Create an account and get 3 free clips per day.
Chapters
MySpine cadaver case final discussion
MySpine cadaver case final discussion
2016anatomybonecadavercaudalcentimeterchapterlevelligamentMedactamidlineminiNASSnoindexpercstenosis
Moderately Hostile Necks (Conical, Angulated, Calcified And With Thrombus) Do Not Negatively Influence EVAR Outcomes With Newer Endografts (Endurant – Medtronic): 4-Year Results
Moderately Hostile Necks (Conical, Angulated, Calcified And With Thrombus) Do Not Negatively Influence EVAR Outcomes With Newer Endografts (Endurant – Medtronic): 4-Year Results
anatomiesanatomyaneurysmangulatedangulationarteriescalcifiedchallengingconicaldifferencedurableendograftendograftsendoleakendoleaksEndurant endograft systemengageevarhostileiliacimplantinstructionsMedtronicmidtermmoderatelyneckneckspatientsperformsproximalregistryrupturesecondarystandardtherapeuticthrombotictypeultimateversus
Treatment Of Complex Central Venous Occlusions: Tips And Tricks To Improve Outcomes And Reduce Complications
Treatment Of Complex Central Venous Occlusions: Tips And Tricks To Improve Outcomes And Reduce Complications
alignedamplatzanatomyAtriumbasicBoston ScientificcardiaccentimetercentralcomplexdeployEliquis by Bristol-Myers SquibbExtensive central venous occlusionfrequencyguidewireicastimagelungoccludedocclusionpatientperformRadiofrequency wire for recanalization of central venous occlusionrecanalizationrecanalizeRF wire technique with image fusionrotationsegmentsnarestenttechniquetherapeuticunderstandveinvenogramvenousvesselswire
Duplex Ultrasound As An Imaging Modality To Replace Angiography And Fluoroscopy In EVAR And Lower Extremity Interventions: Advantages And Limitations
Duplex Ultrasound As An Imaging Modality To Replace Angiography And Fluoroscopy In EVAR And Lower Extremity Interventions: Advantages And Limitations
angiographyarteryballoonbowelchronicclinicalcontrastcreatininedilatationduplexdynamicendovascularevarformationguidewirehabitusiliacinsufficiencypatientpatientspoplitealpublishedrecanalisationreductionrenalstenosisstenoticstentstentstasctreating
A Novel Front-Cutting Atherectomy Device With Plaque Fragment Aspiration: How Does It Work And Value In Crossing CTOs And Lowering Plaque Burden
A Novel Front-Cutting Atherectomy Device With Plaque Fragment Aspiration: How Does It Work And Value In Crossing CTOs And Lowering Plaque Burden
accomplishedadequateamputationsatherectomycatheterclaudicationdeviceembolicembolizationfollowhybridHybrid AtherectomyimprovementischemialesionslimbpatientsPhillipsPhoenixPhoenix Atherectomy Systemproceduralrotationalrutherfordstenosistherapeuticunplannedutilizes
Vertebral Artery Dissections: Etiology, Diagnosis And How To Treat Them
Vertebral Artery Dissections: Etiology, Diagnosis And How To Treat Them
acceptableantegradeanteriorarteryaspirationasymptomaticbasicallybasilarbleedBothcerebellarcriticaldilatedissectiondissectionsendovascularEndovascular stententersexitsforamenintracraniallesionocclusionoriginostialpatientsposteriorresultretrogradesituationstenosisstentstentingsubclaviansubsequentlysurgicalsymptomaticthrombosisvertebralvertebral artery
DEBATE: Not So: Advantages And Limitations Of The Supraclavicular And Infraclavicular Approaches For Venous TOS: Which Approach And When But Never Transaxillary
DEBATE: Not So: Advantages And Limitations Of The Supraclavicular And Infraclavicular Approaches For Venous TOS: Which Approach And When But Never Transaxillary
angiogramangioplastyanterioranticoagulationapproachaxillaryballoonBalloon angioplasty/stentsBothcollateralscryocyanosisdecompressionduplexexposurefavorablyFirst Rib ResectionfollowincisionsinnominateintraoperativeinvolveslymphaticneurogenicobstructionographypatientpatientsPlan for Surgical TreatmentposteriorpostoperativereconstructionresectedresectionScalenectomystenosisstentstentssubclavianSubclavian Vein ThrombosissuccessfulswellingthrombolysisThrombolysis / Balloon Angioplastyunderwentveinvenogramvenous
New Concepts For Better Understanding Aortic Arch Pathology, Its Progression And Treatment
New Concepts For Better Understanding Aortic Arch Pathology, Its Progression And Treatment
anatomicallyanatomyangulationaorticarchascendingcohortconceptsdeterminingdissectionentryfocusingforceshematomaintramuralinvolvementleveloptimalorthogonalpatientsproximaltearTEVARtorquetypeVeithvelocityzone
The Risk Of Stroke In Asymptomatic Carotid Stenosis Patients On Good Medical Management Is So Low That All Should Be Treated Medically: Stratification Of Risk Is Of Little Value: Is Stenosis Or Plaque Progression A Reason To Treat Asymptomatic Patients With CEA Or CAS
The Risk Of Stroke In Asymptomatic Carotid Stenosis Patients On Good Medical Management Is So Low That All Should Be Treated Medically: Stratification Of Risk Is Of Little Value: Is Stenosis Or Plaque Progression A Reason To Treat Asymptomatic Patients With CEA Or CAS
asymptomaticatheroscleroticblindedcalcifiedcardiovascularcarotidlifestylelookedpatientsplaquepreventiveprogressionpublicationrevascriskstenosisstenoticstroketomographytransducerstreatmentultrasoundvolume
All This Buzz About TCAR Is Unnecessary: Transfemoral Access With Filters Or Flow Cessation (MoMa) Is Still The Best Way To Perform CAS In Most Patients Needing The Procedure
All This Buzz About TCAR Is Unnecessary: Transfemoral Access With Filters Or Flow Cessation (MoMa) Is Still The Best Way To Perform CAS In Most Patients Needing The Procedure
archarterycalcifiedcardiologistsCarotid StentingcentimetercomplicationcomplicationscoronaryembolicexcludingexperienceincisioninterventioninterventionalinterventionalistlesionpatientsperformingrationalrevascularizationRoad SaversurgicallyTCARTerumo interventional systemstherapeutictransfemoralvascular
COMPARE Pilot RCT: 1 Year Results Of A Randomized Comparison Of RANGER DCB vs. IN.PACT DCB In Complex SFA Lesions
COMPARE Pilot RCT: 1 Year Results Of A Randomized Comparison Of RANGER DCB vs. IN.PACT DCB In Complex SFA Lesions
bailoutballoonballoonsBoston ScientificcalcificationcentimeterclinicallycoatedcoatingsDCBDEBdosageendpointIN.PACT (MEDTRONIC)ischemialengthslesionlesionspaclitaxelpatencypatientspilotprimaryrandomizedrangeRangerscheinertstenosisstentingstratificationstratifystudytherapeutictreat
Operation
Operation "Grey Doc": Using Retired Vascular Surgeons To Train Residents
anatomycadavercentersclinicaldissectionendarterectomyendovascularfacultygrayinstrumentinstrumentsmedicalparticipatepreopproceduresresidentsreviewsimulationstudentssurgeonsurgicalsuturesuturingTherapeutic / Diagnostictrainingvascular
The Restenosis Rate After CAS Is Probably Higher Than After CEA In The RCTs: When Should Restenosis Be Treated Invasively
The Restenosis Rate After CAS Is Probably Higher Than After CEA In The RCTs: When Should Restenosis Be Treated Invasively
carotidclinicaldataduplexendarterectomyfreedomincidenceipsilateralkaplanlatemedicalmeierpeakprimaryproximalpublishedrandomizedrestenosisstenosissymptomsystolictherapytrialultrasoundvalidatedVeithvelocity
Technical Tips And Equipment For Pedal Access: Update On The Value Of The Vasostat Device To Aid Hemostasis After Tibial, Pedal And Radial Access
Technical Tips And Equipment For Pedal Access: Update On The Value Of The Vasostat Device To Aid Hemostasis After Tibial, Pedal And Radial Access
accessadoptionanatomicantegradeanteriorarterybloodbrachialcardiaccatheterizationcentimetercompressiveconcordantdevicedevicesdistalenvironmentevarextremityflowForge MedicalguidewirehemostasisHemostasis deviceHemostasis following catheterizationinflatedinterventionalischemiamultilevelocclusionpatientperfusionprecisepreservingpunctureradialratesrevascularizationrevascularizationsSeeCure Adhesive PadsheathterumoTerumo interventional systemsTEVARtherapeutictibialtitrateVasostat hemostasis device. TR BVeith
Standardized Aquatic Protocol For Phlebolymphedema Patients
Standardized Aquatic Protocol For Phlebolymphedema Patients
activatingactivationambulationanklecentimeterdataenvironmentinsidelowermusclepatientsphlebologypoolprotocolpublicationspecialistsstandardizedstandingstockingsvascularvenous
Celiac Compression Syndrome: Myth Or Reality: How To Diagnose It And Treat It
Celiac Compression Syndrome: Myth Or Reality: How To Diagnose It And Treat It
aortaarcuatearteryceliaccoexistingctasdenervationdividingepigastricexpirationfibersfollowupischemialaparoscopiclaparoscopyligamentmedianmesentericnervesneurogenicOpen repairpatientspostprandialsplanchnicstenosisstentTherapeutic / Diagnosticvelocities
Sandwich Graft Technique For Treating TAAAs: How To Make It Work Even In Urgent Or Ruptured Cases
Sandwich Graft Technique For Treating TAAAs: How To Make It Work Even In Urgent Or Ruptured Cases
a large juxtarenal aneurysmabdominalacuteaneurysmaneurysmsangiogramangioplastyaorticarteryaxillarycarotidcatheterizecatheterizedceliaccentimetercongestivedissectionembolizedendografterectilegraftgraftsiliacsivusleft carotid subclavian bypassleft subclavian artery embolizationlumenluminaloccludedparallelperformedperfusionreasonablerenalrenalssscansegmentstenosisstentssubclavianTEVARtherapeuticthoracicthoracoabdominalType B thoracic dissectionvesselsvisceralwich graft technique
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
angioplastyanteriorarteriographyarteryballoonclinicalcontralateralcorrelatedDESdopplerdrugdrug elutingDrug eluting stentdysfunctionelutingendovascularerectileevaluationHigh grade bilateral internal pudendal artery stenosisiliacimprovementinternalInternal pudendal artery stentingMedtronicmultifactorialpatientsPOBAprocedurepudendalResolutestenosisstentstentedstentingStenting with a drug-eluting stentsystolictherapeutictreatment
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
angioplastyanteriorarteriographyarteryballoonclinicalcontralateralcorrelatedDESdopplerdrugdrug elutingDrug eluting stentdysfunctionelutingendovascularerectileevaluationHigh grade bilateral internal pudendal artery stenosisiliacimprovementinternalInternal pudendal artery stentingMedtronicmultifactorialpatientsPOBAprocedurepudendalResolutestenosisstentstentedstentingStenting with a drug-eluting stentsystolictherapeutictreatment
In-stent Stenosis After Venous Stenting: Guide for Clinical Decisions
In-stent Stenosis After Venous Stenting: Guide for Clinical Decisions
anticoagulationAspirin by BayerbiopsiesbiopsycompressedcoumadinDialysisdiffusefibrinfreshintimalLovenox by Sanofi-AventismaterialorganizingpatientplavixrecanalizationResuming coumadinstenosisstentstentstherapeuticthrombusunderwentvenogramvenous
Moderately Hostile Necks (Conical, Angulated, Calcified And With Thrombus) Do Not Negatively Influence EVAR Outcomes With Newer Endografts (Endurant – Medtronic): 4-Year Results
Moderately Hostile Necks (Conical, Angulated, Calcified And With Thrombus) Do Not Negatively Influence EVAR Outcomes With Newer Endografts (Endurant – Medtronic): 4-Year Results
anatomiesanatomyaneurysmangulatedangulationarteriescalcifiedchallengingconicaldifferencedurableendograftendograftsendoleakendoleaksEndurant endograft systemengageevarhostileiliacimplantinstructionsMedtronicmidtermmoderatelyneckneckspatientsperformsproximalregistryrupturesecondarystandardtherapeuticthrombotictypeultimateversus
Advances For Endograft Treatment Of Type A Aortic Dissections: Why And How Are The Next Generation Endografts Better
Advances For Endograft Treatment Of Type A Aortic Dissections: Why And How Are The Next Generation Endografts Better
accommodateanatomicalaorticarcharteryascendingbiggestcenterlinecentimeterCook MedicaldetectdissectionendograftendograftsentityentryfeasibilityfeasiblegoreGore Tag (Gore Medical)graftinnominatelandinglocationmeasurementsoversizingpatientpatientspreoperativeproximalsizingstentStent graftstent graft systemTEVARtherapeutictypeZenith Alphazone
Simplifying Treatment Of ALI With The Use Of The Indigo Thrombectomy System: When Is Open Surgery Required
Simplifying Treatment Of ALI With The Use Of The Indigo Thrombectomy System: When Is Open Surgery Required
acuteadjunctiveadvanceafibALIangiographyangioplastyarcharterialAspiration SystemballooningcalibercathetercatheterschronicclotcutaneousembolectomyemboliembolicfavorablefogartyiliacipsilateralischemialevellyticsOpen SurgeryPenumbraPenumbra’s IndigopercutaneousperinealpoplitealremoveremovedrunoffsheathstenosissubacutesystemtechniquetherapeuticthrombectomyThrombectomy - XTRACT Techniquethrombithrombustibialtpa
Status Of The Global Vascular Guideline For The Treatment Of CLTI And The Global Limb Anatomic Staging System: How Will They Help
Status Of The Global Vascular Guideline For The Treatment Of CLTI And The Global Limb Anatomic Staging System: How Will They Help
anatomicanatomyarterybasedcalcificationcliniciancomplexityconsensusdiseaseendovascularextensivefailureglassglobalgradegradedgradesgroinintermediatelengthlimbocclusiononlinepatencypatientpedalpoplitealpreferredprimaryrestorationrevascularizationrevascularizesimplifiedstagestagesstagingstenosissystemtargettechnicaltreatmentvascular
ZILVER PASS RCT Comparing ZILVER PTX DES To PTFE Fempop Bypasses: For TASC C And D Lesions: Zilver PTX Is As Good Or Better At 2 Years
ZILVER PASS RCT Comparing ZILVER PTX DES To PTFE Fempop Bypasses: For TASC C And D Lesions: Zilver PTX Is As Good Or Better At 2 Years
armsbenefitbinarybypassbypassescentimeterclaudicantsclinicalcomparingcomplicationendovascularfemoropoplitealfreedomhypercholesterolemialesionocclusionspatencypatientsprimaryprostheticrandomizedrestenosisshorterstenosissurgicalsustainedtasctrialvascularversusviabahnzilver
DEBATE: Not So: If Careful Technique Is Used, Completion Duplex Or Angiography Control Is Unnecessary And May Be Misleading
DEBATE: Not So: If Careful Technique Is Used, Completion Duplex Or Angiography Control Is Unnecessary And May Be Misleading
aschercarotidCarotid endarterectomyclampcompletioncomplicationdiagnosticexternalexternal carotidimaginglesionlesionsneurologicalpostoperativeratesresidualstenosisstrokesurgeonstechnicalunnecessary
DEBATE: This Study Is Misleading Because Many Patients Benefit From An Open Revascularization First Policy And Are Harmed By An All Endo First Policy
DEBATE: This Study Is Misleading Because Many Patients Benefit From An Open Revascularization First Policy And Are Harmed By An All Endo First Policy
anatomicanatomybasedbasilbypasscomparedataendoendovascularfailedlimbpatientsPercutaneous vascular interventionpreviousregistriesseveritytherapeuticthreattissuetreatmentsvascularversus
Imaging Tools To Increase The Safety/Accuracy Of Endovascular Procedures And Reduce Radiation And Contrast Media
Imaging Tools To Increase The Safety/Accuracy Of Endovascular Procedures And Reduce Radiation And Contrast Media
anatomyangioplastyarterialBaylis MedicalcontrastCVOdefinediagnosticfusedfusiongraftguidewireiliacLeft CIA PTA using Vessel ASSISTocclusionoutlinepatientphasePowerWire RFprettyPTAradialsnarestenosisstentstentstotallyveinsVessel ASSIST (GE Healthcare) - Fusion Imagingvesselswire
Venous Issues in Thoracic Outlet Syndrome: Lysis, Venoplasty, First Rib Resection: Staged Or Same Setting
Venous Issues in Thoracic Outlet Syndrome: Lysis, Venoplasty, First Rib Resection: Staged Or Same Setting
admissionanatomicangiojetangioplastyanticoagulationBoston ScientificbrachialCatheter-directed thrombectomycatheterscenterschroniccolorcompressiondecompressiondocumentedembolizationendoextrinsichospitalizationhypercoagulableinadequatelysismaximaloccludedoccludingocclusionoutletpatencyPatentpatientspercutaneousperipheral thrombectomy systemPTAresectionsinglestenosisstentingsubclaviansurgicallysymptomsyndromesystemictherapeuticthoracicthrombolysisthrombosistreatmentunderwentveinveinsvenogramvenographyvenousVenous angioplasty never with a stent
Delayed vs. Early Intervention (CEA/CAS) In Patients With Carotid Stenosis And Recent Strokes: Patients Should Be Individualized: In What % Is The Stroke Not Due To The Carotid Lesion
Delayed vs. Early Intervention (CEA/CAS) In Patients With Carotid Stenosis And Recent Strokes: Patients Should Be Individualized: In What % Is The Stroke Not Due To The Carotid Lesion
arterycarotidcryptogenicdiagnosedendarterectomyentityintracranialmedicalminorneurologicalpatientsplaquerecurrentriskrisksstenosisstentingstrokessymptomatictherapytreatmenturgent
Styloid-Carotid Artery Syndrome Can Cause TIAs: What Is It: How Should It Be Diagnosed And Treated
Styloid-Carotid Artery Syndrome Can Cause TIAs: What Is It: How Should It Be Diagnosed And Treated
anastomosisanatomicallyangiogramanteriorarteryboneBone resectioncarotidcarotid arteryCarotid ReconstructionCEAcentimeterclassicalconditionEnd-to-End Anastomosisentityhyperplasiainternalinternal carotidkinkingneckoccludedpatientprocessresectedscanstenosisstentsurgeonssymptomssyndromeTherapeutic / Diagnostictriadvascularweakness
Transcript

