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Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
Value Of CO2 DSA For Abdominal And Pelvic Trauma: Why And How To Use CO2 Angiography With Massive Bleeding And When To Supplement It With Iodinated Contrast
Value Of CO2 DSA For Abdominal And Pelvic Trauma: Why And How To Use CO2 Angiography With Massive Bleeding And When To Supplement It With Iodinated Contrast
"Acquired" AVMs: More Common Than We Think
acquiredarterialarteriogramarteriovenousavmscoilcollateralsconnectionsDeep vein trombosisduralDVTentityepisodeevarextensiveextremityfemoralFistulahistoryiliacinflammatorylesionlesionsocclusionpelvicpriorstentingstimulationswellingthrombosistreatedtreatmentuterineveinvenouswayne
Yakes Type I, IIb, IIIa And IIIb: The Curative Retrograde Vein Approach
Yakes Type I, IIb, IIIa And IIIb: The Curative Retrograde Vein Approach
Update And Results Of The REBOA Ongoing Trials In Europe, Japan And The US
Update And Results Of The REBOA Ongoing Trials In Europe, Japan And The US
Continued Tobacco Use Is Bad For PAD Patients But Does Not Negatively Affect Outcomes Of Endo Treatments For Intermittent Claudication
Continued Tobacco Use Is Bad For PAD Patients But Does Not Negatively Affect Outcomes Of Endo Treatments For Intermittent Claudication
New Developments In The Diagnosis And Treatment Of Popliteal Adventitial Cystic Disease
New Developments In The Diagnosis And Treatment Of Popliteal Adventitial Cystic Disease
REBOA Can Save Lives But . . . When Can REBOA Cause Spinal Cord Ischemia And Intermittent Partial Balloon Deflation Can Prevent It: How To Do It
REBOA Can Save Lives But . . . When Can REBOA Cause Spinal Cord Ischemia And Intermittent Partial Balloon Deflation Can Prevent It: How To Do It
Surgical Results Of Treating Hepatic Hemangioma And Literature Review
Surgical Results Of Treating Hepatic Hemangioma And Literature Review
adenomaasymptomaticbenignbleedbleedingbloodcapillarycavernouscenterdiagnosisdiagnosticdifferentialexperiencehemangiomahermannlivermalignantmortalityMRIperformsurgeonsurgerysymptomaticsymptomsTherapeutic / Diagnostictransplantationtumorsvessels
Carotid Interventions After Ischemic Strokes Should Be Delayed 6-8 Weeks Only If The Cerebral Lesion Is Large (>4000 mm<sup>3</sup>) On CT
Carotid Interventions After Ischemic Strokes Should Be Delayed 6-8 Weeks Only If The Cerebral Lesion Is Large (>4000 mm3) On CT
Yakes Type IV Infiltrative AVMs Curative Treatment Strategies: A New Entity
Yakes Type IV Infiltrative AVMs Curative Treatment Strategies: A New Entity
Measures Of Frailty And Their Importance In PAD Patients
Measures Of Frailty And Their Importance In PAD Patients
Value Of IVUS And Other New Techniques To Improve The Diagnosis And Treatment Of Popliteal Entrapments
Value Of IVUS And Other New Techniques To Improve The Diagnosis And Treatment Of Popliteal Entrapments
Complications Of REBOA When Performed By Inexperienced Operators Can Be Disastrous: What Can Be Done To Avoid The Problem
Complications Of REBOA When Performed By Inexperienced Operators Can Be Disastrous: What Can Be Done To Avoid The Problem
aortaballooncathetercomplicationcomplicationsdeathsiliacinflatedischemialeadperformedpicturespreventpromotingsheathsurgeonsurgeonstraumavascularvascular surgeonsVeith
Lymphatic Intervention: Thoracic Duct Embolization, Pulmonary Lymphatic Perfusion Syndrome, And Hepatic Lymphatic Disorders
Lymphatic Intervention: Thoracic Duct Embolization, Pulmonary Lymphatic Perfusion Syndrome, And Hepatic Lymphatic Disorders
accesscontrastductembolizationembolizingglueinduceinterventionalInterventionsleakagelipiodolliverlymphlymphangiographylymphaticlymphaticsneedlenodepercutaneousperfusionperiportalrefluxTherapeutic / Diagnosticthoracicultrasoundvariationvenousvesselsvisualize
Update On Indications For Invasive Treatment Of Carotid Disease (Symptomatic And Asymptomatic) By CEA Or CAS Before Major Surgery Or Coronary Bypass
Update On Indications For Invasive Treatment Of Carotid Disease (Symptomatic And Asymptomatic) By CEA Or CAS Before Major Surgery Or Coronary Bypass
Non-Fasting Lipid Profiles Are A Simplification With No Negative Consequences For Diagnosis, Risk Evaluation And Treatment
Non-Fasting Lipid Profiles Are A Simplification With No Negative Consequences For Diagnosis, Risk Evaluation And Treatment
DEBATE: Not So: Why Open Bypass First Is Best In Some CLTI Patients: Which Ones: What Percent Of CLTI Patients Will Require An Open Procedure At Some Point In Their Course
DEBATE: Not So: Why Open Bypass First Is Best In Some CLTI Patients: Which Ones: What Percent Of CLTI Patients Will Require An Open Procedure At Some Point In Their Course
advancedamputationbypasscentercontemporarydataendoendovascularevarextremityfailedlimblimbsocclusionsOpen Bypassoutcomespatencypatientpatientspercentrevascularizationrisksecondarystagesurgerytolerate
Advantages And Technical Tips For Mini-Incision CEAs
Advantages And Technical Tips For Mini-Incision CEAs
anesthesiaanterioranticoagulationarterybifurcationbladecarotidclopidogrelcranialendarterectomyincisionincisionsinternalinternal carotidinterventionalischemicmicenervepatientspediatricplaquepreoperativeproximalproximallystandardstentingtransversetypicallyVeith
Limb Salvage And Functional Outcome After Traumatic Acute Limb Ischemia (ALI)
Limb Salvage And Functional Outcome After Traumatic Acute Limb Ischemia (ALI)
Why CREST 2 And ACST 2 May Have Little Definitive Value Although They May Provide Useful Information
Why CREST 2 And ACST 2 May Have Little Definitive Value Although They May Provide Useful Information
Early Experience With The New Gore Conformable Excluder With Active Neck Angulation Control: It Provides Better Treatments For AAAs With Severely Angled Necks: How It Works And IDE Trial Results
Early Experience With The New Gore Conformable Excluder With Active Neck Angulation Control: It Provides Better Treatments For AAAs With Severely Angled Necks: How It Works And IDE Trial Results
advantageamplatzanatomyangulatedConformable AAA endoprosthesisdeploydeploymentdesigneddeviceevarexcluderfenestratedfloppyfusionGORE ExcluderGORE Medicalmanipulationneckpatientsposteriorprimaryproximalproximallyregistryrepositionsteeringstifftherapeuticthrombustrialutilizewire
Non-Interventional Management Of CLTI: With Optimal Medical Treatment And Good Wound Care Many Amputations Can Be Prevented: When Is It The Best And Most Cost Effective Treatment
Non-Interventional Management Of CLTI: With Optimal Medical Treatment And Good Wound Care Many Amputations Can Be Prevented: When Is It The Best And Most Cost Effective Treatment
BKAcareendovascularhealhemodynamicischemiaischemiclimblowmultiplepatientpatientspredictproceduresrevascularizationSFA/PTA StentingVeithwound
Current Treatment Options For Limb Threatening Hand Ischemia: How Good Are Their Results
Current Treatment Options For Limb Threatening Hand Ischemia: How Good Are Their Results
DCB + Focal scaffolding: The New Concept For Optimized BTK Angioplasty?
DCB + Focal scaffolding: The New Concept For Optimized BTK Angioplasty?
biomechanicscalcifieddevicedissectionDissection repair devicedissectionsevarguessimplantIntact MedicalkneelesionlesionsmetalminimalmultiplepatencypatientsprimaryproceduralregardrepairrutherfordstentsuccessTack endovascular devicetherapeutictreatingvesselvessels
A New System For Treating Prosthetic Arterial And Aortic Graft Infections
A New System For Treating Prosthetic Arterial And Aortic Graft Infections
abdominalanastomosisaneurysmbiofilmcomorbiditydebridementendovascularenterococcusexplantfasterfavorFemoro-femoral PTFE Bypass infectionfoamgraftinfectedinfectioninstillationintracavitarymalemortalitynegativeNPWTobservationalpatientpreservepressureprostheticptferadiologistremovalspecimensurgicaltherapythoracictreatmentvascularwound
Treating Complex AVM Cases With Multiple Embolic Agents
Treating Complex AVM Cases With Multiple Embolic Agents
Treatment Of Recurrent NTOS: Role Of The Pectoralis Minor: Tips And Tricks In Diagnosis And Treatment
Treatment Of Recurrent NTOS: Role Of The Pectoralis Minor: Tips And Tricks In Diagnosis And Treatment
anteriorAnterior Axillary approach for PM Tenotomyaxialaxillarycentimeterdefinedfewerfrequentimprovementincisionindividualsinducinginjectisolatedmaneuversminormuscleneckneurogenicneurovascularoccurspalpationpatientspersistentposteriorprovocativerecurrentsymptomssyndrometendernesstypicallyulnar
DEBATE: Endo-First Is Best For All CLTI Patients: Rarely Are Open Bypasses Helpful: How Often
DEBATE: Endo-First Is Best For All CLTI Patients: Rarely Are Open Bypasses Helpful: How Often

no chemotherapy. And that's a lady 57 year old with press carcinoma, multiple bone meds/g multiple liver meds/g and that's the CA level, the cancer level how they go down over the time and she has not

received chemotherapy . She didn't want to have chemotherapy . She came from North America over to Europe and she didn't like she said no chemotherapy for me and these are the breasts, the liver meds/g in a January 2004,

here they got six cycles treatments that we are talking September 2004 and we talk October 2006.

- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.

So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift

could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.

For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.

Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting

that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.

Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.

So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.

Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.

Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient

and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people

that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug

by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.

And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.

So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,

but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.

Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite

and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents

of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.

Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.

Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.

4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,

that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.

I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.

If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,

if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.

So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.

Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.

- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.

Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.

Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.

Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.

It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,

you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations

so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times

and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.

It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.

If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2

travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail

for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,

with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.

So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast

before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.

CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries

and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see

actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.

There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.

You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.

This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver

with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss

with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.

We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.

- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.

CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo

t air contamination during the CO2 angiograms. Thank you.

- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.

And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,

as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,

presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,

as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.

So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.

Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,

and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.

Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there

in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,

but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,

but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,

but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion

that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer

and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.

And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.

And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,

treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.

And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.

We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat

with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,

and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.

So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.

Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen

and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.

(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.

Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.

And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily

arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,

it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this

florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.

We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation

in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,

which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen

of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.

- [Narrator] Okay, very interesting hypothesis.

- Talk to you a little bit about again a major paradigm shift in AVMs which is the retrograde vein approach. I mean I think the biggest benefit and the biggest change that we've seen has been in the Yakes classification the acknowledgment

and understanding that the safety, efficacy and cure rate for AVMs is essentially 100% in certain types of lesions where the transvenous approach is not only safer, but easier and far more effective. So, it's the Yakes classification

and we're talking about a variety of lesions including Yakes one, coils and plugs. Two A the classic nidus. Three B single outflow vein. And we're talking now about these type of lesions. Three A aneurysmal vein single outflow.

Three B multiple outflows and diffuse. This is what I personally refer to as venous predominant lesions. And it's these lesions which I think have yielded the most gratifying and most dramatic results. Close to 100% cure if done properly

and that's the Yakes classification and that's really what it's given us to a great degree. So, Yakes one has been talked about, not a problem put a plus in it it's just an artery to vein.

We all know how to do that. That's pulmonary AVM or other things. Yakes two B however, is a nidus is still present but there is a single outflow aneurysmal vein. And there are two endovascular approaches. Direct puncture, transarterial,

but transvenous retrograde or direct puncture of the vein aneurism with the coil, right. You got to get to the vein, and the way to get to the vein is either by directly puncturing which is increasingly used, but occasionally transvenous. So, here's an example I showed a similar one before,

as I said I think some of these are post phlebitic but they represent the archetype of this type of lesion a two B where coil embolization results in cure, durable usually one step sometimes a little more. In the old days we used to do multiple

arterial injections, we now know that that's not necessary. This is this case I showed earlier. I think the thing I want to show here is the nature of the arteriovenous connection. Notice the nidus there just on this side of the

vein wall with a single venous outflow, and this can of course be cured by puncture, there's the needle coming in. And interestingly these needles can be placed in any way. Wayne and I have talked about this.

I've gone through the bladder under ultrasound guidance, I've gone from behind and whatever access you can get that's safe, as long as you can get a needle into it an 18 gauge needle, blow coils in you get a little tired, and you're there a long time putting in

coils and guide wires and so on. But the cures are miraculous, nothing short of miraculous. And many of these patients are patients who have been treated inappropriately in the past and have had very poor outcomes,

and they can be cured. And that a three year follow-up. The transcatheter retrograde vein is occasionally available. Here's an example of an acquired but still an AVM an acquired AVM

of the uterus where you see the venous filling on the left, lots of arteries. This cannot be treated with the arterial approach folks. So, this one happened to be available

and I was having fun with it as well, which is through the contralateral vein in and I was able to catheterize that coil embolization, cured so. Three A is a slightly different variant but it's important it is different.

Multiple in-flow arteries into an aneurysmal vein wall. And the important identification Wayne has given us is that the vein wall itself is the nidus and there's a single out-flow vein. So, once again, attacking the vein wall by destroying the vein, packing

and thrombosing that nidus. I think it's a combination of compression and thrombosis can often be curative. A few examples of that this was shown earlier, this is from Dr. Yake's experience but it's a beautiful example

and we try to give you the best examples of a singular type of lesion so you understand the anatomy. That's the sequential and now you see single out-flow vein. How do you treat this?

Coil embolization, direct puncture and ultimately a cure. And that's the arteriogram. Cured. And I think it's a several year follow-up two or three year follow-up on this one.

