- [Presenter] Thank you very much, Mr. Chairman, thank you Dr. Veith, for inviting me to beautiful New York again. This patient presented with a symptomatic aneurysm of 65 millimeters, 10 years after an EVAR, in the follow-up he had a slow aneurysm expansion which we left alone, because there was
an absence of endoleak. On the CT angiogramic presentation, there is a clear type III endoleak, which is probably coming from the body of the endograft, which was treated with two Nellix stents, with an excellent follow-up and exclusion of the endoleak.
This patient is a somewhat older male, 79 year old, who presented with a large aneurysm six years after an Endurant stent graft. He had already been treated for a type IB endoleak and was now referred for treatment of a proximal endoleak, which is visible
on this CT angiogram, dorsally in the aorta. We tried to treat this with endoanchors, but were not successful, and deemed a fenestrated graft no option because of the Endurant top strut sticking into the lumen, therefore he was treated with two Nellix stents, and three chimney grafts,
where we needed an extra celiac rescue stent. The endoleak was treated successfully, however on the first CT angiogram, the SMA stent appeared to be crushed, which therefore had to be treated with kissing balloons. The first paper on endovascular aneurysm sealing
after previous EVAR described 15 patients, with high technical success, and no reinterventions at eight months follow-up. We collected, or we're currently collecting the Dutch experience of EVAS relining for failed AAA repair, we have now seven centers included,
and we have 35 patients in our cohort. 11 patients patients presented after open repair, around 200 months after the initial repair. 24 patients presented after EVAR, half of them had a type I endoleak, approximately 60 months after the initial repair,
and these are the grafts that failed. There were no Nellix in Nellix patients in this series. Patients presented symptomatically in seven cases, and four with a rupture. We performed 18 EVAS procedures, with two Nellix stent grafts, four unilateral,
four iliac extensions for type IB endoleaks, and 13 chimney procedures. The technical success was 97%, there was one patient who had a persistent type I endoleak at completion. Two out of four ruptured patients
died pre-operatively from multi organ failure, and we had 9% complications. Buttock claudication was expected for the iliac extension patients. Mean follow-up was around one and a half year, with three more aneurysm related mortalities,
one patient ruptured four months after relining due to a type III endoleak, of rubbing of the... the existing endograft, which had a subsequent type III endoleak, one patient died from conversion after a symptomatic aneurysm seven months after relining for endotension, and one patient ruptured
for the second time, seven months after the initial rupture with a type I endoleak. If we look at reinterventions, there were three reinterventions done for type IA endoleak, they were all successful, two were endovascular and one was an explantation.
We relined the SMA stent, as I showed before, and one stenosis in the Nellix graft was bilaterally stented. If we split it out to the type IA endoleak subgroup, there were 10 patients, three were symptomatic, seven had chimney grafts with
a 90% technical success rate. And all the reinterventions that adjust this graft are patients in this group. Interestingly, four out of 10 had a type II endoleak, which is probably the outflow vessel. So, the conclusions from the Dutch experience
would be that this is a challenging patient group, where no open or fenestrated options were available. High technical success was achieved, however, a high reintervention rate for type IA endoleaks. It's a technically demanding procedure, and there were several technical lessons learned,
mostly about the specific filling protocol, which includes pre-pre-fill, separate filling, beware of protrusion of the endobags, which is also described in the field safety notice of Nellix from October 2017. It's off label, of course.
So the take home messages would be that chimney EVAS relining is a new technique to treat failed previous AAA repair. You should be experienced with the system, and use advanced endovascular techniques. There's more reinterventions in type IA endoleaks
or migration, this can be due to insufficient fixation of the endograft, which may be treated with endoanchors simultaneously, and there are no durable data. Thank you very much.
- [Lecturer] Thank you, Frank, for your kind invitation to be part of this meeting again. So, it's a long title. I have no disclosure. I tried to fix it with our experience, and I will have second talk a little bit later this morning when I can address different views.
But you see we have fixed a cohort of hundred patients we treated, and this to 2014, and we do follow this cohort to see what is the long term effectivity of the procedure. So we had a mortality of 2%, 3% stroke
and 4% of endolic type one, three at beginning. We identified in our experience some factors that may be critical for patency and for good outcomes. The one is the procedures in a nonreactive setting where planning is not maybe so optimal, maybe a risk factor for increased mortality
and reintervention during follow up. Using multiple chimneys at the one landing zone may also be a risk factor for mortality and reintervention. Stent grafts that are parallel grafted or compressed or that are too short, this is obvious, but may happen will occlude or require reintervention.
And finally, if the target vessels are stenotic or less than four millimeters in diameter, this might lead to occlusion or reintervention. A factor that we did not analyze but that was looked on in the literature, and we have seen also just before that this may matter,
this is angulation of the branches coming inside the target artery that may be more favorable but natural for fenestrated that springs just perpendicularly to the aorta. We updated our results from our paper from last year
to forty-three mean follow-up 2017, and you can see that the mortality of this population is increasing by time, but aneurism related mortality remains stable, and the patency of the branches remains good. So because I have to address
the thoracoabdominal pathology too, I looked at the 31 with each trait, and you can see the figure here. Mortality zero, 3% stroke, 2% of endolic with a mean follow-up of 39 months. That shows a figure that is quite similar
to the whole cohort with a good patency of the branch. In this group of 31 patients, there were of course patients that did not fit for placing a stent graft in because of the access vessel or a too complex abdominal manala to me.
So to make the endovascular part easier, we did perform some conduits in the branching in some patients like this one. Then we had 19 patients with 100% endovascular parallel graft procedure, and you see at 43 months of follow-up,
we have also no big issues with our branches. But we had reintervention 37%. Some related to the branches in the procedure and some that were not related to the abdominal reconstruction. We had some branch occlusion as you can see one here.
This is a patient that came 2009 with a ripped occlurenal that we fixed that works well with the soliact occluded in an asymptomatic way. So if we compare this both group with hybrid plus stent graft,
parallel graft and 100% parallel graft technique, you'll see there is no big differences. But again, if we look a the whole cohort, we can't say there are no problems, no reintervention. You'll see the course of the right and the top and left down,
this reintervention, and some of them are due to endolic injuries. This patient has an so-called sandwich aneurism in between two parts that have been repaired, the descending and the abdominal aorta that was fixed with an open graft,
and we repaired these with a new kind of device that is customized and has an anti gutter protection and that you'll see immediately on table, the reconstruction. Maybe this will show to have some advantages in the future. So, on conclusion, this technique can lead to good results
in selected patients. The anatomy has to be good. Patient should have an expected life of more than two years, and it behave durable up to four years but taking into account a substantial number of reinterventions to maintain seal and/or branch patency.
Thank you very much for your attention.
- [Riambau] Thank you, thank you very much Joan Karlo. It's a pleasure to share with you this kind of new device but it's not a really new device. The most important difference is starts in the design of the balloon itself with its platform for the Luminor from the iVascular company.
The Oceanus 14 and 35 has a very long tip has a very high crossing capability, with very short shoulders and very quick inflation and deflation time. Importantly the docs is the same. The PTX as usual for this quite common drug coating balloon
but the excipient is water reduced ester with a proportion of the drug excipient ratio 80 to 20. And the transfer technology is applied in order to distribute more uniformly the drug over the balloon. I would like to share with you the first preliminary results
from a Spanish perspective, an observational multicenter study single-arm in order to evaluate this particular device in the lesions in the femoro-popliteal and below the knees vessels. Taking into account the primary endpoints are rated
to the primary patency, death, amputation and TLR up to 12-month follow-up period. Also we recorded another kind of secondary endpoints. A total of 214 validated Rutherford two to five cases have been recruited during a 15-month period following an intention to treat basis.
All the procedures were followed by instructions for use. Primary stenting or atherectomy were excluded. The adjuvant drug treatment was applied to all up to one month and just aspirin for after. So that from this cohort we extracted the critical limb ischemia patients
that represent 155 patients and almost 200 lesions treated with a prominent of males over females. And this kind of regular demographic for those kind of pathology. Diabetes represent 70% of the cases
and one third of the patients has a chronic renal failure in the stage three or over. And 85% of the cases represent Rutherford class five. About the lesion characteristics 76 millimeters in length was the average and the chronic total occlusion
represent 56% of the total cohort and stenosis is 43% BTK lesions 50% of the cases and with severe calcification in more than a half of this cohort of patients. About the results
all-cause mortality for clinical limb ischemia in this particular core was 3.2% major amputations 2.6% TLR 1.6% At one-year follow-up we can see here is a high volume of patients at risk
is 88.5% About the patency rate of that particular cohort the survival was 84.5% and the freedom from amputation 85% and the freedom from TLR so high is 92.5 % in this cohort patients.
So in summary initial primary outcomes in clinical limb ischemia population are encouraging taking into an account the severe ischemic status of this fragile cohort of patients. That is the contribution list for this particular registry.
Thank you very much for the attention.
- [Robyn] Good, morning, thank you, Dr. Veith, for asking me to speak. I have no disclosures over 40,000 people in the United States annually are diagnosed with head and neck cancer, 75% of these patients undergo radiation therapy. Almost 80,000 patients in the US population annually
are diagnosed with lymphoma and about 20 to 30% of these patients undergo radiation therapy to the head and neck. This gives us about 50,000 patients annually undergoing head and neck radiation. With a 25% incidence of carotid stenosis
we are diagnosing about 12,500 patients with radiation arteritis annually. This occurs due to direct endothelial cell damage from the radiation beam, which then causes platelet aggregation, fibrin deposition, obstructed capillary lumens,
and vaso vasorum, focal necrosis, and finally extrinsic compression and luminal narrowing. Patients present similar to atherosclerosis with asymptomatic disease or TIAs and strokes. Recommendation is to screen these patients with ca
there is currently no consensus on when this screening should begin after completion of the radiation therapy. Most physicians recommend five to 10 year later. Once a patient is diagnosed and if surgery is considered,
due to the uncommon location and diffuse lesions of these radiation arteritis patients, patients should undergo either MRA, CTA, or catheter-based arteriogram for preoperative planning. Management options include medical management with traditional risk factor modification
and surgical management should be considered in patients with a symptomatic lesion greater than 50%, an asymptomatic lesion greater than 60%, or deemed to be a low peri-procedural risk. However, due to the more stable morphology of radiation arteritis, most asymptomatic patients
should wait until about 80% stenosis. Looking at the Society for Vascular Surgery guidelines pertaining to carotid disease, they find that a history of neck radiotherapy, the resultant local fibrotic changes of the skin and soft tissues, to be an anatomic criteria
to consider carotid stenting. However, they do feel that carotid endarterectomy remains a safe option. When deciding between carotid endarterectomy and carotid stenting there are many anatomic and physiologic factors to help make that decision.
Carotid endarterectomy should be favored in patients aged greater than 70, those with a type III arch or severe arch calcification, those with carotid artery tortuosity, severe plaque calcification, ulcerated plaque, near-occlusive lesions or extensive lesions.
Carotid stenting should be favored in patients with a history of prior neck radiation or radical neck dissection, those with a tracheostomy, those with prior carotid endarterectomy or cranial nerve injury,
those with a common carotid artery stenosis proximal to the clavicle, or distal internal carotid artery stenosis distal to C2 and those with a large amount of cardiac comorbidities. If carotid endarterectomy is decided upon there are several technical tips we can recommend.
First, given the difficulty of dissection, general anesthesia is preferred. The groin should always be prepped for potential greater saphenous vein harvest, particularly if the patient has a tracheostomy or previous extensive neck dissection.
A longitudinal neck incision is preferred for the ability to extend either proximally or distally. The surgeon should anticipate a more tedious dissection and take careful time to identify the cranial nerves. Once starting the operation the surgeon should anticipate that possibly the endarterectomy plane could be obliterated
and they may require a common to internal carotid artery bypass with greater saphenous vein. If there is significant involvement of the common carotid artery a subclavian to internal carotid artery bypass maybe done with PTFE,
and the patient may need a myocutaneous flap for coverage at the end of surgery. If carotid stenting is considered, the procedural steps are identical to that used for atherosclerosis. However, the surgeon should anticipate,
due to the extensive nature of the plaque, that multiple stents may be required and there's a higher occurrence of filter clotting. Looking at results for carotid endarterectomy, most reports are single institution case reports or case series.