way out in a short segment case. And then Have you used these in single level? Yeah. That's kind of one of the nice things. One thing is for sure that you need to have caudal level

fully exposed for the guide to sit down on the spinous process. You don't need to take down the interspinous ligament of the level below because the way they have guides manufactured is the caudal most level has a special configuration where

it doesn't require in the interspinous ligament of the level below it taken down. But you definitely need to have it exposed. So for example if you're really doing a mini midline case and you had this stenosis was at the interspace

you had a mini exposure for your level above. You got in the screws. You still need I'll call it another extra centimeter in order to fully expose the level below but kind of a small price to pay. What you don't need is an extra three

centimeters so that you can see all your landmarks. You know if you're coming right down on the pedicles. So you know if you got a cadaver with nice bone quality you can do all that with just k wires and do it perc mini-open. But if you don't have all that have guides is nice. For my

patients you can't see pedicles on an AP. You know they're old. They're highly spondylotic. There's bone everywhere but yet they're osteopenic. So if it were really a perc case and you had great pedicular anatomy then you know the relative value proposition of the

guides is different. But if you're missing all those things which I am in all my patients then it's kinda handy. Can it be used in an S1? No S1 guides. The spinous processes anatomy in S1 is too variable and they felt that they're unstable. They're being conservative

I know they can make them. Yeah I don't know if you caught that case I showed. It was a 3D spin with a tomogram and then some reconstructed images and 4 and 5 were with this technique and then

- [Dr. Verhagen] Good afternoon everyone, these are my disclosures. So, obviously proximal aneurysm neck still is the Achilles heel of EVAR. Essential for proper fixation and sealing and still the most frequently constraint for EVAR. And there's been many research reports

telling us that hostile proximal neck anatomy challenges a durable seal over time. The question that remains however is: When can standard EVAR be safely and durably performed in patients with hostile necks? And there's actually very few multi-center studies

reported results with sufficient patients numbers on outcomes on hostile neck anatomies. So, we took the ENGAGE Registry probably well known to most of you. It's a very large, multi-center, multi-country registry on the Endurant endograft.

And the objective of the study was to evaluate the midterm results in patients having challenging proximal neck anatomy treated with the Endurant. We took three subgroups, one was a conical neck defined as more than 20% difference

in diameter over the course of the neck. The angulated necks meaning over or under 60 degrees of angulation and the necks with either calcified or thrombotic material in it for more than 20% of the circumference.

And the hypothesis was that the Endurant performs as well in patients with moderately challenging necks as it does in patients with standard necks. So, if you look at the initial implant you can see that the deliveries and deployment success was the same in the three groups.

So, the group, this is the conical group and here's the angulation group and the calcified and thrombotic group. No differences there. Although, this is a .04 significance number meaning that it may be significantly worse in those patients

but if you actually look at the details of the patient it means that five out of seven patients that have problems that was due to calcium in the iliac arteries in the access arteries and on the neck. So, results in four years, migration,

main body migration no difference between the three groups. Type one a endoleak no difference between the three groups and a secondary procedure to correct type one endoleaks. No difference in those groups either. Conversion, basically one of the ultimate failures,

again, no difference in the groups. But if you look at the ultimate failure a rupture there seems to be a little bit more in the ones with calcium and thrombus. But again, it's about four patients only and two of those four actually had

type three endoleaks as a cause of their rupture and had nothing to do with the neck. So, basically it performs as well in standard anatomy as moderately challenging anatomy. So, we thought maybe there's more and more interesting stuff if we

compare on- versus off-label use again using the ENGAGE Registry. So, considering that implanting endografts outside IFU's actually not uncommon at all in everyone's practice it seems to be important to know how these patients actually do.

So, again a on- versus off-label analysis using the ENGAGE Registry. This is a outlook on what kind of patients are actually included in the ENGAGE Registry. And there's 17% of them outside instructions for use, that's over 200 patients.

And 80% of these patients are outside instructions for use because of a proximal neck issue. So, that's about 180 patients. That's quite a big group to study. Again, initial implant no difference between on-label and off-label as expected.

Then at four years migration no difference. Rupture no difference. Conversion and open surgery no difference. It looks as if it's okay to do so but it isn't. Because if you look at type one a endoleaks for the whole group there's a freedom from

type one a endoleaks off-, 96% in four years. But if you break that down in on- versus off-label you see a big difference. There's actually three times as many patients run into trouble if you use outside instructions for use.

And, obviously, if you look at the whole group there's the same amount of secondary procedures. But if you look at type one a endoleak re-interventions only again there's twice as many re-interventions for that cause and that's also significant.

So, in conclusion challenging proximal neck characteristics have historically impacted long-term durability of EVAR. There's only a few studies of significant sample size that can analyze reliably the performance of contemporary endografts in real-world patients. Insights from this ENGAGE Registry demonstrates

that durable performance of Endurant in standard as well as moderately hostile anatomies through four years is actually quite good. But off-label use shows more type one endoleaks and more secondary interventions to correct them and should, again, be strongly discouraged.

Thank you so much.

- [Speaker] Okay, thank you, Frank, for the opportunity to be here again and talk about our experience to fix complex central venous occlusions. These are my disclosures. Um, I'm not able to pass the slide, okay. So every patient that comes

for a complex central recanalization needs to have a CT to understand the correlation between the occluded segment and the adjacent organs. As you can see in the axial image here, there's a very small window between the aorta, between the pulmonary artery, and the lung.

So we need to understand really well, especially in this situation, this image shows that if you use any blunt puncture or if you use radio frequency wire, which is what I'm going to focus on, it goes straight, you're going to create a fistula

across the supra-aortic vessels or across the aorta. So we need to understand anatomy really well. In order to perform these cases, we like to have dual access in the ipsilateral side of the occlusion and in the femoral, and then we perform a simultaneous central venograms

to understand the collaterals, the length of occlusions, and the diameter of the venous stumps. That can be quite complex, as you can see in these two different patients. We always long introducer sheaths to give you stability.

I like to use a long sheath exactly where the RFY's going to come from, and either coming from below or from above. The other basic principle to recanalize central venous occlusions, especially the long ones, is to try to reduce the length of the occlusion

using conventional technique, and leaving the re-entry device, let's say the radiofrequency wire or a needle or the back end of a glide wire, more as a re-entry device than to recanalize all the way through.

You can approach it from a caudal-cranial direction or from a cranio-caudal direction, which is one that I prefer. Why, because it has stable access. If you come from below, you have the heartbeat, which is giving you instability,

you have a larger target, can be either the SVC or the right atrium, however, there's a higher risk of tamponade. The other basic principle is to have whatever technique that you use, in our case, radio frequency wire,

to use that, that has to be aligned with the snare. A snare used as a target, and as long as they are aligned in three views, you are just fine to fire the device. As we can see, those two pictures on the left, they are perfectly aligned, however the last one on the right is not,

so you have to take all the efforts, be meticulous, make sure they align in three views. After forty cases we had one cardiac tamponade and we decided to improve our technique, so since then, we've been doing this to prep and drape the subxiphoid window,

we have a CT and cardiology attending on standby, all the cases are done under general anesthesia, and you always have the pericardium drain and the chest drain handy. So we very frequently now, we're doing spins on our patients to make sure that we can understand well the anatomy

that we need recanalize, and also we developed with GE a specific algorithm to treat these patients which is we use a cat scan to dot lines from the occlusions from one stent to another, and then this orange line is the one that's going to give us a 3-D image where we need to travel.

As we can see in the cat scan, I can advance about one centimeter and a half this straight, but after one centimeter and a half, I need to go down and go around the curve, so that's what we did, and we find exactly the orange line we're able to reach the target, which was a snare,

and then we were able to snare out and then just basic recanalization using stents and angioplasty. Because our RF wire is not stiff enough, what we do is we use a 125 vert catheter to go through and through, using the body floss technique,

then we exchange for a 260 Amplatz, and then we can perform the venogram, and one technique that we improved in our initial description back in 2009 is what we've been doing the past four years, which is over the same guidewire,

we advance from one side the ballon catheter, just a four millimeter for pre-dilation, and over the same guidewire, we advanced our cover stent. This technique is critical from my point of view to avoid cardiac tamponade,

especially if you're going to recanalize the SVC. Not as important as in this case, which is a brachiocephalic vein recanalization, but we do that technique consistently to train our fellows. And here we can see the reconstruction before

and this is the venogram after, showing adequate result. Another complex recanalization, you can see the number of collaterals, long segments, what we did in this case, we did a rotation angiography to understand again the anatomy really well,

and there's something impressive that happened in this case, and I'm sorry feed is a little narrow, but I hope you'll be able to see that, according to the breathing of that patient, the pleura, the lung was on the way of the RF wire, so we needed to make sure that we were firing the device

or in crossing the occluded segment in expiatory breath hold, then we have no pleura, no lung on the way. And then as a basic technique, to simply repeat the snare and we snare out, this combed MTC is to show that we are perfectly aligned

with that 3-D image that we prepared. And then of course, you can snare out, you can do your venogram to check where you are and you apply your stent, and that's the final rotational geography showing in different ways that you are perfectly aligned

and you crossed the right spot without any complication. I want to finalize in a few seconds, showing this case, a very dramatic case patient with extensive collaterals, it was very painful, had a port on the chest on the right side, extensive occlusion on the right, we gave up on that.

We thought well let's try to recanalize the left, the problem is where we should start? There's no pencil tip, so we need to use radio frequency wire to poke a hole outside of the vessel. We did a combed MTC to make sure we were aligned, and then we use a fusion of image

with a existing CT from the space to see exactly where we were going to cross the supra-aortic vessels, we also used an integrated registration to see where the RF wire started and where it needs to go,

and understanding that we had about 11 millimeters between the sternum and the supra-aortic vessels, basically a flat plane, basically what we were doing here in an endovascular stent graft between those two stumps. And here is the integrated registration

showing to us that the RF already crossed the supra-aortic vessels, we are ready to dive into the right atrium, as we can see here, and then we snare out, deploy the stent, and before deploying the stent, we did a rotation in geography

to make sure we didn't cross the supra-aortic vessels neither the aortic arch, and then deploy the stent. Immediate result, no complications, no x-ray showing complications or echocardiogram. Nine months followup, completely patent,

but the best of all is this. The veins are totally decompressed in the vein and the patient is asymptomatic. Thank you.

- [Presenter] Ladies and gentlemen, dear colleagues, first of all I would like to say to the organizer thanks for the kind invitation. I don't have disclosures. As you know, chronic renal insufficiency is a global problem, with the prevalence of 10 to 16% in the general adult population.

For the patients who are receiving an endovascular treatment are having an increased risk for contrast-induced nephropathy, with an incidence of up to 50% in high-risk patient group. Duplex-guided PTA is not a new treatment. It's already published many times in the medical literature,

but mainly it was treating the SFA, and the popliteal artery. Some sporadic reports are treating the dialysis access. The advantages of Duplex PTA that you're puncturing the access artery under ultrasound. It's a dynamic examination.

You don't need pre- and post-hydration, no need of contrast or radiation. The disadvantages, the habitus of your patient, so obesity can be a problem, and intense bowel gas formation can give you problems with the Duplex images

So, first we did officiate the study in 2013. It was published in European Journal of Vascular Surgery. We treated 35 iliac lesions with 94 clinical success. Then, we went on with the randomized control trial between 2013 and 17.

We included 140 patients with an indication of PTA for significant iliac stenotic disease above the 70% stenosis with the TASC A and B lesion. The endpoints for the primary, passing the guidewire through the stenotic lesion with balloon dilatation with or without stent placement.

Secondary endpoints, of course, were measured in the clinical important complications requiring additional care. In the DuPTA group, more than 50% reduction of the PSV was required, and in the PTA group more than 50% reduction of the stenosis grade

on completion angiography was required. We followed the serum creatinine pre and postoperatively on all the patients on the 30th day, postoperatively got the Duplex. Baseline characteristics of both groups were similar. The most important significant results were

that in the DuPTA group, we found an absolute reduction, significantly higher, and the patient group who had more than 50% reduction of the PSV was also significantly higher. We placed significantly more stents in the Duplex PTA group.

The kidney function pre and postoperatively was comparable. We also did officiate the study on Duplex-assisted EVAR, DEVAR. It was published in 2014. Last Monday, I operated on our 12th patient with this method.

Actually, there are two points which are different from the regular EVAR procedure, namely you mark your renal artery with a guidewire supported with an angiocatheter, and then you start to deploy your main device, and at that point the partial opening of your main device,

you control once more with a Duplex, the flow and your renal arteries. Other different point is that you mark the internal iliac artery with the renal balloon under fluoroscopy and Duplex ultrasound. Further deployment is going in the same way

as with the regular EVAR procedure. All our patients get a control on table with CEUS and SonoVue. Here you see in the end stage picture with SonoVue on table, no endoleak, and this is a final CT without contrast.

So, in conclusion, in our hands we saw that directly measurable results indeed seen when you use Duplex-guided PTA. You can immediately see the degree of recoiling or dynamic dissections, and the dynamic of dissections,

and we didn't find limitation by habitus or bowel gas formation of our patients. We found that Duplex PTA is a safe and effective procedure with comparable clinical results to conventional PTA in iliac TASC A and B lesions. Valid alternative in high-risk patients

with chronic renal insufficiency or contrast allergy. The value in the recanalisation of iliac occlusions, it still has to be examined, and we found that DEVAR is a feasible alternative for AAA patients with renal insufficiency. Thank you for your attention.