So a simple lesion, but illustrative of what we're trying to do here. A foot AVM with a single out-flow vein, this is cured by a combination of direct puncture right at the vein. And you know I would say that the beauty of

venous approach is actually something which it isn't widely acknowledged, which is the safety element. Let's say you're wrong, let's say you're treating an AVM and you think okay I'm going to attack

from the vein side, well, if you're not successful from the vein side, you've lost nothing. The risk in all of these folks is, if you're in the artery and you don't understand that the artery is feeding significant tissue,

these are where all the catastrophic, disastrous complications you've heard so much about have occurred. It's because the individuals do not understand that they're in a nutrient artery. So, when in doubt direct puncture

and stay on the venous side. You can't hurt yourself with ethanol and that's why ethanol is as safe as it is when it's used properly. So, three B finally is multiple in-flow arteries/arterioles shunting into an aneurysmal vein

this is multiple out-flow veins. So direct puncture, coils into multiple veins multiple sessions. So, here's an example of that. This is with alcohol this is a gentleman I saw with a bad ulcer,

and this looks impossible correct? But look at the left hand arteriogram, you can see the filling of veins. Look at the right hand in a slight oblique. The answer here is to puncture that vein. Where do we have our coil.

The answer is to puncture here, and this is thin tissue, but we're injecting there. See we're right at the vein, right here and this is a combination arteriogram. Artery first, injection into the vein.

Now we're at the (mumbles), alcohol is repeatedly placed into this, and you can see that we're actually filling the nidus here. See here. There's sclerosis beginning destruction of the vein

with allowing the alcohol to go into the nidus and we see progressive healing and ultimately resolution of the ulcer. So, a very complex lesion which seemingly looks impossible is cured by alcohol in an out-flow vein.

So the Yakes classification of AVMs is the only one in which architecture inform treatment and produces consistent cures. And venous predominant lesions, as I've shown you here, are now curable in a high percentage of cases

when the underlying anatomy is understood and the proper techniques are chosen. Thanks very much.

- Thank you very much, it's an honor to be here. I want to thank Professor Veith for his help with all EVTM movement and everything we're doing in the committee. Thank you very much. I would speak shortly about the trials. We can look at REBOA and what happened in last years and this is a map that's actual around two years ago.

And two years ago there were very few places that did REBOA even few places in the US if I might say, that did these aortic balloon occlusion. These numbers are doubled now, many countries and many institutes are doing it. REBOA is increasing like aortic balloon occlusion

is increasing not only in trauma. There are mainly case serious observation but there is not a lot of data. The new sheaths came, they are much smaller seven french and six french, and it changed the way we use these methods.

And the indications and contra-indications they are not really clear, I have to say. There are new methods, like using partial REBOA or intermittent REBOA on off, it might be better but we don't really know yet. And we know that total REBOA ischemia burden

is more clear than ever. We know that it's invasive method to close the aorta for long time. I think my view is there are more complications of REBOA than reported, around three to five percent and REBOA as a resuscitation tool and part of

endovascular resuscitation and trauma management. If we look at what's published in general we can see there are a lot of case series reviews. Some animal studies, some guidelines, like the pelvic guidelines from the World Surgical Association. Now it's nailed inside,

it's in the guidelines and you can use it. And some registry data, and I will name a bit about it. Currently, I know about more than 300 centers that are using REBOA for trauma. We know that there were done around 34 cases military, pure military REBOA.

Around 18 cases pre-hospital civilian REBOA. And of course, there are a lot of non-trauma that's done and we don't know how many are done. We know it's doable and we know that when you use REBOA you increase the systolic blood pressure and this is very important.

We know that you can do it from the pre-hospital to the ICU, and it's been done in the city in the ICU in different places. About the mortality and thoracotomy, I don't know really if you can compare these things, but used in specific patients, probably better than thoracotomy,

this is controversial. Relative few complications as I mentioned, but I think there are more complication than reported. And as I mentioned, there is severe metabolic effect of prolonged REBOA, if you use a total REBOA for example. This is the ABO Trauma Registry, and this registry is

a multinational or international corporation. The idea is, that people report to this registry the data, trauma REBOA, and can use this data. So this does not belong to me, this belongs to this group reporting in, and you can use it and report from it. It's very interesting what data is coming in.

This is how it looks like, and you can put also photos, cases, not only the report itself. It's quite astonishing what you can see in this. If we look at the two years result that we reported on 28 patients, it was very high ISS, mostly blunt trauma

which is very exciting because these are blunt trauma patients mainly, getting the REBOA and we know what happen if you compare them to thoracotomy. If you do thoracotomy for blunt injuries we know the results are very bad. Interestingly enough, the access was done mainly blindly

and succeeding with one to three attempts. And people sometimes ask, how can you do on a CPR patient the access, but we manage to do it and it worked. And the survival from the ED was 82%, 30 day survival 43%. I just want to show this slide talking about with 138 patients, currently 212 patients.

Even if you divide into impending cardiac arrest, people that have no palpable pulse or going through CPR even some of them can be saved using the balloon and some of them will get blood pressure when using this method, even survival as seen here, down here.

I will speak briefly about the other studies. This is Japanese Registry, they have included some numbers of patient and analyzed it in its published perspective study that will start soon. This is the UK REBOA trial, which is a prospective randomized trial that has now currently

as I know, 24 patients has been included. This is a very special and very exciting trial we will see what it will lead to. I will not report a lot about the AAST study Joe DeBose that sits here is the manager of this and he can report a bit more, but what I would like to say

that probably there is a survival benefit for REBOA, especially as the claim it might be particularly good if performed prior to arrest. The problem with clinical trials, we know this is not homogenous data, and I'm not sure we will ever get evidence.

And the solution in my world would be maybe to have the methods in a virgin teritory and see if you get better results. Thank you very much for being here and have an opportunity to talk. Thank you.

- So PAD affects five million adults in the United States today, and we know the US population is aging. And 15 to 20% of folks 70 years and older have claudication, a minority of these progress to CLI, and the impact on lifestyle is often minimized, as demonstrated in decreased quality of life scores

in these patients. Now with active tobacco use, there is acceleration of disease towards claudication, and there are higher rates of amputation, MI, and death. But prior to open or endo intervention, the SVS Guidelines recommend supervised exercise,

medical therapy with statins, beta blockers, antiantiplatelets, and Cilostazol, and an aggressive multidisciplinary approach to smoking cessation, which should last no less than six months. But what if a patient can't stop smoking?

We've all had these patients. Should patients with lifestyle limiting claudication be denied open surgical or endo-revascularization? So let's look at the open literature. A meta-analysis performed in 2005 of 29 eligible studies. The results were that bypass graft failure

was three times that in smokers versus nonsmokers. There was a dose response relationship in smoking cessation prior to or after bypass, equalized patencies. A more recent study, published in JVS in September, queried the VSGNE, 1789 lower extremity bypasses, 971 were nonsmokers, 818 were smokers,

and what they found was that primary patency at two years was 48% in smokers, versus 61% in nonsmokers, and when they propensity matched these patients, there was even a greater difference. 10 year survival was also decreased. And in another article,

published in August of this year in JVS, again a VSGNE study, over 2,000 patients, almost 3,000 patients with lower extremity bypass for claudication. The results looked at MALE, amputation-free survival, limb loss, death, major limb events or death,

and they found that current smoking was a significant predictor of major adverse limb events, and major adverse limb events or death. But do active smokers have worse outcomes after endovascular interventions? So, let's look at the literature again.

And there is none. The only paper I could find was a Markov decision analysis, in which compared revascularization in active smokers to medical management, this was a retrospective study, and their results demonstrated better quality of life in smokers after revascularization versus medical therapy.

The quality of life was similar, after revascularization in nonsmokers and smokers, and there was no increase in amputation rates up to 36 months. Also, 26% of the folks that were revascularized, quit tobacco use after their quality of life was improved.

So we decided to do a small study at my hospital. The outcome of endovascular interventions in active smokers with lifestyle limiting claudication versus nonsmokers. This was retrospective. 138 total patients with endovascular intervention for claudication, 47 were current tobacco users,

91 were never or former smokers. The primary endpoints were reintervention, secondary endpoints, surgical bypass, limb loss, MI, stroke and death. And here you can see, as in most studies, the smokers were a younger population,

and anticoagulation, in our patient population, was more common. As far as comorbidities, they were more common, as in most studies, in the nonsmoking group. And in a mean followup of 3.6 years for both groups, there was no statistically significant difference

between the two groups for any of the outcome measures. So in conclusion, active smokers with lifestyle limiting claudication, we would advocate, of course, smoking cessation. Outcomes with respect to reintervention, surgical bypass and limb loss appear to be equivalent in these two groups.

We feel that these patients should not be denied endovascular intervention, and improved quality of life after intervention may result in an increase in smoking cessation in this patient population. Limitations are obvious, this was a very small study,

and retrospective, and we are actually extending this study to look at several hundred additional patients. So I thank you for your attention.

- Good morning, for all of you who got up early. It's a pleasure to be here, thank you Frank for the invitation. I'm going to talk about a problem that is extremely rare, and consequently can only be investigated by putting together databases from multiple institutions, called adventitial cystic disease.

Okay, I have no conflicts. So adventitial cystic disease is an extremely uncommon problem, but it's important because it occurs often in young people. Virtually all series of adventitial cystic disease have fewer than five patients in it,

so they essentially become case reports. And yet it's a very treatable problem. There are several theories about why it occurs, you can see this picture here. The mucin-assisting material that occurs in the popliteal artery region most commonly.

The etiology of that and the origin of that is debated, whether it comes from the joint space, whether it comes from rest, whatever. But it's not really known. In addition, what's not known is the best treatment. There are several options.

Some would advocate just simple aspiration of the cystic material, although it's very viscous. Others simply excising the cyst and leaving the vessel in place. Some both excising and either doing

an interposition graft or a bypass. Early results with every one of these options have been reported, but they're quite variable as far as the outcome. And therefore, we really don't know not only the optimal approach,

but also the best outcome. For that reason, we did a study with 13 institutions on adventitial cystic disease using a technique called vascular low-frequency disease consortium.

Where everybody uses a standardized database and similar collection to act like a single institution. The aim of this study, which is one of 20 that we've conducted over the last 15 years, was to determine first of all what people were doing

as far as current practice patterns, and then look at the outcomes with the different treatment options. And this was published in the Journal of Vascular Surgery. Adventitial cystic disease of any site was identified using both the CPT ICD-9 physician logbooks,

pathology databases, and procedure codes. And then we collected epidemiologic data as well as operative and follow-up data, with our primary endpoints being vessel patency and the need for re-intervention, since amputation is extremely uncommon and rare.

This is the process for the low-frequency disease consortium. Where not only is a standardized database used, but each institution collects their data after getting IRB approval. And then deidentifies it

before sending it to a central server. So there's no way that there could be a security breach. And then we do an analysis of the data. The results of this study were that in the small number of institutions, 15 institutions, 47 patients were identified.

The majority were male, and the majority were smokers. What was interesting to us was that not all are in the popliteal region. And actually there were several patients as you can see, who had upper-extremity adventitial cystic disease, although it's far more common in the popliteal space.

And also there was actually one patient who had adventitial cystic disease of the femoral vein. The symptoms were typically claudication, and ischemic rest pain or tissue loss were quite rare. If you look at the risk factors, smoking, which was probably a comorbidity

and would not be claimed to be the etiology but was present. Other than that, this is a typical distribution of patients with vascular disease. As far as imaging here, you can see a duplex ultrasound

showing the cystic mass and how it typically looks. The majority of patients had a duplex, but also they often had an MRA or CTA as well as an angiogram. And the angiogram was typically part of the treatment paradigm.

This is just the typical appearance of an MRA showing what some people would call the scimitar sign, which is that it's not a typical plaque. And this is a picture of a CT angiogram showing a similar view of a vessel. The results,

so there were some that did not treat only the cyst, but also resected the artery. And either bypassed it, as you can see here, or did an interposition graft,

here's just a picture of one of those. And there were others that just treated the cyst, and either aspirated it alone or resected the cyst and patched the artery. Or did cyst drainage and nothing else to the vessel. If you look at the typical incision of these patients,

this is a posterior approach of the popliteal region. And the small saphenous vein as you can see is marked, and uses the conduit for bypass. The outcomes of these patients were similar as far as length of stay, complications. The one you'll notice is that

two of the five with cyst resection had a complication, so that's a little bit higher. But otherwise they're quite similar as far as the short-term outcomes and results. The main problem, and also if we look at the improvement in ABI,

although cyst resection with bypass had a higher increase in ABI, the rest of the treatments were similar. In other words, the initial outcome was similar with any of those different options.

The one thing you can see circled in red is the patients who had simple cyst aspiration. It was not durable, and consequently they often had to have a second procedure. And the resection of the artery was generally, or bypass of the artery,

generally had better long-term outcomes. The follow-up was 20 months, and here you can see the recurrence and the types of modality of follow-up. So I just conclude by saying that our experience from multiple institutions

is that this is an uncommon problem, that cyst recurrence is very high if aspiration alone is used, and either interposition or bypass is the optimal treatment. Thanks very much for your attention.

- [Speaker] Thanks for the opportunity to present today. I'm going to talk about a specific complication of REBOA, a spinal cord injury. These are my disclosures. REBOA utilization for trauma and hemorrhagic shock has really increased greatly over the last decade, as you've heard.

Comparative data with resuscitative thoracotomy, although not easy to do, appears favorable. Case series and some meta-analyses have suggested that there is a clinical benefit, as Dr. Hur also stated, an ideal time for balloon occlusion though is not clear. Less is better, but what is the optimal time frame?