All of them have similar results showing 30-day stroke and death rates ranging between zero to 3%, which is similar to that what we see for atherosclerosis. However, cranial nerve injury rates up to 22% and wound complication rates up to 8% are higher. Of note, in patients that do have cranial nerve injuries,
similar to atherosclerosis, they do resolve in about six weeks. Looking at results for carotid stenting, again, these are single institution case reports and case series and show similar results for death
and stroke rates at 30 days of zero to 9%, which is similar to what we see for atherosclerosis. Here we don't have to worry about cranial nerve injuries, and we do have some groin complications, about 6% of the time. A meta-analysis was done by Davies
that showed similar results with asymptomatic and symptomatic carotid stenting and carotid endarterectomy having similar stroke and death rates at 30 days. However, there is a higher rate of re-stenosis and re-intervention, and most deaths were related to the original cancer.
In conclusion, both carotid endarterectomy and carotid stenting are technically feasible in patients with radiation arteritis. Both carotid endarterectomy and carotid stenting are just as safe as in patients with atherosclerotic disease,
and while considering carotid intervention the patient's oncological prognosis should also be considered. Thank you.
- [Presenter] Ladies and gentlemen, dear colleagues, first of all I would like to say to the organizer thanks for the kind invitation. I don't have disclosures. As you know, chronic renal insufficiency is a global problem, with the prevalence of 10 to 16% in the general adult population.
For the patients who are receiving an endovascular treatment are having an increased risk for contrast-induced nephropathy, with an incidence of up to 50% in high-risk patient group. Duplex-guided PTA is not a new treatment. It's already published many times in the medical literature,
but mainly it was treating the SFA, and the popliteal artery. Some sporadic reports are treating the dialysis access. The advantages of Duplex PTA that you're puncturing the access artery under ultrasound. It's a dynamic examination.
You don't need pre- and post-hydration, no need of contrast or radiation. The disadvantages, the habitus of your patient, so obesity can be a problem, and intense bowel gas formation can give you problems with the Duplex images
So, first we did officiate the study in 2013. It was published in European Journal of Vascular Surgery. We treated 35 iliac lesions with 94 clinical success. Then, we went on with the randomized control trial between 2013 and 17.
We included 140 patients with an indication of PTA for significant iliac stenotic disease above the 70% stenosis with the TASC A and B lesion. The endpoints for the primary, passing the guidewire through the stenotic lesion with balloon dilatation with or without stent placement.
Secondary endpoints, of course, were measured in the clinical important complications requiring additional care. In the DuPTA group, more than 50% reduction of the PSV was required, and in the PTA group more than 50% reduction of the stenosis grade
on completion angiography was required. We followed the serum creatinine pre and postoperatively on all the patients on the 30th day, postoperatively got the Duplex. Baseline characteristics of both groups were similar. The most important significant results were
that in the DuPTA group, we found an absolute reduction, significantly higher, and the patient group who had more than 50% reduction of the PSV was also significantly higher. We placed significantly more stents in the Duplex PTA group.
The kidney function pre and postoperatively was comparable. We also did officiate the study on Duplex-assisted EVAR, DEVAR. It was published in 2014. Last Monday, I operated on our 12th patient with this method.
Actually, there are two points which are different from the regular EVAR procedure, namely you mark your renal artery with a guidewire supported with an angiocatheter, and then you start to deploy your main device, and at that point the partial opening of your main device,
you control once more with a Duplex, the flow and your renal arteries. Other different point is that you mark the internal iliac artery with the renal balloon under fluoroscopy and Duplex ultrasound. Further deployment is going in the same way
as with the regular EVAR procedure. All our patients get a control on table with CEUS and SonoVue. Here you see in the end stage picture with SonoVue on table, no endoleak, and this is a final CT without contrast.
So, in conclusion, in our hands we saw that directly measurable results indeed seen when you use Duplex-guided PTA. You can immediately see the degree of recoiling or dynamic dissections, and the dynamic of dissections,
and we didn't find limitation by habitus or bowel gas formation of our patients. We found that Duplex PTA is a safe and effective procedure with comparable clinical results to conventional PTA in iliac TASC A and B lesions. Valid alternative in high-risk patients
with chronic renal insufficiency or contrast allergy. The value in the recanalisation of iliac occlusions, it still has to be examined, and we found that DEVAR is a feasible alternative for AAA patients with renal insufficiency. Thank you for your attention.
- Thank you for the kind introduction and to Frank Veith and the colleagues to invite me to this important meeting. So I had the chance here to talk about Vector Velocity Ultrasound, a new technique. This is my conflict of interest. You know all that the Doppler-Angle-Dependent flow imaging fails to estimate, at flow at 90 degrees.
So, this is a factor that's really operator dependent and angle dependent. So, if you have 90 degrees, you see to the right how the doppler image would look like and with the new vector flow imaging technique that was developed during the late 90s
in the Danish Technical University by Professor Jensen and coworkers. They can actually give a good image at 90 degrees, beam to flow angle. So, giving both velocities and also the ratios within stenosis.
You see these vectors here? They are actually pinpointed to 2D image but it gives 3D image cells in it's pixels. So, how does this work? This is a picture of the carotid artery. As I said, it's angle independent velocity estimation.
It has no assumptions of flow angle. It makes estimation of flow at 90 degrees. It also make visualization of complex flow patterns even in heart where we have started doing this in small kids as well. So, we have the transverse oscillation
with VFI works with the same. First doppler beam imaging goes into. It uses that one but then it gives three echoes back. One echo is actually the same as a doppler flow imaging. The other twos give you like the CT, cone beam CT. It gives you two different angulations and from that
it can translate into velocities. And, that's the way it works. So, in atherosclerotic arteries, it may be a challenge to evaluate quantitatively using spectral Doppler Ultrasound due to the turbulent flow conditions and therefore, we tested this for chronic obstructives
diseases in the limbs. So, we took 16 patients to our cath lab and we looked on the vector flow imaging derived velocity ratios and compared them with DSA. And what we could find was that there was a non-linear correlation with the DSA with the stenosis
and a linear one with velocity. So, the VFI recordings, they were analyzed off-line in an in-house MATLAB scripts. It takes some time. It's still in a development phase.
They use a point-and-click interface for providing the velocity and the direction for each pixel. And, this is the way they work. They engineers with this, they find the box, a row of the vector flow imaging and then it takes them roughly 20 hours to do this kind of estimations
in the math lab afterwards. So, the vector flow imaging, they measure laminar flow at any angle up to complex flow. Its replace/improve measures already available by conventional Doppler ultrasound such as velocity and flow estimation.
It's less operator dependent. It has no angle dependency. It has new insonation windows and give you more data for flow estimations. It measure laminar flow at any angle up to complex flow. It offers new parameters for flow characterization
using angle independent vector velocities. For flow complexity, vorticity, shear stress, and pressures. So, to circumvent the angle dependence of the conventional doppler, the angle independent ultrasound technique that was proposed by Jensen and coworkers provides simultaneously, the axial and transversal velocity
components of the blood flow. A conventional ultrasound pulse for flow estimation is transmitted and the received echos are beam fold by three beams in parallel. One use is conventional beam forming for estimating the axial velocity and the other two beams are used
for estimating the transverse velocity components. And by combining the velocity components along the two axis, the 2D velocities are obtained. And, for the moment we can reach down to five centimeters in penetrations for this. Thank you.
- [Yves] Thank you Frank, again, for your kind invitation. Okay, I have no disclosure. So as it was mentioned, there is a high rate of a stroke, early stroke after endarterectomy, which may be due to technical difficulties,
clamp or shunt lesions and sometime in bleeding. In our series of almost 1200 patients treated for endarterectomy in the university center, we are always performing an intraoperative angiogram at the end of the procedure. And we had in 20 patients severe lesions,
which was treated by carotid stenting in complementary of the carotid endarterectomy. It was 17 male, with a mean age of 74 years old. Six patients were symptomatic before the procedure. The initial procedure was endarterectomy with patch in 10 patients, and eversion in three,
and seven patients had a bypass. In these 20 patients, 14 had a shunt, which is twice the rate of the whole series of the patients treated for endarterectomy in our department. And in the five first patients of this series, a second surgical procedure was performed before stenting.
So which lesion was stented? In 16 cases it was carotid stenosis due to clamp, shunt, or dysplasia, and in four patients due to distal atheromatous lesion which was not seen pre-operatively. Three patients had a severe intimal flap,
and one patient had the distal artery rupture on clamp. So what was our technique? Heparin and then antegrad ponction of the common carotid, placement of a 6-French sheath on the Terumo Guide, and then the clamping of the common carotid in order to reverse the carotid flow.
We then placed an auto-expansive stent and in each case we did complementary TLA. The patient was placed in the double anti-platelet treatment for one year after the procedure. What were our results? The mean operative complete duration was two hour and half.
We had one severe complication. One patient had stroke at day two. This is the antegrade before stenting, this is the antegrade after stenting, but died at day six. We had also an intra-petrous asymptomatic
internal carotid dissection which was treated successfully medically. Late results. After three years of follow-up all the patients had 100% secondary patency. But one patient had one intraoperative stent
which was successfully treated by TLA balloon. In the literature, four series were published on that subject. We can see that the percentage of patients treated for stenting was between one and four per cent in the whole series
of treated for endarterectomy. As we are doing, Tameo is also doing common carotid clamping before placement of the stent and all the patient had good follow-up except one in the series of Ross. So in conclusion we think that when you find
a severe complication when doing a complete, an angiogram after a carotid endarterectomy the best treatment should be placement of the stent, which is a feasible and safe technique with excellent long term patency. Thank you for your attention.
- [Presenter] Good morning to everybody. Thank you for everything, Frank. This is my disclosure. Now in literature, I was able to find only four cases, single cases described of dorsalis pedis entrapment.
The first case is claudication. In case of active dorsiflexion, entrapment by the extensor hallucis brevis. Second case was blue toe syndrome, always extensor hallucis brevis tendon compression. Claudication, forced plantar flexion
for constriction by tissue bands. And anterior tarsal tunnel syndrome with dorsalis pedis artery thrombosis. So few single case reports are heterogeneous. What are the cases I want to show you. This was my first dorsalis pedis artery entrapment patient.
It was a patient with a diseased foot. I made a very long subintimal angioplasty going to the plantar arch, very close. And here you can see, I found this persistent stenosis despite multiple balloon inflation.
The patient had spontaneously changed the angulation of the foot, and the stenosis disappeared. So we have a different behavior depending of the angulation of the ankle joint. Dorsalis pedis entrapment
is a functional obstruction observed in plantar flexion of the foot released in standard position. This is the second patient. This is a baseline angio. You can see the baseline angio.
And with this plantar flexion, there is a stenosis that disappears in this case. So also in the baseline angio, there was this system after angioplasty,
it was the same. So dorsalis pedis artery entrapment is an anatomical condition and is not related to the endovascular treatment. It is not a spasm or dissection. This is patient three.
Observe how dorsalis pedis artery has a very, very slow flow and how it is normal when you change the angulation. So dorsalis pedis artery entrapment can affect the tarsal artery also.
Because in this patient, we have a huge tarsal artery. This is patient number four. Below-the-knee vessel disease. And you can see again with plantar flexion of the foot spontaneously,
there is an obstruction of this level that disappear completely when you change the angulation of the foot. So DPA-E can lead to functional total occlusion of the artery. This is patient number five, you can see.
Patient number six. Observe how this artery's perfect, absolutely perfect in this position and is stenotic in this position. So the dorsalis pedis artery entrapment is an anatomical condition
that can affect the true dorsalis pedis or the tarsal artery. It must be considered when there is a shorter stenosis at the passage anterior tibial artery, dorsalis
in the majority of the cases, the dynamic obstruction is in correspondence of the distal astragalus. In some cases, it is higher at the ankle level. What is the clinical significance
of this condition? How many people have dorsalis pedis artery entrapment? We made some Duplex scanning for the six legs, comparing the blood flow of the distal anterior tibial artery and in the distal dorsalis pedis artery.
And in eight patients, there was a functional obstruction in the forced plantar flexure. So in this initial analysis, dorsalis pedis artery entrapment seems to be present
in 6% of the symptomatic population. Can dorsalis pedis artery become symptomatic? Many patients, especially old, bedridden, neuropathic patient, assume a plantar flexed foot position as the resting position while lying on the bed.
We cannot exclude that dorsalis pedis artery entrapment could play a role in developing or maintaining CLI. What can we do in dorsalis pedis artery entrapment? Heel protectors can save heel and patency of the artery. Thank you very much for your attention.
