- Thank you for the opportunity to present this arch device. This is a two module arch device. The main model comes from the innominated to the descending thoracic aorta and has a large fenestration for the ascending model that is fixed with hooks and three centimeters overlapping with the main one.
The beginning fenestration for the left carotid artery was projected but was abandoned for technical issue. The delivery system is precurved, preshaped and this allows an easy positioning of the graft that runs on a through-and-through wire from the
brachial to the femoral axis and you see here how the graft, the main model is deployed with the blood that supported the supraortic vessels. The ascending model is deployed after under rapid pacing.
And this is the compilation angiogram. This is a case from our experience is 6.6 centimeters arch and descending aneurysm. This is the planning we had with the Gore Tag. at the bottom of the implantation and these are the measures.
The plan was a two-stage procedure. First the hemiarch the branching, and then the endovascular procedure. Here the main measure for the graph, the BCT origin, 21 millimeters, the BCT bifurcation, 20 millimeters,
length, 30 millimeters, and the distal landing zone was 35 millimeters. And these are the measures that we choose, because this is supposed to be an off-the-shelf device. Then the measure for the ascending, distal ascending, 35 millimeters,
proximal ascending, 36, length of the outer curve of 9 centimeters, on the inner curve of 5 centimeters, and the ascending model is precurved and we choose a length between the two I cited before. This is the implantation of the graft you see,
the graft in the BCT. Here, the angiography to visualize the bifurcation of the BCT, and the release of the first part of the graft in the BCT. Then the angiography to check the position. And the release of the graft by pushing the graft
to well open the fenestration for the ascending and the ascending model that is released under cardiac pacing. After the orientation of the beat marker. And finally, a kissing angioplasty and this is the completion and geography.
Generally we perform a percutaneous access at auxiliary level and we close it with a progolide checking the closure with sheet that comes from the groin to verify the good occlusion of the auxiliary artery. And this is the completion, the CT post-operative.
Okay. Seven arch aneurysm patients. These are the co-morbidities. We had only one minor stroke in the only patient we treated with the fenestration for the left carotid and symptomology regressed completely.
In the global study, we had 46 implantations, 37 single branch device in the BCT, 18 in the first in men, 19 compassionate. These are the co-morbidities and indications for treatment. All the procedures were successful.
All the patients survived the procedure. 10 patients had a periscope performed to perfuse the left auxiliary artery after a carotid to subclavian bypass instead of a hemiarch, the branching. The mean follow up for 25 patients is now 12 months.
Good technical success and patency. We had two cases of aneurysmal growth and nine re-interventions, mainly for type II and the leak for the LSA and from gutters. The capilomiar shows a survival of 88% at three years.
There were three non-disabling stroke and one major stroke during follow up, and three patients died for unrelated reasons. The re-intervention were mainly due to endo leak, so the first experience was quite good in our experience and thanks a lot.
- 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.
- Thank you, thank you Frank for inviting me, again. The ascending aorta, as you know, is still the holy grail of endovascular aortic therapy. Especially, when dealing with true aortic aneurysms. There are a lot of contraindications to ascending stenting as we have listed here. So, these are all good cases for aortic surgery.
On the other hand there isn't a reason to treat some of these patients as partially high-risk patients with Endo. What about the technique? Transvalvular manipulation is essential. You basically have to do what cardiologists
are doing when they perform a TAVI procedure. And you have to know how to get across the aortic valve. There are straight forward cases like pseudo aneurysms as you can see here, which you can treat with coronary angioplasty and subsequent stenting. But the problem
or the real challenge are true ascending aneurysms. So, there are two options, bending of the ascending aorta in order to create a proximal landing zone or bending of all the ascending aorta. What about the technical details? Of course, a mediastinotomy is required.
You can use a mediastinotomy and we prefer a polypropylene mesh, which you see here. Which is additionally covered with a PTFE wrap. Just in case a recent otomy is required to prevent adhesions between the posterior
surface of the sternum and the ascending aorta. This creates downsizing of the aorta and facilitates endo-grafting here. Here typical example, the usual configuration of the true ascending aortic aneurysm wrapping with polypropylene mesh is what you get.
So, here you have your landing zone for the stent graft. When you dissect you have to circumferentially dissect the aorta. You have to make sure that you don't get into too close contact with the pulmonary artery. Here again, mediastinotomy in most cases,
is sufficient to do the procedure. Diameter reduction can be calculated according to this formula then I do know the length of my graft. You can combine this with supraoptic de-branching or bypass procedures whatever is
necessary in order to deal with this. In a lot of these cases get a landing zone for complete endo-treatment of the aortic arch with Sandwich grafts or similar techniques. We do know from these bio-mechanical studies that wrapping of the aorta reduces shear stress.
The whole concept only works in an ascending aorta up to a diameter of 6.5 cm, but no more. Here typical example, downsizing all the proximal landing zone. Subsequently, what you do get in some of these cases is in falling through here a stent graft makes sense
and then you can treat these patients with a stent graft. You would use a chimney in order to avoid compromising the origin of the innominate artery. Again, a typical example. The question is why do I have to use a stent graft at all after wrapping.
The answer is because you want to get a smooth inner surface and you don't want to have thrombus inflammation where the wrapping causes in-folding, but in all these cases you get very good results. Durable result, in term of the mediastinotomy. The mediastinotomy is very well tolerated
by these high risk patients. When you look at the age of these patients we have no neurological complications. No severe adverse events. This is a procedure, which can be offered to high risk patients
who have a lot of contraindications for open aortic surgery. Of course, this will be the future but not until maybe in ten years from now. Thank you very much.
- Good afternoon. So as we've already heard, traumatic injuries are the leading cause of death and disability in children over the age of one. Fortunately, these types of injuries are relatively infrequent, most commonly involving the lower extremities, for example femur fractures,
causing disruption of the SFA or popliteal artery, or the upper extremities, supracondylar humeral fractures will cause damage to the axial or to the brachial artery. Retrospective review of a children's registry from 1993-2005 with 103 patients all of whom were under the age of 18, most were males.
The majority are penetrating wounds. And most frequently, the extremities were involved. Open surgical repair was favored, primary repair when possible, vein patches for use for those under the age of six, and an interposition graft or bypass was used
for those over the age of 12. Non-operative management was selectively chosen in about 10%, and the outcome in this cohort, 10% mortality, 11 amputations, and limb length discrepancy did become a problem over time, necessitating revascularization in 23%.
A nationwide Swedish registry from 1987-2013 looked at 222 patients, children under 15. In this scenario, 2/3 were male, 2/3 had blunt trauma. Once again, upper extremity injuries were more commonly seen in those under 10. Lower extremity injuries more frequently seen
in those between the ages of 11-15. With that cohort that we talked about, 96% were treated with open surgical repair, similar to what we saw before. Interposition grafts, vein patches for the young, and primary repair whenever possible. However, endo therapy was introduced in this scenario,
with eight patients undergoing intervention for axillary, subclavian artery, iliac, and aortic trauma. A summary of four large series was pooled here, and essentially shows you once again the majority of the injuries are in the extremities. The gold standard to date remains open surgical repair,
either with patch, endo anastomosis, or interposition graft, depending on the age and the location. Lajoie presented this abstract, which is a single center retrospective review, nine years, 60 patients, all under the age of 18. And once again with vascular trauma pediatric group,
majority of treatment is with open, however 16% underwent endovascular intervention with embolization, stents, and stent grafts utilized. None of the stents were implanted in anyone under the age of 13. Follow-up six weeks showed no difference
in the amputation rates or the mortality rates, however reinterventions were certainly higher in those who underwent endovascular therapy. National Trauma Databank from 2007-14 of pediatric trauma under the age of 16. 35,000, so it's a very large cohort.
And you're going to see here, it's not just a trend. This was statistically significant. There is an increase endovascular therapy utilization across the board in that time frame, and specifically for blunt trauma, increasing from 5.8% up to 15.7%.
And what you can take away from this is that the increased endovascular therapy was utilized in children over 12, larger hospitals, level one trauma centers, and those who resided in northeast. In addition to that, those who had a higher
injury severity score also underwent endovascular therapy. The most common procedures, embolization of the internal iliac, and TEVAR for blunt aortic trauma. Unfortunately, despite this, the in-hospital survival failed to improve.
