. But what about cases where you can't
or you shouldn't do open? For example, 44 year old IV drug user, recurrent staph aureus endocarditis, bacteremia, had a previous aorto-bifem which was occluded, iliac stents, many many laparotomies ending in short bowel syndrome and an ileostomy.
CT scan and a positive tag white cell scan shows this. It's two centimeters, it's okay, treat it with antibiotics. Unfortunately, 10 days later it looks like this, so open repair. So, we tried for hours to get into the abdomen. The abdomen was frozen and, ultimately,
we ended up going to endografts so I added rifampin to it, did an aorta union and a fem fem and it looked like this and I said well, we'll see what happens. She's going to die. Amazingly, at a year the sac had totally shrunk. I remind you she was on continuous treatment.
She had her heart replaced again for the second time and notice the difference between the stent at one year to the sac size. So adding rifampin to prosthetic Dacron was first described in the late 1980's and inhibits growth in vivo and in vitro.
So I used the same concentration of 60 milligrams per milliliter. That's three amps of 600, 30 CC's water injected into the sheath. We published this awhile back. You can go straight into the sheath in a Cook.
Looks like this, or you can pre deploy a bit of little Medtronic and sort of trickle it in with an angiocatheter. So the idea that endografts in infected aortas immediately become infected, make it worse. I don't think it's true.
It may be false. What about aorto-enteric fistulas? This person showed up 63 year old hemorrhagic shock, previous Dacron patch, angioplasty to the aorta a few years ago, aorto-duodenal fistula not subtle. Nice little Hiroshima sign
and occluded bilateral external iliac arteries. Her abdomen looked like this. Multiple abdominal hernias, bowel resections, and had a skin graft on the bowel. Clearly this was the option. I'm not going to tell you how I magically got in there
but let's just leave it at that I got an endograft in there, rifampin soaked, sealed the hole and then I put her on TPN. So the idea that you have to resect and bypass, I'll get back to her soon, I think it's false. You don't necessarily have to do it every time. What about aorto-esophageal hemorrhagic shock, hematemesis?
Notice the laryng and esophageus of the contrast, real deal fistula. Put some TEVARs in there, and the idea was to temporize and to do a definitive repair knowing that we wouldn't get away with it. On post update nine, we did a cervical esophagostomy
and diverted the esophagus with the idea that maybe he could heal for a little while. He went home, we were going to repair him later, but of course he came back with fever, malaise, and of course gas around the aneurysm and we ended up having to fix him open.
So the problem with aorto-enteric fistulas is when you put an endograft in them it's sort of like a little boomerang. You get to throw them out and it's nice and it sails around but in the end you have to catch it. So, in the long term the lady I showed you before,
a year and a half later she came back with a retroperitoneal abscess. However, she was in much better shape. She wasn't bleeding to death, she'd lost weight, she'd quit smoking. She got an ax-bi-fem, open resection,
gastrojejunostomy and she's at home. So, I think the idea's, I think it's false but maybe realistically what it is, is that eventually if you do aorto-enteric fistulas you're going to have to do something and maybe if you don't remove the infection
it may make it worse. So in conclusion, endografts for mycotic aneurysms, they do save lives. I think you should use them liberally for bad cases. It could be a bad patient, a bad aorta, or bad presentation. Treat it with antibiotics as long as possible
before you put the endograft in and here's the voodoo, 60 milligrams per mil of rifampin. Don't just put in there, put it in with some semblance of science behind it, put it on Dacron, it may even lead to complete resolution. And I've also added trans-lumbar thoracic pigtail drains
in patients that I literally cannot ever want to go back in. Put 'em in for ten days wash it out. TPN on aorto-enterics for a month, voodoo, I agree, and I use antibiotics for life. Have a good plan B because it may come back in two weeks or two years, deploy them low
or cut out the super renal fixations so you can take them out a little easier. Thank you.
- Thank you, Mr. Chairman. Good morning ladies and gentleman. I have nothing to disclose. Reportedly, up to 50 percent of TEVARs need a left subclavian artery coverage. It raises a question should revascularization cover the subclavian artery or not?
It will remain the question throughout the brachiograph available to all of us. SVS guidelines recommend routine revascularization in patients who need elective TEVAR with the left subclavian artery coverage. However, this recommendation
was published almost ten years ago based on the data probably even published earlier. So, we did nationwide in patient database analysis, including 7,773 TEVARs and 17% of them had a left subclavian artery revascularization.
As you can see from this slide, the SVS guideline did affect decision making since it was published in 2009, the left subclavian artery revascularization numbers have been significantly increased, however, it's still less than 20%.
As we mentioned, 50% of patient need coverage, but only less than 20% of patient had a revascularization. In the patient group with left subclavian artery revascularization, then we can see the perioperative mortality and morbidities are higher in the patient
who do not need a revascularization. We subgroup of these patient into Pre- and Post-TEVAR revascularization, as you can see. In a Post-TEVAR left subclavian revascularization group, perioperative mortality and major complications are higher than the patient who had a revascularization before TEVAR.
In terms of open versus endovascular revascularization, endovascular group has fewer mortality rate and major complications. It's safer, but open bypass is more effective, and durable in restoring original profusion. In summary, TEVAR with required left subclavian artery
revascularization is associated with higher rates of perioperative mortality and morbidities. Routine revascularization may not be necessary, however, the risks of left subclavian artery coverage must be carefully evaluated before surgery.
Those risk factors are CABG using LIMA. Left arm AV fistula, AV graft for hemodialysis. Dominant left vertebral artery. Occluded right vertebral artery. Significant bilateral carotid stenosis.
Greater than 20% of thoracic aorta is going to be or has been covered. And a history of open or endovascular aneurysm repair. And internal iliac artery occlusion or it's going to be embolized during the procedure. If a patient with those risk factors,
and then we recommend to have a left subclavian artery revascularization, and it should be performed before TEVAR with lower complications. Thank you very much.
- Ladies and gentlemen, I have nothing to disclose when regarding this topic. We know that TIAs are independent predictors of long-term mortality in the general population, however, they've been left underreported in almost all the randomized clinical trial. And we don't know the effect of TIAs on long-term survival
in patient with carotid disease. So what we have done, we have performed a study, looking at the effect of TIAs in populations submitted to carotid revascularization, either with endarterectomy, or stenting, and we achieved a pretty good long term result.
However, patient's with TIAs had a significantly lower survival compared with the patient without cerebral events. Similarly, patient with stroke, these reduce survival, and TIA behaves exactly like stroke in this population.
So, by multivariate analysis, TIA together with stroke, chronic renal failure, and age were independent predictors for late mortality. So, we have seen that TIAs have this effect in patient with carotid disease, but what about silent cerebral event?
The silent cerebral infarction has small, radiologically detected infarction without a history of acute dysfunction. And they're usually associated with a variety of condition. In the general population, these cerebral infarction are present in almost
one fifth of the population, 21%. And they are associated with significantly reduction in the stroke free survival in this population. For that reason, they are considered a high risk of stroke in patient with carotid disease.
So looking at the series of patient submitted carotid revascularization, we have seen that the presence of these silent brain infarction was significantly associated with either transient ischemic event and stroke. So, the important factors,
we wanted to further expand these experiences just looking at these phenomenon. In another series of 743 patients submitted to endarterectomy are looking at all the preoperative CT scan in this population. And again, we have found that significantly
association between silent cerebral infarcts and stroke. And by logistical regression analysis, this feature was independently associated with postoperative stroke. At long-term, this effect was also present in association with ipsilateral stroke.
And stroke combined stroke and death. Again, these effect was independent from all other feature. So what about their effect in stenting? Actually, there are no papers in the literature looking at this effect. So we perform a retrospective analysis on
420 patient submitted to a stenting procedure. And all patients were selected with preoperative evaluation of the brain. So, again, 30 day outcome, was not significantly affected by the presence of silent cerebral infarcts, however, when we look at the patient
with endarterectomy and stenting, we see that while in the endarterectomy group, there is a clear decrease of the stroke rate in patient without silent cerebral infarction. This effect is less pronounced
in the stenting group. So in conclusion, silent cerebral infarction increases the risk of postoperative events in carotid endarterectomy. This increased risk should be considered when in indication to revascularization is given.
In stenting, the effect is less pronounced, due to the higher overall risk of neurological event. Thank you.
