- Thank you Chairman, and thanks to Frank and Enrico for the invitation. I have no disclosures. So where are we in 2018? If you look at the indications for which we would be performing distal bypasses, then we get critical ischemia in the form
of rest pain or tissue loss. In terms of rest pain, the revascularizing a single level of disease may be sufficient to eliminate debilitating ischemic pain symptoms. But in tissue loss, the goal is to reestablish inline, pulsatile flow to the distal extremity
to ensure healing. And it may require staged surgical or hybrid procedures to treat multilevel inflow and outflow disease. So the first consideration is an indication, in terms of tissue loss or gangrene,
and that would be an indication for bypass. Looking at comorbidities and high perioperative risk, obviously high perioperative risk patients go for endovascular intervention. But recent studies have also indicated that patients with high cardiac risk
are equal in cardiac risk when you compare endovascular versus bypass, the results are no different. And in fact, the study supported the effectiveness of primary leg bypasses. So in my practice, if there is a patient
high perioperative risk, he gets endovascular intervention. And if not, then a bypass. When you look at 30 days and one year mortality, there is an advantage to endovascular in the first 30 days, but it peters out
to equivalency at one year, between distal bypass and angioplasty. And going forward, to three and five years, the equivalency is maintained, with no statistically significant difference. What about life expectancy?
Now the considerations are that life expectancy with CLI is very poor, 40% for two years. Open bypass in this frail group will lead to a decline in QOL, due to post-op recovery issues. And return to independent ambulation at one year
is poor with open surgery compared to endovascular. So if a patient has got a life expectancy of greater than two years, then it's reasonable to go for bypass surgery. Amputation free survival, again, there is
an advantage, although not by much, for distal bypass compared to angioplasty. And this at one, three, and five years, although initially, an advantage for bypass surgery, gained some form of equivalency or no statistical difference
at five years. What about anatomy? Long segment lesions greater than 20 centimeter, lesions lent occluded popliteal trifurcation and severe common femoral artery disease are all indications where bypass
can be considered. Of course, you need the autogenous venous conduit to be present to be able to do that. In certain cases, you have done a bypass or an endovascular procedure for a particular artery but the wound is not in the same
angiosomal area, and therefore, it doesn't heal. And in those cases, you may need to do a bypass to get better exposure and would allow the combination of endovascular to help the patient.
And lastly, previous failed endovascular interventions will undergo traditional or bypasses through extra-anatomical roots or non-traditional pathways to be able to deliver blood to the areas where there is tissue loss.
So ladies and gentlemen, in conclusion, the role of distal bypass is definitely complementary. In my own practice, endovascular comes first. But the current indications for distal bypass can be patients with tissue loss, patients who've
got good physiological risk factors, long lesions, greater than two years life expectancy, and endovascular failure to recanalize. No endovascular direct revascularization with poor inflow in angiosomal artery
is also an indication. We will wait for the trials. Thank you for your attention.
- Thank you very much Neil. I would like to thank Dr. Veet for having placed this talk in the program. I have no disclosures. Duplex scan is a very cheap methodology. I'm always surprised how people are not using it more. We have a dedicated ultrasound machine
in the operating room, and that makes it much easier for us to use it. We also learned that it's extremely sensitive to low flow. It can detect bleeding vessels when the arteriogram shows an occluded vessel.
It's better than a CT also for low flow situations. There's several advantage for ultrasound guided interventions. There's no radiation. No nephrotoxic contrast material. Multi-planar, magnification,
and you can visualize the arterial wall in addition to the lumen. You can perform a balloon angioplasty, as we've shown and reported before, as well as stenting and arterectomies. Basically, if there is a complication,
you can also treat the complication on the ultrasound alone without requiring x-ray. At the end of the procedure, you can confirm the adequacy of your technique, both anatomically and hemodynamically. The arterial mapping is very important
because it reliably identifies in inflow and outflow vessels, whether it's an acute situation or chronic occlusion. It selects the best site for an anastomosis if you're going to do a bypass, because you can select the least calcified segment.
Identifies the causes of occlusion, and occluded popliteal aneurysm versus arterosclerotic occlusive disease, and visualizes a low flow patent arteries that are not seen by arteriogram. We have done over a thousand cases,
and we're going to concentrate on the femoral popliteals that we perform on the duplex scan alone. Basically, the same demographics as you have in your own practice, with the age being of 73. The technical success was 95% on these patients.