Many reports don't even include occlusion times, although that's getting better as data matures. Animal studies have suggested a significant morbidity mortality with end-points increased at 60-and 90-minute occlusion times. In human studies, when balloon occlusion times have

been compared, they're shorter in survivors than in patients who died. We know that surgical cross-clamp of the aorta has long been associated with spinal cord ischemia risk. In a large metanalysis of blunt traumatic aortic injury repaired with open surgical techniques

and no distal perfusion adjunct, there was 19% risk of paralysis in humans. In porcine studies and sheep studies, prolonged REBOA has been associated with spinal cord injury as well. But rarely reported in humans and whether

that's a reporting bias because of mortality it's not clear. The advantage of studying defined times for REBOA in a non-human primate model were why we undertook this study. The bipedal model really analogous to human

in most respects with the spinal cord anatomy being very similar and the coagulation cascade being the same. Here was our design. We had three groups, one was an initial survival study and model development phase.

Group two and group three were comparing 60- and 30-minute REBOA in the olive baboon with a ten-day survival and particular intent to look at the end point of spinal cord ischemia. This is an example of a pre and during balloon inflation.

You can see the brachial and femoral pressures on the screen on the left show very low blood pressures and soon after balloon inflation you get restoration of normal tension in the brachial arterial line. For our study, we saw these end points that in the

60-minute balloon inflation that animals become quite hypertensive rather than normal tensive. First 30 minutes we had no animals that were in hypertension phase. There was a significantly higher metabolic price to pay with prolonged balloon inflation at

60 minutes with the average base deficit delta of about 18 per millimoles liter. We also saw elevated troponins in the 60-minute occlusion group compared to the 30-minute group. Some had values even over five nanograms per milliliter as well as systolic evidence of myocardial injury.

All animals in the 60-minute REBOA group had histological evidence of renal injury, although none of them had creatine elevated of greater than 1.5 base line at the 10-day end point. Thirteen percent of the animals had histologic and laboratory evidence of myocardial injury.

And 50% of the animals in the 60-minute group had paralysis and histologic evidence of spinal cord injury. These are some representative images that show cavitation in the ventral horns of the spinal cord with severe inflammatory infiltrate. These are some more unexpected findings that show

ischemic injury to the dorsal horns as well as the dorsal columns in some of the animals. Wide spread spinal cord injury are not confined to the anterior spinal artery distribution. In summary, 60-minutes of REBOA balloon inflation after profound hemorrhagic shock in a

nonhuman primate model has high survival, but high morbidity. Fifty percent spinal cord ischemia, metabolic derangement, myocardial strain and injury and renal histologic injury. But in this study, all of these major morbidities

were essentially mitigated by limiting balloon inflation time to 30 minutes. With this in mind, we recommend that zone 1 REBOA be limited to 30 minutes in humans and after 30 minutes, every effort should be made to intermittently deflate the balloon as tolerated to allow

some reperfusion to occur. Thank you so much.

- (speaks French) liver surgeon I perform hepatobiliary surgery and liver transplantation. Maybe I don't belong here, I so probably more rested than anybody in the room here. But today I will present about liver surgery and hepatectomy. I work at The Royal Free where I have the honor and pleasure to have seen Krassi. We are in the

little island in the North Sea. There is many things going wrong there including Brexit but, the guys uh, we have a major advantage. The NHS favors centralization. Centralization look there: London is bigger than New York Uh, eight million, 50 million greater London

and we drain about six millions of people with our HPB center. In the center we perform about 2,000 operations, of major surgery. In five years, half of them are liver surgery. And most of them have uh, benign, malignant tumor. A very small percentage have benign tumor.

I count here for complications uh, and mortality look there, 3.1% of only the malignant because the benign are young people and we perform a different strategy, they have no mortality. Today Hepatic Hemangioma, look there it is uh, 1898 is a key year. Not only the first description

of the lady that died after bleeding out in an autopsy but also, Hermann Pfannenstiel uh, Professor Pfannenstiel. I will introduce you to him. He described the first operation. Now, we're talking of congenital malformations, they uh, lesions occur in the liver and they may grow,

but only 20% they grow. They have a chaotic network of vessels and they have fibrotic, fibrotic development within it. I introduce you Hermann Pfannenstiel, he was a gynecologist, famous, famous, important incision that we still use today.

Remember him, we'll talk to him later. Microscopically, the microscopic is our well-circumscribed lesion, they're compressible. Important you see down there that they compress the liver that is normal close to it. This has an implication because if you operate,

you fill find a blood duct or a vessel and it will bleed or leak by. Microscopically, they are ectatic blood vessels and they are fed by arteries. This is also an important point, for therapy. Separated by fibrous septa, this is also important

because they become harder and they become bigger. And they have distorted blood vessels. They're more frequent uh, benign tumor. Prevalence up to 7%, they have non-neoplastic this must be clear, they are non-cancer. The proliferation of endothelial cells, women

have more and particularly pregnant women, more pregnancy or contraceptive. We divide them in cavernous and capillary and we'll have a word on that. Symptomatic being half of the cases, multiple in 10%, they rarely bleed and they rarely rupture.

Capillary Hemangiomas cells small, I show you an MRI here. The differential with HCC liver cancer is most important. They both are theorized but they continue to appear on late face. They are asymptomatic please, do not touch them, they do no harm.

And so we will not speak of them. We speak only of the cavernous hemangioma. And here, the cavernous hemangioma bleeds Oh my God, no, it's not true. There are 83 reports of bleeding since the report of Hermann Pfannenstiel. Uh, 97 cases, adenomas bleed more frequently.

Frequently, in the past they were confused. Hemangioma and adenoma, adenoma does bleed. There are only true cases, 46 in the literature. Size is not important and they are very rare in elderly people.

This is what we see when they are giant cavernous hemangiomas, they're serious, they are rather easy to diagnose. Diagnostic criteria, uh, look up typical for uh, cavernous hemangioma. How do you point here? Yep, you stop. If you then see that you have

an atypical hemangioma, you jump over to an MRI. MRI is too nowadays, diagnostic and uh, the important thing is you stop. Once you have the diagnosis with MRI, you stop, do nothing yet, do not follow, bye-bye. Treatment modalities surgery: Selective TAE, Radiotherapy, Medication: two classes,

Propranolol, to decrease the hyper circulation. Bevacizumab as a class of drugs of inhibitors of inferior growths and endories, eventually are cold. This is seminal paper, about 35 years ago "Do not treat asymptomatic patients." This is a key: do not bother with hemangioma.

If you do have the algorithm, you look at complaints that can present incidentally when they have complained, not complained, no treatment of abdominal pain. Unrelated to no treatment, we have to eventually make sure that the pain is not related to the cavernous hemangioma. If there is other futures

like compression giant, you can do surgery. If you have a doubt in diagnosis, today rare with MRI, then you can perform a biopsy. The surgical indication then remain progress, severe, disabling symptoms. Diagnostic uncertainty nowadays not the case, with MRI.

Consumptive coagulopathy or Kasabach-Merritt syndrome is a serious, we will see when you perform human transplants. Spontaneous rupture with bleeding as an emergency. Rapid growth in 25%. This is a paper that shows that the size of the cavernous hemangioma is here,

and you can see that operation has been performed for larger size, however, look that even in non-symptomatic or partially asymptomatic patients, you can reach sizes up to 15 centimeters. And this a review of the literature from a Chinese group where they revised a thousand to a hundred cases,

no mortality in the series and enucleation versus the anatomic resection is better. Less complications, less blood less, less time of surgery, and less hospital stay. So please, in this case of surgery, we do enucleation. I was asked by my society the HPBA to speak

about transplantation for liver tumor. You can that an indication is unresectable disease, severe symptoms and mass occupying effects. Pre-cancerous behavior is not for hemangioma only for adenoma differential diagnosis with HCC. And you have to be attentive that you avoid

liver insufficiency during your resection. So, in conclusion, for benign lesions, hemangioma technically is the only indication. And now the systematic review that shows around several emothing United States UNOS and the ELTR Several, several benign tumors but if you break down

for type of tumors you see that most of them are Polycystic disease or partly cavernous hemangioma are very low. 77 in Europe, out of 97,000 operation of transplantation. So, let's get an old paper. The pioneer of transplantation again, extremely low,

one out of 3,200. An extremely low percentage. It's my personal experience I was working at Essen, Germany. Almost a thousand transplants we performed. Unfortunately most of them I did and we never transplanted one hemangioma, my experience for transplantation is zero because it should not be done.

So, my advice for hemangioma. Biopsy not advised, see a liver surgeon in a serious center, diagnosis is done my MRI, observe doubt symptoms and observe. Let the patient beg you for surgery, if significant increase in size and symptoms, we can do surgery. Embolization is possible.

Sometimes it's harmful. The role of the surgeon is to confirm the diagnosis, differentiate it from cancer, exclude causes of other symptoms and avoid unnecessary surgery that's the main thing. Surgery for severe symptoms of Kasabach-Merritt. Only for complicated symptomatic lesions, or where the

diagnosis is uncertain. Ladies and gentleman, I will conclude with a couple of questions. If you have a daughter or son with a liver tumor, would you go to a center or a competent surgeon or to a gynecologist. Professor Pfannenstiel for instance or another doctor. If your car has a problem,

would you go to a good mechanic once for all, or to a small shop for 20-40 times. It is a matter of experience and a matter of costs. And with this, I am ready for your questions. - [Audience Member #1] When have you personally operated on these lesions?

- [Speaker] I am. And the experience that I have in the past I seemed young but I practiced for many years. When I started 25-30 years ago, we were operating many of these because we were not so certain. Then MRI came, and MRI basically made the diagnosis so easy and straight-forward and we started observing

patients. We still do operate today, but they are very large tumors and when I do personally, I avoid the androbolization before because you have more skylotec reaction, just (grainy sound effect) to peel it away from the normal parenchymal.

This is our experience. - [Audience] Thank you. - [Speaker] Thank you very much, yes? - [Audience Member #2] Yes, one question. When you operate, and with all of the experience you have, what are the complications of

(mumbles) - [Speaker] The main, so first of all, there has been also an evolution in the type of operation we don't do anymore the resections where you have some bi-leaks. If you operate correctly, it's bleeding and one infection not one born. If you have to watch bi-leak is the one

that you have to watch and that's because the tissue is pushed away and you may miss something during the enucleation.

- Thank you chairman, thank you again to Dr. Veith for this kind invitation. Ladies and gentlemen I have no disclosure. Actually I have a problem with my mouse, it doesn't really go. Yes I know it is the green button but it doesn't work, okay now it works.

I'm sorry, okay. So again, one year ago we published a paper to evaluate the impact of cerebral lesions and their volume on carotid revascularization outcome. In that paper, not only we looked at the presence of cerebral ischemic lesion but also

we measure the volume of that lesion. While there was no effect of the presence of the cerebral ischemic lesion in the outcome of those patients, if we look at the patient who suffered a post operative stroke, we saw that the amount of the volume of the

lesion was significantly greater compared with patient with no post operative event. And also by combining stroke and death in those populations, the volume was still greater than the other patient. ROC analysis, the cut off point was set

at 4,000 cubic millimeters in that population. BY examining patients with ischemic lesion volume greater than 4,000 cubic milimeters the incidence of post operative stroke was significantly higher compared with patient with a smaller lesion. A multivariate analysis, a volume greater than

4,000 cubic millimeter was an independent predictor of post operative stroke in that population. So the conclusion of this study was that the presence of a cerebral ischemic lesion has no overall effect on the revascularization outcomes. However, if the cerebral ischemic lesion volume

is greater than 4,000 cubic millimeter then the risk of stroke is significantly increased. We wanted to further expand these conclusion and we look at the benefit of a deferred carotid revascularization only in patient with a moderate disabling stroke.

We presented this data at the last ESVS meeting in Spain. So the study endpoint where perioperative 30-day stroke death after endoctorectomy just in patient with a large cerebral ischemic lesion and we investigated the best timing to reduce the post operative complication rate.

So we just extrapolated a small portion of our patient, 126 patient with moderate disabling stroke and a very large ischemic lesion. As you can see from the table here, the volume of the ischemic cerebral lesion in that population was pretty high.

Overall stroke and death in that population was 70.1% and time from symptoms to revascularization was a mean of 7 weeks. ROC analysis, the cut off point was set at four weeks in which you add the maximum differences in the result. So looking at patient operated within four weeks

and after four weeks from symptoms we didn't find any difference in the two groups. However, stroke and death was significantly greater in the patient operated within four weeks compared with patients operated later. And the multivariate analysis, timing to endorectomy

less than four weeks was an independent predictor of stroke after endoctorectomy. So, endoctorectomy after disabling stroke has a high risk of post operative major adverse event which was 7.1% in our series but can be as high as 26% in the literature.

The take home message is that the patient with large cerebral lesions greater than 4,000 cubic millimeters have a better outcome if operated four weeks after symptoms. Thank you for your attention.

- This is a little bit more detailed explanation of the pathophysiology behind Type IV AVM's. Medical disclosures are none. And this is the Yakes classification and this is Type IV lesion we are going to talk about now. So, this angioarchitecture has not been described before, and was first described in the Yakes classification.

What is so unique? It has multiple arteries, arterioles, but these arterioles form innumerable fistulas that are of a microsize, and they infiltrate the affected tissue. So, this is, this can affect every kind of tissue,

skin involvement and muscle involvement, and other than brain AVM, bleeding occurs if mucosa involvement is present or if an ulcer is present. So, we have to think about the definition of an AVM, which is an artery to vein connection

without an intervening capillary bed. But, what applies in Type IV? As you can see here, very nice example of this infiltrating type is that the tissue where the AVM is located is also viable, so the assumption is that

normal capillary beds are interspersed into these innumerable AVMs existing next to the malformed AVM fistulas, and this is a new definition of AVM. So, how to access this lesion? Of course, transarterial is possible

with a catheter or micro catheter. If anatomy doesn't allow transarterial approach, direct puncture is an option. Also, as you can see, in the direct puncture in the lower video, you can see the venus drainage of these fistulas,

and direct puncture of the vein compressed to reflux ethanol into the fistulas is also an approach. But, what is the challenge here? If you want to treat this lesion, you have to keep in mind

that you don't want to occlude the capillaries that are supplying the tissue. So, to find the right treatment approach, the physiologic concept is often important to understand that the arteriovenous fistulas drain into multiple veins and arterialize these veins

so we have a high pressure on this venus outflow site. The normal capillaries have a normal outflow too but this is of lower pressure, and this comes to competition between the arterialized veins and the normal venus outflow, which is, which is inferior to the normal capillary outflow.