- [Henrik] Thank you very much, thank you Frank. I don't know what I did to get that title, for it's certainly long. If some of you were here 6:40 this morning you may recognize some of the slides, because I had a similar title at that time. The risk of stroke in asymptomatic patients
is low, and you can see from this publication that shows the annual risk declining, with the year of the publication. Just a few months ago there was this publication from Kansas where a group looked at 864 with 1400 Stenotic Carotid arteries,
followed them for seven years, and they looked at how many goals of risk reduction were accomplished, and you can see that the step-wise reduction in the black bar, which is the combined end point of Stroke TIA or Carotid Revasc, how that is lowered
from 3.5 to .6% annually if you reach all the goals of healthy lifestyle and take the right drugs. Interestingly also looked at how the risk of stenosis progression similarly was reduced step-wise. They concluded that the risk of TIA, Stroke and Revasc becomes extremely low if risk factors are treated
appropriately, and I would say progression of carotid stenosis is a sign of insufficient risk factor control, and preventive treatment rather than sign of increased risk of stroke. And similarly, we looked at 7,000 patients in the bio image study, where we scanned the carotids,
and we found that 6% had a carotid stenosis, they were followed for three years, and four had a stroke, of which two were ipsilateral. However, a lot had cardiovascular events, which we know. For Asymptomatic Carotid Stenosis, very, very low risk of stroke, maybe .3 to .4%.
It's a high risk of cardiovascular events instead, so therefore, it's very important with preventive treatment and the lifestyle adjustment. And Carotid endarterectomy, or CAS, in general is not warranted, unless a high risk plaque can be identified, of course.
And together, with one of the Chairman, we looked at that a couple of years ago, and published in European journal, and notice how stenosis progression is actually the least important of those listed here. However, these data are also ancient since most of these studies included patients that were gathered
or investigated 10 - 20 years ago, so the risk today is probably less than half of what is shown there or maybe even less. Presence of Carotid Stenosis does not tell it all. We need 3D Ultrasound. And the previous speaker
is a pioneer of this and up in the zeros, published a number of papers, and this is just one of them, using a research tool as you can see in the top left, is handheld, but demonstrated to be very reproducible, but now we can get these as what's called Matrix Transducers where we instead of having just
one array as you see here, we have multiple arrays in both dimensions, and therefore we can do volume imaging, or we can have two plain simultaneously as you see in this slide. We recently looked at how accurate can you measure plaque volume using an instrument like this, and it's simply
tomography as you're used to with CT, you take slices and you look at the area in each slice, you know the difference, sorry the distance in between you can calculate the volume. We did that, and this is what came out when we had two blinded investigators scan the same 37 PAD patients.
The patient was up standing in between exams, the ultrasound machines was reset, so this is fully blinded two independent acquisitions. This is actually much more accurate than if you do two LDL blood tests, what you see here. I shall admit that these patients were a little bit
selected because patients with calcified plaques were excluded. 3D will improve plaque qualification, both volume and morphology. Assessment of degree of stenosis, will be better because the angle-compensation can be done
more accurately in 3D. Speed of examination will increase, and will be more easy to perform a good scan. What can we use it for? For risk assessment in carotid disease , who to operate will be more accurate, we can do better morphology
using this technique, and we can also monitor if we treat the patients appropriate with general prevention. Is the plaque stabilized? And maybe more important, has the atherosclerotic burden stopped growing, and I would suspect or expect
that this method may replace LDL measurement in the future when you want to see if the preventive treatment works. Thank you for attention. (clapping)
- Thank you for the opportunity to speak this morning. I have no disclosures. For my part in this vigorous debate, I would like to present a clinical case and keep on the antidotal level that my colleague has set a precedent for. This is a patient who is a 51 year old critical care nurse. Who developed right arm swelling and cyanosis
of the subclavian vein. She underwent an venogram and successful thrombolysis and balloon angioplasty. There was a residual stenosis at the first rib, and she was maintained on anticoagulation in preparation for surgery.
My colleagues and I recently reviewed the various treatment options for Venous TOS and this publication in the journal of Vascular Surgery lymphatic, venous lymphatic disorders. And in this paper we summarized the results of three different protocols the transaxillary and infraclavicular
paraclavicular based on our review of the best available evidence, we concluded the transaxillary first rib resection and balloon angioplasty is a reasonable approach in which 79% of patients can expect a successful outcome at three months follow up. That was indeed the choice selected for our patient,
she underwent a right transaxillary first rib resection. The intraoperative venogram showed here. Showed obstruction of the vein that was not, that was resistant to balloon angioplasty attempts and she was maintained there after on long term anticoagulation.
The patient recovered well after treatment for wound infection, and six months later she continued to have significant arm swelling symptoms and was not happy with long term anticoagulation treatment. A venous duplex was negative for thrombosis, but a CT angiogram demonstrated central subclavian vein
occlusion. A chest x-ray showed long posterior and anterior rib remnants as highlighted here. And at this point we recommended paraclavicular decompression with possible subclavian vein reconstruction. The approach we would typically recommend
for any primary patient with transaxillary Venous TOS. During the super clavicular exposure, we resected the remaining scalene muscles and posterior rib remnant from the interclavicular exposure we resected the anterior first rib remanent and the subclavius muscle. Working between the two incisions we traced the subclavian
vein below the clavical to its junction with the innominate vein and removed the surrounding scar tissue. But the intraoperative venogram showed persistent obstruction of the vein, indicating the need for further venous reconstruction. Our patient underwent a bypass with a cryo preserved
femoral vein graft from the axillary vein to the innominate vein and the completion venogram demonstrates the wide bypass with rapid flow, no filling of collaterals and the patient has done well in relatively early follow up with no arm swelling. From our review in this previous paper we found a
paraclavicular decompression has an excellent outcome with 96% of patients having a successful results at three months recovery time follow up. And this compares favorably to the 79% success rate for transaxillary and intra clavicular approaches. So in conclusion,
there are several distinct advantages of the paraclavicular approach for venous TOS. It is applicable to all patients with Venous TOS and involves a single operation and is not dependent on postoperative interventions. It provides the most thorough and direct exposure of all
relevant anatomy. And allows the surgeon to complete a first rib resection, scalenectomy and external venolysis. It is ideal for direct subclavian vein reconstruction when needed and involves no sternotomy, claviculectomy or disruption of the sternoclavicular joint and involves
no placement of stents in the subclavian vein. The main disadvantage of the paraclavicular approach is it is not always and easy operation. Particularly for surgeons who don't treat TOS on a frequent basis. It does require a appropriate level of training and
experience, and this expertise is not often locally available, even in a city of eight and a half million people. I have several suggestion and tips for my transaxillary colleagues. First know the limitations of transaxillary first rib
resection and consider the alternatives. Especially if subclavian vein reconstruction appears to be likely. In general if you don't treat neurogenic TOS, you probably don't do enough cases of TOS to feel comfortable and consistent treating Venous TOS.
Do a complete first rib resection all the way to the sternum, do an intraoperative or postoperative venogram to identify patients who need further reconstruction and use balloon angioplasty if you must. But please don't place a stent in the subclavian vein. To improve your outcomes, use venous duplex for follow
up rather than being ography because you may not want to know what the subclavian vein really looks like. And if the vein is not patent use anticoagulation to preserve the collaterals. And lastly don't hesitate to refer early and refer often for patients that might be better treated by
paraclavicular decompression. Thank you for your attention.
- [Speaker] These are my disclosures which are none, but I want to say thank you to the patients, co-investigators, and the Dutch government who made this trial possible. As the chairman told you, it's about intermittent claudication due to an iliac artery obstruction,
and we wanted to make a comparison between going to the gym and work hard or have a quick fix by doing an angioplasty. And this is necessary because there is little evidence available on this field. You know of course the CLEVER trial
that recruited patients during a four-year period in the US. They targeted to include 217 patients, but the trial was prematurely terminated. 46 were included in the endovascular arm, and 43 in the supervised exercise arm, and the outcome at 1 1/2 years follow-up
showed that, surprisingly, the peak walking time was longer in those who were allocated to SET, whereas the quality of life was better in the patients who were allocated to the endovascular revascularization. In a separate publication, they calculated
that endovascular is far more costly than SET. Now, we did a similar trial in the Netherlands. We included patients over four-year, five-year period, and they were allocated to SET according to a standardized program, and endovascular revascularization
and a stent was inserted when indicated, and all patients were put on secondary prevention, were advised to stop smoking and to keep walking. The outcomes were at 12 months the maximum walking distance on a treadmill and disease-specific quality of life,
as measured with the VascuQol questionnaire, and we recorded the range of secondary outcomes. The baseline characteristics are shown here. We included 114 patients to SET and 126 to endovascular revascularization. And you can see there's a disbalance
in proportion of males, and those with a cardiac history, and this was corrected for in the analyses, and 1/2 of the patients had an occlusion or stenosis of the SFA. This is the trial profile, showing that after one year,
some 80% of the patients were available for follow-up in both groups. There were issues with compliance to SET because, at six months, only 50% of the patients completed the program in some way, and this had to do with motivation,
there were reimbursement issues because the government decided that supervised exercise therapy was temporarily no longer reimbursed, and a lot of patients had musculoskeletal disorders, and only 1/3 of the patients
completed the program as we had planned. These are details for the endovascular group. Some 8% of the patients did not have the intervention for various reasons. In 3/4 of the patients, a stent was inserted, and there were of course complications
which were minor in 6% and in 4% of the patients in endovascular a surgical procedure was necessary to resolve the complication. There were additional interventions during the 12 months follow-up,
especially in the SET group because 1/3 of the patients crossed over to an endovascular revascularization. With regard to the endovascular group, 8% of the patients had an additional endovascular intervention.
2% of the patients in the SET group were operated upon finally, and 8% of the endovascularly treated patients needed an extra operation. Now these are the outcomes at one year, and with regard to the maximum walking distance,
we did not find any differences except for at one month, but there were no differences at six and 12 months. With regard to quality of life, both groups improved more than the minimally important difference, with a slight benefit over those
who were treated endovascularly. And the only significant secondary outcome was in pain-free walking distance, which was better in the endovascular group at all times. There were limitations to this study, because also we had to terminate this study prematurely
after we had randomized 240 patients, whereas we wanted to include 360. There was a high crossover rate. There was attrition, 80% of follow-up at 12 months, and attrition might have been selective. Putting it all together, the CLEVER and SUPER trial,
I think that they both showed that endovascular and SET improved the maximum walking distance on a treadmill, and disease-specific quality of life in patients with intermittent claudications due to an iliac artery obstruction, I'm sorry, and therefore, it seems reasonable
to start with SET in all patients and accept a 30% failure rate, especially because endovascular, as first-line treatment, is costly. Thank you very much.
- [Henrik] First of all, thank you very much to the organizers, Frank for bringing me back to this lovely city. So whereas the Doppler velocity measurements for assessment of stenosis is very reproducible, imaging of carotid plaques is actually not. So what's the value of plaque morphology? Interestingly, the signal in plaque morphology is so
strong that when we test at first assessments, it's actually quite good and we see there is some evidence behind it. But if you look at morphology over time, it's not so good. And the reason is the impact of what's called the fixed elevation focus just like when you focus your camera
to make a certain image sharp, the same thing we do with ultrasound. Meaning that we only see a thin slice of the carotid artery as illustrated here. And for instance if you're going to scan this patient, what you see with this angle is nothing, and then with
the patient turns his neck a little bit, you're going to see this plaque. So this is the caveat of reproducibility of 2D, that's why we need 3D. And actually 3D is not new, David Spence's group has been pioneers in this and used it for 10 years, however,
their equipment has been research equipment. You can see handheld 3D on the top left, which is not really good for daily practice. And that equipment is actually getting out there now. The transducer seen in the middle is a so-called matrix transducer where you can do volume imaging
in real time. And what you get is, for instance, two planes, simultaneously that you see here. So when you want to do volumes, you simply do tomography like you do with a CT and you can calculate the area of the plaque in each cross section, and if you know the
distance in between, you can calculate the volume. The problem is, where does the plaque begin and where does it end? And if you look at this image, you can see it's not that easy to define where it begins and ends. So we did some work on this and I'm going to give you
the short story. This is what we ended up with, defining a patch of plaque volume centered around the thickest part, calculated from the true center line derived from the 3D image. And this work is being published in the Ultrasound in
Medicine and Biology, where we looked at the volume defined one centimeter around the thickest part of the plaque, we had two investigators scanning 37 plaques. They were blinded from each other's findings. Patients were standing in between exams. And the ultrasound machines were reset.