- [Presenter] I'll be discussing a device that is viewed as what we believe to be hybrid atherectomy, given the fact that it utilizes multiple effects that have been seen in different other atherectomies, fused now into one. I do some consulting for Phillips,

and so that is a role of that slide. This device is called the Phoenix atherectomy system. It can treat a different range of lesions and it goes from a five to a six to a seven French device. And it's cutter will then remove the fragments

and encase them in the back as it captures and clears. So when you put it on a grid against directional, laser, orbital, rotational that are also all available in the market, this is really the one that has

only the front cutting, the continuous plaque removal, the directional cutting ability to single insertion, and the fact that there's no capital equipment. Here you can see the three commercially available options from two four, to the two two millimeter, to the 1.8.

The two four is one that actually has a deflecting catheter, so you could actually increase the area of removal, making it adequate for bigger lesions. Now, I'm here to share a little bit more on the nation wide registry that we're leading at the ideas that we're going to try to get

600 subjects, as of now from 17 sites. And we're going to try to do a follow up of up to 12 months, particularly on those patients that have limb limb-threatening ischemia. Primary endpoints, of course, are going to be safety and efficacy.

And some secondary endpoints related to the TLR, TVR, Wifi, and target limb amputation rates. As of now, we have an interim group of patients that we've accomplished to get 250 all-comers. This includes Rutherford classes two to six, with follow up at 30 days regarding

the safety of this device. Potentially, I mean, primarily focusing on the embolization rates that we've found. Those that have limb-threatening ischemia are in number of 142 patients, which means 60% of these with Rutherford class four to six.

And these, we will follow up to 12 months. As could be predicted, most of these patients are smokers and or have diabetes. And looking at the lesions, we are looking at, these are kind of what we call real all-comers, so we have long

lesions with a mean lesion length of 86 and those Rutherford's two to four. But all the way up to 114 in those that have critical limb ischemia. If you look at the anatomical distribution,

as would be expected, those that do have limb-threatening ischemia are in the greater percentage of those that have below-the-knee disease. And you can see that we do have a fair amount CTO's. Now, this is a very important slide. It shows that the procedural success

with less than 30% stenosis at the end of the procedure was accomplished in 99% of these patients. But more importantly, also and very noteworthy is the fact that there were no distal embolic events present. Now, this device particularly

does not include the availability of putting it on, of using it in combination with embolic protection device. And so, it still is, obviously, a saving procedure when it comes to the financial aspects. The TLR was .5 and the unplanned amputations were .9. Most of these were related to

very large wounds in patients with Rutherford's class six. There was an improvement in the majority of these patients up to two classes. And when you see the Wifi grid, also there was an improvement from those that started a high risk for amputation, and at 30 days,

were diminished to .5. Most of them did, however, be in the low category, showing that some of these facilities are probably adding more of baseline patients that have claudication rather than critical limb ischemia. On the CLI group, the procedural success was 99%.

And the unplanned target limb amputations were higher, were 12.5%, as you can see, and this was because most of them were at baseline, a Rutherford class six. 100% of these patients at 12 months had improvement in their Rutherford classes

and the CLI group. Obviously, avoidance of those that had a limb loss due to extensive tissue issues. So in summary, the Phoenix hybrid atherectomy system has a performance and the interim analysis that shows that it's consistent with those

of the EASE study, showing low embolization and safety. The results are safe and efficacy, safety and efficacy are also adequate in the CLI, which is the subgroup that tend to have higher risks.

The improvements have been adequate in the Rutherford, and as you can see, this has made it the number one tool that we've now utilized in our group. Thank you very much.

- [Mark] Thank you very much, and thank you again, Frank. The vertebral artery of all the extracranial vessels gets very little attention. It's by the fact that there's some major, major complications from ischemia, dissection, and thrombosis.

So, alright, my disclosures. So, let's see here. Alright basically then the vertebral artery has four segments. This is the first segment, second segment, I'll explain this later,

third second, fourth segment. So four segments of the vertebral artery, and diagrammatically this explains it somewhat better. So, the vertebral artery enters right from the subclavian and C6, and then transverses in the transverse foramen,

extends up to C3, where it exits. It exits here, and this is a mobile section here, where dissection can occur. This mobility here, and then it enters through the foramen magnum and then joins to form the other vertebral, to form the basilar.

So, critical basilar here. You can see the basilar just anatomically showing you the anterior inferior cerebellar and the posterior cerebellar. So the anterior spinal artery. Obviously, the basilar artery's critical

in terms of the dissections. It'll bleed. I'll show you a few examples of that. So, basically what happens is a tear occurs in dissection and there's intra bleeding within a wall. Causes a little hematoma.

And then obviously if asymptomatic, these patients all resolve without any interventions, so they're treated medically and have not become an issue. Now, intracranial, that's a different story for dissection. Basically emboli and atherosclerosis

can result in basilar stroke. Dissection is the most common cause in the younger age group and responsible for stroke in these patients younger than 45 years of age. The most common site for vertebral dissection is at the most mobile site, which is at C2-C3,

where it exits to enter the foramen magnum. In terms of imaging, we still think that gold standard is angiography, but nonetheless MRA and CTA also, quite impressive in terms of overall evaluation. But for all purposes, to see detailed evaluation

of extra and intracranial, vertebral, we like angiogram. Basically, that at least gives you an idea of here, you can see the dissection and the double lumen here, and obviously the occlusion on this vertical CTA examination. So it gives you an idea how valuable the CTA is.

So in this situation here, origin vertebral. And then subsequently, dissection. Dissection because a Guide Wire perforated here. But the patient's asymptomatic. So there's nothing to do and obviously in three months it's back to normal dimensions.

So that's the secret in terms of the vertebral proximal artery. They don't really require anything. On the other hand, you can see here, this is an ostial lesion. So most ostial lesions may or may not

need therapy if the contralateral side supplies. But in this situation you have the ostial lesion which is treated but in addition there's a basilar. The basilar has about a 90 percent stenosis. So in this situation we would dilate the ostial first and then subsequently

dilate and stent the basilar and then subsequently come back and stent the ostial lesion. So that's how we handle a combined lesion with an acceptable result. Except, we leave this one alone, this component here, on this vertebral

is not significant enough to interfere. So we took care of the high grade stenosis in the basilar of course, and then subsequently in the origin ostial vertebral. So sometimes in symptomatic bilateral vertebral stenosis we ask ourselves,

what can we do with this? So we can do nothing with this, I mean, maybe the surgical situation proximally but certainly there's no endovascular intervention for this complex occlusion. Especially when the other side

also has a critical stenosis here, at its origin and we stent that with a satisfactory result and then on that obviously supplies adequate intracranial circulation. So again in stenting, you have to be certain that the stent's in a proper position

so it doesn't migrate otherwise it's very difficult to re-enter. So intracranial bleed is a different situation with dissection, about here you can see obviously a huge infarct to the left cerebellum and so intracranial bleed here,

so obviously then, dissection intracranially is totally different than the extracranial. And obviously significant bleed has a very high morbidity. So here you can see just a very rapid transition. You can see a high-grade stenosis in the origin that is carotid.

And stenting is a great result, stenting, but notice in the meantime that prominent occipital branch occurring because subclavian is occluded, so we obviously demonstrate that by retrograde injection here and then subsequent coming down you see

the occlusion here, and then with acceptable stenting you can see now a normal result with antegrade flow now in the vertebral. So do we have to do that? Well, we do that because there's a shunt from the basilar junction down retrograde

so obviously if we can stent that and correct that then you have antegrade flow normally in that left vertebral. So another situation, this was a patient. We had a stroke on the table while getting a coronary intervention.

So we didn't have to move the patient at all. We just then approached this with initially aspiration which wasn't totally successful but improved somewhat and then we put a Trevo in. And did not great but the sciatic would markedly improve. In all this you can see basilar filling,

posterior cerebral filling, cerebellar filling and the pica filling as well so it improved flow, not the greatest result but acceptable. So in conclusion we say endovascular treatment has largely replaced surgery for most dissections and certainly thrombus

as well and asymptomatic patients. So, best managed conservatively. Symptomatic patients with thrombosis, anticoagulants, respiration, are all acceptable in thrombosis and obviously intracranial situations are difficult.

Surgical possibility, but not much in the way of endovascular intervention intracranially. So basically then stenting, aspiration and anticoagulant is the approach we use when there's significant thrombosis where it's symptomatic, but asymptomatic

patients with dissections are best managed conservatively with best medical management. Thank you.

- Thank you for the opportunity to speak this morning. I have no disclosures. For my part in this vigorous debate, I would like to present a clinical case and keep on the antidotal level that my colleague has set a precedent for. This is a patient who is a 51 year old critical care nurse. Who developed right arm swelling and cyanosis

of the subclavian vein. She underwent an venogram and successful thrombolysis and balloon angioplasty. There was a residual stenosis at the first rib, and she was maintained on anticoagulation in preparation for surgery.

My colleagues and I recently reviewed the various treatment options for Venous TOS and this publication in the journal of Vascular Surgery lymphatic, venous lymphatic disorders. And in this paper we summarized the results of three different protocols the transaxillary and infraclavicular

paraclavicular based on our review of the best available evidence, we concluded the transaxillary first rib resection and balloon angioplasty is a reasonable approach in which 79% of patients can expect a successful outcome at three months follow up. That was indeed the choice selected for our patient,

she underwent a right transaxillary first rib resection. The intraoperative venogram showed here. Showed obstruction of the vein that was not, that was resistant to balloon angioplasty attempts and she was maintained there after on long term anticoagulation.

The patient recovered well after treatment for wound infection, and six months later she continued to have significant arm swelling symptoms and was not happy with long term anticoagulation treatment. A venous duplex was negative for thrombosis, but a CT angiogram demonstrated central subclavian vein

occlusion. A chest x-ray showed long posterior and anterior rib remnants as highlighted here. And at this point we recommended paraclavicular decompression with possible subclavian vein reconstruction. The approach we would typically recommend

for any primary patient with transaxillary Venous TOS. During the super clavicular exposure, we resected the remaining scalene muscles and posterior rib remnant from the interclavicular exposure we resected the anterior first rib remanent and the subclavius muscle. Working between the two incisions we traced the subclavian

vein below the clavical to its junction with the innominate vein and removed the surrounding scar tissue. But the intraoperative venogram showed persistent obstruction of the vein, indicating the need for further venous reconstruction. Our patient underwent a bypass with a cryo preserved

femoral vein graft from the axillary vein to the innominate vein and the completion venogram demonstrates the wide bypass with rapid flow, no filling of collaterals and the patient has done well in relatively early follow up with no arm swelling. From our review in this previous paper we found a

paraclavicular decompression has an excellent outcome with 96% of patients having a successful results at three months recovery time follow up. And this compares favorably to the 79% success rate for transaxillary and intra clavicular approaches. So in conclusion,

there are several distinct advantages of the paraclavicular approach for venous TOS. It is applicable to all patients with Venous TOS and involves a single operation and is not dependent on postoperative interventions. It provides the most thorough and direct exposure of all

relevant anatomy. And allows the surgeon to complete a first rib resection, scalenectomy and external venolysis. It is ideal for direct subclavian vein reconstruction when needed and involves no sternotomy, claviculectomy or disruption of the sternoclavicular joint and involves

no placement of stents in the subclavian vein. The main disadvantage of the paraclavicular approach is it is not always and easy operation. Particularly for surgeons who don't treat TOS on a frequent basis. It does require a appropriate level of training and

experience, and this expertise is not often locally available, even in a city of eight and a half million people. I have several suggestion and tips for my transaxillary colleagues. First know the limitations of transaxillary first rib

resection and consider the alternatives. Especially if subclavian vein reconstruction appears to be likely. In general if you don't treat neurogenic TOS, you probably don't do enough cases of TOS to feel comfortable and consistent treating Venous TOS.

Do a complete first rib resection all the way to the sternum, do an intraoperative or postoperative venogram to identify patients who need further reconstruction and use balloon angioplasty if you must. But please don't place a stent in the subclavian vein. To improve your outcomes, use venous duplex for follow

up rather than being ography because you may not want to know what the subclavian vein really looks like. And if the vein is not patent use anticoagulation to preserve the collaterals. And lastly don't hesitate to refer early and refer often for patients that might be better treated by

paraclavicular decompression. Thank you for your attention.

- Dear Chairman, dear colleagues, thanks again to Dr. Veith for the very kind invitation. So, what about new concepts for better understanding of aortic pathology, progression and treatment? I would like to start from here.

I'm going to show you some new things that we have been able to publish very recently, and one is focusing on the forces, anatomy and forces that play, at least for us, a very important role in the level of the arch.

This is the beginning of this story. It means we have been able to show that when we move from arch Type I to arch Type III, of course, we have an increased torque velocity and angulation at the level of the arch. This was intuitive,

but it's the first time that we have a numerical definition of this torque velocity. The second step is that the torque velocity has been associated with an increase in forces that are drag forces

and may cause a migration or TEVAR failure, as we are focusing on this topic. And these forces has been evaluated using computational fluid of dynamics. And you can see, in a very interesting way,

here these forces act in an orthogonal way, most importantly, the level of the ascending aorta, which is the zone zero and that the level of the zone two and three. In particular, in the zone of the arch three, zone two at zone three,

means the very distal part of the aorta, just surrounding the origin of the LSA. So this two concepts also has been associated to another thought and the thought is that, this is, anatomically speaking, the same location

where usually there is the proximal entry tear for the Type B dissection. So, we try to understand if the anatomy might potentially play a role in determining the B dissection. And we collected over 250 patients from different European institutions

and it was interesting to compare these group of patients affected by Type B aortic dissection and, or intramural hematoma with up to 8000 patients that came from an ad hoc literature search, available in 11 different studies.

It was interesting to know, to show it has the prevalence of the Type III arch in patients that are affected by Type B dissection. It's much higher than in the control patients. As you can see over here, there is a 41% versus 15.5%.

So, if the concept is that the, potentially, if the question, I would say better, is that the anatomy might play a role in this setting in terms of determining sub optimal results or even determining the disease or the determining in the feedback to our procedure

that is not what we would like to know, probably yes, probably anatomy matters. The other point that I would like to show in this presentation is the very reason I write observations. That we presented last April, just in the same hotel,

the AATS Aortic Symposium. It means that we look at those patients who presented with the proximal entry tear, located into the arch. I also said that the aretinoid is stationed into the ascending all day presented

only in the integrated with the no ascending involvement. These are the numbers as you can see over here. And, in an interesting way, we noted that those with the not ascending involvement are managed literally like a Type B dissection as a patient specific way.

Many people said to our proposal that this was a radiobuse. But, this was not because there was a gap in evidence to observe that those with the proximal entry tear into the arch are considered a Type A dissection. And Type A dissection, based on the guidelines,

should be managed in a all day cohort of these patients with an open procedure. In terms of mortality, these patients with the not ascending intersection have a mortality higher, compared with those who have an ascending involvement.

And based on these observations, we proposed that, a kind of sub classification, for specifically for these patients with the proximal entry tear into the arch. Naming those, with the ascending involvement as Arch A, compared with those that

do not present ascending involvement and naming this as Arch B. So, coming to the conclusion, we think that the anatomy matter in determining results for extreme TEVAR means when we face with patients who present a really sub optimal anatomy.

And that, we probably might take in consideration, also is the anatomy might become an important, a potential variable to understand why some patients develop a dissection and some others not. In addition, probably, we are trying to fix a little bit better,

a gap in evidence related specifically to this cohort with proximal entry tear into the arch. Thank you very much for your attention.