So, what follows is a restriction of normal tissue flow with back-up to the capillaries, and backing up into the arterial inflow. So, we have the situation that the arterial venus fistulas have a lower pressure, lower resistance, and an increased arterial flow

compared to the normal capillaries, and this has to be taken into advantage for treatment. How can this be achieved? Thicken the fluid and dilute the ethanol by creating a mixture of 50/50 contrast and ethanol. So, this mixture will follow the preferential flow

into the arteriovenous fistulas in transarterial injections bearing the normal capillaries. So, if it's possible to puncture into the fistulas, pure ethanol can be used, but especially in transarterial access where normal nutrient vessels can be filled,

50:50 mixture contrast is the key to treat a Type IV AVM, Type IV Yates AVM, and here, you can see, using this approach, how this AVM can partly be treated in many several treatment sessions. And here you can see the clinical result. So, this huge ulcer, after seven treatments, healed

because of the less venus hypertension in the lesion. So the additional benefit of 50/50% ethanol contrast mixture is that your injection is visible on flouroscopy so you can see if which vessels you are including. You can react and adjust the pressure you're injecting. So, it also has to be considered

that the more you give diluted, the more total ethanol can be needed, but it's not efficient in larger vessels. This is also the advantage that you just treat the microfistulas. It's of importance that you use non-ionic contrast

as ionic contrast precipitates in the mixture. So here, you can see again, see the Type IV AVM of the arm and hand, which I already showed in my first talk, and here, you see the cured result after multiple sessions showing good arterial drum without fistulas remaining.

So, the conclusion is that Yakes Type IV is a new entity. It's crucial to understand the hemodynamics and the concept of 50/50 contrast ethanol mixture to treat this lesion with also a curative approach. Thank you very much.

- Thank you very much. So as I said, I'll start by talking on Measures of Frailty and Their Importance in PAD Patients. These are my disclosures, none of them relevant to the talk. But you can obviously ask me about them later if you wish. You know, we all talk about frailty

in our everyday clinical lives, and we make decisions based on frailty. But at least for me, I don't think I've put the number on it, I haven't looked at it in a scientific manner before preparing for this talk,

and I'm very lucky to have be able to kind of learn more about it through this, and I want to share with you what I've learned. So, obviously walking has a lot more to do than just the arteries. There's muscle mass, muscle tone, stability,

overall energy, you just need the energy to get going, systemic medical limitations, and psychological drive, which for the younger ones of us, I should have put as the first one. And you know not all elderly patients are the same of course.

And you know this gentlemen here is very healthy and can perform activity as much as he wishes, while this gentlemen here is obvious more frail and activity is more difficult for him, but how do we measure that? Well, frailty means low physiological reserves,

increased vulnerabilities to acute stressors, and functional decline as a result of that. So there's something called the Fried scale that helps us measure that. Well, first of all, self reported, you can ask the patient,

have they lost weight unintentionally? Do they feel exhausted? Or are they just not performing any physical activity anymore? And then objectively, you know, you can shake their hand assess their grip strength.

That's something I definitely incorporate into my everyday clinical practice, and you can observe their walking and if it is slow, then it's abnormal. And the more points you get,

the more frail your patient is obviously, and frailty is important. It's associated with mortality. And when, this slide I realize is difficult to understand from afar, but what the slide shows you

is patients with and without PAD, and with and without frailty. And what it shows you is that frailty contributes to walking limitations in a specific manner. In other words, there's the PAD contribution to walking limitations,

but on top of that, there's also a layer of frailty. And so frailty has an important effect on walking in elderly patients that is separate from just PAD, separate from just the arteries. Not only that, because frailty

obviously affects multiple domains, it has the potential to not only effect walking ability, but also critical limb ischemia in particular and what this study just published recently showed that frailty is independently associated with survival and with amputation in patients with critical limb ischemia.

And you know, I don't have the time, unfortunately, to go into all the details of this study but I really recommend looking at it, and what you, despite multiple limitations, one thing I do want to mention is that frailty obviously overlaps with many things that we view as risk factors

in patients with critical limb ischemia anyway. And parsing them out is difficult but it just goes to show how much frailty is incorporated into the everyday sort of assessment of our PAD patients. So, remember that frailty may equate to futility.

So if you have a very frail patient, you may opt not to do something. But think about a different concept. What if you identify a patient a being frail, if you have the time, you may think of prehabilitation.

Maybe strengthening that patient, make them less frail before the procedure, and by doing that you'll be able to bring them into a procedure or into a new intervention in a stronger way. Well, by now you're like, "Whoa Ido, you blew our minds.

Frailty is Awesome. But how do I assess frailty in my office?" Well, thank you for asking that. There's this really easy test that you can do that does not take to much time. It's called the timed get up and go test.

So now ask me, "Well how do we do that?" Well, there's a movie, a little clip to show you. You basically ask the patient, they have to do this on their own, they get up from a chair, they walk, they get back, and you're timing them as they do it.

And if they, you know, make sure they don't fall but don't help them. And if the patient does that slowly, that is strongly associated with PAD. This has not been validated specifically in PAD patients, frailty, I'm sorry,

but it's not been validated in PAD patients, but it's a very useful test to assess frailty. So as I said, so in conclusion, frailty should be a tool that you should use in your PAD patients.

- Thank you, thank you for the opportunity to talk. And I'm going to go quickly through some of the background slides 'cause we've heard some of this. I have no disclosures. So we've heard a little bit about popliteal entrapment already.

The population it affects. But where I'm going to point out that I think IVUS and some of these newer techniques may be more useful are in these patients because they, if they get repetitive compression they can get occlusion, embolism, and aneurysm.

So I think in these functional patients that we just heard about and in some of these patients who have maybe more subtle findings than a standard type one or type two, that's where I think these techniques are particularly helpful.

Additionally, we have seen a huge rise in women, female athletes over the past decade like you saw on the last slide. They seem to be the more predominant type. And functional, we, Doctor Ali just reviewed all of this. But functional seems to be a more common type.

And that's where, at least at Michigan, we find IVUS to be most useful. For that, and then also for type three, where the muscle, accessory muscle slip may not be as visible on conventional imaging. So, we just heard again about functional entrapment,

I'm also going to talk about at Michigan how we distinguish that between recurrent compartment syndrome, which is another common diagnoses that we see a lot of people coming in with. But it's important to mention too

that all these diagnostic tests are positive in a certain percentage of normal patients. So you really have to be looking at the specific patient population that has these symptoms before you're kind of pursuing this diagnostic algorithm. So our typical work-up and diagnosis,

again, is not always straightforward. We usually start with exercise ABIs. If that's abnormal we have an MRA protocol. And provocative angio that we will pursue. If it's normal, we'll typically do a duplex as has been shown up here previously

to help us distinguish between chronic compartment syndrome and functional entrapment. But it's important also to think of some of the other causes like cystic adventitial disease, endofibrosis, and some other things that can present with similar symptoms.

This is just showing a provocative MRA, which is sort of the next thing in our algorithm. We have patients do active plantar flexion, although, as has been reported in lots of literature, there's a really high false negative rate here because it's very dependent on the protocol.

Patients have to hold this plantar flexion for a long period of time. And so it can be very easy to miss these type three, type four, and functional on the MRA. And we see that quite a bit at Michigan. So we often then proceed to provocative angiogram,

which is shown here in one of our swimmers. He's in neutral position here, and then in this second angiogram you can see he's in active plantar flexion. We often have to use vasodilators in these patients to sort of simulate the amount of exercise

that they're used to getting. But again, these, we only go to this step if we're really convinced that the symptoms are specific for this diagnoses. Now where I think IVUS is particularly useful is these long segments, like you can see over here,

where you can't identify the exact compression point. That's where we're using it. So, again, kind of in these type three, four, and six. But we found it to be a very good adjunctive tool. We're using it all the time in these patients now. And it helps us both identify the exact location

of compression, what specifically is compressing, and it allows us to do a more precise surgical approach and completely identify that area and resect it. And we're also using it postoperatively to confirm that we have indeed relieved all of the compression.

So here's, you saw a video of this already, but here's a patient essentially in neutral position, you can see the artery. When they go into plantar flexion you can see how this is being compressed here. And we will run this down the whole way

and find the maximal areas of compression. And as you can see over here, we'll kind of mark them based on bony landmarks with angiography pictures so that we can identify these exact areas. And then we'll pull that up when we're doing our operative treatment.

So we will also then, after we have done whatever operative treatment we're doing, we will then wake them up, have them do a provocative angio again with us and an IVUS just to confirm before we leave the operating room that we have indeed relieved all of the compression.

And this, we've found, has really significantly minimized the amount of patients that don't get relief postoperatively. So this is a very busy slide, but it's basically just our algorithm at University of Michigan for these patients.

They all come in, they get exercise ABIs. Depending on if they're normal or abnormal they sort of go toward the MRA protocol. As you can see, unless they have a clear type one or type two entrapment, they're all getting this provocative angio and IVUS.

In patients that are a little less clear, they're all getting exercise compartment pressures, meaning that they're running prior to getting compartment pressure measurements. If it's greater than 25 they're getting a fasciotomy. If their results are positive,

depending on whether we think it's functional or true popliteal entrapment, we'll either do a standard posterior release or a musculotendinous resection. But again, this technology, I think, is very useful. We need to be more vigilant in diagnosing these patients.

And I think newer technologies will also aid in this. Thank you.

- Thanks Dr. Veith for the invitation. It's a privilege to be here. My only disclosure is that like Jo, I was a trauma surgeon before I became a vascular surgeon, so that informs part of this talk. As you know Dr. Veith promoted REBOA for aorta aneurysm ruptures long ago.

But there has been a resurgence of this as the military has seen that the majority of deaths on the battle field, preventable deaths on the battlefield is due to hemorrhage. And almost 90% of those were due to non-compressible torso hemorrhage,

not amendable to tourniquets. It's said necessity is the mother of invention and it was really the military vascular surgeons here today and John Eliason and Todd Rasmussen who wanted to prevent non-compressible hemorrhage and created an easy to use low profile catheter

that's have been called the ER-REBOA catheter in recognition of their contribution. It's also been the military vascular surgeons here today, Chuck Fox and Jo DuBose who have been the leaders in promoting and teaching this technology across the country and across the globe.

Like any new technology, however, it can lead to complications if used in an unexperienced hands. And the reported complication rate in the literature is only 5%. My belief is that this is vastly under reported.

It's predominantly performed by trauma surgeons currently. However, ER positions are increasingly using this wanting to use it for a non traumatic indications. However, the lack of experience of catheter and wire skills in these two groups can lead to devastating complications and errors in management.

And that can happen in every step along the way. You've seen some of these pictures earlier but we all can be placed in any number of places, any wars, any branch vessels. Here you see in ascending aorta, internal iliac, left carotid, left subclavian and these are

some of the great pictures from one of Jo's papers but I've seen this in several instances that I didn't think to take pictures myself. Additionally, if it's over inflated in a wrong location that can lead to a vessel rupture. And probably the most common complication

is the access site issues. So, if this is not recognized and dealt with earlier, it can lead to profound leg ischemia and ultimately end up in amputation which is a tragedy after you save the patient's life. Unfortunately, I've seen this in

more than one occasion already. Obviously, there is plenty of other complications including thrombosis, embolism, iliac dissection. I've seen aortic rupture, prolonged visceral and renal ischemia and balloon migration. A tragic example was given to me by

a prominent vascular surgeon who has consulted after a REBOA has been left in the aorta for 12 hours partially inflated which led to aorta, iliac complete thrombosis and despite revascularization had such a severe pelvic & lower extremity ischemia that ultimately led to the patient's death.

This is a shocking example of inexperience that can be prevented by involving people who know what they are doing. So, how can these complications be avoided? Well, certainly training and practice is critical. But also X-ray confirmation because misplacement is common

and it's important to recognize that all patients who have REBOA in place should go directly to the operating room because stopping at the CV scanner is not really an option. The patient is ischemic. You're on the clock.

And also teamwork is critical because while you're performing the procedure, you should have some other person ideally doing the trauma resuscitation because you need to focus entirely on the procedure to prevent complications. I have three basic recommendations for everyone.

One, is that, all trauma patients who are hypotensive should have femoral arterial line catheter placed. This is the longest and most difficult part of the procedure. But, once it is performed and if the patient remains hypotensive, you can easily upsize

to six, seven French sheath and then place REBOA if necessary. Secondly, use teamwork. This is a team effort and trauma surgeons are clearly at the tip of the spear and they are the boots in the ground who need to know

how to do this procedure. However, they do not have the vascular and endovascular experience that trauma surgeons all would've had. And, therefore, it's my recommendation that the vascular surgeons should be involved in 100%

of these cases after a ballon is placed. Especially, in centers that are not doing this very frequently. And it should trigger an automatic vascular consultation, the balloon should be taken down as soon as possible, and the sheath removed as soon as possible

and then bilateral ABIs should be performed because you need to act, you need to recognize complications early in order to prevent the onset of complications. Lastly, the military vascular surgeons have been the leaders in this,

promoting this technology and teaching it world wide and the rest of our civilian vascular surgeons need to step up and a take a leadership role. We need to learn and teach REBOA in our community. We need to help our hospitals to determine who should be credentialed.

And we need to evaluate all REBOA complications collectively, so we can learn from them and prevent them in the future.

- Lymphatic, so it's fun, actually, not to talk on venous interventions for once. And, naturally, the two systems are very different. But, on the other hand, they're also related in several ways and I will come back to that later. I have no disclosures, maybe only my gratitude to this man, Dr. Maxim Itkin,

who actually got me started in the field, and was gracious enough to supply me some of his material. And who is also responsible for making our lives way easier over the last years. Because in former times, we needed to do, to visualize the lymphatic system,

we needed to do pedal lymphangiography and that was very, very cumbersome. It took a long time and was very painful for the patient. And he introduced the ultrasound guided intranodal lymphangiography,

and that's fairly easy for most of us. With ultrasound you find a lymph node in the groin, you puncture that and you can control the needle position with contrast enhanced ultrasound and once you establish that position, you might do a MR lymphangiography.