So now there's a plethora of data out there, and multiple single-site institutional reviews of their own experience. Here's what I can say. I think there are some select indications for which endovascular therapy appears to be advantageous.
Without question, as you've heard already, the blunt thoracic aortic trauma. Here's a 17-year-old, fell from a seven-story building and successfully underwent endovascular intervention. Another case, a 16-year-old gunshot wound to the thigh, injury to the profunda femoris was a large
false aneurysm in the anteromedial thigh, who underwent coil embolization successful exclusion of this area where the pseudoaneurysm happened to be, but maintained perfusion through the SFA and the remaining branches of the profunda. Is there a role here for blunt femoral trauma in the child?
Well, I'm not a big fan of it, doing it in adults, but there is a paper on it. 13-year-old popliteal artery trauma, high ISS score, this occlusion was recanalized and a self-expanding stent placed. And I will note that a bridging technique was utilized.
Once the other injuries were addressed, the patient underwent bypass. 12-year-old with polytrauma, iatrogenic orthopedic screw injury to the SFA, successfully treated with a Jomed stent, and then planned bridging procedure,
who underwent open repair a few days later with an interposition vein graft from the contralateral leg. One more case, 14-year-old polytrauma, self-expanding covered stent placed for an axillary artery injury, and this was a planned procedure as a bridging technique. He, unfortunately expired prior to that opportunity
to perform the bridging technique on him with a bypass. So, in summary, I do think pediatric vascular injuries are uncommon. Open repair, once again, remains the gold standard. Endovascular therapy appears to be increasing, especially TEVAR and embolization.
Endovascular therapy in the extremities is an option as a bridge in older people over 12 who have higher ISS scores. And a nationwide pediatric database for arterial trauma would be beneficial. Thank you.
- 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.
- [Speaker] I wanted to talk about a specific subset of what we've just been talking about, last we talked, so traumatic aortic injuries. I have no relevant disclosures. As you know, most of these occurred just distal left subclavian, which has a fixation point and then the more mobile distal thoracic aorta,
which leads to the tear with blunt trauma. The purpose what we looked at is the traumatic aortic injuries of the chest that are distal to that first five centimeters by the subclavian. So we looked at our trauma registry for a little over six years and included patients that had
blunt trauma either car crash, motorcycle, pedestrian versus auto or falls. And on their trauma center CTA had evidence of an aortic disruption in adult patients. We did divide the groups based on five centimeter length from the take off of the left subclavian artery.
Measuring the distal point to the left subclavian to the first point of the intimal injury seen on the CTA. We did this measurement on the modified sagittal view of the CTA in order to standardized the measurements. And these were all the CTA's done within the trauma center. We chose this five centimeter length based on
radiologic data from a number of studies, two of which are listed here. That generally show the entry that usually occurs somewhere around 15-16 millimeters from the left subclavian and then all stop before five centimeters or most all stop at four centimeters.
That way we had two separate groups that truly appear to be different, different subsets of the same problem. This is a typical lesion that you would see and most of these were further down from the arch so that was very little trouble separating these two groups.
So we found 74 patients and the total 60 of which were in the usual zone what we call the first five centimeters. And then the interest group what we called the Unusual Site there were 14 patients or 19% of the 74. We looked at a number of characteristics
the first thing that came evident, was that although age and race made little difference, this was a disease that predominated by women. Two thirds of the women with unusual location injuries. Two thirds of the patients with unusual location injuries were women, where the standard for the
usual location was about 75% male. We then looked at the mechanism have a role in this unusual site of injury at car crashes and all the usual mechanisms found no difference in their statistical p value. You saw the age was around 40 median age.
And so we thought maybe preconditions.. Premedical conditions might have a role but that was not found either. Then we looked at basic physiologic characteristics as they came in and they are all listed here. And you can see none of these were statistically different.
You can note that the most of them were slightly tachycardic but as a rule were not hypotensive. We also looked at solid organ entries associated with these unusual unusual location aortic tears. And we found no difference in pulmonary, cardiac, spleen or liver entries.
We did find a difference in looking bony fractures in that we found thoracic spinal fractures were present in 50% of time with these aortic injuries in unusual locations. Which was the only fractures that we found statistically different between the two groups.
Again we used SVS classification and here was a major difference in that the unusual site had 80% were grade one or grade two, and most of them were grade one. Where as the usual location we had over half were grade three so there was a significant difference there.
And that results in a difference in management for 14% of the patients with blunt injuries at the unusual locations actually ended up getting a stent graft, where 66% at the usual location did. And then we have talked about grade two being somewhat arbitrary and judgmental,
we found that none of these patients grade two lesions had unusual side needed a stent graft or it was a side that they didn't need one. Where three out of seven at the usual location did. As far as mortality is concern it was also a higher mortality with the unusual location.
Although the length of stay was less, just possibly the effect of those patients died early on. They did not die though from aortic injury. They died from other cause, particularly traumatic brain injury and then later on in the ICU. So our conclusion are that when you look at these injuries
of the thoracic aorta. We didn't include abdominal. They can be divided into two groups. Those that are within five centimeters and those distally. The unique group tend to be lower grade, they tend to not need intervention,
they do have a worse mortality not related to the injury itself, they are associated with thoracic spinal fractures, and more common in female patients. So I think we need to look at this as two different entities.
- 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.
- Thank you again for the opportunity to discuss this topic on acute or chronic vein. Acute or chronic ovarian vein thrombosis. No financial relationships for this particular topic. An etiology is generally obstetric, although even in the obstetric population, it's rare about one in 2000 deliveries.
It's tends to be associated with infectious etiologies including postpartum sepsis, group B strep, ruptured ectopic, hydatidiform mole. There are other potential non-obstetric causes as well. Inflammatory processes that tend to affect the pelvis or the retroperitoneum including pelvic surgery,
certain malignancies, pelvic inflammatory disease, appendicitis, diverticulitis and inflammatory bowel disease. So the pathophysiology in pregnancy and why it occurs is you get significant fluctuations in the ovarian vein itself. The diameter of the ovarian vein
increases up to three times. This corresponds to over 60 fold increase in ovarian blood volume which may lead to ovarian vein incompetence. This incompetence and stasis coupled with Virchow's Triad and pregnancy, particularly in the postpartum period
with stasis in volume contraction, endothelial injury from the delivery itself and just the overall, hypercoagulability of pregnancy, result in this pathology. The clinical features are that, unlike chronic reflux and pelvic congestion syndrome,
this tends to be more frequently right-sided 70 to 90% of the time in the majority of case series. It's bilateral in a small percentage of 11% and left-sided in two to three percent. The reason again being that this is typically a postpartum issue and there was a dextroposition
of the gravid uterus, this results in typical retrograde flow in the left ovarian vein. However, the right ovarian vein which may be compressed and have difficulty draining results and integrated flow stay stasis,
and then this postpartum ovarian vein thrombosis. When it does occur, tends to occur within a week or so within the first 10 days postpartum. And it has a classic triad of where the majority of patients will have fever because there was some infectious component
to what's going on, chills, right lower quadrant pain in more patients than left lower quadrant pain. Again, corresponding with the anatomic distribution of the disease. In certain dramatic instances, it's been described that you can palpate
a sausage shaped tender mass, although this may be challenging in a postpartum patient and in someone, who has an elevated BMI. And if it's asymptomatic, potentially it's not pregnancy related but malignancy related.
The differential diagnosis is all other causes of acute abdomen including appendicitis, adnexal torsion, tube ovarian abscess, pyelonephritis, etc. Imaging is critical. Complications from this include septic emboli,
IVC or renal vein thrombosis. Again, propagation of thrombus into the respective draining veins, pulmonary embolis, ureteral obstruction just from the adjacent inflammatory process and mass effect and chronic pelvic pain in the long run.
So the diagnosis, you have to have a high index of suspicion. A Diagnostic laparoscopy is frequently done by the gynecologist and it may determine the source of abdominal pain and identify this.
And then a duplex ultrasound will identify a hypoechoic, hydrogenous, and it's tube shaped mess with inner echos, again adjacent to the psoas muscle as shown on this diagram. The sensitivity is about 52% of duplex ultrasound. So really the diagnosis ends up getting made
by CT scan or MRI, as seen in the upper right hand corner. The CT scan will show this sausage shaped mass running along the paracolic gutter. MRI is nearly a 100% sensitive and it has the added benefit of determining the acute or subacute of the disease process.