- [Henrik] Thank you very much, thank you Frank. I don't know what I did to get that title, for it's certainly long. If some of you were here 6:40 this morning you may recognize some of the slides, because I had a similar title at that time. The risk of stroke in asymptomatic patients

is low, and you can see from this publication that shows the annual risk declining, with the year of the publication. Just a few months ago there was this publication from Kansas where a group looked at 864 with 1400 Stenotic Carotid arteries,

followed them for seven years, and they looked at how many goals of risk reduction were accomplished, and you can see that the step-wise reduction in the black bar, which is the combined end point of Stroke TIA or Carotid Revasc, how that is lowered

from 3.5 to .6% annually if you reach all the goals of healthy lifestyle and take the right drugs. Interestingly also looked at how the risk of stenosis progression similarly was reduced step-wise. They concluded that the risk of TIA, Stroke and Revasc becomes extremely low if risk factors are treated

appropriately, and I would say progression of carotid stenosis is a sign of insufficient risk factor control, and preventive treatment rather than sign of increased risk of stroke. And similarly, we looked at 7,000 patients in the bio image study, where we scanned the carotids,

and we found that 6% had a carotid stenosis, they were followed for three years, and four had a stroke, of which two were ipsilateral. However, a lot had cardiovascular events, which we know. For Asymptomatic Carotid Stenosis, very, very low risk of stroke, maybe .3 to .4%.

It's a high risk of cardiovascular events instead, so therefore, it's very important with preventive treatment and the lifestyle adjustment. And Carotid endarterectomy, or CAS, in general is not warranted, unless a high risk plaque can be identified, of course.

And together, with one of the Chairman, we looked at that a couple of years ago, and published in European journal, and notice how stenosis progression is actually the least important of those listed here. However, these data are also ancient since most of these studies included patients that were gathered

or investigated 10 - 20 years ago, so the risk today is probably less than half of what is shown there or maybe even less. Presence of Carotid Stenosis does not tell it all. We need 3D Ultrasound. And the previous speaker

is a pioneer of this and up in the zeros, published a number of papers, and this is just one of them, using a research tool as you can see in the top left, is handheld, but demonstrated to be very reproducible, but now we can get these as what's called Matrix Transducers where we instead of having just

one array as you see here, we have multiple arrays in both dimensions, and therefore we can do volume imaging, or we can have two plain simultaneously as you see in this slide. We recently looked at how accurate can you measure plaque volume using an instrument like this, and it's simply

tomography as you're used to with CT, you take slices and you look at the area in each slice, you know the difference, sorry the distance in between you can calculate the volume. We did that, and this is what came out when we had two blinded investigators scan the same 37 PAD patients.

The patient was up standing in between exams, the ultrasound machines was reset, so this is fully blinded two independent acquisitions. This is actually much more accurate than if you do two LDL blood tests, what you see here. I shall admit that these patients were a little bit

selected because patients with calcified plaques were excluded. 3D will improve plaque qualification, both volume and morphology. Assessment of degree of stenosis, will be better because the angle-compensation can be done

more accurately in 3D. Speed of examination will increase, and will be more easy to perform a good scan. What can we use it for? For risk assessment in carotid disease , who to operate will be more accurate, we can do better morphology

using this technique, and we can also monitor if we treat the patients appropriate with general prevention. Is the plaque stabilized? And maybe more important, has the atherosclerotic burden stopped growing, and I would suspect or expect

that this method may replace LDL measurement in the future when you want to see if the preventive treatment works. Thank you for attention. (clapping)

- [Instructor] Thank you. After this very positive expression, I have maybe to make some negative remark about this technology and I don't have any disclosure and you know how the system work and is surgically inspired system

with a so-called Neuroprotection and the rational for the TransCarotid Artery Revascularization is the fact that you have to pass the calcified arch in many patients and this is considered the main cause for the number of peri-procedural stroke in CAS.

It's really important for our cardiologists as I am, it's very difficult to understand this rational because and to follow this hypothesis because every day thousand and thousand of patients are subject for coronary interventional diagnostic of interventional of the coronary artery

and to be passing at least three time per intervention the aortic arch and complication with cerebral embolic are absolute rarity. I saw that, I cannot understand this rational and my question is,

is TCAR only a tool for Vascular Search without experience in the manipulation of guide wires and catheters? And we're readily excluding automatically all cardiologists from carotic intervention because they cannot make an incision

to two centimeter particularly if you may blocks or complication and if you look at the data up to now published, they are not really robust and if you look at the number, of total number of patients reported is 317 patients only.

So, and if you look at the results of the ROADSTER and you can ask Peta are really sure. At the end of the story, you have 3.5% of complications and this is same complication we published this already in 2010. In 1,300 patients with the mobile system,

and we had the complication rate at 30 day of 1.3% and if you look also in patient over 80 years, we could collect more than 200, nearly 200 patients, and they had a complication greater of 2.5% and if you look at the Armour Study, then it's the complication rate in the range below 3%

and if you can see in the middle, that in symptomatic patients accepting any type of arch, not excluding some type of arch, was several percent. So, why you need to a new technology and if you look at the meta-analysis from the Bersin published in 2012,

the number of complication in nearly 2,400 patients was 1.7%. So, if you look at the next potential complication of new lesion in the inner eye, and you look at these studies, including 56 patients, but MRI has been performing only in 10 patients

so that is nothing in comparison to the Deverse Study campaigned looking at the new lesion in one out of 27 patients and in the same range because we're doing 18 and 26% looking at this 10% 10 patients,

but it's not a significant difference. And what is extremely important is to go back to a relatively old studies, nearly 10 years ago, that more than 80% of the complications after CAS occurring after the intervention.

So, at the time when we do not have any protection anymore. So, then the solution could be to have a new stint and if you look at these Italian study in 150 patients using the RoadSaver, no complication in 150 patients. However, we took interventionalist with a very high experience

and you see that we have also some disadvantage of the procedure because it have a very short walking distance to access to the lesion. You may have an access dissection and the interpretation on this is for me

extremely important of reversed-flow is very difficult for me practically, not possibly and of course again, limitation for non-surgical interventionalist. So, as last lecture, if use the newest technology,

it's okay for a vascular surgeon. If you the catheter technology, then remember to this old slide to Cremonesi. If you have an experience below 100 cases then avoid arch two and three. You cannot treat such patient

only if you have an experience of more than 200 cases and you have performing more than 50 per year, then you can use the transfemoral approach. Thank you for your attention.

- Thank you. Unfortunately Dr. Scheinert couldn't come. So, thanks for letting me take over here, his presentation. So, I'm going to present the first year results of a randomized trial comparing as a first head-to-head comparison, two different Drug Coated Balloons. These are our disclosures.

So, this is the first head-to-head randomized comparison, between two different paclitaxel coated balloons. Different coatings and, also, of course, different dosage. The range a balloon has a dosage of two micrograms per square millimeter. The impact is in the higher range three point five

microgram per square millimeter. So, will also lower dosage work here to treat or to effectively treat resenoles or prevent resenoles. This is a investigator initiated trial by Professor Scheinert. It's sponsored by the University.

However, there is a fund, research fund by Boston Scientific. There is an independent monitoring with 100% source data verification. So, clearly independent. So, the study design is prospective.

It's multicenter, randomized again. One-to-one. It's a pilot study 150 patients. However, there's an extension up to 414 patients, to test formal non-inferiority hypothesis. This, I think is important it will stratify to different legion lengths and to the outcome

as followed up to two years. The 150 patients. The first ones. Their one year results I can present today. These are the centers, which we are including and treating the patients. Allowed we are to include rutherford two-to-four.

Stenosis and occlusions. De-novo entry stenosis however, no instant re -tenosis, no severe calcification because, (talking to low) balloon is clearly not devised to treat severe calcification. Lesions were allowed up to 30 centimeters

and a stratification was done in a group. Less than 10 centimeter long. Ten-to-twenty and twenty-to-thirty, to also, have more information about how it works in longer lesions compared to shorter ones and, of course, have more equal distribution

(mumbling) over the two groups. Primary endpoint was patency at 12 months. Defined as absence of clinically driven TLR or drop of ABI more than 20% or more than one point five. Zero one five compared to post-procedure

or resteniosis (mumbling) took with PVR of two point four. Primary safety was a combination of death due to the procedure, major amputation or clinically driven revascularization. There were also, of course, some secondary endpoints for example.

Sustained clinical improvement and also walking capacity. Questionnaires. This 150 patients were disembogue 74, 76. Loss of patients was I think equal to any other studies not too much. Here you can see the distribution.

The base-line demographics. Risk factors were the same. No significant difference qualifications. Most of them critical limb ischemia or other(mumbling). There were some few patients. You can see here, target lesion lengths. No difference here. Longer than many other studies investigating

drug covered balloons. There were also more total occlusions. There were in fact, also, some moderately and serve calcifications. So, altogether these were quite real world lesions. Bailout stenting was in disregard

also, higher than many other studies. These are the results. At 12 months. These are the primary efficacy rates. You can see here. First of all for both balloons these results are again I think really quite good. So, with regard to the complexity of the cases.

It was patency rates here over 89 (mumbling) and 84% at one year. Here with late comers maybe a little better for range but, due to the fact that it was only a pilot study, I think that

this is not robust to say this. So, to summary, this is a first head-to-head comparison between two different balloons. These were really complex real-world lesions. Lesion lengths around 12 centimeters. CTO's around 40%.

Again, to emphasis is that the results are really excellent for both balloons after one year. They were similar for both formulations with different doses and recruitment of the full study 414 patients has just being finished

and now we have to wait for this full cohort. Thank you.

- Thank you very much, I appreciate the opportunity to be here and thanks to the program committee. I have no disclosures. I am not retired yet, so I am not seeking a position. Currently training (mumbles) paradigms mandated rapid acceleration in technical proficiency. We're not taking medical students and turning them

into vascular surgeons in five years. And what we often see now are fellows even after general surgical residency have not had extensive operative experience. To bridge that gap, simulation training has been touted as the method.

And its been incorporated into every training program. But, issues arise as to who has the time to effectively teach these sessions. The barriers for the surgeon educators are increase demands on clinical productivity, research obligations, EHR issues,

location of the simulation centers are often not conducive to clinical responsibilities. They are generally not located next to the operating room or next to your office. So there are opportunities, last year in the ACS surgical bulletin,

they put out, they discussed the retired surgeons, and there's currently 18,000 retired surgeon members in the ACS. Most live in proximity to the hospitals with training programs. They often seek out teaching opportunities.

At the University of Washington, we have Dr. John Arthur, who is in the crowd today. He should be giving this talk, but he was, he wanted me to do it. He's a retired surgeon from Bremerton, Washington. At the 2012 ACS meeting, he asked our division chief,

Dr. Ben Starnes, "Do you have anything a retired vascular surgeon can do?" And he said, "Oh boy, do we." And so we created a curriculum two days a week. Every Wednesday, we do a chapter review and Dr. Arthur participates in that,

then takes our first and second year residents for an additional hour-and-a-half and does skill training with them. He does vascular exposure, suturing techniques, things that we don't have time for. On Friday, he then does open training exposures,

VSIG training and once a month he has an industry representative come in with their product to review the IFU. Then our big course is the cadaver course that we do every December. And its cadaver dissection week, he coordinates all of the procedures that we do on this.

Including getting the instruments and having the faculty members participate in mock procedures. Didactics and reviews, so the instruments are laid out. The medical students and residents participate in this. They go over anatomy.

They go over every instrument so they understand open surgery. The endovascular portion, we have a representative come to our simulation center. They bring a simulator. They then practice deploying the graft,

review the IFU with a specific device so that they can learn this. But he oversees this. The anatomy and instrument review again is done with our vascular surgery interest group, which has really blossomed with his presence.

They have an anatomy review, the suture lab, and he teaches our medical students to basically be scrub techs during our dissection week. During the cadaver lab week, and this is an annual event, we have preop white board sessions, procedures with the residents,

and students serving as assistants. Here you can see the pre-procedure review for a median sternotomy and a thoraco-phreno laparotomy. And going over the details. Then we kind of get after here you can see Dr. Sterns with our residents doing this

with the medical students assisting under the supervision of Dr. Arthur, making sure all the instruments and all the people are where they need to be. And again the residents then perform these procedures as if they are doing an operation,

obviously without the mask. But, you can see that being a faculty member, you get called away. And so that's when Dr. Arthur is able to take over and be there. And this is the issues that we're always faced with.

Coordinating the sessions here, we're talking about endovascular access. I was able to do the endovascular portion. Dr. Kohler then comes in and helps out. And they do procedure-based learning. They will take a person through a carotid endarterectomy

and actually remove a plaque. So this is fantastic stuff that they're doing with this. We've had five years of doing this. And the faculty are all available, but now our simulation happens as scheduled. Its increased involvements of our medical students,

the VSIG members have grown, and its really corrected bad habits that we've noted in the operating room. And its led to an additional recruitment of another Gray Doc, which is Dr. Ted Kohler or salt and pepper. So there's opportunities to engage

with enthusiastic teachers. We need to utilize these resources. They are a wealth of experience. They share their experiences not only clinical, but in their practice and life experiences. It allows us this great group a chance

to further impart their wisdom on the next generation of surgeons. Thank you very much.

- [Speaker] Thank you Dr. Moore, Dr. Veith, ladies and gentleman. Nothing to disclose. Carotid in-stent stenosis varies between 1 up to 30% Most studies have, unfortunately, short follow-up, which may lead to under-estimation. So therefore, we conducted this study to analyze the

incidence of both above 50% and above 80% carotid in-stent stenosis and its clinical implication. This retrospective analysis of prospectively collected data of 450 out of 498 CAS procedure

done over 10 year period in our institution, all had post operative duplex ultrasound within month, 6 month, and every 6 to 12 month thereafter. Kaplan Meier analysis was used to estimate freedom from above 50 and above 80 in-stent restenosis and if you notice between parentheses,

these are validated data published at the JVS few years ago. I see a peak systolic of above 224 was consistent with above 50%, and I see a peak systolic of above 325 was consistent with above 80%. The demographics and clinical characteristic are as expected

in this population, but I'd like to lead you to the bottom of the slide, there are roughly half and half symptomatic versus asymptomatic. 65% were primary CAS and 35% were done for post CA restenosis.

Late outcome, mean follow-up was 41 month, above 50% in-stent stenosis was in 101, 23% above 80% was 7.4%, late TIA was 4.3%,

late stroke was less than 1%, late re-intervention was 5%. And this show the freedom from above 50% restenosis, looking at the bottom, it was 70% freedom from above 50% at 5 years. Looking for above 80%,

it was roughly around 89% freedom from above 80%. Reintervention, around 91% at 5 years freedom from reintervention. Survival, fortunately if you notice 90% of them were alive by 5 years. Late result,

now when you compare this to the same institution and actually I only included data from randomized prospective carotid endarterectomy trial with patching, I'll emphasize with patching, 94% at 5 years. So compare 70% vs. 94%. Now, forget AbuRahma's data,

let's see what other data from other randomized trial. This work is done by my friend and buddy, Dr. Naylor, down look at this meta-analysis of prevalence of restonsis above 70% or occlusion, patch endarterectomies, 5 of them mean follow up 32, the restenosis rate is 4.1%,

and that's very comparable to our own randomized trial. Looking to the CAS data, 5 of them 10%. Now, meta-analysis by Cochrane review, published few years ago, showed CAS was associated with

significantly higher above 70% restenosis rates than CEA, impressive p value, but when you look to meta-analysis which was confined to the 5 randomized trial, there was no statistically significant difference. To me, I don't like that game,

because still the odds ratio is almost 2 after restenting. Now, to answer the final question which Dr. Veith me wants to answer, what do you do with these people? If it's symptomatic, definitely you treat them as primary disease, mean best medical therapy plus a redo PTA and or stenting,

very rarely redo surgery and if you do, you might consider interpositional graft. Now, what do you do with the asymptomatic? I need to refer you to this slide before I tell you my recommendation, from this study published just recently,

CAS of a randomized trial with a mean follow-up of 50, only 1 out of 125 with above 70% having stroke ipsilateral to above 70% and that tell you something. Perhaps we don't need to do anything at all. Now, with that in mind,

I'm going to give you my recommendation, as you know its controversial what you do with these. However, no randomized trial comparing best medical therapy verses PTA/CAS or redo CEA, all should have best medical therapy. High risk, definitely observe them.