Thereby showing, in this case, a beautiful, normal anatomy of the thoracic duct. I need to say, the variations in lymphatics are extreme. So, you can also visualize, naturally, the pathology, like for example, pulmonary lymphatic perfusion syndrome.

What's going on there. Normally, lymph courses up through thoracic duct, but in this case, you kind of have a reflux in the bronchial tree and lymph leakage. And you can image that again, beautifully with MR, which you can show extensive leakage

of lymph in the lung parenchyma. So you can treat that. How can you treat that? By embolization of the thoracic duct. But first we need to get into there, and that's not a very easy thing to do.

But now, again, with access to a lymph node in the groin, you can push lipiodol, and then visualize the cisterna chyli and access that transcutaneously with a 21/22 gauge needle and then push up a O-18 wire high up in the thoracic duct.

First you deploy some coils to prevent any leakage of glue inside the venous system, and then by microcatheter, you infuse glue all the way down, embolizing the thoracic duct. So, complete different group of lymphatic disorders is oriented in the liver and hepatic lymphatic disorders.

And maybe not everybody knows that, but 80% of the flow in the thoracic duct is caused by the liver and by the intestine. And many times in lymphatic disorders, there needs to be a combination of two factors. One factor is a venous variation of a,

sorry, an anatomical variation in lymph vessels and the other one is that we have an increase in lymph flow. And in the liver, that can be caused by a congestion of the liver, for example, cirrhosis, or a right side, that's congested heart failure.

What happens then is you increase the flow, the lymph flow, tremendously and if you also have a variation like in this case, when the vessels do not directly course towards the cisterna chyli, but in very close contact to the abdomen,

then you can have leakage of the lymph and leakage of proteins, which is a serious problem. So, what is then, to do next? You can access the lymph vessels in the liver by percutaneous access in the periportal space,

and induce some contrast and then later, visualize that one back, visualize that with dye that you can see with an endoscopy, thereby proving your diagnosis, and then, in a similar way,

you can induce lipiodol again with glue, embolizing the lymph vessels in the liver, treating the problem. In summary, popularity of lymphatic interventions really increased over the last years mainly because novel imaging,

novel interventional techniques, new approaches, and we all gained more experience. If you would like, I would guess that, we are at a phase where we were at venous, like 10, 15 years ago. If we are a little bit positive,

then the future is very bright. And within 10, 15 years, we find new indications and probably have much more to tell you. Thank you for your attention.

- Thank you very much Frank and thanks for the invitation. My first thing is to deal with the patient who's awaiting CABG who's had a previous stroke or TIA. This is the only study of it's kind showing that if you proceed with isolated CABG, the risk of stroke is extremely high and if you look at the meta-analysis that we've done of whether you do endarterectomy or

stenting in symptomatic patients, this is all the literature there is. And what you can clearly see is that the death and stroke rates in patients undergoing CAS followed by CABG are much higher than after carotid and endarterectomy. And that lead us to recommend that a stage of

synchronous carotid intervention should be considered in CABG patients with a history of stroke or TIA and who have a 50 to 99% stenosis. But advise that for now, if you're going to do that such an intervention, surgery should probably be considered instead of stenting.

But 96% of all interventions of the CABG and carotid variety are in asymptomatic patients, so what about them? Well, this is all the literature there is on stroke risk in patients undergoing isolated CABG with a unilateral asymptomatic stenosis of 70 to 99 or 80 to 99 and you can see there is an awful lot of zeroes

in that table and if you go at patients with bilateral significant disease, the death and stroke rate is much higher but again there is not too many strokes here. And if you look critically at the literature and ask yourself okay we've had so many strokes, how many of them can be attributable to underlying

carotid disease by looking at the CT scans or the distribution of lesions, you'll see that between 85 and 95% of all strokes cannot be attributed to an underlying significant carotid stenosis. And if you look at all the death and stroke rates and this is a multiple meta-analysis that our

group have done over the last 15 years, these are the death and stroke rates depending on how you treat the patients, and 80% of these are asymptomatic and 80% have got unilateral stenosis and the death and stroke rates are far in excess of the risk of stroke if you just perform an

isolated CABG in patients with unilateral asymptomatic disease. There have been two randomized trials. This is one, the Iluminati trial that Jean-Baptiste was involved in, 30-day death and stroke rates not significantly different.

There is quite an astonishing trial from Germany, which was again unilaterally asymptomatic stenosis with a near 20% death and stroke rate with synchronous carotid CABG and a 10% definite stroke rate with medical therapy, ah isolated CABG, sorry. So the ESVS have advised that a staged synchronous

carotid intervention is not recommended in CABG patients with an asymptomatic unilateral, 70 to 99% stenosis for preventing stroke after CABG. A staged synchronous intervention may be considered in patients with bilateral disease, the evidence is not brilliant but it's such a rare thing that it's

probably not worth arguing about. Now what about patients who are undergoing non-cardiac surgery? This is quite an interesting group, because if say, a gastrectomy, a hip replacement or whatever, if they've had a previous history of stroke or TIA

they should undergo carotid imaging and if they've got a significant stenosis they should undergo prior carotid revascularization prior to undergoing their gastrectomy et cetera. But what about the asymptomatic patient? This is quite interesting.

First of all, let's just look at a very large study by Jorgensen, 4 nearly 500,000 elective non-cardiac operations and 7,000 had suffered a prior stroke or TIA, and the most important thing was, the stroke risk was directly related to the time from the onset of the TIA to doing the operation.

So if you did it within three months of the stroke or TIA there was a 12% peri-operative stroke rate, but if you managed to get out to six months, the stroke rate was only 0.1% so the lesson learned there is that if it's possible to delay surgery in patients who've had a prior stroke or TIA

or a recent one, you should delay it for six months. Only two studies have looked at whether asymptomatic carotid stenosis increased the stroke risk in patients undergoing non-cardiac operations. Ballotta did a randomized trial, and Sonny, which is a very large observational study,

looked at the impact of asymptomatic carotid stenosis on outcome and found that there was no evidence that a pre-existing carotid stenosis increased the risk of stroke in patients undergoing major non-cardiac surgery. Similarly, in a huge study on TAVI patients,

no evidence that carotid disease was a risk factor for perioperative stroke. So in our recommendations we advised routine carotid imaging in asymptomatic patients undergoing major non-cardiac surgery is not recommended and prophylactics and arterial stenting is not

recommended in patients with asymptomatic carotid stenoses undergoing non-cardiac/vascular procedures. And if you'd like to look at all the literature and data that we came to in using to our conclusions, the guidelines are free to access on the internet.

Thank you very much.

- Thank you very much. So, this audience certainly knows that the higher the triglyceride, the greater the cardiovascular morbidity mortality, similarly if you have a low HDL that same relation holds, and certainly for the non-HDL-C or LDL-C calculated the higher the worse outcome and there's

multiple drugs related to this. Similarly with stroke, triglyceride the same relationship. Ischemic stroke increased with low HDL and again LDL-C correlates. So the historical precedent has been that you should get a fasting lipid level

when you first encounter the patient, but to make this simple that's really probably not true. So there's various things that are measured and that are calculated, but LDL is generally calculated, HDL is measured and then the triglycerides are calculated as remnant cholesterol.

So if you compare just the measured LDL compared to calculated LDL in a non-fasting state, it's a little bit of a wider linear relationship here as compared with the fasting, it's a little bit tighter. But when you look at this in more depth, and this reference here really nicely puts it all together

but the total cholesterol really doesn't vary if you've fasted one hour or 16 hours, similarly between men and women. The only thing that varies a little bit is triglycerides and we'll go on to that in just a little bit of depth.

But again that's variable, triglycerides go up if you eat really not much difference with the other lipid levels. And if you look just in terms of triglycerides, they overlap between non-fasting and fasting, really at almost all levels

so there's not really discrepancy. Similarly with LDL, same amount of overlap here whether or not you have diabetes it doesn't seem to make a difference. So for lipid panels, profile testing, in most patients you can get a non-fasting

initial lipid profile in any patient for cardiovascular risk assessment, I'd say that's where it's most commonly done in most of our practices. Similarly with acute coronary syndrome, if preferred by the patients et cetera.

But really it's where the non-fasting triglycerides are highly elevated that you want to get a fasting lipid panel. So what causes secondary hyperlipidemia related particularly to hypertriglyceridemia? Certainly certain diet factors, certain drugs,

cyclosporins for example, biliary obstruction and hypothyroidism. And so, one algorithm is that in terms of screening with non-fasting, and if it's less than 200 you're good to go, you really don't need to do anything further,

and if it's greater than 200 then probably a fasting lipid profile, lipoprotein panel is indicated. So reasons that non-fasting lipid measurement is fine most of the time is that again most trials have used non-fasting levels for determination of effectiveness of various medications.

This Friedewald formula actually uses total cholesterol, HDL, and triglycerides to calculate LDL-C, and LDL really is not directly measured, it's not standardized by the CDC such as these other cholesterol moieties are. And again most CV risk factor calculators don't use LDL-C.

So again, non-fasting is acceptable for the initial risk estimation in untreated and primary prevention screening. For patients with genetic hyperlipidemia probably fasting is required. Diagnosis of metabolic syndrome, non-fasting is fine.

And again some other more highly specialized scenarios you may want a fasting profile. Thank you.

- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery

and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely

at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer

or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.

Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.

There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking

at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?

And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,

this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients

with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.

I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,

and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients

who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually

living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,

you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data

over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,

more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.

These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?

I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.

I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at

the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,

such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time

camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.

If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.

Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.

There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series

where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,

limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.

But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.

So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.

So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.

If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.

- Good afternoon. On behalf of my co-author Danielle Lyon I'd like to thank Dr. Veith for allowing us to present our data. No disclosures are relevant to this talk. So, why a small incision carotid endarterectomy? I actually came on to it maybe a decade ago when in debates for carotid stenting versus

carotid endarterectomy my interventional colleagues would show pictures like this. And pictures like this, with big incisions which is how I was trained from sternal notch to the angle of the mandible and above. Then I started thinking you know, maybe this could be done

through a smaller incision safely. So it's a smaller incision, it's cosmetically much more acceptable especially in ladies. Endarterectomy typically only involves about three centimeters of artery anyways. And, there's decreased tissue trauma

with a smaller incision. All of my patients are operated on clopidogrel and aspirin and we also operate on patients on full warfarin anticoagulation without reversal which we published in the annals a few years ago. So first, rely on the preoperative imaging.

So I always get a CTA to confirm the duplex ultrasound. Here you can see a very focal plaque in the proximal internal carotid artery. Here's a more heterogeneous plaque and opposite a carotid stint. I typically do these with,

under general anesthesia with EEG monitoring. The self-retaining retractor I use to stretch the incision would be, I think, a challenge in an awake patient. I image the carotid bifurcation, just like our previous speaker, with ultrasound ahead of time. Just a regular Site-Rite ultrasound,

you don't need a duplex. I typically call my friend Russell who comes with the ultrasound, and doing both longitudinal and transverse views to identify the carotid bifurcation and confirm the extent of the plaque. The incision is typically around three centimeters,

but clearly less than four centimeters, and it's centered over the previously marked carotid bifurcation. I use a standard incision along the anterior border of the sternomastoid muscle. And then use a self-retaining retractor to stretch the incision a bit.

This is a pediatric omni retractor which works really well for this purpose. It's very important, especially for the more-sef-full-ab blade to make sure that you identify the hypoglossal nerve as you can put a fair bit of traction on that upper blade and sometimes the incision is small enough that I actually

make a little counter incision for the proximal clamp. I've found that the use of a shunt can be challenging with this technique. There's one case out of 124 that I had to extend more proximally in order to safely put a shunt. I do, though, use acute ischemic preconditioning.

So typically the mean blood pressure is 90 or above, the patient's fully anticoagulated. I'll clamp the distal internal carotid artery and if there are EEG changes I'll unclamp it, raise the pressure just a little bit more and in most occasions the second or sometimes third time the internal

carotid artery is clamped the EEG does not change. And again, you can extend the incision if necessary as patient safety is absolutely paramount. So the technique is safe. In 124 consecutive patients there were no strokes or deaths.

There was one temporary cranial nerve injury which was the marginal mandibular. A complete endarterectomy can be achieved. Again, no increase in cranial nerve injury compared with a standard incision. And it really is a superior cosmetic result.

So here's a photo that I received from silk road, you probably did too. So here's the TCAR incision compared with a standard carotid endarterectomy incision on the other side. Here's a couple of my recent patients, so you can do this operation with an incision

that is about the same size as that utilized for TCAR. Thank you.

- Thank you very much. I appreciate the opportunity to present and I'd like to thank the program committee and Doctor Veith. I have no disclosures. So Traumatic Limb Ischemia is uncommon. Demtriades looked at this with the national trauma database and found that it only occurred in about one point six

percent of patients. And the majority, or 51 percent, are penetrating injuries. These are often managed by the trauma surgeons at tertiary centers. But with the change in training paradigms, with general surgeons not doing as much vascular procedures

and open vascular surgery not being done as much by many of the trauma surgeons. Vascular surgeons are being called upon to do this, more and more often. The objective of our study is to describe a contemporary series of patients with acute limb ischemia

secondary to trauma that were managed by the vascular surgeon. In identified factors that were accossiated with limb salvage and functional outcomes. We did a retrospective review of our institution over a three year period and looked at several factors,

including the preoperative imaging the level of aclusion, limb salvage, and functional limb outcomes. We identified 68 patients in our study and the majority of these patients had moderate ISS scores and Rutherford Class two ischemia. 53 percent were from an outside hospital

and 62 percent had blunt injury, while 38 percent suffered penetrating injury. If you look at the mechanism again, the majority were motor vehicle accidents for the blunt and gunshot wounds and stab wounds for the penetrating injuries.

Median ages would be expected as fairly young with at 36 and 46 and the majority of these people are males. As is the cases with most trauma series. 58 percent were transferred from an upper, from another hospital in the upper extremity series and 51 percent in the lower extremity series.