So the treatment it's typically anticoagulation, for a full anticoagulation course for DVT as well as antibiotics. Interventional treatments are kept to a minimum and it can be an IVC filter which would have to be placed suprarenal in these instances,
partIcularly for the right gonadal vein. And then percutaneous thrombectomy and surgical techniques. Again, this is exceedingly rare but retroperitoneal or transparent neal exposures of the gonadal vein are relatively straightforward.
The treatment of chronic tends to be that for refluxing ovarian vein and pelvic congestion syndrome, and that's already been delineated. So to conclude, you have to have a high index of suspicion. MRI is the most sensitive study. It can tell you about acute and subacute.
It's the standard of care anticoagulation with antibiotics and for refractory patients, endovascular versus surgery, and then for chronic, the treatment for pelvic congestion syndrome. Thank you.
- Thank you for the opportunity again to discuss this topic on Angiovac Venous Thrombectomy. A large component of the talk was already completed and very eloquently. But, hopefully I can add a little bit extra. No financial relationships to disclose. This is just, briefly, to reinforce that
there are plenty of guidelines for dealing with medical management for deep veined thrombosis. For invasive treatment the attract trial has brought on additional insight into what's appropriate and certain considerations in terms of risks and benefits. But there's still questions, and so, ultimately, there's,
it's always a discussion about the risks versus the benefits, and the treatment is tailored to the patient. And what happens when you're, when you get to eliminate the risk of TPA, that certainly changes things. Some of the considerations are the severity of presentation,
certainly, like the picture, most of us would treat symptom duration. We would prefer to treat acute if we can. That's at least two weeks, at least for an acute component of an acute on chronic disease. But potentially longer.
Life expectancy, activity level, bleeding risk is what is in the back of our minds, even for patients who have to be heparinized, even if they don't have to be on TPA. And then it's a discussion. So, the patient has to be on-board. So, Angiovac when and where?
So, in general some of the patients whom we've trended towards treating, are those with contraindications. Either relative or a strict lytic therapy, acute thrombus, less than two weeks, but subacute thrombus can also potentially be dealt with, a thrombus that's been there for greater than two weeks.
In general, in terms of anatomic factors, it's really designed to take out intervascular foreign material from the venous system. And, it's generally starting to trend towards the right atrium. Whether it's PEs in-transit, pacemaker lead vegetations,
perhaps at the time of complex lead extraction. There have been additional case reports of tricuspid endocarditis and debulking that. And then large volume thrombus in the intravening cava, and in particular with filter thrombosis, and the cases, such as in the image here, where thrombus extends cephalad
to the filter. But again, all patients with ilio caval thrombus may be considered for this treatment. We had some combined data, that needs to be put forth. But, essentially 23 procedures, between two institutions. Most of them with strict contraindications to thrombolysis,
three of them with thrombus cephalad to filter. But as well, two aortic cases, and one right atrial case. And the results, were technically successful in 19 out of the 23 cases. In four cases, the thrombus was just too chronic, probably wasn't a patient who was, probably a patient
selection issue. And there were two mortalities on the three months follow up. And remember these are some of the most significant and advanced versions of disease. There is a registry data base still,
where data is still being accrued by Dr. Moriarty. But again, the tendency now is to move towards the cardiac, the right atrial, pathology. And most recently there is a series of case reports, on, that pertain to this approach for management of right-sided endocarditis and debulking
in addition to administration of antibiotics. So, how do you plan? A lot of it is just pre procedural imaging, knowing your inflow, outflow, and conduit with ultrasound, CAT scan and MR. A T, TE or a TEE maybe useful to determine if there is a
patent PFO microemboli that could potentially shower during these procedures. And so it's something to take into account. The reports are minimal, but something that be theoretically concerned about. IVC filters are sometimes utilized. Simultaneously,
with the filter placed in the super-renal location adjacent to the sheath. But, it's not necessarily because of the low risk for PE. And then, the crux of the procedure, is venovenous bypass. Typically with jugular, femoral, and, at least most individuals that I talk to who do this,
and myself included, get bilateral, jugular, and femoral vein access. Both for the circuit, as well as, for having additional access for utilizing your tools. Again, the goal is inflow, outflow and conduit. So, this is the proprietary portion of the procedure.
The Angiovac cannula is at 22 French cannula. It's the second generation, the third generation's coming out in a few months, most likely. It fits nicely through a 26 French dry seal sheath. It's got a ballon actuated angled funnel tip. Any reinfusion cannula is adequate, 18 French tends
to be appropriate. And you typically get a circuit with a bubble trap that gets your thrombus. You can run the venovenous bypass for up to six hours, recording into the IFU. And there's heavy utilization of adjunctive tools
to clear the thrombus. So, just some examples, with the a cannula in the right jugular and the reinfusion cannula in the left jugular bilateral, femoral vein access, and this is what the entire circuit might look like. And these are the kinds of results you get.
You get, you do one pass from the top and may do another pass from the bottom. Get your thrombus in the bubble trap and those are the results. So, who do we treat? It's a risk to benefit ratio discussion.
Ilio caval, right atrial thrombus, and mobile intravascular object pathologies. Less than two to four weeks ideally and venovenous bypass with extensive use of adjunctive tools. This was a patient with a super-renal filter
thrombused in renal failure and it all recovered, and the stent was plastered to the side. Thank you.
- When stenting are not enough, venoplasty stenting is undoubtedly the treatment of choice in relieving iliocaval obstruction and we have no doubt on what we can technically today obtain with this technique. But open surgery still has a place. The place for the iliocaval segment is today limited
only to oncological patients, their trauma. The disease, given by PTS, is not justifying an open surgery on those segments. But in some cases, at least less than ten percent in our federal center like we are, endovascular technique alone may be not sufficient
to provide durable patency of the iliocaval stenting. An open surgical approach, limited to the common femoral vein, can be required in addition to iliocaval stenting. And I would like to underline that open surgery should not be confused with open access
in event of catheterization failure. It's completely different. At the end, what we apply is endophlebectomy, which is the surgical removal of intraluminal fibrotic tissues. And contrapulizes of the extraluminal damage.
After endophlebectomy, the caliber of the vein is restored by means of bovine pericardium patch. In order to go back to the normal anatomy. Which are the indications for this type of operation? The main indication is to improve the inflow. When the deep femoral system confluence
is inadequate or the axial system is not preserved we have to try to improve the inflow at that level. And it is an essential moment to get a stable patency in the iliocaval segment. The second indication is to provide sufficient room for adequate stent expansion.
If there is lots of rubber and hard tissues that occupies the commofemoral vein, maybe in the long term, the stent can be sufficiently, adequately expanded. And if we remove this tissue we can get a better stent deployment.
The third indication is to reconstruct the vein conduit when it has been lost. This may happen after trauma, after drug injection, and after heterogenic problem. When the vein wall is too damaged, to be treated only by stenting or
only by endophlebectomy, a new conduit can be maybe the better option. What we apply today is a tubulization of bovine pericardium in order to obtain a correct way. And this is probably what we have to underline much more than everything else,
it is a type of hybrid procedure. The operation of endophlebectomy on new oxcilization are rarely performed alone today. We should go down with the stent if required to cover the endophlebectomy area and to treat iliac obstruction in the same moment.
As we listen before, the endophlebectomy limits is to open up the deep femoral conference and the stent usually stop over there. And it is essential because at the present, if we do not apply this, we can say, a kind of protection way to treat
the endophlebectomy segment, its difficult to maintain a long term patency. In this type of operation at the present, we do not apply anymore AV fistula which was limited in our historical work. I would say that today, open surgery
and hybrid procedures are essential in post traumatic treatment strategy. Outcomes in complex cases can be strongly improved. And I would like to underline that it is complex cases. This is not a surgery that is applied in every case of iliocaval stenting.
Its, there has to be attentively, selected because this type of surgery is undoubtedly very delicate, but we can get very good results and despite what we can think, get a good patency over time. It can really today be something
that we can obtain quite attentively. Thank you so much.
- Just going to do a little bit of a deeper dive into the types of nutcracker syndrome. I think most everyone knows this one. The anterior nutcracker syndrome in which the left renal vein is compressed as it passes between the aorta and the SMA, and this is definitely the most common
and certainly the most written about, but there's also posterior nutcracker syndrome in which there's a left renal vein which is retroaortic, and in this case it's compressed between the aorta and the spine, and then even more rare is the atypical nutcracker
in which there is a truncular vascular malformation trapping the left-sided IVC and renal vein between the SMA and aorta. Why do I mention these? I mention these because they inform the decision for open surgical repair when necessary.