- Thank you very much for the opportunity to speak. I will admit that I don't think we've got it all figured out, yet. But we'll go ahead anyway. So, persistent type two endoleaks do occur with some regularity and only about a third of them will resolve spontaneously, but fortunately
rupture is rare. A persistent endoleak with a sac expansion is our most common indication for treatment. We've got multiple treatment modalities, typically with a high initial, technical success, but the overall clinical success is not quite as good.
And so as we've learned the natural history is poorly understood, and there's no real strong evidence to guide our treatments. We tend to use CT image fusion to help us perform transarterial lumbar embolization as well as this is a transarterial from a hypogastric to coil
both lumbars and an IMA as well as the sac. We'll also use a direct sac puncture occasionally from a translumbar approach with the fusion guidance and also use that to guide us in terms of placing our embolic agents and then we'll also perform the transcaval embolization more recently.
This has become preferred over the translumbar approach and we can use that to then guide treatment and we use coils and glue combined typically now. We've performed over 100 procedures in 56 patients averaging two per patient. The average time from the endoleak to the procedure was
37 months and our follow-up is 27 months, about half had their EVAR performed at our institution and then the other half outside and about one in four of those had already had some sort of type two endoleak treatment. At our initial treatment, it's typically a trans, or it's been most commonly, a transarterial lumbar embolization
followed by IMA, followed by transcaval, and then direct sac puncture. Freedom from re-intervention is not perfect, so by one year it's about 50% we'll have a re-intervention for ongoing sac growth. For our secondary procedures, open repair has actually
become more common, followed by transcaval embolization then transarterial lumbar, IMA, direct sac puncture, and then also relining proximal extension with modified graft or anchors or cuffs. We have 10 patients that underwent open repair with a one year freedom from open repair of 94%.
Early on, we performed graft explantation for persistent growth with the type two endoleaks, then we switched to sacotomy initially without a proximal reinforcement. One of these was a patient who did rupture from an isolated IMA type two endoleak. We ligated the IMA, opened the sac, found no other bleeding,
closed the sac, and he's been fine for five years. We've taken to reinforcing the proximal attachment prior to opening the sac. One patient already had a PMEG for a type one and then more recently, we've been placing endoanchors for the proximal attachment prior to opening the sac.
Our clinical success from a single intervention is only 33% with multiple interventions it goes up to 67% and if you include the open repairs with sacotomy it goes up to 88%. This is for sac stabilization or decrease. So, I do still believe that large type two endoleaks
with sac expansion should be treated for lumbars. We will still typically go transarterial for the IMA. We'll go from the SMA. If we can't do those, or we failed, then we'll go transcaval as our next approach followed by translumbar. We like to treat both the nidus and the source feeding
vessel and if we fail with all of those, we proceed to sacotomy then will now place the proximal endoanchors for fixation. What we have been seeing, though, more commonly is this where there's poor attachment at the proximal end or distal end and a patient who we've performed
multiple procedures for type two endoleak and there's ongoing sac growth and even though there's no definitive type one leak, clearly if there were we would just go ahead and treat that, but in those patients who don't have a defined type one or three, but they have poor apposition, then we'll consider relining them,
extending them, anchoring, etc. And then, only then, if they still have problems would we consider treating the small type two endoleak. I'm looking forward to the discussion 'cause I think we've got it all figured out. Thanks.
- Thanks (mumbles) I have no disclosures. So when were talking about treating thoracoabdominal aortic aneurysms in patients with chronic aortic dissections, these are some of the most difficult patients to treat. I thought it would be interesting
to just show you a case that we did. This is a patient, you can see the CT scrolling through, Type B dissection starts pretty much at the left subclavian, aneurysmal. It's extensive dissection that involves the thoracic aorta, abdominal aorta,
basically goes down to the iliac arteries. You can see the celiac, SMA, renals at least partially coming off the true and continues all the way down. It's just an M2S reconstruction. You can see again the extent of this disease and what makes this so difficult in that it extends
from the entire aorta, up proximally and distally. So what we do for this patient, we did a left carotid subclavian bypass, a left external to internal iliac artery bypass. We use a bunch of thoracic stent grafts and extended that distally.
You can see we tapered down more distally. We used an EVAR device to come from below. And then a bunch of parallel grafts to perfuse our renals and SMA. I think a couple take-home messages from this is that clearly you want to preserve the branches
up in the arch. The internal iliac arteries are, I think, very critical for perfusing the spinal cord, especially when you are going to cover this much. And when you are dealing with these dissections, you have to realize that the true lumens
can become quite small and sometimes you have to accommodate for that by using smaller thoracic endografts. So this is just what it looks like in completion. You can see how much metal we have in here. It's a full metal jacket of the aorta, oops.
We, uh, it's not advancing. Oops, is it 'cause I'm pressing in it or? All right, here we go. And then two years post-op, two years post-op, you can see what this looks like. The false lumen is completely thrombosed and excluded.
You can see the parallel grafts are all open. The aneurysm sac is regressing and this patient was successfully treated. So what are some of the tips and tricks of doing these types of procedures. Well we like to come in from the axillary artery.
We don't perform any conduits. We just stick the axillary artery separately in an offset manner and place purse-string sutures. You have to be weary of manipulating around the aortic arch, especially if its a more difficult arch, as well as any thoracic aortic tortuosity.
Cannulating of vessels, SMA is usually pretty easy, as you heard earlier. The renals and celiac can be more difficult, depending upon the angles, how they come off, and the projection. You want to make sure you maintain a stiff wire,
when you do get into these vessels. Using a Coda balloon can be helpful, as sometimes when you're coming from above, the wires and catheters will want to reflux into that infrarenal aorta. And the Coda balloon can help bounce that up.
What we do in situations where the Coda doesn't work is we will come in from below and a place a small balloon in the distal renal artery to pin the catheters, wires and then be able to get the stents in subsequently. In terms of the celiac artery,
if you're going to stent it, you want to make sure, your wire is in the common hepatic artery, so you don't exclude that by accident. I find that it is just simpler to cover, if the collaterals are intact. If there is a patent GDA on CT scan,
we will almost always cover it. You can see here that robust collateral pathway through the GDA. One thing to be aware of is that you are going to, if you're not going to revascularize the celiac artery you may need to embolize it.
If its, if the endograft is not going to oppose the origin of the celiac artery in the aorta because its aneurysmal in that segment. In terms of the snorkel extent, you want to make sure, you get enough distal purchase. This is a patient intra-procedurally.
We didn't get far enough and it pulled out and you can see we're perfusing the sac. It's critical that the snorkel or parallel grafts extend above the most proximal extent of your aortic endograft or going to go down. And so we take a lot of care looking at high resolution
pictures to make sure that our snorkel and parallel grafts are above the aortic endograft. This is just a patient just about a year or two out. You can see that the SMA stent is pulling out into the sac. She developed a endoleak from the SMA,
so we had to come in and re-extend it more distally. Just some other things I mentioned a little earlier, you want to consider true lumen space preserve the internals, and then need to sandwich technique to shorten the parallel grafts. Looking at a little bit of literature,
you can see this is the PERCLES Registry. There is a number of type four thoracos that are performed here with good results. This is a paper looking at parallel grafting and 31 thoracoabdominal repairs. And you can see freedom from endoleaks,
chimney graft patency, as well as survival is excellent. This was one looking purely at thoracoabdominal aneurysm repairs. There are 32 altogether and the success rates and results were good as well. And this was one looking at ruptures,
where they found that there was a mean 20% sac shrinkage rate and all endografts remained patent. So conclusion I think that these are quite difficult to do, but with good techniques, they can be done successfully. Thank you.
- Thank you Mr. Chairman. Thank you, Dr. Veith for you kind invitation. Okay, there we go. Excuse me. DEVASS stands for Dutch EVAS study Group. We all know that women have a twofold, increased risk frequency of rupture.
The average aortic size at rupture is five millimeters smaller. They have a higher rate of undiagnosed cardiovascular diseases. They have smaller ileofemo
more concomitant iliac aneurysms They have a more challenging aortic neck. Smaller proportion is eligible for EVAR and, therefore less likely to meet EVAR IFU. They have a longer length of hospital stay after EVAR, a higher re-admission rate, more major complications,
a higher mortality rate. So, women and AAA is a challenging combination. The rationale behind EVAS is known to you all, I think. The DEVASS cohort is from three high volume centers in The Netherlands. It's a retrospective cohort of 355 patients,
included from April, 2013 to December 2015. So I have two years of result data. If you look at the baseline characteristics, 45 females were in this cohort, with the age of 76 and with some known comorbidities. They were within the instructions for use of 2013, at 28.9%
and even less in the IFU of 2016. These are some more anatomical characteristics with the AAA outer diameter 5.6 centimeters. This is the procedure, most of the patients were under general anesthesia, with the cutdown and the procedure time
was about 100 minute. Straight forward procedure 33 cases out of these 45. Let's have a quick look at the clinical outcomes. The re-intervention's done in the first 12 month. One patient had to conversion to open repair at month 11 due to type 1A Endoleak, and the others were not directly
related to the procedure itself. Although, there was thrombus in approximate stand. In the second month we saw, in the second year we saw some more type 1A migrations and a Stenosis that needed relining, and two out of these patients were within IFU.