With a median time of transfer about three hours. The median time to the operating room was about four and a half hours in this patient population. And most of these patients did receive some kind of preoperative imaging, either a CAT scan with 55 percent of the upper extremity

and 68 in the lower extremity. And the Rutherford classification of ischemia was, generally, two B and below. We looked at the location and the majority in the lower extremity were the Femoropopliteal region and in the upper extremity where the Axillary

and Brachial artery region. So, looking at the number of operations these patients underwent, and the upper extremity and lower extremity both of them underwent a median number of three operations and 84 percent of the patients upper extremity injuries went an open procedure

and 69 percent in the lower extremity. So, open procedures are the modality of choice for repair of these injuries. 58 percent of the lower extremities went on to have Fasciotomies, as well. In some of the details, the open repair

was a dominant treatment as stated. Shunts were only utilized in two of our patients, with Fasciotomies only occurring in 25 percent 58 percent of the lower extremity injuries. And we think about some of the details, we had eight patients who underwent Fasciotomies

during the first operation with dead muscle encountered in three of those patients. Three patients underwent a delayed Fasciotomy with dead muscle encountered in one of those patients. Limb salvagery overall is 94 percent in the upper extremity and 78 percent in the lower extremity.

And again, with the amputation patients, we had 12 patients that underwent an amputation, one primary amputation. The overall limb salvage was 94 percent for upper extremity and 78 percent for lower extremity. The predictors or amputation of functional limb,

in a functional limb where the number was a Rutherford Classification and the number of procedures these patients undergo. The length of stay was 11 days, 25 percent were discharged to a skilled nursing facility and follow up occurred in 59 percent of the patients, as the case

with many of the trauma type studies. When you think about functional deficits, the patients that had no functional deficits in the upper extremity were about 57 percent and the lower extremity 68 percent. But major deficits occurred in one third of the patients

with an upper extremity injury versus six percent. Whereas amputation occurs much more frequently in the lower extremity versus the upper extremity. So, Traumatic Acute Limb Ischemia is uncommon outside of trauma centers, vascular surgeons are extremely well equipped

to deal with this, majority of extremities can be salvaged, transfer times to a tertiary center may explain some of the correlation with limb salvage, and rehabilitation and follow up can be difficult in this patient population. Again, we only had 59 percent follow up, you know,

in the literature it's around 60 and 66 percent in this patient population. It can be managed with very high rates as limb salvage by vascular surgeons. So I think that we can do this and we do it quite well. Limb salvage doesn't equate to functional outcomes,

particularly in the upper extremity. And in the future, I think that we need to probably get better about the follow up and identify some patient centered functional status and quality of life questionnaries post salvage, to see truly what the outcome is and the functional status

is of these patients. Thank you very much. (applause)

- Thank you. I have no conflict of interest. Now the first burning question in carotid artery disease management. I agree with the previous speaker somewhat. Is that is who if anyone with asystematic Carotid Stenosis is likely to benefit from a carotid procedure

in addition to current optimal medical intervention? Where I have to ask this question because of significant advances in medical revascularization over the last three to four decades. Particularly since ACAS was published.

Now at most about 4% of persons with asystametic cartonied stenosis will have a stroke caused by the lesion as explained on Tuesday. We just know that its overall harmful and wasteful to do a procedure on all of them.

But stoke risk stratification cannot identify those who now benefit from carotid endocardectomy and stenting is overall more harmful than endocardectomy. There are many proposed markers of high stroke risk in asymptomatic carotenosis patients given just medical treatment.

Including those some of the European society vascular surgeons. But we already know that each of these markers used in isolation they lack sufficient specificity to identify those most likely to benefit from a procedure. In other words they are to common.

And also the event rates with these individual markers are too low. Particularly considering that all of these studies of these markers were done with suboptimal medical treatment. The second burning question.

Is will prevailing carotid trails find a current procedural indication in stroke prevention? Well the answer with respect to ACST-2 is no. Because its just a trail of stinted verse endocaretomy There is no medical treatment only arm. So its not testing the efficacy of these procedures.

It will help to measure harm of one procedure versus another. But this is of little value without a procedurual indication in the first place. The answer of CREST-2 is not too. Because unfortunately there randomizing

average risk patients like those in ACAS. And we already know that to do a procedure on all of these people is going to be futile and harmful. There's no stroke risk stratification before recruitment. An although they are doing some sub group analysis with markers.

Are these powered sufficiently? I haven't seen that is the case so far. If you look at the CREST-2 sample size. There is approximately 85% power to detect differences in peri-procedural stroke or death or later ipsilateral stroke with endocardectomy versus stent

or stenting versus medical treatment. If the average annual event rate in the medical intervention arm is greater than 2.1 or less than .2 compared to .9 in those procedural arms. Now we know from CREST-1 that they did achieve and average annual event rate of .9 with endocardectomy

but not with stenting. The risk there was about twice as high at 1.6. And its highly likely that they will get an annual event rate in the medical intervetion arm within that range. So that means that the overall role

CREST is most likely to show that stenting causes harm and endocardrectomy knows significant difference with the respect to medical intervention on its own. In other words no procedural indication because if stenting is more harmful we won't do it. And if endocardectomy adds no benefit we won't do it.

The same response for ESCT-2 because like CREST-2 its randomizing average surgical risk patients. No stroke risk stratification before recruitment. Not pre-powered for high stroke risk markers that we have been talking about. ACTRIS has the best chance of finding a procedural role

in asystematic carotid stenosis because they are doing stroke restratification before recruitment. Using embolize detection, errands of impaired to cerebral vascular reserve, errands of intraplaque hemorrhage on MRI

and errands of rapid and severe stenosis progression. But the outcome of this will depend on how the data is analyzed. For example these markers be tested separtly or combined. We already know that markers individually lack specificity. And at the moment the trail does appear to underpowered

with the total of only 700 total patients expected. Mean while TCAR is being accessed only in registries plus or minus input in CREST-2. So it appears we have absent or underpowered comparisons with current medical intervention.

So a clinical indication is unlikely to be established with the current research that is planned. Actually procedural trails are premature when it comes to asystametic cartonid stenosis. What we should be doing is first defining current optimal medical treatment.

Measuring its impact. Risk stratifying people. Using procedural trials only if we find a sub group with an ipsilateral stroke rate that is high enough despite current optimal medical treatment. So if anyone would like to help on this path.

Please speak to me afterwards.

- Good morning. It's a pleasure to be here today and I wanted to let you know that a lot of this work that was being done earlier were really driven by physician need. As you can see, the trial as well as the EXCEL registry is finally on the way, so it's very exciting.

I'm not going to spend a lot of time on this but everybody knows the primary predictor of EVAR failure is really short necks and angulated necks. The first generations have been pretty good but they were really not intended for this type of anatomy. We see a lot of patients with really distorted anatomy

but they still have a relatively lengthy or 10 mm neck. In fact, about 80% of the EVARs treated in the United States have at least a 10 mm proximal neck. They may not be of the highest quality but they're there. So, how could be achieve better results? Basically we need to use every millimeter

of this landing zone, so that we can use the 10 mm neck to its fullest advantage and I believe when you do that, the results are fairly comparable to doing any type of above renal repair, like a fenestrated or branch graft. The stabilization of the device

during delivery is absolutely crucial. So essentially what you want to do is have a device that is able to utilize every neck angle and every millimeter of that available neck. And we know that 80% of all the patients, do have that neck. So, the new conformable endovascular device

has been around for the last five years or so but recently went into trial in December of last year. It's very different proximally than the current EXCLUDER in that the fixation system is single and it has a series of nested stents very similar to a conformable C-TAC device.

As you can see, this allows the device to conform to the anatomy, but not only that you're able to adjust the device inside too and that's actually Frank Veith's terminology, is that you're able to adjust this so that you can inch it up and utilize the entire neck.

16 French, proximal fixation, trunk length's a little bit longer than the current EXCLUDER at 5.5 to 6.5. This allows further treatment in the future going forward if you need to do a fenestrated device or branch graft device above it.

This device was designed to conform up to 90 degree angles and it's designed to seal at 10 mm necks. And, the most important aspect of it is, you're able to reposition the device once you deploy it. The mechanism is really one of being able to angle the device with a steering system

before the deployment and also afterwards and also be able to restrain the device up and down. Another major difference is that it has a 30% restraining secondary sleeve just like a ZFEN device so you're able to move this device up and down the angulated neck

and I'll show that with a case. The clinical trial in the U.S. began in December of last year and so far, I'll show you the update but unfortunately the FDA disallows us to give you any data. I can give you some of the demographics but I'll show you

that the preliminary results look excellent. The goal is to implant 80 patients in the short arm which is complete and 110 patients in the high neck arm is partially complete at almost 30 patients. The trial update objective is as outlined, there are 48 U.S. sites

and the current study enrollment is 106 patients, the short neck arm again I said is complete. Primary safety endpoints, not unlike any other device. Primary effectiveness endpoints, again freedom from all of these aspects. The first device was in 2017,

this was a relatively straightforward patient. The device performed well, this is a six month follow-up. The device had no migration issues, confirmed beautifully. But this is not really what the device was designed for. So, I'm going to give you a case of a patient that was enrolled in the high risk arm.

This patient had an 8.5 cm aneurism, 82 degree angulation, 11 mm proximal neck, turned down for EVAR or fenestrated at two other institutions in the New York City area and basically came for a third opinion as most New Yorkers do.

The aneurism looks like this and it's kind of a very angulated proximal neck with extremely torturous iliacs. This is the case that we did. You can see the device being configured here with the steering wire and when you do this,

you can see the device being able to be easily moved proximally and distally and the next portion of the video shows that steering wire kind of implanting the device into the lesser curve. - [Moderator] The device is deconstrained right? - Yes.

You can restrain it and it's a combination of being able to restrain it and open it which allows you the flexibility and as you can see with this maneuver, the device looks like it's perfectly opposed but in fact, the posterior aspect did not oppose very well.

So, we adjusted it further by increasing the posterior coverage and this is the post-op and we got a seal. There was no ballooning. This device, the ballooning is optional. So, the results have been excellent so far

with the highly angulated neck arm and we'll only see, there's only 30 patients so far but the results have been excellent so far. - [Panel Member] Rob and for you and for also Mark who presented that last case last week. When you deploy this device

it seems that you have a stiff wire, you're almost fighting the very advantage you're proposing. Do you ever consider swapping out for a floppier wire so you can then really get the native anatomy configuration? Because now that fusion image is presumably the pre-op fusion without the stiff wire.

So, I just wondered whether there's any value to that. - That's a great question. In fact, if you look at this video again, not this one but, let me see, this one, there's no wire, that the tip of the Amplatz wire is right at the tip of the device.

So that device is almost unsupported at this level, so you're able to freely flex that device back and forth without the constraints of a stiff wire. - [Panel Member] Is that your personal style or is that something that's part of it. - It's actually a recommended

and the part of the deployment process is to bring the floppy wire. So, you can use like a Glidewire Advantage or an Amplatz Super Stiff or whatever wire you like to use but it has to have a very floppy unsupported section in the proximal segments

to be able to get this kind of maneuverability. - [Moderator] So for the panel who've used this device, with all this manipulation of the proximal neck and especially in a diseased neck, is there any evidence of embolization of thrombus into the renals or distally?

- [Panel Member] Of course there is the potential for that but we haven't seen it yet and I think that the FDA IDE Trial and the registry will address that. I think that you should be careful. If there is a lot of neural thrombus in that neck

then this manipulation could be a potential risk. Actually what you're doing is, it's not that easy to get it into position in just one angulation. Sometimes you have to angulate, push it a little bit, restrain it again and reposition it to come in the perfect position,

especially for high angulation. - Yes. There's definitely a learning curve here but the learning curve actually can be achieved with just a couple of cases to be able to see how the device behaves

in the human anatomy.

- Thank you very much, and thanks Dr. Veith for the invitation back this year. So, the head of our growing ACO at University of North Carolina came to me the other day, actually it was a few months ago and said, "PAD patients, they're expensive And you know, we don't know why but eventually you

guys are going to need to figure this out and get more value in the care for these patients. You're way down the list after hip replacements and stemmies, but someday, we're going to come to you and ask you to give us better value for the care you're doing." So we're going to have to avoid multiple readmissions,

multiple procedures and failed procedures in these patients and a premium is going to be placed on decision making. The status quo that we have now of endovascular first and again and again, and if it fails we can always move on to bypass is probably not going to fly in

a value based world. So this is typical critical limb ischemia case in our health care system and the one good thing about epic that I can find is that I can now see what happens at all the hospitals in our system. And this patient, a pretty typical heel ulcer, low

ABI patient, was seen at least three hospitals in our system had procedures done by a multitude of interventionalists, including cardiologists, vascular surgeons, and others. And for some reason, it's not advancing. (clicking)

- [Woman] One second. - Okay, thank you. So you can see all these different procedures that were done: PTA/stenting, lysis, SFA extensions, toe amputations, and eventually went on that within four years this patient ended up having a BKA after

12 different procedures. Next slide please, and next one. (clicking) Next. And so the choices for CLI patients are complex. Severity of symptoms, depth, complexity of wound,

and the key question is, will this wound be able to heal without revascularization procedures? And you can see the wound on the left is far different from the one on the right. You can see that wound even though the patient may have a hemodynamic criteria of limb ischemia is not a

critical ischemic wound. Next slide. Other key considerations include patient's suitability and risk for revascularization and should we be discussing life expectancy with these patients who we know have a very limited life expectancy?

Next slide. In some of the studies of stem cell therapies, the amputation rate in CLI patients is not as high as expected at less than 25% in one of these studies. Next slide. So at UNC, we studied a large series of patients

with CLI that did not undergo revascularization. Next slide. And these are patients with an ABI of less than 0.5 or a toe pressure of less than 50. Next slide. And these were the results.

If you look by toe pressure, those who had a toe pressure of 30 to 50 had actually a low incidence of limb loss. 82% still had the leg without revascularization at three years, now if they had a very low toe pressure less than 10, yes, the rate of limb loss was much higher. Next slide.