All treatment options for nutcracker are directed to reduce venous hypertension, and we have the generally armamentarium of vascular procedures as I've listed here. Today my task is to discuss the open surgical options and really the two most important ones
are the versions of left renal vein transposition that I've listed here and have been discussed by Dr. Gloviczki and then gonadal vein transposition which, in our institution, is preferred if the anatomy is suitable. So since I'm following Dr. Gloviczki
I had to list all the papers from his institution, but this is the one that's most (mumbles) to my talk. This is their experience with left renal vein transposition versus conservative management in 23 patients, about 50/50, and what they found, if you look at their results and the characteristics of the patients that they treated,
were that if they selected their patients well, and by that I mean patients with appropriate anatomy and appropriate symptoms, they had excellent results when using left renal vein transposition to treat nutcracker syndrome. This is the other manuscript that Dr. Gloviczki mentioned,
so this is a version of open repair that includes stenting plus left renal vein transposition with suturing the stent in place that I think they hope will deal with the issues of migration in renal vein stenosis. So far their early results are excellent.
And then this is a meta-analysis, also mentioned by Dr. Gloviczki, and one of the elements of this meta-analysis was a surgical arm, if you will, although it wasn't really an arm since it's not a study, but they describe those patients
that were treated surgically. So what did that look like? Well in this meta-analysis they found that open surgical approach was associated with resolution of symptoms in the majority of patients, there were very few complications,
no renal failure or mortality, few postoperative complications in this manuscript as well as in our experience. By far (mumbles) the most common postoperative complications are ileus and hematoma, and freedom from re-intervention was fairly good.
75% at a year and 70% at 12 months. So with regard to surgery, I think the selection of the surgical approach needs to based on the patient anatomy and the patient clinical characteristics. Ideally, master all techniques
so you can offer all of them to the patient. I'd like to highlight my favorite operation for this condition which is gonadal vein transposition. I'll go over how to do it in just a moment, but the idea is that you transect the gonadal vein. You mobilize it completely from
the pelvis to the left renal vein, and you transpose it onto the inferior vena cava, and this both achieves a decrease in pelvic hypertension and it decompresses the left renal vein beautifully but doesn't put the left renal vein itself at risk for thrombosis.
It also, which is important in young people, does not require a great saphenous vein harvest which sometimes may be necessary in certain versions of the left renal vein transposition. So here's the technique. You make a mini-laparotomy,
do standard retroperitoneal exposure, mobilize the gonadal vein, and implant it onto the IVC. Here is a case of posterior nutcracker syndrome. You can see that renal vein transposition would be really hard here. There's the gonadal vein.
This patient was successfully treated, and then another patient with atypical anatomy who was successfully treated with a right gonadal vein transposition, and we actually wrote this up in case reports. So lastly, I just wanted to quickly review our experience.
We've done 15 gonadal vein transpositions. We've had excellent success, 100% technical and 93% clinical. The caveat with that is we have a really short follow-up, so it's hard to say yet whether we'll have the problems with clinical recurrence and restenosis.
So in summary, I think we are waiting a good renal stent, but gonadal vein transposition currently, I think if it's a large gonadal vein, is the treatment of choice if you're going to go this surgical route. Thank you.
- [Presenter] Dear colleagues, good afternoon. I present an update on the double-blinded trial on CCSVI Brave Dreams. This is my disclosure. The first data coming out from the Brave Dreams trial were affected by the (mumbles). Where venous PTA did not demonstrate additional effect
on the measure of disability and the new MRI lesion in relapsing remitting (RR) Multiple Sclerosis group at 12 month follow up. The major limitation of the trial is the inefficiency of balloon angioplasty in restoring flow in all the presentation of CCSVI
because in the prime, the flow was restored just in 79% of people. It means in favor of gravity and CCSVI criteria were solved in only 54% of the PTA arm. However, the technique demonstrated to be safe. Pre-operatory morphology affects the effectiveness
of PTA in jugulars, and Giaquinta demonstrated that patients who exhibit hypoplasia, external compression, or longitudinal endoluminal defects did not respond very well to the treatment. And commenting on this, Moneta proposed an additional post hoc analysis focusing
on the PTA responder group identified by Giaquinta in the materials of Brave Dreams trial. So Ladies and Gentlemen, is the hypothesis to be rejected? The CCSVI hypothesis could be considered valid if the subgroup with restored flow
following balloon angioplasty shows benefits compared to the subgroup in which the PTA did not work. So we performed a sub-analysis by comparing the patients with jugular flow not Doppler detectable in upright at 12 months, respect to those
who presented a mono-directional phasic jugular flow. The flow data of the balloon angioplasty arm was matched with a caffeine point, which have accumulation of new lesion on MRI. And the result was extraordinary because 91% of people with restored flow in upright
showed no lesion accumulation. This time the analysis was significant also at 0-12 months where we found 77% of people with restored flow, lesion free. And more than 20% of people protected by PTA were near follow up.
So Ladies and Gentlemen, in conclusion, PTA is safe but restored the flow in favor of gravity in the jugulars in just 79% of patients. However, a post-hoc analysis demonstrates a significant decreased risk of new lesion development at MRI in patients with restored jugular flow
following balloon angioplasty, as compared to those with absent flow and/or to sham. Further analysis and investigation may provide the pre-operatory ID of such a subgroup of responders. Thank you very much.
- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.
They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression
if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.
Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.
This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,
and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients
who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,
and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,
symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.
There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,
again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,
six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,
it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse
if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective
in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.
This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent
because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common
in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.
So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,
those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,
like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.
And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,
get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.
If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners
over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,
it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,
look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.
That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,
then I would do something endovascular. Thank you.
- Good morning. Happy to discuss with you some of the issues of the currently available stents. Nutcracker Syndrome patients most frequently present with left flank pain, pelvic pain, hematuria, usually due to a significant narrowing in front of the aorta between the aorta and the superior mesenteric artery.
Open surgical treatment has been kind of a gold standard. Left renal vein transposition done most frequently followed by gonadal vein procedures or even renal auto-transplantation. Renal vein stenting, in this country, has been done using Wallstents or SMART stents.
In our experience, where we reported 37 surgical patients. We used stents only for secondary procedures. Three of the six stents had problems of either migration or in-stent restenosis. There is a systematic review in the JVS-VL, recently published, 180 patients, 7 series.
Interestingly, 175 were treated in China with good clinical results in 6-126 months. Stent migration was observed from 0 to 6.7%, depending on the series. We have seen stent migration, sometimes it's immediately during t
and that's obviously the easiest to take care of. Or immediately after, before any healing, that is also a more favorable situation. The problem is when it travels to the heart. It is not frequent, but it happens.
This is the largest series, 75 patients, stented, 5 of them had migration. Two of them to the right atrium, one of them required a medium sternotomy to remove it. Stents not only migrate, although again it's rare,
but even one patient is too frequent in this series that usually involves young, female patients. Stents in this position unfortunately can also fracture. If they don't fracture, they can thrombos. If they don't thrombos, they can be compressed.
If they don't compress, that's a stiff stent, it practically always will perforate their renal vein because of the arching configuration of the renal vein and because the unavailability of less than four centimeter long stance. So it is a problem.
It can actually cause significant, severe migration, completely occluding the inferior vena cava together with perforation of the renal vein. Obviously these cases require open surgical repair,
and have a chance to remove a few of these stents. Percutaneous retrieval, fortunately, is possible in about 90% of the cases, and sometimes, if it doesn't cause significant cardiac injury even from the heart or the pulmonary artery and
we had several case reports, of stents, especially after the TIPS procedure, early on, that migrated into the central circulation that would be removed with different types of techniques, of snaring and pulling the lost stent into a large sheath,
whether you snare it at the end or you snare it in the middle. There are good case reports. This patient that we had, we could use a balloon, pull it down to the vena cava, and then from above and below, we could remove it
with a large sheath. Current stents, if you really don't want it to migrate, the only option we see is transposition patch and using hybrid procedure to fix the stents in the renal vein.