99.6% for stenoses and 87% for occlusions. We did have some complications. We're going to concentrate on the thromboembolic complication of these cases. We have 12 out of 237 cases. Also, we added another 15 cases for these presentations,
where we have done duplex guided procedures and patients did embolize or occluded. 12 are infainguinal arteries, and three were bypasses. The treatment was mechanical thrombectomy in 64% of the cases,
thrombolysis alone in 20%, mechanical thrombolysis in 8%. Thrombolysis, suction, thrombectomy, and a new stent in 8% of the cases. Overall results were excellent. 88% of the patients did not require any further study,
and any further methodology for visualization of the vessels. Here's an example of a patient that had an embolus at the the tibioperoneal trunk. We placed a catheter. We injected tPA and 20 minutes later,
we did a duplex scan and was widely patent. This was done, did not require any further studies. This patient had a impossible case, was a clot that formed on top of the balloon, as you see here. On top of the balloon the clot,
so injected tPA here approximately before we deflate the balloon, and then we waited again. Then after, once we deflate the balloon, there were no more clots. This patient had an embolus to the SFA
and the popliteal, and the entire SFA was occluded. We puncture on ultrasound guidance and you can see the wire going through. You can visual, I'm sorry. Can you work it up again? Next? There you go.
Sorry, he was just showing the area of the puncture. We're placing the wire and the sheet, of course. Over the wire, we're going to put a suction thrombectomy device without going below the popliteal. You can see clearly the tip of the wire.
And now, we bring the suction thrombectomy device all the way to most distal portion where the occluded segment occurred. Now we're doing suction thrombectomy after injecting tPA. First we did thrombolysis,
now we're doing suction thrombectomy. Now we can see that it's not perfect, because the volume flow is very low. The peak systolic is very low. Obviously, there's a stenosis somewhere and we detected the stenosis in the SFA.
We had a wire cross, so that was easy. We did a balloon angioplasty and stenting, because the balloon angioplasty alone was not enough. He required the lesion. You can see, even with the stent, there's an area of stenosis that needs to be re-ballooned.
Now we ballooned it and we're basically done. Now the volume flow and peak systolic velocity are great, as I show you here, and we're done with that procedure. Just to finalize. Just the stent that was occluded acutely, and here's the suction device.
Again, the same thing. Look at the power of the suction device. It's going to bring the stents together, actually. All the way and I'm sure Dr. Veet's going to stop my talk any moment now. Here we go and see, and basically it's done.
So, the conclusion's obvious. You avoid the nephrotoxic agents. You visualize the low flow arteries. You identify the cause of occlusion. Those are unique to duplex scanning. Patients with acute arterial ischemia of diverse etiology
can be safely treated by various endovascular procedures under duplex guidance alone. Thank you very much.
- Thank you, I'd like to start by thanking Dr. Veith, not only for the privilege of the podium, but for many years ago teaching me how to do these exposures. If you've missed some of the pictures, many of these were published by Enrico, Dr. Veith, and myself not too long ago in JVS.
So vascular exposure through scarred or infected wounds, as we know, leads to increased OR time, increased risk of blood loss, infection, and damage to vessels and nerves. This afternoon I'm going to show you how to avoid going back into those scarred groins.
On the scarred groin which is seen in the left lower-hand corner, a good inflow vessel is the external iliac artery. It's very easily dissected out in thin patients through a very small incision, about two breaths above the inguinal ligament.
Once you go through the internal and external oblique, you can gently pull up the retroperitoneum, and they're easily exposed. Sometimes even more difficult than the exposure is tunneling through the scarred tissue. You want to tunnel deep to the inguinal ligament
and anterolateral to the artery, usually involving a counterincision to avoid injury to the venous branches. If it's for infection and you're tunneling through the obturator canal, please remember to tunnel inferomedial
to avoid the neurovascular bundle that is superiolateral. The profunda femoris in its mid and distal portions can be a good inflow or outflow vessel. As you see on the left, it lives right underneath the sartorius muscle. The picture on the right shows incision to expose it,
either medial or lateral to the sartorius muscle. Lateral is usually for more distal. The picture on the left shows the course of the dissection once you get deep to the superficial femoral vessels. There is a fibrous band between the adductor longus and vastus medialis,
and once you get through that tissue plane, the profunda vessels are right there. Here you can see the sartorius muscle and superficial femoral artery pulled laterally. When there's scarring medially, you need to get to the popliteal artery.