Good risk with above 70%, there is question whether rePTA/stenting, specifically if our MCA velocity below 15 based on TCD monitoring or if you want to go all the way, neuro symptom during balloon inflation proximal to flow reversal.

In conclusion, ladies and gentleman, validated duplex ultrasound velocity criteria should be used for diagnosing in-stent stenosis, incidence of above 80% in-stent stenosis higher than, I believe than, post-CEA with patch, which is atleast two fold,

and above 50% in-stent stenosis is even higher. Treatment, symptom as primary disease. Asymptomatic, mainly should be observed. Thank you very much for listening.

- [Timothy] Thank you Mr. Chairman. Thank you to Dr. Veith and the organizers of this year's meeting for the opportunity to speak to you this morning. These are my disclosures. Extra-femoral or non-femoral arterial catheterization is rapidly gaining adoption

in particularly the cardiac space. Over 36% of all cardiac caths, whether for diagnostic or PCI purposes in the United States are done transradially in 2017. We've seen also that in lower extremity complex, critical limb ischemia patients the use of transpedal

and transtibial access for either standalone access for guidewire rendezvous for revascularizations and then a variety of applications for brachial access for TEVAR and EVAR and PAD and dialysis work. So for these devices, for these puncture sites, you can't use femoral devices.

And so there are dedicated radial devices that have been on the market for some years, and they essentially are a bladder inflated with a syringe, and that presses along the whole volar surface of the wrist. This lack of precision confers relatively long times to hemostasis,

they're quite uncomfortable, they may have to remain in place for as long as four hours after PCI. And they've even now, in contemporary literature, have been shown to have radial artery occlusion rates which are substantial.

And they're quite challenging to adapt these radial bands to other anatomic vascular puncture sites. So the concept of the VasoStat is quite simple. You simply take the human mechanics of a person holding focused, precise pressure directly over the puncture site,

and because we typically in an interventional environment aren't going to find someone willing to do that for an hour or two. If you render that in the form of a device, that's the concept behind the VasoStat. It's a ratcheting mechanism so you're allowed to,

you're enabled to titrate the amount of pressure specifically right over the arteriotomy, and then there's a stretchable pad that goes over the device. So in a cath lab environment if you've got a sweaty, diaphoretic STEMI patient where adhesion

is particularly important, or if you're doing a transtibial or transpedal wrapping it around the entire ankle or foot. So this is what it looks like in radial application, again, with the sheath still in place, the device is aligned right over the arteriotomy.

It's a pressure-activated adhesive system, and then over top goes this stretchable pad called the SeeCure pad. And that can be whether you're doing a 350-pound patient or a 90-pound patient, so it allows you to use one device for the entire spectrum of patient anatomy.

Once that's been done the sheath is then removed with simultaneous ratcheting of the central compressive plunger, thereby achieving hemostasis. And more importantly, patent hemostasis. Where preserving flow in the target artery,

in this case, the radial artery. With transpedal catheterization or transtibial catheterization, again, the versatility of this device allows one to gain hemostasis irrespective of the puncture site. This is what it's in the environment

after a multilevel revascularization with an anterior tibial approach, and you can see that we have immediate hemostasis. So whereas other devices with deprive the distal limb, be it the hand or the foot, of blood flow, we have continued to accrue data here.

This is a study from Japan where the device is widely used in cath labs, comparing with the TR band, the Terumo TR product. Preinflation we have a 40 cubic centimeter, centimeter per second velocity in the radial artery, which goes down to 12 with the inflated device

compared to the VasoStat where we start out at 58 and go down to only 51. So a 75% reduction with a radial band versus only a 12% reduction. Concordant with the perfusion studies that have been done with

high-resolution laser speckle imaging showing that preservation of blood flow to the hand, you can see in the top panel of thumbnails compared to the bottom with the Terumo TR band product, 75% reduction in blood flow to the hand. Outcomes, just to touch on those briefly,

showing that even in more complex patients with high quantities of heparin their VasoStat functions very effectively. And occlusion rates are the lowest among any of the published results with radial or other devices. And this holds true in the tibial population,

again, in a complex cohort of patients. So to summarize, and this is the latest kid on the block, is the rapid adoption of the distal snuffbox access for radial access. So the precise focused pressure mechanism can shorten time to hemostasis in these patients,

preserving antegrade flow and more importantly distal perfusion. We think this is why we're seeing lower rates of access artery occlusion and further evaluation is underway in a prospective randomized trial. Thank you very much.

- This one is an easier publication we did, but I do think it's interesting because there are no data for real in the use of the aquatic environment for our lymphedema patients. I have no conflicts of interest to declare, but I declare that I'm really interested in this topic because if you look at the Global Spa & Wellness Summit report,

every single year this is the amount of money that are spent in the business of the aquatic environment and of the spa centers. And we are not behaving so well as vascular specialists because what you're looking at over here is a vision of the literature showing that muscle skeleton system data

are out there in the literature for the benefits of the effects of the aquatic environment, but we as vascular specialists are not producing so much data. Before the publication we put on Phlebology on this topic, just these six papers were dealing with the use

of the aquatic environment for lymphedema patients, and all of them are basically on quality of life measurements, not really on objective data of drainage, so every single day in nice hotels also like this one, you have people going inside the pool

and doing all of these activities, not really knowing what's going on inside their venous system, and something cool could actually happen because if you really think about that every single centimeter of water is performing 0.7 millimeters of mercury in terms of standing load,

so when I have a patient standing up inside the pool at 120 centimeters of depth, his feet is actually over one by 88 millimeters of mercury, so four times the stockings we are usually prescribing. We also know that, of course, activating the muscle pump is fundamental, so what we did was activating

the muscle pump inside the aquatic environment, creating a standardized protocol of exercises that we tested on 32 lower limbs of 16 patients affected by bilateral lymphedema. These patients went inside the pool for doing the standardized protocol:

50 minutes per session, twice per week, for a total of five sessions. The protocol is published on Phlebology, so you can download that for free. Basically it's an activation of all the joints of the lower limb.

What you can have after five sessions of this protocol is a significant reduction of the lower limb volume, that by more than 300 mils. The circumferences of the leg and the subcutaneous thickness measured by ultrasound is significantly decreasing, but the interesting part is this one, I think.

You see over there Michael Jackson with the Moonwalk because we were having patients walking backward because you have the biggest activation of the ankle at that point, and it was interesting to notice that the range of motion of the ankle was increase of up to four degrees, and if you put that into statistics,

it's really interesting to notice that the volume reduction was directly related with a 0.4 correlation to the increase in the ankle motion. The evidence of feeling of the leg was decreased from 7.3 to 5.5 out of ten as a score. The functional ambulation classification,

which is a score for debility of walking, was not significantly changed. Again, everything is on Phlebology if you want to download it, and now we are doing other investigations because of course we could bring some about not just the physical property

of the aquatic environment, but also the chemical properties of the kind of water we are using and on the temperature that we want to use over that. So at the current moment I cannot discuss that. We are under a grant of investigation, but for sure I do think this is a way to go

because it's like killing two birds with one stone because indeed you can have patients that are hypomobile or that are, for example, obese that can perform exercises inside the aquatic environment that they could not perform outside the pool, but I have to say that we didn't find anything new because the guy you see

over there is Conrad Jobst. There is a nice quote by van der Stricht. He was saying we should know the history so to avoid wasting our time trying to open doors that were already opened by others, and the door was already opened by Jobst

because as you know he was an engineer. He was affected by an ulcer and in reality he noticed that when he was standing inside his pool, his ulcers was getting better. Being an engineer he understood that it was related to the standing though and so he created the concept

of the graduated pressure that you have inside the water in the stockings we are now prescribing that are then son of the aquatic environment.

- Thank you very much mister chairman and Dr. Veith. It's interesting to myself and John Ide have been given the same subjects. We haven't actually discussed it with each other, so if we come to a different conclusion that'll make for some good discussion. And I have no disclosures

and no potential conflicts of interest. This is often called median arcuate ligament syndrome, or MAL syndrome, and it's very much an evidence-free area. There was some work in the 70s with xylose absorption tests showing that ischemia of the intestine

was an underlying cause, but there's no doubt there's also neurogenic causes to this disorder and whether or not exists is very much up for discussion. I think it still is a diagnosis of exclusion, and it really relies on pressure

of the median arcuate ligament you can see in the middle of that picture going over the aorta and compressing the celiac artery as it comes off the aorta. And these patients tend to present with postprandial epigastric pain, nausea, and vomiting. And they also complain of food fear.

But not all of them are thin, which is of interest. Now there are tremendous vascular and also neurogenic elements to this disorder, and you can see there the greater, lesser, and least splanchnic nerves going into the celiac artery ganglion.

And I do believe in addition to removing the pressure from the celiac artery you need to skeletonize the whole of the front of the aorta there and get rid of those nerves and nerve plexuses. And whether it's the compression that helps these patients or whether it's the denervation that helps these patients,

I don't think anyone knows. So myth or reality? You can see there the normal anatomy of the median arcuate ligament going over the front of the aorta and it doesn't encroach upon the celiac artery. You can see then when that median arcuate ligament is low,

it can actually compress that artery and it can cause the artery to run rather that at right angles to the aorta in a downwards position a little bit like the superior mesenteric artery. And you can see the diagrams there and also the scan on the right-hand side

whereas the normal on the left and the abnormal on the right and you can see how the celiac artery is hooked up by the median arcuate ligaments and fibers of the diaphragm, quite often the left crus of the diaphragm, and how it causes a stenosis or a pseudostenosis on the CT or MRI scan.

And the trick here is to divide that ligament and I don't believe that I've ever had to reconstruct a celiac artery because usually that stenosis actually disappears by itself. Now there's also a physiological abnormality as well. And if you do duplex scanning on expiration and inspiration

you can see high velocities in the celiac artery indicative that there is a flow problem. But unlike with mesenteric ischemia, it's only one vessel and it's not two or three vessels, and this is why some people do not believe that this is the only cause of this condition.

Now, most of us in the UK have done very few of these cases. And this is my experience since 2005 in our center, and we've only done 16 cases. It's about one or two a year. But it's extremely important that you select these patients very very carefully if you're going to get good results

and you exclude any other cause for their symptoms. And as I said, it's extremely important that you skeletonize the aorta totally, take all the tissue off and all the nerves, and you divide that celiac plexus as well as dividing the ligament itself.

And of those we've had improvement in about 88%. Now followup is difficult because if they get improvement they don't come back to see you. But the ones that do come back to see us with abdominal pain we know haven't had improvement. One needed an SMA stent

and one needed a division of adhesions. And that lady had had operations for numerous difficulties in the past as well. And we've got two with ongoing symptoms but with normal CTAs and ultrasound scans. The current guidelines and practices,

you can either do laparoscopy, open repair, or some people are now doing robotic. But there are conversion rates up to 9% if you do the minimally invasive techniques or they do work. And you can see a lovely picture there

of the image you can get with laparoscopic techniques. So is this a reality? Yes, I think it is, but in only selected patients. You have to be very careful who you take on. It's mainly females. They quite often have complex disease

and coexisting diagnoses as you mentioned earlier on. But it is essential that you deal with the pain and take away the nerves as well as dividing the ligament. Thank you very much indeed.

- Thank you Tim, Manny, Dr. Veith. Again thank you for the kind invitation. Um, here are my disclosures. The Chimney Snorkel Sandwich technique is really one that's been used and discussed many times throughout this great meeting in years past.

I've been asked to kind of see how we expand the use for thoracoabdominal aneurysms. Um, basically it's a matter of putting a parallel graft and then having an inner graft that will help seal the aneurysm sac itself by maintaining

perfusion to the visceral vessels. Um, the number of parallel grafts has been shown to be of note, and generally if you get beyond two parallel grafts at any one location, that tends to dramatically increase the incidence of

gutter leaks and potential for continued perfusion of the aneurysm sac. Here again showing at two, they still keep a reasonable aortic diameter, but once you start going three and four parallel grafts you tend to have significant compression

of the main aortic graft itself, as well as the potential for gutter leaks. Um, the PERICLES Registry certainly looked as I know has been discussed earlier in this meeting, and basically what it showed was that this was a reasonable way of treating

some of these complex aneurysms with a durable outcome going out to two to three years, uh, at a survival rate of over 70 percent. So, to show how we use this for patients with thoracoabdominal aneurysms, this was a 67 year, I use the term is,

a 67-year-old gentleman presented urgently with a sudden onset of back and abdominal pain. Apparently he was, uh, had a new wife and was trying some sexually enhancing medications from the DR. Had a history of coronary artery disease,

erectile dysfunction, and congestive heart failure, and CT scan revealed a type four thoracoabdominal dissection with a eight centimeter juxtarenal aneurysm, and he was in acute pain. Uh, here is the CT scan as we go through,

and you can see obviously the very complex dissection. You had a small segment of perfusion still around the level of the celiac going down into the SMA, uh, and then this rather, again the renals were

also with a small luminal area, and then a large aneurysm going up to eight centimeters going down into the abdominal component, and then reasonable access vessels from below. This shows the dissection extending down

through the thoracoabdominal segment, and again, he was in acute pain. Uh, so we came in and did an angiogram and IVUS, uh, and here we show the area of the dissection going down as well as the take-off of the subclavian artery.

Again, the true lumen being here. This was confirmed with IVUS. The IVUS sash, and this is the true lumen here, the false lumen being around the periphery, and as you go through you can see there's almost complete collapse of that

true lumen throughout the cardiac cycle. Uh, we performed a left carotid subclavian bypass, and embolized the left subclavian artery and put a thoracic endograft in, covering that lead point as you go in and taking it really almost up to the level of the left carotid artery.

There you can see the occluded subclavian. Uh, with that in place we then prepared to do a four vessel sandwich, or double sandwich, technique. Here we came down, we brought the grafts down to about the level of the takeoff of the celiac access with thoracic endografts.

Lateral shows the takeoff of the celiac and the SMA. Uh, we were able to catheterize both those vessels from the axillary region and put stents going out in this two sandwich technique, uh, and then actually put our stents going out from both the celiac and SMA.

We then were able to do that once we had those stents in place with adequate overlap and no real gutter leak, we then came down and similarly put another graft down to the takeoff of the renal vessels and then selectively catheterized

the right and left renal. Here you can see the stenosis near the origin of the right renal artery. With that we then performed balloon angioplasty with covered stents, I believe these were VBX stents going out,

and then covered that further down as we went down into the area of the eight centimeter aneurysm. And here we come in building down from that area and the perivisceral segment down and then to the iliacs showing good perfusion down to the takeoff of the

hypogastric, and then finally angiogram showed we had good perfusion to celiac, SMA, both renal vessels, and then down through the aneurysm sac itself. This is, uh, he remains stable. His postoperative course actually was uneventful.

He was discharged from the hospital at day four. He's been seen back now at one year follow up at six and 12 month follow up and he's remained stable with no evidence of endo-leak. So I appreciate the opportunity to try and present a more novel way of managing

these patients in the acute setting. Thank you very much.

- [Dr. N N Khanna] Good morning everybody. Today I'm going to be speaking about endovascular treatment of erectile dysfunction, when is it indicated and justified, and I'll be discussing about the techniques and results of Pudendal Artery Stenting in this regard. These are my disclosures.