And you can see this very very nice correlation in these 37 cases. I will admit that there was some selection because cases with calcification were omitted from this analysis. So, looking at the declining stroke risk in asymptomatic stenosis, it is down to below 1%, and in a recent study
from Kansas where they looked at 860 patients followed over six years, all with carotid stenosis, they found that patients who were optimally treated for risk factors and preventive medications had a combined stroke TIA and revasc rate of 0.6%. It's almost gone guys.
And we in the BioImage Study for scans 6,000 Americans and followed them for three years, and among those 6,000, there were 349 with carotid stenosis, and over four years, sorry, three years, four people develop a stroke, only two of them being ipsilateral. But a lot of them had cardiovascular events.
So asymptomatic carotid stenosis has very very very low risk of stroke, but a high risk of cardiovascular events, so therefore it's very important with the aggressive medical management. It is difficult to see where carotid endarterectomy and stenting has its place there today, unless of course,
high risk plaque can be identified. So 3D is a game changer because plaque volume can be reliably measured. Plaque volume may be the new surrogate to observe and follow. It allows for accurate repeated measurements,
plaque morphology can probably be assessed accurately and followed over time. Thank you for your attention.
- Dr Veith assigned me this topic, but it was interesting to think about. So the global guidelines are about to come out soon, in the first quarter of 2018, but basically, they start out with the premise of what factors should impact the outcome
in limb threatening ischemia patients and should also potentially influence the choice of procedure. So obviously, there's the patient risk and longevity, what's the limb status, that's the L, and the anatomic complexity, so plan.
And then what about angiosomes, where do they fit in? So there's no question that the concept of angiosomes started from Dr Taylor and there's no questions that there's regional blood supply to the foot that certainly have an influence if you're going to do a flap.
So if your flap's dependent on moving that tissue, there's no question the underlying angiosome is important and there's beautiful pictures that have helped us understand pedal anatomy in normal patients and the question is, how does this apply to patients
with chronic limb-threatening ischemia? And if you look at different publications, you can get answers from it has a huge influence, to it doesn't have any influence at all, to well maybe it has some but only in selected patients. So the consensus right now is probably
that when you can do it, you should and that it probably expedites wound healing, but whether it influences limb salvage or not is unclear. So why is that? I think the first answer is that limb threat is a spectrum, so there's not a standardization,
especially when all we had was Rutherford and Fontaine, particularly with regard to how bad the wound was and whether or not there was any infection present. So I didn't put this here for you to read it but for those of you who are watching later or want to look at it online or when the brief comes out,
these are all the publications that correlate WIfI with both amputation risk and wound healing time. So the question could be, could there be some interaction between WIfI and angiosome? So if you look, WIfI just stages the limb, but when the patient gets staged
they haven't even had an angiogram yet, and these are the first series that came out of over 2,000 patients that analyzed outcomes by WIfI. In four of these series, the patients were evascularized and the other two, they took all comers that came in
with diabetic foot infection, but they all show that your initial limb stage correlates with your amputation risk, particularly stage four patients have up to 40% amputation rates in some series and the median is about 30%.
So those patients are destined from the start to have a higher risk. So this was a study from Japan that was just published, so most of what I'm going to show you now is all published in the last two or three years, and basically for the higher-risk WIfI wounds,
especially if they had infection, if they had endo first they did worst. So WIfI has something to say about that. This paper from Jean Baptiste Rico just came out, it was very interesting, they looked at perineal bypass patients
and stratified them by angiosome directed or targeted versus indirect revascularization and the graph on the left there shows there was really no difference in outcome when looked at in that way but the patients who were WIfI stages three and four
did worse than the patients who were WIfI stages one regardless of angiosome target. So how can WIfI be used to maybe answer this angiosome question? So the graph on the left is from Japan, these patients got only endovascular therapy
and as you progressed on the left here from low-stage WIfI one all the way to four, what you see is the limb salvage rate goes down, the wound healing rate goes down, and the number of repeat interventions goes up as you progress in complexity.
So patients in WIfI stages three and four are more likely with endovascular therapy to lose their leg and they're also more likely to have non-healing wounds. And the stage four group, of those who still had their leg, 44% had non-healed wounds.
This paper from Dr Conti's group on the right looks at WIfI stage four patients for bypass versus endo, again strongly in favor of bypass. Let me skip over that. So what does this mean?
Limb salvage, limb stage matters a lot and it's got a predictive ability by itself before you get to the anatomy as far as what happens. Now how could this interact with angiosome? Well I would propose that angiosome is probably important
in higher stage WIfI patients and also in specific subsets where the foot circulation is compartmentalized. So we've actually called this Orphan Heel Syndrome, 'cause the most common situation we see this is patients with diabetes and renal failure
and they may have totally adequate forefoot profusion including a DP pulse but they have regional foot ischemia in the heel. So this is a classic patient, over 20 years I took every one of his toes off, he always had a DP pulse,
they always healed, he went into renal failure and came in with advanced heel necrosis and infection and you can see here on his initial angiogram he has no blood flow to the heel and this is after recanalization
of his post tree tibial artery. But you can see on his endo sign in green here his forefoot lights up great and his heel doesn't light up at all. Another classic example, this patient had a non-healing foot wound
with a palpable DP pulse for 15 months, failed total contact cast, had to walk with a prosthesis on his other leg and this is his initial endo signing green angiogram which shows really slow uptake and what he had was a TP trunk stenosis
and then a origin with a perineal stenosis and this nubbin of a posterior tibial that I just couldn't recanalize. So I reluctantly treated his TP trunk and his perineal lesion and all I got to fill on the heel was collaterals
there's no name plant or vessels here. And look at his spy afterwards, this is indirect revascularization, went from really slow uptake to rapid uptake so I think in some sets of patients getting regional profusion back is really important.
So in conclusion I think if people will now use WIfI and start using the concept of angiosome, we may be able to find selected patients where it's critical to do that and others where it doesn't matter so much. Thank you.
- Thank you Mr. Chairman, and thank you to Frank and his team for inviting me to talk about one tool which can be used for screening. Here's the conflict of interest for this talk. We know that ultrasound blood flow estimation is well established and it has three different modes, spectral, power, and color doppler,
but is that the common denominator, that is incapable of detecting blood flow perpendicular to the direction of the emitted ultrasound beam, as you can see from this textbook alike picture here. So the background for this talk is atherosclerotic vessels are a challenge to evaluate
quantitatively using spectral doppler ultrasound due to the complex flow phenomena in the vessels, and therefore vector velocity ultrasound, it's an angle independent, and provides flow information that may potentially improve diagnosis and treatment in future.
So you look on the right part you can see a doppler, where you don't can see the flow, while in the vector flow imaging on the left part you can see how the velocity is actually marked in each and every pixel with both the flow and also the flow volume.
The same goes for this picture, where you see the vector flow imaging in an arterial venous fistula, there is an in vivo example of a stenosed fistula with quite complex flow, and after it didn't PTA you can see a more harmonized vector flow imaging in this. So transverse oscillation as exemplified here by the
carotic arteries, it gives you an angle independent velocity estimation with no assumptions of flow angle, and it can really show you the complex flow, that you can see even more in this picture, where you have a stenosis and also poststenotic disturbed flow afterwards, which you can interpret.
This recording contained flow both in the lesion and proximal and distal to the lesion, and disturbed flow was defined as vortices, flow in multiple directions, or suddenly occurring aliasing indicating increased flow velocities. So from this we can, from each and every point we can make
a new algorithm, and this is called vector concentration from an angle-independent vector velocity to give a quantitative index, which is simple to calculate and can differentiate and laminar and complex flow. Like in this picture, it's illustrated with changes in intravascular pressure along a streamline,
and found using 2D flow estimation in the carotid bifurcation of a healthy volunteer, and the pressure is plotted along the course of the streamline in this picture. Here is then, we need to go further on to 3D vector flow, which gives full access to the blood flow in all planes
within the scan region. The left part shows a full volume representation of the carotid flow, with streamlines indicating the flow tracts. And on the right part, you can see three cross sectional views, which can be interpreted. This vector flow imaging can thus measure laminar flow
at any angle up to complex flow, and it can replace or improve measures already available by conventional doppler ultrasound technique. So it gives you new insonation windows and more data for flow estimations, and this can be a new marker for assessing diseased aorta as well,
we move from carotids to the aortic, where you can see the vorticity, the shear stress, and also can give pressure measurements. As you can see on the left part, you have a healthy volunteer, and you have the aortic valve there,
and in B you see a stenotic valve with very complex flow which can be interpreted, and then C is after treatment with a new valve, and you can see that now it has a more laminar flow and a more, picture looking roughly the same as on the healthy volunteer on the left side. So the future of vector flow imaging, we propose is in 3D.
And the flow vectors features a ring formation in the ventricle of the heart, or the shear stress along a vessel walls could be detected through 3D flow. And in summary, vector flow techniques with their many advantage over conventional doppler techniques are a powerful alternative.
It can visualize complex flows, as I said, and you get new flow parameters, and you have a free insonation window. And these factors will reduce operator dependency, improve the logistical work, and diagnostic accuracy for patients.
- I'm going to be speaking about indirect access sites for access intervention. I'm going to be focusing on the transjugular approach. So access interventions, typically we perform them through a direct puncture of the fistula. Sometimes you place two introducers. There are some disadvantages to the direct approach.
The crossing catheters technique that we generally use for declots is awkward and cumbersome. The introducers can obstruct flow, there's dead space behind the introducers that can trap clot, and there's radiation exposure or the direct exposure
or scatter radiation from hands near the field. Admit it, we've all had access-site complications, suture-site necrosis and infection, as well as pseudoaneurysms. There's also prolonged procedure time related to needing to obtain hemostasis
in the high-pressure segment. There are also problems particularly to immature fistulas, such as hematoma formation, spasm at the introducer site causing pseudo-stenosis, decreased flow, and fistula thrombosis. Now, the good news is that we do have options
for alternative access sites. I'm sure many of you here use arterial access for immature fistulas in particular. Brachial access can be used to, this can be used for diagnostic or therapeutic purposes. We can also utilize radial or ulnar access.
Rarely, femoral access is used, as we saw in the last presentation. But there's also pendula venous access sites. You can sometimes, as a fortuitous tributary, what I call a target of opportunity, and also, the internal jugular vein.
Now, the transjugular approach was first reported in 1998. It does have some definite advantages over direct puncture technique. You can avoid the cumbersome access, you can keep your hands away from the beam, and there's no dead space as compared
to crossing sheaths for your declot. And if the intervention is unsuccessful, you can convert your IJ access to a catheter if you already have a wire in it. There are some technical challenges associated with this technique.
You do have to overcome the valves. It can be difficult to access the cephalic vein, but you can get around this by using a snare. And there's possibly a risk of IJ thrombosis if you're using large introducers. When to use this technique?
Well, when direct puncture's going to be difficult or cumbersome, when there's a short cannulation segment, when it's an extensively stented access, and when there's inflow pathology requiring a retrograde approach or arterial empathalogy, and it's a good option for clotted access.
The technique, micropuncture access of the jugular vein, ipsilateral or contralateral, place a sheath, and an important thing to use is a reverse-curve catheter, followed by glidewire. So here, we've cannulated the jugular vein going down,
glidewire out into the arm. If you're unable to cross into the cephalic vein, you can use that snare technique. And you can get a long, stable access in this way. It's been reported about, there's about 10 publications on transjugular approach, seven retrospective studies.
There's a large study that's reported thrombectomy. Also a large study looking at immature fistulas. Smaller studies looking at dysfunctional access and pseudoaneurysms. Two case reports, one review article, but there's of course no randomized studies.
There's a recent study from this year from Ferral and Alonzo. This was a retrospective study. Over two years they performed 30 transjugular AV access interventions. This accounted for 5% of their access experience
and this series was all fistulance. Indications for the procedure, 43% were declots, 43% were arterial and fistual pathology, there were two immature fistulas and two bleeding pseudoaneurysms. The access approach was 29 for ipsilateral,
only one contralateral. The results, 97% technical success, a snare was required in 4 cases, a catheter was inserted in two of the cases. There were no episodes of jugular vein thrombosis. In the remaining time, I'd like to show
a couple of case studies. Again, from Ferral and Alonzo. This is a case of an immature fistula. This was a partially occluded, immature left upper arm fistula. The initial fistulagram shows outflow stenosis
with a multiple stenosis in thrombus, and there's an arterial in stenosis that's distal to the access point, so you're not going to be able to treat that. They performed four millimeter angioplasty. Follow-up fistulagram shows a small, but patent vein
and the arterial end could not be treated. They brought the patient back in two weeks for a staged transjugular approach. And you can see the jugular catheter coming down. The vein diameter's improved, but there's still the untreated arterial end stenosis,
which is easily treated through the jugular approach. This is a study from, a case from Dr. Rabellino, ruptured pseudoaneurysm. This is a basilic transposition with a ruptured pseudoaneurysm at an infiltration site. Pretty ugly arm, swollen, skin necrosis.