The above-knee popliteal artery is easily exposed through an incision between the iliotibial tract and the biceps femoris tendon. Once you get through this tissue plane, you can bluntly get into the popliteal fossa and dissect out the above-knee popliteal artery.
The below-knee popliteal artery is a little more difficult. You have to worry about the peroneal artery, I'm sorry, the peroneal nerve that is there, as long as the fibula. You have to dissect off the common peroneal nerve, detach the biceps femoris tendon,
divide the rest of the ligamentous attachments. But once you get out that fibula which causes almost no disability, the below-knee popliteal artery is right there. When tunneling to these, we usually tunnel in a subcutaneous fashion
across the thigh and laterally. If you have lateral infection or scarring and you need to get to the very origin of the anterior tibial artery, you can get there medially. You would dissect the below-knee popliteal artery as usual,
as well as the tibia peroneal trunk. You can almost always see the anterior tibial artery poking through the interosseous membrane. You can put a right-angle clamp in there and very carefully divide that interosseous membrane and expose about the first five centimeters
of the anterior tibial artery. This was used, as you can see here, in a medial vein bypass to the origin of the anterior tibial artery. Lastly I'm going to show you a lateral approach to all three tibial arteries.
It does require a fibulectomy. I have only actually done two out of the three. An incision is made over the fibula in the lower leg. One you get through the fascia, I usually take the Bovie cautery right down onto the fibula. A combination of Bovie cautery and periosteal elevator
will clear all the tissues off of the fibula for at least about eight to 10 centimeters. You have to be very careful posteriorly because the peroneal vessels sit right there. When you divide the fibula as seen in the lower right-hand corner,
you have to protect the peroneal vessels. I usually put an Army-Navy in there, and you can divide it any number of ways. But once you divide the fibula, the peroneal vessels are immediately behind it. That's a very easy exposure.
If you pull down the posterior tibialis muscle, you can very easily get to the anterior tibial artery, and posterior and deep to the peroneal vessels you can get to the posterior tibial artery. Here is just a scheme showing the peroneal artery, anterior tibial artery,
and posterior tibial artery with the fibula resected. And one last picture is a peroneal bypass, you can see the absence of the fibula here. And I thank you for your time.
- Good afternoon. I have no disclosures. I was going to say that the bulk of this work was done by Johnston Moore who's a 3rd-year medical student with us and my partner, Ben Pearce does the novel work that's in this. As you all know there are a number of risk factors
for peripheral vascular disease and diabetes is certainly one of the more important ones. And that's what I'm going to talk about in this talk. This image here shows you the odds ratio increase for peripheral vascular disease with each of these risk factors.
Why should we care? If you look at this map in 1995, it was all yellow, in the 0-6.5% rate of diabetes and now much of the country is getting to look like Alabama, where we say we're in the heart of the biscuit belt.
This is the increasing rate of diabetes diagnosed in the country over a 50-year time span, over 50 years, and you can see that it seems to be ever increasing. The importance of limb preservation, I don't need to tell this group for patients
that get a higher level of amputation more often go to nursing homes and more often end up in a wheelchair. So limb preservation is very important. This slideshow is a functional outcome after amputation, which decreases with a higher level of amputation. And diabetes is known to be associated
with higher levels of amputation. As you may know, Hemoglobin A1C has been linked to lower extremity amputation in diabetic patients and worsened Hemoglobin A1C increases the risk of amputation and higher level of amputation. This is a nice meta analysis that shows multiple papers
that demonstrated that an increasing Hemoglobin A1C over 7 increases the risk of amputation by 26% for every 1% rise in A1C level. Another interesting paper about insulin-sensitizers. So these are the glitazone drugs and Metformin. There is some suggestion that patients
that are on a sensitizing agent in addition to insuin have a lower risk of amputation. They also have a lower risk of peripheral arterial disease in general. Comparison to patients that are on insulin only they have a lower risk of requiring revascularization
and a lower risk of amputation as I said. So we did a project at UAB, looking at these questions about A1C and a choice of diabetic control regimen, and thus impact on amputation and amputation-free survival. When we pulled patients who had A1C levels within three months of their procedure
we ended up with 306 limbs. And we looked at patients that had amputation and/or death, both endo and open revascularization. And what we found was a simple diagnosis of diabetes, and this is not new, increased the risk of amputation pretty significantly.