If you look at the total cohort of type 1A Endoleak, one patient was not operated on and the other were, either open conversion or relining, and one patient was within IFU. A quick look at the death characteristics. Only one patient was within IFU,
and died after open procedure. So the re-interventions, once again, the first year four patients, in the second year five patients. Conversion to open repair, in total three patients. Endovascular re-intervention was performed
in the first year in two patients and in the second year there were three relinings performed. Endoleak 1A, in total six as stated before. No type two Endoleak reported, and in the first year five patients died, which one was aneurisym related, as in the second year, two patients died,
which one was aneurysm related. If we compare this data with the EVAS Global data, of two years not the three year data, this is the freedom from all persistent Endoleak, close to 98% which is good. Freedom from type 1A Endoleak is within IFU, 97% in the global and outside IFU 85%,
and remind these patients 71% were outside IFU. Freedom from secondary interventions, we had to re-intervene in nine patients and its comparable with outside IFU. Freedom from mortality at two years, a bit higher, aneurism related mortality is 95% which is higher, and also the all cost mortality is higher in women.
So to conclude, this is the first cohort that focuses on women after EVAS. The majority of the patients was outside IFU, and as in EVAR women do not that very good in result, appear to be very much like an EVAR. Thank you.
- Well, thank you Dr. Veith, and thank you very much for allowing me to speak on the topic. I have no disclosures. This is a nice summary that Dr. Veith is actually second author, that summarize what we know about predicting who will benefit from intervention among the patients with asymptomatic aortic disease.
You look at this eight means that we have, you realize that only one of those related to the fluid deprivation. The rest of them are related to embolic events. And that's very interesting because we know that antiplatelets have very little effect
on prevention of this. That's summarizing that review. Partially because what we focused on is that mechanism of thrombosis which requires platelet activation and attachment to the wall.
And that's where those antiplatelets that we use, act upon. However, you realize if you just look at the any ultrasound, that because of the velocities that we have and the lengths of the stenosis in carotid disease there is no way how the platelets can be attached to that
due to that mechanism. They just fly away too fast and don't have any time to do this. And it's even more because all the studies, basic science, show that at those shear rates that we have in carotid disease
that is more that 70%. There is very little probability of either platelet attachment or Von Willebrand factor attachment, or as a matter of fact even fibrinogen attachment in that particular area. So on the other hand we also know
that at those shear rates that we have, the Von Willebrand factor molecules unfold revealing tens of thousands more adhesive sites that allow them, not only to the platelets but also to the wall at that particular spot. And then the most likely mechanism
of what we dealing with in the carotid disease is this that the Von Willebrand factor attach and this unactivated platelets form conglomerates which can easily, because they don't attach to each other, easily fly. And that is probably one of
the most likely causes of the TIA. So if you look at the antiplatelet that we use on this particular mechanism, is right here. And those aspirin and clopidogrel, and combination of those we usually use, have very little, if any, effect on this particular mechanism.
So if, on the other hand, you can see that, if you specifically address that particular site you may have a much substantial effect. Now, how can we identify it? Well actually, the calculation of near-wall shear rate is quite simple.
All you need is just highest velocity and smallest diameter of the vessel. Of course, it is an estimate and actual shear rate is much higher but that's even more, because you, better than you prevent, more higher rate. Just to demonstrate, you can have the same velocity,
similar velocity, but different diameters. This stenosis technique will give different shear rate, and vice versa. So it's not really duplicating neither one of them. So we decided to look at this. We did a case control study that was published,
still online in the Journal of Vascular Surgery. And what you can see on the ROC curve, that in fact shear rate predicts symptomatic events much better than either velocity or the degree of the stenosis. And we look specifically at this group
with this thresh point of 8,000 per second and you can see that those patients who have those shear rates and the stenosis are 12 times more likely to have ischemic events. We look at the other means like microembolism. It's ongoing study, it's unpublished data that I show you.
And it's a very, very small sample but so far we have the impression that those microemboli that we can decide for, make a decision for intervention, actually happen only in this category of patient that have high shear rate. Based on this, this is our proposed algorithm,
how we deal with this. If you have asymptomatic patients with more than 70% degree of their stenosis and shear rate that exceeds certain level, we think it's about 8,000 per second, that may be an indication for intervention.
On the other hand if you a have lower shear rate then you can use other means. And what we use is microembolis per hour. Then you can duplicate their areas. If TCD on the other hand is normal you can continue best medical therapy and repeat the ultrasound in a year.
It's arbitrary. This is proposal agreed and based on our studies and that's, I'm thankful for the opportunity to share it with you. Thank you very much.
- Thank you Robbie, and I'd like to thank the meeting organizers and especially Dr. Veith for the generous invitation. As Dr. Norm Rich would say, war is my rule, conflict of interest but I am a consultant for Prytime Medical. Despite compelling research by Morrison and others
on translational research demonstrating effectiveness of aortic balloon occlusion in controlling pelvic hemorrhage. Introducing change is not easy in an institution and we are going to go into a little bit about how to implement those changes in practice.
We want to describe a process for the implementation of REBOA technology into modern practice. And our approach was several steps. We identified key innovators and early adopters in our own institution, conducted a literature review of best evidence,
outline criteria for proficiency and credentialing, and performed an analysis of our consecutive patients, and finally define measurements of success. It's important to research the literature before adopting a new technology and my partners and I published what we perceive to be our role
in controlling exsanguinating torso hemorrhage. And reported that it's important that this new technique be evaluated rigorously and transparently evaluated before widespread adoption. We developed a box where we thought this was the safest indications,
patients in shock with a torso hemorrhage, and pasted that to our cart of supplies and enlisted the support of the nursing staff in our emergency department. And then taking what we learned from John Eliason and Todd Rasmussen in the E Stars program,
developed our own workshop locally to advance the skillsets of our trauma surgeons to ensure that they were comfortable performing ultrasound guided access. This included an eight hour workshop at the Center for Surgical Innovation
at the University of Colorado. We focused our emphasis on ultrasound guided techniques using micropuncture sets and spent a considerable amount of time with emphasis on simulation training. We expanded those simulator trainings
to include knowledge of the zones of the aorta and careful placement of the balloon and measuring to avoid unintended zone placement. And then transition to a live animal model technique where we feel as we learned in the E Stars program that having live tissue gives proper feedback
for introducing sheaths and wires and catheters and such into the femoral vascular tree. At the time we began our course, we used the CODA with a Glidewire advantage and as soon transitioned. We felt that the best patient cohort
was the patients that we studied the most in Denver. Over a 10 year period, we saw almost 2,000 patients, 6% were in severe shock, and we predominantly pack and take those patients to the O.R. for external fixation. We expanded REBOA to include it
in our clinical practice guidelines for refractory shock. And our clinical experience is that we place this under strict ultrasound guidance under proctoring and mentoring with an attending that's attended this course. And we confirm the zone of placement in the operating room,
correction in the emergency department, with a digital X-ray. The balloon occlusion mean time is approximately 30 to 45 minutes. These patients are going expeditiously to the operating room for prepared neopolic packing
and external fixation and their mortality is significant. Despite that, our outcomes amongst the last 75 cases had a survival rate of 72%. A subgroup analysis of just pelvic injuries was a mortality of approximately 21%. We mostly use the balloon for blunt abdominal pelvic trauma
but we have done this for a few ruptures and penetrating injuries as well. As I mentioned, we transitioned from the older system, which required a 12 French sheath and femoral artery repair. And that has probably broadened the use of this catheter now that it's a seven French fluoroscopy-free
and wireless system with a balloon of 32 millimeters. We take caution to teach to avoid unintended zones of placement. Our average length is 28 to 29 millimeters and we inflate to eight, taking care not to overinflate the balloon.