So, in general, open surgery remains the first line of intervention. Stents have a reported high mid-term success rate but migration, fracture, perforation, thrombosis, restenosis are problems and if you go to the FDA website, you see that there are much more cases than
those that are reported. So what do we need? We need dedicated renal vein stents that are short, flexible, resist fracture and migration, and we need them urgently. Thank you.
- My disclosures are not relevant. Joe showed this slide, this is the original SVS guidelines, which really, as he mentioned, is a lesion-based evaluation of what the trauma looks like. And, for the purposes of this discussion, we'll be focusing on grade three injuries. Which really means there's blood outside the aortic wall.
There is loss of integrity of all layers and there's a pseudoaneurysm. We've all transitioned to delayed TEVAR for grade one and two. But, what do we do with these grade three injuries? Where's the boundary between medical therapy
that puts the patient at risk of interval rupture and early repair? Which may, as I'll show, put them at risk of other problems. This is a pretty widely adopted prac the idea of treating traumatic pseudoaneurysms,
at least initially, with some medical therapy. This is a review of 18 studies, almost 1,000 patients. It showed really one in five were managed non-operatively. There is a very low rate of aorta-related mortality which will be a recurring theme on all the data I show you. And, there's a really low rate
of required late interventions. As true for many of our trauma-related literature, there's a really poor long-term follow-up rate. The AAST studies have shown us that delayed repair really can improve outcomes. There's a significant selection bias in
these are non-randomized trials for, I think, exclusively. But the reality is, if a patient can wait until stabilization of their other injuries, they do better if you can wait on repairing the aorta, both mortality and the paraplegia rates are lower.
But, it's not just completely a selection bias. There are maybe some other benefit here. And, one of the things that plays into play is: What are their other injuries like? What is their traumatic brain injury look like? And, we use this as a defining point at Grady
about figuring out whether someone really should be figured for early repair or not. If you look at this series of 300 patients with traumatic aortic injury, 248 had a concomitant brain injury, and those are obviously of a variety of different grades,
from a little blip on the CT scan to a potentially devastating neurologic insult. But, it's not uncommon to have to manage both injuries at the same time. That is the rule rather than the exception. They can be pretty significant
and, again, there's significant selection bias in this series out of Maryland. But, there's about a one third, one third, one third early repair, delayed repair or non-operative strategy. If you look at the non-op patients and the delayed patients, you can see
that we get to that very, very low mortality rate. The early repair patients, as you can imagine, are often associated with a fatal outcome. Now, that fatal outcome is not always a it is usually related to something else
and highlights the selection bias of series like this one, that show us that if you're sick when you come in with an aortic tear, you're going to continue to be sick regardless of whether we fix your tear or not. But, there is some other benefit, potentially. The traumatic brain injury is one piece that I've mentioned,
but it's not uncommon, I think we've all experienced situations like this where the trauma physician and the orthopedic physician and everyone who is taking care of these patients is really focused on a grade three aortic injury. And, it oftentimes allows for neglect
or missing of other injuries that may be more life-threatening. How do we avoid delay? There's a few areas where we can think about intervening. The first thing is getting a good radiographic grade, as Joe alluded to, and there's a variety
of different scoring systems. This ultimately amounts to a simplification of the Harborview scoring system which is the one that I personally have gravitated to over the last two years. Which demonstrates that for the old grade one and two
there is probably no benefit of repeat imaging, there is probably no benefit of intervention, and pseudoaneurysms should be fixed when they are stable and severe ongoing-rupture patients should be fixed right away. That assessment of stability is an important part of this.
Part of Dr. Crawford's interest, in particular, was evaluating the size of the pseudoaneurysm and the size of the hematoma. And so, all of these are things that we've seen before but they all probably behave a little bit differently. So, how do we look and see:
Are there specific types of injury that are more prone to rupture with non-operative therapy? And one of the things that's been assessed is the diameter ratio. I think Joe showed this data a second ago. Another is the size of the periaortic hematoma.
In this large series, if you had two of these three factors: a lactate greater than four, a mediastinal hematoma greater than 10 millimeters or a lesion to normal aortic ratio of greater than 1.4. That was 90% accurate in terms of theoretically predicting early rupture.
Which, if you just look at clinical judgment alone, goes down to 65%. Keeping in mind that clinical rupture, true rupture is very often a fatal event. There is a lot of value in moving that number from 65 to 90. If we can get good modeling that tells us
who is at particularly high risk of rupture in this selected group, there is a lot of potential benefit. Just as importantly, as I've mentioned earlier, if you have a higher aortic grade of injury, you are more likely to die but it does not predict aorta-related mortality.
Much of that is the selection bias that people with higher grades of aortic injury are fixed sooner and therefore are not candidates to die from aorta-related mortality. Let's skip through this. And then again, (audience member coughing)
the idea that we need additional information and we need better imaging, better physiologic data that predicts the need for early repair is the take-home message. The answer, as you can imagine, is more information. Part of what the Aortic Trauma Foundation is doing
is going to be evaluating: Are patients really going to do better with non-operative therapy if they have very specific criteria that allows them to be selected out? Are there high-risk criteria that we can figure out besides just eyeballing the CT scan and saying:
This is someone who's not going to do well if we sit on them. Thank you very much.
- 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, 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.
- Thank you so much. Seattle, like many other cities in the U.S. is facing a terrible, heroin epidemic crisis. We are the safety net for these patients. I was honored, when I was asked to came and share with you how we manage these patients at Harrow View Medical Center. Over the last few years, we have educated our ED doctors,
in order to avoid over-head page to vascular surgery. That they don't do any I&Ds at the bedside. If a patient with a history of IV drug use present with induration or pain on the groin. On those patients, they get triaged for sepsis, they get an IV access, can take some time.
They take labs, including blood cultures. If we can, we do ABIs, this is during the day, and we start the patient on broad-spectrum antibiotics. After that, the patient goes for a CAT Scan. The CAT Scan is really useful for us, it help us not only see the anatomy,
see if the cell is coming close to the external iliac or close to the bifurcation. But maybe even more important, it help us, and you can see the upper emissions, find a lot of needles that have broke and left over by the patients that --
It's a huge hassle for your team in the operating room. So once we have the CAT Scan. We go to the operating room, we get the patient under general anesthesia, we puncture the contralateral side, and this is our preferred method to
take care of this patient. We go up and over, we put the sheath at the end of the external iliac artery, we give some heparin, we do an angiogram that shows exactly where is the injury and we put an occlusion balloon,
usually like a 7 by 60 does the job. Once we have the ballon, we can then ride directly in the pseudoaneurysm. When you open, you take out all the clot and puss and all that tissue. And once you irrigate and debride,
you will see at the bottom, your wound. Usually you see the balloon inside the artery, with a rupture wall, and the proximal ends of the artery. So what we do with with arterial ligation, we resect to help the artery until we gain control, we paralyze vessel loops, remove the balloon
and we do the ligation both the stems and usually we try to preserve the bifurcation. It is a long puncture, it's not possible, we try to preserve our zincuflex, so the patient will have a collateral pathway to their leg. After that, we try to approximate the tissue on top,
or we do an sartorius flap. Now our patient that use black tar heroine, sometimes there's too much inflammation, too much puss, we just put the dressing and we come back in a couple of days for a wash out, to take care of the wound.
After that, the patient goes to intensive care unit, and you will notice that I didn't mention, we ever raise the foot. We don't put any pulse oximeters or do any studies. The foot is going to be okay. The patients usually have some kind of chronic compression
previously and they will tolerate ischemia pretty well. Patient goes to the ICU and the first thing that we do, we avoid hypotension, but we call ID and Pain Service. This patient's outcomes are going to be better if the pain is going to be well controlled, because they will be compliant with the treatment.
ID recommends that antibiotics treatment and helps with management other comorbidities. I know we're starting to have a lot of patients that have PE's during admission, so we try to rule out DVT study and we'll start the patients in treatment.
When we look at our cases, we have more than 50% patient that present with bacteremia, and of those, almost 40% was due to MRSA, so it's a very severe condition that the patient require several weeks of IV antibiotics. Post OP ABI, immediately,
we have a median of 0.41, so the leg is viable. And our amputation rate for these patients is very low. We have only lost 4 legs and of those 4 legs that we have to amputate, 2 patients we revascularized the immediate post-op period and both were infected.