Conversely, patient survival is very poor in this group. 44% at three years in all, and only about two-thirds live for one year. Next slide. So we really need to get a better method of determining who really needs revascularization, who's not going to

live long enough to benefit from it. So the WIFI criteria, which were developed by Joan Mills, David Armstrong, and others and subsequently validated, next slide. Can help predict which patients will do well without revascularization.

I highly recommend using this to predict outcomes in this group of patients. Next slide. Next slide. So, in summary when is non-interventional care a good choice?

Toe pressures that are low but not that bad if it's greater than 20 or so, most of the time you're going to be able to get that wound to heal. If it's a less extensive wound and if it actually looks like the capillary supply is reasonably good even though patient has low toe or ABI pressures,

you can probably get it to heal without surgery. Also if there's a high risk of procedural care or early mortality. Is it actually less expensive? We don't know yet and it depends what you use to take care of the patients.

Next slide. And then finally, we've got to really do a better job at thinking about these patients like cancer patients. The patient has end stage renal disease and CHF and is unlikely to live for a year, but we really want to be doing three or four procedures on that patient before they die.

Thank you very much.

- Good afternoon to everybody, this is my disclosure. Now our center we have some experience on critical hand ischemia in the last 20 years. We have published some papers, but despite the treatment of everyday, of food ischemia including hand ischemia is not so common. We had a maximum of 200 critical ischemic patients

the majority of them were patient with hemodialysis, then other patients with Buerger's, thoracic outlet syndrome, etcetera. And especially on hemodialysis patients, we concentrate on forearms because we have collected 132 critical ischemic hands.

And essentially, we can divide the pathophysiology of this ischemic. Three causes, first is that the big artery disease of the humeral and below the elbow arteries. The second cause is the small artery disease

of the hand and finger artery. And the third cause is the presence of an arterial fistula. But you can see, that in active ipsillateral arteriovenous fistula was present only 42% of these patients. And the vast majority of the patients

who had critical hand ischemia, there were more concomitant causes to obtain critical hand ischemia. What can we do in these types of patients? First, angioplasty. I want to present you this 50 years old male

with diabetes type 1 on hemodialysis, with previous history of two failed arteriovenous fistula for hemodialysis. The first one was in occluded proximal termino-lateral radiocephalic arteriovenous fistula. So, the radial artery is occluded.

The second one was in the distal latero-terminal arteriovenous fistula, still open but not functioning for hemodialysis. Then, we have a cause of critical hand ischemia, which is the occlusion of the ulnar artery. What to do in a patient like this?

First of all, we have treated this long occlusion of the ulnar artery with drug-coated ballooning. The second was treatment of this field, but still open arteriovenous fistula, embolized with coils. And this is the final result,

you can see how blood flow is going in this huge superficial palmar arch with complete resolution of the ischemia. And the patient obviously healed. The second thing we can do, but on very rarely is a bypass. So, this a patient with multiple gangrene amputations.

So, he came to our cath lab with an indication to the amputation of the hand. The radial artery is totally occluded, it's occluded here, the ulnar artery is totally occluded. I tried to open the radial artery, but I understood that in the past someone has done

a termino-terminal radio-cephalic arteriovenous fistula. So after cutting, the two ends of the radial artery was separated. So, we decided to do a bypass, I think that is one of the shortest bypass in the world. Generally, I'm not a vascular surgeon

but generally vascular surgeons fight for the longest bypass and not for the shortest one. I don't know if there is some race somewhere. The patient was obviously able to heal completely. Thoracic sympathectomy. I have not considered this option in the past,

but this was a patient that was very important for me. 47 years old female, multiple myeloma with amyloidosis. Everything was occluded, I was never able to see a vessel in the fingers. The first time I made this angioplasty,

I was very happy because the patient was happy, no more pain. We were able to amputate this finger. Everything was open after three months. But in the subsequent year, the situation was traumatic. Every four or five months,

every artery was totally occluded. So, I repeated a lot of angioplasty, lot of amputations. At the end it was impossible to continue. After four years, I decided to do something, or an amputation at the end. We tried to do endoscopic thoracic sympathectomy.

There is a very few number of this, or little to regard in this type of approach. But infected, no more pain, healing. And after six years, the patient is still completely asymptomatic. Unbelievable.

And finally, the renal transplant. 36 years old female, type one diabetes, hemodialysis. It was in 2009, I was absolutely embarrassed that I tried to do something in the limbs, inferior limbs in the hand.

Everything was calcified. At the end, we continued with fingers amputation, a Chopart amputation on one side and below the knee major amputation. Despite this dramatic clinical stage, she got a double kidney and pancreas transplant on 2010.

And then, she healed completely. Today she is 45 years old, this summer walking in the mountain. She sent to me a message, "the new leg prostheses are formidable". She's driving a car, totally independent,

active life, working. So, the transplant was able to stop this calcification, this small artery disease which was devastating. So, patients with critical high ischemia have different pathophysiology and different underlying diseases.

Don't give up and try to find for everyone the proper solution. Thank you very much for your attention.

Thank you very much, as I'm tiny and small, therefore I am fancy of small tools, just kidding. Dissection, this is the primary mechanism of angioplasty, and we know right now that lesions with dissections have a TLR rate 3.5 times higher than lesions without dissections and the current tools for dissection repair are stents, they have limitations.

Especially for below the knee, when it comes to dissection repair, I guess we all think we should leave minimal metal behind, we should minimize the vessel wall inflammation, it's not about how much metal, you want to leave behind, but I guess the issue is if you leave a lot of metal behind,

we have a higher degree of inflammation. On the other hand, we also want to maintain the normal vessel biomechanics and also preserve anything there for future treatment options. One device, something to help us with that is the Tack Endovascular System,

the Tack Implant it's adaptive sizing, so it adapts to tapering diameter of the vessels from 1.5 to 4.5mm. It's very good visible because it has nitinol with gold markers for visibility on both edges of the Tack, and it's a 6mm implant

when it's deployed. The delivery system is a four French over .014 guide wire system, and four implants are pre-loaded on a single catheter. I'll throw this out that these Tacks are so tiny, you can really deploy them in a highly accurate way.

The TOBA below the knee study design, it was a prospective single-arm, multi-center study. Six sites in Europe and New Zealand, only in patients with Rutherford 4-5 and CLI patients and up to two tibial arteries could be treated with a length up to 15cm.

We had the usual endpoints, safety, device success and procedural success. Now I want just to go into the data we have created. It was really challenging patient cohort with complex lesions as this was a CLI cohort, so the mean age of the patients was higher than in

Claudicant cohort, it was nearly equal distribution of males and females and 80% of our patients were patients with diabetes. What's even more interesting is the lesion characteristics, the mean lesion length was 51.4mm, so we had around one-fifth of patients

with total occlusions, we had all kind of dissections, but more than 80% of dissections higher than grade B. We had really a broad anatomical distribution and we also had calcified patients. With regard to safety and performance, with regard to device success we achieved

a high device success of around 91%, and the procedural success around 97%. Primary safety at 30 days, we only had one re-intervention at 30 days, so this was very encouraging, no major amputation, no death. With regard to the long-term effect,

you have to have in mind, this is a CLI cohort, where we only treated patients with dissections after vessel prep. So, with that, and this was treatment, we had a 12 month patency of 78.4% at 12 months, and the primary assisted patency of 89%.

And once again the amputation free survival was encouraging with 84.5%, and freedom from clinical driven TLR 93.5%. There is the TOBA II BTK study ongoing, once again a single arm, multi-center prospective study once again, only with CLI patients,

up to 60 sites in US, Europe and New Zealand. And we will see, hopefully, these patients finish with enrollment soon, and then we can hopefully present this data within one of the next meetings, at the end of next year. So this is just one case study,

it was a 72 year old male, hypertension, hyperlipidemia, and coronary vascular intervention two years ago, no prior peripheral intervention, WIfI score 3, Rutherford 4, we did a 6 French antegrade access, he was on daily ASA and clopidogrel and he had IV heparin for the procedure.

You see a very nice in-flow vessels which didn't need any treatment, but you saw far below the knee arteries, we had deeper lesions smaller vessels and poor runoff, we did the PTA with a 2.5 120cm balloon with 90 second inflation up to 8 atmospheres. Once again another balloon, once again the same

inflation time and post PTA, with the use of magnification, I think this is one of the most important things, you would not see when you look at this picture, that there are dissections, but when you use multiple magnification, multiple angles, this is critical for identification of dissections.

And we see here two dissections, which would then, we are treating with, here you can see it with magnification, Then we're treating the dissections with the Tacks, just with three Tacks. And this was just the final result. When we did the full out procedure, and angiogram we did not

see any recurrence of the disease there. Just to conclude this Tack system is new therapy for dissection repair, first trials to enroll 100% dissected vessels, so this is not the vessels with no dissection after any kind of vessel repair or after TCP and it's precise vessel dissection

repair system, it leaves minimal metal behind, minimizes the vessel inflammation and maintains normal vessel biomechanics and so therefore also preserves the vessel for further treatment options. Thank you very much.

- (applause) - Thank you very much for this very nice presentation. Any questions? - So, we see dissections every time we balloon, but I think we see them more often in SFAs than in below the knee. - I agree, but I guess we are not used to look

at the dissections below the knee and we learned a lot from above the knee to below the knee, we did OCT and all the other issues, and I guess for below the knee it's very critical to use this magnification and look at dissections with multiple angles, and then you are also able

to see the dissections for below the knee, and I guess we underestimated dissections for below the knee, then there are the bonus structures, people are not lying quietly on the cath lab table, they are moving around, so there are a lot of issues with dissections for below the knee.

- I think, especially when we treat bifurcations, we can see a lot of dissections, which are difficult to treat, is it also possible to tack this? - Yes, we did it, you know, we did also bifurcation, whatever, I didn't show an example of that,

but in our experience of this below the knee study, we placed the Tacks everywhere, just to summarize that. - Very nice. - Could this device be considered for some form of recoil after DCBU incisions, possibly? - Yeah, but we did not investigate that,

yes, I think it could be a new study. It would be interesting to look at that. - Do you have any details with regard to the deformation of the stent in vertical two point lesion? We know that the normal stent you have in one that seems to be totally open, and if you perform the angiography,

and you see a compression of the stent, I suppose of this stent is not very high. - Yeah, I agree, but on the other hand we had patients, and this has all been shown in the TOBA II data already that we had there patients with heavy calcified lesions and we were only treating the dissections in these vessels

and the outcome was very good. This still for sure needs further analysis, in regard to the calcified lesions that we treated, but anyway, the outcome was good, maybe we'll have an update on that next month, with further analysis

- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.

Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen

and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol

at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.

If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.

But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,

We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.

You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.

That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month

we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with

Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,

One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,

the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,

straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,

according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy

If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy

and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.

Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.

So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.


- So, my talk now, is about treating with multiple agents and I think there is a lot of consensus here. We have multiple agents out there, you normally use liquid agents, and you combine it with some mechanical thing for flow modulation.

So you can use coils or plugs, but you never use something like particles. That's not really, in any way, worth while. And, I knew what my role is here. My role is I'm always here as a counter-part to all these alcohol things, and we will discuss it later.

We have, and I just want to make one point here. You have to use this thing, this Onyx, or Squid, or PHIL- or whatever it is. You have to actively inject it, and you have to know the technique, and you have to do it like pressure cooker or plug and push technique, otherwise it won't work.

Otherwise, you will make things worse. So, just show me some failed cases where you used the plug and push techniques. Don't show me cases where you did it wrongly. Of course, that doesn't prove anything. Um, and I think, well you know all of this about

the plug and push technique, here, and I want to go too much into the details. I just want to show you two examples here, and this ght-sided, it's a dominantly venous thing,

it's something that we really like to treat because we'll cure it. There is definitely, regardless with which technique you do, you occlude the vein- you will cure the patient. But, the patient was totally Asymptomatic at the time. So I decided, we wait, he's asymptomatic.

Even if it's something we can do, you mustn't do everything. And, that's interesting because this was 2007, and this is how it looked like in April this year. So, 11 year later, you can see a huge... oh we'll have to go back because it's interesting. You see it, the same patient, after 11 years,

and this is something that is speaking for your hypothesis. That, is an acquired thing, because he's quite old. He's like 40ish/50ish this patient. And he is for us, for an AVM patient, it's brutally old. I mean, I'm really thinking about 'should I treat him?'. (Audience laughs)

Yeah, you know, and this is after 11 years, the sort of venous flow-related aneurysm, it really dilated, and it not only dilated, the venous outflow dilated as well. And, this is how it looked like, here at the perineum pod. You can see, he developed some draining veins

under pressure here at the perineum. So, this is something you have to treat now. I think we all agree, and, my topic here is to do it in the mixture, you can see of course, this is a predominantly venous AVM. Here is the one venous outflow, and the other venous outflow

is up there, it's fed by multiple feeders from the right iliac and of course, at this stage, even from the left internal iliac artery. This is one venous drainage, and this is the other venous drainage. First of all, you occlude the venous drainage.

Because, I don't want to fill this giant aneurysm with coils. You could've done it, and it would be obviously successful. So this is an occlusion of the distal part, with coils, and the proximal venous outflow occluded with an Amplatzer Vascular plug, and this is retrograde

transvenously injection of the venous pouch. So, there was almost no outflow, but there was a little bit left. So, you have to go for it, because otherwise, it will be recanalized. So then, I injected from the transarterial,

so, this is why I have to call about mixed agents. So, we put in an AVP, we put in plugs. And this is some, in this case, squid, in into the venous pouch, and that's at the end.

That's the result in one session. First, block the venous outflow, and then push enough material in that it clots, and its done. So, you don't need to use any ethanol in these cases. You could just do it, just with coils,

but you'd need hundreds. I prefer to do it with some coils, or a plug into the venous outflow. Then I'd push some Onyx into the venous cast, it thrombosis, and it's done, and it's very safe. This is another mixed method,

this is really a failed Onyx case. And, I call this a failed Onyx case, because its really properly done. It's not just some arteries filled with Onyx, but you see some residual like capillary shunts there. And, if you have this small vessel type, or type 4 AVM,

you can never cure it with Onyx alone. Or, I'm not even doing it. This is an ethanol case, you can just kill it, and with this 50/50 mixture, this is very helpful. And, what I do in these, formally type three b, with (mumbles).