I don't think we want to be sticking that arm. They initially went with a femoral approach for the fistulagram, demonstrated the pseudoaneurysm. As you can see here, tandem outflow stenoses. Coming up from below with the femoral artery diagnostic catheter.
Down and into the arm through the jugular approach. And here, you can see the venous outflow after angioplasty, covered stent deployed through the jugular access. So in summary, the transjugular approach is a useful but underutilized technique. The advantages include single-puncture intervention,
does not involve the outflow vein directly, simplified hemostasis, it's a low pressure system. It does have the advantage that you can use large introducers, there's less radiation for the operator, and you can convert to a catheter easily if needed. It is a useful technique for fistula maturation,
thrombectomy, and access maintenance. I say go for the jugular.
- [Presenter] Thanks very much. So I'm giving this talk on behalf of Ian Loftus, from St. George's in London, who couldn't be here today. I got some disclosures for this. These are Ian's slides. So in Europe, there's been some experience using the Nellix system,
endovascular aneurysm seeding with parallel grafts for complex aneurysms on the premise that gutter endoleaks may be reduced using polymer-based technology. In terms of the St. George's group, these would be indications for possible use of chEVAS. So patients with pararenal or juxtarenal aneurysms,
those that are outside the IFU for an infrarenal Nellix, and actually the majority of patients would be those who are either anatomically unsuitable for a fenestrated custom-made graft or unsuitable on the grounds of emergent surgery. In terms of the early lessons,
St. George's has about 80 cases and the early lessons were that it's absolutely essential to plan to achieve an aortic neck in the suprarenal aorta of at least 15 millimeters, important to have a strategy for upper limb access, as I'll show you in subsequent slides,
and avoid patients who have upgoing renal arteries using a suprarenal approach. The choice of the parallel graft, whether balloon expandable or self expandable, is also crucial, and a dual anti-platelet regime
has been instituted in this institution. It's also important to realize that chEVAS is done on the same basic platform as Nellix, and therefore we know that the graft does best in aneurysms that have a large flow lumen and relatively little thrombus.
So I'll just show you some clinical results from the ASCEND registry, so this was a retrospective registry, 154 patients with primary chEVAS for suprarenal and juxtarenal aneurysms. So upper limb access strategies,
crucial in all of these cases, the George's group tends to use a brachial approach when it's one chimney, and an infraclavicular axillary approach when two or more, and the technique has evolved from sewing a conduit
on to actually doing individual punctures for each chimney with a purse-string graft. If you look at data from the ASCEND registry, having a strategy for your upper-limb access in placement of chimneys is clearly very important, you can see here on the far right-hand side,
if you do more than two chimneys, blood loss is excessive. And actually in terms of significant complications of chEVAS, you have to take into account of strokes, so there were four cases of stroke
in the 154 in the ASCEND registry, and three out of the four cases of stroke were posterior circulation, clearly reflecting manipulation around the vertebral artery. In terms of visceral artery considerations, cranial or upgoing renal arteries
are a real problem in terms of access. One obviously has to use all the adjunctive methodology that's available for cannulating the renal arteries and the visceral arteries. But a consideration is that patients do best with a minimum length of 10 millimeter seal and again,
the choice of whether to use balloon expandable or self expanding stents is crucial in ongoing strategies. In terms of durability, one sees probably better durability in the long term with patients who get self expanding stents but clearly the procedure
is easier if you use a balloon expandable stent. Most of the patients in the ASCEND registry had balloon expandable stents and you can see that nine patients required reintervention for a renal artery stenosis but overall the patency of these vessels after intervention was good.
So just to sum up then, EVAS for complex aortic disease, it's a promising use of new technology, there does appear to be a therapeutic gap, I think what's important in terms of proof of concept is testing of component interaction and understanding which branch graft to use.
In terms of good results, patient selection is absolutely key, with achieving a neck of at least 1.5 centimeters and a strategy for the management of upper limb access is absolutely crucial to avoid stroke. Clearly, the role of this therapy
is going to be defined by its long-term durability, and in the US, we hope actually to be instituting an IDE sometime next year. Thank you very much.
- [Anthony] Good morning ladies and gentlemen. Frank thank you, again, for the privilege of being here. Sherif, that was a fascinating anecdote and a case, and I think it's a tribute to your technical expertise. However, I don't think we can generalize from that. I have no disclosures. We know by personal observations
and review of the literature that single center reports show the benefit of carotid patching, and registry data also show the benefit of patching in a statistically significant manner. Randomized trials, as already been discussed, have shown significant benefit from carotid patching,
and that benefit surfaces by reduced operative stroke rate, reduced operative stroke rate and a reduced recurrent stenosis. And as already been alluded to and specifically stated, Dacron patches, however, have shown much less benefit and an increased risk of infection.
But let's look at a systematic review which was performed by Bond and his colleagues and published in the journal Stroke. Almost 1200 patients with 1281 carotid endarterectomies, they were either patched or closed primarily. When you look at the data,
and I'm not going to show you large tables, but I'm going to show you the data that were generated from patch angioplasty was associated with a 67% reduction in operative stroke. And that's the endpoint we're trying to achieve, obviously, the avoidance of stroke with this operation.
60% reduction in stroke and death. 88% reduction in perioperative carotid occlusion. 87% reduction in recurrent stenosis over time. And a 46% reduction in stroke and death over the long-term. So there was long-term benefits, and you can see the P values for each of these endpoints.
And then that led to a Cochrane Review a number of years later, and that was also shown to you by Dr. Sultan. And what he did, and for those of you that read Cochrane Reviews, they do present the data, and then they present some qualitative statements.
And yes, studies are never the quality that they want when they're included in the Cochrane Review. But they reviewed 10 trials, almost 2000 patients, 2157 carotid endarterectomies. And a patch closure resulted in a 69% reduction in ipsilateral stroke.
82% reduction perioperative occlusions. And a 76% reduction in restenosis. And you can see the power of these observations as reflected in the P values. So those observations and those reports are six, seven years old.
Do we have anything that's contemporary? And yes, we do. Let's look at the CREST trial data and the subset of patients that had carotid endarterectomy. And an analysis of how that endarterectomy was closed was published in Stroke.
Specifically addressing, does patching affect the outcome of carotid endarterectomy? And when you look at the operative stroke rate, defined by stroke within 30 days of the operation, is there any question of the benefit of patching? Almost three times the risk of stroke
when patients were closed primarily. And that translated into a significant difference in stroke and death. Now what about four year outcomes? Well the difference, the significant difference in stroke is preserved at four years
when patients were patched, and that translates into a benefit of a reduction in stroke and death in patients who had carotid patching. Well what about restenosis because that's one of the main reasons why we patch also. Look at the difference in restenosis.
A three-fold, more than a three-fold difference in restenosis in those patients who had a carotid patch in this randomized trial. Now obviously, patients were not randomized to patching versus no patching, so this is an observational study. And then when you look at who patches and who doesn't,
in terms of specialty, vascular surgeons in CREST performed 65% of the operations, they patch 89% of the time. Thoracic surgeons patch 76% of the time, but neurosurgeons essentially don't patch. And the question is, is that reflected in operative stroke rates, and I rather suspect it is.
So patch closure should be routine for all carotid endarterectomies. It's associated with a significant reduction in operative stroke, occlusion, stroke and death, recurrent stenosis, and long-term outcomes. Thank you for your attention.
- [Enrique] Thank you Dr. No disclosures. So the basis for my opinion on this is three decades of treating thoracic outlet syndrome surgically and my collection of my personal cases on Venous TOS done during the last 12 years
in the the state of Michigan. The anatomic basis for Thoracic Outlet Syndrome is that of chronic subclavian vein injury produced by repetitive dynamic compression at the costoclavicular space. So you can see on the right side with the arm abduction.
You can see that the vein is compressed severely between the first rib subclavius muscle and the clavicle. So my treatment algorithm is that when I suspect the Axillo-subclavian vein thrombosis, confirm by duplex, immediate anti-coagulation with Heparin,
Expeditious venogram with thombolysis, maximum 3 or 4 weeks perhaps. If the vein becomes patent and is recognizable I proceed immediately with surgery and percutaneous balloon angioplasty. After decompression, if I fail to recolonize and open the vein I just use anticoagulation.
So the treatment consists of systemic antigcoagulation, restoration of the venous lumen, with catheter directed thrombolysis. I've been using the Angiojet for the last decade and infusion catheters as needed. Never had chronic or any renal failure in my experience.
And, this is important, lysis these veins several veins, not just the brachial vein. You have to access all the veins that are involved with thrombus. The brachial, the basillic and the cephalic, you have to put several sheaths, not just one, that's a common mistake.
Then you remove the extrinsic compression typically by a first rib resection or the bone anomaly and then you do a venous angioplasty and I never put a stent. I do the thoracic decompression with two incisions. One above the color bone and
one in the parasternal aspect of the infraclavicular space and following that, as you can see on the right hand side, I still have the sponges in the wound with the wound open and through the sheaths in the arm I proceed to do a completion venogram
and I post dilate the vein to accomplish the maximal delectation of the vein after the decompression. Now, why two incisions? Well this is a patient I saw years ago, where you can see he underwent trans-axillary resection of the first rib
and returned with unresolved vinous occlusion . You can see on the CT scan on the right that is a fragment of the first rib, which was resected through a trans-axillary approach that is still remaining and continued to squeeze the subclavian vein against the clavicle.
So that's why I do two incisions, one above and one below the clavicle. Now over 12 years treated 72 patients. Mostly with single stage. 68% of the patients with a single admission treatment and the pathology was vein thrombosis in almost all of them.
Just vein Stenosis in 4 of them. About 18% had documented hypercoagulable state and only 8 had a pulmonary embolization documented on admission. I did a diagnostic Venography in all of them. Thrombolysis pre-operatively was done in 75% of the cases, About 1.5 trips to the endo suite
per patient, all of them underwent rib resection and PTA and I anti-coagulate everybody for 6 months unless they're hypercoagulable when I do it for life. The anatomical results of these cases were 60% of the veins were widely patent, but 1/3
had partially occluding thrombus. Only 4 remain occluded and the clinical results are about 2/3 the symptoms were completely resolved and about 1/3 felt improved. If you look at the patients who had widely patent vein. Those had less days of delay to Lysis.
They had a much less time from diagnosis to decompression. And the incidence of post drug treatment at thrombosis was much lower. Less trips to the endo suite and lower hospital stay. If you look at patients here with a single admission the symptom resolution was higher during
single admission treatment, the venous patency was better, and the cost was about $8,000 less. The typical causes of treatment failure are late diagnosis, late initiation of treatment, incomplete thrombosis with lysis, PTA and Stenting without the compression of the
thoracic outlet, inadequate rib resection, and inadequate anticoagulation. Therefore I conclude the delay in lytic treatment and surgical decompression appears to be associated with lower venous patency rates. The treatment of VTOS during a single admission
has higher rates of arm symptom resolution, less hospitalization and significant cost savings. Referral to centers where single stage treatment is feasible, may improve the results and reduce the cost of treatment in these patients. Thank you
The third (mumbles) for intervertebral disc herniation includes four steps. We can start with conservative therapy course of four to six weeks. We can move on to percutaneous infiltrations
then to percutaneous decompression techniques and finally to endoscopic or surgical techniques. Obviously we can combine infiltrations with conservative therapy or with percutaneous decompression techniques. Starting with injections in the spine, do we actually need the imaging guidance?
According to the literature, imagine guidance increases the technical and clinical efficacy and decreases potential complication rate. It has been written that blind interlaminar epidural infiltrations are inaccurate in more than one third of the cases.