Here this is one year amputation-free survival, 78% of non-diabetics and 61% in diabetics. As I said, just a simple diagnosis of diabetes was actually the more important risk factors. But an insulin only diabetic was the most significant risk factor for amputation and increasing level of A1C
was approaching statistical significance. A multivariate logistic regression, Creatinine, insulin-only management, and age were associated with amputation. So in summary, the diagnosis of diabetes increases overall mortality, that's known.
Decreases amputation free survival and in a small cohort there was a trend towards higher amputation rates for poor glucose control measured by Hemoglobin A1C. The glycemic control strategy was significantly associated with amputation free survival. So those patients with only insulin control
had higher rates of amputation. The strongest predictor of poor amputation free survival, as I mentioned, is diabetes, but the modality of glycemic control does impact the outcome and insulin sensitizers may improve patient outcomes over time.
- Thank you. I would like to thank staff and Dr. B, for inviting me here to here to give this talk. I have no disclosures. So, before I get into how the BEST Trial changed our practice, I just kind of want to give a brief overview of our practice at USC, when it comes to limb salvage. We are a reversed vein center, we don't use
in situ bypasses very often. And we try to stay autogenous as much as possible. We do believe in tourniquet occlusion for inflow occlusion of tibial vessels, especially so we don't have to clamp them or singe them up with vesselutes.
And we do bring the doppler in, the duplex in right away after completion of a bypass, so we can see the hemodynamic changes. So, intraoperative duplex is a big part of our practice. And in terms of endo, I'd say we're probably 50%-60% endo first with limited use of atherectomy.
We're mainly with the balloons and stents. So, if you look at my practice prior to the trial, this was basically how it was. With Cardiology on one side and Vascular on the other side. And the two sides basically didn't interact at all. And if we did, it sometimes got pretty heated.
And if we had some crossover of patients or arguments about different discussions. Then enter the trial, the BEST-CLI Trial, and as many of you are aware, this trial has been constructed out of Boston with Dr. Farber, Rosenfeld and Menard,
to look at the best treatment for patients with CLTI, either open or endovascular treatment. So, for us at our center, now our Co-PI, was an interventional cardiologist. So, I had to pretty much embrace him and move forward with him and with this trial,
if we wanted to be successful. And I, it actually like I said was a little bit contentious at first, but it has turned harmonious. And proof is, that we've combined our services, especially at our county hospital.
The vascular medicine fellow that they have, has been integrated into all of our practice. And the cath-lab doors have finally been opened, I've finally been able to see what's been going on in there, and actually perform some cases with them. And we've kind of gained this mutual respect
that's led to some research projects and it had been very beneficial. Second thing that was beneficial and really changed in our practice was the construction of a CLI Team. One of the recommendations of the trial,
was to move forward with a team, constructed to discuss these patients. This is how we started with our team, basically the physicians, and then some of the fellows, as well as a nurse practitioner, and research coordination to complete our CLI Team.
What would we do? Well, first thing we would discuss, should this patient even be offered limb salvage and then if so, should they be placed in the trial. Cause that was the question for many of our difficult patients. Then,
we would look at vein ability, co-morbidities, the reliability of the patient was a big thing as well as discharge planning. And for us, Los Angeles' big urban center, we wanted to make sure that we weren't discharging these patients after a complex
reconstruction out to the community. And as a border city, we didn't want to discharge them outside of the country, which can happen sometimes. Since the construction of our CLI Team, we have expanded it quiet a bit. We've moved forward with hiring two podiatrists,
which has really helped and helping us understand the anatomy of the foot and what we can or what we should not do when it comes to foot amputations. We've also moved forward and integrated one of our plastic surgeons, whose very interested in performing flaps down to the lower extremity.
We now have a wound care team that comes to our clinic, and they are there with us to see the best approaches to manage these wounds, as well as nutrition. And finally, physical therapy, cause after you do all this reconstruction, you still want that patient to get up and start moving. And the last thing
you want, is for them to just be stuck in a chair. So that completes pretty much our CLI Team, and it has expanded and been very helpful. Last thing, Diagnostic Angio, if I was to stand up here four years ago, I think I probably performed a diagnostic angio, just very rarely.