This is our current adoption curve where we see a doubling over the last three years of its use. And the potential problems will be spoken to by Dr. McGee who's put together a talk on complications but we've essentially seen this
in almost every branch vessel. The key to success is partnership with the trauma surgeons and having a senior mentor who understands innovation. And in summary, I'd say there needs to be a commitment for the innovation, training and proctoring, credentialing, and clinical practice
guidelines for safe use. Thank you for your attention.
- Good morning, I want to thank Professor Vitta for the privilege of presenting on behalf of my chief, Professor Francesco Speziale, the result from the EXTREME Trial on the use of the Ovation stent graft. We know that available guidelines recommend to perform EVAR in patient presenting at least a suitable
aortic neck length of >10mm, but in our experience death can be a debatable indication because it may be too restrictive, because we believe that some challenging necks could be effectively managed by EVAR. This is why when we published our experience 2014,
on the use of, on EVAR, on the use of different commercially available device on-label and off-label indication, we found no significant difference in immediate results between patient treated in and out IFU, and those satisfactory outcomes were maintained
during two years of follow-up. So, we pose ourself this question, if conventional endografts guarantee satisfactory results, could new devices further expand EVAR indication? And we reported our experience, single-center experience, that suggests that EVAR by Ovation stent-graph can be
performed with satisfactory immediate and mid-term outcomes in patient presenting severe challenging anatomies. So, moving from those promising experiences, we started a new multi-center registry, aiming to demonstrate the feasibility of EVAR by Ovation implantation in challenging anatomies.
So, the EXTREME trial was born, the expanding indication for treatment with standard EVAR in patient with challenging anatomies. And this is, as I said, a multi-center prospective evaluation experience. The objective of the registry was to report the 30-day and
12 month technical and clinical success with EVAR, using the Ovation Stend-Graft in patient out of IFU for treatment by common endograft. This is a prospective, consecutively-enrolling, non-randomized, multi-center post market registry, and we plan to enroll at least 60 patients.
We evaluated as clinical endpoints, the freedom from aneurysm-related mortality, aneurysm enlargement and aneurysm rupture. And the technical endpoint evaluate were the access-related vascular complications, technical success, and freedom from Type I and III endoleaks, migration,
conversion to open repair, and re-interventions. Between March 17 and March 18, better than expected, we enrolled 122 patients across 16 center in Italy and Spain. Demographics of our patient were the common demographic for aneurysm patients.
And I want to report some anatomical features in this group. Please note, the infrarenal diameter mean was 21, and the mean diameter at 13mm was 24, with a mean aortic neck length of 7.75mm. And all grafts were released accorded to Ovation IFU. 74 patients out of 122
presented an iliac access vessel of <7mm in diameter. The technical success reported was 98% with two type I endoleak at the end of the procedure, and 15 Type II endoleaks. The Type I endoleak were treated in the same procedure
by colis embolization, successfully, and at one month, we are no new Type Ia endoleaks, nine persistent Type II endoleaks, and two limb occlusion, requiring no correction. I want to thank my chief for the opportunity of presenting and, of course, all collaborators of this registry,
and I want to thank you for your attention, and invite you, on behalf of my chief, to join us in Rome next May. Thank you.
- Thank you Rod and Frank, and thanks Doctor Veeth for the opportunity to share with you our results. I have no disclosures. As we all know, and we've learned in this session, the stakes are high with TEVAR. If you don't have the appropriate device, you can certainly end up in a catastrophe
with a graph collapse. The formerly Bolton, now Terumo, the RelayPlus system is very unique in that it has a dual sheath, for good ability to navigate through the aortic arch. The outer sheath provides for stability,
however, the inner sheath allows for an atraumatic advancement across the arch. There's multiple performance zones that enhance this graph, but really the "S" shape longitudinal spine is very good in that it allows for longitudinal support.
However, it's not super stiff, and it's very flexible. This device has been well studied throughout the world as you can see here, through the various studies in the US, Europe, and global. It's been rigorously studied,
and the results are excellent. The RelayPlus Type I endoleak rate, as you can see here, is zero. And, in one of the studies, as you can see here, relative to the other devices, not only is it efficacious, but it's safe as well,
as you can see here, as a low stroke rate with this device. And that's probably due to the flexible inner sheath. Here again is a highlight in the Relay Phase II trial, showing that, at 27 sites it was very effective, with zero endoleak, minimal stent migration, and zero reported graph collapses.
Here again you can see this, relative to the other devices, it's a very efficacious device, with no aneurism ruptures, no endoleaks, no migration, and no fractures. What I want to take the next couple minutes to highlight, is not only how well this graph works,
but how well it works in tight angles, greater than 90 degrees. Here you can see, compliments and courtesy of Neal Cayne, from NYU, this patient had a prior debranching, with a ascending bypass, as you can see here.
And with this extreme angulation, you can see that proximally the graph performs quite well. Here's another case from Venke at Arizona Heart, showing how well with this inner sheath, this device can cross through, not only a tortuous aorta, but prior graphs as well.
As you can see, screen right, you can see the final angiogram with a successful result. Again, another case from our colleagues in University of Florida, highlighting how this graph can perform proximally with severe angulation
greater than 90 degrees. And finally, one other case here, highlighting somebody who had a prior repair. As you can see there's a pseudoaneurysm, again, a tight proximal, really mid aortic angle, and the graph worked quite well as you can see here.
What I also want to kind of remind everybody, is what about the distal aorta? Sometimes referred to as the thoracic aorta, or the ox bow, as you can see here from the ox bow pin. Oftentimes, distally, the aorta is extremely tortuous like this.
Here's one of our patients, Diana, that we treated about a year and a half ago. As you can see here, not only you're going to see the graph performs quite well proximally, but also distally, as well. Here Diana had a hell of an angle, over 112 degrees,
which one would think could lead to a graph collapse. Again, highlighting this ox bow kind of feature, we went ahead and placed our RelayPlus graph, and you can see here, it not only performs awesome proximally, but distally as well. And again, that's related to that
"S" shaped spine that this device has. So again, A, it's got excellent proximal and distal seal, but not only that, patency as well, and as I mentioned, she's over a year and a half out. And quite an excellent result with this graph. So in summary, the Terumo Aortic Relay stent graph is safe,
effective, it doesn't collapse, and it performs well, especially in proximal and distal severe angulations. Thank you so much.
- (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.
- Good Morning. Thank you very much Dr. Veith, it is an honor and I'm very happy to share some data for the first time at this most important meeting in vascular medicine. And I do it in - oops, that's the end of my talk, how do I go to the --
- [Technician] Left button, left, left. - Okay. So, what we heard on Tuesday were some opinions, of course opinions are very important in the medical field, we heard some hypothesis.
But what I think is critical for the decision-making physician is always the facts. And I would like to discuss some facts in relation to CGuard and the state of the field of carotid revascularization today. One of the most important facts for me,
is that treating symptomatic patients is nothing to be proud of, this is not a strength, this is the failure of the system. Unfortunately today we do continue to receive patients on optimum medical therapy
in the ongoing studies, including the paradigm study that I will discuss in more detail. So if you want to dismiss large level scale level one evidence, I think what you should be able to provide methodologically is another piece of large level one scale evidence.