I treat them with the safest way I know, with a polymerizing agent, and at the end, if it's necessary, you have these (undistinguishable), you add some ethanol injections, I call that finishing, and then it's done as well. So, at the end, and this is the most important slide here.

We do have different agents, and sometimes we have to mix them. And, ethanol is not everything. A type one, direct connection, whatever classification system you use, a type one, a direct connection,

you can use any mechanical things, and you will cure it. A dominant venous outflow thing, you have to occlude the venous side, and you have to occlude it as close to the arteriovenous connections, or whatever you call it, as you can, and you will be successful.

And, from my point of view, I never use ethanol in these cases, because I think it's dangerous. But anyway, you have to occlude the veins, and in the type three ones, you have to use ethanol in some cases, I call that finishing, before I've done something safer.

And, maybe, we have something more like the MEK1 Inhibitors, that's really something I hope that will be helpful for all of us. And, of course, if you use the wrong technique, and if you use Onyx like glue, you will make things worse. Thanks for your attention.

(Audience claps) - [Audience member One] I just wanted to make one comment, when you talk about ethanol, using it as finishing, I would sort of, think that more as the start of the case. In that, you're doing all of these other things, which I do too, to shut down flow.

What you are doing is occupying space within the venous side of things, what you are doing it basically maximizing the concentration of ethanol to where at's the definitive part of the therapy, and that everything you're doing

up to that point... Like, I mean, granted some of them you're curing without it. But, I mean, when you're giving that ethanol then, I've had a number of cases where you're sort of filling that type two- B Nitus or type three situation, what you then are actually enveloping that with the ethanol,

it's actually going to where it's exactly meant to go, and that's the critical manoeuvre. - (Lecturer) That would be true, if the only cases where it was successful were with a mixture. - [Audience Member] Mhm. - But this is for just for maybe 30% of the patients.

- Well, I guess what I'm trying to say is if, that up to that point on those cases though, it seems that the ethanol is the thing that's probably finishing the job. I mean, help me out here Wayne. (Laughter)

- [Wayne] We will have that discussion later. We will have that discussion later. - [Audience Member two] (mumbling) Can't we stick to a specification lets say (mumbles), not because I like it so much, but type two b, three a, three b, if we throw in some other specifications then

we can (mumbles). - [Audience Member One] But then, I just have to say, please publish it. Because you can't look up everywhere, there is no publication, so if you publish it I could use it.

- Few aspects of vascular surgery are more controversial than the management of neurogenic TOS as you heard earlier from Dr. Illig. I will propose that recurrent neurogenic TOS and persistent neurogenic TOS are even more of a challenge to deal with. Persistent neurogenic TOS

occurs in 10 to 15% of patients, and it's really the individual who fails to show any improvement following decompression. Recurrent, 15 to 30% of individuals who have some degree of partial or complete relief after the initial decompression.

This may be insidious or acute, and most often occurs somewhere within a two-year time frame. It could be a missed original diagnosis. Or it may be a secondary insult, a new stretch injury to the plexus,

incomplete rib resection, ectopic bands, scar tissue formation around the plexus, or pec minor syndrome. Pec minor syndrome is a frequent cause of recurrent and/or persistent neurogenic symptoms.

Its co-existence is over 50% of patients with neurogenic TOS. Sanders recognized in 2003 that pec minor causes the majority of recurrent neurogenic TOS symptoms. What is it?

Well the pec minor originates in the second, third, fourth, and fifth ribs, inserting on the coracoid process, which is part of the scapula. Muscle hypertrophy, spasm, and fibrosis will constrict those structures underneath,

which would be the axial artery vein and posterior to that will be your plexus. This was first described in '45 by Wright. Lord and Stone did five decompressions for what they defined as "hyperabduction syndrome." It was lost at some point,

rediscovered by Thomas then Doctor Sanders in 2004, who studied it prolifically, defined it as a sub-set of neurogenic TOS. There's a plethora of literature in this present day and age supporting pec minor syndrome.

Etiology: majority of people have trauma, most often in motor vehicle accident with a whiplash type of injury. Repetitive shoulder strain and spontaneous events can occur, inducing hyper-induction of the shoulder. Clinical symptoms are similar

between neurogenic and pec minor: weakness, pain in the neck, clavicular, anterior chest wall, trapezius region and then paresthesias, most often in the ulnar distribution. Isolated pec minor does happen. Typically these individuals

have fewer head and neck symptoms. And you'll notice the intensity of symptoms are significantly less. On your examination it's your standard TOS examination. Unfortunately provocative maneuvers are not as rewarding. You'll find that with isolated pec minor,

these individuals have fewer head and neck symptoms, typically with rotation, tilt, scalene compression. There's nothing really to see. But they do have point tenderness over the infraclavicular region, directly on top of the pec minor.

And you'll notice that with contraction of the pec major, the symptoms will be minimized. Sanders noted the three most common findings with pec minor syndrome are: tenderness to palpation in the subcoracoid space, ULTT and EAST.

You'll notice that in some of these patients who do have persistent or recurrent symptoms, quite likely, pec minor tenderness was missed in the original diagnosis. A thorough history and physical certainly is beneficial. Unfortunately there's no test or exam

that is pathognomonic for this. Appropriate imaging should be completed to rule out other pathology. And then a selective pec minor muscle block not a plexus block, but a minor block, a muscle minor block,

should be considered. EMG testing has mixed results. When you look at your muscle block, typically done with a baseline examination, you'll then inject lidocaine 4 cc with ultrasound guidance 45 degree angle to avoid dropping in the lung.

Inject in a two to three centimeter area. And what you're looking for is resolution of your tenderness, improvement of your symptoms, at rest and with provocative maneuvers. For those ones who have an unsuccessful block

you may want to consider repeating it, or consider performing a scalene block. For those individuals that do have pec minor syndrome, conservative therapy, which is range-of-motion and stretching, tends to work well, 50% resolution in eight-week window.

For those individuals who fail pec minor tenotomy, low-risk out-patient procedure, relatively quick recovery time. A variety of approaches have been defined in the literature. Here's one approach with a patient

previously undergoing neurogenic decompression with a superclavicular approach, this is the anterior axillary approach, with a two to three centimeter vertical incision in the anterior axillary line. The subcutaneous divide at the pec fascia

is open and the muscle is elevated with a Deaver retractor. You'll trace this up to the coracoid process, and with that being the case, you'll transect two to three centimeters of the pectoralis minor muscle,

and then release any fascial bands or accessory muscle around the neurovascular bundle. These patients have done well. With isolated tenotomy you'll see that there's an improvement anywhere from 90 to 100%. However, you need to take into consideration

a good number of these people have combined neurogenic TOS and pec minor syndrome. And with that being the case, the success may be a little bit less. So in summary, pec minor syndrome is a frequent cause

of recurrent or persistent neurogenic TOS. Isolated pec minor tends to have fewer head and neck symptoms. Diagnosis is aided with a block. And tenotomy appears to be safe and effective. Thank you.

- Thank you Mr. Chairman, thank you Dr. Veith for the kind invitation. I have no disclosures relevant to this particular lecture. But I think we ought to talk about what critical limb ischemia is. Obviously it's what we call Rutherford four through six. It's most commonly associated with multi-level disease.

About 1/3 or so of the cases are infrapopliteal only, mostly in diabetic patients. There's very poor overall life expectancies. We look at this group of patients in multiple studies, it ranges somewhere between three and four years of average life expectancy,

and there are substantial differences in outcomes within critical limb ischemia, with far worse outcomes in those with poor overall health, advanced stage presentation, or poor runoff at the level of the foot. Now, what is the rationale for endovascular therapy

in critical limb ischemia? Well first, patients are often old and infirmed, and many aren't really considered candidates for open surgery because of poor overall health. Surgery requires inflow, usually attainable. Outflow, not always so easy.

A conduit, which typically should be vein, if we want durable results, and an incision. Active infection is problematic, as there may be graft infection or sepsis. Extensive surgical scarring may compromise future rescue intervention,

and this is a progressive disease, that often requires additional treatment. Now, there have been multiple publications, and this is just a recent one, which came out in the Journal of the American Heart Association. It's a multidisciplinary,

retrospective analysis of Medicare data in people who had presented with critical limb ischemia. This is not perspective, it's not sited in many areas, but I ask you to look at this conclusion. It was there was lower major amputation rates following endovascular therapy.

Both surgery and endovascular did better than primary amputation, in terms of outcomes. But again, this is not a perfect study. Now, we have many publications which have shown very good limb salvage rates in patients using interventions.

Here we see this from Faglia, again showing very low major amputation rates. This from Sam Ahn, once again, very good limb salvage rates. But in truth, we have only one randomized, control trial, level one data, comparing intervention with surgery. And that was the BASIL Trial.

The BASIL Trial is an old trial, it's criticized, appropriately, because the only treatment used was sub-intimal angioplasty. And with sub-intimal angioplasty, often, the sub-intimal tract in crossing is far greater than the area of total occlusion,

resulting in much longer treatment zones. In addition, this trial did not allow some of the new and better treatments that are now available for having better patency to be performed. Nonetheless, in the BASIL Trial, despite very primitive treatment,

that being only sub-intimal angioplasty, we can see that one year out, and in fact out to two years, angioplasty and surgery were relatively equal in terms of limb salvage. At five years, there seemed to be a major advantage to surgery,

in terms of both quality of life, and in terms of less need for reintervention. So then we have to ask, what has changed since BASIL? Well now we have far better crossing. We have re-entry tools that stop us from having to go 10 centimeters

beyond the area of occlusion to get back in. Dedicated crossing tools, better wires, retrograde access, this is important, we have markedly improved patency, with drug coated balloons, drug-eluting stents, wire interwoven nitinol stents, and stent grafts, which have shown in the SFA all of these things,

better SFA patency, and if indeed, we can maintain SFA patency in multi-level disease, often, if there's recurrence, the patients do well. We also have improved Tibial patency in the proximal tibial vessels. However, we do not yet have a great endovascular solution

for long distal tibial vessel occlusions, and that's just the truth. I have to go back here, one, but we have better medical therapy too. As we look at PCSK9 inhibitors, in the GLAGOV Trial, we see in other parts of the body,

a 30% reduction in atherosclerotic volume out at 70 weeks, indeed will this change what we're doing. This has launched this decade of endovascular interventions. So what about this taking away surgical options? BASIL, I think, doesn't apply because the sections went far beyond where they should.

That's bad technique. Stenting across the common femoral or patent popliteal, in my opinion, bad technique. Distal embolization, we've not done enough preparation. I will also caution that sometimes, surgery has bad outcomes as well.

So, the rationale is we really don't want to perform anything that hurts a patient. Entire procedures performed via a sheath, remote from the site, there's less pain, shorter recovery, no extensive scar, and the argument that intervention

takes away surgical options, I think is no longer so valid. Bad intervention or bad surgery, take away options. Where is distal bypass indicated? In large non-healing ulcers in patients with good life expectancy, good quality vein, good outflow, and excellent surgical expertise.

Densely calcified long segment infrapopliteal disease, or disease from the common femoral all the way to the ankle. I think these clearly are going to do better with surgery, certainly in today's world. But even these areas may change. If more effective tools solve the patency problems,

with long segment infrapopliteal disease, and there are trials now aiming at this, such as SAVAL, DCB trials, and Lithoplasty. I thank you for your attention.

- Okay, is thermal ablation obsolete? No. My disclosures. Are nontumescent ablation procedures ready to take over? This is an article in 2014 by Michael Sadek and myself. No in 2014, no in 2019, and no in 2020, and I predict no in 2023. That's about as far as I can go.

So every time I hear this, I scratch my head, "oh my God." So, there's similar arguments regarding open surgery versus minimally invasive surgery. We know that they're both needed, in terms of different particular incidences of pathology. Risk/benefits, insurance coverage?

So if we look at everything, does size matter? And I would submit to you that right now, in terms of the non-thermals, size does matter. So if we look at 12mm or less, I think that's where the sweet spot for non-thermals are. If we look at trials, clinical correlation of success

in acute thrombotic of lower extremity endovenous thermal ablation, the subset showed that there was no real differences between RF and laser. If we look at this prospective study, looking at 1470 laser and radiofrequency, again, no difference.

If we look at this study, no difference, it all works. So in this particular paper by Professor Davies and his group, he looked at certain things and his summary for this article was thermal treatment with RFA and EVLA is the mainstay of varicose vein treatment at present.

Both RFA and laser appeared to have similar efficacies. If we look at this trial that was a pivotal trial in terms of cyanoacrylate and RFA, there's no inferior with regard to efficacy, etc. If we look at a multi-center randomized controlled trial comparing radiofrequency and mechanical occlusion

chemically assisted ablation of varicose veins, again, pain secondary to truncal ablation is less painful with MOCA than RFA with similar short-term technical and quality of life and safety outcomes. If we look at this trial we heard earlier today of partial exposing of this, mechanochemical ablation

versus cyanoacrylate adhesive for the treatment of varicose veins, study protocol for a randomized controlled trial, there is really no difference across the board. Just when you thought new RFA devices are now coming out. We know we talked earlier about

RFA continuous and segmental, and just understand that if it was obsolete, why would they come out? So Kabnick the fortune teller, better known as Carnac, is thermal ablation obsolete? I would submit to you in my crystal ball,

between the times of 2018 and 2023, the answer is no. And then I got my ouija board out, because I didn't understand what I was thinking about, and really the ouija board went "no." So ladies and gentlemen, in conclusion, as of now and 2023, there is not one perfect modality for

venous ablation, each has their sweet spot. Thermal long track records and larger veins, perforator approval, with thermal. Non-thermal, no tumescent, perhaps a shorter procedure and nerve sparing. Recommendation, most of us agree, if you can only

afford one device, I would do thermal. My recommendation would be to have thermal and non-thermal. Thank you very much.

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