Now, it's a part of our practice. And the interventional cardiologist, the Co-PI, agrees with it. Why? Cause I think you're able to now do the angio, stop go talk to the patient, show the films
to my Co-PI, or he shows them to me, we talk about what we should enroll the patient in the trial and if so, what's the best approach. I think you get staged radiation exposure for the patient, and you can do some very g
am I going to go antegrade, retrograde, retrograde from the pedal or what. And have all that stuff available, so that you're just not all of a sudden doing that at the patient. And I think
you have a chance to address the co to decide should this patient even be in the trial, and if they are, how do we need to maximize those co-morbidities? Now, you may say, well what about length of stay?
You know we have to move things along. And here, this is our tracker here for our, we're a member of VQI since 2011, if we just look at the patients that had a length of stay greater than 7 days, you can see,
we were pretty high at some point. This is where the trial started, and we got a little bit worse, but since then, we've corrected things, we've put some things in place to move patients through the system.
And now to date, we are still below the benchmark for the whole national VQI. So, I think it's been very effective. So, how has it changed my practice? Collaboration, it's been very important especially with cardiology and it's helped
immensely with understanding some of the co-morbidities in these patients. Especially with STAT treatment afterwards, antiplatelet therapies and so forth. CLI Team, and like I said, we started fairly small, and we've expanded it
and it's been very beneficial for the patients to get a one stop treatment area and a diagnostic angiogram. Which I never believed was going to be helpful but I do stand by at this point. Thank you!
- I'd like the thank Doctor Veith for inviting me back to speak. I have no disclosures, we will be discussing some slight off-label use of the anitcoagulants. As we all know, acute limb ischemia occurs as a result of acute thrombosis of a native artery or bypass graft or embolism from a proximal
source, dissection, or trauma. The incidence is not insignificant, 15 cases per 100 000 persons per year, or interestingly about 10 to 16% of our vascular workload. Despite the relative frequency of this condition, there are relatively few guidelines to
guide us for anticoagulation therapy. The last set of guidelines for the American College of Chest Physicians regarding PAD gives some very brief, generic recommendations from 2012. They state, suggest immediate systemic anticoagulation with unfractionated heparin.
We suggest reperfusion over no reperfusion, which seems pretty obvious to an audience of vascular specialists. One of the challenges with acute limb ischemia is that it is a fairly heterogenous group. It can be thrombosis or embolism to the aorticiliac segments to the infrainguinal segments, and
there's also the patients who develop ALI from trauma. So we actually looked at the various phases of anticoagulation for acute limb ischemia and then we do, as with many institutions, utilize intravenous heparin at the time of the diagnosis, as well as obviously at the time of surgery,
but we found that there was a significant variation with regard to the early, post-operative anticoagulation regimens. One option is to give therapeutic intravenous heparin on an adjusted dose, but what we found in a significant minority of patients across the country actually,
is that people are giving this fixed mini-dose 500 unit an hour of heparin without any standardization or efficacy analysis. Then, obviously you go the long-term anticoagulation. We reviewed 123 patients who had ALI at our institution, who underwent surgical revascularization.
And they had the typical set of comorbidities you might expect in someone who has PAD or atheroembolism. In these patients, the Rutherford Classification was viable or marginally threatened in the majority, with about 25% having immediately threatened limb.
Various procedures were performed for these patients, including thromboembolectomy in the majority, bypass operations, angioplasty and stenting was performed in the significant minority and then primary amputation in the various selects few. We divided these patients into
the first four days of anticoagulation. Therapeutic with unfractionated heparin early on versus subtherapeutic or this mini-dose unfractionated heparin and we found that 29% of our patients were receiving the mini-dose unfractionated heparin, again without much efficacy analysis.
We used the International Society for Thrombosis and Haemostasis Anticoagulation Outcome Guidelines to look at the ischemic complications, as well as major and minor bleeding for these patients, and we identified actually not a significant rate of difference between the
subtherapeutic category and the therapeutic category of patients, with regard to mortality, with regard to recurrent limb ischemia, MI, VTE, or stroke, major amputation, and we actually didn't find because it's a fairly small study, any significant difference in major or minor bleeding for these patients.