The third fact is conventional carotid stents do have a problem, we heard about this from Dr. Amor. This is the problem of carotid excess of minor strokes, say in the CREST study. The fact # 4 is that Endarterectomy excludes the problem of the carotid block from the equation
so carotid stents should also be able to exclude the plaque, and yes there is a way to do it one of the ways to do it is the MicroNet covered embolic prevention stent system. And there is intravascular evidence from imaging we'll hear more about it later
that yes it can do this effectively but, also there is evidence from now more that 3 studies with magnetic resonance imaging that show the the incidence of ipslateral embolization is very low with this system. The quantity of the material is very low
and also the post procedural emoblisuent issue is practically eliminated. And this is some examples of intervascular imaging just note here that one of the differences between different systems is that, MicroNet can adapt to simple prolapse
even if it were to occur, making this plaque prolapse protected. Fact # 6 that I think is also very important is that the CGUARD system allows routine endovascular reconstruction of the carotid bifurcation and here is what I mean
as a routine CEA-like effect of endovascular procedure you can minimize residual stenosis by using larger balloons and larger pressure's than we would've used with conventional carotid stent and of course there is not one patient that this can be systematically achieved with different types of plaques
different types of protection systems and different patient morphologies Fact # 7 is that the level of procedural risk is the critical factor in decision making lets take asymptomatic carotid stenosis How does a thinking physician decide between
pharmacotherapy and intervention versus isolated pharmacotherapy. The critical factor is the risk of procedure. Part of the misunderstandings is the fact that we talk often of different populations This contemporary data the the vascular patients
are different from people that we see in the street Of coarse this is what we would like to have this is what we do not have, but we can apply and have been applying some of the plaque risk criteria Fact # 8 is that with the CGUARD system
you can achieve, systematically complication level of 1%, peri procedurally and in 30 days There is accumulating evidence from more than 10 critical studies. I would like to mention, Paradigm and Paradigm in-stent study because
this what we have been involved in. Our first 100 patient at 0.9% now in nearly 300 patients, the event rate is 1.2% and not only this is peri procedural and that by 30 days this low event rate. But also this is sustained through out
now up to 3 years This is our results at 36 months you can see note here, very normal also in-stent velocities so no signal of in-stent re stenosis, no more healing no more ISR signal. The outcome Difference
between the different stent types it is important to understand this will be driven by including high risk blocks and high risk patients I want to share with you this example you see a thrombus containing
a lesion so this patient is not a patient to be treated with a filter. This is not a patient to be treated with a conventional carotid stent but yes the patient can be treated endovascularly using MicroNet covered embolic prevention stent and this is
the final result. You can see that the thrombus is trapped behind the stent MicroNet and Final Fact there's more than that and this is the data that I am showing you for the first time today, there are unmet needs on other vascular territories
and CGUARD is perfectly fit, to meet some of those need. This is an example of a Thrombus containing a lesion in the iliac. This is the procedural result on your right, six months follow up angiogram. This is a subclavian with a lot of material here
again you can preform full endoovascular reconstruction look at the precession` of the osteo placement This is another iliac artery, you can see again endovascular reconstruction with normal 6 month follow up. This is another nasty iliac, again the result, acute result
and result in six months. This is another type of the problem a young man presented with non st, acute myocardial infarction you can see this VS grapht here has a very large diameter. It's not
fees able to address the native coronary issue here So this patient requires treatment, how to this patient: the reference diameter is 7.5 I treated this patient with overlapping CGUARD's This is the angio at 3 months , and this is the follow up at 6 months again
look at the precision of the osteo placement of the device ,it does behave like a balloon, expandable. Extending that respect, this highly calcific lesion. This is the problem with of new atherosclerosis in-stent re stenosis is wrongly perceived as
the proliferation of atheroscleroses tissue with conventional stents this can be the growth of the atherosclerotic plaque. This is the subclavian, this is an example of the carotid, the precise stent, 10 years down the line, symptomatic lesion here
This is not re stenosis this is in-stent re stenosis treated with CGUARD and I want to show you the final result at 2 years. I want to thank you for your attention. Say that also, there is the issue of aneurism that can be effectively addressed , Thank you
- Thank you, and thanks to Dr. Veith for the opportunity to share some of our data. These are my disclosures, some devices presented here are investigational and I want to acknowledge my friend Gustavo, who actually shared some of the slides that we'll show. And I want to reference some of his papers. So a spinal cord ischemia has been presented here
as a devastating complication, after both open and endovascular repair of thoracoabdominal aortic aneurysms. The spinal drains are routinely used to ameliorate the frequency and also the severity of spinal cord ischemia, the problem with this trains is that they may result inherent morbidity and mortality.
Now, intraoperative neuromonitoring has been used to not only monitor, but also to manage potential cases of spinal cord ischemia, this is a study by the group at the Mayo Clinic, led by Gustavo. 49 patients, of which 90% had thoracoabdominal aortic aneurysms, all these patients have spinal drain splice,
spinal cord ischemia was seen in six patients. But interestingly, 63% of the patients had significant decrease in the amplitude of both motor and somatosensory evoked potentials. And interestingly all of these changes came back to baseline except in one patient once
their lower legs were reperfused. However, and despite all of these papers that have, you know, talk about the use of spinal drains for endovascular reparative thoracoabdominal aortic aneurysms against the effectiveness of the spinal drains has not been shown.
And the aim of our study was to assess the outcomes of spinal cord protection without the routine use of spinal drains. We actually has some complications in this report, we decided that we were going to use only selectively in our series, the device is used for this in patients
were all part of a physician-sponsored investigational device exemption, demonstrating branch devices were used including the drainage device. We use a similar protocol as the one described by the Mayo Clinic group, which rely on permissive hypertension maintaining the maps above 90 or 100,
and the systolic pressures above 140. However, as mentioned, we did not place spinal drains routinely, the spinal drains were only considered in those patients that had persistent motor evoked potential deficits, at the end of the procedure. Once the legs have been reperfused, we did not use
conduits, we did percutaneous access in all patients. But of note, we did use endo conduits in all patients that have significant iliocclusive disease, not only to be able to deliver the device, but also to maintain flow to the lower extremities, to avoid distal ischemia. So 34 patients were enrolled in this study,
all patients had intraoperative neuromonitoring, and select spinal drains were placed. 10 patients, 29%, were extent 4 thoracoabdominal repairs, and 24 were extent type one to three. Important all patients with type one and three thoracoabdominal aneurysms underwent a staged repair.
We use in 20% of the cases off-the-shelf device is specifically the debranch, and 80% underwent custom made devices, all these devices were pre-loaded with wires. So, of these patients, 73 were male, 9% Type I, 38% Type II, 24% were Type III,
and 29% were Type IV. We saw significant changes in the evoked potentials in 80% of the patients. In all of them those changes came back to baseline except in one patient, who actually had a spinal drain at the end of the procedure.
30-day mortality in two patients, spinal drain was required eventually in only four patients, that's 12%. One because of sustained changes in the motor evoked potentials, spinal cord ischemia occurred in four patients, in all cases secondary to hypertension. After a procedure, in these cases two were permanent,
the cases had spinal drain splice, however, the deficit persisted, two had transient paraplegia, one resolved with permissive hypertension, and one resolved with a spinal drainage, I mean, the spinal drain was only effective in half of those patients. We did have two cases of intracranial bleeding,
associated with hypertension. So in conclusions, we don't believe that the spinal drains are necessary in all patients. A standard protocol that relies on perioperative maintenance of adequate blood pressure in intraoperative neuralmonitoring is however required.
And we believe that tight blood pressure control is mandatory to avoid possible complications related to uncontrolled hypertension, thank you.
- Thank you, good afternoon. I have no disclosures. Well, obesity really is a worldwide epidemic, but among all of the industrialized nations the United States seems to lead the league in terms of the percentage of our population overweight and/or obese.
We're all aware of the adverse health effects of obesity including predisposing to diabetes, itself an epidemic problem, at least in this country. In fact the AMA has suggested obesity should now be declared a disease state with its own ICD-10 code. If that's true as this article in time magazine said
if obesity is a disease why are so many obese patients seemingly healthy? We do know that obese patients tend to have smaller myocardial infarct size, they have improved survival after episodes of heart failure, there's improved survival
after CABG and coronary angioplasty procedures, and there's reduced early and late mortality after acute stroke. In fact we're seeing this so-called obesity paradox play out in vascular surgery. This was an early review of 7500 patient undergoing
a variety of vascular surgical procedures and what you see is this U-shaped curve where is overweight, mildly and moderately obese patients have significantly lower operative mortality. This was a similar NSQIP analysis of over 5000 patients undergoing AAA repair and among all procedures
again you see that same U-shaped curve largely reflected the reduced mortality for open surgery for overweight, mildly and moderately obese patients. We became interested in whether this would play out on a low risk procedure, relatively speaking, carotid endarterectomy.
We investigated 23000 patients undergoing carotid endarterectomy in the NSQIP database. Only a quarter of our patients were normal weight, about 40% over weight, and then nearly 30% were obese. And we found the very same thing, although mortality is exceedingly low, 0.6%,
it was significantly lower in overweight, mildly and moderately obese patients. The overall stroke rate was 1.4% and again that very same U-shaped curve. Stroke rate lower in overweight, mildly and moderately obese patients.
In the most recent and the largest data set ever analyzed, 92000 patients undergoing the spectrum of vascular surgical procedures. A third of the patients only normal weight, about a third overweight, and more than a quarter severely overweight.
We found that mortality was actually higher in underweight compared to normal weight individuals. So it's not good to be thin, many of us take comfort in that. We found that, they found that mortality was lower in overweight compared to normal weight individuals.