So we actually avoid actively doing revascularizations in the accurate period. In conclusion, the vascular emergencies due to IV drug use are increasing and we as vascular surgeons should be prepared to deal with this and educate our colleagues
on how to treat them. Femoral artery ligation is well tolerated and we recommend not performing an immediate revascularization. The amputate rate is low and ID and Pain Service collaboration is essential for these procedures. Thank you so much.
- I have no disclosures that are relevant to this discussion. What I would start off with is, maybe you don't do it at all. Be careful what you ask for. This is very unforgiving work and know that going into it. The technical considerations a
absence of arteriosclerosis, it's a small vessel diameter and as we heard Dr. Eslami talk about, very high risk of vasospasm. The local clinical experience, I'm going to credit Dr. Jeff Friedman
who's one of our local reconstructive plastic surgeons, 10 patients underwent open surgery for repairs, eight arterial, two venous injuries. The age range 36 weeks of gestation to 12 months, Eight of the nine patients, 13 weeks of age or less. 90% of the injuries,
and we saw that again in Dr. Eslami's talk, are injuries that are iatrogenic as a result of invasive procedures performed on the effe cardiac catheterizations, arterial line placement,
direct arterial ligation, femoral vein injury, intra-arterial infusion or trauma. Most of these are like I menti femoral arterial lines, any sort of umbilical catheterizations,
femoral catheterizations and so on. One of the most important things is to do a real thorough evaluation, so in 70% of these cases they had a color flow doppler examination. Six patients had operative intervention. Doppler results verified intraoperative results
or ultrasound results in all cases and in one patient with preoperative arteriogram demonstrating accuracy of the diagnosis as well. No significant limb loss in these 10 patients, of course a small series despite prolonged ischemia times and I think that's probably one of the primary lessons
to take home is that kids tolerate ischemia fairly well and so to follow these would kind of be expectant treatment. Only one patient had toe amputations. Seven of the 10 patients survived, one early postop mortality, one late postop mortality and one nonoperative mortality.
Functional results were good, two with limb growth discrepancies. This is just to identify what you're looking at, make sure you're doing a good intraoperative ultrasound exam and know what you're getting into. This is just some examples of one child,
with obviously an ischemic limb there, this was from access from catheterization. You can see what the arm looks like, the hematoma down around the brachial artery and a microvascular repair there as you see. Going down and a little fasciotomy
all the way down into the hand, with a reasonable result. Of course, a nasty scar but a functional hand. The diagnosis am, doppler evaluation we place heavy weight on, the color doppler examination,
real time assessment of vessel patency, determine the level of occlusion. And then acutely the treatme acute intervention if obvious injury, discontinue the local catheter that's caused the injury,
anticoagulation with heparin, if possible, and really wait about six to eight hours before going unless the limb is totally threatened, warm packs, elevation, intervention if no improvement. And so, the operati
wide proximal and distal control, as you saw in that one case that I presented, complete division of the affected vessel, usually it's severely injured from the catheterization, proximal and distal thrombectomy using a #2 Fogarty, direct vascular repair if possible, vein grafts rarely.
I think Dr. Singh also mentioned that primary repair is better and we certainly believe the same way. And then fasciotomy is used liberally, postoperative anticoagulation again if possible.
suture usually with a microscope, interrupted sutures are a mainstay, papavarin and nitroglycerin generally work fairly well for vasospasm, again back to the ultrasound and then determine the appropriateness for operative intervention. You kind of need to know that going into it.
Operative intervention only in the case of no improvement and venous injuries are usually a little more difficult to treat and often surgical intervention gives poor results. If you just look at t am and doppler, suspected spasm or thrombosis,
conservative management first, if fails, six to eight hours eventually go to the operating room, if it resolves, obviously no care after that. In the future I think development of a team approach with plastic surgery, pediatric cardiology, pediatric surgery and neonatology is important,
establish early intervention program, and determine the possibility avoiding long term sequelae. Thank you very much.
- Thank you. Thank you again for the invitation, and also my talk concerns the use of new Terumo Aortic stent graft for the arch. And it's the experience of three different countries in Europe. There's no disclosure for this topic.
Just to remind what we have seen, that there is some complication after surgery, with mortality and the stroke rate relatively high. So we try to find some solution. We have seen that we have different options, it could be debranching, but also
we know that there are some complications with this technique, with the type A aortic dissection by retrograde way. And also there's a way popular now, frozen elephant trunk. And you can see on the slide the principle.
But all the patients are not fit for this type of surgery. So different techniques have been developed for endovascular options. And we have seen before the principle of Terumo arch branch endograft.
One of the main advantages is a large window to put the branches in the different carotid and brachiocephalic trunk. And one of the benefit is small, so off-the-shelf technique, with one size for the branch and different size
for the different carotids. This is a more recent experience, it's concerning 15 patients. And you can see the right column that it is. All the patients was considered unfit for conventional surgery.
If we look about more into these for indication, we can see four cases was for zone one, seven cases for zone two, and also four cases for zone three. You can see that the diameter of the ascending aorta, the min is 38,
and for the innominate artery was 15, and then for left carotid was eight. This is one example of what we can obtain with this type of handling of the arch with a complete exclusion of the lesion, and we exclude the left sonography by plyf.
This is another, more complex lesion. It's actually a dissection and the placement of a stent graft in this area. So what are the outcomes of patients? We don't have mortality, one case of hospital mortality.
We don't have any, sorry, we have one stroke, and we can see the different deaths during the follow-up. If we look about the endoleaks, we have one case of type three endoleak started by endovascular technique,
and we have late endoleaks with type one endoleaks. In this situation, it could be very difficult to treat the patient. This is the example of what we can observe at six months with no endoleak and with complete exclusion of the lesion.
But we have seen at one year with some proximal type one endoleak. In this situation, it could be very difficult to exclude this lesion. We cannot propose this for this patient for conventional surgery, so we tried
to find some option. First of all, we tried to fix the other prosthesis to the aortic wall by adjusted technique with a screw, and we can see the fixation of the graft. And later, we go through the,
an arrangement inside the sac, and we put a lot of colors inside so we can see the final results with complete exclusion. So to conclude, I think that this technique is very useful and we can have good success with this option, and there's a very low
rate of disabling stroke and endoleaks. But, of course, we need more information, more data. Thank you very much for your attention.
- Thank you Michael and thank you Dr. Veith for the invite. These are my disclosures. The one really (mumbles) is that I'm the study PI for the ACCESS PTS trial. So when we talk about DVT and post-thrombotic sequelae. If you take one to two patient, patients per thousand
who develop acute DVT in the US. You look at the numbers of population in the US and globally. Extending out these data, you can estimate there's about 2.5 million patients in the US with PTS and about 61 million globally.
The pathophysiology of venous disease is whether you talk about obstructive or not obstructive issues. And they're not advancing. That everything around the pathophysiology of venous disease and the sequelae
is about venous hypertension. When we talk about fem-pop occlusions, femoral, the axialization that comes from femoral vein occlusion may not always be adequate to decompress the elevated venous pressures, and when we see popliteal complete occlusions
that can cause severe PTS below the knee into the calf. So the rationale of intervention was if you can reduce the luminal obstruction and restore flow you should be able to reduce the venous hypertension, reduce the severity of PTS sequelae, and improve quality of life.
And this is just a movie showing on the left what access into a tibial vein with an occlusion and chronic DVT, chronic thrombosis, shows with the hypertension compared to the second day when we had that catheter in still from the tibial vein
and the decrease in the pressure and flow. So changing the chronic DVT paradigm was about ACCESS PTS. This was a steering committee that I was very honored to work with. This was a multicenter prospective study of 29 sites that had lower extremity DVT for at least 6 months
documented by ultrasound who had a minimum of femoral DVT and who had failed three months of conservative therapy including therapeutic anticoagulation and compression with a Villalta score of at least eight. The protocol here was basically
crossing the obstruction with CTO techniques, balloon angioplasty, the size of the expected vessel, placing the ecosystem in overnight for 12 hours minimum, and then doing a follow-up the next day with additional therapy if needed. On discharge they were given activity instructions,
blood thinner, and compression. Enoxaparin was the drug of use for one month before they were transitioned to an oral anticoagulant. So here are the demographics. 78 patients, 82 limbs, four of which were bilateral.
Separated by at least a month. The DVT mean age was 13.2 months. Advancing is very bad. The patient enrollment you can see here. What's that? Okay, thank you.