So, we do feel that this small study did justify some efficacy of mini-dose unfractionated heparin because we didn't find that it was causing recurrent lower extremity thromboembolsim in these patients. Now on to long-term anticoagulation, for these patients, after that first three or four days
after the surgery, the options are long-term vitamin K antagonists, the DOAC's or vitamin K antagonists if you have atrial arrhythmia, or in the patients who had no other comorbidities, there really is not much guidance until recently. The compass trial was recently published in 2018
in stable PAD and carotid disease patients, identifying that rivaroxaban plus aspirin had a significant benefit over aspirin alone in patients who had stable PAD. And then, an upcoming trial, which is still ongoing currently in patients who underwent recent
revascularization, whether open or endo, is hopefully going to demonstrate that rivaroxaban, again has a role in patients with lower extremity ischemia. So in conclusion, there is relatively a scarcity of clinical data to help guide anticoagulation after acute limb ischemia.
Unfractionated heparin pre and intraop are standardized, but postop anticoagulation is quite variable. The mini-dose, we consider to be a reasonable option in the first few days to balance bleeding versus rethrombrosis, and fortunately we are having larger randomized clinical trials to help demonstrate the benefit of the DOACs and
aspirin in patients who are stable or post-revascularization for PAD, thank you.
- Good afternoon to everybody. This is my disclosure First of all, literature. In literature I found only four cases, single cases, of dorsalis pedis artery entrapment. Claudication, in case of active dorsiflexion, blue toe syndrome by extrinsic compression
of the extensor hallucis brevis tendon, claudication, forced plantar flexion, anterior tarsal tunnel syndrome with DPA thrombosis. So few single-case reports, heterogeneous. Now I think that the reason more common situation of
dorsalis pedis artery entrapment, this was my first case. It was a patient with critical limb ischemia, with occlusion of anterior tibial artery. I tried to do balloon intimal angioplasty of the anterior tibial artery,
and was about to find residual dorsalis pedis artery. But despite the multiple inflation of balloons there at this level, the stenosis always remained. Then suddenly the patient spontaneously
changed the position of the foot. The stenosis disappeared. So I understood that this was a functional obstruction observed in plantar flexion of the foot and released in standard position.
I started to look at the patient, and this is a baseline angio, so it's not related to a subintimal angioplasty or something like that. With the plantar flexion, there is stenosis,
and here the stenosis released. So the subintimal entrapment is an anatomical condition and is not related to the endovascular treatment like spasm dissection. This is another the case, and you can see that here
we have an occlusion, so DPA-E can lead to functional total occlusion. This is another patient with perfect entrapment, and you can see that the entrapment is stuck in this position by
something compressing the artery. So DPA-E is a rare anatomical condition that can affect pedal and tarsal arteries. It must be considered when there is a focal stenosis at the passage of the anterior tibial and dorsalis pedis artery,
and the patients has a plantar flexion of the foot. In the majority of the cases the dynamic obstruction is in correspondence of the distal astragalus. In some cases, is higher at the ankle level, like in this case.
Now what is the prevalence of this condition in the population? We decided to do duplex scan flow dynamic evaluation in more than 200 patients with asymptomatic legs. We measured at 90 degree ankle joint
and in forced plantar flexion, the blood flow to the dorsal pedis artery. Five patients, we found functional obstruction which resembled dorsal pedis artery entrapment condition. So in the general population, it seems that about two percent of people
has an asymptomatic entrapment of the pedal artery. The problem is, can this entrapment become symptomatic, because many patients, especially bedridden and neuropathic patients assume a plantar flexion as the resting position
while lying on the bed. In these patients, we cannot exclude that DPA-E could play a role in developing or maintaining CLI. In my last six years I made about 4,000 angios on CLI patients,
and I found that in 15 cases, this dorsal pedis artery entrapment, so zero point four percent. This is an example of a patient, I studied this patient for critical limb ischemia. We have a long occlusion of the superficial femoral artery.
And in the distality, we have a part in the anterior tibial artery, and here I have seen this condition. So I started to think about, but critical limb ischemia, why we have only superficial femoral artery occlusion,
a good popliteal artery, anterior tibial artery is good, we have a good foot vessel. And here, we have this small entrapment, the typical entrapment. So I decided to start to treat the superficial femoral artery.