Mortality was lower in obese compared to normal rate individuals and this reflected the fact that cardiac complications occurred significantly less often in obese compared to normal weight individuals. And respiratory complications occurred less often
in obese compared to normal weight individuals. How do you explain this? Well this was a fascinating report from the Health Professionals Follow-Up Study. 38000 individuals, men middle-aged who have been followed for up to 25 years, and if you look at overall
mortality, again that very same U-shaped curve. But what they did in this study was they divided BMI into lean body mass and fat body mass and as you can see there is that U-shaped relationship with respect to lean body mass, but when they ferreted out statistically fat body mass
there was a direct proportional correlation with mortality. How do we explain this? Well we're learning that adipose tissue is more than just a storage depot for energy, it is also an endocrine organ. Adipose tissue produces molecules called adipokines
the most important of which is adiponectin. An elevated BMI is associated with reduced levels of adiponectin which has a positive impact on cardiovascular complications. So in summary, the impact of weight on vascular outcomes is complex.
Modest excess weight appears to be protective for perioperative mortality and cardiorespiratory morbidity. Excess weight is a risk factor for wound complications but the obesity paradox may be related to the endocrine function of adipose tissue. Thank you.
- [Neil] Thanks Tom and thanks Jose and Lowell for inviting me to participate in this great symposium. And I have no relevant disclosures to this talk. Clinical decision making, communication amongst ourselves, in the literature, and to some extent prognosis of patients is dependent a bit on the pattern of reflux in a given patient.
So that's the topic of today's talk for me. Those can be categorized into three rough bins, great saphenous vein reflux, small saphenous vein reflux, and non-saphenous vein or non-truncal reflux. More than one pattern can exist in a given patient, and that obviously has implications
in terms of what needs to be done in recurrence. Even great saphenous vein reflux can be divided into different components based on a variety of elements such as the source of the reflux, which we typically think of
as saphenofemoral junction derived. But the source can be below the junction, either from perforating veins or tributary veins. Sometimes those tributary veins are pelvic derived as in the image on the right. The extent of reflux is obviously very variable.
Sometimes it ends in varicose veins in the thigh and calf and obviously those patients are different than those that have reflux going all the way down to the malleolus or reflux that would be segmental, where it involves the trunk, leaves the trunk into tributaries,
and then comes back into the trunk. The anterior accessory great saphenous vein and saphenofemoral junction can be a cause of great saphenous vein reflux as well as depicted in this diagram where varicose veins shunt the flow from the anterior accessory great saphenous vein
to the great saphenous vein, leading the saphenous vein reflux. Some of the co-panelists for today's session, Dr. Chastanet and Dr. Pitaluga have looked at 1800 patients and categorized their ultrasounds to look at the patterns that exist
in great saphenous vein reflux and identified five different types. The most common type was great saphenous vein reflux with saphenofemoral junction incompetence leading to varicose veins. The second most common type was great saphenous vein
tributary reflux alone. And the third most common type was great saphenous vein reflux with varicose veins without saphenofemoral junction incompetence. This is more than just an academic exercise because if we look at these two types,
type three and type four we'll see that there's a difference in these patients in terms of the phenotypes that they present with their venous disease, specifically in the absence of saphenofemoral junction incompetence,
although, the great saphenous vein and varicose veins are both reflux in the incidence of advanced C4 through C6 venous disease is only 1%. But if you add the saphenofemoral junction component to that patient, the incidence of C4 through C6 disease is 10%.
So that's where the prognosis comes in. Small saphenous vein reflux can be categorized as well. The typical form is derived from the saphenofemoral, sorry, saphenopopliteal junction and leads to sapheno, sorry small saphenous vein reflux and varicose veins.
But that reflux can begin at a higher level, in this case in a perforating vein on the posterior thigh involving the thigh extension and then the small saphenous vein with downward reflux. And it could also begin even in the pelvis with varicose veins leading
to thigh extension reflux downward into the small saphenous vein. Or even at the saphenofemoral junction with reflux through the posterior circumflex vein into the thigh extension and down into the small saphenous vein.
A unique form of what we might call paradoxical reflux that involves the posterior circulation of the venous system superficially would be saphenopopliteal junction where that reflux, in essence, decompresses upward and leads to great saphenous vein reflux and varicose veins.
So all of these different patterns likely have different means to treat, but certainly also may have different long-term prognoses. And then finally varicose veins can be coming from non-saphenous veins. Up to 30% of patients have
non-saphenous related varicose veins. The majority of these patients are female and a lot of these are pelvic-derived varicose veins as you see in the diagram on the right. And many of these are also related to incompetent perforating veins in a number of locations,
particularly the mid thigh, lateral thigh, and popliteal fossa. So in conclusion categorizing reflux in patterns
- Thank you friends who have invited me again. I have nothing to disclose. And we already have published that as far as the MFM could be assumed safe and effective for thoracoabdominal aneurysm when used according to the instruction for use at one, three, and four years. Now, the question I'm going to treat now,
is there a place for the MFM? Since 2008, there were more than 110 paper published and more than 3500 patient treated. 9 percent of which amongst the total of published papers relating the use of the MFM for aortic dissections. So, we went back to our first patients.
It was a 40 year old male Jehovah Witness that I operated in 2003 of Type A dissection and repair with the MFM in 2010 because he had 11 centimeter false aneurysm. Due to his dissection, this patient was last to follow up because he was taking care full time off of
his severe debilitated son. When we checked him, the aneurysm seven years later shrunk from 11 to 4 centimeters wide. And he's doing perfectly well. Then the first patient we treated seven years ago, same patient with Professor Chocron
Type A dissection dissection repair in 2006. Type B treated with MFM in 2010. We already published that at one year that the patient was doing fine. But now, at three and seven years, the patient was totally cured.
The left renal artery was perfused retrogradely by aspiration. That's a principle that has been described through the left iliac artery. So what's next? Next there was this registry
that has been published and out of 38 patients 12 months follow up, there were no paraplegia, no stroke, no renal impairment, and no visceral insult. And at 12 month the results looked superior
to INSTEAD, IRAD and ABSORB studies. This is the most important slide to us because when you look at the results of this registry, we had 2.6 percent mortality at 30 days versus 11 30 and 30.7 no paraplegia, no renal failure, and no stroke vessel
13 to 12.5. 33 and 34 and 13 and 11.8 percent. With a positive aortic remodeling occurring over time with diminishing the true lumen increasing the true lumen and increasing the false lumen.
And so the next time, the next step, was to design an international, multicenter, prospective, non-randomized study. To treat, to use the MFM, to treat the chronic type B aortic dissection. So out of 22 patients to date,
we had mainly type B and one type A with no dissection, no paraplegia, no stroke, no renal impairment, no loss of branch patency, no rupture, no device failure, with an increase in true lumen and decrease in false lumen that was true at discharge.
That was true at one, three, and six and 12 month. And in regards with the branch occluded from the parts or the branches were maintained patent at 12 and all along those studies. So, of course these results need to be confirmed in a larger series and at longer follow up,
yet the MFM seems to induce positive aortic remodeling, is able to keep all branches patent during follow-up, has been used safely in chronic, acute, and subacute type B and one type A dissection as well. When we think about type B dissection, it is not a benign disease.
It carries at 20 percent when it's complicated mortality by day 2 and 25 percent by day 30. 30 percent of aortic dissection are complicated, with only 50 percent survival in hospital. So, TEVAR induces positive aortic remodeling, but still causes a significant 30 day mortality,
paraplegia event, and renal failure and stroke. And the MFM has stabilized decreased the false lumen and increase the true lumen. Keeps all the branch patent, favorize positive aortic remodeling. So based on these data, ladies and gentleman,
we suggest that the MFM repair should be considered for patients with aortic dissection. Thank you very much.
- Thank you so much for having me here. I must confess it's not my talk. It's Professor Veroux's talk. Veroux couldn't join us, so I hope you will forgive me if I cannot read it properly as he would have done. It's just a friendship act of being here.
Talking with you about the potential of these treatment of ventricular veins for relief symptoms, headache like. Professor Veroux published on PlosOne Single-center open label observational study was conducted from January 2011 to December 2015.
Basically focused on 113 headache positive patients. As you see there were different kinds of MS patients involved. 82 were relapsing emitting. 22 were secondary progressive. Nine were primary progressive.
Basically the including criteria included headache resistant to the best medical therapy. There was a bilateral internal jugular vein with a stenosis bigger than 50% of moderate to severe insufficiency of the flow. The stenosis of course were suitable for treatment
and they were followed up at least for 12 months. Basically the followup included a variation of the MIDAS, Migraine Disability Assessment Score. It was preformed the day before angioplasty. Then three months after angioplasty and then at the end of the follow-up.