Erectile dysfunction is the recurrent inability to achieve and maintain an erection satisfactory for sexual intercourse. It's an important and growing health issue both in India and United States. It's estimated that in the United States alone,

50% of the men between the age of 40 to 70 years have varying degrees of erectile dysfunction. And also what's very important is that the erectile dysfunction actually predates coronary artery disease by five years. There are many causes of erectile dysfunction, of which,

80% of cases would be attributable to vasculogenic causes. And after vasculogenic causes arterial inflow problem is even able to endovascular treatment. While you are attempting to do internal pudendal artery stenting,

we should be very familiar with the anatomy and the anatomical variations in the internal pudendal artery. Usually it's the longest branch of the anterior division of internal iliac artery. Arteriography is a third line study

reserved for the evaluation of complex ED after a good clinical and psychological evaluation and a good Penile Doppler Study performed after Intracavernosal Injection of papaverine or papaverine and phentolamine, in which the peaks systolic penile velocity

fails to rise above 25 centimeters per second. This is one of our first patients who had a Complex Erectile Dysfunction because of bilateral, high-grade internal pudendal artery stenosis and a 90% lesion in LAD which was stented

with a drug eluting stent and then both internal pudendal arteries were subjected to internal pudendal artery stenting. We went contralateral, employed mother and child technique, passed in the 0-4 with spercondiview guide wire across the lesion,

and then predilated with a two millimeter, noncompliant balloon, and stented with a 2.5 millimeter Endeavor Resolute Medtronic Stent. This is the final result which we achieved, and then we did a simpler procedure

on the contralateral side. We have done about 50 patients up til now, but we are reporting a series of 32 patients where we have a follow up of about one year. 11 patients had the balloon angioplasty done by a simple balloon or by a drug eluting balloon.

21 patients had drug eluting stents. We followed our patients in three headings. The first one was safety of the procedure where we found it was very safe as there was no death, perennial or penile gangrene, and we had person technical success.

The other heading was the clinical improvement in erectile function. We followed the IIEF-6 scoring system. We found that there was an incremental improvement over three to 12 months of follow up in terms of erectile function

and this correlated very well with increase in peak penile velocity. This has correlated very well with the results of 25 patients published in the Zen Trial, and at one year the improvement here was 84%.

So, in conclusion ladies and gentlemen, stenting of focal stenosis of internal pudendal artery is safe, feasible and leads to a sustained improvement of male erectile dysfunction in about 75% of carefully selected cases. However, many cases are still ineligible for this treatment

as they have multifactorial etioligies for Erectile Dysfunction. Some of them may have good post procedure erections but may suffer from premature ejaculation which is a different disease entity in itself. Larger studies are required

to be able to accept this form of treatment as the standard treatment for male Erectile Dysfunction because of Pudendal Artery Stenosis. Thank you.

- [Dr. N N Khanna] Good morning everybody. Today I'm going to be speaking about endovascular treatment of erectile dysfunction, when is it indicated and justified, and I'll be discussing about the techniques and results of Pudendal Artery Stenting in this regard. These are my disclosures.

Erectile dysfunction is the recurrent inability to achieve and maintain an erection satisfactory for sexual intercourse. It's an important and growing health issue both in India and United States. It's estimated that in the United States alone,

50% of the men between the age of 40 to 70 years have varying degrees of erectile dysfunction. And also what's very important is that the erectile dysfunction actually predates coronary artery disease by five years. There are many causes of erectile dysfunction, of which,

80% of cases would be attributable to vasculogenic causes. And after vasculogenic causes arterial inflow problem is even able to endovascular treatment. While you are attempting to do internal pudendal artery stenting,

we should be very familiar with the anatomy and the anatomical variations in the internal pudendal artery. Usually it's the longest branch of the anterior division of internal iliac artery. Arteriography is a third line study

reserved for the evaluation of complex ED after a good clinical and psychological evaluation and a good Penile Doppler Study performed after Intracavernosal Injection of papaverine or papaverine and phentolamine, in which the peaks systolic penile velocity

fails to rise above 25 centimeters per second. This is one of our first patients who had a Complex Erectile Dysfunction because of bilateral, high-grade internal pudendal artery stenosis and a 90% lesion in LAD which was stented

with a drug eluting stent and then both internal pudendal arteries were subjected to internal pudendal artery stenting. We went contralateral, employed mother and child technique, passed in the 0-4 with spercondiview guide wire across the lesion,

and then predilated with a two millimeter, noncompliant balloon, and stented with a 2.5 millimeter Endeavor Resolute Medtronic Stent. This is the final result which we achieved, and then we did a simpler procedure

on the contralateral side. We have done about 50 patients up til now, but we are reporting a series of 32 patients where we have a follow up of about one year. 11 patients had the balloon angioplasty done by a simple balloon or by a drug eluting balloon.

21 patients had drug eluting stents. We followed our patients in three headings. The first one was safety of the procedure where we found it was very safe as there was no death, perennial or penile gangrene, and we had person technical success.

The other heading was the clinical improvement in erectile function. We followed the IIEF-6 scoring system. We found that there was an incremental improvement over three to 12 months of follow up in terms of erectile function

and this correlated very well with increase in peak penile velocity. This has correlated very well with the results of 25 patients published in the Zen Trial, and at one year the improvement here was 84%.

So, in conclusion ladies and gentlemen, stenting of focal stenosis of internal pudendal artery is safe, feasible and leads to a sustained improvement of male erectile dysfunction in about 75% of carefully selected cases. However, many cases are still ineligible for this treatment

as they have multifactorial etioligies for Erectile Dysfunction. Some of them may have good post procedure erections but may suffer from premature ejaculation which is a different disease entity in itself. Larger studies are required

to be able to accept this form of treatment as the standard treatment for male Erectile Dysfunction because of Pudendal Artery Stenosis. Thank you.

- [David] I thank our meeting organizers for the invitation. I'm going to be talking about in-stent stenosis after venous stenting, a guide for clinical decisions. We use aspirin in all our patients, so we really don't have a mechanism for teasing out the role of platelets in this. My disclosures are here, the histology slides are courtesy

of Dr. David Gordon, who's a cardiovascular pathologist at Michigan. So the evolution of in-stent stenosis proceeds from a fresh procedural thrombus, of course, then organizing a clot, which represents ingrowth of myofibroblasts, old thrombus,

by which Dr. Gordon means compressed fibrin, which is largely acellular, and by experience I know this can persist in stents for months. Organized thrombus, sometimes called mature thrombus, myointimal proliferation, intimal hyperplasia, lots of words for this depending on your local vocabulary.

Organizing thrombus from a wall of a six month old venous stent obviously raises questions about adequate anticoagulation. At Michigan, our venous stent management consists of discharge from the hospital after recanalization stenting on Lovenox twice a day,

Plavis for two months, and then aspirin. Clinic visit in two weeks, whereupon they're transitioned to Coumadin, preferably, because of the availability of an efficacy test, the INR, and they get transjugular venography at six, twelve, and 24 months, and any in-stent stenosis that we see, we biopsy.

How can a biopsy help management? I give an example of this patient who was referred for recanalization two years after an episode of DVT, he underwent recanalization and then four months later had repeat angioplasty and stent extension. He then had a venogram eight months after that,

after the stent extension, and two months, again, after stopping anticoagulation. Here he is after stopping anticoagulation in July 2014. You can see his venogram showing very thick in-stent stenosis here, D-dimer was elevated, INR was reflected being off heparin,

the biopsy was read as early organizing thrombus. That was at eight months. And then four months later, after Coumadin was resumed, you can see the venogram now shows some resorption of that thrombus, either lysis or organization, or something, but in any case, decreased stenosis,

so that biopsy was the cause of our resuming the Coumadin and of course, the shrinkage of the stenosis. This is a nurse with IVC agenesis and underwent iliocaval stenting. Stents replaced in February 2016, biopsied a little over a year later, you can see in-stent stenosis here.

Here are the biopsy specimens. You can see this whitish material with flecks of red. Diffuse intimal thickening was the reading on one of them, and you can see these spindle cells and there's very full collagen, very cellular material. Organizing thrombus shows right here,

with still a mixture of fibrin and some collagen, and here's some compressed fibrin there. This is the same patient with the other leg, and you can see this is much redder than that material and of course the biopsy reflects that as well. Organizing thrombus as well as some fresh thrombus.

Here's a sample of old thrombus being compressed fibrin. In summary, that patient had every stage of thrombus from her two iliac stents. This is a dialysis conduit upper arm, or this is in a patient who has a dialysis conduit, has this SVC innominate subclavian stenting,

and you can see here in the blowup that the stent has been sequentially extended further and further peripheral because of stenoses that were refractory to angioplasty. A biopsy of this stenosis again shows largely whitish material, pearly white material like that with little flecks

of red, and the reading of that was transition here, where the flecks of red representing organizing thrombus transitioning into this diffuse intimal thickening. This case emphasizes that a biopsy is a sampling exercise, and its findings depend on getting the right tissue in the right orientation on the slide.

Many unknowns in the biopsy, for example, how long does it take, when do you expect fresh thrombus to be completely organized, does organization reflect anticoagulation, does organizing thrombus mean you're anticoagulation is inadequate or is there turnover of stable thrombus within the stent?

We don't know that. I'm beginning several months ago, I started working with Dr. Gordon who was involved in some of the pathology of coronary artery stents. We're now classifying our biopsies in terms of percent fresh, organizing, old,

and organized thrombus, hoping to correlate them with long-term stent patency. This is just an example, these are points in six patients. These three patient with old thrombus retrieved from the stent, three of them had zero organizing thrombus, and several of them had very large amount

of organizing thrombus, it's easy to say this patient's an outlier, but in terms of getting to finer discriminations in the setting of, should we resume anticoagulation in a specific patient, we need of course a much larger group. In conclusion, biopsy of in-stent stenosis is inadequately

understood, it varies among patients. In-stent stenosis due to early organizing thrombus can diminish after anticoagulation. Staining suggests that stenosis begins with early clot deposition followed by gradual organization. And as I said, we're now classifying biopsies

in hopes that we can make some inference based on the thrombus distribution to long-term stent patency and the need for anticoagulation. Thank you.

- [Dr. Verhagen] Good afternoon everyone, these are my disclosures. So, obviously proximal aneurysm neck still is the Achilles heel of EVAR. Essential for proper fixation and sealing and still the most frequently constraint for EVAR. And there's been many research reports

telling us that hostile proximal neck anatomy challenges a durable seal over time. The question that remains however is: When can standard EVAR be safely and durably performed in patients with hostile necks? And there's actually very few multi-center studies

reported results with sufficient patients numbers on outcomes on hostile neck anatomies. So, we took the ENGAGE Registry probably well known to most of you. It's a very large, multi-center, multi-country registry on the Endurant endograft.

And the objective of the study was to evaluate the midterm results in patients having challenging proximal neck anatomy treated with the Endurant. We took three subgroups, one was a conical neck defined as more than 20% difference

in diameter over the course of the neck. The angulated necks meaning over or under 60 degrees of angulation and the necks with either calcified or thrombotic material in it for more than 20% of the circumference.

And the hypothesis was that the Endurant performs as well in patients with moderately challenging necks as it does in patients with standard necks. So, if you look at the initial implant you can see that the deliveries and deployment success was the same in the three groups.

So, the group, this is the conical group and here's the angulation group and the calcified and thrombotic group. No differences there. Although, this is a .04 significance number meaning that it may be significantly worse in those patients

but if you actually look at the details of the patient it means that five out of seven patients that have problems that was due to calcium in the iliac arteries in the access arteries and on the neck. So, results in four years, migration,

main body migration no difference between the three groups. Type one a endoleak no difference between the three groups and a secondary procedure to correct type one endoleaks. No difference in those groups either. Conversion, basically one of the ultimate failures,

again, no difference in the groups. But if you look at the ultimate failure a rupture there seems to be a little bit more in the ones with calcium and thrombus. But again, it's about four patients only and two of those four actually had

type three endoleaks as a cause of their rupture and had nothing to do with the neck. So, basically it performs as well in standard anatomy as moderately challenging anatomy. So, we thought maybe there's more and more interesting stuff if we

compare on- versus off-label use again using the ENGAGE Registry. So, considering that implanting endografts outside IFU's actually not uncommon at all in everyone's practice it seems to be important to know how these patients actually do.

So, again a on- versus off-label analysis using the ENGAGE Registry. This is a outlook on what kind of patients are actually included in the ENGAGE Registry. And there's 17% of them outside instructions for use, that's over 200 patients.

And 80% of these patients are outside instructions for use because of a proximal neck issue. So, that's about 180 patients. That's quite a big group to study. Again, initial implant no difference between on-label and off-label as expected.

Then at four years migration no difference. Rupture no difference. Conversion and open surgery no difference. It looks as if it's okay to do so but it isn't. Because if you look at type one a endoleaks for the whole group there's a freedom from

type one a endoleaks off-, 96% in four years. But if you break that down in on- versus off-label you see a big difference. There's actually three times as many patients run into trouble if you use outside instructions for use.

And, obviously, if you look at the whole group there's the same amount of secondary procedures. But if you look at type one a endoleak re-interventions only again there's twice as many re-interventions for that cause and that's also significant.

So, in conclusion challenging proximal neck characteristics have historically impacted long-term durability of EVAR. There's only a few studies of significant sample size that can analyze reliably the performance of contemporary endografts in real-world patients. Insights from this ENGAGE Registry demonstrates

that durable performance of Endurant in standard as well as moderately hostile anatomies through four years is actually quite good. But off-label use shows more type one endoleaks and more secondary interventions to correct them and should, again, be strongly discouraged.

Thank you so much.

- This is my talk today, but we don't actually have the access to these new endografts. So I will only talk about the anatomical feasibility in my presentation today. These are my disclosures, my friends. And entry tear closure with the TEVAR

has been successful, and TEVAR for type B aortic dissection has been the first in treatment, especially for cases with proper fusion. But when you look at the TEVAR for type A aortic dissection, there are having only few cases reported in the literature.

This is because there are many problems to be solved for TEVAR to be feasible for type A aortic dissection. Biggest problem is that the dissection is present near the STJ, so there is no healthy proximal landing zone, and the sizing of stent graft is sometimes difficult.

And also, sometimes the location of entry is unclear. And also, if we use conventional endograft, most of the time we need to reconstruct the aortic branches. And also, most of all, any complication may fatal in this area.

So I focus on next generation endografts these branched endografts for arch aneurysm, because these arch endografts, branch endografts can reconstruct the innominate artery and also, at the same time, make a closed entity. So, this is my grave question.

How will these next generation endografts accommodate type A aortic dissection? So this is what we did. We reviewed 172 type A aortic dissection patients and we excluded 41 patients for inadequate preoperative CT scans

or location of entity unclear, even using the operating record. So this left us with 131 type A aortic dissection patients. 63% male, median age 63 and mean height 162 centimeter, indicating small body size of Japanese patients. And we use the centerline flow technique

created by Vincent Workstation and we always used this for our measurements. And this is our anatomical results. So, we had dissection at STJ in 81% of patient and more than 60% of patient had the entity at the ascending aorta or the STJ.

This slide shows the length, and mean length between the STJ and the innominate artery was 8.2 centimeter, which is quite small. When we defined the proximal landing zone as 2 centimeter distal to the STJ,

mean diameter of the proximal landing zone was 4.4 centimeter, so it has quite an enlargement. So when we used these measurements for the feasibility study, this is the IFU proposed by the Cook for the Zenith A branch.

This is for the arch aneurysm. When we apply this IFU to the measurements this is where we are at. Only 6.9% of patients fit the IFU, and the biggest limitation was the aortic diameter, with 24-38 millimeter

at the landing zone. Only 24% of patients fit the IFU. On the other hand, this is the IFU provided by Gore for TAG TBE, and we applied this IFUs, 46% of patients fit the IFU. Biggest difference, of course,

was the Gore TAG TBE was able to fit up to 48 millimeter in diameter. So this is my first summary. It seems that larger devices are not being more feasible for the treatment of type A aortic dissection,

but we all know that this is not the answer. Placing the larger endograft into the type A aortic dissection has the risk of stent graft in this new entry. This report by Dr. Pantaleo stated that the area oversizing ratio of more than 3.5

is a significant risk factor for stent graft in this new entry. In the patient cohort, more than 12% of patient had the area oversizing ratio of more than 3.5. Also, detection of entry tears is a big problem. Even with good quality CT scan

analyzed with latest three dimensional workstation, we could not detect 61 entry tears. And also size and location is a problem. So this is my final slide and take home message. For TEVAR to be feasible for type A aortic dissection, we need new design stent graft that can

accommodate these characteristics: dilated ascending aorta, collapsed true lumen, and small aortic radius. We also need proper sizing method, to place the endograft safely in the descending aorta. And we also need a better way to detect entry tear.