And if we go to clinical cases, these are two examples of injections which were performed blindly. On the upper row you can see it was an attempt for an ozone injection of the facet joint by an orthopedic surgeon. It was a blind attempt and you can see that the oxygen,
ozone transforms to oxygen after three minutes, is everywhere in the retroperitoneal space, but it's not in the facet joint. And the lower row you can see a blind attempt of epidural infiltration by anesthesiologist. The patient after the injection was reporting
severe headache, that is the center scan and you can see air inside the ventricular system of the brain. Percutaneous infiltrations can be performed through a trans-foraminal access to an interlaminar paramedial access through the sacro-coccigial hiatus and in all cases, you can use contrast or air control
before your steroid injection. These injections they go way back to 1950s and in 1970s you have the first trans-foraminal nerve root blocks. What we're actually injecting is long-acting corticosteroid and we do need the imaging for particulate ones because they can cause some complications
as we will see later. We do tend to combine corticosteroids with local anesthetic and we need contrast medium to verify the proper position of the needle. In all cases, when you are using contrast medium, you should be using agents approved for myelography.
Corticosteroids actually provide an anti-inflammatory effect, a direct neural membrane stabilization effect and they do modulate peripheral nociceptor input. On the other hand, local anesthetic interrupts the pain-spasm cycle, interrupts the transmission of the noxious stimuli and resets the nerve itself.
Contraindications include the patient who is unwilling to consent to the procedure, local or systemic infection, hemorrhagic diathesis or anticoagulant therapy and an allergy to any component mixture. As far as I'm concerned, I do prefer to apply three to four sessions of steroid injections
within 12-months period with a maximum of two infiltrations per session. And in all cases, we are using imaging guidance. We can use fluoroscopy, we can use CT or even MRI guidance and here we are using air or contrast medium to verify proper needle position.
And proper needle position does not mean only in the right spot, but you should have the needle outside a vessel. You will cause complication and problems to the patient if you perform intervascular injection of particulate corticosteroids.
What is worth saying is that trans-foraminal infiltrations they may result in higher pain reduction
when compared to interlaminar epidural infiltrations. Additionally, they seem to be superior to placebo therapies and to blind interlaminar epidural infiltrations for both short- and long-term pain reduction. In one-third of the patients, trans-foraminal infiltrations are surgery-sparing interventions.
And concerning evidence-based medicine, we know that these kind of injections they have a good level of evidence for radiculitis caused by disc herniation, a fair level of evidence for radiculitis caused by spinal stenosis and things are not so good with limited level of evidence to post-surgery syndrome.
And this is a patient, he had a herniation back in 2011. He was treated with a spinal injection, a trans-foraminal infiltration. On May of 2012, you can see that the herniation was gone and what we actually did was give some time to the nature to do its job.
- [Presenter] Thank you, Mr. President. Totally different subject, totally different part of the world. And difficult for a non-surgeon to talk in a surgical audience about this question. And it raised the other face of the other side of the question,
meaning that interventional treatment is not always indicated and not always justificate, and not always associate with good items. No disclosure for this presentation. And we have many recent data
that allowed us to understand better physiopathology of Takayasu arteritis and let use powerful inflammatory drug with good results. This is chronic systemic vasculitis that affect mainly outer an its branch
with chronic inflammation granular matters inflammation with this chronic specific thickening of artery walls. Many challenges and unmet needs in this pathology, but we will discuss especially activity assessment. We know that evolution of this disease is a succession of active and quiescent phases.
And we also recognize quite early that there were no correlation between vascular inflammation and systemic inflammation, meaning that we can evolution of the disease without any marker, biological marker or radiological marker, which is a real problem for us.
Even TEP scan, there was hopes using this new radiological findings, but as you can see in this meta-analysis, the sensitivity and specificities are not that good, that we cannot, did not allowed us to use this radiology to assess the inflammation
of the Takayasu. For vascular intervention, and for treatment as vasculitis, all vasculitis, steroids, immunosuppressant and biological agents improves the outcomes of this disease. And we always need a long-term treatment for those patient.
But for fixed and fibrotic lesions, intervention are needed. We also note that the results of vascular intervention are worse than in atherosclerotic and occlusive diseases. And we also know that after initial good photography of intervention, the long-term patency are poor
with a high rate of re-stenosis. And last sentence is that we know also that the failure of intervention are related to inflammation and the persistent of the inflammation in the wall before the procedure. So this is a summary of absolute revascularizations.
And about half of patient will need intervention in the Takayasu's. We will not discuss about that. We will discuss about what is the best technique in those patients choosing angioplasty or surgery. You have here
some of importance the items that we can use. First, for endovascular procedure, we know that it's world widely used. It's less invasive, safe, easy to do. But the long-term after a good initial
photography, once again, the re-stenosis rate are not acceptable. And 50 to 80% of patient will need another procedure. The best result are seen in short sessions, especially in renal artery and subclavian artery and stenting is not useful in those patients
and anti-platelet used before and after procedure may decrease the rate of re-stenosis. The result with surgery are better with a best long-term patency rate. As you can see the re-stenosis rate are very acceptable.
But not only the re-stenosis rate, we can also say that in severe patient, the long-term survivor increased with surgery in some cases. And especially for patients having long segment stenosis and extensive fibrosis or occlusion. How to choose?
In my opinion, we can see that we can choose specially regarding of local expertise an local availability. This is the best way to choose which technique we can use to save those patient. Last sentence that we can talk about
is about the medical treatment in those patients. As you can see, the rate of complication is as much higher than seven fold in patient without medical treatment. Two example for that, to illustrate that quickly, French experience.
And you can see with this slide that people who have higher ESR, CRP an fibrinogen before procedure will significantly have more and will significantly experience more complication. And secondly, this publication also find that we have three time more complication
with endovascular procedure than in surgery. And second publication, interesting publication from UK, will confirm the data about the difference between surgery an endovascular procedure will also confirm the fact that the complication, vascular complication,
are significantly reduced in patient receiving immunosuppressive treatment for the procedure. So, as a general rule, both endovascular intervention and surgery should be only used after suppression of inflammation wall, in the vessel wall,
in Takayasu disease, especially after a powerful treatment in those patient. So, in conclusion, we can say that Takayasu disease is a challenging disease with a changing face. And the use of new biological agent
can help us to change the face and will probably reduce the vascular procedure. Thank you.
- [Michael] Thank you very much, Giancarlo, and as George just told you, the overall bioresorbable vascular scaffold up look got a punch to the solar plexus recently when Abbott decided to withdraw it from the market. Nonetheless, I'm going to share with you the results, three year results of the Esprit trial.
Well, bioresorbable scaffolds, as you heard from George, there are advantages, there's obviously no permanent device left behind, eventually they resist to the last recoil. It can treat flow limiting dissections like any other stent as opposed to a balloon.
It's a method that can use to deliver more than one drug to the wall of the intima to prevent re-stenosis. It may allow treatment of areas not suitable for a permanent stent. May decrease procedure time and it's potential to reduce late lumen loss.
The disadvantages, well, those are the unknowns. What we don't know can certainly hurt us. And that involves inflammation, embolization of material, and the unknown time that we really understand when we need that support of a stent scaffold. Nonetheless, let's look at the biodegradable stent
landscape. These are some of the stents. The first was the Igaki-Tamai. This was the GAIA study Which was used in 30 patients in the SFA with the mean lesion length of 5.9 cm. You can see a binary re stenosis rate of 67%, TLR at 57%,
certainly not that impressive. They married it with a drug-coated balloon. So again, the same stent with the drug-coated balloon and we reduced the binary restenosis about 10% to 57.9% TLR 42%, still nothing to knock your socks off. There are other types of bioresorbable stents such as
metallic bioresorbable, such as magnesium stent, the AMS stent which showed at six months, a reasonable patency of 80% but look at PTA was 88.1. So it doesn't appear to offer a relative advantage in this group of patients. So now let's get to the Esprit clinical study and three
year result. This is a Bioresorbable scaffold made up Poly(L-lactide) (PLLA), if you will, with a coating of Poly (D&L-lactide) (PDLLA). The drug is Everolimus at 100 micrograms per centimeter squared.
It was on an Omnilink Elite delivery system. Single arm study. There were 35 patients enrolled. Short lesions, less than 5 centimeters and again it was being treated with a single device which was a 6 millimeter stent.
Key inclusion criteria we have already gone through but it also involved iliac arteries which was a minority of cases, about 10%. The rest were SFA. As you can see here in the SFA the majority of cases were in the distal segment of the SFA with a mean lesion
length of about 36 millimeters. Total occlusions about a quarter of patients. A couple cases just to show you. Again, pre-treatment, pre-dilatation and there's post-treatment and you can see the residual stenosis of 20% and then post the placement of the scaffold down
to 11%. And this is one with just some follow-up. A similar short discreet focal lesion, after treatment again at six months you can see the CTA and doplar ultrasound and this is the 12 month angio. In terms of the results, freedom from re stenosis at
one year was at 93.8%. Now, that's certainly comparable with many other technology. I think the thing that got people's attention was going out between two years and three years there was virtually no change in that. In point of fact, there were no events between two year
and three years and this curve as we talked in the last session is essentially flat between those two time points. So in conclusion, the 3-year results of the first inman clinical evaluation with this particular bio-resorbable scaffold with Everolimus showed good results and SFA and iliac lesions with no new events between
two and three years. So where are we now? Well, this is just my own sort of perspective and take on things. On the positive side, the hopes and promises we have these very versatile platforms that we're well familiar with of
these polymers. Obviously non-metallic temporary stents may be better solution than having a permanent implant. And it again allows the resumption of normal phase of motion to the vessel wall so it can relax to its native state and respond to stimuli as a native vessel
without a permanent implant. I've received these various scaffolds to permit some sort of tuning of things and allowing you to get the right or optimal recipe for strength flexibility. And again, I think this idea of resuming normal phase of motion may have some merit but it remains unproven.
The deal-breakers and what I think people are starting to realize is that all these current materials may not be the ideal thing. We can see here that going forward there are limited opportunities to really get the secret sauce right when we're manipulating a number of different things.
This is radial force, flexibility, dissolution kinetics. We can get something that may be passable but it may not be super. Then in closing I'll just share with you this article from the coronary literature that came out earlier this month showing the reasons behind late bioresorbable
scaffold thrombosis the most common being scaffold discontinuity. What does that mean? Well, this is an example from the editorial of the company the piece showing these breaking as the stent starts to dissolve.
The dissolution of the polymer we get these fractures and discontinuity. Here we see here a typical bioresorbable scaffold versus a bare-metal stent. Again, the struts have to be thicker, the vessel wall coverage has to be greater, and I think going forward
what we're going to see with these devices is have to be a re-engineering. And this might involve the entire polymer itself, it might include stent thickness, and strut thickness, excuse me. Because I think we're going to have to have a better way to reduce the frequency of malaposition, improve and
hasten healing, but right now I think the outlook for these bioresorbable scaffold group as a whole remains very uncertain. Thank you.
- [Ross] Thank you very much, Mark. Thank you Frank for inviting me to speak. If you look at the literature, I have no disclosures. If you look at the literature, and look simply at what is the evidence for stroke after cardiac bypass surgery, you'll find that most of them have greater than 50,
greater than 70 or greater than 80% and the greater than is the clue, but if you look at this data, it looks very compelling that the risk of stroke is significant. However, beware of an uncritical analysis where occlusions are combined with stenoses,
symptomatic with asymptomatic, and unilateral with bilateral. If you get rid of the occlusions and the symptomatics, this is what you have if you look at either unilateral or bilateral 50% disease and unilateral or bilateral greater than 70% disease,
the risks of stroke in asymptomatic patients drop dramatically. If we now just want to look at stenoses in asymptomatic patients who got unilateral disease, this is all the literature there is in the world and there's hardly any patients suffering
a post-operative stroke. Down there in the 80-99%, you'll see one patient from Shwartz with a 2.9%. What about bilateral asymptomatic disease? Well, our meta-analysis identified that the risk of death of any stroke was 6.5%,
but again, that only came from one study done 30 years ago. The death and stroke rate is higher at 9% and this reflects the burden of vascular disease and the increased risk with them because most of the deaths are cardiac. If you look at four series of almost 30,000 CABG patients,
and then where we look back and said, okay, was the stroke attributable or ipsilateral to the underlying carotid stenosis? In between 90 and 95% of patients, they were not. There've been two randomized trials. This was the Illuminati study
where there was no significant difference in 30 day death/stroke between synchronous CABG and delayed carotid endarterectomy after CABG and the most recently published German study that was published two months ago in Stroke, which showed an alarmingly high,
this is a national study, an alarmingly high death and stroke rate on intention to treat analysis with synchronous surgery, and if you looked the per protocol rates, the rates of ipsilateral stroke was only 5.9%. My understanding is I've got more experience
with reading all the literature on this, is that carotid disease is a marker for severe aortic arch disease, and indeed, the presence of a carotid bruit and the presence of a greater than 70% stenosis were the only significant predictors
for finding severe aortic arch disease, which is now considered to be the main cause of stroke after coronary bypass. What about the symptomatic patients? I was asked to comment on that by Frank. There's only been one paper that was D'Agostino,
20 years ago, who showed that if you have got symptomatic disease and the unilateral or bilateral disease, then you are in trouble and you need to think about doing something with them. What should you do with them? Well, we've recently published a meta-analysis
in the European journal earlier this year and when we compared the data with a meta-analysis I did some 15 years ago, you will see that after stenting and CABG, whether it's staged or same day, the risks of stroke are very much higher
at present than surgery, so I think in symptomatic patients, surgery is preferable to stenting unless you can prove that you can do it safer. Now, these may change with time, but there's limited literature available to us.