It seems a bad question, this one. But look at the foot. After the opening of the superficial femoral artery, we have not one red blood cell going into the foot. Because the foot is in a plantar flexion position. What to do in this case?
The only thing to do is to say to the patient, please rise your foot. And you can see that immediately, this ligament or something, I don't know, I was a cardiologist, not a vascular side but there is something there compressing the artery.
So in the typical position, so what to do? I think that in DPA-E patients, heel protectors can save the heel and the patency. Thank you very much for your attention.
- Great thank you very much. It's great to be here at Veith and talk to you about optimally deploying the Supera interwoven stent. This is a stent which is very unique and different from other stents. Slotted-tube stents are laser
cut from nitinol tubes with an open cell geometry compared to Supera which incorporates six pairs of elastic nitinol wires into an interwoven helical closed cell geometry.
This design gives it vascular-mimetic like properties in the dynamic vessel that we treat. And it has four times the radial strength of slotted-tube stents so it is resistant to compression from outside. That said its physiologically conformable
and essentially fracture-proof and it has by far the lowest chronic outward force of any of the nitinol-like stents. This just shows the off the-chart radial strength of Supera compared to nitinol and it is this
outward radial force which may generate some of the neoplastic hyperplasia. This gives the clinical advantages. You can use it in flexion points, calcified lesions with no recoil, long lesions with its conformability
and lack of fractures and if you want to convince yourself I encourage you do either intervascular ultrasound or bent-knee angiograms and compare them in this type of stent to the slotted-tube stents.
It's a unique stent so it has unique deployment. It's a ratchet delivery rather than a conventional mechanisms. The stent length is not at exact and depends on who well you implant it. It's not oversized.
You must aggressively pre-treat all segments that you're going to implant the stent. It is a slower deployment, a two-handed which is kind of an art-from if you will. It's a great stent but you have
more potential for trouble if you don't do it correctly. Here are the three important easy steps you must have documented. Aggressive pre-dilation to all of the segments where you're
going to put the stent. It's got to be one-to-one sizing. And you have to deploy it slowly on high magnification after that pre-treatment. That's it, those three steps. The pre-treatment we usually do
on Roadmap with focal force or regular balloons at least one-to-one what we're going to implant and usually a little bit higher. After that, the stent deployment, we use a Roadmap for the distal edge only.
Once we have the distal edge released, we take the Roadmap off, mag up and go slowly. The right hand throws the ratchet system, the left hand adjusts the tension. If the stent elongates a little bit, you slow down and push forward.
If it packs too much slow down, pull backwards. Here's a typical but illustrative case long disease, CTO, calcified disease in the adductor canal and the popliteal. Here's the pre-treatment with a 6 O ballon before a 5 5 superium
to make sure that it's well-expanded. Here is the mag-ed up slow deployment but you can see how beautiful it looks immediately on delivery and how well it stands up without post-dilation in this heavy calcium in the adductor canal.
Now here's the final AP angiogram. We're used to seeing good angiograms in the AP view but here's a bent-knee angiogram just showing the conformability of this stent and its strength in calcified lesions. It has great data.
Eighty-six point three primary patency in the superb trial with no fractures. Furthermore if you deploy it properly and nominally the primary patency was more than ninety percent. Extremely durable at three years
if you nominally deploy the stent, ninety-four percent freedom from TLR. Some things to remember. Again, pre-treat every vessel segment where you're going to put the stent, not just the tight part.
If you don't get pre-dilation with a longer balloon go to a shorter more aggressive focal force or non-compliant balloon. After you pre-medicate the patient don't use the small Superas.
And I can summarize mag up and slow down when you deploy the stent. We don't post dilate unless there's issues but if it does elongate or pack that's when we post dilate. What not to do with a Supera stent.
Don't use it if precision is needed at the back end for example an ostial SFA lesion from above. Again it's not an exact stent length. If there's a lot of mismatch it's not your stent.
You must adequately pre-treat, if you can't pre-treat it, don't put a Supera or in my opinion and stent. And of course you would never primary stent with this type of stent. So in conclusion the Supera stent
is a unique interwoven design giving it vascular mimetic qualities uniquely suited for the femora-popliteal lesion. Has excellent clinical results that seem to be independent of the stent length. All that said proper lesion preparation
and stent deployment techniques are essential to the success of this device. And I thank you very much for your attention.