Thank you.

- Thank you for the opportunity to give this presentation. It is the last presentation of the session. So, I hope I'm not regurgitating everything that was said prior to this. As we know, the Indego system. There's my disclosures.

As we know, the Idego system has been available now for many years. Why we use percutaneous embolectomy and how it allows us to remove thrombi and emboli in one setting. Also, to treat the underlying stenosis given

if there is a SFA arterial lesion that requires ballooning, angioplasty or, some other therapy. Additionally, given the fact that it can be used in a single setting, it certainly does have the ability to reduce cost for the hospital system.

Which is obviously of importance these days. Easier access to the below-the-knee vessels. Additionally, reduce the use of lytics which has it's own set of complications. Additionally, if this does fail. We still have the ability to perform

open thrombectomy embolectomy if needed. The Indigo system that's previously been stated, comes in a very number of different catheter sizes. These sizes allow you to treat the entire Arterial tree. From the petiole arch all the way up to the iliac vessels.

My recommendation is to always use the largest catheter possible for that particular vessel. Here's a nice video showing the CAT 3 system, traversing the entire petiole arch with great ease. These catheters are highly designed but they are somewhat fragile.

So, it's important to be careful with the tip. My technique for acute lymphocythemia is very similar to what we've previously heard. Essentially we advance the sheath all the way up to the level of clot. On some occasions, we actually do traverse

the clot given the scenario. We do infuse TPA in a pulse spray manner. Either, with an infusion catheter or with a jet stream catheter depending on the scenario. We advance the largest caliber sheath into the system

or into the clot itself and using an extract technique which has been previously demonstrated. Adjunctive techniques which often utilize include, ballooning angioplasty, Fogartys and potentially even stints. Here's a reiteration of the extract technique

again the catheters advance up to the level of the thrombus itself. The system is engaged for roughly 90 seconds and again the clot is corked until it can be fully removed through the sheath system. This is an example of a very nice piece

of cloth that was removed from the SFA. In a cork technique fashion. So starting from the Iliac system we'll work our way down. Here's a patient with a subacute thrombus, an embalis in the left iliac distribution. We used a ipsilateral retrograde crossing technique

to reestablish flow. The CAT 8 system was then used to engage the thrombus within the iliac artery. It was removed in whole and on completion angiography there was a residual stenosis which, did require stinting.

Here's an example of a cronic or subacute SFA lesion. Again, we advance the catheter up to the level of clot, engaged it and we were able to remove the thrombus in whole through the sheath system. Finally, the next case include a popliteal artery thrombus and a post knee surgery patient.

Again, this is an acute thrombus, which is actually very nice 'cuz it's very soft. We advance to CAT 6 catheter up to the level of the thrombus itself and removed it in whole. Afib Occlusions, obviously these patients are often times quite sick.

Not great candidates to go to the operating room. Percutaneous technique is often very favorable for their overall outcome and here we see popliteal and distal tibial perineal trunk disease and thrombus. We were able to remove this in whole and reestablish three vessel runoff to the patient.

Here's an example of a patient who's post-atherectomy within the SFA with a significant plaque burden. We often see embolic debris of this nature using the CAT 6 system, we were able to remove that thrombus from the tibial-peroneal trunk. So, when is open surgery necessary or the best option?

When the clock burden is extensive, when it's multilevel, when percutaneous techniques are going to be inadequate. Obviously, when there's dense ischemia with motor and neuro muscular compromise. Additionally, a compartment syndrome

would probably not be a great candidate for a percutaneous thrombectomy and additionally when the chronic or the clot appears to be chronic it is less responsive to cutaneous techniques. Thank you.

- This morning I'm going to give you an update on the Global Vascular Guideline, which has been supported by the global societies, the SVS, the European Society, and the World Federation of Vascular Surgery, to promote evidence-based care in the treatment of patients

with limb threatening conditions. I have no disclosures for this talk. So in the development of a plan for evidence-based practice in CLI, we describe structured decision-making as putting the patient first,

then staging the limb, and then finally staging the anatomy, and that's the basis for, the foundation for the guideline document. This morning we're going to focus on a new anatomic staging system and its rationale

for the treatment of CLTI. The current schemes that we have for staging anatomy in the treatment of CLTI are inadequate because they're generally single lesion based, or they look at the overall burden of disease, which is really not useful for the clinician

in planning the revascularization in these patients who usually have multi-segment disease. Restoration of in-line flow to the foot is the primary technical goal of revascularization in these patients, especially those with tissue loss. And so we need an integrated groin to ankle system

that allows us to make evidence-based decisions for how to revascularize these patients. It's also clear that a system can't fully encompass both endovascular and open bypass surgery because the factors that determine success are intrinsically different,

such as the type of conduit employed. So the Global Limb Anatomic Staging System employs a few basic assumptions. The focus of this system is on infrainguinal disease, which is defined as from the SFA origin to the foot. And a key principle or concept here

is the Target Artery Path, wherein the clinician decides the primary infra-popliteal target that they're selecting to revascularize the foot. The femoro-popliteal and infra-popliteal segments are separately graded on a zero to four scale,

and then they're combined into three overall stages for the limb using a consensus-based matrix, which I'll show you. Pedal disease is graded in this system, but is used as a modifier only. Calcification is graded as severe,

severe enough to impede endovascular treatment or not. It's a simplified approach. We'll go through a few examples. Some of the key points here, again, restoration of in-line flow is viewed as the primary target.

Target artery path is the route continuous from the groin to ankle. It usually involves the least diseased artery, but it could be angiosome-based. It's the clinician's decision. A primary factor that was used to create

the three stages is the concept of limb-based patency, which means continued patency of the entire target artery path, which would be lost if there's an occlusion or critical stenosis anywhere in the path, or if there's hemodynamic failure

such as recurrence of symptoms with a drop in the toe pressure. So the grades and stages were determined over an iterative period over the last couple of years by expert consensus supported by a comprehensive evidence review.

Three stages were created based on the following complexity of the treatment of the target artery path. Low complexity disease with expected technical failure of endovascular treatment of less than 10% and greater than 70% one year limb-based patency, intermediate complexity disease,

and high complexity disease, where expected technical failure rates might be 20% or more, and one year patency might be under 50% for the entire target artery path. So the way this works is you obtain

a high-quality angiogram from groin to foot. You define your target artery path for the case. You grade the femoro-popliteal segment. You grade the infra-popliteal segment and then you look up the overall stage for the limb on a table.

These stages have been integrated in the PLAN system into an overall preferred revascularization strategy for the patient based on patient risk, WIfI stage as well as anatomy. We don't have time to go through all the individual aspects of the stages.

This will be online very shortly, hopefully this week, actually, it'll be posted online for public comment. There is a zero to four scale for femoro-popliteal disease, and a zero to four scale for infra-popliteal disease based on the length of lesions,

the presence of stenosis or occlusion, and their location. One then looks at this grade and then this is the consensus matrix for assigning an overall limb grade based on the femoro-popliteal

and the infra-popliteal grades individually. You can summarize these as saying the stage one disease is short to intermediate length fem-pop disease and/or IP disease, but no or minimal popliteal disease. Intermediate-length disease, including popliteal stenosis

or short-intermediate length IP disease is stage two, and stage three are extensive occlusions, alone or in combination with any disease in the other segment, or a popliteal CTO. Pedal disease is described using a simplified three system, three scale system here,

but is not included in the staging as this data is limited on the relationship to overall outcomes. So here's an example of a case with limited short occlusion of the SFA and an anterior tibial target

that has two lesions in it. The FP grade would be one, the IP grade would be two, and the overall GLASS stage would be two. Here's another example of more extensive fem-pop disease with actually extensive calcification in this segment,

and a peroneal disease. The FP grade is four, the IP grade is two, and the overall GLASS stage is three. And here's a grid that shows, for example, in an average risk patient who has an adequate vein, how you might use both the GLASS stage

and the limb severity stage to determine the preferred approach for revascularization, and you can see that for very high complexity disease and very severe limb threat, open bypass may be preferred. Endovascular is preferred by most of the panel

for most of the other disease, and there's a large area of gray which really has no consensus as yet. These are the folks who were involved in the anatomy section. This was a multi-specialty group

and all of this was then vetted through the entire, roughly 60 individual writing group of the steering committee and the rest of the writing group of the GVG. Thank you.

- Thank you, Frank, for inviting me to this congress again. With always your beautiful long titles which everybody appreciates. So first of all, bypass has been for years the golden standard to treat TASC C and D lesions. And as a vascular surgeon, we're very happy with the results

we achieved after one year. But of course there was a difference in reporting primary patency in the endovascular and the surgical field. In the surgical field it was open or closed. Endovascularly, we were looking at binary restenosis. That's why we looked in our surveys after 100 bypasses

which were presumed to be open in the surgical world and we saw that still 11 of those bypasses had restenosis in the endovascular world. So based on that and the good results we had with the Zilver PTX in the long lesion arm of the sub-study which with primary patency rates of 77%,

we decided to do the Zilverpass Trial. The Zilverpass trial which is a randomized trial randomizing the Zilver PTX versus prosthetic bypass in long lesions. And we included 220 patients who were randomized in four countries

over 13 clinical centers. And I'm very happy to announce to you that we extended the trial with a follow up up to five years with Cook which is very important. We need long-term data as Gary already has mentioned.

So the inclusion criteria was every Rutherford classification two and five with a lesion length of at least 15 centimeter and of course no previous endovascular or surgical intervention in that leg. And we compared apples with apples in these studies.

So both devices were addressed with the same definition of primary patency being the absence of binary restenosis. So looking at the demographics there is a slightly more CLI patients in the bypass group but for the rest it was quite similar.

We also saw more patients with hypertension, obesity, and hypercholesterolemia in the bypass group but when we looked at the lesions, we saw very complex lesions in both arms with 95% occlusions and a mean lesion length of 25 centimeter. So basically,

so the first difference we saw in both arms was looking at procedure characteristics was that not only the hospital stay was longer in the bypass arm, 2.5 versus eight days. But also the time of doing the procedure was shorter

in the endovascular arm. More importantly, if we looked at the 30 day freedom of complication rate, this is with the significance P value of .004, we saw that the Zilver PTX had far less complications than the bypass group.

Looking at 12-month primary patency of 180 out of the 220 patients, and I'm very happy to announce to you that we will present the full data set for the first time at the LINC Congress in Leipzig in January. We see that there is a slightly benefit

of the Zilver PTX over the bypass. And of course you can say, okay, but there were more CLI patients in the bypass group. That's why we did the sub-analysis looking at claudicants versus CLI and indeed you see that especially in claudicants

the benefit of the Zilver PTX is a little bit higher but also in CLI patients the results are equal. Freedom from TLR also here sustained benefit of the Zilver PTX over bypass and also at in 12 month secondary patency no difference between both arms.

And now we start looking now at two years results because that's what we really want to see as a vascular surgeon, long-term data. And also here you'll see sustained benefit with almost 70% primary patency for the Zilver PTX at two years in those challenging long lesions.

Freedom from TLR 80% for the Zilver PTX versus 70% for the bypass arm. This is real clinical data, daily practice. Secondary patency again almost the same. Is there something comparable, has been something comparable published yet?

Yes, Michel Reijnen has published the SuperB Trial comparing the Viabahn versus femoropopliteal bypass and he came basically to the same conclusions. First of all admission days shorter for the endovascular procedure, with a significantly less mobility

and complication rate at 30 days. And then if we looked at TVR and TLR comparing both studies also here in the Viabahn study, an advantage of the Viabahn versus the bypass group. So in conclusion we can say that Zilver PTX

obtained outstanding primary patency rates. And we're going to follow them up for the next five years. That the patency rate analysis was, they're both the same in both arms looking at absence of binary stenosis and that those preliminary results

show at least non-inferiority of the Zilver PTX versus prosthetic bypass with similar patency rates, less complication rates, and a shorter hospital stay. Thank you for your attention.

- [Lecturer] Well, thank you. As you can tell, I have a terrible cold. So, I've incorporated two people to help me with this talk today. One will be David Letterman who used to be a famous TV late night host. And, I've also asked Billy Joel.

He's a famous singer, to help me with this talk, if my talk should go away. (audience laughing) So, I have no disclosures other than the fact that I have this cold. So really, can I really argue against this premise?

It would seem quite self evident that this approach would lead to elimination of all technical defects, and result in an almost negligible incidence of postoperative stroke. And I must say, I did hear from Hans, that a lot of what he's been doing is

with the E Version technique and I think, if I did the E version technique, I may want to do one of these postoperative procedures. But, in our practice, we do standard endarterectomy, and we feel that this is not necessary. So Hans, I think that all that you really showed me

is that what you want to do, is just do the procedure. And then, you want to do it again. So, here is David Letterman helping me with the top 10 reasons why, I think that it's wrong. - [David] Coming, here tonight's top ten list. Got number 10 then.

- [Lecturer] So, I think there's no guarantee that it'll correct the problem. After re-exploration, another completion imaging will be required which will probably further add to the operative time and cost. Number nine, studies show re-exploration actually does

lead to more complications. It's only natural that you've re-operating on the carotid, you have the potential to cause more trouble. And, some postoperative events, are not related to technical error at all. For example, we've just heard about Hyperperfusion syndrome

and platelet thrombi, can occur not only, in the immediate postoperative period, but the following day. And, a completion arteriogram is not going to show this. Furthermore, I think we're unsure of which findings require correction.

Many of us know, when you go in to do these procedures, you see all sorts of things. And the question is, should you go chasing them and adding to the duration of the operation, for an unneccessary chase for a lesion that would never ever have caused a problem?

And then of course, accessing the degree of stenosis is a problem. So, if you re-explore because you see a residual stenosis, should you re-explore for a 50% stenosis? Should it be a stenosis in the external carotid artery? And, can you really be sure about a diameter reduction,

if all you're doing is a straight AP x-ray, where you're not doing two multiple projections? Most reported defects are actually in the external carotid artery. Got nothing to do with the internal carotid artery. And, we actually looked at postoperative

external carotid occlusions and we found that they were extremely unusual in our practice. Only 24 out of almost 2,000 cases, 1.2%. In fact, Enrico Ascher over here, has presented similar data showing that the external carotid lesions are really not that important.

And, in no patient could we involve these external carotid lesions in early or late neurological events. So, chasing the external carotid is a waste of time. Patients will undergo, as we say, unnecessary re-exploration and this is going to expose them

to increased risk. And on top of it, we now have preoperative duplex to prevent technical errors. So, we can evaluate the common carotid artery to make sure we don't clamp it by mistake and put a clamp through a big area of plaque that can could ultimately disrupt.

And so, we no longer have to worry about unrecognized proximal injuries. And again, Enrico Ascher has demonstrated that residual common carotid lesions did not result in postoperative strokes. So why go chasing a lesion in the common carotid

with your arteriogram? And, I really believe that meticulous surgery prevents technical errors. I think, in competent hands, neurological complication rates in carotid endarterectomy by modern vascular surgeons, is so low, that it's unlikely that adding completion imaging

can achieve clinically relevant improvement in outcome. Most of us are getting excellent results with stroke rates of under 1%. I just think, it's just not necessary. As I've said, most surgeons do not utilize completion imaging yet, they report complication rates

easily as good, if not better than those reported by surgeons who routinely do imaging. So, as I've said, our stroke rate in our almost 2,000 endarterectomies are done standard endarterectomies, not E version, have a stroke rate of 0.8%. Are we really going to be able to reduce the stroke rate

by doing a whole lot of unnecessary diagnostic arteriograms? So as I've said, I've asked Dr, Mr. Billy Joel, the famous singer, to help me make the final statement. And, here it goes. [Music] Get it right the first time

That's the main thing Oh, Oh I can't afford to let it pass Get it right the next time That's not the same thing Oh, oh

Going to make the first time last - [Lecturer] I couldn't say it any better. Thank you.