The patient enrollment you can see here. Of the 73 patients that were evaluable by the protocol at 30 days was 77 limbs. If you look at the breakdown of the DVT, 2/3 of them were infrainguinal only disease. The primary endpoint was a goal of
greater than or equal to four point reduction in the Villalta at 30 days in more than 50%. The actual was we reached that goal by 66% of the patients had an at least four point reduction in Villalta for p-value as you see. When you look at the Villalta results
there was a mean improvement of 49% over one year from 15.5 to 7.8. Now notice the 15.5 indicates a severe PTS. When you look at VCSS results there was reduction, or excuse me, an improvement of 43% alt one year from enrollment and treatment.
When you look at the VEINES Quality of Life. Again, a 36% improvement from 61 to 80. When you look at doppler patency of the femoral segments including the popliteal you can see alt one year, 365 days. The percent of patency was seen
basically at the 90+ percentile rate. Washout was seen to be no different between baseline and post PTA. After EKOS there was a slight improvement, not statistically significant, but after the adjunctive therapy the second day
there was a significant improvement from baseline to the end of treatment in the washout phase. When you look at the venous scoring. Thrombus, which really was occlusion scores, all three venous scoring methods of Marder, AVR, and Ouriel were all improved
through the end of completion. The safety endpoint. There were 78 patients, one major bleed from epistaxis during intubation, and there was a recurrent DVT in three, one PE was out of the hospitalization.
Just an example of a two-year-old clot in the femoral popliteal segment, and this was after the follow-up. You can see that flow is restored. This was the two year follow-up doppler. That patient was a marathon runner, couldn't walk very well,
had venous claudication, was unable to run at all, and 6 months after treatment she went back to running a marathon, and this was her two year follow-up doppler showing patency. The conclusions are that ACCESS PTS was statistically significant,
the primary endpoint was reached, the Villalta VCSS, and VEINES Quality of Life improvements were all statistically significant, improvement in time-to-washout was significantly improved, and the persistent patency on doppler, you can see, was about 90+%.
So can ACCESS PTS change the paradigm of chronic DVT treatment? I think so. Removing luminal obstruction, restoring flow, seeing vein function as a conduit, improving on doppler ultrasounds,
with continuous and persistent reduction/resolution of venous hypertension, showing significant improvement in PTS sequelae after 365 days would suggest so. This is a safe and effective treatment for recanalizing chronic venous occlusions,
and hope is here for chronic DVT, post-thrombotic patients, that hopefully will lead to further studies and treat the, change the paradigm treatment. Thank you.
- Thank you Dr. Melissano for the kind interaction. TEVAR is the first option, or first line therapy for many pathologies of the thoracic aorta. But, it is not free from complications and two possible complications of the arch are the droop effect and the bird-beak. I was very interested as Gore came up with the new
Active Control System of the graft. The main features of this graft, of this deployment system are that the deployment is staged and controlled in putting in the graft at the intermediate diameter and then to the full diameter. The second important feature is that we can
optionally modify the angulation of the graft once the graft is in place. Was very, very interesting. This short video shows how it works. You see the graft at the intermediate diameter, we can modify the angulation also during this stage
but it's not really used, and then the expansion of the graft at the full diameter and the modification of the angulation, if we wished. This was one of the first cases done at our institution. A patient with an aneurysm after Type B dissection. You see the graft in place and you see the graft after
partial deployment and full deployment. Perhaps you can appreciate, also, a gap between the graft and the lesser curvature of the arch, which could be corrected with the angulation. As you can see here, at the completion angiography we have an ideal positioning of the graft inside the arch.
Our experience consisted only on 43 cases done during the last months. Mostly thoracic aneurysm, torn abdominal aneurysm, and patients with Type B aortic dissection. The results were impressive. No mortality, technical success, 100%,
but we had four cases with problems at the access probably due to the large bore delivery system as you can see here. No conversion, so far and no neurological injury in this patient group. We have some patients who came up for the six months follow-up and you see here we detected one Type 1b endoleak,
corrected immediately with a new graft. Type II endoleak which should be observed. This was our experience, but Gore has organized all the registry, the Surpass Registry, which is a prospective, single-arm, post market registry including 125 patients and all these patients
have been already included in these 20 centers in seven different countries in Europe. This was the pathology included, very thorough and generous, and also the landing zone was very different, including zone two down to zone five. The mean device used per patient were 1.3.
In conclusion, ladies and gentlemen, the Active Control System of the well known CTAG is a really unique system to achieve an ideal positioning of the graft. We don't need to reduce the blood pressure aggressively during the deployment because of the intermediate diameter
reached and the graft angulation can be adjusted in the arch. But, it's not reversible. Thank you very much for your attention.
- 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.
- 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.
- 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.
- The only disclosure is the device I'm about to talk to you about this morning, is investigation in the United States. What we can say about Arch Branch Technology is it is not novel or particularly new. Hundreds of these procedures have been performed worldwide, most of the experiences have been dominated by a cook device
and the Terumo-Aortic formerly known as Bolton Medical devices. There is mattering of other experience through Medtronic and Gore devices. As of July of 2018 over 340 device implants have been performed,
and this series has been dominated by the dual branch device but actually three branch constructions have been performed in 25 cases. For the Terumo-Aortic Arch Branch device the experience is slightly less but still significant over 160 device implants have been performed as of November of this year.
A small number of single branch and large majority of 150 cases of the double branch repairs and only two cases of the three branch repairs both of them, I will discuss today and I performed. The Aortic 3-branch Arch Devices is based on the relay MBS platform with two antegrade branches and
a third retrograde branch which is not illustrated here, pointing downwards towards descending thoracic Aorta. The first case is a 59 year old intensivist who presented to me in 2009 with uncomplicated type B aortic dissection. This was being medically managed until 2014 when he sustained a second dissection at this time.
An acute ruptured type A dissection and sustaining emergent repair with an ascending graft. Serial imaging shortly thereafter demonstrated a very rapid growth of the Distal arch to 5.7 cm. This is side by side comparison of the pre type A dissection and the post type A repair dissection.
What you can see is the enlargement of the distal arch and especially the complex septal anatomy that has transformed as initial type B dissection after the type A repair. So, under FDA Compassion Use provision, as well as other other regulatory conditions
that had to be met. A Terumo or formerly Bolton, Aortic 3-branch Arch Branch device was constructed and in December 2014 this was performed. As you can see in this illustration, the two antegrade branches and a third branch
pointing this way for the for the left subclavian artery. And this is the images, the pre-deployment, post-deployment, and the three branches being inserted. At the one month follow up you can see the three arch branches widely patent and complete thrombosis of the
proximal dissection. Approximately a year later he presented with some symptoms of mild claudication and significant left and right arm gradient. What we noted on the CT Angiogram was there was a kink in the participially
supported segment of the mid portion of this 3-branch graft. There was also progressive enlargement of the distal thoracoabdominal segment. Our plan was to perform the, to repair the proximal segment with a custom made cuff as well as repair the thoracoabdominal segment
with this cook CMD thoracoabdominal device. As a 4 year follow up he's working full time. He's arm pressures are symmetric. Serum creatinine is normal. Complete false lumen thrombosis. All arch branches patent.
The second case I'll go over really quickly. 68 year old man, again with acute type A dissection. 6.1 cm aortic arch. Initial plan was a left carotid-subclavian bypass with a TEVAR using a chimney technique. We changed that plan to employ a 3-branch branch repair.
Can you advance this? And you can see this photo. In this particular case because the pre-operative left carotid-subclavian bypass and the extension of the dissection in to the innominate artery we elected to...
utilize the two antegrade branches for the bi-lateral carotid branches and actually utilize the downgoing branch through the- for the right subclavian artery for later access to the thoracoabdominal aorta. On post op day one once again he presented with
an affective co arctation secondary to a kink within the previous surgical graft, sustaining a secondary intervention and a placement of a balloon expandable stent. Current status. On Unfortunately the result is not as fortunate
as the first case. In 15 months he presented with recurrent fevers, multi-focal CVAs from septic emboli. Essentially bacteria endocarditis and he was deemed inoperable and he died. So in conclusion.
Repair of complex arch pathologies is feasible with the 3-branch Relay arch branch device. Experience obviously is very limited. Proper patient selection important. And the third antegrade branch is useful for later thoracoabdominal access.