- This work has been done by in my hospital with collaboration of the University of Bologna in Italy. We have no financial disclosures. So all starts from the result of a new TECCO study, but it was published last year showing that stenting was equivalent or even be better in surgery for the de novo common femoral and deep femoral arterial stenosis.
This was a small randomized study of around 117 patients with common femoral artery stenosis. Interestingly enough, 86% of his patients were claudicants, so the applicability of a randomized control trial should be limited to claudicant. The primary outcome was on the patency,
but it was with complication. The combined rate of morbidity and mortality that was 26% in the open surgical arm, and 12.5% in the stent population, and this was just significant. After a median follow up of 24 months, the rates of primary
patency target lesions and system clinical improvement were similar in the two groups. There was no mortality in every group, but one stroke in the endovascular arm. Minor complication were more often seen in the surgical arm with hematoma, delayed wound healing, temporary lymphatic
leakage, paresthesia, but no infection of a graft. The follow up in this small study was not powered enough to assess secondary endpoint, and only 46 patients were available at 24 months for analysis. And the length of stay in the stent group were three days, and six days in the surgical group.
So if you go through the Vascular Quality Initiative published by (mumbling) last year, we find that the 30-day mortality was 1.6%. And the access site hematoma was 5.2%, with a risk of arterial dissection. We have a total rate of complication of nearly 10%.
And interestingly enough in this Siracuse study, was where mostly claudicants were taken care of. You see that the result depends on the symptomatology. If you have a patient with critical infracting ischemia, you have real operation and bad result with the endo first technique.
We have studied our result. In a retrospective study of nearly 150 open revascularizations, half claudicants, half rest pain, and our 30-day result we had 98% of primary patency, three occlusion, 1.7% of mortality at 30 days, 1.4% of cardiovascular complication MI,
groin wound complication was seen in five percent of cases, and in multivariate analysis, only tissue loss and infection, wifi three-four was a predictive factor for wound complication at the groin. This is perhaps the most important aspect of the study. This is what we're seeing in these patients.
As you see here, most of the lesion were at the orifice of a deep femoral artery in more than 73% of the cases. So if you do endo in this application, you can jail or covered the deep femoral artery. Inside of this by open surgery you can clean both artery and leave a good vascularization.
In our practice result in claudicants are excellent, are shown here. They are not so good in patient with rest pain and gangrene because obviously these patients with CLTI and occlusion of the popliteal and infrapopliteal artery needs a popliteal or tibial revascularization
in addition to that of a deep femoral artery to save a foot. So we think that until now open surgery is still the best option in most cases. Thank you.
- [Moderator] Anybody have any burning questions? So Enrico, who do you not do duplex-guided interventions on? - [Enrico] Ah that's a very good question. When I don't have somebody adept to help me. If I'm doing it by myself, I'm not going to do it at this point. Hopefully there's a couple of companies
that are working on devices where you'll be able to do it by yourself. But at this point, you need someone that's going to handle the probe while you handle the catheter so. And the second contraindication
would be a severely calcified, sicofriend calcified vessel. If you have this calcification for about two centimeters and the rest you can see, segmentally it's okay, but if it's a long calcified occlusion
where you cannot see anything, of course it's not going to be acceptable to do on the ultrasound guidance. - [Panelist] I have a question for Dr. Rico. But is the problem here is that so many of those groins have been used and abused forever
with closure devices and all that. So when you go back to that groin, it looks like it been operated four times. There's a lot of inflammation around. I realized that my fellow is staying away from those groins now.
He call in sick when I tell him tomorrow we have a groin to do. So do you think that the results just, I understand first time around, but for those patient with much pulled sticks before and devices.
Should we consider a stand instead? - I have no scientific argument to answer to you, because what we have done these of novel groin incision. If you have a patient with a very fat weave of free producent divention of the groin.
This could be a problem, but in this case I mean if you have a careful surgical technique I mean you kind of already have a complication growing infection (mumbling) like this. I think it's alright if you're really safe even.
But you have to take time and to do everything right. I think to put a (mumbles). When you see oh important is deep feminal aheartery. I think it's quite dangerous. And if it jail. And if he trembles.
I mean you are really in a bad situation. - Okay I think that wraps it up.
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