- [Michael] Thank you Joe, thank you, Dr. Veith and the committee, again, for the opportunity to be here. I was preparing to debate the former president of the SVS, and a distinguished scientist, which is daunting enough, however, given the topic, this really is a slow-pitched softball for me, I would say.

So let's get to the meat of it. This is the paper that was just presented. You heard the data that they showed. Here's another paper from the NSQIP database, equally as big, that came to the opposite conclusion, and here is yet a third paper,

all within the last two years, looking at a meta-analysis suggesting that open and endo are basically the same. So what do you make out of all this stuff? Depends what you feel like reading, and you got to dig into the data.

So here's the bottom line thing I want you to remember, that large registry-based comparative studies often lead to incorrect conclusions, and I'll tell you why. First and foremost, selection bias. Statistical adjustments, including

this propensity score measurement shown here, can only attempt to balance measured variables. But there are many key factors that were unmeasured, including things that we normally use to select procedures, such as the severity of the anatomy, the severity of

the limb threat or tissue loss, and previous treatments that had been done. And then there's the common problem of incomplete data, were there previous vascular procedures done on the treated leg? Lack of long-term follow-up, and actually,

these are all admissions, but are they really unique patients, unique limbs, and is it the same leg that we're talking about? The bottom line is that these large registries give us a very large and it gives you a very low P value, and that doesn't always

equal good science, I'm sorry to say. So how do we normally pick, we normally pick by assessing patient risk, and in that case, you might just be able to compare things like postoperative events, but typically we pick our revascularization strategy

based on looking at the leg and how much tissue loss there is, how severely it's threatened, and of course, the anatomic pattern of disease. Patients who have anatomy that's good for endo versus patients who don't, and whether or not they have a good-quality vein.

Unfortunately, none of that data is available in the study. So the severity of limb threat and the anatomy are just not available in claims data, NSQIP, or actually, in VQI. So every time you see these registries trying to compare the outcomes between these two approaches, take it with a grain of salt.

And I'll give you an example. Would you actually compare PCI versus CABG without knowing anything about the coronary anatomy or the left ventricular function? Absolutely ridiculous, so, but here we are today. Patients getting open bypass surgery

in the endovascular era have greater anatomic complexity, more advanced tissue loss, and a growing proportion of them are getting their operation after a previous failed intervention. None of that data's in this paper. Here's the data about WIfI, which basically

just shows that, based on the severity of limb threat or the degree of tissue loss, we know that has a major effect on outcomes. So all of these series have been involving patients who got different types of revascularization, but yet the amputation rates vary quite significantly

depending on what kind of limb you're starting with. So if you're talking about minor tissue loss versus two toes with gangrene, it's a very different story. We already heard about the BASIL trial, but we also know that the BASIL trial taught us, and others have confirmed, that if you don't get

the right procedure first, you're paying a penalty. Patients who got their bypass after a failed endovascular treatment simply did not do well on the BASIL trial. Almost as bad as if they got a prosthetic graft. And this has been mirrored in other studies.

This is from the VSGNE, showing that if you had a bypass after a previous failed intervention or previous failed bypass, you did equally poorly. So a previous failed, a secondary bypass operation, regardless of the first intervention, is simply not as good, whether it's the patient

or whether it's something that happened from the procedure, we don't know. But we do know that this is happening more and more. And, in fact, when we last looked in 2011, about 40% of bypass operations were the second or third procedure in that leg.

My friends, this is the new vascular epidemic. It's restenosis, and we're currently operating more and more in legs that have seen previous treatment. That may be okay, but we need to know that those patients do not do as well as a first-time bypass. And this is what this data has shown us,

is that if we adjust for all these other confounders, when we compare a first-time bypass to a secondary bypass after failed endo, that the patients just don't do as well in regard to reamputation, reintervention, or MALE-free survival. And this is what we're going to end up with if we only

do bypass after endovascular treatments have failed. So, in conclusion, fortunately, we do have some level-one evidence coming. We have the BEST-CLI trial, we have the UK BASIL 2 and BASIL 3 trials. There is no way to mimic randomization,

because randomization controls for the variables we know and also the ones that we don't, and make sure that they're balanced. And trying to do pseudo-randomization based on registry data is fraught with inaccuracies. So currently, based on the current evidence,

this is how I practice, if patients have low surgical risk, severe anatomy, and a good vein, they're likely to get a bypass, about a 30 to 40% of those patients, and in other cases, endovascular is favored, and I think that's currently

the state of the art, thank you.

- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro

or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire

because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,

or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,

very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D

in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--

radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about

to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.

So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where

the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist

to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here

to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric

reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I

mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic

close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to

understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.

Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use

Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.

We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.

You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.

Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial

phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,

the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,

very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone

and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.

In other words can offer higher value in patient care. Thank you.

- [Enrique] Thank you Dr. No disclosures. So the basis for my opinion on this is three decades of treating thoracic outlet syndrome surgically and my collection of my personal cases on Venous TOS done during the last 12 years

in the the state of Michigan. The anatomic basis for Thoracic Outlet Syndrome is that of chronic subclavian vein injury produced by repetitive dynamic compression at the costoclavicular space. So you can see on the right side with the arm abduction.

You can see that the vein is compressed severely between the first rib subclavius muscle and the clavicle. So my treatment algorithm is that when I suspect the Axillo-subclavian vein thrombosis, confirm by duplex, immediate anti-coagulation with Heparin,

Expeditious venogram with thombolysis, maximum 3 or 4 weeks perhaps. If the vein becomes patent and is recognizable I proceed immediately with surgery and percutaneous balloon angioplasty. After decompression, if I fail to recolonize and open the vein I just use anticoagulation.

So the treatment consists of systemic antigcoagulation, restoration of the venous lumen, with catheter directed thrombolysis. I've been using the Angiojet for the last decade and infusion catheters as needed. Never had chronic or any renal failure in my experience.

And, this is important, lysis these veins several veins, not just the brachial vein. You have to access all the veins that are involved with thrombus. The brachial, the basillic and the cephalic, you have to put several sheaths, not just one, that's a common mistake.

Then you remove the extrinsic compression typically by a first rib resection or the bone anomaly and then you do a venous angioplasty and I never put a stent. I do the thoracic decompression with two incisions. One above the color bone and

one in the parasternal aspect of the infraclavicular space and following that, as you can see on the right hand side, I still have the sponges in the wound with the wound open and through the sheaths in the arm I proceed to do a completion venogram

and I post dilate the vein to accomplish the maximal delectation of the vein after the decompression. Now, why two incisions? Well this is a patient I saw years ago, where you can see he underwent trans-axillary resection of the first rib

and returned with unresolved vinous occlusion . You can see on the CT scan on the right that is a fragment of the first rib, which was resected through a trans-axillary approach that is still remaining and continued to squeeze the subclavian vein against the clavicle.

So that's why I do two incisions, one above and one below the clavicle. Now over 12 years treated 72 patients. Mostly with single stage. 68% of the patients with a single admission treatment and the pathology was vein thrombosis in almost all of them.

Just vein Stenosis in 4 of them. About 18% had documented hypercoagulable state and only 8 had a pulmonary embolization documented on admission. I did a diagnostic Venography in all of them. Thrombolysis pre-operatively was done in 75% of the cases, About 1.5 trips to the endo suite

per patient, all of them underwent rib resection and PTA and I anti-coagulate everybody for 6 months unless they're hypercoagulable when I do it for life. The anatomical results of these cases were 60% of the veins were widely patent, but 1/3

had partially occluding thrombus. Only 4 remain occluded and the clinical results are about 2/3 the symptoms were completely resolved and about 1/3 felt improved. If you look at the patients who had widely patent vein. Those had less days of delay to Lysis.

They had a much less time from diagnosis to decompression. And the incidence of post drug treatment at thrombosis was much lower. Less trips to the endo suite and lower hospital stay. If you look at patients here with a single admission the symptom resolution was higher during

single admission treatment, the venous patency was better, and the cost was about $8,000 less. The typical causes of treatment failure are late diagnosis, late initiation of treatment, incomplete thrombosis with lysis, PTA and Stenting without the compression of the

thoracic outlet, inadequate rib resection, and inadequate anticoagulation. Therefore I conclude the delay in lytic treatment and surgical decompression appears to be associated with lower venous patency rates. The treatment of VTOS during a single admission

has higher rates of arm symptom resolution, less hospitalization and significant cost savings. Referral to centers where single stage treatment is feasible, may improve the results and reduce the cost of treatment in these patients. Thank you

- [Mr. Donati] Thank you, dear colleagues, and dear professor Veith, thank you very much for the invite, and for the opportunity of being here today. I have no disclosures. So, the interest for expedite treatment for symptomatic carotid patients

has been sparked by studies published almost 10 years ago, based on data collected 20 and 30 years ago. And, the reality is that there is a lack of recent high-quality literature to support our current practice. What do we really know about symptomatic carotid stenosis,

and timing of surgery? What we think we know, is that every patient, who is who is diagnosed with a moderate to severe carotid stenosis, and presents with a minor stroke or a TIA, should have a symptomatic carotid plaque.

Then we are told that patients have a high risk of recurrent neurological events the first few hours and days after surgery, and that justifies expedited treatment. We also still believe that patients that undergo any treatment

that can provide a perioperative risk below 6% receive a treatment which is beneficial for them, and of course, we all know that patients should be on something called Best Medical Therapy. But what we think we know, but probably don't know that well,

is that if we look into the literature for minor strokes and TIAs, well, approximately 60% of the patients, probably more, do not have any carotid stenosis at all. Then, if we look at patients with carotid stenosis, a sub (mumbles) analysis from the next trial

looking at patients with any symptomatic stenosis that develop symptoms during follow-up, and they were all some Best Medical Therapy, they actually developed cardioembolic lacunar strokes. There is then an entity which is not well-defined, which is the entity of cryptogenic strokes,

and intracranial carotid stenosis. Intracranial carotid stenoses are considered a leading cause of distal emboli, and they have been reported to be present in as many as 80% of patients with extracranial carotid disease.

Cryptogenic strokes, those unidentified flying objects, although by definition excluded the presence of a carotid stenosis, well, this population of patients have an average age of 65 years, and they share the same risk factors

of patients with carotid stenosis, and it would be naive to think that a carotid stenosis is protective against cryptogenic strokes. So, being generous, I think that approximately a third of patients who presents with a minor strokes or a TIA,

and are diagnosed with a moderate-to-severe carotid stenosis, have a symptomatic carotid plaque at presentation. And although this might only look a game of numbers, I think that it's telling us a big truth, and the truth is that we know very little

about which plaque is symptomatic, and which is not. And these has significant implications. The first one is that a large proportion of patients undergoing urgent carotid endarterectomy and carotid artery stenting are likely to be treated for the wrong condition.

The second implication is that, different subgroup of patients might actually benefit from different Best Medical Therapy. When we have to make a decision about urgent treatment for one of our patient, we also need to keep in mind

that recent improvements in drug therapy has reduced, significantly, the risk of surgery, but also the risk of recurrent neurological events, and that 6% is probably not acceptable any more. What we need to understand is,

which plaque is symptomatic, and which is not. And hopefully, imaging, functional studies, and biomarkers will come to our rescue, and the day we will understand which plaque is symptomatic and which is not, that day, we will probably know also

which plaque we have to operate before it becomes symptomatic. We also need to understand what Best Medical Therapy is for our patients. We now have available different combination of drugs, we have new antiplatelets, new anticoagulants,

and then there is the question of, which is not well understood, of drug resistance in this population of patients. A number of studies are looking, or have been looking into different combination of drugs in patients with minor strokes and TIA

of non-cardioembolic origin, and there will be lessons to learn from each one of them. What we need to know and remember in our everyday practice, is that initiation of Best Medical Therapy as soon as possible is the single most important measure

to reduce the risk of recurrent neurological events, not surgery. That Best Medical Therapy, according to the available literature, should probably include statins and dual antiplatelet therapy.

That it is safe to treat patients in the first two weeks, but risks compared to the current results of Best Medical Therapy are probably too high in the first 48 hours. And we also need to know that contemporary complication rates

for carotid endarterectomy in symptomatic patients are around 3%, below 2% for TIAs. And this is the new benchmark for Best Medical Therapy: carotid artery stenting and urgent carotid endarterectomy. To conclude, dear colleagues, my recommendations are: do not rush intervention.

You might be treating the wrong condition, and you might offer your patient risks which are too high. Do not wait, they need Best Medical Therapy as soon as possible, and they need to be thoroughly investigated for diverse source of emboli,

and stay tuned, because it has to, and it will certainly change. Thank you very much for your kind attention. (audience claps)

- Mister Chairman, ladies and gentlemen it's a pleasure to be here. I have no disclosure. Although Eagle syndrome is a well known condition to ENT and maxfax surgeons, vascular surgeons are less familiar with this entity and it presents with multiple symptoms

and the symptoms are associated with an abnormal styloid process. Doctor Eagle in 1937 described two clinical presentation, the classical and the stylocarotid syndrome. Anatomically the stylohyoid complex include hyoid bone, the styloid ligament and the styloid process

and both evolves from the Reichert's cartilage of the second branchial arch. The styloid process provide anchor to important muscles, the styloglossus, the stylopharyngeal and the stylohyoid. It is a rare condition and only four to 10%

of patient became symptomatic. Anatomically usually it's bilateral but the symptoms are mainly unilateral and the main aetiological factor is trauma leading to hyperplasia and metaplasia. The classical Eagle syndrome presented

with a triad with neck pain, otalgia and foreign body sensation in the pharynx while the stylocarotid syndrome is mainly caused carotid artery dissection. In this paper it seems to be an elongated styloid process give a four times risk to develop carotid artery dissection.

Also cartoidstyloid syndrome is we now associate it with the standard TIA and stroke and the carotid stent fracture as well. CT angiogram is paramount to making the diagnosis but duplex scan and TCD are very important in the technique and multi dynamic significant stenosis due

to the compression. I was lucky enough two years ago to be referred for a third opinion. A young patient who had been experiencing for the past three years left arm weakness after keeping the neck rotated to the right

for a few minutes so while I was trying to figure out if these symptoms were genuine I went with him to the vascular lab department and scanning the patient in the neutral position showed a normal common carotid artery,

a double kinking of the internal carotid artery and normal flow in the MCA but when we asked the patient to rotate the neck to the right the patient after two minutes genuinely experienced weakness in the left arm.

You can see the dramatic decrease in the flow in the MCA so I requested a CT angiogram. You can see the massive elongated styloid process with a double kinking of the internal carotid artery. This picture is very nice, only a picture

but you can see that this is bilateral. So I decide to take him to theater and I prefer the anterior approach. You can see the internal carotid artery kinking is quite well evident. While I was dissecting the elongated styloid process

I was very aware to see where the intersection of the three mass were where and also before resecting the bone I wanted to leave one centimeter behind to not to be very close to the facial nerve. This one is the bone resected

and while double kinking I thought at the time the resected internal carotid and perform an endo anastomosis was the right thing to do. This CT angiogram shows the bone resected and the carotid straightened.

So in conclusion ladies and gentlemen, it is a very uncommon entity but vascular surgeons should be aware of this because it can cause carotid dissection which is one of the most important cause of stroke and TIA in young adult

and also we should think probably while in one case was reported, identifying this condition prior occluded artery stenting. There are no treatment guidelines so surgery should be decided on individual basis with all the symptomatic patient

and also the patient with the CT scan you see evident compression of the styloid process on the carotid artery. Anterior approach for us, as a vascular surgeon, is the most common approach rather than transoral and what I recommended as well.

Thank you very much for your attention.

Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.