As it was appears,. Of curse we can add the different kinds of lesions of the juvenile level. As it was previously reported, the Professor Veroux ended selection. It is mandatory in these kinds of procedures.
Adding the transversal defect the single most important criteria for determining if the PTA would be successful or not. Of course, again, transversal rather than longitudinal defects are preferred in the treatment of
this kind of patients. The exclusion criteria were the possibility of hypoplasia or extreme muscle compression. In particular, as you know there is the omohyoid possibility of compression.
Looking at a followup that is significantly of three years or more. The clinical results in these patients affected by headaches lead to significant reduction. And 86% of them with an improvement of the MIDAS scores in the three months following up.
At the same time, the improvement was maintained throughout the followup period up to three years. Mainly in the relapse remitting and the secondary progressive patients. So the conclusion of the investigation you can again (mumbles)
is that patient selection is mandatory, of course, again, on the transverse lesion mainly. Balloon valvuloplasty is feasible in these patients and has succeeded with a good result at three years followup in the MIDAS score. Of course, these findings are suggesting
that it could be a useful intervention for selected MS patients with persistent headaches and of course, non-thrombosis stenosis of the IJVs. Thank you so much.
- This is a controversial topic. Basically we have been following standard set-up on the arterial side to grade venous stenosis. But duplex, many people would look at the stenosis either by venogram or duplex and then compare it to the adjacent normal segment.
In arteries the stenosis is usually focal so this approach works well. But in iliac veins particularly, does not work well. On venogram this looks normal but actually on IVUS it's a severe stenosis, 67 square millimeters,
it should be somewhere around 200. So, you are looking at a 70% stenosis. So, just the standard does not work well in veins. You have, does not happen, that type of rokitaskis stenosis does not happen, all the time but is present in varying degrees in about 20% of patients.
Another standard that we have applied, without thinking too much, is so-called critical threshold. Most major arteries, as we know, is not hemodynamically significant until is is somewhere around 70% or so. If the region of resistance is low,
it maybe a little bit low, somewhere around 60%, 70%, 80% depending on local resistance. Why does that happen? It happens because of autoregulation. As increases stenosis there is pressure flow of arterial dilation.
At some point, usually somewhere around 70%, 80% the pressure flow of compensating vasodilation is maxed out. So as increases stenosis the flow goes down and the pressure goes up. I want to point out that the pressure going up is proximal, not downstream.
The pressure goes down downstream. And pressure does go up upstream but is so well compensated on the arterial side by off-load to other areas. Another way to look at it is consider peripheral assistance, as a stenosis in aggregate.
Now there's a fall of blood pressure from 100 mean to somewhere around 30 millimeters post arterial. So that represents a very high-grade stenosis. So any proximal stenosis, by the principle of tandem stenosis, has to exceed
this high value to become hemodynamically significant. So that's why the 70% critical threshold. On the venous side there's no autoregulation. And the only distal downstream stenosis is abdomen. Not very much, about five millimeters of mercury pressure. So, on the venous side, pressure rises
with incremental stenosis. There's no critical threshold, it's nonlinear but no sudden inflection point. So this theory of 70% should not hold on the venous side. As a practical matter, most stenosis are in that range. They are in the 60%, 70% range.
But every once in awhile, say about 10%-15% of cases, where you will come across a 20% or 30% stenosis, which is clinically significant, because the veins are post-thrombotic and they have poor compliance. So even a slight stenosis will increase the pressure.
This is a concept of inflow outflow. If the inflow matches outflow, then the pressure will be normal. So you can calculate from the size of the outflow, we know what is the optimal outflow, you can calculate from the outflow size
whether the stenosis is significant or not. Critics will say this is a morphologic method. Yes and no. It's morphologic but it is tightly connected to flow. So it is a quasi hemodynamic method to measure the outflow size.
And again, calculated by various, by flow femoral size. Thank you.
- Yeah, thank you Mr. Chairman. These are my disclosures. Well, we know that the Heli-FX EndoAnchor System provide fixation and seal in aortic necks, and it can prevent or resolve migration or endoleaks. It's important to have an even spacing around aortic circumference and
to resolve type 1A endoleaks, you need successful, of course, deployment of EndoAnchors and adequate penetration into the aortic wall. The objectives for this study was to quantify the EndoAnchor penetration into the aortic wall in patients undergoing EVAR
and to assess the predictors of successful penetration and to associate that with postprocedural type 1A endoleaks. We searched in the ANCHOR database, and we included patients that has been treated for a type 1A endoleak, and we had to have a good quality
first postprocedure contrast-enhanced CT scan without any artifacts due to metal or glue, and without implantation of adjuvant aortic extension cuffs or stents. And then we selected two patient cohorts, patients with successful treatment
after the implantation of EndoAnchors for a type 1A endoleak, and patients with a persistent type 1A endoleak after the EndoAnchor implantation. Well, this is to show how we determined the position of the EndoAnchors, this is a good penetrating EndoAnchor
more than two millimeters in the aortic wall. This is borderline, and this means there is still a gap between the endograft and the aortic wall or the EndoAnchor itself is penetrating less than two millimeters. And this of course, a non-penetrating EndoAnchor.
The good ones are green, the borderlines are orange, and the non-penetrating are flagged red. Here are results, the anatomical criteria to predict type 1A endoleaks, as you can see here, at the left, in the type 1A endoleak patients, there is a larger aortic diameter
with a median of 30 millimeters, and neck length is shorter, less than one centimeter, compared to the patients with no endoleak. Then about the EndoAnchor penetration, in the patients with a persistent type 1A endoleak, there are significantly more EndoAnchors
which are borderline or non-penetrating. What are the predictors for a successful EndoAnchor penetration. Well, protective factors, oversizing of the endograft compared to the diameter of the infrarenal aortic neck, and the use of the endurant stents.
Independent risk factors are the aortic diameter at the lowest renal artery, and five and 10 millimeters below more than 30 millimeters, a significantly neck thrombus and calcium around the circumference and also a more than two millimeter thickness.
Predictors for a type 1A endoleak, protective factors is the neck length more than one centimeter, and good penetrating EndoAnchors and risk factors for a type 1A endoleak is, again, the aortic diameter five millimeters
below the lowest renal artery more than 30 millimeters, and also boerderline and non-penetrating EndoAnchors and in this logistic regression model, a non-penetrating EndoAnchor is really predictive for a type 1A endoleak, or a persistent type 1A endoleak. A few cases, this is an excellent job,
there are four EndoAnchors placed, and they all penetrate well, although they are not circumferentially divided around the circumference. The majority of the problems in the patients in the ANCHOR database, if a persistent type 1A endoleak
is mainly due to an incorrect indication, these are EndoAnchors red and orange, non-penetrating and borderline. That is because they are above the fabric, or they are in a no-neck aneurysm, so the indication is not correct.
This is again, a patient with an undersized endograft, of course, the EndoAnchors will never penetrate the aortic wall at a post-serial part of the aorta. This is another example of misdeployment, a huge load of calcium and thrombus, and again, to defined a no-neck aneurysm,
and again, well it's obvious that the EndoAnchors will not do their job. These are then the EndoAnchor distribution in successfully treated type 1A endoleaks at the left, 332 EndoAnchors, but if you select only the patients
with an EndoAnchor which are inside recommended use at the right, you can see that more than 90% of those EndoAnchors are good penetrating. Here are the patients at the left with a persistent type 1A endoleak, 248, and you can see the majority is red or orange,
and that means that majority of those patients had an EndoAnchor deployment beyond the recommended use. So to conclude, good EndoAnchor penetration is less likely when there is large aortic diameter, the EndoAnchor is not perpendicular to the stentgraft during deployment,
and it's beyond the recommended use, more than two millimeters of thrombus, not in the infrarenal neck, or a gap more than two millimeters. And in borderline or non-penetrating EndoAnchor, it's predictive for a type 1A endoleak.
Thank you very much.