The European Society of Vascular Surgery published its carotid guidelines in August of this year online, they're free to access from the ESVS website. And we've addressed all the issues relating to combined carotid and cardiac disease.
We concluded that a staged or synchronous carotid intervention should be considered in CABG patients with a history of stroke or TIA, and who have a 50-99% stenosis, and in that situation, where they are symptomatic, we feel that at present, surgery is safer than stenting,
but that well may change in the future. We advised against staged or synchronous interventions in patients with unilateral asymptomatic 70-99% stenosis, as the evidence that it reduces the risk of stroke is negligible, but we did recommend that a staged
or synchronous carotid intervention may be considered in CABG patients with bilateral asymptomatic disease or a severe stenosis with contralateral occlusion and when I say carotid intervention, I mean both surgery or stenting, as the meta-analysis published earlier this year
showed that the outcomes in asymptomatic patients between surgery and stenting were virtually identical. Thank you very much indeed.
- [Manju] I have no relevant financial disclosures. The prevalence of proximal vascular claudication is known in patients with peripheral arterial disease as about 15% and about a third of patients following aortobifemoral bypass graft or EVAR with internal iliac artery embolization.
However, prevalence in the general population is unknown. And as we all know hip and buttock pain can have multiple nonvascular etiologies, and sometimes it is literally and figuratively a pain in the butt to figure this out. Arterial flow to the pelvis is complex,
not only direct inline flow but also flow through multiple proximal and distal collateral circulations, and standard noninvasive evaluation, which is more axial, does not really evaluate this adequately in any way. So in addition to standard evaluation,
additional modalities that have been studied up in our brachial index as well as near Infra-Red Spectroscopy, which measures muscle O2 saturation. Exercise transcutaneous pCO2 is a newer addition. It was first studied
in the pulmonary literature in the 1980s when a drop in TcPO2 was noted in patients with chronic lung disease. It was Dr. Abraham from France who actually automated correction of peripheral TcPO2 values to central changes during exercise by software
and published in circulation in 2003. One of his fellows, Dr. Mahe, actually visited us in 2013, and we got the software as well as learned the technique from them. This is from Dr. Abraham's original publication
where you see the TcPO2 levels falling in various parts of the lower extremity, as well as the baseline lead in the chest and then a calculation of the drop index with greater than 15% being cut off for ischemia. And this is the final result.
In that original publication, comparison with CT scan showed detection of a greater than 75% stenosis in arterial flow to the internal iliac artery to be fairly satisfactory in terms of sensitivity and specificity. But most importantly the negative
predictive value was really high. So we adopted this protocol in our lab in 2013 using the same criteria, and the patient is placed on the treadmill. The TcPO2 probes as well as EKG leads are placed. The patient stands for two minutes for probe stabilization
and then starts walking at a gradient of 10 degrees and two miles per hour for a maximum of 12 minutes or as much as symptoms will allow. And then after they stop walking they stand for another 10 minutes for recovery to baseline. The data is directly imported into the software
and the drop index corrected and displayed. Reproducibility has been shown not only in proximal claudication but also in distal claudication as I will demonstrate. And we have used this to study to tease out patients with and without true and pseudoclaudication
using CT angiography, otherwise, another imaging as clinically indicated. 68 patients are included in the analysis thus far. And this is the distribution of pain that they have presented with. Majority of them the pain in multiple areas.
As expected 80% of them had a history of peripheral arterial disease and current or prior smoking. And about 30% overall had a known history of lumbar spine stenosis or hip arthritis. Resting ABIs were not very informative.
And if you look at the breakdown of the studies, about 42% of them were positive, 34 negative, and 22% were indeterminate. This is an example of a 71-year-old gentleman with left buttock and right calf claudication and you can see the dip below the baseline in the tracing.
The left common iliac artery could be stented successfully, and you can see the green line moved up into the normal area, but right popliteal intervention was unsuccessful. Another patient with bilateral buttock and thigh claudication,
you can see the green and blue lines below the threshold. He underwent distal aortic and proximal common iliac artery stenting. Note the residual stenosis in the right internal iliac artery. And a post-procedure study shows improvement
but not resolution on the right side but resolution on the left. This is a comparison of our results with the previous studies, and as you can see the most impressive is the negative predictive value of 93%.
We have performed this study in 137 patients so far and are still analyzing those results. So to conclude, non-invasive evaluation of buttock claudication with exercise TcPO2 is safe and cost effective with ability to reserve imaging for patients only with positive studies.
A high negative predictive value promises good ability to differentiate from other nonvascular causes of buttock and hip discomfort. However, it is time consuming. Automation is not yet there and is essential, and the current software is proprietary.
I thank you for your attention.
- [Instructor] Dr. Almeida, Dr. Kabnick, Dr. Wakefield, I want to thank you gentlemen, and particularly Dr. Veith for asking me to be here. At a fundamental level venous pressure is interaction between flow and conduit caliber. More flow, higher pressure.
Smaller the conduit, higher the pressure. These are all Penroses of different sizes. And you can see the small Penrose has higher pressure than the three-fourths larger Penrose, at the bottom. And this relationship retains at each
tributary and confluence level, which surprisingly remains more or less constant in the lower limb. Iliac flow is 11% of cardiac index, about 700 cc's per minute in adults. It's a fixed fraction of cardiac output.
As you know, cardiac output is, at resting, is remarkably uniform. And that is the case with lower limb flow. We are interested in veins, this is outflow, inflow is fixed. Now this is the open channel flow.
In open channel, flows like like a reservoir. The depth is an analog of venous pressure in conduit flows. So, if the outflow is small compared to the inflow, you are going to have higher pressure, and you'll get overflow collaterals.
If the outflow is big compared to inflow, remember inflow is fixed, the pressure will be lower. And normal pressure is obtained when the outflow equally balances inflow. Now, optimal iliac vein caliber can be calculated
from this constant inflow, that's same for everybody, with variation for surface area and body mass. Optimal iliac vein caliber can be calculated from flow equations and corresponds to IVUS measurements in normals. These calibers must be established after initial stenting
and reinterventions. CFV familiar range should be 12 millimeters in diameter, 14 for EIV, 16 for CIV. And if you use areas, you can get a little bit more sophisticated measuring the areas.
125 square millimeters for CFV, 150 for EIV, and 200 for CIV. If you want to normalize venous pressure, after all, venous hypertension is the basis of CVD, this parameter should be established after initial stenting and after reinterventions.
This is the famous figure, which I have borrowed from Dr. Sumner's book, that's arterial stenosis and flow. There's percent stenosis, we know this by heart, right, instinctively. The flow does not go down 'til you reach about 80% stenosis,
it's drilled into you, true of most major arteries. Well, the point is, why is that? Why does that happen? And the reason is this, the reason is peripheral resistance in arterioles.
Now, if you calculate by degradation of pressure, this resistance, probably in a person's, somewhere around 70% stenosis. So it's a tandem stenosis to anything that develops above. So you are not going to get flow reduction unless that 70% threshold is exceeded.
Now, of course, flow is a critical thing in arterial regions. In veins, it's venous pressure, and there's no peripheral stenosis here, that factor is not that, abdomen is somewhat of a weak,
acts like a peripheral venous pressure, only two to five millimeters, so it doesn't matter much. So in veins, any reduction in caliber, given a normal flow, will raise venous pressure. In experimental systems, as little as 13% will do it. It all depends upon Poiseueille equation, right?
r four, fourth power of radius, so caliber size is very important. Another thing is, because of Poiseueille equation, it's impossible to equalize flow and maintain normal pressure with numbers alone. The numbers become very, very impossible.
But if you have the same size, you can equalize pressure that happens at the calf level, the thigh level, the inferior vena cava with the azygos system, but iliac veins is a bottleneck. Another thing is this minor stenosis, 16 millimeters to 14, it's about 13% stenosis,
it doesn't matter in arteries. But in veins, the geometric factor, the Poiseueille equation, r four, will almost double, which means the pressure will rise. So, in veins, even minor, what we think is minor, is really not minor.
In arteries, maybe. So, we have to get to the, many of these arterial, physiologic concepts, which are being inappropriately applied to the venous system. Thank you.
Moving on to percutaneous decompression techniques for the discs, we can have decompression and we can have regeneration techniques for the discs. Specifically for the decompression techniques we can have thermal techniques using laser, continuous or pulsed radiofrequency and plasma energy ablation.
We can have mechanical decompression using a wide variety of devices and we can have chemical decompression by means of Discogel or ozone intradiscal injections. All these techniques, what they are actually based on is that fact that a intervertebral disc is a closed hydro-ablic space and when you are removing a small
part from the nucleus, you are actually causing a significant decrease in the intradiscal disc and this disc pressure actually is what makes the herniation move inwards. And we have these techniques from back in the 1940s. The indications for these kind of treatments
in the intervertebral discs include patients who are capable of providing consent with a symptomatic small to medium-sized herniation and when we are speaking about the size of the herniation, if you have a theoretical line between the facet joints, all herniations which do not cross this line,
they can be percutaneously treated. And when we are speaking about symptomatic cases, symptoms should be consistent with the segmental level where the herniation is located on the MR imaging. For example, if you have a left L4-L5 foraminal herniation, you are expecting the patient
to report a left L4 root neuralgia. Absolute contraindications include sphincter dysfunction, extreme sciatica and progressive neurologic deficit. And actually all these are indications for surgery. Additional absolute contraindications include sequestration or the presence
of asymptomatic herniation, local or systemic infection, spondylosthesis and stenosis of the vertebral canal, anticoagulants, coagulation disorders and the patient refusing to provide informed consent. Most of these techniques are performed under fluoroscopy so we (mumbles) projection with 45-degrees angulation
of the fluoroscopy beam and as far as the lumbar spine is concerned, we perform a direct posterior lateral (mumbles) in the disc. In the final position, we need to have the needle in the anterior third of the disc in the lateral projection towards the midline in the AP projection and you can see
how important the technologist is because we need to have good visualization of what we are doing. Once you are there, you have access to the disc and you can insert any kind of product that you are familiar with, starting from thermal, going to mechanical or chemical decompression.
The magic number for all these techniques concerning success rate is around 80%. The complication rate is very low, between 0.5%. What we do know so far from the literature is that there are no studies of evidence of superiority of one technique over the other.
As we've already said, complications are really rare. Spondylodiscitis is the most fearsome one with a percentage of 0.24% per patient.
- [Presenter] Thank you very much Mrs. Chairman, ladies and gentlemen. Yesterday morning we had a session about treatment of lung SFA lesions Task C and D, and one of the conclusions was that the best that you can do for treatment of Task C and D, lung lesions in SFA, is debul
king, relining the SFA, and try to leave nothing behind. So, in this purpose we set up the Definitive AR study, it's a multicenter, randomized, pilot study for SFA and popliteal lesions. We randomized almost 120 patients, direct endarectomy
or direct atherectomy, and DCB, the drug-coated balloon, or drug-coated balloon alone. We had also when you have severe calcifications, a group separate you see on the right side, that goes directly in the direct atherectomy and DCB group. The inclusion criteria,
Rutherford classification two through four, more than 70% stenosis, and the target lesion was 7 to 15 centimeters. Exclusion in-stent restenosis, and aneurysms like always in these studies. The device we used for the endartectomy or atherectomy was a
SilverHawk TurboHawk, well known in the United States, was owned by Covidien and is now a Medtronic device. And the DCB balloon was the Bayer Paclitaxel Paccocath Technology balloon. You see here the baseline characteristics. The first group, the DAART group,
is direct atherectomy with drug-coated balloon, the second the drug-coated balloon, and on separate the very calcified group, and you'll see the lesion length is almost 11 centimeters, the calcifications were severe, also 70-74% in the first two groups.