- Thank you Lowell. - Good morning, and thanks Lowell and Jose, for the invitation to come back this year. I don't have any disclosures. Well, what we're going to talk is imaging the female pelvic veneous system. And the female pelvic venous system is a complex arrangement
of four interconnected venous systems, and really you have to understand the anatomy to understand the keys to imaging it and treating it, and that's the connections between the renal vein, both the left and the right ovarian veins, the tributaries of the internal iliac veins,
and the superficial veins of the lower extremity through the saphenofemeral junction. And central to all of this are the tributaries of the internal iliac vein. Which functions as a gateway between the pelvis and the leg, and really are exactly analogous to perforating veins,
connecting the deep veins of the pelvis to the superficial veins of the leg, and you have to have an intimate knowledge of this anatomy both to image it adequately, as well as to treat it. So classically, the internal iliac vein is thought as the confluence of three tributaries.
That is, the obturator vein anteriorly, tributaries of the internal pudendal vein, sort of in the middle of the pelvis, and the superior and inferior gluteal veins, and these communicate with the legs through four escape points
that the anatomists describe anteriorly as the obturator point or the "O" point, where the round ligament vein comes through the abdominal wall, the "I point. And medially in the thigh, pudendal or the "P" point, and posteriorly the gluteal point,
which communicates both with the posterior thigh as well as with the sciatic nerve and gives rise to sciatic varices. (coughs) From our standpoint today, I'm more interested in atypical, varices, that is, pelvic source lower extremity varices,
arising from the pelvis, anteriorly for the obturator vein, and from the round ligament vein, which communicate with the vulva, branches of the internal pudendal vein, which communicate with the perineum, and the medial thigh, and posteriorly, with branches of the superior and inferior gluteal vein.
So as far as imaging goes, we're interested primarily in two clinical scenarios which the imaging requirements are somewhat different. That is, atypical pelvic source varices without any pelvic symptoms, and atypical varices with pelvic pain, and the way that we study these with venography
are quite different. Although some people do pursue blind sclerotherapy from below, I do think imaging with venography adds substantially to both the control of the sclerosant, as well as how thoroughly you're able to embolize the pelvic tributaries.
And I personally like to do sclerotherapy of the varices with venography, and use direct puncture venography using either a 23 or a 25 gage butterfly needle, that's placed under ultrasound guidance. Contrast is then injected to calibrate both
the variceal bed as well as to track the tributaries, as I'll show a minute, up into the pelvis, and usually you can embolize about to the level of the broad ligament. Simultaneously, foam sclerotherapy is performed, using a combination of Sotradecol,
and Ethiodol as a contrast media, and then is followed both by Flouroscopy, using a reverse road mapping technique to subtract the bone and other things out, and follow the contrast through as well as with ultrasound as shown here.
And just as an example, here's some vulvar varicosities, that communicate both with the obturator vein up here, with the round ligament vein through the "I" point, as well as with the saphenofemoral junction here. And although you could do this blindly, I do think you get a much better understanding
of the anatomy and the volume of sclerosant required, doing it with venography. These are posterior thigh varicosities, that communicate through the "G" point here, and you can actually see the contrast refluxing into the inferior gluteal vein shown here,
and all of this can be treated with sclerosant. The second clinical scenario, is that of atypical varices with pelvic pain, in which case you do want to make sure you treat the pelvic variceal bed completely. And for this, the venography techniques are
balloon occlusion venography performed from above. My preference is right internal jugular vein approach, because it's easier to place the occlusion balloon into the right and left internal iliac veins, which a sequentially selected, and then I use a Berenstein occlusion balloon
and then place it just below the confluence of the internal iliac vein and the external iliac veins, inflate the balloon, inject contrast, which both blocks antegrade flow, and allows reflux into the varices. Most of the time you can't see these varices if you don't have an occlusion balloon,
and then as you see the varices, sequentially select more distal tributaries with a glide wire, put the balloon down, inflate it, and perform sclerotherapy and occasionally, depending on the size of the vein, use coils if you need to. Here is an example of the balloon
in the internal iliac vein, you see the "O" point. We've already sclerosed the contralateral obturator vein, and you see this classical obturator hook here, which is classical for the obturator vein. Here the occulsion balloon is in tributaries of the internal pudendal vein,
you see it communicating through the "P" point with varices in the medial thigh, and then with the great saphenous vein here, with a type two junction. Here the balloon is in the inferior gluteal vein. You see communication with the "G" point here,
as well as communication with sciatic varices, this classic horsetail look shown here. So in conclusion, understanding anatomy is critical to the treatment of pelvic venous disorders, you do clearly have to understand the anatomy of the internal iliac vein, as well as the escape points,
and vary your venographic technique, based on the patient's symptoms. Thank you very much.
- Folks always ask if you can do saphenous vein ablation in the presence of Deep Venous Obstruction. So, we'll talk about that a little bit. So, deep vein thrombosis, as we know, acutely, the danger, or the pulmonary embolus
is what we worry about anti-coagulation is the standard for that, but the longer fate of a DVT may be the post-thrombotic syndrome of which this is from scarring and valve damage, as we know. Mark Meissner showed us in this study back in '97
that more proximal DVT, femoral DVT fares worse than calf vein DVT as far as symptoms, and that goes out to about four years in this study. And we know that the worse actor of all is probably ileo femoral DVT,
so the more progressable the deep vein thrombosis, the greater the obstruction, the greater the symptoms. So, I always show, I like this study by Lois Killewich that she did back in 1989 basically showing the recanalization of deep vein thrombosis on a timeline.
And the message here is, that around three months, 86% of the recanalization has occurred. So, that's kind of my trigger as far as the earliest that I would even consider doing intervention on a post-thrombotic, would be at least three months to allow recanalization to occur.
We know that folks with, post thrombotic folks, do worse as far as receipt scores at five years if you compare primary deep veinous disease with post thrombotics, the post thrombotics fare poorly. And that's really the rationale between these
clot removal strategies in the ileo femoral segment to try and mitigate post-thrombotic syndrome. So, when you have a patient in front of you, the way I kind of line these things up, there going to be either obstruction dominant or reflux dominant.
You're not going to get a limb assymetry. A big, you know, one leg just clearly, larger than the other from saphenous vein reflux. It's just not going to happen. So, if you got true limb assymetry, and a saphenous vein that's 10mm and incompetent,
you're not going to improve their limb assymetry from saphenous vein ablation. So, you got to look at your indications. This patient should be looking for something ileo femoral that you can stent, but I don't think the saphenous is going to be much of a contribution.
The other thing, these folks don't have a lot of vericose veins they have more advanced skin damage. Whereas with reflux dominant, saphenous vein incompetent patient will usually present with vericose veins,
they won't have the limb assymetry, and that's why the C-3 gets a little hazy. It's swelling from superficial vein disease. It's usually just some fullness in the malleolus, maybe around the ankle, but you're not going to get full-blown edema
from saphenous vein incompetence. So, know why you're doing saphenous vein ablation. Not all refluxing saphenous veins need to be treated. Can you do saphenectomy in the presence of deep vein obstruction? We've shown this before.
This old Raju study that he did saphenectomy stripping in two groups, those with and without previous thrombosis, and they both did fairly well, did not seem to be impaired by the presence of obstruction.
This study by Puggioni on RFA ablation. She looked at some patients with DVT in a larger group that were all treated with RF ablation, and the bottom-line of her study was that RF ablation in patients with previous DVT is safe. Again, I wouldn't do it until after three months.
Does prophylactic anti-coagulation have any effect on post-thrombosis rates after saphenous vein ablation? Well, not in the study by Knipp. They used low molecular-weight heparin in folks going saphenous vein ablation, and it just increased the risk of bleeding,
and it had no effect on thrombosis. Can you do combined iliac vein stenting and saphenous vein ablation in the same setting? This is another iconic study by Neglen showed that, yes, you can. Patients with advanced disease
that underwent iliac vein stenting and saphenous vein ablation in the same operation had good symptom relief and very few complications. So, in conclusion, saphenous vein ablation may benefit
patients with previous DVT. Clearly, you're not going to do this in the acute phase of the DVT. When is it safe? I'd say the earliest you would do it, or even consider it is three months
because that's when recanalization starts to peak out. Limbs with concomitant superficial vein reflux and deep vein obstruction can be safely treated by combined treatment, at least in the Neglen series, and the DVT prophylaxis should be
administered at the surgeon's discretion. Thanks.
- 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 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.
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