- Thank you, thanks to Dr. Veith and the program committee for allowing me to present this morning. My disclosure. So, uh, I think that there's been an abundance of literature over the years that is suggested that venography may have poured diagnostic sensitivity for identifying iliac and, and
common femoral vein obstruction. Uh, in uh published literature, 34% of patients who have chronic venous symptoms of a severe degree had iliac vein obstruction on imagining techniques other than venography such as IVUS with normal venograms and often times
patients have significant outflow obstruction and there are no pelvic collaterals present so this is not a reliable though maybe specific indicator of outflow obstruction. The video study was designed to prospectively compare multiplanar venography vs. IVUS
to address the question if you do enough views on venogram do you find the same lesions that you might detect with IVUS. And we also wanted to look, does the imaging that you do to look for iliac and common femoral vein outflow track obstruction
effect your clinical decision about intervention. These are the patients in the video trial CEAP 4 through CEAP 6. And so 100 patients were randomized in this or not randomized, but rather entered entered this prospective multi-center single-arm study
at 14 sites in the US and Europe. This was half CEAP 6 patients and the remainder were CEAP 4 and 5. The patients underwent multiplanar venography. The site investigator was asked to make a decision about whether there was a significant lesion
and how they would treat that lesion and then once that was recorded IVUS was preformed and then again after the pull back the investigator was asked to make a decision about whether there was a significant lesion and how they would treat it.
We standardized venography with a hand injection in 3 views as noted. A 30 degree RAO and LAO and an AP view and the catheter was placed at the cranial portion of the femoral vein we adopted the standards and the literature
of a 50% diameter stenosis. And venography in a 50% CSA reduction on IVUS as a significant lesions. The uh, study cohort was approximately 43 women. The left leg was the index limb and 2 to 1 ratio to uh, to the right.
The age average 62 and you can see the majority of the patients were CEAP 4 and CEAP 6. What we identified with IVUS is a 21% greater (mumbling) identification of outflow obstruction. Venography was a lot less sensitive
at identifying these lesions and therefor suggesting that IVUS is a more sensitive imaging modality for identifying outflow obstruction vs. multiplanar venography. And when you looked at the core lab over read
this was for both the IVUS imaging and for the venography. And we at first calculated the diameter stenosis for both modalities we saw that with the multiplanar venography you tended to underestimate
the degree of diameter stenosis compared to IVUS and this resulted in missing about a quarter of the lesions that were greater than 50% diameter stenosis. And in part IVUS intended to score the lesions more severe for the same lesions compared to venography and this was statistically significant.
When we looked at CSA measurements from the IVUS system and also calculated off the venography in the core lab we saw again that venography missed about 18% of the significant greater than 50% CSA lesions even with reviews.
And this resulted in a change of procedure in about 60% of the patients there was a change in the decision about whether to treat of not and in 50 of the patients the number of stents changed from either no stent to 1 stent or 1 stent to 2 stents.
So without IVUS your likely under treating iliac and common femoral vein obstruction. This was the uh, rVCSS scores after treatment in this group. On the right here in green is the improvement on the left worsening.
And you can see in large part these patients all improved uh, expect for this outlier here and then some patients there was no improvement and when you looked at a score a VCSS score greater than 4 as being significant at 1 and 6 months there was a significant improvement post intervention.
And we see here in this receiver operating curve that IVUS best predicted clinical improvement at 6 months. And so we see that IVUS was more sensitive accurate for identifying significant lesions and the iliac and common femoral vein segments. It was the best guide for stent intervention
and it appears that if use a 50% cut off either diameter or CSA reduction it best predicts that intervention will lead to an improved clinical outcome at 6 months. Thank you.
- Yeah, thank you very much. Unfortunately Dierk Scheinert couldn't come, so thankfully he's allowed me here to take this presentation over so thanks a lot for this. So these are the latest 5-year results of the INCRAFT device from Cordis Devices currently under FDA review not yet approved
in the US, but in Europe. These are the conflict of interests, this is (mumbles). So this device is a three-piece modular system, low porosity polyester. You can bilaterally in-situ length adjust it up to 3cm. And the main feature I think with this device
is it's a low-profile device, 13 Fr inside 14 Fr outside except the biggest body which has an outer diameter of 16 Fr. The innovation study that was 60 patients, you can see here some objectives. So the question was whether you could deploy it
accurately where you wanted to have it without any type I, III, and IV endoleaks and of course there were also some other primary and secondary endpoints and again follow-up had to be done up to five years. This is a busy slide just showing you,
please look to the right side, to show you that there were quite some violations of the recommendations in which kinds of anatomies to implant this craft. Here for example neck lengths less than 10mm, here were some patients implanted.
Also angulations over 60 degrees, three patients, there were some thrombus in the neck, and here you can see aortic bifurcation smaller than 18mm, there were quite some patients and especially the iliac sealing length was shorter than 10mm in nearly 50% of the patients
and also the diameter of the external iliac arteries were nearly 50% lower than 7mm. Here the freedom from endoleaks type I was one at 30 days which has been resolved and another one developed after 30 days which also has been involved. No type III.
Stent graft patency after 30 days also 100% and otherwise also no other adverse events with this device at thirty days. So to answer the question with this device to the first question of (mumbles) will lighter fabrics and stent material decrease EVAR durability?
Will there be more endoleaks I, III, or IV? You can see here the long-term data so no Ia endoleak developed over four and five years, there was one Ib endoleak which developed at four years which also was apparent at five years. No type III endoleak.
One graft patency failure with a (mumbles) occlusion here at four years which also was here at five years. No migration, one fraction of the (mumbles) proximal third graft, otherwise it was very safe. You can see here once again the Kaplan-Meier curve for type I endoleaks through five years here
with type Ib here later on, and this is the patency Kaplan-Meier curve also showing here the good patency at five years, and this is freedom from second large vent. Here I don't have any data whether this is type II endoleak or not so this still has to be reported and clarified.
So to conclude the INCRAFT performed well on long-term while overcoming more difficult access morphologies. The endograft can be utilized in patients with demanding access and vessel morphology, and there are more studies ongoing.
There is one in the US and Japan where we wait for long-term data, 190 patients and also from Europe's 180 patients also there we still wait for long-term data. Thank you.
- Thank you very much. Thank you, Frank, for inviting me again. No disclosures. We all know Onyx and the way it comes, in two formulas. We want to talk about presenter results when combining Onyx with chimney grafts. The role of liquid embolization or Onyx is listed here.
It can be used for type I endoleaks, type II endoleaks and more recently for treatment of prophylaxis of gutters. So what are we doing when we do have gutters? Which is not quite unusual. We can perform a watchful waiting policy, pro-active treatment in high flow gutters,
pro-active treatment low flow gutters, or we can try to have a maximum overlap, for instance with ViaBahn grafts 15 centimeters in length or we can use sandwich grafts in order to reduce these gutters in type I endoleaks. Here, a typical example of a type I leak treated with Onyx.
And here we have an example of a ruptured aneurysim treated with a chimney graft. And here is what everybody means when they're talking about gutters. Typical examples, this is what you get. You can try to coil these
or you can try to use liquid embolization. Here's the end result after putting a lot of coils into these spaces. What are these issues of the chimney-technique type I endoleak? Which are not quite infrequent as you see here.
Most of these resolve, but not all of them. So can we risk to wait until they resolve? And my bias opinion is probably not. Here, the incidents of these type endoleaks is still pretty high. And when you go up to the Arch
the results can even be different. And in our own series published here, type I endoleak at the Arch were as high as 28%. A lot of these don't resolve over time simply because it's a very high flow environment. Using a sandwich technique is one solution
which helps in a lot of cases but not all of these simply because you have a longer outlet compared to a straightforward chimney graft. You can't rely on it. So watchful waiting? There are some advocates who
prefer watchful waiting but in high flow gutters this is certainly not indicated. And the more chimneys you have, like in a thoracoabdominal aneurysm with four chimneys, the less you can wait. You have to treat these very actively,
like you see here, in these high flow areas. Here a typical example, again symptomatic aneurysm with sealing. Here Onyx was used but without any success. So what we did is we had to add another chimney and plus polymer sealing and then we had a good result.
Here some results, only small serious primary gutter sealing using Onyx with good results in a type I leak. But again, this is only a small series of patients. Sandwich technique already mentioned. When you use, like we did here for chimney grafts in the arteries, you do need Onyx otherwise you
always get problems with these gutters and they do not seal over time. Another example where liquid polymer was used. And here again, you see the polymer. The catheter in order to inject the polymer is very difficult to see but with a little bit of experience
you know where you are. And again, here it is, the Onyx, a typical example. Here another example of the Arch, bird beacon effect, extension, chimney graft. Again the aneurysm gets bigger. And so a combination of using proximal extensions
plus chimneys plus liquid embolization solves this problem after quite a long period of time. And here typically is what you see when you inject the Onyx. This does not work in all cases. Here we used Onyx in order to seal up the origin of the end tunnel.
This works very nicely but there is so ample space for improvement and in some cases it's probably better to use a fenestrated branch graft or even the opt two stabler instead of using liquid embolization. Thank you very much.
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