You see here one of the total occlusions of the SFA, and you see here 20 centimet and we tried, we used the first, the transluminal catheterization with a remote guidewire, afterwards pre-ballooning
TurboHawk and drug-coated balloon, and you see the result at the end. But for now, the procedural outcomes. You see here that we had distal embolizations in the DAART group, three patients and two perforations in this group in a drug-coated balloon.
We had to cross over bail-out stenting for two patients, and very severe dissections in 10 patients. You can see it here stressed. Now, the results, the Duplex ultrasound patency at 12 months: the whole group is 93% of the endarterectomy and lining up
with drug-coated balloon, and almost 90% for the other group. You see the two cohorts, one to another, and you see always a slight little difference for the endarterectomy in favor of endarterectomy group. Angiographic patency you see on the other slide
why the shivers are different of the duplex ultrasound is because not all patients showed up for an angiography after one year. So you see very good results. Clinically-driven TLR, three patients in the DAART group and four patients in the DCB group.
In the very calcified group, we haven't had any clinical TLRs. We had two deaths in the DAART, and two deaths in the other groups. The deaths are not related to the device, not to the therapy.
These patients died of cancer. So as conclusion, Mrs. Chairman, ladies and gentlemen, DCB offers promising results in the treatment of femoro-popliteal lesions. However limitations exist in complex lesions with severe calcifications, acute residual stenosis
and lesion lengths. Lining up atherectomy, first do an endartectomy or direct artherctomy of the SFA and lining up of the drug-coated balloon is a very good therapy for SFA lesions. Thank you for your attention.
- [Martin] Good morning. Thank you Dr. Veith for the invite again this year. These are my general disclosures, none specific for this talk. I'm going to speak regarding how complex carotid interventions which I would define in the middle of the slide there as treatments involving the carotid bifurcation
with carotid endarterectomy combined with treatment of longer length or tandem specific lesions of the common carotid artery, tortuous internal carotid arteries with long length disease, recurrent stenosis that require redo procedures, symptomatic posterior circulation disease
requiring a simultaneous intervention, prior head and neck cancers and radiation effects and combined opened cardiac surgery with carotid endarterectomy is a higher risk group that's been relative non-controlled and ill-defined with smaller studies done
describing singular techniques. We know certainly that carotid endarterectomy and carotid stenting have low stroke and death rates. When they're performed with these more complex groups have not been analyzed. So this is a person audit
of 325 consecutive interventions since 2009. 28% of these involving a complex carotid intervention by that definition with those treatments listed there. Comparative groups, 185 standard carotid endarterectomies, 21 carotid case during that case, during that time, and also isolated innominate
or proximal common carotid artery stenting for aneurysm or occlusive disease. Some of these patients followed with duplex imaging, many of those for the aneurysms with a chimney technique for the occlusive disease with a bare stent treatment.
Carotid repair details. My preferred technique, arteriotomies extending beyond the endarterectomy end points, routine use of a balloon tip Pruitt-Inahara shunt, conventional endarterectomy, thin wall patching in all cases,
and completion duplex scanning. Carotid stenting done transfemorally with a neuroprotective filters, IVUS-guiding with general use of larger diameter balloons at the repair sites. The specifics for the complex carotid group.
With the combined radiated or recurrent stenosis saphenous vein patch is used preferentially. Some interposition grafts used. Combined posterior circulation, these are bypasses of the subclavian or vertebral reimplants.
With long length and tortuous ICAs I'll describe briefly a technique of ICA shortening. And with ipsilateral common carotid disease, the long length mid and distal portion of the common carotid artery can be treated with a eversion endarterectomy technique
which I'll quickly describe. Near occlusions or multilength obliterations of the common carotid will require interposition grafts or bypassing from the subclavian artery. And proximal or origin stenosis done over the retrograde bare stent,
preferentially a Boston Scientific Express stent, general lengths less than three centimeters. Stenting performed first before the endarterectomy. The ICA shortening technique done after arteriotomy is made. An endarterectomy, approximately centimeter length segments cut out of the proximal ICA and then reimplantation
of the posterior wall, with a continuous suture, then patching across that site. The eversion endarterectomy technique done by dividing at the distal common carotid artery and the performing an eversion endarterectomy of the common carotid artery.
Insertion then of the shunt into the distal vessel. Endarterectomy completed up the internal carotid artery and then patching across the whole segment. With the more proximal disease, again stenting of focal disease at the arch origin vessels and complete occlusions treated with
carotid-carotid bypasses. These are the comparative results a cohort here that has 40% symptomatic presentations. Fairly rigorous image capturing and followup with mean followups out to nearly three years in this group, showing relatively equal outcomes
in the 30 day period between complex carotid group and the standard CEA subgroup, of no strokes in the carotid endarterectomy groups, either complex or standard CEA. The complications primarily in the standard CEA group due to cardiac complications.
Composite severe perioperative outcomes were equivalent and restenosis occurred at the carotid bulb in all of those cases, both complex and standard groups. One group to note is isolated common carotid artery stenting or innominate stenting for occlusive disease, up to a 10% recurrence rate, requiring reintervention.
So, can be done safely, these complex intervention with a more aggressive technique treating all of the disease on the ipsilateral side. Recurrent stenosis can be a problem, either at the bifurcation or in the proximal common intervention sites
and duplex surveillance imaging is indicated. Thank you very much.
- [Domenico Valenti] I would like to thank Frank Veith for the kind invitation. I have no disclosure to make. Almost 14 years ago, Doctor Archie stated very well, in his invited commentary on Ross Naylor's Camiade paper. The carotid bypass is an acceptable alternative method of carotid reconstruction, and it should be
in the repertoire of every surgeon undertaking a carotid endarectomy. Few years later, Doctor Ricco validated Doctor Archie's statement in his very large prospective study where carotid bypass should be a durable and safe procedure,
with a primary patency rate of 97.9%. Recently, carotid stenting has been advocated as a complimentary technique, but mainly for technical defect detected during the, after the carotid endarectomy, on completion study or immediately post-op
rather than a bail-out procedure for a failed endarectomy. At King's, we are indeed adding bypasses in our repertoire and all the bypass were performed mainly for a bail-out procedure but two, were post radiation stenosis.
We are all familiar with the Gore Hybrid Graft, which is a novel technique, probably natural evolution of the aortic technique as an heparin-bounded PTFE, we've got a Nitinol stent, this constrained and allowed a sutureless anatomosis. Almost three years ago,
after a disaster carotid endarectomy, I decided to use a hybrid graft instead of the standard PTFE, and last year I presented here our initial experience with the hybrid graft. The implantation technique is very straightforward,
the graft is surgeon-friendly, and basically with a constrained stent, it's almost the same size of a pretty narrow shunt, is inserted under direct vision inside the internal carotid artery. Then when the stent is in place,
almost two and half centimeter inside the internal carotid artery, the deployment line is pulled, keeping parallel to the PTFE, and sutureless anastomosis is performed. The proximal anastomosis is done in the usual fashion,
end-to-end, using 6-0 prolene suture, I tend to re-implant the external carotid whenever it's possible. This is what it looks like in real life, it's patient with postural degradation, severe contralateral occlusion,
the carotid hybrid graph, and you can see the immediate post-op CT angio with the pen that show the good patency of the graft. So far, we implanted the 19 cases and in this table you can see the reason for conversion. All the patients were enrolled in very strict
surveillance programs with DuploScan and CT angiogram. We completed 36 months of follow-up and during the follow-up, three cases occluded, one at six, one at 12 and one at 24 months. The common denominator for the ones occluded at 12 and 24 months is both patients
had stopped clopidogrel at six months. During the follow-up period, four stenosis for re-stenosis were detected, there were two minor, one moderate, one severe, and again, the common denominator on the severest and restenonsis was the patient stopped clopidogrel after six months.
This one is particularly the case, you can see in the post-op CT angiogram will show a good patency of the hybrid graft in 2015 and last September the patient developed quite severe 95% restenosis. The Capper-Meyer analysis on the hybrid graft
in carotid surgery shows 78% primary patency rate. In conclusion, ladies and gentlemen, carotid endarectomy still remains the gold standard, a carotid bypass with a standard PTFE graft is a safe and durable procedure, Gore Hybrid Graft for carotid surgery
is a novel technique with a reasonable 36 months patency rate, in our experience, why all the occlusion were probably associated with the stop of one of the dual antiplatelet treatment, we recommend to continue the dual antiplatelet treatment
long term, and the long term follow-up is necessary in order to establish the durability of this novel graft for carotid surgery. Thank you very much indeed for your attention.
- [Roberto] Good afternoon to everybody. This is my disclosure. First of all, the anatomical variability of foot arteries. Marco probably should speak better and essentially, the distal distribution pattern in 1,624 legs was described. And we have two key points in the distality.
The first key point is that the vascular abnormalities are a variation of the ankle vessel distribution. We can have in the majority of the cases a balance, see a circulation like this, but we can have an anterior dominant peroneal artery, posterior dominant peroneal artery,
or a single peroneal artery giving both dorsalis pedis artery and the plantar system. Also, in the foot, more distally, we have a foot distribution pattern which can change from patients. We have in about 80% a standard balance of circulation, but we can't have a dominant dorsalis perdis artery,
a dominant lateral plantar artery, or the tarsal loop with the absence of the pedal-plantar loop. So, every patient is different. Follow patient's anatomy and not book pictures. Second, what is the pathology of foot arteries? Today, I have shown you the key point of what I think
of the pathology: foot arteries are the border between two different worlds, two different diseases in terms of biology and clinical evolution, and I call them "bad" and "sad," BAD is Big Artery Disease and SAD is Small Artery Disease. In BAD patients, outflow is good.
We can do angioplasty looking for the healthy foot distribution system. The majority of BAD patients can be revascularized, either surgically or percutaneously. In SAD patients, below-the-ankle outflow is obstructed and angioplasty can be dangerous,
because there is disease of the foot distribution system. In the vast majority of the cases, SAD is an untreatable disease, either surgically or percutaneously, and is able to jeopardize the fate of the leg and of the patient.
What is the value of angiosome? We described this angiosome and today we know we have three meta-analysis, a lot of paper demonstrating that direct revascularization according to the angiosome concept seems to be better than indirect revascularization
in terms of wound healing and limb salvage. I have one fundamental critique. The value of an angiosome-oriented revascularization is inversely related to the function of collateral vessels. When we have BAD without SAD, collateral vessels are generally spared, and we have a good foot distribution
system, and this is a peroneal artery, with these three distal branches, giving blood to the tiptoe despite a total occlusion of dorsalis pedis and of the plantar system. When we have SAD with or without BAD, collateral vessels are generally involved.
We have the failure of the foot distribution system. This is a patient with no peroneal tibial artery, but with the lesion in the first two, you can see that we have a loneliness of this foot two, because every vessel is occluded here. And only going with a very small balloon here,
in the distal metatarsal artery of the first and of the second two, totally calcified, and dilated with a 1.5 and then a 2.3 drop in the balloon, we were able to get the healing of this toe, because this was the only way. In some patients, angiosome-oriented revascularization
when possible, it depends from the degree of the SAD disease is the only way to get healing. Finally, is there a rule for bypass? Now, look at this lesion. Is this focal lesion critical? Has this lesion a role in the pathophysiology
of CLI in this patient? According to a defined group, the hemodynamic significance of a lesion is 50% diameter stenosis by visual estimation or by quantitative vessel analysis software assessing at least two different angiographic projections. So, this lesion is not critical.
We cannot rid this lesion. Angioplasty must be confined to critical lesions or occlusions. In the vast majority of CLI patients, angioplasty leaves behind a not-critical diffuse disease. Due to this hemodynamic reason, and due to patency rates,
a good bypass will always, always be better than angioplasty in treating CLI patients with diffuse multilevel obstructive disease. However, in Italy we wrote this consensus document, and we said that short lesion, angioplasty first strategy.
Long lesion, bypass first strategy. But we have to consider the bypass visibility and this means to consider four steps. Fundamental, the patient clinical status, is the patient a good candidate for bypass surgery? Foot evaluation, is the foot a possible
there is a possible site for anastomosis. Bypass conduit, that is saphenous for bypass And finally the outflow vessel, is a BAD patient or a SAD patient? Can we revascularize this patient? If you're able to get four, yes,
you can go for a bypass first strategy. But if you get also only one no, you must go back to an angioplasty first strategy. So is there a rule for bypass? Sure, however, every revascularization strategy must be tailored on the global patient status.
Thank you very much for your attention.
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